Which statement describes a potential hemodynamic effect of norepinephrine when titrated to treat septic shock at high doses?

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Multiple Choice

Which statement describes a potential hemodynamic effect of norepinephrine when titrated to treat septic shock at high doses?

Explanation:
High-dose norepinephrine can constrict both arterioles and venous capacitance vessels. While its primary goal in septic shock is to raise arterial pressure by increasing systemic vascular resistance, the intense venous constriction at high doses can reduce the venous reservoir’s capacity and raise right atrial pressure, narrowing the pressure gradient that drives venous return to the heart. That can lead to a decrease in venous return (and preload) despite an elevated mean arterial pressure. So, the possibility of reduced venous return is a real hemodynamic effect at high doses. The other statements don’t fit because norepinephrine typically increases systemic vascular resistance and often raises mean arterial pressure; it is not expected to decrease SVR or have no effect on MAP.

High-dose norepinephrine can constrict both arterioles and venous capacitance vessels. While its primary goal in septic shock is to raise arterial pressure by increasing systemic vascular resistance, the intense venous constriction at high doses can reduce the venous reservoir’s capacity and raise right atrial pressure, narrowing the pressure gradient that drives venous return to the heart. That can lead to a decrease in venous return (and preload) despite an elevated mean arterial pressure. So, the possibility of reduced venous return is a real hemodynamic effect at high doses.

The other statements don’t fit because norepinephrine typically increases systemic vascular resistance and often raises mean arterial pressure; it is not expected to decrease SVR or have no effect on MAP.

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