Lauren A. Plante
•Maternal cardiac arrest occurs in 8–8.5 per 100,000 delivery hospitalizations
•Manual chest compressions with rescue breaths is inherently inefficient with respect to generating adequate cardiac output
•Additional differential diagnosis of maternal cardiac arrest includes amniotic fluid embolism, magnesium toxicity, and local anesthetic systemic toxicity
•In most cases of maternal cardiac arrest, the initial rhythm is not shockable
•Preparations for early resuscitative cesarean delivery should occur in parallel to maternal resuscitation to affect delivery within 5 minutes of maternal cardiac arrest
The incidence of cardiac arrest in pregnancy is between 1:12,000 and 1:36,000 pregnancies. Population-based estimates of the incidence of maternal cardiac arrest show about 8–8.5 cases per 100,000 delivery hospitalizations in North America [1,2]; however, these data do not distinguish between antepartum, intrapartum, and postpartum cardiac arrests. Similar rates have been reported in the United Kingdom, i.e., 6.3 per 100,000 (1:16,000).
Maternal cardiac arrest may result from any of the factors associated with adult cardiac arrest. Pregnancy-specific etiologies must be included in the differential, such as amniotic fluid embolism, magnesium toxicity, and local anesthetic systemic toxicity.
Analysis of 56 million U.S. delivery hospitalizations between 1998 and 2011, containing 4843 cases of maternal cardiopulmonary arrest , showed that overall survival to hospital discharge was 59%, which is about three times higher than the cardiac arrest survival of women of childbearing age who are not pregnant (19%) . Survival varies with the etiology of cardiac arrest, with highest rates (86%) noted in arrest due to magnesium toxicity and 82% due to anesthesia-related causes. Maternal survival after cardiac arrest due to anesthetic complications from the UK was reported excellent (100%), while lower in etiologies . Furthermore, survival was much lower when the arrest occurred at home or in an ambulance rather than in the hospital (summarized in Box 21.1).
Box 21.1 Etiology and Survival of Maternal Cardiac Arrestc
Proportion of Maternal Cardiac Arrests (% of total)
Survival to Hospital Discharge (%)
Amniotic fluid embolism
Aortic aneurysm, dissection, or rupture
0–25 (this 25% represents 1 of 4 reported)
Note: Rounded to nearest integer; may not sum to 1 because differentially partitioned in different datasets.
a Category as “obstetric embolism” in , where it includes both venous and air embolism.
b Category appears in only one reference.
A direct comparison of women who received CPR in-hospital, drawn from the U.S. National Inpatient Sample, showed that pregnant women who received CPR were more likely to survive than nonpregnant women in the same age cohort (71% vs. 49%) . There was no survival advantage to pregnancy when the arrest was due to trauma or traumatic injuries . In a separate analysis of the American Heart Association’s voluntary registry, survival for in-hospital maternal cardiac arrest was 41% .
Out-of-Hospital Cardiac Arrest
Limited information is available specifically on out-of-hospital cardiac arrest (OHCA) in pregnancy. In a Toronto database of OHCA between 2010 and 2014, there were six maternal OHCAs, all in the third trimester, out of a total of 1085 reproductive age women . Only one woman (17%) and two newborns (33%) survived to hospital discharge, even though return of spontaneous circulation (ROSC) was achieved in 50% of pregnant women, a rate three times higher than in nonpregnant counterparts. A retrospective study identified two survivors among 16 pregnant women who sustained OHCA between 2009 and 2014; both women were in their first trimester who had arrested due to a cardiac cause with ROSC prior to arrival at the hospital . The sole fetal survivor was born at term to one of these women. These small studies suggest that the outcome for OHCA in pregnancy is poor for both mother and baby. Nonpregnant young adults who experience OHCA also have a poor prognosis, with 6%–10% probability of survival [10,48].
