Vasodilators in ADHF Flashcards
Vasodilator benefit in ADHF
increase venous capacitance, resulting in lower preload to reduce myocardial stress.
Limits ischemia and helps preserve cardiac tissue Produces rapid symptomatic benefit by reducing pulmonary congestion
Sodium Nitroprusside MOA
Nitric oxide–induced stimulation of GC to convert GTP to cGMP
Sodium Nitroprusside Clinical effects
Balanced arterial and venous vasodilator
Sodium Nitroprusside Indications
Warm and wet ADHF, alternative to inotropes in cold and wet ADHF, hypertensive crises
Sodium Nitroprusside Dosing in ADHF
0.1–1 mcg/kg/min IV
Sodium Nitroprusside Elimination
Half-life < 10 min, Cyanide hepatically metabolized,
thiocyanate renally excreted (accumulation in dysfunction)
Nitroglycerin Mechanism of action
Combines with sulfhydryl groups in vascular endothelium to create S-nitrosothiol compounds that mimic nitric oxide’s stimulation of GC and production of cGMP
Nitroglycerin Clinical effects
Preferential venous vasodilator > arterial vasodilator, arterial vasodilation at high doses
Nitroglycerin Indications
Warm and wet ADHF, ACS, or hypertensive crises
Nitroglycerin Dosing in ADHF
5 -100 mcg/min, 200 mcg/min max
Nitroglycerin Elimination
Half-life = 1–3 min, Inactive metabolites in urine