Chapter 17: Advanced Cardiac Life Support of the Pregnant Patient

Cardiopulmonary arrest in pregnancy is uncommon, occurring once in every 20,000 to 50,000 pregnancies. Even at the busiest medical centers, this will only total a few cases per year. Most of what we know regarding cardiopulmonary resuscitation (CPR) in pregnancy is based on animal experiments or observational studies in humans. There are no published randomized controlled clinical trials of CPR during pregnancy and few clinicians have had the experience of running many obstetrical codes. The mortality of obstetrical arrest is over 90% in some studies.

Advanced cardiac life support (ACLS) guidelines have been developed with a focus on sudden death from ischemic heart disease. Although acute myocardial infarction can occur during pregnancy, arrest in a previously healthy woman is more likely related to acute events such as pulmonary embolism or hemorrhage. The unpredictability and rarity of sudden death during pregnancy makes preparation difficult. The single most important factor for improving the survival of mother and baby is a well-prepared, time-conscious, team approach.

The focus of this chapter will be to help you plan such an approach. We will review (1) pertinent pathophysiology, (2) preparation for ACLS response, (3) how to run a code from the aspect of the bedside clinician, (4) the causes of Obstetric arrest, and (5) postresuscitative care. It should be noted that the ACLS guidelines published by American College of Cardiologists are the standard in the United States. These are available online at http://circ.ahajournals.org/content/122/18_suppl_3.toc. Nothing in this chapter should be interpreted as conflicting with these guidelines, but I have taken the liberty of offering simplification in a few areas, while expanding in a few others.

Review of the ACLS guidelines reveals 3 major modifications for the pregnant patient that we will explain in detail: (1) focus on early endotracheal intubation, (2) leftward displacement of the uterus during chest compressions, and (3) consideration of perimortem cesarean delivery within 4 minutes of onset of arrest. These few items are easy to remember and are the most important contents of this chapter. ACLS guidelines have changed since our last edition, with stronger emphasis on minimally interrupted, high-quality CPR, and on postresuscitative care.

Fetal and maternal circulation interface at the placenta, driving gas exchange between mother and fetus. Maternal cardiopulmonary adaptation to pregnancy allows balanced delivery of oxygen to the mother’s tissues and the fetus. Synergistic physiologic changes protect oxygen delivery in normal pregnancy. Maternal plasma volume and red blood cell mass increase, augmenting blood volume by 40% (>1000 mL). The left ventricle dilates and becomes more compliant, increasing stroke volume and cardiac output by 40%. The high oxygen affinity of fetal hemoglobin facilitates oxygen exchange across the placenta. Uterine contractions during labor result in maternal autotransfusion, enhancing oxygen delivery when it is needed most. Clinical experience and animal experimentation indicate that during normal pregnancy, maternal systemic and uterine oxygen delivery far exceed the minimal level necessary to sustain maternal and fetal life—with a remarkable reserve to compensate for life-threatening conditions. During cardiopulmonary arrest, however, oxygen delivery to maternal tissue and the uterus is dramatically reduced or eliminated. Maternal or fetal adaptations to severe insult are insufficient to sustain tissue viability. Death happens in minutes.

Pathophysiologic Rationale for CPR Recommendations in Pregnancy

Some normal physiologic changes of late pregnancy may have deleterious effects on oxygen delivery. By approximately 20 to 24 weeks’ gestation, the gravid uterus begins to compress abdominal and pelvic blood vessels, particularly the inferior vena cava and aorta. This diminishes preload to the heart, decreases maternal stroke volume, and may decrease uteroplacental oxygen delivery. In about 10% of women, these effects are so profound that the patient will become hypotensive in a supine position, even in the absence of illness. Uterine aortocaval compression has 2 important clinical consequences during maternal arrest: (1) it must be temporarily relieved to optimize the effectiveness of CPR and (2) it provides an opportunity to definitively improve maternal survival, since emergent delivery can have a profound benefit on maternal hemodynamics.

