Respiratory System PDF

Dr.
Azam’s
Notes in Anesthesiology
Postgraduates appearing
Updated up to December 2013, 3rd Edition for MD, DNB & DA Exams
Respiratory System
Edited by:
Dr. Azam
Consultant Anesthesiologist
& Critical Care Specialist
! !
www.drazam.com
! !
! 2
Dr Azam’s Notes in Anesthesiology 2013
Dedication
To Mohammed Shafiulla, my father, my oxygen, companion, and best friend; for

being my major pillar of support and making this vision a reality. Thank you for your
continual sacrifices with boundless love and limitless gratitude, for the sake of your
children. I owe you a debt I can never repay.
I also would like to thank my mom (Naaz Shafi), my wife (Roohi Azam), my two lovely
kids (Falaq Zohaa & Mohammed Izaan), for their support, ideas, patience, and
encouragement during the many hours of writing this book.
Finally, I would like to thank my teachers (Dr.Manjunath Jajoor & team) & Dr T. A. Patil . The
dream begins with a teacher who believes in you, who tugs and pushes and leads you to the next
plateau, sometimes poking you with a sharp stick called "truth."

A NOTE TO THE READER
Anesthesiology is an ever-changing field. Standard safety precautions must be followed, but as new research and clinical experience
broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the
most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the
method and duration of administration, and contraindications.
However, in view of the possibility of human error or changes in medical sciences, neither the author nor the publisher nor any other party
who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect
accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information
contained in this work. Readers are encouraged to confirm the information contained herein with other sources. It is the responsibility of the
licensed prescriber, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual
patient. Neither the publisher nor the editor assumes any liability for any injury and/or damage to persons or property arising from this
publication.
Dr. Azam

Respiratory System - Contents Dr Azam’s Notes in Anesthesiology 2013
1.Respiratory Physiology And Its Changes During Anesthesia - 7 28. Oxygen Toxicity - 83
2.Control Of Breathing - 36 29. Complications Of Oxygen Therapy - 85
3.Oxygen dissociation curve - ODC - 38 30.Pulmonary Function Test - 86
4.Oxygen Cascade - 40 31.Bedside pulmonary function test - 89
5.Oxygen Flux - 41 32.Describe functional residual capacity & Closing volume. Describe
6.Lung Compliance - 42 their clinical significance - 90
7.Discuss the anatomy of diaphragm with a diagram. How will it 33.Closing Capacity & Closing Volume - 92
behave under different stages of anesthesia - 45 34. Enumerate the effects of chronic smoking & the anesthetic
8.Describe the Anatomy of larynx? Discuss the effect of damage to implications - 93
recurrent laryngeal nerve vocal cord palsies - 47 35.Describe the techniques of chest physiotherapy? What is its role in
9.Respiratory Mechanics - 52 the post surgical period - 97
10.Respiratory movement in Anesthesia. - 53 36.Incentive Spirometry - 99
11.Abnormal Chest & Lung Movements - 54 37.Flow Volume Loops - 100
12.Changes in lung volume in various positions in anesthetized 38.Scoliosis -102
patient - 56 39. Discuss the assessment, preparation and problems of anesthesia
13.Surfactant - 57 in a chronic smoker for cholecystectomy - 107
14.Tracheo-Bronchial Tree with Diaphragm - 58 40.Enumerate Post operative Complications - 110
15.Hypoxic Pulmonary Vasoconstriction - 60 41. High Altitude & Anesthesia - 111
16.Hering–Breuer inflation reflex -62 42.Hyperbaric Oxygen Therapy (HBO) - 114
17.Airway Resistance - 63 43.High Altitude Pulmonary Edema - 118
18.Working of Breathing - 65 44.Anesthetic Management of patient with COAD - 117 & 186
19.Carbon-Di-Oxide Dissociation Curve - 66 45.Describe the causes & management of venous air embolism - 120
20.Dead Space - 68 46.Pulmonary embolism - 122
21.CO2 Response curve - 70 47.Deep Vein Thrombosis - 125
22.Mixed venous Oxygen saturation (SVO2) - 71 48.Amniotic Fluid Embolism - 127
23.Flail Chest - 73 49.Describe pathophysiology, clinical features diagnosis &
24.Tissue Oxygenation - 74 management of fat embolism - 129
25.Metabolic function of the lung - 77 50.Define Pulmonary Edema. What are the Clinical Features &
26.What are the major causes of Hypoxemia? What is Hypoxic Management of Pulmonary edema - 131
Pulmonary Vasoconstriction? How can general anesthesia 51.Bronchial Asthma - 133
worsens V/Q mismatch - 78 52. Bronchial Asthma in Pregnancy - 146
27.Humidification - 81 53.A 50 year patient with history of Emphysema posted for excision of
emphysematous bullae by VATS (Video Assisted Thoracic surgery).
Describe anesthetic management - 150
54.Options for Lung Isolation - 154
5

Respiratory System - Contents Dr Azam’s Notes in Anesthesiology 2013
55.Bronchial Blockers - 155

56.Complications of Thoracoscopy - 156
57.Double lumen tubes (DLT) - 158
58.One lung anaesthesia- problems and management - 162
59.Describe the Pathophysiology, diagnosis, clinical features &
current trends in management of ARDS - 165
60.Permissive Hypercapnia - 171
61.AUTO-PEEP - 172
62.Intercostal Chest Drain - 174
63.Broncho-pleural fistula - 177
64.Laryngospasm - 179
65.Bronchospasm - 180 .
66.A 30 year old female ASA grade I following exploratory
laparotomy is not maintaining oxygen saturation in the post
operative period. Discuss the causes & Management - 181
67.Discuss the preoperative evaluation and preparation of 55 year
old male with bronchiectasis scheduled for right lower lobe
excision - 182
68.Bronchography - 185
69.Pulmonary Aspiration - 189
70.Extracorporeal Membrane Oxygenation - 192
71.Pulmonary Hypertension - 194
72.What is Oxygen Delivery? Classify Oxygen Delivery systems.
Discuss the role of venturi Mask in oxygen therapy? - 197
73.Difference between the ODC curve & CO2 Curve?
74.Modes of Ventilation during Bronchoscopy
75.Indications, Contraindications, Preoperative consideration&
Anesthetic Management of Mediastinoscopy? - 200

1. Respiratory Physiology And Its Changes During Anesthesia. Dr Azam’s Notes in Anesthesiology 2013
Introduction: Pharynx:
• Anesthesiologists are directly involved in manipulating airway • Extends from posterior aspect of nose at base of skull down to level
and pulmonary function to a great extent than any other organ of lower border of cricoidʼs cartilage (C6). It is 10 cm long in adults
system. Thus, a sound and thorough working knowledge of and funnel shaped.
pulmonary physiology is essential to the safe conduct of Importance:
anesthesia. 1. Large adenoids can cause airway obstruction
Functional anatomy: 2. Pharyngeal bursa often impede passage of an E.T tube, if force is
• Structure and function of the respiratory system in relation to used the E.T. tube may penetrate the mucosa and create a false
anesthesia passage which can lead to bleeding, sepsis and post-op collection
Nose: of secretions.
• Deflection of normal septum may diminish lumen of respiratory 3. Peritonsillar abscess (quinsy) may cause difficult nasal intubation
airway and in some cases it is sufficiently severe to prevent the and dangerous as E.T. may be deflected sharply forwards or it may
passage of all but the smallest of E.T tubes. Before attempting impinge and rupture the abscess and lead to aspiration and
nasal intubation it is advisable to test patency of each nostril, the pneumonities.
side where the obstruction is greatest anteriorly often proves the • An unconscious patient following anesthesiashould be nursed on his
easiest to intubate. side unless contraindicated. In this position the tongue tends to fall
• Warming and humidifying the inspired air. away from the posterior pharyngeal wall and foreign material is less
• Endotracheal anesthesiais followed by a mild tracheitis. likely to enter the larynx.
Humidification of fresh gas flow can prevent it. Larynx:
• In most anaesthetic systems, the temperature of gases reaching • Lies at C3-6 in midline of neck. It is formed by a cartilaginous
the patients is approximately the same as the room temperature. skeleton held together by ligaments, lined by mucous membrane and
• To and fro system: where the temperature of canister may moved by muscle.
rise to as high as 450C and in which no time is available for • Larynx is made up on 3 unpaired & 3 paired cartilaginous structure:
cooling of gases enroute to the patient this system provides
3 Unpaired 3 paired
very efficient humidification.
• Circle absorption system: Here inspired mixture consists not Thyroid Cartilage Arytenoid cartilage
only fresh dry gases but some expired gases containing
water vapours at room temperature, but by the time they Cricoid cartilage Corniculate cartilage
traverse the apparatus they will have cooled to room
temperature and loose the water content in the apparatus, Epiglottis Cuneiform Cartilage
(exothermic reaction).

Describe the Anatomy of larynx?
Respiratory Physiology And Its Changes During Anesthesia. Continuation: Discuss
Dr Azam’s Notesthe effect of damage
in Anesthesiology to rec
2013
vocal cord palsies? Continuation:
Measurements Male Female Describe the Anatomy of larynx? Discuss the effect of damage to recurrent la
Ligaments:
Length 44 mm 36 mm
Blood Supply to Larynx:
Transverse 43 mm 41 mm
• Superior Laryngeal Artery: • Branch of
Diameter Cricothyroid
•Intrinsic Artery: superiorExtrinsic Ligaments:
• Supply up to
Dr Azam’s Notes in Anesthesiology 2013 Ligaments: the vocal cord
t of damage to recurrent laryngeal nerve • Cricovocal membrane thyroid •artery
Thyrohyoid membrane
AP Diameter 36 mm 26 mm
•• Quadrangular
Inferior laryngeal membrane • Cricotracheal membrane
• Cricothyroid
artery membrane • Branch •ofHypoepiglottic ligament
by ligaments • Supplies below
Inferior thyroid
Muscles of Larynx: the vocal cords.
artery
C3 to C6)
Cavities:
• Vestibule
• ventricle
Extrinsic Muscles: • Subglottic
Intrinsic Muscles:
• Abductor: • Sternothyroid Nerve Supply:
• Posterior cricoarytenoid • Thyrohyoid
Inlets of Larynx:
• Adductors: • Inferior constrictor ! • It extends from the laryngeal inlet to the! lower border of cricoid cartilages.
• Stylopharyngeus !"#$%&'()!(
• Lateral cricoarytenoid
• Transverse arytenoid • Palotopharyngeus Folds:
• Cricothyroid* • Aryepiglottic fold - Space between the aryepiglottic fold forms the larynge
!!!"#$%&'(&!)*&+,-%*).!/! !!!0%1#&&%,2!)*&+,-%*).!/!
• Thyroarytenoid * • Vestibule fold - Space between the vestibule fold is called as Rima Vestib
• Relaxors: • Vocal fold - Space between the vocal fold is called as Rima glottidis
• Thyroarytenoid* • Vallecula: Shallow space present in front of the epiglottis behind the base
• Vocalis !!!!!3,2%&,*)!4&*,15!!!!!!!!!!!
tongue. 9:2%&,*)!4&*,15!6;(2(&8! ?(2(&!4&*,15! "%,7(&+!4&*,15!
• Tensors: 67%,7(&+8!
us • Cricothyroid *
"#$$)'%7!)*&+,:! "#$$)'%7!25%! "#$$)'%7!*))!',2&',7'1! "#$$)'%7!*))!
*4(<%!)%<%)!(=!<(1*)! 1&'1(25&+('>!;#71)%7! %:1%$2!1&'1(25+&('>! 7#4-)(22'1!&%-'(,!!!
GRID: Question to be answered under following headings:
1(&>!
1. Definition
2. Measurements
3. Cartilaginous
4. Muscles
5. ligaments
6. Folds Dr Azam’s Notes in Anesthesiology 2013 8
7. Blood Supply Dr Azam’s Notes in Anesthesiology 2013
Dr Azam’s Notes
8. Nerve in Anesthesiology 2013
Supply
9. Nerve Supply & Nerve Palsies
Respiratory Physiology And Its Changes During Anesthesia. Continuation: Dr Azam’s Notes in Anesthesiology 2013
• During phonation, the vocal cord meets in midline, on inspiration Trachea: C5 to C 6

they abduct returning to midline on expiration, in order to • It is a tube made up of cartilage and enclosed posteriorly by tracheal
minimize risk of any trauma to cords, intubation and extubation muscle and lined interiorly by ciliated columnar epithelium. It is about
should be carried out during inspiration. 18mm in diameter and 10-11 cm in length in an adult.
Laryngeal paralysis may be classified as: • It extends from lower part of larynx C6 to T5, where it divides into
right and left bronchi.
• Organic Tracheo-bronchial tree:
A. Motor: unilateral/bilateral • Tracheal bifurcation occurs at a distance of approximately 25cm from
i) Incomplete: only abductors paralyzed upper incisor teeth in adults. Carina is a sharp shining ridge formed
ii) Complete: abductors and adductors paralyzed as a result of bifurcation of trachea into 2 principal bronchi.
B. Sensory: unilateral / bilateral • Carina acts as an anchor for double lumen tube. The trachea divides
i) Functional: functional aphonia: bilateral adductors into right and left principal bronchus. The right (25) is wider, shorter
paralyzed. about 2.5cm long more nearly vertical than left bronchus (45°) is
narrower, 5cm long.
• Thus there is much greater tendency for ET tubes and suction
Paralysed Position of catheters to enter this lumen and foreign bodies are more likely to
Extent Voice RespirationSwallowing enter it.
laryngeal.N vocal cord
Unilateral - Incomplete Median Normal Normal Normal • Each principal bronchus enters the lung through the hilum and
recurrent (abductor Hoarse divides into secondary (lobar) bronchi, one for each lobe of lungs
laryngeal.N palsy) Para median / Normal (3 on right and 2 on left side) each lobar bronchi divide into tertiary
- Complete
(segmental bronchi), one for each bronchopulmonary segment.
Bilateral Median / Normal Dyspnea Normal
recurrent Para median • Tertiary (segmental) bronchi divides repeatedly to form very small
(bilateral branches called terminal bronchioles and still smaller branches are
abductor called respiratory bronchioles.
palsy) • From the proximal part of terminal bronchioles gas exchange begins
Superior Uni / bilateral Cadaveric, Feeble Normal Aspiration and extends throughout succeeding generations of airways to the
with slack, wary / rough into larynx alveoli. This corresponds to the anatomical dead space and alveolar
recurrent
laryngeal.N dead space respectively. Each respiratory bronchiole aeriates a small
part of lung known as pulmonary unit or terminal respiratory unit /
acinus.
• The respiratory bronchiole ends in microscopic passages: Alveolar
ducts containing 2 or more pulmonary alveoli, atria, air saccules.
•

• These irregular dichotomous branching for about 23 generations

are called "Weibel's classification."
• There are about 300 million alveoli and 15 million alveolar ducts.
The acinus is the fundamental gas exchange unit of the lung.
• There are about 1,50,000 acini in human lungs it is 5mm in
length and 20-40 µl volume when lung is at functional residual
capacity.
There are 3 types of cells covering the alveolar surface.

Type I Alveolar cells:
• Occupy 80"% of surface for gas exchange spread a wide area,
provide a very thin layer of cytoplasm. They are derived
from type II cells, highly differentiated, metabolically limited,
and susceptible to injury, they have tight intercellular junctions.
Type II Alveolar cells:
• Extensive metabolic and enzymatic capacity, manufacture
surfactant, has tight ICJ, impermeable to fluids.
Type III alveolar cells:
• Are alveolar macrophages and play important role in lung
defenses, they contain proteolytic enzymes which are released
duringlung injury. Thus contributing to pulmonary damage.
Collateral ventilation: !
• Alveoli have holes in their walls called "pores of kohn" which
permits collateral ventilation between neighbouring alveoli;
similar large 30μm diameter ducts allow collateral ventilation
between respiratory bronchioles.
Alveolar capillary membrane:
• It exists between alveolar space and capillary lumen, consists of
alveolar epithelium, interstitial tissue and endothelium.
10

Functions: Major division of lungs:

1. Gas exchange across blood gas barrier Lung side/lobe Classification of Bronchopulmonary segment.
2. Fluid exchange between alveolar interstitial tissue and the I. Right (10)
capillary lumen. A. Upper Apical, Anterior, Posterior
Blood gas barrier:
B. Middle Medial, lateral
• It is barrier between alveolar gas and pulmonary capillary blood,
across which gas exchanges takes place. C- Lower Superior, Medial Basal. lateral basal, anterior basal, posterior
• It has 3 components: basal
• Alveolar epithelium, which is a thin layer of type I alveolar cell II. Left: -9
cytoplasm. Interstitial tissue consisting of fused alveolar and
A. Upper Apical posterior, anterior
endothelial basement membrane.
• Pulmonary capillary endothelium. B. Lingual Superior, Inferior
LUNGS C. Lower Superior, Posterior basal, Antero medial basal, Lateral basal.
• Each of these structures has the shape of a half cone; right side
weights 600 gms, Left side 550 gms in a healthy adult.
• They contain a high proportion of elastic tissue; this elasticity is Broncho-pulmonary segments: (BPS)
responsible for most of expiratory force in quite respiration. The • These are well-defined sectors of the lung, each one ofwhich is
loss of elasticity as in emphysema leaves the lungs permanently aerated by a tertiary/segmental bronchus. Each segment is
distended unless expiratory muscles are brought into play - a pyramidal in shape with its apex directed towards the root of the
situation causing expiratory embarrassment. lung. Each segment has its own separate branch of pulmonary artery
• Each lung lies free in its own pleural cavity, attached only to the and each segment has more than 1 vein and each vein drains more
mediastinum by its root. than 1 segment. Each segment is surrounded by connective tissue
Lobes of lungs: and thus each BPS are independent respiratory units. Thus
• Both right and left lung contain oblique fissures that separates pulmonary pathology initially tends to remain segmental.
upper and lower lobes, in addition the right lung has a horizontal • Working knowledge of BPS is important for localizing lung
fissure separating middle and lower lobes. pathology, interpreting CXR, operating on lungs, identifying lung
regions during bronchoscopy. Segments are no barriers to the
spread of Bronchogenic Ca.
• Abscesses are more common in posterior segment of right upper
lobe and apical segment of right lower lobe and its drainage of
infection by postural drainage (dependent portion).
• The lung parenchyma can be divided into 3 categories based on
functional anatomy.
11

Arterial supply of lungs: Clinical significance of surfactant:

Right side: Bronchial artery arising from 3rd posterior intercostal • Deficiency of surfactant causes respiratory distress syndrome.
artery. ( RDS)
Left side: 2 bronchial artery both arising from descending thoracic • Decrease in surfactant is seen in pulmonary embolism, drowning
aorta. hypoxia, acidosis, CPB, pulmonary lavage.
Venous drainage: • Surfactant replacement therapy as now been considered the
• Majority by Pulmonary veins and 2 bronchial veins for first and standard of care for those neonates with RDS who require
second divisions. mechanical ventilation.
Nerve supply: • Ex: Survanta. Exosurf neonatal.
• Parasympathetic: vagus. Nerve. RESPIRATORY MECHANICS
• Sympathetic: Spinal segments T2-T5. Respiration as the term is generally used includes 2 processes:
SURFACTANT: I. External respiration: The absorption of O2 and removal of CO2.
• Naturally occurring surfactant composed of several II. Internal respiration; the utilization of 02 and production of CO2 by
phospholipids, lipids and 4 or more specific apoproteins. cells and the gaseous exchange between the cells and the fluid
• Surfactant is secreted by type II alveolar cells, which lines the medium. It is also called "cellular respiration".
alveoli and acts mainly by reducing surface tension, tl/2: 14 III. Internal respiration includes; aerobic metabolism and anaerobic
hours. Approximately 90% of surfactant is dipalmitoyl metabolism.
phosphatidylcholine (DPPC) remaining phospholipids are Respiratory system:
phosphotidyl glycerol, phosphotidyl inositol. Cholesterol is the • It is made up of a gas exchange organ - the lungs and a pump that
predominant natural lipid in surfactant. ventilates the lungs.
• The 4 surfactant proteins A, B, C and D make up 5-10% of the Respiration is divided into 2 components:
total, their presence is essential for proper activity of pulmonary • Inspiration: an active process in which muscles of inspiration
surfactant. In the fetal lung surfactant appears at about 6months contract due to arrival of impulses from the respiratory centre, during
of gestation. which air from the atmosphere enters the lung. The muscles of
Actions: inspiration have to overcome the elastic recoil and the chest wall has
• Reduction of surface tension. to be moved out.
• Stabilization of small alveoli. • Expiration: a passive process, it occurs due to relaxation of
• Prevents transudation of fluid from capillary to alveoli. contracted muscles of inspiration, during which air moves from
• In the normal lungs due to the presence of surfactant the alveoli the lungs to the atmosphere. The elastic recoil of the lungs brings
are coated with surfactant which causes a decrease in surface them back to resting position.
tension as the alveoli deflate, the amount of surfactant per unit
area of alveolar membrane increases and so surface tension is
reduced even further and the contrary to what would be
predicted just on the basis of Laplace's law, the smaller alveoli
inflate more easily than the larger ones.
12

RESPIRATORY MECHANICS Muscular forces needed to expand the respiratory system:

Respiration as the term is generally used includes 2 processes: • Thorax: It is shaped like a truncated cone with small superior and
I. External respiration: The absorption of O2 and removal of large inferior openings and diaphragm attached at the base. The
CO2. predominant ventilatory change in thorax occurs in the A P.diameter
II. Internal respiration; the utilization of 02 and production of CO2 in the upper thoracic region and in the lateral direction in the lower
by cells and the gaseous exchange between the cells and the portion of the thorax.
fluid medium. It is also called "cellular respiration". Muscles of ventilation:
Internal respiration includes; aerobic metabolism and anaerobic A. Muscles of inspiration:
metabolism. • Diaphragm about (75-80%) - major muscle of inspiration
Respiratory system: • External intercostals about (15-20%) - it elevates ribs for inspiration
• It is made up of a gas exchange organ - the lungs and a pump • Accessory muscles, which will work only when pulmonary ventilation
that ventilates the lungs. increases by 100lit/min. They include: sternocleidomastoid, scalene
Respiration is divided into 2 components: muscle, pectoral muscles, back muscles, muscles of posterior neck.
• Inspiration: an active process in which muscles of inspiration • Other muscles that decrease the resistance of airflow include
contract due to arrival of impulses from the respiratory centre, mylohyoid, digastric, alaenasi, platysma, cheek and laryngeal
during which air from the atmosphere enters the lung. The muscles.
muscles of inspiration have to overcome the elastic recoil and B. Muscles of Expiration:
the chest wall has to be moved out. • They begin to function only when pulmonary ventilation increases by
• Expiration: a passive process, it occurs due to relaxation of 70 to 90 L/min.
contracted muscles of inspiration, during which air moves • Abdominal muscles - rectus abdominis, external and internal oblique,
from the lungs to the atmosphere. The elastic recoil of the transverse abdominis; facilitate active expiration.
lungs brings them back to resting position. • Internal intercostals muscles - lower ribs for forced expiration.
Respiratory mechanics refers to the study of factors involved in Diaphragm:
altering lung volume, which includes: (A) Muscular forces needed • Dome shaped muscle that separates the thoracic cavity from the
to expand the respiratory system. (B) Mechanics of ventilation. (C) abdomen. It is a major muscle of inspiration. It has 3 portions:
Determinants of lung volume and its subdivisions. • Crural part: Stabilize central tendon and generates downward
movement of diaphragm.
• Sternocostal part: Acts to lift and expand the lower rib cage.
• Central tendon: into which both muscular parts are inserted have a
complex bi-domed shape and a central narrow portion so that 2
halves can act independently.
13

Adult diaphragm is composed of 3 types of skeletal muscle fibers. Abnormalities of movement of diaphragm:
1. Type I fibres (55%): slow oxidative, red resistant to fatigue, A. If diaphragm is paralyzed on one side due to damage/blockade
these contain high concentrations of mitochondria, oxidative of phrenic. N, the negative intrathoracic pressure will cause
enzymes, numerous capillaries high myoglobin content which paralyzed portion to move up instead of down.
gives the muscle a dark red colour. They are endurance fibres, B. Pressure form below- as in advanced pregnancy, obesity, and
resistant to fatigue and are deficient in infants. intra abdominal pathology will impede free movement of
2. Type IIa (Fast oxidative) (20%) diaphragm.
3. Type II b (Fast glycolytic white fibres) (25%): they have few C. Following upper abdominal surgery, pain limits movement of
mitochondria, high concentration of glycolytic enzymes, and diaphragm.
large stores of glycogen. They are white due to fewer blood D. Advanced emphysema, increases lung volume causes
vessels, little myoglobins. They are larger, can generate more diaphragm to be pushed down in resting phase, so that it is at a
force, but fatigue easily. mechanical disadvantage, works inefficiently and increase in
Actions: Contraction of both costal and crural fibres causes WOB.
diaphragm to descend, decreasing pleural pressure and raising E. The supine position and induction of anesthesia has been
abdominal pressure, which associated with basal atelectasis because the closing capacity
in turn expands the lower ribcage and contributes to inspiration. encroaches on FRC so the FRC decreases and increase in A-a
• In normal subjects, the diaphragm is approximately a gradient leads to hypoxemia.
hemispherical dome at the end of expiration: but as the central F. In ICU patients on prolonged mechanical ventilation,
tendon descends and the zone of apposition decreases, it diaphragmatic dysfunction can be reduced by giving adequate
resembles a flattened sheet. time to relax the diaphragmatic fibers and this helps in
Functions: increasing the blood supply to the diaphragm, which is helpful in
• Most important inspirarory muscle. weaning the patient.
• Responsible for 60-75% of tidal volume during quite breathing. Basic mechanism of breathing: !
• In quadriplegics, high neuraxial blocks we see that intercostals • The periodic exchange of alveolar gases with fresh gas from upper
muscles do not act during inspiration. Decrease in airway reoxygenates desaturated blood and eliminates CO2. This
intrapleural pressure leads to paradoxical inward movement of exchange is brought about by small cyclic pressure gradients
ribcage and fall in tidal volume. established within the airways. This includes intrapleural pressure
and alveolar pressure.
14

• Spontaneous ventilation: at the start of inspiration intrapleural

pressure is -5cm, H2O during inspiration it decreases to -7.5cm H2O
and during expiration the diaphragmatic relaxation returns
intrapleural pressure to - 5cm H2O. At the start of inspiration
alveolar pressure is 0 cm H2O during inspiration it decreases to -3 to
-4 cm H2O, which causes air into the lungs until pressure becomes
zero. And during expiration alveolar pressure changes to +1 to +3 cm
H2O, this causes elastic recoil of lung, so there is movement of air
from lungs to atmosphere, which continues till alveolar pressure,
becomes zero.
Ptranspulmonary = Palveolar – Pintrapleural
Mechanical ventilation:
• IPP is used at upper airway, during inspiration, the gas flows into
alveoli, until alveolar pressure reaches that in upper airway. And
during expiration phase of the ventilator, positive airway pressure is
removed and the gradient reverses allowing gas flow out of the
alveoli.
ABNORMAL CHEST AND LUNGMOVEMENTS
When the stability of the thoracic cage is destroyed either by trauma/
surgical intervention, then abnormal movements of both chest wall and
underlying lung may occur.
There are 3 principle conditions that must be considered.
a) Paradoxical respiration: due to crush injury of the chest /surgical
removal of part of ribcage, the affected chest wall collapses in
wards. On inspiration, the unaffected side will expand in the normal
fashion but the injured side will be sucked in. On expiration, the
reverse takes place. So thus called "paradoxical respiration".
b) It is seen in patients breathing spontaneously and abolished by
controlled ventilation. It is an indication for artificial ventilation.
b) Pendelluft: signifies pendulum like movement of air that occurs
from one lung to the other in the presence of an open pneumothorax in
a patient breathing spontaneously.
The lung on normal side fills with air partly from the trachea and partly
from the partially deflated lung on the affected side due to loss of
intrapleural pressure. On expiration, the converse takes place and
some expired air form the normal lung passes over into the other 15 side.
Consequence: rebreathing increases, alveolar CO2 tension increase.
c) Mediastinal flap: When pleural cavity is opened, lung Induction of anesthesia activates expiratory muscles and expiration
collapses and the pressure around it becomes atmospheric, the becomes active. So it necessitates Selicks maneuver during induction
negative intrapleural pressure on the other side, will pull the heart of anaesthesia.
and great vessels in the mediastinum towards the sound lung, 2. Tracheal tug: in deep anesthesia inspiration is associated with a
seen maximum during inspiration. On expiration the intrapleural trachea tug. This is a sharp downward movement of the trachea on
pressure becomes less negative and mediastinum passes back to inspiration due to sharp contraction of the central part of the diaphragm
its original position. or failure of elevator muscles of larynx to standup to the forceful
Consequences: It is dangerous in lateral position, as the whole contraction of the diaphragm It is seen in deep anesthesia, respiratory
weight of mediastinal contents is compressing the dependent obstruction. It is an indication for E.T. tube suction or bronchoscopy.
normal lung. It interferes with the filling of great veins, leading to 3. Sigh: For every 7 normal breaths one deep inspiration is taken this
decreased cardiac output. is known as sigh. It is seen in conscious and deep anesthesia.
Management: 4. Hiccup: It is an intermittent clonic spasm of the diaphragm, of
• All three abnormal chest and lung movements can be treated by reflex origin. It is transmitted via vagus nerve. It can be caused by
mechanical ventilation (IPPV). inflation of stomach with anaesthetic gases irritation below diaphragm
Diffusion respiration: (DR)! due to blood or pus.
• If the N2 in the lung is replaced by O2, there is adequate uptake • It is a reflex response of the partially anaesthetized respiratory
of O2 in the blood, in the absence of respiratory muscle activity. centers and incompletely paralyzed peripheral musculature to vagal
This process is known as "diffusion respiration". stimulation.
• The CO2 is not removed form blood and tension of CO2 Management:
increases rapidly to 46 mm Hg. But there after more slowly at • Block the reflex pathway by deeper level of anesthesia with
approximately 3mm Hg/min. This is seen during "Jet supplementation with analgesic, potent inhalational anesthetic.
ventilation". • In post op period: phenothiazine, initiation of following reflex with
RESPIRATORY MOVEMENTS IN ANAESTHESIA both nose and ears blocked and patients sips repeatedly from a
• During spontaneous ventilation, halothane has an enormous glass of water.
effect on the • Local anesthetic infiltration of phrenic .N. in the neck should be
• rib cage contribution but little effect on the diaphragm of the total considered.
respiratory movement.
• When a patient is placed supine from an upright position, the
proprotion of breathing from rib cage expansion decreases
and abdominal breathing predominates, diaphragm contracts
more effectively.
• Lateral decubitus position, ventilation favours, the dependent
lung because dependent-hemi diaphragm takes a higher position
in the chest.
16

Breath holding: Compliance:

• Most adults with normal lung and gas exchange can hold their Elastic recoil is usually measured in terms of compliance (C)#
breath for approximately 20 to 30 sec, when breathing room air
previously without hyperventilating. The breakpoint at which Compliance(C)= = Change in volume/ change indistending
normal people feel compelled to breath is constant at a PaCO2 pressure ΔV/ΔP
of 50 mm Hg. • The lungs and thoracic wall function as a single unit, and provided
• Prior 100% O2 breathing, breath holding can extend to 2-3 mins the tidal volume is in the normal range. Compliance can be obtained
and prior, hyperventilation can extend apnoeic period to for either the chest, or the lung or both together.
6-10mins.
• The duration of breath holding is directly proportional to the
oxygen stores alveoli and rate at which PaCO2 rises. A) Lung compliance (CL) =
• Mild hyperventilation during G.A. will produce prolonged apnoeic CL = 150-‐200 ml/cm.H2O, CL is inversely proportional to WOB.
period. The pressure gradient is measured between airway and pleural space.
Importance: CLcan be measured by: #
• It indicates the individualsʼ cardiopulmonary reserve, if breath a) Static compliance b) Dynamic compliance.
holding less than 10 sec it indicates poor cardiopulmonary a) Static compliance or elastic resistance: is measured when there is
reserve. no air flow. It reflects elastic properties of the lung and chest wall.
B) MECHANICS OF VENTILATION:
• The movement of the lungs is passive and determined by
impedance of the respiratory system, which can be divided into: Static compliance (CST) =
I. Elastic resistance of tissues. – compliance Change in static compliance invokes similar change in the dynamic
II. Gas liquid interface. compliance. Eg. Atelectasis, ARDS, tension pneumothorax, retained
III. Non-elastic resistance to gas flow. – Airway resistance secretions.
I) Elastic resistance of tissues: b) Dynamic compliance: Is measured when air flow is present. It
• Both the lungs and chest have elastic properties, the chest has a reflects both airway resistance (non elastic resistance) and elastic
tendency to expand outward, while the lungs have a tendency to properties of the lung and chest wall (elastic resistance).
collapse. The recoil properties of the chest are due to structural
chest wall muscle tone. CDYN =
• The surface tension forces tends to decrease area of inter face • Change in dynamic compliance is independent without
and favours alveolar collapse. Alveolar collapse is directly corresponding change of static compliance. Eg. Bronchospasm,
proportional to surface tension but inversely proportional to the Kinking of ET rube, airway obstruction.
alveolar size.
Laplace formula: Pressure = 2 x wall tension / radius.
17

PRESSURE VOLUME LOOP FOR THE RESPIRATORY SYSTEM

B) Chest wall compliance: 200mlcm. H2O
• If a pressure volume curve for the respiratory system is plotted
• Tran thoracic pressure = Atmospheric pressure - intrapleural through a cycle of inspiration and expiration, a loop is obtained. As
pressure. the inspiratory and expiratory limbs of the curve do not exactly
! coincide. This loop effect is known as "Hysteresis", the area of loop
C) Total thoracic compliance (CTOTAL): representing the energy expanded / wasted, as heat is moving
• It is the sum of reciprocal of lung and chest wall compliance. through the inspiratory-expiratory cycle.
• 1/CTOTAL= 1/Cw+ 1/Cl= 100 ml /cm. H2O • In emphysema: lung compliance increases, during inspiration,
• The pressure gradient to be measured is that between the airway resistance is almost normal and lungs inflate easily. The equal
airway and the atmosphere. pressure point occurs at a more distal location in smaller airways.
• It is measured in a patient who is relaxed and ventilated, either • The Trans pulmonary pressure is low. It may proceed to ventilatory
with the aid of a: (a) tank ventilator, (b) E.T. tube method. insufficiency and finally to failure of the gas exchange function of the
Work of breathing (WOB): ! lungs.
• WOB is the energy required to ventilate the lung. WOB = P x V. • Pulmonary fibrosis: lung compliance decreases, limits expansion of
The work of inspiration can be sub divided into: a) work the lung and decrease in VC and decrease RV. Here the, flow
required to over come elastic resistance of lung. b) Work volume curve is narrow and shifted to the right compared to the
required to over come air way resistance. c) Work required to predicted normal curve for that patient. Here the PEFR and flow rate
over come tissue resistive work. are WNL. The down slope of the curve, showing the decline of flow
• In ideal elastic lung: inspiration and expiration would occur along rate as volume decreases, is steep because lung volume is small
the straight line AFB and equalamounts of inspiratory work done and the slope is nearly linear.
and expiratory work is represented by area AFBCD. Non-elastic resistance:
• In real lung with tissue and airway losses, inspiration occurs Gas flow in the airways: Movement of gas in and out of the lungs is
along curve AGB; the inspiratory work done (AGBCD) is thus > produced by the transpulmonary pressure and is conducted through
than ideal case. Total wasted energy due to tissue and airway the airways. The ease with which gas moves through the airways
losses is thus, the sum of the shaded and hatched areas or the depends on: a) Airway resistance b) Pattern of gas flow.
area of the loop. a) Airway resistance: It is the degree of airflow obstruction in the
airways. It is the pressure needed to generate a given inspiratory flow.
Airway resistance (Raw) = Pressure change (deltaP) / Flow (V) =
0.6-2.4 cmH2O/L/sec.
Increased airway means increase WOB.
• Poiseuille's law: deltaP = γ/r4 The driving pressure (deltaP) to
maintain the same an flow (V) must increase by a factor of 16-fold
when the radius (r) of the airway is reduced only half of its original
size.
18

• Raw proportional with length of ET tube and Raw inversely • Turbulent flow: Characterized by random movement of gas
proportional with diameter of ET tube. molecules down the air passages
Location of Raw: Principal sites of resistance to gas flow are the • Pressure gradient = flow2 X Gas density /r4
nose, major bronchi. • Occurs in laryngeal opening, trachea, large bronchi (generations
Factors affecting Raw: 1-5). It is usually audible.
1. Lung volume: increased LV leads to decrease Raw, thus • Turbulent / laminar flow occurring can be predicted by the
patients with high Raw often increase their FRC by position / "Reynoldsʼs number" = Linear velocity x diameter x gas density /
pursed - lip breathing, (emphysema). gas viscosity. Low Reynoldsʼs number ( < 1000) is associated with
2. Bronchial smooth muscle tone: Vagal stimulation, Hypoxia, laminar flow, whereas > 1500 produces turbulent flow.
histamine causes bronchoconstriction and increases airway • Orificial flow: depends on density of the gas, it occurs at larynx
resistance(Raw). either absolute/relative size may reflect the effects of
3. Lower airway obstruction: Like mucosal edema, mucous cardiopulmonary disease.
plugging, foreign bodies, increase Raw. • The term "volume" refers to one of the 4 primary
4. Upper airway obstruction: secondary to decreased level of (nonoverlapping) subdivisions of the total lung capacity. The term
conscious, position of head, neck /jaw, adenoids / tonsils: "capacity" refers to one of the 4 lung compartments that is measured
increase Raw. by tests of pulmonary function. Each capacity consists of 2 or more
5. Anaesthesia: Raw doubles during anesthesiadue to decrease primary volumes.
FRC, E.T. tubes, connection of circuit. Cyclopropane, • Most of the lung subdivisions are measured from resting midposition-
morphine: increases Raw. Ether, Halothane: decreases Raw. the respiratory level of a resting subject, who is paralyzed.
Measurement of Raw: Midposition defines the volume of gas in the lungs at end of a
1) by simultaneous recording of airflow and the spontaneous expiration. Lung volumes vary with age, sex, and body
pressure gradient between mouth and alveoli. size related to height.
2) Body plethysmograph • In 1846 Hutchinson devised the first spirometer and
3) FEV1, PEFR, midexpiratory flow rate. described the compartments of lung volume and measured Vital
Pattern of gas flow: capacity.
3 types: i) Tubular / Laminar ii) Turbulentiii) Orificial.
• Tubular / Laminar: Consists of concentric cylinders of gas
flowing at different velocities, velocity is highest in centre and
decreases towards the periphery It occurs in small airways (< 1
mm)
• Laminar flow = pressure gradient / Raw
• Raw = 8 x length x gas velocity / πr4
19

DETERMINANTS OF LUNG VOLUME AND ITS SUBDIVISIONS:

• They are basically anatomic measurements; however, alterations in
either absolute/ relative size may reflect the effect of
cardiopulmonary disease.
Lung capacities:
Vital capacity:
• Is determined by the strength of the respiratory muscle and chest
and lung compliance. VC<10ml/kg is indicative of impending
respiratory failure. It is decreased in chronic bronchitis, pregnancy,
abdominal splinting, and myasthenia gravis.
Inspiratory vital capacity:
• Defined as maximum volume of air that can be inhaled after the
fullest possible expiration. In obstructive pulmonary disease, FVC /
VC > 10% difference is said to have air trapping during expiration.
Functional Residual capacity:
• At this volume, the inward elastic recoil of lung approximates the
outward elastic recoil of chest. It can be measured by nitrogen wash
out / helium wash-in technique, body plethysmography. FRC
decreases with age, posture, anaesthesia, surgery, pulmonary
edema, obesity, decrease muscle tone. FRC increases with
emphysema, asthma.
Closing capacity:
• Lung volume at which airway begins to close in the dependent parts
of the lung.
• CC = Closing volume + Residual volume = 900+1200 - 2100 ml.
20

• FEV1: Volume expired in the first sec, FEV1/FVC: normal > 95%
and declines with age and 85% may be acceptable in an elderly
patient.
Maximum breathing capacity:
• Maximum volume of air that can be breathed per minute, usually
measured for 15 seconds. Normal: 100-200-lts/ min. It is decreased
with the age, emphysema, and bronchospasm.
Peak expiratory flow rate:
• After maximum inspiration, the patient expires forcefully as much as
he can and maximum flow rate of air is measured. It is done by
pneumatochography, Wright peak flow meter.
• Normal: men 450-700 1/min, women: 300 - 500 1/min.
Changes in lung volume in various positions inflicted upon
anaesthetized patient:
• Supine position: When conscious person changes from erect to
supine position, FRC decreases by 0.5 - 1L, because abdominal
viscera press against the diaphragm and 4 cm cephaloid shift of
• CV = closing capacity - residual volume = 2100 - 1200 = 900 ml. diaphragm occurs.
CC is measured using a tracer gas Xe-133 and N2 wash out • During anaesthesia, cephaloid shift of diaphragm is due to muscular
technique. It is unaffected by posture. paralysis. During IPPV, gas moves along the line of least resistance,
Significance: to the less congested and more compliant substernal units of the
• As CC rises FRC, arterial hypoxemia occurs due to intra - superior lungs are inflated preferentially.
pulmonary shunting of deoxygenated blood. It can be avoided by
• Horizontal position: Gravity increases perfusion of dependent i.e.,
1) PEEP application. 2) Airway collapse occurs. posterior lung segments. Spontaneous ventilation favors dependent
• CC increases with aged, smokers, obesity, LVF, asthma, lung segments and controlled ventilation favors independent i.e.,
emphysema CC decreases with supine posture, anaesthesia. anterior segments. FRC decreases and may fall below C.V.
CC = FRC in elderly, infants.
• Prone position: Compression of abdominal and thorax decreases
Dynamic lung volumes:
total lung compliance and increase WOB. Mechanical ventilation in
• Lung volumes can also be measured by its dynamic prone position improves oxygenation in ALI / ARDS, as it re-aerates
performance during active inflation / deflation it includes: 1)
the dorsal lung units, which are collapsed - consolidated, when in
Forced VC (FEV): is the total volume of gas that can be forcibly
supine position, due to weight of overlying heart and high pleural
expired after maximal inspiration, it is described by the maximum
pressures dorsally. V/Q matching and oxygenation are improved in
mid expiratory flow rate which applies to the gas volume expired
prone position, which leads to decrease in inspired oxygen
between 25 and 75% of the total (MMEFR25-75).
concentration and decreases the MAP and increases
outcome in ALI / ARDS.
21

• Lateral decubitus: There is decrease volume of dependent • Apneustic centre: lies in lower pons, it is excitatory and is
lung but there is increase in perfusion. Increase ventilation of overridden by the pneumotaxic centre.
dependent lung in awake patients, while there is decrease • The pontine centers appear to fine tune R.R and rhythm. Transection
ventilation of dependent lung anaesthetized patient. of pons just below pneumotaxic centre causes slow gasping.
• Trendelenburg position: decrease in lung capacities due to • Expiratory centre: situated ventrally on each side of medulla,
shift of abdominal viscera, increase V/Q mismatch and stimulated causes expiratory muscle activity.
atelectasis, decrease FRC, decrease pulmonary compliance. • The primary goal of respiratory control is to maintain homeostasis of
• Reverse trendelenburg position: increase FRC, spontaneous blood gases, allowing speech, enable coughing, sneezing, yawning,
ventilation requires less work. minimize WOB, protect airway during eating, drinking, vomiting.
• Lithotomy position: VC decrease, more chance of aspiration.
• Sitting position: increase in LV, increase FRC, increased
WOB.
CONTROL OF BREATHING
• Spontaneous ventilation is the result of rhythmic neural activity in
respiratory centers within the brainstem. This activity regulates
respiratory muscles to maintain normal O2 and CO2tensions.
• The basic neuronal activity is modified by inputs form other areas
in the brain: volitional, autonomic as well as various central and
peripheral receptors (sensors).
Central respiratory centers:
• Inspiratory centre: lies in the dorsal part of the medulla on each
side, they generate basic rhythm of respiration.
• 2 medullary groups of neurons are recognized they are i) dorsal
respiratory group: Primarily active during inspiration, ii) ventral
respiratory group: active during expiration.
• Close association of the dorsal group of neurons with tractus
solitarius may explain reflex changes in breathing from vagal /
glossopharyngeal. N stimulation.
• Pneumotaxic centre: lies in upper pons, it is inhibitory and
transmits impulses to the inspiratory area and produces a faster
respiratory rate.
22

Central sensors: (central chemoreceptors – CR) Golgi tendon organs:

• They respond to changes in CSF H+ ion concentration. They lie • Are plentiful in intercostal muscles are involved in pulmonary stretch
on anterolateral surface of medulla. It is effective in regulating reflex that inhibits further inspiration.
PacO2 because BBB is permeable to dissolved CO2 but not to Muscle spindles:
HCO3 ions. • In the inspiratory muscle and diaphragm contribute to depth and
• Increase in PaCO2 causes increase in CSF H+ ion concentration effort during inspiration. They sense dyspnea and are activated in
which in turn activates the central CR, which stimulates the airway obstruction.
respiratory' medullary centre and increases alveolar ventilation RESPIRATORY TRACT REFLEXES
which decreases PCO2 back to normal. The reverse occurs Inflation: (Herring - Breuer in 1868)
during decrease PCO2. • Pulmonary stretch receptors are responsible for this reflex; these
• The PaCO2 at which ventilation is zero is called receptors are found in the airway smooth muscles without end
"apnoeic threshold". Spontaneous respiration is absent under organs.
Anesthesia when PaCO2 falls below "apnoeic threshold". • Inflation of the lung inhibits the spontaneous contraction of the
Peripheral sensors: diaphragm.
Peripheral chemoreceptors: Deflation
• They include carotid bodies and aortic bodies. They are sensitive • During expiration the tonic discharge of stretch receptors diminishes
to change in PaO2, PaCO2 pH and arterial perfusion pressure. so that inspiration can start again. These receptors lie principally in
They interact with central respiratory centers via alveoli, terminal bronchioles.
glossopharyngeal nerve producing reflex increase in alveolar Paradoxical reflex
ventilation due to hypoxia, increase in H+ ion, and increase • Described by Head, it can only be demonstrated when vagus nerve
PaCO2, cyanide, nicotine, and doxapram. is partially blocked. Inflation of lungs under this conditions leads to
• If PaO2 decreases below 50mm Hg, the peripheral CR activity is strong diaphragmatic contraction, it is opposite of normal inflation
increased. reflex, so it is termed as paradoxical. This reflex may account for the
Lung receptors: primitive gasp in newborn when the lungs are first inflated.
• Impulses from these receptors are earned centrally by vagus PULMONARY GAS EXCHANGE
nerve. • The function of respiratory system is to provide an adequate supply
Irritant receptors: of O2 to the tissues and to regulate excretion of CO2, so as to help
• In the tracheobronchial mucosal react to noxious gases, dust, maintain a normal acid base state. 3 principal factors are concerned
smoke, cold gases. Activation of these receptors causes in their function, namely: I) Ventilation II) Pulmonary blood flow /
increase in R.R., bronchoconstriction, coughing. Pulmonary circulation. Ill) Diffusion of gases.
J- receptors:
• Located in interstitial space within the alveolar walls, they induce
dyspnea.
23

Ventilation: Alveolar VD:

• It is the process of fresh gas reaching the areas of the lung • It contributes to wasted ventilation, it occurs when the ventilated
where gas exchange takes place. Gas exchange is dependent alveoli are not adequately perfused by the pulmonary circulation. It is
on total / minute ventilation = RR x tidal volume = 5 L/min. in an negligible in normal physiological condition. Alveolar VD is increased
average adult at rest. in pulmonary embolism, CHF, pulmonary vasoconstriction.
Physiological dead space:
DEAD SPACE (VD): • It is sum of anatomic and alveolar dead space volumes. Under
• That part of tidal volume not participating in alveolar gas normal conditions, the physiological VD approximately equal to
exchange is known as VD / wasted ventilation. A condition in anatomic VD.
which ventilation is in excess of perfusion. It includes 3 types of Conditions that increase physiological VD:
VD: • NM Disease, CHF, pulmonary embolism, old age, upright posture,
Anatomic VD: atropine, asthma.
• It corresponds to the conducting airways, which contribute to Bohr's equation: VDphys/ VT = PaCO2 - PECO2 / PACO2 = 0.25-0.40 or 33%.
about 30% (150ml) of dead space in an adult, i.e., 2ml / kg, of Apparatus dead space:
their volume is wasted since it does not take part in gas • Gas contained in any anaesthetic apparatus between the patient and
exchange. that point in the system where rebreathing of exhaled CO2 ceases to
Increase Anatomic VD: occur. This may add upto VDphys further decreasing alveolar
• Old age, protrusion of jaw with extension of head, ventilation and it is very hazardous in anaesthetized pediatric patient.
anticholinergics, upright posture, and asthma Upto 125 ml of VD can be added to the space in a Magill system.
Decrease Anatomic VD: • Importance of Dead space: 1) VD/VT = 0.3-0.45 in ventilated,
• Young women, tracheostomy, and supine posture. intubated, anaesthetized patients. 2) VD is more when mask (0.68) is
• It is measured noninvasively by Fowler's method: Patient takes used as compared to intubation (0.5). 3) If VD/VT< 60% reflects
a single VC breath of 100% O2, exhales through a rapid N2 normal ventilatory function upon weaning from mechanical
analyzer. Expired N2 concentration is then plotted against ventilation. 4) If VD/VT>60% causes inefficient ventilation, muscle
expired volume. It has 3 phases: fatigue, ventilatory and oxygenation failure.
• Phase - 1: Free of N2 being pure oxygen,
• Phase - II: N2 concentration increases with introduction of
alveolar gas
• Phase - III: alveolar plateau achieved. Anatomical VD = Phase
II / Vertical line such that Area A = Area B and measuring the
volume from zero.
24

DISTRIBUTION OF VENTILATION • Normal blood flow within the lungs / total perfusion (Q) is 5 lt/min.
• Regardless of body position, alveolar ventilation is unevenly Normal pulmonary arterial pressure has systolic value of 20-30 mm
distributed in the lungs. The Rt. Lung receives (53%) ventilation Hg and diastolic pressure 8-12 mm Hg, mean pulmonary capillary
than the left one (47%) and lower (dependent) areas of both pressure is 10 mmHg with a pulmonary venous pressure of 4mm Hg
lungs tend to be better ventilated than do upper areas because at heart level.
of a gravitationally induced gradient in intrapleural pressure. The • Pulmonary artery and right ventricle pressures are not increased by
- normal VA is 5250 ml/ min. increase in CO demonstrating the distensibility of the pulmonary
• Because of a higher transpulmonary pressure, alveoli in upper vasculature. Increased pulmonary blood volume is seen in: Supine
lung areas are near maximally inflated and relatively non- position, over transfusion, LVF. Decrease pulmonary blood volume is
compliant, and they undergo little more expansion during seen in: upright posture, valsalva's maneuver, after haemorrhage.
inspiration and smaller alveoli in dependent areas have a lower Measurement of pulmonary flow: 4 principal methods: I. Use of
transpulmonary pressure and are more compliant, and undergo radioactive gases, 2. Direct Fick method 3. Indicator - dilution method.
greater expansion during inspiration. 4. Body plethysmograph.
Lung inflation = Total compliance x Airway resistance. Hypoxic pulmonary vasoconstriction (HPV):
Pulmonary circulation; • It is an important mechanism to improve the match between V and Q
• It is a low pressure, low resistance system in series with the right by diverting blood from poorly ventilated areas to better-ventilated
ventricle. The cardiac output from right ventricle passes through areas. Alveolar hypoxia, results in vasoconstriction and a decrease in
the pulmonary artery, which is a thin walled structure and it blood flow in those vessels supplying the hypoxic area, so that the
divides immediately into right and left branches and then blood is diverted to oxygenated parts of the lung.
dividessuccessfully following the conducting airways down to • HPV maintains the V/Q balance on a breath-to-breath basis. The
terminal bronchioles, these small branches give rise to a dense predominant site of HPV lies in the small pulmonary arteries
capillary network that maintain stability of the alveoli. (30-50µm), capillary bed and venous system. Low PAO2 levels are
• The oxygenated blood is collected by venules that run between responsible for generalized HPV in the fetus, which leads to
the lobules and then unite to form 4 pulmonary veins that drain decrease blood flow through the pulmonary vascular bed to about
into left atrium. The pulmonary musculature is supplied by 10-15% of the foetal cardiac output and also at high altitude. Exact
sympathetic N.S with α-adrenergic fibres producing mechanism of HPV is unknown.
vasoconstriction and β-adrenergic fibres vasodilatation. Drugs modifying HPV reflex:
Parasympathetic via vagus N causes vasodilatation. • Decrease HPV: volatile anaesthetic agents, nitrates, SNP, Ca2+
• Bronchial arteries from thoracic aorta supply oxygenated blood channel blockers, bronchodilators.
to supporting tissues of the lung, bronchi and drains into • Increase HPV: cyclooxygenase inhibitors, propanolol.
pulmonary veins contributing to the anatomical shunt.
25

Pulmonary vascular resistance (PVR):

• Increase PVR: by hyproxia, NO, β-blockers, histamine,
endothelins, acidosis, angiotensin -II, chronic lung disease.
• Decrease PVR: α-blockers, β-sympathomimetics, PGE1; E2,
aminophylline, SNP.
Hypoxia:
• It occurs when PaO2 < 60 mm Hg and PaCO2> 40mm Hg. It is
oxygen deficiency at the tissue level.
It is divided into 5 types.
• Hypoxic hypoxia: In which the PO2 of the arterial blood is
reduced. Eg. Cyanotic congenital heart disease, emphysema,
asthma, pulmonary emboli, altitude.
• Anemic/Hemic hypoxia: in which the arterial PO2 is normal.
But the amount of haemoglobin available to carry oxygen is
reduced. Eg. CO poisoning, anemias.
• Stagnant / Circulatory hypoxia: the blood flow to a tissue is so
low that the adequate oxygen is not delivered to it despite the
normal PO2 and haemoglobin concentration. Eg: CHF, MI,
dehydration.
• Histotoxic hypoxia: in which the amount of oxygen delivered to
a tissue is adequate but because of the action of the toxic agent,
the tissue cells can not make use of the oxygen supply to that.
Eg. Cyanide poisoning.
• Demand hypoxia: increase oxygen consumption. Eg: Fever,
Seizures.
Management:
• supplemental oxygen, CPAP / PEEP
Distribution of pulmonary perfusion / pulmonary blood flow:
• Pulmonary blood flow is also not uniform and it is mainly gravity
dependent. Thus, blood flow depends on the relationship
between pulmonary artery pressure (Ppa), alveolar pressure (PA)
and pulmonary venous pressure (Ppv). West created a lung
model that divides the lung into 3 zones, but the Modified west
lung model divides lung into 4 zones; they are as follows:
26

• Zone 1: occurs in most gravity independent part of the lung • It is now evident that as Ppa and Ppv increases; 3 important changes
above the level where Ppa = PA. Pulmonary artery pressure is takes place in the pulmonary circulation namely; a) Recruitment /
sub atmospheric in zone -1, the alveolar pressure that is opening of previously unperfused vessels, it is the principal change
transmitted to the pulmonary capillaries promotes their collapse as Ppa and Ppv increase from low to moderate levels; b) Distension /
and thus zone -1 receives ventilation in the absence of perfusion widening of previously perfused vessels, it is the principal change
and creates alveolar dead space ventilation, normally zone-1 when Ppa and Ppv increases from high to moderate levels, c)
areas exist only to a limited extent. PA >Ppa> Ppv (Ppa - PA). Transudation of fluid from very distended vessels, it is the principal
Zone 1 enlarges in hypovolemic shock change when Ppa and Ppv increases from high to very high levels.
• Zone 2: Occurs from lower limits of zone-I to the upper limit of Thus, as mean Ppa increases; Zone-1 arteries may become zone 2
zone 3, where Ppa > PA>Ppv. Flow in zone 2 is determined by arteries and as mean Ppv increases zone 2 veins become zone-3
Ppa = PA and has been likened to an upstream river water fall veins and the increase in both mean Ppa and Ppv distends zone 3
over a dam; here the Ppa increases down Zone 2 and PA vessels according to their compliance and zone 3 vessels may
remains constant, the perfusion pressure increases and flow become so distended that they leak fluid and become converted to
steadily increases down the zone. Well-matched V/Q occurs in zone-4 vessels.
zone 2, which contains the majority of alveoli. So, Zone 2; Ppa Ventilation: perfusion ratio:
>PA > Ppv. The phenomenon of Ppa -PA determining blood flow • Efficient gas exchange in the lung requires the gas flow, in and out of
has names like; the water fail, starling resistor, weir and each functional unit to be matched by the blood flow through it i.e.,
sluice effect. ventilation (V) must match perfusion (Q).
• Zone - 3: Occurs in most gravity dependent areas of the lung, • At rest V/Q = 5250/ 5000 ml / min is about 1. Thus, it is normally
where Ppa> Ppv > PA and blood flow is determined by Ppa- Ppv assumed that optimum V/Q ratio for any unit of lung tissue is 1.
difference. Because gravity also increases pulmonary venous When a unit of lung tissue is inadequately ventilated V/Q < 1, some
pressure, the pulmonary capillaries become distended, thus of the pulmonary capillary blood perfusing it, effectively bypasses the
perfusion in zone 3 is lush, resulting in capillary perfusion in lungs, since there is too much perfusion for the blood gases to
excess of ventilation / physiologic shunt. equilibrate adequately with alveolar gas. This increases the
• Zone - 4: Occurs also in the lower most gravity dependent "'physiological shunt" effect in the lungs.
areas of the lung, where Ppa>PISF > Pv > PA. The expansion of • When a lung unit is under perfused V/Q > 1, the expired gas from the
pulmonary interstitial space by fluid causes PISF to become +Ve unit contains a lower than normal concentration of CO2, since excess
and exceeds Ppv. So that blood flow in zone 4 is governed by fresh gas is supplied which does not exchange gases with pulmonary
pulmonary arterial - pulmonary interstitial space pressure capillary blood. This increases the "alveolar dead space" effect on
difference (Ppa - PISF) which is less than Ppa - Ppv difference the lungs.
and therefore zone 4 blood flow is < than zone 3 blood flow.
27

Distribution of V/Q ratios in the lung: Diffusion of gases:

• At the top of the lung V/Q ratio is estimated to be 3.3, and this It includes: A) Alveolar gas transfer B) Transport of gases in blood.
value decreases passing down the lung to the bottom, where the A) Alveolar gas transfer: The exchange of gases within the lung occurs
V/Q ratios are about 0.3. through a process of passive diffusion across the alveolar capillary
• Importance of V/Q ratios: ! membrane.
• V/Q ratios relates to the efficiency with which lung units OXYGEN
resaturate venous blood with O2 and eliminate CO2. 1. Alveolar O2 tension (PAO2) = PIO2 - PaCO2 / RQ = 106 mm Hg. It
determines the partial pressure gradient driving O2 across AC-
SHUNTS membrane.
• Shunting denotes the process whereby desaturated, mixed 2. Arterial O2 tension (PaO2) = 102 - Age/3 = 60-100 mm Hg.
venous blood from the right heart returns to the left heart without 3. A-a gradient = < 15mm Hg upto 20-30 mm. Hg with increase in
being resaturated with O2 in the lungs. The effect of shunting is age.
to decrease arterial O2 content and this is referred as Rt-to-Lt. 4. Pulmonary end-capillary O2 tension (PcO2) is 106mm. Hg
Shunt. However Lt to Rt shunt do not produce hypoxemia. 5. Mixed venous O2 tension: is 40mm .Hg and it represents the
overall balance between O2 consumption and O2 delivery.
Type of shunts: OXYGEN CASCADE
Absolute/anatomic shunt: • The O2 content in air (at sea level) is about 159.6mm Hg. (760 mm
• Extra pulmonary: via thebesian.v, congenital heart disease, ii) Hg x 0.21), gradually falls to 10-15 mm Hg. (0.5 KPa) in the
intrapulmonary: bronchial veins, atelectasis. It refers to lung mitochondria where it is utilized.
units where V/Q is zero; also called "True shunt". It cannot be • The transport of O2 down this concentration gradient is described as
corrected with increase in the inspired O2 concentration. "Oxygen cascade". It involves different transport mechanisms,
• Relative / physiological / venous admixture shunt fraction: it convection, diffusion through gas and liquid media and transport
is an area of the lung with a low but finite V/Q ratio because i) bound to Hb.
venous blood may bypass the lungs entirely via intracardiac • The same process occurs in the reverse direction for CO2.
shunts, thebesion veins, bronchial circulation, ii) blood may
pass through areas of true shunt- iii) blood may pass through
parts of lung which are not ventilated adequately V/Q < 1.
• Shunt equation = Qs / QT = CcO2-‐ CaO2 / CcO2 -‐ CVO2
• = Shunt flow / total flow = reduction in O2 content due to shunt /
total O2 content added by lungs
Importance:
• l) The shunt fraction is usually quoted as a % and is a useful
clinical index ofoxygenation efficiencyin critically ill patients. 2)
Shunt fraction > 30% are associated with poor survival. 3) Iso-
shunt diagram is helpful in following clinical progress and in
adjusting O2 therapy. ID. 28

Factors influencing oxygenation at different levels: ! Transport of Oxygen in the blood:

• The inspired gas is humidified at body temp (370C). 2) inspired • Inalveolar air, the O2 tension is 106 mm Hg and in venous blood
gas mixes with the existing alveolar gas. 3) O2 is constantly entering the pulmonary capillary is 40 mm Hg. because of this
being taken up by pulmonary capillary blood. 4) Return of blood pressure gradient difference of 66 mm Hg O2 diffuses rapidly across
from bronchial veins and consumption by myocardium; V/Q the alveolar capillary-membrane, on reaching the blood, the O2 first
mismatch, true shunt. 5) The PO2 falls progressively from the dissolves in plasma and finally combines with Hb for its carriage to
arterial to the venous end of the capillaries and from capillaries the tissues.
to the cell and is lowest in the mitochondria; depending on blood a) Dissolved O2 in plasma: Only a small quantity of O2 about (3%)
flow, Hb concentration and cardiac output.6) O2 consumption 0.3ml / 100 ml of blood at a PaO2 of 100 mm Hg is physically dissolved
occurs in the body at the mitochondrial level but below 1-2 mm in the plasma. This is of vital importance because: i) it reflects the PO2
Hg of PO2, oxidative phosphorylation cannot take place and in the blood, ii) Acts as a pathway for supply of O2 to Hb. iii) At tissue
anaerobic metabolism sets in. this critical value of mitochondrial levels, it is first transferred to the cells, while its place is rapidly being
PO2 of 1 -2 mm. Hg is known as "Pasteur point". taken up by more O2 liberated from the Hb. iv) Dissolved O2 is a linear
• The most important variable in considering the diffusion of O2 is function of PAO2.
the partial pressure gradient across the capillary wall, as O2 b) O2 combined with Hb: Most of the O2 (97%) in the blood is
passes across the membrane, the PO2 of blood rises which is in transported in combination with Hb.
turn determined by the rate of gas transfer and its rate of Haemoglobin: Consists of the protein globin joined with the pigment
combination with Hb. RBC takes about 0.75 sec to traverse a haem, which is a Fe- containing porphyrin. Normal adult Hb consists
capillary. of: Hb (A1): 98% and Hb (A2): 2%.
Oxy-hemoglobin: reaction of Hb with O2 occurs in 4 stages on basis
of law of mass action: Hb4 + O2⇔ Hb4O2, Hb4O2 + O2⇔ Hb4O4, Hb4O4
+ O2⇔ Hb4O6, Hb4O6 + O2⇔ Hb4O8.
1gm of fully oxygenated Hb would be expected to contain 1.39 ml of
O2, in practice, it has been found that 1gm of Oxy-Hb carries 1.31 ml
O2. At a PaO2 of 100 mm. Hg, Hb is 97.5% saturated, thus 15 gm of
Hb in 100 ml blood can carry approximately 19 ml of O2. Every 100 ml
of blood passing through the lungs take up 5ml of O2. (19 ml arterial -
14 ml venous = 5ml).
29

Characteristic of HbO2 binding: Oxygen Hb dissociation curve: (ODC)

• It is determined primarily local O2 tension. It is affected by pH, • The percent of Hb saturation with oxygen (PO2) at different partial
temperature, CO2, 2, 3-DPG. It produces an allosteric change in pressures of O2 in blood is described by the "ODC". It expresses the
the structure of Hb to a "Relaxed form", while deoxygenated Hb relation between oxygen tension taken on the X axis and % of Hb
has a "Tense form". This switching between R and T forms saturation taken on the Y axis at 37° C, pH: 7.4, PCO2 40 mm. Hg. It
underlies the oxygenation and delivery mechanisms. De- is a sigmoid curve.
oxygenation of Hb increases the affinity of several protein- • It shows that at a normal arterial value of 100 mm Hg, Hb is 97%
binding sites on its molecule, which increases its ability to saturated, at PO2 of 60mm Hg saturation is still 90%. When the PO2
transport CO2 from the tissues to the lungs and underline the role is < 60 mm Hg, the saturation falls steeply, so that the amount of Hb
of Hb as a major buffer in acid-base regulation. uncombined with O2 increases greatly for a given decrease in PO2.
Oxygen flux: • Mixed venous blood has a PO2 of about 40mm. He and is
• The amount of O2 leaving the Lt. Ventricle per minute in the approximate 75% saturated, this is indicated by the middle of the
arterial blood has been termed the "oxygen flux". It represents ODC. The position of the ODC is best described by P50. The PO2
O2 delivers to the tissues. level at which Hb is 50% saturated (P50). The normal adult P50 is
O2 flux = CO x Arterial O2 saturation x Hb concentration x 1.31. 26.7 mm Hg. A low P50 implies the ODC is shifted to left and vice
• = 5000 ml/min x 98/100 x 15.6/ 100g / ml x 1.31 ml/gm. versa. Changes in P50 have a main consequence on the release of
• O2flux = l000ml/min. O2 to the tissues. A low P50 decreases O2 availability to the tissues
• Normally about 250ml of this O2 is used up in cellular metabolism and may therefore lead to cellular hypoxia. Unconsciousness is likely
and the rest returned to the lungs in the mixed venous blood, to occur in a normal person with a PO2< 26.7mm Hg.
which is therefore about 75% saturated with O2. FACTORS INFLUENCING THE ODC
• The 3 variables in the equation: Cardiac output, arterial O2 • The P50 is a way of describing any shift of the ODC to the left or
saturation and Hb concentration are multiplied together; a right. Right shift of ODC: lowers O2 affinity, displaces the O2 from
relatively trivial reduction of each may result in a catastrophic Hb and makes more O2 available to the tissues. Eg: Acidosis
reduction in O2 flux. The body can tolerated any one of these 3 (Increase H+ ions), hyperthermia, ↑CO2, ↑2, 3 - DPG high altitude,
factors: hypo perfusion, arterial desaturation, anaemia but not a exercise propranolol, isoflurane. Left shift of ODC: ↑ Hb affinity for
combination of all 3 or even 2 factors. Lowest tolerable value of O2, reducing O2 availability to the tissues. Eg Alkalosis, hypothermia,
O2 flux is 400 ml/min. ↓ CO2, ↓ 2, 3, - DPG, carboxy Hb, meth - Hb, Fetal Hb, CO
• Oxygen flux is decreased in: anaemia, CCF, metabolic acidosis, inhalation.
respiratory acidosis. Oxygen flux is increase in exercise, • Clinically important factors altering O2 binding include: H+ ion
thyrotoxicosis, halothane shakes, pain and shivering. concentration CO2 tension, temperature, 2, 3 - DPG these molecules
influences the position of the ODC as follows:
30

PH (Bohr Effect): Oxygen stores:

• Shift in position of ODC caused by ↓pH and ↑in CO2 entering / • Is important concept in anaesthesia.
leaving blood is called "Bohr effect". A fall in pH shift the ODC to • When the normal O2 flux is interrupted by apnea, existing O2stores
the "right" and ↑ in pH shifts ODC to the left. PH change may be are consumed by the cellular metabolism, if stores are depleted,
produced by either metabolic / respiratory disturbances. hypoxia and cell death follows. Normal O2 stores in adult 1500 ml /
Double Bohr Effect: 1.5 lts. (Includes O2 remaining in lungs (30%), O2 that is bound to Hb
• The ODC of the adult and fetal Hb are influenced by the acid (50%), O2 bound to myoglobin (20%) and O2 dissolved in body fluids.
base status, described by "HUGE". The transfer of H+ ions from The O2 contained with in the lungs at FRC therefore, becomes the
the fetal blood into the maternal intervillous spaces causes the most important source of O2.
fetal pH to rise and increase the affinity of fetal blood to O2 (shift • Apnea in a patient breathing room air previously leaves ≈480 ml of
to left): at. The same time H+ ions acids passing to the maternal O2 in the lungs and the metabolic activity of tissues rapidly depletes
circulation causes the maternal pH to fall, thereby reducing the this reservoir and severe hypoxemia usually occurs with in 90
affinity of maternal blood for O2 (shift to right) so further O2 is seconds. The onset of hypoxemia can be delayed by ↑ the FiO2 prior
released to the fetus. to the apnea. Following ventilation with 100% O2, FRC contains 2300
• 2, 3-DPG: It combines with globin and modifies O2 access to the ml of O2, this delays hypoxemia following apnea for 4 - 5 minutes.
haem chain, an increase in 2, 3 DPG being associated with a This concept is the basis for preoxygenation prior to induction of
reduction in the affinity of Hb for O2. Therefore a high anesthesia
concentration of 2, 3-DPG shifts ODC to right and vice versa. 2, Significance of ODC:
3-DPG level in increase in anaemia. 1) ODC relates the saturation of Hb to the PaO2
• Temperature: fall in temperature, shifts ODC to left. 2) ODC relates the O2 content to the PO2.
• Storage of blood: in Acid Citrate Dextrose (ACD) -blood, there is 3) ODC relates the O2 transport (L/min) to the peripheral tissues to the
a rapid fall in concentration of 2, 3-DPG in the RBC's and the PO2.
ODC shifts to left, so that recently transfused blood is reluctant to 4) ODC relates the O2 actually available to the tissues as a function of
give up O2 to the tissues. It may take 2-3 days to recover after PO2.
infusion. The use of CPD as an anticoagulant in stored blood
delays the fall in 2, 3-DPG for about 10 days.
• At the steep lower portion of the ODC changes in PO2 has a
very marked effect on the % saturation, so facilitating the transfer
of O2 tissues very easily. At the upper flat part of the ODC
changes in PO2 have relatively little effect on Hb saturation and
therefore blood O2 content. It assists the diffusion of O2 across
the blood gas barrier in the lungs, thus loading of O2 by the
blood.
31

CARBONDIOXIDE
• CO2 is a by product of aerobic metabolism in the mitochondria.
There are gradients for CO2 tension from mitochondria to
cytoplasm, ECF, venous blood, alveoli, where CO2 is finally
eliminated.
1. Mixed venous CO2 tension (Pv CO2): 46 mm Hg normal
2. Alveolar CO2 tension: (PACO2) = VCO2 / VA = 40 mm Hg.
3. Pulmonary end-capillary CO2 tension (PcCO2) = 40mm Hg.
4. The rate of diffusion of CO2 across the Ac-membrane is 20
times that of O2.
5. Arterial CO2 tension: 38 + 4 mm Hg i.e. 40 mm Hg is
considered normal
6. End-tidal CO2 tension (PETCO2): is an estimate of PaCO2.
Carbon dioxide transport in blood:
• CO2 diffuses passively down its concentration gradient from the
mitochondria to the capillaries. The tissues produce CO2 and this
is then given up to the blood circulating through the capillaries. It
rapidly enters the plasma and then passes in to the red cells. On
reaching the pulmonary capillaries the PCO2 in venous blood is
46 mm Hg and PACO2 is 40 mm Hg therefore a pressure
gradient of 6 mm Hg, driving CO2 across the AC- membrane.
• In normal circumstances each 100 ml of arterial blood caries 48
ml of CO2;. CO2 is transported in blood in 3 forms:
Dissolved CO2: - (in solution in plasma):
• CO2 is more soluble in blood than O2, with solubility co-efficient
of 0.067 ml / dl / mm Hg at 37°C. Only 5% is carried in this
manner. The majority of CO2 is present in physical solution in the
plasma, but a very small proportion is combined with water to
form H2CO3. This dissolved CO2 form is very important because
it is responsible for determining the CO2 tension in the blood, it
acts as the intermediary between the air in the alveoli and the
inside of the RBC.
32

As bicarbonate: • The major component of the Haldane effect is the increase carriage
• 70% of the CO2 passes to the RBC's and combines with H2O à of CO2 by reduced Hb as carbamino Hb. In addition, CO2 is carried
carbonic acid which is accelerated by the presence of the as by HCO3 is increased. Due to the Haldane effect, the up take of
enzyme. "Carbonic anhydrase" with in the RBC's and CO2 by the capillary blood is facilitated. When this blood reaches
endothelium and then carbonic acid dissociates into H" and the lungs and becomes oxygenated, the elimination of CO2 is
HCO3 ions. As a result HCO3- represents the largest fraction of facilitated.
the CO2 in the blood. The HCO3 diffuses out of the RBC into the • The CO2 response curve is a sensitive index of respiratory
plasma so to maintain ionic equilibrium Cl- ions diffuse into the depression and also it is used to study the respiratory effects of
RBC, this is called the "Chloride shift/ Hamburger effect". narcotic drugs.
• In the pulmonary capillaries, the reverse occurs chloride ions Methods are used to measure the CO2 response curve:
move out of RBC's as HCO3" ions reenters the RBC's for a) Steady state method
conversion back to CO2 and H2O by carbonic anhydrase and b) Rebreathing method
CO2 diffuses out into the alveoli. Thus plasma HCO3- plays a • Shift to right:
very important role as the principal store house and earner of • Pethidine, morphine, emphysema, metabolic alkalosis.
CO2 in the blood. • Shift to left:
As a carbamino compound: • Metabolic acidosis, hypoxia. Progressive reduction of the CO2
• About 25% CO2 can combine with the amino -group of the Hb to dissociation curve is seen with inhalational agents, in appropriate
form "carbamino - Hb". components in the anaesthetic circuit.
• In the tissues deoxygeneration of Hb enhances carriage of CO2 • The CO2 response curve changes from person to person and
by activating proton finding and carbamino formation sites. time to time in the some individual.
Correspondingly, oxygenation of Hb causes the reverse effect, CO2 stores:
displacing H+ and CO2, thus facilitating the "unloading" of CO2 in • The CO2 stores in the body are about 120 lts, primarily in die form of
the lungs. This dependency of CO2 carrying capacity on the dissolved CO2 and HCO3. It requires 20 - 30 mins for a new CO2
oxygenation state of Hb is known as the "Haldane effect". equilibrium to occur between imbalance in CO2 production and
• The Haldane effect is the shift in the relationship of PCO2 to the elimination. During apnoea PaCO2 increased by about 1 kPa in the
total CO2 caused by altered levels of O2. Low PO2 shifts CO2 DC first minute and then decrease to a rate of 0.4 kPa / min, as alveolar
to left so that the blood is able to pick up more CO2 and high PO2 PCO2 levels buildup and CO2 elimination by diffusion through the
shifts"CO2 DC to right so that unloading of CO2 in the lungs airways increase.
occurs.
• CO2 dissociation curve: It relates to the CO2 content of blood
to the PCO2 to which it is exposed. The position of this curve
depends upon the degree of oxygenation of the blood. The more
deoxygenated the blood becomes, the more CO2 it carries at a
given PCO2 this is called the "Haldane effect".
33

Blood filtration:
• Pulmonary vasculature acts as filter in the circulation, particles > 8
μmare filtered during their passage through the lungs Small clots are
dissolved by fibrinolytic system. Lungs are rich source of
endogenous heparin, thromboplastins which play a role in the overall
control of coagulation.
Metabolic functions: refer the Table
RESPIRATORY PHYSIOLOGY DURING ANESTHESIA
• Spinal anesthesia (SA): VT and respiratory not affected in quite
breathing ↓ SA. 50% ↓in FEV and ↓ expiratory reserve volume,
inspiratory capacity is normal. When paralysis of abdominal muscles
occurs.
• G.A. affects the pressure volume and flow of the respiratory system.
Under GA in supine position FRC ↓ by 15 -20 % occurs with in 1 mm
of induction of anesthesia due to increase closing capacity, cephaloid
displacement of diaphragm, ↓ out ward chest wall recoil, increase
lung recoil. Pulmonary resistance increase following intubation.
Effect of nonvolatile anaesthetic agents on respiratory function: -
• Barbiturates: They ↓ medullary respiratory centers, which in turn
decrease ventilatory response to hypoxia, hypercapnea. Transient
apnoea occurs after an induction dose. VT↓, RR↓, bronchospasm in
asthmatics, laryngopasm in slightlyanaesthetized patients can occur
following airway manipulation.
• Benzodiazepines: ↓ ventilatory response to CO2,apnoea can occur
following IV administration.
• Opioids: ↓RR prevents adequate ventilation by causing chest wall
rigidity, restingPaCO2 increases, apnoeic threshold increases and
hypoxic drive↓. Morphine, pethidine can cause histamine-induced
bronchospasm.
• Ketamine: potent bronchodilator increases bronchial secretions
upper airway reflexes remain intact and can cause bronchospasm on
airway manipulation.
• Propofol: ↓ RR and apneoa following induction dose, it inhibits
hypoxic ventilator/ drive and depress the response to hypercarbia.
34

Inhalational anesthetics: Type to enter text

• Nitrous oxide: increases RR ↓VT due to CNS stimulation and
activation of pulmonary stretch receptors. It depresses hypoxic
drive and ventilatory response to arterial hypoxia mediated by
peripheral chemoreceptors in carotid bodies.
• Halothane: causes rapid shallow breathing, increases RR,
decreases VT, PaCO2 and apnoeic threshold are increase,
minute ventilation decreases due to medullary depression and
intercostals muscle dysfunction.
35

2. Control Of Breathing Dr Azam’s Notes in Anesthesiology 2013
• Spontaneous ventilation is the result of rhythmic neural activity in respiratory centers within the brainstem. This activity regulates respiratory
muscles to maintain normal O2 and CO2tensions.
• The basic neuronal activity is modified by inputs form other areas in the brain: volitional, autonomic as well as various central and peripheral
receptors (sensors).
CONTROL OF BREATHING
Peripheral chemoreceptors:
Central respiratory centers:
d) Expiratory centre: situated ventrally

on each side of medulla, stimulated
a) Inspiratory centre: lies in the causes expiratory muscle activity.
dorsal part of the medulla on The primary goal of respiratory control is
each side, they generate basic b) Pneumotaxic centre: to maintain homeostasis of blood gases,
rhythm of respiration. lies in upper pons, it is allowing speech, enable coughing,
• 2 medullary groups of neurons inhibitory and transmits sneezing, yawning, minimize WOB,
are recognized they are impulses to the protect airway during eating, drinking,
i) dorsal respiratory group: inspiratory area and vomiting.
Primarily active during produces a faster
inspiration, respiratory rate.
c) Apneustic centre: Peripheral sensors:
ii) ventral respiratory group:
lies in lower pons, it is Peripheral chemoreceptors:
! Active during expiration.
• Close association of the dorsal excitatory and is • They include carotid bodies and aortic bodies.
group of neurons with tractus overridden by the • They are sensitive to change in PaO2, PaCO2 pH and
pneumotaxic centre. arterial perfusion pressure.
solitarius may explain reflex
• They interact with central respiratory centers via
changes in breathing from The pontine centers
glossopharyngeal nerve producing reflex increase in
vagal / glossopharyngeal. N appear to fine tune R.R alveolar ventilation due to hypoxia, increase in H+ ion,
stimulation. and rhythm. Transection and increase PaCO2, cyanide, nicotine, and
of pons just below doxapram.
pneumotaxic centre • If PaO2 decreases below 50mm Hg, the peripheral CR
causes slow gasping. activity is increased.
36

Control Of Breathing. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Central sensors: (central chemoreceptors – CR)

• They respond to changes in CSF H+ ion
concentration.
• They lie on anterolateral surface of medulla. It is
effective in regulating PacO2 because BBB is
permeable to dissolved CO2 but not to HCO3
ions.
• Increase in PaCO2 causes increase in CSF H+
ion concentration which in turn activates the
central CR, which stimulates the respiratory'
medullary centre and increases alveolar
ventilation which decreases PCO2 back to
normal. The reverse occurs during decrease
PCO2.
• The PaCO2 at which ventilation is zero
is called "apnoeic threshold". Spontaneous
respiration is absent under Anesthesia when
PaCO2 falls below "apnoeic threshold".
GRID: Question to be answered under

following headings:
1. Introduction
2. Central Respiratory Center
3. Central Sensors - Central
chemoreceptors CR
4. Peripheral Sensors - Peripheral
chemoreceptors
37

3. Oxygen dissociation curve - ODC Dr Azam’s Notes in Anesthesiology 2013
Significance of ODC:
Oxygen Hb dissociation curve: (ODC) 1) ODC relates the saturation of Hb to the PaO2
Definition:The percent of Hb saturation with oxygen (PO2) at
2) ODC relates the O2 content to the PO2.
different partial pressures of O2 in blood is described by the
3) ODC relates the O2 transport (L/min) to the peripheral tissues to the PO2.
"ODC". 4) ODC relates the O2 actually available to the tissues as a function of PO2.
Graph:
• It expresses the relation between oxygen tension taken on the
X axis and % of Hb saturation taken on the Y axis at 37° C, pH:
7.4, PCO2 40 mm. Hg. It is a sigmoid curve.
3 Points:
The three main points to indicate on the curve are:
• Arterial point: pO2 100 mmHg with SaO2 = 97.5%
• Mixed venous: pO2 40 mmHg with SaO2 = 75%
• P50: pO2 26.6 mmHg with SaO2 = 50%
• P50 increases , the affinity to oxygen decreases & hence

release of O2.
• P50 decreases , the affinity to oxygen increases & hence holds
O2.
38

Oxygen dissociation curve - ODC. Continuation: Dr Azam’s Notes in Anesthesiology 2013
FACTORS INFLUENCING THE ODC

• The P50 is a way of describing any shift of the ODC to the left
or right.
• Right shift of ODC: lowers O2 affinity, displaces the O2 from GRID: Question needs to be answered
Hb and makes more O2 available to the tissues. under following headings:
• Acidosis (Increase H+ ions), 1. Definition
• hyperthermia, 2. Graph + Diagram
• ↑CO2, 3. 3 Points on ODC
4. Significance of ODC
• ↑2, 3 - DPG
5. Shift: Right & Left shift of ODC.
• high altitude,
• exercise
• propranolol,
• isoflurane.
Left shift of ODC: ↑ Hb affinity for O2, reducing O2 availability to
the tissues.
• Alkalosis,
• Hypothermia,
• ↓ CO2,
• ↓ 2, 3, - DPG,
• carboxy Hb,
• meth - Hb,
• Fetal Hb,
• CO inhalation.
39

4. Oxygen Cascade Dr Azam’s Notes in Anesthesiology 2013
• Oxygen like any other gas, moves down a partial pressure gradient Series of steps of PO2 from atmospheric air to mitochondria
from air via the respiratory tract. and the factor effecting them
• Arterial blood, systemic capillaries and cells to finally reach the Dry atmospheric air 160mmHg (21 kPa)
mitochondria- where it is consumed.
Factors effecting are barometric pressure and FiO2
Definition: The steps by which the partial pressure of oxygen
gradually decreases from a high level in the inspired gas to a low Atmospheric. pressure x FiO2
level in the mitochondria is called oxygen cascade. 760 x 0.21 = 160mmHg
Humidification at 370C 150mmHg (19 kPa)
! =(atmospheric pressure – saturated vapour pressure of H2O at
body temperature 370C) x FiO2
(760 – 47) x 0.21 = 149.3 mmHg
Alveolar gas 106 mmHg (14 kPa) PAO2

Due to:
• Dilution of atmospheric air by alveolar air
"!#$%!&!'()!**+,! • Constant uptake of O2 - O2 consumption VO2
Arterial O2 tension PaO2 100mmHg (13.3 kPa)

Due to
• Ventilation perfusion mismatch (venous admixture)
• True shunt of pulmonary arterial blood
Cell PO2 40mmHg (6 – kPa)
High altitude -‐ ↓ in barometric • Drops from 100mmHg in arterial blood to the 40mmHg at
pressure à↓ PIO2 . so PIO2 should capillary level – factors affecting blood flow, Hb, CO
GRID: Question need to to answered
Mitochondria 5-22 mmHg
be ↑ to avoid hypoxemia under following headings:
Atmospheric pressure X FIO2 1. Definition • Most of the oxygen is used in the mitochondria. If the PO2
1. 760 x 0.21 = 160 = 21 kPa 2. Diagram here fills to below 1-2mmHg (0.2 kPa) – PASTEUR POINT
3. calculation of Oxygen Cascade
Atmospheric Pressure – SVP then aerobic metabolism stops.
4. Steps
x FiO2 • Reductions of PO2 at any stage results in reduction of PO2
5. Pasture Point
2. (760 – 47) 0.21 = 150 = 19 leading to anaerobic metabolism below the Pasteur point.
kPa 1 kPa = 7.6mm Hg
40

5. Oxygen Flux Dr Azam’s Notes in Anesthesiology 2013
Definition:
• The amount of oxygen leaving the left ventricle per minute in the arterial It should be noted that various conditions in which
blood. Oxygen carrying capacity or O2 control, oxygen flux can be
• Normal = 1000ml of O2 / minute decreased. #
Calculation: • Anaemia
# Oxygen Flux = CO x SaO2 x Hb% x 1.31 (clinical practice) • CCF
• Metabolic acidosis
• Respiratory acidosis
• Various respiratory diseases leading ↓ alveolar Ventilation
= 5000ml/min x x x 1.31 / g (1.39: molecular basis)
OF = 1000ml / min 1000ml/w. Consider the value in normal adult.
Oxygen demand may be increased – physiologically in patients
• g is the amount of oxygen carried in 1gm of haemoglobin. • Exercise
• O2 content of plasma is ignored here or the O2 content is small is 0.003ml • Thyrotoxicosis
of O2 / mm of Hg / 0.1L of PO2. • Pain and shivering
# = 0.003 x 100mm of Hg • Halothane shakes
# = 0.3ml / 100ml of plasma. In 3500ml of plasma, O2 content = 10.5ml • Malignant Hyperthermia
• On molecular basis • PaO2 of 100mm of Hg à 98%
• 1gm Hb caries à 1.39 ml of O2 700mm of Hg à 100%
• But in clinical practice it caries 1.31ml (still controversial)
• Normally 250ml of this oxygen is used up in cellular metabolism.
• Rest returns to the lungs in mixed venous blood which is therefore 75% • But plasma O2 content is increased:
saturated with oxygen. # 0.003ml / mm of Hg / 100ml of blood
Importance: # 0.003 x 700 = 2ml / 100ml of blood is carried
• Because the three variables in the equation CO, arterial O2 saturation and • Normal – with 100mm Hg PaO2 = 0.3ml / 100ml
Hb concentration are multiplied together, a relatively trivial reduction of
each may result in a water temperature reduction in oxygen flux.
GRID: Question need to to answered under
following headings:
1. Definition
2. Formula
3. calculations
4. Factors increasing & decreasing Oxygen flux
41

6. Lung Compliance. Dr Azam’s Notes in Anesthesiology 2013
Definition: Total compliance is determined by adding the reciprocal of the individual

• Stretch ability of the lung is called Compliance compliances (1/ Ctotal = 1/ Cl + 1/Cw).
• Change in volume per unit change in pressure.#
C= ΔV # Low compliance: -
ΔP# # ΔV= Volume Change (lung expansion) • Means that volume change is small per unit pressure change
# # # ΔP= Pressure change (work of breathing ) • (↑WOB): The lung are stiff and non complaint
Lung compliance: - • (↓FRC): The work of breathing is↑ - this might be responsible for refractory
hypoxemia in some of the clinical situations.
• Change in lung volume per unit pressure change
• It is 200ml per cm of water pressure changes (0.2L/cm H2O) • Patients with low compliance is usually related to conditions that reduce
Transpulmonary pressure(Ptp) = Alveolar pressure(Palv) - Intrapleural pressure(Ppl) FRC.
Pulmonary blood volume, Extravascular lung water & fibrosis affect • They usually have restrictive lung defect, low lung volume , low minute
lung compliance. ventilation with compensatory ↑ in respiratory rate.
1. ARDS
Chest wall compliance: 2. Fibrosis
It is 200 ml per cm of water pressure changes
3. Pulmonary oedema
It is assumed that lung - chest wall compliance is equal 0.2 L /cm of
4. Tube kinking
H 2O
5. Retained secretion
Transthoracic pressure(Pt) = Atmospheric pressure(Pbs) - Intrapleural pressure(Ppl)
6. Bronchhospasm
Total compliance: 7. Obesity
Lung + Chest wall Together 8. Pneumothorax
The total compliance = 0.1 L /cm of H2O change, this means the lung
expand 100 ml for every 1cm of H2O pressure increase in the alveoli. GRID: Question need to to answered under following
headings:
1. Definition
2. Different compliance
3. Types of Compliance
4. Cause of Low & high compliance
5. Factors affecting Compliance
42

Lung Compliance. Continuation: Dr Azam’s Notes in Anesthesiology 2013
High compliance: Conditions that decrease compliance

• Volume change is large per unit pressure change High compliant lung is Static compliance is ↓→ atelectasis, ARDS, pneumothorax, obesity,
usually related to conditions with ↑FRC. retained secretions.
• With Extreme high compliance- lungs often have obstructive lung defect, air Dynamic compliance is ↓: bronchospasm , kinking of ET tubes
flow obstruction, incomplete exhalation poor gas exchange . # # # Airway obstruction
# Ex: 1) Advanced age or in neonates
Factors affecting the compliance:
2) Emphysema:
Types: • Posture: In supine position – FRC is ↓ -so is the compliance
• Pulmonary: Congestion →↓ compliance reduction of expansion of
Static compliance: - the chest
It is measured when there is no air flow. In absence of air flow, airway • IPPV - airway obstruction due to accumulation of cellular debris
resistance is not a determining factor. So it reflect the elastic properties of and secretions due to decrease ciliary activity and ↓ compliance
lung & chest wall. • GA → It ↓ses compliance because of posture, shallow breathing
Measurement: Measurement of compliance – that is volume change ↓ broncho motor tone and of external intercostals.
measured at different point of pressures. • Disease status: ARDS, pulmonary edema, inflammatory
Static Compliance = corrected Vt/Plateau pressures - PEEP = 40-60 ml/CMH2O condition, pulmonary fibrosis, these all ↓ compliance
Dynamic compliance: • Infants and emphysema: → increased compliance
Measured when air flow is present, airway resistance becomes a critical • Upper abdominal surgery ↓ Compliance .
factor in the measurement of compliance. So it reflects airway resistance as
well as elastic properties of lung & chest wall.
Measurement: -It is measured during quiet breathing when lung volume is
displayed against intra pleural pressure ( esophageal pleasure ) continually
Dynamic Compliance = corrected Vt/Peak airway pressures - PEEP = 30-40 ml/CMH2O
(Change in C- dynamic can occur independently of C- static, eg- Tube kinking)
Collected tidal volume = tidal volume – tubing volume
# Tubing volume =peak airway pressure– PEEP x 3ml/ cm H20
[Measurement of static & dynamic compliance is obtained after obtaining
above values – when patient connected the ventilators after paralyzing].
43

Lung Compliance. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Conditions that decrease Compliance:

Static Compliance •Atelectasis
•ARDS
•Tension Pneumothorax
•Obesity
•Retained secretions
Dynamic Compliance •Bronchospasm
•Airway obstruction
•Kinking of ET-Tube
44

7. Discuss the anatomy of diaphragm with a diagram. How will it behave under different Dr Azam’s Notes in Anesthesiology 2013
stages of anesthesia?
• Diaphragm about (75-80%) - major muscle of Actions:

inspiration
• Contraction of both costal and crural fibres causes diaphragm to descend,
• Dome shaped muscle that separates the thoracic cavity decreasing pleural pressure and raising abdominal pressure, which in turn
from the abdomen.
expands the lower ribcage and contributes to inspiration.
It has 3 portions:
• In normal subjects, the diaphragm is approximately a hemispherical dome at the
• Crural part: Stabilize central tendon and generates
end of expiration: but as the central tendon descends and the zone of
downward movement of diaphragm.
apposition decreases, it resembles a flattened sheet.
• Sternocostal part: Acts to lift and expand the lower rib
Functions:
cage.
• Central tendon: Into which both muscular parts are • Most important inspirarory muscle.
inserted have a complex bi-domed shape and a central • Responsible for 60-75% of tidal volume during quite breathing.
narrow portion so that 2 halves can act independently. • In quadriplegics, high neuraxial blocks we see that intercostals muscles do not
act during inspiration. Decrease in intrapleural pressure leads to
Adult diaphragm is composed of 3 types of skeletal paradoxical inward movement of ribcage and fall in tidal volume.
muscle fibers.
• Type I fibres (55%): slow oxidative,resistant to fatigue,
these contain high concentrations of mitochondria,
oxidative enzymes, numerous capillaries high myoglobin
content which gives the muscle a dark red colour. They GRID: Question need to to answered under following
are endurance fibres, resistant to fatigue and are headings:
deficient in infants. 1. Introduction
• Type II a (Fast oxidative) (20%) 2. 3 Portions
• Type II b (Fast glycolytic white fibres) (25%): they 3. Composition & types of Skeletal muscle fibers
have few mitochondria, high concentration of glycolytic 4. Actions
enzymes, large stores of glycogen. They are white due 5. Functions
to fewer blood vessels, little myoglobins. They are 6. Abnormal movement of diaphragm
larger, can generate more force, but fatigue easily. 7. Diaphragm under anesthesia.
45

Discuss the anatomy of diaphragm with a diagram. How will it behave Dr Azam’s Notes in Anesthesiology 2013
under different stages of anesthesia? Continuation:
Abnormalities of movement of diaphragm:

• If diaphragm is paralyzed on one side due to damage/blockade of phrenic. N, the negative intrathoracic pressure will cause paralyzed portion to move
up instead of down.
• Pressure form below- as in advanced pregnancy, obesity, and intra abdominal pathology will impede free movement of diaphragm.
• Following upper abdominal surgery, pain limits movement of diaphragm.
• Advanced emphysema, increases lung volume causes diaphragm to be pushed down in resting phase, so that it is at a mechanical disadvantage,
works inefficiently and increase in WOB.
• The supine position and induction of anesthesia has been associated with basal atelectasis because the closing capacity encroaches on FRC so the
FRC decreases and increase in A-a gradient leads to hypoxemia.
• In ICU patients on prolonged mechanical ventilation, diaphragmatic dysfunction can be reduced by giving adequate time to relax the diaphragmatic
fibers and this helps in increasing the blood supply to the diaphragm, which is helpful in weaning the patient.
Diaphragm Under Anesthesia:

• Stage I (Analgesia & Amnesia): Diaphragmatic movement will be normal
• Stage II (Dream - Unconscious): There will be irregular moments
• Stage III:(Surgical)
• Plane 1: Respiration is full & normal followed by decrease in respiration &
minute volume
• Plane 2: A longer pause between the inspiration & expiration may be
detected.
• Plane 3: Diaphragm & intercostal muscle contract simultaneously to
produce coordinated inspiratory effort. Abdominal bulge is noted as well.
• Plane 4: Diaphragm movement is gradually depressed. The sternocostal
portion is paralyzed first followed by crural portion. irregularities in
diaphragmatic respiration followed by complete cessation.
• Stage 4 (Medullary paralysis): Respiratory Arrest
46

8. Describe the Anatomy of larynx? Discuss the effect of damage to recurrent laryngeal nerve
vocal cord palsies?
Definition: Larynx is the cartilaginous skeletal held together by ligaments

and muscles. Muscles of Larynx:
• Extends from root of the tongue to the first tracheal ring (C3 to C6)
Intrinsic Muscles: Extrinsic Muscles:

Measurements Male Female • Sternothyroid
• Abductor:
• Posterior cricoarytenoid • Thyrohyoid
Length 44 mm 36 mm
• Adductors: • Inferior constrictor
Transverse 43 mm 41 mm • Lateral cricoarytenoid • Stylopharyngeus
Diameter • Transverse arytenoid • Palotopharyngeus
• Cricothyroid*
AP Diameter 36 mm 26 mm • Thyroarytenoid *
• Relaxors:
• Thyroarytenoid*
• Vocalis
• Tensors:
• Larynx is made up on 3 unpaired & 3 paired cartilaginous • Cricothyroid *
structure:
3 Unpaired 3 paired GRID: Question to be answered under following headings:
1. Definition
Thyroid Cartilage Arytenoid cartilage
2. Measurements
Cricoid cartilage Corniculate cartilage 3. Cartilaginous
4. Muscles
Epiglottis Cuneiform Cartilage 5. ligaments
6. Folds
7. Blood Supply
8. Nerve Supply
9. Nerve Supply & Nerve Palsies
10. Diagram
47

