Maternal death is a rare complication of pregnancy. Despite this fact, pregnancy-related mortality in the United States is increasing as women delay childbearing into their third and fourth decades of life. Pregnancy at advanced maternal ages unmasks underlying medical problems, and maternal heart disease is currently the main cause of death.

Once the diagnosis of maternal Code Blue is made in an unresponsive pregnant woman, acute intervention with CPR and Basic Life Support (BLS) can help maintain maternal circulation while preparing to perform a potentially lifesaving PCMD. Despite the data on poor maternal survival rates after a PCMD, the potential benefits to the fetus make this procedure indicated.

This chapter will explore the epidemiology of maternal mortality in the United States, followed by a discussion about the physiologic changes of pregnancy that result in the necessary changes for effective CPR in the pregnant population. The discussion will conclude with an in-depth discussion on the issues surrounding the PMCD and ways to maximize fetal and maternal outcomes.

Maternal mortality is defined as “the death of a woman during pregnancy up to 42 days after delivery or termination of pregnancy.”¹ According to the Centers for Disease Control and Prevention (CDC), the rate of maternal mortality has increased from 7.2 deaths per 100,000 live births in 1987 to as high as 17.8 deaths per 100,000 live births in years 2009 and 2011 (Fig. 38-1).² The main causes of maternal death in the United States are cardiac disease, infection, hemorrhage, embolism, and hypertensive disorders (Fig. 38-2).² This chapter will focus on cardiac arrest.

The frequency of cardiac arrest in pregnancy is 1 in 20,000 pregnancies and approximately 1 in 12,000 hospitalizations.^3,4 Poor survival rates were previously described at approximately 6.9%.⁴ However, recent literature has described survival rates as high as 58.9%, demonstrating the importance of rapid identification and proper management of cardiac arrest in the pregnant patient.¹

With regard to maternal mortality, the most common cause is cardiac disease, including cardiomyopathy, followed by infection, underlying medical conditions, and hemorrhage (Fig. 38-3).⁵ There has been an overall increase in maternal deaths due to heart disease (Fig. 38-4).⁶ This increase in cardiac deaths is because more women with preexisting cardiac diseases are becoming pregnant as well as an increased incidence of maternal cardiac risk factors such as smoking, advanced maternal age, and obesity. There is also a stark difference in maternal mortality rates between racial-ethnic groups, with an almost tripled pregnancy mortality ratio for non-Hispanic black patients (Fig. 38-5).⁵ Non-Hispanic black women had a 3.2-higher risk of maternal death compared to non-Hispanic white women. This group of women were less educated, were unmarried, initiated later prenatal care, and were younger on average. Other considerations include a higher rate of hypertension, diabetes, and obesity as well as less insurance coverage.

Physiological changes in pregnancy occur in practically every organ system due to mechanical and hormonal factors. Cardiac output increases by 20% from approximately 8 to 32 weeks gestation, and can be up to 50% above baseline at the time of labor. This is due to increased preload from a rise in blood volume, decreased afterload from decreased vascular resistance, and increased heart rate by 15 to 20 beats per minute (Figs. 38-6 and 38-7).^7–9 Uterine blood flow increases to support the growing fetus, shifting from 3% to 6% of cardiac output early in pregnancy to 12% of cardiac output at term.¹⁰ These hemodynamic changes must be taken into account when performing CPR.

Pregnant women have an increased tidal volume to overcome the physiologic and anatomic changes in pregnancy, resulting in a higher minute ventilation. However, this change also results in a chronic respiratory alkalosis (Fig. 38-8).^11,12 With increasing metabolic demands, oxygen consumption increases by approximately 20%.^13,14 Later in gestation, the gravid uterus elevates the diaphragm, resulting in reduced functional residual capacity, end expiratory volume, and residual volume.¹⁵ To compensate for this, there is an increase in the chest anteroposterior and transverse diameters and an overall decrease in chest wall compliance.¹² Given these changes, oxygen reserves are lower and metabolic demands are higher, making the pregnant patient more susceptible to hypoxemia and less tolerant of apnea.¹

Other physiologic changes during pregnancy include hyperemia and edema of the upper airway.¹⁶ These changes make intubation more difficult, with increased bleeding and decreased visualization.¹⁷ The pregnant airway is also narrower as a result of edema, which should be taken into account when choosing the size of the endotracheal tube for intubation.¹⁸

Finally, the pregnancy plasma volume increases by 50% at 32 weeks gestation, but total red cell mass increases only by 20% to 30%.^19,20 This results in a relative hemodilution and “anemia of pregnancy.”²¹ Platelet counts may be slightly lower than in the nonpregnant population, but this usually does not have maternal sequelae.²² There are increased levels of coagulation factors and decreased levels of coagulation inhibitors, resulting in a hypercoagulable state.²³ As such, thromboembolism should be high on the differential as a cause of maternal cardiac arrest, and elevated prothrombin/time/international normalized ratio (PT/INR) levels or low-normal levels of fibrinogen should prompt consideration of disseminated intravascular coagulation in differential diagnosis.

