Cardiopulmonary Resuscitation in Pregnancy
Carolyn M. Zelop
Edward P. Grimes
Cardiopulmonary resuscitation of the pregnant victim is surprisingly similar in many respects to advanced cardiac life support (ACLS) protocols for nonpregnant patients. However, the unique physiologic changes of pregnancy require special consideration and necessitate some modification of standard algorithms. There are two patients, and pregnancy also requires a multidisciplinary approach and coordination of specialties: emergency medicine, obstetrics including perinatology, neonatology, and possibly cardiothoracic surgery.
Causes of cardiac arrest include those found in nonpregnant patients as well as those unique to pregnancy.
Pregnancy results in a myriad of physiologic, anatomic, and metabolic changes.
Cardiopulmonary resuscitation (CPR) involves a number of modifications, including the left lateral uterine displacement position and removal of all fetal monitoring leads prior to defibrillation.
Any medication that would be utilized in the nonpregnant patient should be utilized in the pregnant cardiopulmonary arrest patient.
Emergent delivery of the fetus, open-chest cardiac massage, and cardiopulmonary bypass.
The Setting
You are a physician called to the emergency department to help evaluate a pregnant patient involved in a motor vehicle accident.
Paramedics at the scene noticed blood on her clothing, apparently from her groin, as they secured her neck in a cervical spine collar. They reported the following: HR, 140; BP, 80/palp; RR, 24; SaO2, 96%. Abdominal exam revealed marked diffuse tenderness. Several dark clots are passed per vagina. For volume replacement, a second large-bore IV is placed, infusing lactated Ringers (LR) as the patient is transported. Upon arrival at the hospital, assessment continues. In the emergency department (ED), fetal monitoring is initiated, revealing a fetal heart rate in the 130s with no decelerations. Fundal height is consistent with 32 weeks’ gestation. The obstetric and neonatology services are called STAT. BP now falls to 60/palp and the patient becomes unresponsive. Shallow respirations are noted after 100% O2 is administered by face mask. Rapid sequence intubation is performed using succinylcholine and cricoid pressure. A cardiac monitor attached to this patient reveals sinus tachycardia. BP can no longer be measured, pulses are found to be absent. Cardiopulmonary resuscitation (CPR) is initiated after moving the patient into left lateral uterine displacement. Cardiac monitors reveal deterioration into a wide-complex rhythm consistent with ventricular tachycardia, which progresses quickly to ventricular fibrillation. After fetal monitors are removed, defibrillation sequence is attempted at 200, 300, and 360 J. Cardiac rhythm returns to sinus tachycardia after the third attempt at defibrillation, but pulses are still not palpable. CPR continues. Epinephrine 1 mg is given using IV above the groin. Vital signs do not improve. With no response to resuscitation, an emergency cesarean section is performed by the obstetric team at the bedside. With continued volume replacement and incremental doses of epinephrine, peripheral pulses become palpable. The mother improves hemodynamically and is transferred to the intensive care unit. Although the fetus requires intubation, the neonatology staff report improving hemodynamic and metabolic parameters.
This clinical vignette describes the rare but catastrophic occurrence of cardiopulmonary arrest during pregnancy. The complexity of dealing with altered physiology and the unique clinical scenario of treating two patients simultaneously often paralyzes the clinician when time is of the essence. This chapter should enable the clinician to generate a differential diagnosis and to modify ACLS protocols to respond appropriately to this specialized rescue situation.
Epidemiology and Clinical Spectrum
The differential diagnosis of cardiopulmonary arrest is expansive. The etiologies are related to causes found in the nonpregnant population as well as conditions unique to the pregnant state.
Maternal mortality has been increasing during the new millennium. In 2004, maternal deaths in the United States reached a new high with 13.1 deaths per 100,000 live births.1,2,3,4 Reportedly, the prevalence of maternal cardiac arrest is estimated to be 1 per 30,000; however, this figure may be rising.5,6 Advances in medical technology open the door to reproductive options for women with chronic illness who previously could not consider pregnancy. The escalating cesarean birth rate will give rise to increased rates of accreta and other obstetric conditions, which elevate the risk of maternal hemorrhage.7 The obesity epidemic is rampant, especially during pregnancy, leading to medical and surgical complications in the mother and fetus which can become life-threatening.8
The differential diagnosis of cardiopulmonary arrest is expansive. The etiologies are related to causes found in the nonpregnant population as well as conditions unique to the pregnant state. The clinician assessing the pregnant patient with sudden cardiopulmonary collapse must consider hemorrhage, embolism, and other unique etiologies (Table 35-1).9,10,11,12
Physiologic Changes of Pregnancy and Their Impact on Cardiovascular Collapse
Pregnancy results in a myriad of physiologic, anatomic, and metabolic changes that allow successful maternal adaptation to the fetal–placental unit.
Pulmonary and Airway Changes
Estrogen induced hyperemia and edema of the upper airway may alter the usual anatomic landmarks of the pharynx and larynx. The level of the diaphragm rises 4 cm, but the excursion remains normal. Thoracic compliance, however, decreases, especially in the third trimester, although respiratory muscle function remains unchanged. The rise in the diaphragm leads to a 20% decrease in functional residual capacity, mainly due to a decrease in residual volume. Lung volume changes result in a more rapid oxygen desaturation in the setting of oxygen deprivation. Progesterone-induced increase in minute ventilation, mainly due to increased tidal volume, produces a respiratory alkalosis accompanied by a compensatory renally induced metabolic acidosis. While this facilitates excretion of fetal CO2, decreased serum bicarbonate renders the pregnant woman less capable of neutralizing the acid load that may arise during anaerobic respiration. The increased metabolic rate requires that oxygen consumption increase by 20% to 40%. The parameters are different for interpreting a normal arterial blood gas in pregnancy: PH, 7.40 to 7.45; PCO2, 28 to 32; PO2, 101 to 106; and HCO–3, 18 to 21.
Table 35-1 • Causes of Cardiopulmonary Arrest in Pregnancy | |
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Gastrointestinal Changes
Progesterone decreases the motility of the gastrointestinal tract and weakens the competency of the lower esophageal sphincter. Therefore, upon loss of consciousness, the pregnant patient has a higher risk of aspiration.
Hematologic Changes
There is a 40% increase in blood volume beginning at 6 weeks and plateauing at 30 weeks of gestation. Erythropoietin and reticulocyte count increase at a slower rate but contribute to the overall expansion of the red cell mass. The increased circulatory volume protects the mother against hypotension and hemorrhage. It perfuses the expanded vascular system created by the vasodilation and low resistance of the uteroplacental unit. The disproportionate increase in volume over red cell mass creates the physiologic anemia of pregnancy.
Cardiovascular Changes
Cardiac output increases 40% starting as early as the first trimester. This increase in cardiac output is primarily due to an increase in stroke volume. However, increased heart rate does contribute secondarily. One of the primary functions of the increase in the cardiac output is to perfuse the uteroplacental unit, which requires 20% of the overall cardiac output, and to sustain the increased metabolic requirements of tissue throughout the body during pregnancy.
Paradoxically, the enlarging uteroplacental unit mechanically compresses the great vessels, thereby decreasing venous return from the inferior vena cava and increasing afterload through compression of the aorta. This physiologic aberration, due to the enlarging uterus, begins at about 20 weeks and is exacerbated with increasing uterine distention, which would be magnified in certain clinical settings such as multiple gestations. These cardiopulmonary changes render the pregnant patient more vulnerable to any cardiopulmonary insult and require special consideration during any resuscitation sequence.15,
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