Core MGMT PDF

Schedule of Lectures
Friday
8:00-9:55 Physics;; anesthesia delivery systems;; monitoring
10:05-11:45 Pharmacology — local anesthetics, inhalation agents
11:55-12:30 Pharmacology — general principles of

pharmacokinetics/dynamics;; fluid management
1:15-2:20 Cardiovascular review
2:30-3:05 CV Pharmacology – sympathomimetics, alpha and

beta blockers, antihypertensives, vasodilators
3:15-4:20 Obstetric review
4:30-5:25 Regional anesthesia and pain management
5:35-6:45 Pharmacology — intravenous induction agents,

opioids, benzodiazepines
Saturday
7:30-8:10 Respiratory review I
8:20-9:30 Respiratory review II
9:40-10:45 CNS review
10:55-12:15 Pharmacology — ANS, anticholinergics,

anticholinesterases, NMBs
1:00-2:15 Pediatric review
2:25-4:00 Hematology;; musculoskeletal review;; MH

4:10-4:45 Geriatrics;; surgical procedures
4:55-6:00 Surgical procedures cont’d;; co-morbidities
Sunday
7:45-8:50 Endocrine review
9:00-10:45 Renal/hepatic review
10:55-12:00 Pharmacology — diuretics, psychotropics,

antiemetics, H2 blockers, chemotherapeutics,
antimicrobials, herbals
12:45-1:45 Anatomy/positioning review*
1:50-3:45 Study/test taking skills and workshop, Q & A, wrap-

up
*End of CRNA lectures

**Professional/legal aspects and statistics administered as a self-study module
NCE Content Outline
I. Basic Sciences (25%)
A. Anatomy, physiology and pathophysiology
1. Cardiovascular
a. Dysrhythmias
b. lschemic heart disease/angina
c. Myocardial infarction
d. Hypertension
e. Congestive heart failure
f. Endocarditis
g. Valvular heart disease
h. Cardiomyopathy
i. Peripheral vascular disease
j. Congenital heart disease
k. Pericardial diseases
2. Respiratory
a. Bronchitis
b. COPD/emphysema
c. Asthma
d. Pneumonia
e. Tuberculosis
f. Pulmonary embolism
g. COR pulmonale
h. Pulmonary hypertension
i. Upper respiratory tract infection
j. Acidosis
k. Adult respiratory distress syndrome
l. Epiglottitis
m. Sleep apnea
3. Central nervous system
a. Seizures
b. CVA
c. Hydrocephalus
d. Parkinson’s
e. Multiple sclerosis
f. Myasthenia gravis
g. Alzheimer’s/dementia
h. Demyelinating disease
i. Intracranial hypertension
j. Intracranial tumor
k. Intracranial aneurysm
l. Autonomic hyperreflexia
m. Neuropathy/myopathy
n. Psychiatric disorders
o. Cerebral palsy
p. Spinal cord injury
4. Musculoskeletal
a. Fractures
b. Rheumatoid arthritis
c. Lupus erythematosus
d. Muscular dystrophy
e. Scoliosis
f. Malignant hyperthermia
5. Endocrine
a. Diabetes mellitus
b. Diabetes insipidus
c. Hypo/hyperthyroidism
d. Cushing’s disease
e. Addison’s disease
f. Pituitary dysfunction
g. Parathyroid dysfunction
h. Pheochromocytoma
i. Acromegaly
j. Hypo/hyperaldosteronism
6. Hepatic
a. Hepatitis
b. Cirrhosis
c. Hepatic failure
d. Porphyria
7. Renal
a. Kidney stones
b. Acute renal failure
c. Chronic renal failure
d. Uremia
e. Nephritis
8. Hematologic
a. Anemia
b. Sickle cell/hemoglobinopathies
c. Polycythemia
d. Platelet disorders
e. Hemophilia
f. von Willebrand’s disease
g. Disseminated intravascular coagulation
9. Gastrointestinal
a. Peptic ulcer disease
b. Ulcerative colitis
c. Diaphragmatic hernia
d. Hiatal hernia
e. Gastroesophageal reflux disorder (GERD)
f. Gallstones/gall bladder disease
g. Pancreatitis
h. Splenic disorders
i. Carcinoid syndrome
j. Pyloric stenosis
k. Bowel obstruction
10. Immune
a. Allergic responses and anaphylaxis
b. AIDS/HIV
c. Immunosuppression
d. Latex allergy
e. Sepsis
f. Angioedema
11. Other
a. Abnormal lab tests
b. Cancer
c. Glaucoma
d. Thermoregulation
e. Trauma
f. Shock
g. Substance abuse (alcohol, tobacco, other)
h. Airway difficulties
i. Diagnostic data
(1) Chest X-ray
(2) Pulmonary function tests
(3) Echocardiogram
(4) Cardiac catheterization
(5) CAT/MRl
(6) Ultrasound
(7) Electrocardiogram
(8) Stress tests
j. Burns
B. Pharmacology
1. General principles
a. Pharmacodynamics
b. Pharmacokinetics
c. Anaphylaxis
d. Drug interactions
2. Inhalation anesthetics
a. Nitrous oxide
b. Isoflurane
c. Desflurane
d. Sevoflurane
3. Intravenous agents
a. Barbiturates
(1) Thiopental
(2) Methohexital
b. Opioid agonists
(1) Morphine
(2) Fentanyl
(3) Alfentanil
(4) Sufentanil
(5) Meperidine
(6) Remifentanil
(7) Hydromorphone
c. Opioid agonist-antagonists
(1) Nalbuphine
(2) Butorphanol
d. Benzodiazepines
(1) Diazepam
(2) Midazolam
(3) Lorazepam
e. Other sedative/hypnotics
(1) Propofol
(2) Ketamine
(3) Etomidate
f. Dexmeditomidine
4. Local anesthetics
a. Procaine
b. Chloroprocaine
c. Tetracaine
d. Cocaine
e. Benzocaine
f. EMLA
g. Bupivacaine
h. Lidocaine
i. Mepivacaine
j. Ropivacaine
5. Muscle relaxants
a. Succinylcholine
b. Pancuronium
c. Vecuronium
d. Atracurium
e. Rocuronium
f. Cisatracurium
6. Antagonists
a. Edrophonium
b. Neostigmine
c. Naloxone
d. Flumazenil
e. Pyridostigmine
f. Physostigmine
7. Neuraxial analgesics
a. Opioids
b. Clonidine
8. Anticholinergics / Cholinergic agonists
9. Nonsteroidal Antiinflammatory Drucs
10. Miscellaneous oral analgesics
a. Acetominophen
b. Codeine
c. Oxycodone
d. Hydrocodone
e. Tramadol
11. Sympathomimetics
12. Digitalis and related drugs
13. Alpha and beta receptor antagonists
14. Antihypertensives
a. Sympatholytics
b. Clonidine
c. ACE inhibitors
d. Angiotensin II receptor inhibitors
e. Nitrovasodilators
f. Nitric oxide
15. Antidysrhythmics
16. Calcium channel blockers
17. Bronchodilators
18. Psychopharmacologic therapy
a. Selective serotonin reuptake inhibitors
b. Tricyclic antidepressants
c. MAO inhibitors
d. Lithium
19. Prostaglandins
20. Histamine receptor antagonists
21. Serotonin antagonists
22. Insulin
23. Oral hypoglycemics
24. Diuretics
25. Antacids
26. Gastrointestinal prokinetic medications
27. Anticoagulants
a. Heparin
b. Heparin reversal (Protamine)
c. Low molecular weight heparins
d. Oral anticoagulants
e. Oral anticoagulant reversal
f. Thrombolytics
g. Thrombin inhibitors
28. Antimicrobials
29. Chemotherapeutics
30. Antiepileptic drugs including gabapentin
31. Antiparkinsonian drugs
32. Drugs used to treat lipid disorders
33. Herbal remedies and dietary supplements
34. Minerals and electrolytes
35. Dantrolene
36. Corticosteroids
37. Tocolytics
38. Uterotonics
C. Applied chemistry, biochemistry, physics
1. Chemistry
a. Aqueous solutions and concentrations
b. Acids, bases and salts
2. Biochemistry
a. Hepatic metabolism
b. Cellular mechanisms for action
c. Drug receptor interaction
3. Physics
a. Units of measurement
b. Gases and gas laws
c. Solubility, diffusion and osmosis
d. Pressure and fluid flow
e. Electricity and electrical safety
f. Vaporization and humidification
g. Measurement of oxygen, carbon dioxide and hydrogen ion
II. Equipment, instrumentation, and technology (15%)

A. Anesthetic delivery systems
1. High/low pressure gas sources
2. Regulators/manifolds
3. Flowmeters, valves, floats
4. Vaporizers
5. Proportioning systems
6. Pressure failure safety devices
7. “Fail-safe” devices
8. Ventilator
9. Carbon dioxide absorbent
10. Anesthetic circuits
a. Rebreathing, circle system
b. Non-rebreathing
c. Modified non-rebreathing
11. Pneumatic and electronic alarm devices
B. Airway Devices
1. Face masks
2. Laryngoscope
a. Rigid
b. Flexible/Fiberoptic
c. Videoscope
3. Endotracheal tube
4. Endobronchial tube including double lumen tubes
5. Airways
a. Oral
b. Nasal
6. Tracheostomy tubes
7. Laryngeal mask airway
8. Intubating laryngeal mask airway
9. Jet ventilation
10. Lighted stylet
11. Other
a. Retrograde wire
b. Eschmann catheter
c. Combitube
d. Cook exchange catheter
C. Monitoring devices
1. Central nervous system
a. Evoked potential
b. Intracranial pressure
c. Modified EEG monitor (e.g BIS, etc.)
d. Cerebral oximetry
2. Cardiovascular
a. Electrocardiogram
b. Arterial pressure monitoring
c. Noninvasive blood pressure monitoring
d. Central venous pressure monitoring
e. Pulmonary artery pressure monitoring/SVO2
f. Cardiac output
g. Precordial/esophageal stethoscope/doppler
3. Pulmonary/airway monitoring
a. Capnography
b. Airway gas analysis
c. Pulse oximetry
d. Airway pressure
e. Blood gas analysis
4. Peripheral nerve stimulator
5. Urinary output monitoring
6. Temperature monitoring
7. Maternal/fetal monitoring devices
8. Others
a. Fluid/blood warmers
b. Forced air warming blanket
c. Heat and moisture exchanger (HME)
d. Blood salvage (cell saver)
III. Basic principles of anesthesia (30%)

A. Preoperative assessment and preparation of patient
B. Fluid/blood replacement
1. Fluid therapy (crystalloids and colloids)
2. Hemotherapy (blood component therapy)
C. Positioning (Technique, Physiologic alterations, Complications)
1. Prone
2. Supine
3. Lithotomy
4. Lateral
5. Sitting
6. Beach chair
7. Trendelenburg
8. Reverse trendelenburg
D. Interpretation of data
1. Lab tests
2. Diagnostic data
3. Intraoperative monitoring data
E. Airway management
1. Mask
2. Cricothyrotomy
3. Fiberoptics
4. Intubation
5. Supralaryngeal management
F. Local/regional anesthesia (Technique, Physiologic alterations,
Complications)
1. Infiltration
2. Topical
3. Regional blocks
a. Subarachnoid block
b. Epidural block
c. Combined spinal/epidural
d. Caudal block
e. Brachial plexus block
f. Airway blocks
g. IV regional block (Bier)
h. Retrobulbar/peribulbar block
i. Ankle block
j. Digital block
k. Wrist block
l. Sciatic block
m. Femoral block
n. Popliteal block
4. Ultrasound guided nerve block
5. Nerve stimulator guided nerve block
G. Monitored anesthesia care/conscious sedation
H. Pain management
1. Epidural analgesia
2. Infiltration nerve blocks
3. Intrathecal narcotics
4. PCA management
I. Others
1. Hypotensive
2. Hypothermia
J. Postanesthesia care/respiratory therapy
K. Pain Theory (Anatomy, physiology & pathophysiology)
IV. Advanced principles of anesthesia (30%)

A. Surgical procedures and procedures related to organ systems
1. Intra-abdominal
a. Gall bladder
b. Liver
c. Pancreas
d. Spleen
e. Stomach
f. Renal
g. Diaphragm
h. Intestine
i. Herniorrhaphy
j. Bladder
k. Abdominal/gyn
l. Prostatectomy
m. Laparoscopy
n. Bariatrics
2. Extrathoracic
a. Breast biopsy
b. Mastectomy
c. Plastic and/or reconstructive
3. Extremities
a. Lower
b. Upper
c. Total joint replacements
d. Vein stripping
4. Genital and urologic
a. Transurethral resection
b. Cystoscopy
c. D and C
d. Hysterectomy
e. Hysteroscopy
f. Anal/rectal
g. Penis/testes
5. Head
a. Extracranial
(1) Cranioplasty
(2) Rhizotomy
(3) Ear
(4) Eye
(5) Face
(6) Nose
b. Intracranial
(1) Decompression (burr holes)
(2) Space-occupying lesion
(3) Vascular
(4) Transsphenoidal hypophysectomy
(5) Stereotactic procedures
c. Oropharyngeal
(1) Fractures
(2) Reconstructive
(3) Orthodontic/dental
(4) Pharynx
(5) Reconstructive and/or plastic surgery
6. Intrathoracic
a. Diaphragm
b. Esophagus
c. Heart
d. Lung
e. Mediastinoscopy
f. Thoracoscopy
7. Neck
a. Cervical spine (anterior and posterior approach)
b. Larynx/trachea
c. Lymph node biopsies
d. Parathyroid/thyroid
e. Neck tumors
f. Radical neck
g. Rigid laryngoscopy
h. T&A
8. Neuroskeletal
a. Laminectomy
b. Fusions
c. Spinal cord procedures
d. Surgical sympathectomy
e. Vertebroplasty
9. Vascular
a. Carotid
b. Thoracic
c. Abdominal
d. Upper extremity
e. Lower extremity
f. Porto-systemic shunts
g. Renal artery
h. Vena cava filter
i. Endovascular procedures
10. Diagnostic/therapeutic
a. Venous/arterial catheterization
b. Cardioversion
c. CAT scan
d. MRI
e. Electroconvulsive therapy
f. Interventional radiology
g. Electrophysiology
h. Steroid therapy
i. Radiation therapy
j. Endoscopy
k. Bronchoscopy
l. Esophagoscopy/gastroscopy
11. Management of complications
a. Anesthetic
b. Surgical
12. Other
a. Trauma
b. Burns
c. Resuscitation
d. Pacemakers
e. Lithotripsy
f. Organ transplants
g. Organ harvest
(1) Living donor
(2) Cadaver
h. Laser
B. Pediatrics
1. Anatomy, physiology, pathophysiology
a. Normal
b. Prematurity
c. Congenital anomalies
2. Pharmacology
3. Anesthesia techniques/procedures
C. Obstetrics
1. Anatomy, physiology, and pathophysiology
2. Pharmacology
a. Caesarean section
b. Vaginal delivery
c. Labor epidurals
d. Intrathecal
e. Postpartum tubal ligation
f. Vaginal birth after caesarean section
g. High risk
h. Non-obstetric surgery in the parturient
D. Geriatrics
1. Anatomy, physiology, pathophysiology
2. Pharmacology
E. Obesity
1. Anatomy, physiology, and pathophysiology
2. Pharmacology
Anesthesia Equipment Review
Ideal Gas Laws

• Boyle’s Law:
PV = Constant
Allows us to apply pressure to reservoir bag to
ventilate patient
• Charles’ Law:
V/T = Constant (Temperature Always in Kelvin)
Heating a gas causes it to expand
• Gay-Lussac’s Law:
P/T = Constant (Temperature Always in Kelvin)
Heating a gas causes an increase in pressure
• Combined Gas Law:
PV/T = Constant (Temperature Always in Kelvin)
Solubility Coefficients
Agent Blood-Gas MAC Vapor
Pressure
Desflurane 0.42 6.3 690

Isoflurane 1.4 1.15 250
N2O 0.48 104% 745psi
Sevoflurane 0.59 1.71 185
Blood-Gas Coefficient inversely correlates with induction speed

Calculating Percents & Pressures
• Atmospheric Pressure:
1 ATM = 760 mmHg = 14.7 psi
• Calculating Maximum Agent Concentration:

Max % = VP/ATM x 100
Ex: Max % sevoflurane = 185/760 x 100 = 24.34%
(VP dependent on substance and temperature – does not
vary with changes in atmospheric pressure)
• Calculating Concentration in mmHg:

mmHg = ATM x % Concentration
Ex: 7% desflurane = 7% x 760 = 53.2 mmHg
Diffusion
• Fick’s First Law
– For a given solute, the major determinant of
the rate of diffusion is the concentration
gradient
• Graham’s Law
– The rate of diffusion is proportional to the
square root of the molecular weight
• Large molecules diffuse more slowly
Medical Gases
• E-cylinders:
Measures 2’ x 4”
Internal volume of 5000 cc
Specific wall thickness for the gas to be stored
• H-cylinders:
Measures 4’ x 9”
Holds about 10x the volume of an e-cylinder
• Features:
Pin Index Safety System
Pressure relief system
Yoke assembly
Oxygen Cylinder
• Must be stored as a gas
– critical temperature is -118 C
• Follows Boyle’s Law
• Full cylinder contains 660 liters
• Full cylinder at 2000 psi
• Tank pressure correlates linearly with tank
volume
• Tank should be changed if < 1000 psi
Nitrous Oxide Cylinder

• 90-95% filled with liquid N2O
• Critical temperature is 36.5 C
• Does not follow Boyle’s law until all liquid
in the cylinder is consumed
• Pressure gauge does not correlate with
volume until all liquid is consumed
• Full E-cylinder contains 1590 liters
• Full E-cylinder pressure = 750 psi
The Anesthesia Machine

Machine Components
• Oxygen supplies
• Nitrous and other gas supplies
• Gauges
• Regulators
• Fail-Safe Valve, Oxygen supply alarm
• Flow meters
• Oxygen ratio proportioning systems
• Flush valve and gas outlet
Oxygen Supplies
• Wall supply at 40-60 psi
uses labeling, color coding and DISS
• Tank supply
from E-cylinder on yokes
• Oxygen flows to 5 places:
Flush valve
Oxygen supply failure alarm
Fail-Safe valve
Flow meters
Pneumatically powered devices e.g. ventilator
Nitrous & Other Gas Supplies

• Nitrous and other gases also supplied by
wall outlets or E-cylinders
Also uses labeling, color coding and DISS
• Nitrous oxide flow is only to the flow
meters, through the fail-safe valve
• Other gases, e.g. air, follow similar
pathway, but may not be involved in the
fail-safe valve
Gauges
• Uses the Bourden principle
curved metallic tube that straightens with increased pressure
• Designed to read 33% higher than

maximum working pressure
• Heavy metal case and plate glass front in

case of Bourden tube rupture
Regulators
• Converts variable high pressure to
constant low pressure
Machines have 2nd stage regulator after inlet of the
pipelines to further reduce pressure and maintain a
constant pressure even if wall outlet pressure varies
• E-cylinder regulators designed to deliver

less pressure than the wall outlet
If tanks are accidentally left on, wall supply is used
preferentially
Fail-Safe Valve, O2 Alarm

• Fail-Safe Valve
shuts off other gas flow if O2 pressure falls below 25 psi
does not prevent delivery of hypoxic mixtures
• Oxygen Supply Failure Alarm

oxygen pressurizing a cylinder with a whistle device at
entrance
fall in pressure allows oxygen to flow past whistle
simple, but effective. May be heard when turning
machine off
Flow Meters
• Tapered glass tubes larger at top
this allows constant pressure with variable flow
• High flow rate
produces turbulent flow
density of gas is the major flow rate factor
CO2 and N2O have similar densities
• Low flow rate
produces laminar flow
viscosity of gas is the major flow rate factor
O2 and Helium have similar viscosities
• Effect of changing barometric pressure
decreased pressure = rotameter too low,
underestimating flow
increased pressure = rotameter too high, overestimating
flow
Oxygen Proportioning Systems
• Machines are equipped with devices to

prevent delivery of FiO2 < 25%
• Proportioning systems only linked to N2O

if other gases are used, hypoxic gas mixtures could be
delivered
Flush Valve & Gas Outlet
• Flush valve bypasses on-off switch

• Delivers oxygen at 40-60 psi
risk of barotrauma under certain conditions
• Estimated rate of delivery: 30-70 Liters/Min
• Common gas outlet
15 mm size; different from breathing circuit or scavenger
Often equipped with check valve to prevent retrograde
gas flow
Vaporizers
Current vaporizers use a variable bypass design
Vaporizer dial
Vaporizer Output Regulation

• Using Dalton’s Law, saturated vapor
pressures are:
desflurane = 91%
isoflurane = 31% sevoflurane = 24%
• Variable bypass design allows a fraction of

the input gas to go to the vaporization
chamber and the remainder of gas to not
receive volatile agent
Vaporizer Characteristics
1. Variable bypass allows a fixed
concentration regardless of the flow
2. Vaporizers are vapor pressure specific –
only agents with identical vapor pressures can be
interchanged
3. Vaporizers must have a mechanism to
compensate for temperature variation
4. Vaporizers must have an efficient heat
transfer system
Vaporizer Use Variables
• Most volatile agents produce about 200 cc of
gas for each cc of liquid
• How long will 100 cc of sevoflurane last when
given at 3L/min at 2%?
3000 cc x .02 = 60 cc/minute of sevoflurane used
60cc / 200 cc per 1 cc liquid = 0.3 cc liquid used each minute
100 cc / 0.3 cc/min = 333 minutes
100 cc of sevoflurane will last 333 minutes at 3L/m

at 2%
Barometric Pressure Effects
• Decreases in barometric pressure cause

an increase in vaporizer output
• Conversely, increases in barometric

pressure cause a fall in vaporizer output
Desflurane Vaporizer
• Desflurane’s high vapor pressure (690
mmHg) makes variable bypass impossible
• Desflurane vaporizer heats the agent to 39º C
• This increases the vapor pressure to 1500
• Pressure sensors determine the fresh gas
flow rate and the output is calculated
• Desflurane is then introduced into the fresh
gas flow as a gas
Circle System Components
• CO2 absorber
• APL “Pop-off”
• Unidirectional valves
• Reservoir bag
• Circuit hoses
• Fresh gas supply
CO2 Absorber
• Can be either sodalime or Amsorb
• Chemical reaction to eliminate CO2
CO2 + Ca(OH)2 Ö CaCO3 + H2O
(Sodalime uses NaOH or KOH as catalyst)
• Exothermic reaction, in all 3 phases
solid, liquid & gas
• Irregular granules, 4-8 mesh
– provides maximal surface area with minimal airway
resistance
• 1000 gm canister can absorb 200 L of CO2
• Canister 50% airspace, 50% absorbent
• Indicator (ethyl violet) indicates exhaustion
APL & Unidirectional Valves

• APL vents excess gas to scavenger
Vents when set pressure is exceeded
Set fully open for spontaneous ventilation
Set fully closed for patients on ventilator
Can be used as a PEEP valve
• Unidirectional valves
Disk valves
Prevent rebreathing of CO2
Reservoir Bag & Circuit Hoses
• Reservoir Bag
Serves as reservoir to buffer high inspiratory & exhaled
gas flows
Serves as a shock buffer
Serves as a means of giving positive pressure
Volume should exceed inspiratory capacity
• Circuit hoses
22mm fitting – different from gas outlet or scavenger
Compliance is about 3cc/cmH2O/meter
Large diameter offers almost no resistance
Dead space only in areas of bi-directional flow
– Dead space ends at the Y-piece of the circuit
Mapelson Circuits
• Mapelson A
Fresh gas flow and exhaust exactly opposite of
Mapelson D
Very effective for spontaneously ventilating patients
Fresh gas flows can be as low as 0.6x minute ventilation
(spontaneous ventilation)
• Mapelson D
Used in pediatric cases because of very low resistance
Requires about 200-300 mL/Kg/m fresh gas flow for
spontaneous ventilation, 70-100 mL/Kg/m for controlled
ventilation
Bain modification places fresh gas tubing within the
expiratory hose
Waste Anesthetic Gases

• Chronic low-level exposure to N2O:
Spontaneous abortion
Fetal malformation
Cancer
Neuropathy
Behavioral changes
• NIOSH recommendations:
N2O < 25 ppm
Halogenated agents < 2 ppm
Halogenated agent + N2O < 0.5 ppm
OR Ventilation Systems
• Air turnover is the single most important
factor in reducing anesthetic air pollution
• 10 exchanges per hour or more is required
• Fresh air enters the OR through ceiling

vents and leaves through floor vents
Scavenging Systems
• Required by JCAHO
• Reduce anesthetic loss to OR by 90%
• 19 mm hose, rigid enough to hold 10kg/cm
• Scavenger interface
Closed reservoir
Open reservoir
• Disposal Routes
Active – to specialized wall suction at > 30L/min
Passive – to floor vents
Scavenger Systems
Closed Scavenger Open Scavenger
Ventilator Classification
• Volume limited
Delivers a fixed volume
Not affected by changes in compliance or resistance
Loss of ventilation in cases of leak
• Pressure limited
Delivers a predetermined pressure
Affected by both changes in compliance and resistance
Unaffected by leak
• Jet Ventilator
Narrow catheter placed in trachea
Oxygen at 25 – 30 psi delivered for 1 – 1.5 secs x 12/min
Tidal volumes of 400 – 700 mL obtained
• High-frequency ventilator
Gas transport by diffusion rather than convection
Volume Ventilators
Commonly used on anesthesia machines
• 2 components
Bellows assembly
Control box
(Hanging bellows ventilators don’t meet standard of
care)
• Ventilatory cycle
Closure of relief valve (to scavenger)
Pressurization of bellows chamber
Discontinuation of pressurization to begin exhalation
Refilling of bellows from exhaled volume and fresh gas
flow
Opening of relief valve to vent excess gases to
scavenger
Fresh Gas Flow Coupling

• During inspiratory phase, fresh gas flow
adds to the tidal volume
• High FGF may significantly increase TV
and minute ventilation
• Usually not seen with newer piston-driven
ventilators, which can deliver very
accurate TVs to patients with poor
compliance or very small patients
High-frequency Ventilators
• Small tidal volumes – at or less than dead
space
• Rapid rates – 60 or more breaths/minute
• CO2 retention corrected by decreasing rate
• Indicated for bronchopleural fistula, to
improve oxygenation during one-lung
anesthesia, tracheal reconstruction and
extreme loss of lung compliance
Capnography
• Two types available
Side stream – gas sample brought to machine
analyzer
Main stream – analyzer positioned in gas flow
• Measurement techniques
Infrared – infrared light is strongly absorbed by CO2
Mass spectrometry
Chemical indicators
The Capnogram
I. The inspiratory baseline

Fresh gas rushes past the sampling site
CO2 concentration approaches zero
The Capnogram cont’
II. Expiratory upstroke

Exiting alveolar gas contains CO2 and causes rapid
upstroke
Airway obstruction may produce a decrease in slope
Capnogram cont’
III. Expiratory plateau

Capnogram plateaus as a stable amount of CO 2 is
exhaled
May have a slight incline as lung units with lower V/Q
ratios empty
Capnogram cont’
IV. Inspiratory downstroke

Fresh gas drawn past sampling site
Downstroke may be slowed by an incompetent
inspiratory valve
Abnormal Capnograms
Increased Airway Resistance

Slowed expiration shown in phases 2 and 3
Abnormal Capnograms cont’
Rebreathing
Elevated baseline – phase 1
Caused by failed expiratory valve, exhausted CO2 absorber
Can be caused by inadequate fresh gas flow in Mapelson
circuits
Cardiac Oscillations
Changes in intracardiac volume resulting in gas movement
Rhythm corresponds to pulse
Spontaneous ventilation
Sometimes called “Curare Clefts”
PaCO2 – PeCO2 Differences

• Normally 3 – 5 mmHg
• Changes in V/Q ratio

Shunt has very little impact on end-tidal CO 2
Changes in dead space have a large impact on end-tidal CO 2
• Sample size
Very small children will have small exhaled volumes. Dilution from
fresh gas flow may reduce apparent end-tidal CO 2
• Machine errors
Oximetry
• Oxyhemoglobin dissociation curve
P50 = 27 mmHg
PaO2 40, 50, 60 = Sat 70, 80, 90%
PaO2 > 90 Ö Saturation independent of PaO2
• Functional saturation
O2 Hb
Sat = ---------------------- x 100
O2 Hb + R Hb
Pulse Oximeters
• Makes use of light absorbance
• Tissue contains many absorbers of light
Blood pulsations used to determine arterial absorbance
• Absorbance of 2 wavelengths of light to
determine oxyhemoglobin and reduced
hemoglobin
• Ratio formed and saturation determined
Accuracy and Error Sources

• Accuracy r 2% x 1 standard deviation
Accuracy within 2%, 68% of the time
• Dyes can cause large decrease in

measured saturation
• Carboxyhemoglobin causes false

elevation in measured saturation
• Methemoglobin results in sat of 85%
Oxygen Analyzers
• Galvanic (fuel) cell
Output voltage proportional of O2 partial pressure
• Polarographic sensors
Current applied reduces O2. Changes in current reflect
O2 concentration
• Paramagnetic analyzers
Magnetic field applied to stream of gas. Changes in
stream pressure reflect O2 content
Principles of Electricity
• Ohm’s Law
E = IR (E = voltage, I = amperage, R = resistance)
• Power
E x I = power (measured in watts)
• DC vs. AC
Electron flow only in one direction = DC
Electron flow reverses at regular intervals = AC
AC Electricity
• Impedance Æ resistive force in AC circuit
• Impedance (Z)
Z = frequency x inductance
Z = 1/(frequency x capacitance)
• The greater the frequency the less the
impedance
• Inductance Æ electrical current can be
induced in a separate wire or iron core
Electrical Shock Hazards

• AC has greater propensity to cause V-fib
• Tissue damage occurs:
Disruption of normal cellular electrical activity
Thermal injury – may be internal along path of
conductivity
• Shock occurs when patient completes
circuit
• Macroshock (at 60Hz)
1mA = threshold of perception
10-20 mA = “let go” current
50 mA = pain
100-300 mA = V-fib
Grounded Electrical Power
• As supplied by electric utility, power is
grounded
• In a grounded system current will flow
between the “hot” wire and any conductor
(patient) with ground
• If patient is touching ground only contact
with the “hot” wire is needed for shock to
occur
Ungrounded Power
• In the OR power is ungrounded
• Isolation transformer is the device that

“ungrounds” the power
• Line isolation monitor monitors the

integrity of the isolated power system
Alarm is usually set to 2-5 mA
Microshock
• A catheter or wire in the heart can deliver
high current density
• As little as 20 microamps may induce V-fib
• Isolation transformer does not prevent
microshock
• Isolation monitor will not detect risk of
microshock
Lasers
• Laser reactivity depends on wavelength:
CO2 – absorbed by water, limited tissue penetration
Nd:YAG – transmitted through clear materials, deep
penetration
Argon – absorbed by hemoglobin and melanin
• CO2 laser blocked by any type of clear
glass or plastic
• Nd:YAG and Argon lasers require special
protective eyewear
• Airway fires a risk from ETT ignition
Airway Fire Management

• Primary Response
Discontinue O2 source
Remove endotracheal tube
Mask ventilate with lowest possible FiO2
• Secondary Response
Recommendations vary from author to author
Re-intubation
Short term steroid administration
Antibiotic administration
Bronchoscopy
Ventilatory support
Temperature Monitoring
• Hypothermia – body temperature less than
36o C
• Postoperative shivering increases oxygen
consumption by a factor of 5
• Radiation accounts for 40% of heat loss.
Convection and evaporation account for
about 30%
• Conduction accounts for 30% of heat loss
• One MAC decreases vasoconstriction and
shivering threshold by 2 – 4o C.
Temperature cont’
• Three phases of intraoperative hypothermia:
1) Redistribution of heat from core to periphery.
Occurs in 1st hour and results in a 1 – 2o fall
2) Steady decline occurs in following 2 – 3 hours
3) Equilibration – losses equal metabolism
• Accurate core temperatures can be obtained from:
PA, distal esophagus, tympanic membrane,
nasopharynx
• Mouth, rectum, bladder, axilla are reasonable
alternatives except during cardiopulmonary bypass
Warming Methods
• Treatment of hypothermia is ideally focused on
intraoperative prevention
• Active rewarming – application of an external heat
source:
-Heated blankets – conductive heat source
-Radiant warmers – radiant heat source
-Forced air warmers – convective heat
source. Forced air warmers have been
shown to be the most effective
• Burn injuries have been associated with all types of
active rewarming devices
– Use of external heat sources are contraindicated in pts
with severe PVD or during hypoperfused states (i.e. aortic
cross-clamping)
Blood Salvage (Cell Saver)

• Device anticoagulates blood as it leaves the
surgical field
• Cells are washed in NS and centrifuged to a
HCT of 45 – 65%
• Contraindications – presence of infection,
malignant cells, urine, bowel contents and
amniotic fluid
• Washing process removes platelets and
coagulation factors, but not bacteria
• Leukocyte filters often used to trap bacteria
Bispectral Index Monitoring
• BIS ranges
– 100 - 90 = awake, unanesthetized patient
– 90 – 70 = light to moderate sedation
– 70 – 60 = deep sedation (probable amnesia)
– 60 – 40 = general anesthetic state
– 40 – 10 = deep anesthetic state & burst suppression
– 10 – 0 = flat-line EEG pattern
• Causes of unexpected BIS results/changes
– Change in level of surgical stimulation
– Change in level of anesthesia or sedation
– Change in body temperature
– Change in level of neuromuscular blockade & shivering (falsely Ĺs EMG)
– Presence of high-frequency electrical device e.g. Bovie, pacemaker
– Placement of temporal lead over temporal artery
– Use of pressors, ketamine
**BIS lags behind real-time by approximately 10-15 seconds
Notes
Notes
Pharmacology Review:
Local Anesthetics
.
Inhalation Agents
Local anesthetics
• drugs which prevent nerve depolarization,
thereby causing loss of sensation
– they produce a reversible interruption of

neural impulses along sensory and motor
pathways
– they do not produce a loss of consciousness

or CNS depression (under normal
circumstances)
The nerve membrane

• a biphospholipid membrane punctuated
with Na+ channels
– found distributed throughout the membrane of
unmyelinated nerves
– found only at the nodes of Ranvier of
myelinated nerves
• myelinated nerves are more resistant to the effects
of locals; must block at least 2 successive nodes to
block transmission
Most sensitive to
From Lange, Clinical Anesthesiology
the effects of LA
Effect of local anesthetics on the

neural action potential
• locals prevent the opening of Na+
channels, thereby preventing the
membrane potential from increasing
sufficiently to reach threshold potential
• the Na+ channel acts as a specific receptor

site for local anesthetic molecules
The Na+ channel
• locals affect that part of the Na+ channel which
leads to the intracellular portion of the nerve
cell—A.K.A. “The H gate”
(@ RMP) during depolarization
activation gate inactivation gate

nerve axoplasm
The Na+ channel

• locals cross the nerve membrane and
gain access to the interior portion of the
Na+ channel rendering it inactive by
activation of the H gate
nerve axoplasm
Threshold
potential
Effect of locals on threshold
potential
locals do not alter RMP or TP
dissociation of drug
results in complete,
spontaneous return of
neural transmission
Chemical configuration of local

anesthetics
essential for ester or amide 2º or 3º
anesthetic activity intermediate amino
linkage portion
Ester local anesthetics

• chloroprocaine (Nesacaine)
• procaine* (Novocaine)
• cocaine
• tetracaine (Pontocaine)
• benzocaine (Cetacaine)
– *denotes most frequently used ester LA for infiltration anesthesia
Ester local anesthetics, cont’d
• hydrolyzed by both plasma cholinesterase
and non-specific RBC esterases
– cleavage of ester LA yields PABA (para-
amino benzoic acid) and an alcohol; PABA is
excreted unchanged in the urine
– PABA is responsible for a greater potential of
the esters for producing allergic reactions
– elimination of esters may be prolonged with
cases of plasma cholinesterase deficiency
(genetic or acquired)
Cocaine
• In contrast to other ester LAs:
– is partially metabolized by N-methylation and
ester hydrolysis in the liver
– is excreted partially unchanged in the urine
• Cocaine blocks reuptake of norepinephine

by the adrenergic nerve terminal causing
an increase in SNS tone
Amide local anesthetics

• lidocaine* (Xylocaine)
• bupivacaine* (Marcaine)
• levobupivacaine (Chirocaine)
• mepivacaine (Carbocaine)
• prilocaine (Citanest)
• etidocaine (Duranest)
• ropivacaine (Naropin)
• dibucaine (Nupercaine)
– *denotes most frequently used amide LAs for infiltration anesthesia
Amide local anesthetics, cont’d
• metabolized by microsomal enzymes in
the liver; hepatic disease and enzyme
induction alters pharmacokinetics
• hepatic metabolism is generally slower
than the hydrolysis of the esters; may
result in sustained/cumulative effects of
amides
Amide local anesthetics, cont’d

• prilocaine
– metabolized to ortho-toluidine
• an oxidizing compound which converts
hemoglobin to methemoglobin
• methemoglobin does not carry O2
efficiently; high
plasma concentrations lead to cyanosis
• readily reversed using methylene blue 1-2
mg/kg IV (reduces methemoglobin back to
hgb by oxidizing itself to methylene white)
Pharmacodynamics of local
anesthetics
• depend on 3 attributes of the drug:
– pKa (the pH @ which drug is
ionized:unionized 50:50)--responsible for
onset of local anesthetic
– lipid solubility—responsible for potency of
local anesthetic
• probably plays a role in the duration of the LA as
well
– protein binding—responsible for duration of
local anesthetic activity
pKa of local anesthetic
• locals are weak bases commercially
prepared in acid solutions with pKa values
slightly above physiologic pH
• onset of activity of local is more delayed if:
• the drug’s pKa is further from 7.4 (more of the drug
exists in the ionized form)
• the pH of the environment the drug is administered
into is < 7.4 (i.e. infected or hypoperfused tissues)
– remember—the unionized form of the drug is

necessary to cross the neural cell membrane; the
ionized form of the drug interacts with the H gate
pKa of individual local

anesthetics
• mepivacaine 7.6
• etidocaine 7.7
• lidocaine 7.9
• prilocaine 7.9
– these pKa values are closest to physiologic

pH therefore the onset is believed to be
relatively quicker
pKa of individual local

anesthetics
• bupivacaine 8.1
• ropivacaine 8.1
**onsets of these
• tetracaine 8.5 agents (excluding
• cocaine 8.7 chloroprocaine)
• chloroprocaine 8.7** are considered to
be relatively slow
• dibucaine 8.8
• procaine 8.9
Lipid solubility of local
anesthetics
• generally speaking, the more lipid soluble
a local anesthetic is, the more potent it is
– potency does not necessarily correspond to
onset time
• generally speaking, lipid solubility parallels
protein binding
– agents with higher lipid solubility may also last
longer because they are less likely to be
cleared by blood flow
Protein binding of local

anesthetics
• generally speaking, the more highly
protein bound an agent is, the more
difficulty it has dissociating from the Na+
channel
• therefore, the longer the agent’s duration
of action
– chloroprocaine possesses virtually no protein
binding
Protein binding of local anesthetics

• short acting locals:
– procaine (6%)
– chloroprocaine (N/A)
• intermediate acting locals:
– lidocaine (64%)
– mepivacaine (77%) Remember: “LMP”
– prilocaine
• long acting locals:
– bupivacaine (and ropivacaine)(95%)
– etidocaine (95%) Remember:
“you can BET
– tetracaine (75%) on them”
Frequency-use dependence
• locals with higher pKa values are highly ionized
at physiologic pH and depend on diffusing
through open (activated) Na+ channels to gain
access into the axoplasm and exert their effects
• nerves which undergo depolarization more

frequently (i.e. autonomic and sensory nerves)
are more susceptible to blockade by agents with
higher pKa values than those which fire less
frequently (i.e. large motor nerves)
Minimum concentration (Cm)

• the amount of local anesthetic necessary to
produce conduction blockade
• nerve fiber diameters directly relate to an
agent’s Cm for those fibers—larger,
myelinated nerves (i.e. A fibers) require a
greater [ ] of LA to produce blockade than
do smaller, unmyelinated nerves (i.e. C
fibers)
*Progression of blockade: “ATP, TP, MVP”
(Autonomic, Temperature, Pain, Touch, Pressure, Motor, Vibratory ,
Proprioception fibers)
Local anesthetic toxicity

• locals are absorbed systemically from their
sites of injection
• if plasma [ ] of LA becomes high, toxic
effects may ensue (i.e. lidocaine induced
seizures, bupivacaine cardiotoxicity)
• significant initial pulmonary uptake of
injected LA (A.K.A. “first pass pulmonary
extraction”) is protective against toxicity
Local anesthetic toxicity
• plasma [ ] of LA related to:
– total dose administered
– vascularity of the injection site
• certain techniques produce higher plasma [ ] of LA
– airway
– intercostal
– caudal
– epidural
– brachial plexus or other major nerve blocks
– peripheral (subcutaneous infiltration)
– spinal
Local anesthetic toxicity, cont’d

• plasma [ ] of LA related to:
– use of epinephrine
• when mixed into LA, it produces vasoconstriction
of the injection site resulting in:
– less systemic absorption
– probable quicker onset
• avoid use in “fingers, ears, tip of nose, toes, hose”;
vasoconstriction may cause gangrene
• the physicochemical properties of the drug

t
• toxic effects (early symptoms) cu
ra e
s oc 3X th of
– circumoral/tongue numbness s/ ly ion
ac te rat es
a rdi xima cent aus
– metallic taste in mouth C ro on at c
p c
ap ma e th s/s
– tinnitus s in ro
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– vertigo, blurred vision
– restlessness, muscular twitching Neuro
bupiva s/s from
– drowsiness caine m
rapidly ay
follo we be
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• later symptoms cardiac
s/s!
– loss of consciousness Ö coma
– seizures (dangerous--CMRO2 is not lowered by LA)
– apnea tre
a
su tme
– CV depression pp nt
or is tiv
e
• cardiotoxicity—effects from interaction of
LA with cardiac Na+ channels seen with
higher plasma [ ]s
– first manifested as hypotension
– depression of conduction and automaticity
– depression of contractility
– dysrhythmias
– high grade A-V block
– ***bupivacaine is selectively cardiotoxic; effect
magnified in the parturient***
20% intralipid
• A modality for the treatment of
bupivacaine-induced cardiotoxicity/CV
collapse
– Lipids accelerate the removal of the local from
the circulation
'RVHĺPONJLQIXVHGRYHUWKHst
minute while continuing CPR
– Repeat every 3-5 minutes to a maximum of 3
ml/kg
– Continuous infusion of 0.25 ml/kg/min until
hemodynamic recovery
Dosage limits for ester LA

based on patient weight of 70 kg
• procaine 1000 mg
• chloroprocaine 800/(1000) mg
• benzocaine 200 mg
• cocaine 200 mg
• tetracaine 200 mg *For
infiltration,
epidural, or
peripheral
**remember the “200 or 800 rule” blocks
Dosage limits for amide LA*
plain/(with epi)
• lidocaine 300/(500) mg
– 4-5 mg/kg (plain)
– 7 mg/kg (with epinephrine)
• bupivacaine 175/(225) mg
– 2.5 mg/kg (plain)
– 3.5 mg/kg (with epinephrine)
• ropivacaine 300 mg *For
infiltration,
• prilocaine 400/(600) mg epidural,

or
peripheral
• mepivacaine 300/(500) mg blocks
Ion trapping
• noted with the use of paracervical blocks
• local crosses the placenta and becomes
more ionized in the relatively acidemic
fetus
• essentially becomes “trapped” in fetal
tissues; may cause systemic toxicity in the
fetus
Ion trapping, cont’d

• less likely to occur with
– highly protein bound locals which diffuse
slowly across the placenta
– ester locals—rapid hydrolysis responsible for
smaller quantity of drug able to cross the
placenta
• seen chiefly with the use of mepivacaine,
prilocaine (amide locals which are not
highly protein bound)
miscellany
• locals (especially lidocaine) will blunt the hypoxic
drive at doses significantly below analgesic
doses—use cautiously in COPDers
• “carbonation” of local (addition of NaHCO3 to
LA) will raise the pH of the solution; speeds
onset of block because more of the LA exists in
the unionized form (A.K.A. buffering)
– lidocaineÖ1mEq/10 ml of local
– bupivacaineÖ0.1mEq/20 ml of local (will PPT
with higher volume of bicarb)
• Lidocaine has two active metabolites:
– MEGX - monoethylglycinexylidide
– GX - glycinexylidide
Miscellany, cont’d
• EMLA
– a topical cream
– a eutectic mixture of lidocaine and prilocaine
– 5% EMLA cream topically applied for 45
minutes or more greatly reduces the pain
associated with venipuncture in the pediatric
population
– methemoglobinemia possible but rare
• Methemoglobinemia a concern in GI suites or
during AFI 2º the overuse of topical sprays (i.e.
cetacaine)
Notes
Anesthetic Agents
Minimum Alveolar
Concentration (A.K.A. “MAC”)
• that percentage of anesthetic agent which

obliterates movement in response to
noxious stimuli in 50% of subjects
• each anesthetic agent has its own MAC
MACs of Anesthetic Agents
• isoflurane (Forane) 1.15%

• sevoflurane (Ultane) 1.71%
• desflurane (Suprane) 4.58-6.3%
• N2O 104%
Factors Affecting MAC
• increase in MAC (pt requires more anesthetic
agent)
– hyperthermia
– hypernatremia
– chronic ETOH ingestion
– pts with red hair
– drug-induced elevations in central catecholamines
(produced with the use of MAO inhibitors, tricyclic
amines)
– 1-6 months of age, except with sevoflurane (1-2
months of age)
Decreases in MAC
• hypothermia • acute ETOH
• hyponatremia ingestion
• pregnancy • anemia
• lithium • increasing age
• lidocaine • use of pre-op meds
• neuraxial opioids • drug-induced
• PaO2 < 38 mmHg decreases in central
catecholamines
• SBP < 40 mmHg (antipsychotics)
• alpha-2 agonists
• CPB
No Change in MAC
• duration of anesthesia
• hyper or hypokalemia
• anesthetic metabolism
• thyroid gland dysfunction
• gender
• PaCO2 15-95 mmHg
• PaO2 > 38 mmHg
• SBP > 40 mmHg
MAC Awake
• that percentage of volatile anesthetic at

which 50% of patients respond
appropriately
• approximately 1/3rd of the MAC value for

the volatile anesthetics; N2O 60%
MAC BAR
• The minimum alveolar concentration of an
anesthetic which will Blunt Autonomic
Responses to surgical or other noxious
stimuli
• Typically thought to be ~ 1.3 MAC;
addition of N2O or opioids reduces this
value significantly
Ostwald Solubility Coefficients
• Any liquid/gas ratios in which

gas is the denominator
• Used to predict the
pharmacokinetic profile of an
anesthetic
Blood-Gas Solubility
• describes how soluble an anesthetic agent
is in the blood
• inversely related to induction time of the
anesthetic agent
**The less soluble an agent is in the blood,
the more quickly it will induce anesthesia
via inhalation
Blood-Gas Solubilities
–desflurane 0.42
–N2O 0.47
–sevoflurane 0.69
–isoflurane 1.4
FA/FI of Anesthetic Agents

Determinants of FA/FI
• FI determined by:
– fresh gas flow
– circuit volume
– circuit absorption (loss) of agent
• FA determined by:
– uptake (loss) of agent
– ventilation
– concentration effect
– second gas effect
Factors affecting FI
• Ventilatory
– Need increased minute ventilation
– Need increased flows from the anesthesia machine
– Need higher concentration of the anesthetic agent
(called “overpressure”) exercises the concentration
effect
• Remember--the speed of induction is dependent upon the

speed at which FA (alveolar [ ]) approaches FI (inspired [ ])
The Concentration Effect

• The higher the inspired concentration of
an anesthetic agent, the more rapid the
relative rise in alveolar concentration of
that agent
The anesthetic follows its concentration
gradient from machine to alveoli to blood
to brain
Uptake (A.K.A.”Loss”)
Alveolar to venous
B:G difference in agent
solubility partial pressure
coefficient
Into the blood Flow Barometric

(CO) pressure
(760
mmHg)
Factors affecting FA
• The Second Gas Effect: the ability of the large

volume uptake of one gas (first gas) to
accelerate the rate of rise of alveolar partial
pressure of a co-administered second gas.
– exercises the concentration effect
***N2O is used as the first gas

(more applicable to agents with higher B:G solubilities)
Factors affecting speed of

inhalation induction
• cardiac output—directly related to agent
uptake into the blood
Higher cardiac output correlates with greater

uptake into the blood; results in slower
(inhalation) induction time
inhalation induction, cont’d
• Functional Residual Capacity (FRC)
– the amount of air left in the lungs at the end of a normal expiration
• increased FRC (emphysema) = slower

• decreased FRC (pregnancy, neonates,

large abdominal tumors) = quicker

inhalation induction, cont’d
• intracardiac shunts
– L Ö R shunt = little effect on induction time
– R Ö L shunt (cyanotic lesions) = slower

(inhalation) induction time (blood bypasses lungs
therefore less agent is picked up)
Oil/Gas Solubility
• reflects how soluble the agent is in the
lipid bilayer
• generally speaking, the more lipid soluble
an agent is, the less polar it is
• the importance of polarity of anesthetics

found in 1899 by Meyer and Overton;
known as the Meyer-Overton theory
Oil/Gas solubility is inversely
related to MAC
**The higher the oil/gas solubility,

the more potent the agent,
therefore, the lower the MAC
Oil/Gas Solubilities
• N2O 1.4
• desflurane 19
• sevoflurane 55
• isoflurane 91
Tissue/Gas Solubility
• this ratio is concerned with the lean
tissue’s (i.e. skeletal muscle) affinity for a
given anesthetic agent
• it predicts emergence times from
anesthesia
lower tissue/gas ratios indicate that the
gas is relatively insoluble in tissues thus
emergence will be more rapid
Tissue/Gas Solubilities
• N2O 1.22
• desflurane 35
• sevoflurane 99
• isoflurane 110
Diffusion Hypoxia
• occurs after the use of N2O
– when discontinued , insoluble N2O diffuses rapidly out
of the tissues, into the blood, and into the alveoli
– the rapid movement of N2O into the alveoli dilutes
existing alveolar gas, thereby displacing O2 and
causing hypoxia
**Dilution of alveolar gas may also cause a dilutional

hypocarbia; net result Ö hypoventilation
Stages of General Anesthesia
• historically noted with the use of ether
• A.K.A. Guedel’s eye signs
Stage I
• amnesia
– begins with the induction of anesthesia
– ends with loss of consciousness (loss of

eyelid reflex)
– pain perception threshold not lowered

Stage II
• delirium/excitement
– characterized by uninhibited excitation
– pupils are dilated, gaze is divergent
– potentially dangerous responses to noxious

stimuli can occur during this stage
Stage III
• surgical anesthesia
– characterized by central gaze with pupillary
constriction
– respirations are regular
– depth of anesthesia is sufficient when noxious
stimuli fails to produce untoward sympathetic
response or somatic reflexes
Stage IV
• anesthetic overdose
– onset of apnea
– pupils are dilated and non-reactive
– hypotension leads to complete CV collapse if
left unchecked
– commonly referred to as “too deep”
Comparative
Pharmacology of the
Inhaled Anesthetics
CNS Effects
• agents do not cause permanent memory
loss or impairment of cognitive function
• EEG activity and CMRO2 are both

decreased at approximately 0.4 MAC by
all agents
– sevoflurane may cause an Ç in EEG activity
CNS Effects, cont’d

• all agents produce dose-dependent
increases in CBF with concomitant
increase in ICP
• this effect may be offset by
hyperventilation; responsiveness of
cerebral vasculature to changes in PaCO2
is unchanged by volatile agents
• N2O also increases CBF but may actually
increase CMRO2 as well
• autoregulation of CBF is best preserved
with isoflurane
• isoflurane may actually provide cerebral
protection in face of transient ischemic
events
• may ultimately produce an isoelectric EEG

• desflurane may impair cerebral
autoregulation at clinical concentrations
(>0.5 MAC) (Anesth Analg 2000; 91:152-5)
• EEG stimulation
– sevoflurane > isoflurane > desflurane
@ 2 MAC @ 12 MAC
CV Effects
• CO, BP, SVR all decreased, HR increased
during spontaneous ventilation
• effects magnified in pts with pre-existing
cardiac disease
• concomitant use of cardio/vasoactive
drugs may magnify depressant effects
CV Effects, cont’d
• may be due to:
– direct myocardial depression
– inhibition of CNS outflow
– peripheral autonomic ganglion blockade
– attenuated carotid sinus activity
– decreased formation of cyclic AMP
– decreased release of catechols from the adrenal
medulla
– decreased influx of Ca++ ions from cardiac slow
channels
– depressant effects on the SA node and the
conduction system
Blood Pressure and SVR

• all volatiles produce dose-dependent
decreases in BP
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• isoflurane > desflurane > sevoflurane
• N2O does not cause BP decrease when

administered alone
– N2O produces cutaneous vasoconstriction
and an overall increase in SVR
Cardiac Output and Index

• CO and CI are only modestly diminished with the
use of isoflurane, desflurane and sevoflurane in
appropriate anesthetic dosages
– decreases ultimately noted in a dose-dependent
fashion
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– noted least with sevoflurane
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maintain CI somewhat; baroreceptors are preserved
• N2O causes an increase in CO when
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SVR
Heart Rate
• difficult to quantify secondary to many
confounding factors
• HR increased most with the use of
desflurane, closely followed by isoflurane
– baroceptors preserved
– from possible intrinsic beta adrenergic activity
– effect attenuated by administration of fentanyl
– cardiac stimulation:
• desflurane > isoflurane > sevoflurane
@ 6 – 9%
Coronary Blood Flow

• isoflurane is the most potent coronary
vasodilator
– historically implicated in causing a “steal”
phenomenon
• later shown that individual needed “steal-prone
anatomy” for this to occur; only found in
approximately 9% of the general population
• desflurane does not cause steal in the
canine model
Cardiac preconditioning
• All potent anesthetics noted to have a
protective effect on the myocardium
– when administered prior to an ischemic
cardiac event (i.e. hypoxia, coronary
occlusion), they afford protection against
myocardial injury
• evidenced by stable troponin levels post-insult
• desflurane > isoflurane > sevoflurane
Dysrhythmias
• Isoflurane, desflurane, sevoflurane do not
sensitize the myocardium to the effects of
endogenous and exogenous epinephrine
to the extent that the older agents did
• Dose limit for exogenous epinephrine is

6 mcg/kg
for isoflurane, desflurane and sevoflurane
Pulmonary Vascular Resistance

• N2O causes a modest increase in PVR in
the normal pt; increases may be clinically
significant in the pt with pre-existing
pulmonary HTN
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• Volatile agents decrease PVR
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Hypoxic Pulmonary
Vasoconstriction
• the ability of the pulmonary vasculature to
constrict in response to regional
hypoxemia, resulting in a more optimal
ventilation/perfusion match
– all of the volatile agents only mildly attenuate
HPV
• shown to only modestly reduce oxygenation, even
at 1 MAC
– N2O markedly attenuates HPV
Ventilatory Effects
• all volatiles produce dose-dependent
increases in the frequency of breathing
• all volatiles produce concomitant
decreases in VT
• overall effect is a decrease in minute
ventilation and increase on PaCO2 from
markedly reduced tidal volumes
Response to CO2 and Hypoxemia

• all volatiles produce a dose dependent
depression of the ventilatory response to CO2
– ventilatory depression from
• depression of medullary ventilatory center
• selective weakening of intercostal muscles
• all agents, including N2O, profoundly depress
the ventilatory response to hypoxemia
***1.1 MAC produces 100% suppression of the
carotid body response to hypoxemia
Bronchodilation
• the volatile agents all produce

bronchodilation; sevoflurane is the most
effective of the newer agents
– desflurane appears to cause less

bronchodilation than sevoflurane and may
actually cause bronchoconstriction in smokers
(Anesthesiology 2000; 93:404-8)
Airway Resistance and Irritation
• Increases in airway resistance with the use of desflurane
may be secondary to increased vapor density within the
airways 2° higher concentrations of desflurane
necessary to achieve anesthetic concentrations
• Irritation
– desflurane > isoflurane > sevoflurane
@ 6-9% @1.8-2.2% @ 6-8%
just > 1 MAC > 1.5 MAC > 4 MAC
± ,UULWDWLRQĻ ZLWK
• Ĺ hours of anesthesia
• Ĺ age
• opioid administration
• absence of smoking
Hepatic Effects
• hepatic blood flow and O2 delivery is best
preserved with the use of isoflurane
• all volatiles interfere with hepatic drug
clearance from
– reduction of hepatic blood flow
– suppression of metabolizing enzymes
• although the least metabolized, desflurane
has been implicated in causing a
hepatotoxicity resembling halothane
hepatitis
Renal Effects
• all volatile agents produce similar
reductions in renal blood flow, GFR, and
U/O (Important to maintain intraoperative U/O
@ at least 0.5 cc/Kg/hr)
– desflurane noted to cause the least renal impairment
of the volatile agents
• BUN remains stable
• little to no production of inorganic fluoride ion (Fl-)
• fluoride-induced nephrotoxicity occurs at

ȝPROUHVXOWVLQDSRO\XULF UHQDO
insufficiency
Renal Effects, cont’d
• fluoride ion production noted from the
metabolism of sevoflurane
• pentafluoroisopropenyl fluoromethyl ether

(A.K.A. Compound A), a vinyl ether, is formed
when sevoflurane interacts with soda lime in a
closed anesthesia circuit (it is a degradation product of the
CO2 absorber, not a metabolite of biotransformation of sevoflurane)
Compound A
• higher [ ] of sevoflurane = higher [ ] of
Compound A
• FGF rate must equal or exceed 2l/minute when

using a semi-closed circuit to prevent buildup
(newer reports study use of lower FGFs with no
untoward effects)
Compound A, cont’d
• higher expired CO2 = higher temperature
in absorber = higher production of
Compound A
• peak [ ] of Compound A @ 2 anesthetic
hours, relatively constant thereafter
***Compound A has been shown to be
nephrotoxic in rats; studies to date do not
support this finding in humans
Other by-products
• Desflurane may be degraded to CO in
desiccated sodalime
– usually occurs on Monday AM, 1st case of the day
– leads to carboxyhemoglobinemia
• may potentially occur with all methyl ethyl ethers
– isoflurane > sevoflurane
• Sevoflurane degraded to hydrogen fluoride by
Lewis acid-mediated reaction; acids etch glass
containers and corrode vaporizers
– reaction is inhibited by the addition of H2O to
sevoflurane
Canister fires
• Rare reports emerging re: extreme
heat/fire occurring in the CO2 absorbent
canister
• common elements of occurrence
– use of Baralyme (no longer available)
– presence of desiccated soda lime
• color change does not occur as a result of
desiccation
– use of sevoflurane
• lack of correlation between vaporizer setting and FI
of sevo may be associated with excessive heating
of the CO2 absorber (FI exceeds ET [ ])
Canister fires, cont’d

– typically noted the 1st case of the day
– byproducts of sevoflurane degradation include
methanol, formaldehyde and CO, all of which
are potentially combustible
– important to discontinue FGF when machine
is not in use, even between cases, to limit
desiccation of soda lime
– periodic monitoring of canister temperature
may be warranted
Skeletal Muscle Effects
• all volatiles except N2O produce skeletal
muscle relaxation and enhancement of
NDNM blockade
– sevoflurane > isoflurane; desflurane has been
shown to be equal to both in different studies
• all volatiles except N2O may trigger
Malignant Hyperthermia; none to the
extent that halothane does
Obstetric Effects
• volatile anesthetics produce similar and
dose dependent decreases in uterine
blood flow and tone
– significant at > than 1 MAC
• N2O does not affect uterine contractility
• all volatile agents rapidly cross the
placenta
Metabolism (A.K.A. Biotransformation)

• volatiles are metabolized to varying degrees
via hepatic microsomal enzymes; N2O is
metabolized by anaerobic bacteria in the
bowel
– N2O 0.004%
– desflurane <0.1%
– isoflurane 0.2%
– sevoflurane 2-3%
Nitrous oxide (N2O)
• Produces significant analgesia