Describe the Anatomy of larynx? Discuss the effect of damage to recurrent laryngeal nerve Dr Azam’s Notes in Anesthesiology 2013
Ligaments:
Intrinsic Ligaments: Extrinsic Ligaments:

• Cricovocal membrane • Thyrohyoid membrane
• Quadrangular membrane • Cricotracheal membrane
• Cricothyroid membrane • Hypoepiglottic ligament
Cavities:
• Vestibule
• ventricle
• Subglottic
Inlets of Larynx:
• It extends from the laryngeal inlet to the lower border of cricoid cartilages.
Folds:
• Aryepiglottic fold - Space between the aryepiglottic fold forms the laryngeal inlet.
• Vestibule fold - Space between the vestibule fold is called as Rima Vestibuli
• Vocal fold - Space between the vocal fold is called as Rima glottidis
• Vallecula: Shallow space present in front of the epiglottis behind the base of the
tongue.
48

Describe the Anatomy of larynx? Discuss the effect of damage to recurrent laryngeal nerve
Blood Supply to Larynx:
• Superior Laryngeal Artery: • Branch of

• Cricothyroid Artery: • Supply up to
superior
the vocal cord
thyroid artery
• Inferior laryngeal
artery • Branch of • Supplies below
Inferior thyroid the vocal cords.
artery
Nerve Supply:
! !"#$%&'()!(!
!!!"#$%&'(&!)*&+,-%*).!/! !!!0%1#&&%,2!)*&+,-%*).!/!
!!!!!3,2%&,*)!4&*,15!!!!!!!!!!!
9:2%&,*)!4&*,15!6;(2(&8! ?(2(&!4&*,15! "%,7(&+!4&*,15! Lymphatic Drainage:
67%,7(&+8! • Supraglottic lymph vessels: Upper deeper cervical glands
• Subglottic lymph vessels: Pre-tracheal ( lower deep cervical
glands)
"#$$)'%7!)*&+,:! "#$$)'%7!25%! "#$$)'%7!*))!',2&',7'1! "#$$)'%7!*))!
*4(<%!)%<%)!(=!<(1*)! 1&'1(25&+('>!;#71)%7! %:1%$2!1&'1(25+&('>! 7#4-)(22'1!&%-'(,!!!
1(&>!
49

Describe the Anatomy of larynx? Discuss the effect of damage to recurrent laryngeal nerve vocal Dr Azam’s Notes in Anesthesiology 2013
cord palsies? Continuation:
Vocal Cord Palsies:
Paralyzed laryngeal Extent Position of VC Voice Respiration Swallowing

nerve
Unilateral recurrent Incomplete Median Normal Normal Normal
laryngeal nerve
Complete Paramedian Hoarse of normal Normal Normal
Bilateral Median or Normal Dyspnea Normal
paramedian
Superior with RLN Unilateral or Cadaveric slack, Feeble or rough Normal Inhalation into larynx
Bilateral wavy
• Semonʼs Law: States that in a progressive lesion of recurrent laryngeal

nerve, the abductors are paralyzed before the adductors.
• Functional lesion: Adductor paralysis is almost always bilateral and
due to functional change in CNS.
50

Discuss the effect of damage to recurrent laryngeal nerve vocal cord palsies? Continuation: Dr Azam’s Notes in Anesthesiology 2013
Neurological lesions:
Vocal Cord palsy
General Causes
Vagus Nerve Recurrent Laryngeal nerve
• DM
Supra-nuclear lesions: • Syphilis
in the motor cortex • viral Disease
Left RLN Palsy:
• Aneurysm of Right recurrent laryngeal nerve:
aorta • Aneurysm of subclavian artery
• Lungs: TB, • Lungs: TB, apical carcinoma
Nuclear lesions: Malignancy Bilateral RLN Palsy:
• stroke • Esophagus: •Pulmonary tuberculosis
• Tumor malignancy • Esophageal malignancy
• MS
Peripheral
neurological
lesions
Intra Cranial: Lesions in the neck:

• Posterior fossa • Trauma
tumors • metastatic nodes
• Basal fractures
51

9. Respiratory Mechanics. Dr Azam’s Notes in Anesthesiology 2013
Respiratory mechanics: Refers to the study of factors involved in Determinants of lung volume
altering lung volume, which includes: MECHANICS OF and its subdivisions.
VENTILATION:
1. Muscular forces needed to expand the respiratory system.
2. Mechanics of ventilation.
3. Determinants of lung volume and its subdivisions.
Muscular forces needed to • Elastic resistance of

expand the respiratory system. tissues. – compliance
• Gas liquid interface.
• Non-elastic resistance to
gas flow. – Airway
resistance
• Thorax
• Muscles of ventilation
• Muscles of inspiration
• Diaphragm about #(75-80%) - major # muscle of
inspiration.
• External intercostals about (15-20%)
• Accessory muscles: sternocleidomastoid, scalene • Lung Volume
muscle, pectoral muscles, back muscles, muscles of • Lung Capacities
posterior neck
• Muscles of Expiration: GRID: Question to be answered under following headings:
• They begin to function only when pulmonary 1. Muscular forces needed to expand the respiratory system.
ventilation increases by 70 to 90 L/min. a. Muscles of ventilation - Inspiration & Expiration
• Abdominal muscles - rectus abdominis, external and 2. Mechanics of ventilation.
internal oblique, transverse abdominis; facilitate active b. Compliance
expiration. c. Gas liquid interface
• Internal intercostals muscles - lower ribs for forced d. Airway resistance - Non-elastic resistance to gas flow.
expiration. 3. Determinants of lung volume and its subdivisions.
e. Lung Volume & Capacities
52

10. Respiratory movement in Anesthesia. Dr Azam’s Notes in Anesthesiology 2013
1. When a patient is placed supine from an upright position, 5. Hiccup:

the proprotion of breathing from rib cage expansion • It is an intermittent clonic spasm of the diaphragm, of reflex origin.
decreases and abdominal breathing predominates, • It is transmitted via vagus nerve.
diaphragm contracts more effectively. • It can be caused by inflation of stomach with anaesthetic gases irritation
2. Lateral decubitus position, ventilation favours, the below diaphragm due to blood or pus.
dependent lung because dependent-hemi diaphragm takes • It is a reflex response of the partially anaesthetized respiratory centers
a higher position in the chest. and incompletely paralyzed peripheral musculature to vagal stimulation.
Induction of anesthesia activates expiratory muscles and Management:
expiration becomes active. So it necessitates Selicks maneuver • Block the reflex pathway by deeper level of anesthesia with
during induction of anaesthesia. supplementation with analgesic, potent inhalational anesthetic.
• In post op period: phenothiazine, initiation of following reflex with both
3. Tracheal tug: nose and ears blocked and patients sips repeatedly from a glass of water.
• This is a sharp downward movement of the trachea on • Local anesthetic infiltration of phrenic .N. in the neck should be
inspiration due to sharp contraction of the central part of the considered.
diaphragm or failure of elevator muscles of larynx to standup
to the forceful contraction of the diaphragm.
• In deep anesthesia inspiration is associated with a trachea
tug.
• It is seen in deep anesthesia, respiratory obstruction. GRID: Question to be answered
• It is an indication for E.T. tube suction or bronchoscopy. under following headings:
1. Supine Position
4. Sigh: For every 7 normal breaths one deep inspiration is 2. Lateral Decubitus position
taken this is known as sigh. It is seen in conscious and deep 3. Tracheal Tug
anesthesia. 4. Sigh
5. Hiccup
53

11. Abnormal Chest & Lung Movements Dr Azam’s Notes in Anesthesiology 2013
Introduction:
c) Mediastinal flap: When pleural cavity is opened, lung collapses
When the stability of the thoracic cage is destroyed either by
and the pressure around it becomes atmospheric, the negative
trauma/surgical intervention, then abnormal movements of both
intrapleural pressure on the other side, will pull the heart and great
chest wall and underlying lung may occur.
vessels in the mediastinum towards the normal lung, seen maximum
during inspiration. On expiration the intrapleural pressure becomes
There are 3 principle conditions that must be considered.
less negative and mediastinum passes back to its original position.
a) Paradoxical respiration: due to crush injury of the chest /
Consequences: It is dangerous in lateral position, as the whole
surgical removal of part of ribcage, the affected chest wall
weight of mediastinal contents is compressing the dependent normal
collapses in wards. On inspiration, the unaffected side will
lung. It interferes with the filling of great veins, leading to decreased
expand in the normal fashion but the injured side will be sucked
cardiac output.
in. On expiration, the reverse takes place. So thus called
"paradoxical respiration". Management:
It is seen in patients breathing spontaneously and abolished by • All three abnormal chest and lung movements can be treated by
controlled ventilation. It is an indication for artificial ventilation.
mechanical ventilation (IPPV).
b) Pendelluft: signifies pendulum like movement of air that
occurs from one lung to the other in the presence of an open
pneumothorax in a patient breathing spontaneously.
The lung on normal side fills with air partly from the trachea and
partly from the partially deflated lung on the affected side due to GRID: Question to be answered under
loss of intrapleural pressure. On expiration, the converse takes following headings:
place and some expired air form the normal lung passes over 1. Introduction
into the other side. 2. Paradoxical respiration
Consequence: rebreathing increases, alveolar CO2 tension 3. Pendelluft & its Consequence
increase. 4. Mediastinal flap & its Consequence
5. Management.
6. Diagram
54

ABNORMAL CHEST AND LUNGMOVEMENTS Dr Azam’s Notes in Anesthesiology 2013
Pendelluft
Mediastinal Flap
55

12. Changes in lung volume in various positions in anesthetized patient Dr Azam’s Notes in Anesthesiology 2013
1. Supine position: 5. Trendelenburg position:

• When conscious person changes from erect to supine position, • Decrease in lung capacities due to shift of abdominal viscera, increase
FRC decreases by 0.5 - 1L, because abdominal viscera press V/Q mismatch and atelectasis, decrease FRC, decrease pulmonary
against the diaphragm and 4 cm cephaloid shift of diaphragm compliance.
occurs during anaesthesia, cephaloid shift of diaphragm is due to 6. Reverse trendelenburg position:
muscular paralysis. • Increase FRC,
• During IPPV, gas moves along the line of least resistance, to the • spontaneous ventilation requires less work.
less congested and more compliant substernal units of the superior 7. Lithotomy position: VC decrease by 18%, more chance of
lungs are inflated preferentially. aspiration.
2. Horizontal position: 8. Sitting position: increase in LV, increase FRC, increased WOB,
• Gravity increases perfusion of dependent i.e., posterior lung Fatigue, Paralyse & ventilate to decrease WOB.
segments. Spontaneous ventilation favors dependent lung
segments and controlled ventilation favors independent i.e.,
anterior segments.
• FRC decreases and may fall below C.V. GRID: Question to be answered under following headings:
3. Prone position: 1. Supine position
• Compression of abdominal and thorax decreases total lung 2. Horizontal position
compliance and increase WOB. 3. Prone position
• Mechanical ventilation in prone position improves oxygenation in 4. Lateral decubitus position
ALI / ARDS, as it re-aerates the dorsal lung units, which are 5. Trendelenburg position
6. Reverse Trendelenburg position
collapsed - consolidated, when in supine position, due to weight of
7. Lithotomy position
overlying heart and high pleural pressures dorsally. 8. Sitting position.
• V/Q matching and oxygenation are improved in prone position,
which leads to decrease in inspired oxygen concentration and
decreases the MAP and increases outcome in ALI / ARDS.
4. Lateral decubitus:
• There is decrease volume of dependent lung but there is increase
in perfusion.
• Increase ventilation of dependent lung in awake patients, while
there is decrease ventilation of dependent lung anaesthetized
patient.
56

13. Surfactant Dr Azam’s Notes in Anesthesiology 2013
Definition:
Clinical problems associated with deficiency:
“A chemical substance in the alveolar lining fluid which varies the surface
- Gas exchange deteriorates within 24-36hrs.
tension as alveolar volume changes is called pulmonary surfactant”.
- Arterial hypoxemia is the first clinically observable indication.
Production / synthesis: - Decrease compliance
• Synthesis in utero occurs during the 2 trimester of pregnancy (24 wks of - Alveolar hypoventilation
gestation)
- Serious V/Q abnormalities
• pulmonary surfactant is produced by type II granular pneumocytes in the
lung( type II epithelial cells) formed by the synthesis of fatty acids which - Respiratory acidosis
are incorporated into the phospholipids such as Dipalmitoyl lecithin.
- Patchy atelectasis produces regions of shunt like (venous
Contents: admixture like) effect aggravating arterial hypoxemia.
Surfactant contains
• Dipalmitoyl phosphotidyl choline (DPPC): 62%
• Neutral lipids: 13% Surfactant therapy: Dose 3ml/kg
• Proteins: 8% • use of surfactant greatly assists in the management of infants with
• Carbohydrates 2% respiratory distress syndrome.
• Other phospholipids 10% • It can be used to prevent or treat RDS in premature infants of low
Importance of surfactant: birth weight.
• A number of verities seem to influence the result of surfactant
• By decreasing the surface tension it increases the lung compliance and
therapy in ARDS. They are,
thereby favors even distribution of inspired gas.
1. Timing of treatment.
• Alveolar stability 2. Mode of administration
• Significant for alveolar liquid balance 3. Type of surfactant preparation
• Most of the “ELASTANCE” of the lung is determined by the surface 4. Dosage
tension phenomenon. 5. Ventilatory strategy used in combination with surfactant. Early
• Significant in alveolar clearance and alveolar configuration. treatment may be more beneficial.
6. Nebulization is not effective.
GRID: Question to be answered under following headings: 7. Bronchoscopic or direct intratracheal instillation of aerosols more
1. Definition effective.
2. Production & synthesis • Natural surfactants are less vulnerable for inactivation by the
3. Contents plasma components filling the alveoli.
4. Importance of Surfactant • Artificial surfactants are to the used in LARGE doses.
5. Deficiency • Surfactant therapy and PEEP together produce the largest and most
6. Surfactant Therapy sustained effect. #
57

Single left lung Right DLT BB/Left DLT/
14 . Tracheo-Bronchial Tree with Diaphragm. Whole lung lavage Dr Azam’s Notes

Left DLT in Anesthesiology 2013
Independent lung ventilation Left DLT Right DLT
BB, ipsilateral bronchial blocker; DLT, Double-lumen tube; EBT, contralateral single-lumen endobronchial tube.
Trachea:
• Tube formed of 15 to 20 C – shaped cartilage, which are incomplete posteriorly.
Right lung Left lung
• Adult trachea 11-13 cm, 1.5 to 2.5 cm wide. 19
Extends:
• From C6 to T5 (level of cricoid cartilage to sternomanubrial joint) Apical Apical posterior
• Lined by ciliated columnar epithelium Upper lobe Posterior 22

50
16
• Moves with respiration and with alterations in position of head. Deep inspiration Anterior 10
13
Anterior
– carina descends as much as 2.5cms Upper lobe
• Extension of Head and Neck - ↑ length of trachea by 23 to 30% Lower lobe Superior
Lingula
Superior 9 Inferior
Lateral Superior
Middle lobe
Medial Anterior
basal
Medial
Anterior basal
Angle of main bronchus: basal Posterior Lateral
basal basal
Lateral
basal Posterior
basal
Lower lobe
Millers: Page # 1842

Figure 59-20 Diagram of the tracheobronchial tree. Mean lengths and diameters are shown in millimeters. Note that the right middle lobe bronc
A directly anteriorly while the superior segments (some authors refer to these as the “apical” segments) of the lower lobes exit directly posteriorly.
apical designation on the right side the segmental bronchi in a rostral to caudal sequence give the mnemonic “A PALM A MAPL.” (From Youngber
Vascular and Thoracic Anesthesia. Philadelphia, Churchill Livingstone, 2000.)
Generations: Dichotomous division

• The Bronchi divides 23 times in total, and 23 generations “Weibel
Classification” in order to increase the surface area available for gas
Difference between right and left main bronchi: exchange.
1. Right main bronchus wider and shorter – 1-2.5cm longer • The first 16 Generations are termed as conducting Zone.No bronchi in
2. Left main bronchus narrower and longer – 5cm this region takes part in gas exchange. This forms the anatomical dead
3. Diverges right main bronchus at 250 space. Its around 150 ml.
• Generation from 17 to 23 is the Respiratory Zone - Where gas exchange
4. Left main bronchus at 450
takes place. The volume is around 2-3 liters.
5. Right divides into upper, middle and lower branches • Turbulent flow occurs from Generations 1 - 5 & laryngeal opening.
6. Left divides into upper and lower lobe branches • Larynx - Orificial flow.
58

Tracheo-Bronchial Tree with Diaphragm. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Anesthetic implications:
1. Right main bronchus is more nearly vertical than left main bronchus –
Right Left tendency for ETT and suction catheter to enter RMB is high.
Upper lobe Upper lobe 2. If the ETT is inserted too far, the beveled end of the tube may become
1) Apical 1) Apical blocked off by its lying against the mucosa on the medial wall of RMB.
2) Posterior 2) Posterior 3. The short length of RMB makes the lumen difficult to occlude during
3) Anterior 3) Anterior thoracic anesthesia.
Middle lobe Lingular lobe
4. Posterior segment of right upper lobe and apical segment of right lower lobe
4) Lateral 4) Superior
5) Medial – common sites for development of lung abscess.
5) Inferior
Lower lobe Lower lobe 5. Patient lying wholly or partly on the side – inhaled material gravitates to into
6) Apical 6) Apical basal lateral portion of posterior segment particularly right side.
7) Medial basal 7) Anterior basal 6. patient lies on his back – inhaled material accumulates in apical segment of
8) Anterior basal 8) Lateral basal lower lobe.
9) Lateral basal 9) Posterior basal 7. When the patient lies supine – apical segment, of either lower lobes.
10) Posterior basal
8. Right sided endobronchial tubes must have a slit in the bronchial cuff for
ventilating the right upper lobe. Anatomic variations between individuals in
the distance between the right upper lobe and the carina often result in
difficulties in ventilating that lobe with right sided tubes.
Drugs influencing bronchial smooth muscle tone:
Broncho dilatation Broncho constriction GRID: Question to be answered under following
headings:
• Salbutamol, adrenaline, • Neostigmine,histamine and 1. Trachea
isoprenaline, aminophylline, histamine releasing drugs, 2. Extent
halothane amylnitrate, atropine PG inhibitors,atracurium, 3. Angle of left & right main bronchus with Diagram
and hyoscine β - blockers 4. Difference between right & left main bronchi
5. Generations & Dichotomous divisions
6. Diagram with Labelling
7. Drugs influencing bronchial smooth muscles.
8. Anesthetic implications.
59

15. Hypoxic Pulmonary Vasoconstriction Dr Azam’s Notes in Anesthesiology 2013
Definition: Hypoxic pulmonary vasoconstriction is a paradoxical, Factors influencing HPV in hypoxia or atelectatic lung:
physiological phenomenon in which pulmonary arteries constrict in the 1. Vasodilator such as NTG, nitroprusside, β-adrenergic
presence of hypoxia without hypercapnia, redirecting blood flow to
alveoli with a higher oxygen content. agonists dobutamine, salbutamol, Glucagon, ↓HPV.
(aminophylline ,hydralazine may not ↓ HPV )
Alveolar Hypoxia leads to 2. Very high or very low pulmonary artery pressure
Mechanism:
3. Very high or very low mixed venous oxygen tension
{SvO2 }.
4. Decreased FiO2
! !"#$%"#&'%'($)'*)+&&),-,./+*-$) 5. Pulmonary Infection
6. hypocapnia
!"#$%"#&'%($)*+,* 7. Volatile Anesthetic agents.
0/+1"'(#*'1)+1'()) Mechanism:
-'%#973)2($)** :76&##973)2($)*** • Alveolar hypoxia stimulate metabolic activity of pulmonary vascular
5!;8* smooth muscle directly and ↑ production of ATP.
-)./#01')2)$** !1#$0(3&(24'2$*5%1#$0(676&'28** • This low O2 tension also causes membrane of pulmonary vascular
smooth muscle cell in a state of partial depolarization and
influences the role of calcium in excitation – Calcium contraction
!2&,#*+/3)4+$#1#*$5/'15#/) !2&,#*+/3)4+$#('&+5+5'#*)) coupling.
• Thus alveolar hypoxia may directly causes ion fluxes which cause
contributes to vasoconstriction.
! )6!7) " )6!7)
60

Hypoxic Pulmonary Vasoconstriction. Continuation: Dr Azam’s Notes in Anesthesiology 2013
I (-) HPV II. Factor ↓ blood flow in ventilated lung and divert or ↑
• Very high or very low pulmonary artery pressure blood flow to hypoxic or atelectatic lung
• Hypocapnia • PEEP in ventilated lung
• High or very low PVO2 • Low FiO2
• a) Vasodilator (NTG, nitroprusside) • Vasoconstrictor - vasoconstriction in normoxic lung
• b) Calcium channel blocker • Intrinsic peep
• c) β agonists (Dobutamine, aminophylline)
• Pulmonary infection
• Inhalation anaesthetics
• N2O ? refer.
Factors Increasing ↑ Pulmonary Vascular Resistance Factors Decreasing ↓ Pulmonary Vascular Resistance
• 3A – Angiotensinogen II • α-blockers
• -Acidosis • β-sympathomimetic
• - α-sympathomimetic • PGE1 and PGE2
• B – beta-blocker • Ach
• C – Cyclopropene • Aminophylline
• D – Diethyl Ether, N2O • Alkalemia
• 2H - Hypoxic & Hypercapnia • Sodium Nitroprusside
Summary:
61

16. Hering–Breuer inflation reflex Dr Azam’s Notes in Anesthesiology 2013
Hering and Breuer in 1868 showed that inflation of lungs, reflexly inhibited the spontaneous contraction of diaphragm and
concluded that pulmonary stretch receptors are responsible for initiation of this reflex.
Stretch receptor:
• Unencapsulated
• Without end organ
• Found in airway smooth muscles
• Abundant near the carina.
-Stimulus:
• Stretching
• Changes in lung volume
- Increases in lung volume increases afferent nerve traffic via vagus nerve to the respiratory centre. This inhibits further
inspiration.
- This limitation of inspiration determines the relationship between tidal volume and respirator frequency.
- These pulmonary stretch receptors are generally responsible for signaling changes in the mechanical state of the lungs
to the brain.
Hering – Breuer reflex:

• Cannot be demonstrated in awake resting human beings during normal tidal breathing.
• Anaesthesia abolishes this reflex
• Barbiturates – low dose, depresses this reflex high dose abolishes this reflex.
62

17. Airway Resistance Dr Azam’s Notes in Anesthesiology 2013
Definition:
Conditions that Increases Airway resistance:
• Raw is the degree of airflow obstruction in the airways.
• It is the pressure needed to generate a given inspiratory flow. Type Clinical condition
• ΔP / ΔV
1) COPD Emphysema
Chronic bronchitis
Airway Resistance = Alveolar pressure(intra-pleural pressure)/
Asthma (chronic and acute)
Flow
Bronchiectasis
2) Mechanical obstruction Post intubation obstruction
• Normal value: 0.6 -2.4 cm H2o /lt /sec ( at flow 30 lt / min i.e 0.5lt/
Foreign body aspiration
sec )
Endotracheal intubation
• Measurement:Driving pressure may be measured by body
plethesmography, pneumotachygraph. Condensation in ventilator
circuit
Factors affecting airway resistance: 3) Infection Croup
# Airway resistance causes obstruction of airflow in the airways. It Epiglottitis
is increased when the patency or diameter of the airways is reduced. Bronchiolitis
Obstruction to airflow may be caused by (i.e. diameter is decreased in)
i) Inside the airway # (ex. Retained secretion)
# ii) In the airway wall (ex. Neoplasm of bronchial muscle)
# iii) Outside airway (ex. Tumour surrounding and compressing) Raw and length of ETT:
lymph node enlargement hematomas.
According to simplified form of poiseuilles law, (laminar flow) Raw α Length α 1/Diameter4
Low lung volume à radial traction produced by lung parenchyma
surrounding the airway, and which holds them open is reduced à
ΔP =
decrease diameter à increase Raw
ΔP: Driving pressure, r = Radius of airway, V = Air^low.
(Note: in clinical setting, ↑ raw is one of the most frequent cause of
increased WOB).
(If flow is turbulent then, pressure gradient is proportional to r5).
If flow is orificial (i.e. ex. constrictions like larynx, flow rate will be
proportional to density).
63

Airway Resistance. Continuation: Dr Azam’s Notes in Anesthesiology 2013
-Bronchial muscle tone

• Vagus stimulation
• Hypoxia ( these all three cause bronchoconstriction )
• Histamine
-Effect of anaesthesia

• Increased during anaesthesia
• Because of Bronchospasm
o Reduction in FRC, lung volume
o Tubes, connection of circuit.
• Cyclopropane, morphine → increases Raw
• Ether, halothane, atropine → decreases Raw
Posture: Flexion of neck à increase raw (twice).
Smaller airways: of size < 2 mm diameter are very large in number
• Therefore contribution to Raw is minimal.

• Increased density, viscosity of gas à increase Raw.
• Medium sized airways contribute maximum to Raw.
• A patient does not experience dyspnea unless the resistance is

increased about 3 times while 5-15 times in SEVERE
DYSPNEA.
64

18. Working of Breathing. Dr Azam’s Notes in Anesthesiology 2013
• It comprises all the energy required to ventilate the The air resistance in laminar ^low can be lowered by reducing the viscosity,
lungs. whereas in turbulent ^low it is the density that must be lowered.
• Because expiration is normally entirely passive, both the I. Effect of work breathing:
inspiratory and expiratory work of breathing is • Increases in the work of breathing 1) anaesthesia-most often because of
performed by the inspiratory muscles. (Primarily the reduced lung, chest wall compliance less commonly, increase in airway
diaphragm). resistance.
• It equals the product of pressure change across the • The problems of increased work of breathing are usually circumvented by
lung and volume of gas moved. controlled mechanical ventilation.
II. Measurement of work of breathing:
• The pressure change ΔP in the equation Raw = • Total work of breathing is difficult to measure in spontaneous respiration,
can be treated as the amount of work of breathing. In volume may be measured with a pneumatograph, esophageal pressure
quite breathing it ranges from 0.3-0.8 kg Nm/minute. indicating intrerpleural pressure, may be measured with an esophageal
• Elastic resistance: Defined as force tending to return balloon.
the lung to its original size after stretching. It is not the • Normally the WOB accounts for less than 3% of the total body O2
force required to expand the lung. consumption, at rest but may be much higher in diseases.
• The work required to overcome elastic resistance # # # Ex: # COPD
increases as tidal volume increases.i.e ERαTV, lung # # # # Cardiac failure.
volumes # # # # Exercise, anesthesia.
• The structural resistance: is composed of the
• Thocacic wall WOB and anesthetic circuits.
• The diaphragm • Expiratory valve in anesthetic breathing systems increases work of
• The abdominal contents. expiration, particularly when not fully open.
• is related to speed of the flow of air. Therefore when
It • Coaxial anesthetic breathing systems increase expiratory resistance, the
speed of flow of air increase, structural resistance lack by virtue of its small caliber expiratory tube, and the Bain because of
increase. the high flow rate of fresh gas directed at the patients mouth.
The air flow resistance:
• Depends on length and size of lumen of bronchial tree.
• E.T.T.: increase air flow resistance.
• Particularly important in a young child for whom too
small an ETT may increase the air resistance
enormously.
65

19. Carbon-Di-Oxide Dissociation Curve Dr Azam’s Notes in Anesthesiology 2013
• CO2 diffuses passively down its concentration gradient from the mitochondria to the
capillaries.
• The tissues produce CO2 and this is then given up to the blood circulating through
the capillaries.
• It rapidly enters the plasma and then passes in to the red cells.
• On reaching the pulmonary capillaries the PCO2 in venous blood is 46 mm Hg and
PACO2 is 40 mm Hg therefore a pressure gradient of 6 mm Hg, driving CO2 across
the AC- membrane.
• In normal circumstances each 100 ml of arterial blood caries 48 ml of CO2;. CO2 is
transported in blood in 3 forms:
• Dissolved CO2: - (in solution in plasma): This dissolved CO2 form is very important
because it is responsible for determining the CO2 tension in the blood, it acts as
the intermediary between the air in the alveoli and the inside of the RBC.
• As bicarbonate: 70% of the CO2 passes to the RBC's and combines with H2O à
carbonic acid which is accelerated by the presence of the enzyme. "Carbonic
anhydrase" with in the RBC's and endothelium and then carbonic acid dissociates
into H" and HCO3 ions. As a result HCO3-‐ represents the largest fraction of the CO2 in
the blood. The HCO3 diffuses out of the RBC into the plasma so to maintain ionic
equilibrium Cl-‐ ions diffuse into the RBC, this is called the "Chloride shift/
Hamburger effect".
• As a carbamino compound: About 25% CO2 can combine with the amino -‐group of
the Hb to form "carbamino -‐ Hb".
• In the tissues deoxygeneration of Hb enhances carriage of CO2 by activating
proton finding and carbamino formation sites. Correspondingly, oxygenation of Hb
causes the reverse effect, displacing H+ and CO2, thus facilitating the "unloading"
of CO2 in the lungs. This dependency of CO2 carrying capacity on the oxygenation
state of Hb is known as the "Haldane effect".
66

Carbon-Di-Oxide Dissociation Curve. Continuation:
CO2 Transport
3 forms
• The Haldane effect is the shift in the relationship of PCO2 to the
total CO2 caused by altered levels of O2. Low PO2 shifts CO2 DC
to left so that the blood is able to pick up more CO2 and high PO2 Dissolved As
Bicarbonate
As Carbamino
compound
shifts"CO2 DC to right so that unloading of CO2 in the lungs form 70%
25% CO2
occurs. co2 + H2O - Carbonic acid
+ amino
It determines In presence of carbonic
• CO2 dissociation curve: It relates to the CO2 content of blood to the
anhydrase
group of
the PCO2 to which it is exposed. The position of this curve CO2 tension in H+ & HCO3 Hb
depends upon the degree of oxygenation of the blood. The more blood HCO3
Carbamino Hb
diffuses out
deoxygenated the blood becomes, the more CO2 it carries at a Of RBC
given PCO2 this is called the "Haldane effect". To maintain

ionic
• The major component of the Haldane effect is the increase Equilibrium
carriage of CO2 by reduced Hb as carbamino Hb. In addition, CO2 Cl ion

is carried as by HCO3 is increased. Due to the Haldane effect, the Diffuses into
RBC
up take of CO2 by the capillary blood is facilitated. When this It's called chloride
blood reaches the lungs and becomes oxygenated, the Shift
Or Hamburger
elimination of CO2 is facilitated. Effect
• The CO2 response curve is a sensitive index of respiratory
depression and also it is used to study the respiratory effects
of narcotic drugs.
Methods are used to measure the CO2 response curve:

a) Steady state method
b) Rebreathing method
Shift to right:
• Pethidine, morphine, emphysema, metabolic alkalosis.
Shift to left:
• Metabolic acidosis, hypoxia. Progressive reduction of the CO2
dissociation curve is seen with inhalational agents, in
appropriate components in the anaesthetic circuit.
• The CO2 response curve changes from person to person and time
to time in the some individual.
67
20. Dead Space Dr Azam’s Notes in Anesthesiology 2013
Defined: Is defined as wasted ventilation or a condition in which ventilation is in Alveolar dead space:
excess of perfusion or high V/Q ratio. • It contributes wasted ventilation, their the ventilated
Types: alveoli are not adequately perfused by the
I. Anatomical Dead space pulmonary circulation.
II. Physiological dead space • In normal physiological condition it is negligible
III. Alveolar dead Space • factor influencing.
IV. Apparatus Dead space • Alveolar dead space is increased (where V/Q is
I. Anatomical Dead space high).
• Anatomical dead space (VD anat) compromises the volume of respiratory 1. Decrease CO (CCF) and blood loss
passages extending from the nostril and mouth down to (but not including) (hypotension)
respiratory bronchioles as there is no exchange of gases between blood and 2. Pulmonary vasoconstriction
air. (Nostrils to terminal bronchioles) 3. Pulmonary embolism
• Value: for a given total volume 500ml anatomical dead space is 150ml or
Physiological dead space:
30% of total volume or 2ml/kg body weight. (POUNDS)
# It is the sum of anatomical and alveolar dead
Factors inGluencing Anatomical dead space: space. Under normal condition, the physiological
Anatomical dead space varies with age dead space equal anatomical dead space.
• In young women it may be as low as 100ml
Normal value: It accounts for 1/3rd or 30% of tidal
• In old men it may be more than 200ml
volume or 2 ml/kg.
1. Position of the lower jaw • The relationship between physiological dead space
• Depression of the jaw, flexion of the head (common cause of respiratory and total volume (VT) remains fairly constant when
obstruction in anesthetized patient) reduces dead space by 30ml. tidal volume is altered, the VD physiological. is
• Protrusion of the jaw with extension of the head increases dead space often expressed as a fraction of the tidal volume.
by 40ml • VD/VT ratio: normal -0.25-0.4
2. Pneumonectomy or tracheostomy ↓ volume of dead space
3. Artificial airway or intubated patients – it ↓ dead space
4. Anti-cholinergic agents à↑ dead space
5. Posture – upright à↑, Supine à↓
6. Lung diseases and bronchitis, asthma à↑
7. Positive pressure ventilation à↑
8. ↓ in tidal volume increases dead space
68

Dead Space. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Apparatus dead space: Factor Dead space

Consists of gas contained in any anesthetic apparatus between the patient
1) Posture
and that point in the system where rebreathing of exhaled CO2 cease to
occur.
Upright ↑(VD anatomical)
Supine ↓
# This may add up to VD physiological further decreases the alveolar
ventilation it is very hazardous in anesthetized pediatric patients. 2) Position of airway
Neck extension ↑
Neck flexion ↓
Effect of anaesthesia on dead space: 3) Age ↑
VD physiological appears to be variable – but as a general rule VD phs a 4)Artificial airway, intubation ↓
VD/VT ratio is increased in patient under anaesthesia after taking into account
5) IPPV ↑
of apparatus dead space.
During IPPV: ↑ is VD physiological is approximately compensated or by 6) anti cholinergic reagents ↑
7) Lung diseases(Bronchitis, asthma) ↑
intubation (which reduces dead space by 70 ml). so
8) ↓ pulmonary blood flow (VD
1. Ventilated + intubation and anesthetized patient à VD/VTà 0.3 – physiological).
Pulmonary vasoconstriction
0.45
Pulmonary embolism ↑
2. If corrected VD by intubation is not taken into account, then VD/VTà 0.4
Hemorrhage (hypotension)
– 0.6.
Cardiac failure
-IPPV à zone I (↑ VD/VT).
Comparative study: Dead space is more when mask is used, when compared
to intubation
• VD/VT with mask à 0.68
• VD/VT intubation à 0.51 maská,intubation↓ by 70 ml
- Thus a difference in total functional dead space of 82 ml between
intubated patients and anesthetized with mask.
- Dead space during anesthesia with passive ventilation can be roughly
estimated by.
VD/VT = 33+ %
69

21. CO2 Response curve. Dr Azam’s Notes in Anesthesiology 2013
Definition:
FACTORS INFLUENCING THE CO2 RESPONSE
The carbon dioxide response curve is a sensitive index of respiratory
CURVE:
depression and as such has been used in the study of respiratory effects of
Alterations in the CO2 response curve may be two types
narcotic drugs.
• Slope may be increased or decreased indicating an
Methods: alteration in CO2 sensitivity.
The ventilatory response to CO2 is usually measured using either • The curve may be displaced either to the left or right.
1. Study state method Both types may be of course be seen together.
2. Rebreathing method
Following factors which influence the CO2 response:
1) Study state method: • Individual responses: vary from person to person and
The patient inspires 3 different concentration of CO2---- 2%, 4% and 6% each time to time in a same individual.
for about 20 mins or until ventilation is steady. Towards the end of each period • Hypoxia: in presence of hypoxia, the CO2 response
the ventilation to end tidal CO2 are measured .points relating to ET PCO2are curve become steeper. Hypoxia therefore reinforces the
derived. The time of benefit is obtained. ventilatory response to CO2.
• Metabolic acidosis and alkalosis.
2) Rebreathing method:
The Patient re-breaths for 4 min from a 6 liter bag which is filled with initial 7% In steady method:
CO2, 50%O2 and 43% N2. During first half minute equilibration occurs between • Metabolic acidosis shifts the curve to the left
CO2 in the bag and the subject. During the next 3-5 mins there is a linear • Metabolic alkalosis shifts the curve to the right –
increase in PCO2 and consequent increase in ventilation. Time relating although slopes remain unchanged.
ventilation to end tidal PCO2 is derived from measurements made during this
time.
For comparable levels of PO2 the rebreathing and steady state method give
similar results for the CO2 sensitivity except during metabolic acidosis and
alkalosis.
The advantages of the rebreathing are that it is rapid but distressing to the
subject and it can more readily be repeated.
Points relating to ventilation to end tidal PCO2 are derived from these method
and the time of best fit is obtained.
The is called CO2 response curve inspite of being straight line.
The slope of the line (1 min–1 kpa–1) is measure of the subjects ventilatory
sensitivity to CO2. 70

22. Mixed venous Oxygen saturation (SVO2) Dr Azam’s Notes in Anesthesiology 2013
Mixed venous oxygen saturation is a PAC (pulmonary artery catheterization) based monitoring technique. Fick’s equation forms the basis for PAC
based monitoring termed continuous mixed venous oximetry.
Rearrangement of Fick equation reveals the following determinants of SVO2.
SVO2 =
SaO2 = Arterial O2 saturation (%)
VO2 = O2 consumption (ml O2/min)
13.9 = constant (O2 combining power of Hb).
Hb = Hemoglobin concentration (g/dl).
• As long as arterial O2 saturation, O2 consumption and haemoglobin concentration remains stable ,mixed venous O2 saturation can be used as an
indirect indicator of cardiac output.
• Mixed venous oxygen saturation varies directly with arterial O2 saturation and hemoglobin concentration and varies inversely with O2
consumption.
• SaO2 and Hb% =

• SVO2 provides comprehensive information about the balance of O2 delivery and consumption by the body, not just cardiac output but also
adequacy of cardiac output.
Measurement:
Although mixed venous oxygen saturation can be determined by intermittent blood sampling from pulmonary artery, a specially designed PAC
can provide this information more reliably and continuously. Fibreoptic bundles incorporated into the PAC determine the Hb saturation in pulmonary
artery blood based on principles of “REFLECTANCE OXIMETRY”.
A special computer connected to this PAC displays SVO2 continuously and allows standard thermodilution cardiac output measurements.
Low SVO2 (< 60%) may sensitively re^lect an abnormality of one or more of the factors on the right hand side of equation.
71

Mixed venous Oxygen saturation (SVO2). Continuation: Dr Azam’s Notes in Anesthesiology 2013
Factors artifactual elevate SVO2:

• Wedging of the catheters. Interpretation of Mixed venous
Oxygenation (SVO2)
• mitral regurgitation
• Improper PAC tip positioning
• Inaccurate calibration
• sepsis, L-R shunts.
• In summary, SVO2 oximetry is an appealing, well Normal Low
established technology, but catheters are more > 70% < 70%
expensive than PAC and studies have not defined
appropriate clinical indications for their use.
Do nothing
SaO2
Mixed Venous
Oxygenation
Low (Hypoxia Normal > 95%
(Increased O2 Extraction Ratio
Low Mixed Venous Oxygen Therapy

High Mixed venous
oxygenation Increase PEEP
Oxygenation
Cardiac output
Decreased Increased Decreased Others

Oxygen Usage
Low Cardiac output
Oxygen Oxygen
usage High Cardiac output ( < 2.5 L/min/m2)
Delivery
(> 2.5 L/min/m2)
Impaired Oxygen
Hypoxia Delivery Pulmonary artery
Fever CN Poisoning
Anaemia Sepsis / Burns Occlusion pressure
Increased Metabolic Hypothermia
Decreased Cardiac Mitral repair Hemoglobin
State
output Shivering
Alkalosis
Meth Hb
> 18 mm Hg
Myocardial Dysfunction < 18 mm Hg
> 8 gms/dl
(Stress, anxiety, pain or High VO2)
< 8 gms/dl (Anemia) Fluid Challange

Dobutamine
Analgesia/Sedation 72
Blood Transfusion
23. Flail Chest Dr Azam’s Notes in Anesthesiology 2013
• A flail chest occurs when two or more adjacent ribs are fractured in two or Management:
more places resulting in a segment of the thoracic cage becoming • Stabilization of injured patient:
detached. Flail chest--also called floating or crushed chest. • O2 supplementation
• On inspiration there is encroachment of the injured segment upon the lung • Ventilatory support if V/Q mismatch on ABG
due to paradoxical movement leading to impairment of ventilation & • External traction on the injured segment is done
oxygenation. • Pain management
• It is common with blunt injury or trauma to the chest wall involving antero- • intercostal blocks
lateral aspect. • Thoracic epidural
• Commonly seen in elderly age group because of more calcification & • Intravenous injections of Fentanyl/Morphine.
brittleness of the chest wall. • Appropriate antibiotics
• intramedullary pinning of the ribs
Diagnosis:
• History of blunt trauma to the chest & clinical assessment - pain, erythema,
edema, tender to touch, subcutaneous emphysema
• cardio-respiratory insufficiency
• V/Q mismatch on serial ABG analysis
• Mediastinal air indicates injury to bronchi or trachea.
• Pendelluft Phenomenon: To & fro movement of air from damaged lung to
normal lung - leads to inadequate oxygenation.
Monitoring:
• ECY for Dysrrhythmias
• Frequent ABG & other lab test like Hb, TC Ultrasound abdomen to R/O any
abdominal injury.
• FiO2 Analyzer
• Pulmonary artery pressure to measure pulmonary artery shunting
• Blood pressure
73

24. Tissue Oxygenation. Dr Azam’s Notes in Anesthesiology 2013
Definition: Factors which increases VO2:

• IV Methylene blue (1mg/Kg)
• The adequacy of tissue oxygenation is determined for methemoglobinemia
by balance between oxygen delivered (VO2) into the • Increased Cardiac Output:
Patient with Sepsis • Prompt correction of
tissue and O2 required to sustain aerobic •
Metabolic acidosis.
metabolism (MRO2). • Left to right shunts
• AV fistula
• Excess of inotropes
• When VO2 is equivalent to MRO2, glucose is
completely oxidized to yield 36 ATP molecule (673 • Inflammatory conditions
kcal) per molecule of glucose. • Increased hemoglobin:
• High Hematocrit due to chronic hypoxia
• When VO2 cannot match MRO2 some of the
• Increased SaO2:
glucose is diverted to form lactate, with energy yield
• Weaning or recovery from hypoxia
of 2ATP(47 kcal) molecules per glucose molecule.
Factors which Decreases VO2:
• VO2<MRO2 = Shock/Dysoxia Cyanide toxicity
•
• Methemoglobinemia
• Dysoxia can be result of an in adequate supply of Hypothermia
•
oxygen as occurs in hypovolemia shock and
• Sepsis
cardiogenic shock or it can be caused by a defect in
• Carbon monoxide poisoning
mitochondria O2 utilization as occurs in septic
• Anemia to hemolysis
shock.
• Decreased CO - Hypovolemia, MI & CCF
• VO2 can be calculated by: VO2 can be improved by:
• VO2 = Cardiac output ( Cao2 - Cvo2) - Fick equation • Volume resuscitation to be done in patients
# # or with decreases Cardiac index, low CVP < 4
• VO2 = QX1.34XHbX(SaO2-SvO2) mm of Hg or PCWP < 6 mm of Hg
• Aim CVP > 10 mm of Hg & PCWP > 15 mm of
Tissue oxygenation is affected by:
Hg
• Cardiac output • Use of Dobutamine in patients with low
• Hb Concentration ejection fraction or CCF.
• Difference in O2 Hb saturation between arterial • Anemia Hb < 7gm/dl - Correction with blood.
blood & venous blood (SaO2 - SvO2)
• If SaO2 is less than 90% - give Oxygen
• Antibiotics in Sepsis
An abnormally low VO2 ( < 100ml/min/m2 ) can be a • Normothermia to be maintained
marker of impaired tissue oxygenation, in patients with • Hyperbaric Oxygen therapy
no sepsis or inflammation.
74

Tissue Oxygenation - Continuation Dr Azam’s Notes in Anesthesiology 2013
1. Inhibition of Oxidative
Phosphorylation Cardiac
2. Mail distribution of blood flow output
3. Oxygen Dysfunction
Oxygen
consumption
Oxygen
content
Factors influencing Tissue

Oxygenation
Oxygen
delivery
Oxygen
transport
Oxygen
DO2 = CO X SaO2 X 1.59
uptake
VO2 = CI X Hb X ( CaO2 - CvO2 )
75

Tissue Oxygenation. Continuation. Dr Azam’s Notes in Anesthesiology 2013
Heart Rate
Pulse Blood Pressure
Oximetry
Lactate Urine
levels Output
pH Measurement of
tissue
Oxygenation
Clinical Signs
SvO2
ABG
76

25. Metabolic function of the lung. Dr Azam’s Notes in Anesthesiology 2013
Whilst the main function of the lung is for respiratory gas

exchange, it has several other important physiological roles
These Include:
• Reservoir of blood available for circulatory compensation
• Filter for circulation:
• Thrombi, micro-aggregates etc
• Metabolic activity:
• Activation:
• Angiotensin III
• Inactivation:
• noradrenaline
• bradykinin
• 5 H-T
• some prostaglandins
• Immunological:
• IgA secretion into bronchial mucus
• Pulmonary surfactant - formed in Type II alveolar cells.
77

26. What are the major causes of Hypoxemia? What is Hypoxic Pulmonary Vasoconstriction? How
can general anesthesia worsens V/Q mismatch?
Five Causes of Hypoxemia (↓ PaO2):

1. Hypoventilation
2. Low inspired Oxygen
3. Right to Left shunt
4. Ventilation-Perfusion mismatch
5. Diffusion impairment
Five Causes of Hypoxemia (↓ PaO2):
Hypoventilation: Low inspired Oxygen:

• P(A-a)O2 is normal Right to Left shunt: Ventilation-Perfusion
• A decrease in Barometric
• PaCO2 is elevated ( Hypercapnia) pressure (High Altitude) • Healthy Individuals: mismatch:
• A portion of the bronchial • V/Q mismatch is the
• A decrease in FIO2 - circulation (blood supply most common cause of
Causes of Hypoventilation: accidental disconnection
• Depression of CNS by drugs to the conducting zone hypoxemia in disease
of the ETT, leak or of the airways) venous state.
• Upper airway obstruction exhausted central supply blood drains into the
• Disease of Neuromuscular of O2 pulmonary vein
junction
• A portion of coronary
• Disease of respiratory muscles circulation venous blood Diffusion impairment:
• Abnormality of the chest wall drains through the
• Disease of motor neurons of the • PaCO2 is normal
thebesian veins into the
brain stem/Spinal cord left ventricles
• P(A-a)O2 is normal at rest
• Inflammation, trauma or but may be elevated
• Congenital abnormalities:
hemorrhage in the brain stem • TOF,
during exercise
• VSD + PAS
• Intrapulmonary
Hypoxic pulmonary vasoconstriction is a paradoxical, physiological fistulas
phenomenon in which pulmonary arteries constrict in the presence of
hypoxia without hypercapnia, redirecting blood flow to alveoli with a higher
oxygen content.
78

