MED-SURG: SA node sends

Cardiovascular/
impulse

Right and Left

Hematologic Conditions
Right and Left atria
ventricles
contracts
pumps/contracts

CARDIOVASCULAR SYSTEM
 HEART  Controls BLOOD  Carries
OXYGEN  Promotes TISSUE PERFUSION Passes to Purkinje AV node sends
Fibers impulse
4 CHAMBERS
Right Atrium Left Atrium
Right Ventricle Left Ventricle
Unoxygenated Blood Oxygenated Blood
divides signals to
passes to Bundle of
Right and Left
His
AV Valves ventricles

Bicuspid Valve/ Tricuspid Valve

Mitral Valve
LBM = Left is Bicuspid/Mitral valve 1) SINOATRIAL NODE
 The natural pacemaker of the heart
Semilunar Valves  LOCATION: Upper portion of right
Pulmonic Valve Aortic Valve atrium
2) ATRIOVENTRICULAR NODE
Locations of Valves  The gatekeeper of the heart
“Please Answer My Telephone”  It decides what impulses to let
through
Pulmonic valve Left side, 2nd  LOCATION: border of the right
intercostal space atrium and the right ventricle
Aortic Valve Right side, 2nd 3) BUNDLE OF HIS
intercostal space 4) RIGHT AND LEFT BUNDLE BRANCHES
Bicuspid/Mitral Left side, 4th-5th 5) PURKINJE FIBERS
Valve intercostal space
NSAIDs or COX Inhibitors
Tricuspid Valve Left side; 3rd-4th (Carbonic Oxidase Inhibitors)
intercostal space
COX-1 Inhibitor COX-2 Inhibitor
Receptor of body that Receptor of the body that
Conduction System of the Heart (PROCESS)
produces protective produces
lining prostaglandins.
 GI lining
 Kidneys
NEPHROTOXIC = prone Prostaglandin
to renal failure  carries stimuli
Prone to ULCERS Brain = interprets stimuli
 Pain
 Fever
 Inflammation
WITH meals ANALGESIC
(prevent ulcers)
ANTIPYRETIC
Increase Oral Fluid
Intake ANTI-INFLAMMATORY
(prevent renal problems)
 Atherosclerosis Arteriosclerosis 2) Unstable
Fat deposits/Plaque Hardening of blood Angina/Preinfarction
vessels
 Unexpected
 Duration: >15 minutes
 Not relieved by REST
 This can lead to Myocardial
Infarction
3) Variant Angina/Prinzmetal
 PAIN during REST
4) Nocturnal Angina
 PAIN occurs at NIGHT
5) Silent Angina
 NO PAIN
 Observed at the ECG tracing:
Myocardial Injury Elevated ST Segment
Myocardial Ischemia Inverted T Wave
Myocardial Infarction Pathologic Q Wave

Angina Pectoris Atherosclerosis Fat deposits

Poor Oxygen Poor Blood

Narrowing  MANAGEMENT: BACONS
Supply Supply
a) Beta-Adrenergic Blockers “-olol”
Beta-1 (B1) Beta-2 (B2)
Stimulates Stimulates LUNGS
HEART
Poor Tissue Anaerobic Increase HR
Ischemia
Perfusion Respiration

Increase Bronchodilation
Cardiac
Workload
produces lactic Increase BP
CHEST PAIN (+) Pain
acid  BETA-BLOCKERS are:
 GOOD for the HEART
 BAD for the LUNGS
ANGINA PECTORIS  Blocks stimuli:
 Decreases BP
(Antihypertensive)
 Decreases RR
 Levine’s Sign: Cardinal Sign/Hallmark Sign (Bronchoconstriction)
 TYPES:  Decreases HR (Anti-
arrhythmia)
1) Stable Angina b) Aspirin “Acetylsalicylic Acid”
 Predictable/Expected  NSAID and Antiplatelet
 Duration: <15 minutes
 Relieved by REST
 Occurs during strenuous activities
 d) OXYGEN Supplementation
has e) Nitroglycerin (Drug Of Choice)
ASPIRIN NSAIDS Anticoagulant  ROUTES:
Effect a. SL (under the tongue)
 EFFECTIVENESS: burning
sensation under the
tongue (Stingy taste)
Decreases
decreases  Doses: 3 MAX doses
Platelet Antiplatelet
blood viscosity  Interval: 5 minutes
coagulation
 MAXIMUM: 15 minutes
 Container: Dark/amber
container (photosensitive)
 Expiration: 6 months
PREVENT CLOT prone to
FORMATION BLEEDING  Change tablets TWICE a
year
 Monitor Signs & Symptoms of  S/E:
BLEEDING:  Hypotension
a. Epistaxis through Headache
b. Hematemesis  Dizziness
c. Petechiae  PRIORITY: Safety
d. Ecchymosis b. PO (tablets)
e. Hematuria c. IV
f. Melena d. PATCH
g. Hematochezia  Place: PROXIMAL to
Melena Hematochezia HEART (Non-hairy area)
Dark-red Bright-red  ROTATE the sites
Old RBC Fresh RBC (prevents tolerance and
UPPER GI LOWER GI skin irritation)
 EFFECTIVENESS:
absence of chest pain
 S/E:
 Hypotension
c) Calcium Channel Blockers “-dipine” through Headache
 Examples:  Dizziness
a. –dipine medications  PRIORITY: Safety
b. Diltiazem f) SETUP resting time
c. Verapamil  Schedule resting periods with the
patient

