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Cardiology PDF
Cardiology PDF
3. Aorta anterior to and to the right of the pulmonary artery is diagnostic of transposition of
great arteries (It's quite obvious really: Failure of neural crest cell migration
4. ECG physiology:
a. Ventricular response in AF depends on the AV node refractory period
i. Narrow QRS
ii. Irregularly irregular R-R
b. Bundle branch conductivity - determines duration of QRS
5. Catheter placement:
a. Hand washing ensures central lines are not infected
i. Staph aureus
ii. Staph epidermidis (coagulase negative)
b. Use subclavian
c. Catheter replacement doesn’t really work
d. Antibiotic prophylaxis doesn’t work
6. Amyloidosis
a. Localised amyloidosis list of precursor proteins:
i. Senile cerebral - A beta
ii. Thyroid - Calcitonin
iii. Pancreatic islets - Amylin
iv. Heart - ANP
v. Pituitary - Prolactin
7. Acute LVF:
a. Dyspnea
b. Tachypnea
c. CXR findings:
i. Cardiomegaly; LVH (RVF would show RVH)
ii. Alveolar edema / batwing
iii. Kerley B lines
iv. Blunt costophrenic angles (effusion)
1) COPD - Flat diaphgragm
d. 3rd heart sound due to increased LV end systolic volumes
8. Atherosclerosis:
a. Endothelial injury activates platelets
i. Release of PDGF, and increased expression of VCAM-1 on endothelium
ii. PDGF from endothelium + platelets + infiltrating macrophages (monocytes that
emigrate)
1) Migration of smooth muscle cells into intima from the media
2) Proliferation of smooth muscle cells
a) Reactive intimal hyperplasia
iii. TGF-Beta
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Cardiology Page 1
iii. TGF-Beta
1) Chemotactic for SMC
2) Induces interstitial collagen production
b. Smooth muscle cells synthesize the fibrous cap, not fibroblasts
c. When coronary arterial occlusion >75% it can may cause angina of effort
10. Complications of MI
a. Day 1 : Cardiogenic shock, arrhythmias
b. Day 1 - 3 : Pericarditis
i. Serofibrinous
ii. Localised: over the necrotic myocardium
iii. Rx: Aspirin, and short lived
c. Day 3 - 14 : Ventricular free wall rupture, cardiac tamponade
d. 2 weeks: Dressler's pericarditis
i. New pericardial, pleural effusions
ii. Autoimmune, diffuse involvement
iii. Fever, pleuritis, leukocytosis
iv. Responds to Aspirin, NSAIDS, Glucocorticoids
11. Sharp pleuritic pain radiating to neck, worsened with swallowing; relieved by leaning forward -
phrenic nerve involvement (close to the heart, and irritated in pericarditis)
12. Conduction speed of atrial fibers is faster than that of ventricular fiber.
a. Know the anatomy; locations of these fibres/nodes/
b. Purkinje fastest
c. AV node slowest (causes a delay of 0.13 seconds) 0.05 m/s
d. SA node --> 1.1 m/s
e. Purkinje (and bundles of His) > Atrial > Ventricular > AV node
14. A change in O2 saturation while blood moves into the atria to the ventricles - VSD
a. 75% SpO2 = 45mm Hg O2
b. 96% SpO2 = 96 mm Hg O2
15. Phenoxybenzamine:
a. Non selective irreversible alpha 1 and 2 blocker.
b. Norepinephrine can't overcome blockade hence, Emax is reduced (efficacy is reduced)
18. HOCM:
a. Asymmetrical septal hypertrophy + dynamic outflow obstruction
b. AD with variable expression
i. Mutation in beta-myosin heavy chains
c. Can lead to sudden death
d. Increased blood flow (increased preload) = less murmurs
e. Decreases blood flow (decreased preload) = more murmurs because of AV closure
25. IV drug abusers infective endocarditis: right valves are affected; otherwise 90% are left sided
28. Proximal 2-3 cm of pulmonary veins have cardiac muscle, and function as sphincters during
systole.