• Produces minimal muscle relaxation
– does not potentiate NMBDs
• The only inhalational anesthetic to
increase pulmonary vascular resistance
• Activates the SNS
• Does not trigger MH
N2O, cont’d
• Is 34X more soluble in the blood than
nitrogen
– Diffuses into air-filled spaces
• body cavities:
– inner ear
– bowels
– pulmonary cysts, blebs, bulla
– will expand pneumothorax
– will expand air embolism
– will expand ETT, LMA cuffs
N2O, cont’d
• Contraindicated for use in pregnancy
– may increase incidence of SAB
– interferes with synthesis of methionine synthase
(forms myelin) and thymidylate synthase (forms
DNA)
• Contraindicated for use in immunosuppressed
– causes megaloblastic changes, agranulocytosis
– impedes hematopoiesis
• Overuse may lead to peripheral neuropathy
Miscellany
• “phases” of GA
– I Ö induction
– II Ö maintenance
– III Ö emergence
• halogenation decreases an agent’s
flammability and enhances chemical
stability of an agent
Notes
Notes
Pharmacokinetics & Dynamics;
Fluid Replacement
Pharmacokinetics
• Zero order elimination
– Constant amount of drug is eliminated per unit time
– Implies saturation of metabolic pathway
– Occurs with several important drugs: ethanol,
phenytoin, salicylates, theophylline, high dose
thiopental
Pharmacokinetics Cont'
• First order kinetics
– Constant fraction of drug is eliminated per unit time
– The rate of elimination is proportional to the amount of
drug in body
– The vast majority of drugs are eliminated this way
Triexponential Decay Curve
58
• First order kinetics terms
– Volume of distribution (Vd) – amount of drug in the
body divided by the concentration in the blood
Large volumes of distribution imply lipid solubility
Small volumes of distribution imply lipid insolubility
Usually expressed in Liters/Kg
– Clearance (Cl) – the volume of plasma from which
the drug is completely removed per unit time
– Elimination half-life (T1/2ȕ) – the time taken for
plasma concentration to reduce by 50%
After 4 half-lives, elimination is 94% complete
• Relationship of Cl, Vd and T1/2ȕ
– A relationship exists between the rate of clearance,
the amount of volume of plasma that needs to be
cleared, and the half-life
T1/2ȕ = ln(2) x Vd / Cl
T1/2ȕ = 0.693 x Vd / Cl
– If the clearance is increased, the half-life is reduced
– If the volume of distribution is increased, the half-life
is increased
• Multicompartment model
– Distribution of lipid soluble drugs follows the
blood flow
• Organs receiving the majority of the cardiac output
receive the most drug during initial distribution –
vessel rich group
• Later, other tissues take up drug and redistribute
the drug from the vessel rich group
• Finally, after full redistribution, the plasma level fall
as a result of elimination
59
• Distribution and elimination half lives
• Context-sensitive half-times
– Time and dose dependent half-times
– As total amount of drug increases, duration of action
increases
e.g. fentanyl
T1/2ʌ – 2 mins
T1/2Į – 12 mins
T1/2ȕ – 240 mins
– Fentanyl given at 2 mcg/kg has a duration of action of
8 – 10 min
– Fentanyl given at 10 mcg/kg has a duration of action
of 60 min
– Fentanyl given at 50 mcg/kg has a duration of action
of 16 hrs
– The context-sensitive half time of low dose fentanyl is
2 min
• Protein binding
– Most drugs bind to proteins to some extent
– Albumin, alpha-1 acid glycoprotein & transcortin are
the most common proteins that drugs bind to
– Highly bound drugs have a lower Vd and low Cl
– Drugs can compete with protein binding sites
– Important drugs that are highly protein bound:
coumadin, diazepam, propranolol & phenytoin
– Competition for binding site can significantly affect
free drug levels:
e.g. Patient on coumadin is given phenytoin.
Coumadin with 97% binding suddenly frees another
3% from displacement by phenytoin. This doubles
free coumadin level and raises INR
60
Pharmacodynamics
• A drug’s ability to change physiological,
bio-chemical or pathological processes is
called its mechanism of action
• Most drugs work by activation or inhibition
of a receptor
• Maximum effect does not always require
occupation of all receptors
Pharmacodynamics Cont'
Types of antagonism
Competitive reversible -
Types of antagonism Cont'
Competitive Irreversible -
61
Types of antagonism Cont'
Noncompetitive antagonism – changing levels of agonist
have no effect at all at any point of therapy
Notes
Notes
62
Fluid Management
Body Fluid Compartments

• Total body water (TBW) is 50 – 60% of
weight
• Total body water is divided into 2
compartments:
1. Intracellular – 2/3 of TBW
2. Extracellular (ECF) – 1/3 of TBW
a. Interstitial – 2/3 of ECF
b. Intravascular – 1/3 of ECF
Body Fluid Compartments
63
Hydrostatic/osmotic pressures
Basics of Fluid Therapy

• Basal adult fluid requirements
3000 cc / day or 125 cc / hour
• Exposed viscera: 7–10 cc / kg / hour
• Infants and children
4 cc / kg / hour for first 10 kilograms
2 cc / kg / hour for second 10 kilograms
1 cc / kg / hour for subsequent weight
– Ex: 25 kg child
4 x 10 = 40 cc / hour +
2 x 10 = 20 cc / hour +
1 x 5 = 5 cc/ hour = 65 cc hour
Basics of Fluid Therapy Cont'

• Serum osmolality
– Normal = 285 – 295 mos / Liter
• Dehydration will cause the loss of free
water and increased osmolality
• Acute blood loss does not alter osmolality
• Calculation of osmolality
– Osmolality = (2 x (Na + K)) + (BUN / 2.8) + (glu / 18)
• Osmolality of intravenous fluids:
Hypotonic < 260 – 340 > Hypertonic
Isotonic
64
IV Fluids
Solution Tonicity Na+ K+ Ca ++ Cl- Glucose
mEq/L mEq/L mEq/L mEq/L gm/L
D5W 253 (-) 0 0 0 0 50
NS 308 (0) 154 0 0 154 0
D5 1/4NS 330 (0) 38.5 0 0 38.5 50
D5 1/2NS 432 (+) 77 0 0 77 50
D5 NS 561 (+) 154 0 0 154 50
LR 273 (0) 130 4 3 109 0
D5 LR 525 (+) 130 4 3 109 50
Plasmalyte 294 (0) 140 5 0 98 0
Basics of Fluid Therapy

• Available crystalloid replacements
– Normal Saline
• osmolality = 308 = (Na+)154 + (Cl-)154
• largely confined to extracellular fluid (ECF)
• about 1/3 of fluid remains intravascular, remainder
is distributed to ECF

• Available crystalloid replacements cont'
– Ringer’s Lactate
• Osmolality = 274 = (Na+) 130 + (K+) 4.0 + (Ca++)
2.7 + (Cl-) 109 + (lactate) 28
• Lactate added to offset negative charges from
plasma proteins
• Similar distribution of fluid as with NS
65
• Available crystalloid replacements cont'
– D5W
• Osmolality = 253
• Dextrose is rapidly metabolized
• Delivers free water which is distributed throughout
total body water
• Only about 15% remains in the intravascular space

• Osmolalities are additive
– D5 NS = 253 + 308 = 561
– D5 0.2 NS = 253 + 308/4 = 330
• Selection of crystalloid replacement
– Based on patient needs:
• Free water – D5W, D50.2NS
• Intravascular replacement – Ringer’s

• Available colloid solutions
– Plasma protein derivatives
• Albumin and plasma protein fraction
– Synthetic colloids
• Hetastarch, dextran
• Uses
– Used to keep a larger fraction of fluid in the
intravascular space
– Effective when a rapid Ç in intravascular
volume is needed
66
• Albumin
– Available as 5% and 25%
– In absence of capillary leak, may mobilize
extracellular fluid to the intravascular space
– Expensive
– Carries little risk of transmitting viral disease
• Heated to 60ºC for at least 10 min to minimize the
risk of transmitting viral diseases

• Hetastarch
– Available as a 6% solution
– Average molecular weight - 450,000 daltons
– Nonantigenic; anaphylaxis very rare
– May cause platelet dysfunction at doses > 15 ml/kg
– Relatively contraindicated in renal transplant pts as
small amounts may be filtered and alter tubular
function
– 2 forms available
• Hespan
• Hextend-Contains additional sugar and Ca 2+; may
cause less inhibition of platelets

• Dextran
– Two different molecular weights available
• Dextran 70
– Has significant antiplatelet function and may
interfere with blood typing
• Dextran 40
– Used to improve microcirculation by reducing
blood viscosity
– Inhibits platelets and interferes with blood
typing
• Both dextrans are antigenic and have been
associated with severe anaphylactic and
anaphylactoid reactions
– Dextran 1 acts as a hapten to bind circulating
Dextran antibodies; reduces incidence of
allergic reactions
67
Cardiovascular Review
The Cardiac Cycle
Normal Cardiac Pressure-Volume Loop

Hemodynamic Monitoring
• Central Venous Pressure
– a wave Ö rise in pressure due to atrial contraction
• a waves are larger in the presence of any resistance
to RV filling, (tricuspid stenosis, RV failure, cardiac
tamponade); these cause an increase pressure as the
atrium attempts to contract and eject blood
• c wave Ö rise in pressure due to ventricular
contraction and bulging of the closed tricuspid valve
• v wave Ö rise in pressure during atrial filling
Hemodynamic Monitoring Cont'
– x descent Ö fall in pressure due to atrial relaxation

– y descent Ö fall in pressure due to the opening of the
tricuspid valve and the beginning of ventricular filling
Normal intracardiac pressures

Cardiac Formulas
• Body Surface Area =
• Cardiac Index = CO / BSA Normal = 2.2 – 4.2
• Stroke Volume = CO x 1000 Normal = 60 – 90
Rate
• Stroke Index = SV / BSA Normal = 20 – 65
• SVR = (MAP – CVP) x 80 Normal = 1200 – 1500
CO
• PVR = Mean PA – PCWP x 80 Normal = 100 – 300
CO
• LVSWI = .0136(MAP – PCWP) x SI Normal = 46 - 60
Mechanisms of Arrhythmias
• Reentry accounts for most premature
beats and tachyarrhythmias
• Reentry requires two pathways:

– Antegrade pathway
– Retrograde pathway where antegrade conduction is
blocked
• Automatic Dysrhythmias
– Refers to the slope of phase 4 depolarization
– Increased slope causes increased rate and
ventricular irritability
Events that Alter Phase 4 Slope

• Increased slope:
Hypoxemia
Hypercarbia
Hypokalemia
Hyperthermia
Sympathomimetic drugs
Systemic hypertension
• Decreased slope:
Vagal stimulation
Positive airway pressure
Hyperkalemia
Hypothermia
Normal ECG Intervals
• PR interval – 0.12 to 0.20 seconds
• QRS complex – 0.05 to 0.12 seconds
• QT interval – normally less than one-half

of the preceding RR interval
Arrhythmias
• Atrial Fibrillation
– Most common sustained dysrhythmia – 0.4% of
population
– Incidence increases with age – 10% if over 80
– Result of multiple intra-atrial reentry pathways
– ECG shows chaotic atrial rhythm often with a rate >
400/min
giving rise to irregular input to the AV node and an
irregular heart rate
– Symptoms vary from none to angina and CHF
– Will decrease CO approximately 25%
– Treatment: cardioversion is the most effective
treatment, amiodarone and sotalol
Arrhythmias Cont'
• Supraventricular Tachycardia
– Any tachyarrhythmia requiring atrial or AV junctional
tissue for its initiation and maintenance
– PAT – term no longer recommended since most
arise in AV node
– Usually a reentrant rhythm
– 3 times more frequent in women
– Rates of 160 – 180/min common
– Treatment: adenosine, calcium channel blockers
Arrhythmias Cont'
• Atrial Flutter
– Paroxysmal arrhythmia that usually converts
spontaneously
– Atrial rates of 250 – 300/min common
– Regular ventricular rhythm common with varying
degrees of block
– Seen most commonly in patients with pulmonary
disease, cardiomyopathy, ETOH intoxication, and
thoracic surgery
– Treatment of choice is cardioversion
Arrhythmias Cont'
• Classification of Heart Block
– First Degree – PR interval greater than 0.2 seconds
– Mobitz Type 1 (Wenckebach) or second degree block

type 1
• Progressive prolongation of the PR interval until a beat is
entirely blocked. Reflects disease in the AV node
Arrhythmias Cont'
• Classification of heart block, Cont'
– Mobitz Type 2 or second degree block type 2
– PR interval remains unchanged but
periodic blocked beat occurs
– Reflects disease in His-Purkinje system
– More serious than type 1 and will not respond to
atropine
Arrhythmias Cont'
– Classification of Heart Block Cont’
– Third-degree block
– Complete absence of conduction from the atria to the
ventricles. Will not respond to atropine and requires
pacing
Arrhythmias Cont'
• Classification of Heart Block Cont’
• Ventricular Tachycardia
– 3 or more consecutive PVC’s at a calculated rate of
more than 120/min
– Treatment: cardioversion
Arrhythmias Cont'
• Ventricular Fibrillation
– Chaotic asynchronous contraction of the ventricles
with no visible QRS complexes and no associated
cardiac output
– Often preceded by v-tach
– Most common cause of sudden death
– Treatment: immediate defibrillation
Arrhythmias Cont'
• Torsades de pointes
– Ventricular arrhythmia associated with sudden deaths
– Associated with a prolonged Q-T interval usually > 600
ms
– Most commonly a result of inherited prolonged Q-T
syndrome
– May also be drug induced: droperidol implicated
– Usual antiarrhythmic agents will worsen Torsades
Intravenous magnesium treatment of choice
Cardiac anatomy
1) Right atrium 14) Pulmonary trunk
2) Right ventricle 15) L pulmonary artery
3) Left atrium 16) R pulmonary artery
4) Left ventricle 17) L pulmonic veins
5) Tricuspid valve 18) R pulmonic veins
6) Pulmonic valve 19) Chordae tendinae
7) Aortic valve 20) Papillary muscles
8) Mitral valve 21) ligamentum arteriosum
9) Superior vena cava 22) R brachiocephalic
10) Inferior vena cava 23) L common carotid
11) Ascending aorta 24) L subclavian
12) Aortic arch 25) Septum
13) Descending aorta
Coronary Circulation
• Anatomy
– Myocardial blood supply entirely from right and left
coronaries
– Blood flow is epicardial to endocardial
– Majority of venous return is to the right atrium via the
coronary sinus
– Small amount of venous return can enter the cardiac
chambers directly through the Thebesian veins –
causes a small shunt
– The RCA:
• supplies the RA, RV, some LV, SA node (60%) &
AV node
• the RCA usually gives rise to the PDA supplying a
small part of
the septum and inferior wall – this is a “right
dominant” circulation
Coronary Circulation Cont
– The LCA:
• Supplies the LA, LV and most of the septum
• The LCA splits into the LAD and circumflex (CX)
arteries
• The LAD supplies the anterior wall, septum & SA
node (40%)
• The CX supplies the lateral wall
Coronary Circulation Cont'

• Physiology
– Coronary flow is about 250 ml/min and intermittent
– Force of LV contraction occludes myocardial
perfusion
• LV perfused almost entirely during diastole
• CPP = diastolic pressure – LVEDP
– Endocardium sees highest pressures and most
vulnerable to ischemia
– Coronary flow is regulated largely by metabolic
demand although alpha and beta receptors present
Coronary Circulation Cont'
• Myocardial oxygen balance
– High level of oxygen extraction (65%) as compared to
usual (25%)
– Saturation of coronary sinus blood about 30%
**Factors affecting oxygen demand: basal

requirements, rate, wall tension, contractility
Ischemic Heart Disease

• Estimated to be 30% of surgical patients
• Angina
– Angina reflects intracardiac release of adenosine
– Diagnosis:
• History
• ECG – greater than a 1mm ST segment
depression
• ECHO
• Nuclear stress Imaging
• Coronary angiography
– Treatment
• CABG for left main or 3-vessel obstruction
• Antiplatelet/antithrombin drugs, E-blockers, Ca++
channel blockers, organic nitrates
Ischemic Heart Disease Cont'

• Acute Myocardial Infarction
– Acute Coronary Artery Syndrome – a
hypercoagulable state
• Plaque rupture causes local coagulation
– Atherosclerosis may be an inflammatory disease
– Diagnosis – requires at least 2 of 3 criteria
• History of angina
• Serial ECG changes indicative of infarction
• Rise and fall of cardiac enzyme markers
– Treatment
• Acutely with oxygen, nitrates, aspirin
High flow oxygen may be associated with
increased infarct size
• Reperfusion therapy – angioplasty, stenting, IIb/IIIa
inhibitors CABG
• Medical therapy – E-blockers, ACE inhibitors,
antiarrhythmics, nitrates, heparin
ECG Changes with MI

• Acute MI associated with ST elevation
– This is a current of injury from leakage of ions
– Reciprocal ST segment depression may occur
• Q-waves appear with evolution of MI
– Q-waves a later finding
– Result from an “electrical window”

Complications of Ischemia and Infarction
– Ventricular fibrillation/tachycardia – 3 to 5% of
infarcts
• Peak incidence – 4 hours after infarction
– A-fib – 10% of infarcts
– Heart block and bradydysrhythmias – 20% of inferior
infarcts
– Pericarditis (Dressler’s Syndrome) – 3% of patients
– Mitral regurgitation – from injury to papillary muscles
with inferior infarct
– CHF
Ischemic Heart Disease cont
• Preop
– Delay surgery??? May no longer be indicated
– E-blocker therapy
– Nitrate therapy
– Monitor leads II, V5
– ST trend analysis
– Art-line, central pressure monitoring, ECHO
• Intraop
– Induction – heart rate control is most important
(<90)
– Tachycardia, hypovolemia, anemia (<28%) can
cause ischemia
– No agent or technique proven superior
– Minimize stress response at time of extubation
– Anticipate and treat post-op pain
Systemic Hypertension
• Blood pressure > 140/90 on 2 or more
occasions at least 1 week apart
• Most common circulatory disease in US
affecting 24% of adults
• Significant risk factor for:
– CAD, CVA, CHF, aneurysms, renal disease
• Essential hypertension – no cause can be
found – 95% of cases
Hypertension Cont'
• Treatment
– Diuretics
± ȕEORFNHUV
– Calcium channel blockers
– ACE inhibitors, ARBs
± Į EORFNHUV
Hypertension Cont'
• Secondary hypertension causes:
– Renovascular
– Hyperaldosteronism
– Pheochromocytoma
– Cushing’s syndrome
– Increased ICP
– Drugs – glucocorticoids, mineralocorticoids,
cyclosporine, MAO inhibitors, nasal decongestants
– Thyrotoxicosis
– Hyperparathyroidism
• Treatment is aimed at source of secondary
hypertension
Hypertension Cont'
• Anesthetic considerations
– Preop evaluation
• Determine adequacy of control – diastolic < 110
• Expect blood pressure fluctuations
• Assess end-organ damage – LVH, CAD/angina,
PVD, renal insufficiency
• Check cardiac function – ECG, stress testing,
ECHO, CXR, cardiac cath
Hypertension Cont'
• Treatment pharmacology: ACE inhibitors,
angiotensin II antagonists, diuretics, beta-blockers,
calcium channel blockers, alpha-blockers
• ACE inhibitors associated with episodes of severe
hypotension
– Should be held the day of surgery
• Continue antihypertensive meds
• Consider art line, monitors of volume status
Hypertension Cont'
• Intraop
– Requires careful volume control
– Expect labile blood pressure
– Consider E-blockade, lidocaine pre-laryngoscopy;
avoid tachycardia
– No technique advantageous over another
– Nitroprusside for severe intraop HTN
– Provide analgesia prior to end of anesthetic
– Additional BP control at time of extubation
• Post-op
– Promptly resume BP meds
– Adequate pain management
Congestive Heart Failure
• Alternate Terms:
– Preload – LVEDV, LVEDP, LAP, PCWP, PAOP
– Work - LV stroke work, cardiac output, blood pressure
Congestive Heart Failure Cont'

• Normal myocardial function
– As muscle starting length increases, contractility
increases(Starling)
– The most important determinant of contractility is
PRELOAD
– There is an optimum fiber length (A)
A
B
Failing myocardial function
– Lesser increase in contractility for a given preload
(B)

• Compensatory mechanisms
– Increased preload
– Increased sympathetic tone
• Catecholamine levels parallel degree of LV
dysfunction
• Chronically elevated levels cause receptor
downregulation
• Acute decrease in catecholamine levels, e.g.
general anesthesia, can precipitate decompensation
• Activation of renin-angiotensin system
– Causes retention of sodium and water increasing
preload
– Causes vasoconstriction and increased afterload
• Vasopressin levels increased
• Ventricular hypertrophy

• Risk
– Major determinant of perioperative risk
– Single greatest risk factor for cardiac surgery
– Up to 8x greater mortality
– Median survival after diagnosis: Men – 1.7 yrs,
Women – 3.2 yrs
• Types
– Left vs. right
– Systolic vs. diastolic
• NYHA classification
– I Ö No limitation,
– II Ö Slight limitation,
– III Ö Marked limitation,
– IV Ö Unable to carry out any physical activity
• Preop
– Stabilize patient before surgery
– Continue any inotropic support, neseritide
– Consider art-line, central pressure monitor, TEE
• Intraop
– Be aware of possibility of hypovolemia, hyponatremia,
hypokalemia as a result of diuretic therapy
– Avoid anesthetic techniques that depress myocardium
i.e. barbiturates, propofol, volatile agents, meperidine
– Extubation may be hampered by pulmonary insufficiency
• Postop
– Inotropic support may be needed
– Pulmonary edema in as many as 16% of patients
Shock
• Definition – Poor tissue perfusion
• Types
– Hypovolemic
– Cardiogenic – end-stage of CHF regardless of
etiology
– Distributive – septic, anaphylactic, neurogenic
• Pathophysiology
– Vital organ hypoperfusion causing acidosis
– Release of cytokines increases capillary permeability
– Development of ARDS or MODS
– Inability of the heart to pump sufficient quantity of
blood with sufficient pressure to perfuse organs,
despite high cardiac output
Shock Cont'
• Preop
– Remove inciting agent if possible
– Optimize preload and oxygenation
– Monitor to assess preload, SVR, and CO
• Intraop
– Select appropriate inotropic therapy – controversial
– Minimize use of agents with negative inotropic effects
– Aggressive fluid therapy to maintain preload
• Postop
– Consider use of lower tidal volumes with increased
rates
Valvular Heart Disease
Mitral Stenosis
• Result of fusion of mitral leaflets and narrowed
mitral aperture
• Obstructed LV filling Ö increased LA and
pulmonary pressures Ö thrombus formation, a-fib,
pulmonary edema
– Preop:
» Optimize fluid status
» Control ventricular rate, give ventricle time
to fill
» Maintain sinus rhythm
» Assess bleeding risk if patient on coumadin
Valvular Disease Cont‘ (MS)

• Intraop
– Careful ECG monitoring and treatment of atrial
arrhythmias
– Maintain control of ventricular rate
– Maintain preload central pressure monitoring and
TEE can help
– Prevent increases in pulmonary vascular resistance
by avoiding hypoxia, acidosis, hypercarbia, N2O
– Avoid sudden decreases in SVR since CO may be
fixed
• Postop
– Provide adequate analgesia
– Be alert to increased risk of pulmonary edema
Valvular Disease Cont'
• Yellow area represents effects of MS on

Pressure-Volume Loop
• Mitral Regurgitation
– Result of incompetent mitral valve with reverse blood
flow into LA
– Regurgitant fraction > 0.6 is severe
– 2 types
• Acute 2o chordae rupture – poorly tolerated
• Chronic most commonly from rheumatic fever
• Pathophysiology
– Increased LA pressures Ö pulmonary
hypertension/edema Ö RV failure
– Factors affecting regurgitation – rate, SVR, valve
orifice
Valvular Disease Cont‘ (MR)

• Preop
– Continue medications
– Consider antibiotic prophylaxis
• Intraop
– Consider central pressure monitoring and TEE
– Avoid bradycardia, maintain preload, reduce afterload
(“fast, full, vasodilated”)
– Avoid causes of pulmonary vasoconstriction
– Avoid excessive PEEP
– Optimize CO with fluids, vasodilators, inotropes
• Postop
– Pain management is critical
– Continue monitoring and treatment of cardiac output
• Yellow area represents effects of MR on

• Aortic stenosis
– Result of narrow aortic valve orifice
– This limits CO and increases LV work
– Usually the result of congenital bicuspid valve or
rheumatic fever
• Pathophysiology
– Aortic obstruction Ö LV hypertrophy Ö ischemia/CHF
– CO is essentially fixed
• Preop
– Continue meds especially antiarrhythmics
– Antibiotic prophylaxis
Valvular Disease Cont‘ (AS)

• Intraop
– ECG – evaluation of ST segment may be difficult with
LVH
– Central pressure monitoring - less helpful because of
still LV causing pressure swings
– TEE- may differentiate diastolic from systolic failure
– Avoid tachycardia to allow LV to empty
– Maintain adequate filling pressures
• Postop
– Extubation is potential time of ischemia
– Adequate pain control to minimize risk of tachycardia
• Yellow area represents effects of AS on

• Aortic Regurgitation
– Incompetent valve allows backflow of blood into LV
during diastole
• Acute – following dissecting aneurysm, SBE, trauma
– Unprepared LV quickly overloaded
– Immediate AVR usually required
• Chronic- following rheumatic fever, hypertension
– Ventricle has time to accommodate
– Eventual AVR usually required
• Pathophysiology
– Regurgitation Ö volume overload & decreased diastolic
pressure Ö LVH Ö increased oxygen demand with
decreased perfusion
Valvular Disease Cont‘ (AR)

• Preop
– Optimize LV performance with inotropes, vasodilators
– Avoid reduction in diastolic pressure
– Balloon pump contraindicated
• Intraop
– Arterial catheter needed
– Central pressure monitoring and TEE often indicated
– Use induction & maintenance techniques that avoid
bradycardia
– Maintain diastolic pressure
– Bradycardia & increased SVR will increase regurgitation
• Postop
– Hypertrophic LV may require high filling pressures
• Yellow area represents effects of AR on

Flow-Volume Loop Summary
Mitral Stenosis Mitral Regurgitation
Aortic Stenosis Aortic Regurgitation
Cardiomyopathy
• 3 Types
– Dilated – ETOH, ischemic, viral
– Hypertrophic – hypertension, AS, genetic, high-output
syndromes
– Obstructive – formerly known as IHSS
• Dilated cardiomyopathy
– Decreased systolic ejection (decreased EF)
– May have a diastolic component as well
– Associated arrhythmias common
– Intracardiac thrombosis may occur
– Valve regurgitation a possibility
• Anesthetic care
– Same as CHF and/or valvular disease
Cardiomyopathy Cont'
• Hypertrophic & Obstructive
– Dynamic outflow obstruction in 25 - 50% of cases
– Ejection fraction may exceed 80%
– Increased risk of ischemia
– Diastolic dysfunction
– Diagnosis by ECHO
• Preop
– Replace fluid deficits to maintain filling volumes
– Consider beta-blockers, calcium channel blockers
– Sedate to prevent anxiety (provokes sympathetic
stimulation)
Cardiomyopathy Cont'
• Intraop
– Prepare phenylephrine for pressor
– Avoid ketamine
– Avoid prolonged laryngoscopy
– Consider volatile agents that decrease LV function
– Maintain beta-blockade, calcium channel blockade
– Promptly replace fluid/blood loss
– Avoid positive chronotropic/inotropic meds – atropine,
pancuronium
– Cardioversion for a-fib
• Postop
– Adequate pain control
– Maintain adequate hydration
Pacemakers
• 2 parts
– Electrical pulse generator
– 2 electrodes – negative electrode is stimulator (bipolar
vs. unipolar)
• Pacing modes
– Fixed – pacemaker fires at a fixed rate whether there is
native activity or not.
• × risk of v-tach or v-fib
– Synchronous – pacemaker inhibited by native activity
Pacemakers Cont'
• 5-letter pacemaker code
– 1st letter – chamber being paced (Atrium, Ventricle,
Dual)
– 2nd letter – chamber monitored (Atrium, Ventricle,
Dual, O = none)
– 3rd letter – how pacer responds to activity (Triggered,
Inhibited, Dual, O = none)
– 4th letter – programmable functions (P = output only,
M = multiprogrammable, C = communicating, R = rate
modulated, O = none
– 5th letter – type of anti-tachycardia function (P =
pacing, B = bursts, D = dual (pacing and shock), N =
normal, S = scanning or shock, E = external)
Pacemakers Cont'
• Indications for a pacemaker
– Tachy-brady syndrome
– Sick sinus syndrome
– AV conduction defects (Mobitz II or 3rd degree
block)
• may externally pace emergently (i.e. Zoll)
• Factors that alter pacer function
– Electrocautery – can inhibit demand pacers
– Lithotripsy – can inhibit demand pacers
– MRI – can convert into fixed mode
– Electrolyte abnormalities – hypo/hyperkalemia
Pacemakers Cont'
• Electrocautery recommendations
– Consider converting to fixed mode using
• magnet placed externally converts to fixed mode
– Use bipolar cautery if possible
– Place ground pad as far away from generator as
possible
– Use lowest current possible
– Apply cautery in short bursts
Pericardial Tamponade
• Excessive fluid in the pericardial sac
• Pathophysiology
– Increased pericardial pressure Ö increased CVP,
LVEDP Ö Coronary artery compression Ö decreased
perfusion
– Increased pericardial pressure Ö decreased diastolic
filling Ö decreased CO Ö tachycardia, hypotension
• Diagnosis
– ECHO – the best
– Equalization of chamber pressures
– Decreased voltage on ECG
– Electrical alternans
– Pulsus paradoxus (> 10 mmHg drop with inspiration)
Pericardial Tamponade Cont'

• Preop
– Place appropriate monitors – central pressure
monitoring, TEE
– Support hemodynamics – “full and fast”
– Consider transthoracic drainage under local
– Positive pressure will worsen hemodynamics
– Consider placing external pacing patches
• Intraop
– Avoid loss of preload (ketamine, etomidate)
– Avoid positive pressure ventilation if possible
– Hemodynamic effects resolve promptly with
decompression
• Be prepared for rebound hypertension
Notes
Cardiovascular Pharmacology
Antidysrhythmic Drugs
• Lidocaine
– Reduces phase 4 slope and decreases excitability
– Eliminates unidirectional blockade
– Effective in treating PVC’s, V-tachyarrhythmias, V-fib
– Not effective in atrial arrhythmias
• Adenosine
– Interacts with specific adenosine receptors
– Shortens action potential duration, causes
hyperpolarization
– Effects blocked by methylxanthines – eg. Caffeine
– Effective for reentrant supraventricular tachycardias
– Very short half-life – 12 seconds
– Quickly metabolized by vascular endothelial cells
Antidysrhythmic Drugs cont’

• Digoxin
– Increases vagal activity
– Inhibits Na+, K+ -ATPase that increases intracellular calcium
– Causes hyperpolarization, shortening of atrial action
potential, decreased phase 4 slope
– ECG effects: prolonged PR interval, T-wave
flattening/inversion
– Effective in treating: a-fib, a-flutter by reducing AV
conduction
– Digoxin toxicity includes complete heart block, CNS
depression
– Digoxin toxicity enhanced by hypokalemia
• Amiodarone
– Analog of thyroid hormone. Mechanism of action
unknown
– Effective in treating almost all arrhythmias including:
supraventricular dysrhythmias, ventricular
tachydysrhythmias including V-fib and V-tach
– Prevents recurrence of atrial fibrillation
– Improves response to defibrillation
• Bretylium
- Interferes with release of norepinephrine from
adrenergic nerve terminals
- Now used only in treatment of CRPS

• Calcium channel blockers
– Calcium channels are pores in cardiac and smooth
muscle membranes
– Calcium enters cell through voltage-dependent channels
• 3 Types of channels
N – neuronal
T – transient
L – long lasting (site of action of CCB’s; responsible
for Phase 2 of the cardiac action potential)
– Reduction of intracellular calcium Ö myocardial
depression, depression of automaticity, depression of AV
node conduction, vasodilation
– May potentiate NMBs
Cardiac action potential

1 CCBs exert their effects here 0 -rapid
depolarization
2
1 - overshoot
2 – plateau (ST
3 segment)
0
3 - repolarization
4 – RMP
(diastole)
4
• Sotalol
– Non-selective beta blocker
– Inhibits K+ currents
– Prolongs QRS and lengthens QT interval
– Effective in treating: ventricular and atrial
tachyarrhythmias including a-fib and a-flutter
• Magnesium
– May interfere with Ca++ influx
– Effective in treating digitalis induced arrhythmias
– Possibly effective in treating Torsades de pointes
Antidysrhythmics
Class Mechanism Agents

Ia Blocks fast sodium quinidine, procainamide,
channels, × action disopyramide
potential duration
Ib Blocks fast sodium lidocaine, tocainide
channels,Ø action mexiletine
potential duration
Ic Marked depression of flecainide, propafenone
myocardial maximum
velocity
II Blocks beta-adrenergic propranolol, metoprolol,
receptors esmolol
III Prolongs repolarization amiodarone, sotalol,

ibutilide, bretylium
IV Blocks slow calcium verapamil, dilitazem
channels
V (miscellaneous agents) digoxin, adenosine
SNS pharmacology
Sympathomimetics (A.K.A. pressors)
– Classified by:
• Receptor(s) stimulated
• Interaction with receptor
–Direct vs. Indirect
»Direct stimulate adrenergic receptors
»Indirect stimulate the release of
norepinephrine from sympathetic
nerve terminals but also stimulate the
adrenergic receptors directly
Direct-acting D1 agonists
Phenylephrine (Neosynephrine)
– 1º stimulates D1, minimal D2 and E2
– Useful in treating hypotension
• Historically contraindicated for use in
parturients; presently accepted for use
– Also used as a topical vasoconstrictor &
mydriatic
Centrally-acting SNS agonists

• Clonidine (Catapres)
– Stimulates postsynaptic D2 receptors in the brainstem
located in medullary vasomotor center
– Overall inhibitory effect; sedation, analgesia is
potentiated; produces anxiolysis
– Stimulates peripheral presynaptic D2-receptors
involved in (-) feedback
– Results in Ø release of NE from SNS terminals
– Used to treat HTN
– *Rebound hypertension will occur if clonidine is
d/c’d suddenly Ö due to the effect of accumulated
renin, angiotensin II, catecholamines
• Dexmedetomidine (Precedex)
– Used for sedation in the OR, ICU
Direct acting E-agonists

• Epinephrine (Adrenaline)
Stimulation of E1,2 at lower doses; D1,2 at higher
doses
• × myocardial contractility
• Resuscitation med in CPR
• Treatment of anaphylaxis
• Nebulized to treat croup
• Vasoconstrictor in local anesthetics
• Norepinephrine (Levophed)
Stimulates D1,2 and E 1
• Used as a (+) ionotrope
• Isoproterenol (Isuprel)
Stimulates E1,2
• Useful in the treatment of complete heart block
Direct Acting E-agonists
• Dopamine (Inotropin)
Stimulation is dose dependent
• 2-5 µg/kg/min Ö stimulation of dopaminergic
receptors in renal, mesenteric beds
• 5-10 µg/kg/min Ö E1, minimal E2 stimulation
• >10 µg/kg/min Ö D1,2
Useful in treating hypotension by increasing
myocardial contractility while increasing urine
output (@ low dose)
• Dobutamine (Dobutrex)
Stimulates E1,2, minimal D1
• Increases myocardial contractility; optimizes output
by decreasing SVR
**Meds may be used in conjunction with each other
E2 agonists
• Uses:
– Treatment of bronchospasm:
• Metaproterenol (Alupent)
• Albuterol (Ventolin, Proventil)
• Terbutaline (Brethine, Bricanyl)
– Cessation of premature labor (A.K.A.
tocolytics):
• Terbutaline (Brethine)
• Ritodrine (Yutopar)
Side effects may include hyperglycemia,
tachycardia, hypokalemia from potentiation
of the Na+/K+ pump, pulmonary edema
Indirect Acting D and E-agonists

• Ephedrine
E1,2; D1,2; direct/indirect agonist
ED effects approximately 7:1
Useful for the parturient; does not cause
placental hypoperfusion
Adverse reactions include: HTN,
tachycardia/arrhythmias, transient ÇK+,
anxiety, pulmonary edema,
Ç Incidence of tachyphylaxis after repeated
doses
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• Phenoxybenzamine
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– Onset 60 min; elimination half-time ~ 24 hrs
– Prominent orthostatic hypotension
– Used in the preop treatment of pts with
pheochromocytoma
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• Phentolamine
– Competitive, reversible, non-selective inhibitor
$FWVDWSRVWV\QDSWLFĮ1 DQGSUHV\QDSWLF Į2
receptors; also has direct action on
vascular smooth muscle
– Given intravenously
• Onset 2 min; DOA 10 -15 min
– Causes vasodilation, postural hypotension,
diarrhea, reflex tachycardia
– Principally used to treat acute hypertensive
emergencies
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• Prazosin
± Į1 selective blocker
– Less reflex tachycardia noted
• Terazosin
± Į1 selective blocker
– Used to treat BPH
E-blockers
• All derivatives of isoproterenol
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antagonists
• Block catecholamine effects on cardiac
conduction system, reduce inotropy
• Reduce sinus rate, rate of depolarization,
increase refractory period
• Shown to reduce CV morbidity and mortality
when used perioperatively for major surgery
• May precipitate bronchospasm, CHF,
hypotension, bradycardia
• Effective in treating: a-fib, a-flutter, PVCs,
digitalis-induced arrhythmias
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Direct-acting vasodilators
• Nitroglycerine (NTG)
– Organic nitrate that activates guanylate cyclase
Ö cGMP levels in smooth muscle Ö increased
nitric oxide Ö vasodilation
– Arteriolar vasodilation less profound than with
SNP
– Used in treatment of MI, angina, CHF, variant
(Prinzmetal’s) angina, uterine spasm
– Prophylactic NTG not shown to reduce
intraoperative MI
– Rapid onset and termination of effect when given
intravenously
– Direct effect causes dilation of cerebral
vasculature and possible ischemia
Direct-acting vasodilators, cont’
• Sodium nitroprusside (SNP)

– Direct acting vasodilator
– Mechanism of action similar to NTG with
increase in nitric oxide formation
– Causes more arteriolar vasodilation than NTG
– Causes release of cyanide anion (CN) during
metabolism
Cyanide Toxicity
Cyanide binds to ferric ion (Fe+++) found in
cytochromes, not hemoglobin
• CN then prevents aerobic metabolism
resulting in:
– Metabolic acidosis
– Increased mixed venous sat
– Confusion
– Death
CN toxicity may first present as
tachyphylaxis to the effects of the
SNP infusion
–Treatment: amyl nitrate, thiosulfate
Direct-acting vasodilators, cont’

• Hydralazine (Apresoline)
– Acts mainly at the arteriolar level with little
venodilation
– Reduces calcium levels in smooth muscle
– Can cause significant reflex tachycardia and
precipitate myocardial ischemia
– Much longer acting than NTG or SNP with
half-life of 3 -7 hours
– Causes increased renin production
ACE Inhibitors
• Enalapril is class prototype - lisinopril, benzapril,
quinapril, captopril, others available
• Interfere with the conversion of angiotensin I to
angiotensin II by inhibiting angiotensin
converting enzyme (ACE)
– overall effect = Ø vasoconstrictive effect
• Delay breakdown of bradykinin and associated
prostaglandins
• Only medication shown to increase survival in
patients with CHF (regression of LVH/cardiac
remodeling)
• Also shown to improve M&M after MI
ACE Inhibitors Cont’

• Can precipitate acute renal failure in patients with renal
artery stenosis
– ØGFR
• ×K+ associated with decreased production of
aldosterone
• Angioedema has been reported with use
• Fetal anomalies reported – cannot be given during
pregnancy
• Have been implicated in profound hypotension during
induction of anesthesia (should be held the AM of
surgery)
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allergic-like symptoms
Angiotensin II Receptor Inhibitors

• Agents include losartan, valsartan
• Block the vasoconstrictive activity of angiotensin II
without affecting ACE activity
– Selectively interferes with the binding of angiotensin II to
the AT1 receptors found in vascular smooth muscle
• May also cause profound intraoperative
hypotension; should be d/c’d the day before
surgery
• Cough is significantly less than with ACE inhibitors
Statins
• Atorvastatin (Lipitor)
– Most commonly prescribed drug in history
• Mechanism of action
– Competitive inhibitors of HMG-CoA reductase
– Results in decreased hepatic formation of cholesterol
• Beneficial effects
– Reduce total cholesterol levels and improve HDL/LDL
ratio
– Reduce atherogenesis
– Decrease inflammation
– Improve endothelial function
– Maintain plaque stability
– Reduce thrombus formation
Statins Cont’
• Adverse reactions
– Elevated liver enzymes (0.5%)
– Rhabdomyolysis
• Can precipitate myoglobinuria and renal
failure
– Myalgia
– Hepatic and pancreatic dysfunction
– Contraindicated in pregnancy and during
breast feeding
– Peripheral neuropathy
Phosphodiesterase (PDE) Inhibitors

• Amrinone (Inocor)
• Milrinone (Primacor)
– Inhibit phosphodiesterase
• Enzyme which breaks down cAMP
Ç circulating levels of cAMP cause an
adrenergic
effect from Ç Ca++ transport
Stimulation of E1 and E2 receptors
(+) Ionotropy
(+) Vasodilation
May cause a È in platelet aggregation (E2 effect)
amrinone > milrinone
Nesiritide (Natrecor)
• Recombinant B-type natriuretic peptide
• Binds to guanylate cyclase receptor of
vascular smooth muscle
– Increases cGMP concentration
• Causes vascular relaxation
• Dose-dependent fall in PCWP and BP in
patients with CHF
• IV administration, with half-life of 18 min
• Indicated for decompensated CHF
Vasopressin
• Also known as arginine vasopressin, ADH
• Causes contraction of vascular and GI smooth
muscle
• Recommended as equivalent to epinephrine in
treatment of v-fib, PEA and asystole
• Used only one time during resuscitation
• Given as single 40 U dose during resuscitation
or via continuous infusion
– May result in H2O intoxication
• Also used to treat diabetes insipidus, GI
hemorrhage
• Elimination half-life of 10 – 20 mins
Tolvaptan
• Competitive vasopressin inhibitor
• Indicated for treatment of CHF, SIADH,
hyponatremia, polycystic kidney disease
Aliskiren
• Direct renin inhibitor
• Indicated for use in essential hypertension
• Contraindicated in patients with DM and
renal insufficiency
• Contraindicated in pregnancy
• Hypotension with induction remains
uncertain
Clevidipine (Cleviprex)
• Dihydropyridine calcium channel blocker
• Lowers blood pressure through peripheral
vasodilation
• May cause some reflex tachycardia
• Administered as an infusion.
• Very short elimination half-life – 1 minute
- destroyed by plasma esterases
• Shown superior to SNP or NTG for post-
bypass hypertension
Notes
Obstetric Review
Physiologic changes during pregnancy: respiratory

parameter effect causative factors
minute ventilation Ç50% ÇRR: progesterone causes
È paCO2 (from 40 to 30) increased sensitivity to
VE pH remains unchanged due CO2; metabolic rate
increased
to increased renal excretion
of HCO3 ions ÇVT (1º causative factor)
O2 consumption Ç 20% Ç metabolic rate
O2 delivery Ç Ç 2,3 DPG; facilitates

unloading of O2 to fetus
FRC È 20% (largest Ìof all) abdominal distention from

(VC, TLC, and CV remain unchanged)
gravid uterus; pushes
diameter of thorax Ç
diaphragm cephalad
airway resistance È progesterone causes
bronchiolar and pulmonary
pulmonary vascular È
vessel dilation
resistance
Physiologic changes during pregnancy:

cardiovascular
parameter effect causes/effects
ÇHR (10-15 bpm by mid 2nd
cardiac output Ç particular to stage of trimester)
Ç10% 1st trimester pregnancy or labor: greatest
increase (60-80%) occurs ÇSV
Ç 40% 3rd trimester
with umbilical cord clamping ÈSVR
Ç RBC 15-20% *disproportionate rise in

blood volume plasma volume to RBC
Ç plasma volume 45-50%
Çtotal volume by 1500 ml mass; causes “dilutional
anemia”
ÈHgb/HCT (11/33%)
Increased H/H may signify
Çvessel engorgement low volume state
Çplatelets parturient considered
coagulation hypercoaguable
Çcoagulation factors,
especially fibrinogen PIH may result in
hypocoaguable state
Physiologic changes during pregnancy:
other systems
system effect cause/effect
Ç sedation effect of progesterone
neurologic
È in MAC
Ç RBF È in BUN and creatinine by

renal 50%
Ç GFR
pyloric displacement from gravid uterus

gastrointestinal
incompetent GE sphincter progesterone
È gastric emptying (as **parturient highly prone to
early as 12 wks gestation) regurgitation/aspiration
Èplasma cholinesterase SCH duration clinically

hepatic levels unchanged 2º large initial
Ç hepatic enzymes VD of drug
È albumin
Uteroplacental flow
***the placenta has no
autoregulation***
Uterine perfusion is directly proportional to maternal

MAP and inversely proportional to uterine vascular
resistance:
uterine blood flow = uterine arterial pressure - uterine venous pressure

uterine vascular resistance
**UBF = 500-700 ml/min at term (10% of CO)
Uteroplacental flow
– maternal factors which contribute to uterine
hypoperfusion:
• **maternal hypotension (from hemorrhage,
hypovolemia, aortocaval compression)
• increased catecholamines (from stress of labor, pain,
PIH)
• supine hypotensive syndrome (A.K.A. aortocaval
compression)
• seizures
– iatrogenic factors which contribute to uterine
hypoperfusion:
• hypocarbia
• uterine tetany (from hyperstimulation)
• hypotension from GA or regional anesthesia
• phenylephrine was thought to cause uterine
hypoperfusion however use is widely accepted for the
tx of hypotension (overuse of ephedrine may lead to
neonatal acidosis)
-maternal blood
is carried via
placenta
uterine arteries
-blood flows
from arteries
into the
intervillous
spaces
-bathes fetal villi
then drains
back into
uterine veins
-umbilical vein
carries nutrient
rich blood to
fetus, fetal
blood is drained
via umbilical
arteries (2)
Internet source: dgking@siu.edu with permission
Supine hypotensive syndrome

• A.K.A. aortocaval compression
– occurs from 18th - 20th week of gestation on
– gravid uterus compresses the IVC when parturient is
supine
• È venous return, BP, CO
• n/v
• diaphoresis
• lightheadedness
– lower abdominal aorta may also be compressed
• È uteroplacental perfusion
• treatment Ö left uterine displacement (LUD) by
10-15 cm elevation of the R hip
• ephedrine 5-10 mg IV, phenylephrine 50-100
mcg IV, fluids if needed
Determinants of placental transfer of drugs
• physiologic (maternal factors):

– placental perfusion
– maternal to fetal concentration gradient
– total dose of drug administered
– vascularity of administration site
– maternal pH
– maternal protein binding
– metabolism of drug
Determinants of placental transfer of drugs
• pharmacologic
– dependent on drug diffusion constant (Fick)
• placental transfer will be greater if:
– È degree of ionization of drug
» ion trapping—an unionized agent crosses the
placenta and becomes ionized/”trapped” in the
relatively acidemic fetus—may be noted with the
use of paracervical anesthesia
– È molecular size of drug
– È protein binding of drug
– Ç lipid solubility of drug
» NMBs, glycopyrrolate, insulin, heparin do
not X placenta
Transfer of locals across placenta

• lower doses of LA needed in the parturient
2º:
– engorgement of epidural vessels
– ×sensitivity to the effects of LA (progesterone)
– maternal CSF pH favors unionized portion;
enhanced diffusion across nerve cell membrane
Placental transfer of locals from greatest to least:

mepivacaine>etidocaine>lidocaine>ropivacaine>bupivacaine
Fetal circulation
• allows nutrients and oxygen to be transferred
from the mother to the fetus, and for
deoxygenated blood to be returned to the
mother
• shunts are in place to allow the majority of blood
flow to bypass the fluid-filled lungs
– shunting from RÖL occurs 2º × fetal pulmonary
vascular resistance from:
• relative hypoxemia
• compression of pulmonary vasculature by fluid-
filled alveoli
Fetal response to drug transfer
• due to the nature of fetal
circulation, drugs which
cross the placenta have
limited distribution
systemically and to the CNS
– 75% of umbilical venous
blood immediately
passes through the fetal
liver and is metabolized
(first pass effect)
– remainder of drug is
diluted by remaining fetal
blood
• vital organs are protected
from exposure to high [ ] of
drugs
Internet source:www.clem.mscd.edu
Fetal circulation
desaturated blood is carried from blood enters the RA from the SVC
and IVC; is shunted from RÖL
the fetus by umbilical arteries (2) to •*blood in the across the foramen ovale into the
the placenta for oxygenation
carotid artery LA
and descending
aorta has a PO2
oxygen and nutrient rich blood is of
blood from the pulmonary artery is
returned to the fetus via the approximately shunted across the ductus arteriosus
umbilical vein (1) 23-25 mmHg to the aorta, bypassing lungs
the majority of umbilical vein blood

enters the IVC from the ductus oxygenated blood goes from the LA
venosus; mixes with desaturated into the LV, exits the heart by the
blood from the lower extremities ascending aorta to the coronary,
carotid*, and subclavian arteries
the remainder of
umbilical vein blood approximately ½ of the blood in
enters the liver via the the descending aorta perfuses
portal vein the abdomen and lower
extremities; the rest is returned
to the placenta
stages of labor
Stage of labor pain analgesia
1st early Ö cx 1-3 cm visceral and parenteral
active Ö cx 4-7 cm cervical (opioids)
transition Ö cx 8-10 cm T10 Ö L1 epidural
combo spinal/epid
2nd pushing/ lower vagina, paracervical
delivery perineum caudal
S2 Ö S4 pudendal
3rd
delivery of placenta
**T4 level necessary for adequate anesthesia for C/S via spinal or epidural
Obstetric monitoring
• parameters followed:
– FHR (120-160 BPM considered normal)
• patterns (i.e. beat-to-beat variability, accelerations,
decelerations)
• loss of baseline variability may indicate beginning
distress (fetal hypoxia/acidosis); may treat with O2
and ephedrine
» other factors which may È variability include
narcotics, locals, benzodiazepenes, barbiturates,
inhalational agents, and anticholinergics
– uterine activity (contractions)
• early decelerations (Type I)
-signifies fetal head compression with resultant vagal stimulation

-occurs during the 1st 1/3rd of the contraction
-U-shaped, FHR usually remains > 100 BPM
-may be treated with atropine (CONTROVERSIAL)
• late decelerations (Type II)
-ominous; signifies fetal distress from uteroplacental insufficiency

-occurs late in the contraction; FHR may remain low even after ctxn is
resolved
-U-shaped, FHR usually remains > 100 BPM
-may be treated with O2, fluids, ephedrine, LUD; definitive tx is delivery
• variable decelerations (Type III)
-occur at different points of contraction
-shape varies; FHR may be <100 BPM

-signifies cord compression; may resolve with maternal position
change
-generally considered to be benign unless FHR remains low
Scalp pH values
• 7.25-7.45 Ö normal
• 7.20-7.24 Ö indicates mild distress
• <7.20 Ö indicates severe distress;

immediate delivery required
Fetal distress
• A.K.A. “persistent fetal asphyxia” or “non-

reassuring fetal tracing”
– early s/s:
• loss of beat-to-beat variability
• bradycardia
• meconium staining of amniotic fluid
Transition from intrauterine to
extrauterine life
• lungs transition from fluid filled to air filled
to facilitate gaseous exchange
– the neonate must generate (-) intrathoracic
pressures of 50-70 cm H2O
• surfactant is necessary to maintain inflation of
alveoli
– majority of fluid is expelled by fetal chest
compression during vaginal delivery;
remainder is drained via lymphatics over the
next 24º
• some may be retained with C/S requiring chest
physiotherapy and monitoring

extrauterine life, cont’d
• Circulatory changes:
– pulmonary vascular resistance is decreased by 80%
from:
• expansion of the lungs with air
• release of vasoactive substances and arachadonic
acid metabolites
• ×PO2 to 60 mmHg
– increases pulmonic circulation and oxygenation
– the ductus arteriosus is sensitive to ×PO2
× pH, and ØPGE1 synthesis from placenta;
• it will constrict in 90% of full term infants over the
1st 3 days of life; permanent closure takes
approximately 2-3 weeks

extrauterine life, cont’d
– flow through the foramen ovale ceases with ØPVR;
blood fills the LA causing FO flap closure
• probe patency of the FO persists in approximately
30% of the adult population
– umbilical cord clamping results in ×SVR
Apgar Scoring
0 1 2
color completely body pink with completely pink
cyanotic and/or cyanotic
pale extremities
heart rate absent <100 BPM >100 BPM
(BPM)
reflex no response grimace cry, cough,
sneeze
irritability*
breathing apneic slow; weak cry crying
muscle limp minor flexion of active;

extremities extremities well-
tone flexed
Apgar Scoring, cont’d

• 1 minute Apgar score directs resuscitative
efforts; 5 minute score relates to long-term
outcome 2º cerebral hypoxia/damage
• Apgar scoring 8-10
– most newborns fall into this category
– suction PRN, maintain temperature
– monitor for decline in condition
• Apgar scoring 4-7
– indicative of mild asphyxia
– O2 via mask (BBO2), external stimulation
– bag/mask ventilation if no improvement in condition
Apgar Scoring, cont’d

• Apgar score 0-3
– bag/mask ventilation; LMA insertion vs.
tracheal intubation
– external cardiac compressions if HR < 60
BPM
– may administer drugs via umbilical vein or
ETT*
• *Remember ALIEN V2:
– atropine, lidocaine, isoproteronol, epinephrine, naloxone
valium, vasopressin
Neonatal resuscitation
• medications:
– epinephrine 1:10,000 dilution Ö 0.1 ml/kg
– calcium gluconate 50 mg/kg
– NaHCO3 diluted 1:1 Ö 1mEq/kg slowly
– atropine 0.02 mg/kg
– naloxone 10-100 mcg/kg
– lidocaine 1.0 mg/kg
– defibrillate with 2j/kg
– question need for volume expansion with albumin or
blood (10 ml/kg), dextrose (D10) 0.2g/kg
pregnancy induced hypertension

(PIH)
• A.K.A. preeclampsia, toxemia
• manifests after the 20th week of pregnancy;
approximately 10% occurrence rate
• multisystemic involvement; etiology unknown
• major cause of premature labor 2º uterine
hyperreactivity
• major cause of obstetric and perinatal m/m
• primary causes of maternal death:
– cerebral hemorrhage
– pulmonary edema
manifestations of PIH:
– HTN—BP 140/90 or greater
– proteinuria
– edema
• peripheral
• airway
– intravascular depletion
– ÇÇ sensitivity to endogenous and exogenous
catecholamines
– CNS disturbances
• headache
• visual field disturbances
• hyperreflexia
• seizures (eclampsia)
– *Èuteroplacental perfusion
complications of PIH
• HTN
• progressive thrombocytopenia
• liver dysfunction
• renal dysfunction
• preeclampsia (premonitory sx of
development of eclampsia)
• fetal distress
HELLP
• PIH may evolve into this syndrome
• acronym for:
– Hemolysis
– Elevated Liver enzymes
– Low Platelets, ÇFSPs,
• may lead to DIC
• *definitive treatment is delivery of the fetus
– PIH typically resolves within 48º of delivery
treatment of PIH
• magnesium sulfate (MgSO4)
– relaxes smooth muscle of the vessels, uterus,
and bronchioles
• interferes with Ca++ transport
• È muscle membrane excitability
• È motor end plate sensitivity
– inhibits release of ACH; enhances effects of NDMBs
• may also be utilized in the treatment of pre-term
labor as a tocolytic
– Loading dose 4-6 gm/30 min; maintenance 1-
2 g/hr for up to 24° post partum
magnesium sulfate
• toxic effects
– skeletal muscle weakness
– uterine atony
– hyporeflexia- this is the earliest sign of impending
Mg++ toxicity
– vasodilation/hypotension
– AV block, prolongation of P-Q intervals and widened
QRS
• may lead to cardiac arrest
– CNS depression
• apnea
• paralysis
– MgSO4 crosses the placenta with ease; all effects,
especially hypotonia, may be seen in the fetus
– treatment is with Ca++, supportive
– *therapeutic plasma level Ö 4-6 mEq/L
problems associated with PIH

• acute hypertension with laryngoscopy, addition
of epinephrine to local for regional anesthesia
– may lead to:
• seizures
• cerebral hemorrhage
• pulmonary edema
– hydralazine, labetalol usually the antihypertensives of
choice; may use esmolol pre-intubation
• difficult airway 2º edema
– Ç risk for aspiration
problems associated with PIH,

cont’d
• coagulopathy may be present
– check coags; may preclude the use of regional
anesthesia
– may need to administer FFP, platelets, cryoprecipitate
• regional (specifically spinal) anesthesia may ppt
profound hypotension
– preload with 1-2 liter crystalloid (LR, normosol)
• may need invasive monitoring
• follow U/O carefully
– should be > than 1ml/Kg/hour
– may administer loop diuretics, mannitol
• Èplasma cholinesterase
– probably clinically insignificant
maternal hemorrhage
• multiple causative factors
• placenta previa
– an abnormally low implantation of the
placenta
– causes a partial to complete obstruction of
the cervical os; may necessitate C/S
– 1º symptom Ö painless vaginal bleeding
occurring on or around 32nd week of
gestation
maternal hemorrhage, cont’d

• abruptio placenta (A.K.A. placental abruption)
– premature separation of placenta from uterine wall
• risk factors:
– HTN, abdominal trauma, ETOH or cocaine use,
multiparity
– *1º cause of DIC in the parturient
– vaginal bleeding may be overt or occult
– may manifest as sudden maternal decompensation
• severe abdominal pain
– quickly leads to shock, fetal distress
– necessitates emergency C/S
maternal hemorrhage, cont’d

• retained placenta
– usually from fragmentation of the placenta
– bleeding occurs from resultant uterine atony (2-5% of
vaginal deliveries)
– EBL may be as much as 2 liters/5mins
– necessitates manual uterine exploration/removal of
retained fragments
• GA vs. sedation
• NTG 80-120 mcg IV given to relax uterus
– may be 2º abnormal implantation
• accreta, increta, percreta
– may be the result of intrauterine infection
– may necessitate uterine artery embolization, emergency
hysterectomy
“The Four T’s”
• Tone - atonia of the uterus from multiple
gestations, polyhydramnios
– the 1° cause of postpartum hemorrhage
• Trauma - cervical or vaginal lacerations;
placental abruption, uterine inversion
• Tissue - retained placental fragments,
placental malimplantations (accreta, increta,
percreta)
• Thrombosis - abnormalities of coagulation,
either underlying or acquired
Placental implantation
treatment of uterine atony

• oxytocin
– posterior pituitary hormone which increases uterine
tone
– may cause vasodilation, hypotension, tachycardia if
rapidly administered
– may cause SIADH
• results in H2O intoxication and hyponatremia
• unlikely with the use of synthetic oxytocins which do not
contain vasopressin
• methergine
– may cause hypertension, N/V; contraindicated in PIH
• PGF2D (Hemabate)
– may cause bronchospasm
uterine inversion
• necessitates GA with RSI
– ketamine preferred indxn agent (supports BP)
• large bore IV, blood products
• uterine relaxation
– low dose volatile anesthetics
– NTG 50-100 mcg IV boluses
• oxytocin gtt is started after uterus is
replaced; prevents recurrence
uterine rupture
• 80% occur spontaneously with no predisposing factors
• 1% incidence
• may be noted in:
– grand multiparous pts
– precipitous delivery
– uterine overstimulation
– VBAC (1º concern)
• manifests as:
– sudden, continuous, intense abdominal pain, even despite
epidural anesthesia
– change in uterine tone/contraction pattern
– maternal hypotension
– fetal bradycardia/distress
• Çincidence of perinatal mortality (fetal mortality ~ 80%)
amniotic fluid embolus