How can general anesthesia worsens V/Q mismatch? Continuation:
Book Text Pagina 2 di
V/Q Ventilation Perfusion:
Definition: It is relationship between alveolar
ventilation & total perfusion.
In zone 1:
• Alveolar pressure (PA) > pulmonary artery pressure (Ppa) >
pulmonary venous pressure (Ppv).
In zone 2:
• Pulmonary artery pressure (Ppa) > Alveolar pressure (PA) >
pulmonary venous pressure (Ppv).
• Flow in zone 2 is determined by the Ppa-PA difference (Ppa - PA) and
has been likened to an upstream river waterfall over a dam.
• Because Ppa increases down zone 2 whereas PA remains constant,
perfusion pressure increases, and flow steadily increases down the
zone.
In zone 3:
• Pulmonary artery pressure (Ppa) > pulmonary venous pressure (Ppv)
> Alveolar pressure (PA).
In zone 4:
• Pulmonary artery pressure (Ppa) > Pulmonary interstitial pressure
Figure 17-1 Schematic diagram showing the distribution of blood flow in the upright lung. In zone 1, alveolar pressure
(PISF) pulmonary venous pressure (Ppv) > Alveolar pressure (PA). (PA) exceeds pulmonary artery pressure (Ppa), and no flow occurs because the intra-alveolar vessels are collapsed by th
compressing alveolar pressure. In zone 2, Ppa exceeds PA, but PA exceeds pulmonary venous pressure (Ppv). Flow in
zone 2 is determined by the Ppa-PA difference (Ppa - PA) and has been likened to an upstream river waterfall over a dam
Because Ppa increases down zone 2 whereas PA remains constant, perfusion pressure increases, and flow steadily
increases down the zone. In zone 3, Ppv exceeds PA, and flow is determined by the Ppa-Ppv difference (Ppa - Ppv),
• Ventilation (V) is approximately = 4 liters, & total perfusion (Q) = 5 liters which is constant down this portion of the lung. However, transmural pressure across the wall of the vessel increases
• V/Q = 4/5 = 0.8 liters/min down this zone, so the caliber of the vessels increases (resistance decreases), and therefore flow increases. Finally, in
zone 4, pulmonary interstitial pressure becomes positive and exceeds both Ppv and PA. Consequently, flow in zone 4 is
determined by the Ppa-interstitial pressure difference (Ppa - PISF). (Redrawn with modification from West JB:
Ventilation/Blood Flow and Gas Exchange, 4th ed. Oxford, Blackwell Scientific, 1970.)
In this region, alveolar pressure (PA) then exceeds Ppa and pulmonary venous pressure (Ppv), which
is very negative at this vertical height. Because the pressure outside the vessels is greater than the
pressure inside the vessels, the vessels in this region of the lung are collapsed, and no blood flow
occurs (zone 1, PA > Ppa > Ppv). Because there is no blood flow, no gas exchange is 79possible, and
the region functions as alveolar dead space, or "wasted" ventilation. Little or no zone 1 exists in the
Dr Azam’s Notes in Anesthesiology 2013 lung under normal conditions,[2] but the amount of zone 1 lung may be greatly increased if Ppa is
reduced, as in oligemic shock, or if PA is increased, as in the application of excessively large tidal
How can general anesthesia worsens V/Q mismatch? Continuation:
General anesthesia worsens V/Q mismatch
FRC & Compliance Curve:

• V/Q mismatch occurs very commonly during anaesthesia because the FRC falls leading to a change in the position of the lung on the compliance
curve.
• The apices, therefore, move to the most favorable part of the curve whilst the bases are located on a less favorable part at the bottom of the
curve.
Dead Space:
• At the extremes of V/Q mismatch, an area of lung receiving no perfusion will have a V/Q ratio of (infinity) and is referred to as alveolar dead-
space, which together with the anatomical dead-space makes up the physiological dead-space.
• Ventilating the dead space is, in effective, wasted ventilation, but unavoidable.
Shunt:
• Area of lung receiving no ventilation, owing to airway closure or blockage, its V/Q ratio will be zero and the area is designated as shunt.
• Blood will emerge from an area of shunt with a PO2 unchanged from the venous level (5.3kPa or 40mmHg) and produce marked arterial
hypoxemia.
• This hypoxemia cannot be corrected by increasing the FiO2, even to 1.0, as the area of shunt receives no ventilation at all. The well-ventilated
parts of the lung cannot compensate for the area of shunt because Hb is fully saturated at a normal PO2 .
• Increasing the PO2 of this blood will not increase the oxygen content substantially.
Treatment of Shunt:
• In the case of shunt, adequate oxygenation can only be re-established by restoring ventilation to these areas using measures such as
physiotherapy, PEEP or CPAP, which clear blocked airways and re-inflate areas of collapsed lung.
• Because closing capacity (CC) increases progressively with age, and is also higher in neonates, these patients are at particular risk during
anaesthesia as the FRC may fall below CC and airway closure result.
80

27. Humidification. Dr Azam’s Notes in Anesthesiology 2013
Definition: Devices for humidification:

Absolute humidity = mass of water held in a given volume of gas 1. Devices adding water to gases
Relative humidity = amount of water vapour expressed as a percentage of • Vaporizers (unheated)or cold water humidifier
the amount which that volume of gas could hold at the same temperature if • Heated vaporizers or hot water humidifier
it was fully saturated • Nebulizers
2. Devices retaining water from inspired gases e.g. heat
Consequences of inadequate humidification: moisture exchangers
Ventilation of the lungs with dry gases produces heat loss, moisture loss
from the respiratory passages and alters pulmonary functions. 1. Devices adding water to gases
• Heat loss causes fall in body temperature and increases O2 consumptions A. Bubble humidifier / cold water humidifier
• Moisture loss leads to drying / dehydration of respiratory mucosa • In this O2 is bubbled through a large surface of water. This makes the
• Reduces mucociliary activity and causes sputum retention. Airways will temperature of O2 to fall below ambient temperature.
get blocked by secretions and result in V/Q mismatch. • Used with nasal prongs/face mask
• Vapor saturation=20-25%
Consequences of excessive humidification B. Hot water humidifier
• Mucosal heating and burns leading to pulmonary oedema and airway
stricture formation (heated humidifiers) • Air/O2 from a blower or mechanical ventilator is passed over a surface
• Inspired gases are not heated but large amounts of water are administered of water whose temperature is maintained at 45-550C
to the respiratory tract may be a fall in body temperature due to loss of • Vapour saturation =70-90%
latent heat of evaporation • Over heating of water is the major disadvantage
• Water overload
• Impaired function of mucociliary elevator. May result from an increased
volume of mucus requiring clearance so that the capacity of the
mucociliary elevator may be exceeded.
To prevent all these complications:
• The air/O2 inspired by the patient should be saturated with water vapour at
370C or
• The inspired air/O2 should be supersaturated by suspending water
droplets in it at room temperature.
81

Humidification. Continuation: Dr Azam’s Notes in Anesthesiology 2013
C.Nebulizer
They can be:
• Gas driven
• Mechanically ventilated
• Ultrasonic#
They work on Bernoulliʼs principle
2. Devices retaining water from inspired gases:

Examples—heat and moisture exchanger ( HME ) / artificial
nose.
• It is a device, that when connected to an artificial airway ,
will extract heat and moisture from the expired gas, and
will return this heat and moisture to the inspired gas during
inspiration. It retains about 70% of expired moisture.
• The modern version consists of a replaceable condenser
that can be taken out and cleaned.
• Types: E.g. condenser humidifiers, hydrophobic
condenser humidifier, Hydroscopic condenser humidifier.
Advantages:
GRID: Question need to to answered under following
• Satisfactory humidification with artificial airways.
headings:
• The breathing circuit remains dry.
1. Definition
• Comparatively inexpensive, disposable and do not require
2. Consequences of inadequate humidification:
an extra power source.
3. Consequences of excessive humidification
Disadvantages: 4. Devices for humidification
• Canʼt provide very high levels of humidification. a. Devices adding water to gases
• Ventilation can get obstructed if sputum falls on exchange b. Devices retaining water from inspired gases
membrane. 5. Diagram
• Produce a slight increase in the resistance to breathing
and increases the dead spaces.
• Bacterial contamination.
82

28. Oxygen Toxicity Dr Azam’s Notes in Anesthesiology 2013
Definition: Its a complex phenomenon where O2 molecule is Pathological findings:

Exudative phase
capable of subtle modifications, which transforms it into a range
of free radicals and other highly toxic substances. E.g. • Interstitial oedema
superoxide ions, activated hydroxyl ions, hydrogen peroxide, • Destruction of Type I pneumocytes
Proliferative phase
singlet O2 etc.
• Proliferation of type II pneumocytes
Free Radicals Damage:
• Thickening of air blood barrier there by decreasing alveolar space
• DNA • Hyaline membrane formation
• Lipids Signs and symptoms:
• SH containing proteins • Earliest symptom is substernal distress, cough and chest pain
The oxygen toxicity can present as: • Decrease in vital capacity is the most sensitive indicator. As toxicity
• Pulmonary toxicity (Lorren-Smith effect) progresses MV, Respiratory rate/Compliance of lung etc. all will deviate from
• CNS toxicity (Paul-Bert effect) normal.
• Retrolental fibroplasia in neonates / retinopathy of prematurity
(RLF / ROP).
Pulmonary toxicity: (Lorren-Smith Effect) CNS Toxicity: ( PAUL- BERT EFFECT )

• It was first described by Paulbert in 1878. Lambertsen and colleagues have
• First described by a pathologist Lorren-Smith in 1899. For explained this in detail. Exposure to oxygen at partial pressure in excess of
causing this type of injury PAO2 is more important than PaO2.
2 ATA result in convulsions.
• It appears when O2 is administered at pressure varying from
• Frank convulsions are preceded by warning signs as-twitching of muscles
0.7 to 3 ATA.
around the eyes, mouth and forehead, dilation of pupils, visual “dazzle”
Mechanism: vertigo or nausea etc.
Mechanism:
• Oxidation of SH groups on essential enzymes e.g. CO-A.
• In activation of SH containing enzymes controlling levels of GABA
• Peroxidation of lipids – inhibits cell functions
• Inhibition of the pathway of reversed electron transport possibly Treatment:
by inhibition of iron and SH containing flavo proteins • Gradual /sudden withdrawal of high pressure O2 and allowing the patient to
breath room air.
• These changes lead to loss of syntheses of pulmonary
surfactant, encouraging the development of absorption collapse
and alveolar oedema.
• The onset of pulmonary toxicity occurs after approximately 30
hours exposure to PIO2 of 100kPa (patient can tolerate 100%
O2 up to 10-12 hours). Absorption atelectasis and CVS
depression will also contribute for pulmonary toxicity.
83

Oxygen Toxicity. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Retrolental fibroplasia /Retinopathy or prematurity

• When patient with RLF comes for surgeries like eye
• RLF is the result of O2 induced retinal vasoconstriction. It occurs in examination, under anesthesia photocoagulation scleral
premature neonates especially < 30 weeks gestation, with birth weight
buckling etc, and if the infant is <44 weeks, then SaO2
<1200gm, exposed to high concentration of O2 i.e. 150 mmHg for >2
should be kept between 87-92%.
hours.
• N2O should be avoided/ turned off 30minute before air
• This disease is multifactorial in nature, with O2 being only one of the bubble is injected in the eye.
factors involved. PREVENTION OF O2 TOXICITY:
• Occurrence of RLF correlates better with PaO2 than PAO2 . PaO2< 1. Use of lowest possible o2 conc. for shortest period of time
140mmHg are considered as safe. consistent with sustaining of life .
Pathophysiology:
2. Early use of PEEP to decrease large shunt fraction .
• Hyperoxia constricts retinal arterioles and causes swelling and 3. Reduction of o2 consumption .
degeneration of the endothelium of the arterioles and capillaries.
4. Toxic effects can be inhibited by
• Spindle cells in the retina when get stressed, they secrete angiogenic 4.1. SH compounds - Glutathione , cysteine
factor which is responsible for vascular proliferation between the
4.2. Antioxidants - vit C & E
vascular and avascular portion of the retina. This leads to proliferative
4.3. Acid –base
retinopathy.
This is divided into five stages.
• Stage 1: A thin white line separating posterior vascularized and GRID: Question needs to be answered under following
anterior avascularized portions of the retina. headings:
• Stage 2: The demarcation line increases in volume and elevates. It is 1. Definition
then known as ridge, 80% of patients with stage 1 and 2 regress to 2. Types
normal by 2-3 months. 5-10% will progress to stage 3. 2.1. Pulmonary Toxicity
• Stage 3: Tissue proliferation develops from the ridge, usually i. Mechanism
posteriorly. It can be mild, moderate / severe. It can regress ii. Pathological findings
spontaneously by ≥6 months iii. Treatment
• Stage 4: ( 4a and 4b ): Partial retinal detachment occurs with the 3. CNS Toxicity
macula still attachment (stage 4a) stage 4b – Macula gets detached iv. Mechanism
• Stage 5: Total retinal detachment . v. Treatment
• stage 4 and 5 result in blindness or limited vision. 4. Retrolental fibroplasia of prematurity
vi. Mechanism
vii. Pathological findings
viii.Treatment
84

29. Complications Of Oxygen Therapy Dr Azam’s Notes in Anesthesiology 2013
Complications Of Oxygen Therapy:
Progressive hypercapnia: Drying and

•# If the respiratory center of the Circulatory depression: Crusting of Fire
patient is comparatively insensitive secretions: • O2 support combustion, O2 tents
• Significant depression is seen in
to increasing PCO2 and his patients with preexisting CVS This occurs if and pressure chambers are most
respiratory drive is significantly disorders, otherwise it is a rare hazardous forms of O2 therapy in
dry O2 is
dependent on hypoxic stimulus, complication. this respect.
administered.
then inhaling high concentration of • Increase PaCO2 (>30kPa)
O2 will cause hypoventilation and causes peripheral, cerebral,
hypercapnia, CO2 narcosis coronary, hepatic vasodilation
develops and patient may become and renal vasoconstriction. Depression of Hemopoiesis
drowsy and comatose. Hyperbaric O2 has got direct Absorption atelectasis:
• This is commonly seen in patients myocardial depressant action. • When 100% O2 is administered to a patient with
with COPD. • It is especially seen in patients in obstructive airway disorders, O2 displaces all the N2 in
• An increase in V/Q ratio with an whom the circulation is the airway. O2 has got high solubility coefficient and
increase in dead space also maintained by excessive gets absorbed fully rendering the alveoli to collapse.
contributes to CO2 retention sympathetic activity and This leads to atelectasis. The perfusion to such
following O2 therapy. excessive catecholamine collapsed alveoli to continues and causes
• To prevent this, O2 should be discharge induced by the severe intrapulmonary shunt. The chest X-ray findings of
administered in a controlled hypoxia. Sudden relief of atelectasis starts to appear after 24 hours of start of
concentration (of 24-30%) in all hypoxia abolishes the exposure but the changes occur within 6 minute with
COPD patients, with careful sympathetic over activity and 100% O2 administration and within 60 minute with 85%
monitoring. causes temporary hypotension O2 administration.
and circulatory collapse. This is
treated by IV fluids and infusion Also Write about
of sympathomimetic agent. • Pulmonary toxicity
• CNS Toxicity
• Retrolental Fibroplasia of prematurity
85

30. Pulmonary Function Test Dr Azam’s Notes in Anesthesiology 2013
Non-Specific - Bed Side Test
Specific Test - PFT
Test of Ventilation Test of Distribution of Ventilation Test of Diffusion Test of Perfusion Other Tests
Single Breath N2 elimination Test

Multi-breath N2 wash out test Carbon Monoxide Diffusing
Radio-active Xenon distribution Capacity
radio-active Xenon
Static Test injection#
Dynamic Test
Radio-nucleotide
Non-Specific - Bed Side Function:
Macro-aggragated iodine
•Anatomical • Breath Holding test
Measurements • Sniderʼs Match Blowing test •Split Lung Function Test
•Do not evaluate • De Bonoʼs Whistle test •Bronchospirometery
Measures rate of flow of Gas • Auscultation over the trachea
Function •radio-active Scanning
• Sphygmomanometer •Pulmonary artery occlusion
• Walk test test
4 Volumes 4 Capacities MBC/MVV
• Stair case test. •ABG
TV VC FEV
IRV TLC PEFR •A-a Gradient
ERV FRC MMEFR 25 to 75 % •Raw
RV IC Respiratory Muscle Strength •Compliance
Fixed Obstruction
Variable Extra-Thoracic Obstruction
E-Expiration is normal
Flow
Volume Variable Intra-Thoracic Obstruction
Loops I-Inspiration is normal
Restrictive Lung Disease
86
Dr Azamʼs Notes in Anesthesia

FRC Dynamic Tests
Pulmonary Function Test
• Spirometer can measure - VT,IRV, • Volume of air remaining in the lung MBC or MVV
ERV, VC, IC, FEV & MBC after normal expiration • Max volume of air that can be breathed per
• Cannot be measured by Spirometer • measured by: minute by voluntary effort
- RV, TLC & FRC • N2 washout technique • normal - 160L/min to 180 L/min
• Helium dilution MBC is decreased in:
Static Test • Body Plethysmograph • old age
VT - Tidal Volume • FRC increased: • emphysema
• Total Volume of air inspired & Expired in each breath • Obstruction of airways • bronchospasm
• measured by wrightʼs Respirometer • Emphysema • bronchiolar obstruction
• PEEP
IRV - Inspiratory reserve volume FVC & FEV
• FRC decreased:
• Volume of air that can be inspired after normal FVC
• Under Anesthesia
inspiration. • Assess the expiratory ability
• post op old age
ERV - Expiratory reserve volume • max volume of air that can be
• obesity
• Volume of air that can be expired after normal exhaled forcefully and rapidly after
• smoking
expiration maximum inspiration
• Lithotomy
• It reflects the thoracic muscles, abdominal muscle • measured by Spirometer and fast
• Abdominal distention
& thoracic mobility moving Kymograph
• Lap surgeries
RV - Residual Volume • FVC done over 4 sec
TLC • reflects the relationship between
• Volume of air remaining in the lung
after maximum expiration • Total volume of air in lung after Flow & resistance
maximum inspiration. FEV1
• Measured by
• TLC decreased: • Max volume of gas exhaled during
• N2 washout technique
• Pulmo fibrosis the 1st second of FVC maneuver
• Helium dilution technique
VC - Vital Capacity • obesity • FEV1 = 83% of VC
• weakness of inspiratory muscle
• Most commonly measured
• volume of air that can be expired after maximum inspiration FVC is decreased in:
• can be measured by - spirometer • Atelectasis
• BSA: Male- 2.6l/m2 Female - 2.1l/m2 • Fibrosis
• A given VC is abnormal if < 80% of predicted value • muscle weakness
• VC: decreased - in pregnancy, Pulm fibrosis • abdominal swelling
• Emphysema • pain
• ch.Bronchitis In healthy patients
• asthma FVC=VC
• Abdominal pain
• can be < 70 to 75% in upper abdominal surgery
• < 50 to 55% in lower abdominal surgery
• Position: Lithotomy Vc < 18% 87
• VC= 3 X VT for effective cough
• Decrease in VC means decreased ability to cough and post operative complications Dr Azam’s Notes in Anesthesiology 2013
PEFR:
• After max inspiration patient exhales as forcefully
as he can and the max flow rate is measured
and expressed in lt/min and lt/sec
• Normal: Condition FEV1 FVC FEV1 /FVC
• 450-600 L/min
Airway obstruction (asthma, bronchitis) Decreased Normal Decreased
• 300 - 500 L/min
• Measured by Wrightʼs Respirometer Stiff lungs (pneumonia, pulmonary edema) Decreased Decreased Normal
# # Pneumotachygraph
Respiratory muscle weakness (myasthenia, Decreased Decreased Normal
PEFR is decreased in:
myopathies)
• Obstructed Airway
Values less that 200 lt/min suggest impaired cough
and increased likely hood of post op pulmonary
complications
MMEFR ( 25% to 75%): Obstructive Restrictive
• Flow measured in middle half of FVC FEVI Decreased Decreased
• obtained by dividing the volume of gas FVC Normal Decreased
between 25 - 75% by corresponding FEV1/FVC Decreased Normal
elapsed time FRC Increased Decreased
• Normal = 4 to 5 L/sec TLC Increased Decreased
Importance
(Raw)airway resistance Increased Normal
• more sensitive of small airway
obstruction or disease MMEFR Decreased Normal
MBC Decreased Normal
Respiratory Muscle weakness: PEFR Decreased Decreased
• It is evaluated and measured by
maximum static respiratory
pressure
• PImax = -125 cm of H2O - normal Flow-‐Volume Loops
• If PImax = -25 inability to take deep • Provide a graphic analysis of flow at various lung volumes
breath • Used to differen:ators between pa:ents with upper airway and lower airway obstruc:on
• PEmax = + 200 cm of H2O - normal • Flow is charted on Y-‐axis
• If PEmax = + 40 cm of H2O • Volume is charted on X axis
severely impaired coughing ability • Pa:ent is asked to inhale fully to TLC and then perform a FVC maneuver. This is followed
• seen in Emphysema
immediately by a maximum inspira:on back to TLC
• predictor of successful weaning
• The ra:o of expiratory flow to inspiratory flow at 50% of VC is normally 1 (mid VC ra:o)
• Evaluation of NM disorder
88
31. Bedside pulmonary function test. Dr Azam’s Notes in Anesthesiology 2013
Bed-side tests: De Bonoʼs whistle tests:

Breathe holding test by: (SABREZ TEST) • This instrument has a tube with adjustable holes
• Roughly reveals the cardio-pulmonary status and a whistle at the end.
and ventilatory capacity. • Patient is asked to exhale forcefully into the tube.
• Patient is asked to take a deep breath and hold • Measures peak expiratory flow rate up-to 300 lt/
it as long as possible. > 30 sec is normal. < 15 mt.
sec-decrease ventilatory capacity. Auscultation over the trachea:
Sniderʼs Match-blowing test: • Performed during a forced expiration
• Patient is asked to inspire maximally and then • Normal value is 3-4 sec.
expire rapidly with his mouth open in an attempt • 6 sec – suggestive of obstructive airway disease.
to extinguish a burning match (Patient is asked
Non-Specific - Bed Side Function:
to blow out the match without pursing the lips.) Sphygmomanometer Blow test:
• Breath Holding test
• Held 6 inches or 15 cm from his mouth. • A normal patient can blow into • Sniderʼs Match Blowing test
• A lighted match stick is held 6 inches or 15 cms sphygmomanometer tube, keep it blown & raise
• De Bonoʼs Whistle test
from the patients mouth. Roughly shows the the mercury level up to 40 - 50 mm of Hg.
• Auscultation over the trachea
expiratory capacity and MBC of the patient. • Inability to do so indicate reduced expiratory • Sphygmomanometer
• These patients have FEV1 > 1.60 L and MBC > flow.
• Walk test
60 L/min
• Stair case test.
• Patient who can blow out the match can safely STAIR TEST
undergo thoracic or non-thoracic surgery. • 3 flight steps, Each flight step are 20 steps, (60
• If the patient cannot blow out the match, MBC < Steps totally) 15 cm each step.
60L/min and FEV1< 1.6 Liters. Distance less
than 8 cm FEV1< 1L. WALK TEST
• Brisk walk (Richter test)
• Normally: 160-180 L/min
• 600 mts in 6 min
• ARC - Mumbai:Ability to blow the candle off at
22 cm from the mouth indicates MBC > 150L/
min (MBC >100L/min at 15 cms & MBC > 50 L/
min at 7.5 cms)
89

32. Describe functional residual capacity & Closing volume? Describe their clinical significance?
Definitions:
FRC: The volume of air remaining in the lung after normal expiration. Males – 3300ml, Females –
2300mlFRC = ERV + RV
Clinical Significance:
Factors decreasing FRC Factors increasing FRC

1) Supine, trendelnburg posture 1) Increased intrathoracic pressure
2) Anaesthesia – intraoperative Eg. PEEP, CPAP
3) Upper AbL and thoracic surgery 2) Emphysema ,asthma
(post operative due to pain)
4) Pul. fibrosis, pulmonary oedema
5) Obesity
6) Abdominal swelling – pregnancy,
tumour, ascites
7) Thoracic cage distortion Relationship of FRC and CC:
8) Reduced muscle Tone • FRC = CC #Neonate and infants
9) Smoking • FRC = CC #in supine position at 45 years (40-45)
• FRC = CC #in upright position at 65 yrs.
Anesthetic Implications of FRC: GRID: Question needs answered under following

1. Decreased FRC - hypoxemia headings:
2. If closing capacity > FRC ,airway closure occurs with V/Q mismatch. 1. Definition
2. Factors increasing & decreasing FRC
3. FRC serves as O2 reserve, decreased FRC leads to decreased O2 reserve.
3. Anesthetic Implications of FRC
4. The FRC O2 store helps to prevent large swings in arterial PO2 during respiration. 4. Measurements of FRC
5. Decreased FRC reduces lung compliance and increases pulmonary vascular 5. Relationship between FRC & CC
resistance. 6. Diagram
6. If FRC ↓ importance is - Pre-oxygenate for 5 to 7 min.
7. Increased FRC is usually associated with in RV and limits the inspiratory capacity
and hence limits the patients ability to increase ventilation on demand.
8. If FRC is increased it limits the patients ability to increase ventilation on demand.
90

Describe functional residual capacity & Closing volume? Describe their clinical significance? Dr Azam’s Notes in Anesthesiology 2013
Measured by
a. Nitrogen washout technique
b. Helium dilution method
c. Body plethysmography
Nitrogen washout techniques:
• Originally done by Fowler in 1949
• Patient makes a full inspiration from RV to TLC with 100% O2 – then slowly expires into a spirometer. By knowing the concentration of
N2 in the spirometer, the lung volume during the beginning of the test can be calculated.
Helium dilution method:

• Patient breaths in and out from a reservoir with a known volume of gas, containing a trace amount of Helium. The Helium is diluted by
the gas previously present in lungs. From knowledge of the reservoir volume, and initial and final helium concentration, the volume of
gas present within the lungs can be calculated.
Body plethysmography:
• Helps to measure the collapse portion of the lung. Comparison of the results indicates the degree of collapse.
91
33. Closing Capacity & Closing Volume. Dr Azam’s Notes in Anesthesiology 2013
Definition:
Lung volume at which airway closure occur mainly in the dependent part
of the lung is called closing capacity.
It is a sum of CV+RV (N) 2000 ml # # #
# ( If CC > FRC then greater hypoxia occurs)#
CC is usually well below FRC thus airway closure does not occur during
normal quite breaking but greater than RV.
-RV < CC < FRC

-CC can be measured using a bolus of marker gas, such as helium
inspired at RV. After completing a full inspiration, the subject exhales his
vital capacity slowly. Expired volume and helium concentrations are
measured. CC increased:
# Closing capacity is the lung volume at which there is a sharp rise With age. This increase in CC may be responsible for age
in the alveolar plateau of helium concentration. related decline in O2 tension.
# CC = FRC in neonates and infants
N2 washout technique: # CC = FRC in supine position at 45 yrs
While breathing air the subject slowly expires to residual volume and # CC = FRC in upright position at 65 yrs
then slowly takes a single breath of oxygen to maximum inhalation. The
breath is held for a few (10 sec) seconds and then slowly and evenly Obesity
expired. During this phase the instantaneous nitrogen concentration and Increased in asthma, smokers (due to loss of elastic recoil)
volume of the expired are recorded and a characteristic curve is LVF, MI, post-op period
obtained. It has 4 phases 1) dead space gas 2) fixed dead space and
CC decreased:
alveolar gas 3) mixed alveolar gas 4) phase in which sudden rise in
• Supine position
concentration of N2.
• Anaesthesia
CC is the volume at which phase 4 begins .
Significance:
As CC rises more than FRC arterial hypoxaemia occur.
PEEP application can prevent this airway collapse.
92

34. Enumerate the effects of chronic smoking & the anesthetic implications. Dr Azam’s Notes in Anesthesiology 2013
Definition: RS:
• Average packs/day times of year smoked. Nicotine Levels: 15 to 50 • Mucosal Hypersecretion
microgram / ml in smokers • Impaired tracheobronchial clearances - Cilio-static action
• 1 cigarette = 1mg to 4 mg of nicotine • Narrowing of small bronchial airway
• Segmental atelectasis, COPD, Bronchospasm
• 1 Cigar = 40 mg nicotine
• Bronchitis
Grading: • Induces bronchospasm
• Non smoker CVS:
• Ex smoker • Coronary vasospasm
• Smoker - 1-14 mg / day of nicotine (1-14 cigarettes) • Increase in BP and ↑ HR
• Smoker – 15-24 mg / day (15-24 cigarettes) • ↑ Myocardial O2 demand
• Smoker - > 25 mg/day cigarettes
• 3 cigarettes = 1 bedi. GIT:
• ↑ acid secretion
Effects of smoking: • ↓ LES
Carbon monoxide Nicotine • ↓Gastric emptying
200 times more affinity for HB 15 to 50 microgram / ml Immunity:
than O2 in smokers • Immunity is impaired
Carboxy Hb, Half life is 6 hours½ life of one cigarette is Liver:
30min. (nicotine) • Induces hepatic enzyme system (cytochrome P450)
ODC - Left Shift It stimulate sympatho Endocrinology:
Absolute decrease in O2 content adrenal axis. • Hormonal levels of epinephrine, GH, Cortisol increases
• The oxygen cost of breathing is increased (12-19%)
• Carboxy Hemoglobin Levels:
• Normal = 1%
• Smokers = 8 to 10%
Effects on Various systems:
Hematology:
• Increased red cell mass - due to hypoxia
• Platelet survival time is reduced
• Increased platelet aggregation
• Increased thromboembolic episodes
93

Enumerate the effects of chronic smoking & the anesthetics implications.Continuation: Dr Azam’s Notes in Anesthesiology 2013
INTERACTIONS BETWEEN SMOKING AND DRUGS BASED ON ALTERATIONS IN DRUG METABOLISM

73. Goals of preoperative pulmonary preparation Refer
Drug class Metabolic response Page # 20
Analgesics - • To reduce the respiratory secretions.
Pentazocine Higher maintenance dose needed • To reduce the reversible factors such as airway narrowing.
Xanthimes - • To eradicate the respiratory tract infections.
• To improve the general well being of the patient.
Theophyllene Significantly accelerated metabolism
Tranquilizers - Peri-operative Management:
Diazepam CNS depression less frequent (Probably due to ↑ rate of 1. Pre-oxygenation & FIO2
metabolism) 2. Dosage & frequency of the drugs need to be increased
Chlorpromazine Reduced drowsiness. because of accelerated metabolism ( enzyme induction)
3. Antacids & H2 blockers are less effective
4. Regional anesthesia is preferred
5. If General Anesthesia is indicated then LMA is preferred
Goals include: Induction & maintenance of General Anesthesia:
• Elimination and control of acute or chronic Monitoring: • When ever possible endotracheal tube should be avoided as
pulmonary infections • ECG it may precipitate bronchospasm.
• Reversal of bronchospasm • NIBP • LMA is preferable
• Improvement of secretion clearance SaO2 Goal:
•
• Expansion of collapsed or poorly ventilated alveoli • EtCO2 • Smooth induction
• Hydration • Adequate depth of anesthesia
• Correction of any electrolyte imbalance
Preoxygenation: 100% oxygen for 3 - 5 min
Investigations: Induction Agents:

• CBC Pre-medications: • Propofol 2 - 2.5 mg/kg IV in hemodynamically stable patients.
• ECG • BNZ - Anxiolysis • ketamine 1 - 2 mg/kg IV has bronchodialtory effect in
• Bronchodilators hemodynamic unstable patients.
• PFT - decrease FVC, decrease
FEV1, Decrease PEFR • Anti-cholinergics • After unconsciousness is produced lungs can be ventilated
• Antibiotics with either Halothane ( More effective bronchodilator effect)
• LFT
• Anticoagulants or Isoflurane
• Lipid profile
• Chest X - ray
Volatile Anesthetics:
• Halothane shown to be more effective bronchodilator than
isoflurane but may sensitize the myocardium to cardiac
dysrrhythmic effect of catecholamines & theophylline.
94

Enumerate the effects of chronic smoking & the anesthetics implications.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Preoperative Preparation:
• Stop Smoking Time course BeneKicial effects
• Dilate the airway using: 12-24 hours Decrease carbon monoxide and nicotine levels
• Beta agonist 48-72 hours Normalizes carboxy Hb levels. Improves ciliary
• Anti-cholinergics
function, tissue oxygenation.
• Theophylline
• Steroids 1-2 weeks Decrease sputum production & improves smaller
• Cromolyn Sodium airway function.
• Loosen the Secretions by: 4-6 weeks Improves PFT
• Airway hydration ( Humidification/Nebulization) 6-8 weeks Normalizes immune function, drug metabolism and
• Systemic hydration orally - 3 Liters hepatic enzyme activity
• Mucolytic agents & Expectorant drugs 8-12 weeks Reduces overall post-operative pulmonary
• Antibiotics
Remove secretions: complications.
•
• Postural drainage
• Coughing
• Chest physiotherapy(percussion & Vibration) Post-operative Management:
Ancillary Measures: Goals:
• Treatment of co-existing disease • To promote adequate analgesia
• Treatment of Cor-Pulmonale • To minimize the incidence of postoperative complications
• Pre-operative Digitalization • To prevent infections
Patient Education, motivation & facilitation of • Chest physiotherapy & deep breathing exercise.
post operative care: Continuation: • Consider CPAP - Decreases WOB, Improves LV Compliance.
• Psychological preparation • Continuous administration of Local anesthetic with low dose opioids via
• Incentive spirometry & deep breathing exercise epidural catheter for post operative pain relief.
• Exposure to secretion removal maneuvers
• Exercise
• Weight gain/reduction
• Diet supplements.
95
GRID: Question need to to answered under

following headings: Smoking
GRID: Question need to to answered under following headings:
1. Definition Right Lobectomy. Refer Page 25 & question 11
2. Importance of Carboxy Hb & Nicotine 1. Pre-operative Evaluation
3. Systemic effects of smoking 2. Investigations
4. Pre operative Respiratory care & Goals 3. PFt 3 Phase testing
5. Investigations 4. Pre-operative lab criteria for pneumonectomy.
6. Benefits of cessation of smoking. 5. Preoperative preparation
7. Perioperative management 6. Anesthetic consideration
8. Post operative care Goals. 7. Monitoring.
96

35. Describe the techniques of chest physiotherapy? What is its role in the post surgical period? Dr Azam’s Notes in Anesthesiology 2013
Definition: Techniques which promote clearance of excessive respiratory Bronchial drainage:

secretions • Purpose of bronchial drainage is to facilitate removal of
Following therapeutic measures are commonly used in chest physiotherapy. secretions with aid of gravity from peripheral portion of the
Components of Chest Physiotherapy: RBC - BSA lung into larger bronchi, from where it can be expectorated or
1. Relaxation removed by suction.
2. Breathing exercise
3. Coughing Indications:
4. Bronchial drainage • Pre existing supportive lung disease.
5. Splinting, support and positioning • Prophylactic drainage post operatively.
a. Percussion • Aspiration
b. Vibration • Patient on prolonged artificial ventilation
6. Activities of daily living and breathing control. • Diagnosis of bronchitis, bronchiectasis, lung abscess
• Patients with atelectasis
Relaxation: • Unconscious patients
• Various positions like sitting, standing and lying down are used. • Paralyzed patients
• Aim of these positions is to enhance ability of patient to breath more efficiently Contraindications:
and effectively during rest and to cope with dyspnoea after physical activity. • Acute medical / surgical emergency
Breathing exercise: • Pain / discomfort restricting patients cooperation
• Purpose is to improve the function of respiratory muscles and to increase chest Regimen: Before meals
wall compliance. Also through a conscious effort, the patient will increase the • Few secretions – drain in A.M and PM (2 times)
volume of air moving in and out of his lungs. • Large amount of secretions – 3-4 times/day (Always before
• Breathing exercises should be practiced in several positions, since the meals)
distribution of air and pulmonary circulation varies according to what position the Duration of treatment:
chest is in. • If all lung fields need drainage, total time > 30 – 40 mins and if
only 3-5 lung fields are involved patients should remain 5 – 10
Coughing: min in each desired position.
• Is most effective method of removing secretions but it needs adequate VC and Technique:
adequate power of abdominal muscles. For Effective Cough VC = 3XVT • Two techniques are commonly employed to move secretions
• Patient is asked to take deep breaths, hold it for fraction of second and then from peripheral lung field to main bronchi.
perform cough by firm contraction of abdominal muscles and by flexing his trunk I. Percussion
slightly forward. II. Vibration
I. Percussion: The therapist claps with cupped hand on the
chest wall over the draining lung field for 30-45 sec, while the
patient breaths normally.
97

Describe the techniques of chest physiotherapy? What is its role in the post surgical period? Dr Azam’s Notes in Anesthesiology 2013
continuation:
Indications: percussion is needed in Post operative chest physiotherapy helps in:

• Thick and viscid secretions. • Decreases the incidence of PPCs
• Bronchitis, bronchiectasis, lung abscess and postoperative • Reduces length of hospital stay & cost
secretions. • Increases oxygen-hemoglobin saturation
Contraindications: • Improves chest wall mobility and lung ventilation
• Acute medical and surgical emergency (MI, thrombi AF). • Decreases incidence of atelectasis
• Patients not cooperative • Decreases incidence of Pneumonia
• Deep breathing (Inspiration) improves FRC and hence gas exchange
• Trauma to chest / abdomen (incision)
• Helps in coughing out secretions.
• Pneumothorax / Pl. effusion
II. Vibrations: Role in Post surgical period:
# The therapist vibrates and applies gentle pressure on chest The incidence of atelectasis and pneumonia was decreased using a
wall over the draining lung field during phase of exhalation. combination of therapies including:
# When percussion, vibration cycle is repeated 2-3 times. The • Deep breathing
patient is encouraged to cough effectively. If productive, procedure • Postural drainage
• Directed cough
is repeated.
• Incentive Spirometry
Indications:
• To follow percussion during bronchial drainage
• If secretions are loose and liquid
Contraindications: Same as percussion GRID: Question need to to answered
under following headings: Smoking
1. Definition
2. Components & explanation
3. Indications
4. Technique
5. Role of Chest physiotherapy in Post
operative period.
98

36. INCENTIVE SPIROMETRY Dr Azam’s Notes in Anesthesiology 2013
The intensive spirometry is an effective and inexpensive prophylactic

bronchial hygiene tool that provide a visual goal or incentive for the
patent to achieve and sustain maximal inspiratory effort. ! !"#$%"&%! %'(%)'$*+%,*&*,'$-%*(.%/01%
Method: it is a type of voluntary deep breathing, in which the patient is

given inspired volume as a goal to achieve. It also emphasizes holding !""2%,"345%*(.%26$6($'"(% 8$6+6,$*#'#%
"7%#6,26$'"(#%
the inhaled volume to provide sustained inflation important for expanding
collapsed alveoli. It is done in hourly basis.
!(639"('*%
Types of devices: 82$62'*+%5-&":69'*%
Volumetric incentive spirometer:

# It has volume indicator and counter. 8,3$6%26#&;%7*'+326%
# It is a original device that required the patient to inhale deeply and Etiology of Post-operative Complications:
sustain the inhalation for several seconds.
Other uses of incentive spirometry:
A flow rate sensitive incentive spirometer:
# It can also be helpful in diagnosis of acute
# Recent device which do not require that a preset inhaled volume
pulmonary disease, in that a sudden decrease in the
be taken and do not ensure that deep breath will be sustained.
ability of patient to perform at a previously established
Drawbacks: for incentive spirometry to be effective
level may herald the onset of severe atelectasis,
• The patient must be co-operative, motivated and well instructed in pneumonia or other pulmonary disorders.
the technique.
• VC of >15ml/kg or inspiratory capacity > 12ml/kg should be GRID: Question to be answered under following
obtainable. headings:
• The patient should not be tachypneic or receiving high FiO2 (that 1. Introduction
2. method
is patient should not have respiratory failure).
3. Types of devices
• The things which patient should not be doing is the expiratory
4. Draw backs
maneuvers, such as inflating balloons, use of blow bottles or 5. Etiology of PPC
performing FVC. 6. Other uses of Incentive Spirometry.
Since performance of these events cause patient to exhale to below the
FRC, causing alveoli to become smaller or to collapse.
99

100. Flow Volume Loops Dr Azam’s Notes in Anesthesiology 2013
Flow Volume Loops: Fixed Obstruction:

• Provide a graphic analysis of flow at various lung volumes • e.g., benign stricture of trachea following tracheostomy/intubation,
• Used to differentiators between patients with upper airway and tumour or a mass such as goiter.
lower airway obstruction • No significant change in airway obstruction during inspiration or
• Flow is charted on Y-axis expiration. Since both are decreased nearly to same extent, the mid
• Volume is charted on X axis VC ratio remains nearly 1.
• Patient is asked to inhale fully to TLC and then perform a FVC
maneuver. This is followed immediately by a maximum
inspiration back to TLC
• The ratio of expiratory flow to inspiratory flow at 50% of VC is
normally 1 (mid VC ratio)

Variable Extra-thoracic Obstruction:

• e.g., vocal cord paralysis, pharyngeal muscle weakness, chronic NM
disorders, severe obstruction, sleep apnea etc.
• In these conditions, inspiratory flow is decreased while expiratory
flow remains normal and VC ratio > 1.
100

Flow Volume Loops. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Variable Intra- Thoracic Obstruction: Type to enter text

• e.g., tumors of trachea and major bronchi during forced
expiration the high pleural decreases airway diameter and may
increase obstruction.
• Hence expiratory flow is reduced while inspiratory flow may
remain normal. Because mid VC ratio E/1 <1
101

38. Scoliosis Dr Azam’s Notes in Anesthesiology 2013
Introduction: Means crooked Post trauma:

Definition: a) Vertebral fracture or post surgery
• Is a complex 3D deformity characterized by coronal, sagittal and b) Post thoracoplasty
horizontal plane deviations of spine associated with rotation of c) Post radiation
vertebrae, resulting in deformed rig cage. d) Post burns
• Can be associated kyphosis.
Syndromes:
Incidence: 0.13 % a) Vater syndrome
Classification b) Neurofibromtosis
• Non structural or Flexible scoliosis c) Marfans syndrome
• Structural d) Rheumatoid Arthritis
e) Ehler danlos syndrome
Non structural:
• Ex: Sciatica, leg length, discrepancy and pelvic tilt due to hip Pathophysiology:
contracture, which disappears with postural modification. CVS:
Associated with
Structural scoliosis: 1. Mitral valve prolapse
Idiopathic: 2. Marfan syndrome
a. Infantile < 3 years 3. Cyanotic heart disease
b. Juvenile > 3 yrs – 10 yrs Alveolar hypoventilation
c. Adolescent > 10 yrs ↓
Congenital: V/Q mismatch
a. Hemivertebrae ↓
b. Fused ribs Hypoxia
c. Spina dysmorphism ↓
Neuromuscular: ↑ HPV and pulmonary HTN
a. Cerebral palsy ↓
b. Poliomyelitis Right ventricular hypertrophy
↓
c. Muscular dystrophy
Right heart failure
d. Friedreichʼs ataxia
e. Meningo-myelocele.
102

Scoliosis Continuation: Dr Azam’s Notes in Anesthesiology 2013
Respiratory System: Management:

• X-ray PA and lateral view of spine.
• Cobbʼs angle: used to assess severity of scoliosis.
Due to compression • Angle < 200 – benign and no surgical Rx but monitored every 4
of lung & it's vasculature
months by x-ray to known progression.
• Angle > 60 – respiratory impairment (+) i,e restrictive lung disease.
(RID).
• Angle > 1000 severe impairment needs correction.
Decrease in Compliance Other indications:
• Pain
• Neurologic involvement
• Cosmetic purpose
• 25-400 orthotic braces, > 400 – surgical correction.
Surgical technique
Decrease lung • Posterior spinal fusion with herrington rod.
Muscle Volume • Anterior approach
Increased in Work of
Weakness o Thoracotomy
Breathing
o Trans diaphragm.
o Trans abdominal
• Combined
Anaesthetic management:
Preoperative evaluation and planning:
Hypoxia
I. Consider cardiac respiratory status and neuromuscular status.
II. Neurologic deficits
Failure III. Cobbʼs angle
IV. Associated congenital anomalies
V. Also discuss
a. Autologous transfusion
b. Awake intubation / tracheostomy if need
c. Rehearsal of wake up test
d. Postoperative ventilation
e. Post operative chest physiotherapy and pain management
f. Sleep apnea syndrome
g. Unable to lie flat
h. Prone position
103

Anaesthetic consideration: Intraoperative management:

Preoperative investigations: Consider: #
• PFT 1) Long duration
• ABG 2) Blood loss
• 2D Echo 3) Hypothermia
• ECG: changes due to cor pulmonale 4) Pressure points
• Hb: à↑ Hematocrit due to chronic hypoxia 5) Problems of prone position like
• CT thorax • Induction: on trolley with all monitors.
• X-ray spine • Thiopentone, propofol, volatiles, etomidate, fentanyl etc.
• All other radio tests • Intubation: Fiberoptic / Trachostomy
• Avoid scoline in post with muscle dystrophy.
Premedication: with caution • Maintenance: O2, N2O, fentanyl, vecuronium
Antisialogauge: to ↓ secretion in prone position which can
displace. E.T.T. Wakeup test:
Antibiotics: of any cardiac pathology and respiratory infection • To monitor motar component of spinal cord.
Steroid: In any neurologic deficits. • Hence should use short acting agents to facilitate this test.
Monitors: Disadvantages:
• ECG 1. One time indicator only
• Pulse Oximeter 2. Cannot be done in childrens or mental retarded.
• urine output 3. Extubation
• EtCO2 4. Dislodgement of instruments and monitor lines
• Neuromuscular Monitoring 5. VAE
• Neuro Monitoring - SSEP, MEP 6. Pain
• Wake up Test
• Respiratory Rate • SSEP: Monitors ascending sensory tract in posterior column.
• ABG. • MEP: Monitors descending motor tracts situated antero laterally in
the column.
• SSEP: - Non invasive.
• Brief S - wave electric stimulation (100-200 µ sec)
• Stimulus intensity 20 MA.
• Electrodes:
• Subcutaneous needle
• Standard EEG
104

• Amplitude 1-3 µv. Autologous transfusion

• Stimulus frequency: 3-0 – 5-0 HZ. • iso volemic haemodilution – to haematocrit 20-25%
• Artifacts – noise, diathermy, electric sources. • Cell salvage
• Ischemia - ↑ latency, ↓ amplitude (> 50%). • Antifibrinolytic agent (aprotinin)
• Hypothermia of anesthetic agents can all interfere with SSEP Postoperative complications:
recording. Management
MEP: • Pneumothorax / haemothorax: ICD, IPPV.
• Electric or magnetic transcranial stimulus • V/Q mismatch:Preparative O2 and physiotherapy
• Recorded over lower limb muscles. • Hypoxia: O2
• Factors influencing SSEP and MEP: • Failure of respiration: IPPV
1. Subcortical and spinal EP are insensitive to agents. • Pain : PCA, epidural analgesia, enyoanalgsia.
2. Cortical SSEP and myogenic MEP are sensitive. • Bleeding and ↓ BP: Blood and Fluids
3. Sevoflurane is compatible with SSEP. • SIADH: 12 hr Na estimation
4. N2O ↓ amplitude of SSEP and MEP by 40-50% • DIC
5. opiods, barbiturates, benzodiazepines, propofol: slightly ↓ • Neurologic deficits: assessment
amplitude SSEP. • Paralytic ileus: NG tube
6. Etomidate: Increase SSEP amplitude • Infection: Antibiotics
7. Bottom line: Avoid volatiles and N2O Postoperative monitoring: !
8. institute opioid / propofol • Oxymeter, ABG, HR, BP
• X-ray, urine output etc.
MEP à Volatile, N2O, iv agents, NM blocking agents, hypothermia:
all interfere with MEP.
• Spinal cord stimulation (thoracic or cervical) preferred over
cortical because former is less sensitive to agents.
• Etomidate / opioids / ketamine à preferred
• Delibrate ↓BP, hypothermia: can affect monitoring.
Blood salvage:
• Deliberate hypotension: MAP 60-70 mm Hg
• Epinephrine instillation
• Normothermia and normocarbia
105

Cobbʼs Angle
• Cobb's angle, a measurement used for evaluation of curves in
scoliosis on an AP radiographic projection of the spine (Fig.1).
• When assessing a curve the apical vertebra is first identified; this
is the most likely displaced and rotated vertebra with the least
tilted end plate.
• The end/transitional vertebra are then identified through the
curve above and below.
• The end vertebra are the most superior and inferior vertebra
which are least displaced and rotated and have the maximally
tilted end plate.
• A line is drawn along the superior end plate of the superior end
vertebra and a second line drawn along the inferior end plate of
the inferior end vertebra.
• If the end plates are indistinct the line may be drawn through the
pedicles.
• The angle between these two lines (or lines drawn perpendicular Cobbʼs Angle
to them) is measured as the Cobb angle. In S-shaped scoliosis Measuring Cobb's Angle
where there are two contiguous curves the lower end vertebra of
the upper curve will represent the upper end vertebra of the
lower curve.
• Because the Cobb angle reflects curvature only in a single plane
and fails to account for vertebral rotation it may not accurately
demonstrate the severity of three dimensional spinal deformity.
• As a general rule a Cobb angle of 10 is regarded as a minimum
angulation to define scoliosis.
106