29. Warfarin administration requires monitoring of PT/INR (maintain INR between 2 - 3.5)
a. Most common long term anticoagulant to prevent venous thrombosis and pulmonary
embolism.
b. Long term anticoagulant in aortic valve replacement
c. Blocks Vit K dependent gamma carboxylation of glutamate residues
i. II, VII, IX, X
d. Typically longer onset of action (long half lives of clotting factors)
e. Factor VII has the shortest half life hence deficiency is seen first
31. SVC forms behind the first costal cartilage, Descending aorta echo = rotate TEE posteriorly
32. Valve findings:
a. Aortic regurgitation:
i. Early diastolic crecendo murmur
ii. Amyl nitrite reduces preload >> Reduces murmur
b. HOCM - increases while standing (reduced preload)
c. AS - decreases while standing (reduced preload)
d. Non splitting murmur (ASD)
e. Wide S1 splitting - mitral stenosis/bundle branch block
f. Mitral / tricuspid stenois - diastolic murmur with presystolic accentuation Tyrosine is essential in PKU, since mcc is
deficiency of phenylalanine hydroxylase.
33. Anterior uveitis: (Enzyme that converts Phe to Tyr)
a. HLA-B27 linked diseases
b. Lyme disease Asparagine formed from aspartate
c. Syphilis (Asparagine synthetase; Glutamine as
d. Herpes virus amino donor). Essential for rapidly
dividing tumour cells that cant produce
34. Beta 1 selective blockers - no hyperkalemia its own Asparagine.
a. Hyperkalemia is a beta 2 blockade effect due to blockade of insulin release >> 1. Asparaginase >> lysis of tumour
hyperkalemia cells
38. Severe MR = S3 gallop (diastolic component may also be indicative); intensity of murmur isnt
very useful
a. S3 = high ventricular filling rate during mid diastole
b. Pulmonary edema (if acute)
c. Functional MR - improves with diuretics --> Decrease in LV size decreases size of mitral
valve annulus
i. Holosystolic murmur at the heart apex
ii. Maximum intensity at the beginning of systole
d. Calcific Mitral annulus - doesn’t decrease in size
e. MR due to chordae rupture - doesn’t magically go away with drug therapy
39. Beta blockers decrease mortality in patients with acute coronary syndrome; watch out for
exacerbation of asthma / COPD due to B2 blockade causing bronchoconstriction
a. Acute increase in TPR (B2 blockade) but that’s transient
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Cardiology Page 4
a. Acute increase in TPR (B2 blockade) but that’s transient
b. Contraindicated in asthma / COPD
40. Renin is inhibited by (B1 receptors on JG cells) B1 selective beta blockers; reduces ATII,
Aldosterone; useful in hypertension
a. But - plasma renin levels have little to do with antihypertensive efficacy of beta blockers.
Main mechanism of action is negative chronotropic and inotropic effect
b. Basically YMMV
41. B2 receptor mediated vasodilation in muscular vessels (increases blood flow during exercise);
Epinephrine
42. Beta blockers - good for reducing reflex tachycardia when administering vasodilators; more
effective that non-DHP CCB's too.
a. Beta blocker + non-DHP --> Significantly reduced heart rate (sinus bradycardia)
i. Depressed AV node, contraction
ii. Bradycardia + Hypotension
b. Other drugs that will reduce heart rate:
i. Digoxin
Sturge-Weber syndrome :
ii. Pilocarpine / Rivastigmine
1. Encephalotrigeminal angiomatosis
iii. Amiodarone & Sotalol
2. Skull radio-opacities tram track
calcifications
43. Glucagon:
3. Nevus flammaeus
a. Directly acts on Gs proteins on cardiac myocytes
b. Increases intracellular cAMP
c. Bypasses beta receptors, hence useful in beta blocker overdose
i. Reverses the following - bradycardia, hypotension, CVS collapse
cAMP cGMP
55.
4 protein subunits Receptor + guanylyl cyclase in single protein
a. cGMP:
i. Transmembrane receptor - ANP
ii. Free cytosolic receptor - NO
b. Increased cGMP - Increased Myosin Light chain phosphatase >> Relaxation
56. FA = produce more ATP than glucose, but uses more O2 per ATP than glucose
69. Angiotensin II - Gq
70. ADH:
a. V1 - Gq
b. V2 - Gs
73. Patients with noncoronary atherosclerotic disease, diabetes, or chronic kidney disease are at
the same risk for MI / Stroke as patients with known heart disease. Coronary disease --> mcc of
death in diabetics.
75. Spironolactone inhibits action of aldosterone, and hence prevents cardiac remodeling and
fibrosis that way. Hence increases overall survival [RALES trial, significant reduction in
mortality in CHF III and IV; spironolactone + standard therapy]
82. Ventricular and outflow tract maximum pressures are almost equal
b. Increase in TPR - reduces the slope of both Venous return and CO curves
i. Veins - decreases the amount of arterial blood entering veins; venous return
decreases
ii. Arteries - increases afterload, which decreases SV = Decreased CO.
c. Arteriovenous fistula
i. Acute - only decrease in TPR (since arterioles are bypassed)
ii. Chronic
1) Decreased TPR
2) Increased CO (due to sympathetic overdrive and renal fluid retention?)
