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Although cardiac arrest in pregnant patients is rare (it is estimated to occur once in every 30,000 deliveries), the incidence of maternal death has been increasing recently in the U.S. In 2005, there were 15.1 deaths per 100,000 live births1 However, the National Health Promotion and Disease Prevention Objectives of Healthy People 2010 identified a rate of no more than 3.3 maternal deaths per 100,000 live births as a national goal.2 Factors associated with a higher risk of pregnancy-related death include advancing maternal age, race, increasing live birth order, lack of prenatal care, and being an unwed mother.3

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The leading causes of maternal death in the U.S. are pulmonary embolism, hemorrhage, pregnancy-induced hypertension, and infection3 (Table 16-1). Although pulmonary embolism is the most common medical cause of death in pregnant women, homicide is the most common overall cause of maternal death.4 Interpersonal violence indicators should be examined in all pregnant patients as a preventive measure.

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Table 16-1 Pregnancy-Related Causes of Maternal Cardiopulmonary Arrest 
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Uteroplacental blood flow is directly related to maternal blood volume and arterial pressure. Support of maternal blood volume and oxygenation is the best way to prevent fetal hypoxia. With this principle in mind, a detailed understanding of cardiac arrest physiology is important. A more complete discussion of fetomaternal physiology can be found in Chapter 103, Normal Pregnancy, but several points are discussed and put in perspective here.

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The maternal cardiovascular system undergoes dramatic changes during pregnancy. Cardiac output increases 30% to 45% above baseline levels by the 20th week of gestation and remains at that level until delivery. In addition, the mean arterial blood pressure gradually falls throughout the first two trimesters of pregnancy and returns to baseline levels by term. This change is a result of decreased resistance in the pulmonary and uteroplacental circulations. The uteroplacental mass increases and requires 10% of systemic blood volume by term, compared with a baseline of 2%. By the second half of pregnancy, the uteroplacental vascular bed functions as a passive low-resistance system, with flow determined by maternal perfusion pressure. Thus, in a state of cardiac compromise, uterine blood flow is greatly diminished. The addition of vasopressors with α- and β-adrenergic effects can cause significant vasoconstriction, thereby ...

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