In nonpregnant patients, chest compression is estimated to produce cardiac output approximately 30% of normal. Although the effectiveness of chest compressions in pregnancy is unknown, it is likely diminished by aortocaval compression. In healthy late-term pregnancy, the gravid uterus can be shifted off the inferior vena cava if the patient is positioned in left lateral decubitus position, increasing cardiac output by 25%. However, CPR force generation is reduced by left decubitus positioning during arrest. When performing CPR on patients with gestational ages more than 20 weeks, manual displacement of the uterus to the left is a better first option (Fig. 17-1). If left lateral positioning during CPR is attempted, a 27 to 30 degree angle is recommended—but this may be difficult to maintain during chest compressions.

The most recent update to ACLS guidelines (2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care) emphasizes the importance of high-quality CPR. Rapid initiation of CPR increases survival to discharge. Even a few seconds of delay between interruption of chest compressions and shock significantly reduces defibrillation success rates. CPR should be started immediately once pulselessness is identified and should not be interrupted—even for intravenous line placement or cesarean delivery—except as briefly as possible (<10 seconds) when indicated by ACLS protocol (eg, to perform rhythm determination, to administer shock, or to rotate CPR providers). Hands should be placed slightly higher on the sternum than usual, accounting for the anatomy of the gravid abdomen and thorax. The optimal rate of compression is 100/min, with a compression depth of 2 in. Complete recoil of the chest should be allowed between compressions. If waveform capnography is used to monitor CPR effectiveness, the partial pressure of end-tidal CO₂ should exceed 10 mm Hg. If an arterial line is present, diastolic pressures should exceed 20 mm Hg.

Pathophysiologic Rationale for Perimortem Cesarean Section—the 4-Minute Rule

See Fig. 17-2.

Although the maneuvers discussed above may partially relieve aortocaval compression, perimortem cesarean delivery should theoretically be even more effective. It has been shown that cesarean delivery immediately increases cardiac output by 30% in healthy women. Delivery drastically reduces the perfusion demands of the uterus and placenta, which consume approximately 30% of maternal cardiac output near term; it also provides an approximate 500-mL autotransfusion. Delivery also allows resuscitative access to the infant.

Katz and colleagues have reviewed all published data on perimortem cesarean deliveries from 1900 through 2004. Their combined analyses show that 71% of babies who survived maternal arrest with good neurologic outcome were delivered in 5 minutes or less (Table 17-1) and that the rate of neurologic injury among survivors increases dramatically if delivery is further delayed. Maternal benefit of perimortem cesarean delivery is less well documented, but many case reports describe maternal recovery from refractory shock upon perimortem cesarean. Publication bias should be considered when interpreting these reports, though.

There is no rule that says delivery cannot be initiated before 4 minutes. If CPR is ineffective or the cause of the arrest is unlikely to be reversed within 4 minutes (eg, abruption, pulmonary embolism), it is prudent to proceed immediately to cesarean birth.

As pregnancy progresses, increasing aortocaval compromise by the enlarging uterus and improving viability of the fetus leads to 3 clinically important pathophysiologic states, as seen in Table 17-2. At less than 20 weeks, significant aortocaval compression is unlikely, the fetus is not viable, and perimortem cesarean delivery is unlikely to benefit mother or child. From 20 to 24 weeks, maternal hemodynamic benefit and fetal viability are both questionable. At greater than 24 weeks, perimortem cesarean delivery is most likely to benefit mother and infant.

If the patient’s obstetrical dates are unknown, they can be estimated by bedside examination. The uterine fundus is usually palpable at the level of the umbilicus at approximately 20 weeks’ gestation and grows cephalad at a rate of 1 cm/wk. Therefore, perimortem cesarean is supported when the uterine fundus is palpable at least 4 cm above the umbilicus in the supine position. Fundal height can be misleading in many cases (eg, multiple gestation, intrauterine growth retardation, oligohydramnios, fibroids, etc) but may be the best available data in a dire emergency. Portable ultrasound can be useful for determining gestational age but should not interfere with resuscitation.

Exact measurements are not necessary in a code situation; the American Heart Association supports intervention on an “obviously gravid uterus,” which describes situations when the clinician decides that the uterus is causing aortocaval compression and the fetus is viable.

A great deal of preparation before and during a code is necessary to successfully perform a perimortem cesarean within 5 minutes, and it is likely that a few achieve this goal. However, maternal survival has been reported after up to a 15-minute delay to perimortem cesarean and infant survival has been noted after up to a 30-minute delay. It is important to remember that when rapid delivery is impossible to achieve, a delayed procedure might still provide benefit.

