cards

Question 1

wide splitting

Answer 1

exaggeration of normal split: split on expiration, and incr on inhalation. 2/2 delay in RV emptying (pulmonic stenosis, RBBB)

Question 2

JVP

Answer 2

v wave = slow incr 2/2 atrial filling against closed Valve
y descent = blood flow from atrium to ventricle after opened valve
a wave = Atrial kick
c wave = RV Contraction and bulging of TV
x descent = atrial relaxation and downward displacement of TV during ventricular contraction

Question 3

CO

Answer 3

SV*HR = (rate of O2 consumption)/ (arterial O2 - venous O2)

Question 4

Ohm’s law

Answer 4

MAP = CO*TPR

Question 5

MAP

Answer 5

⅔ diastolic pressure + ⅓ systolic pressure

Question 6

fixed split

Answer 6

pulmonic closure delayed regardless of breathing

2/2 ASD

Question 7

paradoxical split

Answer 7

delayed A2, so split on inspiration. on expiration, P2 comes later and no longer split
2/2 delayed LV emptying (aortic stenosis, LBBB)

Question 8

cardiac AP vs skeletal AP

Answer 8

1. plateau (from calcium influx). Contraction of myocyte is triggered by this influx of Ca
2. nodal cells depolarize spontaneously due to funny current (slow, inward Na/K mixed current)
3. Cardiac myocytes electrically coupled by gap junctions

Question 9

pacemaker potential

Answer 9

Phase 0 upstroke = Vgated Ca channels (vs Na channels in muscle). slower upstroke → AV delay. Fast v-gated Na channels are permanently inactivated b/c resting potential is less negative than in muscle
Phase 1 initial repol and phase 2 plateau are absent
Phase 3 repol is inactivation of Ca and activation of K
Phase 4 slow depol is If from mixed Na/K inward current. Slope determines heart rate. sympathetic activation → incr If channels open → incr HR

Question 10

Class Ia antiarrhythmics

Answer 10

Quinidine, Procainamide, Disopyramidine.
Na+ channel blockers
decr slope of phase 0 and phase 3
state dependent! incr threshold for firing in abnormal pacemaker cells.
incr AP duraction, incr ERP, incr QT
Reentrant/ectopic SVT, VT
Hyperkalemia causes incr toxicity.
Quinidine: cinchoism–headache, tinnitus.
Procainamide: reversible SLE-like syndrome
disopyramide: heart failure.
All have thrombocytopenia, torsades

Question 11

Class Ib antiarrhythmics

Answer 11

Lidocaine, Mexiletine, Tocainide
Na+ channel blockers
decr slope of phase 0 and incr slope ofphase 3
state dependent! incr threshold for firing in abnormal pacemaker cells.
decr AP duration.
Preferentially affect ischemic or depolarized purkinje/ventricular tissue.
Ventricular arrhythmias, especially post-MI, and digitalis toxicity
Hyper-K incr toxicity
Local anesthetic effects, CNS stimulation/depression, CV depression

Question 12

Class Ic antiarrhythmics

Answer 12

Flecainide, propafenone
Na+ channel blockers
decr slope of phase 0 and no change to slope of phase 3
state dependent! incr threshold for firing in abnormal pacemaker cells.
No effect on AP duration
Vtach progressing to VF, intractible SVT. Last resort.
contraindicated post-MI and in pts with structural heart dz
Hyperkalemia incr toxicity
proarrhythmic, esp post-MI. Significant prolongation of ERP of AV node

Question 13

Class II antiarrhythmics

Answer 13

beta blockers
metoprolol, propranolol, esmolol, atenolol, timolol
Decrease SA/AV node activity by decr cAMP, decr Ca current.
Suppress abnormal pacemakers by decr slope of phase 4
Incr PR interval (AV node)
Esmolol – short acting
VT, SVT, rate control
Toxicity: impotence, asthma, bradycardia, AV block, CHF, sedation. May mask signs of hypoglycemia
Metoprolol – dyslipidemia. Treat OD with glucagon.
Propranolol – exacerbates vasospasm in prinzmetal’s angina

Question 14

Class II antiarrhythmics

Answer 14

K channel blockers
amiodarone, ibutilide, dofetilide, sotalol
incr AP duration, incr ERP. decr slope of phase 3
Used when other drugs fail. incr QT interval
Toxicity:
sotalol – torsades
ibutilide – torsades
amiodarone – pulm fibrosis, hepatotoxicity, hypo/hyperthyroidism (iodine), corneal deposits, skin deposits (blue/gray), photodermatitis, neuro effects, constipation. (Check PFTs, LFTs, TFTs)

Question 15

amiodarone

Answer 15

Class III. but has class I, II, III, and IV effects because it alters lipid membrane

