USMLE

Description:	CV Pharm 2
Category:	USMLE
Created by:	Asclepius on 2008-10-19

Question	Answer
goal of antianginal therapy	reduce myocardial oxygen consumption
name 5 determinants of antianginal therapy	end diastolic volume, blood presure, heart rate, contractility, and ejection time
how do nitrates effect end diastolic volume, blood pressure, contractility, heart rate, and ejection time	decrease EDV, decrease BP, increase contractility (reflex), increase HR (reflex), decrease Ejection time
how does beta-blocker affect end-diastolic volume, blood pressure, contractility, heart rate, ejection time	increase EDV, decrease BP, decrease contractility, decrease HR, increase ejection time
name 3 factors that combo beta-blockers + nitrates will decrease	blood pressure, heart rate, and overall myocardial oxygen consumption
for calcium channel blockers, what drug is similar to nitro	nifedipine
for calcium channel blockers, what durg is similar to beta-blockers	verapamil
define bioavailability, protein bound percentage, where excreted, and 1/2 life for digoxin	75% availability, 20-40% bound, excreted in kidney, 40 hours t(1/2)
mechanism for digoxin	block Na/K ATPase, increase Na, slow Na/Ca antiport, increases Ca in ECM, positive inotrope
how does digoxin affect ECG readings	vagal effects increase PR, decrease QT, T wave inversion on ECG, and scooping of ST segment
name 2 uses for digoxin	CHF (increase contractility) and A-Fib (decrease conduction at AV node)
5 major general digoxin side efects	nausea, vomiting, diarrhea, blurry yellow vision, arrhythmia
name 3 contraindications with digoxin	renal failure, quinidine (will displace dig on protein, potentiate effect), hypokalemia (potentiate effect)
what is the antidote for digoxin	slowly normalize K, lidocaine, cardiac pacer, anti-dig Fab fragments
describe function that all class I antiarrhythmics have	decrease slope of phase 4 depolarization by blocking Na channels
define state dependency and state what drugs are state dependent	class I antiarryhtmics. selectively depress tissue that is depolarized
name 4 class Ia antiarrhythmics	Queen Amy Proclaims Diso's pyramid: quinidine, amiodarone, procainamide, disopyramide
name 3 mechanisms of class Ia antiarrhythmics	increase AP duration, increase ERP, increase QT interval
what do you use class Ia antiarrhythmics for?	atrial and ventricular arrhythmias
quinidine toxicities	cinchonism: headache, tinnitisum, thrombocytopenia plus torsades
procainamide toxicity	reversible lupus like side effect
name 3 class IB antiarrhythmics	lidocaine, mexiletine, tocainide
mechanism for class IB	decrease AP duration by blocking Na channel
where does class IB affect?	affect ischemic or depolarized purkinje and ventricular tissue.
what is class IB useful for?	acute ventricular arrhythmias (post-MI) and digitalis induced arrhythmia
name 4 side effects of class IB	local anesthetic, cns stimulation, cns depression, cardiovascular depression
name 3 class IC antiarrhythmics	flecainide, encainide, propafenone
name mechanism of class IC	no effect on AP
what is class IC sueful for?	v-tach that progress to V fib and also for SVT. usuaully only last resort for refractory tachyarrhythmias
class IC toxicities	proarrhythmitic, especially post-MI (contraindiciated)
name 5 class II antiarrhythmics	propanolol, esmolol, metoprolol, atenolol, timolol
mechanism of class II antiarrhythmics	Beta-blockers; decrease cAMP, decrease Ca currents, decrease slope phase 4, increase PR interval at AV node
what is a short acting class II	esmolol
name 5 side effects of class II drugs	mask hypoglycema, impotence, asthma, CV effects (bradycardia, av block, chf). sleep alterations
name 4 class III antiarrhythmics	sotalol, ibutilide, bretylium, amiodarone
mecanism of class III	block K channels; increase AP duration, increase ERP, increase QT, used when others fail