Etiology and Risk Factors for Maternal Cardiac Arrest
Box 21.2 Etiologies of Maternal Cardiac Arrest
Local anesthetic systemic injury
Aortic dissection or rupture
Congenital heart disease
Licit (oxytocin, magnesium, insulin, opioids)
Illicit (opioids, others)
Amniotic fluid embolism
Venous air embolism
H’s & T’s
Hydrogen ion (acidosis)
Thrombosis (coronary or pulmonary)
HELLP syndrome (hemolysis, elevated liver enzymes, low platelets)
Source: Jeejeebhoy FM et al. Circulation. 2015;132:1747–73; Zelop CM et al. Am J Obstet Gynecol. 2018;219(1):52–61.
•In most cases of maternal cardiac arrest, the initial rhythm is non-shockable, with 50% being pulseless electrical activity and 25% being asystole .
•Preexisting medical conditions are associated with higher odds of maternal cardiac arrest .
•The majority of cases of maternal cardiac arrest are preceded by respiratory insufficiency and/or hypotension .
Challenges in Performing CPR Pregnancy
Conventional cardiopulmonary resuscitation (CPR) is inherently inefficient with respect to generating cardiac output , and that is without the additional challenges imposed by pregnancy. In addition, there may be legal, sociologic, or cultural factors at play when a pregnant woman suffers a cardiac arrest .
Normal pregnancy requires maternal physiologic adaption in all organ systems. The growing uterus, fetus, and placenta impose mechanical and metabolic demands, which have the potential to complicate critical situations such as cardiac arrest and resuscitation. An understanding of pregnancy anatomy and physiology is crucial in recognizing and responding to critical situations (see Box 21.3).
Box 21.3 Pregnancy Physiology that Affects Maternal Resuscitationa
Total cardiac output increases by 30%–50% with 20% of this directed to the uterus
Following delivery, this portion of cardiac output is redirected away from the uterus into maternal circulation that potentially may contribute to maternal resuscitation
Increased venous capacitance and vasodilation leading to decrease in systemic vascular resistance
Decrease in blood pressure and contributing to dependent edema
Decreased sensitivity to both endogenous and exogenous vasopressor substances
May affect response to vasopressors
Increased anteroposterior diameter of the chest
May affect efficacy of chest compressions
Increased airway edema and mucosal capillary fragility
Increased minute ventilation and oxygen consumption, and decreased functional residual capacity
Increased oxygen demand and quick desaturation when oxygenation is interrupted
Decreased thoracic compliance due to elevation of diaphragm and mammary growth during pregnancy
May affect efficacy of chest compressions
Compensated respiratory alkalosis with decrease in carbon dioxide, serum bicarbonate, and buffering capacity
May affect acid−base balance during resuscitation
Relaxation of the lower esophageal sphincter and slowed transit time through the stomach and intestine
Increased risk of aspiration
Decreased production of binding proteins
Increase in free concentration of protein-bound drugs
Increased renal blood flow and glomerular filtration rate
Drug clearance may be affected
Decreased tubular absorption of protein and glucose
Protein and glucose spills in the urine at lower thresholds
Relaxation of ureteric smooth muscle, compression of ureters at the pelvic brim by enlarging uterus
Decreased colloid oncotic pressure and decrease in hematocrit
Increased sensitivity to local anesthetics
Dose adjustment may be necessary
A key point in pregnancy physiology is the decrease in cardiac output (CO) in the supine position past mid-pregnancy because of compression of the IVC by the enlarged uterus, which has been known for over 50 years . More recently, cardiac magnetic resonance imaging (MRI) studies demonstrate an incremental effect of pregnancy-induced IVC compression in later gestation and the variation in cardiac output from supine to left lateral position. There is an increase in ejection fraction by 11%, left ventricular end diastolic volume by 21%, stroke volume by 35%, left atrial volume by 41%, and cardiac output by 24% by shifting the patient from supine to left lateral position . MRI shows the inferior vena cava is almost completely occluded in the supine position when a pregnancy is at term , which can be remedied by lateral tilt positioning to a minimum of 30 degrees or more [16–18], a position which tends to see patients sliding off the underlying surface. Indirect methods also show a modest variation in CO ; however, these methods have not been validated for use in pregnancy [20,21].