39. Discuss the assessment, preparation and problems of anesthesia in a Dr Azam’s Notes in Anesthesiology 2013
chronic smoker for cholecystectomy.
Preoperative Evaluation:
Problems:
Goal: 1. Polycythemia - DVT
2. Chest X-Ray - presence of Bullae leading to Pneumothorax
• To determine the severity of disease
3. Bronchospasm - Pre operative & peri operative.
• To elucidate any reversible components such as bronchospasm
or infection. 4. Post pulmonary Complications:
a. Hypoxemia
Basic pulmonary assessment b. Atelectasis
History: c. Hypercarbia
- Cough # # -Smoking 5. Cor-pulmonale - Right heart failure
- Sputum # # -Occupational and 6. Tachyarrhythmias: patients on theophylline.
7. Laryngospasm & Bronchospasm.
- Dyspnea # # -Family history
8. Pulmonary Infection
- Fever ## # -Exercise limitation 9. Delayed extubation
- Medications 10.Mechanical Ventilation - Post operative.
Thorough cardiovascular and respiratory system examination is
mandatory to detect signs of COPD and/or RHF.
1. COPD - definitions of Chronic bronchitis & Emphysema
2. Preoperative Management
Lab Investigations:
a. Pre operative evaluation
1. Complete Hemogram- may be suggestive of raised b. Laboratory Investigations
haematocrit c. Pre operative respiratory care
2. Total Counts - Infection 3. Anesthetic Management
3. Urine examination d. Problems
4. RBS, BU, SC e. Anesthetic Technique
5. Blood grouping and Rh typing f. Premedication
g. Induction
6. Serum electrolytes –in suspected digitalis toxicity
h. Maintenance + Inhalation Agents
7. ABG analysis-Hypoxemia, hypercarbia, acidosis i. Intraoperative bronchospasm & management
8. Chest X-ray j. Reversal & Extubation
9. ECG-Suggestive of Rt. Heart failure 4. Postoperative Management.
10. Spirometry and PFT: Differentiate Between
obstructive or Restrictive lung Disease
107

Discuss the assessment, preparation and problems of anesthesia Dr Azam’s Notes in Anesthesiology 2013
in a chronic smoker for cholecystectomy. Continuation:
Anesthetic technique of choice:
Pre-operatively respiratory Care. • Regional Anesthesia by avoiding instrumentation of airway &
• Stop Smoking tracheal intubation is preferred when operative site is on the
• Dilate the airway using: extremities or below umbilicus.
• Beta agonist • Sensory block must not exceed T6 - COPD
• Anti-cholinergics • Sensory block must not exceed T10 in Kyphoscoliosis.
• Theophylline
• Steroids Monitoring:
• Cromolyn Sodium • ECG, NIBP, SpO2, EtCO2, RR, Plateau pressures, & ABG if need be.
• Loosen the Secretions by:
• Airway hydration ( Humidification/Nebulization) Induction & Maintain General Anesthesia Volatile anesthetic agent
• Systemic hydration orally - 3 Liters of choice:
• Mucolytic agents & Expectorant drugs Induction & maintenance of General Anesthesia:
• Antibiotics • When ever possible endotracheal tube should be avoided as it may
• Remove secretions: precipitate bronchospasm.
• Postural drainage • LMA is preferable
• Coughing Goal:
• Chest physiotherapy(percussion & Vibration) • Smooth induction
Ancillary Measures: • Adequate depth of anesthesia
• Treatment of co-existing disease
• Treatment of Cor-Pulmonale Preoxygenation: 100% oxygen for 3 - 5 min
• Pre-operative Digitalization
Patient Education, motivation & facilitation of post Induction Agents:
operative care: Continuation: • Propofol 2 - 2.5 mg/kg IV in hemodynamically stable patients.
• Psychological preparation • ketamine 1 - 2 mg/kg IV has bronchodialtory effect in hemodynamic
• Incentive spirometry & deep breathing exercise unstable patients.
• Exposure to secretion removal maneuvers • After unconsciousness is produced lungs can be ventilated with
• Exercise either Halothane ( More effective bronchodilator effect) or Isoflurane
• Diet supplements. Volatile Anesthetics:
• Halothane shown to be more effective bronchodilator than isoflurane
• Monitoring: but may sensitize the myocardium to cardiac dysrrhythmic effect of
• ECG, NIBP, SpO2, EtCO2, RR, Plateau pressures, & ABG catecholamines & theophylline.
if need be.
108

Discuss the assessment, preparation and problems of anesthesia in a chronic smoker for Dr Azam’s Notes in Anesthesiology 2013
cholecystectomy. Continuation:
choice of Neuro muscular blocking agents -Reversal:

Neuro muscular agent: • Injection: Neostigmine 0.05mg/kg IV
• Succinylcholine 1 - 2 mg/kg or Rocuronium Rapid sequence # # +
intubation: 0.6 to 1.2 mg/kg • Injection: Glycopyrrolate 0.01 mg/kg IV
• AVOID - Atracurium & Mivacurium as they release
histamine.
• Vecuronium 0.05 mg/kg or Rocuronium Tracheal intubation: -Extubation:
Recommended initial dose is 0.6 mg/kg. is safe. • Deep extubation may be advantageous.
• IV Lidocaine 1.5 mg/kg may be administered 1-3 min before • Prophylactic administration of inhaled β2 agonist; Ipratropium and
laryngoscopy. IV lidocaine minimizes reflex bronchospasm during emergence.
Precautions will you take while controlled Mechanical Post operative management & ventilatory support.
ventilation? • Post operative Pain Relief:
Controlled Ventilation: IPPV • If inadequate analgesia - it may lead to diaphragm splinting &
• Humidification of inspired gases - to prevent drying of impaired coughing ability.
secretions • Oxygen Therapy:
• Adequate intravenous fluid is administered to prevent • Low flow - venturi mask may be used.
dehydration & drying of secretions. • CPAP with low concentration of oxygen if hypoxemia present.
• Ventilator setting: to avoid Hypercapnia & Auto PEEP • Humidifications of inspired gases:
• Tidal volume: 6ml to 8ml/kg • Maintains cilliary function
• High inspiratory flow rates 1L/kg - to prolong the E Time. • Reduces viscosity of secretions
• Respiratory rate 10 to 12 breaths per minute - No • Facilitating their expectoration.
Hyperventilation • β2 agonists
• Increased E time - prolonged E time for emptying of the • Methylxanthines
alveoli. Mucolytics
•
• Respiratory Stimulants:
109

40. Enumerate Post operative complications? Dr Azam’s Notes in Anesthesiology 2013
• Post operative respiratory Complications are: Mechanism for Post operative pulmonary complications:
1. Airway obstruction: • VC is ↓ by 25% ( <15ml/kg - vital capacity): Decrease ability to
a. Laryngospasm, bronchospasm - Treatment of cause, Oxygen cough.
supplementation, bronchodilators. • Residual Volume ↑ by 13% following GA
2. Hypoxemia: SaO2 < 90% • ERV ↓ by 25% after lower abdominal surgery & 60% after upper
• Immediate ( 1 to 2 Hrs): abdominal and thoracic surgery.
• Opioids, • Risk increases as duration of surgery exceeds 3 hours to 4hrs.
• Loss of pulmonary vasoconstriction,
• shivering Pathogenesis:
• V/Q mismatch, Post operative decrease in Vital capacity
• Diffusion Hypoxia
• Late ( > 2 Hrs):
• Atelectasis,
• Pulmonary Embolism,
• Pneumothorax,
• Pulmonary Edema Poor cough &
3. Cor-Pulmonale: Digitalization & Diuretics retention of Atelectasis
Secretions
4. Pulmonary infection:
• Pneumonia
5. Hypoventilation.
• Hypercarbia: Alveolar hypoventilation secondary to pain, inadequate
analgesia, inadequate reversal of NMB. - Oxygen supplementation. Pneumonia
6. Aspiration:
Arterial Hypoxemia
7. Atelectasis:
• Decreased FRC,
• Pain,
• splinting of diaphragm,
• decrease sputum clearance.
8. Delayed ambulation Acute Respiratory Failure
9. DVT & PE:
• Polycythemia Treatment of PPC: • Non - Invasive Ventilation - CPAP.
• intraoperative hypothermia & Dehydration: • Oxygen supplementation • Early Mobilization
• LMWH, TED Stockings, early mobilization and • Incentive Spirometry & Deep • Early Nutrition
Hydration breathing exercises Cor-pulmonaleDiuretics, Digoxin
•
10. Need for Mechanical ventilation, prolonged ICU stay/ • Chest Physiotherapy - Percussion & Avoiding Respiratory depressants.
•
hospital stay vibration. • Antibiotics & Analgesics 110
• Bronchodilators • Invasive ventilation - Lastly
41. High Altitude & Anesthesia Dr Azam’s Notes in Anesthesiology 2013
Levels of altitude: Pulmonary HTN at HA:

1. Base line à 3000 M above mean sea level 1. Normal PAP is 12 mm Hg
2. Mild HA à 3000 – 3600 M 2. At HA PAP is 28 mm Hg due to HPV
3. Moderate HA à 4200 – 4800 M HAPO (high altitude pulmonary oedema) is due to
4. Extreme HA à above 4800 M 1. hydrostatic pressure
2. permeability of pulmonary vasculature.
Pathophysiological changes: 3. Coagulation defect.
BAROMETRIC 4. free O2 radicals.
ALTITUDE IN ALVEOLAR WATER
PRESSURE IN MM Po2 PAO2 PaCO2
FEET VAPOUR TENSION
HG
At 0 feet Neurogenic pulmonary oedema:
760 159 103 40 47 mm Hg
# ↑ ANS activity à ↑ PAP à oedema.
10,000 523 109 61 35 47 Body temperature: hypothermia (+) at HA < 350C core temperature is
20,000 349 73 35 30 47 called hypothermia.
It leads to
Pasteur point: At which anaerobic metabolism begins. (PO2 < 1. Decrease BP
1-2 mm Hg) (0.2 Kpa) 2. Arrhythamias
1. O2 gradient is decreased and cross atmosphere and 3. AV block
alveolar and also cross alveolar to capillary 4. Decrease contractility.
2. Hypoxia à hypoventilation via central and peripheral • MAC decreased by 5% fall in temperature due to decrease CNS activity
chemoreceptors and increased solubility of anaesthetic vapours at low temperature.
3. Increased diffusion capacity à CNS: vasodilation.
4. i.e, normally it is 2.1 ml/mm Hg/min. 1. Altered behaviour
5. At AA it increases by 3 folds same like in strenous exercise. 2. Lack of judgement
3. In coordination
CVS: 4. Speech sleep disturbances
1. Hypoxia à↑ erythropoitin àincreased erythropoisis. 5. drowsiness
6. Inconsciousness
2. ↑ Hematocrit > 65%
7. Increased ICP
3. ↑ 2-3 DPG à ODC shifts to Rt.
8. Increased CBF
4. ↑ blood volume by 30%
111

High Altitude & Anesthesia. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Anaesthesia at HA Preoperative preparation:

General principles: • Psychological preparation – important because patients are lovely,
1. Due to decrease PIO2 risk of perioperative hypoxia is apprehensive about monitoring of the place and isolation.
increase. • Premed – opiates and other depressants abolishes compensatory
2. Surgical teams usually not available at severe high altitude. increase in HR and RR to maintain, normal oxygenation at high altitude
They are available at mild HA. when given at higher doses. Hence these should be used when
3. Do not operate on new comer before he/she is necessary (like preoperative pain state) along with O2 administration of
acclimatized. If emergency operate at mild HA. monitoring.
4. Preload: Use crystalloid / colloid / blood which are warmed • Benzodiazepines, NSAIDS, barbiturates etc used.
to body temperature Be cautious not to overload patients. • Atropine / Glycopyrrolate can be used.
5. Bleeding: oozing is due to • induction: Thiopentone has slower onset due to prolonged correlation
a. Increase venous pressure time at HA.
b. Increase blood volume • Etomidate, propofol, benzodiazepines can be safely used.
c. Venous dilation • Inhalational agents
d. Increase capillary density. • O2 high concentration of O2 should be given, atleast 40% higher than at
e. Coagulation defect. sea level during perioperative period, due to following reasons.
1. Anaesthesia deprives compensatory mechanisms.
1. Increased risk of infection and pollution: due to lack of 2. Hypoxic brain damage may occur at low PaO2.
properly built O.T at HA. 3. Compensation for acidosis is reduced at HA
2. Fire and explosion – decrease due to PIO2, but it can still 4. Decrease PIO2 and PAO2 at HA
exist due to decrease of kerosene lights. Ether should be 5. N2O – potency of anaesthetic gases is proportional to their partial
avoided in presence of open flames. Battery operated lights pressure and not the percentage in mixture of O2 is important.
can be used in O.T. 6. N2O has to be given at 50% to be effective. At HA its effectiveness
3. Hypothermia – common. decreases due to decrease BP. Since 50% O2 has to be given at HA
• Maintain O.T temperature at 240C and more at 3000 M above sea level N2O will not be sufficient and
• Use blankets, hot air blower, heater etc. effective in low concentration.
7. Ether – induction is slow and require high concentration risk of
explosion present
8. halothane – suitable agent can also be used.
9. NDMR: prolong action due to hypothermia.
10. Reversal – has to be complete.
112

High Altitude & Anesthesia. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Regional anaesthesia:
• Increase incidence of PDPH, bladder and bowel
distension after spinal anaesthesia.
• Increase PDPH is due to increase ICP.
• Duration shortened.
TIVA: Ketamine: Very useful for small procedure. useful where
O2 supplementation cannot be given. Useful in field
anaesthesia remote place it causes less depression of
ventilation.
Equipment:
• Flowmeter are calibrated at sea level.
• At high altitude they show low reading at high flows.
• The error is about 20% at 3000 M from sea level.
• Use O2 analyser if low flow technique is used.
• Use spirometer to calibrate flow meters at low BP at HA.
• Vaporizer: SVP of any agent does not change with change of
ambient pressure but changes with temperature. vapours
delivered at HA get dissolved in blood readily due to
decrease in temperature hence the dial setting has to be
slightly adjusted according to the clinical response.
• Venture mask designed to deliver FIO2 of 35% at sea
level will deliver 41% O2 at 10,000 feet.
• Pressure gauge reading - same
• EMO apparatus is a drawn over ether vaporizer and can
be used with oxford miniature vaporizer for IPPV at
isolated localities.
• Apparatus boyles type F.
• This is a field type portable model of Boyleʼs apparatus
with Goldman vaporizer for halothane
• Triservice anaesthetic apparatus (penlon) is a drawn
over system, utilises atmospheric air for O2. It has got
miniature oxford vaporizer for use of halothane and
trilene as volatile agents.
• Suboptimal equipment at HA: is an important
consideration while choosing the anaesthetic technique.
113

42. Hyperbaric Oxygen Therapy (HBO) Dr Azam’s Notes in Anesthesiology 2013
• Regional Hypoxia: Large O2 gradient, allows at least some degree

Definition: It means administration of O2 at higher than of O2 delivery by increasing PaO2 in the hypoxia zone.
atmospheric pressure Eg: Compromised Surgical flap, Wound Ulcers, Crush Injuries.
Effects: • Global hypoxia: CO poisoning: CO has high affinity for Hb and
• Higher the PIO2, higher is the PAO2. shifts ODC to the left. It inhibits cytochrome oxidase enzyme.
• Higher the PAO2, higher is the actual amount of O2 carried Hyperbaric O2 in CO poisoning acts by three mechanisms:
in physical solution Hence by increasing PIO2 we can 1. Compete with CO molecules for Hb binding sites on COHb and
increase the amount of dissolved O2. eliminates CO.
• By administering O2 at high atmospheric pressure, we can 2. Provides sufficient dissolved O2 for tissue use
increase the dissolved O2 content of the blood which will be
3. Moves ODC to the right
sufficient to meet tissue demands.
Eg: CO, CN intoxication, Severe anemia.
• Increasing O2 stores in the body thus allowing tissues to
survive anoxia for much longer periods. • Infections: Inhibits growth of anaerobic organisms e.g. Cl, Welchi,
Cl-tetany.It inhibits Clostridial alpha toxins
Factors: • Aerobic organisms which are sensitive to HBO are
• PaO2 I. Staphylococcal aureus
• Hb II. Pseudomonas pyocyaneus
• Cardiac output • Leukocyte oxidative killing mechanisms operate, when the O2
Indications: tensions > 30mmHg. Improve osteoclastic function therefore
4C: useful in osteomyelitis
• CO/CN poisoning • Gas lesions:
• Clostridia infection • By increasing arterial hydrostatic pressure, decrease the volume
• Cancer therapy of emboli
• Caissonʼs disease • Produce hyperoxia which improves O2 delivery to tissue
downstream of the obstructing emboli
Current Indications: • This also maximizes the gradient for elimination of gas in the
• Regional Hypoxia emboli
• Global hypoxia
• Infection
• Gas-lesion conditions
114

Hyperbaric Oxygen Therapy (HBO). Continuation: Dr Azam’s Notes in Anesthesiology 2013
Methods of administration:
1. Single person chamber /Mono-place
• Only the patient is subject to compression and the staff
GRID: Question to be answered under following
remains outside. It is made up of transparent acrylic. headings:
2. Large operating room pressure chamber / multi-place 1. Definition
• Encloses both the patient and medical attendants. Can be used for 2. Factors
surgery. Medical attendants breathe compressed air, while patient 3. Indications
breaths 100% O2 at pressure from a mask/ETT. a. 4C
• Chamber made of steel & aluminum. b. Current Indications
4. Explain Current Indications
5. Method of Administration
Complications:
6. Complications
• Barotrauma
• Decompression sickness
• O2 toxicity
• Visual function disturbances: e.g. progressive myopia because of
effect of either O2 pressure on lens shape/RI. Retrolental
fibroplasia in neonates. Cataract formation.
• Claustrophobia poses problem for therapy.
• Nausea, Vertigo, Tinnitus, Parasthesia, anxiety and involuntary
muscle movement.
• Factors influencing the onset of toxicity – duration of exposure and
atmospheric pressure, (can tolerate 3 ATM for 30 minutes)
115

43. High Altitude Pulmonary Edema Dr Azam’s Notes in Anesthesiology 2013
A type of pulmonary edema seen in young adult who have quickly ascended to an altitude in excess of 2400 m or 8000 ft and engage
themselves in strenuous physical activity before acclimatization.
It is primarily a disorder of pulmonary circulation induced by a relatively sustained alveolar hypoxia.
Pathophysiology:
• Initiating event is HPV due to alveolar hypoxia.
• Increase pulmonary capillary permeability due to increased pulmonary artery pressure.
• Transudation of fluid into alveoli.
Prevention:
• Gradual acclimatization around 300m/day.
• Staging in which several days are spent at an intermediate altitude of around 2000 m.
• Avoidance of strenuous physical work for 2-3 days at high altitude.
• These patients within one day develop cough, dyspnea, chest pain and cyanosis
• O/E: tachycardia and b/L rales.
• Chest x-ray: discrete patches of pulmonary infiltrates.
Treatment:
1. Administrating of supplemental inspired oxygen (O2).
2. Prophylactic administration of nifedepine to lower pulmonary artery pressure which prevents pulmonary edema.
3. A portables hyperbaric chamber which is pressurized to about 120 mm Hg above ambient pressure can be used for rapid simulation
of descent.
4. Lasix
5. Steroids
116

44. Anesthetic Management of patient with COAD. Dr Azam’s Notes in Anesthesiology 2013
Chronic obstructive airway disease Lab Investigations:

1. Complete Hemogram- may be suggestive of raised haematocrit
2. Urine examination
3. RBS, BU, SC
Chronic Bronchitis Emphysema
4. Blood grouping and Rh typing
5. Serum electrolytes –in suspected digitalis toxicity
Anesthetic Management: 6. ABG analysis-Hypoxemia, hypercarbia, acidosis
7. Chest X-ray
Preoperative Evaluation: 8. ECG-Suggestive of Rt. Heart failure
9. Spirometry and PFT.
Goal:
• To determine the severity of disease
• To elucidate any reversible components such as The pre-operative respiratory care:
bronchospasm or infection.
• Stop Smoking
Basic pulmonary assessment • Dilate the airway using:
• Beta agonist
History: • Anti-cholinergics
- Cough -‐Smoking • Theophylline
- Sputum -‐Occupational and • Steroids
- Dyspnea -‐Family history • Cromolyn Sodium
- Fever -‐Exercise limitation • Loosen the Secretions by:
- Medications • Airway hydration ( Humidification/Nebulization)
• Systemic hydration orally - 3 Liters
Thorough cardiovascular and respiratory system
• Mucolytic agents & Expectorant drugs
examination is mandatory to detect signs of COPD • Antibiotics
and/or RHF. • Remove secretions:
• Postural drainage
• Coughing
• Chest physiotherapy(percussion & Vibration)
Ancillary Measures:
• Treatment of co-existing disease
• Treatment of Cor-Pulmonale
• Pre-operative Digitalization
Patient Education, motivation & facilitation of post 117
operative care Continuation next page:
Anesthetic Management of patient with COAD. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Patient Education, motivation & facilitation of post

operative care: Continuation: • Steroids:
• Physiological preparation • 100 mg of hydrocortisone is given IV before induction & post
operatively 100 mg 8th hourly for 48 hours.
• Incentive spirometry & deep breathing exercise
Monitoring:
• Exposure to secretion removal maneuvers
• Exercise • ECG, NIBP, SpO2, EtCO2, RR, Plateau pressures, & ABG if need be.
• Diet supplements. Induction & maintenance of General Anesthesia:
• When ever possible endotracheal tube should be avoided as it may
Anesthetic Management: precipitate bronchospasm.
• Problems: Pulmonary mechanics following • LMA is preferable
anesthesia & Surgery: Goal:
• Vital capacity Decreased by 20 - 25 % • Smooth induction
• Residual Volume increased by 13% • Adequate depth of anesthesia
• Expiratory reserve volume decreased by 25%
• Surgery duration exceeding 3 hours Preoxygenation: 100% oxygen for 3 - 5 min
These changes are responsible for atelectasis,
hypoventilation, hypoxemia & pulmonary infection. Induction Agents:
• Propofol 2 - 2.5 mg/kg IV in hemodynamically stable patients.
• Proper Selection of Anesthesia technique: • ketamine 1 - 2 mg/kg IV has bronchodialtory effect in hemodynamic unstable
• Regional Anesthesia by avoiding patients.
instrumentation of airway & tracheal intubation • After unconsciousness is produced lungs can be ventilated with either
is preferred when operative site is on the Halothane ( More effective bronchodilator effect) or Isoflurane
extremities or below umbilicus.
• Sensory block must not exceed T6 Volatile Anesthetics:
• Halothane shown to be more effective bronchodilator than isoflurane but
Premedication: may sensitize the myocardium to cardiac dysrrhythmic effect of
• Benzodiazepines for anxiolysis & opioids for pain catecholamines & theophylline.
may be used - with careful attention to avoid
respiratory depression. Neuro muscular agent:
• Morphine is avoided - causes Histamine release • Succinylcholine 1 - 2 mg/kg or Rocuronium Rapid sequence intubation: 0.6 to 1.2
induced bronchoconstriction. mg/kg
• Antichoninergics depresses mucociliary activity & • AVOID - Atracurium & Mivacurium as they release histamine.
impair secretion clearance. • Vecuronium 0.05 mg/kg or Rocuronium Tracheal intubation: Recommended initial
• H2 receptors are avoided dose is 0.6 mg/kg. is safe.
• Bronchodilator to be continued till induction. • IV Lidocaine 1.5 mg/kg may be administered 1-3 min before laryngoscopy.
118

Controlled Ventilation: IPPV Reversal:

• Humidification of inspired gases - to prevent drying of • Neostigmine 0.05mg/kg + Gylcopyrolate 0.01 mg/kg IV.
secretions
• Adequate intravenous fluid is administered to prevent Extubation:
dehydration & drying of secretions. • Trachea should be extubated while anesthesia is still sufficient to
• Ventilator setting: to avoid Hypercapnia & Auto suppress hyperactive airway reflexes.
PEEP
• Tidal volume: 8ml/kg Post-operative Management:
• High inspiratory flow rates 1L/kg - to prolong the E Goals:
Time. • To promote adequate analgesia
• Respiratory rate 10 to 12 breaths per minute - No • To minimize the incidence of postoperative complications
Hyperventilation • To prevent infections
• Increased E time - prolonged E time for emptying of • Chest physiotherapy & deep breathing exercise.
the alveoli. • Consider CPAP - Decreases WOB, Improves LV Compliance.
• Continuous administration of Local anesthetic with low dose
Intraoperative bronchospasm: Identification & Management: opioids via epidural catheter for post operative pain relief.
To R/O other causes of high Deepen Anesthesia:

airway pressure & • Give 100% oxygen
wheezing: • Inhalation Anesthetic
• ET - Tube Kinking agents if BP is normal.
• Thick secretions • Low BP - Ketamine
• Pulmonary edema
• tension pneumothorax
• Aspiration Pneumonitis Beta2 Agonist:
• Pulmonary edema • Rapid acting albuterol through
• Endobronchial intubation meter dose inhaler directly in
• bucking breathing circuit.
• Aminophylline 0.5mg/kg -
tachyarrhythmias
• Terbutaline S/C 0.25mg every 20
min for 3 doses.
• Epinephrine: 0.1 - 0.5 ml of 1:1000
S/C may be the last resort.
• Steroids: hydrocortisone 4mg/kg
followed by 3mg/kg. 119

45. Describe the causes & management of venous air embolism.
Investigations:
• Doppler ultrasound technique: Can detect 0.10 ml of Air.
• Air enters the venous circulation whenever there is sufficient gradient
• Cardiac auscultation - Mill Wheel murmur when 30 ml is present.
between the right atrium and the point of entrance of air. It is found that
• End Tidal Carbon-dioxide - Sudden fall in EtCO2
5cm gravitational gradient is sufficient for air to enter venous circulation.
• Pulmonary Artery Pressure Increases
• Entry of 100ml of air into venous circulation can be fatal.(2ml/kg to 5ml/kg)
• Trans Esophageal Echocardiogram - Can detect 0.02 ml/kg.
Causes of Air embolism:
1. Surgery: Operation involving veins in head and neck, thorax, abdomen, Management:
neurosurgical procedures (Posterior fossa surgeries in sitting position).
Prevention:
Open heart operation, Obstetrics and Gynecology procedures like- Delivery
! In those operations where embolism is a known hazard, special care must
in presence of placenta previa, Insufflation of fallopian tube and
be taken by surgeon and adequate monitoring with facilities for specific therapy
laparoscopy. should be available for anesthesiologist.
2. Diagnostic procedures: Air encephalogram, Angiocardiography, Air 1. CVP should be maintained at a level which is just less than that which
myelography, Bronchoscope. causes troublesome oozing.ʼ
3. Therapeutic: IV therapy, Antral washouts, pneumoperitonium, IPPV, blood 2. Use of air as a contrast medium in radiology should be replaced by more
transfusion, haemodialysis and ECMO soluble gas such as CO2.
4. Accidental –Rapid decompression. a) CO2 should be used to inflate during laparoscopic procedures instead of
air.
Signs and symptoms: b) N2O should be avoided as part of anesthetic technique when air
• Gasping respiration in spontaneously breathing patients. embolism is likely complication.
• Increase CVP and PAP.
Treatment:
• Dysrrhythmias.
• Hypotension • Stop N2O
• Abnormal heart sounds-Mill wheel murmur. • The hallmark of the treatment of air embolism lies in early
• Alteration in heart rate –Bradycardia or tachycardia detection, rapid aspiration of embolised air and sealing of source
• Cyanosis of entry.
• Mill wheel murmur – caused by agitation of blood and air in right • Prevention of further entry of air: First act is a compress and ligate the
ventricle. It is often not heard at all or is audible for only short open vessel. Raising CVP or local venous pressure may help
period of time. 30 ml of air produces characteristic mill wheel identification of vessel.
murmur. • Removal of air: Air is aspirated through central venous catheter in
the right atrium. When large amount of air is present it is
sometimes necessary to aspirate several 100ml of blood in order
to capture the air. This act may produce blood volume depletion.
Using large syringe containing 3-4 ml of heparnised saline so that
the deareated blood can be returned to circulation can minimize
this.
120

Describe the causes & management of venous air embolism. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Supportive treatment:
Posture:
The classical posture of head down in left lateral decubitus position places the right
atrium and tricuspid values above the right ventricle. This position.
• Minimizes passage of air into pulmonary artery.
• Improves cardiac output and venous return as heart is dependent.
• Minimizes the possibility of developing an air lock.
• Volume expanders and vasopressors used for persistent hypotension.
• Natural absorption of air is increased by ventilation with 100% oxygen.
• Whole body compression greater than atmospheric pressure may be valuable to
force the gas into solution, particularly in case of systemic air embolism involving
brain.
GRID: Question needs answered under following headings:

1. Introduction
2. Causes
3. Sign & Symptoms
4. Investigations
5. Management
a. Prevention
b. Treatment
c. Supportive Treatment.
121

46. Pulmonary embolism. Dr Azam’s Notes in Anesthesiology 2013
PTE is the most common cause of death in hospitalized patients. Pathophysiology:
Virchow Triad: Emboli occlusion in pulmonary circulation increases dead space

The triad of risk factors described by Virchow over a century ago still
apply.
• Stasis
• Hypercoagulability Hypoxemia & increase in PaCO2
• Endothelial injury
The risk of DVT and PTE is higher in presence of advanced age,
obesity, malignancy, CCF, acute MI, prolonged immobilization.
ORIGIN OF EMBOLI: Acute increase in Pulmonary Vascular resistance by reducing the
1. Venous thrombi in larger lower extremity: Most commonly they cross sectional area of the pulmonary vasculature causing reflex &
begin as calf vein thrombosis which can propagate into the vasoconstriction
larger popliteal, femoral and pelvic venous system.
2. Right heart: thrombi may also embolize from right heart as a
result of CCF, atrial fibrillation and endocarditis. Net increase in Pulmonary shunt & hypoxemia
3. Rarely emboli can also originate from renal, hepatic, or upper
extremity veins.
4. Occlusion of more than 50% of pulmonary circulation (massive
PE) is necessary before sustained pulmonary hypertension is
Affected areas looses its surfactant with in hours & may
seen
become atelectatic with in 24 - 48 hours
5. Sustained increase in right ventricular after-load precipitate
acute right ventricular failure.
Clinical features & Diagnosis:
• Tachypnea, dyspnea, chest pain or hemoptysis, wheezing on ECG:
auscultation. • Tachycardia
• ABG: Hypoxemia, respiratory alkalosis ( because of increase • Right axis deviation
minute ventilation ) • RBBB
• Chest X-Ray: Areas of oligemia (radiolucency), Wedge shape • S1,Q3 & T3
density with infarct, atelectasis with an elevated diaphragm, • Tall T Waves
enlarged pulmonary artery. • Peaked P- waves
• AF.
Pulmonary Angiogram: Gold standard for PTE.
122

Pulmonary embolism. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Risk Factors associated with DVT & THROMBOEMBOLYTIC THERAPY:

PTE: • Thrombolytic therapy should be considered for PTE with hemodynamic
• Prolonged bed rest instability, in which rate of clot lysis is critical.
Urokinase:
• postpartum state
• Fracture of lower limbs • Loading dose – 4400 IU/kg over 10 min.(t ½ 10 to 15 min)
• Surgery of lower extremities • Maintenance – 4400 IU/Kg every 12 hours
Streptokinase:
• Carcinoma
• Loading dose – 2,50,000 U (over30 min)
• CHF
• Maintenance – 1,00,000 U every 24 hours (t ½ 30 to 80 min)
• Obesity Tissue plasminogen activator (TPA)
• Surgery > 30 min
• 25-50mg – every 2 hours after loading dose of heparin. Heparin
• Hypercoagulability ( protein C & protein S increases the efficacy of TPA.(t ½ 3 to 4 min)
deficiency)
Advantages of TPA: Less systemic fibrinolysis
• Dehydration # # # Rapid improvement in haemodynamic condition
Treatment of PTE: Contraindication for thrombolytic therapy:
Supportive Treatment: Absolute: Active internal bleeding
# # Recent CVA (within 2 months)
• Oxygenation and ventilation
Relative:
• Volume administration
Inotropes • Recent major surgery (within 10 days)
Isoproterenol: • Recent GI bleeding
Which functions as a pulmonary vasodilatory, bronchodilator and β- agonist • Arterial HT (systolic more than 200 mm/Hg &
is appropriate for treating mild haemodynamic compromise from PTE. • Diastolic more than 110 mm/Hg)
Nor-Adrenaline, DOPAMINE & DOBUTAMINE: • More than 75 years, Diabetic haemorrhage retinopathy
Definitive Treatment: PULMONARY EMBOLECTOMY:
Heparin: • Reserved for patients with greater than 55-60% of pulmonary
• Heparin decreases mortality from PTE. Death rate has seen found to be vasculature occlusion
8% for treated and 32% for untreated patients.
• Heparin bolus (5000 units) is recommended even before definitive
diagnosis is made, to prevent additional accumulation of platelets and
thrombi on the embolus.
• Continuous infusion of heparin started at rate of 1000-1500 units / hr to
maintain APTT at 1.5 to 2.0 time normal.
• Infusion: Inj Heparin 2500 U in 250 ml NS, 1ml = 100 U, 10ml = 1000 U
123

Pulmonary embolism. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Anesthetic Consideration for PTE:

Pre-operative consideration: Intraoperative PE: May present as
• Patient comes to OT for placement of Caval filter/thrombectomy • Unexplained hypotension,
• May present for unrelated surgery. • Hypoxemia
• If acute episode of PE is > 1 year old, the risk of stopping anticoagulant • Bronchospasm
therapy is less. • Increased Airway resistance/pressure
• In case of chronic PE, PFT would have returned to normal • Sudden decrease in EtCO2 production
• The goal should be prevention of new episode of PTE. • Raised CVP & Pulmonary artery pressure
Intraoperative management:
• IVC filter (greenfield filters) are placed percutaneously under local
anesthesia with sedation. GRID: Question need to to answered
• Decrease venous return during device placement can precipitate under following headings:
hypotension. 1. Introduction
• The use of Neuraxial block is Contraindicated in patients with residual 2. Virchow Triad
anticoagulation or prolonged BT or INR. 3. Origin of emboli
• If GA is given shorting acting drugs to be used which may allow early 4. Clinical features
post operative ambulation. 5. Pathophysiology
• Patients presenting for pulmonary embolectomy are critically ill. They 6. Risk factors
are usually already intubated but tolerate PPV poorly. 7. Treatment
• Patients may require Inotropic support - Isoproterenol - Reduces PVR, a. Supportive Treatment
Increases contractility may also decrease diastolic blood pressure may b. Definitive treatment
require dopamine & dobutamine c. Pulmonary embolectomy
• Small doses of anesthetic agents to be used. 8. Anesthetic consideration
• CPB is required usually 9. Recognition of intraoperative PE.
• Monitoring of right atrial pressure for fluid administration
• N2O is avoided and high FiO2 to be considered
• Avoid drugs releasing histamine
• During removal of embolic fragments from distal pulmonary artery PPV
to be applied when surgeon applies suction through the arteriotomy
placed in pulmonary trunk.
124

47. Deep Vein Thrombosis. Dr Azam’s Notes in Anesthesiology 2013
Clinical Features:
Definition: • Changes in skin color (redness) in one leg
• Deep venous thrombosis is the formation of a blood clot in • Increased warmth in one leg
a vein that is deep inside a part of the body, usually the • Leg pain in one leg
legs. • Leg tenderness in one leg
• Blood clots may form when something slows or changes • Skin that feels warm to the touch
the flow of blood in the veins. • Swelling (edema) of one leg
Risk factors include: Diagnosis:

• Any catheter which have been passed through the vein in The following tests may be done:
the groin • D-dimer blood test
• Prolonged Bed rest • Doppler ultrasound examination of the legs
• Cigarette smoking • Plethysmography (measurement of blood flow) of the legs
• Family history of blood clots • X-rays to show veins in the affected area(venography)
• Fractures in the pelvis or legs • Blood tests to check if there is increased chance of blood
• Giving birth within the last 6 months clotting (hypercoagulability). Such tests include:
• Heart failure • Activated protein C resistance (checks for the Factor V Leiden
• Obesity mutation)
• Recent surgery (especially hip, knee, or female pelvic • Antithrombin III levels
surgery) • Antiphospholipid antibodies
• Blood that is more likely to clot (hypercoagulability) • Genetic testing to look for mutations that make more likely to
• Cancer ( Because Malignant cell contain cysteine develop blood clots, such as the prothrombin G20210A mutation
proteinase which activates factor X) • Lupus anticoagulant
• Taking estrogens or birth control pills. This risk is even • Protein C and protein S levels
higher if you smoke. • Screening for disseminated intravascular coagulation (DIC)
• DVTs are most common in adults over age 60, but can
occur at any age.
• Sitting for long periods when traveling can increase the
risk of DVTs.
125

Deep Vein Thrombosis. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Treatment of DVT: (unfractionated or Low molecular weight

heparin) III. Prevention of DVT:
I.Anticoagulation: • Early mobilization
Heparin: • DVT - Elastic stockings
• Heparin bolus (5000 units) is recommended even before • Physiotherapy with active leg exercise
definitive diagnosis is made, to prevent additional • Shortening the surgery time
accumulation of platelets and thrombi on the embolus. • Mini dose of heparin 5000 U 8th hourly.
• Continuous infusion of heparin started at rate of 1000-1500 • Intermittent external pneumatic compressions with inflatable cuffs.
units / hr to maintain APTT at 1.5 to 2.0 time normal. • Central neuraxial / Regional anesthesia has beneficial effects over General
• Infusion: Inj Heparin 2500 U in 250 ml NS, 1ml = 100 U, anesthesia.
10ml = 1000 U • Sympathectomy induced increases in lower extremity venous blood
flow
Warfarin: (Oral Vitamin K Antagonist) • Systemic anti-inflammatory effects of local anesthetics
• Initiated with in 24 hours of Heparin therapy according • Decreased platelet reactivity
prothrombin time, which is expressed as INR. • Attenuated post operative increase in Factor VIII & vWF
• Monitoring of INR & to be targeted between 2 to 3 • Attenuated post operative decrease in anti thrombin III
• Heparin needs to be discontinued after 48 hrs after starting • Alters stress hormone release
Warfarin therapy.
• To be continued for 3 months or longer.
II. Restoration of venous patency:

• IVC filters (Greenfield Filters) for patients with recurrent
pulmonary embolism. GRID: Question need to to answered
• Thrombolytics treatment under following headings:
1. Definition
2. Risk factors
3. Clinical features
4. Diagnosis
5. Treatment of DVT
6. Prevention of DVT.
126

48. Amniotic Fluid Embolism Dr Azam’s Notes in Anesthesiology 2013
• Rare (1:20,000) catastrophic and life threatening Pathophysiology:

complication of pregnancy that occurs in the setting of a ! !"#$%&$'()*+$,(-".%*$/"(
disrupted barrier between the amniotic fluid and maternal -----".%*$/"(
circulation.
• 80% mortality. And 50% mortality in the first hour. 0-'12#$'2*(%./&3+'&$%#(( 4+"%32*(%./&3+'&$%#((
• 3 common sites of entry of amniotic fluid into maternal
circulation are endocervical veins, Placenta and Uterine 53$&$'2*(6+*"%#237(8-//-*(%./&3+'&$%#! 9+*"%#237(:-//-*(82/%/62/"((
trauma site.
• Can occur during labour or delivery, cesarean section or post
partum. !'+&-(9+*"%#237(4;<(=(476%>-"$2((
Contains of Amniotic Fluid:
• Amniotic fluid contains, Desquamated fetal debris,
?-8-3-(#-+3%*%@$'( ?6%#&2#-%+/(3-/%*+&$%#(( B:C((
Prostaglandins and leukotrienes.
$"62$3"-#&A,-2&1(
Alternative term “anaphylactoid syndrome of pregnancy”
suggested to emphasize role of chemical mediators in this
syndrome.
Diagnosis: Signs of symptoms.
Signs and symptoms: • Increase pulmonary artery pressure.
• Onset – dramatic and abrupt. • Decrease cardiac output.
• Dyspnoea, Arterial hypoxemia, • Amniotic fluid material in the parturient blood aspirated from a
• Cyanosis, Seizures, central venous or pulmonary artery catheter - Confirmatory.
• Loss of consciousness, Hypotension (Disproportionate to • Autopsy lung biopsy.
blood loss)
• Acute pulmonary embolism, Uterine atony, Differential diagnosis:
• Fetal distress is present at the same time, - Aspiration of gastric contents (bronchoconstriction)
• Cardiopulmonary arrest in 80%, - Pulmonary embolism (chest pain)
- Venous air embolism
• Coagulopathy resembling DIC with associated bleeding, May
be the only presenting symptom. - Local anesthetic toxicity (high spinal level)
- High epidural anesthesia
- Total spinal anesthesia
127

Amniotic Fluid Embolism. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Treatment: Arrest – CPR

1. Tracheal intubation and mechanical ventilation of lungs with 100%
O2. PEEP is often helpful. GRID: Question need to to answered under
2. Inotropic support – guided by CVP and PAC dopamine, dobutamine following headings:
and norepinephrine – to treat acute LVF and hypotension. 1. Introduction
2. 3 Common sites of entry of amniotic fluid.
3. Fluid therapy – guided by CVP. - Prone for pulmonary edema.
3. Contains of amniotic fluid
4. DIC treated with FFP, cryoprecipitate and platelets. 4. Signs & symptoms
5. Uterine atony – oxytocin and methylergometrine. 5. Pathophysiology
6. Expeditious delivery appears to improve maternal and fetal 6. Diagnosis
outcome - immediate cesarean delivery. 7. Treatment of AFE
CPR:
1. Before delivery of fetus – difficult.
2. Chest compressions marginally effective.
3. Aortocaval compression impairs resuscitation in supine position.
4. Chest compressions are less effective in a lateral tilt position.
128

49. Describe pathophysiology, clinical features diagnosis & management of fat embolism?
Definition: Fat embolism is a pathological entity characterized by occlusion of multiple blood

vessels with fat globules that are too large to pass through the capillaries.
Clinical presentation: Fat embolism syndrome (FES) has
Etiologic factors: three presentations:
• Traumatic factors: Fractures, burns, subcutaneous and adipose tissue 1. Subclinical: This characterized be the presence of
injuries, surgeries like IM nailing, total hop arthroplasty, total knee arthroplasty, laboratory abnormalities only and non specific symptoms
CPR. such as tachycardia (>100 beats/minute), tachypnea (>25
• Non traumatic factors–Cryosurgery of bone, interosseous fluid and drug breaths/min), pyrexia (>37.80C), hypoxemia (room air
administration, liposuction, lymphangiography. PaO2< 80 mmHg)are common findings.
• Diseases– Sickle cell anemia acute pancreatitis fatty liver 2. Non-fulminant subacute:Characterized by Respiratory
• Drugs– Lipid emulsion, intra-arterial cisplatin, long term steroid insufficiency or failure.Fever, tachycardia (> 110 beats/
administration. minute).
• Petechiae: is pathognomonic sign of FES. It appears on
Pathophysiology: upper anterior portions like chest, neck, arms, axilla,
# Two theories are proposed to explain pathophysiology of fat embolism. shoulders, oral mucous membrane, conjunctive. The
• Mechanical theory: According to this theory syndrome of fat embolism incidence varies from 25% - 95%. The petechiae results
results from physical obstruction of pulmonary and systemic vasculature with from occlusion and distention of dermal capillaries by fat
embolised fat. Increased intramedullary pressure after injury forces marrow globules. The petechiae are localized to upper anterior
into injured venous sinusoids from which fat travels to lung. After reaching the portions of body because the fat which is lighter than blood
lung, fat can obstruct the pulmonary vessels and cause corpulmonale if floats.
adequate compensatory pulmonary vasodilation does not occur. The fat that • Neurological signs –usually nonspecific, includes acute
has gained access to systemic circulation may obstruct vessels of brain, confusion, stupor, coma, decerebrate rigidity and
myocardium kidney and other organs. convulsions. Cerebral hypoxia is probably responsible for
• Biochemical theory: According to this theory which a supported by the the neurological signs.
development of fat embolism in non traumatic conditions, fat globules in the 3. Fulminant acute: it is an accelerated and more severe
pulmonary and systemic circulation originates from lipids normally present in variant of non fulminant subacute form. Angina pain may be
the blood. Physicochemical alteration of these compounds can lead to fat present as a result of corpulmonale or from sudden
embolism embolization of fat globules into coronary vessels.
129

Describe pathophysiology, clinical features diagnosis & management of fat embolism? Dr Azam’s Notes in Anesthesiology 2013
Continuation:
Diagnostic criteria:
Gurd and Wilson criteria: Lindeque Criteria: !

