-inhibits Na-K-ATPase and increases intracellular Ca2+
-used for heart failure as an ionotropic agent
-increased contractility, stroke volume, and blood flow to kidney
-decreased LV end diastolic volume
-decreased ventricular size and tension
-can also decrease heart rate by increasing vagal tone = slows SA firing an AV
conduction
-USED IN PTS WITH ATRIAL FIBRILLATION OR FLUTTER
-limitations: t1/2 is 36 hr, renal elimination, and low therapeutic index
-can cause nausea, vomiting, diarrhea, visual changes
-can cause arrhythmias = bradycardia, AV block, ventricular premature
beats/tachycardia
Digoxin toxicity treatment
-lower dose or drug withdrawal
-potassium if pt has low serum K+
-atropine = blocks vagal effects
, -lidocaine = ventricular arrhythmias
-glycoside antibodies = DIGIBIND
Digibind
-antidote for digoxin toxicity
digitalis interactions
-serum potassium
-hypercalcemia = additive effects so serum Ca2+ must be low prior to treatment
-hypomagnesemia = sensitizes to arrhythmias
Captopril, Enalapril, Lisinopril
-ACE inhibitors
-Reduce levels of angiotensin II (blocks conversion of ANGI to ANGII)
-increased levels of bradykinin (vasodilation?)
-decreased afterload = increased stroke volume
-decreased preload and congestion due to venodilation
-decreased aldosterone = decreased blood volume
-SLOWS progression of hypertrophy/remodeling = decreased mortality
-ENALAPRIL IS PRODRUG (metabolized to enalaprilat)
-used in heart failure as a neurohormonal modulator
Losartan, Valsartan, Candesartan
-ANG II receptor blockers (ARBS)
-blocks RAAS system
-increased levels of bradykinin (vasodilation?)
-decreased afterload = increased stroke volume
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