CPR in a tilted position results in inefficient compressions , whereas CO is compromised in the supine position. Proposed solutions range from the Cardiff wooden wedge , preformed foam wedge , and the “human wedge” in which the patient is supported on the thighs of a kneeling rescuer . The American Heart Association (AHA) and European Resuscitation Council (ERC) recommend that an additional rescuer manually displace the uterus, either pulling it from the left or pushing it from the right, with upward and lateral pressure [11,25,26] (see Figures 21.1 and 21.2). The International Consensus on Cardiopulmonary Resuscitation (ILCOR) guidelines, however, differ from most others, stating that there is inadequate evidence to make a recommendation about left lateral tilt or uterine displacement during CPR in a pregnant patient .
Fetoplacental Perfusion and Oxygenation
In humans, the uterine arteries dilate during pregnancy and increase in diameter by nearly fivefold , which makes placental perfusion largely dependent on a pressure head, with very limited or absent vasoreactivity. Oxygen (O2) and carbon dioxide (CO2) transfer across the placenta along the pressure gradient between maternal intervillous blood and the fetal blood in villous capillaries . As CO2 diffuses into maternal blood, its decreasing pH favors release of O2 and enhances O2 transfer to the fetus. Fetal hemoglobin has inherently higher O2 affinity, further favoring uptake.
The fetal response to impaired perfusion and asphyxia manifests by bradycardia and redistribution of blood flow , which are compensatory responses to allow defense against moderate hypoxia. The preterm fetus has a less robust cardiovascular response to interruption of blood flow, however, and may be able to survive longer primarily due to greater cardiac glycogen reserve compared to the term fetus . Human studies are not feasible, but fetal lambs show a failure of compensatory responses by about 12 minutes following complete umbilical cord occlusion . The fetus is clearly at risk of injury and/or death when uteroplacental blood flow is interrupted; however, maternal CPR takes precedence and delivery is advisable as a resuscitative measure for the mother.
Approach to Cardiac Arrest in the Pregnant Patient
ILCOR and AHA guidelines were revised in 2010 to emphasize circulation (rather than airway or breathing) as the initial step in resuscitation after cardiac arrest , and the most recent guidelines in 2015  reiterate this focus. After verifying the scene is safe and the patient is unresponsive, the health care provider should call for help, activate the emergency response team, and either get the AED or send someone else to do so. The uterus should be displaced manually as soon as a second rescuer is available , but another method of uterine displacement is needed when there is only one rescuer.
If the patient has no pulse and respiratory effort is absent or gasping, the immediate intervention is to begin CPR, cycling 30 compressions and 2 breaths. A firm underlying surface is required, such as a backboard. The AHA considers that actions in the basic life support (BLS) sequence should be simultaneous rather than sequential in maternal cardiac arrest , so the order of ventilation versus defibrillation is unclear in this population. In adults generally, immediate defibrillation is indicated if the rhythm is shockable [32,33]. Ventilations are delivered by bag-valve-mask with FIO2 of 1.0 at an O2 flow rate of ≥15 L/min, at a rate of 2 ventilations to every 30 compressions; or an advanced airway is inserted (endotracheal or supraglottic device) and ventilations are delivered at a rate of 10 per minute, without coordinating or interrupting chest compressions (see Figure 21.3).
Old iterations of BLS suggested an A-B-C (Airway-Breathing-Circulation) order of tasks, but since 2010 the recommendation has been C-A-B (Circulation-Airway-Breathing) [34,35]. When the arrest victim is pregnant, experts have suggested C-A-B-U (Circulation-Airway-Breathing-Uterine displacement)  or C-A-B-D (Circulation-Airway-Breathing-Delivery). A shockable rhythm should always be defibrillated.
