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Cardiovascular - Pharmacology


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vasodilator with lupus-like syndrome as side effect?
mechanism of hydralazine?
increases cGMP - smooth muscle relaxation; vasodilates arterioles > veins; reduces afterload
what calcium channel blocker is most selective for peripheral vasculature?
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?
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?
what happens to contractility and HR in nitrate therapy?
increase - reflex response
what do beta blockers affect in antianginal therapy?
how do nitrates affect ejection time and MVO2?
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?
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?
what are the class IA antiarrythmics?
Na+ channel blockers:
quinidine, amiodarone, procainamide, disopyramide
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this class IA antiarrhythmic can cause cinchonism (headache, tinnitus, thrombocytopenia), torsades de pointes (due to increased QT interval)
what class of antiarrhythmics are contraindicated post-MI
class IC - proarrhythmic
what beta blocker is very short acting?
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?
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?
what is the drug of choice for diagnosing/abolishing AV nodal arrhythmias?
what depresses ectopic pacemakers, especially in digitoxin toxicity?
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?
in patients with wolff parkinson white and atrial fibrillation, what can digitoxin do?
enhance transmission through accessory pathways that can predispose to v tac

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