Cardio Flashcards
rate of possible pacemakers in the heart
SAN = 60-100 AVN = 40-60 His/BB/Purkinje = 25-40
what is Ortner syndrome
-sxs?
mitral stenosis causing so much LA dilation that it impinges on recurrent laryngeal nerve
-hoarseness, left vocal cord paresis
IVC is to the ___(side) of abdominal aorta
right
causes of nonbacterial thrombotic endocarditis
deposition of sterile platelet rich thrombi
valve damage from inflamm cytokines in setting of hypercoagulable state
- advanced malignancy (esp mucinous adenocarcinoma)
- SLE
what is most common murmur associated with rheumatic heart disease?
-describe
what other murmurs can be heard?
Mitral stenosis most common
OS and mid-diastolic rumbling
also:
- mitral regurg (blowing holosystolic)
- aortic valve
describe murmur of mitral stenosis
opening snap at beginning of diastole, mid-diastolic rumbling (best over cardiac apex)
describe murmur of mitral regurg
blowing holosystolic
HCM inheritance pattern
what are possible gene mutations
AD
beta-myosin heavy chain
myosin-binding protein C
mutation in long QT syndrome? what causes long QT?
K+ channel mutations
decr in repolarizing K+ current prolongs QT
what is most common cause of death 2-3 days after MI?
Ventricular arrythmia (eg vfib)
what is supine hypotension syndrome
usu pregnant women >20 weeks
bp drops when lying down b/c gravid uterus compresses the IVC
describe murmur of aortic regurg
diastolic decrescendo
describe concept of coronary steal
pharm vasodilators (eg adenosine, dupyridamole) that cause coronary arteriolar dilation can cause redistribution of blood flow from ischemic to nonischemic areas of myocardium
b/c arterioles that supply v ischemic myocardium are already max dilated at rest. with pharm vasodilators -> no change in blood flow to ischemic myocardium, but sig incr blood flow to nonischemic myocardium, amplifying the ischemia (makes it easy to detect on myocard perfusion imaging which uses these vasodilators
describe murmur of aortic stenosis
crescendo-decrescendo
what is best auscultatory indicator of mitral stenosis severity? why?
A2-OS interval
shorter interval = more severe stenosis
in worse MS, higher LA pressure causes the valve to open more forcefully/earlier
Hyperlipidemic agents MOA:
- fibrates
- omega 3
- ezetimibe
- statins
- bile binding resins
- fibrates: activate PPARa –> decr hepatic VLDL prod and increased LPL activity
- omega3: decrease VLDL prod and inhib synthesis of apolipopro B
- ezetimibe: blocks intestinal cholesterol absorption
- statins: decrease hepatic cholesterol synthesis by inhibiting HMG CoA reductase
- bile binding resins: incr fecal loss of cholesterol derivatives by binding bile acids in intestine and disrupting enterohepatic bile acid circulation
PCSK9 inhibitors: monoclonal Ab that reduce LDL receptor degradation in liver
what is pulsus paradoxus and explain why it happens in cardiac tamponade
normally have <10 drop in SBP with inspiration (decr pressure in pleural space and lung interstitium, increasing pulm vasc capacitance = decr venous inflow to left heart = decr LV SV and drop in SBP)
> = 10mmHg drop in SBP with inspiration
cardiac tamponade -> external compression of ventricles which equalizes LV and RV diastolic pressures -> intraventricular septum bulges into LV as resylt if insp increase in RV filling.
this further reduces LV stroke vol, leading to a drop in systolic BP >100mHG
what are two causes of holosystolic murmur
MR or VSD
what medication should be started on pts w/ stable angina?
what is a good alternative if they’re allergic to it?
aspirin! inhibition of COX1 in platelets prevents synthesis of ThromboxaneA2, a potent stimulator of platelet aggreg and vasoconstriction.