1. PaO2< 60 mmHg on room air.
Major features– petechial rash, respiratory 2. PaCO2> 55 mmHg or pH<7.3
insufficiency, cerebral signs.
3. Spontaneous respiratory rate
Minor features– Pyrexia, tachycardia, retinal
changes, jaundice, renal changes. >35 breaths/minute.
4. Clinical signs of increase work
• Positive diagnosis requires at least one of breathing (dyspnea and
major and four minor clinical features. accessory muscle action).
TREATMENT:
1. Fluid resuscitation: The severity of FES is directly related to degree and duration
of associated shock. Shock by producing pulmonary damage of its own can
intensify the lung injury caused by FES. Aggressive fluid resuscitation must be GRID: Question needs answered under
initiated early to restore intravascular volume, improve preload establish optimal following headings:
cardiac output. Appropriate monitoring should be used to avoid fluid overload. 1. Definition
2. Albumin has been recommended for volume resuscitation along with balanced 2. Etiology
electrolyte solution, as it not only restore blood volume but also binds fatty acids, 3. Pathophysiology - Theories
reducing their potential for lung damage. 4. Clinical features
3. Ventilatory support: Lung is the primary target organ in FES necessitating the use 5. Diagnosis
of aggressive ventilatory therapy. Mechanical ventilation preferably with PEEP must 6. Management.
be instituted whenever simple oxygen administration with or without CPAP is
insufficient to maintain adequate oxygen saturation.
4. Drugs: Steroids-Limits free fatty acid induced inflammatory reaction in lungs.
5. Aprotinin – A protease inhibitor decreases aggregation of platelet and release of
serotonin and thus limits lung injury.
130

50. Define Pulmonary Edema. What are the Clinical Features & Management of Pulmonary edema. Dr Azam’s Notes in Anesthesiology 2013
Definition: Pulmonary edema defined as abnormal accumulation of Investigations:

fluid in the interstitial and air spaces of the lungs. ECG:
• Sinus tachycardia – most common.
Etiology: Initiation & Development of Pulmonary edema. • Any cardiac arrhythmias (AF, SVT, VT)
• Evidence of any acute change in ST (MI/angina)
! !"#$%&'%()*+($,'-&-.#)/$%''0$%) • Evidence of underlying heart disease.
ABG:
63,7)/$,4$%''.8%)."#$%&'%).") • Typically ↓ PaO2: ↓ PaCO2 (hyperventilation)
1%#$%&'%(),"#,-.#)/$%''0$%))
8,302%),9)."-%$'-.-.&3)'/&#%)) • (Pulse oximetry may be inaccurate if peripheral shut down is
!2/&.$%()3+2/*&-.#)($&."&4%)) present).
) 1.'-,$-.,")&"()."#$%&'%() Full blood count:
1%#$%&'%()."-%$'-.-.&3)/$%''0$%)) /%$2%&5.3.-+),9)&38%,3&$)%/.-*%3.02)) • Anaemia; leucocytosis indicating the precipitant.
Echo:
!"#$%&'%()#&/.33&$+)/%$2%&5.3.-+)) • Look for LV function / value abnormalities / VSD / effusion.
:&-&'-$,/*.#)93,,(."4),9)&38%,3&$) • Cardiac enzymes
&.$'/&#%)) • LFT, albumin, total proteins.
• Chest radiograph:
Clinical Features: Management of pulmonary oedema can be

• Tachypnea discussed under three heading:
• Tachycardia 1. General supportive measures.
• Desaturation 2. Identification of the precipitating factors and
• Orthopnea treatment of the same, if possible.
• PND 3. Detection and treatment of underlying disease
• On Auscultation: process.
• Crepitations (bilateral, coarse)
• Rhonchi
Classification of Pulmonary Edema:
• Crackles 1. Imbalance of starling forces (hemodynamic pulmonary oedema)
• Progressive Hypoxia 2. Altered alveolar capillary membrane permeability (Acute respiratory distress syndrome)
• Hypotension (permeability pulmonary oedema)
• Cyanosis 3. Lymphatic insufficiency:
4. Unknown or incompletely understood:
131

Define Pulmonary Edema. What are the Clinical Features & Management of Pulmonary edema. Dr Azam’s Notes in Anesthesiology 2013
Continuation:
Management of pulmonary oedema can be discussed under three heading:
2. Identification of the precipitating factors 3. Detection and treatment of

1. General supportive measures: and treatment of the same, if possible. underlying disease process.
• Stop IV Fluids
Events which may precipitate
• Head up The best form of management would
Oxygen therapy pulmonary oedema include:
• be to block the inappropriate
• Reduction in pre-load • Myocardial infarction/ischaemia.
activation and progress of the
• Morphine - 0.1 to 0.5 mg/kg watch for • Dysrrhythmias
condition which is responsible for the
respiratory depression • Tachycardia
condition.
• Diuretics - 0.1 to 1 mg/kg • Bradycardia
• NTG - 5 µg/min infusion • Hypertensive crisis
• Reduction in After load • Fluid overload
• Sodium Nitroprusside - 5 µg/min infusion • Pulmonary embolism
• Thyrotoxicosis
• Digitalis - 0.8 - 1.2 mg IV; 0.1 mg
• Severe anaemia
maintenance
• Inotropes
• Dopamine - 5 to 10 µg/kg/min
• Dobutamine - in left Ventricular Failure Post operative pulmonary oedema:
5 µg/kg/min • Increased BP
• Aminophylline • Hyperadrenergic state
• Bolus: 5 mg/kg • Shivering
• Infusion: 0.5 mg/kg • In adequate reversal
• In adequate Analgesia
• Respiratory Therapy
• Anxiety
• IPPV with PEEP
• Laryngospasm & Bronchospasm
• CPAP • Blood transfusion:
132

51. Bronchial Asthma Dr Azam’s Notes in Anesthesiology 2013
Definition: Pathophysiology:
!
• Asthma is a disease of airways characterized by reversible !""#$%&'()*+,$&-.&'/( 01&2.3-'$4,&'(!"#$!"%!&''
expiratory airflow obstruction due to increased !-,&%#-&'(( 52-(!-,&%#-&'((
responsiveness of the trachea-bronchial tree to a number
()%#'' 2"3-&#!+"''
of stimuli. *+,,-"' *+,,)#!+"'
Clinical features: ."!/0,'10"1-$'' 45-$&!%-''
• The diagnosis of asthma is based largely on a history of 6+,1'
periodic paroxysms of dyspnea, usually at rest as well as *%7&8+9-"!&'''
on exertion, interspersed with intervals of complete or
nearly complete remission. 294'
• Clinical manifestations are – wheezing, cough and
dyspnea
:-,-0%-'+3'#$!99-$'09-"#%'
Physical findings: <-)=+#$!"-%'6>?'(>?'4>' G-)$+9-"!&'$-3,-5'HC090,;'
!;
• Tachypnea !!; @!%#0/!"-'
• Hyperresonance on percussion !!!; *$+%#09,0"1!"%'AB?'4B?'(B'
Inspiratory and expiratory rhonchi !C; D$017=!"!"'
•
C; E8$+/F+50"-'.B'
• Wheeze C!; *,0#-,-#'0&#!C0#!"9'30&#+$''
• Decreased breath sounds
• Prolonged expiration.
@7I-!$$!#0F,-'!"3,0//0#+$7'0!$J07'''
In severe attacks: '
• Wheezing may not be apparent.
• Clinical picture being – ʻAir hungerʼ K; D$+"&8+,I0%/''
• Use of accessory muscles of respiration B; 41-/0'+3'F$+"&8!0,'L'!"3,0//0#+$7''
• Diminished breath sounds without rhonchi. ''''''&-,,'!"3!,#$0#!+"'
• Pulsus paradox M; N)&)%'%-&$-#!+"'!'#8!&='0"1'#-"0&!+)%''
• Cyanosis
:-%),#%'!"''
O; 2"&$-0%-'!"'0!$J07'$-%!%#0"&-''
P; (-&$-0%-'!"'3+$&-1'-5I!$0#+$7' K; @7I-$!"3,0#!+"'+3',)"9%?'0"1'#8+$05''
C+,)/-'0"1'3,+J'$0#-%'' B; 2"&$-0%-1'J+=%'+3'F$-0#8!"9H'QRD';''
M; .,#-$0#!+"'!"'$-%I!$0#+$7'/)%&,-'
3)"&#!+"''
>; 680"9-%'!"'-,0%#!&'$-&+!,'''''
133

Bronchial Asthma. Continuation Dr Azam’s Notes in Anesthesiology 2013
Severity of expiratory airflow obstruction & Grading: Classification of Bronchial asthma:

FEV FEF 25-75 Pao2 Pa Co2 Characteristics Mild Moderate Severe
Severity
(% predicted) (% predicted) (mm Hg) (mm Hg)
Mild 65-80 60-75 > 60 < 40 1) A pre-treatment Exacerbation of cough Moderate exacerbations Virtually daily
(asymptomatic) frequency of and wheezing no more of cough and wheezing exacerbations, frequent,
2) Moderate 50-64 45-59 > 60 < 45 exacerbations often than 1-2 times/wk more frequent. often severe. Tends to
Severe exacerbations have sudden severe
infrequent, urgent case urgent visits to
3) Marked 35-49 30-44 < 60 > 50 treatment required <3/ emergency department
year on doctorʼs office > 3/
4) Sever (status < 35 < 30 < 60 > 50
year, hospitalization > 2/
asthamaticus)
year
2) Frequency of Few clinical signs / Cough and low grade Continuous symptoms
symptoms symptoms between wheezing between of cough and wheezing
• FEV1 – Forced expiratory volume in 1 second. exacerbation acute exacerbations almost always present
• FEF25, 75 – Forced exhaled flow at 25% to 75% of forced vital often present
3) Degree of exercise Good, may not tolerate Diminished Very poor, marked
capacity.
tolerance vigorous exercise like activity limitation
Diagnosis:
prolonged running
• No single laboratory test can confirm the diagnosis. A test for 4) Frequency of Not more than 1-2 times 2-3 times/week Considerable almost
bronchodilator responsiveness can provide supportive evidence – nocturnal asthma per month nightly sleep
more than 15% increase in expiratory air flow when asthma is interruption. Early
suspected on clinical ground. morning chest tightened
Non specific: Pulmonary function >80% predicted normal 60-80% predicted < 60% predicted
1. Haemoglobin and haematocrit à increase in proportion to the PEFR or minimal airway airway obstruction substantial degree of
degree of chronic hypoxemia and extent of dehydration. obstruction. evident. Flow volume airway obstruction.
Normal expiratory flow curve, Shows reduced Flow volume curve
2. Total WBC count à Leucocytosis is present due to fever, infection
volume curve expiratory flow at low shows marked.
or dehydration. Lung volumes not lung volumes/often Concavity spirometry
3. Blood eosinophil count increased. Usually a increased usually 15% may to be normalized
4. Sputum examination 15% response to acute response to aerosol even with steroids. May
5. Chest x-ray (hyper inflation) aerosol bronchodilator bronchodilator have substantial
even with near normal increase in lung
baseline values. volumes and marked
uneveness of
ventilation. Incomplete
reversibility to acute
aerosol bronchodilator <
2 mg/ml.
134

Bronchial Asthma Continuation: Dr Azam’s Notes in Anesthesiology 2013
Treatment: Albuterol (Salbutamol)

Management of asthma includes • Oral – 0.10-0.15 mg/kg QID 4-6 hrs
• Avoidance of allergens. • Nebulization – 2.5 mg QID 4-6 hrs
• Desensitization or immunotherapy • Aerosol inhalation – 100 µg-200 µg QID 4-6 hrs
• Drug therapy Terbutaline (β2)
• Oral – 2.5 mg QID 4-6 hrs
Goals of treatment are: • Subcutaneous – 250 µg QID
• To achieve normal % of predicted values of FEV and PEFR. • Salmeterol inhaled (long acting)
• To reduce diurnal variability of PEF and symptoms. • MDI – 25 µg/puff- 2 puffs 12 hrly
• To minimize the use of β2 agonists drugs. Blister – 50 µg/blistter - 12 hrly
•
• To optimize quality of life. Isoproterenol – Inhaled – 1: 200 solution, 5-15 inhalations QID 4-6
• To reduce the risk of life threatening asthma. hours I.V-0.05-5 μg /min infusion.
Isoetharine (β2)
Drugs:
• Inhaled – 0.5 ml of 1% solution diluted 1: 3 with saline 3-4 hrly.
Bronchodilator drugs include:
Epinephrine
1. Sympathomimetic drugs.
• Subcutaneous – 0.3-0.5 ml of 1: 1000 solutions QID
2. Methylxanthines Inhaled β2 agonists are highly effective in preventing
3. Anticholinergics bronchoconstriction due to exercise or allergens:
Anti inflammatory drugs include: Methylxanthines:
1. Corticosteroids • Theophytlline
2. Mast cell stabilizers • Aminophyline (85% theophyline + 15% ethylenediamine)
3. Leukotrine inhibitors Mechanism of action of methylxanthines:
Sympathomimetic drugs: • Inhibition of phosphodiesterase à increase in C-Amp.
• These drugs produce bronchodilation via β2 agonist activity on • Antagonism of adenosine
receptors in airway smooth muscle, mast cells and cholinergic • Stimulation of endogenous catacholamine release
nerves. • Anti inflammatory action
Mode of action: • Improved mucociliary clearance.
• Activation of β2 receptor causes an elevation in C-AMP via G3-protein. • Stimulation of ventilator drive
A number of proteins then become phosphorylated by protein kinase A. • Increased diaphragm contractility
one such protein is the calcium activated potassium channel. (Maxi-K • Diuresis
channel). Phosphorylation of Maxi-K channel leads to membrane • Positive inotropy
hyperpolarisation and smooth muscle relaxation. . • Reduction in cardiac preload and after load.
• Chronic use of β2 agonists may relieve symptoms without treating the
underlying chronic inflammatory process which is responsible for
asthma. This leads to irreversible thickening of the airway wall and
increased hyperreactivity.
135

• Theoplytine has a narrow therapeutic range i.e (10-20 µg/ml of Corticosteroids:

blood) (dose > 30 µg/ml à seizures and cardiac dysarrythimas). • Corticosteroids are the most effective pharmacologic therapy for
• Oral theophyline is relatively weak and high doses are needed. treating asthma.
Dose: IV 5-6 mg/kg loading dose over 20 mins. 1 mg/kg/hr • They act in a relative non-specific manner by inhibiting a variety of
infusion. inflammatory cells, cytokine expression and transcription factors
• Side effects à Nervousness, nausea, vomiting, anorexia, which are involved in the inflammatory disease process.They also
headache, seizures, cardiac arrhythmias tremors. increase the number of β receptors and thus may increase the
Decreased clearance! Increased clearance sensitivity of β2 receptor agonists. By inhalation a higher
concentration of steroid can be achieved in the airway while
- Erythromycin - Barbiturates minimizing the side effects associated with the systemic
- Quinolones - Phenytoin administration.
- Allopurinol - Cigarrate smoking Medication Dose Comments
- Cimetidine - Marijuana addicts
- Propanolol Systemic 7.5-60 mg PO daily For long term treatment of
- Elderly corticosteroids severe asthma
- CHF Prednisolone 40-60 mg PO daily Effective for initiating therapy
Liver disease
Inhaled corticosteroids
Anticholinergics:
Beclomethosone 4-20 puffs/day
• Produces bronchodilation by blocking muscarinic receptors in
42 μg/puff
airway smooth muscle leading to decreased vagal tone.
Budesonide 1-3 inhalations/day
• Ipratropium bromide is a synthetic derivative of atropine
200 μg/puff
administered by metered dose inhales (MDI).
Tramcinolone 4-20 puffs/day
• Onset of bronchodilator effect 15-30 mins.
100 μg/puff
• Effect lasts for 4-6 hrs.
• Inhales – 20 μg/puff ,1-2 puffs QID Adverse effects:
• Others – Oxitropiums, flutropium.
• Local effects: Dysphonia (Hoarsess), glossitis, pharyngitis
• Act on larges airways. oropharyngeal candidiasis.
136

Systemic effects – Dose related systemic effects. Leukotriene inhibitors:

• Adrenal suppression ! +,"-!.!/'0)1234*$%4!
Osteoporosis "#$%&'()*'%!$%'(!!!
• $%5'6$5'*3!0#)54'*!!!!!
• Growth suppression !
• Skin bruising ! .=/'0)123'*$@4!! +,"-!! +,"-!'*&'7'5')*!!
• Cataracts 839:!!;<!=!>>?!!!!!
• Hypertention ,A"B!
• Na and Cl retention F2@54'*32/!H!,A!
• Psychosis $*5)34*'@5@!!
• Gastritis 839!I$J#'/KL$@5!$*(!
,ACB!"*5$3)*'@5! ,AFB! M)*54/KL$@5!!
• Inhaled corticosteroids in doses of 1500 µg/day – in adults ,AGB!
# # # # # 400 µg/day – in children. 4939!D=E.! ,A8B!
• Have lesser effect on pituitary adrenal function. • !"#$%&#%#$'(")%(#"*
Mast cell stabilizers: NO I'/K45)*!H!?PP!M3!-Q!R'(!! • +,%#,'*-.%".()#$*
• Cromolyn sodium SO I$J#'/KL$@5!SP!M3!-Q!CTG!'*!
• /0.12*
• Nedocromil 0$5'4*5@!U!NS!24$#@!!
• 345."*".'5#$'.*
• Acts as an inhibition of inflammation by inhibiting the release of
chemical mediators from mast cells (eosinophils and • /#')$#5&)66)2**
macrophages) perhaps by membrane stabilizing effect (by
preventing calcium entry). Management of chronic asthma:
• Pretreatment with these agents inhibits bronchospasm produced Inhaled anti-inflammatory drugs are the first line treatment for chronic
by antigen and by exercise. asthma.
• Dose: MDI: 1 mg/puff 2-4 puffs tid – qid 1. Corticosteroids
• One dose prior to exercise or allergen exposure good for 1-2 2. Chromolyn sodium
hours. 3. Leukotriene inhibitors
• Nebulizes 20 mg solution – 1 amp tid – qid. • If symptoms persists despite low doses of inhaled corticosteroids,
• Improves – lung functions, reduces symptoms and lower airway inhaled β2 agonists or theophylline may be added.
reactivity Acute severe asthma (status asthmaticus)
Supportive measures:
• (May block volume dependent chloride channels in endothelial
cells). • Supplemental oxygen – by nasal prong or face mark to correct
hypoxemia.
• Antibiotics
• Hydration
• To correct any fluid deficit
• To make secretions less viscous
137

Chest physiotherapy – if severe mucous hyper secretion chest Need for intubation and mechanical ventilation:
physiotherapy and postural drainage may help in clearing • Many, but not all acute severe asthmatics will need ventilatory
secretions. support. intubation and ventilation are measures of last resort since
Specific measures: endotracheal intubation introduces another potential source of
• Inhaled β2 agonists are the main stay of bronchodilator therapy bronchospasm. Positive pressure ventilation is frequently inefficient
salbutamol. during small airway constriction resulting in frequent episodes of
• Systemic corticosteroids pneumothorax or pneumomediastinam.
• Hydrocortisone 3-4 mg/kg IV. Indications:
• Effect of drug-will be seen after few hours. 1. Exhaustion and unconsciousness
• Methylxanthines 2. Refracting hypoxemia PaO2< 60 mm Hg.
• Aminophylline– 6 mg/kg IV slowly over 20 mins. 3. Rising PaCO2 5-10 mm Hg/hr. Despite maximum medical therapy.
• Later 0.5/mg/kg/hr IV infusion. . 4. Absolute PaCO2 of 50 mm Hg greater with respiratory acidosis.
Criteria for admission and observation of asthmatics in intensive 5. Established or imminent cardiac or respiratory arrest.
care unit. 6. If the FEV1/FVC ratio less than 40% (ventilatory failure should be
Patients with severe airflow obstruction. anticipated in the postoperative period).
• Use of accessory muscles of respiration. Non-invasive ventilation:
• Pulsus paradoxus of more than 12 mm hg .. • Face mask mechanical ventilation ( CPAP ) is a short term ventilatory
• Diaphoresis support in patients with hypercapnic ventilatory failure who are not
• Inability to recline • Responding adequately to drug therapy and
• Hypercapnia • Where immediate intubation and mechanical ventilation are not
• PEFR less than 40% predicted indicated. Patients with encephalopathy or with a need of airway
• Tachycardia (HR > 110/min), tachypnoea (> RR 28/min). protection are not suitable for this form of therapy.
Poor response to initial therapy.# Advantages:
• Less than 10% improvement in PEFR. • Decreases need of anaesthesia.
• Those who deteriorate despite therapy. • Decreases need of sedation and paralysis.
• Respiratory arrest • Decreases incidence of nosocomial infections.
• Altered mental status • Decreases incidence of sinusitis and otitis
• Patients with imminent life threatening features like • Better comfort
• Unconsciousness confusion, drowsiness. • Usually a nasal CPAP of 5-7.5 cm H2O will be necessary.
• Hypoxia (PaO2< 60 mm Hg despite 60% FiO2) or patients with a • Nasal CPAP 5 t 7.5 cm of H2O.
raised PaCO2.
138

• Disadvantages: • Patients with bronchial asthma are very difficult to ventilate. Large
• Aspiration of gastric contents due to gastric insufflation. tidal volumes increase the tendency to dangerous hyperinflation and
• Facial pressure necrosis high flow rates dissipate energy in narrowed airways.
• Less control of patientʼs ventilatory status. Ventilator settings are based on:
Intubation: 1. Low tidal volume, 6-8 ml/kg body weight.
• Should be performed by experienced anesthesiologists, as 2. Low frequency, 8-12 breaths/minute.
manipulation of the upper airways may precipitate laryngospasm. 3. Long inspiratory time which allows adequate time for expiration.
Oral intubation preferred to nasal intubation because nasal route 4. PEEP is contra indicated as it increases the tendency to
requires smaller ETT and high incidence of nasal polyp and hyperinflation.
sinusitis in asthmatics. 5. Asthmatics are difficult to wean because they are anxious and the
Sedation: ETT may precipitate bronchospasm if sedation is light. .
• Is required in awake patient to prepare for intubation and to allow Anaesthetic management:
for effective mechanical ventilation. • 5 steps to safe and successful conduct of anaesthesia in asthmatic
• Improves patients comfort, facilitates various procedures, patients.
decreases oxygen demand and consumption, decreases formal I. A through preanaesthetic evaluation (History, physical examination
carbon di oxide production besides decreasing the risk of and relevant laboratory tests).
barotrauma. II. Adequate pre-operative preparation
Muscle paralysis: A. Psychological
• Muscle paralysis is required in patients fighting with the ventilator B. Physical and
despite sedation and those who continue to have asynchronous C. Pharmacological
breathing which is a grave risk factor for quantum of high airway III. Proper selection of patients
pressure. Paralysis helps to reduce oxygen consumption, CO2 IV. Proper selection of anaesthetic agents and anaesthetic
production and lactic acidosis and also decreases the risk of techniques.
barotrauma. Because the expiratory effort is eliminated there is V. Provision of adequate post operative pain relief.
less airway collapse. Aims:
• Muscle relaxants of choice are vecuronium and atracurium with I. To detect the presence of clinically significant respiratory
cardiovascular stability properties. They are given either dysfunction.
intermittently by bolus injection or by continuous IV infusion, but II. To assess the effectiveness of therapy in order to maximize
the disadvantage of prolonged muscle paralysis include greater preoperative therapy before reaching operating room.
danger of developing DVT, disuse muscle atrophy and myopathy,
which is more pronounced in the presence of concomitant use of
high dose steroids.
139

a) History: History should be obtained regarding. Pulmonary function test shows reduction in
• Duration of disease (acute or chronic). I. FVC – normal but may be reduced during sever attack
• Frequency and severity of symptoms, hospitalization II. FEV1 – decrease
• Any recent episode of bronchospasm, respiratory tract infection. III.FEV1/FVC – reduced
Elective surgery should be post poned for atleast 4-6 wks after IV. FEF25-75% - reduced
last episode because of hyperesponsiveness of airways). V. FRC and TLC – increased
• Review of medication, (dosage, frequency, steroid therapy. Chest x-ray – often normal in mild asthma in severe asthma
• Previous anaesthetic record. hyperinflation.
• Smoking history. - Flattening of diaphragm
• History allergy to drugs and food. - Increased lung marking
b) Physical examination:
- Peribronchial thickening
• General appearance and mental status – exhausted / confused /
unconscious. • ABG – Hypoxia (PaO2) and hypercarbia seen in serve asthma
• Posture – sitting upright / unable to lie down because of • ECG – sinus tacchycardia.
breathless. • FEV1 = max vol. of gas exhaled during the 1st second of a FVC
maneuver.
• Diaphoresis / dehydration.
• Respiratory system à# During bronchospasm • FEV1 = 83% of VC
• Respiratory rate increases.
• Increased AP diameter
• Decreased breath sounds = 0.8 is normal (80.33%)
• Prolonged expiratory phase and wheeze during expiration. Preanesthetic medication:
• Cardiovascular system – tachycardia • Anxiety may precipitate an acute attack of asthma so preoperative
• Pulsus paradoxus greater than 12 mm Hg. sedation is desirable in asthmatic patients.
Investigations:
• Benzodiazepines – diazepam 5 mg orally night before surgery
I. Haemoglobin and haematocrit à increased due to hypoxemia children 1-10 years-midazolam 0.5 mg/kg orally before surgery.
and dehydration. • Inj promethazine HCl 25 mg Im
II. Total leucocyte count à increased during infection eosinophil • Diphenhydramine – H1 receptor blocking drug and sedative effect.
count > 5% - implies allergic cause. • Hydroxyzine HCl – because of sedative, antihistaminic and
III. Total eosinophil count [normal 250 cell/cumm] more than bronchodilator effect.
normal suggests allergy. • Bronchodilators should be continued upto the time of surgery.
IV. Sputum examination – numerous eosinophils – charcot leyden
crystals.
V. Blood investigation – RBS, urea, S. creatinine.
140

Peri-operative hydrocortisone supplementation guidelines: Monitors:

Anticipated 1. Pulse oximeter
Preoperative Intraoperative Post-operative
surgical stress 2. NIBP
Minor 25-50 mg or 1-2 None unless Resume usual 3. Capnography
times usual dose complication replacement 4. Precordial stethoscope
POD1 5. ECG
Major 100-150 mg or 50 mg IV = 8th 50 mg IV and 8th 6. Arterial line
usual steroid hrly after initial hourly or 150 mg Choice of anaesthesia:
dose which ever dose continuously over Factors governing the choice of anaesthesia.
is higher within 2 24 hours for 2-3 Patient characteristics:
hour of start of days then reduce 1. Adult asthmatic
procedure dose by 50% per 2. Paediatric asthmatic
day until 3. Pregnant asthmatic
preoperation 4. Trauma patient with asthma
regimen is 5. Cardiac patient with asthma
reached. 6. Asthmatic with full stomach
Site of operation
Steroid treatment regimens: • Cardiac
Patients taking < 10 mg/day à assume Additional steroid • Non-cardiac (peripheral, extremities, upper and lower abdomen)
steroids normal (prednisolone) coverage not required • Nature of operation
à > 10 mg/day à 25 mg hydic cortisone at • Elective or emergency
minor surgery à induction status
Major surgery à Usual pre-operative • Acute or chronic
steroids and 25mg Duration of surgery
hydrocortisone at Type of patient – inpatient or day care patient.
induction + 100 mg/day Type of anaesthesia:
for 48-72 hrs • General anaesthesia – (a) by mask, (b) by ETT (c) by LMA.
• Regional anaesthesia – (a) subarachnoid block (b) continuous
lumbar epidural anaesthesia, caudal, peripheral nerve blockade.
General anaesthesia:
Induction agents:
• Choice of induction agents in asthma is controversial ability to rapidly
and smoothly inducing deep levels of anaesthesia is for more
important to the asthmatic patient than the particular induction agents
to achieve that depth.
141

• Induction agents are two types. Inhalation agents:

• Intravenous and inhalation. • Inhalational anaesthetics are potent bronchodilation and prevent
bronchospasm.
Thiopentone: • By depressing neural pathways which mediate these reflexes (vagal
• Thiopentone occasionally induce bronchospasm as a result of pathway).
exaggerated histamine release. • By direct effects on airway smooth muscles.
• But its cause is likely to be instrumentation of the airway under Halothane:
light planes of anaesthesia. Merits:
Demerits: • Being non-irritant provides rapid smooth and pleasant induction.
• Leaves airway reflexes largely intact. • Deep levels of anaesthesia can be rapidly attained which is a distinct
• Does not block irritant induced reflex bronchospasm. advantage or bronchospasm appears more frequently in very light
• Bronchodilation occurs at greater doses, more than 5mg/kg body level of anaesthesia.
weight. • Provides rapid recovery.
Ketamine: • Decreases pulmonary resistance and improves gas exchange during
• Is the only I.V. agent with bronchodilating properties. asthma attack.
Merits: Demerits:
• Increases circulating concentration of epinephrine. • Deep levels of anaesthesia produce profound condiovascular effects.
• Inhibits muscaranic receptors. • Sensitizes myocardium to catacholamine and aminophylline.
• Blocks re-uptake of endogenous catecholamine. • Pulmonary vascular response to hypoxia is abolished leading to
• Directly dilates tracheal smooth muscle. ventilation perfusion imbalance.
• Depresses afferent irritant vagal pathways. • Depresses mucociliary function
• Eliminates bronchospasm during anaesthesia. • Can not be used in hepatitis patient (hepatotoxic)
Demerits: Muscle relaxants:
• Contraindicated in patients with increased serum theophyline • Succinylcholine: may also causes histamine release but to a lesser
concentration (causes seizures). extent therefore it can be used.
• Recovery prolonged NDMR:
• Hallucinatory effects. • Neuromuscular blocking agents that cause histamine release should
Propofol: be avoided, namely d-tubocuorrine mivacurium, metacurine and
• Provides rapid smooth induction with prompt complete recovery. atracurium.
• It directly relaxes airway smooth muscle. • Preferred relaxants are pancuronium, vecuronium, and rocuronium.
Reversal agents:
• Neostigmine can cause bronchospasm but when used with
anticholinergic agents like atropine and glycopyrolate, neostigmine
does not significantly change airway resistance. .
142

Opioids: Analgesia:
• Should be avoided as they are known to release histamine and • Injection fentanyl is preferred, given in incremental doses 1-2 μg/kg
cause bronchopasms. They also causal respiratory depression. B.W.
• Fentanyl < morphine < pethidine. Maintenance of anaesthesia:
Lignocaine HCl: • N2O + O2 + NDMR + IPPV.
• IV lignocaine can be given 1-2 minutes before intubation to • NDMR à injection vecuronium 0.05 mg/kg B.W.
prevent reflex-induced bronchospasm. Topical spray of # # Or
lignocaine endotracheally may provoke reflex • Injection pancuroninum 0.05 mg/kg B.W.
bronchoconstriction if adequate depth of anaesthesia has not • Injection rocuronium 0.05 mg/kg B.W.
been achieved. Inhalational agent:
General anaesthesia: • Isoflurane is the agent of choice for maintaining patients with reactive
• The goal of anaesthesia in the patient with asthma is to depress airway. It does not sensitize the myocardium to catacholamines.
airway reflexes with anaesthetic drugs so as to avoid • In presence of toxic levels of theophylline, halothane is known to
bronchoconstriction of the hyper reactive airways in response to cause ventricular dysrrhythmias.
mechanical stimulation. Ventilation:
Pre-oxygenation: 3-5 minutes with 100% O2. • Spontaneous ventilation during general anaesthesia in patient with
• Induction severe obstructive disease is more likely to result in hypercarbia than
• Intravenous agents in patients with normal pulmonary function.
• Thiopentone sodium 5-7 mg/kg
• • Intra-operative best arterial oxygenation and ventilation are provided
Ketamine or 2 mg/kg B.W. by controlled mechanical ventilation of the lungs preferably a volume
• Propofol 2-5 mg/kg B.W. cycled ventilator with ventilatory rates less than 10/min to prevent
Inhalational agents:
hypercarbia, minimize VQ mismatch and allowing for exhalation.
• Agents like halothane and sevoflurane can be used for induction Lower ventilatory rates necessitate larger tidal volumes (10-12 ml/kg)
of anaesthesia because of direct bronchodilator effect and
which may predispose the patient to pulmonary barotraumas
smooth induction.
because of high pulmonary airway pressure.
I. Anticholinergics
• PEEP is not ideal because adequate exhalation may be impaired in
• Inj atropine 0.02 mg/kg B.W. presence of narrowed airways.
• Inj Glycopyrolate 0.01 mg/kg B.W.
• Relatively long inspiratory and expiratory times allow more uniform
• Blunting reflex bronchospasm prior to intubation by injection distributing of gas flow to both lungs and avoid air trapping.
lignocaine (xylocard) 1-2 mg/IV 1-2 min before tracheal
• Humidification is necessary if ventilation is prolonged.
intubation.
143

Reversal: Regional anaesthesia:

• Injection neostigmine 0.05 mg/kg B.W. • Suitable for lower abdominal, perineal, extremity and superficial
• Injection atropine 0.02 mg/kg B.W. procedure in adults and children old enough to accept and tolerate
# # Or this.
• Injection glycopyrolate 0.01 mg/kg Merits:
• Emergence and extubation: • Being awake, easy to diagnose intra-operative bronchospasm.
• Emergence and extubation: At the conclusion of the anaesthesia • Avoids manipulation of trachea
for elective surgery, emergence from anaesthesia should be slow De-merits:
and smooth to minimize the risk of bronchospasm. • Scope limited by awake patient and site of operation.
• Two methods of extubation – Extubation under deep anaesthesia • Bronchospasm likely to occur under spinal anaesthesia.
# Awake Extubation Perioperative complication:
• Extubation under deep anaesthesia à unless contraindicated by • Intraoperative bronchospasm – incidence of intraoperative wheezing
other conditions, a sufficient depth of anaesthesia maintained after intubation is 6.4% which is more common than during either
with inhalation anaesthetic to depress hyper reactive airway general anaesthesia by mask or regional anaesthesia.
reflexes and then ETT removed allowing the patient to emerge Differential diagnosis of intraoperative bronchospasm / wheezing:
gradually. 1. Mechanical obstruction of ETT by kinking or secretions.
• Awake Extubation à If a deep extubation is contraindicated the 2. Foreign body in the airway à localized wheeze
patient is left intubated although the presence of ETT may 3. Endobronchial intubation
stimulate bronchospasm as airway reflexes return but a slow 4. Aspiration of gastric contents
emergence from anaesthesia achieved by the use of intravenous 5. Carinal irritation
opiod, which may improve then patientʼs tolerance of ETT and 6. Tension pneumothorax
decrease the incidence of severe bronchospasm. A small dose of 7. Pulmonary embolism
narcotic given intraoperatively or lidocaine 1 mg/kg given 8. Pulmonary oedema
intravenously upon emergence minimizes tracheal stimulation as 9. Anaphylactic reaction
the patient awakes. 10. Acute asthmatic attacks
144

Management consists of:

• Establishing the diagnosis
• Prevention and
• Treatment of intraoperative bronchospasm includes
1. 100% O2
2. Deepen anaesthesia
3. Ketamine 0.5 mg/kg/IV
4. Institute / increase concentration of halothane / isoflurane
5. Sedation – droperidol 0.22 ml/kg IV
6. Paralysis
7. Suction airway
8. IV lidocaine 1 mg/kg to all coughing and straining patients.
9. Beta 2 agonist aerosol (MDI) into patients airway with the
piece.
10. Anticholinergic aerosol (Ipratropium)
11. Steroids (i) beclamethasone aerosol (ii) Hydrocortisone IV
Aminophylline: (i) Loading dose 5-6 mg/kg over 15-20 minutes
(ii) Drip 0.5 to 1 mg/kg/hr
Post operative management:
• Management consists of close respiratory monitoring treatment
of bronchospasm and provision of adequate analgesia,
humidified O2 and physiotherapy.
• Appropriate management of post-operative pain.
• Epidural analgesia
• Patient controlled analgesia
145

52. Bronchial Asthma in Pregnancy. Dr Azam’s Notes in Anesthesiology 2013
• The national asthma education programme (1993) estimates that • Women with most severe asthma before their pregnancy were most
1 to 4% of the pregnancies are complicated by asthma, which likely to suffer a deterioration of their disease, during the 3 months
progresses to status asthmaticus in about 0.2%. postpartum, asthma reverted towards its pre pregnancy course.
Respiratory changes in pregnancy:
• Capillary engorgement of the mucosa throughout the respiratory Deterioration in asthma:
tract, causing swelling of the vocal cords and oropharynx, larynx • Due to relative tissue hyperesponsiveness to cortisol and a
and trachea. progressive rise in the level of other steroids. Eg. Aldosterone,
1. O2 consumption – Increased by 20-50% desoxycorticosterone.
2. Minute ventilation – Increased by 50% • ↑ in PGF2 – known bronchoconstrictor accounts for deterioration in
3. Tidal volume – Increased by 40% symptoms.
4. Respiratory rate – Increased by 15% • Another reason is that many women reduce or stop their medication
5. PaO2 – Increased by 10% during pregnancy.
6. PaCO2 – Increased by 15% (10-11mmHg)
7. FRC – Decreased by 20% Effect of Asthma on pregnancy:
8. RV – Decreased by 20% • The goal of asthma therapy in pregnancy should aim to improve
No changes in dead space, lung compliance, arterial PH, vital pulmonary function in addition to achieving symptomatic control.
capacity and closing volume. Goal of 90% of predicted normal.
Effect of pregnancy on asthma: • In pregnant asthmatics, there is increased incidence of
• Symptoms of asthma in pregnant patients, improves in 1/3rd, preeclampsia, preterm labor, low birth weight baby, perinatal
remained unchanged in 1/3rd and worsened in 1/3rd. mortality.
• Peak incidence of exacerbation occurs between 24th and 36th • Steroid dependent pregnant asthmatics had a significantly increased
weeks of gestation in those when asthma worsened during risk of gestational diabetes.
pregnancy.
• Attacks seldom occurs in last 4 weeks of pregnancy and in well Effects of drug therapy:
managed patients, attacks during labour are very rare, probably • Most medications used for asthma are safe for mother and foetus,
related to the further rise in free cortisol. some may have mild potential adverse foetal and neonatal effects.
• Increasing levels of circulating progesterone and oestrogen
account for gradual improvement in Asthma as pregnancy
progress.
1. Progesterone – has a direct relaxant effect on smooth muscle
2. Oestrogen – potentiates β-adrenoceptor
3. PGE2 – known bronchodilator is also increased
4. Free cortisol – Improvement in symptoms.
146

Bronchial Asthma in Pregnancy.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Drug Effect Pharmacologic step therapy of chronic asthma during pregnancy

1) Systemic corticosteroids Impaired foetal growth Pulmonary
Frequency / severity
Category function Step therapy
2) Theophylline Foetal tachycardia (maternal level > of symptoms
(untreated)
20 μg / ml). Mild < 3 times per week. > 80% Inhaled beta agonists as
Neonatal jitteriness, vomiting Nocturnal needed
tachycardia (maternal level > 12μg/ml) symptoms < 2 /
3) Systemic beta 2 agonists Foetal tachycardia, neonatal month
tachycardia, hypoglycaemia, tremor. Moderate > 3 times per week. 60-80% Inhaled beta 2 agonists
4) Topical sympathomimetic Foetal heart rate alterations attributed Exacerbations affect + chromolyn. substitute
decongestants to uterine vasoconstriction seen at sleep or activity inhaled
high doses. beclomethasone. Add
oral theophyline
• Use of oral corticosteroids may be associated with an increased Severe Daily activity limited. < 60% Above + oral
risk of PIH and weakly associated with cleft palate. Frequent nocturnal corticosteroids (Burst for
• Following drugs should be avoided in asthmatic pregnant symptoms and active symptoms
patients. acute exacerbations alternate day or daily if
Prostaglandin F2α Aspirin / other NSAIDS necessary)
Prostaglandin E2 Histamine – releasing drugs
Ergometrine e.g., atracurium, tubacurare. Pharmacologic management of acute asthma during pregnancy:
• Nebulized beta 2 agonist bronchodilator, Upto 3 doses in first 60-90
minutes. Every 1-2 hours thereafter until adequate response.
Treatment of asthma during pregnancy:
• Intravenous methyl prednisone (with initial therapy in patients on
• The ultimate goal of management of asthma during pregnancy is regular corticosteroids and for those with poor response during the
to maintain adequate oxygenation of the foetus by preventing first hour of treatment). 1mg/kg BW every 6-8 hours. Taper as patient
acute asthmatic episodes and maintaining optimal pulmonary improves.
functions.
• Consider intravenous Aminophylline (generally only if, patients
• Asthma medications are considered safe during pregnancy. requires hospitalization). If it is to be used, 6 mg/kg loading dose
• Under treatment of asthma during pregnancy may be more • 0.5 – 1mg/kg/hr initial maintenance dose
dangerous for mother and foetus than potential side effects of
• Adjust rate to keep theophilline level between 8-12 µg/ml
medications.
• Consider SC terbutaline 0.25mg of patient not responding to above
• Treatment should be inhaled bronchodilators rather than oral therapy.
medications.
• Breast feeding is safe for asthmatic mothers.
147

Anaesthetic management: Regional anaesthesia:

The goals of managing a woman with asthma include; • Is the preferred technique in patients with asthma undergoing
• Ensuring optimal pre operative pulmonary status. caesarean section.
• Providing adequate analgesia during labour or caesarean Advantages:
delivery, to facilitate a painless and stress free child birth. • Obviates the need for airway instrumentation
• Preventing bronchospasm or aggressively treating any • Reliably blocks maternal stress responses to delivery
respiratory problems that may arise. • Does not block fetal stress response in a new born for adaptation to
Pre-operative evaluation extra uterine life.
Aim of the pre operative evaluation is to: • Smooth transition from operation to recovery, provision of analgesia
1. Determine the efficacy of therapy and control of asthma. with no additional sedation and respiratory depression from residual
2. Identify those at risk of developing acute attacks before, during anaesthetic agents.
and after anaesthesia. Additional benefits of epidural:
3. Derive an anaesthetic plan tailored to both patient and clinical • Provides Postoperative pain relief with LA or narcotics.
situation such as analgesia for labour and anaesthesia for • Epinephrine containing LA solutions provide bronchodilation.
caesarean section. • Respiratory function better with epidural
Management during labour and delivery: General anaesthesia for caesarean section:
• Epidural analgesia (Bupivacaine or bupivacaine + Fentanyl) • Premedication – Inj Metaclopromide 10mg I/V, Inj Ranitidine 50mg I/
Offers advantages to the women in labour. It decreases the rate V or 30 ml of 0.3 M solution of sodium citrate ½ hr before surgery.
in O2 consumption and minute ventilation that occurs with • Preoxygenation with 100% O2 for 5 mins.
uterine contractions and during II stage of labour. Induction –# Inj. Thiopentone 4-6mg/kg BW I/V,
• Ergometrine and PGF2αcause bronchoconstriction, therefore Or
should be avoided. # # Inj.Ketamine 1.5-2mg /kg BW I/V
Anaesthesia for caesarean section: # # # # # +
• Antiasthmatic therapy should be continued in the immediate pre- # # Inj.Atropine 0.02mg / kg B.W. I/V
operative period. # # # # Or
• Choice of anaesthesia for caesarean section depends on both # # Inj. Glycopyrolate 0.01 mg / kg B.W. I.V.
foetal and maternal factors. • Inj. Lignocaine 1-1.5 mg/kg I.V. given 1-2 mins before intubation to
attenuate both airway reflexes and hemodynamic responses
associated with endotracheal intubation.
• Rapid sequence intubation is followed by, Relaxant – Inj. Succinyl
choline 1-2 mg/kg BW I/V
148

Maintenance of anaesthesia: Extubation:

• O2 + N2O + non depolarizing muscle relaxants + IPPV • Termination of general anaesthesia in the non pregnant asthmatic is
• Inj. Vecuronium 0.05mg / kg I.V. usually accomplished with extubation of the trachea during deep
# # # Or anaesthesia.
• Inj. Pancuronium 0.05mg / kg I.V. • This is not possible in parturients since the risk of aspiration is high.
• Inhalational agents should be given after delivery of baby but Hence emergence from general anaesthesia requires a balance
high concentration can decrease uterine tone and increase blood between reducing the risk of aspiration and that of bronchospasm.
loss. • Adequate dose of opioids or lignocaine (1-1.5mg/kg) before
• Halothane and isoflurane are approximately equipotent emergence can help minimize airway reactivity before extubation
bronchodilators at high concentrations (1.7 MAC) halothane
produces greater bronchodilation than isoflurane at lower
concentration (0.6 MAC) and therefore may be preferred for
anesthesia for caesarean section.
• But it sensitizes the myocardium to the arrhythmogenic effects of
catecholamines and has a potential for causing cardiac
arrhythmias in the settings of high catecholamine states or in
conjunction with aminophylline.
• Isoflurane, Sevoflurane and Enflurane on the other hand do not
cause arrhythmias in the presence of catecholamine or when
combined with aminophylline.
Monitors:
• Intra operative ventilation should be controlled to maintain
ETCO2 between 27-32 mmHg. Large slowly delivered tidal
volume with a long expiratory time can limit peak inspiratory
pressure and prevent air trapping.
• After delivery of the baby, depth of anaesthesia should be
increased with Opioids, preferably Fentanyl to limit reflex
responses to ETT.
Analgesia – Inj. Fentanyl 1-2 µg/kg IV.
Reversal – Inj. Neostigmine 0.05 mg/kg IV
# # Inj. Atropine 0.02 mg/kg IV
# # Inj. Glycopyrolate 0.01 mg/kg IV
149

53. A 50 year patient with history of Emphysema posted for excision of emphysematous
bullae by VATS (Video Assisted Thoracic surgery). Describe anesthetic management.
Indications of VATS: Contraindications:

Diagnostic Therapeutic • Hemodynamic unstable
• Myocardial Ischemia
Pulmonary Lung Biopsy, Etiology of Drainage of empyema, • Recurrent or persistent pneumothorax
recurrent pleural effusion. decortication • Evidence of endobronchial tumor.
Physiology in Awake Paralyzed closed & open chest:

Volume reduction, • Awake closed chest in LDP:
Resection of mass, cyst • The lower lung is better perfused & upper lung &
etc. one lung ventilation. V/Q ratio is not much altered.
• Awake, open chest & Spontaneous ventilation:
Pericardium & Heart Pleurodesis, • Opening of non dependent hemithorax causes
Pneumoplasty imbalance of of pressure on both sides of
mediastinum.
Pericardial drainage • During inspiration, the mediastinum gets shifted
Pericardiectomy towards dependent lung, due to negative pressure
in that lung.
• During expiration, because of positive pressure in
Pacemaker implant dependent lung mediastinum is pushed upward
out ward of the dependent hemithorax, causing
Mediastinum LN Biospy, Tracheo-esophageal
decreasing tidal volume in the dependent lung.
fistula repair, thoracic
sympathectomy, • This is called Mediastinal shift.
Mediastinal cyst excision. • During inspiration, the decent of diaphragm &
negative pressure on the dependent chest allows
the gas to enter from non dependent lung to
Thoracoscopy in Techniques of lung separation: dependent lung, & during respiration reverse
anesthetized • Double lumen tube occurs.
patient usually • Endobronchial sing tubes. • This is called paradoxical respiration.
requires one lung • Bronchial blockers (preferred in pediatric patient)
ventilation. • Fogartyʼs catheter
• Foleyʼs Catheter
• Magillʼs ballon tipped luminal blocker
• Pulmonary Artery catheter.
150

A 50 year patient with history of Emphysema posted for excision of emphysematous bullae
by VATS (Video Assisted Thoracic surgery). Describe anesthetic management. Continuation.
Physiology of One Lung Ventilation:

• In LDP: Management of Intra-operative Hypoxemia:
• If the non dependent lung is not ventilated then any • High Fio2 - Prevention & treatment.
blood flowing to this lung becomes shunt flow. • PEEP to Ventilated lung
• The dramatic reduction in the blood flow is due to • Maintain Cardiac output.
Hypoxic Pulmonary Vasoconstriction (HPV). • Re-inflation of non ventilated lung
• One lung creates an obligatory R to L transpulmonary
shut through non-ventilated lung. Capnothorax:
• This leads to larger P(A-a) O2 difference & lower • Co2 is used
PaO2. • It helps in the collapse of lung
Management of One Lung Ventilation For Emphysematous Acts as retractor.
•
bullae:
• Low pressure insufflation of 2-10 mm of Hg is used.
• Low tidal volume: Small tidal volumes.
• Low peak airway pressure: low airway pressures during Problems:
positive-pressure ventilation until the airway is isolated. • Sever Hypotension
• Low plateau pressure • Bradycardia
• For induction of anesthesia it is optimal to maintain • CO2 Embolism
spontaneous ventilation until the lung or lobe with the • Subcutaneous emphysema.
bulla or bleb is isolated. Risk of aspiration is very high. Preoperative Evaluation:
• Detailed history
Etiology of Hypoxia during one lung Ventilation:
• Cor-pulmonale - Inability to tolerate major lung resection
• HPV • Deviation of the trachea may signify presence of
• V/Q Mismatch pneumothorax, hemothorax, empyema.
• Pressure differences in thoraces. • Presence of clubbing, cyanosis, type and pattern of breath.
• Physical collapse of operative lung (30 - 40 % shunt
Investigations:
approximately)
• Hb, PCV
• Increase in pulmonary vascular resistance. • Renal function test
• Use of small tidal volume in relatively non-Compliant • Pulmonary function test & ABG
dependent lung along with decreased FRC will lead to • RBS,
increase PVR & alveolar collapse. • PT, INR
• ECG
• Chest X-ray
151

A 50 year patient with history of Emphysema posted for excision of emphysematous bullae by Dr Azam’s Notes in Anesthesiology 2013
VATS (Video Assisted Thoracic surgery). Describe anesthetic management. Continuation.
Pre operative Respiratory Care: Monitoring: Advanced Monitoring:

• Stop Smoking • ECG • Arterial Blood pressure - LV
• Dilate the airway using: • Pulse Oximetry Dysfunction, CAD, Severe COPD
• Beta agonist • Capnography & Emphysema
• Anti-cholinergics • Blood pressure • TEE
• Theophylline • Temperature • Pulmonary artery
• Steroids • Urine out put
• Cromolyn Sodium • precordial stethoscope
• Loosen the Secretions by:
• Airway hydration ( Humidification/
Nebulization) Anesthetic Management: Types of Anesthesia
• Systemic hydration orally - 3 Liters • Local Anesthesia
• Mucolytic agents & Expectorant drugs • Regional - Ipsilateral inter costal nerve block, paravertebral block & epidural
• Antibiotics anesthesia
• Remove secretions: • General Anesthesia: Therapeutic vats procedure is performed with the patient
• Postural drainage under GA with controlled ventilation.
• Coughing • Goals for GA are:
• Chest physiotherapy(percussion & • Satisfactory levels of GA
Vibration) • Adequate muscle relaxation
Ancillary Measures: • Rapid reversal with spontaneous ventilation at the conclusion of surgery.
• Treatment of co-existing disease • Pre-oxygenation
• Treatment of Cor-Pulmonale • Induction - based on the patients medical condition
• Pre-operative Digitalization • Muscle relaxant tailored to the expected duration of the procedure.
Patient Education, motivation & facilitation • Maintenance of anesthesia with volatile provides several desirable effects
of post operative care: Continuation: including bronchodilation, early extubation.
• Psychological preparation • Subcutaneous infiltration with LA at the entry port.
• Incentive spirometry & deep breathing
exercise Positioning:
• Exposure to secretion removal maneuvers • Lateral Decubitus position
• Exercise • Proper padding of pressure points
• Weight gain/reduction • Final confirmation of position of ETT with fibreoptic bronchoscope
• Diet supplements.
152

A 50 year patient with history of Emphysema posted for excision of emphysematous bullae by Dr Azam’s Notes in Anesthesiology 2013
VATS (Video Assisted Thoracic surgery). Describe anesthetic management. Continuation.
Extubation:
Post operative pain relief:
• Chest tube drain
• Local Anesthetic at port entry site.
• Endotracheal or endobronchial suction
• Intercostal nerve blocks
• Re-expand the lung - the key is to increase the
• NSAIDS
tidal volume slowly without creating high peak
• Epidural Analgesia
airway pressure.
• Patient controlled analgesia.
• Reversal of NM blockade
• Early extubation to be considered to prevent
suture line rupture & air leak due to IPPV
• If post operative ventilation is considered then Post operative complications:
endotracheal tube to be changed over to single • Persistent Air leak
lumen tube is preferred. • Down lung syndrome: Increased secretions, atelectasis & pneumonia that
can develop post operatively following one lung ventilation. This can occur
either on the same side or opposite side.
Post operative management & ventilatory • Infection
support. • Hornerʼs syndrome
• Early Ambulation • Dissemination of malignant disease.
• Post operative Pain Relief: • Chronic pain
• If inadequate analgesia - it may lead to • Lung herniation through the chest wall
diaphragm splinting & impaired coughing • Venous air embolism.
ability. • Bronchopleural fistula
• Oxygen Therapy:
• Low flow - venturi mask may be used.
• CPAP with low concentration of oxygen if
hypoxemia present.
• Humidifications of inspired gases:
• Maintains cilliary function
• Reduces viscosity of secretions
• Facilitating their expectoration.
• β2 agonists
• Methylxanthines
• Mucolytics
• Respiratory Stimulants:
• Nutrition
• CPAP/NIPPV/IPPV 153

54. Options for Lung Isolation Dr Azam’s Notes in Anesthesiology 2013
V 1834 Adult Subspecialty Management
Table 59-9 Options for Lung Isolation
Options Advantages Disadvantages
Double-lumen tube Quickest to place successfully Size selection more difficult

1. Direct laryngoscopy Repositioning rarely required Difficult to place in patients with difficult airways
2. Via tube exchanger Bronchoscopy to isolated lung or abnormal tracheas
3. Fiberoptically Suction to isolated lung Not optimal for postoperative ventilation
CPAP easily added Potential laryngeal trauma
Can alternate OLV to either lung easily Potential bronchial trauma
Placement still possible if bronchoscopy not
available
Bronchial blockers (BB) Size selection rarely an issue More time needed for positioning
Arndt Easily added to regular ETT Repositioning needed more often
Cohen Allows ventilation during placement Bronchoscope essential for positioning
Fuji Easier placement in patients with difficult airways Nonoptimal right lung isolation due to RUL
and in children anatomy
Postoperative two-lung ventilation by withdrawing Bronchoscopy to isolated lung impossible
blocker Minimal suction to isolated lung
Selective lobar lung isolation possible Difficult to alternate OLV to either lung
CPAP to isolated lung possible
Univent tube Same as BBs Same as for BBs

Less repositioning compared with BBs ETT portion has higher air flow resistance than
regular ETT
ETT portion has larger diameter than regular ETT
Endobronchial tube Like regular ETTs, easier placement in patients Bronchoscopy necessary for placement
with difficult airways Does not allow for bronchoscopy, suctioning or
Longer than regular ETT CPAP to isolated lung
Short cuff designed for lung isolation Difficult right lung OLV
Endotracheal tube (ETT) advanced into bronchus Easier placement in patients with difficult airways Does not allow for bronchoscopy, suctioning or
CPAP to isolated lung
Cuff not designed for lung isolation
Extremely difficult right OLV
CPAP, continuous positive airway pressure; ETT, endotracheal tube; OLV, one-lung ventilation; RUL, right upper lobe.
154

55. Bronchial Blockers Dr Azam’s Notes in Anesthesiology 2013
Anesthesia for Thoracic Surgery 1839 59

Table 59-13 Characteristics of the Cohen, Arndt, and Fuji Bronchial Blockers
Cohen Blocker Arndt Blocker Fuji Uniblocker
Size 9 Fr 5 Fr, 7 Fr, and 9 Fr 5 Fr, 9 Fr
Section V Adult Subspecialty Management

Balloon shape Spherical Spherical or elliptical Spherical
Guidance mechanism Wheel device to deflect the tip Nylon wire loop that is coupled with the None, preshaped tip
fiberoptic bronchoscope
Smallest recommended ETT for coaxial use 9 Fr (8.0 ETT) 5 Fr (4.5 ETT), 7 Fr (7.0 ETT), 9 Fr (8.0 ETT) 9 Fr (8.0 ETT)
Murphy eye Present Present in 9 Fr Not present
Center channel 1.6 mm ID 1.4 mm ID 2.0 mm ID
ETT, single endotracheal tube; ID, internal diameter.

