CV 6
Help!
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| flow of blood through PDA? | aorta to left pulmonary artery
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| ACE inhibitors can cause what type of electrolyte disturbance? | hyperkalemia
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| small mass on mitral valve with finger-like projections; non-neoplastic | papillary fibroelastoma
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| calcium channel blocker associated with accelerated progression of CHF? | verapamil
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| drug to slow ventricular response in Wolff-Parkinson White? | ibutilide
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| hypersensitivity angiitis or microscopic polyarteritis nodosa (can be caused by penicilin) | leukocytoclastic angiitis
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| in which part of the systemic circulation does the greatest decrease in blood pressure occur? | arterioles
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| vasodilator with lupus-like syndrome as side effect? | hydralazine
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| mechanism of hydralazine? | increases cGMP - smooth muscle relaxation; vasodilates arterioles > veins; reduces afterload
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| what calcium channel blocker is most selective for peripheral vasculature? | nifedipine
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| mechanism of calcium channel blockers? | block voltage-dependent L-type calcium channels of cardiac and SM and thereby reduce contractility
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| which calcium channel blocker is not used to treat arrhythmias? | nifedipine
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| 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
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| what do nitrates affect in antianginal therapy? | preload
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| what happens to contractility and HR in nitrate therapy? | increase - reflex response
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| what do beta blockers affect in antianginal therapy? | afterload
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| how do nitrates affect ejection time and MVO2? | decrease
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| how do beta blockers affect ejection time? | increase it
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| what do beta blockers do to EDV? | increase it
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| what do beta blockers do to BP, contractility, and HR? | decrease them
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| what is digitoxin used for? | CHF (increases contractility) and atrial fibrillation (decreases conduciton at the AV node)
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| toxicities of digitoxin are increased by what? | renal failure, hpokalemia, and quinidine
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| blurry yellow vision is side effect of what? | digitoxin
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| what is the antidote for digitoxin? | slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments
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| lupus-like syndrome is associated with what class IA antiarrythmic? | procainamide
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| what are the class IA antiarrythmics? | Na+ channel blockers: quinidine, amiodarone, procainamide, disopyramide (queen amy proclaims disco pyramids)
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| this class IA antiarrhythmic can cause cinchonism (headache, tinnitus, thrombocytopenia), torsades de pointes (due to increased QT interval) | quinidine
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| what class of antiarrhythmics are contraindicated post-MI | class IC - proarrhythmic
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| what beta blocker is very short acting? | esmolol
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| 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
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| toxicity of amiodarone? | pulmonary fibrosis, hepatotoxicity, hypo/hyperthroidism;corneal deposits, skin deposits resulting in photodermatitis, neuro effects, constipation, bradycardia, heart block, CHF
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| K+ channel blockers that can cause torsades de pointes | soltalol, ibutilide
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| K+ channel blocker that can cause new arrhythmias and hypotension? | bretylium
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| wha type of cells do Ca2+ channel blockers primarily affect? | AV nodal cells
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| what type of antiarrhythmics are used for prevention of nodal arrhythmias? | class IV - Ca2+ channel blockers
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| what class IV antiarrhythmic can cause torsades de pointes? | bepridil
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| what is the drug of choice for diagnosing/abolishing AV nodal arrhythmias? | adenosine
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| what depresses ectopic pacemakers, especially in digitoxin toxicity? | K+
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| Mg+ is effective for treating what? | torsades de pointes and digitoxin toxicity
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| drug for hypertension in patient with PKD? | ACE inhibitor
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| anti-hypertesive for pregnant woman? | methyldopa
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| in patients with wolff parkinson white and atrial fibrillation, what can digitoxin do? | enhance transmission through accessory pathways that can predispose to v-tach
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