• manifests as a sudden onset of respiratory distress
and ÈBP
– ÈSaO2, ÈETCO2,
– leads to complete CV collapse
• greater incidence in multiparous pts during precipitous
delivery
• dx confirmed by the presence of amniotic fluid/fetal
material in maternal blood sample
• may lead to development of DIC, uterine atony
• treatment is supportive (CPR, pressors, aminocaproic
acid to tx DIC, NaHCO3, steroids, correction of
hypoxemia, HOB slightly Ç with 15º L lateral tilt, LUD)
• mortality rate 86% (50% during 1st hour)
• 3rd leading cause of maternal mortality
polyhydramnios
• An overabundance of amniotic fluid;
associated with:
– TE fistula
– umbilical cord prolapse
– breech presentation
– malpresentation with multiple gestations
– uterine atony
anesthesia for emergency

Cesarean section
• may be done under spinal anesthesia in
certain cases; indwelling epidural catheter
may be dosed with carbonated lidocaine
2% or 2-3% chloroprocaine (rapid onset)
– must achieve a T4 level
• GETA necessary for truly emergent
scenario
– maternal hemorrhage, persistent fetal
bradycardia
emergency c/s, cont’d

• preoxygenate with FiO2 1.0
– anticipate airway difficulties
• have a variety of blades, small (#6.5) ETT, stubby
laryngoscope handle, bougie, Proseal LMA, Fastrach
or ILA, cricothyrotomy set, Glidescope, fiberoptic
bronchoscope
• place pt supine with (+) LUD
• pt is prepped/draped before induction
– surgeon makes incision immediately after verification of
ETT placement; allows for minimal fetal exposure to
anesthetics
• rapid sequence induction
– HOB Ç 30º
– suction available
– stylet in ETT
– (+)/(-) use of Na+ citrate
– Pt is at high risk for aspiration
– Pt is at high risk for failed airway
induction for emergency C/S
• may use sodium thiopental 2-4 mg/kg IV
– lowest fetal brain [ ] of all indxn agents
• may use propofol
– reported neonatal hypotonicity associated with use
• ketamine 1.0 mg/kg if the pt is hypovolemic
– follow immediately with SCH 1.0-2.0 mg/kg
• may use glycopyrrolate, NDMBs
• *maintain cricoid pressure until placement of ETT is
verified by (+) ETCO2 and BBS
• do not hyperventilate pt
– hypocarbia results in placental hypoperfusion
• anticipate need for volume resuscitation
• VAE a risk, especially if the uterus is exteriorized and
above the level of the heart during repair
• may need to assist with neonatal resuscitation as well
anesthesia for non-obstetric surgery

• surgery during pregnancy are usually
– cholecystectomy
– ovarian cystectomy
– appendectomy
– cervical cerclage
• primary concerns:
– avoidance of fetal hypoxia/acidosis
• 1º fetal risk Ö uterine asphyxia
– avoidance of potentially teratogenic anesthetic
agents, especially in 1st trimester
• N2O
• benzodiazepines
– 1º overall risk Ö development of premature labor
• usually 2º underlying pathology/surgical procedure
• treat with E agonists (terbutaline, ritodrine), MgSO4
anesthesia for non-obstetric

surgery, cont’d
• anesthetic goals
– delay surgery if possible until 2nd trimester
– left uterine displacement (LUD) after 20th
week gestation
– maintenance of maternal BP
• fluids
• *ephedrine
– monitoring of FHR and uterine activity
– conduction anesthesia if possible
• limits fetal exposure to anesthetics
Other core concepts for obstetrics
• average EBL after delivery
– vaginal: 400-600 ml
– cesarean: 1000 ml
• parturient is always considered a “full stomach” and at
risk for aspiration
– always needs RSI, even for non-obstetric procedures
• parturient has airway edema and friable tissues
– magnified in the 3rd trimester
– may lead to difficult airway scenario
• infant born to mom with gestational diabetes at × risk for
macrosomia, hypoglycemia
• ? use of atropine; may mask fetal distress
• all tocolytics cross the placenta; E agonists may lead to
hyperglycemia, tachycardia, hypokalemia from
potentiation of the Na/K+ pump, pulmonary edema
Other core concepts for obstetrics

• most common musculoskeletal complaint
of the parturient is low back pain
• lumbosacral nerve is most commonly
injured after vaginal delivery
• major complications of dilation/curettage
– uterine perforation
– hemorrhage
• most drugs are safe during lactation
– exceptions are lithium and ergotamine
airway scenarios
• Routine C/S, GETA planned, no fetal
distress, can ventilate but can’t intubate?
– Wake pt up; attempt AFI
• Emergency C/S, GETA necessary, fetal
distress, can ventilate but can’t intubate?
– LMA (pro seal, fast trach, ILA good choices)
• Can’t ventilate/can’t intubate?
– LMA 1st, cricothyrotomy
Regional Anesthesia Review
Peripheral Nerves
Dermatomes
121
Dermatome Landmarks
• C2 – first palpable spinous process

• C7 – vertebra prominens (most prominent)
• T7 – parallel to inferior edge of scapula
• T10 – level of umbilicus (prostate and uterus)
• L4 – highest points of iliac crests
• S2 – level of posterior iliac spines
Spinal Anesthesia
• Landmarks
– Spinal anesthesia most commonly given at L3 - L4
– Cord ends at L2, subarachnoid space ends at S2
– Anterior iliac crests parallel to body of L4
– Anesthetic deposited between arachnoid and pia
Spinal Anesthesia Cont'

• Spread of local anesthetic
– Level obtained depends mainly on:
• Specific gravity & patient position
• Dose
• Site of injection
• Length of vertebral column
• Barbotage not a factor in spread
122
• Physiologic effects of spinal anesthesia
– Preganglionic sympathetic blockade Ö venodilation,
arteriolar dilation with fall in both preload and
afterload
– If level extends to T2, depression of cardiac
accelerator fibers seen
– Nausea secondary to unopposed parasympathetic
stimulation to gut
• Anticholinergic treatment may be effective
– Decreased tidal volume as intercostal muscles relax
• Minute ventilation preserved by increased rate

• Dural puncture headache
– Secondary to loss of CSF through dural puncture site
– Seen in about 2% of cases – more common in young
patients and in females
– Headache is postural with relief in the supine position
– Incidence less with “pencil point” spinal needles
• Spreads dural fibers vs. cutting
– 6th cranial nerve palsy possible

• Dural puncture headache cont’
– Treatment
• Conservative therapy: hydration, caffeine,
analgesics, abdominal binder, sumatriptan
• Epidural blood patch – if conservative therapy not
successful 20 mLs of autologous blood or until
sensation of back pressure occurs
– Once puncture is closed, patient recovers quickly –
CSF made rapidly (approximately 400 cc/day with
150cc in CNS at any time)
123
Spinal Local Anesthetics
• Hyperbaric solutions
– Tetracaine 0.5% in 5% dextrose
– Bupivacaine 0.75% in 8.75% dextrose
– Lidocaine 5% in 7.5% dextrose
– Procaine 10% in water
• Isobaric solutions
– Tetracaine 0.5% in water
– Bupivacaine 0.75% in saline
– Lidocaine 2% in saline
• Hypobaric solutions
– Tetracaine 0.2% in water
– Bupivacaine 0.3% in water
Maximum Spinal Dosage
• Lidocaine 60 mg
• Procaine 100 mg
• Bupivacaine 9-15 mg
• Tetracaine 10 mg (hypobaric)
12 mg (hyperbaric)
15 mg (isobaric)
Epidural Anesthesia
• Landmarks
– Same as for spinal anesthesia
– Dura and arachnoid not
punctured
– Anesthetic deposited outside
of the dural sac in epidural
space
• Space is potential; filled
with fat, vessels, wider in
lumbar region than cervical
• May leave catheter in
place
124
Spinal/Epidural Structures
• Midline approach: skin Ö subcutaneousÖ
supraspinous ligament Ö intraspinous
ligament Ö ligamentum flavumÖ epidural
space
• Paramedian approach: skinÖ
subcutaneous Ö ligamentum flavum Ö
epidural space
Epidural Anesthesia Cont'

– Level much less affected by patient position
– Level determined by volume of anesthetic – each
increase in dermatome is 1.5 – 2 cc of volume
• Physiologic effects of epidural
anesthesia
– Identical as spinal anesthesia for given dermatome
level; onset slower
Epidural Anesthesia Cont'

• Complications of epidural anesthesia
– Inadvertent dural puncture – 3% of epidurals with
70% of headache
– Epidural hematoma – suspect in patient with
persistent block and well defined level that fails to
regress
• More common in elderly patients
125
Combined Spinal Epidural
• Two techniques employed:
– Single level needle-through-needle, or specialized
needle
– Sequential technique can be at same or different level
• Offers rapid onset and density of block with advantages
of epidural catheter
• Complications
– Catheter migration into subdural space – especially if
larger needles used
– Increased spinal level after administration of epidural
– Metal particles – one study found needle-in-needle
technique resulted in metal particles in epidural and
subdural spaces
Caudal Anesthesia
• Landmarks
– Triangle formed by the superior posterior iliac spines to
sacral hiatus
– Caudal canal contains nerves from the cauda equina
Caudal Anesthesia Cont'

– Almost entirely determined by volume of local
anesthetic
– 15 – 20 ml of local gives “saddle block”
– 30 ml of anesthetic may give up to a T10 level
• Indications
– Suitable for variety of perineal, anal procedures
– Also used for analgesia during latter part of labor
126
Interpleural Block
• Landmarks
– Vertical line drawn about 8 cm lateral to spine
– Intercostal neurovascular bundle found beneath
inferior edge of rib
• Technique
– Epidural needle placed between visceral and parietal
pleura
– Catheter placed for continuous block
Interpleural Block Cont’

• Distribution of analgesia
– Chest wall and upper abdomen
– Depends on volume and catheter location
• Complications
– Pneumothorax, sympathetic block, local anesthetic
toxicity
– Avoid in patients receiving positive pressure
ventilation
Upper Extremity Block

• Innervation of hand
Median nerve
127
Upper Extremity Block Cont'
Radial nerve
Upper Extremity Block Cont'

Ulnar nerve
Brachial plexus block

• Four approaches:
– Interscalene
• Local deposited on roots of brachial plexus (BP)
• May block phrenic nerve
– Supraclavicular
• Local deposited on trunks, divisions of BP
• 2-5% incidence of pneumothorax
– Infraclavicular
• Local deposited on cords of BP
– Axillary
• Most frequently performed
• Local deposited on branches of BP;
musculocutaneous nerve sometimes missed
128
Interscalene Block
• Block placed between anterior and middle scalene
muscles
• Anesthesia most intense at C5 – C7 level
• Some sparing of C8 – T1 making block effective for
shoulder surgery, but not hand surgery
• Multitude of side effects & complications:
Stellate ganglion block Venous injection
Recurrent laryngeal nerve Epidural injection
block Subarachnoid
Phrenic nerve block injection
Vertebral artery injection Pneumothorax
Failed Block (most
common)
Axillary Block
• Landmarks
– Axillary nerves lie in the neurovascular bundle in
axilla
– Using nerve stimulator or US, entrance into
neurovascular bundle is confirmed
– Distal tourniquet is often used to promote cephalad
spread
Axillary Block Cont'

– With use of tourniquet and volume > 20 ml,
anesthesia of musculocutaneous nerve can be
achieved to allow use of tourniquet
• Complications of upper extremity blocks
– Upper extremity blocks, excluding IV regional, carry a
29% complication rate
– 15% of blocks fail or are inadequate
– Other complication (14%) include nerve damage,
pneumothorax, hematomas, subarachnoid injection,
intra-arterial/intravenous injection, phrenic nerve
paralysis, vagal nerve paralysis
129
Assessment of UE blockade
• “The Four P’s”
– Push
• Assesses motor blockade of radial (innervates
triceps)
– Pull
• Assesses motor blockade of musculocutaneous
(innervates biceps)
– Pinch (index finger)
• Assesses sensory blockade of the median nerve
– Pinch (pinky finger)
• Assesses sensory blockade of the ulnar nerve
Intravenous Block
• Also known as Bier Block
• Limited duration Ö 45 to 60 min
– Sustained cuff pressure may become painful; lack of
perfusion to the limb should not exceed 120 min
• Lidocaine 0.5% 40 – 50 cc used
– Must be preservative free
• Tourniquet must remain up for 15 – 20 min to
allow tissue binding of lidocaine and reduce
incidence of systemic effects upon cuff deflation
Wrist Block
• Anatomy
– The radial nerve branches and travels in the
subcutaneous tissues across the dorsum of the wrist
– The medial nerve is found between the palmaris
longus and flexor carpi radialis tendons
– The ulnar nerve passes medially to the ulnar artery
and between the ulnar artery and the flexor carpi
ulnaris
• Technique
– Block of all 3 nerves gives complete anesthesia of the
hand
– Each nerve requires 5 – 7 ml of anesthetic for
blockade
130
Digital Nerve Block
• Anatomy
– Digital nerves run in tissue on both sides of
phalanges
• Technique
– 1 – 3 ml of anesthetic is injected at base of each side
of finger
Femoral Nerve Block

• Anatomy
– Femoral nerve lies
lateral to the femoral
artery
– Anatomy of the femoral
neurovascular bundle
Ö NAVEL
Nerve, Artery, Vein,
Empty space, Lacunar
ligament
Femoral Nerve Block Cont’

• Femoral nerve branches
– Anterior division:
• Middle cutaneous
• Medial cutaneous
• Muscular (sartorius)
– Posterior division:
• Saphenous nerve (most medial)
• Muscular (individual heads of the quadriceps
muscle)
• Articular branches (hip and knee)
131
Femoral Nerve Block Cont'
• Distribution of anesthesia
– Usual volume 15 – 20 ml
– Block delivered at ileoinguinal fold just lateral to
femoral artery
– Femoral block results in anesthesia of:
• Entire anterior thigh
• Most of the femur
• Knee joint
– The block also confers anesthesia of the skin on the
medial aspect of the leg below the knee joint
(saphenous nerve - a superficial terminal extension of
the femoral nerve)
Sciatic Nerve Block

• Anatomy
– Sciatic nerve is a continuation of the sacral plexus
– Largest nerve trunk in the body
– Innervates posterior thigh, lower leg, foot
– Divides into the internal and external popliteal nerves
Sciatic Nerve Block Cont'

• Technique
– Patient placed in Sims position
– Line drawn from posterior superior iliac spine to
greater trochanter
– Line is drawn from sacral hiatus to greater trochanter
– Perpendicular line is drawn at center of line 1 and
needle is inserted at intersection point with line 2
– Using a nerve stimulator, flexion of foot is noted with
< 0.5 mA
20 ml of local anesthetic injected
132
• Distribution of anesthesia
– Sciatic nerve blockade results in anesthesia of the:
• Skin of the posterior aspect of the thigh
• Hamstrings and biceps muscles
• Part of hip and knee joint
• The entire leg below the knee, except for medial
aspect
Popliteal Block
• Anatomy
– Popliteal nerve runs lateral to the popliteal artery and
vein, behind the knee
– The popliteal nerve supplies the lower third of the leg,
with the exception of the medial skin (saphenous
nerve)
• Technique
– A line is drawn over the tendon of the femoris biceps
muscle (laterally)
– A second line is drawn over the tendon of the
semitendinous muscle (medially)
– A third line is drawn through the popliteal crease and
a mid-point perpendicular is drawn cephalad 7 – 10
cm
133
Popliteal Block Cont'
• Technique Cont'
– The nerve is located with a stimulator looking for foot
flexion 30 – 40 ml of anesthetic is required
Ankle Block
• 5 nerves supply
sensation to the foot:
– Deep peroneal, superficial
peroneal, posterior tibial, sural
& saphenous
– Deep peroneal nerve between
dorsi-flexor tendons of foot
– Posterior tibial nerve lies
posterior to the artery
– Remaining nerves in
subcutaneous tissues
– All are branches of the sciatic
system except the saphenous
nerve
Stellate Ganglion Block

• Landmarks
– Transverse process is sought
between sternocleidomastoid
and trachea
• Most easily felt at C6
– Carotid artery &
sternocleidomastoid moved
laterally, trachea medially
– Needle inserted to touch
transverse process and
withdrawn 1mm
– 20 ml of local anesthetic
injected
134
Stellate Ganglion Block Cont'
• Indications
– Regional circulatory insufficiency
– Complex regional pain syndrome of upper extremity
– Inadvertent intraarterial injection of thiopental
• Horner’s Syndrome
– Ptosis, miosis, enophthalmosis, facial anhydrosis
• 2o to loss of sympathetic innervation to face
– Does not ensure block of sympathetics to arm
– Arm skin temperature increase only certain indicator
of sympathetic block of arm
• Complications
– Hematoma, intravascular injection, dural puncture,
pleural puncture
Airway Blocks
• Superior laryngeal nerve
block
– Provides dense block of
supraglottic region
– Nerve pierces the thyrohyoid
membrane just below cornu of
hyoid
– Needle is inserted into
thyrohyoid membrane and 2 ml
of anesthetic is injected
– Aspiration of air implies needle
is is too deep
Airway Blocks Cont'

• Transtracheal block
– 22 to 24 gauge angiocath is placed through the
cricothyroid membrane – presence confirmed with
aspiration of air
– Patient instructed to inhale and 5 ml of 2% lidocaine
is injected. Coughing is precipitated, which sprays
anesthetic onto cords
135
Retrobulbar Block
• Anatomy
– Orbital cone contains optic and cranial nerve III and V
branches to the eye
• Technique
– Blunt-tip 25 gauge needle enters between globe and
orbit by inserting needle at junction of medial and
lateral third of the lower lid
– Depth of needle determines of block is retrobulbar
(deep to the cone of extraocular muscles) or
peribulbar (superficial to cone of extraocular muscles)
– 2 to 7 ml of anesthetic required
– Because of location, peribulbar block has a slower
onset, but fewer complications
Retrobulbar Block Cont'

• Technique Cont'
Celiac Plexus Block

• Indicated for the treatment of visceral pain
• Celiac ganglia are clustered at L1
• Most common complication is orthostatic
hypotension from sympathetic block
• Usually done with CT or fluoroscopic
guidance
• Often done bilaterally
136
Celiac Plexus Block Cont'
• Block is done with patient prone
• Needle inserted at 45o and passes under
the 12th rib to the anterior aspect of L1
• 15 – 20 ml of anesthetic on each side
Hypogastric Block
• Many common characteristics with celiac
block
• Used to treat pain from pelvis and
perineum
• Same technique used as celiac block, but
done at the L5 level
• May cause transient bowel and bladder
dysfunction
Pain Syndromes Review
137
Transmission of pain
• Transmitted from the periphery to the
cortex
– Stimulation of nociceptors by trauma
– Secretion of nociceptive substances which activate
nerves carrying pain signals
» Substance P
» Bradykinin
» Histamine
» Serotonin
Transmission of Pain Cont’

– Transmission to the spinal cord via:
• A-delta fibers (myelinated)
– Rapid transmission of sharp, well defined pain
– Short duration
– Secrete neurotransmitter glutamate
• C fibers (unmyelinated)
– Slow transmission of dull, diffuse pain
– Sustained duration
– Secrete neurotransmitter Substance P
Transmission of pain, Cont'

• A-delta and C fibers enter into the
dorsal horn of the spinal cord
– Ascends/descends via Tract of Lissauer
– Passes through substantia gelatinosa (A.K.A.
Rexed’s lamina II)
– Crosses cord via the midline and ascends via lateral
spinothalamic tract
• Dull pain passes through reticular formation of
brain stem and terminates in the thalamus
• Sharp pain ascends directly through thalamus to
the cortex
138
Spinal cord tracts
Antinociception/modulation of
Pain
• Descending fibers from the reticular formation project to
the dorsal horn of the cord and suppress relay of pain
signals to the brain
– Travel through the nucleus raphe magnus through the
dorsolateral funiculus
– Activation of inhibitory interneurons
• Release of enkephalin and other endogenous
opioids
– Suppression of pain signals by binding to
opioid receptors in substantia gelatinosa
» Decrease substance P
» Inhibit pain relay
Complex Regional Pain

Syndrome
• Terms
– Allodynia – pain from a stimuli that does not normally
provoke pain
– Anesthesia Dolorosa – pain in an anesthetic area
– Hyperpathia (Hyperesthesia) - increased reaction to a
painful stimulus
– Paresthesia - An abnormal sensation, whether
spontaneous or evoked
– Radiculopathy - A disturbance of function or
pathologic change in one or more nerve roots.
139
Syndrome Cont’
• Pathophysiology
– Unknown, but involves altered peripheral/CNS
response thresholds to afferent stimuli
– Sympathetic dysfunction present
– No definitive diagnostic test available, diagnosis on
clinical basis
– Associated with antecedent trauma
– Characterized by burning neuropathic pain, allodynia,
hyperpathia, decreased range of motion, edema, skin
and hair atrophy
– No correlation between severity of injury and severity
of symptoms

Syndrome Cont’
• Treatment
– Physical Therapy
– Sympatholytic medication, sympathetic
blocks, neuropathic pain medications
CRPS Type I
• Formerly known as Reflex Sympathetic
Dystrophy
• Usually follows minor trauma
• 3 Phases
1) Acute – localized severe burning, warm & dry
extremity. Lasts 1 – 3 months
2) Dystrophic – diffuse throbbing pain, cold & cyanotic
extremity, osteoporosis 3 – 6 months
3) Atrophic – pain lessens, severe muscle & skin
atrophy, severe osteoporosis
140
CRPS Type II
• Formerly known as “Causalgia”
• Follows injury to large nerves
• Onset of pain is immediate
• Allodynia, hyperpathia and vasomotor
dysfunction present
• Dramatic pain relief from sympathetic
block
Myofascial Pain
• Pathophysiology
– Also called “Trigger Points” – very common
– Often begins with acute muscle injury
– Pain can last for years, described as aching muscular
pain with tender areas
– Compression of the “Trigger Point” produces severe
pain
• Thought to be secondary to reflex muscle spasms
Æ muscle fatigue Æ muscle ischemia
Myofascial Pain Cont’

• Treatment
– Injections of local anesthetic are both
diagnostic & therapeutic
– Depo-steroids may also be beneficial
– Stretching exercises may help prevent
recurrence
141
Radiculopathy
• Pathophysiology
– Lower back and cervical pain most common
complaint at pain clinics
– Radicular pain from nerve root irritation is sharp,
aching and may “shoot” to distribution of nerve root
– Sensory loss, weakness, hyporeflexia may be present
– Must rule out other causes of root compression:
spinal stenosis, tumor, herpes zoster, arachnoiditis
• Treatment
– Conservative therapy – bed rest, analgesics, local
heat, support
– Epidural steroids - effective in 2/3 of patients
– Surgical decompression
Cancer Pain
• Pathophysiology
– Present in up to 80% of cancer patients
– Two types:
• Patients with chronic benign pain and extended life
expectancy
• Terminal patients with severe, intractable pain –
these patients should receive prompt and
aggressive therapy
– Underlying levels of pain often have acute
exacerbations
Cancer Pain Cont’

• Treatment
– Pharmacologic elevation of pain tolerance –
narcotics/non-narcotics
– Modulation of pain pathways – TENS, acupuncture
– Interruption of pain pathways – blocks, surgical
ablation
– Attack of pathologic condition
142
Pharmacology
IV Induction Agents, Opioids,
Benzodiazepenes
IV induction agents
5 major classifications
barbiturates isopropylphenol carboxylated benzodiazepenes phencyclidine

imidazole
thiopental propofol etomidate diazepam ketamine

thiamylal midazolam
methohexital lorazepam
Þ Ø Ø Ý Ø
interaction with GABA (Cl- channel) interaction
with NMDA
Barbiturates
• 2,5 substitutions of barbituric acid
• Produce sedation by interaction with GABA (1º
inhibitory neurotransmitter in the CNS)
– ×Cl- conductance through GABA channel causes
hyperpolarization of the membrane
• Depression of the reticular activating system
(responsible for wakefulness)
• ØSNS transmission; depression of the medullary
vasomotor center; dilation of venous
capacitance vessels with pooling
– ØBP with reflex × in HR; particularly in hypovolemic
pt
– Causes (-) ionotropy
Barbiturates
• Produce unconsciousness within 30
seconds after IV injection due to rapid
uptake by the brain
– Follows bi-exponential decay curve
• D phase Ö redistribution to inactive (non-CNS),
highly perfused sites; accounts for rapid
awakening
– Skeletal muscle
– Fat; may become sequestered after repeated doses and
re-released into system
• E phase Ö metabolism (hepatic microsomal
enzymes); ½ time thiopental approximately 11
hours
Barbiturates
• Potent cerebral vasoconstrictors
– Used to treat × ICP
– Offers cerebral protection in face of focal
ischemia
– Ø CMRO2
– Utilized as anticonvulsants
• May produce an isoelectric EEG
– Methohexital an exception—may activate epileptic foci
Barbiturates
• Depress medullary ventilatory centers
– Øventilatory response to CO2
• Cough reflex is not attenuated
• Provides no analgesia; may actually have an
antianalgesic effect
• Do not trigger MH
• May cause hepatic enzyme induction after
repeated use
• Highly protein bound
• *Contraindicated in pts with acute intermittent
porphyria
Acute intermittent porphyria
• An autosomal dominant disorder; females > males
• Results from an error in pyrrole metabolism due to
deficiency of porphobilinogen deaminase
• Characterized by recurrent attacks of abdominal pain*,
gastrointestinal dysfunction, and neurologic disturbances
– Attacks precipitated by
• Barbiturates
“ Cr
• Sulfonamides a zy
lad
• Starvation yw
i th
bel
• Infection ly p
ain
”
• ETOH
• Excessive amounts of aminolevulinic acid and
porphobilinogen in the urine; may lead to paralysis/death
Barbiturates
• Inadvertent intraarterial injection can be
devastating
– pH of solution 11; barbiturate crystals
precipitate in blood
• Causes intense pain; vasospasm of limb; may
ultimately lead to gangrene
– Treatment through existing IV catheter (do NOT
remove!):
» Injection of D blocker (phentolamine or
papaverine)
» Dilution with saline
» Lidocaine
» May require brachial plexus or stellate
ganglion block; urokinase to lyse clot
Sodium Thiopental
• IV induction dose:
– 3-5 mg/Kg (adult)
– 5-6 mg/Kg (children)
– 7-8 mg/Kg (infants)
• Onset—10-20 seconds; peak—30-40 seconds
• Duration of action (time until consciousness)
5-15 min due to rapid redistribution
• Does release histamine
– Contraindicated in pts with status asthmaticus
• Allergic reactions manifest as anaphylaxis
Propofol (Diprivan)
• A diisopropylphenol
• Interacts with GABA channels
– Ø rate of dissociation of GABA from channel receptor
• Leads to ÇCl- conductance through channel and subsequent
hyperpolarization of membrane
• 1º side effect Ö pain upon IV injection
– Drug dissolved in a fat emulsion (egg lecithin,
soybean oil)
• May be administered to pts with egg allergy
– Allergy typically to egg albumin; lecithin is a yolk derivative
• Fat emulsion may support microbial growth
– Strict aseptic technique needed; discard after 6 hours
• Some generic formulations contain sulfites as a preservative
– Avoid in atopic or bronchospastic pts; use Diprivan
Propofol cont’d
• *Clearance exceeds hepatic blood flow
– Rapid awakening from initial redistribution to
highly perfused, non-CNS sites (D phase)
– E phase from hepatic and extrahepatic
(pulmonary) extraction
• Pharmacokinetics not altered greatly in pts with
hepatic disease
• Plasma ½ time less than 1/3 of thiopental
– No cumulative effects
• May be administered as a continuous infusion
Propofol cont’d
• CV effects
– ÈÈ SBP, SVR to a greater degree than thiopental
from direct myocardial depression
• ÈSNS activity
• Ç vagal predominance
• HR remains unchanged
• Respiratory effects
– Apnea with larger doses
– Bronchodilation
– ÈÈ airway reflexes
Propofol cont’d
• CNS
– È CMRO2
– È CBF, ÈCPP
• Use with caution in pts with Ç ICP, space
occupying lesions
– May stimulate epileptogenic foci
– Potentiates effects of other sedative-
hypnotics, volatiles, narcotics
• Does not possess intrinsic analgesic properties but
is not anti-analgesic like STP
Propofol cont’d
• Ø rate of PONV
– Sub-hypnotic doses (10 mg IV) may possess anti-
emetic effect
– May be used as sole anesthetic for pts with strong hx
of PONV
• May cause a transient adrenocortical
suppression
– Not sustained as with etomidate
• Should be used cautiously in the parturient
– Ç incidence of infant myotonus, lower Apgar scores
• Potentiates effects of NDMBs
Propofol cont’d
– 2.0-2.5 mg/Kg
• Decrease in elderly or hypovolemic pts
– Onset—40 seconds; peak effect—within 1
minute
– DOA—5-10 minutes
• May release histamine
• Allergy manifests as anaphylaxis; greatest
antigenicity of all of the IV induction agents
– Propofol > thiopental > midazolam
Etomidate (Amidate)
• A carboxylated imidazole derivative
• Enhances the effects of GABA at the receptor
site
• Produces a rapid induction of unconsciousness
followed by a rapid awakening
– Return to consciousness approximately 5X quicker
than STP
• Drug undergoes hepatic metabolism and
hydrolysis in the plasma
• Provides no analgesia; not anti-analgesic
Etomidate cont’d
• *Known for its cardiovascular stability
– È SBP modestly from slight È in SVR
– Minimal changes in CO, HR
– Minimal direct myocardial depression
• Produces less apnea than noted with STP
or propofol
• Causes pain upon IV injection 2° addition
of propylene glycol
• PONV more common
Etomidate cont’d
• Potent cerebrovasoconstrictor
– ÈCMRO2, CBF, ICP
• Produces excitatory spikes on EEG
– Causes myoclonus in 33-50% of pts
• May be attenuated with premedication with benzodiazepenes
or opioids
• *Causes adrenocortical suppression
– Inhibits 11-E-hydroxylase (converts cholesterol Ö
cortisol)
• Dose dependent
• May last for 4-8 hours after injection
Etomidate cont’d
• IV induction dose
– 0.1-0.4 mg/Kg
– Onset--30-60 seconds; peak—1 minute
– DOA 3-10 minutes
• Does not release histamine
Ketamine (Ketalar)
• A phencyclidine derivative
• Antagonizes the effects of N-methyl-D-aspartate (NMDA)
– A mediator of the long-term excitatory effects of
nociception
• Also interacts with other voltage gated Ca++ channels
– NE, muscarinic, serotonergic receptors
• *Produces a dissociative anesthesia
– Resembles a catatonic state
• Eyes open; slow, nystagmic gaze
– Amnestic
– *Intense analgesia
– Ç incidence emergence delirium
• Seen in adults 16-65 years old
• May be attenuated with premedication with
benzodiazepenes
Ketamine cont’d
• CNS effects Ö excitatory
– ×CBF 60-80%
– ×CMRO2
– ×ICP
• CV effects
– ×SNS tone
• Inhibition of reuptake of catecholamines
• ×HR, BP, CO
– ×myocardial O2 consumption
Ketamine cont’d
• Respiratory effects
– Potent bronchodilator
• *IV induction agent of choice for asthmatics
– Minimum respiratory depression
– Does not depress laryngeal reflexes; may be
slightly enhanced
– Chemoceptor response to CO2 preserved
– ×airway secretions from stimulation of
muscarinic receptors
• Should be co administered with an anticholinergic
Ketamine cont’d
– 1.0-2.5 mg/Kg
– Onset--<30 seconds; peak—1 minute
– DOA—5-15 minutes
• Undergoes hepatic metabolism
• Does not release histamine
• Çuterine tone but preserves placental blood flow
IV Induction Agents Miscellany

• CV depression
– Propofol>STP>etomidate>ketamine
• Respiratory depression
– Propofol>STP>etomidate>ketamine
• CNS excitation
– Ketamine>etomidate>propofol>STP
• Production of PONV
– Etomidate>STP>ketamine>propofol
Opioids
• Derived from the poppy plant (Papaverum
Somniferum); A.K.A. narcotics (narc = numbness/stupor; otic
= like)
• The drugs of choice for the control of moderate to
severe pain
– Produce analgesia without loss of proprioception or
consciousness
• 3 classes
phenanthrenes phenylpiperidines benzylisoquinolones
(synthetic) (lack opioid activity)
-morphine -meperidine
-papaverine
-codeine -fentanyl
-noscapine
-fentanyl analogues
-sufentanil, alfentanil,
remifentanil
Opioids cont’d
• Opioids are stereospecific agonists (ligands) for
opioid receptors
– Receptors found primarily in CNS
• Cerebral cortex, brain stem, spinal cord
– Also found in peripheral tissues
– Prototype is morphine
• Endogenous ligands Ö A.K.A. endorphins
– E endorphins
– Dynorphins
– Enkephalins
– Neoendorphins
Mechanism of Action of Opioids

stereospecific
agonist binds to
opioid receptor
presynaptic
inhibition
activation of anti-
nociceptive
systems
bradykinin substance P glutamate
È neuronal
transmission of
afferent ÇK+ hyperpolarization
neurons conduction of membrane
È pain
Opioid Receptors
• Mu1
– *Primary effect of stimulation Ö supraspinal
analgesia
– Spinal analgesia
– Euphoria
– Miosis
– Urinary retention
• *Most clinically useful opioids are highly specific
ligands for this receptor
Opioid Receptors cont’

• Mu2
– *Primary effect of stimulation Ö spinal
analgesia
– Pruritis
– Respiratory depression
– Emesis
– Bradycardia
– ÈÈGI motility
– Physiologic dependence

• Delta
– Supraspinal analgesia
– Respiratory depression
– Urinary retention
– ÈGI motility
– Physiologic dependence
• Kappa
– Supraspinal analgesia
– *Sedation
– *Dysphoria
– Miosis

• Sigma
– No longer classified as an opioid receptor
- Dysphoria
- Hypertonia
- Tachycardia
- Tachypnea
- Mydriasis
Opioids
• Pharmacokinetic differences between opioids

is 2º variation in individual agent’s lipid
solubility
• Clearance of all opioids is principally via
hepatic conjugation
– Exception Ö remifentanil
• Cleared entirely by non-specific plasma esterases
Opioids cont’
• È CBF, CMRO2
– Fentanyl, sufentanil, alfentanil’s effects on
CBF and ICP insignificant
• X the BBB, placenta
– May cause neonatal depression following
maternal parenteral dosing
• Cause depression of ventilation
– Shift the CO2 response curve to the R
• Cause sphincter of Oddi spasm
– fentanyl > morphine > meperidine
Relative potencies of opioid

agonists
0.1 1 10 20 100 1000
meperidine morphine hydromorphone alfentanil fentanyl sufentanil

(prototype) remifentanil
Morphine
• Causes arteriolar and venous dilation
– Dilates capacitance beds
– Useful in the treatment of pulmonary edema
• *Causes histamine release
• Causes adrenocortical suppression at high doses
• Suppresses the cough centers in the cerebral medulla
• Emetogenic
• May reactivate herpes simplex following intrathecal or
epidural administration
• Active metabolite-morphine-6-glucuronide
– May actually be responsible for most of morphine’s
analgesic effects
Meperidine (Demerol)
• Contraindicated in pts taking MAOIs as it Ès
reuptake of serotonin
– May cause serotonin syndrome
• Has an atropine-like effect
– may Ç HR
• Contraindicated in pts with history of seizures
– Active metabolite normeperidine is a cerebral
stimulant
– May accumulate after repeated doses
• Specifically binds to opioid receptors in
substantia gelatinosa
– Also has potent local anesthetic properties
– Provides excellent spinal analgesia
– Useful for tx of post-operative shivering
Fentanyl (Sublimaze), Sufentanil (Sufenta)

• Rapid onset, short DOA
– 2º high lipid solubility
• Depression of ventilation may outlast analgesia
• CV stability even at high doses
• Intense suppression of laryngeal/cough reflexes
• Chest rigidity noted
• Fentanyl may be administered transdermally or
transmucosally
• Sufentanil may cause ÈÈ HR
• Devoid of histamine release
Fentanyl Dosage Ranges

• 1-5 mcg/kg—low dose
• DOA approximately 8-30 minutes
• 6-10 mcg/kg—moderate dose

• DOA approximately 60-90 minutes
• > 10 mcg/kg—high dose

• DOA longer than morphine—approximately 16º
Alfentanil (Alfenta)
• Alfentanil has a rapid onset 2º low pKa
– approximately 90% of the drug exists in the
nonionized form @ physiologic pH
• Associated with >er È in HR, BP than fentanyl,
sufentanil
• Smaller VD
– Lower lipid solublilty
– Higher protein binding
• Non-cumulative
• May elicit an acute dystonic reaction in
Parkinson’s pts
Remifentanil (Ultiva)
• Unique pharmacokinetic profile allows for rapid
onset and rapid dissipation of the drug’s effects
– Elimination ½ time 6 minutes
• Cleared by plasma esterases
– Unchanged by renal or hepatic failure
– Not affected by plasmacholinesterase deficiency
• Causes intense chest wall rigidity
• May cause Ç SNS activity due to rapid
dissipation of analgesic effects
Neuraxial Opioids
• Opioids may be given intrathecally or via
epidural
– Bind with receptors found in substansia
gelatinosa (Rexed’s lamina II); produce spinal
analgesia
• Morphine is hydrophilic
• Greater rostral spread
–Slow onset, longer DOA
–May cause a delay in respiratory
depression
• Fentanyl and its analogues are lipophilic
–Less rostral spread
–Quick onset, short DOA
Side Effects of Neuraxial Opioids
• 1º respiratory depression
• Pruritis
• N/V
• Sedation
• Urinary retention
Opioid Antagonists
• Will fully reverse the analgesic effects and
untoward side effects associated with
opioids by competitive inhibition of ligand
effects at the opioid receptor
• May be used in the differential dx of the
unresponsive OD pt
• May ppt acute withdrawal in narcotic
addicted pts
Naloxone (Narcan)
• Pure opioid antagonist
– Devoid of agonist activity
• Rapid onset after IV dose (<1 minute)
• DOA 20-60 minutes
– Effect of opioid may outlast naloxone’s effects
– May need to re-administer
– Naltrexone (ReVia, Trexan) oral, DOA 24-72º
– Nalmefene (Revex) 10-20 X as potent as
naltrexone
Rapid Reversal of Narcotics
• HTN
• Ç HR
• Dysrhythmias (VT, VF)
• Pulmonary edema
– From SNS stimulation 2º rapid reversal of
analgesic effect of opioids and abrupt onset of
pain
S/S of Opioid Withdrawal

• Dysphoria
• N/V
• Muscle aches
*N
• Lacrimation de ee d
• Rhinorrhea mi finiti 3 or
sta ve m
• Mydriasis ke dx ore
n f ; m s/
or a s
• Piloerection i n f y b fo r
l ue e
• Sweating nz
a
• Diarrhea
• Yawning
• Fever
• Insomnia
Narcotic Agonist/Antagonists
• Displace opioid from the Mu2 receptor
• Agonist at kappa receptors
• Known for minimal production of respiratory
depression
– “Ceiling effect”
• Useful in the tx of pruritis from intrathecal opioids
• Nalbuphine (Nubain)
– Antagonist @ Mu, agonist @ kappa
– Equipotent with morphine
– 25% of activity of naloxone
• Butorphanol (Stadol)
– As above with only 15% potency of naloxone
Benzodiazepenes
• High therapeutic index
• Production of anterograde amnesia
• Specific site of action as anticonvulsants
• Muscle relaxation, sedative, and anti-anxiety
properties
• Easily reversible by a specific benzo reversal
agent—flumazenil
• Still remain the drug of choice when treating
anxiety
• Do not cause enzyme induction to the same
extent that barbiturates do
• Low physiologic dependence
Benzodiazepenes cont’d
• Prototype for the class is diazepam (Valium)
• Benzos of clinical importance in the U.S. are:
– Diazepam (Valium)
– Midazolam (Versed)
– Lorazepam (Ativan)
• Structurally formed around a basic benzene ring
fused to a 7-membered diazepene ring
• All important benzodiazepenes have a 1,4
diazepene ring and a 5-aryl substituent
• Many benzodiazepenes have active metabolites
The Benzodiazepene Receptor

• Identified in the CNS in 1977
• Occur almost exclusively on post-synaptic
nerve endings
• Found in various areas of the brain and
spinal cord
– Highest number found in the cerebral cortex,
particularly in those areas associated with
memory formation
The Benzodiazepene Receptor
• Sequestration of
receptors in the CNS
responsible for the
relative lack of side
effects peripherally
• The receptor is an
integral part of the
GABA receptor
– GABA is an inhibitory
neurotransmitter in
the CNS
Mechanisms of Benzo Activity
Diazepam (Valium)
• Insoluble in H2O; dissolved in organic solvents
• pH 6.6-6.9—causes pain upon IM injection
– Absorption unreliable
• May cause venous thrombosis/phlebitis when
administered IV
• Implicated in higher incidence of birth defects
– Cleft palate and lip
– Should not be administered during the 1st
trimester of pregnancy
Diazepam (Valium) cont’
• Pharmacokinetics
– Rapidly absorbed from the GI tract
– Initial rapid uptake by the brain, followed by
redistribution to inactive sites
– Highly protein bound, highly lipid soluble,
rapidly crosses the placenta
– Large VD from extensive tissue uptake
– Decrease in plasma protein levels cause a
magnified effect of the drug

• Metabolism
– Metabolized by microsomal enzymes
• Oxidative pathway
• Loss of a methyl group (N-demethylation)
– 2 metabolites
• Desmethyldiazepam—principle metabolite;
slightly less potent than parent compound; slow
rate of metabolism
• Oxazepam—rapidly conjugated by glucuronic
acid

• Elimination half-times
– Diazepam
• 21-37 hours
– Desmethyldiazepam
• 4-96 hours
– Significant prolongation of the above T1/2
seen with:
• Hepatic disease
• Advanced age
• Effects on organ systems:
– Ventilation
• Minimal depressant effects when administered
alone
• Only slight increases in PaCO2
• CO2 response curve not shifted to the right as
seen with opioids
• Exaggerated depression when co-administered
with opioids, ETOH, other CNS depressants, or
to elderly, COPD, or otherwise debilitated pts

• Cardiovascular
– Therapeutic doses cause minimal reductions
in BP, CO, and SVR
– No effect on the SNS
– No orthostatic depression
– Combination with opioids cause negative
ionotropy (a dose related, additive response)

• Skeletal muscle
– Relaxation caused from a glycine-like activity
• Spinal effect on internuncial neurons; no
effect at the NMJ
• Direct effect on the gamma-efferent
system (a reduction in output from the
cord reduced muscle tone)
• Drug interactions
– ETOH
• Depressant effects of benzodiazepenes are
greatly magnified
• Possibly due to a common site of action at the
GABA receptor for the two drugs
• Cross tolerance occurs
– Benzodiazepenes useful in the treatment of
the delirium tremens
– Cimetidine/ranitidine
• Cimetidine delays hepatic clearance by interfering
with the oxidative-reductive pathway
• Both drugs increase the bioavailability of the
benzodiazepenes

• Drug interactions
– Anesthetics
• MAC of all inhalational anesthetics is
decreased
• Induction does of thiopental and propofol
are reduced
• CNS depressant effects are additive when
given in conjunction with anesthetics,
opioids, and other sedatives
– Contraindicated in pts with acute narrow-
angle or open-angle glaucoma
Midazolam (Versed)
• H2O soluble due to the presence of an
imidazole ring
– Stable in aqueous solutions
– Rapidly metabolized
• 2-3X as potent as diazepam
• Shares all of the same effects as the
other benzodiazepenes
Midazolam (Versed) cont’
• pH of parenteral solution 3.5
– Imidazole ring is open at pH <4.0
– Closes at pH above 4.0 (i.e. @ physiologic
pH)
• Compound becomes highly lipid soluble
• Causes no pain upon IM or IV injection

• Rapidly absorbed via the GI tract
• Extensively protein bound
• Highly lipid soluble; rapidly crosses the
BBB and placenta
• Rapidly redistributed to inactive sites and
available for hepatic metabolism
– Undergoes hydroxylation; metabolites have
minimal potency

• Effects on organ systems
– Cerebrovascular
• Dose-dependent reductions in CBF and
CMRO2
• Produces no increase in ICP
• Affords greater cerebral protection than
diazepam (but less than barbiturates) in
face of ischemia
• Effects on organ systems
– Cardiovascular
• Produces a greater increase in HR and
decrease in BP than diazepam
• Similar to effects produced by thiopental
– Respiratory
• Similar effects as from diazepam
• COPD pts may have more of an adverse
effect
– Contraindicated in pts with acute narrow-
angle or open-angle glaucoma
Lorazepam (Ativan)
• Intermediate onset and duration of action
• Similar to diazepam in irritation/production
of arteriospasm if improperly injected
– Propylene glycol or benzyl alcohol as a carrier
• Used as a sleep aid, anti-anxiety or
amnestic agent, tx of or prophylaxis
against delirium tremens, antiemetic
• Greatest production of amnesia
• Contraindicated in pts with narrow-angle
glaucoma
Clinical Uses for the

Benzodiazepenes
• Pre-operative medication
• Induction/maintenance of anesthesia
• IV sedation
• Anticonvulsants
• Treatment of delirium tremens
• Production of skeletal muscle relaxation
• Sleep aids
• Treatment of night terrors
• Attenuating emergence delirium noted with the
use of ketamine
Adverse Effects of the
Benzodiazepenes
• Age and dose dependent
– Ataxia, drowsiness, prolonged sedation,
especially when co-administered with other
sedatives
– Paradoxically increased anxiety
– Increased confusion/amnesia
– ODs rarely fatal; treatment is supportive
Benzodiazepene Reversal
• Flumazenil (Romazicon)
– Approved for use in the U.S. in 1991
– A specific, exclusive benzodiazepene
receptor antagonist
• Competitively inhibits agonist activity
• High affinity for the benzo receptor
• Some weak intrinsic agonist activity
Flumazenil
• Does not produce symptoms of abrupt
reversal
– Anxiety
– HTN
– Tachycardia
– Neuroendocrine evidence of a stress
response
• Probably secondary to flumazenil’s weak
agonist activity
• May produce seizures (chronic users,
tricyclic poisoning)
Flumazenil, cont’d
• Does not alter MAC
• Does not reverse effects of ethanol,
opioids, barbiturates
• Dose 0.2-1.0 mg IV
• Onset 2 minutes, peak effect 6-10
minutes, DOA brief (alpha T1/2 7-15 mins,
beta elim T1/2 41-79 mins
• 50% of drug is protein bound; hepatic
clearance predominant
Flumazenil, cont’d
• Extent/duration of reversal secondary to
plasma level of benzo agonist
• Pt should be monitored for resedation
• Other side effects:
– Seizures Agitation
– N/V Headache
– Dizziness Cutaneous vasodilation
– Pain upon injection Paresthesia
– Emotional lability Abnormal vision
– Fatigue Benzo w/d in dependent pts
Notes
Opioid Fact Sheet Receptor Types
Mu Mu2 Kappa Delta
Site supraspinal spinal supraspinal supraspinal

spinal spinal spinal
Ca +2
Mediator K+ channel K+ channel channel K+ channel
Endogenous agonists endorphin endorphin dynorphin enkephalin

(met- and leu-)
Exogenous agonists morphine morphine UO488H DPDPE

all commonly all commonly
known synthetic known synthetic
opioids opioids pentazocine
Antagonists naloxone naloxone naloxone naloxone
(low dose) (low dose) (high dose) (medium dose)
naltrexone naltrexone naltrexone naltrexone

Nor-BNI
Physiologic Effects
Pain analgesia analgesia analgesia analgesia
Psychotropic euphoria dysphoria
Ventilatory depression depression
Pupilary miosis miosis
GI constipation mild constipation
Chronotropic bradycardia
GU urinary retention
physical physical
Dependence dependence dependence
Respiratory Review I
O2 Content of Blood Ö CaO2

• O2 content is the sum of two factors:
1) O2 dissolved in solution
• 0.003 ml O2 dissolved per 100 ml of plasma
– The solubility coefficient of O2 at 37º C
2) O2 bound to hgb
• 1.34ml O2/g Hgb
– O2 content of the blood per 100 ml:
(0.003 X PaO2) + (SaO2 X hgb X 1.34)
Arterial (CaO2) = [(0.003 X 100) + (0.98 X 15 X 1.34)] = 20.00

Venous (CvO2) = [(0.003 X 40) + (0.75 X 15 X 1.34)] = 15.19
Arterial to venous difference = CaO2-CvO2 approximately 5 ml
O2-Hgb Dissociation Curve

HGbF
carboxyHGb
metHGb
È2,3 DPG
50
26.6
×
× P50: PaO2 26.6 mmHg @ SaO2 50%
168
SaO2 – PaO2 Correlation
“40, 50, 60 = 70, 80, 90”

PaO2 of 40 = Sat of 70%
Factors Influencing the O2-Hgb

Dissociation Curve
• Rightward shift of curve
– O2 has a decreased affinity for Hgb; delivery to
tissues is facilitated
• Occurs with hyperthermia, Ç2,3 DPG, ÇCO2,
ÈpH
– 2,3 DPG is increased during pregnancy,
anemic states
– Bohr effect Ö delivery of O2 to tissues is
increased with Ç[H+]
Remember “RIGHT”
+
Right shift Increase in: 2,3 DPG H ions Temperature
Factors Influencing the O2-Hgb

Dissociation Curve Cont’
• Leftward shift of curve
– O2 has an increased affinity for Hgb; delivery
to tissues is reduced
• Occurs with hypothermia, È2,3 DPG, ÈCO2, ÇpH,
fetal hgb, methemoglobin, carboxyhemoglobin
169
Oxygen delivery (DO2)
Oxygen consumption (VO2)
• O2 delivery Ö DO2
– The amount of oxygen delivered to the tissues
• A factor of the CaO2 and cardiac output (Q)
– 20.00 X 5L/min = 1000 ml O2/min
• O2 consumption* Ö VO2
– The amount of O2 utilized by the tissues
• Dependent on variables including metabolic need,
rate, etc.
• Typical 250 ml O2/min
– Fick equation
• A relationship between O2 content and O2
consumption
Respiratory Quotient
• The ratio of carbon dioxide diffusing from blood
into alveoli (CO2 production) to oxygen diffusing
in the opposite direction (O2 consumption)
» CO2 production (200)

O2 consumption (VO2) (250)
• Normal value is approximately 0.8 (0.7-1.0)

• May be used to calculate the basal metabolic
rate
Alveolar to Arterial (A/a) O2

Gradient
• The difference between the PAO2 and PaO2
– Typical A/a gradient 4-10 mmHg
» Age + 10
4
– Secondary to normal physiologic shunt
produced by the return of deoxygenated blood
from bronchial veins directly into the
pulmonary vein
– A/a gradient will increase from respiratory
distress, interstitial lung disease, with aging
170
CO2 Content and Transport
• CO2 found:
– As HCO3- (73%)
– Attached to hgb; forms carbamino (23%)
– Dissolved in blood (24 X more soluble in fluid
than O2) (7%)
• CO2 combines reversibly with H2O; forms
carbonic acid
– CO2 + H2O H2CO3
• Haldane effect: O2 consumption by the
tissues favors uptake of CO2 into the blood
Arterial Blood Gas Values

• pH Ö 7.40 (7.35-7.45)
• PaO2 Ö 80-100 mmHg
• PaCO2 Ö 35-45 mmHg
• HCO3- Ö 22-26 mEq/L
• O2 saturation Ö 95% or greater
• Base excess (BE) -2-+2
Mixed Venous Blood Gas Values

• pH Ö 7.36 (7.31-7.41)
• PvO2 Ö 35-40 mmHg
• PvCO2 Ö 41-51 mmHg
• HCO3- Ö 22-26 mEq/L
• O2 saturation Ö 70-75%
• Base excess (BE) -2-+2
• The best assessment of cardiac output is
mixed venous O2 saturation
171
Interpretation of ABGs
• For every 10 mmHg È CO2, pH will Ç
approximately 0.1
– PaCO2 30 mmHg Ö pH 7.50*
• For every 10 mmHg Ç CO2, pH will È

approximately 0.05
– PaCO2 50 mmHg Ö pH 7.35*
*Based on normal pH of 7.40 and PaCO2 40 mmHg
Acid-Base Balance
• Regulation of H+ ions in body fluids

– Respiration (rapid response to × [H+])
• Production of CO2 from metabolism; combines with
H2O to form carbonic acid
– Other metabolic acids formed from dietary
intake
» Sulfuric, Phosphoric, Organic acids
Acid-Base Balance Cont’

• Regulation of H+ ions in body fluids cont’
– Chemosensitive area in medulla senses È blood pH;
stimulates ventilatory center to Ç RR, thereby
removing CO2
– When CO2 removal exceeds HCO3- excretion,
resultant alkalosis ensues
– If ventilatory centers are depressed; CO2 builds
up, leads to carbonic acid production and È
pH; acidosis ensues
172
Respiratory Acidosis/Alkalosis
Acidosis from: Alkalosis from:

-Hypoventilation -Hyperventilation
-oversedation with -Anxiety
sedatives, narcotics -Iatrogenic (Ç vent
-COPD, pneumonia settings)
-CNS depression -Pregnancy
(physiologic) -ASA overdose
-
*pH will correct over time 2º renal excretion/retention of HCO3
Acid-Base Balance, Cont'd

• Buffer systems-pairs of substances which
resist changes in acidity of solutions
– Bicarbonate/carbonic acid is the 1º buffer pair in the
body
• H+ + HCO3- H2CO3 H2O + CO2
– Increases in H2CO3 lead to acidosis 2º Ç [H+]
– Increases in HCO3- lead to alkalosis 2º È [H+]
• Normal ratio of HCO3- to CO2 20:1
Renal Regulation of pH
• 90% of bicarbonate (HCO3-) is reabsorbed by the
proximal tubules
• H+ and Na+ are exchanged
– Facilitates H+ excretion via Na+ and HCO3-
reabsorption
– Ammonium (NH4+) also excreted
• Carbonic anhydrase (secreted by renal brush border)
catalyzes formation of HCO3- from CO2 and H2O
– Also found in RBCs
– When HCO3- decreases and H+ increases, metabolic
acidosis ensues
– If HCO3- retention exceeds H+ excretion, metabolic
alkalosis ensues
173
Anion Gap
• Determined from measurement of plasma
Na+, Cl-, and HCO3-
– Anion gap = [Na+] – [Cl-] – [HCO3-]
• Normal value 12 mM/L
• Used in the differential dx of metabolic
acidosis
– Hyperchloremic acidosis
• Diarrhea, renal tubular acidosis
– Wide-anion gap acidosis
Metabolic Acidosis/Alkalosis
Acidosis from: Alkalosis from:
-Diabetic ketoacidosis -Overdose of diuretics
-ASA, ETOH, ethylene -Cushing’s disease
glycol poisoning -Exogenous
-Lactic acidosis 2º corticosteroids
hypoperfusion -Aldosteronism
-Renal failure -From Ç excretion of
H+, K+, Cl-
-Fluid losses from upper
GI tract (ÈH+ 2º HCl
loss)
Physiologic Effects of Acidosis vs. Alkalosis
Acidosis Alkalosis
-Rightward shift of O2- -Leftward shift of O2-
Hgb dissociation curve Hgb dissociation curve
-Increase in K+ -Decrease in K+
-Vasodilation -Decrease in ionized
-Myocardial depression Ca++
-Vasoconstriction
(cerebral/coronary/systemic)
-Bronchoconstriction
174
Lung Volumes Defined
• Tidal volume (TV) is the volume of air
moved in and out of the respiratory tract
during each ventilatory cycle
• Inspiratory reserve volume (IRV) is the
additional volume of air that can be forcibly
inhaled following a normal inspiration
• Expiratory reserve volume (ERV) is the
additional volume of air that can be forcibly
exhaled following a normal expiration
Lung Volumes Defined Cont’

• Residual volume (RV) is that volume of
air remaining in the lungs after a maximal
expiration. It cannot be expired no matter
how vigorous or long the effort
» RV = FRC – ERV
• Minute volume (A.K.A. minute ventilation)
is the volume of air exhaled per minute
» MV = RR X VT
Lung Capacities Defined

• Vital capacity (VC) is the maximal volume of air
that can be forcibly exhaled after a maximal
inspiration
» VC = TV + IRV + ERV
• Functional residual capacity (FRC)* is the
volume of air remaining in the lungs at the end
of a normal expiration
» FRC = RV + ERV
• Total lung capacity (TLC) is the volume of air
in the lungs at the end of a maximal inspiration
» TLC = FRC + TV + IRV = VC + RV
175
Lung capacities, Cont'd
• If vital capacity is measured to be < 30%

of predicted, this is an ominous sign
– Pt may need post-op ventilation
• FRC may be:
– Diminished with pregnancy, GA, positioning
– Increased in the elderly, COPD, asthma,
chronic bronchitis
• Will ultimately affect speed of induction and breath
to breath changes of volatile agent
TLC (total lung

capacity) 5800 ml
Lung Volumes and Capacities
VT (tidal volume)
500 ml
IRV (inspiratory
reserve volume)
3000 ml
ERV (expiratory
3000 reserve volume)
1100 ml
500 4600
VC (vital capacity)
4600 ml
FRC
2300 RV (residual
FRC volume) 1200 ml
2300 1100
FRC (functional
residual capacity)
1200 2300 ml
Closing Volume and Capacity

• During a forced expiration, small airways begin to close
– Remaining volume that can be exhaled is known as
the closing volume
– Closing volume (CV) + residual volume (RV) =
closing capacity (CC)
• Closing volume may = or exceed FRC

– Seen in RDS, ARDS, morbid obesity, elderly
– Premature closure of airways leads to atelectasis,
hypoxia, hypercarbia
176
Closing Volume/Capacity
3000
500
airway closure begins here FRC
1100 CV
CC
1200
Pulmonary Function Tests

• PFTs are typically reported in both
absolute values and as a predicted
percentage of normal. Normal values vary,
depending on gender, race, age, and
height
– Maximal breathing capacity (also called "maximal
voluntary ventilation") is the maximum volume of air
that can be exhaled by voluntary effort in a 15 second
interval. This volume is multiplied by 4 and expressed
as liters per minute
– Forced expiratory volume 1 (FEV1) - the volume of
air that is forcefully exhaled in one second
– Forced vital capacity (FVC) - the volume of air that
can be maximally forcefully exhaled
Pulmonary Function Tests

• PFTs cont’
– Ratio of FEV1 to FVC (FEV1/FVC) - expressed as a
percentage; normal values are around 80%
– Forced expiratory flow (FEF25 -75) - the average
forced expiratory flow during the mid (25 - 75%)
portion of the FVC
– Peak expiratory flow rate (PEFR) - the peak flow
rate during expiration.
Restrictive (fibrosis): ratios normal or slightly increased

Obstructive (asthma, COPD): ratios usually low
177
Flow-Volume Loop
Adapted from Yao & Artusio’s

th
Anesthesiology, 5 ed; pp 11
Abnormal Flow-Volume Loops
Adapted from Yao & Artusio’s

Anesthesiology, 5th ed; pp 12
Zones of the Lung
*V/Q optimal in this zone
shunt = perfusion without ventilation deadspace = ventilation without perfusion
178
Notes
Notes
179
Respiratory Review II
Chronic Obstructive Pulmonary

Disease-COPD
• overall features:
– loss of lung elasticity
• breakdown of parenchyma
• development of blebs, bullae
• coughing ((+/-) productive)
• dyspnea
• inspiration not typically affected; obstruction to
expiration noted
– expiratory wheeze
• subclasses:
– chronic bronchitis
– emphysema
Chronic bronchitis vs. emphysema

“blue bloater” “pink puffer”
glandular hypertrophy Ö loss of lung parenchyma
Çsecretions few secretions
Çobese thin
ÇPaCO2, ÈPaO2 PaCO2 WNL
bronchospastic Ö ØPaO2 only in advanced cases
(+) response to bronchodilators not bronchospastic
Çincidence of cor pulmonale HCT WNL
ÇHCT
PFT’s, volumes, capacities

ÇCC with air trapping ÇCC with air trapping
ÇFRC ÇFRC
ÈFEV1/FVC ÈFEV1/FVC
ÇRV/TLC ÇRV/TLC
VT usually unchanged
Pre-op care of COPD pt
• 3baseline ABGs, PFTs
• d/c smoking if possible
– Ècarboxyhemoglobin levels Ö improved
oxygenation
• chest physiotherapy
• bronchodilators
• ABX
– more applicable for chronic bronchitis pt
Anesthetic concerns for COPD