Pathophysiologic Rationale for Early Endotracheal Intubation

Perimortem cesarean delivery usually requires maternal intubation. The physiologic changes of late pregnancy increase the risk for life-threatening complications during endotracheal intubation roughly 10-fold. Maternal oxygen consumption is significantly increased, lung compression by the gravid uterus reduces functional residual capacity by 20%, and intrapulmonary shunting increases 3-fold. These factors result in rapid oxygen desaturation if gas exchange is interrupted. Edema and hyperemia of the upper airway make airway bleeding more common and visualization of the vocal cords more difficult. Furthermore, if preeclampsia is present, airway edema can be further exacerbated with fluid overload. Additionally, progesterone causes decreased gastric motility while simultaneously relaxing esophageal sphincter tone, thereby increasing risk for aspiration.

Thus, the decision to forego bag-mask ventilation and proceed directly to endotracheal intubation is often more appropriate in the pregnant patient. Intubation should be performed by the most experienced person available and equipment for difficult airways needs to be at the bedside. Aspiration risk can be reduced by avoiding prolonged bag-masking, which causes gastric distention, and by application of cricoid pressure during intubation, which can diminish passive aspiration. Use of neuromuscular blocking agents and rapid sequence intubation can help prevent vomiting that leads to aspiration. Proper “sniff position” of the head and neck facilitates direct laryngoscopy. Airway edema may necessitate the use of slightly smaller endotracheal tubes, and the Bougie endotracheal tube introducer can be helpful when laryngoscopic view is difficult.

Nonemergent intubation during pregnancy may actually cause arrest if airway difficulties arise. Therefore, the obstetric team and a physician experienced in airway management should be notified prior to intubation of all pregnant women. Assessment of the airway for potential difficulty during endotracheal tube placement should be performed and a plan should be formulated for the 3 most favorable methods to secure the airway. Equipment necessary to carry out these alternatives, such as a laryngeal mask airway, video laryngoscope, and percutaneous cricothyrotomy kit, should be present prior to proceeding. Additionally, placement of a nasogastric tube to reduce the risk of aspiration pneumonitis (Mendelson syndrome); preoxygenation with 100% FIO₂ should also be performed prior to intubation.

Code Pharmacology and Cardioversion

Little information is available regarding the use of code medications in pregnancy. Vasopressor agents commonly used in ACLS protocols, such as norepinephrine and vasopressin, are known to decrease uterine blood flow. However, the infant’s best chance of survival is maternal survival. Therefore, in full arrest, ACLS pharmacology protocol is not altered by pregnancy. Standard defibrillation/cardioversion energies and electrical impedence of the chest wall are not altered by pregnancy. Moreover, deleterious effects of maternal defibrillation/cardioversion have not been reported in infants.

Much of the work involved in successfully conducting ACLS for a mother and perinate occurs well before arrest. An institution should have a protocol in place to immediately—and at all hours—provide the required personnel and equipment (Fig. 17-3). At our institution, oversight of this process is provided by a medical staff committee that meets monthly.

Each individual team member should be an expert at his or her particular assignment. However, studies have shown significant deficiencies in the knowledge base of most caregivers in regards to obstetrical arrest. ACLS certification, renewal and simulation are all helpful to educate and practice code responses, especially for the rare maternal occurrence.

Personnel not assigned a specific task on the code team should not be present in the patient’s room. Onlookers increase ambient noise and stress of the code, detracting from the code team’s performance. One exception may occur in teaching institutions, where residents and other trainees are incorporated to do only tasks that they are well trained in, such as providing chest compressions and obtaining vascular access.

Although many experienced clinicians are likely to be present and have good suggestions during a code, the sequence of events runs best when there is one established leader giving all orders. Establishing authority for code leadership requires some forethought and discussion between specialties before a code.

It is the responsibility of the code leader to make sure each member of the team is doing his/her job. The code leader should anticipate the needs of the mother and baby during the code to ensure that all equipment and personnel necessary to deliver and resuscitate the baby is available within the first 4 minutes of the code. Without proper protocols and preparation in place, this will not be possible.

Obviously, it is preferable to prevent an arrest rather than manage one, and close communication and cooperation between obstetric and critical care services in an institution can be an effective strategy for offering high-quality care and to minimize risk for mother and fetus.