How Should CPR Be Modified in Pregnancy?
There are no randomized trials focused on cardiac arrest care modifications for pregnancy. A 2011 systematic review of cardiac arrest in pregnancy only addressed maternal physiology as it pertains to resuscitation . They identified five pertinent articles: two on perimortem CS [37,38], two on the effect of lateral tilt on chest compressions [22,24], and one on thoracic impedance during pregnancy , from which they concluded that defibrillation energy requirements should not be altered in pregnancy.
Basic Life Support
The importance of high-quality chest compressions remains the utmost priority in national and international guidelines [32,49,50], as survival rates are directly linked to good-quality chest compressions.
The Society for Obstetric Anesthesia and Perinatology  and the European Resuscitation Council  had previously suggested hand placement higher on the sternum in pregnancy because of the elevation of the diaphragm. The current 2015 AHA guidelines [11,25] do not recommend higher hand placement on the sternum, nor do the ILCOR guidelines . Cardiac MRI demonstrates no difference in cardiac position in a woman’s third trimester compared to 3 months postpartum .
Chest compressions should be performed at a rate of 100–120 times per minute, with a compression depth 5–6 min, and recoil of the chest wall should be allowed between compressions, which means the rescuer cannot lean his/her weight on the chest [32,49,50]: inadequate recoil interferes with right heart filling and coronary perfusion . These recommendations are not altered in pregnancy.
Ventilation and Oxygenation
The airway must be kept open during CPR either with head-tilt chin-lift, or jaw-thrust maneuver, or with the use of an oral airway; nasal airways are avoided in pregnancy because of edema and friability of nasal mucosa.
Hypoventilation or apnea causes hypoxemia faster in a pregnant woman, because of increased oxygen demand and reduced functional residual capacity. It takes only about 4 minutes of apnea for SaO2 to drop below 90% (compared to more than 7 minutes in a nonpregnant adult) when neither preoxygenation nor passive oxygen insufflation is provided . Options for oxygenation and ventilation are listed below.
•Bag-valve-mask ventilation does not protect the airway, and therefore there is risk of aspiration in pregnancy.
•Endotracheal intubation is more difficult in a pregnant woman because of anatomic alterations and airway edema, and therefore it must be undertaken by the most experienced provider. Cricoid pressure is neither required nor recommended for intubation .
•Supraglottic airway devices (e.g., laryngeal mask airway) should be considered if intubation cannot be easily accomplished.
Excessive attention to ventilation may compromise high-quality CPR, and therefore chest compressions should continue without interruptions for ventilation . ILCOR recommends that <10 seconds be allotted for interruption of chest compressions in order to deliver 2 breaths, if no advanced airway is in place . Guidelines continue to recommend a compression-to-ventilation ratio of 30:2 if no advanced airway is in place. Once an advanced airway has been achieved, ventilations should be delivered at a rate of 10 per minute (every 6 seconds) in parallel to chest compressions . The ideal tidal volume during CPR is unknown.
A high-flow rapid-insufflation device used to preoxygenate prior to a general anesthetic for emergency cesarean delivery is thought to be useful in delaying time to oxygen desaturation . Apneic oxygenation is an established way of maintaining oxygen saturation without ventilation, albeit accompanied by respiratory acidosis, and in a validated computational model of pregnancy physiology, delivering high-flow FIO2 of 1.0 during a period of apnea increased to nearly 60 minutes, the time required for SaO2 to fall below 90% . Thus, it would seem that providing at least a high flow of oxygen by facemask or high-flow nasal cannula might be helpful in maternal cardiac arrest until a more secure airway can be achieved.
