Drugs to Treat CHF Flashcards
Vasodilators
Hydralazine, Organic Nitrates, Nitroprusside
Drug Options
Vasodilators, ACE Inhibitors, ARBs, Beta-blockers, Positive Inotropic Drugs, Phosphodiesterase Inhibitors, Diuretics
Positive Inotropic Drugs
Digoxin, Dobutamine, Dopamine
Positive Inotropic and Vasodilator Activity
Phosphodiesterase Inhibitors
Effects of Vasodilators in CHF
venodilators: decrease preload –> decrease LVEDV –> decrease CO –> decrease LVEDP –> decrease edema
arteriodilators: decrease TPR –> decrease after load –> increased SV –> increased CO –> increased tissue perfusion; CO improves so much that it does not affect the BP and HR
Nitroprusside
venous=arterial vasodilation
balanced decrease in preload and after load
increases cardiac output with minimal changes in BP and HR in CHF
only given IV
Organic Nitrates
ventilation > arteriodilation
low doses: decrease preload –> decrease congestion and edema by decreasing CO
high doses: decrease preload and after load
acute Tx with nitroglycerin tablet, chronic Tx with ISDN or Nitroglycerin patch
decrease mortality when ISDN combined with hydralazine
Hydralazine
arteriodilator
decrease after load leading to an increase in SV and an increase in CO
decrease mortality when combined with ISDN
ACE Inhibitors/ ARBs
decrease after load and preload
decrease afterload –> increase SV –> increase CO
decreases LVEDP: (ventilation, decreased RAA leading to a decrease in salt and water retention)
minimal changes in BP and HR
decreases detrimental remodeling
decrease mortality in CHF
Nesiritide
recombinant human B-type natriuretic peptide, activates guanylyl cyclase increasing cGMP causing vasodilation
decreased after load and decreases preload
IV Tx acute decompensated CHF
Type III Phosphodiesterase Inhibitors
increase cAMP in heart causing an increase in cardiac contractility and an increase in CO
increase cAMP in vascular smooth muscle causing vasodilation and increasing CO
increasing CO and vasodilation causes minimal BP and HR changes
Drug: Milrinone - used as short term IV Tx of severe acute CHF - can cause pro arrhythmic effect, thrombocytopenia, and hypotension
Beta- Blockers
Carvedilol, Metoprolol, and Bisoprolol
slow AV nodal conduction, negative inotropic, slow progression, antiarrhythmic effect
decreases mortality and morbidity
inhibits detrimental cardiac remodeling
initiate dosing gradually with careful monitoring
Tx for compensated CHF
Digoxin
Mechanism: directly increases contractility
inhibits Na-K ATPase increasing intracellular Ca increasing contractility
Vagomimetic effects: decrease automaticity in SA node decreasing HR, decreases AV nodal conduction leading to an increase in PR interval causing an AV block)
can lead to tachyarrhythmias and arrhythmias at high doses
DOES NOT DECREASE MORTALITY
Low therapeutic index, Renal Excretion (must be adjusted for renal function)
t1/2= 1.5 - 1.7 days
Effects of Digoxin
increase cardiac contractility
increase CO
decrease venous pressure and decrease heart size
decrease HR
diuresis
decrease O2 demand
decrease sympathetic tone decreasing the TPR
Uses of Digoxin
CHF with A. fib
decrease V rate in A flutter and A fib