| Question |
Answer |
| flow of blood through PDA? |
aorta to left pulmonary artery |
| ACE inhibitors can cause what type of electrolyte disturbance? |
hyperkalemia |
| small mass on mitral valve with finger-like projections; non-neoplastic |
papillary fibroelastoma |
| calcium channel blocker associated with accelerated progression of CHF? |
verapamil |
| drug to slow ventricular response in Wolff-Parkinson White? |
ibutilide |
| hypersensitivity angiitis or microscopic polyarteritis nodosa (can be caused by penicilin) |
leukocytoclastic angiitis |
| in which part of the systemic circulation does the greatest decrease in blood pressure occur? |
arterioles |
| vasodilator with lupus-like syndrome as side effect? |
hydralazine |
| mechanism of hydralazine? |
increases cGMP - smooth muscle relaxation; vasodilates arterioles > veins; reduces afterload |
| what calcium channel blocker is most selective for peripheral vasculature? |
nifedipine |
| mechanism of calcium channel blockers? |
block voltage-dependent L-type calcium channels of cardiac and SM and thereby reduce contractility |
| which calcium channel blocker is not used to treat arrhythmias? |
nifedipine |
| what is the goal of antianginal therapy? |
reduce myocardial O2 consumption by decreasing 1 or more of the determinants of MVO2: EDV, BP, HR, contractility, ejection time |
| what do nitrates affect in antianginal therapy? |
preload |
| what happens to contractility and HR in nitrate therapy? |
increase - reflex response |
| what do beta blockers affect in antianginal therapy? |
afterload |
| how do nitrates affect ejection time and MVO2? |
decrease |
| how do beta blockers affect ejection time? |
increase it |
| what do beta blockers do to EDV? |
increase it |
| what do beta blockers do to BP, contractility, and HR? |
decrease them |
| what is digitoxin used for? |
CHF (increases contractility) and atrial fibrillation (decreases conduciton at the AV node) |
| toxicities of digitoxin are increased by what? |
renal failure, hpokalemia, and quinidine |
| blurry yellow vision is side effect of what? |
digitoxin |
| what is the antidote for digitoxin? |
slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments |
| lupus-like syndrome is associated with what class IA antiarrythmic? |
procainamide |
| what are the class IA antiarrythmics? |
Na+ channel blockers: quinidine, amiodarone, procainamide, disopyramide (queen amy proclaims disco pyramids) |
| this class IA antiarrhythmic can cause cinchonism (headache, tinnitus, thrombocytopenia), torsades de pointes (due to increased QT interval) |
quinidine |
| what class of antiarrhythmics are contraindicated post-MI |
class IC - proarrhythmic |
| what beta blocker is very short acting? |
esmolol |
| what is the antiarrhythmic action of beta blockers? |
decrease cAMP and calcium currents; suppress abnormal pacemaker by decreasing slope of phase 4 - AV node particularly sensitive - increased PR interval |
| toxicity of amiodarone? |
pulmonary fibrosis, hepatotoxicity, hypo/hyperthroidism;corneal deposits, skin deposits resulting in photodermatitis, neuro effects, constipation, bradycardia, heart block, CHF |
| K+ channel blockers that can cause torsades de pointes |
soltalol, ibutilide |
| K+ channel blocker that can cause new arrhythmias and hypotension? |
bretylium |
| wha type of cells do Ca2+ channel blockers primarily affect? |
AV nodal cells |
| what type of antiarrhythmics are used for prevention of nodal arrhythmias? |
class IV - Ca2+ channel blockers |
| what class IV antiarrhythmic can cause torsades de pointes? |
bepridil |
| what is the drug of choice for diagnosing/abolishing AV nodal arrhythmias? |
adenosine |
| what depresses ectopic pacemakers, especially in digitoxin toxicity? |
K+ |
| Mg+ is effective for treating what? |
torsades de pointes and digitoxin toxicity |
| drug for hypertension in patient with PKD? |
ACE inhibitor |
| anti-hypertesive for pregnant woman? |
methyldopa |
| in patients with wolff parkinson white and atrial fibrillation, what can digitoxin do? |
enhance transmission through accessory pathways that can predispose to v-tach |