3) Increased Psf and Venous return
84. AV fistula:
a. Congenital
b. Acquired -
i. Secondary to penetrating injury
ii. Dialysis
c. Pulsatile mass with a constant bruit
85. Antiarrhythmics:
a. Sodium channel blockade effect:
i. Ic > Ia > Ib
b. Class Ia
i. Moderate Na channel blockade effect
ii. Extend the AP duration
c. Class Ib
i. Very weak Na blockade
1) More selective for ischemia induced ventricular arrhythmias
ii. Associate and dissociate rapidly from Na channels
iii. Reduces AP
d. Class Ic
i. Most potent effect
ii. Strongest Na channel blockade
1) Can promote arrhythmias; speed on conduction slowed more than the ERP
iii. Slowest dissociation from the channels
iv. AP duration stays same
92. Internal thoracic artery and veins are between the trasversus thoracis and internal intercostal
muscle.
93. Pulmonary trunk may be pierced by penetrating injury to 2nd intercostal space at left sternal
border
94. IVC injury --> Stab to the back, just to the right of the vertebral bodies
95. Restrictive cardiomyopathy:
a. Sarcoidosis
b. Amyloidosis
c. Radiation damage
d. Hemochromatosis
96. Anthracyclines: Doxorubicin, Daunorubicin, epirubicin, idarubicin - Cause ROS generation -->
Dilated cardiomyopathy - Systolic failure
a. CHF Symptoms:
i. Dyspnea on exertion
ii. Orthopnea
iii. Peripheral edema
b. Presents many months after discontinuing drug
c. Swelling of sarcoplasmic reticulum
d. Loss of cardiomyocytes
e. Prevention:
i. Dexrazoxane - Fe chelating agent (decreases ROS formation)
98. Right ventricular overload will lead to widening of S2 split (increased ejection time)
102. Fibrinolytics are also used for pulmonary embolism, and arterial thrombosis
109. Dihydropyridines - causes peripheral vasodilation, has little action on the heart - watch out for
reflex tachycardia
110. Verapamil and Diltiazem - Rate control for Atrial fibrillation (Slows AV conduction)
a. Constipation/nausea
b. Flushing
c. Hypotension
113. Dicrotic pulse: Two peaks in the pulse (systole + diastole); extremely low systolic output
114. Hyperkinetic pulse: rapid ejection of a large stroke volume against decreased afterload [figure
this out later?]
a. PDA
b. AV fistula (dialysis one)
123. Mitral regurgitation - increased regurgitant flow with increased afterload [logical, think about
it]. Hence arterial vasodilators and beta blockers can help (Reduces afterload), surgery
definitive treatment.
125. Cardiac output/Blood flow for left and right heart = same (both rest and exercise)
126. Pericytes around capillaries regulate the blood flow into that vascular bed
129. Monckebergs medial calcific sclerosis - calcific deposits in tunica media muscular arteries;
age >50; asymptomatic because no luminal narrowing
f. PDA - isn't really cyanotic; may cause differential cyanosis (later in life)
135. SVC syndrome -bilateral edema of body and engorgement of veins of face; mcc is malginancy
136. Jugular venous pulse (jvp)
a Right atrial contraction Prominent - RVH, Tricuspid
stenosis, pulmonary
hypertension
Absent - AF
c Bulging of tricuspid valve during RV
contraction
a.
x Atrial relaxation
v Gushing in of blood into atria during late
systole, early diastole
y Passive emptying of RA after tricuspid opens Deep in pericarditis
in diastole
b. Giant c-v wave: No x descent; Tricuspid regurgitation
141. CABG
a. Single LAD - Internal mammary artery
b. Multiple coronary arteries - Great saphenous veins
i. Accessed at the medial leg, or at it's point of termination in the femoral triangle of
the upper thigh
143. Popliteal artery is more likely to be damaged than the tibial nerve or whatever in a posterior
tibial displacement or any other traction force.
a. The artery is deep in the popliteal fossa
b. The artery is tightly fixed proximal and distal to the popliteal fossa by: adductor magnus
and the soleus muscles.