MYOCARDIAL INFARCTION
CALCIUM-CHANNEL goes to Blood
BLOCKERS Vessels

MI Atherosclerosis

Increases Blood Vasodilation

Supply (Vasodilator)
Uncontrolled Angina
Ischemia (Unsatable
Angina/Preinfarction)

Decrease HR (Anti- Decrease BP

arrythmia) (Antihypertensive)

Infarction Necrosis
  SIGNS & SYMPTOMS: DANCEPAD
a) Dyspnea Tissue Death of Left
b) Anxiety (Feeling of doom) AP, HPN, MI, CHF, Ventricle
Atherosclerosis
c) Nausea & Vomiting CVA
d) Crushing Chest pain (radiating to the LEFT
shoulder and LEFT arm)
e) Elevated Temperature
f) Pallor
g) Arrhythmia
h) Diaphoresis
 DIAGNOSTICS
a) ECG Narrowing Fat deposits
Myocardial Injury Elevated ST Segment
Myocardial Ischemia Inverted T Wave
Myocardial Infarction Pathologic Q Wave
b) Cardiac Enzymes (Troponin I)
 Confirmatory test
c) CK-MB
d) Lacto dehydrogenase
BEFORE:
e) Myoglobin
Anticoagulant
 MANAGEMENT: MONATAS Blood Clot
a) Morphine Sulfate (Drug of Choice) Aspirin
PREVENTS Clot
 Class: Opioid Analgesics/Narcotics
 Use: Treats SEVERE chest pain
 S/E: CNS depressant
 Affects: Medulla Oblongata
Depression
a. HR AFTER:
b. BP
c. RR (Respiratory Depression) Thromoblytic
 MANAGEMENT: Streptokinase
DISSOLVES Clot
a. Check RR BEFORE administering
b. Check Reflexes (DTR reflexes) e) Thrombolytic
b) Oxygen Supplementation  DISSOLVES Clot
c) Nitroglycerin  E.g. Streptokinase, Urokinase
d) Aspirin

f) Anti-arrythmias
 DIGITALIS (Digoxin)
a. (+) INOTROPIC effect
 Increases force of contraction
 DIURETIC effect (increases
urine output)
 Potassium must be within
NORMAL levels (3.5-5.5
mEq/L)
b. (-) CHRONOTROPIC effect
 Decreases PR (Bradycardia)
 Withhold if PR is < 60 bpm
c. CUMULATIVE effect
 Has TOXICITY
 Signs of TOXICITY: VANDAB
1) Vision changes
(flickering flashes of
light/halo visions)
 2) Anorexia
3) Nausea & Vomiting
4) Diarrhea
5) Abdominal cramps
(earliest sign) Target: Reason of
6) Bradycardia RAAS Vasoconstriction Activation: Low
d. Slows conduction through AV node (Increase BP) BP
e. MAJOR CONCERN: DIGITALIS
TOXICITY
f. ANTIDOTE: Digoxin Immune fab
(DIGIBIND) Produces Renin by Poduces
g. Most reliable indicator of BETTER Angiotensinogen
juxtaglomerular Angiotensinogen
goes to kidneys
TISSUE PERFUSION: cells in Kidneys by Liver
 Urine output
h. Contraindications (potentiates
TOXICITY):
 Old age
 Acute MI Converts to Angiotensin I goes converts to
 Severe arrhythmia Angiotensin I to Lungs by ACE Angiotensin II
g) Stool Softeners
 Prevents Valsalva maneuver

