During pregnancy, cardiac output, stroke volume, and heart rate increase beginning as early as the sixth week of gestation. These changes peak at 16 to 20 weeks and then plateau.⁵ Later in pregnancy, as the uterus increases in size, aortocaval compression begins to affect maternal hemodynamics, particularly when the patient is in the supine position. Some aortocaval compression has been noted as early as 12 to 14 weeks’ gestational age; however, it is considered to have a significant impact on maternal hemodynamics by 20 weeks’ gestational age. Maternal stroke volume progressively decreases as the size of the uterus increases. Cardiac output remains roughly the same due to the gradual increase in heart rate of 20% to 25% above baseline beginning at 20 weeks.⁶

Despite the increase in plasma volume, cardiac output, and heart rate, mean arterial pressure declines gradually throughout pregnancy before plateauing at 20 weeks’ gestational age. Systemic vascular resistance is greatly reduced in order to maintain blood flow to the placenta, likely due to increased production of relaxin and nitrous oxide, which begins in very early pregnancy. Therefore, a pregnant patient may be relatively hypotensive and tachycardic at baseline, and in cases of shock the ability to compensate by increasing peripheral vascular resistance is compromised. The placenta itself has a high sensitivity to the effects of catecholamines released during stress. Blood flow may be rapidly diverted away from the placenta, causing the fetus to suffer significant insult from decreased oxygen availability very early in maternal resuscitation.⁷

The cardiovascular hemodynamic changes are exacerbated by significant changes in maternal pulmonary physiology in late pregnancy. Maternal functional residual capacity is significantly reduced due to elevation of the diaphragm from displacement by the gravid uterus. Maternal oxygen demand is also increased by 20%. These changes result in rapid desaturation during maternal shock states. Oxygen diffusion across the placenta is dependent on a relatively high maternal partial pressure of oxygen in the alveoli (PaO₂) in order to create an oxygen gradient. If the maternal PaO₂ is less than 60 mm Hg, this gradient ceases to exist and the fetus is no longer able to extract oxygen from the maternal bloodstream, causing significant fetal distress.⁸

In addition, airway management in the pregnant patient is made challenging by increased mucosal edema, fragility, capillary congestion, and reduced lower esophageal sphincter tone, increasing the likelihood of aspiration during intubation.⁹ Failed intubation is eight times more likely in pregnant patients than in nonpregnant patients,¹⁰ and there is less time for intubation due to decreased maternal oxygen reserves as well as poor fetal tolerance to hypoxia and respiratory acidosis. Intubation should therefore be performed by the most experienced physician available, with difficult airway equipment available at the bedside.

Management of the unstable or arresting pregnant patient is further complicated by the effects of the gravid uterus on the major vessels. Aortocaval compression significantly decreases preload and increases afterload, reducing cardiac output by a significant amount when the patient is in the supine position¹¹ (Figure 24.1). At 20 weeks, stroke volume is increased by 27% when the patient is placed in the left lateral decubitus position. At 32 weeks, stroke volume is increased by 35% in the left lateral decubitus position.¹² The changes in preload and afterload with aortocaval compression can cause chest compressions to be significantly less effective, as there is less available circulating blood volume and an increased resistance to cardiac output.

The marked improvement in cardiac output seen in the left lateral decubitus position suggests that relief of aortocaval compression is a crucial step in cardiopulmonary resuscitation (CPR) in late pregnancy; however, there are obvious limitations to positioning a patient in the left lateral decubitus position during active chest compressions. There are no physiologic studies showing that chest compressions are as effective in the left lateral tilt position. In existing studies, there is significant variability in the level of tilt provided. Attempts by providers to position the patient appropriately may cause unnecessary delays in resuscitation.¹³ Given this variability and the importance of high-quality chest compressions, CPR should be performed with the patient supine. Because of
the hemodynamic effects of aortocaval compression, the AHA guidelines recommend continuous manual left uterine displacement (LUD) when the uterine fundus is at or above the umbilicus.² However, the only method of completely relieving aortocaval compression is delivery of the fetus.

In the case of maternal arrest, pregnancy-related etiologies should be considered. Cardiac disease is the most common cause of death in pregnant women. Pregnancy is a hypercoagulable state that increases the risk of venous thromboembolism; massive pulmonary embolism should always be considered as a potential etiology for cardiac arrest during pregnancy. Other potential etiologies specific to pregnancy include eclampsia, amniotic fluid embolism, hemorrhage, and peripartum cardiomyopathy.¹⁴ Pregnant women are also at a higher risk of intimate partner violence, and occult trauma should be considered in the differential of any unstable pregnant patient.¹⁵