From Campos JH: Which device should be considered the best for lung isolation: Double-lumen endotracheal tube versus bronchial blockers. Curr Opin Anaesthesiol 20:
30, 2007, with permission.
exposure. Bronchial blockers are most commonly used intralumi- blockade, the Arndt blocker can be advanced independently of
nal (coaxial) with an SLT. They can also be placed separately the wire loop by observing its entrance into the right mainstem
thorough the glottis or tracheostomy exterior to an SLT. This bronchus under fiberoptic visualization. The optimal position of
allows the use of a smaller SLT and is often an option in pediat- the Arndt blocker in the left or in the right bronchus is achieved
rics. Another advantage of the bronchial blockers is when post- when the blocker balloon’s outer surface is seen with the fiberop-
operative mechanical ventilation is being considered after
prolonged thoracic or esophageal surgery. In many instances
these patients have an edematous upper airway at the end of the
procedure. If a bronchial blocker is used there is no need to
change the SLT and there is no compromise of the airway if
mechanical ventilation is needed in the postoperative period.
Table 59-13 describes the characteristics of current bronchial
blockers. The smallest internal diameter (ID) of an endotracheal
tube that will allow passage of both a bronchial blocker and a
fiberoptic bronchoscope depends on the diameters of the bron- 155
choscope and blocker. For standard adult 9-Fr blockers, an
Dr Azam’s Notes in Anesthesiology
endotracheal tube greater than2013
or equal to 7.0 mm ID can be used 1
56. Complications of Thoracoscopy Dr Azam’s Notes in Anesthesiology 2013
The complications of thoracoscopy are:

• Intra-operative complications
• Post operative complications
Intra-operative Complications: Post-Operative Complications:

• Complications related to intubation • Early:
for single lung ventilation. • Persistent Air Leak
• Complications related to single lung • Down Lung syndrome
ventilation • Infection
• Conversion to open thoracotomy • Hornerʼs Syndrome
• Complications of nerve blocks • Recurrent Laryngeal nerve
injury
• Late:
• Dissemination of malignant
disease
• Chronic pain
• Lung herniation
156

Complications of Thoracoscopy. Continuation. Dr Azam’s Notes in Anesthesiology 2013
Intra-operative Complications: • Complications of open thoracotomy:

• Complications related to intubation for • Complications of Nerve Block
single lung ventilation. DLT • Local anesthetic toxicity
• Minor complications like pharyngeal • Adrenaline induced ventricular arrhythmias
trauma & pain, laryngitis & ballon • Nerve root injury
rupture. • Total Spinal anesthesia
• Malposition of the DLT • Pneumothorax
• Tracheobronchial tree disruption • Hemothorax
• Complications related to endobronchial
intubation: Post operative complications:
• Hypoxaemia • Early
• Hypercapnia • Persistent Air leak
• Barotrauma • More common in COPD, Children & steroid users
• Complications related to bronchial • Subcutaneous Emphysema, residual or recurrent
blockers: pneumothorax
• Difficulty in insertion • Management: Pleurectomy control of air leak
• Migration of bronchial blockers • Down lung syndrome:
• Malposition related complications • Atelectasis, infection & increased secretions in either
lung.
• Complications related to single lung ventilation: • Infection
Pulmonary Cardiovascular CO2 Insufflation • Late
Effects Effects Effects • Dissemination of malignant disease
• Chronic Pain
Hypoxaemia Hypotension Hypotension • Lung herniation
Hypercapnia Hypertension Bradycardia
Impaired HPV Arrhythmias Co2 air embolism
Pulmonary Mediastinal Shift Subcutaneous

Edema Emphysema
Atelectasis
Pneumonia
Complications more with Rt Lung as Vascular supply is 10%
more compared to the left side. 157

57. Double lumen tubes (DLT) Dr Azam’s Notes in Anesthesiology 2013
Double lumen tubes (DLT) ROBERT SHAW DLT

• Lung separation techniques of choice
Right sided! # # # # # # # Left sided
Types:
I. Robert Shaw tube – right and left
II.Carlens tube – left
III.Whites tube – right
Techniques of lung separation:

Double lumen tubes
Bronchial blockers
Endobronchial tubes – not often used.
Salient features of Robert Shaw tubes

• 2 catheters bonded together side-by-side.
• D shaped lumen
• The lumen on one side is longer and angulated to
facilitate entry into right / left bronchus. The other
lumen terminates in the trachea.
• They have a proximal tracheal cuff and a distal
bronchial cuff, which separates the two lungs.
• These cuff are high volume, low pressure type.
• The right sided tube has a slot in the part that enters
the right main stem bronchus to allow ventilation of the
right upper lobe
• Two curves in planes that are 90° apart.
• Proximal curve designed to fit oropharyngeal curve.
• Distal curve to facilitate placement of the tip in
appropriate main stem bronchus.
158

Double lumen tubes (DLT). Continuation: Dr Azam’s Notes in Anesthesiology 2013
Carleneʼs Tube: Whiteʼs Tube - Right sided:
Whiteʼs Double lumen tube: - Right side

• The angle of the bronchial portion is 400
in left and 200 in right sided DLT.
• Sizes: 41, 39, 37, 35, 28 and 26 french
(6.5, 6.0, 5.5, 5.0, 4.5 and 4mm interval
diameter of each tube).
• Right sided DLT used for left
thoracotomies, so that only right lung
can be ventilated.
• Left sided DLT may be used and are
preferable for both left and right sided
thoracotomies.
Carlens tube:
• Designed to intubate left main stem bronchus
• Has a carinal hook - which anchors on the carina when the DLT is Contraindications to the use of DLT
placed in position, preventing further downward displacement.
Disadvantages (due to carinal hook) • Distorted anatomy of tracheobronchial tree, which may hinder intubation
and proper positioning of DLT.
I. Increased difficulty during intubation
II.Laryngeal trauma / trauma to carina. • Endoluminal lesions in the main stem bronchus, like exophytic growth,
strictures.
III.Amputation of hook during or after intubation.
IV.Physical interference during pneumonectomy. • Full stomach (risk of aspiration)
159

Placement of a left sided DLT

Conventional DLT intubation technique: (Robert Shaw DLT)
1. Ensure the correct tube (right / left side) is taken.
2. Check both the cuffs and lumen connections
3. The DLT is first passed with the distal curvature concave anteriorly
4. Once the tube tip passes the larynx, with the anterior force on the
laryngoscope continued, the tube is carefully rotated 900 degrees, so that
the distal curve is now concave towards the appropriate side and the
proximal curve is concave anteriorly. This allows endobronchial intubation.
5. Now the tube is advanced until mild resistance to further passage is
encountered or the end of the common moulding of the two limens is at
the teeth.
6. The average depth of insertion for both male and female patients 170cm
tall is 29 cm. For each 10 cm increase or decrease in height, the average
placement depth is increased or decreased by lcm.
Initial position Rotated – 90% Final
Checklist to ensure proper insertion (left DLT )

1. Once intubated, both the cuffs are inflated
Endobronchial cuff: 1-2ml of air Procedure Breath sounds heard
Tracheal cuff: 5 of air.
2. Both the lungs are ventilated Clamp right lumen both Left Left and right Right
Note: l.Appearance of respiratory gas moisture. cuffs inflated
# 2. B/L chest lift Clamp left lumen both None or None or very None of
# 3. Presence of B/L breath sounds cuffs inflated very ↓↓ ↓↓ very ↓↓
3.# If only U/L breath sounds and chest lift are present, then it Clamp left lumen deflate Left Left and right Right
indicates that both the lumen of DLT must have entered one of left cuff
main stem bronchus.
In this situation, withdraw the tube 1-2 cm at a time, until B/L
breath sounds are heard.
4.# When B/L breath sounds are present, clamp the right lumen
(tracheal). Ventilate the left lung.
Breath sounds and chest movement should disappear on the right side and
be present only on the left side.
160

Major malposition of DLT INDICATIONS FOR USE OF DLT:

The proper positioning of DLT may be confirmed by use of:
• Fibreoptic bronchoscopy. Absolute
• Comparison of capnography (Waveform and end-tidal CO2 • Prevention of spillage or contamination from diseased to non
pressure) diseased lung.
• Continuous spirometric data. Infection – abscess, bronchiectasis, hyadatid cyst
• Palpation of DLT by the surgeon from within the chest.
Massive hemorrhage
• Controlled ventilation distribution
Bronchopleural fistula
Bronchopleural cutaneous fistula
Types & Comparison of double lumen tube: Giant unilateral lung cyst, bullous emphysema
Tracheobronchial trauma, rupture, tear
Type Bronchus intubated Carinal hook Shape of lumen • Unilateral bronchopulmonary lavage
Carlen Left Yes Oval Pulmonary alveolar proteinosis
White Right Yes Oval • Thoracoscopy
Robert – Shaw Right or left No D shaped
Relative: (ability to alternate deflation and inflation of lung
help surgeon to visualize lobar and inter segmental planes)
• Surgical exposure – high priority thoracic aortic aneurysm,

pneumonectomy
• Surgical exposure – low priority
• Esophageal reaction, lobectomy (upper), segmental
resection
• Occluding pulmonary emboli miscellaneous:
• Treatment of refractory atelectasis
161

58. One lung anaesthesia- problems and management. Dr Azam’s Notes in Anesthesiology 2013
Physiologic Considerations during Thoracic Anaesthesia.

I. Lateral Decubitus position
II. Open pneumothorax
III. One lung ventilation
Problems During OLV Etiology
Hypoxemia Intrapulmonary shunt during one-lung ventilation
Sudden severe hypotension Surgical compression of the heart or great

vessels
Sudden changes in ventilating Movement of endobronchial tube/ blocker, air

pressure or volume leak
Arrhythmias Direct mechanical irritation of the heart
Bronchospasm Direct airway stimulation, increased frequency of

reactive airways disease
Massive hemorrhage Surgical blood loss from great vessels or inflamed

pleura
Hypothermia Heat loss from the open hemithorax
162

One lung anaesthesia- problems and management. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Open pneumothorax:
• LDP – access to operations on lungs, pleura,
• Spontaneous LDP
esophagus great vessels and other Mediastinal shift:
mediastinal structures and vertebrae.
• -ve pleural pressure in NDL is lost. NDlung collapses
• Increases the risk of Hypoxemia:
• Inspiration – pl. pressure – more negative in DL
• alters the V/q relationship significantly – ↑ by Mediastinum shift done
•
Induction, Mechanical vent, Muscle paralysis
• Expiration - ↓ vP
opening chest and retraction Paradoxical respiration (pendeluft)
• Perfusion more in dependent lung • To and fro gas movement between Non Dependent Lung (NDL) and
• Ventilation more in non dependent lung Dependent Lung (DL)
Awake state:
• Inspiration – pneumothorax ↑ NDL to DL
• V/Q match is preserved • Expiration – pneumothorax ↓ DL à to NDL
• Dependent lung – more perfusion – due to • Imp – these effects can be over come during positive pressure ventilation
gravity More ventilation • ↓ GA
• Contraction of dependent. Hemidiphargm • OLV – intentional collapse of lung on operative side – no ventilation but
more efficient perfusion continues èlarge A-L intra pulmonary shunt èáp(A-a)o2 gradient
• On a more favorable part of compliance curve èhypoxemia
Induction:
• ↓ FRC nondependent lung – more favorable
part of compliance curve
• Dependent lung – less part of compliance
curve
• Ventilation more to non dependent lung
• Perfusion more to dependent lung ventilation
less in D ↓V/Q
• More mismatch
163

most patients, although the peak airway pressures are lower.128
There is a report
One lung suggesting
anaesthesia-that pressure-controlled
problems and ventilation Preoperative
management. Spirometry
Continuation: Dr Azam’s Notes in Anesthesiology 2013
may lead to improved oxygenation in COPD patients.129 Pressure- Studies consistently show that when the previous factors are con-
controlled ventilation will avoid sudden increases in peak airway trolled, patients with better spirometric lung function preopera-
pressures
OLV that-may result from surgical manipulation in the chest. tively are more likely to desaturate and have lower Pa2 values
Management:
Table 59-18 Suggested Ventilation Parameters for One-Lung Ventilation
Parameter Suggested Guidelines/ Exceptions
Tidal volume 5-6 mL/kg Maintain:

Peak airway pressure < 35 cm H2O
Plateau airway pressure < 25 cm H2O
Positive end-expiratory pressure 5 cm H2O Patients with COPD: no added PEEP
Respiratory rate 12 breaths/min Maintain normal PaCO2; Pa-ETCO2 will usually increase 1-
3 mm Hg during OLV
Mode Volume or pressure controlled Pressure control for patients at risk of lung injury (e.g., bullae,
pneumonectomy, post lung transplantation)
Therapies for Desaturation during One-Lung Ventilation:
Severe or precipitous desaturation:

• Resume two-lung ventilation (if possible).
Gradual desaturation:
1. Ensure that delivered Fio2 is 1.0.
2. Check position of double-lumen tube or blocker with fiberoptic bronchoscopy.
3. Ensure that cardiac output is optimal; decrease volatile anesthetics to < 1 MAC.
4. Apply a recruitment maneuver to the ventilated lung (this will transiently make the hypoxemia worse).
5. Apply PEEP 5 cm H2O to the ventilated lung (except in patients with emphysema).
6. Apply CPAP 1-2 cm H2O to the non ventilated lung (apply a recruitment maneuver to this lung
immediately before CPAP).
7. Intermittent re-inflation of the non ventilated lung
8. Partial ventilation techniques of the non ventilated lung:
a. Oxygen insufflation
b. High-frequency ventilation
c. Lobar collapse(using a bronchial blocker)
9. Mechanical restriction of the blood flow to the non ventilated lung
164

59. Describe the Pathophysiology, diagnosis, clinical features & current trends in
management of ARDS.
ETIOLOGY & PATHOPHYSIOLOGY:

DEFINITION:
There are no clearcut etiological factors and hence the
• Acute respiratory distress syndrome (ARDS) is a clinical syndrome of severe
dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading pathophysiology of the syndrome can not be listed down in
to respiratory failure. correlation to the etiology.
• Acute Pao2/Fio2 ≤ 200mmHg The proposed mechanisms are as follows:
• Bilateral infiltrates consistent with pulmonary edema Changes in the lungs can be divided into 3 phases
• No clinical evidence of left atrial hypertension or, if measured, pulmonary Exudative phase: (1-6 days)
artery occlusion pressure ≤18 mm Hg. Characterized by
a. Alveolar edema,
Causes of ARDS classified into ‘direct’ and ‘indirect’ lung injury
b. edema fluid having a high protein content
c. large number of inflammatory cells
d. increased capillary permeability.
Direct Lung Injury Indirect Lung Injury e. Pleural effusion as an important route of clearance of
edema fluid.
Common Pneumonia, Aspiration Sepsis
of Gastric contents Severe trauma with f. Airway obstruction which appears to be mediated by
shock and Multiple blood thromboxane.
transfusion Proliferative phase: (6 to 10 days)
a. Infiltration of the interstitium by fibroblasts and collagen.
Less Common Pulmonary Contusion Drug over dose b. Proliferation of alveolar type-II epithelial cells.
Fat Emboli Acute pancreatitis
Fibrotic phase: (10-14 days onwards)
Nearing drowning Blood transfusion
inhalation injury Pregnancy related a. When there is large destruction resulting in emphysema
Re-perfusion injury ARDS and the dead space increases.
b. Functionally the oxygenation improves; but there is
pulmonary vascular obliteration due to fibrosis.
c. In survivors beyond 3-4 weeks, the lungs are completely
remodeled by sparsely cellular collagenous tissue.
165

Describe the Pathophysiology, diagnosis, clinical features & current trends in management
of ARDS. Continuation:
Multiple organ failure:

! !"#$%&%!' CVS: The important cause is sepsis and the depression of
!()*+*,'(-./0/1(2+3,'043523,'(10436/4)/4(37'
6+465730+/-' myocardial contractility by TNF produced in sepsis.
Cardiac failure occurs when

860+930(.'6/2)7(2(-0':(*);'<=3'3-.'<>3?' - Cardiac index is < 2L / minute. m2
- Mean arterial pressure < 60 mm Hg
- VF or asystole
@(504/)A+7'3BB4(B30+/-'3-.'360+930+/-''
Renal: Caused mainly because of hypotension, nephrotoxic drugs
and sepsis. Renal failure is suspected when
- Rise in serum creatinine > 2 mg/100 ml.
Or
<E0/0/1+6' - Urine output less than 600 ml/24 hrs
C(360+9('/1+.3-0'*)(6+(*'' I4/0(3*(*''
(FF(60*''
D1EB(-'F4(('43.+637*'7+G('AE.4/1E7' J73*03*(,'' Liver: Fulminant hepatic failure occurs only in 10% of patients with
43.+637*,'*+-B7(0'DH'3-.'AE.4/B(-' I73*2+-/B(-'360+930/4,')73*2+-'
ARDS. But reversible enzyme changes occur in almost 95% of
)(4/1+.(''' AE3754/-+.3*('(06;''''
cases. Criteria for diagnosing significant hepatic dysfunction are
- Serum bilirubin > 4 mg/100 ml
- Prothrombin time > 1.5 times the normal
- Serum albumin < 2g/100 ml
K+4(60'(FF(60'' #-.+4(60'(FF(60'' K+4(60'(FF(60'' #-.+4(60'(FF(60'' Hepatic failure causes altered host defense, and also blood borne
- K(*04/E'K@8' J-ME2('+-360+930+/-'' - </773B(-'' - </2)7(2(-0''
substances not being detoxified in the liver can cause damage to
- I(4/1+.3*('7+)+.'' - N'3-0+)4/0(+-3*('' - J73*0+-'' - S3B(23-'F360/4''
- #-L54(' - OP'IK'' - Q+R4/-(60+-'' - T+-+-*' 3-.' /0A(4' the pulmonary endothelium.
(-./0A(7+52'' - <3'8"I3*('' ' )4/0(+-*''
' - <372/.57+-'' ' CNS: manifested as confusion, agitation, seizures and coma.
'
Thought to be present when the Glasgow coma scale is less than
6-8.
Flow Chart: Pathophysiology
166

Describe the Pathophysiology, diagnosis, clinical features & current trends in management Dr Azam’s Notes in Anesthesiology 2013
Endothelial or Parenchymal injury
Causes of CNS dysfunction are
• Can be seen in clinical picture as well as biochemical abnormalities and other
- Production of neurotransmitters associated disorders.
- Direct microvascular injury • Clinical picture: ARDS is suspected and provisionally diagnosed if there is
- Cerebral ischaemia. acute respiratory failure, following one of the predisposing factors. An arterial
Blood: Hematological dysfunction occurs in 26% of cases. O2 tension, below 50 mm Hg when breathing on room air can be taken as a
Diagnosed when diagnostic index.
• The clinical picture being described here occurs during the early phase of
- Platelet count less than 50,000/mm3
development of the syndrome and are divided into:
- White blood cell count<1000/mm3 4 stages.
- Fibrinogen levels<100 mg/100 mls. • Stage I – Hyperventilation is the only clinical abnormality. No cyanosis and
GIT: Occurs in 7-30% of cases and is manifested as# chest X-ray is normal.
- Hemorrhage • Stage II – Hyperventilation persists. But cyanosis ensues.
- Ileus • Stage III – Increasing respiratory distress (with hyperventilation and cyanosis)
CXR shows diffuse consolidations.
- Malabsorption
• Stage IV – hypercarbia, metabolic acidosis and multiple organ failure manifest
- Cholecystitis in this stage.
- Pancreatitis
These abnormalities occur because of mucosal ischemia
and alterations in microvascular permeability.
The multiple organ failure occurs because of
1. Altered blood flow -Oxygenated blood bypasses nutrient
capillary beds. This occurs because of
- Redistribution of blood to skeletal muscles
- Bypassing capillary bed through anatomic pre-capillary
arteriovenous channels.
- Reduction in "recruitable capillary reserves.
167

Describe the Pathophysiology, diagnosis, clinical features & current trends in management of Dr Azam’s Notes in Anesthesiology 2013
ARDS. Continuation:
B) Biochemical and other investigation abnormalities: The final value is obtained by dividing the aggregate sum by the
A four point scoring system for lung injury has been formulated and is as number of components that were used:
follows: • No lung injury # # # 0
• Mild to moderate lung injury # 0.1-2.5
1. Chest radiograph score Score
• Severe lung injury (ARDS) # 2.5
No alveolar consolidation 0 Management:
Alveolar consolidation in one quadrant 1 # Aims primarily at prevention and when the condition is
Alveolar consolidation in two quadrants 2 established, treatment of the condition.
Alveolar consolidation in three quadrants
3 Prevention:
Alveolar consolidation in all four quadrants 1. Injudicious administration and hence overloading of the
4
circulation by crystalloids should be avoided while
2. Hypoxemia score Value Score resuscitating the patient, especially if the CVS is
compromised.
PaO2 / FiO2 > 300 0 2. Use of proper filters during blood transfusion to prevent
PaO2 / FiO2 225-299 1 microthromboembolism.
PaO2 / FiO2 175-224 2 3. Inotropic support - Manipulation the circulation with inotropes
PaO2 / FiO2 100-174 and vasodilators could lead to avoidance of many of the
3
PaO2 / FiO2 < 100 irritating events in ARDS.
4
3. Respiratory system compliance Value Score 4. Good aseptic precautions (esp. while doing invasive
score (when ventilated) monitoring) and broad spectrum antibiotic cover are
Compliance > 80ml/cm. H2O 0 mandatory)
5. Controlled early O2 therapy
Compliance 60-79 ml/cm. H2O 1
Compliance 40-59ml/cm. H2O 6. Avoid hyperoxia and barotrauma.
2
Compliance 20-39/cm. H2O
3
Compliance < 19 ml/cm. H2O
4
4. Peep score (when ventilated) Value Score
PEEP < 5cm. H2O 0
PEEP 6-8 cm. H2O 1
PEEP 9-11 cm. H2O 2
PEEP 12-14 cm. H2O
3
PEEP > 15 cm. H2O
4
168

Describe the Pathophysiology, diagnosis, clinical features & current trends in management of Dr Azam’s Notes in Anesthesiology 2013
ARDS. Continuation:
TREATMENT: • N-acetyl cysteine (supposed to increased lung lymph flow)

• Cryoprecipitate rich in fibronectin for reversal of opsonic
This can be put mainly under 5 headings. deficiencies.
I. Control of infections: - Early detection and treatment of infections according to • Agonist infusion
• Airway instillation of amiloride (which inhibits Na-transport)
the culture & sensitivity with appropriate antibiotics.
• Immunotherapy - Administration of polyclonal antibodies against the core lipid of IV. Improving systemic O2 delivery: this may be achieved by
endotoxin • Optimizing the blood volume, Hb & keeping a watch on the
• Increasing the immunological surveillance by the use of muramyl dipeptides. CVP, PAWP.
II. Improving Gas Exchange: • Inotropes like dopamine & Nor-adrenaline.
• Recent trends in this field are the use of vasodilators like
• Controlled O2 therapy should be started initially. But once the condition has
sodium nitroprusside (SNP) and Glyceryl trinitrate (GTN).
progressed, endotracheal intubation, IPPV with PEEP is thought to be abetter
choice. PEEP is advantageous in such situations because it increases the arterial V. Attenuation of pulmonary or systemic injury:
oxygenation with as little FiO2 as possible. Apart from preventive measures like keeping low FiO2
Intermittent Mandatory Ventilation (IMV) with judicious levels of PEEP, and preventing barotrauma described earlier, solely tried
usually between 5-18 cm H2O is considered .FiO2 should be limited to 0.5 or to the modes of treatment in this perspective are
minimum possible without significant hypoxia, and aiming at SPO2 of 92% and • Extracorporeal membrane oxygenation (ECMO)
above. • Oxygen free radical scavengers
• Anti TNF antibodies
III. Limiting or decreasing alveolar edema: - • Pentoxifylline – acts as rheological agent and may improve
the microcirculation by altering the moulding capacity of
May be done by RBCs.
a. Decrease in hydrostatic pressure - Suggested agents include; prostacyclins, • Attention to other modalities of care (like that of eyes,
prostaglandin E1 nitrates sodium nitroprusside, Ca-channel blockers, bladder, nutrition, and frequent change of position to avoid
diuretics, the last four being used when the patient is haemodynamically bed sores and chest physiotherapy) should be given as in
any other patient admitted in ICU.
stable.
b. Increase colloid osmotic pressure. No effective method till date and whatever
colloids we give in the phase of capillary leak, pass into the interstitium, thus
increasing the edema and worsening the problem.
c. Reduce capillary leak – Recently tried ones are
• PGE and thromboxane synthetase antagonist DAZOXIBEN
169

Describe the Pathophysiology, diagnosis, clinical features & current trends in management Dr Azam’s Notes in Anesthesiology 2013
Mechanical Ventilation ARDS NET Protocol Summary
VI. Acidosis Management GOAL: (pH < 7.30),
I. INCLUSION CRITERIA: Acute onset of
pH 7.30-7.45
1. PaO2/FiO2 ≤ 200 (corrected for altitude)
If pH 7.15-7.30: Increase RR until pH > 7.30 or
2. Bilateral (patchy, diffuse, or homogeneous) infiltrates consistent with
PaCO2 < 25 (Maximum set RR = 35). .
3. pulmonary edema
If pH < 7.15: Increase RR to 35. If pH remains <
4. No clinical evidence of left atrial hypertension
7.15, VT may be increased in 1 ml/kg steps until
II: VENTILATOR SETUP AND ADJUSTMENT
pH > 7.15 (Pplat target of 30 may be exceeded).
I. Calculate predicted body weight (PBW)
May give NaHCO3
a. Males = 50 + 2.3 [height (inches) - 60]
Alkalosis Management: (pH > 7.45) Decrease
b. Females = 45.5 + 2.3 [height (inches) -60]
vent rate if possible.
1. Select any ventilator mode
VII. I: E RATIO GOAL: Recommend that duration
2. Set ventilator settings to achieve initial VT = 8 ml/kg PBW
of inspiration be < duration of expiration.
3. Reduce VT by 1 ml/kg at intervals ≤ 2 hours until VT = 6ml/kg PBW.
4. Set initial rate to approximate baseline minute ventilation (not > 35 bpm).
Monitoring: 5. Adjust VT and RR to achieve pH and plateau pressure goals.
- Heart rate # # - Blood gas
- Blood pressure # - Pulse oxymetry III. OXYGENATION GOAL: PaO2 55-80 mmHg or SpO2 88-95%
- CVP## # - Temperature Use a minimum PEEP of 5 cm H2O. Consider use of incremental FiO2/PEEP
- PAWP # # - Serum electrolytes combinations to achieve goal.
- Urine output # - Cardiac output # IV. PLATEAU PRESSURE GOAL: ≤ 30 cm H2O
• Check Pplat (0.5 second inspiratory pause), at least q 4h and after each
# # # - Lung compliance
change in PEEP or VT.
• If Pplat > 30 cm H2O: decrease VT by 1ml/kg steps (minimum = 4 ml/kg).
GRID: Question to be answered iii. LAE • If Pplat < 25 cm H2O and VT< 6 ml/kg, increase VT by 1 ml/kg until Pplat
under following headings: iv. ISO2D > 25 cm H2O or VT =6ml/kg.
1. Definition v. AP/SI
2. Causes of ARDS - Direct & • If Pplat < 30 and breath stacking or dyssynchrony occurs: may
c. Acidosis Management increase VT in 1ml/kg increments to 7 or 8 ml/kg if Pplat remains < 30 cm
Indirect Injury d. Mechanical Ventilation H2O.
3. Pathophysiology & Etiology - • Inclusion Criteria
Flow chart • Ventilator Setup
4. Clinical Features & Stages • Oxygenation Goals
5. Management • Plateau Pressure Goals
a. Prevention
b. Treatment
i. COI
ii. IGE
170

60. Permissive Hypercapnia.
• Acidosis causes CNS dysfunction, intracrainal HTN, neuromuscular weakness,
CVS impairment & increases Pulmonary vascular resistance.
• Its a strategy used to minimize the occurrence of ventilator
related lung injury. • pH is targeted > 7.30
• Tromethamine (THAM) is a non bicarbonate buffer that helps to compensate for
• This is achieved by ventilating the patient by low tidal volume
metabolic acidosis. THAM decreases H+ ions concentration & indirectly
(4 - 7 ml/kg), thus making it possible to ventilate the patient
decreases CO2 level & increases bicarbonate levels.
with lower peak inspiratory pressure, & to minimize potential
pressure or volume related complications. • Each 100 mL contains tromethamine 3.6 g (30 mEq) in water for injection. The
solution is hypertonic 389 mOsmol/L (calc.). pH 8.6 (8.4-8.7).
• Plateau pressure are targeted (< 30 to 35 cm of H2O) to
avoid alveolar over distention. • THAM Solution (mL of 0.3 M) Required =Body Weight (kg) X Base Deficit (mEq/
liter) X 1.1*
Indications: •
• Status Asthmaticus
• ARDS
Mechanism & physiologic changes in permissive Hypercapnia
Decrease Tidal Volume ( 4 - 7 ml/kg)

Increase PaCO2
Decrease peak inspiratory
Atelectasis Respiratory Acidosis Hypoxemia
Decreases Mean
airway pressure
To reduce PEEp may be pH may be normalized Corrected by
used if airway pressures with sodium bicarbonate or using Higher
are in acceptable range THAM(tromethamine) FIO2
Decreases Barotrauma
171

61. AUTO-PEEP. Dr Azam’s Notes in Anesthesiology 2013
• Also called intrinsic PEEP, inadvertent PEEP occult PEEP and !

ʻbreath-stackingʼ. "#$%&'!()*!
• Auto-peep in mechanically ventilated patients, is defined as an
unintentional positive end expiratory pressure (PEEP) that occurs +,-$./0.1!2++2!!
with patients receiving ventilatory support when a new inspiratory
breath is begun before expiratory flow has ended.
34-#52++2!!!
Auto-PEEP is associated with:
• Airway obstruction
• Rapid respiratory rate (> 20) CONSEQUENCES OF AUTO-PEEP:
• Insufficient inspiratory flow rate • Increases the work of breathing
• In adequate or short E-Time • Worsens gas exchange
• Equal I & E time (1:1) • Can cause hemodynamic compromise
• Can lead to inappropriate treatment
Failure of lung volume to return to passive FRC during expiration • Misinterpretation of central venous and pulmonary artery catheter
increased risk of auto-PEEP. pressure measurements.
1. COPD • Inappropriate fluid administration or unnecessary vasopressor
2. In ventilated patients with high MV (> 10-20 l/m). therapy.
3. Age (> 60 yrs.)
4. Increased airway resistance (small ETT, bronchospasm, Treatment of Auto -PEEP:
increased secretions, mucosal edema) • Reduction in Tidal volume
5. Increased lung compliance • Reduce Respiratory rate
6. High respiratory frequency • Increasing Inspiratory flow rates
7. High I: E ratio i.e., short TE (1: 1 AND 2: 1) • Prolonging E - Time
8. Increased VT particularly with airflow obstruction
Diagnosis of Auto-PEEP:
• If patient develops hypotension due to hyper inflation or Auto
PEEP then do Apnea Test:
• Apnea Test:Disconnect patient from ventilator for 30 sec(Apnea), if
this leads to normalization of blood pressure ( due to increased
Venous return), this confirms the diagnosis of Auto-PEEP.
172

AUTO-PEEP. Continuation: Dr Azam’s Notes in Anesthesiology 2013
In ventilated patients:
Shortening of TE (expiratory time)
↓
Incomplete exhalation
↓
Pressure builds up therefore exhaled volume is less than delivered volume
↓
Progressive high FRC
↓
Tissue recoil increases
↓
Increased force (pressure) pushing air out of lungs (splints the airways open –
diameter increases).
↓
Decreased airway resistance to exhaled flow.
Methods of reducing auto-PEEP: !

• Higher gas inspiratory flows.
• Shorten inspiratory time.
• Allow longer time for exhalation increase E time.
• Longer E-time with smaller VT and low RR.
• Use of low resistance exhalation valves, large ETT-- Reduce air-
trapping.
• Use of spontaneous modes whenever possible – IMV/SIMV, pressure
support and CPAP.
• Set PEEP < 75% to 85% of Auto-PEEP
173

62. Intercostal Chest Drain Dr Azam’s Notes in Anesthesiology 2013
Chest Drain Insertion:

Need for the Chest Drain:
• To evacuate air / fluid into a closed collection system Triangle of Safety
to restore:
• Negative intra-thoracic pressure
• Promote lung expansion Posterior border
• Prevent lethal levels of pressure from developing of pectoralis
Anterior
in thorax. Major
border of
Latismus Dorsi
Components: 3 Components
• Drain Anterior
• Collection chamber Axillary Line
• One way valve
Indications:
• Significant pneumothorax > 30 % 6th Rib
• Lessor pneumothorax - Requiring ventilation,air shifting
• Hemothorax,
• Empyema Chest Tube:
• Chylothorax, Red rubber / Silastic PVC
•
• Pleural Effusion
• Right angled / straight
• Hydropneumothorax
• Sizes 6 - 40 F / Infants: 6 -24 F
Sites of Chest Drain Insertion: • Adults:
• 4th-5th I/C space in Anterior axillary line. • 24 - 28 for air,
• 2nd I/C space in Mid clavicular line. • 32 - 34 for pleural effusion,
• Superior border of the underlying rib. • 36 - 40 for blood / pus.
174

Intercostal Chest Drain. Continuation: Dr Azam’s Notes in Anesthesiology 2013
!"#$%&'()*+",-$&)((((("'.*)(/-$*)(!*-,(((($)-0
Prof. A. K. Sethi’s EORCAPS-2011
Chest Drains: Drainage Bottles:

• Simple system: single bottle
• Large bottle (8in. / 20cm)
• Disadvantage: increasing resistance as bottle fills
• 1 / 2/ 3 bottle systems.
Physics & physiological aspects:

• Under water seal – 0,*")-,(
1,"%.
• A one way valve
• Produces a siphon effect, enhances drainage
23 &
• Drainage tube; 1.8m, 9.5 – 12mm ID
• Distal end of drainage tube 2 cm below water:
The depth determines the hydrostatic pressure needed
to overcome during expiration.
• Collection chamber always 100cm below the chest:
(To prevent the chamber fluid getting sucked up the
tube during obstructed inspiration). Management of Chest Drain:
• Large diameter collection chamber (20cm diameter): • Bubbling chest tube - never to be clamped.
(Minimal resistance to drainage of air, to prevent • Controlled drainage for large pleural effusions.
loss of underwater seal as water moves up the drainage • Avoid clamping in pneumothorax.
tube during deep inspiration). Prof. A. K. Sethi’s EORCAPS-2011
Complications: Avoiding Re Expansion PE: !"#$%&'()&"*+

• Incorrect positioning • Suggestions: Clamp for 1 hour after 1 liter Contraindications:
• Intra thoracic / abdominal injury of drainage. • Lack of Air fluid
• ,*'"--.')/$"+&)&"*&*0
• Inter Costal neurovascular bundle injury • No standard recommendations. • Coagulopathy
• Re-expansion pulmonary oedema • Not more than 1- 1.5 liters ,*)-(/)1"-('&'/2/(34"#&*(%/&*56-7
• at one time.
• Accidental disconnection • 500 ml per hour. • ,2!/*.6-"8(+'6%(-/36*4%./&*56-7
• Infection /Obstruction
• 9.:.;$(*+&"*/$6%#"*(-7/".4.#(
• Hemorrhage
• <''&4.*)(%/4&+'"**.')&"*
175
• ,*=.')&"*/2>3+)-6')&"*
Intercostal Chest Drain. Continuation: Dr Azam’s Notes in Anesthesiology 2013
CHEST DRAIN CARE:

• Avoid clamping, examine daily
• Keep below the level of patient GRID: Question to be answered under following headings:
1. Need for the Chest Drain
• Tight fittings connections / no kinking
2. Components
• Milking with caution 3. Indications
• Pain 4. Sites of Chest drain
• Serial X-rays - Proximal holes 5. Triangle of Safety
6. Chest Tube
7. Drainage bottle
Removal of chest drains: 8. Physics & Physiology of Chest drain
• Clamping 9. Complications
• 24 hours after drainage stopped 10. Avoiding Re-expansion pulmonary edema
• At removal ask patient to inhale deeply 11. Contraindications
12. Chest drain care
and perform Valsalva
13. removal chest drain.
• Chest drain removed swiftly
• Purse string suture closed
• Check CXR
176

63. Broncho-pleural fistula Dr Azam’s Notes in Anesthesiology 2013
Definition: Bronchopleural fistula (BPF) is a sinus tract Goals for ventilation

between the bronchus and the pleural space.
• Maintain adequate oxygenation while reducing the fistula flow
Presentation:
• Positioning: BPF is dependent
• Failure to re-inflate lung despite chest tube drainage
• Lowest possible tidal volume
- trauma, infection, carcinoma.
• Fewest mechanical breaths IMV > Assist control
• Complication of diagnostic / therapeutic procedure /
• Lowest PEEP / Shortest inspiratory times
mechanical ventilation.
Mechanical Ventilation: issues

Predisposing Factors: • Adequate sized chest drainage system
• Residual carcinoma • Ventilation: Pressure controlled
• Previous radiotherapy • Independent lung/ High frequency
• Underlying inflammatory lung disease • Synchronized closure / positive pressure to chest tube.
• Gross pleural contamination • Consider permissive hypercapnia
• Sputum culture positive for TB • FOB Instillation of sealant
• Long dependent stump
Signs & Symptoms: Anesthesia implications:

• Fever / Dyspnoea / Productive cough/ serosanguinous Optimization
•
fluid Chest drain / Hydration
•
• Radiology & FOB confirmation Antibiotics
•
• Diagnosis - Methyl blue / Bronchography/ Radioactive • Sitting upright
aerosol Diseased hemithorax dependent
•
177

Broncho-pleural fistula. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Anesthetic Implications:
• Prevention of spill into healthy lungs GRID: Question to be answered under following headings:
• Obtaining control of distribution of ventilation 1. Definition
• Potential of enlargement of fistula with DLT / 2. Presentation
Bronchial Blocker. 3. Predisposing factors
4. Signs & symptoms
5. Goals for Ventilation
Induction - Options available are:
6. Mechanical Ventilation issue
7. Anesthetic Implications
• Bronchoscope and intubation under local 8. Anesthetic Management.
anesthesia.
• Bronchoscopy and intubation under G A
maintaining spontaneous respiration
• Bronchoscopy and intubation under GA and muscle
relaxation.
• Patient upright and affected side dependent.
178

64. Laryngospasm Dr Azam’s Notes in Anesthesiology 2013
Definition: a closure of the larynx that blocks the passage of air to the
lungs In laryngospasm, the very entry of oxygen into the lungs is impeded. Management:
Incomplete Obstruction:
Etiology: • The first to remove the irritant stimulus.
• By an irritant stimulus to the airway under lighter planes of anaesthesia. • SecondDeepen the level of anesthesia.
• Thirdly Facilitate ventilation by applying gentle positive airway
• Volatile anesthetic agents—ether, Desflurane & Isoflurane is more irritant
pressure with 100% oxygen via a tight-fitting face mask may
than halothane which itself is more irritant than enflurane.
“break” the spasm.
• Secretions - Vomitus, Blood
• If spasm does not break, a small dose of suxamethonium (10 mg
• Presence of nasogastric tube. Inhalation of pungent volatile anaesthetics, or 20 mg in an adult)will relax the striated muscles of the larynx.
• Placement of an oropharyngeal or nasopharyngeal airway,
• Powerful peripheral stimuli Complete Obstruction:
• Peritoneal traction, mesenteric pull etc. • This spasm cannot be “broken” by bag pressure through a mask:
• Barbiturates instead, it will fill the stomach.
• Chronic smokers- having a hypersensitive respiratory tract. • Succinylcholine plus ventilation will help break the spasm.
Pathophysiology:
• During laryngospasm the reflex closure of the vocal cord ensues. GRID: Question to be answered under following headings:
• It may be partial or Complete 1. Definition
• Complete Obstruction: 2. Etiology
3. Pathophysiology
• May not be able to ventilate the lung
4. Clinical features
• Partial Obstruction:
5. Management.
• Manifests as crowing respiration or stridor and when complete, by a
“rocking” obstructed pattern of breathing
• Abdominal wall rises with contraction of the diaphragm during
inspiration, but because air entry is blocked, the chest sinks and fails
to expand.
Clinical Features:
• Hypoxia,
• Hypercarbia and acidosis causing hypertension initially.
• Tachycardia
• Hypotension,
• Bradycardia, ventricular arrhythmias leading to cardiac arrest.
• Children are particularly prone to these complications because of their
small functional residual capacity and relatively high oxygen consumption. 179

65. Bronchospasm. Dr Azam’s Notes in Anesthesiology 2013
Definition of Bronchospasm: Bronchospasm is an abnormal Deepen Anesthesia:

contraction of the smooth muscle of the bronchi, resulting in an • Give 100% oxygen
acute narrowing and obstruction of the respiratory airway. • Avoidance of the precipitating factors
Etiology: • Inhalation Anesthetic agents if BP is normal.
• Reflex bronchiolar constriction may be centrally mediated; as • Low BP - Ketamine
asthma or it may be a local response to airway irritation.
• Bronchospasm is common in anaphylactoid reaction due to drug Beta2 Agonist:
and blood transfusion as well as in cigarette smokers and those • Rapid acting albuterol through meter dose inhaler directly in
with chronic bronchitis. breathing circuit.
• Histamine releasing drugs (e.g. Morphine, d-tubocurarine, • Aminophylline 0.5mg/kg - tachyarrhythmias
atracurium or metocurine) and beta-adrenergic antagonists may • Terbutaline S/C 0.25mg every 20 min for 3 doses.
exacerbate bronchospasm. • Epinephrine: 0.1 - 0.5 ml of 1:1000 S/C may be the last resort.
• Steroids: Hydrocortisone 4mg/kg followed by 3mg/kg.
Clinical Features:
• Wheezing (usually more pronounced on expiration)
In anesthetized patient it may be: GRID: Question to be answered under following headings:
• Difficult to ventilate due to diminished compliance, Stony hard 1. Definition
reservoir or AMBU bag. 2. Etiology
• The marked increase in airway pressure required for ventilation 3. Clinical Features
4. Management.
• Air trapping,
• Hypoxemia,
• Tight bag,
• Tachycardia,
• ↓ SPO2,
• Prolonged expiration,
• Hypoxia,
• ↓ compliance,
• Air trapping,
• ↑CO2,
• ↓ CO.
180