HYPERTENSION Angiotensin II
 Increase of Blood Pressure promotes
activates adrenal Detects Adrenal
 TYPES: cortex glands Increases BP
a) Primary/Essential HPN (potent
vasoconstrictor)
 Unknown Cause
b) Secondary/Non-Essential HPN
 Known Cause
adrenal cortex
CAUSES of HYPERTENSION: Aldosterone
produces promotes water
promotes sodium
a) SMOKING mineralocorticoids :
retention retention
ALDOSTERONE
 due to vasoconstricting effects of
nicotine
 Secondary HPN
b) ELDERLY
 Primary HPN
increases BP
c) COARCTATION OF AORTA
d) OBESITY
 Primary HPN
e) Na+ EXCESS (Na+ Retention)
 Secondary HPN  TYPES: ABCD
f) DIABETES 1) ACE INHIBITORS “-pril”
g) ATHEROSCLEROSIS  Blocks ACE
h) RENAL FAILURE  Promotes Vasodilation (Decrease
i) INCREASE THYROID & ADRENAL BP)
FUNCTIONS 2) BETA-ADRENERGIC BLOCKERS
3) CALCIUM-CHANNEL BLOCKERS
MANAGEMENT of HPN: 4) DIURETICS
a) ANTIHYPERTENSIVES:  Use: Promotes Urine Excretion
 Decrease BP  S/E: Increase Urine Output
 Body fluids: DOWN
 Blood Volume: DOWN
 Blood Pressure: DOWN
 TYPES:
 1) POTASSIUM-SPARING  The Rh NEGATIVE person will regard
E.g. Aldactone, the (+) D antigen blood as an
Spironolactone INVADING ORGANISM.
Increases Na+ and Water  DEFENSE MECHANISM of the Rh (-)
excretion; Retains K+ person:
2) LOOP DIURETICS  Forms ANTIBODIES to the (+) D
E.g. Furosemide antigen blood
Most potassium wasting  In the 1st pregnancy of the Rh (-)
diuretics mother to a Rh (+) fetus:
3) OSMOTIC DIURETICS  NO COMPLICATIONS; NORMAL
E.g. Mannitol  The beginning problem comes in the 3rd
DOC for Increased ICP Stage of LABOR (PLACENTAL STAGE)
4) THIAZIDE DIURETICS  In the separation and expulsion
E.g. Hydrochlorothiazide of the placenta, the placental
For LONG TERM use of barrier dissipates.
diuretics  The fetus Rh (+) blood gains
5) CARBONIC ANHYDRASE access to the mother’s Rh (-)
INHIBITORS blood
DOC for Glaucoma  This time, the Rh (-) mother will
form ANTIBODIES against the
BLOOD TYPING (Going DOWN ONLY) fetus Rh (+) D antigen blood.
O  WHY is it SUCCESSFUL for the Rh (-)
mother to have a NORMAL delivery of an
(Universal Donor) Rh (+) fetus?
A  REMEMBER: The baby is out in
B the 2nd Stage of LABOR (Delivery
AB of the Baby)
 Meaning, the baby is out before the
A B placenta had dissipated in the
uterus.
A B
AB AB  The ACTUAL PROBLEM comes in the 2nd
pregnancy of the Rh (-) mother with Rh
(+) fetus.
AB  The maternal blood of the Rh (-)
(Universal Recipient) mother was pre-exposed before
O during her 1st pregnancy;
A ANTIBODIES HAVE ALREADY
B FORMED!
AB  The ANTIBODIES can now CROSS
ABO INCOMPATIBILITY (ISOIMMUNIZATION) THE PLACENTAL BARRIER!
 Rh NEGATIVE mother carries a Rh POSITIVE  The ANTIBOIES can now
fetus DESTROY the fetus’ RBCs,
 What is the meaning of the (+) and (-) in blood resulting to a EXCESSIVE LOSS OF
typing? RBCs (Hemolytic Anemia), leading
 Indication of whether or not the person to a condition called
has a D antigen ERYTHROBLASTOSIS
 Protein that is found in the cell walls
of every RBC FETALIS!
 If have D antigen: Blood type is  Why do people have Rh NEGATIVE blood?
POSITIVE  85% of people have Rh POSITIVE
 If have absence of D antigen: Blood Blood
type is NEGATIVE  15% of people will have Rh
 How does Rh Incompatibility Happens? NEGATIVE blood.
 When an Rh NEGATIVE person exposed  This happens when the MOTHER
to a (+) D antigen blood ONLY! is HOMOZYGOUS(Rh NEGATIVE
 gene) and the FATHER is  Congestion of the heart