Most initial rhythms in maternal cardiac arrest are non-shockable, either pulseless electrical activity or asystole . Nevertheless, quick rhythm analysis and defibrillation where indicated are important components of resuscitation. Both the pre-shock and post-shock pause in chest compressions should be limited to less than 5 seconds . Shocks should be single rather than stacked, and defibrillators with a biphasic rather than monophasic waveform are preferred . Manufacturer’s recommended energy dose should be used for the first shock if known; if it is not known, the responder may provide the initial shock at the maximum dose . Similarly, if the manufacturer’s recommendation for fixed versus escalating energy in a subsequent shock is known, guidance should be followed; if not known, a higher-energy subsequent shock should be used [27,54].
There has been no study of the efficacy of various defibrillation strategies in pregnancy. Thoracic impedance and trans-myocardial current delivered is unchanged in pregnancy [11,39]. The fibrillation threshold of the fetal heart is unknown , and it is unlikely that much of a transthoracic current delivered to the mother would be transmitted to the uterus.
Electronic fetal monitors if already in place should not be removed for the purpose of electrical safety in defibrillation [11,51]. Either the standard hospital defibrillator or an automated external defibrillator (AED) may be used with pads or paddles placed in the anterolateral position, with care taken to ensure the lateral pad is placed under the left breast .
Advanced Cardiac Life Support
In addition to BLS interventions (chest compressions, defibrillation, ventilation), advanced cardiac life support (ACLS) involves additional monitoring (such as capnography), endotracheal intubation, and pharmacologic therapies. Despite known alterations in volume of distribution, protein binding, and other pharmacokinetics of pregnancy, ACLS drug doses are no different. The potential for transplacental passage or fetal effects of ACLS drugs is irrelevant. These drugs are given IV, so venous access should be established, preferably large-bore venous access above the diaphragm. Any drugs that may have contributed to or precipitated maternal cardiac arrest such as oxytocin or magnesium should immediately be discontinued. If the arrest is attributed to magnesium toxicity, 1 gram of calcium should be administered IV, usually as 10 mL of 10% calcium gluconate .
Vasopressors require central rather than peripheral access. Standard-dose epinephrine (1 mg every 3–5 min) is a common intervention for patients in cardiac arrest and should be considered [11,27,54]. Benefits include both ROSC and improved survival with standard-dose epinephrine [54,59] in adult cardiac arrest. High-dose epinephrine (0.1 mg/kg and above) is not recommended.
Sodium bicarbonate is not a routine part of ACLS. Indications may include hyperkalemia or tricyclic overdose . It may cause intracellular acidosis in both the maternal and fetal compartment [12,59].
Antiarrhythmic drugs are used when ventricular fibrillation or pulseless ventricular tachycardia is refractory to one or more defibrillation attempts. In contrast to effective CPR and defibrillation, antiarrhythmic drugs have not been shown to increase survival, though they may increase the probability of ROSC .
•Lidocaine (100 mg) is an alternative 
Note that both these drugs cross the placenta with potential fetal/neonatal side effects. Amiodarone may affect the fetal thyroid , and fetal plasma lidocaine levels may exceed maternal, especially when acidosis is present . Neither of these is a reason to avoid giving the drug when it is indicated in maternal cardiac arrest.
Intravenous lipid therapy may be used when cardiac arrest is attributed to local anesthetic systemic toxicity (LAST), though there are neither experimental nor observational studies in humans , let alone in pregnancy. The Society for Obstetric Anesthesia and Perinatology recommends lipid emulsion as adjunctive therapy in the case of local anesthetic-induced maternal cardiac arrest , dosed as a bolus of 1.5 mL/kg 20% lipid emulsion (Intralipid®), followed by 0.25–0.5 mL/kg/min infusion . The majority of maternity units in both the United Kingdom and the United States keep lipid emulsion in stock for this indication [62,63] recommended by both the Association of Anesthetists’ of Great Britain and Ireland  and the American Society of Regional Anesthesia and Pain Medicine . Successful resuscitation from LAST-induced cardiac arrest may take 1 hour or more. Lidocaine must be avoided as an antiarrhythmic when LAST is suspected.
