Which of the following is NOT a primary mechanism by which isoproterenol increases cardiac output?

Which of the following is NOT a primary mechanism by which isoproterenol increases cardiac output?

• A. Direct beta-adrenergic activation
• B. Increased heart rate
• C. Increased contractility
• D. Increased systemic vascular resistance

Answer: (D)

Isoproterenol is a nonselective beta-adrenergic agonist, so its primary actions come from stimulating beta-1 receptors in the heart and beta-2 receptors in vascular smooth muscle. On the heart, beta-1 activation increases the rate of firing at the SA node (positive chronotropy) and enhances calcium availability in cardiac myocytes (positive inotropy), both of which raise cardiac output. In addition, beta-2 activation causes vasodilation in many vascular beds, especially skeletal muscle, which lowers systemic vascular resistance and reduces afterload, further supporting an increase in output. Therefore, the ways isoproterenol raises cardiac output are direct beta-adrenergic stimulation of the heart (increasing heart rate and contractility) and reduced afterload from vasodilation. Increased systemic vascular resistance would oppose the rise in cardiac output, so it is not a primary mechanism by which isoproterenol works.

Isoproterenol is a nonselective beta-adrenergic agonist, so its primary actions come from stimulating beta-1 receptors in the heart and beta-2 receptors in vascular smooth muscle. On the heart, beta-1 activation increases the rate of firing at the SA node (positive chronotropy) and enhances calcium availability in cardiac myocytes (positive inotropy), both of which raise cardiac output. In addition, beta-2 activation causes vasodilation in many vascular beds, especially skeletal muscle, which lowers systemic vascular resistance and reduces afterload, further supporting an increase in output.

Therefore, the ways isoproterenol raises cardiac output are direct beta-adrenergic stimulation of the heart (increasing heart rate and contractility) and reduced afterload from vasodilation. Increased systemic vascular resistance would oppose the rise in cardiac output, so it is not a primary mechanism by which isoproterenol works.