Question 16

class IV antiarrhythmics

Answer 16

Ca channel blockers
verapamil, diltiazem
decr conduction velocity, incr ERP, incr PR. Prevention of nodal arrhythmias, especially SVT
Reduce contractility (decr phase 2), but allow body to retain adrenergic control, unlike beta blockers
Toxicity: constipation, flushing, edema, CHF, AV block

Question 17

adenosine

Answer 17

incr K out of cells → hyperpolarization and decr Ca current. diagnosing/abolishing SVT. Very short acting.
Tox: flushing, hypotension, chest pain
Blocked by theophylline, caffeine

Question 18

hyperkinetic pulse

Answer 18

rapid ejection of large stroke volume against decr afterload. Exercise or high-output conditions eg PDA, AV fistula

Question 19

Mg

Answer 19

torsades and dig toxicity

Question 20

layers of artery

Answer 20

intima – endothelial cells sitting on BM
media – smooth muscle
adventitia – connective tissue

Question 21

Temporal arteritis

Answer 21

large vessel vasculitis
branches of carotid (temporal → HA, ophthalmic → visual sx, jaw claudication)
ESR > 100, PMR
granulomatous inflammation with intimal fibrosis of vessel
Segmental lesions (need long bx, negative bx does not exclude dz)
Tx: corticosteroids. tx early to prevent blindness

Question 22

Takayasu’s arteritis

Answer 22

large vessel vasculitis

asian females

Question 23

polyarteritis nodosa

Answer 23

medium vessel vasculitis: muscular arteries supplying organs
necrotizing, segmental, spares lungs
HTN (renal), GI Sx (mesenteric) skin lesions
Transmural inflammation with fibrinoid necrosis (pink vessel wall) → massive fibrosis (nodosa)
associated with HBsAg positivity
immune complex mediated
Tx: steroids or cyclophosphamide (fatal if untreated)

Question 24

Kawasaki dz

Answer 24

medium vessel vasculitis: muscular arteries supplying organs

kids

Question 25

buerger’s dz (thromboangiitis obliterans)

Answer 25

medium vessel vasculitis: muscular arteries supplying organs
necrotizing vasculitis of digits
ulceration, gangrene, autoamputation
Reynaud’s 
highly assoc with smoking
Tx: cessation

Question 26

Wegner granulomatosis

Answer 26

small vessel vasculitis: arterioles, capillaries, venules
nasopharynx (septal perf, ulceration), lungs (b/l nodular infiltrates), kidneys (RPGN) (“C distribution)
Bx: large necrotizing granulomas with adjacent necrotizing vasculitis
c-ANCA
Tx: Cyclophosphamide, Corticosteroids

Question 27

microscopic polyangiitis

Answer 27

small vessel vasculitis: arterioles, capillaries, venules
lung and kidney
no granulomas
p-ANCA
Tx: cyclophosphamide, corticosteroids
relapses common

Question 28

Churg strauss

Answer 28

small vessel vasculitis: arterioles, capillaries, venules
lung, heart
asthma, peripheral eosinophilia (vs MPA)
p-ANCA
path: necrotizing granulomatous vasculitis with eos (vs GPA)

Question 29

HSP

Answer 29

small vessel vasculitis: arterioles, capillaries, venules
palpable purpura (inflammation along with bleeding) in buttocks, legs
GI pain and bleeding
hematuria (IgA nephropathy)
follows upper respiratory tract infection
Tx: self limited, but can recur. steroids if severe

Question 30

path atherosclerosis

Answer 30

Intimal plaque (necrotic lipid core) with fibromuscular cap
injury → Lipid enters intima → oxidation → macrophages form “fatty streak” → thickening, necrotic core → proliferation of SM and fibrosis → fibromuscular cap

SMC proliferation (derived from media) is responsible for intimal thickening **

Question 31

atherosclerosis

Answer 31

Intimal plaque (necrotic lipid core) with fibromuscular cap
injury → Lipid enters intima → oxidation → macrophages form “fatty streak” → thickening, necrotic core → proliferation of SM and fibrosis → fibromuscular cap

SMC proliferation is responsible for intimal thickening **

Question 32

phases of MI

Answer 32

1 wk – granulation tissue (plump fibroblasts, collagen blood vessels). Gross: red border coming from outside (vascular)
>1 month – fibrosis type I collagen. gross: white scar. aneurysm, mural thrombus, Dressler syndrome.

Question 33

Liebman-Sacks endocarditis

Answer 33

SLE
sterile
both sides of mitral valve
results in MR

Question 34

Class III antiarrhythmics

Answer 34

K channel blockers
amiodarone, ibutilide, dofetilide, sotalol
incr AP duration, incr ERP. decr slope of phase 3
Used when other drugs fail. incr QT interval
Toxicity:
sotalol – torsades
ibutilide – torsades
amiodarone – pulm fibrosis, hepatotoxicity, hypo/hyperthyroidism (iodine), corneal deposits, skin deposits (blue/gray), photodermatitis, neuro effects, constipation. (Check PFTs, LFTs, TFTs)