During normal pregnancy at 28-32 weeks, cardiac output increases by approximately 40-50% above pre-pregnancy values. The primary hemodynamic driver of this increase (in order of contribution) is:
- A Increased heart rate (75%) > increased stroke volume (25%)
- B Reduced systemic vascular resistance due to progesterone-mediated vasodilation is the only driver; cardiac output changes are secondary
- C Increased erythropoiesis drives oxygen delivery increase independent of cardiac output
- D Increased stroke volume (due to expanded plasma volume and increased preload) contributes more in early pregnancy; heart rate increases contribute more in the third trimester ✓
Explanation
The 40-50% rise in cardiac output during pregnancy is achieved by both increased stroke volume and heart rate, but their relative contributions differ by trimester. In the first and second trimesters, plasma volume expansion (up to 50%) increases preload and stroke volume predominantly (Starling mechanism). In the third trimester, compression of the inferior vena cava by the gravid uterus reduces venous return (especially supine), so heart rate increase (from ~70 to ~85-90 bpm) becomes proportionally more important. The progesterone/relaxin-mediated fall in SVR facilitates (rather than drives) the increase by maintaining low afterload, allowing the augmented output to be sustained.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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