c. Tibial nerve - doesn’t pass through the adductor magnus (vs artery)
Acute MI
Reduced ventricular
compliance:
- Aortic stenosis
- Hypertensive heart disease
- HOCM
152. Hypokalemia
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152. Hypokalemia
a. ECG findings:
i. ST depression
ii. T wave flattening
iii. Prominent U waves
b. Premature atrial / ventricular contractions
c. VT / VF (profound hypokalemia)
153. Carvedilol (beta blocker, with alpha blocker) - Improves all cause mortality in CHF
156. Alpha agonism --> increases sytolic and diastolic bp; decreased renal and splanchnic blood flow
157. Norepinephrine may be useful in shock
161. Pulmonary artery hypertension leads to RHF, (elevated RH pressures) which can lead to
coronary sinus dilation. Coronary sinus dilation is not a normal finding, and is dilated by any
factor that causes atrial dilation
162. Coronary artery disease --> reduced drainage into coronary sinus
163. Amiodarone:
a. Class III antiarrhythmic
b. Prolongs QT; but has a much lower likelihood of causing Torsades de pointes
i. Less QT dispersion, whatever the hell that means
c. Drug of choice for post MI Ventricular fibrillation
d. Toxicity:
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Cardiology Page 18
d. Toxicity:
i. Blue gray discoloration of skin
ii. Photosensitivity
iii. Pulmonary fibrosis
iv. Thyroid dysfunction
166. Cocaine
a. Reuptake inhibitor
i. Hypertension
ii. Tachycardia
iii. Mydriasis
iv. CNS activation
b. Vasoconstrictor
i. MI, Coronary artery vasospasm
ii. Intranasal use --> Mucosal atrophy, nasal septal perforation
169. Cushings syndrome and SLE - Increase the risk of coronary artery disease
170. Atropine - treats bradycardia
171. RCA - gives off the posterior descending artery in 90% of the population; 10% LCX
a. Right dominant circulation
b. AVF, II, III - ST elevations + Sinus node dysfunction (bradycardia) = RCA thrombosis
i. Rx Bradycardia:
1) Atropine (inhibits Vagal influence)
a) Toxicities - Can precipitate acute angle glaucoma in pts with shallow
anterior chambers
172. Anticholinergic drugs - reduce pain & prevents adhesions of iridocyclitis (uveitis)
173. Coronaries:
a. LCX - runs between the left atrium and ventricle (AV groove, kinda close to the rear of
the heart)
b. LAD - runs in the anterior interventricular groove
c. Remember the heart apex is tilted
177. Urokinase
a. Treatment for myocardial infarction and pulmonary embolism
b. Plasminogen --> Plasmin; Plasmin degrades Fibrin into its degradation products
179. Restrictive cardiomyopathy --> mcc of death is CHF that develops due to it
a. Decreased ventricular compliance (dV/dP)
180. Eccentric hypertrophy of LV in Mitral regurgitation
a. Because increased regurgitant flow during systole = amount of blood returning to the LV
during diastole
b. Volume overload
181. Hypertrophic cardiomyopathy - important cause of VF in individuals <30 and mcc of sudden
cardiac death in young athletes.
a. Massive cardiac hypertrophy
b. Septal involvement
c. Normal coronaries
183. Alpha 1 selective agonists - Don’t cause much reflex tachycardia (wha?)
184. Adult type aortic coarctation:
a. Post-ductal coarctation
b. Hypertension in head + upper extremities
i. LVF
ii. Berry aneurysms - rupture due to htn
iii. Aortic aneurysms
c. Hypoperfusion in lower extremities
i. Low exercise tolerance / muscle weakness
d. Large palpable intercostal vessels
i. Sign of development of collateral circulation
ii. Notching of ribs
187. Place filter in the IVC in patients with DVT treatment complications (GIT bleeds)
a. Renal veins join IVC at L1/L2
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a. Renal veins join IVC at L1/L2
b. Common iliac veins merge to become IVC at L4
200. Orthopnea
a. Supine dyspnea that is relieved by sitting up; specific sign of LHF
b. LHF progresses to:
i. Pulmonary interstitial edema, widening of alveolar septa
ii. Intra alveolar accumulation
201. Cardiac asthma - exercise induced wheezing in LHF. Exercise = increased venous return to the
heart, but failing heart cant increase CO appropriately. Hence pulmonary pressures rise.
a. Not a specific sign
b. Seen in COPD and Asthma
206. Isoproterenol - b2 agonism can cause increased blood flow in skeletal muscles, renal and
mesenteric vascular beds. Not useful for increasing perfusion in the skin though.