66. A 30 year old female ASA grade I following exploratory laparotomy is not maintaining oxygen
saturation in the post operative period. Discuss the causes & Management.
Definition: Hypoxia is defined as inadequate oxygen supply to the cells and tissues of the body. Decreased FRC:
Values: Sao2 < 90%, PaO2 < 60% • Seen in Pulmonary edema (Treatment will be fluid
restriction, diuretics & oxygen therapy Positive
Causes of Post operative Hypoxia & its treatment: ( 12 Causes) pressure ventilation.), Infections( Antibiotics),Obesity
Low Inspired concentration of O2: (incentive spirometer & deep breathing exercises),
• When FIO2 is < 0.21%. The treatment would be giving high inspired oxygen through Venturi aspiration(postural drainage, nebulization incentive
mask. spirometer & deep breathing exercises.)
Airway obstruction: Right to left intrapulmonary shunts:
• Pharyngeal obstruction: Treatment would be Head tilt & chin lift.# • Most common cause is Atelectasis. Treatment would
• Laryngeal obstruction: treatment: Lift the chin while the head is on a pillow or displace #jaw be Deep breathing exercise, Chest physiotherapy
forward. Alternating lifting and relaxing the chin will, relax the strap muscle of the neck. humidification of inspired gases, coughing &
• Attempt to facilitate ventilation of gentle positive pressure via mask. When conservative incentive spirometer.
measures are not effective in breaking spasm within 1min, then a muscle relaxant should be Drug Overdosage:
given I.V. Scoline 1.5mg/kg injected • Like opioids, muscle relaxants, in adequate reversal.
• Bronchospasm: Bronchodilators like Beta agonist, Anticholinergics, Theophylline Treatment would be titrated dosage of opioids & to
andSteroids wait for adequate reversal.
Post operative shivering: Pulmonary Embolism:
• May also cause hypoxia. Treatment is Oxygen therapy • Lower limb surgeries, prolonged
Sudden reduction in cardiac output: immobilization.treatment would be DVT stocking,
• Can contribute to hypoxemia. Treatment: Watch out for bleeding & dehydration. Give IV early mobilization, DVT prophylaxis.
fluids, blood replacement. Pneumothorax:
Diffusion Hypoxia: • Result of direct injury to lungs or rib fracture.
• At the end of surgery when both oxygen & nitrous oxide stopped at the same time. Where • Treatment is 100% oxygen, insertion of chest tube &
N2O diffuses back into the alveoli. Treatment is to give oxygen after cutting off N2O. intercostal drainage & IPPV.
Type of Surgery:
• Patients with abdomino-thoracic procedures will not respire adequately because of pain on
deep inspiration. Treatment would be adequate analgesia with opioids or NSAIDS or
through the epidural.
Ventilation Perfusion Mismatch:
• Usually seen under Anesthesia. GRID: Question needs answered under
following headings:
1. Definition
2. values
3. 12 Causes of Post operative Hypoxia &
its management.
181

67. Discuss the preoperative evaluation and preparation of 55 year old male with bronchiectasis
scheduled for right lower lobe excision.
Pre-operative evaluation 5).Pulmonary function tests

Respiratory system It is divided into three phases: First Phase (whole lung test)
A). Bronchopulmonary manifestation # # # # second phase (split lung test)
• Cough:Indicate bronchial irritation & duration, onset, severity, # # # # Third phase testing
amount of sputum, associated with blood staining as frank blood. First Phase: (whole lung test)
• Dyspnoea:Indicate some V/Q mismatch, duration and severity It consists of ABG + Spiromety at room temperature to evaluate
(limitation of daily work) triggering factors & relieving factors. lung volume.
• Chest pain:Difference between cardiac & pleuritic or • Room air : PaCO2 > 45mm of Hg
musculoskeletal. FEVI < 50% of predicted
MBC of < 50%
• It is non invasive, it suggested that the patient needs to go through
B). Intrathoracic Metastatic Manifestation
the next phase of testing.
Pleural effusion, pneumothorax, SVC obstruction
Flow volume loops: Obstructive disease
Phrenic nerve involvement, Hornerʼs syndrome, brachial plexus
# # # Restrictive disease
involvement
• Look for position & the shape of the loop; help you to differentiate
between the obstructive & restrictive. The slope of expiratory curve
C).Extra thorax manifestation
between the 25% & 75% flow, despite the MMEFR (maximum mid
Metastasis into liver, bone, brain, kidney
expiratory flow rates) and gives a good indicator of the effort
Any neoplastic syndrome, (Cushingsʼs, hypercalcemia)
independent small airway obstruction (which responds to
Bronchodilation)
Investigations:
1. Hb HCT = Polycythemia
Phase Two (Split lung Function)
2. TC, DC, ESR = Any lung infection
•
3. BUN, S. Creatinine, LFT = to rule out organ involvement**
Radio isotope ventilation perfusion scan help in quantifying
4. Chest X-ray : antero-posterior, lateral
ventilation & perfusion. Technetium 99, xenon 133
Look for Predicted post FEV 1 = Pre op FEV1 x Perfusion percentage of the remaining
a). Upper airway deviation or obstruction (intubation difficulty could be lung
anticipated) • A predicted post op FEV1 of 800ml is considered as lower limit for
b). Pleural effusion lung resection.
c). Cardiac enlargement • A better index would be a predicted post op. FEV1 of atleast 35 to
d). Bullous Cyst 45%.
e). Parenchymal, Lung disease
182

Discuss the preoperative evaluation and preparation of 55 year old male with bronchiectasis Dr Azam’s Notes in Anesthesiology 2013
scheduled for right lower lobe excision.Continuation:
Phase Three: Preoperative Preparation:

Invasive procedure: Occlusion of main pulmonary artery by Pre-operative Respiratory Care: also refer page 20 (Smoking)
ballon. • Stop smoking: 8 to 12 weeks
• Increase in mean pulmonary artery pressure above PAP > 40 • Dilate Airway: β2 agonist, Theophylline, Steroids, Mart cell stabilizer
mg Hg. • Loosen secretion: Airway hydration, Systemic hydration, Mucolytic expectorant,
• Increase in PaCo2 above 60mm of Hg. antibiotics
• Decrease in PaO2 below 45mm of Hg • Remove Secretions : Postural drainage, chest physiotherapy & Coughing
• All this indicates the Patients inability to tolerate the removal • Education, Motivation & Facilitation of post operative case
of this amount of lung tissue. # -# Psychological Prep
• PVR is found to be above 190 dyne / sec / cm5, results # -# Incentive spirometry
associated with severe morbidity & mortality. # -# Exposure to secretion removal maneuver
# -# Exercise
Preoperative Lab Criteria for Pneumonectomy # -# Weight loss / gain
# # -# Stabilize other medical problems
• CVS: ECG, Echo
Test High risk patient
• Dobutamine stress echocardiogram
ABG (Room air) PaCo2> 45mm • Other co-morbidities.
PaO2< 50mm
FEV1 < 2L • Anesthetic consideration: Refer COAD/COPD Notes

Pre-medications: According to individual lung function.
(Prediction post op < 0.8 L or 40% Increase
Poor Lung: No sedation
FEVI)
Good lung function: Narcotic + benzodiazepine
FEV1 / FVC < 50% of predicted • Double lumen tube Intra-operative.
Monitoring:
MBC < 50% of increase • CVS: ECG, NIBP, CVP, (PCWP - Dependent lung & Intra-arterial Blood Pressure
in sick patients)
Max VO2 (O2 < 10 ml/kg/min • Respiratory: Stethoscope on the dependent lung
consumption) -Pulse Oximeter
With these finding the morbidity & mortality is very high. -Fio2 analysis
-ETCO2
• Nerve: Peripheral nerve stimulator
• Temperature, ABG, urine output
183

Discuss the preoperative evaluation and preparation of 55 year old male with bronchiectasis Dr Azam’s Notes in Anesthesiology 2013
scheduled for right lower lobe excision.Continuation:
Induction: Reversal:
A mid thoracic epidural catheter before induction on after induction to Neostigmine 0.05mg/kg + Glycopyrrolate 0.01mg/kg
be put Intraoperative Complications:
Thiopentone 3 to 5 mg / kg 1. Hypoxemia
Gyclopyrrolate 0.01 mg / kg 2. Lower Lung Syndrome: Gravity dependent pleural fluid
trasduation into the dependent lung.
Relaxant: 3. Pneumothorax on the dependent lung.
Inj. Scoline 2 mg /kg Postoperative Ventilation:
Short acting is preferred if difficult intubation is anticipated. • Only in chronic lung disease.
Intubation: Robertshaw DLT confirm the air entry (refer DLT Notes) • Air leak from the bronchial stump.
• Mechanical ventilation to be done with the single lumen
Patient positioning tube.
Lateral decubitus with disease lung on the non dependent portion. All • Vt = 6 to 8 ml/kg
positional hazards to be avoided. • RR = to maintain the ETCO2 around 40
Maintenance: • FiO2 = initially start with 100% later reduce it to 40% with
O2 + volatile inhalation agents + Narcotics (Fentanyl 1-3mg/kg /hr + Muscle
Saturations of 90 to 92%
relaxants (Inj Vecuronium 0.05mg / kg)
Management of one lung ventilation: Post Operative pain Relief:

Conventional Management: • Thoracic epidural for poet operative pain relief.
1). Maintain two lung ventilation as long as possible • Other option
2). Use FiO2 to 100%
3). One lung ventilation is started with larger tidal volume 8-10 ml/kg
4). RR is adjusted to get ETCo2< 40 Torr
5). Vasodilate dependent lung (O2 is the best pulmonary vasodilator)
Differential lung management

1). Dependent lung PEEP
2). Differential lung PEEP & CPAP
3). Apneic Oxygenation
4). Selected non-dependent lung high frequency ventilation
5). Selective dependent lung nitric oxide
6). Pressure control ventilation to non-depend lung
184

68. Bronchography. Dr Azam’s Notes in Anesthesiology 2013
Definition: G.A for bronchoscopy in children:

• It is a method of delineating the bronchial tree with radio • Pre-op preparation: treatment of infection, physiotherapy, postural drainage
opaque contrast medium. • Induction: IV or inhalation
Indication: • Relaxation: Scoline
• Mainly used for diagnosis and evaluation of • Maintenance: O2; N2O; halothane; IPPV.
bronchiectasis. • Once anesthesia has been established, contrast medium is introduced
• Dye: iodine containing radio-opaque substance Dionosil through a catheter placed down the ETT via ETT connector. Right side is
(Propyl iodine B.P) is used in its oil based form. studied first when both lungs are to be examined during one procedure.
Anesthesia (LA / GA): • The patient is placed in right lateral position initially for filling upper lobe and
• Local anesthesia is safer then catheter is advanced to the opposite the opening of the right middle
• But children or nervous adult require G.A. lobe with slight head up tilt. After taking x-ray thorough suctioning is done.
Drawback of G.A: • For examining left lung put patient in left lateral position.
• First: R.S function is unlikely to be optimal further • At the end of the procedure NMB is reversed and after suctioning and return
impaired with introduction of contrast medium into the of active cough reflex ETT is extubated.
tracheobronchial tree.
• Second: hazards associated with poorly illuminated x-
ray room. GRID: Question need to to answered under following headings:
• Third: because of hypoxia and airway obstruction 1. Definition
bronchoscopy should be avoided in children below 1yr 2. Indication
(only one lung if required). 3. Dye used
4. Anesthesia for bronchoscopy
5. GA for Bronchoscopy in children
6. Draw backs of GA
185

69. Anesthetic Management of patient with COAD. Dr Azam’s Notes in Anesthesiology 2013
Lab Investigations:
Chronic obstructive airway disease
1. Complete Hemogram- may be suggestive of raised haematocrit
2. Total Counts - Infection
3. Urine examination
Chronic Bronchitis: Emphysema: Defined as a 4. RBS, BU, SC
Defined by the presence pathological disorder with 5. Blood grouping and Rh typing
of production of cough on irreversible enlargement of the 6. Serum electrolytes –in suspected digitalis toxicity
most days for 3 airways distal to the terminal
7. ABG analysis-Hypoxemia, hypercarbia, acidosis
consecutive months for at bronchioles with destructive
least 2 consecutive years. process involving the lung 8. Chest X-ray
parenchyma resulting in loss of 9. ECG-Suggestive of Rt. Heart failure
elastic recoil of the lungs. 10. Spirometry and PFT: Differentiate Between obstructive or Restrictive lung
Disease
Anesthetic Management:
The pre-operative respiratory care:

Preoperative Evaluation: 1. Stop Smoking
2. Dilate the airway using:
Goal: a. Beta agonist
• To determine the severity of disease b. Anti-cholinergics
• To elucidate any reversible components such as c. Theophylline
bronchospasm or infection. d. Steroids
Basic pulmonary assessment e. Cromolyn Sodium
3. Loosen the Secretions by:
History: f. Airway hydration ( Humidification/Nebulization)
- Cough # # -Smoking g. Systemic hydration orally - 3 Liters
h. Mucolytic agents & Expectorant drugs
- Sputum # # -Occupational and
i. Antibiotics
- Dyspnea # # Family history 4. Remove secretions:
- Fever ## # -Exercise limitation j. Postural drainage
- Medications k. Coughing
Thorough cardiovascular and respiratory system l. Chest physiotherapy(percussion & Vibration)
examination is mandatory to detect signs of COPD 5. Ancillary Measures:
and/or RHF. 6. Treatment of co-existing disease
7. Treatment of Cor-Pulmonale
8. Pre-operative Digitalization 186

9. Patient Education, motivation & facilitation of

post operative care: Continuation: • Steroids:
j. Physiological preparation • 100 mg of hydrocortisone is given IV before induction & post
k.Incentive spirometry & deep breathing exercise operatively 100 mg 8th hourly for 48 hours.
l. Exposure to secretion removal maneuvers Monitoring:
m.Exercise • ECG, NIBP, SpO2, EtCO2, RR, Plateau pressures, & ABG if need be.
n.Weight gain/reduction
o.Diet supplements. Induction & maintenance of General Anesthesia:
• When ever possible endotracheal tube should be avoided as it may precipitate
Anesthetic Management: bronchospasm.
• Problems: Pulmonary mechanics following • LMA is preferable
anesthesia & Surgery: Goal:
• Vital capacity Decreased by 20 - 25 % • Smooth induction
• Residual Volume increased by 13% • Adequate depth of anesthesia
• Expiratory reserve volume decreased by 25%
• Surgery duration exceeding 3 hours Preoxygenation: 100% oxygen for 3 - 5 min
These changes are responsible for atelectasis, Induction Agents:
hypoventilation, hypoxemia & pulmonary infection. • Propofol 2 - 2.5 mg/kg IV in hemodynamically stable patients.
• ketamine 1 - 2 mg/kg IV has bronchodialtory effect in hemodynamic unstable
• Proper Selection of Anesthesia technique: patients.
• Regional Anesthesia by avoiding • After unconsciousness is produced lungs can be ventilated with either
instrumentation of airway & tracheal intubation Halothane ( More effective bronchodilator effect) or Isoflurane
is preferred when operative site is on the • LMA is preferred as it avoids instrumentation of the airway and hence
extremities or below umbilicus. bronchospasm.
• Sensory block must not exceed T6 Volatile Anesthetics:
• Halothane shown to be more effective bronchodilator than isoflurane but may
Premedication: sensitize the myocardium to cardiac dysrrhythmic effect of catecholamines &
• Benzodiazepines for anxiolysis & opioids for pain theophylline.
may be used - with careful attention to avoid
respiratory depression. Neuro muscular agent:
• Morphine is avoided - causes Histamine release • Succinylcholine 1 - 2 mg/kg or Rocuronium Rapid sequence intubation: 0.6 to 1.2
induced bronchoconstriction. mg/kg
• Antichoninergics depresses mucociliary activity & • AVOID - Atracurium & Mivacurium as they release histamine.
impair secretion clearance. • Vecuronium 0.05 mg/kg or Rocuronium Tracheal intubation: Recommended initial
• H2 receptors are avoided - Causes bronchospasm dose is 0.6 mg/kg. is safe.
• Bronchodilator to be continued till induction. • IV Lidocaine 1.5 mg/kg may be administered 1-3 min before laryngoscopy.
187

Controlled Ventilation: IPPV Reversal:

• Humidification of inspired gases - to prevent drying of • Neostigmine 0.05mg/kg + Gylcopyrolate 0.01 mg/kg IV. Careful
secretions monitoring of bronchospasm.
Extubation:
• Adequate intravenous fluid is administered to prevent
dehydration & drying of secretions. • Trachea should be extubated while anesthesia is still sufficient to
suppress hyperactive airway reflexes.
• Ventilator setting: to avoid Hypercapnia & Auto
PEEP • Prophylactic administration of inhaled β2 agonist; Ipratropium and
• Tidal volume: 8ml/kg IV lidocaine minimizes reflex bronchospasm during emergence.
• High inspiratory flow rates 1L/kg - to prolong the E Post-operative Management:
Time. Goals:
• Respiratory rate 10 to 12 breaths per minute - No • To promote adequate analgesia
Hyperventilation • To minimize the incidence of postoperative complications
• Increased E time - prolonged E time for emptying of • To prevent infections
the alveoli. • Chest physiotherapy & deep breathing exercise.
• Consider CPAP - Decreases WOB, Improves LV Compliance.
• Continuous administration of Local anesthetic with low dose
Intraoperative bronchospasm: Identification & Management: opioids via epidural catheter for post operative pain relief.
To R/O other causes of high Deepen Anesthesia: GRID: Questions needs answered under following
airway pressure & • Give 100% oxygen headings:
wheezing: • Inhalation Anesthetic 1. COAD - definitions of Chronic bronchitis &
• ET - Tube Kinking agents if BP is normal. Emphysema
• Thick secretions • Low BP - Ketamine 2. Preoperative Management
• Pulmonary edema a. Pre operative evaluation
• tension pneumothorax b. Laboratory Investigations
• Aspiration Pneumonitis Beta2 Agonist: c. Pre operative respiratory care
• Pulmonary edema • Rapid acting albuterol through 3. Anesthetic Management
• Endobronchial intubation meter dose inhaler directly in d. Problems
• bucking breathing circuit. e. Anesthetic Technique
• Aminophylline 0.5mg/kg - f. Premedication
tachyarrhythmias g. Induction
• Terbutaline S/C 0.25mg every 20 h. Maintenance + Inhalation Agents
min for 3 doses. i. Intraoperative bronchospasm &
• Epinephrine: 0.1 - 0.5 ml of 1:1000 management
S/C may be the last resort. j. Reversal & Extubation
• Steroids: hydrocortisone 4mg/kg 4. Postoperative Management.
followed by 3mg/kg. 188

70. Pulmonary Aspiration Of Gastric Contents Risk & Management. Dr Azam’s Notes in Anesthesiology 2013
Definition: Risk Factors:

• Aspiration can be defined as the inhalation of material into Predisposing factors for aspiration under general anaesthesia:
the airway below the level of the true vocal cords.
• Patient factors
Pathophysiology: • Increased gastric content
• Barrier pressure is the difference between LOS pressure a. Intestinal obstruction
(normally 20-30mmHg) and intragastric pressure (normally b. Non-fasted Drugs
5-10mmHg) and both are influenced by a number of factors. c. Delayed gastric emptying
• Lower oesophageal sphincter incompetence
LOS pressure is reduced: a. Hiatus hernia
• LOS pressure is reduced by peristalsis, vomiting, during b. Gastro-oesophageal reflux
pregnancy (a progesterone effect) as well as pathological c. Pregnancy
conditions such as achalasia, and various drugs d. Morbid obesity
(anticholinergics, propofol, thiopentone, opioids) e. Neuromuscular disease
• Decreased laryngeal reflexes
Intragastric pressure is influenced by: a. Head injury
• Intragastric pressure is increased if the gastric volume b. Bulbar palsy
exceeds 1000ml, and with raised intra-abdominal pressure • Gender
such as that occurring with pneumoperitonium during a. Male
laparoscopy. • Age
• The resulting drop in barrier pressure may increase the risk a. Elderly
of aspiration, although it should be pointed out that studies
have shown a concomitant increase in LOS pressure in • Operation factors
anesthetized patients undergoing laparoscopy, thus • Procedure
maintaining barrier pressure. a. Emergency
• The rate of gastric emptying for non-caloric clear fluids is b. Laparoscopic
rapid – the half-time being about 12 minutes. Solids however, • Position
require six hours or more to be cleared from the stomach, a. Lithotomy
displaying zero-order kinetics.
• Anaesthetic factors
• Airway
a. Difficult intubation
b. Gas insufflation
• Maintenance
a. Inadequate depth
189

Pulmonary Aspiration Of Gastric Contents Risk & Management. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Classification: PREVENTION
Aspiration pneumonitis: Preoperative fasting
• Known as Mendelsonʼs syndrome, as described by the • The commonly quoted figures of a critical volume of 25ml of aspirate,
obstetrician in 1946, this condition involves lung tissue with a pH < 2.5 being sufficient to cause aspiration pneumonitis are
damage as a result of aspiration of non-infective but very derived from unpublished work by Roberts and Shirely on Rhesus
acidic gastric fluid. monkeys, and extrapolated to humans.
• pH of < 2.5 & volume of 25 ml is required. • Current guidelines are
This usually occurs in two phases • 2 hours for clear fluids,
• Firstly desquamation of the bronchial epithelium causing • 4 hours for breast milk, and
increased alveolar permeability. This results in interstitial • 6 hours for a light meal, sweets, milk (including formula) and non
edema, reduced compliance and VQ mismatch. clear fluids.
• The second stage, occurring within 2 to 3 hours, is due to an Reducing gastric acidity:
acute inflammatory response, mediated by proinflammatory • Histamine (H2) antagonists and proton pump inhibitors (PPIs) are
cytokines such as tumour necrosis factor alpha and commonly used to increase gastric pH, although they do not affect the
interleukin 8 and reactive oxygen products. Clinically, this pH of fluid already in the stomach.
may be asymptomatic, or present as tachypnoea, • Oral sodium citrate solution reliably elevates gastric pH above 2.5, but it
bronchospasm, wheeze, cyanosis and respiratory increases gastric volume, and is associated with nausea and vomiting.
insufficiency. • H2 antagonists act by blocking H2 receptors of gastric parietal cells,
thereby inhibiting the stimulatory effects of histamine on gastric acid
Aspiration pneumonia: secretion.
• This occurs either as a result of inhaling infected material or • PPIs on the other hand, block the ʻproton pumpʼ of the same cell,
secondary bacterial infection following chemical pneumonitis. inhibiting the stimulatory actions of histamine, gastrin and acetylcholine.
• It is associated with typical symptoms of pneumonia such as An oral H2 antagonist must be given 1-2 hours before anaesthesia, and a
tachycardia, tachypnoea, cough and fever, and may be PPI, 12 hours in advance.
evidenced by segmental or lobar consolidation (classically • A recent meta-analysis by Clark et al suggested that ranitidine was
right middle lobe) on chest radiography. superior to PPIs in both reducing gastric fluid volume and acidity. Its use
• The disease process is similar to a community acquired is recommended in patients at risk of aspiration only, not routinely.
pneumonia although the complication rate is higher, with • Metoclopramide has a prokinetic effect promoting gastric emptying, but
cavitation and lung abscess occurring more commonly. there is little evidence to support its use.
• It does however, remain part of the usual pre-medication for Caesarean
Particulate-associated aspiration: section under general anaesthetic.
• If particulate matter is aspirated, acute obstruction of small
airways will lead to distal atelectasis.
• If large airways are obstructed, immediate arterial hypoxaemia
may be rapidly fatal.
190

Pulmonary Aspiration Of Gastric Contents Risk & Management. Continuation: Dr Azam’s Notes in Anesthesiology 2013
Rapid Sequence Induction (RSI) Nasogastric tube placement

• It has been shown that most cases of aspiration occur on • Patients for emergency theatre with intestinal obstruction frequently have
induction and laryngoscopy, hence the following is of the a nasogastric tube in situ.
utmost importance. • There is evidence from cadaver studies that this does not alter the
• For patients at high risk of aspiration, a RSI is the induction of efficacy of cricoid pressure.
choice unless presented with a sufficiently difficult airway to • Furthermore it can be useful to empty the stomach before induction of
warrant an awake fibreoptic intubation. anaesthesia.
• The patient should be on a tilting trolley, with suction to hand. • Studies have shown that there is no significant difference between the
• Three minutes of pre-oxygenation precede the administration incidence of gastroesophageal reflux with large or small bore tubes.
of an induction agent, cricoid pressure (discussed below) and
the rapidly acting muscle relaxant succinylcholine. MANAGEMENT
• This avoids the need for bag-mask ventilation and the • Head down tilt
possibility of gastric insufflation. • Oropharyngeal suction
• Adequate depth of anaesthesia is important to avoid • 100% oxygen
coughing, laryngospasm and vomiting. • Apply cricoid pressure and ventilate
• Cricoid pressure is not released until confirmation of • Deepen anaesthesia/perform RSI
appropriate placement of the tracheal tube with the cuff • Intubate trachea - Mechanical Ventilation with PEEP and FIO2
inflated. management.
Cricoid pressure • Release cricoid once airway secured
• First described by Sellick in 1961, cricoid pressure remains an • Tracheal suction
essential manoeuvre performed as part of RSI despite significant • Consider bronchoscopy
controversy. Bronchodilators
•
• The aim is to compress the oesophagus between the cricoid ring
cartilage and the sixth cervical vertebral body thus preventing
reflux of gastric contents.
• The force recommended is 30N, or that required to close the
oesophagus without distorting the airway.
• This latter complication is the greatest limiting feature of the
manoeuvre, causing malalignment, distortion of the cricoid ring and
possible closure of the vocal cords.
• Even when applied correctly there is doubt as to its efficacy, simply
causing anatomical displacement of the oesophagus in some
people, and non compression in others.
• In addition, manometry studies have shown it to reduce LOS tone
thus reducing barrier pressure.
• Cricoid pressure should be released in the case of active vomiting
to avoid oesophageal rupture.
191

• This method not only oxygenates the blood, but also supports the
Indications:
71. Extracorporeal Membrane Oxygenation ( ECMO) cardiac function of the patient,Dr
because
Azam’sthe blood
Notes in return to the aortic
Anesthesiology 2013
(clinical criteria used to select infants for ECMO) arch is supplied by ECMO machine. Hence this route is most
commonly used.
• Those infants who are at 80% risk or greater of mortality if
Definition: Veno-venous:
conventional
• ECMO meansmethods are used. of blood, outside the body through a
oxygenation In this route, blood is removed from the RA via a catheter inserted in
•Veno-venous:
• Candidates should have
membrane oxygenator. a reversible
It is usedlung diseasein whom adequate
in patients # the right IJV. The
In this oxygenated
route, blood is returned
blood is removed to the
from the RA RA
viathrough a
a catheter
• Should be free of significant
oxygenation cardiac
by conventional disease.have failed.
methods catheter inserted via the femoral vein. It doesnʼt support cardiac
• P(A-a)O gradient.
Indications:
2 605 to 620mm at 100%O2,for 4 to 12 hours. inserted in the right IJV. The oxygenated blood is returned to the RA
output
• -Oxygen index
(clinical =Mean
criteria usedairway pressure
to select infants ×FiO /PaO2 = 0.3to 0.6 for
for 2ECMO) through a catheter inserted via the femoral vein. It doesnʼt support
½ to• 6Those
hrs infants who are at 80% risk or greater of mortality if cardiac output
• PaO2 conventional
35 to 50 mm methods
of mg forare
2 toused.
12 hrs. pH < 7.25 for 2hrs.
• Candidates should have a reversible lung disease Patients IJV (Out)
Contraindications:
• Should be free of significant cardiac disease.
1. Infants <34 weeks of gestation.
• P(A-a)O2 gradient. 605 to 620mm at 100%O2,for 4 to 12 hours.
2. Weighing <2000gms.
• Oxygen index =Mean airway pressure ×FiO2 /PaO2 = 0.3to 0.6 for
3. Having
½ toevidence
6 hrs of intracranial Hemorrhage (because of heparin Carotid Artery (In) Reservoir Bladder
use).
• PaO2 35 to 50 mm of mg for 2 to 12 hrs. pH < 7.25 for 2hrs.
4. Mechanical ventilation used for >2 weeks prior to initiation of
Contraindications: ECMO Circuit
ECMO
1. Infants <34 weeks of gestation.
5. Coagulopathy.
2. Weighing <2000gms.
3. Having evidence of intracranial Hemorrhage (because of Roller Pump
Heat Exchanger
heparin use).
!"#$%&'()) )
4. Mechanical ventilation used for >2 weeks prior to initiation of Membrane
! "#$%&'()#(*'+,
ECMO
! "#$%&-#$%./, Oxygenator
5. Coagulopathy.
Methods: # #
• Veno-arterial
• Veno-venous
Veno-arterial:
• Blood is drawn from the right atrium via IJV. The oxygenated
blood is returned to the aortic arch via the right CCA.
• This method not only oxygenates the blood, but also supports 6
the cardiac function of the patient, because the blood return to
Dr Azam’s Notes in Anesthesiology
the aortic 2013
arch is supplied by ECMO machine. Hence this route
is most commonly used.
192

Extracorporeal Membrane Oxygenation ( ECMO). Continuation: Dr Azam’s Notes in Anesthesiology 2013
Complications:
ECMO circuit:
• It utilizes a modified heart lung bypass machine,
consisting of a venous blood drainage reservoir, a blood Physiologic:
pump, the membrane oxygenator where the exchange of Mechanical:
• CNS: Intracranial Hemorrhage (14%), bleeding ;
O2 and CO2 takes place, and a heat exchanger to seizures • Failure of pump,
maintain temperature. rupture of tubing,
• Respiratory: Pulmonary oedema, pulmonary
failure of the
hemorrhage
membrane and
• CVS: hypo/hypervolemia leading to hypo/HTN
difficulties with
• Alteration in R-Angiotensin – aldosterone cycle,
the cannulas.
secondary to the non pulsatile perfusion, may
lead to Renal complications.
• Hematological: Anaemia, leucopenia,
thrombocytopenia (because of consumption in
membrane oxygenator)
• Infections.
Disadvantages: "
• Expensive, complex
• Needs monitoring with specially trained personnel. One of the
patient and one for the circuit (IVOX needs only one)
• Requires daily use of blood and blood products (none in IVOX)
193

72. Pulmonary Hypertension Dr Azam’s Notes in Anesthesiology 2013
ESC Guidelines 2497
Definition: Classifications:
• It528
is defined as Increased in mean pulmonary Clinical
Artery pressure
Table 3 Haemodynamic definitions ofResearch in Cardiology,Table
pulmonary Volume 96, Number
4 Updated 8 classification
clinical (2007) of pulmonary
(PAP) ≥ 25 mm Hg at rest and >
hypertension30
a mm Hg on ©exercise.
Steinkopff Verlag 2007 hypertension (Dana Point, 20081)
Pathophysiology:
Definition Characteristics Clinical group(s)b 1 Pulmonary arterial hypertension (PAH)
................................................................................ 1.1 Idiopathic
Pulmonary
postcapillary
hypertension
Mean PAP
!25 mmHg
All Genetic variations that are particularly found in
1.2 Heritable
1.2.1 BMPR2
(PH)
................................................................................
cases of familial (FPAH) and idiopathic PAH (IPAH)
1.2.2 ALK1, endoglin (with or without hereditary
Pre-capillary PH Mean PAP 1. Pulmonary arterial include the signaling pathways of transforming
haemorrhagic telangiectasia)
1.2.3 Unknown
mmHg hypertension
Diseases !25
of left heart
PWP "15 mmHg 3. PH due to lung diseases
growth factor-! (Bone Morphogenic Protein Recep-
1.3 Drugs and toxins induced
1.4 Associated with (APAH)
LVEDP , PCP
CO normal or 4. Chronic tor 2; BMPR2) and serotonin (5-hydroxitryptamine
1.4.1 Connective tissue diseases
Grading of PAH:
reducedc thromboembolic PH 1.4.2 HIV infection
5. PH with unclear and/or transporter; HTT) [53, 54]. Nevertheless,
1.4.3 Portal hypertension • Mild =since the
26 to 40 mm Hg
multifactorial
mechanisms
mutations of BMPR2 and 5-HTT are •only
1.4.4 Congenital heart disease
1.4.5 Schistosomiasis
15 to= 20%
Moderate 41 to 55 mm Hg
................................................................................
Post-capillary PH Mean PAP 2. PH due to left heart
penetrant, they may only be considered
1.4.6 Chronic haemolytic anaemia
1.5 Persistent pulmonary hypertension of the newborn
• as predis-
Severe = > 55 mm Hg
!25 mmHg disease posing
. . . . . . . . . . . . . . . .factors,
. . . . . . . . . . . . . . . . . . . . . and
1 Pulmonary veno-occlusive disease and/or pulmonary
0
. . . . . . . . . . . . .gene-gene
. . . . . . . . . . . . . . . . . . . . . . . . . . . .interactions
.. and/or
PWP .15 mmHg
CO normal or
gene-environment
capillary haemangiomatosis interactions (risk factors, asso-
................................................................................
precapillary reducedc ciated
2 Pulmonary diseases) hypertensionare due torequired left heart diseasefor the development of
PAP
Passive
Reactive (out of
TPG "12 mmHg
TPG .12 mmHg
the 2.2 disease
2.1 Systolic dysfunction
Diastolic dysfunction in both familial and sporadic PAH [19].
. . .The
. . . . . . . . . . early
. . . . . . . . . . . . .stages
. . . . . . . . . . . . . . . .of
. . . . . PAH
. . . . . . . . . . . .are
. . . . . . . . .characterized by primar-
2.3 Valvular disease
Right heart proportion)
failure ............
Cor pulmonale
a
b
All values measured at rest. ily functional
3 Pulmonary hypertension due to lung diseases and/or
hypoxia
alterations of the pulmonary vasculature
Death
According to Table 4.
c
High CO can be present in cases of hyperkinetic conditions such as (vasoconstriction).
3.1 Chronic obstructive pulmonary Progression
disease of the disease at the
systemic-to-pulmonary shunts (only in the pulmonary circulation), anaemia, 3.2 Interstitial lung disease
hyperthyroidism, etc. later3.3stages Other pulmonary is associated diseases with mixed restrictive with and morphological changes
CO ¼ cardiac output; PAP ¼ pulmonary arterial pressure; PH ¼ pulmonary
Fig. 1 Pathogenesis of pulmonary hypertension. Postcapillary PH, in which
hypertension; PWP ¼ pulmonary wedge pressure; TPG ¼ transpulmonary particularly obstructive pattern
3.4 Sleep-disordered breathing
of the small pulmonary arteries (“vascular
pressure gradient (mean PAP – mean PWP).
diseases of the left heart (atrial, ventricular, valvular) cause pulmonary ve- remodeling”) 3.5 Alveolar hypoventilation
3.6 Chronic exposure to high altitude
that share disorders a relatively homogeneous his-
nous congestion, which leads to secondary elevation of PCP and PAP, is dis- tomorphological
3.7 Developmental abnormalities pattern. This process of pulmonary
tinguished from precapillary hypertension
PH, where(PAH, group 1). In this case the diagnosis requires
an isolated elevation of PAP occurs ................................................................................
with normal PCP. Precapillary
the exclusion of all other groups of PH. vascular
4 Chronic thromboembolic remodeling pulmonary involves hypertension all layers of the vessel wall
† PAH (Tables 4 and 5) representspulmonale,
PH may lead to cor the condition right heart ................................................................................
described more
failure, and death extensively due to the availability of specific treatments. Based on
and5 PHis withcomplicated
unclear and/or multifactorial by cellular mechanisms heterogeneity within
5.1 Haematological disorders: myeloproliferative disorders,
the publication of recent randomized controlled trials (RCTs) a each compartment splenectomy. (reviewed in [33, 34]). Indeed, each
new treatment algorithm with updated levels of evidence and
grades of recommendation and the current approval status in differ-
cell type (endothelial cells, smooth muscle cells, fibro-
5.2 Systemic disorders: sarcoidosis, pulmonary Langerhans cell
histiocytosis, lymphangioleiomyomatosis,
and/or above 30 mmHg during exercise in the setting
ent geographic areas have been provided. Definitions for the evalu- blasts), as well asvasculitis
neurofibromatosis,
5.3 Metabolic disorders: glycogen storage disease, Gaucher
inflammatory cells and platelets, may
of normal or reduced cardiac output and normal PCP
ation of a patient’s severity, treatment goals, and follow-up strategy play a significant disease, thyroid disorders role in this condition. The pathogenic
have been also included. The specific characteristics of the different
[6, 8, 23, 24]. Pulmonary vascular resistance (PVR) is
types of PAH including paediatric PAH have been highlighted. processchronic is renal driven
5.4 Others: tumoural obstruction, fibrosing mediastinitis,
failure on dialysis by several mediators including en-
elevated above 3 mmHg/l/min (Wood units). This de-
† The other four main clinical groups of PH, i.e. pulmonary dothelin-1,
ALK-1 ¼ activin receptor-like prostacyclin,kinase 1 gene; APAH ¼ associated and nitric pulmonary oxide-mediated sig- 194
veno-occlusive disease (PVOD, group 10 ), PH due to left heart
finition is based on invasive measurements by right
disease (group 2), PH due to lung diseases (group 3), and
nals, that all play a
arterial hypertension; BMPR2 ¼ bone morphogenetic protein receptor, type 2;
HIV ¼ human immunodeficiency virus; PAH ¼ pulmonary arterial hypertension.
central role (reviewed in [44]). These
Dr heart
Azam’scatheterization.
Notes in However, the initial diagnosis
Anesthesiology 2013 pulmonary hypertension (CTEPH,
chronic thromboembolic factors represent the therapeutic targets of the currently
of PH is mostly based on non-invasive tests such as
group 4 ) have been discussed individually while the heterogen-
available
PAP at rest is 14 medical
+ 3 mmHg, with treatment an upper limit options of normal of (Fig. 2).
Pulmonary Hypertension.Continuation: Dr Azam’s Notes in Anesthesiology 2013
2514 ESC Guidelines
Clinical Features: Treatment:

• Breathlessness
• Weakness
• Fatigue
• Pulmonary Insufficiency
• Features of Heart Failure
(Graham - Steell Murmur)
Diagnostic Work up:

• Chest Radiography
• Prominent pulmonary arteries
• Right atrial & Ventricular enlargement
• Parenchymal lung disease
• 2D ECHO
• P - Pulmonale - Right Atrial Hypertrophy
• Right Axis deviation
• Right Ventricular Strain/Hypertrophy
• Complete / Incomplete RBBB
• PFT:
• Obstruction or Restriction
• Low diffusion capacity
• V/Q Scan:
• Ventilation/Perfusion Mismatch.
Figure 2 Evidence-based treatment algorithm for pulmonary arterial hypertension patients (for group 1 patients only). *To maintain arterial blood
O2 pressure !8 kPa (60 mmHg). †Under regulatory review in the European Union. §IIa-C for WHO-FC II. APAH ¼ associated pulmonary arterial
hypertension; BAS ¼ balloon atrial septostomy; CCB ¼ calcium channel blocker; ERA ¼ endothelin receptor antagonist; IPAH ¼ idiopathic pulmon-
ary arterial hypertension; PDE5 I ¼ phosphodiesterase type-5 inhibitor; WHO-FC ¼ World Health Organization functional class.
195
three times higher.131,132 It is, however, more convenient for the the ERA bosentan or the phosphodiesterase type-5 inhibitor silde-
Dr Azam’s Notes in Anesthesiology 2013 patient because the reservoir can be changed every 48 h as com- nafil was recently completed, and preliminary data show improve-
pared with 12 h with epoprostenol. A phase III RCT (TRIUMPH) of ments in exercise capacity.133 Oral treprostinil is currently being
Pulmonary Hypertension.Continuation: Dr Azam’s Notes in Anesthesiology 2013
Anesthetic Management: Post operative:

• Anesthetic Consideration: Increased Risk of sudden death due to worsening PAh, Embolism
• Increased risk of right heart failure Dysrrhythmias
• Medication should be continued throughout the perioperative Aggressive postoperative monitoring required.
period.
• Avoid Hypoxia, Hypercarbia & acidosis must be controlled, as
they increase PVR.
• Availability of NO (OR) Prostacyclin to be kept available.
Monitoring: 1. Definition
• ECG, Pulse Oximetry, NIBP, EtCO2, CVP, Urine output & 2. Pathophysiology
invasive blood pressure monitoring & Temperature. 3. Classification & Grading
4. Clinical Features
Regional Anesthesia: 5. Diagnostic Workup
• Should be considered when ever possible. 6. Medical Management
7. Anesthetic Management
General Anesthesia: 7.1. Anesthetic Consideration
Induction: 7.2. Monitoring
• Propofol, Thiopentone & Fentanyl 7.3. Regional Anesthesia
• Avoid - Atracurium - Histamine release. 7.4. General Anesthesia
7.4.1. Maintenance
Maintenance: 7.4.2. Vasodilators
• Inhalational agents, NM Blockers can be used. 7.4.3. Post operative Management.
• Intraoperative hypotension may be treated with either Nor-
Epinephrine & Phenylephrine.
Vasodilators: To be kept ready.

• NTG
• NO
• Milrinone
• Prostacyclin
196

73. What is Oxygen Delivery? Classify Oxygen Delivery systems. Discuss the role of venturi Mask Dr Azam’s Notes in Anesthesiology 2013
in oxygen therapy?
Oxygen Delivery (DO2): Advantages:

• Is the amount of oxygen delivered to the whole body from the • FIO2 is predictable and accurate
lungs ml/min. • No need for airtight fitting mask
• No rebreathing
Calculation: • No apparatus dead space
Oxygen Delivery = Cardiac Output X Hb Conc. X % of saturation X 1.31 • The enrichment ratio is fixed and independent as patient ventilating
• 1.31 (ml of O2/gm Hb) patters
• Easy to use
Classification of Oxygen delivery systems: • Economical because low flow of O2 can be used.
Oxygen Therapy
Indications of Venturi Mask:
Classification
• For documented hypoxia to increase PaO2
• Inadequate ventilating efforts
• Increased shunt e.g: COPD
• Pulmonary edema
Variable Fixed performance
performance devices
• Pulmonary Consolidation
devices • ARDS.
Disadvantages:
Facial Discomfort
No capacity – nasal
Cant be worn during feeding coughing or speaking
catheters, cannulae Large capacity – device / FiO2 can be increased if entrainment ports are obstructed by the
mask with bag
patient.
Role of Venturi Mask in Oxygen Therapy:

• Comes in 6 different oxygen concentrations 24% to 50%.
HAFOE systems
• Colour coded devise
Small capacity – Anaesthesia circuits • It increases the rate of flow of oxygen & air to above the patients
masks Ventilators inspiratory flow rates.
• It can provide a constant O2 concentration no matter how quickly or
slowly the patients breath.
• May decrease work of breathing & dyspnea.
• May correct hypoxia and decrease the stimulus to Increase CO.
197

74. Difference between the ODC curve & CO2 Curve? Dr Azam’s Notes in Anesthesiology 2013
Hb Oxygen Dissociation Curve CO2 Dissociation Curve
Carries Oxygen from lungs to tissue Carries CO2 from tissue to lungs
Oxygen is carried in Dissolved & Oxyhemoglobin form. Its carried in 3 Forms:

1. Dissolved CO2
2. As bicarbonate (70%)
3. As Carbamino compound (25%)
No Haldane effect Haldane effect seen (to be explained)

No Chloride shift Chloride shift seen (to be explained)
No Hamburger effect Hamburger effect Seen (to be explained)
Bohr Effect is seen & Explain Double Bohr Effect.
198

75. Modes of Ventilation during Bronchoscopy. Dr Azam’s Notes in Anesthesiology 2013
There are four basic methods of ventilation management for rigid

bronchoscopy:
1. Spontaneous ventilation: The addition of topical anesthesia or
nerve blocks to the airway decreases the tendency to breath
hold and cough when volatile anesthetics are used.
2. Apneic oxygenation: (with/without insufflation of oxygen). This
requires thorough pre-oxygenation, and the anesthesiologist will
have to interrupt surgery to ventilate the patient before
desaturation occurs. This should allow the surgeon working
intervals of 3 minutes or longer depending on the underlying
condition of the patient.
3. Positive-pressure ventilation: via a ventilating bronchoscope
(Fig. 59-36). This allows the use of a standard anesthetic circuit
but may cause significant air leaks if there is a discrepancy
between the size of a smaller bronchoscope and a larger airway.
4. Jet ventilation: This can be performed with a handheld injector
such as the Sanders injector or with high-frequency ventilator.
These techniques are most useful with intravenous anesthesia
because they entrain gas from either the room air or an
attached anesthetic circuit and the dose of any volatile agent
delivered will be very uncertain.
199

76. Indications, Contraindications, Preoperative consideration& Anesthetic Dr Azam’s Notes in Anesthesiology 2013
Management of Mediastinoscopy.
Mediastinoscopy: Anesthetic Management:

• Performed via the central approach, entering through 3 cm Preoperative Preparation & Pre-Medications:
incision in the suprasternal notch. 1. Stop Smoking & 10 Points to be written. (Refer page 108)
2. Short acting Benzodiazepines - Caution use. Avoid if tracheal
Indications of Mediastinoscopy: obstruction is suspected.
1. Inter Bronchial & Inter tracheo-bronchial opacities.
2. Poly-lobulated Mediastinal opacities Anesthesia:
3. The isolated opacity 1. IV - Large Bore
4. Pulmonary lesion - To look for mediastinal node for diagnosis. 2. Blood to be kept ready - Risk of Hemorrhage.
5. In bronchopulmonary cancer & staging of lung cancer. 3. Pre-oxygenation
4. IV Induction
5. If respiratory obstruction - an awake intubation under LA technique
Contraindications: 6. 20° Head up position to decrease venous congestion & drainage.
• SVC Syndrome 7. Armoured tube can be used or At times double lumen endotracheal
• Distended veins tube to be used.
• Cardiovascular disease 8. Long standing mass FOB to be performed prior extubation to rule
• Cervical Spine disease out tracheomalacia
• Radiation
Monitoring:
Preoperative Consideration: 1. Pulse
1. Most of the patients are smokers, co-existing morbidity 2. ECG
including HTN, IHD, PVD & pulmonary disease. 3. Blood pressure
2. LArge mediastinal mass may compress the adjacent 4. Pulse oximeter - Right hand - Because innomiate artery supply the
structures. right arm & is commonly compressed. ( Bracheocephalic
3. Respiratory tract infection. Compression)
5. EtCO2
Investigations: 6. Urine output
• Hb, biochemistry, ECG, Chest X - Ray, CT - scan for location of 7. Ventilator Graphics: PAP, Plateau pressure.
the tumour. Tracheal complications, PFT, 2DEcho & ABG.
200

Indications, Contraindications, Preoperative consideration& Anesthetic Management of Dr Azam’s Notes in Anesthesiology 2013
Mediastinoscopy. Continuation:
Anesthetic Management of Mediastinoscopy Hemorrhage:

1. Stop Surgery and pack the wound - Risk of hemodynamics
collapse.
2. Begin the resuscitation and call for help both anesthetic &
surgical.
3. Obtain large bore vascular access in the lower limb.
4. Place arterial line
5. Prepare for massive hemorrhage protocol & blood warmers
and rapid infusion.
6. Obtain cross matched blood in the operating room.
7. Place a double lumen tube or bronchial blocker if the surgeon
believes thoracotomy is possible.
8. Once the patient condition is stabilized and all the preparations
are made, the surgeon can re - explore the cervical incision.
9. Convert to sternotomy or thorocotomy if indicated.
201

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What are the indications for mediastinoscopy?

What are the indications for mediastinoscopy?

What are the contraindications for mediastinoscopy?

What are the contraindications for mediastinoscopy?

Dr.

To Mohammed Shafiulla, my father, my oxygen, companion, and best friend; for

Dr Azam’s Notes in Anesthesiology 2013

A NOTE TO THE READER

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

55.Bronchial Blockers - 155

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

• During phonation, the vocal cord meets in midline, on inspiration Trachea: C5 to C 6

Dr Azam’s Notes in Anesthesiology 2013

• These irregular dichotomous branching for about 23 generations

There are 3 types of cells covering the alveolar surface.

Dr Azam’s Notes in Anesthesiology 2013

Functions: Major division of lungs:

Dr Azam’s Notes in Anesthesiology 2013

Arterial supply of lungs: Clinical significance of surfactant:

Dr Azam’s Notes in Anesthesiology 2013

RESPIRATORY MECHANICS Muscular forces needed to expand the respiratory system:

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

• Spontaneous ventilation: at the start of inspiration intrapleural

Dr Azam’s Notes in Anesthesiology 2013

Breath holding: Compliance:

Dr Azam’s Notes in Anesthesiology 2013

PRESSURE VOLUME LOOP FOR THE RESPIRATORY SYSTEM

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

DETERMINANTS OF LUNG VOLUME AND ITS SUBDIVISIONS:

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Central sensors: (central chemoreceptors – CR) Golgi tendon organs:

Dr Azam’s Notes in Anesthesiology 2013

Ventilation: Alveolar VD:

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Pulmonary vascular resistance (PVR):

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Distribution of V/Q ratios in the lung: Diffusion of gases:

Dr Azam’s Notes in Anesthesiology 2013

Factors influencing oxygenation at different levels: ! Transport of Oxygen in the blood:

Dr Azam’s Notes in Anesthesiology 2013

Characteristic of HbO2 binding: Oxygen Hb dissociation curve: (ODC)

Dr Azam’s Notes in Anesthesiology 2013

PH (Bohr Effect): Oxygen stores:

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Dr Azam’s Notes in Anesthesiology 2013

Inhalational anesthetics: Type to enter text

Dr Azam’s Notes in Anesthesiology 2013

d) Expiratory centre: situated ventrally

Dr Azam’s Notes in Anesthesiology 2013