- See: -
Inotropic Agents - Inotropic agent (not vasoconstrictor); - Useful in pt w/ poor
CO output, elevated left ventricular filling pressures (PAOP > 18mm Hg), & marginal systemic blood pressures; - For Shock syndrome as result of
MI, endotoxins, trauma, Renal failure; - Selective B1 stimulator; - Causes direct iotropic stimulatorwith reflex vasodilation & increase
CO; - SBP remains constant; - Causes less
Tachycardia than Dopamine - at higher doses, beta-2 activity increases, resulting in
Tachycardia and peripheral vasodilation; - w/ high systemic vascular resistance, dobutamine dose can be increased to give beta 2 mediated arterial vasodilation;
- Use w/ Myocardial Infarct: - dobutamine's lack of induction of endogenous
Norepinephrine minimizes its effect on myocardial oxygen demand; - when titrated to avoid significant increases in heart rate, dobutamine does not increase infarct size or elicit arrhythmias; - heart rate may decrease as hemodynamics improve; - since vasodilation occurs in response to increased cardiac output, blood pressure may change very little; - hence, dobutamine is agent of choice w/ hemodynamically signficant Rt. ventricular infarction;
- Dosage: * infused at 2.5 - 10 ug/kg/min (Diluted: 250mg/250ml of D5W); * maximum dose of 30 ug/kg/min - must decrease dosage if SBP > 130mm Hg - note
Tachycardia ( > 10% may get Ischemia) and ectopic ventricular beats, evaluate BP, volume status; *
dopamine and dobutamine have been used together; - combination of moderate doses of both drugs maintain arterial pressure better with less of an increase in wedge pressure and, thus, less pulmonary congestion than dopamine alone;
- Precautions: * Must correct hypovolemia Before use, consider Swan Ganz; * Decrease dosage with
MAOI use; * Note Dobutamine produces little vaso-constriction at usual doses and has no role in the absence of spontaneous circulation; Check BP & HR;