• slower inhalation induction time
– ÇFRC dilutes out agent; slows rate of rise of
FA/FI
• peak inspiratory pressures elevated 2º
bronchospasm, fibrous lung tissue
• ventilator settings:
– large VT (10-15 cc/Kg)
– I:E with a more sustained expiratory phase
(I:E 1:2.5, 1:3)
– slower RR
• maintain PaCO2 near baseline values
Anesthetic concerns for COPD, cont’d

• FiO2 should be < 50%
– COPDers rely on hypoxic drive to ventilate
(esp “blue bloaters”)
• high O2 concentrations may cause
hypoventilation/apnea
• avoid N2O
– may rapidly expand blebs, bullae Ö
pneumothorax risk
– ÇPVR
• anticipate need for post-op ventilation
– avoid post op residual NM blockade
– use sedatives, narcotics, local with care
asthma
• reactive airway disease
– bronchial inflammation
– expiratory obstruction
• wheeze, productive cough, dyspnea
– Çincidence in females, African-Americans
– individuals typically atopic
• asthma, nasal polyps, ASA allergy Ö Sampter’s
triad
• 1º finding Ö hypoxemia
Intraoperative concerns
• airway manipulation may lead to bronchospasm
– may be difficult to reverse
– use bronchodilators, IV lidocaine pre-
laryngoscopy
– volatiles have bronchodilating properties
• sevoflurane most potent bronchodilator
• desflurane may cause Ç in airway
resistance, especially in smokers
• N2O Ç PVR, ÈFiO2
– limit dose of anticholinesterases
• increases cholinergic tone
– avoid non-specific E-antagonists
Respiratory pharmacology
• E-adrenergic agonists
– mainstay of asthma/bronchospastic disease
treatment
• facilitate bronchodilation via E agonism
– albuterol (Ventolin, Proventil)
• aerosolized
– terbutaline, epinephrine sq
• may be used in the tx of status asthmaticus
– A sustained bronchoconstriction with severe
dyspnea, hypoxia, hypercarbia leading to
respiratory/cardiac arrest
Respiratory pharmacology
– aminophylline (Theophylline)
• phosphodiesterase (PDE) inhibitor; × cAMP,
[NE], overall × in sympathetic activity
–IV intraoperatively, PO available
»IV dose for bronchospasm: 5-6 mg/Kg
bolus followed by maintenance infusion
of 0.5-1.0mg/Kg/hr
-
p ro
2° to of
y
»caution in pts with CAD, arrhythmias,
ited icit
lim gen
e is mo
Us rh yth drug
cor pulmonale, CHF
ar
»check serum theophylline level before
loading dose
»therapeutic level 10-20 mcg/ml
respiratory pharmacology, cont’d

• ipratropium (Atrovent)
– a synthetic congener of atropine, administered as an
aerosol
– used in conjunction with E-adrenergic agents
• corticosteroids
– may be inhaled or PO
– pt may need stress-dose steroid coverage
intraoperatively
• montelukast (Singulair)
– inhaled or PO
– non-steroidal; leukotriene receptor antagonist
– prophylactic/daily maintenance
restrictive airway disease

• two types
– extrapulmonary origin
• mechanical restriction of respiration
– kyphoscoliosis, scleroderma, ankylosing
spondylitis, obesity, pleural effusion
– pulmonary origin
• mechanical restriction of respiration with
interference with gas exchange
– tuberculosis, sarcoidosis, asbestosis, fungal
infection, chemical or radiation pneumonitis,
pulmonary fibrosis
restrictive airway disease
• PFTs
– ÈTLC, ÈVC, ÈFEV1
– ***FEV1/FVC within normal limits***
• anesthesia adds to hypoventilation
– caution with use of sedatives, narcotics,
NDMBs
– ÇRR, ÈVT; monitor PIP closely
• avoids barotrauma
ARDS
• a.k.a. “shock lung”, hyaline membrane disease
• pathophysiology 2° complement activation
– lung capillaries become increasingly permeable
• leakage of plasma proteins, RBCs, WBCs into
alveoli and interstitium
• × platelet aggregation leads to pulmonary
microemboli
• ØFRC
• ×shunt
• ×PVR (may lead to CV decompensation)
• ×secretions
• severe hypoxemia, hypercarbia
– mortality 50%
triggers for development of ARDS

• massive trauma
– direct lung injury
• massive transfusion or volume resuscitation
• chemical inhalation
• burns
• shock
• sepsis
• aspiration
• post pulmonary embolus
• pancreatitis
care of the ARDS pt
• pts are intubated/mechanically ventilated
– settings:
• ×× VT, RR
– ultimately leads to barotrauma
» high frequency jet or oscillating ventilation
more desirable
» inhaled nitric oxide (NO) selectively dilates
pulmonary vasculature; × potential for
toxicity, methemoglobinemia
• PEEP is essential
– may Ø venous return, BP, CO
**ventilator on anesthesia machine may be unable to
provide necessary respiratory parameters
Lung Cancer
• 4 major types:
– adenocarcinoma
– bronchogenic CA
– alveolar cell CA
– undifferentiated (large cell, small (A.K.A. oat) cell) CA
• 100,000 cases/year
• leading cause of death from cancer in both
males and females
• 1º risk factor Ö cigarette smoking
– responsible for 85% of cases
lung CA co-morbidities
• COPD
– from long-standing tobacco use
• bronchial obstruction
• atelectasis
• pneumonia/consolidation
• pleural, pericardial effusions
• pulmonary HTN
• respiratory insufficiency
• CAD
• Çincidence of ETOH abuse
– possible hepatic involvement
lung CA co-morbidities, cont’d
• metastasis
– brain, bone 1º sites
• paraneoplastic syndromes (rare)
– associated with small (A.K.A. oat) cell
carcinoma
• SIADH
• Cushing’s, Ç ACTH
• myasthenic syndrome
– Eaton –Lambert Syndrome
– A.K.A. Lambert-Eaton Myasthenic Syndrome –
“LEMS”
lung CA co-morbidities, cont’d

• myasthenic syndrome
–Eaton –Lambert (A.K.A. LEMS)
• etiology unclear; probably due to a È
release of ACh @ the NMJ
• truncal/lower extremity weakness; fatigue
• symptoms improve with exercise; (+)
feedback for the Ç release of Ach
• **highly sensitive to the effects of
NDMBs
– caution with use of defasiculating doses!
One lung anesthesia

• used for lobectomy, pneumonectomy,
esophagogastrectomy, thoracoabdominal
aneurysm resection
• achieved with the use of a double lumen tube or

a bronchial blocker
– placement verified via direct flexible bronchoscopy
– L-sided DLT easier to place; R-sided DLT may
obstruct the RUL bronchus with incorrect placement
– allows for the intraoperative deflation of the non-
dependent lung; facilitates better surgical exposure
One lung anesthesia, cont’d
• *1º concern with OLA is shunt
– may see hypoxemia, hypercapnia
• surgical (non-dependent) lung receives no
aeration but remains perfused until surgeon
ligates the pulmonary artery to the surgical
site
• lateral decubitus adds to the shunt;
dependent lung receives Ç blood flow but
aeration is restricted

• Vent settings for one lung anesthesia
• vent settings: ÈVT, ÇRR
• monitor PIP; airway pressures may be high 2º
OLA, pt disease
– HPV is altered with the use of inhalation anesthetics
@ >1.0 MAC, use of NTG, SNP
– if oxygenation remains poor during OLA, CPAP may
be administered via the ETT to the non-dependent
lung
• not to exceed 5 cm H20; may passively inflate the lung
– Addition of PEEP to the dependent lung controversial
– *Definitive tx of poor oxygenation is re-inflation of
the non-dependent lung (transient)

• before closure, the operative lung is re-inflated with a
Valsalva maneuver to test suture line for air leaks
• chest should be fully closed with chest tube to suction
before the pt is allowed to spontaneously ventilate
– (-) intrathoracic pressure will entrain air through the
wound; may lead to tension pneumothorax
• extubate if possible
– (+) pressure ventilation places pressure on fresh
bronchial stump
– remove DLT and re-intubate with single lumen tube if
pt is to remain intubated
• pts, (particularly pneumonectomy) are at Ç risk for
development of pulmonary edema if overhydrated
– lung is a reservoir for fluid
– may use diuretics (typically furosemide)
prophylactically
pre/intraoperative care
• 3ABGs, PFTs pre-operatively
• use bronchodilators, antibiotics
• lg bore IVs and blood readily available
– Ç risk for intraoperative hemorrhage
• careful fluid management
• lateral decubitus position
– risk of nerve and/or dependent eye/ear injury
• FiO2 should not exceed 30% in pts who have
received chemotherapeutic agents, specifically
bleomycin
• thoracic epidural for post-op analgesia
– may utilize intraoperatively; allows for È use of
inhaled anesthetics; better preservation of HPV
during one lung anesthesia
Parameters for tolerance of

pneumonectomy
• Pre-op PFTs
–CO2 < 45 mmHg
–FEV1 > 2L
–FEV1/FVC > 50%
–Max VO2 > 10ml/kg/min
Bronchoscopy
• used for diagnosis/staging of pulmonary or
bronchogenic tumors or other pulmonary
conditions (i.e. tuberculosis, sarcoidosis)
• may be performed with GETA or with
sedation and topical anesthetization of the
airway
• fiberoptic bronchoscope also used to
facilitate awake intubation in the pt with
anticipated difficult intubation, cervical
spine instability
Bronchoscopy
• may be flexible or rigid
– flexible achieved through a large (at least an #8.0)
ETT fitted with a swivel adaptor
• adapter freely rotates; allows for insertion of the
scope through a sealed port and simultaneous
ventilation through a sideport
• fresh gas flows must be increased to deliver O 2
and anesthetic agent past the partial obstruction
produced by the scope
– ventilation is briefly lost when surgeon uses
suction, removes scope with tissue samples
– propofol gtt is helpful to maintain anesthesia
during periods of apnea
– FiO2 should not exceed 30% if laser is used to debulk
bronchogenic tumors
• airway fire may ensue (O2 and N2O support
combustion)
bronchoscopy, cont’d
• rigid bronchoscopy
– typically utilized to remove aspirated foreign bodies
from the trachea or mainstem bronchi
– requires GETA
– pt is anesthetized; scope is inserted through the
glottis into the trachea
• ventilation is achieved via jet ventilation through a
sideport on the scope
– airway competition with the surgeon; team
approach essential
– pts may desaturate quickly 2º limited reserve
– Ç risk of barotrauma/pneumothorax with
overzealous jet ventilation
flexible/rigid bronchoscopy
• postoperative concerns
– airway bleeding
– tracheal/bronchial laceration
– respiratory insufficiency
– reactive airway; Ç persistent cough
• may use FiO2 with cool steam in PACU, IV opioids,
lidocaine, nebulized racemic epinephrine
– dental damage with use of rigid scope
– pneumothorax
Mediastinoscopy
• a rigid scope is passed through the
suprasternal notch
– allows for direct visualization of the
mediastinal space; sampling of paratracheal
and mediastinal lymph nodes at various levels
– used to stage intrathoracic cancers,
lymphoma, etc.
• contraindicated in pts with aneurysm of
ascending aorta, previous mediastinoscopy
Mediastinoscopy
• 1º problem Ö acute brachiocephalic
compression with mediastinoscope
– may lead to hypoperfusion of the R common
carotid, CVA
– monitor pulsatile waveform of the RUE; notify
surgeon if waveform dampens
• may monitor RUE with pulse oximetry;
insert arterial line in L radial artery
–arterial monitoring may still be achieved
in the event of brachiocephalic avulsion
complications of mediastinoscopy
• hemorrhage 1° concern
– lg bore IV, blood availability a must
– anticipate need for emergency sternotomy
• venous air embolus
• L recurrent laryngeal nerve damage
• phrenic nerve damage
• pneumothorax, pneumopericardium,
pneumomediastinum
• thoracic duct injury
• tracheal compression/injury
• esophageal injury
• CVA from sustained brachiocephalic
compression
• bradycardia, arrhythmias, cardiac arrest
Pneumothorax
• a collection of gas in the pleural space
(between visceral and parietal pleurae)
resulting in collapse of the lung on the
affected side
– tension pneumothorax Ö air within the pleural space
that is entrained/trapped
• creates Ç intrathoracic pressure
• displaces mediastinal structures causing
hypoxemia and compromised cardiopulmonary
function
Pneumothorax, cont’d
• s/s (rapid onset)
– hypotension
– chest pain (90%)
– dyspnea (80%)
– jugular venous distension
– tracheal deviation (late!)
– pulsus paradoxus
– anxiety
– fatigue
• hemothorax Ö blood accumulation in the pleural
space
• causative factors
– any blunt or penetrating injury that disrupts
the parietal or visceral pleura or bronchi (stab
or GSW to the chest, rib fx from MVA, etc.)
– injuries secondary to medical or surgical
procedures
• barotrauma via (+) pressure ventilation
• subclavian, IJ sticks
• nephrectomy
• CPR
– spontaneous pneumothorax
• 6X more prevalent in males
• causative factors, cont’d
– neonates
• post meconium aspiration
• prematurity
– 19% incidence in pts with RDS
– tuberculosis
– pneumonia
– asthma, COPD
– pertussis
– lung abscess
– Cystic Fibrosis
– Marfan’s syndrome
s/s of pneumothorax
• respiratory distress and/or arrest
• hypoxia
• hypercarbia
• decreased or absent lung sounds on affected side
• tachypnea
• hyperresonance of the chest wall on percussion, (+)
transillumination in neonate
• increasing peak airway pressures
• tachycardia
• mental status changes
• abdominal distension (late!)
• CXR shows air in pleural cavity (may not be
immediately evident)
• definitive treatment
– decompression
• emergency needle aspiration Ö @ 2nd intercostal
space, midclavicular line on affected side
– may use a 14g angiocath; typical “whoosh” is
heard
– insertion of a chest tube
• place to suction to evacuate air/heme and re-
expand lung
• d/c N2O if pt is anesthetized
– may rapidly expand pneumothorax
Pulmonary embolus
• the third most common cause of death in the
US; massive PE is probably the leading cause of
unexpected death
• diagnosis difficult; may mimic many other
disease states
– high mortality rate; treatment is CPR,
thoracotomy/CPB, thrombolytic therapy
• leads to complete obstruction of the pulmonary
circuit
– *classic triad of signs and symptoms of PE:
• dyspnea
• chest pain
• hemoptysis
other s/s of PE
• chest pain, chest wall tenderness, painful respiration
• back and/or shoulder pain
• upper abdominal pain
• syncope
• shortness of breath, tachypnea (respiratory rate >16/min)
• wheezing, rales
• cyanosis
• fever (temperature >37.8° C), ÇWBC
• diaphoresis
• thrombophlebitis
• lower extremity edema
• intubated pts:
– ÈETCO2 precedes È SaO2 2º obstruction of pulmonary
circulation
– Ç PIP from Ç PVR
– CV instability
cardiac s/s of PE
• cardiac arrhythmia
• accentuated second heart sound, murmur
• tachycardia (heart rate >100/min)
• ÇÇ pulmonary vascular resistance leading to R
heart strain, acute cor pulmonale
– ECG changes:
• peaked T waves in lead II, RAD, RBBB
• (+/-) atrial fibrillation
• NSST changes
causative factors of PE
• hypercoagulable states
– venous stasis
– prolonged bedrest
– following surgery, long periods of travel
– malignancy, chemotherapy
– pregnancy
– hx of DVT, previous PE
– obesity
Cor Pulmonale
• R-sided heart failure
– 1º causative factor COPD
• from Ç PVR 2º chronic hypoxia/fibrotic changes of
lung structure
– pulmonary HTN
– pulmonary fibrosis
– chronic/acute PE
– sleep apnea
• pts are at risk for peri/postoperative respiratory
compromise; will magnify Ç in PVR
– hypoxia, hypoxemia
– hypercarbia
– acidosis
• co-morbidities
– CAD
– LV dysfunction
Cor Pulmonale, Cont’d

• intraoperative concerns
– *SVR should be maintained or increased in
the face of fixed ÇPVR
• È SVR results in severe hypotension from ÈÈ CO
– caution with regional anesthetics, vasodilators
• Ç PVR from:
– hypoxia
– hypercarbia
– hypothermia
– N2O
Cor Pulmonale, Cont’d
• intraoperative concerns, cont’d
• Ç airway reactivity, bronchospasm may be
noted
–inhalation agents bronchodilate
–NO may be useful to ÈPVR
• E adrenergic agents useful for both
bronchodilation and treatment of CV
instability
Tuberculosis
• incidence in US dropped by 11.8% in
2010; cases continue to escalate
worldwide
– WHO reported 440,000 cases of multi-drug
resistant TB; 1/3rd fatal (2008) (12,898 in US)
• high risk groups Ö homeless, elderly,
prisoners, minorities, immigrants from
Latin America, Asia
• caused by Mycobacterium tuberculosis;
transmitted via droplet
TB concerns
– pt co-morbidities
– extent of organ involvement (pt may have
multisystemic involvement)
– possible toxic response to rifampin and isoniazid
• hepatitis, thrombocytopenia, ototoxicity,
nephrotoxicity, peripheral neuropathies
• *isoniazid may Ç defluorination of volatile
anesthetics
– may choose to avoid sevoflurane
– protection of OR staff
• quiet extubation if possible
• OR masks should fit closely, have capability to
filter aerosolized particles in 1-5µm range (N-
95 mask)
cigarette smoking
• associated risks:
– smoke contains >3000 identifiable toxins and
carcinogens
• CO and nicotine cause acute systemic effects
– nicotine stimulates the SNS; causes Ç in HR,
BP, SVR for approximately 30 minutes after a
cigarette
– 2X Ç risk of CAD than non-smokers
• CV comorbidities also include HTN, PVD
– 6X Ç risk of post-op pulmonary complications
than non-smokers
cigarette smoking
• associated risks, cont’d:
– Ç risk of oral, pharyngeal, lung, and
head/neck cancers
– Ç levels of carboxyhemoglobin (COHb)
• impairs O2 carrying capacity
• may produce falsely high SaO2 readings
– emphysematous changes of the lung with
hyperreactivity
• pts are bronchospastic, have Ç secretions
• Èciliary function
– ÈMAO, Çdopamine (CNS)
cigarette smoking, cont’d

• cessation of smoking overnight:
– reduces levels of CO, carboxyhemoglobin, nicotine
– will not reduce airway hyperreactivity
• need 24-48º for initial reduction; approximately 10
days until normal
• cessation of smoking for 8 weeks:
– decreases incidence of post-op pulmonary
complications
• cessation of smoking >2 years
– decreases risk of MI to that of the nonsmoker
Non-cardiogenic (post obstructive)
pulmonary edema
• occurs following acute complete upper airway
obstruction i.e. post-extubation laryngospasm
– forceful respiratory efforts against a closed glottis
create large (-) intrathoracic pressures
• pulls exudative fluid from pulmonary capillary beds
into the alveoli
– results in hypoxemia, hypercarbia, pink, frothy
sputum from ETT
• treatment
– (+) pressure ventilation
– diuretics (furosemide)
• *may be a causative factor in the development of
ARDS
The difficult airway

adapted from the ASA difficult airway algorithm
• assess the likelihood and clinical impact of

basic management problems:
– difficult intubation
– difficult ventilation
– difficulty with pt cooperation/consent
– difficult surgical airway
• actively pursue opportunities to deliver
supplemental O2 throughout the process of
difficult airway management
The difficult airway

adapted from the ASA difficult airway algorithm
• consider the relative merits and feasibility

of basic management choices
– awake intubation vs. intubation attempts after
induction of GA
– noninvasive technique vs. surgical technique
for initial approach to intubation
– preservation vs. ablation of spontaneous
ventilation
• develop primary and alternative strategies
– difficult airway algorithm
The difficult airway, cont’d
– difficult intubation
• will this patient be a difficult
laryngoscopy/intubation?
– Remember “LEMON”
» L=look externally
» E=evaluate 3,3,2
» M=Mallampati score
» O=obstruction
» N=neck mobility
Attributes of the difficult laryngoscopy pt

• short “bull” neck
• overbite
• retrognathic chin
• goiters (? tracheal compression, deviation)
• “snaggle teeth”, CAPS
– remember presence of deciduous teeth in children
• “3,3,2”
– 1st 3 Ö oral aperture
• can the patient open his/her mouth 3 finger
breadths?
– 2nd 3 Ö hyomental distance
– 2 Ö hyoid to thyroid distance
• If these measurements are short, laryngoscopy
may be difficult

• difficult ventilation
• will this patient be difficult to ventilate via
BMV?
– remember “BONES”
• B=beard
• O=obesity
• N=no teeth
• E=elderly
• S=snores
• difficult surgical airway
– will this patient be a difficult
cricothyrotomy?
• remember “SHORT”
– S=surgery
– H=hematoma/infection
– O=obesity
– R=radiation
– T=tumor
• **surgical airway (cricothyrotomy) is the

definitive treatment in the “can’t intubate,
can’t ventilate” scenario
*always confirm intubation with exhaled CO2
Fiberoptic bronchoscopy
• useful in pts with:
– known difficult intubation
– tumors, abcesses of airway
– subglottic stenosis
– mediastinal masses
– congenital abnormalities
– neck immobility
– verification of placement of DLT
• may be done in anesthetized or awake pts
**EORRGRUĹVHFUHWLRQVLQDLUZD\"RSWIRUEOLQGLHVXSUDJORWWLF
techniques; do not choose FOB!
preparation of the patient for AFI
• glycopyrrolate 0.2 mg IM/IV at least 20 minutes before
attempts at anesthetizing the airway
– secretions dilute and obstruct application of local
• topical anesthetization
– may be achieved with cetacaine, hurricaine sprays
• use with caution; overdose may lead to
methemoglobinemia
– lidocaine 4% via atomizer or nebulizer
• limit dose to avoid toxicity
– lidocaine 5% ointment applied to base of tongue
– transtracheal injection of lidocaine
• through the cricothyroid membrane
– percutaneous block of the superior laryngeal nerve
(external branch) and recurrent laryngeal nerve
• *sedation must be given cautiously; pt should be
comfortable, cooperative, not obtunded
Intubation
• oral
• nasal
– use vasoconstrictor to nares (typically
phenylephrine)
– soften ETT
– lubricate ETT
– NO stylet
– may do awake/blind
• manipulation of C-spine minimized
• pt remains spontaneously ventilating
– contraindicated in anticoagulated pts, pts with
LeForte II or III facial fractures
Optimal intubation conditions

• reasonably experienced endoscopist
• “sniffing” position
• no significant muscle tone
• “BURP”
– backward, upward, rightward pressure placed
externally on the larynx
• 1st attempt failure
– is pt relaxed enough?
• change something:
– position
– blade (type and/or size)
– endoscopist
Optimal positioning for
laryngoscopy/intubation
Verification of endotracheal
intubation
• visualize
– chest excursion
• “bag-feel” compliance
• CO2 via capnography, E-Z Cap non-OR location
• H2O vapor in ETT(?)
• AUSCULTATE!
– *do not release cricoid pressure if doing RSI
until chest is auscultated, CO2 is present
Rapid sequence induction

• induction sequence for pts who present as “full
stomach”
– indicated for obesity, pregnancy, bowel/gastric outlet
obstruction, emergency surgery
• cricoid pressure is applied to prevent aspiration
of gastric contents from passive regurgitation
– pressure should be released if pt actively retches to
prevent esophageal rupture
– overzealous pressure may displace cervical fractures
• HOB Ç 30º
Rapid sequence induction
• preoxygenation 3-5 minutes with FiO 2 1.0 or 6-8 vital
capacity breaths
• suction readily available
• stylet in ETT
• IV induction agent is rapidly followed with an intubating
dose of SCh or rocuronium
– cricoid pressure is applied upon loss of
consciousness
– bag mask ventilation of airway is held; may open
esophageal sphincter if airway pressure is >
18cm/H2O
cricoid pressure is maintained until ETT
– **
placement is verified by (+) ETCO2,
auscultation
Basic airway equipment

• oral airways
– Berman and Guedel
• nasal airways
– use with caution in anticoagulated, pregnant pts
– precede with topical vasoconstriction; lubricate well
• laryngoscope blades
– MAC
• curved, tip placed in vallecula
– McCoy (A.K.A. “Flexi-tip”)
– Miller
• straight, more direct view of glottis
– better for pediatric pt
supraglottic airway devices

• Laryngeal mask airways
– Basic
– Flexible
• armored tube for ENT, oral, plastic surgeries
– Pro-seal
• allows for passage of an OGT when properly seated
• allows for (+) pressure ventilation
– Intubating LMA—A.K.A. Fastrach
• useful when pt can not be intubated via laryngoscopy
– part of the difficult airway algorithm
• Combitube, King
• **none protect the airway from aspirating
regurgitated stomach contents
– contraindicated for use in full stomach, obese, GERD pts
Alternative airway devices
• Lighted tracheal stylet (Trachlight)
– “blind” technique obviates the need for
laryngoscopy; useful for
• small oral aperture
• blood in airway
– ETT is loaded onto lighted stylet which is
angled at tip
– Room lights are dimmed
– Stylet is inserted midline into the oropharynx
– Transillumination at the level of the thyroid
cartilage indicates proper placement of wand;
tube is advanced into the glottis
Alternative airway devices, cont’d
• Bullard, Upsher scopes

– Allows for intubation of patients will minimal to
no head extension
• small oral apertures
• cervical spine instability
• s/p c-spine fusions
• Halo traction
Complications of laryngoscopy/intubation
• 1º Æ dental damage, lip contusions
• sore throat
• increased sympathetic tone during laryngoscopy
• vomiting/aspiration upon induction
• post-intubation croup (pediatrics)
• POPE from laryngospasm
• endobronchial intubation
– particularly in children; ETT may enter the R
mainstem bronchus
• s/s wheezing, unilateral breath sounds and chest
excursion, hypoxemia, high PIP
• arytenoid dislocation
• Injury to RLN, SLN, hypoglossal nerve
• inability to intubate via conventional means
O2 delivery systems
• nasal cannula
– FiO2 24-44% (dependent on 1-6 liter/min flow;
approx 4% increase with each additional liter)
• partial rebreather face mask
– FiO2 65-75%
• non-rebreather face mask
– FiO2 85-95% (10-15 l/min)
• Venturi mask (high flow)
– FiO2 24-50%
• positive pressure
– bag-valve mask
• FiO2 approaches 100% with reservoir (15l/min
flows required)
Mechanical ventilation modes

• Volume-cycled ventilation
– ventilator delivers a set tidal volume (VT)
• *pressure varies with resistance from and elasticity
of the lungs
– A/C – assist/control ventilation
» ensures a desired respiratory rate; will
assist pt-initiated breath with delivery of the
fixed VT
– SIMV – synchronized intermittent mandatory
ventilation
» delivers set respiratory rate and volume as
in A/C mode but pt-initiated breaths above
the set RR remain unassisted
Mechanical ventilation modes, cont’d

• Pressure-cycled ventilation
– Breaths delivered limited by pre-set peak-
inspiratory pressure over a set inspiratory time
• *tidal volume varies with resistance from and
elasticity of the lungs; changes in respiratory system
mechanics may result in unrecognized changes in
minute volume!
– PCV – pressure control ventilation (similar to A/C;
each inspiratory effort by pt will result in delivery
of full pressure support over a fixed inspiratory
time)
– PSV – pressure support ventilation – minimum
rate is not set; all breaths are triggered by the pt
Alternative ventilation modes
• NIPPV – non-invasive positive-pressure ventilation
– delivery of PPV via a tight-fitting mask covering the nose
or both the nose and mouth
– used in spontaneously ventilating pts; typically pressure-
controlled but may be volume-controlled as well
• CPAP – continuous positive airway pressure –
constant pressure is maintained throughout the
airway cycle
• BiPAP – bi-level positive airway pressure – both
inspiratory (IPAP) and expiratory positive pressure
(EPAP) set; triggered by the pt
– pt must be awake with intact laryngeal reflexes; passive
gastric filling with air/regurgitation/aspiration a concern!
– do not use in hemodynamically unstable pts or those
with GI obstruction
Notes
Notes
LATEX-FR
EE Quick Reference
41
The First LMA™ Airway
Mask *Maximum Cuff Largest ETT
Size Patient Size Volume (Air) ID (mm)
1
11/2 Infants 5-10 kg
2
Neonates/infants up to 5 kg up to 4 ml
up to 7 ml
3.5
4.0
2 Infants/children 10-20 kg up to 10 ml 4.5
21/2 Children 20-30 kg up to 14 ml 5.0
3 Children 30-50 kg up to 20 ml 6.0**
4
5
Adults 50-70 kg
Adults 70-100 kg
41 up to 30 ml
up to 40 ml
6.0**
7.0**
6 Large adults over 100 kg up to 50 ml 7.0**
2
The First Single-use LMA™ Airway
Mask *Maximum Cuff Largest ETT
Size Patient Size Volume (Air) ID (mm)
1 Neonates/infants up to 5 kg up to 4 ml 3.5
11/2 Infants 5-10 kg up to 7 ml 4.0
2 Infants/children 10-20 kg up to 10 ml 4.5
3 Children 30-50 kg up to 20 ml 6.0**
4 Adults 50-70 kg up to 30 ml 6.0**
5 Adults 70-100 kg up to 40 ml 7.0**
41
The Most Versatile LMA™ Airway
Mask *Maximum Cuff Largest Size Largest ETT
Size Patient Size Volume (Air) OG Tube/Salem Sump ID (mm)
11/2 Infants 5-10 kg
Infants/children
2up to 7 ml 10 French/8 French 4.0
2 up to 10 ml 10 French/8 French 4.5
(10-20 kg)
21/2 Children 20-30 kg up to 14 ml 14 French/12 French 5.0
3 Children 30-50 kg up to 20 ml 16 French/14 French 5.0
4 Adults 50-70 kg up to 30 ml 16 French/14 French 5.0
5 Adults 70-100 kg up to 40 ml 18 French/16 French 6.0**
** These are maximum volumes that should never be exceeded. It is recommended the cuff be inflated to
60 cm H2O intracuff pressure.
** = cuffed ID = internal diameter ETT = endotracheal tube OG = orogastric
Never overinflate the cuff!
To place an order, please call (800) 788-7999
-FRE
E Quick Reference
EX
LAT
41
The Intubating LMA™ Airway
Mask *Maximum Cuff
Size Patient Size Volume (Air)
3 2
Children 30-50 kg up to 20 ml
4 Adults 50-70 kg up to 30 ml
5 Adults 70-100 kg up to 40 ml
6.0 mm 6.5 mm
41
LMA Fastrach™ Endotracheal Tube Sizes
7.0 mm 7.5 mm 8.0 mm
2 /
The LMA™ Airway for Head and Neck Cases
Mask *Maximum Cuff Internal
Size Patient Size Volume (Air) Diameter (mm)
2** Infants/children 10-20 kg up to 10 ml 5.1
3 Children 30-50 kg up to 20 ml 7.6
4 Adults 50-70 kg up to 30 ml 7.6
5 Adults 70-100 kg up to 40 ml 8.7
6*** Large adults over 100 kg up to 50 ml 8.7
* These are maximum volumes that should never be exceeded. It is recommended the cuff
be inflated to 60 cm H2O intracuff pressure.
** Coming soon in single use.
*** Available in reuseable mask only. 41
2 Single Use
Never overinflate the cuff!
41 Use Only 40 Times
Consult the instructions for information

2 on indications,
contraindications, warnings, and precautions.
, LMA, LMA Classic, LMA ProSeal, LMA Fastrach, LMA Flexible, LMA Flexible Single Use and LMA Unique
are trademarks of The Laryngeal Mask Company Limited.
LMA North America Inc. www.LMANA.com

Putting Confidence in Your Hands ™
(800) 788-7999 LMA-145 09/04

Nervous System Review
Cerebral Metabolism
• Average adult brain is 1500 g
• CMRO2 = 50 ml/min or 3.5 ml/100 g/min
– 60% CMRO2 for electrical activity
– 40% CMRO2 for cellular integrity
• Brain lacks O2 reserves
– Loss of consciousness within 10 sec
– Hypoxic injury within 3 – 8 min
• hippocampus & cerebellum most
sensitive
Cerebral Blood Flow

• CBF parallels metabolic activity
– Ranges between 10 – 300 ml/100 g/min
– Average CBF = 50 ml/100 g/min
**20% of cardiac output
• Flows below 10 ml/100 g/min associated
with irreversible brain damage
206
Cerebral Autoregulation
Extrinsic CBF Regulators

• PaCO2 – directly proportionate to CBF
– ×CO2 from 20 – 40 doubles CBF
– PaCO2 < 20 may cause ischemia
• PaO2 – only marked changes alter CBF
– Hyperoxia causes little change
– Hypoxia (< 50 mmHg) acutely raises CBF
• Temperature – CBF change 6% / oC
– CMRO2 changes by a factor of 2 for
every 10o C change
Autonomic Control of CBF

• Intracranial vessels receive innervation
– sympathetic vasoconstriction
– parasympathetic vasodilation
• Physiologic function is unclear
May only play a roll in pathologic states
• Pharmacologic control of CBF through the
ANS very limited
207
Extrinsic control summary
Cerebral Perfusion Pressure
• CPP = MAP – ICP (or CVP if greater)

normally 80 – 100 mmHg
• CPP < 40 associated with flat EEG
• CPP < 25 associated with brain damage
Cerebrospinal Fluid
• Found in the ventricles, cisterns and
subarachnoid space
• Formed in the choroid plexus of ventricles
• Adults form 400 – 500 ml/day
• CSF volume is about 150 ml
• CSF flow:
Lateral ventricles Foramina of Monroe
3rd ventricle Cerebral aqueduct (Sylvius)
4th ventricle Foramen of Magendie
Cysterna magna Subarachnoid space
208
CSF Cont'
• CSF is absorbed by the arachnoid
granulations of the cerebral hemispheres
• CSF is isotonic with plasma but contains
lower K+, HCO3-, glucose, protein
• CSF production decreased by
acetazolamide, steroids, furosemide,
isoflurane, spironolactone, vasoconstrictors
CNS Pharmacology Summary

Agent CMR CBF CSF CSF ICP
Production Absorption
Isoflurane --- + +- + +
Desflurane --- + + - ++
Sevoflurane --- + ? ? ++
Nitrous - + +- +- +
Barbiturates ---- --- + + ---
Etomidate --- -- + + --
Propofol --- ---- ? ? --
Benzos -- - + + -
Ketamine +- ++ - - ++
Opioids +- +- + + +-
Lidocaine -- -- ? ? --
Cerebral Aneurysms
• Saccular aneurysms and AVMs are
common causes of nontraumatic
intracranial hemorrhage
• Aneurysms occur at bifurcation of arteries
• 10 – 30% have multiple aneurysms
• 5% of population have aneurysms
• Morbidity/mortality very high from rupture
• > 7mm in size are surgical candidates
209
Cerebral Aneurysms Cont'
• After rupture, 30% have severe
vasospasm (4 – 14 days later)
• Symptomatic vasospasm treated with:
Hypervolemia, Hemodilution, Hypertension
• Unruptured aneurysms associated with
headache, 3rd nerve palsy
• Patients usually 40 – 60 years of age
Cerebral Aneurysms Cont'

• Intraoperative management
– Avoid rupture, induced hypotension
– Avoid rapid decrease in ICP prior to dural
opening – may precipitate rupture
– Maintain adequate CPP
– “Brain relaxation” after dura opened
mannitol, steroids, thiopental(?)
Seizure Disorders
• Grand Mal (Tonic-Clonic) seizures
– Leading cause – idiopathic
– 2o causes – trauma, congenital defects, asphyxia,
CNS infection, drug withdrawal, metabolic pathology
– Usually seizures are benign events, but 2 o injury is
common
– Airway reflexes are usually preserved during and after
seizure
• PreOp
– Ensure adequate anticonvulsant levels
210
Seizure Disorders Cont'
• IntraOp
– Standard induction agents are good
– Benzodiazepines may help reduce incidence of
seizure
– Sudden hemodynamic changes may indicate intraop
seizure
– Patients may show tolerance to opioids
– May show resistance to NMB’s
– Most anesthetics have potential to precipitate
seizures
Postop
– EEG may be required if emergence is slow
– Be alert to possibility of postoperative seizure and
secondary injury
– Possibility of Todd’s paralysis
– Adequate analgesia reduces incidence of
hyperventilation

• Petit Mal (Absence) seizures
– Common seizure disorder of childhood
– Patient appears to be “day-dreaming”; facial twitching
is common
– Little or no post-ictal phase
• Pre-op
– Continue anticonvulsant meds and check adequate
levels
• Intraop
– Some anticonvulsants increase resistance to NMBs
• Postop
– Adequate analgesia reduces incidence of
hyperventilation
211
Hydrocephalus/Intracranial
Hypertension
• Hydrocephalus
– Congenital – aqueductal stenosis, Arnold-Chiari
malformation, Dandy-Walker syndrome
– Post-traumatic – intraventricular hemorrhage
– Neoplastic – Tumor obstructing CSF flow
– Post-inflammatory – meningitis, abscess
Hypertension Cont'
• Intracranial Hypertension
– Intracranial compartment has fixed volume:
Brain = 85%, CSF = 10%, Blood volume = 5%
– Increased volume of any component Ö intracranial
hypertension (ICP > 15 mmHg)
– Cerebral perfusion pressure:
(CPP) = MAP – ICP
- Usually from a 2o process – trauma, tumor,
hemorrhage, abscess, edema
Hypertension Cont'
212
Hypertension Cont'
• Methods of reducing increased ICP
– Reduce PaCO2
– Avoid hypoxia
– Head elevation
– Osmotic diuretic therapy
– Corticosteroids
– CSF drainage
Hypertension Cont'
• Cerebral protection
– Decreases electrical activity Ö CMRO2 Ö CBV Ö ICP
• Indications for cerebral protection
– Global ischemia (cardiac arrest) Ö No outcome
change
– Regional ischemia (stroke) Ö No outcome change
– Initial therapy following head injury Ö No outcome
change
Hypertension Cont'
• Preop
– Hypertonic fluid resuscitation
– Mannitol
– Avoid premedication
• Intraop
– Have patient hyperventilate prior to induction
– Thiopental, etomidate, propofol, lidocaine all reduce
CBV
– Narcotics reduce hemodynamic response to
intubation
213
Hypertension Cont'
Intraop Cont’
– Limit use of N2O, volatile agents – all are vasodilators
– Hyperventilate to CO2 of 27 mmHg
– Additional osmotic diuretic may be indicated
• Postop
– Most require postop hyperventilation
– Early extubation desirable for quick neuro exam
Parkinson’s Disease
• Pathophysiology
– Degenerative extrapyramidal disease
– Dopaminergic failure with cholinergic excess
– Sx – bradykinesia, rigidity, resting tremor, postural
instability
– Dementia in up to 50% of patients
• Treatment
– L-dopa
– Bromocriptine and lergotrile
– Amantadine
– Selegiline
– CNS anticholinergics
– Stereotactic surgery
Parkinson’s Disease Cont'

• Preop
– Continue meds
– Avoid phenothiazines, butyrophenones, metoclopramide
– Assess intravascular volume status
• Intraop
– Close attention to ECG for arrhythmias
– Increased risk of aspiration
– Decreased intravascular volume
– Decreased responsiveness to indirect acting
vasopressors
– Potential hyperkalemia with succinylcholine
• Postop
– Follow CNS state – delirium common
214
Huntington’s Disease
• Degenerative disease of the CNS
• Autosomal dominant transmission
• Basal ganglia affected early, later global cerebral
degeneration
• Does not appear until 35 – 40 years-of-age
• Manifestations: choreoathetosis, dementia, behavioral
changes
• Dopamine excess in basal ganglia
• Treatment: antidopaminergics agents
• Anesthetic management:
– Aspiration risk
– Decreased plasma cholinesterase activity
– Increased effect of nondepolarizing relaxants
Multiple Sclerosis
• Pathophysiology
– Demyelinating disease of the brain and spinal cord
– Almost exclusively upper motor neuron disease
characteristics
– May also have autonomic dysfunction, cranial nerve
involvement
**Increased body temperature will aggravate
symptoms
– Associated conditions: seizures, uveitis, cognitive
dysfunction, memory loss, personality changes
• Treatment
– Steroids, ACTH, immunosuppressant agents
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between attacks
Multiple Sclerosis Cont'

• Preop
– May need steroid coverage
• Intraop
– Standard monitoring
– Spinal anesthesia implicated in causing relapse
– Epidural if clearly indicated
• Need for informed consent regarding worsening of
symptoms
• Use lower concentrations of anesthetics
215
Multiple Sclerosis Cont'
Intraop cont’
– Peripheral block not a problem
– Caution with use of succinylcholine
– NMBs require careful titration
– Caution with extubation in patients with brainstem
involvement
• Postop
– Continue steroids, avoid/treat hyperthermia
Myasthenia Gravis
• Pathophysiology
– Autoimmune disease with IgG antibodies to
neuromuscular (N2) receptors
– Decreased muscle strength, easily fatigued
– Pharyngeal weakness common
– Associated diseases: thymoma,
hyper/hypothyroidism, lupus,
pernicious anemia, RA, scleroderma
• Treatment
– Anticholinesterase agents
– Immunosuppressive drugs
– Steroids
– Plasmapheresis
– Thymectomy
Myasthenia Gravis Cont'

• Preop
– Continue anticholinesterase meds
– Steroid coverage
• Intraop
– Routine monitoring
– Avoid muscle relaxants if possible. Otherwise, careful
titration
– Start IV neostigmine infusion 1 hour before
emergence. Estimate neostigmine dose at 1/30 th of
daily pyridostigmine dose
– Check NIF (> 30 cmH2O), head lift, cough/gag
reflexes
216
• Postop
– Continue neostigmine infusion
– Careful monitoring of ventilatory function

• Cholinergic Crisis
– Anticholinesterase agents have narrow therapeutic
index (TI)
– Too much anticholinesterase agent will also produce
weakness, as well as parasympathicotonia
– Test weakness with Edrophonium (Tensilon test):
• If weakness is from myasthenia, improvement will
be seen
• If weakness is from cholinergic crisis, worsening
will be seen
Alzheimer’s Disease
• Pathophysiology
– Affects 6% over 65, 18% over 75, 50% over 85
– Disease of cerebral cholinergic transmission with
neuron degeneration
– Extensive cerebral atrophy especially of hippocampus
and temporal lobes
• Treatment
– Symptomatic and supportive
– CNS anticholinesterases – tacrine (Cognex) &
donepezil (Aricept)
• 50% have serious side effects
217
Alzheimer’s Disease Cont'
• Preop
– Patient may be unable to give informed consent
– Avoid centrally acting anticholinergic agents
– Benzodiazepines should be avoided
• Intraop
– Use shortest acting agents possible
• Desflurane shown to cause less postoperative
delirium than sevoflurane
• Propofol offers quickest recovery
• Postop
– Expect prolonged emergence
– Delirium & disorientation common
– Poor candidates for PCA
Autonomic Dysreflexia
• Pathophysiology
– Seen in patients with spinal cord transection at T7 or
higher
– CNS inhibition of autonomic activity lost
– Develops 2 – 3 weeks after transection
– Risk declines with lower transections. At T10 or lower
very rare
– Severe hypertensive response with bradycardia
possible with any stimulus below level of transection
• Treatment
– Stop initiating stimulus
– Spinal (but not epidural) anesthetic effective
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– Centrally acting hypotensive agents not effective
– Nifedipine can be used for prophylaxis
Autonomic Dysreflexia Cont'

• Preop
– Nifedipine – given 30 min before procedure
– Assess volume status
• Intraop
– Arterial line for tight BP control
– CVP/PA catheter if volume changes expected
– GA with volatile agents superior to N2O/opioids
– Spinal anesthesia highly effective
– Epidural appears effective in laboring patients
• Postop
– May occur with distended bladder
– With severe HTN, consider possibility of cerebral
bleeding
218
Electroconvulsive Therapy (ECT)
• An electrical current applied to the brain,
producing “therapeutic” seizures
– In use since 1930’s
• Used in the treatment of:
– Depression
– Mania
– Affective disorders in schizophrenics
• Frequency
– 2-3 X week for 6-12 treatments
– Weekly to monthly maintenance prevents
relapse
– Use in US is increasing
Physiologic response to ECT

• Generalized motor seizures
– grand-mal seizures may last several minutes
• two phases:
– 10-15 second tonic-clonic stage
– 30-60 second prolonged clonic phase
– A minimum seizure duration of 25 seconds is

recommended to ensure adequate antidepressant
efficacy
• IV caffeine pretreatment may prolong seizure
activity
Physiologic response to ECT

• Acute cardiovascular response:
– × cerebral blood flow and ICP
– Initial parasympathetic stimulation
• May cause bradycardia Ö asystole (rare)
• Duration 10-15 seconds
– may pretreat with anticholinergic
– Prominent sympathetic response follows:
• HTN, tachycardia
• Untoward events:
– Dysrhythmias
– Myocardial ischemia/infarction
– Neurologic vascular events
219
Anesthetic Considerations for ECT
• Usually carried out outside of the OR suite
in remote locations
• Depressed patients:
– Majority are elderly with co-morbidities
• Requires thorough pre-procedure evaluation
– Medication profile
• MAOIs
• SSRIs
– Note interactions of psych meds with
anesthetics i.e. meperidine and indirect-acting
vasopressors

• Anesthetic requirements:
– Amnesia
– Airway management
– Prevention of bodily injury
• Use of muscle relaxants Ö succinylcholine most
commonly used
– Control of hemodynamic changes
• Labetalol, esmolol
– esmolol has a lesser effect on seizure duration
than labetalol
• Ca++ channel blockers
• Clonidine
– does not effect seizure duration
– Smooth, rapid emergence

• Pharmacology Ö induction agents
– Methohexital is the “Gold Standard”
• Causes least decrease in seizure duration
• ? availability
– Etomidate
• × myoclonus
• May delay recovery
• HTN,× HR may be accentuated
– Propofol
• Attenuates hemodynamic response
• Anticonvulsant; doses < 0.75 mg/kg acceptable
220
Sequelae of ECT
• Short-term memory loss
• Muscle aches
– May be attenuated with pretreatment with
ketorolac
• Fractures/dislocations
• Dental damage
• Headache
• Emergence agitation
• Status epileptcus
• Sudden death
ECT-Other Key Points

• Moderate hyperventilation via BMV after
induction is beneficial
– Improves the quality/duration of seizures
– LMA useful
• A bite guard is placed before application of
current
– Protects teeth/tongue/lips from transient trismus from
current
Coma
• Pathophysiology
Response Score
Coma implies diffuse
cerebral pathology or Eye Opening
Spontaneous 4
dysfunction To speech 3
Many causes including: To pain 2
None 1
hyperosmolar coma,
shock, head trauma, Motor Response
Obeys 6
poisoning, infection, Localizes 5
Withdraws 4
uremia, electrolyte Abnormal flexion 3
imbalance Extensor response 2
None 1
• Glasgow coma scale
Verbal Response
>12 – mild brain injury Oriented 5
9-12 – moderate injury Confused 4
Inappropriate words 3
<9 – severe injury Incomprehensible 2
None 1
221
Pharmacology Review
ANS, Anticholinergics,
Anticholinesterases, Depolarizing and
Non-Depolarizing Muscle Relaxants
Autonomic Nervous
System
Autonomic Nervous System

• involuntary, vegetative processes
– control of HR, BP (arterial tone), sweating, GI
motility, reproduction
• 2 major subdivisions:
1) parasympathetic (A.K.A. “craniosacral”)
– arises from: cranial nerves III, VII, IX, and X
sacral nerves 2,3,4
2) sympathetic (A.K.A. “thoracolumbar”)
– arises from the IML cell column of the dorsal horn of the
spinal cord
» 31 pairs of spinal nerves
***It is imperative that a balance be maintained between these systems!
222
Adapted from Bevan
Major neurotransmitters of the ANS
• acetylcholine (ACh)
– choline + acetyl-Co-A Choline acetyltransferase
ACh
– found at:
• synapses of all autonomic ganglia and post junctional
neurons
– nicotinic receptors (N1) located here
• post junctional parasympathetic to effector organ synapse
– muscarinic receptors located here
• neurotransmitter of the somatic nervous system
– nicotinic receptors (N2) located at the NMJ
– hydrolyzed by acetylcholinesterase
• pharmacologic effect of ACh=“SLUDGE effect”
Cholinergic Nerve Terminal - Synthesis of ACh
223
“SLUDGE”
(pharmacologic effects of ACh)
• S—salivation
• L—lacrimation
• U—urination
• D—defecation
• G—GI motility (increased)
• E—emesis
– bradydysrhythmias, negative inotropy,
bronchospasm, vasodilation also noted
Pharmacologic effects of ACh

• Negative chronotropic effect
• Negative ionotropic effect
• Vasodilation
• × GI motility/secretion
• Contraction of smooth muscle in uterus,
bladder, ureters, and bronchioles
• Stimulation of salivary, lacrimal, and sweat
glands
Cranial nerve X
• A.K.A. the vagus nerve

–Responsible for 75% of
all parasympathetic
activity
224
Major neurotransmitters of the ANS
• norepinephrine
– found at the post junctional sympathetic to
effector organ synapse
– receptor subtypes of sympathetic effector
organs:
• alpha1Ö vascular; responsible for vasoconstriction
• alpha2Ö presynaptic; typically involved with
negative feedback
• beta1Ö cardiac; positive chronotropy, inotropy
• beta2 Ö bronchioles, vessels
• dopamine (DA)1,2,3
Adrenergic Nerve Terminal and Receptors
Synthesis of endogenous catecholamines
225
Termination of norepinephrine
• 3 major pathways
1) Reuptake
• responsible for 2/3rds of termination of action
of NE
2) Diffusion away from receptors
3) Metabolism by MAO, COMT
Catecholamine metabolism
ANS stimulation by systems

Sympathetic NS Parasympathetic NS
Heart (E1)
SA node ÇHR ÈHR
AV node Çconduction velocity (CV) ÈCV
His-Purkinje system Çautomaticity, CV minimal effect
Ventricles Çcontractility, automaticity, CV (+/-) effect
Bronchial smooth muscle (E 2) relaxation constriction
GI tract (D1)
motility È Ç
secretion È Ç
sphincters contraction relaxation
Bladder
smooth muscle (E 2) relaxation contraction
sphincter contraction relaxation
Uterus (E2), (D1) relaxation (E 2) contraction (D1)
Eye (D1) mydriasis miosis
Salivary glands (E2) È ÇÇ
Sweat glands Ç (SNS fibers are cholinergic)
Liver (E 2) Çglycogenolysis glycogen synthesis
Çgluconeogenesis
Arterioles
skeletal muscle (E 2) constriction (D), relaxation (E) relaxation
skin (D1) constriction relaxation
pulmonary constriction relaxation
coronary constriction (D), relaxation (E) (+/-) relaxation
226
effects of SNS stimulation by receptor type
• Alpha1 (postsynaptic)
– vasoconstriction
– mydriasis
– relaxation of GI tract with contraction of sphincters
– contraction of bladder sphincter
• Alpha2 (presynaptic)
– inhibition of norepinephrine release
• Alpha2 (postsynaptic)
– platelet aggregation
– hyperpolarization of cells in the CNS
• Beta1 (postsynaptic)
– Çconduction velocity, automaticity, contractility
• Beta2 (postsynaptic)
– vasodilation
– bronchodilation
– GI, uterine, bladder relaxation
– glycogenolysis
– lipolysis
• Dopamine1 (postsynaptic)
– vasodilation (Çsplanchnic, renal, mesenteric beds)
• Dopamine2 (presynaptic)
– inhibition of norepinephrine release
Anticholinergics
anticholinergics
• this class of drugs competitively
antagonizes the activity of acetylcholine
(ACH) at the post junctional
parasympathetic effector siteÖÖ
The muscarinic receptor
***The prototype for this class of drugs is

atropine***
227
anticholinergics
• exert little or no effect at N1 or N2 receptors
• effects at nicotinic receptors only noted in the presence
of high concentrations of anticholinergics, as in overdose
• do not prevent the release of ACH from cholinergic fibers
• do not chemically alter ACH in any way
• do not affect cellular events which cause cholinergic
symptoms when they bind to muscarinic receptors
• anticholinergics are considered to be selectively

antimuscarinic
therapeutic uses of anticholinergics

• pre-op medication
• treatment of reflex-mediated bradycardia
• bronchodilation
• biliary and ureteral smooth muscle relaxation
• mydriasis/cycloplegia
• antagonism of gastric H+ ion secretion
• use in non-prescription cold remedies
• prevention of motion sickness
• treatment of anticholinesterase poisoning
atropine and scopolamine

• naturally occurring alkaloids; esters which resemble
cocaine
• racemic mixtures of both levo and dextrorotatory
isomers—anticholinergic activity conferred mainly by the
levo forms
• atropine also possesses some intrinsic sympathomimetic
properties
• are tertiary amines; both drugs may cause unwanted
CNS side effects from depression of central ACh
• use with caution in pts with fever, narrow angle
glaucoma, tachydysrhythmias, CHF, acute MI,
contraindicated in pts with GI or GU obstructive disease
228
dosages/pharmacokinetics
• atropine
– treatment of bradydysrhythmias, premedication:
– 0.4-1.0 mg IV/IM/sc (may also be administered via ETT)
– **typical dose .015 mg/Kg; may be co-administered with
anticholinesterase for NDMB reversal
– children 10-20 mcg/Kg
– onset 45 sec, peak 2 min, DOA 1-2 hours
• scopolamine
– used chiefly as a sedative/amnestic, for tx of motion sickness
(transdermal patch)
– 0.4-0.8 mg IV
– onset immediate, peak 50-80 min, DOA 2 hours IV, 4-6 hours
PO
**may potentiate sedative effects of benzos,
narcotics, inhalation agents
– should be avoided in pts with Alzheimer’s, narrow-
angle glaucoma
glycopyrrolate (Robinul)
– a quarternary amine
– synthetic
– possesses significant anticholinergic properties but
lacks CNS effects
– better suited for use in the OR
– used both as an anticholinergic and mixed with
anticholinesterase
• *best matched with neostigmine in both onset & DOA
– dosage:
• .01-.02 mg/kg IM/IV
• peak 5 min, duration 60-120 min
Variation of potencies of
anticholinergics
scopolamine antisialagogue
most potent mydriatic
CNS depressant
atropine heart
exerts greatest effect @ bronchioles
GI tract
glycopyrrolate effects fall somewhere
between atropine’s and
scopolamine’s with no
CNS effects
229
Central Anticholinergic Syndrome
• seen only with the use of the tertiary amine
anticholinergics
• most common in pediatric, elderly populations
• symptoms include:
– rapid, irregular pulse
– restlessness, agitation, excitement
– hallucinations
– somnolence
– coma
• treat with physostigmine
overdose of anticholinergics
• produces symptoms characteristic of muscarinic
blockade; commonly noted in pediatric
population after ingestion of OTC cold remedies
– tachycardia
– mydriasis
– dry mouth
– flushed, warm, dry skin
– rise in body temperature
– restlessness, confusion, disorientation
– skeletal muscle weakness, orthostatic hypotension
– coma, death
• treatment is physostigmine, support of
systems
Anticholinesterases
230
anticholinesterase agents
• inhibit acetylcholinesterase (A.K.A. true
cholinesterase)
– will also inhibit plasma cholinesterase (to a lesser
degree)
• may prolong effects of succinylcholine
• pharmacologic effects synonymous with
effects of acetylcholine
• utilized to reverse pharmacologic effects of
NDMRs
• subgroups based on the mechanism by which
they inhibit acetylcholinesterase
Classification of Anticholinesterases
• Based on the mechanism by which they inhibit
acetylcholinesterase
• Three types:
– Truly reversible inhibition
• edrophonium
– Reversible with formation of carbamyl ester
• neostigmine, pyridostigmine, physostigmine
– Irreversible
• echothiophate, organophosphates, nerve gases,
pesticides
Schematic Representation of
Acetylcholinesterase (AChe)
231
Hydrolysis of Acetylcholine
• Involves 3 steps:
– Alignment
• ACh lines up over active enzymatic sites
– Transesterification
• ACh is cleaved
– Hydrolysis
• H2O is added
• end result = choline + acetic acid
anticholinesterases
agent dosage/pharmacokinetics agent-specific features
edrophonium 0.5-1 mg/Kg IV -truly reversible;

(Tensilon) onset immediate competitive with aCh
peak 1-5 min -effects presynaptic
DOA 5-20 min -best co administered
with atropine
-utilized in dx of MG vs.
cholinergic crisis
neostigmine .04-.07 mg/Kg IV -carbamylates aChe
(Prostigmine) onset 5-7 min -*best co-administered
DOA 40-60 min with glycopyrrolate
pyridostigmine 0.3 mg/Kg -carbamylates aChe
(Mestinon) onset 10 min -longest DOA
DOA 90 min -used in the tx of MG
physostigmine .01-.03 mg/Kg -carbamylates aChe

(Antilirum) onset 3-7 min -*the only
DOA 30-60 min anticholinesterase which
crosses the BBB
Depolarizing and Non-

depolarizing Muscle
Relaxants
232
Physiology of Nerve Transmission
• the motor nerve loses its myelin sheath distally,
dividing into many filaments
– each filament terminates at and innervates a single
muscle fiber
• the area between the nerve terminal and the
muscle fiber in known as a synapse
– the area of the synaptic cleft is 20-30 nm
• the nerve does not physically touch the muscle
fiber—it secretes ACh and stimulates N2
receptors
The Neuromuscular Junction
Nicotinic 2 Receptors
• found on both the post synaptic motor end
plate and on the axon terminal (pre
synaptic)
– presynaptic receptors involved in a POSITIVE
feedback mechanism
• extrajunctional N2 receptors are scattered
over the muscle membrane
– numbers are few with normal muscle innervation
– proliferation occurs with muscle denervation—
exquisite sensitivity to ACh and SCH
233
The Postjunctional N2 Receptor
*MW of D subunits = 40K
Action Potential
• 1) travels down the nerve fiber
• 2) causes a release of a quanta of ACH from the
terminal
• 3) (+) charged ACH binds with (-) charged N2
protein subunit
– opens the ion channel of the N2 receptor
– Na+ rushes in; K+ rushes out
– depolarization causes normal RP of -90 mv to
decrease to -45 mv (TP)
– once TP is reached, action potential will be
propagated over entire muscle fiber
– excitation/contraction coupling Ö muscle ctxn
Classification of NMBDs
• depolarizers
– succinylcholine and decamethonium—
resemble and mimic the activity of ACh,
causing membrane depolarization
• non-depolarizers
– cause paralysis from competitive interference
with ACh’s ability to activate the N2 receptor
– drug classes divided into intermediate and
long-acting agents
234
“autonomic margin of safety”
– the difference between a neuromuscular

blocking drug’s dose which produces
blockade at the NMJ and that which
produces circulatory effects
• CV effects of muscle relaxants usually
secondary to:
– histamine release
– direct activity at cardiac muscarinic receptors
ED50 and ED95

• when referring to NDMBs, ED50 and ED95
express the amount of drug necessary to
decrease baseline twitch height by 50%
and 95% respectively
• used as an index of potency when

comparing non-depolarizers to each other
Succinylcholine
• a depolarizing muscle relaxant
• a highly flexible diester (A.K.A.
succinyldicholine)
• chemically similar to ACh (actually 2 ACh
molecules bonded by an ester linkage)
• 2 quarternary amine ends
• causes a “Phase I blockade” of NM
transmission
235
Succinylcholine, cont’d
• produces rapid intubating conditions Æflexibility of
molecule allows for rapid access to the D subunits of
the N2 receptor
• dose 1-2 mg/kg IV; 2-4 mg/kg IM

