Dobutamine is a synthetic sympathomimetic alpha-1 / beta-1 and beta-2 agonist. Cardiac beta-1 adrenergic stimulation results in increased myocardial contractility and HR ( the inotropic effect being greater then chronotropic effect). The stimulation of alfa-1 and (beta-1) tends to offset the beta-2 effect on the vasculature (arterioles) leading to vasoconstriction, i.e. increase in BP. Thus, by increasing the cardiac workload (demand) the supply (flow) is challenged - testing if supply is sufficient to sutisfy demand.

By gradually increasing the infusion rate, HR and BP can be "titrated" until symptoms or target HR is reached. If target HR can not be reached by Dobutamine infusion alone (most often due to ongoing beta-blocker medication) small doses of Atropine (0.25 - 0.5 mg/push) often brings the HR to target.

Blood t1/2 for Dobutamine is about 2 min. Side effect or severe symptoms are usually easy to control with small doses of beta-blockers IV(Metropolol).

BP fall at higher doses of Dobutamine is relative common (15-20% of patients). This reaction is thought to be a mechano-receptor reflex initiated from LV. A BP fall during Dobutamine stress does not carry the same significance as a BP fall during physical stress test: it occur equally often in patients with CAD and in patients without CAD. Most often no treatment is necessary. If significant symptoms occur, simple leg elevation will help. In rare cases of severe symptoms small doses of beta-blockers are effective.

Ongoing treatment with beta-blockers is often a problem when using the Dobutamine protocol. It can be very difficult (or impossible) to reach the target HR, even after addition of Atropine. Pharmacological vasodilation protocols (Dipyridamole or Adenosine) are the protocols of choice in this situation.

Dobutamine should be used with caution in patient with significant arrhythmia and in patient with psychiatric history.