Which vasopressor increases systemic vascular resistance at both low and high doses, with usually unchanged or decreased cardiac output and decreased renal blood flow?

Which vasopressor increases systemic vascular resistance at both low and high doses, with usually unchanged or decreased cardiac output and decreased renal blood flow?

• A. Dopamine
• B. Norepinephrine
• C. Epinephrine
• D. Isoproterenol

Answer: (B)

Adrenergic receptor effects explain this pattern. Norepinephrine acts mainly on alpha-1 receptors, causing robust vasoconstriction of systemic arterioles and a rise in systemic vascular resistance across both low and high doses. Its beta-1 activity can modestly increase heart rate and contractility, but this often does not translate into a higher cardiac output when afterload is markedly increased; in many situations the overall cardiac output remains the same or decreases. The strong vasoconstriction also reduces renal blood flow because the renal arterioles constrict in response to the drug. Other vasopressors don’t fit this profile as neatly. Dopamine has dose-dependent effects and can improve renal perfusion at very low doses due to dopaminergic receptors, and epinephrine tends to raise cardiac output more noticeably (via beta-1 effects) in addition to vasoconstriction, so its impact on cardiac output is less likely to be unchanged or decreased. Isoproterenol lowers systemic vascular resistance by beta-2 stimulation and increases cardiac output, which contradicts the described pattern. Therefore, norepinephrine best matches the described effect: increased systemic vascular resistance at both low and high doses with usually unchanged or decreased cardiac output and decreased renal blood flow.

Adrenergic receptor effects explain this pattern. Norepinephrine acts mainly on alpha-1 receptors, causing robust vasoconstriction of systemic arterioles and a rise in systemic vascular resistance across both low and high doses. Its beta-1 activity can modestly increase heart rate and contractility, but this often does not translate into a higher cardiac output when afterload is markedly increased; in many situations the overall cardiac output remains the same or decreases. The strong vasoconstriction also reduces renal blood flow because the renal arterioles constrict in response to the drug.

Other vasopressors don’t fit this profile as neatly. Dopamine has dose-dependent effects and can improve renal perfusion at very low doses due to dopaminergic receptors, and epinephrine tends to raise cardiac output more noticeably (via beta-1 effects) in addition to vasoconstriction, so its impact on cardiac output is less likely to be unchanged or decreased. Isoproterenol lowers systemic vascular resistance by beta-2 stimulation and increases cardiac output, which contradicts the described pattern.

Therefore, norepinephrine best matches the described effect: increased systemic vascular resistance at both low and high doses with usually unchanged or decreased cardiac output and decreased renal blood flow.