– 2X ED95 needed due to rapid hydrolysis by plasma
cholinesterase
• onset within 60 sec
Phase I Blockade
• causes:
– decreased contraction in response to a single
twitch stimulus
– decreased amplitude but sustained response
to continuous stimulation (A.K.A. “no fade”)
– absence of post-tetanic facilitation
– augmented by anticholinesterases
• *SCh produces paralysis which is non-
competitive with ACh
Hydrolysis of SCh
• hydrolyzed by plasma (A.K.A. pseudo or
butyrl) cholinesterase
– plasma cholinesterase is so active that only a
fraction of the initial IV dose of SCh actually
reaches the NMJ
• SCh is initially hydrolyzed to
succinylmonocholine and choline, then to
succinic acid and choline
– succinylmonocholine has approximately 1/20
to 1/80 potency of SCh
236
Conditions which interfere with
plasma cholinesterase
• may result in smaller plasma
concentrations and/or attenuated activity
of enzyme Ob
pl es
i
– severe liver disease m asm ty Ç
ef ay c a ch s le
fe a
– starvation cts us olin vel
of e re est s of
SC si er
– advanced pregnancy h stan ase
ce ;
to
– CRF
– following hemodialysis
– decreased in infancy to 50% of normal adult
activity, 70% by age 6, 100% by puberty
Drugs which interfere with

• echothiophate
• organophosphate exposure
• all other anticholinesterases
• metoclopramide
• MAO inhibitors
• cytotoxics
Disadvantages of SCh
• muscle pain/myalgias
• cardiac dysrhythmias
• hyperkalemia
• increases in intraocular, intragastric, and
intracranial pressures
• sustained skeletal muscle contraction/MH
• phase II block
– occurs with overdosage of SCH; resembles a
non-depolarizing block
• anaphylaxis
• “second dose effect”
– bradydysrhythmia noted after a second IV dose of
SCh is administered within a few minutes of original
dose; ? 2° succinylmonocholine
237
Patients at risk for SCh-induced
hyperkalemia
• burn patients
• patients with denervation and muscle
atrophy (including prolonged bedrest)
• severe skeletal muscle trauma (i.e. crush)
• upper motor neuron lesions for first 6
months
• lower motor neuron lesions (i.e. GB
syndrome, ALS, polio)
• patients with severe abdominal infections
“SCh Apnea”
• a prolonged block in patients who have
lower or absent levels of or atypical
– the ability to produce plasma cholinesterase is

transmitted on 2 genes
Dibucaine
• An amide local anesthetic which has the
ability to suppress the activity of normal
plasma cholinesterase by 80%
• It suppresses only 40-60% of the enzyme
produced by the heterozygote
• It suppresses only 20% of the enzyme
produced by the atypical homozygote
• Percentages are translated into the
dibucaine number
238
Genetics of Plasma
Cholinesterase Production
Allele present on **(+) homozygous for plasma
both genes cholinesterase
(normal individual)
DN 80
Allele present on **Heterozygous
one gene only **1 in 480 individuals
DN 40-60 **Produce only 50% of enzyme
Allele missing on **(+) homozygous for atypical

both genes plasma cholinesterase
**1 in 3200 individuals
DN 20
Nondepolarizers
• combine reversibly with the postjunctional
N2 receptor and render it inactive by
binding to only one alpha subunit
– this prevents the interaction of ACh with the
N2 receptor, and channel opening with
subsequent depolarization of the muscle fiber
does not occur
• **Unlike SCh, the nondepolarizers are
competitive with ACH
Nondepolarizers, cont’d
• NDMBs account for ~ 60% of anaphylactic
reactions during GA
• rocuronium was recently thought to be
responsible for the majority of these
reactions, however newer findings uphold
previous findings that SCh has the highest
antigenicity of all (Barash 2009)
– SCh>rocuronium>atracurium
239
Nondepolarizing Muscle
Blockade
• decreased twitch response to a single
stimulation
• fade during continuous stimulation
• post-tetanic facilitation
• potentiation by other nondepolarizers
• antagonism by anticholinesterases
• fasciculations do not occur
• does not trigger Malignant Hyperthermia
Comparison of Depolarizing and Nondepolarizing

NM Blockers
depolarizers non-depolarizers
causes yes no
fasciculations
fade with repeated no yes
stimulation
post tetanic no yes
facilitation
effect of potentiation reversal
anticholinesterases
antagonized by nondepolarizers depolarizers
“Train of Four”
240
Pharmacokinetics of NDMBs, cont’d
• Highly ionized @ physiologic pH
– poor lipid solubility
– do not cross the BBB, placenta, GI epithelia,
renal tubules
• VD is small
– Biexponential decay
• Initially redistributed to highly perfused
organs (alpha phase)
• Beta elimination phase dependent on
individual drug profiles, clearance
mechanisms
Pharmacokinetics of NDMBs,
cont’d
• concomitantly administered anesthetics
have no effect on pharmacokinetics
– volatiles will reduce the dose of NDMB
necessary to achieve relaxation
• extremes of age:
– elderly have decreased rates of clearance
from declining renal function
– neonates have larger VD but need less initial
dose for 50% decrease in twitch height
Enhancement of NDMB Activity

• drugs:
– volatile anesthetics
– aminoglycoside ABX
– local anesthetics
– cardiac antiarrhythmics
– diuretics (specifically furosemide)
– Mg++, lithium
– cyclosporine
– combinations of NDMBs
241
Enhancement of NDMB Activity,
cont’d
• other conditions:
– hypothermia
– acid-base alterations
– changes in serum K+
– adrenocortical dysfunction
– thermal (burn) injury
– allergic reactions
– presence of Myasthenia Gravis or Eaton-
Lambert syndrome
Subtypes of Nondepolarizers
• long acting
– pancuronium (Pavulon)
– doxacurium (Nuromax)
– pipecuronium (Arduan)
• intermediate Acting
– vecuronium (Norcuron)
– rocuronium (Zemuron)
– atracurium (Tracrium)
– cis-atracurium (Nimbex)
Response to NDMBs
• size of initial dose important
– must have 80-90% receptor occupation for
onset of paralysis
• renal disease—alters decline in plasma
concentrations, especially with drugs
which depend chiefly on renal clearance
• hepatic disease—patients have increased
VD, generally need a larger initial dose to
see an effect at the NMJ, more difficult to
clear
242
pancuronium (Pavulon)
• stiff, bulky steroid nucleus (same as sex
hormones); onset 1-3 min, DOA 40-65 min
• no histamine release or ganglionic blockade, but
exhibits a vagolytic effect
• cumulative, 80% renal clearance
• produces a 10-15% increase in HR, MAP, and
CO from selective cardiac vagal blockade
through atropine-like effect at the SA node
• activates the SNS by release of NE (? from
ganglionic stimulation vs. interference with NE
reuptake)
• does not release histamine
• intubating dose 0.04-0.1 mg/kg IV
doxacurium (Nuromax)
• long acting bisquarternary ammonium
• devoid of histamine release or other CV side
effects
• similar duration as pancuronium
• pharmacokinetics largely dependent on renal
clearance mechanisms
• onset approximately 4 minutes, DOA 76 minutes
• may have cumulative effects
pipercuronium (Arduan)
• long acting bisquaternary aminosteroid
• lacks histamine release or other CV side
effects
• pharmacokinetics largely dependent on
renal clearance mechanisms
• onset 3 to 5 minutes, DOA 60-90 minutes
• may have cumulative effects
• intubating dose 0.07-0.085 mg/kg
243
Intermediate acting NDMBs
• introduced in the 1980’s
• compared with the long acting NDMBs, they:
– have a similar onset of rate of maximal blockade
– approximately 1/3rd the duration
– 30-50% more rapid rate of recovery after reversal
– minimal to absent cumulative effects (may be used as
a continuous infusion)
– minimal to absent CV effects
– reliably antagonized with reversal agents 20 minutes
after administration
vecuronium (Norcuron)
• an intermediate acting monoquarternary aminosteroid
analogue of pancuronium
– lack of a methyl group makes it less “ACh like” and
decreases vagolytic properties 20-fold
• *known to have the best autonomic margin of
safety of all of the NDMBs
• onset similar to pancuronium but only 1/3 the duration
(3-5 min, 20-35 min, respectively)
• minimal to absent cumulative effects
• dependent largely on hepatic metabolism
• lacks histamine release, completely devoid of untoward
CV effects
• intubating dose 0.1mg/kg IV
atracurium (Tracrium)
• a bisquarternary benzylisoquinolone
• undergoes spontaneous degradation in vivo
– known as Hoffmann elimination Ö dependent
on physiologic pH and temperature of 37º
Celsius
• secondary route of metabolism is ester
hydrolysis by non-specific plasma esterases
• metabolism is independent of renal and hepatic
mechanisms, and does not depend on plasma
cholinesterase
244
atracurium (Tracrium)
• onset in 3-5 minutes, DOA 20-35 minutes
• exhibits a modest histamine release at
large doses (1 mg/kg and above)
• generates laudanosine as a by-product of
Hoffmann elimination and ester hydrolysis
– metabolized by the liver; may build up with
hepatic disease
– may cause seizure activity in high
concentrations
cis-atracurium (Nimbex)
• an intermediate isomer of atracurium
• same pharmacokinetic profile as
atracurium (i.e. onset, DOA, metabolism,
etc.)
• does produce laudanosine as a metabolite
• no consistent dose dependent increase in

histamine release, even at large doses
Rocuronium (Zemuron)
• an intermediate acting quarternary ammonium—
structurally similar to vecuronium
• approximately 1/5th the potency of vecuronium
• rapid onset time—similar to succinylcholine
– useful for rapid sequence inductions where SCh is
contraindicated
• DOA approximately 31 minutes
• fairly good CV profile but does cause a slight
histamine release at large doses and may be
vagolytic at 5X ED95
• no significant cumulative effects noted
• primary route of excretion is hepatic—75% of the
drug is found unchanged in the bile
245
Pediatric Review
Review of systems-cardiovascular
– stroke volume is fixed 2º non-compliant LV

• *CO is directly proportional to HR (CO = HR X SV)
– bradycardia should be avoided
– propensity of parasympathetic tone (“vagal animals”)
• PNS fully developed @ birth
– immature baroreceptors; minimal reflex activity
• SNS continues to develop during 1st 6 weeks of life
– inability to vasoconstrict in response to hypovolemia
review of systems-respiratory
• O2 consumption is high (4-6 cc/lb; adults 3 cc/lb)
• × alveolar ventilation and CO2 production
• FRC small
– prone to rapid desaturation
• Öbradycardia follows hypoxia
– rapid inhalation induction
– closing capacity may exceed FRC
• prone to atelectasis, hypoxia
– premature infants lack surfactant Ö RDS
• × work of breathing 2º Ç chest wall and È lung
compliance
246
pediatric airway
• airway anatomy:
– larynx anterior; overlies C3-4
– epiglottis stiff, U-shaped
• intubation achieved with Miller blade
– large tongue
– large occiput
– trachea funnel-shaped; narrows below the level of the
vocal cords; should have audible leak @ ~ 16 cm H2O
• prone to post-extubation croup; 10X higher
incidence if leak is absent
• ETT size [ age (in years) + 16]
4
ETT length (cm) [ age (in years)] + 12
2
post-extubation croup
• increased occurrence with:
– prolonged surgery
– repeated attempts @ intubation
– large ETT
– head/neck surgery
– Ç movement of ETT
• treat with nebulized racemic epinephrine
(vaponephrine)
Pedi airway, cont’d

• infants are obligate nose breathers
– choanal atresia
• oral airway is taped in place until surgical repair is done
• breathing is diaphragmatic 2º underdeveloped accessory
muscles of respiration
• infants have small cricothyroid membranes Ö
difficult to secure surgical airway
• airway changes occur during puberty 2º
hormones
247
Periodic breathing
• Infants have less Type I (high oxidative)
muscle fibers of diaphragm/intercostals
– These fibers are responsible for repetitive
motion
– Easily fatigable
• Predisposition to apneic periods
• Chemoreceptors are intact
Review of systems-renal
• ØGFR
– reach adult values at 1-2 years old
• Ø ability to concentrate or dilute urine
– 2º immature tubular cells, È response to aldosterone
– reach adult capability by 1 year old
• ×Na+ excretion
– neonates are obligate Na+ losers, even if
hyponatremic
– sodium excretion is inversely proportional to age
• ADH synthesis/excretion intact
Review of systems-hepatic
• Phase I reactions (oxidative/reductive) fully
functional @ birth
• Phase II reactions (conjugation) immature
– Propensity for developing jaundice
• ÇRBC destruction in face of decreased levels of enzyme
which conjugates bilirubin
• prematurity
• may also be caused by furosemide, diazepam, sulfonamides
(any drug which competes for albumin as a binding site)
• bilirubin levels increase; may lead to kernicterus with
retardation if un tx’ed
– treatment
» phototherapy/hydration
» exchange transfusion in extreme cases
248
Review of systems-neurologic
• immature blood-brain barrier anterior
• immature CNS
– Incomplete myelination
• immature ANS
– parasympathetic predominance
with È SNS tone posterior
• fontanelle closure
– anterior Ö 18 months
– posterior Ö 2 months
– anterolateral Ö 2 months
– posterolateral Ö 2 years
Review of systems-fluids/heme
• total body water content 10-30% > than adults
– ECF 35-40% (adults 20%)
– hydrophilic drugs noted to have large VD; need larger initial dose
• estimated blood volumes:
– preemie Ö 90 cc/Kg
– full term infant < 1yo Ö 80 cc/Kg
– child (until puberty) Ö75 cc/Kg
• HgbF @ birth replaced with HgbA by 4-6 months
– responsible for a transient È in hemoglobin during the initial 6 to
8 weeks of life; known as the physiologic nadir
– HgbF shifts oxy-Hgb dissociation curve Ö L
• compensated for with typical neonatal Hgb of 15, HCT 45-55%
• Hematopoiesis occurs in liver initially, changes to
marrow by 6 weeks
pharmacokinetics
• Neonates are resistant to the effects of

SCh (Large VD)
• Local anesthetics, particularly
mepivacaine, not well metabolized
• Emergence delirium is common
249
temperature regulation
• pediatric pts are × prone to development
of intraoperative hypothermia
– large BSA
– little subcutaneous fat
– inability to shiver
• heat production via non-shivering thermogenesis;
utilizes brown fat stores
– immature hypothalamic temperature
regulation
• poikilothermic tendencies
hypothermia
• effects:
– Ç oxygen consumption
– hypercapnia
– hypoxia
– acidosis
– hypoglycemia
• all lead to × pulmonary vascular resistance; RÖL
shunting
– *CO to brown fat 10% during normothermia;
75% during hypothermia
pre-op fasting guidelines

• clear fluids administered up until 2° pre-op
• breast milk administered up until 4° pre-op
• solids/milk administered up until 6° pre-op
– allows for smaller deficit replacement, less

dehydration, hypoglycemia, irritation 2º
hunger/thirst
– *aspiration is rare in the pediatric population
250
fluid calculations
• “4-2-1 rule” of fluid replacement
– 4cc/Kg/hr for first 10 kg body weight
– 2cc/Kg for next 10 kg body weight
– 1cc/Kg for each kg after 20 kg body weight
• may use LR, 0.45 ns for maintenance
– closely approximates body fluids
• replace blood loss:
– 3:1 with crystalloid
– 1:1 with PRBCs, colloid
fluid calculations, cont’d

• deficit
– maintenance X hours spent NPO
• replace ½ during 1st hour following surgery
• replace ¼ during 2nd, 3rd hours following surgery
• 3rd space losses for pediatric cases
– minimal (ENT, peripheral orthopedic procedures)
• 3-5 ml/kg/hr
– moderate (herniorraphy, appendectomy)
• 5-10 ml/kg/hr
– major (bowel surgery repair)
• 8-20 ml/kg/hr
Glucose replacement
• glucose may be replaced with dextrose
containing solutions
– neonates have È glycogen stores
• pediatric patients prone to hypoglycemia:
– premature infants
– neonates
– *infants of diabetic mothers
– IUGR, SGA
– chronically ill infants/children
– extensive pre-op fasting
• avoid hyperglycemia
251
Vital signs
Age HR SBP RR
Preterm 120-180 40-60 55-60
Newborn 95-145 50-70 35-40
6 months 110-180 60-110 25-30
1-2 years 100-160 65-115 20-24

2-3 years 90-150 75-125 16-22
3-5 years 65-135 80-120 14-20
5-8 years 70-115 92-120 12-20

9-12 years 55-110 92-130 12-20
12-14 years 55-105 100-140 10-14
Cardiac Anomalies
• divided into two subclasses:
– cyanotic lesions (A.K.A. R ÖL shunt—blood bypasses
pulmonic circulation)
• Tetralogy of Fallot
• Transposition of the Great Vessels
• Total Anomalous Pulmonary Venous Return
• Truncus Arteriosus
• Tricuspid Atresia
• Hypoplastic Left Heart Syndrome
– non-cyanotic lesions (A.K.A. LÖR shunt—blood
enters pulmonic circulation but returns in part to R
side of the heart)
• AV canal
• ASD
• VSD
• Patent Ductus Arteriosus (PDA)
• Coarctation of the Aorta
Cardiac anomalies cont’d

• care of the pt usually focused on minimizing
shunting; optimizing oxygenation
• air filters necessary in pts with RÖL shunts
• anomalies may frequently occur with other
syndromes
• IV induction will be delayed in LÖR shunts;
inhalation induction will be slower in RÖL shunts
• antibiotics
• prostaglandin infusions, lower FiO2 necessary
for “ductal dependent” lesions
252
Tetralogy of Fallot
-Most common of
the cyanotic heart
defects;
occurrence males
> females
-R Ö L shunting
increases with:
È SVR
Ç PVR
Çmyocardial
contractility
“TET spells”
(RVH)
-therapy aimed at
ÇSVR; children
will squat to
compensate
Transposition of the Great Arteries
-SVR/PVR
should be
relatively
equal
-*must have
PDA or
ASD/VSD for
*
mixing until
repair
Total anomalous pulmonary

venous return
253
Truncus arteriosus
-rare
-common
trunk is the
only artery
arising from
the heart
-predominant
LÖR shunt;
leads to
excessive
pulmonary
blood flow
-associated
with other
syndromes;
may be a
difficult
intubation
Tricuspid atresia
-agenesis of the
tricuspid valve; no
communication
between RA and
hypoplastic RV
-ASD, small VSD
AV Canal
-Large endocardial
cushion defect
which allows for
complete mixing of
venous and arterial
blood
- Associated with
Down’s Syndrome
254
Hypoplastic Left Heart
Atrial Septal Defect
Ventricular Septal Defect
255
Patent Ductus Arteriosus
• commonly noted in
the premature
infant; persistent
communication
between the
pulmonary artery
and the aorta
• result is pulmonary
edema
• spontaneous
closure from
hyperoxia,
pharmacologic
ligation by
indomethacin
• may require
surgical ligation;
done through a
thoracotomy
incision
Coarctation of the Aorta

• varying degrees of
cyanosis based on
– location of the
stenosis
– severity
(diameter) of the
lesion
– typical finding—
BP lower in LEs;
may have pink
upper body,
cyanosis/mottlin
g of the LEs
Persistent pulmonary hypertension

• A.K.A. persistent fetal circulation
– Çpulmonary vascular resistance from insult causes blood to
shunt RÖL through ductus arteriosis and foramen ovale,
bypassing the lungs
• severe hypoxemia from V/Q mismatch
• more prevalent in full-term infants
• causative factors:
– meconium aspiration
– diaphragmatic hernia
• mortality rate 50%
• treatment:
– mechanical ventilation
• leads to barotrauma, bronchopulmonary dysplasia
– inhaled NO to selectively dilate pulmonary vasculature
– ECMO-bypasses lungs until PVR decreases and shunting
reverses
256
PPH, cont’d
• Primary precipitating factors
– hypoxemia
– acidosis ALL cause
an increase
– hypothermia in PVR
– pneumonia
• Other causative factors:
– meconium aspiration
– diaphragmatic hernia
Surgical emergencies
• Tracheo-esophageal fistula
• Omphalocele
• Gastroschisis
• Pyloric stenosis
• Congenital diaphragmatic hernia
• Myelomeningeocele
• Foreign body aspiration is the most common
surgical emergency in the pedi population
Tracheoesophageal fistula
• anomalous development of the esophagus; may
or may not communicate with the trachea
– 5 subtypes
• I Ö esophageal atresia; no communication with
trachea
• II Ö esophagus fully formed with communication to
trachea
• IIIA Ö esophageal atresia with communication to
trachea
• IIIB Ö upper esophageal atresia with no
communication; distal communication to trachea
(90%)**
• IIIC Ö esophageal atresia with both upper and
lower esophageal communication
257
Tracheoesophageal fistula
**IIIB occurs in
90% of cases
TEF, cont’d
• may be dx’d with first feeding
– leads to coughing/choking
– inability to pass a feeding tube into stomach
• gastric distention with respirations
• *aspiration pneumonia and other pulmonary
issues most frequent complication
• causes of mortality
– *respiratory complications (60%)
– associated anomalies
– post-op complications (i.e. leaking anastomosis)
anesthetic considerations for TEF

• pouch/stomach decompression before induction
• continuous suction for Ç oral secretions
• no (+) pressure ventilation before intubation
• **awake intubation
• tip of ETT should be just above the carina and distal to
the level of the fistula if communication
• hydrate
• warm OR
• post-op gastric tube insertion, neck manipulation may
disrupt surgical repair
• may need staged surgeries
• surgical complications:
– pneumothorax, atelectasis, subcutaneous emphysema
– RLN damage
258
omphalocele vs. gastroschisis
omphalocele gastroschisis
-midline defect arising from the -abdominal wall defect; non-
base of the umbilicus midline
-viscera encapsulated in sac; less -viscera not encapsulated; Ç
insensible loss 2º evaporation insensible loss
-*may be associated with cardiac -rarely associated with other
anomalies or other syndromes (i.e. syndromes
VATER) -1:15,000 live births
-1:5000 live births
VATER syndrome
• acronym for a syndrome of associated
anomalies
– Vertebral defects (i.e. spina bifida)
– Anal anomaly (usually imperforate)
– TracheoEsophageal fistula or Esophageal
atresia
– Radial or Renal dysplasia
• may also be associated with cardiac
anomalies, 1º VSD
Omphalocele vs. gastroschisis
259
anesthesia for
omphalocele/gastroschisis
**decompression of stomach before induction**
**awake intubation not necessary
• N2O contraindicated
• muscle relaxation needed for re-insertion of the
bowel into the abdominal cavity
– surgeries may need to be staged
– post-op (+) pressure ventilation required for 2-3 days
• expect ventilatory compromise
• warm OR
• hydrate adequately
– Ç insensible losses and temperature loss with
exposed viscera
Pyloric stenosis
• manifests at 3-6 weeks; males>females
• non-bilious projectile vomiting noted after meals 2º
gastric outlet obstruction
• olive-shaped abdominal mass
• **eventual development of hypochloremic, hypokalemic
metabolic alkalosis and dehydration
– pt may retain CO2 via hypoventilation to compensate for loss of
H+
• pts treated as full stomachÖRSI or awake intubation;
extubate fully awake
• intraoperative hydration and electrolyte replacement
necessary
Congenital diaphragmatic hernia

• 1:5000 live births
• abdominal viscera herniates into chest cavity
• left sided most common (90%)
• infant should be delivered via C/S to È pressure during
delivery
• features
– scaphoid abdomen
– hypoxia
– radiograph Ö loops of bowel in the thorax
• anesthetic concerns
– decreasing gastric distension
– no bag/mask ventilation; immediate awake intubation
– no N2O
– limit PIP to 28 cm H2O; tension pneumothorax a concern
• infant may require ECMO for persistent fetal circulation
260
Congenital Diaphragmatic Hernia
Congenital Diaphragmatic Hernia
Myelomeningeocele
• A failure of neural tube closure
• Meningeal sac may be occult or
externalized
– Meningeocele-contains meninges
only
– Myelomeningeocele-contains
meninges and neural tissue
• opportunity for large 3rd space
losses, hypothermia, infection
• pt may need to be side-lying for
induction/intubation
• Associated with
– Club foot
– Hydrocephalus
– Dislocated hips
– Klippel-Feil syndrome
– Cardiac defects
– Genitourinary defects
– (eventual) latex allergy
261
Myelomeningeocele
other pediatric surgical emergencies

• volvulus, intussusception, incarcerated inguinal
hernia
• necrotizing enterocolitis (NEC)
– 1º seen in preemies; from hypoxia
• high degree of morbidity/mortality
– sepsis, ARF, CV collapse
• “Prune belly” syndrome
– congenital atresia of abdominal wall musculature
– may be associated with renal anomalies
(cryptorchidism, genitourinary tract abnormalities) and
club foot
– awake intubation
– risk for
• pulmonary complications, *aspiration 2º inability to cough
• airway tumors/anomalies
– hemangiomas, cystic hygroma, choanal atresia
Airway anomalies
• cleft lip and/or palate
– a separation of the segments of the lip or roof of the
mouth
– cleft lip is a separation of the two sides of the lip and
often includes the bones of the maxilla and/or the
upper gum
– cleft palate is an opening in the roof of the mouth and
can vary in severity. A cleft palate occurs when the
two sides of the palate do not fuse during embryologic
development
• may be a difficult intubation
262
Airway anomalies, cont’d
• Pierre-Robin
– a condition in which the lower jaw is
abnormally small
– tongue prolapses backward toward the throat
causing upper airway obstruction
– *cleft lip and a cleft palate may or may not be
present
– difficult intubation based on degree of
micrognathia (A.K.A. mandibular hypoplasia)

• Treacher-Collins
– most common of the mandibular dystoces
– a condition in which the maxilla and mandible are
underdeveloped
• very small mouth
– very small or partially absent cheek bones and
notches in or stretching of the lower eyelids
– ears are frequently abnormal and part of the outer ear
is usually absent
– hearing loss is commonly associated with this
syndrome.
– **very difficult intubation

• Crouzon Syndrome
– a condition in which sutures in the head are
prematurely fused resulting in abnormal growth of the
skull and face
– bulging eyes noted due to abnormal growth of the
mid-face
– may have a receding upper jaw and protruding lower
jaw
– problems with dentition due to abnormal jaw growth
• mask fit usually difficult in these pts
263
• Beckwith-Wiedemann syndrome
– macroglossia
– macrosomia
– *hypoglycemia
– hypocalcemia
– polycythemia
– may occur in conjunction with omphalocele
– may be associated with multiple tumors

• Klippel-Feil syndrome
– cervical spine instability
• may be associated with cardiac anomalies
– VSD, bradydysrhythmias
• 3 major findings
– 2 or more fused cervical vertebrae
– cervical immobility
– low posterior hairline
• may have restrictive lung disease if scoliosis is
present
– **caution during laryngoscopy, positioning

• Turner’s syndrome (gonadal dysgenesis)
– a chromosomal condition that exclusively affects girls and
women, caused by the complete or partial absence of one of the
two X chromosomes normally found in women
– common characteristics:
• short stature
• lack of ovarian development
• HTN
• drooping eyelids
• coarct of aorta
• renal agenesis
• pectus excavatum
• high palate may be a
• micrognathia difficult
• webbed neck (A.K.A. “bed neck”)
intubation
• low hairline in the back of the head
264
• Goldenhar syndrome
– manifests as unilateral mandibular hypoplasia
• associated with eye, ear, and vertebral anomalies
of the affected side
• tracheal intubation may be difficult; varies with
degree of hypoplasia of mandible

• Tracheomalacia
– A softening of the trachea
– May be associated with esophageal atresia
– May follow prolonged intubation
• Main anesthetic concern Ö airway obstruction,
particularly during inspiration
• Necessitates tracheal stenting
Cystic Hygroma
265
Trisomy 21
• A.K.A. Down’s Syndrome
• *the most common chromosomal abnormality
• 1:700-1:1100 live births
– 1:40 live births when maternal age > 45 years
• features
– mental retardation
*1º anesthesia
– generalized hypotonicity concern Ö airway
• *atlantoaxial subluxation
difficulties
– obesity
– large tongue, tonsils, adenoids
– narrow subglottic area
• Ç prone to post intubation croup
– associated cardiac defects involve the endocardial cushion
• VSD, AV canal
– also associated with duodenal atresia
croup vs. epiglottitis

croup epiglottitis
-6 mos-5 years -3-7 years
-usually preceded by URI -sudden onset with a rapid
-familial progression of symptoms
-gradual onset -can lead to acute upper airway
-(+/-) fever and/or Ç WBC obstruction/death
-”barking seal” cough -may necessitate tracheostomy
-”Steeple sign” on CXR; reveals -Ç fever/WBC
subglottic stenosis -severe pain
-self limited; tx’d with -pt extremely anxious
-hydration, humidification of -sitting upright
ambient air -copious oral secretions
-use of steroids controversial -Haemophilus Influenza Type B
causative; incidence È with
advent of HIB immunization
epiglottitis
• diagnosis confirmed with chest radiograph
– epiglottis large
– tracheal narrowing from edema
• requires antibiotic therapy
• if surgical intervention (tracheostomy) is required
– quiet induction (inhalation) with child maintained in sitting
position; use sevoflurane
– surgeon standing by for emergency trach if unable to intubate
– intubate with small tube
– hydration
• if intubated without trach; wait until there is an audible
leak around tube before extubation
– extubate in OR; monitor closely for 1 hour
266
Post tonsillectomy bleeding
• occurrence
– 1st 24º post-operatively or
– 7-10 days post-operatively
• sloughing of eschar from tonsillar beds causes rebleeding
– pts need large bore IV
• may present to OR extremely hypovolemic
• *rapid sequence induction
– Çswallowed blood, emergent status = full stomach
• suction readily available for laryngoscopy
– anticipate possibility of aspiration, post-extubation
laryngospasm
– typical EBL for routine tonsillectomy ~ 100 ml
Upper respiratory infection

• usually viral
• prevalent amongst pedi population; 6% present for
anesthesia with an active URI
• s/s (must have 2 or more for (+) dx of URI)
– sore/scratchy throat
– sneezing
– rhinorrhea
– congestion
– malaise
– non-productive cough
– temp >38.5º C
– laryngitis
• phases of URI
– onset, active, resolution
• important to ascertain which phase the patient is in
URI cont’d
• potential concerns
– respiratory complications 2º Ç airway
irritability, secretions
• post extubation stridor, croup
• hypoxemia
• bronchospasm
• laryngospasm
• *pulmonary changes may persist 4-7 weeks after
resolution of URI
267
Neonatal surgery
• Neonates prone to peri/postoperative
complications:
– High risk pts:
• Premature infants
– should be at least > 46 weeks post-conceptual
age
– not good candidates for same-day surgery
» Cardio/respiratory monitoring for 24º post op
is required
• History of apnea/bradycardia
– Pt may be given prophylactic caffeine 10 mg/kg
• Multiple congenital anomalies
• Chronic lung disease
Notes
Notes
268
Hematology Review
Anemia
• Pathophysiology
– Most commonly from chronic blood loss
• Other anemias: aplastic, hemolytic, sickle-
cell, chronic disease, thalassemia
• Also from iron, folate, cobalamin deficiencies
– Symptoms secondary to inadequate oxygen
delivery: fatigue, angina, claudication, TIAs
– WHO definition of anemia:
Children < 6 yrs Hgb < 11

Children 6 – 14 yrs & non- Hgb < 12
pregnant females
Pregnant females Hgb < 11
Males Hgb < 12
Anemia Cont”
• Treatment
– Treat underlying cause
• Iron
• Vitamin replacement – Folate, B12
– Erythropoietin, transfusion
– Oxygen supplementation
Aplastic Anemia
• Pathophysiology
– Most cases idiopathic
– Drug induced: chloramphenicol, NSAIDs, sulfa, gold
– Infection: AIDS, hepatitis, CMV, EBV, TB,
toxoplasmosis
– All cell lines affected: RBCs, WBCs, platelets
– RBCs older as compared to normal patient, lower 2,3
DPG levels and tighter oxygen binding with
decreased oxygen delivery
• Treatment
– Bone marrow transplant
– Steroids, immunosuppressive drugs
Aplastic Anemia Cont'

• Preop
– Reverse isolation precautions
– Ensure adequate supply of blood products
– Prophylactic antibiotic therapy
– Stress dose steroids
– Avoid IM or rectal premedication
• Intraop
– Monitoring as dictated by surgery
– Avoid nasal intubation
– Anticipate hypotension and increased fluid requirements
– Spinal/epidural contraindicated
– Avoid nitrous – suppresses marrow production
– Normothermia promotes coagulation
Aplastic Anemia Cont'
• Postop
– Immediate post-extubation period with greatest O 2
demands
– Continue to monitor coagulation status
– Continue antibiotic coverage
– Continue steroid coverage
Sickle-Cell Anemia
• Pathophysiology
± 0ROHFXODUOHVLRQRQȕFKDLQRI+JE ± SRVLWLRQJOX Ö
val
– Defect allows deformation and polymerization of Hgb
molecules in face of hypoxia, acidosis, hypothermia,
hypovolemia Ö cell distortion.
• P50 > 27
– 0.2% of African-Americans with disease
Sickle-cell Anemia Cont'

Pathophysiology cont’
– Sickling causes:
• Vasocclusive crises: pulmonary infarction, renal
infarction, hepatic damage, CVA, bone ischemia
• Hemolysis: anemia, hyperbilirubinemia, jaundice,
cholelithiasis
• Sequestration crisis - threatening in the pedi
population
• Aplastic crisis – secondary to viral infection and
shortened RBC life-span
• Acute chest syndrome – probably the result of
pulmonary infarction with infection

• Treatment
– Simple exchange transfusions
– Hydroxyurea – increases fetal Hgb
– Bone marrow transplantation
• Preop
– Simple transfusion to achieve HgbA > 50%, HgbS <
40% (some recent data questions this; suggests to
transfuse to Hgb >10)
– Adequate preop hydration – maintenance x 1.5 prior
12 hours
– Treatment of any existing infections
– No benefit to alkalinization
– Minimal sedation to avoid hypoxia/hypercarbia

• Intraop
– Routine monitoring, art line for ABG’s, central
catheter as indicated
– Avoid hypovolemia, extremes of temperature
– No anesthetic technique shown to be superior
– Avoid tourniquet if possible
– Extubation critical period – possible hypoxia,
respiratory acidosis

• Postop
– Maintain adequate hydration
– Keep patient warm but avoid hyperthermia
– Supplemental oxygen for 12 – 48 hours
– Adequate analgesia
– Incentive spirometry
Sickle-Cell Trait
• Pathophysiology
– Heterozygous form of sickle-cell disease
– Reduced formation of HgbS
• Preop, Intraop, Postop
– Same as for sickle-cell disease
– Much lower morbidity & mortality
Leukemia
• Pathophysiology
– Hematologic malignancy with proliferation of WBCs
– Massive consumption of amino acids Ö fatigue,
metabolic starvation
– WBC invasion in all organs with corresponding
decrease in function
– Immunosuppression
– Coagulopathy
• Treatment
– Variety of antineoplastic agents
– Bone marrow transplantation
Antineoplastic Agents
• Doxorubicin (Adriamycin), Daunorubicin &
Epirubicin
– Toxic to myocardium
– Late toxic effects (up to 5 yrs later) may
appear
– Myocardial damage is permanent and total
dose dependent
– CHF is unresponsive to inotropic drugs
– May predispose patient to MH
Antineoplastic Agents
• Bleomycin
– Pulmonary toxicity with pneumonitis Ö fibrosis
– Pneumonitis may rapidly worsen with
enriched oxygen mixtures – keep FiO2 < 30%
• Vinca Alkaloids
– Peripheral neuropathy
– SIADH
• Cyclophosphamide
– Cholinesterase inhibition
Leukemia Cont'
• Preop
– Assess volume status – many patients with prolonged
vomiting
– Assess effects of antineoplastic agents – myocardial
depression, peripheral neuropathy, stomatitis
• EF indicated in patients treated with doxarubacin
– Assess coagulopathy
– Antibiotic prophylaxis
– Steroid coverage if indicated
Leukemia Cont'
• Intraop
– Routine monitors and additional monitoring as
indicated
– No anesthetic technique shown superior
– Patients at increased risk of MH
• May be secondary to previous doxarubacin
treatment
• Postop
– Continue antibiotic and steroid coverage
AIDS/HIV
• Viral infection attacking and killing T-helper cells
containing CD4 antigen
&'OHYHOVEHORZFHOOVȝ/ DVVRFLDWHGZLWK
significant morbidity
• Anesthetic management determined by type and
extent of underlying diseases
• Healthcare workers should employ universal
precautions with all patients
AIDS/HIV
• Body fluids know to contain virus:
– Saliva
– Tears
– Semen
– Cervical secretions
– Urine
– CSF
– Breast milk
• Methods of viral inactivation
– 1:10 bleach solution
– Sterilization techniques – autoclave, ethylene oxide,
sterilizing solutions
Virus can live 7-10 days outside of host
AIDS/HIV
• Testing for HIV
– Antibody tests: ELISA, Western blot (time from
infection to seropositivity about 3 weeks)
– Antigen tests: PCR, p24 antigen
– CD4 lymphocyte count
• Other important facts
– Needle stick exposure to HIV infected blood – risk is
1:250
– Needle stick exposure to Hepatitis B infected blood –
risk is 1:10
• If stuck, do antibody testing immediately and at 6,
12, 24 weeks
– Prophylactic AZT therapy not shown to be effective
Coagulation Cascade
Coagulation Cascade Cont’

• Thrombin generation begins with vessel
injury resulting in tissue factor exposure
• Tissue factor interacts with Factor VIIa to
generate thrombin
• Thrombin converts fibrinogen to fibrin and
activates factors V, VIII, XI
– These stimulate production of additional
thrombin
• This all results in the hemostatic plug
Coagulation Factors
Foolish People Try Climbing Long Slopes After
Christmas, Some Also Have Fallen
Factor I – Fibrinogen Factor IX –

Factor II – Prothrombin Antihemophilic Factor B
Factor III – Tissue Factor (Christmas Factor)
Factor IV – Calcium Factor X – Stuart Prower
Factor XI –
Factor V – Labile Factor Antihemophilic Factor C
Factor VI – doesn’t exist Factor XII –
Factor VII – Stable Factor Hageman Factor
Factor XIII – Factor XIII –
Antihemophilic Factor A Fibrin Stabilizing Factor
Coagulation Tests
• PT – Prothrombin time
– Measures the extrinsic pathway
– Measures Factors II, VII,IX & X
• INR – International Normalized Ratio
– PT(test) / PT(normal)
• PTT – Partial Thromboplastin Time
– Measures both intrinsic and common pathways
• Bleeding Time –
– Measures platelet function
– No correlation with degree of surgical bleeding
Coagulation Tests Cont’

Condition PT PTT BT
Vitamin K deficiency / Warfarin + 0 0
Hemophilia 0 + 0
von Willebrand Disease 0 + +
DIC + + +
NSAID use / Thrombocytopenia 0 0 +
Liver Disease + 0 0
Thromboelastogram (TEG)
TEG monitoring is used to diagnose different conditions

such as fibrinolysis, thrombocytopenia, and factor
deficiency. Results help to direct transfusion therapy
based on specific coagulopathy.
Thromboelastogram Cont'
Hemophilia
• Pathophysiology
– Hereditary X-linked recessive disorder
– Incidence: 1/10,000 male infants – 15,000 patients in
USA
– Deficiency in Factor VIII (85%) or Factor IX
(Christmas disease)
– Level of deficiency is variable
– Diagnosis by determining factor levels
– PTT is elevated, PT and plt count are normal
– Symptoms: entirely due to complications of bleeding
– Because of frequent factor replacement, up to 15%
will develop antifactor antibodies complicating
treatment
Hemophilia Cont'
• Treatment
– Recombinant factor replacement
– DDAVP for mild cases
– Cryoprecipitate and FFP no longer recommended
Hemophilia Cont'
• Preop
– Attain 40 – 70% of deficient factor level prior to
surgery
– VD(ss) for factors about 100 cc/kg
– Avoid unnecessary IM injections
• Intraop
– Caution with invasive monitoring
– Risk of bleeding may outweigh benefits of regional
– Follow coagulation profile
Hemophilia Cont'
• Postop
– Avoid analgesics with anti-platelet function (ketorolac)
– Patients may have high narcotic tolerance from
previous exposure
Von Willebrand’s Disease

• Types
– I Ö Low levels of Factor VIII:vWf, Factor VIII:C
• Most common form; autosomal dominant
– II Ö Functional abnormality of Factor VIII:cWf.
• autosomal dominant
– III Ö Defective synthesis of Factor VIII
• Role of Factor VIII
– Factor VIII consists of 2 parts:
• von Willebrand factor for platelet function
• Factor VIII:C as part of the intrinsic pathway
• Coagulation studies
– PTT and bleeding time elevated
• Periop Management
– DDAVP – stimulates the production of Factor VIII
Immune Thrombocytopenic
Purpura (ITP)
• Pathophysiology
– IgG antiplatelet autoantibodies
– Antibodies directed against platelet membrane
glycoprotein
– May see during pregnancy (1–2 /1000)
• Treatment
– Corticosteroids initial line of therapy
– Intravenous IgG
– Splenectomy
– Immunosuppressive drugs – azathioprine, vincristine
– Platelets – have shortened half-life, but temporarily
increase count
ITP Cont'
• Preop
– Steroids and IgG to increase platelet count
– Avoid IM injections for premedication
• Intraop
– Avoid nasal intubation
– Theoretical disadvantage to volatile agents 2º
inhibition of platelet function
– Neuraxial anesthesia only if bleeding time and
thromboelastogram (TEG) results are normal
DIC – Disseminated Intravascular

Coagulopathy
• Overview
– Syndrome of activation of clotting cascade and
fibrinolysis
– Widespread formation of fibrin, consumption of
clotting factors
– No pathognomonic test for DIC – lab findings must
match clinical findings
– Lab findings – rapidly falling platelet count,
prolongation of clotting times, presence of fibrin
degradation products (FDPs), decreased clotting
factors, positive D-dimer
DIC Cont’
• Risk factors:
– Sepsis - Burns
– Liver disease - Fat embolism
– Shock - Retained placenta
– Brain injury - Amniotic fluid embolism
– Tissue necrosis - Eclampsia
– Leukemia - Disseminated malignancy
– Hemolysis
DIC Cont'
• Treatment
– Correction of underlying problem
– Administration of blood products
– Heparin – very controversial
– Aminocaproic acid (Amicar) – may precipitate
massive intravascular coagulation
– Tranexamic acid (Lysteda) - may precipitate
massive intravascular coagulation
Blood Component Therapy
• Utilization
– RBCs Ö 22 million, platelets Ö 7 million, FFP Ö 2
million
– Viral infections associated with transfusion – hepatitis
C, hepatitis A, cytomegalovirus, Epstein-Barr virus,
human T cell lymphotrophic viruses (AIDS, hairy-cell
leukemia)
– Cytomegalovirus is the most commonly
transmitted virus associated with transfusion;
Hep B occurs in 1/350,000 units transfused
• RBC’s
– Used to increase oxygen carrying capacity
– Indicated in acute blood loss and anemia
• 1ml/kg will increase hematocrit 1%
Blood Component Therapy Cont'

• RBCs cont’
– Citrate binds calcium to prevent coagulation
– RBCs should be reconstituted with normal saline, no
calcium-containing solutions (e.g. LR)
– Changes during RBC storage Ö microaggregate
accumulation, decreased pH, increased potassium (4
mEq/U), decreased calcium, decreased Factor V and
VIII, decreased 2,3-DPG, increased lactate and
increased free hemoglobin
• RBCs cont’
– Complications of massive transfusion (10 U)
• Citrate toxicity
• Ca2+ should be administered after multiple
transfusions (starting at ~ 6-8 U transfused)
• Metabolic alkalosis
• Dilutional coagulopathy
• Hypothermia, electrolyte abnormalities
– Complications of all transfusions Ö
• Immunosuppression
• Acute & delayed hemolytic reactions
• Febrile reactions
• Anaphylaxis
• Transfusion-related acute lung injury (1:10,000)
• Graft-vs.-host disease
• Viral infections

• Effect of blood loss on HCT calculation
(Estimate allowable blood loss to a specific HCT)
1. Calculate blood volume (70 ml/kg adult (or male 75
ml/kg; female 65 ml/kg))
2. Estimate red cell volume based on starting HCT
(ERCV)
3. Estimate red cell volume of HCT of 30 (ERCV 30)
4. Calculate difference (ERCV - ERCV30 )
5. Multiply difference by 3 (accounts for re-addition of
plasma)

• Example:
– 85 kg man with a starting HCT of 35
1. 85 kg x 70 ml/kg = 5950 ml
2. 5950 ml x 35% = 2083 ml (ERCV)
3. 5950 ml x 30% = 1785 ml (ERCV30)
4. 2083 ml – 1785 ml = 298 ml
5. 298 ml x 3 = 894 ml allowable blood loss to HCT
of 30
• Platelet Transfusion
– Indicated when platelet count < 50,000
Each unit of platelets will increase count by 15,000
– Transfused platelets have decreased survival of
about 7 days
– ABO compatibility desired but not required
• about 70 ml of plasma per unit

• Fresh Frozen Plasma
– Contains all plasma proteins and clotting factors
– Indicated for treatment of factor deficiencies, reversal
of coumadin, and correction of coagulopathy from
liver disease
One unit of FFP increases each clotting factor by 2-
3%
– Goal to achieve 30% of normal coagulation factors
– Usual dosing Ö 10-15 ml/kg
– Same risk of viral infections as with whole blood
Heparin
• Mechanism of action
– Forms complex with antithrombin III allowing inhibition
of Factor X and thrombin
• Elimination
– Metabolized by hepatic heparinase
– Half-life is dose dependent:
100U/kg – 1 hour
400U/kg – 2.5 hours
800U/kg – 5 hours
– Low molecular weight heparins (e.g. Lovenox) have a
longer half-life
• Coagulation tests affected
– ACT, APTT
Heparin Cont'
• Heparin resistance
– Antithrombin III (AT3) deficiency (may be 2º previous
heparin therapy)
– CAD – mechanism unknown
– Old age
– Pulmonary embolus
– Hypereosinophilia
Resistance is managed by increasing heparin dose
and/or administration of antithrombin III
Heparin Cont'
• Complications of heparin therapy
– HIT-heparin-induced thrombocytopenia – an allergic
reaction to heparin with triad of signs:
• Thrombocytopenia
• Heparin resistance
• Thrombus formation
– Treatment Ö discontinue heparin therapy
Enoxaparin (Lovenox)
• A fractionated low molecular weight heparin
• Onset 20-30 min after sc dose, peak effect 3-5º
– Effects for up to 12º from anti-factor Xa activity
• May be administered IV or SQ
• Indicated for:
– Prophylaxis for DVT/PE in pts undergoing
• Major abdominal surgery
• Total joint surgery
– Treatment of DVT/PE in conjunction with coumadin
– Use in pts with unstable angina, non-Q wave MI,
acute ST elevated MI (STEMI), coronary stents in
conjunction with aspirin, atrial fibrillation
• Enoxaparin should be held at least 10-12º before
neuraxial anesthesia; 24º if higher doses are used
Coumadin
• Mechanism of Action
– Reduced amount and activity of vitamin K dependent
factors:
II, VII, IX, X, protein C and protein S
– Effects take days to appear as existing factor levels are
reduced
– Factor VII affected first – shortest half-life
• Toxicity
– Most toxicity is related to bleeding
– Coumadin is teratogenic
– Immediate reversal of anticoagulant effect with FFP
– Intravenous vitamin K is also effective, but requires
hours (up to 24) for effect
Thrombin Inhibitors
Thrombin Inhibitors Cont’

• Thrombin has three domains: one active
site and two exosites.
– Exocite 1 acts as a dock to orient fibrin
– Exocite 2 is a heparin-binding domain
• The bivalent DTIs, bivalirudin and
lepirudin, bind to both the active site and
exosite 1
• The univalent DTIs, argatroban and
dabigatran etexilate, bind only to the active
site.
Dabigatran
• Binds only to the active site, but blocks
thrombin activity
• Has almost minimal of protein binding and
therefore a very dependable profile
• Also has some antiplatelet activity
• No known reversal agent and even FFP
may not reverse anticoagulation.
• Monitor activity with APTT
• Elimination half-life: 7-9 hours
Factor Xa Inhibitors
• Rivaroxaban available as oral preparation
• Competitively binds with Factor Xa
• Both PT & PTT elevated
– Usefulness of these coagulation studies in
assessing anticoagulation is unknown
• Elimination half-life: 6-7 hours
• No know reversal agent
– FFP may not reverse anticoagulation
Fibrinolysis Inhibitors
• Aminocaproic acid (Amicar), Tranexamic
acid
– Binds and inactivates plasminogen
– Results at reducing blood requirements have been
equivocal
Musculoskeletal Review
Hip & Femoral Fractures

• Pathophysiology
– 30-day mortality = 7%
– No shown benefit in GA vs. regional anesthesia
– Cause of fracture may affect anesthetic management
• Syncopal episode, PE, ischemic event, etc
• Treatment
– Surgical correction of fracture offers best results
– Traction alone associated with high M&M due to
pulmonary and septic complications
Hip & Femoral Fractures

• Hip arthroplasty may be done on an
emergent basis
– fractured hip Ö probable femoral head
fracture
• Associated with ÇÇ blood loss (1L or more)
sequestered around the fracture site
– Hypovolemia common
• Full stomach status from pain/delayed gastric
emptying
• Pt may have occult (internal or neurologic) injuries
288
Subtypes of hip fractures
•Blood loss from hip

fracture depends on
the location of the
fracture
•The capsule acts as a
tourniquet, thereby
restricting blood loss
Blood loss from greatest to least:
subtrochanteric, intertrochanteric > base of femoral neck >
transcervical, subcapital
Hip & Femoral Fractures Cont'

• Preop
– Early surgical intervention preferred
– Patients hypovolemic as result of blood loss
– Patients often have multiple other medical problems
• Intraop
– Routine monitors and possible central catheter
depending on underlying disease states
– Consider fluid bolus before regional anesthetic
– Use warming blanket – large exposed surface area
– Possibility of air, fat, bone embolization with insertion
of femoral head
– Anticipate cementing with hydration, increased FiO 2,
vasopressor
Hip & Femoral Fractures Cont

• Postop
– Blood loss of up to 2 units continues
postop
– Maintain Hct > 30 if CV disease present
– Adequate analgesia to promote early
ambulation
289
Total Joint Arthroplasty
– Total hip arthroplasty Ö 2-3% post-op mortality (30
days out)
– Pts are typically elderly with pre-existing co-
morbidities
• Ç Risk for perioperative cardiac events
– MI, CHF, pulmonary embolus
• Arthritis
– Positioning issues
– Difficult airway 2º limited cervical and TMJ
ROM, stiff larynx
– May need stress dose steroid coverage
Total Joint Replacement, Cont'd

• Intraop
– Risk of pulmonary emboli
• 1º cause of early (1-6 day) mortality
• Showers of embolic material occur, especially
while surgeon is reaming long bones
– Fat, bone, marrow, and/or cement may be
embolized
– Cement Ö methylmethacrylate
• May cause severe hypotension up to 30 minutes
after installation
– Causes an exothermic reaction; vapors are
released which vasodilate
» Lower incidence during total knee
arthroplasty 2º tourniquet inflation
Fat embolism
• Fat Embolism Syndrome – petechiae,
neurologic dysfunction, hypoxemia
• Occurs as a result of release of marrow fat
into the venous circulation and secondary
production of inflammatory mediators
• 80 – 100% risk with long bone/pelvic fxs
• Wide range of effects, from minor
pulmonary dysfunction to full FES
290
Fat Embolism Cont'
• Complications of FES
– Hypoxemia
– Poor pulmonary compliance
– Pulmonary HTN with RV failure
– Coagulopathy
• Treatment
– Supportive with PEEP, Ç FiO2, hemodynamic
support, correction of coagulopathy
Total Knee Arthroplasty

• May be unilateral or bilateral
• Ç incidence of forming DVT postoperatively; pts are
typically anticoagulated
• Less risk of intraoperative embolic events than with THR
• Morbid obesity an associated comorbidity
• Performed using a tourniquet; provides a “bloodless”
field
– May cause postop neuropathy if inflation time
exceeds 2º from ischemia
– Hypotension/arrhythmias/CV collapse may occur with
tourniquet deflation
• Ç volume shifts
• Release of vasoactive substances (1º lactic acid),
CO2 and K+ systemically
Anesthetic Concerns for Total Joint

Replacement
• Hypovolemia from blood loss common
– Good IV access needed (lg bore X 2)
– Invasive monitoring, SaO2, ETCO2
– Blood products available
– Regional may be preferable to GETA
• Decreases blood loss
• È incidence of thromboembolic event
• Facilitates earlier mobility
– Avoid hypothermia
– D/C N2O, euvolemia before tourniquet deflation or
installation of cement
291
Facial Fractures
• Overview
– Facial fractures present difficulties with airway
management
– Anatomical changes as a result of fracture
• Edema
• Bleeding and hematoma formation
• Patients require awake fiberoptic intubation
or tracheostomy
• CSF leak not uncommon
Facial Fractures Cont’

• 3 well described facial fractures:
– Le Fort I – maxillary fracture with free-floating
maxilla
– Le Fort II – maxillary fracture with fractures of
zygoma, orbital floor of eye and nose
– Le Fort III – fractures of multiple bones of 2/3
of face
*nasalintubations contraindicated with Le Fort II

and III fractures
Le Fort I, II, and III fractures
292
Rheumatoid Arthritis
• Pathophysiology
– Autoimmune disorder triggered by an antigen in
genetically susceptible patients
– Pathologic changes: hyperplasia of synovium, joint
infiltration by lymphocytes & fibroblasts with ultimate
joint destruction
– Cervical spine often affected with 2o compression
– Myocardial damage may occur
– Pulmonary fibrosis with restrictive lung disease may
also occur
• Treatment
– NSAID’s
– Immunomodulators – azathioprine,
hydroxychloroquine, methotrexate, corticosteroids
Rheumatoid Arthritis Cont'

• Preop
– Check mobility of TMJ and cervical spine
– Check mobility of other joints in regard to patient
positioning
– Check preop meds – steroid coverage may be
required
• Intraop
– Cervical cord damage possible during intubation
– Trachea may be affected and smaller diameter tube
needed
– Greater BP swings as a result of myocardial
dysfunction
Rheumatoid Arthritis Cont'

• Postop
– Laryngeal edema common
– Check carefully for new neurologic
deficits
– Continue steroid coverage if indicated
293
Muscular Dystrophy
• Pathophysiology
– Pseudohypertrophic (Duchenne’s) most common
– X-linked recessive trait
– Defect causes increased membrane permeability and
fatty infiltration of the muscle
– Clinical presentation: males > 2 years with weakness
– Manifestations: weakness, cardiomyopathy,
kyphoscoliosis with secondary restrictive lung disease
– ECG Ö deep Q’s in precordial leads
• Treatment
– Steroids may be beneficial
– Spine rodding and fusion
– Tendon releases
Muscular Dystrophy Cont'

• Preop
– Assess cardiac function
– Mitral valve disease may require antibiotic prophylaxis
– Increased risk of aspiration & delayed gastric
emptying
– Prepare for possibility of MH triggering
– Steroid coverage if indicated
• Intraop
– Central catheter & TEE if cardiac function poor
– Avoid succinylcholine – may result in hyperkalemia
– Consider a “full stomach”
– Titrate NMBs carefully
– Avoid calcium channel blockers – may enhance
muscle relaxation
Muscular Dystrophy Cont'

• Postop
– Potential for prolonged ventilator dependence
• Especially if vital capacity < 30% of
predicted
– Monitor for rhabdomyolysis
– Late ventilatory complications may make
outpatient surgery unadvisable
294
Myotonic Dystrophy
• Pathophysiology
– Triad – frontal baldness, cataracts, mental retardation
– Symptoms begin at age 20 – 30
– Persistent muscle contracture after cessation of
stimulation
– Inherited autosomal dominant trait
– Respiratory muscle weakness and cardiomyopathy
common
– May also have endocrine involvement with
hypothyroidism, DM, adrenal insufficiency
• Treatment
– Quinine, procainamide, phenytoin, tocainamide,
mexiletine – all drugs that depress Na+ influx
Myotonic Dystrophy Cont'

• Preop
– No preop analgesics or sedatives
– Warm OR – shivering can cause severe muscle
contractions
– Ensure NPO status
• Intraop
– Jaw muscle spasm and jaw dislocation common with
intubation
– Avoid succinylcholine Ö severe prolonged
contractions & hyperkalemia
– Anticipate cardiomyopathy and arrhythmias
– Response to non-depolarizing NMBs appears normal
Myotonic Dystrophy Cont'

• Postop
– Be alert to possible pulmonary complications
and ventilatory depression
295
Malignant Hyperthermia
• Pathophysiology
– Incidence: 1/15,000 – 20,000 in children
1/50,000 – 100,000 in adults
males > females
– Genetic basis for MH resembles autosomal
dominant
– Mortality in US < 10%
– Occurs after exposure to triggering agents:
• Volatile agents, succinylcholine
– Defect in calcium release/control leads to
increased intracellular calcium and sustained
muscle contraction
MH Cont'
• Pathophysiology cont’
– Hyperkalemia, acidosis, hypercarbia, rhabdomyolysis,
renal failure, DIC usual cause of death
– SX: hypercarbia (earliest & most sensitive sign),
tachypnea, tachyarrhythmias, fever, muscle rigidity,
electrolyte imbalances
– Associated with: myotonia congenita, central core
disease, SIDS, strabismus, osteogenesis imperfecta
– Differential diagnosis: thyroid storm,
pheochromocytoma, neuroleptic malignant syndrome,
sepsis, hypercarbia/hypoxia, drug reaction
MH Cont'
• Treatment
Majority of patients have no history of disease and
require no treatment
• Preop
– High risk:
• Patients with previous masseter spasm (10 – 20 %
with MH)
• First degree relatives
• Patients with unexplained elevated CPK
– Change circuit and bag, remove vaporizers, flush
machine with O2 at 10 L/min for 20 min
– dantrolene prophylaxis no longer indicated
296
MH Cont'
• Intraop
– Routine monitors:
• Emphasis on capnography
• Follow body temperature (late sign)
– Avoid triggering agents
• Volatiles, succinylcholine
• Use of phenothiazines controversial
– Dantrolene immediately available
• Very hard to mix
• Adequate personnel available
• Postop
– continue close monitoring of temperature and ECG
Treatment of MH episode
• Discontinue triggering agents
• Hyperventilate with 100% O2
• Actively cool; lavage bladder, stomach with cold NS
• Treat acidosis, aggressively hydrate
• Dantrolene – 2.5 mg/kg IV (may need more)
• Avoid calcium channel blockers
– Complete CV collapse if co-administered with
dantrolene
• Maintain U/O – osmotic diuretics if necessary
• Follow coagulation profile
• 25% incidence of recurrence postop
– Continue to monitor for at least 24 hours
– Dantrolene 1 mg/kg IV q 4-6h and continued for 24-
48h after episode
Scoliosis & Kyphosis

• Pathophysiology
– Idiopathic scoliosis from upper & lower motor neuron
diseases and myopathic causes
– May also have a metabolic cause – altered collagen
deposited in end-plates or juvenile osteoporosis
– If diagnosed before age 10, progressive course
– Pulmonary function can be severely impacted by
overall reduction in chest volume Ö appears as
restrictive lung disease
• Treatment
– Bracing
– TENS stimulation
– Surgery
297
Scoliosis & Kyphosis Cont'
• Preop
– Assessment of pulmonary function
– Rodding is associated with large blood loss –
consider pre-donation
• Intraop
– Somatosensory evoked potentials for rodding
procedures
– Expect prolonged ventilator dependence if VC < 30%
of predicted
– SSEP & MEP best test of cord integrity
• Wake-Up test previous gold standard
– Prone position required for extended period of time
• Position carefully; minimize ocular pressure,
sustained hypotension, over-hydration with
crystalloid
Scoliosis & Kyphosis Cont'
• Postop
– Expect delayed extubation
– Check neurologic status as soon as possible
Systemic Lupus Erythematosus

• Multisystem disease
– Fibrinoid substances deposited in multiple tissues
causing inflammation
– Pericarditis, endocarditis, myocardits, CHF,
conduction block, restrictive lung disease, anemia,
nephrosis, glomerulonephritis, thromboembolism,
renal failure, seizures, arthritis, lupoid hepatitis
• Treatment
– Immunosuppression with steroids, azothioprine,
cyclosporine
298
SLE Cont'
• PreOp
– PFTs, ejection fraction
– Renal function
• Intraop
– No specific technique shown to be superior
• Postop
– Continue steroid coverage
– Careful assessment of pulmonary function
Notes
Notes
299
Geriatrics,
Surgical Procedures I
Laparoscopy, Controlled
Hypotension, Ophthalmic
Procedures, Liposuction
Geriatrics
• function of organ systems decline steadily
approximately 1% per year for every year
past 30 years old
– manifests as a multi-systemic loss of reserve
• CV
• renal
• respiratory
• hematologic
• overall body composition
Body composition in the elderly

