- 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