Opioid overdose, either from prescribed or illicit use, may precipitate maternal cardiac arrest. Several cases have been reported in association with remifentanil patient-controlled analgesia (PCA) in labor [66,67].
The primary focus of resuscitation is the pregnant woman, not the fetus. Fetal monitoring is irrelevant in the setting of maternal arrest as it will not contribute to maternal resuscitation and may well distract the team from proper resuscitation performance .
Perimortem Cesarean Delivery (Resuscitative Hysterotomy) and the 5-Minute “Rule”
•AHA recommends consideration of perimortem cesarean delivery or resuscitative hysterotomy  if the initial maternal resuscitative measures are unsuccessful in the presence of uterine size greater than or equal to 20 weeks.
•Guidelines for resuscitation in pregnancy commonly refer to a 5-minute rule or a 4-minute rule: after 4 (or 5) minutes of CPR without return of spontaneous circulation, perform perimortem cesarean (PMCD) with the goal of effecting delivery in the next minute .
Perimortem cesarean, or more precisely “resuscitative delivery,” is primarily performed as a last-ditch attempt to resuscitate the mother. Decompressing the IVC by emptying the uterus has the potential to return CPR to its baseline effectiveness, which may be enough for return of spontaneous circulation and maternal survival. In addition, extraction of the fetus and placenta lowers maternal oxygen demand, increases functional residual capacity and chest wall compliance, and shifts that portion of circulating volume previously diverted to the uterus back into the central circulation. As a way of emphasizing the maternal effects of the procedure, some authors describe it as “resuscitative hysterotomy.” [41,43,45,72–74]
•Maternal survival is clearly better when the interval from cardiac arrest to delivery is shorter. A systematic review of cases in English and German found that maternal survival was inversely correlated with time from arrest to delivery, in a gradual stepwise fashion  but there was no specific breakpoint; the time which marked 50% injury-free survival was 25 minutes. Even after 4 minutes (or more) of CPR without ROSC, there still appears to be maternal benefit in PMCD. The role of contemporary post-arrest care in improving injury-free survival after maternal cardiac arrest remains unexplored.
•PMCD may be associated with survival of the newborn. In a recent review, overall neonatal survival was 76%, and intact survival 57% . Neonatal survival after maternal cardiac arrest is affected by the time elapsed between arrest and PMCD: in the UKOSS CAPS study , 96% of infants survived when PMCD was performed within 5 min, while 70% survived when PMCD was performed at later than 5 min. Infant survivors have, however, been reported when PMCD was performed as late as 30 [75,76] and even 43  minutes after maternal cardiac arrest. In the 2016 review, just as for maternal survival, there was no sharp drop in newborn survival at 4 or 5 minutes after maternal arrest: the threshold for 50% injury-free neonatal survival was almost the same as the mothers at 26 min .
•PMCD should be performed at the site of arrest, because transport reduces success . Transport to hospital is, of course, indicated when the arrest has occurred out of hospital. Little information is available about performing PMCS out of hospital [39,41], and no recommendation can be made here. The technique of PMCD is simple [11,78,79] (see Figure 21.4). If an obstetrician is not available, a general surgeon, family medicine physician, or emergency medicine physician may have the required surgical skills. Speed is of the essence. Though a cesarean tray with instruments should be used if one is at the site, no time should be wasted waiting for one: the operator may proceed with nothing more than a scalpel.
Figure 21.4 Technique of perimortem cesarean delivery, performed via vertical abdominal and uterine incision. (a) Vertical incision through the abdominal wall from the level of the uterine fundus to the symphysis pubis. (b) Retraction to expose the anterior surface of the uterus and retract the bladder inferiorly. (c) Small vertical incision through the lower uterine segment. (d) Extension of the incision superiorly to the fundus by bandage scissors. (e) Delivery of the fetus (suction the nose and mouth; clamp and cut the cord). (From Healy M et al. J Emerg Med. 2016;51:172−7. With permission.)