Dobutamine is an adrenergic drug that primarily functions by stimulating beta-1 receptors in the heart. Beta-1 receptor activation increases cardiac output, which may be useful in the treatment of cardiogenic shock and severe heart failure. Dobutamine also increases myocardial oxygen demand, which makes it useful for cardiac stress testing in the diagnosis of coronary artery disease.

Key Points

  • Dobutamine
    • Beta-1 agonist > Beta 2, Alpha
      • Increases cAMP, resulting in increased cardiac output
        • Positive inotropy (Cardiac Myocytes) → increased contractility, stroke volume
        • Mild positive chronotropy (SA Node), and dromotropy (AV Node) → Increased Heart Rate
        • Dobutamine is a β-adrenergic agonist with predominant activity on β1 receptors and minimal activity on β2 and alpha-1 receptors. It causes an increase in heart rate and cardiac contractility, leading to an increase in myocardial oxygen consumption.
        • Stimulation of β1-adrenergic receptors results in increased production of cAMP in target cells and causes
          • positive inotropy (increased cardiac output and decreased LV filling pressures)
          • weakly positive chronotropic effect (increases heart rate), which combined with the positive inotropic effect increases myocardial oxygen consumption. This can trigger or exacerbate myocardial ischemia. However, in patients with acute myocardial infarction complicated by cardiogenic shock, this drawback may be outweighed by improvement in cardiac output and end-organ perfusion.
          • mild vasodilation (decrease in systemic vascular resistance): alpha1 agonist (vasoconstriction) balances the β2 agonist (vasodilation) resulting in overall mild vasodilation.
    • Clinical Use
      • Heart Failure/Cardiogenic Shock
        • used for management of refractory heart failure associated with severe left ventricular (LV) systolic dysfunction and cardiogenic shock (think of this as poor perfusion/poor cardiac output states)
        • Increased cardiac output addresses the hypoperfusion in “Cold” Heart Failure. Used to manage acute exacerbations, not chronic management
        • Increased cardiac output addresses the cardiogenic shock
      • Increases myocardial oxygen demand (Cardiac Stress Testing)
        • Positive inotropy and chronotropy can induce ischemia