Disclaimer: The American College of Cardiology ACLS guidelines are the gold standard for running codes in the United States. Nothing contained in our chapter is intended to conflict with those algorithms, but we have sought to simplify and focus on the care of the pregnant patient. The reader should refer to the ACLS 2010 guidelines for full details. We provide several summary figures for reference (Figs. 17-4,17-5, 17-6).

An overview of how to run an obstetric code is provided in Fig. 17-7 with a more detailed discussion to follow.

The following 5 things should be accomplished as quickly as possible:

1. Assess the pulse and start CPR, if pulseless.

2. Assess the airway and breathing. Instruct airway team to give 100% oxygen and proceed with intubation.

3. Check the rhythm. Rhythm interpretation in the pulseless patient is simple, since only ventricular fibrillation (VF) and fast ventricular tachycardia (VT) cause pulselessness requiring immediate shock. Figures 17-8,17-9, 17-10 will assist in rhythm interpretation. If the rhythm is pulseless VF/VT, shock the patient (Fig. 17-11). Remove the fetal monitor lead prior to shock.

4. Assess gestational age (related to aortocaval compression and fetal viability). Assign support staff to gather personnel and equipment necessary to perform cesarean delivery and to resuscitate the neonate, if emergent delivery is indicated.

5. Allocate a team member to establish venous access above the diaphragm. A large-bore catheter, such as a 9-French cordis introducer, in the internal jugular or subclavian position is helpful if massive transfusion is required, but it may be difficult to place during CPR. In contrast, a humeral intraosseous catheter can almost always be rapidly placed during CPR for drug administration.

Although these 5 events are listed in order, all should occur nearly simultaneously. In some circumstances, an experienced clinician might choose a different sequence. For example, if the patient has an obvious respiratory arrest secondary to massive aspiration, the first step might focus on the airway. For practical purposes, though, the exact order is not critical as long as CPR is prioritized and all steps occur rapidly.

• 6. Take a deep breath and think. You are doing fine. You have rapidly implemented the initial “CABD" (Circulation, Airway, Breathing, Defibrillation) approach to ACLS and have gathered resources you might soon need.

• 6a. Support the circulation. Be sure someone is manually displacing the uterus to the left while chest compressions are initiated. They should be hard and fast—100 compressions per minute. Have a ready supply of CPR personnel waiting in line to relieve one another, as most people can only provide adequate CPR for about 2 minutes before fatigue degrades their effectiveness. Immediately relieve anyone who cannot provide deep, hard compressions. If waveform capnography is used to monitor CPR effectiveness, the partial pressure of end-tidal CO₂ should exceed 10 mm Hg. If an arterial line is present, the diastolic pressure should exceed 20 mm Hg.

If pulseless, give epinephrine, 1 mg, IV (every 3-5 minutes) or vasopressin, 40 units, IV (every 20 minutes) until pulse is restored, at which time the patient should be placed in a left lateral decubitus position. If she is hypotensive, start a phenylephrine infusion at 100 μg/min or a norepinephrine (Levophed) infusion at 10 μg/min, escalating the dose to effect.

• 6b. If indicated, begin cesarean after 4 minutes. Consider immediate delivery if no pulse is initiated with CPR or if the cause of the arrest is unlikely to be reversible within 4 minutes (ie, abruption or pulmonary embolism).

Perimortem cesarean delivery is a stressful endeavor for all involved. Even the most seasoned care team inevitably will face unforeseen obstacles. Through experience with dozens of perimortem deliveries, our team has evolved through practice-based learning. We recommend utilizing a midline abdominal and uterine incision. This approach provides easier access for the operator to deliver baby and placenta. Additionally, it may facilitate maternal resuscitation by allowing access to the abdominal aorta for assessing adequacy of CPR and to provide aortic compression when appropriate. Compression of the aorta may assist with resuscitation by facilitating the delivery of drugs primarily to the heart and brain as opposed to a lower extremity and torso distribution. The surgeon should not be cavalier while entering the abdomen and must be careful to avoid bowel and bladder, which are often sufficiently distended to interfere with exposure. Closure of the abdomen should await assessment for bleeding that may resume, once the heart regains independent function.

