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Cardiopulmonary arrest occurs in 1/20 000 to 1/50 000 pregnancies. Maximizing survival for all victims requires timely identification of the cause of arrest, prompt initiation of cardiopulmonary resuscitation (CPR) and, in certain circumstances, emergent Cesarean delivery to achieve optimal outcomes for the mother and, potentially, the infant.


While a pregnant patient is usually younger with fewer comorbidities than a nonpregnant patient, there are many causes of cardiac arrest unique to the parturient, often precipitated or exacerbated by maternal physiologic changes of pregnancy (Table 169-1).

TABLE 169-1Common Causes of Maternal Cardiac Arrest

Anesthesia-related causes of cardiac arrest, while steadily declining, relate to failed intubation and the inability to ventilate. More recently, supraglottic devices and videolaryngoscopes have improved outcomes in these situations. Rarely, epidural-associated local anesthetic toxicity can cause complete cardiovascular collapse. The incidence of local toxicity has been declining due to the use of lower concentrations of local anesthetics, increased awareness of toxicity by anesthesiologists, and improved safety measures during the procedure. Despite this, anesthesia-related complications are still the seventh leading cause of maternal death in the United States.


Difficulty in securing the airway is multifactorial. Circulating progesterone leads to airway edema and friability and to decrease lower esophageal sphincter tone, resulting in a higher incidence of gastroesophageal reflux. In addition, the gravid uterus causes a cephalad displacement of the diaphragm, resulting in decreased functional residual capacity. Finally, parturients have greater oxygen consumption. All these factors—altered airway anatomy, increased aspiration risk, and early desaturation—make securing the airway difficult.


Progesterone-induced smooth muscle relaxation and an expansion of maternal blood volume mask signs of maternal hypovolemia. By roughly 20 weeks, the uterus reaches the level of the inferior vena cava and can cause aortocaval compression and decreased venous return leading to hypotension as well as an increased venous pressure below the uterus. This exacerbates pelvic hemorrhage as well as precludes the use of lower extremity intravenous (IV) during resuscitation due to the limited return circulation.


The management of cardiac arrest in the pregnant patient is similar to the nonpregnant patient with a few modifications. In a decompensating patient, interventions to prevent cardiac arrest should be quickly instituted, including placing the patient in a full left lateral position to relieve possible aortocaval compression, administering 100% oxygen, establishing IV access above the diaphragm, assessing for hypotension and treating reversible ...

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