Which statement about the hemodynamic state in cirrhosis is most accurate when SVO2 is high?

Which statement about the hemodynamic state in cirrhosis is most accurate when SVO2 is high?

• A. Low cardiac output
• B. High systemic vascular resistance
• C. Increased cardiac output with low systemic vascular resistance
• D. Intravascular depletion

Answer: (C)

In cirrhosis the circulation often becomes hyperdynamic due to widespread vasodilation, especially in the splanchnic circulation. This causes a drop in systemic vascular resistance and a perceived underfilling of the effective arterial blood volume. In response, the heart ramps up its output to maintain blood pressure and perfusion. Because oxygen delivery to tissues rises with this high cardiac output, the mixed venous oxygen saturation (SVO2) increases. So, when SVO2 is high, the most accurate description of the hemodynamic state is increased cardiac output coupled with low systemic vascular resistance. The other patterns don’t fit this scenario: low cardiac output wouldn’t produce the high SVO2 seen with the hyperdynamic state; systemic vascular resistance remains low rather than high due to NO-mediated vasodilation; and intravascular depletion would tend to lower CO and SVO2 rather than raise SVO2.

In cirrhosis the circulation often becomes hyperdynamic due to widespread vasodilation, especially in the splanchnic circulation. This causes a drop in systemic vascular resistance and a perceived underfilling of the effective arterial blood volume. In response, the heart ramps up its output to maintain blood pressure and perfusion. Because oxygen delivery to tissues rises with this high cardiac output, the mixed venous oxygen saturation (SVO2) increases. So, when SVO2 is high, the most accurate description of the hemodynamic state is increased cardiac output coupled with low systemic vascular resistance.

The other patterns don’t fit this scenario: low cardiac output wouldn’t produce the high SVO2 seen with the hyperdynamic state; systemic vascular resistance remains low rather than high due to NO-mediated vasodilation; and intravascular depletion would tend to lower CO and SVO2 rather than raise SVO2.