indicated when parenteral therapy is necessary for inotropic support in the short-term treatment of patients with cardiac decompensation due to depressed contractility, which could be the result of either organic heart disease or cardiac surgical procedures.
Not useful in ischemic heart disease because it increases heart rate and thus increases myocardial oxygen demand.
Direct-acting inotropic agent whose primary activity results from stimulation of the beta-adrenoceptors of the heart
Produces comparatively mild chronotropic, hypertensive, arrhythmogenic, and vasodilative effects
Does not cause the release of endogenous norepinephrine, as does dopamine
Primary activity results from stimulation of the β1-adrenoceptors of the heart, increasing contractility and cardiac output.
Since it does not act on dopamine receptors to induce the release of norepinephrine (another α1 agonist), dobutamine is less prone to induce hypertension than is dopamine.
Predominantly a β1-adrenergic agonist, with weak β2 activity, and α1 selective activity
used clinically in cases of cardiogenic shock for its β1 inotropic effect in increasing heart contractility and cardiac output.
Administered as a racemic mixture consisting of both (+) and (−) isomers
Half life 2 minutes
In human urine, the major excretion products are the conjugates of dobutamine and 3-O-methyl dobutamine
Increased risk of arrhythmia, including fatal arrhythmias
Hypertension, angina, arrhythmia, and tachycardia
Used with caution in atrial fibrillation as it has the effect of increasing the atriovenrticular (AV) conduction