• 6c. Consider and treat the cause of arrest. A pregnant patient is unlikely to suffer pulseless VF/VT as the solitary cause of her arrest. Maternal survival depends on achieving rapid diagnosis and reversal of the underlying etiology. A list of common causes for obstetric arrest is presented below. Often, there is not enough time to perform laboratory or radiographic studies, requiring the code leader to rely on bedside diagnosis based on targeted history and physical examination. It is imperative to rapidly assess pertinent medications the patient has received that could have precipitated arrest, such as intravenous magnesium infusion or epidural anesthesia. Sudden onset of dyspnea and pleuritic chest pain or unilateral leg edema (usually the left leg in pregnancy-associated deep venous thrombosis [DVT]), for example, should prompt consideration of pulmonary embolism. It is helpful to write out the “Hs and Ts" (Table 17-3) at the bedside during a code in order to verify consideration of all common etiologies.

Bedside echocardiography is helpful in cardiac arrest. A cardiac echo probe positioned during CPR can provide a quick cardiac evaluation when CPR is briefly discontinued for rhythm determination. Interruption of CPR specifically for echocardiography is not recommended, but it might facilitate discovery of the etiology. An echocardiogram showing a dilated, hypocontractile right ventricle would be consistent with pulmonary or amniotic embolism as opposed to a hyperdynamic, underfilled left ventricle seen with hemorrhagic shock. A hypocontractile left ventricle is often seen in peripartum cardiomyopathy or amniotic fluid embolism, as well.

The ACLS algorithm for pulseless arrest (see Fig. 17-4) is divided into 2 pathways, based on the initial cardiac rhythm—pulseless ventricular fibrillation/ventricular tachycardia (VF/VT) or pulseless electrical activity (PEA)/asystole. The key to treating the former is to shock the patient as quickly as possible. The key to treating PEA/asystole is to diagnose and treat the underlying cause. These separate algorithms significantly overlap in pregnancy. Although pulseless VF/VT is often experienced in obstetric codes and requires immediate defibrillation, electrical therapy is unlikely to be sufficient unless the root cause of the arrest is also treated.

The American College of Cardiology has offered the pneumonic “Hs and Ts” to help outline reversible causes of cardiac arrest, but pregnancy entails some causes rarely or never seen in other populations, such as hypermagnesemia and amniotic fluid embolism. Therefore, I have taken the liberty of altering the Hs and Ts so as to facilitate application to pregnant patients (see Table 17-3). It is beyond the scope of this chapter to deal with each exhaustively; however, discussion of a few is vital because they require rapid clinical diagnosis and emergent therapy.

Hypovolemia

In an arrest, hypovolemia indicates massive acute hemorrhage. A memory aid is not necessary if the bleeding is overt, but occult hemorrhage typically requires discernment. The physiologically augmented blood volume of pregnancy can sustain massive blood loss before significant changes in vital signs manifest. Most occult hemorrhages causing maternal arrest are of uteroplacental origin, such as abruption, placenta previa, or uterine atony. Vaginal bleeding is often observable, but up to 2.5 L of blood can be concealed between the endometrium and placenta, creating a severe disparity between hypovolemic signs and apparent blood loss. Subcapsular liver hematoma is another form of occult hemorrhage that can lead to shock or arrest in patients with preeclampsia (+/− HELLP); it is sometimes associated with right upper quadrant or epigastric pain.

If you think the patient is bleeding to death, one of the best single IV catheters for resuscitation is a 9-French cordis introducer placed in the subclavian or internal jugular vein. One must push in vitro fertilization (IVF) rapidly using low-resistance IV tubing (blood transfusion tubing) with a manual pump. A liter of fluid can be given in less than 5 minutes with the appropriate equipment. Standard IV infusion pumps deliver inadequate rates for resuscitation (typically <1 L/h), but infusion pumps purposefully designed for rapid transfusion can be very helpful. Patients that are pulseless from bleeding will likely require large volumes of packed red blood cells (or whole blood), fresh frozen plasma and platelets, so it is imperative that the blood bank is immediately notified of emergently required products. A reasonable balance in massive transfusion is to order packed red blood cells, fresh frozen plasma, and single donor platelets in a ratio of 6:6:1. Hemostasis may require surgical and/or radiologic intervention.

