Cardiac Arrest in Labor and Delivery: A Current Review


The scenario of cardiac arrest is a feared one in the labor and delivery suite; yet, the incidence is 1 in 30,000 pregnancies (1). Parturients tend to be young, healthy patients without previous hospitalizations or medical problems. Unlike the operating suite, the labor and delivery ward is often crowded with family members, walking parturients and families welcoming the arrival of their newest relatives. Not only is cardiac arrest a feared entity in this population, it is often unexpected. For these reasons, it is necessary that the obstetric anesthesiologist be knowledgeable about the risk factors for cardiac arrest, the physical changes in the parturient and the management of cardiopulmonary resuscitation during pregnancy.

Cardiac arrest in the parturient has numerous causes. The most feared and deadly is amniotic fluid embolism (AFE). AFE can present with cardiac arrest, hypotension, bronchospasm, coagulopathy, fetal distress or cyanosis (2). Even with optimal treatment, AFE is associated with a high rate of morbidity and mortality. It has been reported that only 15% of patients who survive AFE are neurologically intact (2). A more common cause of cardiac arrest in the parturient is hemorrhagic shock. Due to the occurrence of placental pathology, some patients are at higher risk for major hemorrhage during labor. These include patients with placental abruption, placenta previa, or abnormalities of placental implantation: placenta acreta, increta or percreta. Other etiologies of cardiac arrest include trauma, pulmonary embolism, anaphylaxis, and congenital or acquired cardiac disease. Complications of tocolytic therapy include cardiac dysrhythmias, myocardial infarction and congestive heart failure (3) Unlike the operating room, many patients will receive multiple infusions of non-anesthetic medications, such as oxytocin, magnesium or antibiotics. Accidental bolus doses of magnesium or vancomycin can lead to severe consequences, including hypotension and cardiac arrest. Case reports have linked ergot derivatives with myocardial infarction and cardiac arrest in the parturient. (4) As increasing numbers of parturients are of advanced age, one must be aware of coexisting medical problems that may complicate tocolysis and treatment of preclampsia. During an operative delivery, surgical complications and persistent uterine atony may lead to massive hemorrhage and cardiac arrest.

Complications of regional and general anesthesia are another cause of cardiac arrest in labor and delivery. Even with routine dosing and testing, epidural catheters can migrate into the intravascular or subarachnoid space, leading to systemic toxicity or total spinal anesthesia, respectively. Drug overdosage can lead to local anesthetic toxicity, particularly in patients who have received multiple top-up doses of local anesthetics during a prolonged labor. Unlike the operating room, patients in the delivery suite receive regional anesthesia for prolonged periods of time without the continuous presence of an anesthesiologist. It is therefore essential that the amount of local anesthetic the patient receives be monitored from shift to shift. Finally, it is critical to remember that induction of either regional or general anesthesia can lead to severe hypotension in hypovolemic patients.

The effective treatment of cardiac arrest during pregnancy requires a complete understanding of the physiologic changes seen in the parturient. These physiologic changes can make the diagnosis and treatment of emergent situations difficult in the labor suite. Cardiac output is greatly influenced by the patient's position, especially during the third trimester. The supine hypotension syndrome can decrease cardiac output by 30% to 40% (3). Many women cannot tolerate the supine position, especially after 30 weeks gestation. For safety, women are encouraged to maintain left uterine displacement either by elevation of the right hip or by positioning themselves on their sides. In the labor suite, patients are frequently positioned on their back to facilitate cervical exams and placement of monitoring devices. If the patients are not reminded to return to their side, especially in the presence of epidural anesthesia, there can be a rapid decrease in venous return, leading to hypotension and possibly cardiac arrest.

After the 10th week of gestation, cardiac output is increased by 1.0 to 1.5 liters per minute (5). Maternal heart rate increases throughout pregnancy, reaching a peak of 15-20 beats above nonpregnant values during the third trimester (5). Maternal blood pressure is less than nonpregnant values, with systolic pressures typically about 10 15 mm Hg lower than non-pregnant values. Because of these cardiac changes, patients can bleed extensively before normally recognizable physical signs such as tachycardia and hypotension will occur. In addition, at about 34 weeks gestation , plasma volume is increased by 40- 50%. A smaller increase in red blood cell (rbc) volume occurs, resulting in a decreased hematocrit and the physiologic anemia of pregnancy (5). Often, a lower hematocrit can be misinterpreted due to this phenomenon, especially in the case of hypovolemia and acute hemorrhage. Because of these compensatory mechanisms, and the tendency for blood flow to be shunted from the uteroplacental circulation under conditions of hypovolemia, the pregnant patient can lose 35% of her blood volume before tachycardia, hypotension, and other signs of hemodynamic instability can be identified (5). A parturient may appear stable when the fetus is severely deprived of blood flow and the patient is greatly compromised.

