In patients receiving beta-blocker therapy, dobutamine is likely to produce which hemodynamic change?

In patients receiving beta-blocker therapy, dobutamine is likely to produce which hemodynamic change?

• A. Increase in heart rate
• B. Increase in contractility
• C. Increase in systemic vascular resistance
• D. Vasodilation

Answer: (C)

Dobutamine mainly raises cardiac output by stimulating beta-1 receptors to boost contractility, with a secondary beta-2 effect that tends to vasodilate and lower systemic vascular resistance. When a patient is on beta-blocker therapy, these beta receptors are blocked, so the drug’s inotropic effect is blunted and the vasodilatory beta-2 action is diminished. With the vasodilation reduced, the vascular tone can shift toward vasoconstriction, and systemic vascular resistance can rise. Since the heart’s contractile response is also blunted, the net effect in this setting is a higher SVR rather than the usual drop in SVR seen without beta-blockade. Hence an increase in systemic vascular resistance is the most likely hemodynamic change.

Dobutamine mainly raises cardiac output by stimulating beta-1 receptors to boost contractility, with a secondary beta-2 effect that tends to vasodilate and lower systemic vascular resistance. When a patient is on beta-blocker therapy, these beta receptors are blocked, so the drug’s inotropic effect is blunted and the vasodilatory beta-2 action is diminished. With the vasodilation reduced, the vascular tone can shift toward vasoconstriction, and systemic vascular resistance can rise. Since the heart’s contractile response is also blunted, the net effect in this setting is a higher SVR rather than the usual drop in SVR seen without beta-blockade. Hence an increase in systemic vascular resistance is the most likely hemodynamic change.