• loss of lean body mass
– decreases in skeletal muscle
– increases in body fat
• overall effect contributes to an × VD, especially of
the highly lipid soluble agents
– loss of tissue elasticity
– thin, fragile skin
– stiff joints, Ç incidence of osteoarthritis
• positioning, nerve injury, airway management, intra
operative temperature loss all issues
300
Cardiovascular changes in the elderly
• × incidence of CAD
• calcification of heart valves
• Ø HR 2º “physiologic E blockade” from
– overall Ø in functioning E receptors
– Ø in cAMP
• slow circulation time 2º decrease in CO
• HTN from
– reduction in arterial compliance
– loss of elasticity of vessels
• effect is an × in SVR and afterload Ö LVH
Cardiovascular changes in the elderly,

cont’d
• Øoverall plasma volume

– dehydration
– electrolyte disturbances (Ç or È K+, ÈNa+)
• ×incidence DVT
• ×incidence of PVD
– claudication of extremities
– stroke
Pulmonary changes in the elderly

• Ølung tissue elasticity
– over distention of alveoli
• development of emphysematous changes within
lung parenchyma
• × V/Q mismatch 2º both Ç physiologic dead space
and shunt
– ØTLC, VC, ×FRC and closing capacity
• CC will continue to × progressively with age
– Øresponse to hypercarbia, hypoxia
– ×incidence of pulmonary emboli
– poor (weak) cough
– Ølaryngeal reflexes
• × aspiration risk
301
Pulmonary changes in the elderly
• PaO2 decreases with age

– PaO2 = 100 – (0.4 X age (yrs))
– typical decreases 0.35-0.5 mmHg/yr
• A-a gradient increases with age
Renal changes in the elderly

• Ø# of functioning nephrons
• ØRBF
• ØGFR
– magnified by a concomitant È in cardiac
function
• development of fluid overload/CHF not uncommon
Hepatic changes in the elderly

• Øhepatic function
– È tissue mass
– È hepatic blood flow
– È albumin production
• È COP, Ç peripheral edema
• Ç free fraction of highly protein bound drugs
– exaggerated pharmacologic responses
– È clearance mechanisms
302
Neurologic changes in the elderly
• × incidence of cerebral syndromes
– organic brain syndromes
• Alzheimer’s, dementia
– confusion
– post-anesthetic delirium
– neurologic deficits from CVA
• hypothalamic dysfunction
– poikilothermic tendencies
• adds to risk for perioperative hypothermia
Laparosopic surgery
• surgery aided by a laparoscope; done through

small incisions
– typically used to perform intra-abdominal procedures;
occurrence increasingly more frequent with newer
instrumentation/techniques
– facilitates quicker recovery time, discharge from
hospital
– requires insufflation with CO2 to displace surrounding
tissues from operative site; increases visibility for
surgeon and allows for surgical manipulation
CO2 insufflation
• creates a pneumoperitoneum
– CO2 is absorbed systemically
• peak absorption time 20 minutes
• dependent on:
– diffusion of gas
– absorption 2º vascularity of site
» Ç intraabdominal pressure creates È
peritoneal perfusion; limits CO2 absorption
» extraperitoneal CO2 insufflation (i.e. for
herniorraphy) leads to Ç CO2 absorption
through adipose tissue
303
Problems associated with laparoscopy
• positioning variables Ö facilitates exposure for
surgeon
– Trendelenberg, reverse Trendelenberg (both may be
steep!), side tilt, lithotomy
• may cause hemodynamic instability
• potential for nerve injury
• Trendelenburg
– Ç ICP
– facial edema, laryngeal edema, difficulty in
extubating
– acidosis 2º CO2 absorption; dependent upon
• rate of absorption
• length of surgery
Pulmonary changes from

pneumoperitoneum
– creation of pneumoperitoneum causes
abdominal distention, cephalad displacement
of diaphragm
• È FRC, VC
• Ç PIP, intrapleural pressure
• È compliance
• V/Q mismatching
• hypoxia
• hypercarbia
problems associated with

laparoscopy, cont’d
• arrhythmias, vasodilation from hypercarbia
– Èvenous return, È CO
– Ç SVR, PVR
• pneumothorax, pneumomediastinum,
pneumopericardium
– may lead to tension pneumothorax, cardiac
arrest
• subcutaneous emphysema
• gas embolus
304
gas (CO2) embolus
• typically noted during initial insufflation
– thought to be the most dangerous phase of the case
• possibility of CO2 embolus, perforation of major
vessels/hemorrhage
• heralded by a sudden, precipitous drop in BP
– hypotension more pronounced with CO2 embolus vs.
air probably 2º vasodilating properties of CO2
• *will see an initial paradoxical rise in ETCO2,
followed by the decrease usually noted during
an embolic event
• may lead to CVA, acute MI, pulmonary edema if
severe
gas (CO2) embolus

• treatment is supportive
– *Ask surgeon to stop insufflation, release
pneumoperitoneum
– place pt in Trendelenberg with L lateral tilt
• decreases ability of embolus to continue to enter
the pulmonary outflow tract
– d/c N2O; FiO2 1.0
– CPR, insertion of CVP catheter for aspiration
• symptoms resolve quickly 2º high diffusivity of CO 2
other complications of laparoscopy

• vascular injury
• visceral injury
– may lead to hemorrhage
• increased incidence of PONV
• absolute contraindications:
– preexisting Ç ICP
– presence of ventriculoperitoneal or
peritoneojugular shunts
• Laparoscopic procedures not limited to
intraabdominal cases; may be
intrathoracic, extremity, etc
305
care of laparoscopy pt
• GETA with (+) pressure ventilation with or without
the addition of PEEP may be better than
spontaneous ventilation
– Ç controlled ventilation offsets the rise in PaCO2
produced by insufflation
• some procedures may be done with regional or
MAC
• decompress pt with OGT
• N2O may be used, however
– bowels may obscure surgical field
– may add to the expansion of a CO2 embolus
• anticipate the need for:
– rapid blood loss/administration of blood products
– conversion to an open procedure
Controlled hypotension
• provides:
– decreased intraoperative blood loss
– better exposure of surgical field
– decreased operative time
– decreased number of blood products
transfused
• indications:
– orthopedics (Harrington rod insertion, total joint
replacement, spinal fusion)
– neurosurgery (aneurysm clipping, AVM resection)
– ENT, plastics, oral surgery (major facial
reconstruction, head and neck tumor resection, neck
dissection)
– gynecology/urology (radical pelvic procedures)
– religious blood refusal, rare blood types, difficult
cross matches
306
• contraindications:
– cardiovascular disease (includes HTN—do
not drop BP more than 20% of pt baseline
– cerebrovascular disease (TIA, carotid
stenosis)
– pregnancy
– spinal cord compression
– aortic stenosis
– renal disease
– severe pulmonary disease
– increased ICP
– severe hypovolemia/anemia
• essential to keep mean BP @ 50-60 mmHg at
all times
• U/O should be closely monitored; should be at
least 0.5 cc/kg/hr for duration of hypotensive
technique
• ? use of hypotensive technique in prone pts
– may lead to central retinal occlusion Ö blindness
• may use inhalation agents, SNP, NTG infusions
to produce hypotension
Ophthalmic surgery
• pt populations
– pediatric patients
• may have concurrent syndromes with
multi systemic involvement
– elderly patients
• frequently have other multi systemic
disease processes
• full pre-op work up necessary, even if
anesthesia is sedation only
307
Intraocular dynamics
• intraocular pressure
– normal range 12-20 mmHg
– determined by:
• volume changes within the globe
• external pressures
• **The most significant determinant of IOP

is change in choroidal blood volume and
dynamics
– arterial blood flow autoregulated
Intraocular dynamics, cont’d

• any increase in CVP will cause resistance
to aqueous outflow
– coughing/bucking/straining
– Valsalva maneuvers
– Trendelenburg position
• hypercarbia causes intraocular

vasodilation and a concomitant increase
in IOP
Anesthetic Effects on IOP

• Agents which facilitate aqueous drainage
causing a decrease in IOP:
– sedatives
– induction agents
– volatile anesthetics, N2O
– non-depolarizing muscle relaxants
• Agents/procedures which cause an increase in
IOP:
– ketamine
– succinylcholine
– laryngoscopy/intubation
308
Anesthesia for ophthalmic surgery
• retrobulbar block with sedation typical

anesthetic technique
– complications of retrobulbar block usually
secondary to pt motion or oversedation
– peribulbar block or “topical only” surgeries
also performed
– most common side effect of RB block is
ecchymosis (2-5% incidence)
• Most common serious complication is retrobulbar
hemorrhage
Retrobulbar block
• primary goal is to immobilize the eye and block
the ciliary ganglion; surgeon may block
superficial facial nerve and eyelid block as an
adjunct
• area is highly vascular and in close proximity to
the CNS
• incidence of serious complications 1/750 blocks
• rare, life threatening complications occur within
2-40 minutes after block with a mean onset time
of approximately 8 minutes; duration 20-60
minutes
Complications of RB Block
• hemorrhage of the retrobulbar space
• central retinal artery occlusion
• intraocular injection
• optic nerve injury
• shivering, agitation, dysphagia, and
tremulousness
• grand mal seizures
• apnea, HTN, tachycardia, bradycardia, cardiac
arrest
• loss of consciousness
• cranial nerve blockade
• total spinal
309
Complications of RB block, cont’d
• toxic or allergic reaction to local anesthetics
• retrograde flow of LA through optic chiasma
leads to:
– contralateral eye signs
– amaurosis
– mydriasis
– nystagmus
– extraocular muscle paresis
• oculocardiac reflex
The Oculocardiac Reflex

• usually from inadvertent pressure on the globe,
traction on extraocular muscles, rapid RB
injection, orbital hematoma
• symptoms include:
– bradycardia, nodal rhythms, ectopy
– hypotension
– diaphoresis
– asystole

• occurs most frequently in children during
strabismus surgery (estimated 32% of cases)
• transient cardiac standstill occurs as often as
1/3200 strabismus cases
• greater than 60 deaths have been reported,
even during local/sedation
• hypoventilation/hypercarbia produce a
significant increase in bradycardia
• reflex fatigues easily
310
• mediated by:
– trigeminal (afferent)
– vagus (efferent)
• A.K.A. “The Five and Dime Reflex”
• first intervention is to stop the stimulus
which is producing the reflex—may need
to give an anticholinergic as well
Strabismus
• A condition in which the visual axes of the eyes
are misaligned
– thought to be due to an underlying myopathy
– the most frequent ophthalmic condition necessitating
surgical repair
• Four main concerns:
– CV effects of ophthalmic medications
– Potential for development of oculocardiac reflex
• pretreatment with atropine is controversial;
glycopyrrolate may be better 2º lack of CNS effects
– Increased susceptibility to MH
– Increased incidence of PONV (50-80%)
• possibly from Ç in vagal tone from OC reflex
• leads to dehydration, inpatient admission
Open Globe Injury

• non-depolarizers may be used for RSI
– rocuronium 0.6 mg/kg provides intubating
conditions in approximately 60 seconds with
no appreciable increase in IOP
– high dose vecuronium (0.15-0.2 mg/kg)
provides intubating conditions in
approximately 90 seconds with no
appreciable increase in IOP
• succinylcholine transiently increases IOP
(probably = to increase from blinking)
– use is now generally accepted
– safer in the patient with questionable airway
311
Open Globe Injury extras
• pt may have other less obvious injuries
(i.e. head trauma) which require further
evaluation
• an inhalation induction may be used in
younger pts to obtain IV access
• intraocular procedures under GA require
an absolutely motionless pt
Intravitreal Gas Injection

• used at the end of vitrectomy or during surgery for
retinal detachment to aid in adhesion of the re-attached
retina and help globe maintain shape
• gases with low diffusivity used
– sulfur hexafluoride (SF6)
– carbon octafluorine
• N2O will diffuse into the gas bubble and cause a rapid
expansion in size
– must be D/C’d at least 20-30 minutes before
intravitreal gas injection occurs
– should be avoided in pts returning to surgery within
8-10 days of gas injection (some sources state up to
4 weeks)
Retinopathy of Prematurity
• approximately 25% of premature infants weighing
<1250 gm develop ROP (A.K.A. RLF)
– results in partial to complete detachment of retina 2º
sclerotic vessels; blindness
• causative factors include:
– hyperoxia
– apneic episodes/hypoxia/hypercarbia
– immature retinas
– IVH
– PDA
– infection
– transfusion therapy
• arterial O2 tension for premature infants should not
exceed 60-70 mm Hg
312
Systemic Effects of Ophthalmic
Solutions
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Miscellany
• Unexpected post operative eye pain
– 2 major causes
• corneal abrasion—most commonly occurring
ocular injury
• acute glaucoma
• 3 goals of retrobulbar block
– Remember the “3 A’s”:
• Akinesia of the eye
• Anesthesia of the eye
• Abolishment of the oculocardiac reflex
Liposuction
• Liposuction
– tumescent (A.K.A. “wetting solution”) utilized
to:
• emulsify fat
• provide anesthesia
• provide hemostasis
– A mixture of 0.9 ns or RL with
• epinephrine 1:1,000,000
• lidocaine 0.025%-0.1%
– large volumes (1-4 cc) are injected for every cc
of fat to be removed
• EBL = approximately 1% of the aspirate removed
313
Liposuction, cont’d
• Problem list:
– Frequently done as an office-based procedure
or in same-day surgery
– Tumescent solution is reabsorbed over 48º
with peak serum levels of lidocaine noted 10-
14º after initial injection
• 35-55 mg/Kg total dose of lidocaine not
uncommon but has been used safely 2º
slow, sustained release of lidocaine from
the fat compartment
Problem list, cont’d

• Ç risk factors for increased incidence of
mortality include:
– multi-liter wetting solution infiltration
– large volume aspiration/massive 3rd spacing
– volume overload vs. intravascular depletion
– multiple concurrent procedures
– anesthetic overdose Æ hypoventilation
– early discharge
Liposuction, cont’d
– **the major cause of postoperative death
following liposuction is pulmonary embolism
• Surgeons should limit total aspirate to 5000 ml
• Careful post-operative monitoring of fluid and
electrolyte status
– 3rd spacing and fluid overload a concern
• look for hypoxia, HTN, pulmonary edema
– Other problems:
• perforation of abdominal viscus
• fat embolism
• infection
• hemorrhage
• anesthetic sequelae
314
Surgical Procedures Review
CABG
• Indications
– >75% stenosis of left main
– Severe angina with multi-vessel disease and poor LV
function
– Persistent angina after failed medical therapy
• Surgical stages
– Large mid-sternal incision
– Aorta cannulated with potential of embolization
– Right atrium cannulated with potential of arrhythmias
– Cardiopulmonary bypass
• Potential for awareness with no vital sign indicators
– Anticoagulation – Bull curve
CABG cont’
• Surgical stages cont’
– Termination of bypass
– Pacing may be required
– Prepare with available inotropes
– Reversal of anticoagulation
– IABP may be necessary
– Chest closure
• New surgical techniques
– MidCAB – done through a smaller incision to
mediastinum
– OPCAB – done without using cardiopulmonary
bypass
315
CABG cont’
• Preop preparation
– Continue all preop meds
• Intraop management
– Narcotics/relaxants/amnestics for less healthy
patients
– Hypnotics/volatile agents with less narcotic for
healthier patients
– Monitoring
• Multi-lead ECG
• A-Line
• Central catheter
• TEE
• ACT to ensure adequate anticoagulation and
reversal
Burns
• Overview
– Second most common cause of accidental
death
– Thermal injury causes loss of microvascular
integrity
• Increased capillary permeability
• Local fluid accumulation, systemic fluid loss
• Decreased local perfusion
• Generalized edema
Burns Cont’
– Inhalation injury depending on material
inhaled
• Possible pulmonary edema and/or CO
poisoning
– Mechanisms of heat conservation lost
– Burns can constrict and cause circulatory or
ventilatory insufficiency
– Electrical burns can cause considerable injury
to vital organs
– Eschar excellent medium for infection
316
Burns Cont’
• Acute treatment
– Large-bore IV access
– Assess extent of burns –
“rule of nines” Ö
• Parkland formula for
fluids:
– 4 ml/kg/% burn
in 1st 24 hrs
– Maintain warm
environment
– Secure airway if
indicated
Burns Cont’
• Preop
– Elevate room temperature
– Ensure adequate venous access
– Prepare warmed IV fluids
Burns Cont’
• Intraop
– Routine monitors
– CVP and UO
– Avoid succinylcholine Ö severe hyperkalemia
– Consider central catheter and TEE depending on
underlying health
– Anticipate airway difficulty – edema, constriction
– Burns create a hypermetabolic state with high O 2
demand
– Liberally replace fluid loss, transfuse blood
– Consider albumin and other colloid expanders
– High narcotic and NMB demands
317
Craniotomy
• Overview
– Done for a variety of lesions – space occupying,
vascular
– CNS accommodates well to chronic processes.
However, even mild symptoms may indicate
exhaustion of compensatory mechanisms
• Loss of compensation can also occur from Ç ICP,
hypoxia, hypercapnea, È venous return, È MAP
Cerebral perfusion pressure = MAP – ICP
• Preop
– Emergency:
• Immediate control of airway to avoid hypoxia,
hypercarbia
• If Cushing’s Triad is present (HTN, bradycardia,
irregular respirations), maintain MAP, establish
hyperventilation
Craniotomy Cont’
• Intraop
– A-line and CVP, possible PA cath
– Processed EEG
– Steroids, osmotic diuretics
– IV induction with barbiturates/narcotics
– Avoid succinylcholine if Ç ICP present
– Support MAP with phenlyephrine
– Avoid nitrous oxide
– Hyperventilation to PaCO2 = 27 – 30mmHg (not less
than 25 mmHg)
• Postop
– Prompt awakening important for neurologic evaluation
– Possible loss of airway reflexes as result of surgery
Craniotomy cont’
• Sitting position
– Patients with infratentorial lesions
– Area of brain stem, cranial nerves
• May see periods of hemodynamic instability,
bradydysrhythmias
– Head elevated above heart – risk of venous air
embolization
– Monitoring and anesthetic management as with
supine crani
318
Craniotomy Cont’
• Sitting position cont’
– Consider multiport RA catheter for removal of air
– Avoid nitrous oxide
– TEE most sensitive to air emboli (precordial doppler
next best choice)
• Sudden onset of hypotension, tachycardia,
arrhythmias indicate possible air embolization
– Cranial nerve dysfunction common – carefully check
airway reflexes prior to extubation
Abdominal Aortic Aneurysm

• Overview
– 3% of male population over 55 yrs
– High incidence of co-existing disease Ö HTN (50%),
CAD (35%), carotid disease (35%)
– Emergent repair has much higher M&M
– M&M also associated with level of X-clamp Ö
infrarenal < suprarenal< supraceliac
• Preop
– Careful assessment of co-morbidities
– Consider epidural for pre-emptive/perioperative
analgesia
AAA Repair Cont’

• Intraop
• A-line, central catheter, TEE
– Large-bore venous access
– No anesthetic technique shown superior
– Blood scavenging indicated
– Consider renal prophylaxis with mannitol, dopamine –
especially for suprarenal clamping or pre-existing
renal disease
319
AAA Repair Cont’
• Intraop cont’
– During X-clamp:
• Control BP with SNP, NTG and/or additional
inhalation agent
• Consider fluid loading as preparation for X-clamp
release
• Maintain normal cardiac chamber size during X-
clamp
• Acidosis can be profound
– Prepare HCO3-2 for clamp release
• Supraceliac clamp will isolate liver – citrate
intoxication a possibility
– Administer Ca2+
AAA Repair Cont’

• Intraop cont’
– Normalize BP, discontinue vasodilators prior to clamp
release
– Acute hypotension can be managed with gradual
release or re-application of clamp
• Postop
– BP and HR control essential
– Analgesia with epidural or PCA
AAA Repair Cont’

Aneurysm repair may be performed as an
endovascular procedure; endoluminal graft is
inserted into the aorta via the groin; obviates the
need for aortic cross-clamping
• Patients must have favorable anatomy
• Blood loss may still be significant through
access ports in groins
• Adequate hydration necessary 2º use of contrast
media
• Period of normotension to slight hypotension is
necessary as graft is launched into the aorta
320
Thoracic Aneurysm Repair
• Overview
– One quarter of all aortic aneurysms are in the thoracic
aorta
– Male:female - 3:1
– Primary risk factors – HTN, atherosclerosis
– Other risk factors – Marfan’s syndrome, syphilis,
coarctation, AS
– DeBakey Classification:
• Type I – Both ascending and descending aorta
• Type II – Ascending aorta only
• Type III – Distal to left subclavian
Thoracic Aneurysm Repair Cont’

• Preop
– May cause tracheal/bronchial compression,
SVC syndrome, laryngeal nerve compression,
spinal cord ischemia
– Premedication should reduce anxiety and
maintain control of rate and pressure

• Intraop
– Full invasive monitoring and TEE
– Be prepared for difficulty with airway
management
– One-lung ventilation usually required
– High-dose narcotics blunt stress of intubation
and incision
– Beta-blockers and SNP/NTG for rate and
pressure control
321
• Intraop cont’
– CSF drainage to improve cerebral/cord
perfusion pressure
– Significant acidosis, vasodilation with release
of cross-clamp
– Renal and mesenteric ischemia certain unless
shunt in place
• Consider pre-clamp mannitol and renal-
dose dopamine
• Postop
– Patients usually kept sedated until extubated
Carotid Endarterectomy
• Overview
– Indicated in patients with > 60% stenosis of CA
– Stroke risk about 2%
• Risk of embolization of plaque debris
• Risk of ischemia during carotid clamping
– Many patients have other vascular insufficiencies –
myocardial, renal, peripheral
– Perioperative mortality highest from cardiac events
• Preop
– Careful preoperative assessment for co-existing
disease
CEA Cont’
• Intraop
• A-line for close BP control
– CNS monitor
• Awake patient (cervical plexus block) – neuro
exam
• Anesthetized patient – processed EEG, SSEP,
transcranial doppler
Stump pressure not helpful
– Avoid exogenous glucose, control glucose in DM
patients
– BP control and elevation with phenylephrine
– Vagal stimulation blocked with application of local to
carotid bulb
322
CEA Cont’
• Postop
– HTN from carotid sinus denervation common
• 66% of patients hypertensive
postoperatively
– Loss of hypoxic drive from carotid body denervation –
bilateral only
Gastric Bypass
• Pathophysiology
– BMI = Kg / Height(M)2
• Underweight: < 18.5
• Normal: 18.5 – 24.9
• Overweight: 25 – 29.9
• Obese: 30- 39.9
• Morbid Obesity: > 40
– Surgical indication: morbid obesity + co-morbidity
(arthritis, urinary incontinence, pseudotumor cerebri,
sleep apnea, ventilatory insufficiency, cardiomyopathy,
GERD, HTN, DM, thromboembolism, pulmonary
hypertension)
– Mortality 0.5%
– Morbidity 10% - anastomotic leak, dilation of bypassed
stomach, wound dehiscence, bowel obstruction, etc.
Gastric Bypass Cont’

• Gastric bypass designed to limit food
intake and desire for food; induces a
malabsorptive state
– Obtains sustained weight loss in 75% of
patients
• Medical management = 2%
323
• Preop
– Patient may require special OR table
– Carefully assess co-morbidities
• DM
• HTN
• Sleep Apnea
• Pulmonary Disease
• Up to 30 % of patients who used “Phen-
Fen” may have right-valve disease and
pulmonary hypertension

• Intraop
– IV access may be difficult; assess need for central
access
– Arterial line a must – BP monitors may be inaccurate
or fail completely
– Central catheter if cardiopulmonary status warrants –
CO of over 10 L/min common
– Careful positioning – shoulders may fall back causing
neuropathy
• Build “ramp” at head of the OR table
– Awake fiberoptic intubation may be indicated
– Very large VD – easy to underestimate drug
requirements
– Mesenteric traction syndrome can cause sudden
hypotension

• Intraop cont’
– Abdominal closure may precipitate high airway
pressures
• Most patients remain intubated and are weaned
from ventilator
– Judicious fluid replacement; U/O may be diminished
• Postop
– Minimal dosing of narcotics – sleep apnea is common
– Extubation with anesthesia care provider present –
limited FRC will cause rapid hypoxemia if airway is lost
• May extubate over exchange catheter until airway
patency is assured
324
Anaphylaxis
• Hypersensitivities
– Type I
• Immediate; 2 types
– Atopic Ö involves the skin and respiratory tract
(i.e. allergic rhinitis, asthma)
– Non-atopic Ö anaphylaxis
– Type II
• Cytotoxic
– Hemolytic transfusion reaction, heparin-induced
thrombocytopenia (HIT)
Anaphylaxis Cont’
• Hypersentivities cont’
– Type III
• Formation of immune complexes
–Serum sickness
– Type IV
• Delayed
–Contact dermatitis, (+) response to
tuberculin testing
Anaphylaxis Cont’
• A rapid, exaggerated response to an
allergen
– Requires prior exposure to the allergen
– Occurs 1:5,000-1:25,000 anesthetics
• High risk pts: pediatric, parturient, atopic, or prior
drug exposure
– Effects are magnified in pts who are ß-blocked
– Death occurs from respiratory distress and/or
profound circulatory shock
– 3 major s/s:
• Hypotension
• Bronchospasm
• Urticaria/flushing
325
Cascade of events for Type I
initial exposure to allergen IgE attaches to mast
cells; basophils
CD4, T-cells stimulate

production of IL4, IL5, IL6,
IL10; granulocytes &
macrophages degranulation
subsequent
exposure to
stimulation of ß allergen release of vasoactive
lymphocytes and substances:
plasma cells histamine
cytokines
leukotrienes
prostaglandins
kinins
platelet activating factor
production
of allergen-
specific IgE
antibodies
anaphylaxis
Anaphylaxis Cont’d
• Leading 5 causative factors in the intra
operative development of anaphylaxis:
– Neuromuscular blockers (60%)
• Succinylcholine > Rocuronium > Atracurium
– Latex (17%)
– Antibiotics (15%)
• PCN > cephalosporins; × cross-sensitivity
between the two
– Colloids (4%)
– Sedative/hypnotics (3-4%)
• Propofol > STP > Etomidate/Ketamine
Anaphylactoid Reactions
• Not IgE mediated
– Previous exposure to allergen not necessary
– Symptoms from direct stimulation of release of
histamine from mast cells and activation of
complement cascade
– May be clinically indistinguishable from anaphylaxis
• Causative factors:
– Synthetic plasma expanders
• Dextran, Hetastarch
– Vancomycin – Red-Man syndrome
– Protamine
– Atracurium
– Opioids
– Contrast
326
Latex Allergy
• × incidence with the advent of universal
precautions
– Huge demand for latex gloves predisposes to
lower quality control standards, rapid
production with more free latex particles
• May manifest as Type I sensitivity after
prior sensitization
– Mediated via IgE-specific latex proteins
– Results in angioedema/anaphylaxis
Latex Allergy Cont’

• Type IV sensitivity common amongst healthcare
workers
– Manifests as cutaneous contact dermatitis 24-48º
after exposure
• Important to provide a latex-free environment
– Latex is an aeroallergen and may be present in the air
at least 1 hour after the use of latex gloves
– Eventual goal is to make all hospitals completely
latex-free, (including the ban of decorative latex
balloons)
Latex Allergy Cont’

• Risk factors:
– Myelomeningocele
– Other congenital defects (esp. urologic) requiring
multiple/staged surgeries
– Atopic or asthmatic individuals
– Healthcare workers (5-10% incidence)
– Food allergies
• Figs
• Papayas
• Bananas
• Avocados
• “Large pit” fruits
327
Treatment of Anaphylaxis/Anaphylactoid
Reactions
• D/C anesthetic
• Administer FiO2 1.0
• Treat hypotension with volume
(SLQHSKULQHȝJ,9IRULQLWLDOV\PSWRPVor 0.5-1.0
mg IV for complete CV collapse
• Diphenhydramine (Benadryl) 25-50 mg IV
– Competitively antagonizes the effects of histamine @
H1 receptors
• Steroids
– Reduce inflammatory response,
• Hydrocortisone 250-1000 mg IV; methylprednisone
1-2 gm IV
• Ca 1 gm IV
++
– × cAMP; useful for treatment of bronchospasm, as a

cardiotonic
• H2 blockers (+/-)
Notes
Notes
328
Endocrine Review
Diabetes Mellitus Type I

• Pathophysiology
– Genetic predisposition to autoimmune destruction
of glucose transporter on islet cells
– Proteins affected from glycosylation
– Increased protein viscosity – impedes blood flow
– Derangement of autoregulation of blood flow in
CNS, myocardium and kidney
– Micro-vascular disease associated with:
autonomic neuropathy (40-50%), gastroparesis,
painless myocardial ischemia, orthostatic
hypotension, atlanto-occipital joint immobility,
PVD, HTN, renal insufficiency, peripheral
neuropathy, and retinopathy
Diabetes Type I Cont'
• Treatment
– Insulin replacement–
• Pancreas no longer secreting insulin
• Normal insulin production is about 50 U/day,
but patients may require much more
– Pancreatic transplant
– Aggressive blood pressure control
– Aggressive control of other atherogenic factors –
cholesterol, triglycerides
329
• Preop
– Consider metoclopramide
– Carefully assess cardiac and volume status
– Silent myocardial ischemia common
– Preoperative glucose < 200 mg/dl
– Assess neck mobility and airway carefully
• May perform ”Prayer sign” to assess joint
mobility (TMJ)
– Patient presses hands together as if
praying. Clinical assessment of degree of
protein glycosylation

• Intraop
– Routine monitors with ST segment trending
– Consider central catheter – volume status key to
preserving renal and myocardial function.
– Osmotic diuresis and dysautonomia make BP
control difficult
– Neuropathy may alter CV and pulmonary drives
– Monitor and treat blood glucose carefully
• Usually requires insulin infusion
• Postop
– Continued careful glucose control indicated
– ANS dysfunction associated with increased
incidence of postoperative sudden death
Diabetes Type II
• Pathophysiology
– 18 million patients in US
– Causes same organ dysfunction as DM Type I
– Ketosis is rare because of the presence of
endogenous insulin
• Patients can develop hyperosmolar nonketotic
coma (“HONK”)
– Patients often have high basal insulin levels
– Cells are resistant to insulin effects
– Eventually pancreatic fatigue occurs
• Preop
– Same as for DM Type I
330
Diabetes Type II Cont'
• Metformin (Glucophage)
– Mechanism of action unknown
• Known to improve glucose tolerance in pts with
Type II DM
• Lowers basal and postprandial glucose
• Decreases hepatic glucose production
• Decreases intestinal absorption of glucose
• Improves insulin sensitivity
• Increases peripheral glucose uptake/utilization
• Does not cause hypoglycemia
Metformin Associated Lactic Acidosis (MALA)

Thought to be due to effect of causing anaerobic cell
metabolism
– 50% mortality
– Any stress and IV contrast shown to precipitate
MALA
– Metformin should held for at least 8 hours preop
– Extended release metformin preparations should
be held for 24 hours preop

• Intraop & Postop
- Protein glycosylation results in the same
pathophysiology as in DM Type
- Same Intraop and Postop management as Type I
331
Gestational DM
• Pathophysiology
– Occurs in genetically susceptible individuals
– Maternal complications are few
– Fetal complications more common:
polyhydramnios, macrosomia, prematurity, birth
trauma, RDS, rebound hypoglycemia
– Maternal risk factors: age > 25, previous
macrosomal infant, unexplained fetal demise,
obesity, family history of GDM
• Treatment
– Diet, exercise
– Insulin controversial (insulin does not cross the
placenta)
Gestational DM Cont'
• Preop
– Full-stomach precautions: non-particulate antacid
– Examine airway for edema
• Intraop
– Regional anesthesia preferred
• Diabetic nerves more sensitive to effects of
local – use lower concentration
– Volume status is key to uterine/organ perfusion
– If GA, awake extubation may be needed
• Postop
- Major postoperative problems concern the fetus –
rebound hypoglycemia, acidosis
Diabetic Ketoacidosis
• Pathophysiology
– Seen in Type I DM, associated with cessation of
insulin
• Coupled with significant physical or emotional
stress (infection)
– Osmotic diuresis will result in severe volume
depletion with electrolyte abnormalities – total
body K+ very low
– Acidosis result of free fatty acid release with
hepatic oxidation to ketones
• Kussmaul respirations, coma
332
Diabetic Ketoacidosis Cont’
• Treatment
– Insulin
– Aggressive rehydration
– Correction of electrolyte abnormalities
– Hemodynamic support
– Correction of precipitating event
Diabetic Ketoacidosis Cont'

• Preop
– Preop central catheter to manage aggressive
volume replacement
– Insulin infusion (0.1U/kg/hr)
– Frequent pH, K+, Na+, U/O measurements
– Check airway for stiff joint syndrome
Caution - rapid correction of DKA can result in
cerebral edema
Diabetic Ketoacidosis Cont'

• Intraop
– Continue frequent monitoring of labs
– A-line for tight BP control – dehydration,
dysautonomia causes wide fluctuations in BP
– Add dextrose to IV infusions once glucose < 300
• Postop
– Hypoglycemia a possibility once cause of DKA is
corrected
– Continue to carefully monitor glucose levels
333
Diabetes Insipidus
• Pathophysiology
– Idiopathic form is sex-linked, recessive
• Nephrogenic DI is very rare congenital disease
– Results from inadequate ADH production from
posterior pituitary
– Most commonly from invading neoplasm or injury
– May be drug induced: lithium, amphoterocin, fluoride
– May be 2o to systemic disease: sickle cell, multiple
myeloma
• Treatment
– ADH replacement
– Chlorpropamide – ADH stimulator
Diabetes Insipidus Cont'

• Preop
– Assess electrolyte and osmolality status
– Rule out additional hormonal deficiencies
– D/C provocative medications (lithium)
• Intraop
– Patient is often hypovolemic
– Electrolyte abnormalities may result in arrhythmias
• Postop
– Continue close electrolyte monitoring
– ADH therapy can cause acute increase in SVR
– Chlorpropamide therapy may result in
hypoglycemia
SIADH
• Sustained release of ADH in the absence of
physiologic stimuli
• Seen in patients with pituitary disease,
pulmonary disease, intracranial disorders,
myxedema, acute intermittent porphyria
• Drugs that cause ADH release: morphine,
barbiturates, beta-adrenergics
• Results in volume overload and severe
hyponatremia
334
SIADH Cont'
• Lab findings
– Urine osmolarity > 300 – 400 mOs/L
– Urine sodium > 25 – 30 mEq/L
– Plasma sodium < 130 mEq/L
– Serum osmolarity < 280 mOs/L
– Creatinine, BUN, albumin, uric acid all low
from dilution
SIADH Cont'
• Preop – careful neurologic assessment
–Must correct hyponatremia
– Fluid restriction
– NS or hypertonic NS
– Loop diuretics
– Caution with rapid correction of hyponatremia
– can lead to central pontine myelinolysis (1 –
2 mEq/hour maximum)
SIADH Cont'
• Intraop & Postop
– Avoid hypotonic IV solutions
– Avoid drugs known to release ADH
– Monitor serum Na+ and osmolarity closely
– Treat volume overload and hyponatremia
335
Hypothyroidism
• Pathophysiology
– May result from disease of the thyroid (95%),
pituitary gland, hypothalamus
– Elevated TSH is hallmark lab finding
– Most cases are subclinical
– Symptoms: hypothermia, hypoventilation,
hyponatremia, hypotension, CHF, hypoglycemia,
fatigue, cold intolerance, weakness
• Treatment
– Oral thyroxin replacement
– Thyroxin (T4) has long half-life (1 week). TSH
takes weeks to stabilize after starting/changing
therapy
Hypothyroidism Cont'
• Preop
– Maintain euthyroid state
• Intraop
– Careful temperature monitoring
– MAC of inhaled anesthetics not significantly
changed
– Drug elimination/metabolism may be delayed
– Cardiovascular instability or collapse
– If severely hypothyroid, pt may have difficulty
weaning from ventilator
• Postop
– Keep patient warm
– Only inadequately treated patients carry risks
Hyperthyroidism
• Pathophysiology
– Multinodular diffuse enlargement (Grave’s
disease)
– Almost never malignant
– Autoimmune disorder with IgGs that bind to TSH
receptors and also cause ophthalmopathy
(exophthalmos)
– Also seen in pregnancy, thyroiditis, thyroid
adenoma, choriocarcinoma, TSH secreting
pituitary tumor, exogenous T 4 administration
– Sx: tachycardia, a-fib, anxiety, weakness,
hypermetabolism
336
Hyperthyroidism Cont'
• Treatment
– Antithyroid drugs (PTU), 131I, surgical thyroid
removal
• Preop
– Risk related to occurrence of thyroid storm
– Pts have a risk of developing thyroid storm even if
euthyroid preop
• Risk decreased by 90% if euthyroid
– If surgery is emergent – use beta-blockers, iodides
– Hydrate liberally if CV status will tolerate
• Intraop
– No technique shown to be superior
– May predispose to post-anesthetic hepatic
dysfunction
– Careful temperature monitoring
– Invasive monitoring if patient has cardiomyopathy,
dysrhythmias
– Consider possible tracheal distortion - ? Awake
intubation
– Avoid sympathomimetic agents, anticholinergics
– Treat hypotension with phenylephrine
• Postop
– Be alert to possibility of thyroid storm
May be difficult to distinguish thyroid storm from MH
intraoperatively
– Wound bleeding may compromise airway
– Recurrent laryngeal nerve injury may cause
hoarseness, acute dyspnea upon extubation
– Late tetany may occur as a result of damage to
parathyroids
337
Thyroid Storm
• Symptoms
– Due to sudden, excessive release of thyroid
hormones
– Usually seen 6-18 hours postop
– Many characteristics in common with MH
• Increased temp
• Increased heart rate
– High-output CHF
– Dehydration & shock
• Treatment
– Cool patient
– Beta-blockers, steroids, PTU, iodide
– Pressors and inotropic support as indicated
Adrenal Physiology
• Adrenal divided into 2 parts:

1.Cortex Ö
• Secretes androgens, mineralocorticoids
(aldosterone), glucocorticoids (cortisol)
2.Medulla Ö
• Secretes epinephrine, norepinephrine,
dopamine
Zones of the adrenal gland

Factors acting on Hormones
the gland secreted
Zona Glomerulosa
Angiotensin and Mineralocorticoids

corticotropin (ACTH) (aldosterone)
Zona Fasciculata
Glucoocorticoids
(cortisol and
Corticotropin corticosterone)
Zona Reticularis
epinephrine (80%) Corticotropin

norepinephrine (20%) Androgens
338
Adrenal Physiology Cont’
• Aldosterone
– Secreted by the zona glomerulosa (outer cortex)
– Angiotensin II and K+ most potent stimulators of
secretion
– Causes retention of sodium and water by increasing
sodium reabsorption at the distal tubule
• Cortisol
– Secreted by the zona fasciculata (middle cortex)
– Under control of ACTH from anterior pituitary
– Causes increases in glucose, sodium reabsorption,
potassium excretion
– Major stress hormone
Cushing’s Syndrome
• Pathophysiology
– Most common cause is exogenously administered
steroids
– ACTH overproduction (Cushing’s Disease)
– Adrenal overproduction (zona fasciculata/reticularis)
– Symptoms: hair loss, DM, stria, osteopenia,
electrolyte abnormalities, centripetal obesity, HTN,
PUD
• Treatment
– Removal of glucocorticoid source
– Then, coverage with gluco/mineralocorticoid, e.g.
hydrocortisone
Cushing’s Syndrome Cont'

• Preop
– Steroid coverage (200 – 300 mg hydrocortisone/day)
– Assess airway
• Intraop
– Routine monitoring
– Care with tape removal
• Postop
– Closely monitor electrolytes and glucose
– Possible occult GI blood loss
– Taper steroids slowly over several days
– CXR for adrenalectomy – 20% incidence of
pneumothorax
339
Addison’s Disease
• Pathophysiology
– Decreased production of gluco/mineralocorticoids
– Autoimmune destruction of adrenal gland (80%)
– Associated with TB, thyroiditis, sepsis, adrenal
hemorrhage
– Sx: hypotension, hypovolemia, muscle weakness,
hyperkalemia, severe dental caries
• Treatment
– Gluco/mineralocorticoid replacement
Addison’s Disease Cont'

• Preop
– Careful airway assessment – loose teeth
– Correct hypovolemia, hyperkalemia,
hyponatremia, hypoglycemia
• Intraop
– Consider art line, CVP/PA catheter
– Frequently check electrolytes, glucose
• Postop
– Steroids to be continued
– Monitor for arrhythmias from hyperkalemia
Pheochromocytoma
• Pathophysiology
– Tumor of catecholamine-secreting tissue 90% in
adrenal gland, 10% bilateral
– Part of : MEN IIa, MEN IIb, von Hippel-Landau
syndrome, neurofibramatosis, Sturge-Webber syndrome
– Stress, pain cause an exaggerated release of
catecholamines
– Associated CV disease: tachycardia, CHF, arrhythmias,
paroxsymal HTN, myocarditis, hypovolemia
340
Pheochromocytoma
– Also associated with glucose intolerance,

hyperparathyroidism
– Diagnosis: 24 hour urine for: free norepi,
vanillylmandelic acid, metanephrines &
normetanephrines, epinephrine
– Clonidine suppression test: 0.3 mg clonidine will
decrease serum catecholamine levels in essential
HTN, but not with pheochromocytoma
• Treatment
– Removal of tumor
Pheochromocytoma Cont'
• Preop
± ,QLWLDWHĮEORFNDGH
– Reestablish intravascular volume
± ȕEORFNDGH LIWDFK\FDUGLDRUG\VUK\WKPLDV
– Serial hematocrits to evaluate volume status
– ECHO indicated if cardiomyopathy suspected
– Carefully monitor electrolytes, glucose
• Intraop
– Art line, central catheter for tight CV control
– No technique or agents superior. Avoid
droperidol, ketamine
– SNP and dopamine ready. Expect exaggerated
responses
– Expect hypertension, tachycardias with tumor
manipulation
– Expect hypotension with control of venous
drainage of tumor
341
• Postop
– Hypotension, CHF common as patients have been on
endogenous inotropes/pressors for many years
– May also be psychiatric changes from removal of
catechols
Acromegaly
• Pathophysiology
– 99% from primary pituitary adenoma
– Secretion of GH after closure of epiphyseal plates
– Also associated with increased BMR,
hyperprolactinemia, hyperthyroidism, glucose
intolerance, hypertriglyceridemia, HTN,
cardiomyopathy
– May have pituitary mass effect – Nelson
Syndrome
• Treatment
– Surgery is primary therapy
– Bromocriptine, somatostatin
Acromegaly Cont'
• Preop
– Careful assessment of airway – macroglossia,
prognathism, enlarged nasal bones
– Evaluate for dysrhythmias, cardiomyopathy,
cardiomegaly, obstructive sleep apnea,
kyphoscoliosis
• Intraop
– Be prepared with large masks, blades
– Fiberoptic intubation may be necessary
– Caution with NMBs if myopathy exists
342
Acromegaly Cont'
• Postop
– Surgical manipulation of pituitary can result in: DI,
CSF leak, anterior pituitary insufficiency (ACTH,
TSH, gonadotropins)
– Careful monitoring of airway, sat
– May see sinusitis, hematomas, cranial nerve
palsies
Hyperaldosteronism
• Pathophysiology
– Primary - mineralocorticoid excess
– Secondary - excess renin release from kidneys
• causes retention of Na+ with depletion of K+
and increased extracellular volume
– Symptoms: diastolic hypertension, cardiomegaly,
hyperglycemia (50%), muscle weakness; obesity
is common
– Diagnosis: increased urinary K+ and aldosterone
with decreased plasma renin (primary)
• Treatment
– K+ supplementation, aldosterone antagonist
– Surgical excision of adrenal glands
Hyperaldosteronism Cont'
• Preop
– Correct hypervolemia, hypernatremia,
hypokalemia, hyperglycemia
– Patient may have decreased gastric pH Ö H2
blocker preop
– Obesity may present airway difficulties
• Intraop
– Art line
– Consider central catheter for major surgery
– No specific technique shown superior
– Avoid hyperventilation
– Prolonged emergence possible if electrolyte
abnormalities are present
– Hypokalemia may potentiate NMB’s
343
Hyperaldosteronism Cont'
• Postop
– Expect delayed emergence
– 20% pneumothorax in patients with adrenalectomy
– Continue close monitoring of electrolytes, glucose
– Hypotension possible
Carcinoid Syndrome
• Pathophysiology
– Most common GI endocrine tumor
• Tumor releases histamine-like substances Ö
hypotension and bronchospasm
• Tumor may also release serotonin Ö
hypertension, hypovolemia
• Systemically active when metastatic to liver or
when released substances avoid metabolism by
liver
• Causes endocardial fibrosis in right heart with
valve lesions
• Treatment
– Surgical ablation or arterial embolization to reduce
tumor burden
Carcinoid syndrome Cont'

• Preop
– Assess fluid balance – chronic diarrhea may have
caused electrolyte imbalance
– Preop somatostatin analogue octreotide has radically
reduced the M&M associated with anesthesia
• Octreotide blocks humoral release of autocoids from
tumor
• Intraop
– Art line – expect rapid changes in BP
– Central catheter – volumes may not be reflected in
pressure changes, however
– TEE will allow evaluation of filling volumes
344
GLAND HORMONE SECRETED TARGET ORGAN/EFFECT
anterior pituitary adrenocorticotropic hormone (ACTH) adrenals; stimulates synthesis/secretion of adrenocortical hormones
follicle stimulating hormone (FSH) ovaries; stimulates estrogen secretion and growth of ovarian follicles
growth hormone (GH) multiple sites; stimulates protein synthesis and overall growth
luteinizing hormone (LH) ovaries; stimulates ovulation, estrogen and progesterone synthesis, formation of corpus luteum
prolactin breasts; stimulates breast development and milk production
thyroid stimulating hormone (TSH) thyroid; stimulates synthesis and secretion of thyroid hormones
posterior pituitary oxytocin uterus, breasts; causes uterine smooth muscle contraction, milk ejection
vasopressin (ADH-antidiuretic hormone) kidney; controls H2O excretion/reabsorption at the renal collecting ducts; serum osmolality
thyroid tri-iodothyronine (T3) multiple sites; stimulates protein, carbohydrate, and fat utilization
L-thyroxine (T4) multiple sites; stimulates skeletal growth, increases O2 consumption and heat production
calcitonin decreases serum Ca++ levels; deposits Ca++ into bones
parathyroid parathyroid hormone increases serum Ca++ levels; decreases phosphate levels
pancreas (D) glucagon liver; increases blood glucose; stimulates conversion of glycogen to glucose
(E) insulin decreases blood glucose
adrenal cortex
glomerulosa aldosterone kidney; increases renal Na+ reabsorption, K+ and H+ ion secretion
fasciculata cortisol liver; stimulates gluconeogenesis; multiple sites; immunosuppression and antiinflammatory
reticularis androgens onset of puberty, secondary sex characteristics
medulla epinephrine (80%); NE (20%) multiple sites; secreted in response to SNS stimulation
gonads
testes testosterone spermatogenesis
ovaries estradiol female reproductive organs; growth/development; causes follicular phase of menstrual cycle
progesterone causes luteal phase of menstrual cycle
Renal and Hepatic
Review
Functions of the kidney

• balance of:
– water
– electrolytes
– acid-base
– osmolarity
• hormone secretion
• maintenance of plasma volume
• excretion
Kidney trivia
• functional unit of the kidney is the
nephron; comprised of 2 units:
– glomerulus
– renal tubule (Bowman’s capsule, proximal tubule, Loop of Henle,
distal tubule, collecting tubule)
• kidneys receive approximately 25% of total

CO; function relies on 2 factors:
– renal blood flow = 1200 ml/min
– glomerular filtration rate (GFR)
Renal Physiology
• 3 basic renal processes:
– Glomerular filtration
• The filtering of the blood at Bowman’s capsule
forming primitive urine
– Tubular reabsorption
• Reabsorption of critical substances from tubules
back into the circulation
– Tubular secretion
• Secretion of substances to be excreted from the
body into the tubule from the blood
Glomerular filtration rate

• normal GFR = 125 ml/min (180L/day)
–entire plasma volume is filtered ~
65X/day
• the first step in urine formation
• proteins not filtered (under normal
conditions)
• net filtration pressure = 10 mmHg
glomerular capillary BP 55 mmHg
minus plasma COP 30 mmHg
minus Bowman’s capsule hydrostatic pressure 15 mmHg
equals 10 mmHg
Glomerular filtration rate, cont’d

• GFR is decreased during anesthesia due
to multiple factors:
– ×E stimulation
– Øplasma volume
– Ømean arterial pressure
– iatrogenic factors i.e. aortic or renal
artery
X-clamping
Response to Ø GFR
• hormonal secretion of renin by the JG
apparatus of the kidney
– triggered by Ørenal perfusion, Ø flow past macula densa, E
stimulation, Ì in Cl- ion [ ] ; inhibited by ANP
renin
lungs
angiotensinogen angiotensin I
angiotensin converting
enzyme (ACE)
angiotensin II
-vasoconstriction -antidiuretic hormone (ADH) secretion

-aldosterone release with Na+/H2O retention from × reabsorption @ distal tubules,
elimination of K+ **Aldosterone also released in response to × K+
Summary of tubular reabsorption/secretion
Proximal Distal Collecting

convoluted convoluted duct
tubule tubule
reabsorbed* secreted reabsorbed* secreted both
•glucose and •variable proton •variable sodium •variable proton •variable
amino acids secretion for (controlled by for acid/base reabsorption*
•67% of filtered acid/base balance aldosterone); balance controlled by ADH
sodium •organic ion chloride follows •variable
•other electrolytes secretion passively potassium •variable proton
•65% of filtered •variable H2O controlled by secretion for
H20 controlled by ADH aldosterone acid/base balance
•50% of filtered
urea
•all filtered
potassium
*Reabsorption occurs by : 1) passive diffusion 2) 1º active transport (Na +) 3) 2º active transport (glucose and AAs)
Schematic of the nephron
The nephron
is the
functional
unit of the
kidney
Formation of urine
• Urine concentration 2º to:
– medullary countercurrent system
• osmotic gradient forms when Loop of Henle
dips into the renal medulla
• 2 limbs of Loop:
descending ascending
•extreme permeability to •actively pumps sodium
H2O out of the tubule to
•no active sodium surrounding interstitial
transport fluid
•impermeable to H2O
– effects of ADH (vasopressin)
Control mechanisms of fluid balance

• Volume sensors
– baroreceptors
• carotid sinus
– stimulates SNS, ADH secretion
• afferent renal arterioles (JG apparatus)
– stimulates renin-angiotensin-aldosterone system
• atrial stretch receptors
– depresses ADH, secrete atrial natriuretic peptide (ANP),
and brain natriuretic peptide (BNP)
» serve as a counter-regulatory system for the renin-
angiotensin-aldosterone system.
» ANP degraded by neutral endopeptidase (NEP)
atrial stretch receptors
– Inhibition of ADH when stimulated
– Atrial natriuretic peptide (ANP)
• synthesized, stored and released by atrial
myocytes in response to atrial distention
– net result Ö arterial vasodilation, × Na+/
H2O excretion, Ø aldosterone, renin
release
– Brain natriuretic peptide (BNP)
• synthesized within the ventricles and the brain;
released by the same mechanisms that release
ANP with similar physiological actions.
• used as a clinical diagnostic marker for heart
failure
atrial stretch receptors

– ANP degraded by neutral endopeptidase
(NEP)
• NEP inhibitors—new class of drug used
alone or in combination with ACE inhibitors
in the treatment of CHF (animal studies)
• nesiritide (Natrecor): recombinant BNP
used to treat acute decompensated CHF
ANP
Tests of renal function
• urine specific gravity (SG)Ö1.003-1.030 (tubules)
– values vary based on pt age, hydration status,
presence of DI, diuretics, ØK+, ×Ca++, ×Fl-
• blood urea nitrogen (BUN)Ö10-20 mg/dL (GFR)
– values vary with dehydration, high protein diet, GI
bleeding, catabolic states
• serum creatinine Ö 0.7-1.5 mg/dL (GFR)
– metabolite of creatine (major muscle constituent)
– values vary with variations in muscle mass
• *usual plasma ratio of BUN/CR = 10:1
Creatinine clearance
• creatinine clearance (GFR)
– *most reliable indicator of GFR/renal function
– 110-150 ml/min Ö normal kidneys
– 50-80 ml/min Ö mild renal dysfunction
– <25 ml/min Ö moderate renal dysfunction
– <10 ml/min Ö anephric; requires dialysis
Acute renal failure

• loss of renal function over hours or days
• 50% mortality rate
• predisposing factors
– preexisting renal disease (1º cause)
– hypoperfused states
• hemorrhage, massive trauma, burns, sepsis
– CHF
– acute renal artery obstruction
– high risk surgery
• AAA, CABG with CPB, renal or hepatic transplant
– advanced age
– DM
– jaundice, myoglobinuria, scleroderma
• **prevent with maintenance of volume and O 2 transport,
pharmacologic therapy with dopamine (+/-), osmotic or
loop diuretics
Subclassifications of ARF
• Prerenal (70%)
– most common cause of ARF 2º ØBP, low
volume states (A.K.A. “ischemic ARF”)
• urine is concentrated, low in Na +
– reflects the kidney’s attempt to conserve H2O, Na+
in hypoperfused state
– treat by
» increasing BP
» administration of crystalloid (LR)
» dopamine (renal dose 2-5mcg/Kg/min)
» ? prostaglandins
• tubular damage from hypoxia may lead to acute
tubular necrosis (ATN)
Subclassifications of ARF, cont’d

• Renal (25%)
– 1º cause acute tubular necrosis (ATN); also
from glomerulonephritis, vasculitis
• urine is dilute, ØNa+, ×K+
• Postrenal (5%)
– mechanical obstruction of urine outflow
(obstructive uropathy)
• nephro or ureterolithiasis
• obstructive clots
– treatment typically surgical
Chronic renal failure/ESRD

• A progressive Ø in the number of functioning
nephrons; may take years to develop; usually 2º
uncontrolled HTN, diabetes
• symptoms occur when 40% of functional
nephrons remain
– manifests as:
• polyuria, nocturia; 2º failure of countercurrent mechanism to
concentrate urine
• fulminant when 90% of nephrons are
dysfunctional Ö uremia with or without oliguria;
requires dialysis
Signs and symptoms of CRF
• anemia
– from Ø production erythropoietin
– ×2,3 DPG
• O2/Hgb dissociation curve shifts Ö R
– × delivery of O2 to tissues
• metabolic acidosis
• hyperkalemia
• HTN
• Øplatelet quality (Øaggregation, ×bleeding time)
• defective Von Willebrand factor
• wide variations in intravascular fluid volume
• dependent on last dialysis; pts may be depleted if
recently dialyzed
• effusions (pleural and/or pericardial)
• pruritis
Most common electrolyte

disturbances of CRF
• hyperkalemia
• hypocalcemia
• hypermagnesemia
• hyperphosphatemia
Anesthetic management of pt with CRF

• hemo vs. peritoneal (CAPD) dialysis
– CAPD pt must be drained prior to
surgery
• intravascular volume labile in
hemodialyzed pts; may be either dry or
overloaded
– ascertain when last HD was
– goal is to have pt 2.5 Kg > dry weight
upon arrival to OR
• expect × lability
– replace fluids prudently
Fluids/CRF
• solutions should not contain K+; 0.9 ns or
D5:IUHTXHQWO\XVHG/5ĺ P(TO
• caution with D5W—free H2O remains after
dextrose is utilized; hypotonic; can lead to
overload
• 3:1 crystalloid:blood loss replacement if blood
loss < or = to 10% TBV
• 1:1 colloid:blood loss if blood loss exceeds
10% TBV
– cases with anticipated large fluid
losses/shifts require invasive monitoring
Anesthetic management of pt with

CRF, cont’d
• correction of serum K+
– most serious physiologic derangement resulting from
CRF
• 2º Ø excretion of K+; metabolic acidosis
– insulin used to carry K+ into cells; glucose used to
avoid iatrogenic hypoglycemia
– alkalosis from hyperventilation, administration of
NaHCO3-
– Ca++ to preserve cardiac function
• *elective surgery should be postponed if K+
is > 5.5 mEq/dL
Volatile anesthetics and CRF

• Sevoflurane is associated with the
production of inorganic Fl- ion
– Causes nephrotoxicity in rats; not evident in
humans
– isoflurane, desflurane acceptable for use
– *1º symptom Fl- induced nephrotoxicity is
polyuria; tubules become poisoned and
unable to [ ] urine
• toxic level Fl- 50 mmol/l
Anesthetics and CRF
• exaggerated responses noted with the use of
anesthetics 2º:
– anemia
• B:G solubility of volatiles reduced; × FA/FI
– ×CV instability 2º hypovolemia
• IV agents
– ×VD drugs with Øclearance rates
– Øprotein binding; ×free fraction of highly bound
drugs
– ×ventilatory depression from opioids
• morphine-6-glucuronide and normeperidine
(active metabolites) dependent on renal
clearance
– uremic disruption of the BBB
Muscle relaxants and CRF

• succinylcholine
– may cause a modest/transient increase in
serum K+ Ö 0.5-1.0 mEq/dL
– not attenuated by pretreatment with NDMBs
– more of an issue in the pt with ARF vs. CRF
• may use with caution in the pt with CRF if the K+ in
5.0 mEq/dL or less
Muscle relaxants and CRF

• avoid long-acting NDMBs with cumulative effects
– these agents are largely dependent on renal
clearance for metabolism
• pancuronium, doxacurium, pipecuronium
• atracurium, cis-atracurium OK for use
• vecuronium, rocuronium OK initially but may
exhibit cumulative effects
– initially takes more drug to reach NMJ 2º × VD
• anticholinesterases primarily excreted by the
kidneys
miscellany
• aminoglycoside ABX, vancomycin are highly
nephrotoxic
• ×incidence of blood-borne pathogens, especially
HepB, HepC, HIV noted with hemodialysis pts
• protection of hemodialysis site(s) intraoperatively is of
utmost importance; avoid direct pressure to AV fistula,
prolonged hypotension
• anticipate × bleeding tendency
• Øplasma cholinesterase activity, especially following
HD
• *most common cause of mortality in the CRF pt is
sepsis; morbidity from infection
Urologic procedures
• Transurethral resection of the prostate
(TURP)
– performed via cystoscopy; prostate is
resected with electrocautery in the presence
of continuous irrigation
– major concerns:
• hyponatremia, H2O intoxication
–A.K.A. “TURP syndrome”
TURP syndrome
• secondary to a number of factors:
– duration of procedure
• longer procedures = more prostatic venous
sinuses opened, greater absorption of irrigant
– height of irrigation container
• greater height above pt = greater hydrostatic
(driving) pressure into open venous sinuses
– type of irrigant
• fluid should be isotonic and non-hemolytic
– sorbitol commonly used
– glycine may lead to blindness
TURP syndrome, cont’d
• Manifestations:
– CV
• hypervolemia
• ×BP
• ØHR
• ×CVP
• pulmonary edema, CHF
– Coagulopathy
• 2º dilutional thrombocytopenia from fluid
overload
• DIC occurs < 1% of cases
TURP syndrome, cont’d

• Manifestations:
– neurologic - from hyponatremia and Øserum
osmolality; leads to cerebral edema
± HDUO\VV ĺKHDGDFKHUHVWOHVVQHVVLUULWDELOLW\
confusion
± ODWHUVV ĺ VHL]XUHVFRPD
• *difficult to assess if pt is receiving GA;
recommended anesthetic for TURP is spinal
anesthesia
– T10 level is necessary for adequate
anesthesia
– may see leg movement 2º direct stimulation of
obturator by electrocautery
Treatment of TURP syndrome

