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USMLE
CV Pharm 2
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 |