Cardiac physiology review
Physiologic changes in acute sepsis
- The cardiac output curve shifts up dramatically, due to two factors. First, arterial vasodilation reduces the afterload on the heart, increasing cardiac output. Second, sympathetic nervous system activation stimulates increased heart rate and contractility.
- The venous response curve shifts to the left, due to multiple factors. First, venodilation decreases the stressed volume of blood within the veins. Second, venodilation may increase the venous compliance. The combination of decreased stressed volume and increased venous compliance causes a reduction in the mean systemic filling pressure, which shifts the venous response curve to the left. There may also be some extravasation of fluid out of the vasculature (“third spacing”), further reducing the stressed volume in the venous system.
What happens if we treat with volume resuscitation?
What happens if we treat with norepinpehrine?
- Norepinephrine stimulates venoconstriction, which increases the stressed volume of blood in the venous system and also decreases the venous compliance. Increased stressed volume and reduced venous compliance increases the mean systemic filling pressure, shifting the venous return curve back to the right.
- The cardiac output curve will shift downward. Norepinephrine does have some beta-agonist activity which will tend to increase contractility. However, the dominant effect in this scenario is often the increase in systemic vascular resistance which increases afterload, thereby decreasing the cardiac output.
Image credits: https://en.wikipedia.org/wiki/Hepatic_vein#/media/File:Gray1121.png
- IBCC chapter & cast – BRASH syndrome - September 28, 2020
- IBCC chapter & cast – Hemophagocytic LymphoHistiocytosis (HLH) - September 21, 2020
- IBCC chapter & cast –Gastrointestinal hypomotility in critical care - September 14, 2020