• aimed at CV stabilization, ventilatory
support, replacement of Na+
– initial treatment (Na+ > or = 120 mEq/l)
• diuretics (mannitol, furosemide)
• fluid restriction
• Na+ replacement with 0.9 ns
– If Na+ is < 120 mEq/l
– hypertonic saline (3%) may be used but can
lead to central pontine demyelination if Na+ is
replaced too rapidly (0.5 mEq/hr; 10-
15mEq/day)
TURP
• other concerns
– pts are elderly; may have co-morbidities
– hypothermia from cold irrigation and ambient OR
temperature
– occult bleeding; difficult to quantify
• formulae for blood loss during TURP Ö
– 2-4 ml blood loss/min resection time
– 20-50 ml/gm prostate tissue resected
– u/o difficult to quantify
– lithotomy position
• Øvenous return
• ×incidence of nerve injury
TURP concerns, cont’d

• bladder perforation – incidence 1%
– s/s
• rigid, tender abdomen
– periumbilical, inguinal, suprapubic, lower abdominal pain
• sudden n/v
• diaphoresis
• intense (referred) shoulder pain from irrigation fluid
extravasation into the peritoneal space
• tachycardia, hypo or hypertension
• hiccups, SOB
• necessitates immediate exploratory
laparotomy
Summary of S/S of TURP

syndrome
Cardiorespiratory CNS Heme/renal
-respiratory distress
-n/v -hemolysis
-cyanosis
-confusion -ARF
-HTN
-twitching -hyponatremia
-hypotension
-visual disturbances -hypo-osmolarity
-wide QRS, ÇST
-seizures -hyperglycinemia
segment
-paralysis -hyperammonemia
-dysrhythmias
-coma -shock
-bradycardia
Nephrectomy
• removal of kidney for neoplasm, directed donation; may
be done via laparoscope with hand assist
• major concerns
– ×intraoperative blood loss
– positioning
• lateral with bed re flexed and kidney rest extended;
leads to compression of IVC, Øvenous return from
LEs, nerve injuries, V/Q mismatch
– ØU/O; goal is to maintain U/O @0.5ml/kg/hr
– pneumothorax
• kidneys sit just below diaphragm bilaterally; pleural
space may be entered during dissection
– ? use of N2O
– ×absorption of CO2/eventual acidosis if laparoscopic
Radical prostatectomy
• open procedure involving removal of prostate;
usually for neoplasm
– major concerns
• elderly pt population with co-morbidities
• *massive bleeding
• difficulty in quantifying U/O intraoperatively
– urethra is transected during case; U/O is lost to the field
• positioning
– pt supine in “re-flex” position; Øvenous return
• hypothermia
– procedure gradually moving towards robotic
prostatectomy
• less blood loss but CO2 insufflation and steep
Trendelenburg issues
ESWL-extracorporeal shock wave lithotripsy

• non-invasive technique utilized to pulverize renal and
ureteral calculi; uses low energy shock waves pulsed
externally directly at calculus
• Shocks occasionally in concert with EKG; timed 20ms
after r wave (absolute refractory period)
– absolute contraindications:
• pregnancy
• coagulopathies
• active UTI
• abdominally implanted pacemakers (i.e. old AICDs)
– relative contraindications:
• AAA (<5 cm)
• morbid obesity
Anesthetic concerns for ESWL
– minimizing pt movement, both corporeal and
diaphragmatic from (+) pressure ventilation; causes
stone movement
– pain
• technique is typically MAC/sedation; may use spinal,
local infiltration at site
– cardiac arrhythmias (PAC, PVC, SVT, VT)
– surgeon may request anticholinergics to × HR if
shocks delivered in sync with ECG
– potential for visceral injury includes:
• pulmonary contusions from direct shock waves (1º
organ injured)
• GI tract, pancreas 2º proximity to the kidneys
Percutaneous nephrolithotomy
• performed when nephrolithiasis is too
large to pass and/or when ESWL is
contraindicated
• pelvis of kidney is accessed percutaneously using
radiography
• once entered, wound is dilated to allow passage of
cystoscope; nephrolithiasis is pulverized directly
• concerns:
– × blood loss
– usually performed in remote location
– prone position with inherent problems
– hypothermia
– use of hypertonic radio opaque dyes; requires
adequate hydration
– ?pneumothorax
Renal transplantation
• replacement of renal function in pts with ESRD
– donor may be cadaver or live directed with
matching blood/tissue type
– may be done under GETA or epidural
anesthesia
• major risks for recipient:
– intraoperative hemorrhage
– untoward cardiac events
– hyperacute rejection of allograft
– postoperative infection (surgical or URI)
• anesthetic concerns for recipient:
– preexisting comorbidities (HTN, IDDM)

• full stomach status
– pre-op volume status 2º recent hemodialysis
– potential for rapid blood loss
– protection of hemodialysis access sites
– euvolemia imperative for adequate perfusion; graft
function/diuresis dependent on careful fluid
maintenance
• diuretics (mannitol, furosemide), renal dose
dopamine (+/-) also promote diuresis
• anesthetic concerns for recipient, cont’d:
– electrolyte (especially K+) abnormalities
– prolonged/magnified effects of anesthetic
agents
– careful aseptic technique
– invasive monitoring
– U/O difficult to quantify
– administration of immunosuppressive agents
before graft unclamping/reperfusion
– evaluate need for stress-dose steroids
• anesthetic considerations for the donor

– essentially the same as for nephrectomy for
live donor
– cadaveric donation:
• maintenance of perfusion pressure to the allograft
until X clamp is applied is key
– use of fluids, pressors, diuretics
Liver trivia
• found in RUQ of the abdominal cavity
– rib level T5-11
• largest gland in the body
– largest source of lymph
• acts as a reservoir for blood
– can store up to 500 ml of blood at any time
• Ç SNS stimulation causes expulsion of blood into
the systemic circulation
• hepatic blood flow = 100ml/min/100gm tissue

– accounts for 25% of cardiac output
Liver trivia
• hepatic blood supply
– hepatic artery
• arises from celiac artery
• 25% of total blood flow to liver
• 45-50% of hepatic O2 supply
• mean pressure approximately 90-100 mmHg
• receptors: D1, E2, DA1, cholinergic
**able to dilate when portal vein flow decreases;

A.K.A. “reciprocity of flow”
Liver trivia
• hepatic blood supply
– portal vein (R and L branches)
• formed by the convergence of the splenic and
superior mesenteric veins
• 75% of total blood flow
• 50-55% of hepatic O2 supply (blood is partially
deoxygenated in pre-portal tissues)
• mean pressure approximately 10 mmHg or less
• receptors: D1, DA1
**blood is rich in nutrients absorbed from the GI tract;
also carries metabolites and toxins to the liver
Pre-portal organs
organ blood supply
stomach
spleen celiac artery
pancreas
pancreas superior
mesenteric artery
small intestine
small intestine inferior mesenteric

artery
colon
**blood from the hepatic artery and portal vein enters hepatic sinuses and
exits into hepatic veins which drain into the IVC
Liver trivia
• innervation
– sympathetic T7-10
– parasympathetic R and L branches of vagus;

R branch of phrenic
– ANS control via the celiac ganglion
Functions of the liver

• bile production and absorption of lipids
from the intestine
– liver produces cholesterol
• forms bile salts (stored in gall bladder)
– bile salts are essential for the absorption of

dietary cholesterol, fatty acids, fat soluble
vitamins A,D,E, and K, and other lipids from
the bowel
• hematologic
– RBCs rupture at the end of their life cycle, releasing
HGb
• metabolized to heme and globin
– heme forms bilirubin
» combines with albumin; undergoes hepatic
conjugation; is then excreted by the kidneys
– the liver is responsible for the storage up to 60% of
the excess iron needed for activity of:
• HGb
• myoglobin
• cytochrome
• catalase

• hematologic, cont’d
– coagulation
• the liver synthesizes factors 2, 5, 7, 9, 10, 11, 12,
13, and fibrinogen
– vitamin K is necessary for the formation of
2, 7, 9, and 10
– Kupffer cells (tissue macrophages found in
sinusoids of liver) remove FSPs from the
circulation
– plasma activators of fibrinolysis are cleared by
the liver

• metabolic activities
– glycogenesis
• conversion of glucose to glycogen for storage
– 100g of total body glycogen stores found in
liver (400g in skeletal muscle)
– glycogenolysis
• breakdown of glycogen to glucose
– gluconeogenesis
• conversion of amino acids, lactate, and glycerol
(A.K.A. non-carbohydrate sources) to glucose
• important source of glucose once glycogen stores
have been depleted (after 12-24º starvation)
• metabolic activities, cont’d
– fat metabolism
• conversion of excess carbohydrates and proteins
to fat
• formation of lipoproteins
– both necessary for fatty acid transport
• oxidation of fatty acids (E-oxidation) to produce
acetoacetic acid
acetoacetic acid acetyl-Co-A Krebs cycle

for ATP production

• metabolic activities, cont’d
– protein production
• synthesis of 10-15 grams of albumin/day
– responsible for 80-90% capillary oncotic
pressure (COP)
– decrease in COP leads to capillary leakage

producing edema and ascites; increases VD
– enhanced effects of highly protein bound
drugs noted

• additional hepatic functions include:
– metabolism of ammonia
– removal of:
• aldosterone
• ADH
• GABA
• cortisol
• sex hormones
– detoxification and removal of exogenous
pharmacological agents
• detoxification and removal of exogenous
pharmacological agents
– biotransformation: production of inactive metabolites
typically by the cytochrome P-450 system via:
• oxidative-reductive pathways (A.K.A.”Phase I”
reactions)
• conjugation of compounds: non-polar, fat soluble
substances are transformed into polar, H2O soluble
substances
– facilitates renal excretion (A.K.A. “Phase II”
reactions)
• production of enzymes responsible for ester
hydrolysis of certain pharmacological agents
Characteristics of the patient with liver failure
• Ascites (1° characteristic)

– abdominal free fluid arising from:
• Portal HTN
– hydrostatic pressure in the portal vein exceeds
usual pressure (< 10 mmHg); fluid leakage
from the liver capsule, lymphatics, or capillaries
from liver outflow blockage
• decreased COP from hypoalbuminemia
– peripheral edema from:
• H2O and Na+ retention from stimulation of the
renin-angiotensin-aldosterone mechanism
**this indicates severe liver disease**
• hepatic encephalopathy
– from:
• elevated serum ammonia levels
• elevated serum bilirubin levels
• buildup of GABA
• formation of false neurotransmitters from
plasma protein imbalance (theoretical)
**encephalopathy may be reversed by

flumazenil
hepatic encephalopathy, cont’d
• precipitated by:
– hemorrhage
– hypokalemia
– CNS depressant meds (i.e. narcotics,
benzodiazepenes)
– hypovolemia
– infection
– following paracentesis
– stress
– alkalosis
– hypoxemia
– hypothermia

• portal hypertension
– portal vein pressure increases in response to increased
liver resistance from damaged hepatocytes
• development of backflow (shunting) to vessels with
lower resistance (i.e. pre-portal organs, esophagus)
– collateral circulation redirects blood flow and
relieves increased pressure
– may be surgically relieved
• portacaval shunt (infrequent)
• transjugular intrahepatic portosystemic shunt (TIPS)
– shunt is inserted transvenously via the IJ under
fluoroscopy
– provides a conduit for portal venous blood flow
directly into the hepatic vein while bypassing the
hepatic parenchyma.
portal hypertension, cont’d
• manifestations of collateral circulation:
– splenomegaly
• may lead to leukopenia, thrombocytopenia
– caput medusae
– dilated paraumbilical veins
– esophageal varices
• blood is shunted to low-resistance
esophageal vessels causing varicosities;
rupture is a leading cause of death
**NGT’s, esophageal stethoscopes
contraindicated
• renal disease
– increased bilirubin levels correlate with
potential for post-op renal failure
– ARF may be due to:
• endotoxins from infection
• hypovolemia from decreased
cortical/medullary flow
**U/O should be maintained at 50 ml/hr, with

judicious use of LR, mannitol, albumin;
assess serum osmolarity, Na+, K+ frequently

• pulmonary
– typical PaO2 of cirrhotic 50-70 mmHg
• probably due to shunts from development of
intra-pulmonic spider vessels
• may also be due to V/Q mismatch from
increased perfusion/decreased ventilation from
ascites, pleural effusions, and lowered lung
volumes
– PaCO2 decreased with respiratory alkalosis
• hyperventilation (possibly due to elevated
ammonia levels)
– HPV is impaired
• pulmonary, cont’d
– hyperventilation is contraindicated due to the
shift of ammonium ion to ammonia:
+
NH3 NH4
with alkalosis, this relationship is shifted to the left; allows for buildup
of ammonia leading to encephalopathy
• cardiac
– CO is typically increased in these patients
• >14 l/min is not uncommon
– peripheral vascular resistance is markedly
decreased
• possibly from vasodilating endotoxins
**contributes to a hyperdynamic circulation;
the myocardium does not respond well to
changes in pre and afterload
• coagulation
– coagulopathy occurs from:
• thrombocytopenia from hypersplenism
• impaired platelet function
• decreased synthesis of clotting factors
• decreased T1/2 of clotting factors
• formation of abnormal factors
• decrease in Vitamin K synthesis/storage
• coagulation, cont’d
– may need to administer Vitamin K+, FFP,
platelets, intraoperatively
– care is taken with line insertion, intubation,
conduction anesthesia, nasal airways
– assess intraoperative blood loss carefully
• peripheral edema
– from:
• decreased COP
• increased aldosterone, ADH secretion
• decreased deactivation of aldosterone,
ADH, and cortisol
• jaundice
– from:
• decreased bilirubin conjugation/excretion
–leads to pruritis and skin breakdown
from accumulation of bile salts in the
skin
**position well intraoperatively; pad bony

prominences
**look for increased bleeding tendencies
• hypoglycemia
– secondary to:
• decreased glycogen stores
• impaired gluconeogenesis
• increased systemic insulin concentrations
with moderate disease, FBS slightly elevated

(approx 140 mg/dl)
**hypoglycemia indicates severe disease
• other characteristics:
– spider nevi
– palmar erythema
all due to increased
– pectoral alopecia estrogen levels
– altered hair distribution secondary to the
– gynecomastia liver’s inability to clear
this and other sex
– decreased libido hormones
– testicular atrophy
– menstrual disorders
Characteristics of the patient with

liver failure
• serum transaminases
– alkaline phosphatase, AST, ALT (previously
known as SGOT, SGPT)
• not good diagnostic tools
– severe liver damage is necessary for even
slight elevations in these values
– albumin, bilirubin, PT are better prognostic

indicators of hepatic function
Effects of anesthesia on the
liver
• all volatile anesthetics diminish hepatic
blood flow
– secondary to diminished systemic blood
pressure
– isoflurane actually dilates the hepatic artery
and preserves reciprocity of flow; desflurane
may have a similar effect
Effects of anesthesia on the

liver
• conduction anesthesia decreases HBF
– secondary to decreases in systemic BP
• barbiturate/N2O/narcotic technique
decreases HBF the least—approximately
15%
Other factors impairing HBF

• surgical packs, retractors, and trauma
• increased sympathetic outflow secondary
to:
– light anesthesia
– hypotension
– hypovolemia
– hypercarbia
– hypoxemia
• hyperventilation
– results in:
• increase in mean intrathoracic pressure,
thereby reducing overall hepatic perfusion
• decrease in portal venous blood flow from
decreased PaCO2
• ammonium conversion to ammonia
• increased urinary K+ excretion from respiratory
alkalosis

• positive pressure ventilation
– may decrease HBF as much as 20%
• PEEP
– 5 cm H2O decreases HBF approximately 26%
– 10 cm H2O decreases HBF approximately
32%
**post-op ventilation should be avoided if
possible
– positioning
Drug handling and the cirrhotic

• drug intolerance results from the following:
– CNS changes secondary to an abnormal
BBB
– increased VD
• leads to an increased T1/2 of drugs
T1/2 = VD/Cl
– decreased CHON binding
Drug handling and the cirrhotic
• decreased drug clearance from:
– decreased HBF
– decreased biotransformation of drugs
• Phase I biotransformation:
– oxidative, reductive enzymes
– hydrolyzing enzymes
– cytochrome P-450 system
• Phase II biotransformation
– conjugation reactions
**the functions of Phase I biotransformation are
impaired at an earlier time than those of
Phase II
Hepatic biotransformation of
drugs
Phase I Phase II
-barbiturates -morphine
-isoflurane, -oxazepam
sevoflurane -propofol
-meperidine
-diazepam
-amide locals
-vecuronium
Hepatic biotransformation
• classically enhanced by:
– steroids
– barbiturates
– benzodiazepenes
– phenytoin
– antihistamines
– ETOH
***A.K.A. “enzyme induction”
Pre-operative evaluation
• labs:
– H/H, platelets
– lytes, glucose
– albumin*
– bilirubin*
– coags (PT*, PTT, bleeding time if possible)
• PT < or = 2.5 seconds of control—mild
cirrhotic
• PT > 2.5 seconds of control—severe
cirrhosis
– serum transaminases not crucial
Pre-operative evaluation, cont’d

• ECG
• chest X-ray
• presence/severity of ascites
– good prognostic indicator
– may need paracentesis before surgery
• presence of co-existing diseases
– cardiac, vascular, pulmonary, etc
– viral diseases i.e. hepatitis, CMV
Intraoperative care
• gowns, gloves, goggles
• strict aseptic technique
• rapid sequence or awake intubation
• careful line insertion—large bore IVs, CVP or PA
catheter
• no nasal airways, NG tubes, esophageal probes
• foley a must
• fluid warmers, humidvent, warming blankets,
increased ambient temperature
• use NMJ monitor
• administer parenteral meds with care, especially
narcotics and benzodiazepenes
Intraoperative care, cont’d
• regional is generally contraindicated secondary
to coagulopathy
• pulse oximeter may give erroneous readings in
the presence of severe jaundice
• maintain U/O with judicious use of LR, albumin,
mannitol
– avoid furosemide; albumin good for binding of
bilirubin
• maintain normotension
• maintain normocarbia
• assess blood loss continuously; check labs
frequently
Anesthetic agents
• thiopental
– use small, incremental doses; may choose
etomidate if CV instability is present
• succinylcholine
– may be used even though plasma
cholinesterase levels may be decreased
• atracurium, cis-atracurium
– good choice for NDMB; metabolized through
extra-hepatic pathways
Anesthetic agents, cont’d

• opioids
– dependent on Phase II for metabolism
– need to weigh risk/benefit for use i.e.
prolonged T1/2 vs. increased SNS tone
secondary to pain
– use sparingly
• benzodiazepenes
– avoid in the encephalopathic patient
• volatile anesthetics
– isoflurane best at maintaining HBF;
desflurane least biotransformed
Orthotopic liver transplantation
• the only curative procedure for non-
malignant, end-stage liver disease
– disease must not reoccur in the allograft
• 1st done successfully in 1967
• orthotopic means “same location”
• surgical time 8-16 hours
• EBL-variable; 8 to >100 U
General contraindications to
organ transplant
• incurable malignancy
• old age
• active systemic or incurable infection
• other major systemic disease
• morbid obesity
• current ETOH, drug, or tobacco abuse
• emotional instability
• unsupportive social milieu
Patient population
• age range -- neonate to 70 yrs
– 1/3rd of cases are pediatric; mostly < 5 years old
• male:female --1:1
etiology
adult pediatric
sclerosing cholangitis - 99%

primary biliary atresia -12%
chronic active hepatitis* - 20%
alcoholic cirrhosis - 13% inborn errors of metabolism - 6%
cryptogenic cirrhosis - 11%
primary biliary cirrhosis - 11%
&KURQLFKHSDWLWLV&LVUDSLGO\EHFRPLQJWKHÛ HWLRORJ\IRUKHSDWLF
transplantation (UNOS 2010)
Associated conditions
• acquired anemia
• coagulopathy
• hypoalbuminemia
• low SVR
• high CO
• cardiomyopathy in alcoholics
• hepatorenal syndrome
• massive ascites
Three phases of OLT

• recipient hepatectomy (A.K.A.
“preanhepatic phase”)
• anhepatic phase
• neohepatic phase
Recipient hepatectomy
• starts at skin incision and ends with the removal of the
recipient liver
• consists of :
– mobilization of the suprahepatic vena cava,
infrahepatic vena cava, and liver hilum (A.K.A. portal
triad)
– establishment of veno-venous bypass
• common problems associated with this phase:
– hemorrhage secondary to portal HTN, scarring from
previous abdominal surgeries
– decreased filling pressures secondary to
hemorrhage/vascular compression
– hyperglycemia
– increasing coagulation problems, both intrinsic and
acquired through massive transfusion
– oliguria
Veno-venous bypass
• markedly decreases blood loss during
recipient hepatectomy
• relieves most of the complications of portal
and IVC cross-clamping:
– decreased venous return
– low CO
– tachycardia
– acidosis
– intestinal swelling
– decline in renal function
Veno-venous bypass
• consists of 2 limbs of flow from the patient
– portal system
– L femoral vein
• blood is returned to L axillary vein
• flow rates low (1-2 l/min)
• heparin bonded tubing used; pt is not
heparinized systemically
• complications include inadvertent
decannulation, air embolism,
thromboembolism
Anesthetic concerns during

recipient hepatectomy
• PRBCs, FFP administered to replace
blood loss
– avoid platelets, cryoprecipitate during veno-
venous bypass; may use aminocaproic acid
• avoidance of sequelae of massive blood
transfusion
– administer Ca++, Mg++ as needed
– treat hyperkalemia
• treat metabolic acidosis with NaHCO3-
• maintain U/O (fluids, mannitol, renal dose
dopamine (+/-))
Anhepatic phase
• begins with clamping of the hepatic vessels and
vena cava and removal of the liver; ends with the
reperfusion of the donor liver
• the donor liver (A.K.A. allograft) is brought onto the
field and sutured into place
• common problems associated with this phase:
– hemorrhage
– increasing coagulopathy and fibrinolysis
– acidosis
– hypothermia
– decreased renal function
– inability to metabolize pharmacologic agents,
including heparin
Anesthetic concerns during the

anhepatic phase
• aggressive replacement of blood loss
– care is taken not to volume overload which will
cause graft congestion upon reperfusion
• acidosis, hypocalcemia, electrolyte and

glucose abnormalities are treated;
coagulopathy is treated once veno-venous
bypass is d/c’d
Neo-hepatic phase
• begins with the unclamping of the portal

vein, hepatic artery, and vena cava and
reperfusion of the donor liver
• typically a period of great hemodynamic
instability; preparation for this phase is key
to the overall success of the procedure
Neo-hepatic phase
• common problems associated with
declamping:
– hypotension
– bradycardia
– dysrhythmias
– hypothermia
– lactic acidosis
– coagulopathy
– hyperglycemia
“Reperfusion syndrome”
• characterized by:
– bradycardia
– hypotension (MAP<70% of baseline)
– conduction defects
– decreased SVR with acutely increased RV
pressures
– pulmonary HTN
– cardiac arrest
• cause is unknown (? autocoids vs. rapid
increase in serum K+ concentration)
Anesthetic considerations for

the neo-hepatic phase
• before clamp removal:
– correct acidosis
– ionized Ca++ should be normal
– K+ should be > 4.5 mEq/L
– have epinephrine and other pressors ready
– anticipate pulmonary edema
– place pt on FiO2 1.0; D/C volatile anesthetics
at least 5 minutes prior to unclamping
– anticipate severe coagulopathy; use TEG
monitoring to guide specific blood product
therapy
Anesthetic care of the OLT patient
• at least 2 large bore IVs; 1 should be #7.0 fr to
facilitate rapid transfusion; have rapid infuser
available
• arterial lines (femoral and radial) and PA
catheter should be used; solutions should be
heparin-free
• aspiration precautions for induction/intubation
• benzodiazepenes may be used to provide
amnesia during periods of hemodynamic
instability
• choose drugs which do not compromise
splanchnic flow (i.e. opioids, isoflurane) for
maintenance
post-operative course
• primary graft dysfunction is rare
• respiratory complications include ARDS,
nosocomial pneumonia, diaphragmatic
injury, pneumothorax
• DIC possible
• ICU stay typically 2-5 days post-op
• triple immunosuppression therapy is
started immediately; early rejection is
common
Other postoperative
complications
• vascular or biliary leaks
• hepatic artery or portal vein thrombosis
• bleeding requiring re-exploration
• abdominal abscesses
• lymphocele at site of veno-venous bypass
• recurrence of Hepatitis B (later)
• development of neoplasm or lymphoproliferative
malignancy 2º use of immunosuppressive
agents
Cyclosporine
• inhibits IL-1, IL-2; blocks activation of CD-4 cells
• may cause toxicity:
– HTN
– renal fibrosis/tubular atrophy
• ×BUN/Cr
– hepatocellular damage
• ×LFTs
• gingival hyperplasia
• tremors
• seizures
– study from 2004 recounts seizure activity in immunosuppressed
pts undergoing liver biopsies while receiving ketamine for sedation
» conclusion was that there should be a relative contraindication
to ketamine administration to pts receiving cyclosporine
Side effects of other immunosuppressive agents

• azathioprine
– leukopenia, anemia, thrombocytopenia
– hepatocellular and pancreatic damage
– ÇNDMB activity
• prednisone
– adrenal suppression
– glucose intolerance
– PUD
– aseptic osteonecrosis
– fragile integument
Notes
Pharmacology
Diuretics, Psychotropics,
Antiemetics, Antimicrobials,
Herbals and Dietary Supplements
Diuretics
• 5 major classifications:
– Thiazide diuretics
– Loop diuretics
– Osmotic diuretics
– Aldosterone antagonists
– Carbonic anhydrase inhibitors
• Used to 1º treat HTN, usually in conjunction with

ACE inhibitors and/or E blockers
Thiazide diuretics
• Prototype Ö hydrochlorothiazide (HCTZ)
– Uses
• Treatment of HTN, mild CHF
– Functions
• Inhibits reabsorption of Na+/Cl- @ the distal tubule
• Increases K+ excretion
• Possesses mild vasodilatory properties
• May cause a hypochloremic, hypokalemic
metabolic alkalosis
Loop diuretics
• Prototype Ö furosemide (Lasix)
• Ethacrynic acid (Bumex)
– Uses
• Treatment of HTN with reduced renal function,
moderate to severe CHF, acute pulmonary edema,
acute/chronic renal failure, hyperkalemia
– Functions
• Acts principally on the loop of Henle
– Inhibits reabsorption of Na+, Cl-
– Increases K+ excretion
• May be ototoxic
Osmotic diuretics
• Prototype Ö mannitol
– Uses
• Treatment of acute renal failure, reduction of IOP,
ICP, preservation of renal function pre X-clamping
of aorta, renal artery
– Functions
• × renal medullary blood flow
• × osmolarity of renal tubule fluid
• Transient × in COP
– Draws interstitial fluid into the intravascular
space
» May precipitate acute pulmonary edema in
pts with a hx of CHF
Aldosterone antagonists
• Prototype Ö spironolactone (Aldactone)
– Uses
• Treatment of renal insufficiency concomitant with
hepatic failure, CHF concomitant with hypokalemia
– Functions
• Blocks effects of aldosterone on the renal tubules
• Spares K+
Carbonic anhydrase inhibitors
• Prototype Ö acetazolamide
– Uses
• Treatment of glaucoma, reduction of CSF
production, prevention of altitude sickness
– Functions
• Inhibition of carbonic anhydrase (an enzyme of the
brush border) @ proximal tubule
– Increases Na+, HCO3- excretion
– Alkalinizes tubular urine
Summary-Diuretic sites of action on the nephron

Osmotic Loop Thiazide K+ Carbonic
Sparing anhydrase
inhibitors
-proximal -Loop of -proximal -distal part -brush
convoluted Henle part of distal of distal border of
tubule convoluted convoluted proximal
-descending tubule tubule tubule
limb of Loop -collecting
of Henle duct/tubules
-distal part
of distal
convoluted
tubule
-collecting
duct/tubules
Diuretic Miscellany
• Diuretics may enhance the effects of
NDMBs due to excretion of K+
• Pts taking diuretics may have exaggerated
responses to the effects of anesthetics 2º
relative intravascular volume depletion
• Concomitant administration of furosemide
in pts taking lithium may precipitate lithium
toxicity
Psychotropic Agents
• Classifications:
– Phenothiazines and thioxanthenes
– Butyrophenones
– Lithium
– Tricyclic antidepressants
– Monoamine oxidase inhibitors (MAOIs)
– Serotonin uptake inhibitors (SSRIs)
– Benzodiazepenes
Psychotropic Agents
• All of these agents are thought to exert their
effects by altering the concentrations of available
central and peripheral neurotransmitters,
primarily:
– Norepinephrine
– Dopamine
– Serotonin
• Drug interactions common with:
– Anesthetic agents
– Sedatives
– Opioids
– Sympathomimetics
Theories of Psychiatric Illness

• Secondary to various chemical imbalances
– Depression-due to a deficiency of
serotonin and NE (A.K.A. “amine hypothesis of
depression”)
– Mania-due to an excess in NE or an
increase in intracellular Na+
– Psychosis-due to an increase in dopamine
activity
– Schizophrenia and disordered thought
processes-also due to an increase in
dopamine activity
Present day therapy
DISORDER AGENTS USED
Schizophrenia Phenothiazines
Thioxanthenes
Butyrophenones
Mania Lithium
(also psychosis) Antipsychotics
Depression Tricyclic amines

MAOIs
SSRIs
Phenothiazines and
Thioxanthenes
• A.K.A. “major tranquilizers”; usually prescribed
for management of psychotic symptoms
• Improve mood/behavior without excessive
sedation
• High therapeutic index
• Do not produce physical dependence
• Commonly used agents include:
– Chlorpromazine (Thorazine)
– Promethazine (Phenergan)
Phenothiazines and
Thioxanthenes Cont'
• Most likely exert their effects by
antagonism of dopamine as a
neurotransmitter in the basal ganglia and
limbic portions of the forebrain
– Dopamine is a central inhibitory

neurotransmitter
Phenothiazines and
Thioxanthenes Cont'
• Other clinical uses include:
– Antiemetics
– Analgesic potentiators
– Antihistamines
– Sedatives
• Capable of producing extrapyramidal
symptoms due to central dopaminergic
receptor blockade; causing × [ ] of Ach in
the basal ganglia
Extrapyramidal Reactions
• Three categories:
– Dystonic reactions
• Neck muscle spasms, trismus, oculogyric crisis,
carpopedal spasm, torticollis, facial grimacing;
occur most frequently in children
– Akathesia
• Feelings of motor restlessness
– Parkinsonian signs and symptoms
• Masklike facies, drooling, tremors, cogwheel
rigidity
Tardive Dyskinesia
• Persistent rhythmic involuntary movements of
the tongue, face, mouth and/or jaw
• Female geriatric patients receiving high-dose

phenothiazines most at risk for development
– May develop in 5-10% of other patients treated for >
than 1 year with major tranquilizers
• No known long-term treatment; increasing

antipsychotic medication or physostigmine
may provide temporary relief
Side Effects of Phenothiazines
• CV—decreases in BP due to:
– Depression of vasomotor reflexes mediated
by the hypothalamus
– Alpha-adrenergic blockade
– Direct relaxant effects on vascular smooth
muscle
– Direct cardiac depression
– May produce orthostatic hypotension
Neuroleptic Malignant Syndrome

• Occurs in a small percentage of pts
treated with antipsychotics
• Typically develops in young males 48-72
hours after initiation of therapy
• Mortality 20-30%; common causes of
death include ventilatory failure, cardiac
failure, or dysrhythmias
• Difficult to differentiate from MH
• Can be treated with dantrium or
neuromuscular blockade
Neuroleptic Malignant Syndrome

Cont'
• Characteristics:
– Hyperthermia
– Generalized hypertonicity of skeletal
muscles
– Instability of the ANS
• Changes in BP
• Tachycardia
• Arrhythmias
– Fluctuating levels of consciousness
– CPKs and hepatic transaminases
increased
Drug Interactions with
Phenothiazines
• Ventilatory effects of opioids are
exaggerated
• Miotic and sedative effects of opioids
increased
• Analgesic effects of opioids potentiated
• Enhanced effects of ETOH
• Interference with activity of exogenously
administered dopamine
Anesthetic Implications for the

Patient Taking Phenothiazines
• Avoid use in Parkinsonian patients
• Do not co-administer agents which cause
dopaminergic blockade (i.e. droperidol,
metoclopramide)
• Avoid use of ketamine, meperidine
• Watch overall narcotic dose
• Use glycopyrrolate if anticholinergic is needed
• Use direct-acting pressors (i.e. phenylephrine,
methoxamine) in the event of hypotension
Butyrophenones
• Prototype for this class is haloperidol (Haldol)
• May reduce anxiety accompanying psychosis
• Pharmacologically resemble the
phenothiazines
• Block dopamine on postsynaptic sites
• Significant extrapyramidal symptoms
associated with use
• Exhibit potent antiemetic properties
• Undergo hepatic metabolism
Droperidol (Inapsine)
• Most commonly utilized as an antiemetic
• Used as an adjunct in neurolept anesthesia
• Increases action of fentanyl (no increase in ventilatory
depression)
• May produce orthostatic hypotension
• May produce dysphoria; produces extrapyramidal
symptoms in 1/100 pts
• Contraindicated in Parkinson’s patients
• Reports of development of ventricular arrhythmias (i.e.
Torsades) noted with use
• Causes severe hypertension in patients with
pheochromocytoma
• Recommended dose < 1 mg, monitor ECG for 2 hours
2nd Generation Antipsychotics

Risperidone is drug prototype
Has antiadrenergic, antiserotonergic &
antihistaminergic actions
Used to treat schizoaffective disorders,
bipolar disease & autism
High specificity for the D2 receptor
This results in a lower incidence of
extrapyramidal side-effects
Lithium Carbonate
• An alkali metal used for the treatment of
mania and manic episodes of bipolar
disorder
– No known physiologic role
– No known receptor site
– Does not bind to plasma proteins
– Normally undetectable in the plasma
– No effect on non-manic individuals
– Same group on periodic table as Na+, K+
Lithium Carbonate Cont'
• Mechanism of action thought to be
related to its inhibition of adenylate
cyclase and the stabilization of
dopamine and beta-adrenergic
receptors
• Li acts as an imperfect Na+ ion
substitute at the cellular level
• Therapeutic level 0.8 – 1.5 mEq/L
Side Effects of Lithium

• Na+ retention with peripheral edema
(noted in initial phases of treatment)
• Nephrogenic diabetes insipidus (DI)
– Inhibition of ADH activity on renal adenylate
cyclase causing reduced H2O reabsorption
across tubules
Anesthetic Implications for Patients

Taking Lithium
• Li prolongs depolarizing and non-depolarizing
muscle blockade
• Li lowers the MAC requirement
• Watch U/O carefully intraoperatively
• Reports of irreversible encephalopathy in
patients receiving Li concomitantly with
Haldol; maybe prudent to avoid droperidol
• Diuretics (especially furosemide) may
precipitate lithium toxicity from increased
excretion of Na+ with H2O
Tricyclic Amines
• These agents potentiate the action of
biogenic amines, particularly NE and
serotonin by interfering with their reuptake
into adrenergic nerve endings, both
centrally and peripherally
Tricyclic Amines
• Amitryptiline
• Desipramine
• Clomipramine
• Nortriptyline
• Imipramine
Side-effects of Tricyclic Amines

• Anticholinergic effects (dry mouth, blurred
vision, etc.)
• CV
– Orthostatic hypotension, reflex increase in
HR, direct cardiac depressant effect
• CNS
– Sedation, evidence of seizure activity on
EEG, seizure threshold lowered
– Extrapyramidal symptoms and ataxia
Drug Interactions/Anesthetic
Implications of Tricyclic Amines
• Extreme hypertension may be noted after
the administration of pressors—use only
direct acting sympathomimetics
• Increased incidence of cardiac
dysrhythmias (ST, VT, VF); increased if
pancuronium co-administered
• Best to avoid ketamine and meperidine as
well
Drug Interactions/Anesthetic
Implications Tricyclic Amines Cont'
• Avoid centrally acting anticholinergics; may lead
to post-op delerium/confusion
• Use direct-acting antihypertensives (phentolamine,
sodium nitroprusside)
• Tricyclics augment the analgesic and ventilatory
depressant effects of the opioids and depressant
effects of the sedative/hypnotics; necessary to
reduce usual dosages
MAO Inhibitors
• Form stable and irreversible complexes with
the enzyme monoamine oxidase which:
– MAO is found in the mitochondria of nerve cell
cytoplasm, liver, intestines, and platelets
– MAO inactivates endogenous and exogenous
catecholamines specifically:
• epinephrine,
• norepinephrine
• tyramine
• serotonin
• dopamine
MAOIs
• Agents include:
– Phenelzine
– Tranylcypromine
– Selegiline (selective MAO-B inhibitor)
MAO Inhibitors Cont'

• Biogenic amine concentrations build up in
brain, intestines, heart, and blood of patients
treated with MAOIs
• Increases in cerebral amines thought to
underlie the antidepressant effects of the
MAOIs
• MAOIs may cause hypotensive effects due to
the production of a false neurotransmitter,
octopamine, which builds up in adrenergic
nerve endings
– Has only a fraction of the vasoconstricting effects
of NE
Side-effects of MAOIs
• Anticholinergic effects such as blurred vision,
dry mouth
• Sedation
• Orthostatic hypotension due to buildup of
octopamine
• No ECG or EEG changes noted as with
tricyclic amines
• Interactions with foods high in tyramine or
medications with SNS activity; may see
severe hypertension (excess tyramine triggers
further release of NE and serotonin)
Anesthetic Considerations for
Patients Taking MAOIs
• Use only direct-acting sympathomimetics
when treating hypotension
• Treat hypertension with direct acting
vasodilators
• MAOIs should be D/C’d 2 weeks prior to
elective surgery if possible
• MAC is increased
• Do not co-administer meperidine with MAOIs
– MAOIs inhibit deamination of serotonin
– meperidine inhibits re-uptake of serotonin
– leads to “serotonin syndrome”
Selective Serotonin Reuptake

Inhibitors (SSRIs)
• Most broadly prescribed class of drug used for
the treatment of depression
– Also used to treat OCD, bulimia nervosa, panic
disorders, chronic pain syndromes
• Inhibit CNS neuronal uptake of serotonin; allows
for greater circulating amounts of serotonin
• Bind much less potently to muscarinic,
histaminergic, and alpha1 receptors than do other
antidepressants
– Less side effects noted than with use of tricyclics,
MAOIs
SSRIs
• Agents include:
– Fluoxetine
– Citalopram
– Paroxetine
– Sertraline
– Fluvoxamine
Anesthetic Implications for SSRIs
• Should not be co-administered with MAOIs
– (? use of meperidine)
• Caution in pts with impaired hepatic or renal
function
• Caution in pts with seizure hx
– ? use of ketamine
• Safety in pediatric population not established
• ? use of ondansetron, granisetron, etc.
Serotonin Syndrome
• Mild:
– Anxiety -Chills
– Ataxia -Insomnia
• severe:
– Hyperthermia
– Hypotension
– Depression of ventilation
– Skeletal muscle rigidity
– Seizures
– Coma
• Treatment is supportive
Vomiting
• Once stimulated, the vomiting center
stimulates efferent motor fibers
responsible for the act of vomiting
– Efferent motor nerves found in:
• Cranial nerves V, VII, IX, X, XI to the
upper GI tract
• Cervical and thoracic spinal nerves to
the diaphragm and the abdominal
muscles
• Stomach plays passive role
Postoperative Nausea and
Vomiting (PONV)
• Occurs after as many as 20-80% of all
cases
• Approximately 30% incidence after one-
day surgeries
• Constitutes the #1 reason for inpatient
admission following one-day surgery
– intractable pain, bleeding follow
Morbidity from PONV

• Straining—may deter a good surgical
outcome in certain cases
• Incisional pain with actual vomiting
• Dehydration—may be especially
deleterious in the pediatric or elderly pt
Emesis Risk Factors

• Age
– pediatric incidence greater than adults
– peak age 11-14 years
• 2º puberty related hormones
• Gender
– females > males
– highest incidence on the 4th and 5th days of the
menstrual cycle
• Obesity
• Hx of postoperative nausea and vomiting
(PONV)
• Hx of motion sickness
• Non-smoker
Estimated Frequency of Emesis
with Adult Procedures
• Laparoscopic ovum retrieval > 50%
• Laparoscopy ~ 35%
• Dental extractions, arthroscopy ~ 15%
• Other surgeries with high frequency of
PONV:
– GI surgery (stomach, duodenum gallbladder)
– Head and neck surgery
Pediatric Procedures with a High

Risk of PONV
• Strabismus surgery Ö 70-80%
• Tonsilloadenoidectomy
• Orchiopexy
• Middle ear procedures
• Otoplasty
Anesthetic Agents which Increase

PONV
• Ketamine
• Etomidate
• Narcotic based technique vs. volatile
anesthetic
– Excludes “high dose” technique
• Nitrous oxide (??)
– Data remains controversial/inconclusive
• Acetylcholinesterase inhibitors (??)
Postoperative Causes of Emesis
• Pain
• Dizziness
• Same-day surgeries
– Sudden postural changes as with early
ambulation
– Premature oral intake
– Motion with transportation home
• Opioids
The Vomiting Center

• Located in the brain in the reticular
formation at the level of the olivary nuclei
• Receives direct input from afferents from
both sympathetic and parasympathetic
nervous systems
• Closely related to and stimulated by the
chemotactic trigger zone (CTZ)
The CTZ
• Located in the medulla on the
floor of the 4th ventricle
– Receptors for several agonists which
produce nausea and vomiting are
found here
• dopaminergic
• serotonergic
• histaminic
• muscarinic
• opioid
The CTZ Cont'
• Causative factors of vomiting from
stimulation of the CTZ:
– Drugs
• Opioids
• Cytotoxics
– Radiation
– Metabolic disturbances
• Each receptor in the CTZ has at least
one specific antagonist which may
reverse nausea and vomiting
Cortical Afferents
• Cortical afferents carry stimuli
directly to the vomiting center
• Hypoxia
• Pain
• Increased ICP
• Noxious odors
• Sight
• Taste
• Psychogenic factors
The Vestibular Apparatus
• Stimulation of the vestibular apparatus

transmits impulses to the CTZ via the
cerebellum
– Motion
– Inner ear surgery
Antiemetics Specific for

Vestibular Disturbances
• Vestibular disturbances from motion, inner
ear surgery
– Scopolamine (Transderm Scop) or IV/IM
– Diphenhydramine (Benadryl)
• both exert a central anticholinergic effect
Visceral Afferents
• Visceral afferents carry stimuli directly to

the vomiting center
– Cardiac disease (i.e. acute MI)
– disturbance of GI or GU tracts
Opioid Receptors of the CTZ
• Stimulated by opioids of all types,
other drugs, and the vestibular
portion of cranial nerve VIII
• Usually depressed by high-dose
narcotic technique
• Naloxone, a specific opioid
antagonist, not accepted as a
treatment for PONV
Antiemetics Specific for the

Peripheral Muscarinic Receptor
• Scopolamine (central actions also)
• Diphenhydramine (central actions also)
• Atropine
• Glycopyrrolate
– Both may used to prophylax against n/v
secondary to:
• Unapposed parasympathetic tone seen with
regional techniques
• Surgeries where vagal stimulation is common

Serotonin (5HT3) Receptor
• High affinity for 5HT3 receptors
• Essentially devoid of unwanted side
effects
• May be costlier than other modalities;
most meds still under patent
• Best used prophylactically; onsets are
slightly delayed
Serotonin (5HT3) Receptor Cont'
• Ondansetron (Zofran)
– Typical dose 4 mg IV
– Onset approximately 10 mins
– Metabolized by the cytochrome P-450 system
– Durtion - 4 (+ or -) hours; may need to re-dose q 4-
8 hours as needed
• Granisetron (Kytril) Most common side
– Duration - 24 hours
effect is headache
• Dolasetron (Anzemet)
– No longer indicated. Likely off market and NCE
soon

Histamine Receptor
• Antihistamines reduce the excitability of
labyrinth receptors; may prevent n/v
secondary to motion
• Antagonism of histamine receptors in the
CTZ adds to antiemetic properties
– Promethazine (Phenergan)
– Dimenhydrinate (Dramamine)
– Meclizine (Antivert)
– Diphenhydramine (Benadryl)
– Hydroxyzine (Vistaril)

Dopamine Receptor
• Many potent antiemetic agents have
dopaminergic blocking properties
– Butyrophenones
• Haloperidol (Haldol)
• Droperidol (Inapsine)
– Phenothiazines
• Prochlorperazine (Compazine)
• Chlorpromazine (Thorazine)
– Benzamides
• Metoclopramide (Reglan)
Metoclopramide (Reglan)
• A gastric prokinetic due to its selective

cholinergic agonism
– Increases upper GI motility enhancing
gastric emptying
– Relaxes the pylorus, duodenum
– Increases motility of the small intestine
– Increases lower esophageal tone
– Has no effect on gastric acidity or H+ ion
secretion
Metoclopramide (Reglan)
• Acts as a dopaminergic receptor
antagonist
• Causes a slight degree of alpha
blockade
• Usual antiemetic dose 10-20 mg IV
– Onset 1-3 mins; DOA short with an
elimination T ½ of 2-4 hrs
• Contraindicated in pts with Parkinson’s,
bowel obstruction; may cause
abdominal cramping in the awake pt if
administered quickly
Aprepitant & Fosprepitant

• Blocks neurokinin I receptors
• Effects both peripheral and central
• Must be given prior to induction of
anesthesia and is only available as an
oral preparation
• Peak plasma concentrations 4 hours after
ingestion
• Comparable effects to ondansetron, but
longer acting & synergistic with other
PONV treatments
Antacids
• Increase gastric fluid pH
– This causes an increase in gastric motility
• Generally contain Mg, Al, or Ca salts
which react with/neutralize HCl
• Divided into two types:
– Particulate – not used for aspiration
prophylaxis
– Non-particulate
Non-particulate antacids
• A.K.A. “clear” or “soluble” antacids
• Mix readily with gastric contents
– Less dangerous if aspirated
• Sodium citrate (Bicitra)
– Use preoperatively is controversial; some
feel that it increases gastric volume and may
actually contribute to development of
aspiration/PONV
– Usually given before Cesarian sections, “full
stomach” cases (30 cc PO)
– May cause hypernatremia after repeated
doses
H2-blockers
• Compete with histamine at H2 receptors
• Cimetidine (Tagamet)
• Ranitidine (Zantac)
• Famotidine (Pepcid)
• Block acid stimulating effects of:
– Histamine
– Pentagastrin
– ACh
• Do not directly increase pH of gastric fluid
H2-blockers Cont'
• Used in the treatment of peptic ulcer
disease, upper GI bleeding
• May ultimately be usurped by the use of proton
pump inhibitors (omeprazole, lansoprazole,
pantozprazole)
– Used in aspiration prophylaxis
– May also be used in prophylaxis against
anaphylaxis in highly atopic individuals
• administered in conjunction with diphenhydramine
(Benadryl Ö blocks histamine @ H1 receptors)
H2-blockers Cont'
• Cimetidine, Ranitidine
– Inhibit the cytochrome P-450 system;
impedes the metabolism of:
• Benzodiazepenes
• Caffeine
• Ca++ channel blockers
• E-blockers
• Tricyclic amines
• Amide local anesthetics
• Phenytoin
• Theophylline
• Anticoagulants (specifically warfarin)
H2-blockers Cont'
– May È serum [ ] of digoxin
– Ç duration of depolarizing and non-
depolarizing muscle relaxants
– May cause bronchospasm in asthmatics
Mendelsohn’s Syndrome
• Aspiration of fluid with a pH of 2.5

or less and a volume of greater
than 25 - 30 cc (0.3 cc/kg)
Antimicrobials
Antimicrobial Anesthetic Implications
Cephalosporins 5 – 10 % cross-sensitivity with penicillin.
Aminoglycosides neuromuscular blockade (neomycin most potent),
(gentamycin) ototoxicity, renal toxicity.
Macrolides Inhibition of cytochrome P-450, clearance of
(erythromycin) benzodiazepines and narcotics.
Glycopeptides May cause massive histamine release (Red-Man
(vancomycin) Syndrome) if infused too quickly. Rate of infusion < 1
gm/hr. Ototoxic & nephrotoxic.
Quinolones Do not use in children or pregnancy (arthropathy).
(ciprofloxacin) May prolong QT interval.
Tetracycline Do not use in children or pregnancy (tooth damage).
Linezolid Reversible MAO inhibition
Herbals and Supplements

• More than 15 million pts take herbals (~1
in 3 adults); may not admit to use during
the pre-operative interview
• Not classified as drugs by the FDA
(considered to be dietary supplements)
– Potential for contamination, wide variations in
preparations and dosages, toxic ingredients
• Herbals should be d/c’d at least 2 weeks
preoperatively
– Abrupt d/c may result in withdrawal syndrome
Herbals and Supplements Cont'
• Major side effects/anesthetic implications include:
– drug interactions
• Anesthetics, sedatives, tricyclics, MAOIs, SSRIs,
immunosuppressants, antihypertensives,
anticoagulants
– CNS depression or excitation
– CV instability
– Hypoglycemia
– Fluid and electrolyte abnormalities
– Hepatotoxicity
– Coagulopathy
– Allergic reactions
– Alterations in drug metabolism
• 2° interference with cytochrome P-450
– Carcinogenicity
Effects of Herbals & Supplements

CV CNS Hepatotoxicity Hypoglycemia Coagulopathy
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PD\DOVRĹ )HYHUIHZĹ Germander Artichoke Dong quai
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Ginseng Ĺ Kava Kava Chromium Garlic
*LQVHQJĹ
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*ROGHQVHDOĹ
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Licorice Ĺ
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<RKLPELQH Ĺ
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+DZWKRUQĻ Fenugreek Echinacea
/DYHQGHUĻ Garlic Fish oil
/HPRQYHUEHQDĻ Ginseng Feverfew
St. John’s Wort Ĺ Grape seed Horse chestnut
Valerian Ļ Juniper Vitamin E
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Periwinkle ? Glucosamine
Yellow root
Notes
Anatomy Review
Lining of the Respiratory Tract

• nonciliated stratified squamous epithelium
– anterior nose, oropharynx, laryngopharynx
• ciliated pseudostratified squamous
epithelium
– posterior nose, nasopharynx, laryngeal mucosa above cords
• ciliated pseudostratified columnar

epithelium
– larynx below cords, trachea, bronchiolar tree
• nonciliated cuboidal epithelium

– terminals and respiratory bronchioles
The Nose
• external nose
• internal nose
– bony septum
– nasal turbinates
– posterior nares
• paranasal sinuses
– maxillary
– frontal
– sphenoid
– ethmoid
• functions
– warms inspired air
– humidifies air
– cleans inhaled air
– organ of olfaction
– resonator for speech
410
The Pharynx
A musculomembranous tube extending from the
undersurface of the skull to the level of C6 and lower
border of the cricoid cartilage where it is continuous with
the esophagus.
• divisions
– nasopharynx
– oropharynx
– laryngopharynx
• innervation
– sensory
• via glossopharyngeal (cranial nerve IX)
– motor
• via vagus (cranial nerve X)
• primary motor function
– swallowing
Esophagus
• upper 1/3 striated muscle
– voluntary
– airway protection against regurgitation via the
cricopharyngeus muscle (A.K.A. upper
esophageal sphincter (UES))
• motor innervation via the RLN
• lower 2/3rds
– involuntary; tone/contraction under ANS control
• distal 3-5 cm Ö lower esophageal sphincter
(LES)
– A functional structure; may be manually opened with ~
18 cm H2O pressure
Divisions of the Pharynx

• nasopharynx
– Behind posterior nares and above soft palate
• oropharynx
– Extends from the soft palate to the base of the tongue
• laryngopharynx
– Extends from the base of the tongue to the opening of
the esophagus
– Contains the landmarks for endotracheal intubation:
epiglottis, vallecula, aryepiglottic folds, arytenoid
cartilages
411
Mallampati Classification of the Airway
Cormack-Lehane laryngoscopic grades
The Larynx
• consists structurally of a framework of articulating cartilages linked
together by ligaments which move in relation to each other by the
action of laryngeal muscles
• location
– adult Ö anterior neck at the level of C 4-6
– child Ö anterior neck at the level of C 3-5
• blood supply
– arterial
• subclavian artery to inferior thyroid artery to inferior laryngeal
artery
– venous
• inferior laryngeal vein to brachiocephalic vein to SVC
The Laryngeal Cartilages

• singular cartilages
– thyroid
– cricoid
– epiglottis
• paired cartilages
– arytenoids
– corniculates
– cuneiforms
412
Thyroid Cartilage
• largest cartilage of the larynx
– two broad sheets of cartilage which unite in a V shape
anteriorly to form the “Adam’s Apple”
– attached to the hyoid bone by the thyrohyoid
membrane
– attached to the cricoid cartilage by the cricothyroid
membrane
– provides the anterior attachment for the vocal cords
Cricoid Cartilage
• consists of the only complete ring in the larynx
which broadens into a plate like structure
posteriorly; A.K.A. “The Signet Ring Cartilage”
• forms the inferior and posterior borders of the

larynx
• is the narrowest portion of the pediatric airway
Epiglottis
• leaf like, elastic
– projects obliquely upward behind the tongue and in
front of the entrance to the larynx
• functions to cover the glottic opening to prevent entrance of
solids and liquids into the airway during swallowing
• attached to the posterior surface of the thyroid
cartilage above the vocal cords
• first cartilage encountered during laryngoscopy
413
Arytenoid Cartilages
• pyramidal in shape; sit on cricoid cartilage
– each has a muscular process which is the
insertion of the posterior and lateral
cricoarytenoids
– each has a vocal process which is the
posterior attachment of the vocal cords
Corniculate, Cuneiform Cartilages

• corniculates
– cone shaped structures situated in posterior
part of the aryepiglottic folds
– each is attached to the apex of an arytenoid
cartilage
• cuneiforms
– elongated structures located slightly posterior
to the corniculates at the base of the epiglottis
Other Laryngeal Structures

• aryepiglottic folds
• ventricular folds (false vocal cords)
• vocal folds (true vocal cords)
• glottis
– *the rima glottis is the narrowest portion of the adult
airway
• cricothyroid membrane
– palpated between the lower border of the thyroid
cartilage and the cricoid ring
– allows for easy surgical access to the airway via
cricothyrotomy in “can’t ventilate, can’t intubate”
scenario
414
epiglottis
hyoid
thyrohyoid
membrane
thyroid
cricoid cricoid corniculates
trachea
arytenoids
cricothyroid
membrane
epiglottis
thyroid
arytenoids
cricoid
1. Epiglottis
2. Hyoid bone
3. Thyrohyoid membrane
4. Aryepiglottic muscle
5. Thyroepiglottic muscle
6. Thyroid cartilage
7. Cricothyroid muscle
8. Cricothyroid articulation
9. Trachea
10. Saccule
11. Transverse arytenoid
muscle
12. Oblique arytenoid muscles
13. Cricoid cartilage
14. Posterior cricoarytenoid
muscle
15. Membranous trachea
415
Muscles of the Larynx
muscle action effect
posterior cricoarytenoids rotate arytenoids outward ABduction
(2) (widens rima)
lateral cricoarytenoids rotate arytenoids inward ADduction

(2) (approximates vocal
cords)
transverse arytenoid (1) approximate arytenoids ADduction

(approximates vocal
cords)
thyroarytenoids (2) draw arytenoids forward relaxes and shortens

cords
cricothyroids (2) draw up arch of cricoid tenses and elongates
and tilt lamina back cords
OPEN CLOSED
thyroid cartilage cricothyroid
cricoid vocal cord

rima glottidis
lateral cricoarytenoid
(contracted)
thyroarytenoid
pivotal axis
of arytenoids
posterior
“Signet ring”
cricoarytenoid
(cricoid plate) (relaxed)
Action of laryngeal muscles
416
Innervation of the Larynx
• superior laryngeal nerve
– a branch of the vagus nerve; contains internal
and external branches
• internal branch supplies sensory innervation above
the vocal cords
– stimulation may precipitate laryngospasm
• external branch supplies motor innervation to the
cricothyroids
Innervation of the Larynx

• recurrent laryngeal nerve
– a branch of the vagus nerve (cranial nerve X)
– supplies motor innervation to all muscles of
the larynx except the cricothyroids
– supplies sensory innervation to the larynx
below the vocal cords
– may be damaged during thyroid/parathyroid
surgery
Damage to the Recurrent

Laryngeal Nerve
• unilateral transection = hoarseness

• bilateral damage from ischemia =
complete airway obstruction from
laryngospastic cords
• bilateral transection = flaccid vocal cords
– may have some passage of air
417
The Trachea
• cartilaginous and membranous tube extending
from the vocal cords to the carina to form the
right and the left mainstem bronchi
• lies anterior to the esophagus and is protected
anteriorly with cartilaginous rings
• posterior wall is membranous
• the carina lies at the level of T5
Airway measurements
distance female male
incisors to 10-14 cm 12-16 cm

vocal cords
incisors to 24-26 cm 26-28 cm

carina
The Bronchi
• mainstem (A.K.A primary bronchus)
– right
• shorter, wider, and less acute angle off trachea
– in adults, forms a 25 degree angle
– in children less than 3 years old, forms a 50 degree angle
• divides into 3 lobar branches
• Inhaled foreign bodies are more likely to enter the right
mainstem bronchus
– left
• longer, narrower, more horizontal than right
– in adults and children, forms a 40-60 degree angle off
trachea
• divides into two lobar branches
418
The Tracheobronchial Tree, Respiratory
Bronchioles, and Alveoli
• continued branching produces:
– segmental bronchi
– small bronchi
– bronchioles
– terminal bronchioles
– respiratory lobules
The Terminal Bronchioles
• the tracheobronchial tree ends at the 16th

level from the trachea at the level of the
terminal bronchioles
• diameter is <1 mm, cilia disappears,
cartilage is absent
• *this marks the end of anatomic dead
space
Anatomic dead space

• equal to approximately 1cc/lb in both
adults and children
• examples:
– 70 Kg pt = 155 lbs
approximate anatomic dead space = 155 cc
- 4 kg infant = 9 lbs
approximate anatomic dead space = 9 cc
419
The Respiratory Lobule
• respiratory bronchiole
– actual respiratory exchange begins here
• muscle layer of bronchial tree is thickest here
(relatively speaking)
– forms a thin band around the openings of the alveolar
ducts
– no muscle is found beyond this point
• alveolar duct
• alveolus (air sac)
Classification of airways by order of

branching
common name generation of airway
trachea 0
main bronchi 1
lobar bronchi 2-3
segmental bronchi 4
small bronchi 5-11
bronchioles, terminal bronchioles 12-16
respiratory bronchioles 17-19
alveolar ducts 20-22
alveolar sacs 23*
The Lungs
• lie free in the pleural cavity attached only
at the hilum
– the bronchi, major vessels, and lymphatics
enter and leave here
• each lung has a concave base
– rests upon the diaphragm
• each lung has an apex
420
• the right lung
– three lobes
• right
• middle
• lower
– broader, shorter than the left lung due to elevation of the
diaphragm from the liver
» the right apex extends further above the clavicle than
the left
• the left lung
– two lobes
• upper
• lower
– smaller than the right due to the position of the heart
The Thoracic Cavity

• three divisions separated from each other
by partitions of pleura
– pleural space
• contains the lungs
– pericardial space
• contains the heart, pericardium
– mediastinal space
• contains the major vessels, lymphatics
The Bronchial Circulation

• feeds the parenchyma of lung
• venous return to the pulmonic vein
– accounts for a normal 1-3% shunt
(deoxygenated blood mixing with arterial
blood)
• not to be confused with pulmonary
circulation
– where respiration occurs
421
The Pleura
• a double layered serous membrane
– parietal
• lines the entire thoracic cavity, inner surface of ribs, superior
surface of diaphragm
– visceral
• adheres to the surface of each lung
– the pleural space is a potential space between the

pleura
• a small amount of serous fluid is present
Muscles of respiration
• diaphragm
– responsible for 70% of VT
• accessory muscles of respiration:
inspiration expiration
sternocleidomastoid external oblique
scalenes internal oblique
pectoralis major rectus abdominus
pectoralis minor lower iliocostalis
serratus anterior lower longissimus
serratus posterior superior serratus posterior inferior
upper iliocostalis
Major nerve plexuses