HETEROZYGOUS  CAUSES:
o one copy is Rh NEGATIVE a) Heart Problems
gene  TYPES of CHF:
o one copy is Rh POSITIVE 1) Right-sided Heart Failure (RSHF)
gene  Unoxygenated blood (SYSTEMIC)
 50% chance to have a Rh  The unoxygenated blood will forced
NEGATIVE baby to go back to the body (lower
MANAGEMENT: extremities) and to the head.
1) Administer RHOGAM within 72 hours  S/Sx:
 Prevents formation of antibodies a. Jugular Vein Distention
(anti-D antigen)  The unoxygenated blood that
 RHOGAM must be administered goes from the heart, forces
every after delivery of the Rh (-) back to the HEAD.
mother b. Bipedal Edema
 RHOGAM lasts only for 2 months  The unoxygenated blood that
 ALL Rh (-) WOMEN with goes from the heart, forces
UNTYPABLE PREGNANCIES must back to the FEET.
take RHOGAM! c. Ascites
2) Anti-D Titer Screening (COOMBS TEST)  The unoxygenated blood that
 Determines if the mother has goes from the heart, forces
ANTIBODIES (Anti-D antigen) back to the STOMACH.
 Types of Coombs Test: d. Hepatomegaly
a) DIRECT COOMBS TEST  The unoxygenated blood that
o Fetal blood sample is goes from the heart, forces
tested back to the LIVER.
b) INDIRECT COOMBS TEST 2) Left-sided Heart Failure (LSHF)
o Maternal blood sample is  Oxygenated blood (PULMONARY)
tested  The oxygenated blood will force to
ASSESSMENT: go back to the lungs.
1) ALL Rh (-) WOMEN should undergo COOMBS  S/Sx:
TEST a. Pulmonary Edema
a) If test is NEGATIVE/LOW:  The oxygenated blood that
1. Receives RHOGAM at 28 weeks goes from the heart, forces
(7 months) back to the LUNGS.
 For PROPHYLACTIC measure
b. Crackles
 To prevent seepage of the
c. Difficulty of Breathing
placenta filled with Rh (+)
d. Hemoptysis
blood
 MANAGEMENT: UNLOAD FASTER
 Prevent sensitization of the
a) Upright Position
mother
b) Nitroglycerin
2. within 72 hours postpartum
c) Lasix (Furosemide)
b) If test is POSITIVE/HIGH:
d) Oxygen
1. The mother is sensitized; TOXIC
e) Aspirin
to the baby
f) Digoxin
2. Do not give RHOGAM
g) Fluid Restriction
3. Fetus is monitored via DOPPLER
h) Aminophylline
VELOCITY
i) Sodium Restriction
c) DOPPLER VELOCITY is ABNORMAL:
j) Thrombolytic
 Indicates child has ANEMIA
k) Edema (reliable indicator of worsening of
 RBCs has been destroyed
CHF)
d) DOPPLER VELOCITY is NORMAL:
 Weigh once a day every morning
 CHILD is likely to be Rh (-)
l) Rest (decrease cardiac workload)
CONGESTIVE HEART FAILURE (CHF)
HOW TO INTERPRET ABG ANALYSIS: a) Back of wrist
1) Label pH b) Outside elbow
 7.35-7.45 = NORMAL c) In front of
 <7.35 = ACIDOSIS knees
 >7.45 = ALKALOSIS  Erythema  Lab abnormalities
2) Find the CAUSE (ROME) Marginatum  Increased WBCs
 R = Respiratory  Pinkish-macular  Increased C-
rashes on skin reactive protein
 O = Opposite  WORSENS by heat (inflammation)
 M = Metabolic  NEVER starts in  Increased ESR
the face
 E = Equal  LOCATION:
 RESPIRATORY = PaCO2 a) Trunk
NORMAL PaCO2 = 35-45 b) Inner thighs
<35 = ALKALOSIS  Sydenham’s Chorea  Previous
>45 = ACIDOSIS  Called St. Vitus rheumatic fever
 METABOLIC = HCO3 dance
NORMAL HCO3 = 22-26  Sudden, rapid,  Arthralgia
<22 = ACIDOSIS purposeless
>26 = ALKALOSIS movements of
3) Determine COMPENSATION extremities
 FULLY COMPENSATED  Involuntary facial
NORMAL pH grimaces
 PARTIALLY COMPENSATED  Present at LATER
ALL ARE ABNOMAL (pH, PaCO2 and part of disease
HCO3)  Relieved by REST
 UNCOMPENSATED & SLEEP
Either PaCO2/HCO3 is NORMAL