Understanding the respiratory changes of pregnancy is essential during the management of cardiac arrest. These changes necessitate quick establishment of oxygenation and ventilation. Tidal volume increases during pregnancy cause an increase in minute ventilation. Increased oxygen consumption leads to increased rates of arterial oxygen desaturation in the parturient who becomes apneic. The expanding uterus and consequent diaphragmatic elevation decreases thoracic volume leading to a decrease in functional residual capacity (FRC). Due to the hormonal and physical changes of pregnancy, patients are at increased risk for difficult ventilation and failed intubation. Increased levels of progesterone lead to delayed gastric emptying, increasing the risk for aspiration during mask ventilation and intubation (1). Though many centers require that patients remain npo during labor, many patients will present in spontaneous labor after consuming a large meal. Edema of the upper airway, increased breast size and generalized weight gain can delay the establishment of adequate ventilation and intubation. It is essential that oxygenation and ventilation be restored expeditiously while maintaining cricoid pressure.

Successful resuscitation in late pregnancy is difficult because the gravid uterus acts like an abdominal binder producing an increase in intrathoracic pressure, diminished venous return, and obstruction to forward flow of blood into the abdominal aorta, especially in the supine position (6). In addition, the gravid uterus accounts for 10% of cardiac output and this massive shunting of blood may hinder efforts at CPR (7) External cardiac massage can at best generate only 30% of a non-pregnant patient’s normal cardiac output and increased oxygen requirements during pregnancy make the parturient much less tolerant to hypoxia (8).

To perform chest compressions one must ensure that left uterine displacement is adequately maintained. The Cardiff wedge, which is made of hard laminated wood on casters, provides both relief of aortocaval compression and a firm surface upon which to perform compressions (1). In the absence of a wedge, a “human wedge” is useful by tilting the patient on the bent knees of a kneeling rescuer (1). Patients can also be “wedged” by using rolled up blankets to tilt the right hip. If the compressions are performed in a hospital bed, the placement of a hard wooden board beneath the patient is also essential for successful compressions. Standard algorithms should be used according to ACLS protocol; they are unaltered by pregnancy (3). Although large doses of alpha-andrenergic and combined alpha and beta andrenergic agents may decrease uterine blood flow, the use of these drugs is absolutely essential to restore maternal circulation and thus save both mother and fetus. To successfully resuscitate a parturient in late pregnancy, a coordinated team approach is essential. Obstetricians, anesthesiologists, neonatologists and nursing staff must work efficiently and in an organized fashion to resuscitate these patients. As these events happen unexpectedly, cooperation is essential to assemble needed equipment and perform resuscitation efforts in the labor suite. Upon commencement of CPR, one must be vigilant to be sure that time is not wasted if chest compressions and medications are not successful. It is now recommended that cesarean section be performed within 4-5 minutes of the arrest (3) It has been shown that the shorter the interval between the onset of maternal cardiac arrest and commencement of CPR, and the shorter the time taken to deliver the fetus once CPR commences, the more likely that the mother will survive and the fetus will be neurologically intact. Timing is the most crucial factor when performing CPR in late pregnancy. Cesarean section, performed in a patient’s room within 10 minutes after arrest, was essential in the successful resuscitation of a full term parturient and her fetus during an amniotic fluid embolism (9). In that case, because of the rapid delivery of the fetus leading to immediate restoration of maternal circulation, both patients survived neurologically intact.

The obstetric anesthesiologist must be prepared to become the team leader in the event of cardiac arrest. It is essential that one be familiar with the most recent ACLS protocols. In addition, all resuscitation equipment must be readily available in the event of cardiac arrest in the labor suite. With preparation and cooperation, the obstetric anesthesiologist can greatly reduce the morbidity and mortality for both mother and fetus.



1. Chestnut DH Ed. Obstetric Anesthesia Principles and Practice Mosby-Year Book: St. Louis, Missouri, 1994.
2. Clark S, Hankins G, Dudley D: Amniotic Fluid Embolism: Analysis of the National Registry. American Journal of Obstetrics and Gynecology 1995; 172:1158-69.
3. Cummins, Richard O. Ed. Textbook of Advanced Cardiac Life Support. American Heart Association, 1994.
4. Tsu BCH, Stewart B et al. Cardiac Arrest and Myocardial Infarction Induced by Postpartum Intravenous Ergonovine Administration. Anesthesiology 2001; 94(2): 363-4.
5. Alexander RH, Proctor HJ. Eds. Advanced Trauma Life Support, Course for Physicians. American College of Surgeons. Chicago, Illinois, 1993.
6. Whitten M, Irvine L: Postmortem and Perimortem Cesarean Section: What are the Indications? Journal of the Royal Society of Medicine 2000; 93:6-9.
7. Whitty JE. Maternal Cardiac Arrest during Pregnancy. Clin J Obstet Gynec 2002; 45(2): 377-92.
8. Lee R, Rodgers B, White L: Cardiopulmonary Resuscitation of Pregnant Women. American Journal of Medicine 1986; 81:311-8.
9. Finegold H. et al Successful resuscitation after maternal cardiac arrest by immediate cesarean section in the labor room. [Letter] Anesthesiology 2002. 96(5):1278

Helene Finegold, MD
Assistant Professor of Anesthesiology
Magee Womens Hospital
Pittsburgh, PA

fessor of Anesthesiology
Magee Womens Hospital
Pittsburgh, PA