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54 Cards in this Set

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what drug given in pt with known CAD to reduce risk of MI/stroke?
statins, esp pravastatin and simvastatin
target LDL value
0-1 RF: <160; 2+ RF: <130; CAD/DM/PAD/AAA: <100, maybe <70
how to convert hba1c to average FSG
HbA1c * 33 - 86
causes of secondary hypertriglyceridemia (4)
DM, Hypothyroidism, alcohol abuse, estrogen use
None
tx for hypertriglyceridemia
if secondary, treat 1' disorder; if 1', use NIACIN, fibric acid derivatives (?fibrates), or omega-3 fatty acids; also, lifestyle changes
use of bile acid sequestrants in hyperTG
contraindicated -- can actually increase TG
what TG level confers risk for pancreatitis?
>1000 (?>500)
classification of TG levels
<150: normal; 150-199: borderline; 200-499: high; >500: very high
what is total chol the sum of?
LDL + HDL + vLDL
what is the non-HDL cholesterol goal?
non-HDL chol = totalchol - HDL = vLDL + LDL; non-HDL cholesterol goals are LDL goals + 30;
what risk with statin-fibrate combo?
myositis
what to do if LDL not adequately controlled on max dose statin?
add bile acid sequestrant or ezetimibe (as long as no hTG)
max dose simvastatin
40mg/d
criteria for metabolic syndrome
>= 3 risk factors (ABCDeFG): 1) Abdominal obesity; 4) BP > 130/85; 3) Cholesterol -- HDL<50 in women; 2) TG>150; 5) fasting glucose > 110
what drugs elevate HDL and decrease TG? Which to use with statin?
niacin and fibrates; niacin-statin preferred b/c of fibrate-statin risk of myositis
dosage of niacin
titrate up to 1500-2000 mg/d, depending on tolerance
ecg findings in pericarditis
diffuse pr depression, st elevation
mgmt of symptomatic aortic stenosis
valve replacement (3-5yr prognosis is poor)
symptoms of chronic pericarditis
dyspnea, signs of R-sided HF; no chest pain
PTCA vs CABG in diabetics
CABG shown to have better long-term mortality
which murmurs increase in intensity with valsalva?
MVP and HOCM
4 causes of CP that can quickly lead to death
1) MI; 2) Aortic dissection; 3) Tension pneumothorax; 4) PE
best rapid diagnostic test for aortic dissection
TEE
when to do echo/nuclear imaging vs electrocardiography in stress testing?
if baseline ECG is abnormal, difficult to interpret ECG changes
risk of thromboembolus with cardioversion in afib? how to avoid?
if afib < 48hrs, cardioversion usu safe; else, need anticoag first; TEE if need to confirm absence of thrombus formation
None
common causes of pleuritis in young people
viral pleurisy; also autoimmune dzs (SLE, RA), drug-induced lupus
VQ scan vs PECT for r/o PE
according to MKSAP, VQ unless high risk pt (not sure this is still true)
which drugs have mortality benefit in CAD?
beta blockers and ACEi (independent of effects on BP and LV function)
what change in heart sounds with WPW?
paradoxically split S2
P-P interval in mobitz I
constant
pathophys of mobitz II
usu a/w L or R BBB; dropped beat when the remaining branch suffers intermittent block
detecting MI in pt with LBBB
cannot assess ST depression in presence of LBBB ==> need to do nuclear imaging
use of class Ia antiarrythmics in pts with frequent PVCs
contraindicated -- proarrythmic effects of class Ia drugs outweighs benefit
in-hospital mortality of cardiogenic shock
50%
most important intervention in cardiogenic shock due to acute MI
restore patency of vessel - angiography/angioplasty
what immediate intervention in acute STEMI?
angioplasty (not thrombolysis)
what does persistent ST elevation very late after acute MI indicate? (3)
1) persistent myocardial injury; 2) ventricular aneurysm formation; 3) localized MI-related pericarditis
what is isosorbide mononitrate?
venous and arterial vasodilator used to tx angina
tx of choice for preventing post-MI remodeling
ACEi (improves LV function, reduces short- and long-term mortality, reduces incidence of heart failure, reduces incidence of recurrent reinfarction)
which cardiac pts benefit most from ACEi tx?
anterior wall MI, systolic dysfunction, or clinical evidence of CHF
when do most post-MI VSDs occur?
2-7 days after infarction (same timing as post-MI papillary rupture)
acute hypotension and bradycardia in setting of acute MI -- whats the cause?
vagal reaction
which vessels usu involved in RV infarction?
right coronary artery proximal to RV marginal branch
what can cause triad of hypotension, elevated JVP, and clear lung fields? (2)
RV infarct or tamponade
None
what kind of arrythmia a/w RV infarct?
bradycardia (from SA or AV node ischemia)
therapy for RV infarct
standard MI tx + volume loading, avoid diuretics/venodilators (eg nitrates), ?pacing
survival rate 24hrs after large VSD/papillary muscle rupture
25% with medical therapy
tx of post-MI VSD
nitroprusside or intra-aortic balloon pump
where does free wall rupture typically occur after MI?
at juncture of infarcted myocardium with normal myocardium; less often in ccenter of infarct
when does free wall rupture occure post MI?
1-4d, rarely up to 3wks after MI
coronary angiography before discharge for which patients?
pts with angina or residual ischemia (at rest or with exertion) after successful thrombolysis; for pts w/o angina/ischemia, stress test sufficient for discharge
what leads involved in lateral MI?
I, aVL, V5, V6
presentation of posterior MI on ecg
prominent R waves + ST depression in precordial leads, often a/w inferior MI
vtach vs vfib
arbitrary distinction based on cycle length; both are fatal if not corrected