• A nerve plexus is a network of intersecting
nerves which combine sets of spinal nerves that
serve the same area of the body into one large
grouped nerve
– Cervical plexus
– Brachial plexus
– Celiac plexus
– Lumbosacral plexus
– Sacral plexus
422
Cervical Plexus (C1-C5)
– Branches
• cutaneous
– Lesser occipital nerve
– Greater auricular nerve
– Transverse cervical nerve
– Supraclavicular nerves
» Sensory to the skin behind the ear, at the angle of the jaw,
in the anterior and lateral triangles of the neck to below the
clavicle
• muscular
– Ansa cervicalis
» Omohyoid, sternothyroid, sternohyoid,
– Thyrohyoid, geniohyoid
» Innervates the scalenes and levator scapulae,longus
capitis and longus colli
• mixed
– Phrenic nerve Ö diaphragm
– Spinal accessory nerve
– Communication with vagus
Cervical plexus cont’d
The Brachial Plexus

• supplies the upper limb with sensory and motor
innervation
• a branching network of nerves derived from the anterior
(ventral) rami (roots) of spinal nerves C5, 6, 7, 8, and T1
• divided into:
– roots “R
a
• C5-T1 dri ndy
n
bla ks c Travi
– trunks ck” offe s
e
• upper, middle, lower
– divisions
• anterior, posterior
– cords
• lateral, medial, posterior
– branches
• musculocutaneous, median, axillary, radial, ulnar
423
The Brachial Plexus
Source: internet
distribution of terminal nerves

cords branches innervation to
UE flexors (m)
lateral musculocutaneous lateral aspect forearm from
elbow to wrist (s); *most difficult
to block
median medial aspect forearm (s)
see below
shoulder (m,s)
posterior axillary
UE extensors (m)
thumb, 2nd finger, inner medial
radial 3rd finger (s)
dorsal-distal half 2nd, 3rd fingers;
medial median medial ½ 4th finger (s)
ventral-thumb, 2nd, 3rd, and ½ of
4th finger (s)
ulnar
4th, 5th fingers, lateral hand (s)
424
Major plexuses, cont’d
• Celiac (solar) plexus
– formed (in part) by the greater and lesser splanchnic
nerves of both sides, and also parts of the right vagus
nerve
– includes a number of smaller plexuses which supply
viscera:
• hepatic
• splenic
• gastric
• pancreatic
• suprarenal
• renal
• testicular/ovarian
• superior mesenteric plexus
• inferior mesenteric plexus

• Lumbosacral plexus
– Lumbar plexus (T12-L4)
• Main branches
– iliohypogastric
– Ilioinguinal nerve
– genitofemoral nerve
• Dorsal divisions
– lateral femoral cutaneous
– femoral nerve Ö adductors of hip, extensors of knee, and
skin over medial surfaces of thigh and leg
• Ventral divisions.
– obturator nerve Ö adductors of hip and skin over medial
surface of thigh
– accessory obturator nerve
425
– Sacral plexus (L4-S4)
• gluteal nerve Ö adductors and extensors of
hip and skin over posterior surface of thigh
• sciatic nerve Ö flexors of knee and ankle,

flexors and extensors of toes, and skin over
anterior and posterior surfaces of leg and
foot
• saphenous nerve Ö skin over medial

surface of leg
The Great Veins of the Neck

• internal jugular
– right IJ best for cannulation and passage of a
PA catheter
– left IJ puncture possible; Ç risk of thoracic
duct injury
• external jugular
– large valve at the junction of the EJ and the
subclavian
• anterior jugular
• subclavian
426
Aortic arch, neck, head vessels
Aortic arch vessels
• 3 major vessels arise from the arch

– brachiocephalic (A.K.A. innominate)
• subdivides into the R common carotid and the R
subclavian
– may be compressed during mediastinoscopy
– left common carotid
– left subclavian
The Antecubital Fossa
*best vein
to pass a
long-arm
CVP
427
The Circle of Willis
An anastomosis of the internal carotids and the
vertebral arteries which is found at the base of
the brain. All cerebral arteries are derived from
this anastomosis.
**this circle is directly responsible for cerebral
perfusion
**during carotid artery X-clamping, collateral flow is
through the vertebral arteries
CPP = MAP – ICP (or CVP)
The Circle of Willis

1) Anterior cerebral
2) Anterior communicating
3) Recurrent artery (of Heubner)
4) Hypothalamic
5) Internal carotid
6) Middle cerebral
7) Anterior choriodal
8) Posterior communicating
9) Posterior cerebral
10) Superior cerebellar
11) Pontine
12) Basilar
13) Anterior inferior cerebellar
14) Posterior inferior cerebellar
15) Vertebral
16) Posterior spinal
17) Anterior spinal
CSF circulation
CSF secreted by choroid plexus
Ø
lateral ventricles 1 & 2
Ø
Foramen of Munro
Ø
3rd ventricle
Ø
lateral
ventricles Aqueduct of Sylvius
4th Ø
Foramen of
Munro
ventricle 4th ventricle
Ø
Aqueduct
Foramina of Luschka & Foramina of Luschka and Magendie
of Sylvius
Magendie Ø
subarachnoid space
3rd ventricle
Ø
reabsorption by arachnoid villi
428
Cranial Nerve (CN) review
# Cranial Nerve Foramen Region Entered Components Target, Function
I Olfactory cribiform plate of ethmoid nasal cavity special sensory olfactory epithelium - smell
II Optic optic canal of sphenoid orbit special sensory retina-vision
levator palpebrae superioris

superior rectus
medial rectus
inferior rectus
III Oculomotor superior orbital fissure orbit somatomotor inferior oblique
preganglionic parasympathetic to:
ciliary ganglion (innervation of
sphincter pupillae and ciliary
visceromotor muscle)
IV Trochlear superior orbital fissure orbit somatomotor superior oblique muscle
V (V1-
3) Trigeminal
ophthalmic
major branches:
V1 lacrimal, frontal
nasociliary, general sensation from skin and
meningeal superior orbital fissure orbit general sensory mucosa in region at and above orbit
maxillary
major branches:
infraorbital,
V2
zygomatic, general sensation from skin and
nasopalatine, mucosa in region from orbit to
palatine foramen rotundum pterygopalatine fossa general sensory mouth
mandibular
major branches:
buccal, muscles of mastication
V3
auriculotemporal, tensor tympani
lingual, inferior tensor veli palatini
alveolar, and foramen ovale with lesser mylohyoid
meningeal petrosal from CN9 infratemporal fossa branchiomotor anterior belly digastric
general sensation from the skin and
mucosa from region at and below
general sensory the mouth
VI Abducens superior orbital fissure orbit somatomotor to lateral rectus
VII Facial
major motor
branches: temporal,
zygomatic, buccal,
mandibular, cervical, internal acoustic muscles of facial expression
and posterior PHDWXVĺIDFLDOFDQDOĺ stapedius, stylohyoid, mylohyoid,
auricular stylomastoid foramen temporal bone branchiomotor posterior belly digastric
IDFLDOFDQDOĺPLGGOH
HDUĺFKRUGDW\PSDQLĺ
petrotympanic fissure special sensory taste, anterior 2/3rds of the tongue
preganglionic parasympathetic to
IDFLDOFDQDOĺPLGGOH submandibular ganglia (innervates
HDUĺFKRUGDW\PSDQLĺ submandibular and sublingual
petrotympanic fissure visceromotor glands)
pterygopalatine ganglia (innervates
greater superficial lacrimal gland, nasal glands, and
SHWURVDOĺSWHU\JRLGFDQDO visceromotor palatine glands)
VIII Vestibulocochlear internal auditory meatus temporal bone special sensory hearing and balance
IX Glossopharyngeal jugular foramen neck branchiomotor stylopharyngeus

pharynx, palate, carotid sinus,
carotid body and posterior 1/3
viscerosensory tongue
special sensory taste, posterior 1/3 tongue
MXJXODUIRUDPHQĺ
W\PSDQLFEUDQFKĺ
W\PSDQLFFDQLFXOXVĺ
middle ear middle ear viscerosensory middle ear and auditory tube
MXJXODUIRUDPHQĺ
W\PSDQLFEUDQFKĺ
W\PSDQLFFDQLFXOXVĺ
middle ear infratemporal fossa visceromotor parotid
X Vagus jugular foramen branchiomotor pharynx and larynx

general sensory auricle, external auditory meatus
viscerosensory mucosa of entire larynx
visceromotor abdomen & thorax
enters by foramen
Accessory (A.K.A. PDJQXPĺH[LWVE\MXJXODU
XI Spinal Accessory) foramen neck branchiomotor trapezius, sternocleidomastoid
all tongue muscles innervated

XII Hypoglossal hypoglossal canal neck somatomotor except palatoglossus
The Cranial Nerves
with regard to their regions of

innervation, are nerves of the head. They
spread through the head-neck region,
except for the parasympathetic portions of
the vagus nerve which pass to the
abdominal organs.
Cranial Nerves I-VI

Cranial nerves Type Function
I. Olfactory S smell
II. Optic S sight
III. Oculomotor M eye movement,

pupil constriction
IV. Trochlear M eye movement
V. Trigeminal B chewing, great

(three branches)
ophthalmic (S), maxillary (S), mandibular sensory of face
(M & S)
VI. Abducens M eye movement
Cranial nerves VII-XII

Cranial nerves Type Function
VII. Facial B taste, great motor

(five branches)
temporal, zygomatic, buccal, mandibular, cervical
of the face
VIII. Acoustic S hearing, balance
(A.K.A. vestibulocochlear)
IX. B swallowing,
Glossopharyngeal afferent carotid
body and sinus
X. Vagus B “Great Wanderer”
(branches: superior laryngeal
and recurrent laryngeal nerves afferent and
may be injured during
intubation)
efferent
XI. Accessory M larynx and
(A.K.A. spinal accessory) pharynx
XII. Hypoglossal M tongue
(may be injured during intubation)
429
The Spine
Spinal Ligaments
Diaphragmatic Innervation
• phrenic nerve (R & L branches)
– arises from C3, 4, 5
• this is the source of motor innervation
(“C3,4,5 keeps a man alive”)
– sensory innervation
• lower 6 intercostal nerves
430
Cardioaccelerator Nerves
• arise from T1-5

• bradycardia usually noted in quadriplegia
or high level of spinal anesthesia
Landmarks for Sensory Levels

T4 nipple
T6 xiphoid
T8 lower border of rib

cage
T10 umbilicus
T7; L4 lower border of

scapula; Iliac crest
Epidural space widens as it

descends; widest at L2-3
431
Spinal cord
• Extends from the foramen magnum to the
level of L1 (adults), L3 (children)
– Terminates to conus medullaris; lower spinal
nerves form the cauda equina
• Blood supply—derived from a single anterior and
paired posterior spinal arteries
– Anterior spinal artery
» formed from the vertebral artery
» supplies anterior 2/3rds of the cord
– Posterior spinal arteries
» Arise from cerebellar artery
Additional blood supply to the cord

• Intercostals (thorax)
• Lumbar arteries (abdomen)
• Artery of Adamkiewicz (great ventral
radicular artery, arteria radicularis magna)
– arises from the aorta, T9-12 (60%)
– unilateral—usually from the L side
– provides the major blood supply to the
anterior, lower 2/3rds of the spinal cord
Blood supply of the hand
432
Sites for arterial cannulation
• Radial artery
– Most commonly selected site
• Ulnar artery
– Major blood supply of the hand
– Difficult to cannulate; deep, tortuous
• Brachial artery
– Large, easy to cannulate
– Risk of median nerve damage
• Axillary artery
• Femoral artery
– Good to use in low flow states
• Dorsalis pedis artery
– May have distortion of waveform; falsely high SBP 2º
distance from aorta
Peripheral Nerve Stimulation

• most common site of placement of PNS is
along the groove of the ulnar nerve; elicits
a response from the adductor pollicis
brevis
• facial nerve monitoring possible if arms
are not accessible; elicits a response from
the orbicularis oculi (correlates well with
larynx and diaphragm) and corrugator
supercilii
positioning
• neuropathies following surgery are from:
– stretching of nerves for sustained periods of time
– pressure on nerves for sustained periods of time
• leads to ischemia of the nerve Öneuropathy
• anesthetized pts are unable to compensate for
awkward/painful positions
– muscle relaxation allows for positioning that would
otherwise not be tolerated by the pt
• proper positioning considered a “shared
responsibility” among OR team
433
positioning
• upper extremity
– *ulnar nerve is the most frequently damaged in pts in
the supine position
– neuropathy may manifest as sensory and/or motor
deficit
• usually transient
– 70-90% of injured pts are male
– other predisposing factors to development of injury:
• extremes of weight (particularly obese pts)
• extended bedrest (before and/or after surgery)
• long surgery
• preexisting neuropathy in the contralateral limb
brachial plexus injury

• most associated with median sternotomy
– particularly with dissection of IMA
• probably 2º uneven retraction of chest wall
• increased risk with
– arm abduction > 90º from side
• compounded if head is turned contralaterally
– prone position with arms on rests beside head
positioning
• lower extremity
– lithotomy position carries a high risk of
perioperative nerve injury
• usually mild/self limiting
• severe Ö footdrop
– common peroneal nerve
• *most commonly injured nerve in the lower
extremities
• relatively superficial
– wraps around the head of the fibula on the lateral aspect
of the knee
434
lower extremity nerves, cont’d
• sciatic nerve
– adjacent to the hamstrings
– stretch from hyper flexion of the hip, especially when
coupled with an extended leg/flexed foot
• femoral nerve
– more commonly injured with deep, lower abdominal
retraction
• sustained compression of the iliac or femoral arteries leads to
ischemia
– pronounced abduction of thigh (frog leg)
lower extremity nerves, cont’d

• obturator
– injured with pronounced abduction of the thigh
– neuropathies are usually sensory (numbness inner
aspect of thigh)
• lithotomy position caveats:
– padding of bony prominences is essential
– position changes of the LEs must be made
simultaneously
• 1º risk factor for the development of neuropathy
following lithotomy is obesity
supine position
• minimal circulatory and ventilatory changes
noted
– FRC may be slightly È due to cephalad displacement
of diaphragm/abdominal contents
– stress on lower back
• may be attenuated with mild knee flexion
– pressure on heels
– upper extremities should be neutral
• if supinated, abduction from body not to exceed 90º
• pronation may cause undue pressure on the ulnar
groove
• individualize to each pt
435
Trendelenburg
• head down; associated with many physiologic
changes
– Ø pulmonary compliance, FRC from diaphragmatic
displacement
– × myocardial O2 demand
• from × preload, slight impedance of forward LVSV
– may ultimately È CO
– ×ICP, IOP
• leads to facial, scleral edema; possible retinal detachment
– × risk of passive regurgitation; possible aspiration
– arms should be secured if abducted
– shoulder braces should be placed on acromio-
clavicular processes with padding
prone
• face down; head and neck should remain

in a neutral position
– turned head may obstruct vertebral artery flow
and jugular drainage
• upper extremities are best placed at sides
– should not be abducted > 90º if extended
alongside the head
• avoid pressure on breasts, genitalia
prone, cont’d
• physiologic changes include
– Ø FRC
– × intraabdominal pressure
• may impede venous return via IVC; thereby
reducing preload/CO
• collaterals via epidural vessels; may see Ç
intraoperative blood loss from congestion
• Ø pulmonary compliance
• pooling of blood in lower extremities
– × risk for airway compromise during position
changes or intraoperatively
• pt should be log rolled after induction with neck
maintained in a neutral position
436
prone, cont’d
– facial/ocular edema
• retinal artery occlusion may lead to
blindness (A.K.A. Post-operative visual loss (POVL))
–risk possibly compounded by
overhydration with crystalloid, prolonged
periods of hypotension, direct pressure
on the orbits, possible anatomic
predisposition
–2 major common denominators:
»length of surgery
»blood loss
**increases in both of these attributes
may be causative factors in POVL
sitting
• venous air embolism (VAE) is the 1º
complication associated with this position
– occurs when the operative site is above the
level of the heart
• treatment:
– have the surgeon flood the operative site with
saline
– discontinue N2O
– aspirate air through a central venous catheter
– resuscitate with fluids, ionotropic support, (+)
pressure ventilation
sitting, cont’d
• other effects of sitting include:
– ØBP, preload, CO from pooling, ØCPP
• Caution when measuring BP via cuff
(brachial)
–NIBP on upper extremity may
significantly overestimate CPP; case
studies emerging of severe brain
damage post-op
–transducer should be placed at the
level of the ear (approximates
location of Circle of Willis)
– Øintrathoracic blood volume; V/Q
mismatching
437
lateral decubitus
• side lying; physiologic changes generally
pulmonary; overall V/Q mismatch from:
– × pulmonary compliance with Ø perfusion to the
upper lung Ö Ç dead space
– Ø pulmonary compliance and FRC with × perfusion
to the dependent lung Ö Ç shunt
• compression of IVC
• pressure on axilla on dependent side
– brachial plexus injury common
– pulse oximetry on dependent hand recommended to
assess perfusion
• pressure on medial aspects of knees
• potential injury to dependent eye/ear
Notes
Notes
438
SPECIFIC
NERVE
INJURIES
NERVE POSITION ETIOLOGY INJURY
Increased intracocular pressure
retinal artery occlusion
*Optic Nerve Prone with head rest Ocular Pressure
* Stimulation of oculocardiac
reflex
Oculomotor/Abducens
Supine/lateral Mask pressure Hypotony of ocular muscles
Nerve
Facial Nerve Mask/headstrap
Supine/lateral Paresis
*Buccal branch pressure
Mandibular branch Supine/lateral Forward traction on jaw Paresis
Pressure from ETT or
Supraobital Nerve Supine Paresis
mask connector
*Recurrent laryngeal Surgical trauma Ipsilateral cord adduction
Compression of plexus Paralysis of deltoid, biceps,

Trendelenberg with as it emerges from the brachialis & brachio-radialis
Brachial Plexus
shoulder brace and interscalenes and muscles;; loss of sensation over
Upper C5 & C6
wrist suspension travels to the deltoid & radial of hand and
subclavicular area forearm
Abduction of arm with
Compression between
hyperextension, Paralysis & atrophy of small
1st rib & clavicle
external rotation;; muscles of hand & flexors of
Lower C8, T1 Stretch over axillary
magnified with wrist (claw hand)
prominence of humeral
contralateral rotation Ulnar type of sensory loss
head
of head
Pressure on outer Wrist drop "Saturday Night
Radial Nerve Prone/supine
aspect of arm Palsy"
*Ulnar Nerve (most
Pressure on medial
commonly injured in Supine Paralysis "Claw Hand"
aspect of arm
upper extremity)
Trauma related to Paresis "Ape Hand"
Median Nerve Any position
antecubital IV insertion (unopposed thumb)
Weakness or paralysis of
Obturator Nerve Lithotomy Acute thigh flexion adductor thigh muscles;; pain
down inner aspect of thigh
Pressure of leg brace on
Saphenous Nerve Lithotomy Loss of sensation
the medial aspect of leg
Acute thigh flexion with Loss of quadriceps function;; gait
Femoral Nerve Lithotomy
abduction abnormal;; may have sensory loss
* Common peroneal Pressure on lateral
Lithotomy or lateral Foot drop;; may have sensory
nerve (most common aspect of knee at head
decubitus stirrups loss over dorsum of foot
lower ext. injury) of fibula
Prone or supine with Pressure on dorsum of Sensory deficit;; loss of position
Deep Peroneal Nerve
crossed feet foot sense;; inability to dorsiflex toes
Sensory loss on lower dorsal
Sural Nerve Crossed feet Pressure on heel aspect of leg, lateral side of foot
and 5th toe
Supine with muscle Flattening of normal
Lumbosacral Muscle spasm with low back pain
relaxants lumbar convexity
Revised 11/21/11
Test Taking Strategies
The “PASS” System
“Study is
nothing else
but a
possession of
the mind.”
Thomas Hobbes, 1651
The “PASS” system
• P--preparation
• A--attitude
• S--stamina
• S--strategy
Preparation
• Studying
– General rote knowledge
– True comprehension of subject matter
•Begin early
Multiple Choice Exams

• MCEs tend to focus on details which are
not typically well retained in short-term
memory
– repetition and learning small amounts each
day allow for a more reliable long-term
memory
• Because MCEs contain many questions,
the student needs to be familiar with a
much broader range of materials
MURDER-a study system

• M--mood
• U--understand
• R--recall
• D--digest
• E--expand
• R—review
• Taken from www.studygs.net

Mood
• Set a positive mood for yourself to study in
• Select the appropriate:
– time
• late PM vs. early AM?
– environment
• home vs. library
– attitude
• Spaced studying is better than cramming
– A recent study of British postal workers showed that
those who studied 1 hour a day learned as much in
55 hours as the 4 hour a day study group did in 80
hours
Understand
• Mark any information you don’t understand
in a particular unit
• Attempt to resolve with further

investigation
– multiple written resources
– instructor
– peers
Recall
• After studying the unit, stop and
put the information into your
own words
– especially helpful when preparing
for oral comprehensives
Digest
• Return to the information that you did not
understand and reconsider the material
• Contact external expert sources if you still
cannot understand the information
Expand
• Ask 3 questions at this point:
– What further questions can I ask about the
topic?
– Would I be able to impart this information to
others?
• If you can teach it, you know it
– How would I apply this information to my area
of interest?
Review
• The most important step
– Go over the material you have covered a final
time
– Review what strategies helped you
understand and/or retain information in the
past and apply these to your current studies
Index card study system
• gives you an accurate perception of how
well you know the material
• forces you to rewrite and think about the
material, rather than just look over it
– memory increases when items are actively
generated and not simply passively read
• portability allows for “anytime, anywhere”
studying
Index card study system, cont’d

• Review your notes and readings frequently, so
that the material is “fresh”
– retention is maximized if notes are revisited within 24
hours of the initial lecture
• Generate questions from the material as if you

were writing the exam; include key words/terms
pertaining to the material

• Write each question/term on the back of
an index card
• Write the answer on the front using key
words in the explanation
– Use notes and text as a reference but use
your own words whenever possible
• Shuffle the index cards
• Look at the card on the top of the deck
– place on the bottom after answering
correctly
– return to the notes/text if your answer is
incomplete or incorrect
• Proceed through the deck of cards
until you “own” the information

• Carry your cards with you everywhere
– take advantage of small pockets of time
• If you think you know the answer but

cannot put it into words, you probably
don’t know it well enough
– can you explain the concept to someone
else?
• Test yourself where no one can

see you (and think you’re nuts);
by reciting answers out loud
– verbalization of answers helps
ensure understanding and
enhances retention
• Study/discuss with a classmate

Other study aids
• Memory builders
– Organization of information
• Writing lists, charts, and tables from notes
and texts
–classification and grouping of items is
highly effective in forming connections and
boosting memory (“chunking” of
information)
– Mnemonics
Other study aids

– Dietary habits/supplements
–Folic acid, Vitamin E
–Gingko biloba (efficacy in question)
–epicatechin, a flavonol found in tea,
grapes, blueberries, and cocoa, enhances
memory in mice; the effect increases
further when coupled with exercise
(Journal of Neuroscience 5/30/07)
– Practice exams
• success on a MCE has to do with both
knowledge and skill in test-taking
Post exam item analysis for

multiple choice tests
• Helps to review past errors on MCEs
– “Why did I answer that way??”
• May aid the test taker in fine tuning study

modalities and test taking strategies
Study Skills Deficiencies
When reviewing errors on MCEs and practice
exams, make the following notations:
• DNK Ö ”did not know” Æ may highlight a

deficiency in study skills
• TM Ö error made secondary to lack of
time before taking the exam
• NT Ö error due to deficiencies in class
notes
• TB Ö errors made secondary to lack of
understanding of assigned text readings
Test Taking Strategy

Deficiencies
• T Ö timing Æ errors made because time
ran out during the exam
• RC Ö reading comprehension was
altered; question was not read carefully*
• C Ö confidence Æ errors made because
the answer was changed from correct to
incorrect
• GS Ö error from a wild guess made
without narrowing down options
P.A.S.S.
• Attitude
– Approach exams with a positive, upbeat
attitude—”I am well prepared; I’m going to ace
this exam!” and other self-fulfilling prophecy-
type statements
– Do you have test taker’s anxiety?
– Relaxation techniques
Relaxation techniques
• Deep breathing
• Visualization
• Mantras
• Repeating S-T-O-P over and
over
P.A.S.S.
• Stamina
– Good sleep is crucial in the days leading up to
the exam
• do not cram until the wee hours
• minimize ETOH and other “mind manipulators” in
the days leading up to the exam
– “You are what you eat”

• don’t go to the exam on an empty stomach
• don’t “carb load”; balance carbs with protein so
that you don’t “crash” mid-exam
P.A.S.S.
• Food
– fresh fruits and vegetables are recommended to
reduce stress
• Stress-inducing foods
– processed or preserved foods
– chocolate
– eggs
– fried foods
– junk foods, chips, similar snack foods
– artificial sweeteners
– pork, red meat
– white flour products
– carbonated soft drinks
– spicy foods
Exam-specific strategies
• Multiple choice exam questions
– usually include a phrase or stem followed by three to
five options
• “distractors”Æ options which mimic the correct
answer and attract attention
• “foils”Æ options which contrast with all others
making it seem as though it is the correct answer
• Be sure to take the time to read the stem
carefully!
– rushing causes “input” errors (Type I)
• Rushing may cause misprocessing of stem

or indicator words (Type II error)
– the student quickly scans the stem and mistakenly
ascribes an incorrect word for the actual indicator
– the student overlooks subtle differences between
related terms in distractors i.e. sympathetic vs.
parasympathetic
• Rushing may cause an “output error”

(Type III error)
– the student quickly hits enter, possibly
choosing the wrong answer
• Probably responsible for most failures on the NCE
Multiple choice exams
• Improve your odds of answering by

thinking critically
1) cover the options, read the stem, and
attempt to answer; choose the option that
most closely matches your original answer
2) read the stem with each option, treating it as
a true-false question; choose the “most true”
Strategies to answer questions

• Immediately eliminate any option(s) that
you know to be incorrect
• Question any option that doesn’t
grammatically fit with the stem
– look for grammatical clues (i.e. “an” at the end
of the stem—correct response begins with a
vowel)
Strategies to answer questions
• Question options that are totally

unfamiliar to you
• Question options that contain
negative or absolute words
Key distractor words
• “absolute” determiners
– Always
– Never
– All
– None
– Must
– Only
• Responses containing these words are less
likely to be correct than those containing
conditional or “gray” terms

• Conditional or “gray” terms
– Sometimes, somewhat
– Some, few
– Frequently Ca
o p re f
– Often, usually be tion ul—
– Generally co m thi
rre ay s
– Many, majority ct!
– On the average
– Probably

• Always read the stem slowly and carefully!
– It is easy to miss the terms:
• not
• except
– May see these on the NCE exam but efforts are
being made by item writers to gradually
eliminate these questions
– May sometimes be italicized, but not always

Strategies to answer
questions, cont’d
• Trust your knowledge if an answer seems
too easy
– Don’t read into questions
– Don’t think that the question is a “trick”
– Do check to make sure that none of the other
answers seems better than your initial
response
Strategies to answer difficult

questions
• “all of the above”
– If you know that at least 2 of the options seem
correct, all of the above is a strong possibility
• don’t fall into the “all of the above” trap, however
– Beware of the “none of the above” option

• frequently the wrong answer

questions
• number answers
– If you have absolutely NO idea
what the answer is, toss out the
high and low and consider the
middle numbers
questions
• “look alike options”
– One may be correct; if so, choose
the one that makes the most
sense
• eliminate choices that mean basically
the same thing, and thus cancel each
other out

questions
• If two alternatives seem

correct, compare them for
differences, then refer to the
stem to find your best answer

questions
• echo options
– If two options are opposite each
other, chances are that one of
them is the correct answer
questions
• Favor options that contain

qualifiers and adjectives
– the result is longer, more inclusive
items that better fill the role of the
answer
• the longest response is often the
correct one

questions
• Look for verbal associations
– A response that repeats key
words that are in the stem is likely
to be correct
If all else fails

• Choose response b or c
– many item writers subconsciously
feel that the correct answer is
“hidden” better if it is surrounded
by distractors
– response “a” is usually least likely
to be the correct one
– don’t look for patterns
• don’t panic if the last 6 answers were
all “b”
Guessing
• Always guess when there is no penalty
• Use common sense or logic when
attempting to select the best possible
answer
• Use hints from previous known questions
to answer questions that you don’t know
• Should you change an answer before
hitting enter???
Changing Answers
• Used to be taboo—i.e. “Go with
your first instinct!”
• Newer thought is to change the
answer if, after further reflection,
you have a strong feeling/doubts
about your response
– recent studies show that students who
change dubious answers usually
improve their test scores
Journal of Personality and Social

Psychology (Vol. 88, 725-235)
• A May ’05 study of 1561 students taking a

midterm in Introductory Psych
• When students changed their answers, they:

– went from wrong to right 51% of the time
– went from right to wrong 25% of the time
– went from wrong to wrong 23% of the time
Multiple choice exams
• Remember:
– The correct answer is guaranteed to be
among the possible responses
– Your first answer is generally correct (unless
you are absolutely sure that it is incorrect)
– You can score points with lucky guesses
– No amount of skill in test taking will
compensate for lack of
studying/preparedness!
Exam day strategies

• Arrive early and take a moment to relax
and reduce your anxiety
• Wear comfortable clothing
• Think positively
– It has been demonstrated that when you
become emotional—i.e. ”I’ve got to pass this
or I can’t work!”, performance ultimately
suffers
• don’t psych yourself out
Exam day strategies

• Anxiety is good (to a point)
– Mild anxiety heightens awareness of the task
at hand and of the external environment;
sharpens senses/concentration
– Moderate to high anxiety causes the opposite
effect; narrowing of the senses, auditory
effects (2º hyperventilation)
Exam day strategies, cont’d
• Take short breaks during the exam

– budget time wisely
• Focus and deep breathe
– relax
• these will all help to boost confidence
• Use of beta blockers?
– generally not a good idea unless you know that you
are able to tolerate them and they work well for you
Exam day strategies

• If you find yourself getting
emotional (angry, upset, weepy,
etc.)
– STOP for a short period of time
– Regain composure/concentration
– Exercise relaxation techniques
Exam day strategies

• Listen for any last minute instructions given by
the instructor/test center attendant
• Read directions carefully
• Change positions to help you relax
• Pay attention to passing time
– Keep a steady pace
• Do not panic if you find the test difficult
National Certification Examination
(NCE)
• Variable length
• Computerized adaptive
– Based on “item response theory”
• Multiple choice
– A stem followed by 4 options
– No “K-type” questions
– Minimal negative or “except” questions
– Newer questions such as multiple correct
response phased in as of 2009
The NCE cont’d

• Minimum-100 questions
– 70 questions from content outline
– 30 pretest questions
• Do not count towards score
• Maximum-170 questions
• Time limit is still 3 hours
• Must register for the exam within
3 months of graduation
– Once application is made,
eligibility period is 90 days
Eligibility policy change 10/07

“Candidates who do not take and pass
the NCE within two calendar years of
completion of the nurse anesthesia
educational program will not be
eligible to apply to take the
Certification Exam unless they enter
and complete another unabridged
accredited nurse anesthesia
program.”
Update for the NCE examination
• New questions released in 2009:
– Multiple correct response (MCR)

• The stem is followed by 4-8 responses;
test-taker must choose all applicable
answers for credit
• The stem will indicate how many responses
are correct
Multiple correct response (MCR)

Which of the following hormones are
secreted by the neurohypophysis?
(choose two):
A) HGH
B) oxytocin
C) prolactin
D) TSH
E) vasopressin
F) FSH

– Computation questions
• Test-taker will be asked to compute an
answer (i.e. calculating SVR based on pt’s
vital signs)
• Rather than having the choice of four
answers, the examinee will be asked to
enter the computed answer in the space
provided
Computation questions
• Response must be entered in the form
of a number (i.e. 1200, not “twelve
hundred”
• Directions will be given as to
rounding, decimal places, etc
• A calculator will be supplied for those
questions that may be computationally
complex; there will be no use of
personal calculators

– “Drag and drop” questions
• A clinical scenario will be given and
interventions will be listed
• Tests an examinee’s ability to prioritize
• May also be utilized in a matching format
• The examinee will be asked to drag the
interventions to the appropriate spot and
drop them so that they are in order of
requested priority

– “Hot spot” questions
• The examinee will be asked to identify a feature
of a graphic
• As the mouse is rolled over the graphic, various
areas will highlight with an “X”
• The examinee will choose the correct answer by
clicking on the “X” that depicts the requested
feature
• The examinee may change the answer before
moving to the next question by clicking on
another region (X) in the image

– Graphics and video
• Any questions may be visually augmented
with the use of graphics and/or video clips
as stimuli for the question
– **newer format questions intended to

test the examinee on clinical
acumen/application of knowledge
Content outline
Basic sciences 25%
Equipment, 10%
instrumentation, and
technology
Basic Principles 30%
Advanced Principles 30%
Professional Issues 5%
Adapted from the 2011 Candidate Handbook
Taking the NCE

• Computer skills not needed
• May have pencil/paper
– no calculators allowed
• Space bar, ENTER key, TAB key
• NO tutorial or practice questions
• Must answer question before proceeding to the
next
• Cannot return to/review previous questions
Taking the NCE
• Test centers:
– Other examinees may be present
– Attempts by staff to keep noise at a minimum
– May bring ear plugs
– May not test privately unless documented
disability requires accommodation
– May take 2-4 weeks to get an appointment at
a specific testing center
Pass fail decision occurs when:

• Candidate clearly demonstrates either
competency or incompetence at any point
between 100-170 questions
• 170 questions have been administered
• Maximum amount of time has been
reached
– Very few candidates time out
Pass Rates 2005-2011

93%
OD Passin
DS
ARE g Scor
92% IN Y e – 4
OU 5
92% RF 0
AVO
R!
90%
89.9%
90%
89.1%
88.9%
87.7%
Time frame following program
completion until exam:
Time frame until % of total Further analysis of
exam examinees test taker
performance on the
< 4 weeks 26.3% NCE in relationship
to the completion
1 month 32.8% date revealed that
the longer the
2 months 21.7% examinee had
been out of
3 months 7% his/her program,
the lower their
t 4 months 11.9% score on the NCE.
As of August, 2009
• Beginning in August 2009, the candidate
receives pass/fail status at the end of the
examination by the testing center
• This is only a preliminary result
– all test results must still be validated by the
Council on Certification (CCNA)
• May not sign as a CRNA until verification
letter is received from the NBCRNA
Why is it only a preliminary

result?
• Need to assure:
– Test center security
• Verifies that the test session occurred under
controlled conditions
– All exams videotaped
– Irregularities reported; investigation ensues;
student’s score is held
– Verification of validity of results by CCNA
– Verification of candidate records
Why is it only a preliminary
result?
• Testing service conducts a series of
analyses
– Three diagnostic tests:
• Verifies that computer functioned properly
– Verifies the final ability estimate
– Verifies that the number of questions
administered was correct
– Verifies the pass/fail decision was correct
based on the ability estimate
VISIT NBCRNA WEBSITE!!

www.nbcrna.com
• Under “resources” tab, you will find:
– Candidate handbook
– FAQs
– Alternative question formats/tutorials/samples
– Updated reports
• Annual report of NCE and SEE
performance
– pass rates
– demographic/satisfaction surveys
– monthly certificant lists
Please contact us at:

support@ccanesthesiareview.com
if we can further help you in
preparing for the NCE!
Professional and
Legal Aspects of
Nurse Anesthesia
Self study
Professional Aspects
• Nurse anesthetists currently
provide 65% of all of the
anesthetics in the U.S., either
autonomously or in conjunction
with an anesthesiologist
• Nurse anesthesia is considered
the oldest nursing specialty
American Association of Nurse

Anesthetists
• Founded in 1931
• Developed and implemented a certification program in
1945
• Instituted mandatory recertification for all practicing
CRNAs in 1978
• Practices under a code of ethics
• Sets forth standards for practice; oversees certification
and recertification of nurse anesthetists, accredits
programs of nurse anesthesia, acts as liasion to the
public and with legislators, provides members with
multiple services, including peer assistance for
chemically dependent members
• Represents >30,000 CRNAs today
465
AANA, cont’d
• Comprised of 3 autonomous councils:
– COA-Council on Accreditation of Educational
Programs in Nurse Anesthesia
– NBCRNA-National Board on Certification &
Recertification of Nurse Anesthetists
• CCNA-Council on Certification of Nurse
Anesthetists
• Council on Recertification of Nurse Anesthetists
– Council for Public Interest in Anesthesia
AANA organizational goals and

objectives statements
• Goal Statement 1:
– AANA and CRNAs support a culture of patient safety
– AANA and CRNAs ensure the future of the nurse
anesthesia profession
– Members value AANA membership
– Organizational performance is a model for
professional associations
adapted from AANA website
Statements – 2011 updates

• Vision Statement
– AANA will be a preeminent professional association
for healthcare and patient safety.
• Mission Statement
– AANA advances patient safety, practice excellence,
and its members’ profession.
• Core Values
– Patient safety; Care for the whole patient, from a
nursing perspective; Professional excellence and
personal well-being; Healthcare policy and
collaboration; Integrity and quality in all professional
and clinical settings
• AANA Motto
– Safe and Effective Anesthesia Care
466
AANA Regional Map
AANA regions
• Region 1
Connecticut, Maine, Massachusetts, New Hampshire, New Jersey,
New York, Puerto Rico, Rhode Island, Vermont
• Region 2
Georgia, Kentucky, North Carolina, South Carolina, Tennessee,
Virginia, West Virginia
• Region 3
Illinois, Indiana, Michigan, Wisconsin
• Region 4
Arkansas, Iowa, Kansas, Minnesota, Missouri, Nebraska, North
Dakota, Oklahoma, South Dakota
• Region 5
Alaska, Arizona, California, Colorado, Hawaii, Idaho, Montana,
Nevada, New Mexico, Oregon, Utah, Washington, Wyoming
• Region 6
Delaware, District of Columbia, Maryland, Ohio, Pennsylvania
• Region 7
Alabama, Florida, Louisiana, Mississippi, Texas
AANA Code of Ethics

• Outlines the principles to which the
profession of Nurse Anesthesia sets its
standards; each certified or recertified
member of the AANA is responsible to
meet these expectations personally and
collectively.
• Ensures the highest possible ethical
standards
467
Key Points of the AANA COE
– Patient Care
– Competence
– Professionalism
– Societal Obligation
– Confidentiality
– Personal Integrity
– Endorsement
– Research Ethics
– Practice Settings
– Employment Relations
Standards of Care for Nurse

Anesthesia Practice
• The highest mandate for clinical behavior
as set forth by the AANA
– assists the profession in evaluating the quality
of care provided by practitioners
– provides a common base for practitioners to
use in their development of quality practice
– assists the public in understanding what to
expect from the practitioner
– supports and preserves the basic rights of the
patient
Standards I-IV
• Standard I Ö Perform a thorough and
complete pre-anesthesia assessment
• Standard II Ö Obtain informed consent
• Standard III Ö Formulate a patient-specific
plan for anesthesia care
• Standard IV Ö Implement and adjust the
anesthesia care plan based on the
patient’s physiologic response
468
Standards V-VII
• Standard V Ö Monitor the patient’s physiologic
condition as appropriate for the type of
anesthesia and specific patient needs
• Standard VI Ö There shall be complete,
accurate, and timely documentation of pertinent
information on patient’s medical record
• Standard VII Ö Transfer the responsibility of
care of the patient to other qualified providers in
a manner which assures continuity of care and
patient safety
Standards VIII-IX
• Standard VIII Ö Adhere to appropriate safety
precautions, as established within the institution,
to minimize the risks of fire, explosion, electric
shock and equipment malfunction. Document
on the patient’s record that the anesthesia
machine and equipment were checked.
• Standard IX Ö Universal precautions shall be
taken to minimize the risk of infection to the
patient, the CRNA, and other staff
Standards X-XI
• Standard X Ö Anesthetic care shall be
assessed to assure its quality and
contribution to positive patient outcomes
• Standard XI Ö The CRNA shall respect
and maintain the basic rights of patients
Adapted from the AANA website
469
Key Historical Figures in Nurse
Anesthesia
• Sister Mary Bernard
– provided the earliest documentation of anesthetic care of
patients by nurses in 1887
• Agatha Hodgins
– the founder of the AANA; pioneer in the use of N2O and O2 in
anesthesia machines; first president of the AANA (1931)
• Helen Lamb
– recognized the need for an organized area of Nurse Anesthesia
studies which initially included educational standardization and
standards of excellence, eventually cluminated in formation of
the Council of Certification
• Alice Magaw
– “The Mother of Anesthesia”; a pioneer in anesthesia research;
she reported the results of greater than 14,000 anesthetics in
1906. Worked @ St. Mary’s (presently the Mayo clinic) in 1889
Professional Responsibilities of
Nurse Anesthetists
• Anesthetists practice under
– nurse practice acts which are overseen by the state in which
they reside/practice
– requirements/standards set forth by the institution they practice
in, and by AANA and JCAHO practice standards
• Anesthetists are required to receive certification from the

Council on Recertification
– initial entry requirement of Master’s degree in Anesthesia or
other related health science
– certification after graduation from an accredited program via
national exam
– recertification every two years with a requirement to earn 40
Council approved Continuing Education Units (CEUs)
Quality assurance
• A process through which health care
providers can monitor the quality and
appropriateness of care provided and
improve care or clinical performance
• QA programs are mandatory according to

JCAHO standards for all institutions which
are JCAHO accredited
470
Quality Assurance
• There are five basic components of the quality
assurance process:
– Monitoring
– Problem identification
– Development and implementation of solution
– Re-evaluation of the solution
– Documentation of the entire process
National Practitioner Data Bank

• Designated by The Health Care Quality
Improvement Act of 1986
– The NPDB is primarily an alert system intended to
facilitate a comprehensive review of health care
practitioners' professional credentials.
– The intent is to improve the quality of health care by

encouraging State licensing boards, hospitals and
other health care entities, and professional societies
to identify and discipline those who engage in
unprofessional behavior; and to restrict the ability of
incompetent physicians, dentists, and other health
care practitioners to move from State to State without
disclosure or discovery of previous medical
malpractice payment and adverse action history.
NPDB, cont’d
• Requires input from five sources:
– Medical malpractice payments
– License actions by medical boards
– Professional review or clinical privilege action
taken by hospitals and other health care
entities (including professional societies)
– Actions taken by the DEA
– Medicare/Medicaid exclusions
471
The Legal System
• 3 basic sources of law
– constitutions
• the basis of governmental power
– statutes
• laws passed either by Congress (federal) or by individual
state legislatures
– regulations
• set forth by regulatory agencies i.e.
– JCAHO-Joint Commission on Accreditation of Healthcare
Organizations
– OSHA-Occupational Safety and Health Administration
– FDA-Food and Drug Administration
– individual medical and nursing boards/associations
• 2 types of law
– civil
– criminal
Malpractice
• Malpractice occurs when there is a deviation
(either willful or inadvertent) from the accepted
standard of care which results in harm to
another person; negligence in the discharge of
professional duties.
• There are four components of a malpractice

case:
– Legal duty
– Breach
– Cause
– Damage
4 components of a malpractice case

• Legal duty Ö the proper care that a practitioner
owes to the patient; a contract between the
patient and the practitioner
• Breach Ö of legal duty; failure of the practitioner
to meet the standard required by law. 2 types:
– error of omission-expected care was not rendered
– error of commission-care was rendered in an
improper manner
• Cause Ö the manner in which the legal duty
was breached
• Damage Ö the result of the breach (injury)
and/or the monetary reward to the plaintiff i.e.
general, special, or punitive damages
472
Malpractice, cont’d
• The burden of proof to assign fault and
prove negligence against the defendant
lies with the injured party, A.K.A. the
plaintiff
• The plaintiff must prove
– beyond a reasonable doubt, with clear and
convincing evidence, that damage has been
done
• Res Ipsa Loquitor
– Literally “the action speaks for itself”. This allows
circumstantial evidence to prove negligence on the part
of the defendant; the injurious event does not need to be
directly witnessed
Res Ipsa Loquitor

• Four elements must be proved when applying
this doctrine:
– The injury is of a kind that typically would not occur in
the absence of negligence
– The injury must be caused by something under the
exclusive control of the anesthetist
– The injury must not be attributable to any contribution
on the part of the patient
– The evidence for the explanation of events must be
more accessible to the anesthetist than to the patient
Legal Terminology, cont’d

• Tort
– A civil wrong; either intentional or accidental in nature.
Tort law recognizes the responsibility of the
healthcare professional to act prudently. If injury
occurs, this would fall under the tort concept of
negligence.
• Negligence
– Failure to act in a prudent manner; carelessness. In
proving an act of negligence, three requirements must
be fulfilled:
• standard of care
• causation
• damages
473
Legal Terminology, cont’d
• Deposition
– An oral question and answer session under
oath where attorneys from both sides seek to
discuss testimony and evidence in a lawsuit
• Expert witness
– A person who has special skill and knowledge
about a subject related to the case
Legal terminology
• Captain of the Ship Doctrine
– A legal theory which ascribes the highest authority in the OR to
the surgeon (nearly obsolete)
• Respondent Superior
– Literally “let the master answer”. An employer is liable for the
employee’s actions within the scope of employment, as well as
for the employee’s legal consequences
• Amicus curiae
– Literally “friend of the court”; a person utilized during the appeals
process who is not involved with the case; provides information
which is relevant to the appellate court on the law to be applied
• Supervision
– the legal relationship between a CRNA and attending
anesthesiologist
• Vicarious liability
– the supervising physician is ultimately responsible for a negligent
act by the CRNA
defenses to negligence
• Statute of limitation
– a lawsuit must be filed within a finite period of time after an incident
occurred or from the initial discovery of damage
• typical statute of limitations for medical malpractice is 2 years from
the time of discovery of the alleged wrongdoing/damage
– 2 exceptions
• The plaintiff is under a disability which keeps him/her from
bringing the suit (e.g. children, persons under legal
guardianship)
– infants who were injured during delivery may seek
damages up until 18 years of age
• The plaintiff may not have been able to discover that there
was an injury caused by negligence before the statute of
limitations expired
**the statute of limitations varies by state, nature and
circumstances of the case
474
defenses to negligence
• Good Samaritan Act
– protection of a person who provides
emergency care to another; suit may not be
filed against the provider in the event of a
poor outcome
Informed Consent
• Consent is the patient’s agreement to
undergo a specified procedure
– Informed consent requires that the patient is
fully apprised of alternative options and
possible complications of the procedure they
are to undergo before making a decision
– The consenting patient must be older than 18
years of age or an emancipated minor
• An emancipated minor is younger than the age of
majority (18) who meets requirements to provide
consent (lives on their own, is married, has a child)
Informed consent
• Should be obtained by the caregiver before and
physical contact is made with the patient
– The duty to disclose is the basis for informed consent;
it is measured by the amount of knowledge the
patient needs
• Patient signs a contract in the presence of a 3rd

party who acts as a witness
– placed in the medical record
– considered a legal document; tampering with it (or
any other documents) is considered a criminal
offense
475
Elements of informed consent
• The patient’s diagnosis
• Explanation of the nature/purpose of the
treatment or procedure
• Possible risks, complications, and
consequences of the treatment/procedure
• Expected benefits of the treatment/procedure
• Prognosis if the treatment/procedure is not
performed
• Alternative forms of treatment (if any)
Consent may be given by:

• The patient
• The relative of a minor patient or of an
incapacitated person
• A person designated by the patient before
incapacitation (i.e. power of attorney)
• A court-appointed designee (i.e. guardian)
• A court order may be obtained if consent is not
attainable and the procedure is deemed to be in
the patient’s best interest
• May be obtained by phone in the presence of a
listening 3rd party
Implied Consent
• Patient’s failure to object to care

– minor procedures performed i.e. IV insertion
in a patient care area
• Patient is unable to respond to give
consent
– intubation during an emergency situation
476
Care without consent
• Battery
– The unwanted (not consented to) physical
contact between two persons
• Assault
– Fear of the eventuality of battery—may be
non-physical (i.e. verbal) in nature
• These may be listed as either civil or criminal
offenses
Slander and Libel

• Slander: words falsely spoken that damage the
reputation of another; an attack on the person’s
reputation
• Libel: a false and malicious publication printed
for the purpose of defaming a living person; a
harmful statement in a fixed medium, especially
writing but also a picture, sign, or electronic
broadcast (the anesthesia chart)
– Anesthesia providers may be sued for charting non-
substantiated facts re: the patient, i.e. subjective or
derogatory statements
– Both are torts: civil wrongs which constitute
“defamation of character”
Miscellany
• Death is the most common anesthetic mishap
followed by nerve injury and brain damage
– common denominator for 34% of anesthetic mishaps
is airway mismanagement
• The most frequent claim made against CRNAs is
for inadvertent dental damage
• Human error accounts for 80% of all anesthetic
mishaps (followed by equipment failure and
other non-human event)
– most common source of patient morbidity is due to
unrecognized circuit disconnection
477
• The incidence of substance abuse among
CRNAs is approximately 10%.
– 70% of reported cases involved abuse of
either fentanyl or sufentanil
• Employers must provide reasonable
accommodation for the recovering
chemically dependent CRNA under The
Americans With Disabilities Act (1990)
• Frank v. South*
• Chalmers-Francis v. Nelson*
• State v. Borah
• Sermcheif v. Gonzales
• Brown v. Allen Sanitarium, Inc. et al.
• Gore v. United States
– *These cases provided the legal foundation
for the practice of nurse anesthesia
• The 10th amendment to the US Constitution
gives states the right to enact laws to protect the
safety and health of their citizens
– Allows states the right to regulate
• public health
• welfare
• safety
– “The powers not delegated to the US by the
Constitution, nor prohibited by it to the States, are
reserved to the States, respectively, or to the people.”
• Dent v West Virginia, 1889
478
Malpractice policies
• Occurrence policy
– This type of policy covers the insured for all
acts within the policy period, regardless of
when the lawsuit was filed. This is generally a
preferred type of coverage.
• Claims made
– The insured must have coverage with the
same company at the time of the incident and
continuously through the date that the claim is
made or the lawsuit is filed.
Malpractice policies, cont’d

• Umbrella policy
– A policy that covers the insured after all other
underlying coverage is exhausted. For
example, if you have a general liability policy
with $1,000,000/event and a judgment is
rendered against you for $1,300,000, the
umbrella policy covers the extra $300,000.
Umbrella insurance does not cover other
claims that are otherwise not insured.
Malpractice policies, cont’d

• Tail policy
– Tails are obtained when policies are cancelled
(i.e. upon retirement or in the event of a job
change or a move to a different state). This
policy provides insurance benefits for events
that may have occurred during the time that
the insurance policy was in effect.
479
Liability coverage
• Typical coverage:
1,000,000/3,000,000
The maximum coverage for

The maximum coverage
any number of events in a
for one event in a policy
policy year Ö ”aggregate”
year
CRNA Scope of Practice

• The scope of practice of CRNAs includes,
but is not limited to, the following:
– Performing and documenting a preanesthetic
assessment and evaluation of the patient,
including requesting consultations and
diagnostic studies; selecting, obtaining,
ordering, and administering preanesthetic
medications and fluids; and obtaining
informed consent for anesthesia
CRNA Scope of Practice, cont’d

• Developing and implementing an anesthetic plan
• Initiating the anesthetic technique which may
include: general, regional, local, and sedation
• Selecting, applying, and inserting appropriate
non-invasive and invasive monitoring modalities
for continuous evaluation of the patient’s
physical status
• Selecting, obtaining, and administering the
anesthetics, adjuvant and accessory drugs, and
fluids necessary to manage the anesthetic
480
• Managing a patient’s airway and pulmonary

status using current practice modalities
• Managing emergence and recovery from
anesthesia by selecting, obtaining, ordering, and
administering medications, fluids, and ventilatory
support
• Discharging the patient from a postanesthesia
care area and providing postanesthesia follow-
up evaluation and care
• Implementing acute and chronic pain
management modalities

• Responding to emergency situations by
providing airway management,
administration of emergency fluids and
drugs, and using basic or advanced
cardiac life support techniques
• Additional nurse anesthesia
responsibilities which are within the
expertise of the individual CRNA
Statistics Review
481
Statistical Analysis Terminology
• Mean, median, mode

• Parametric vs. non-parametric
• Standard deviation
• Student’s T-test
• Analysis of a variance (ANOVA)
• Correlation
• Chi square
Definitions
• Sample Ö a grouping of individual
observations intended to yield some
knowledge about a population of concern,
especially for the purposes of statistical
inference
• Frequency distribution Ö a list of the

values of variables in a sample group
Parametric vs. non-parametric variables

• Parametric (quantitative data)
– Numeric variables
• Interval (no natural zero point; differences between
variables are meaningful but ratio is not)
• Ratio (true zero; both intervals and ratios between
data have meaning)
– Weight of 100 lbs is 50% less than weight of
200 lbs
– Discrete vs. continuous
– discrete: indivisible such as number of children
or episodes
– continuous: infinite number of values such as
weight
482
Parametric vs. non-parametric variables,
cont’d
• Non-parametric (qualitative data)

– Nominal (name)
• Values describe attribute of variables (i.e.
color of car, college major, etc.)
– Ordinal (ranking)
• Values describe ranking of variables; have
some natural order (1st, 2nd, greatest, least,
etc.)
Definitions, cont’d
• Blinding Ö
– prevents the subject, the person administering
the treatment, and those evaluating it from
knowing which treatment is being allocated
– ensures that the patient and/or the person
administering the treatment and/or the trial
evaluators are 'blind to' (don't know) which
treatment is allocated to whom
– avoids prejudice/distortion of the results of the
study – A.K.A. “bias”
• Placebo Ö
– an inactive treatment or procedure
– literal meaning = “I do nothing”
– “placebo effect”
• usually a positive or beneficial response
• attributable to the patient's expectation that the
treatment will have an effect
• occurrence rate of approximately 30%
483
• Randomization Ö
– the process by which experimental subjects
are allocated to treatments
• this process must be completely random and not
by any subjective/possibly biased approach
– randomization is preferable in studies since
alternatives may lead to biased results
Null hypothesis
• A hypothesis set up to be nullified or refuted in
order to support an alternative hypothesis
• The null hypothesis is presumed true until
statistical evidence in the form of a hypothesis
test indicates otherwise
• Used to test differences in treatment and control
groups
– the assumption at the outset of an experiment is that
no difference exists between two groups for the
variable being compared
Values of central location

• Mean - the average of the numbers in the
data set
– may be “skewed” with the presence of outliers
(extremely low or high values)
• Median - the central most number in the
data set
– a better indicator of centrality in the presence of
outliers
• Mode - the most frequently occurring
number in the data set
– best indicator of centrality with use of nominal
data
484
Standard deviation
• Statistic that illustrates how closely all of
the variables are clustered around the
mean in a set of data
– when variables are tightly bunched together
and the bell-shaped curve is steep, the
standard deviation is small
– when the examples are widely distributed and
the bell curve is relatively flat, this would
illustrate a relatively large standard deviation
The Bell Curve

standard deviations from the mean
1 1
2 2
3
3
*Į ± ³FULWLFDO
region” (tail of
distribution)
mean
* When values
fall into the
critical region,
reject the null
hypothesis frequency
Student’s T-test
• The t-test assesses whether the means of two
groups are statistically significantly different from
each other
• Appropriate for use when a comparison of the
means of only two groups is necessary
• May be of 2 types:
– paired—1 group is studied with 2 separate data
measurements (i.e. before and after a drug or
treatment is administered)
– unpaired or two-sample—compares the means of 2
separate groups (i.e. control vs. placebo groups)
485
Analysis of a variance (ANOVA)
• The ANOVA delineates if the mean of a
population is the same (the null hypothesis) or if
it differs between populations (the alternate
hypothesis) by looking at the variances between
2 or more groups
• Useful for larger study groups

– One-way ANOVA Öcompares several independent
groups of observations for variations in their means
– Two-way ANOVA Ö a method of studying the effects
of two factors separately (main effects) and together
(interaction effects)
Fisher’s Exact Test

• A statistical significance test used in the
analysis of categorical data where sample
sizes are small
• The need for the Fisher test arises when
data is divided into two categories in two
separate ways
• The test is used to examine the
significance of the association between
two variables in a 2 x 2 contingency table
Chi Square test

• Most widely used non-parametric test
• Tests a null hypothesis that the relative
frequencies of occurrence of observed
events follow a specified frequency
distribution
• Pearson's chi-square is used to assess
homogeneity, goodness-of-fit and tests of
independence
486
Correlation
• A relationship between 2 variables
• used to assess whether one variable
influences another
– positive correlation: beer sales at the ball park
increase as temperature increases
– negative correlation: beer sales decrease as
temperature drops
– no correlation: data does not follow a linear
pattern; is scattered randomly across the X
and Y ordinates
Correlation
Positive correlation Negative correlation
Notes
487

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Schedule of Lectures

8:00-­9:55 Physics;; anesthesia delivery systems;; monitoring

10:05-­11:45 Pharmacology — local anesthetics, inhalation agents

11:55-­12:30 Pharmacology — general principles of

1:15-­2:20 Cardiovascular review

2:30-­3:05 CV Pharmacology – sympathomimetics, alpha and

3:15-­4:20 Obstetric review

4:30-­5:25 Regional anesthesia and pain management

5:35-­6:45 Pharmacology — intravenous induction agents,

7:30-­8:10 Respiratory review I

8:20-­9:30 Respiratory review II

9:40-­10:45 CNS review

10:55-­12:15 Pharmacology — ANS, anticholinergics,

1:00-­2:15 Pediatric review

2:25-­4:00 Hematology;; musculoskeletal review;; MH

4:55-­6:00 Surgical procedures cont’d;; co-­morbidities

7:45-­8:50 Endocrine review

9:00-­10:45 Renal/hepatic review

10:55-­12:00 Pharmacology — diuretics, psychotropics,

12:45-­1:45 Anatomy/positioning review*

1:50-­3:45 Study/test taking skills and workshop, Q & A, wrap-­

*End of CRNA lectures

II. Equipment, instrumentation, and technology (15%)

III. Basic principles of anesthesia (30%)

IV. Advanced principles of anesthesia (30%)

Ideal Gas Laws

Desflurane 0.42 6.3 690

Blood-Gas Coefficient inversely correlates with induction speed

• Calculating Maximum Agent Concentration:

• Calculating Concentration in mmHg:

Nitrous Oxide Cylinder

The Anesthesia Machine

Nitrous & Other Gas Supplies

• Designed to read 33% higher than

• Heavy metal case and plate glass front in

• E-cylinder regulators designed to deliver

Fail-Safe Valve, O2 Alarm

• Oxygen Supply Failure Alarm

Oxygen Proportioning Systems

• Machines are equipped with devices to

• Proportioning systems only linked to N2O

Flush Valve & Gas Outlet

• Flush valve bypasses on-off switch

Vaporizer Output Regulation

• Variable bypass design allows a fraction of

100 cc of sevoflurane will last 333 minutes at 3L/m

Barometric Pressure Effects

• Decreases in barometric pressure cause

• Conversely, increases in barometric

APL & Unidirectional Valves

Waste Anesthetic Gases

• 10 exchanges per hour or more is required

• Fresh air enters the OR through ceiling

Fresh Gas Flow Coupling

I. The inspiratory baseline

II. Expiratory upstroke

III. Expiratory plateau

IV. Inspiratory downstroke

Increased Airway Resistance

8:00-9:55 Physics;; anesthesia delivery systems;; monitoring

10:05-11:45 Pharmacology — local anesthetics, inhalation agents

11:55-12:30 Pharmacology — general principles of

1:15-2:20 Cardiovascular review

2:30-3:05 CV Pharmacology – sympathomimetics, alpha and

3:15-4:20 Obstetric review

4:30-5:25 Regional anesthesia and pain management

5:35-6:45 Pharmacology — intravenous induction agents,

7:30-8:10 Respiratory review I

8:20-9:30 Respiratory review II

9:40-10:45 CNS review

10:55-12:15 Pharmacology — ANS, anticholinergics,

1:00-2:15 Pediatric review

2:25-4:00 Hematology;; musculoskeletal review;; MH

4:55-6:00 Surgical procedures cont’d;; co-morbidities

7:45-8:50 Endocrine review

9:00-10:45 Renal/hepatic review

10:55-12:00 Pharmacology — diuretics, psychotropics,

12:45-1:45 Anatomy/positioning review*

1:50-3:45 Study/test taking skills and workshop, Q & A, wrap-