| Cardiac output in labor (between uterine contractions) | 10% increase in early first stage | Increase in SV (HR unchanged) | Epidural analgesia reduces but does not fully eliminate the increases in cardiac output |
| 25% increase in late first stage |
| 40% increase in second stage |
| Systolic and diastolic blood pressures | Elevated from the late first stage | Progressive activation of the sympathetic nervous system during labor | Labor epidural analgesia attenuates these changes |
| Aortocaval compression (in the supine position) | - 20% reduction in uterine blood flow
- 50% decrease in lower extremity blood flow
| About 8% of women may develop bradycardia and significant hypotension when lying supine (supine hypotensive syndrome) |
| Uterine blood flow and uterine contractions during labor | Increases to 600–900 mL/min on average (50–190 mL/min preconception) | Uterine contractions augment CO and SV by an additional 15–25% (300–500 mL of blood displaced with each contraction) |
| Compression of the aorta by the uterus increases with contractions | Reduces uterine filling and increases afterload |
| Immediate postpartum hemodynamics | CVP rises and cardiac output increases up to 75% of predelivery values | Relative hypervolemia and increased venous return in this period is a result of relief of caval compression and reduction of vascular capacitance, which exceeds the blood loss of labor (autotransfusion) |
| Further postpartum hemodynamics | - During the first hour postpartum term, CO decreases to 30% above the prelabor value; it reaches the prelabor value about 48 h postpartum
- CO 10% above prepregnant value at 2 weeks, returns to baseline at 12–24 weeks postpartum
- HR normalizes in 2 weeks
- Stroke volume takes much longer and is still 10% above baseline at 24 weeks
- LV hypertrophy regresses gradually and is still appreciable at 24 weeks
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