-will reduce risk of occlusive thrombus formation and subsequent MI
clopidogrel if allergic to aspirin - irreversibly blocks P2Y12 part of ADP receptors on platelet surface -> prevents platelet aggregation
Fenoldopam
- what is it used for
- MOA
- effects
selective peripheral Dopamine-1 receptore agonist
given IV for hypertensive emergency (esp in pts with renal insuff ie high Cr)
effects
- arteriolar dilation
- incr renal perfusion
- promotes diuresis and natriuresis
phenylephrine
- what is it used for
- MOA
- effects
alpha-adrenergic agonist
increases TPR due to arterial vasoconstriction
used in hypotension, shock
Adenosine
- what can it be used for and why
- adverse effects
is a coronary arteriole vasodilator
also an anti-arrythmic.
- hyperpolarizes the nodal pacemaker, briefly blocking conduction through the AV node.
- short lived, but briefly blocking conduction from atria to ventricles often terminates reentrant circuit and leads to conversion of PSVT to NSR
adverse effects
- flushing
- chest burning (bc bronchospasm)
- hypotension
- high grade AV block
what is Eisenmenger syndrome
- cause
- symptoms
initially congenital cardiac defect (eg ASD) causes left to right shunt
over time, pulmonary arteries get hypertrophy so severe that PVR > SVR and instead get right-to-left shunt
- late onset cyanosis
- clubbing
- polycythemia
what does Right Coronary Artery supply
RV and
inferior wall of LV
wide fixed split S2 that does not vary with respiration indicates ?
what happens in this problem?
ASD
higher pressure in LA causes Left-to-right shunt of blood into RA. increased RA pressure causes pulmonary HTN
In formation of an atherosclerotic plaque, what cells release growth factors that trigger smooth muscle cell recruitment?
- platelets (platelet derived growth factor PDGF)
- activated macrophages
- endothelial cells
(T cells release inflamm cytokines, which activate macrophages, SMCs, endothelial cells)
risk of severe myopathy highest when statins given concurrently with?
fibrates
-impair hepatic clearance of statins
two major effects of digoxin
- incr vagal tone (slows rate - slows conduction thru AV node)
- inhibit Na-K-ATPase, increasing intracellular Na and Ca2+ (incr contractility), more extracellular K
AV block can be a side effect of what 3 medications?
digoxin
beta blockers
CCBs
(they slow AVN conduction)
infective endocarditis most commonly causes what valvular condition?
tricuspid regurgitation
difference between dihydropyridines and nondihydropyridines?
dihydropyridines- affect arterial smooth muscle causing vasodilation (little/no effect on heart)
nondihydropyridines- slow HR and reduce contractility
milrinone MOA
PDE3 inhibitor
can be used as inotropic agent in refractory HF due to LV systolic dysfunction
decreases rate of degradation of cAMP in cardiac tissues
increased cAMP = promotes Ca2+ influx into cardiac myocytes = incr myocardial contractility
also inhibits PDE3 in vascular smooth muscles, so can causes systemic arterial and venous dilation leading to decr BP. can’t use in pts with severe hpotension
symptoms of digoxin toxicity
life-threatening arrythmias
GI
fatigue, confusion, weakness
*color vision alterations (esp yellow tinting)
where is digoxin cleared
renally
what is normal
- PR interval
- QRS duration?
PR <200 ms
QRS <120ms
what is most common primary cardiac neoplasm
- where do most originate
- what does it look like on histo
myxoma
80% originate in LA
(sxs can mimic mitral valve stenosis)
can hear mid-diastolic murmr (tumor p;op) heard in early diastole from motion of tumor mass obstructing mitral valve orifice
amorphous extracellular matrix with scattered stellate or globular myxoma cells within abundant mucopolysaccharide ground substance
side effects of CCBs
-why?
peripheral edema
dizziness
CCB preferentially dilate precapillary vessels (ie arteriolar dilation) -> incr capillary hydrostatic pressure and fluid extravasation into interstitium
young patients who get HF after a viral prodrome -> suspect what?
viral myocarditis (is a common cause o f dilated cardiomyopathy)