208. Adjust dose of Digoxin in the elderly, since renal function decreases with age and can lead to
digoxin toxicity.
a. Only a 1/3 of the drug is actually protein bound (so protein binding isn't really a big deal)
b. Not accompanied by increase in creatinine; since muscle mass also falls with age
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Cardiology Page 22
b. Not accompanied by increase in creatinine; since muscle mass also falls with age
c. Muscle mass - lean body weight (important for dosing calculations of digoxin; just not as
important as renal function)
d. Symptoms:
i. Changes in colour vision [neurological sign]
ii. Fatigue and weakness [hyperkalemia]
iii. Delirium
iv. Diarrhoea, nausea, vomiting
v. Arrhythmias
210. Isoproterenol - increases cardiac contractility (b1) and decreases peripheral venous resistance
(b2) at low doses; [understand the axes of the graph and then figure out if effect increasing or
decreasing with x]
212. Intermittent claudication (muscle pain with exercise that remits with rest)
a. Result of atherosclerosis of large arteries, fixed stenotic atheromatous plaques that
bulge into the arterial lumen
i. Blood flow to muscle cant increase during exercise
b. Pain relieved by resting; exacerbated by minimal exercise (ischemic muscle pain)
c. Thigh claudication:
i. Ipsilateral external iliac artery or common femoral artery
ii. Common femoral and profunda femoris artery
217. Chylomicrons - synthesized on the RER and the Golgi apparatus of the small intestinal
enterocytes with Apo B48.
218. LCAT - Esterifies cholesterol
220. Remember diastole --> Coronary vessel perfusion. Increase in diastolic pressure increases
afterload --> Increases cardiac work and increases O2 demand
221. Dobutamine increases myocardial oxygen demand (increases B1 mediated contraction + heart
rate)
a. Hard question that tested on specific knowledge of stuff
b. Dobutamine can also increase conduction velocity; causes arrhythmias
223. Coronary circulation is maximum during diastole, also in stress, the increase in adenosine
vasodilates the coronaries
226. LDL receptors functions by receptor mediated endocytosis; (clathrin pits yada yada)
227. Accentuated P2 - Pulmonary hypertension; Accentuated S2 - Systemic hypertension
231. Remember that cardiac hypertrophy is because of increased mRNA synthesis for myosin/actin
(increased sarcomeres), more mitochondria etc. No increase in mitoses since there is no
hyperplasia
234. Muscarinic receptors are present on the endothelium; on stimulation trigger the release of NO
(EDRF) --> Smooth muscle relaxation.
236. Milrinone - increases cardiac contractility by preventing the degradation of cAMP within the
myocytes [PDE-3 inhibitor]
a. Increased cAMP --> Calcium conductance increases
239. ACE inhibitor therapy - causes characteristic dry cough [you know why]
a. ARBs don’t inhibit bradykinin degradation, hence don’t cause dry coughs
241. Fatty streaks are present in kids, may not always progress to atherosclerosis. But they will be
made of foam cells.
249. ATP depletion in the myocytes, around the contractile elements occurs within 60s of ischemia;
leads to cessation of contractility.
a. Total ATP levels stay normal for the first few seconds
i. ATP --> AMP --> Adenosine (vasodilator)
b. If ischemia is reversed within 30 mins, the contractility impairment is reversed after
prolonged 'stunning'
253. Bile acid binding resins (cholestyramine) useful for treatment of cholesterol; interferes with
bile acid circulation and increases cholesterol excretion
254. Ezetimibe + statin = hepatotoxic
255. Antihyperlipidemics max effect:
Statins Decrease LDL Reduces atherosclerotic heart disease
256. Cyanotic toe discoloration + renal failure after invasive vascular procedure
a. Atheroembolic disease of renal arteries
b. Cholesterol debris gets pushed from larger arteries into the smaller ones --> Ischemia of
the organs and tissues.
c. Other sites:
i. Livedo reticularis
ii. Cholesterol emboli on retinal examination
iii. Skin infarcts
259. Ventricular remodeling - chronic change in mass, volume, shape & myocyte composition of the
heart. Usually adjacent to the ischemic dysfunctional myocardium.
260. DVT risk is high in patients who are undergoing hip/knee replacements and are non-
ambulatory:
a. Heparins (bind to ATIII & Xa)
263. Ivabradine - slows heart rate by blocking sodium channels from the cytoplasmic side, prolongs
the Na+ funny current.
a. No effect on contractility
b. Decreases heart rate
c. Rx for HF with reduced ejection fraction
264. Coronary sinus blood - most deoxygenated blood in the body. Myocardial oxygen extraction
(75 - 90%) is the highest in the body.
a. Mixes with slightly less deoxy blood from the rest of the body at the RA before entering
the PA.