Inotropic Therapy in ADHF Flashcards
Inotropic Therapy Indication in ADHF
Cold and wet (Forester subset IV) or cold and dry exacerbations (Forester III) (if PCWP > 15 mm Hg)
Dobutamine Mechanism of action
β1-Agonist: Stimulates AC to convert ATP to cAMP to ↑ CO; slight peripheral vasodilation
Dobutamine Clinical effects
Positive inotropic, chronotropic, lusitropic effects
Dobutamine Dosing in ADHF
Start 2.5–5 mcg/kg/min IV; max of 20 mcg/kg/min
Dobutamine Elimination
Half life = 2 min, Hepatically metabolized (inactive), renally eliminated
Dobutamine AEs
hypokalemia, myocardial ischemia, tachyphylaxis
Dobutamine over Milrinone in ADHF
Dobutamine may be favored in: Severe hypotension, Bradycardia, Thrombocytopenia, Severe renal impairment
Milrinone Mechanism of action
PDE inhibitor: Inhibits cAMP breakdown in heart to ↑ CO and in vascular smooth muscle to ↓ SVR
Milrinone Clinical effects
Positive inotropic and lusitropic effects,
no direct chronotropic effects
Milrinone Dosing in ADHF
Start 0.1–0.2 mcg/kg/min IV; may titrate to max of 0.75 mcg/kg/min
Milrinone Elimination
half life = 1 hr, prolonged to 2–3 hr if HF or CrCl < 50 mL/min; 90% renal
Milrinone over Dobutamine in ADHF
Milrinone may be favored: To avoid tapering or discontinuing home β-blocker, When pulmonary artery pressures are high