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Pregnancy poses anatomic and physiologic impediments to cardiopulmonary resuscitation. Recent studies have shown that nearly 40% of obstetric providers are unaware of the pronounced differences between the resuscitation of pregnant women versus nonpregnant women.1 This chapter will review physiologic changes that occur in pregnancy, as well as causes of maternal arrest, which will form a foundation for understanding the modifications that must take place when resuscitating pregnant women.


The cardiovascular system changes dramatically throughout pregnancy. By 32 weeks’ gestation, cardiac output has increased 30% to 50% above baseline because of an increase in circulating blood volume (increased preload). Progesterone-induced smooth muscle relaxation decreases systemic vascular resistance, leading to reduced afterload and up to a 15% to 20% increase in heart rate. During labor, cardiac output will increase an additional 10% to 15% above baseline.2 It is imperative to understand that uterine blood flow is at its maximum by late pregnancy and cannot be further increased during hypoxic or low-flow states; thus, during cardiopulmonary arrest, there will be vasoconstriction of the uteroplacental bed, further compromising the fetus.3

A dilutional anemia occurs secondary to a 50% increase in plasma volume and only a 30% increase in red blood cell mass. Because of the increase in plasma volume, a substantial amount of hemorrhage can take place before signs of hypovolemia become apparent.1 This physiologic anemia may have an impact on oxygen delivery to vital organ systems, especially during cardiopulmonary arrest.3

By 20 weeks’ gestation, the uterus reaches the level of the inferior vena cava. With a pregnant woman in the supine position, the uterus may cause compression of the inferior vena cava and decrease cardiac output.2 Quantitative cardiovascular magnetic resonance imaging has shown a 24% decrease in cardiac output at 32 weeks’ gestation in the supine position as compared to the lateral position.4 By the third trimester, the uterus may completely obstruct the inferior vena cava, leading to syncope, hypotension, and bradycardia.5,6 Compression of pelvic veins is also a concern in the pregnant patient. Signs and symptoms of compression in the pelvis are dependent edema, venous stasis, varicose veins, and hemorrhoids.5 This increased venous pressure may lead to rapid blood loss in cases of injuries to the pelvis and lower extremities; therefore, it is best to avoid intravenous lines in lower extremities, especially for resuscitation efforts, because venous return from the lower extremities to the central circulation is not assured.1,5 Most importantly, in addition to compression of major vessels, the gravid uterus exerts pressure on the diaphragm, which may limit forward blood flow during chest compressions (Figure 30-1).3

Figure 30-1.

Aortocaval compression in the supine position and its alleviation with uterine displacement.

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