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