CRITERIA (+) RHD:

RHEUMATIC HEART DISEASE (RHD)
a) 2 Major S/Sx + History of streptococcal
 Autoimmune disorder
infection
 CAUSE: GABHS (Group A Beta
b) 1 Major S/Sx + 2 Minor S/Sx + History of
Hemolytic Streptococcus)
streptococcal infection
 GABHS’s mimics normal tissues
which the immune system destroys
the normal tissues
 Happens after school age
COMPLICATION OF RHD:
SIGNS & SYMPTOMS OF RHD
1) PERMANENT Cardiac damage
MAJOR SIGNS & MINOR SIGNS &
2) Cardiac Arrest
SYMPTOMS (JONES) SYMPTOMS (FEELPA)
MANAGEMENT OF RHD: HEART
 Joints (Polyarthritis)  Fever 1) Heart Valve Surgery:
 Painful joints a) If possible repair: Valvuloplasty
 ABSENT b) If NOT: Valve Replacement Surgery
deformities 2) Erythromycin/Penicillin
 O – shaped Heart  ECG changes 3) Anti-Inflammatory (Corticosteroids)
 Carditis (may  Prolonged PR & 4) Rest
cause permanent QT interval 5) Throat Care
valvular damage)
 Nodular  Evidence of GABHS
(Subcutaneous  Increased ASO PATHOPHYSIOLOGY:
Nodules) titer
 Called Aschoff
Bodies
 Painless
 LOCATION:
 2) Intermittent fingers (expose to
Rheumatic Heart Causative agent: claudication COLD)
Disease GABHS 3) Leg cramps
DOC: Vasodilators DOC: Vasodilators
AVOID: 4 C’s AVOID: 4 C’s

Cold Cold
Caffeine Caffeine
Cigarettes Cigarettes
Infects Upper
Rheumatic Fever
Respiratory Constrictive Clothing Constrictive Clothing
SURGERY: SURGERY:

Debridement Debridement
Amputation Amputation

RHEUMATIC HEART PERNICIOUS ANEMIA

infects to Heart
DISEASE  Vitamin B12 Deficiency
 CAUSES:
a) Unknown
b) Autoimmune
c) GI problem (Stomach)
Valvular Diseases Affects Heart Valves
 Surgery in the stomach
 Parietal cells dysfunction
(production of intrinsic factor)
 NO Intrinsic Factor (absence
of absorption Vitamin B12)
 Vitamin B12 Deficiency
Congestive Heart  Absence of production of
infects Kidneys
Failure
RBCs
 Unhealthy of the nerves
(Paresthesias)

Acute
Glomerulonephritis

BUERGER’S DISEASE RAYNAUD’S DISEASE  S/Sx of Anemia:

Thromboangiitis Arteriosclerotic a. Pallor
Obliterans (TAO) Obliterans (ASO) b. Red, Beefy
Clot and Inflammation Intermittent vasospasms
 Opens and Closes
Tongue (Cardinal
all of a sudden Sign)
Common in MALES Common in FEMALES c. Coldness upon
Smoking Smoking touch
Involves arteries and Involves small arteries
veins (arterioles) ONLY
d. Fatigue
LOWER extremities UPPER extremities e. Dizziness
(Legs) (Fingers)  CONFIRMATORY TEST:
Manifests: Manifests: Schilling’s Test
1) Pain (Anytime) 1) Pain in the
 a. Give radioactive
vitamin B12 via
Oral and IM
b. Collect urine
within 24 hours
c. RESULT:
Greater than 10% NEGATIVE
Vitamin B12
excretion
Less than 10% POSITIVE
Vitamin B12
excretion
 DOC: Vitamin B12 via
IM once a month for life