According to the Advanced Cardiac Life Support (ACLS) guidelines by the American Heart Association (AHA), the major contributing factors to any cardiac arrest are hypovolemia, hypoxia, hydrogen ions (acidosis), hyperkalemia/hypokalemia, hypothermia and toxins, cardiac tamponade, tension pneumothorax, and thrombosis.²⁴ The most common causes of cardiac arrest in pregnancy are pulmonary embolism (29%), hemorrhage (17%), sepsis (13%), peripartum cardiomyopathy (8%), stroke (5%), preeclampsia/eclampsia (2.8%), and anesthesia complications (2%). Other causes include myocardial infarction, preexisting cardiac disease, amniotic fluid embolism (AFE, otherwise known as anaphylactoid syndrome), and trauma (Table 38-1, Fig. 38-3).^5,25

Given the physiological changes in pregnancy, the AHA released guidelines for CPR that were specific to the obstetric population. The most recent guidelines from 2015 include left lateral displacement of the uterus during chest compressions, ventilation with early intubation, and consideration for cesarean delivery after 4 minutes of unsuccessful CPR.

The algorithms discussed in this section should be used as a guide to BLS and advanced cardiac life support in pregnant women (Figs. 38-9 and 38-10).¹

Chest compressions should be performed using a firm surface or backboard, and in the same fashion as in the nonpregnant population, at a rate of at least 100 per minute at a depth of at least 2 in (5 cm), allowing full recoil before the next compression, and at a compression-ventilation ratio of 30:2. Interruptions should be minimized and limited to 10 seconds, except for specific interventions such as insertion of an advanced airway or use of a defibrillator.^1,26 The rescuer should place the heel of one hand on the center of the victim’s chest over the lower half of the sternum, with the heel of the other hand on top of the first so that the hands overlap and are parallel.¹

During CPR in the normal population, only 25% to 40% of normal cardiac output is generated through chest compression.²⁷ The generated cardiac output is even lower in the obstetric population later in gestation, given the aortocaval compression and hemodynamic changes incurred by the gravid uterus. By 20 weeks gestation, the gravid uterus has reached the level of the inferior vena cava, resulting in decreased venous return and then decreased cardiac output.²⁸ To reduce aortocaval compression and increase cardiac preload, the recommendation is for continuous lateral uterine displacement in all pregnant women undergoing cardiac arrest when the uterus is palpable at or above the umbilicus¹. If the uterus is difficult to assess, such as in a morbidly obese patient, manual left uterine displacement should be attempted if technically feasible. Left uterine displacement can be performed manually, from the patient’s left side with the two-handed technique (Fig. 38-11) or the patient’s right side with the one-handed technique (Fig. 38-12). Note that manual left uterine displacement is recommended over left lateral tilt because it allows the patient to remain supine, easing chest compressions, defibrillation, and airway and IV placement.²⁹

There is increased susceptibility to rapid hypoxemia in pregnancy, given the reduced oxygen reserve secondary, increased oxygen consumption, and decreased functional residual capacity.^14,15 As such, proper ventilation with effective chest compressions is essential. Bag-mask ventilation should be initiated early with 100% oxygen, as a higher partial pressure of oxygen is required to achieve the same maternal oxygen saturation.⁴ Two-handed bag-mask ventilation is preferred over the one-handed technique, and it should be performed in a 30:2 ratio with chest compressions to limit interruptions in compressions.^30,31 Responders must be careful not to overventilate the patient, which causes worsening alkalosis, uterine vasoconstriction, and decreased fetal oxygenation.³² Early intubation is recommended and should be done by the most experienced provider given the difficult airway in pregnant patients.³³ Although pregnant patients are at higher risk of aspiration, cricoid pressure is not recommended during resuscitation and intubation.^1,34 Continuous waveform capnography should be used to confirm ETT placement and monitor CPR quality in settings where these tools are available.³⁵

The defibrillation protocol is the same in pregnant patients as in nonpregnant patients.⁴ Transthoracic impedance does not change in pregnancy, so there are no changes in electric shock application.³⁶ Adhesive pads should be placed anterolateral with the lateral pad placed under the breast tissue in the usual fashion.¹ Defibrillation should use 120 to 200 J of biphasic shock energy with subsequent escalation of energy output if the first shock is not adequate and if the device allows this option.³⁷ Chest compressions should resume immediately after delivering an electric shock.

Intravenous (IV) access should be obtained above the diaphragm because aortocaval compression by the gravid uterus can prevent femoral vein medications from reaching the heart quickly. Furthermore, during cardiac arrest or abnormal cardiac rhythm, the chances of any intravenously administered medication reaching the heart muscle are greater when the distance to travel to the heart is smaller. Two large-bore catheters placed in the antecubital veins can be as effective as central lines for volume repletion.³⁸

Medical therapy is also no different in the pregnant patient. In ventricular fibrillation and tachycardia refractory to defibrillation, a rapid infusion of amiodarone 300 mg should be administered, with repeat dosing of 150 mg as needed.^1,39 Epinephrine has been demonstrated to increase the likelihood of return of spontaneous circulation, although it has not been shown to change survival.⁴⁰ Given the short-term benefit, the AHA allows the consideration of administering 1 mg IV or intraosseous epinephrine every 3 to 5 minutes. Epinephrine is preferred over vasopressin; while both have equivalent efficacy, vasopressin can cause uterine contractions.⁴¹ Sodium bicarbonate is often avoided, given that it will cause an increase in fetal pCO₂ faster than the HCO₃ crossing the placenta due to resting maternal alkalosis and decreased respiratory compensation.¹ Although pharmacokinetics may be affected by the physiological changes of pregnancy, no change in the dosage or route of administration is suggested.¹ While some providers abstain from using potentially teratogenic medications, the AHA advises use of any indicated medication during a life-threatening arrhythmia.⁴²