Hypermagnesemia

Elevated magnesium levels typically occur in patients receiving intravenous magnesium for preterm labor or preeclampsia, especially with renal insufficiency. Weakness, respiratory depression, and hyporeflexia/areflexia are findings of severe hypermagnesemia. Electrocardiographic findings are similar to those seen in hyperkalemia, including peaked T-waves, and broadening of the QRS. Ultimately, the ECG will demonstrate a sine-wave morphology as the QRS and T merge. Myocardial and respiratory muscle failure and life-threatening ventricular arrhythmias lead to arrest.

If the patient was receiving intravenous magnesium prearrest, stop magnesium and give IV/IO calcium chloride 10 mL (10% solution) or calcium gluconate 10 mL (10% solution).

Pulmonary Embolism

Pregnancy poses a 5- to 10-fold increased risk for venous thromboembolism. Pulmonary embolism is the most common cause of death in pregnancy in most series, accounting for up to 30% of maternal mortality. Some patients with pulmonary embolism present with syncope or sudden death without prominent dyspnea or hypoxemia. Although bedside echocardiogram is not useful for the diagnosis of pulmonary embolism in general, it is sensitive during arrest because a patient in severe shock from a pulmonary embolism will have a dilated and hypocontractile right ventricle. Acute right heart failure is usually the proximal cause of death.

If you suspect pulmonary embolism, give intravenous fluids to optimize preload of the right ventricle. Norepinephrine infusion can be used to support the circulation. If the patient is pulseless and the baby is viable, emergent cesarean delivery should be performed, since any specific therapy for pulmonary embolism is unlikely to provide benefits in less than 4 minutes. If delivery does not restore maternal circulation, the situation is nearly hopeless, but several desperate measures can be considered. None are of proven benefit or superiority to others.

1. Tissue plasminogen activator (tPA), 50 to 100 mg, may be given as an intravenous bolus. Massive hemorrhage from the C-section site and all venipuncture and arterial puncture sites will ensue, but tPA may temporarily restore maternal circulation. The obstetricians at our facility have achieved reasonable surgical hemostasis during cesarean delivery in a patient receiving tPA. The operative team, including a skilled general or vascular surgeon, should administer or be alerted of the decision to give thrombolytics, as it may subsequently befall them to ligate the uterine arteries or temporarily cross-clamp the aorta if uncontrollable bleeding ensues. Preparations for massive transfusion should be made immediately in accordance with institutional and blood bank criteria, if tPA is given.

2. Other options for pulmonary embolism treatment include venoarterial extracorporeal membrane oxygenation, surgical pulmonary thrombectomy, and percutaneous pulmonary artery interventions. Unfortunately, many of these are not available in most institutions, and will rarely occur quickly enough to save the mother’s life.

If a pulse can be recovered and sustained by resuscitative measures, a fourth option becomes available which is simply starting intravenous heparin at a therapeutic dose (unfractionated heparin: 80 U/kg bolus, 18 U/kg/min initial infusion rate). Choosing between these options in a patient who has just suffered an arrest is very difficult and strong empirical evidence is lacking to support any as dominant. Echocardiography is often helpful in this situation since severe acute right heart failure is predictive of poor prognosis, which favors aggressive therapy. Inhaled nitric oxide (iNO), introduced through a mechanical ventilator circuit at 20 to 40 ppm, may partially relieve life-threatening acute pulmonary hypertension secondary to pulmonary embolism in some patients.

Amniotic Fluid Embolism

Amniotic fluid embolism is an unpredictable and unpreventable event that can occur anytime during pregnancy but predominates during the peripartum and immediate postpartum period. Patients usually present with sudden cardiorespiratory collapse and coma, sometimes associated with disseminated intravascular coagulation (DIC) and seizures. There is no available diagnostic test, rendering clinical history and physical examination as superior for diagnosis. The pathophysiology of amniotic fluid embolism is complex, and studies suggest that, both, right and left heart failure, and an anaphylactic-like reaction may all play a role.

If you think the patient has amniotic fluid embolism, support the circulation as described above. Echocardiography might be helpful, as acute pulmonary hypertension and right heart failure have been treated successfully in some cases with iNO (20-40 ppm). Cardiogenic shock from left heart failure might improve with a dobutamine infusion (beginning at 10 μg/kg/min) once an adequate blood pressure has been recovered. Some patients have been successfully treated with cardiopulmonary bypass or extracorporeal membrane oxygenation.

Anesthesia-Related

Anesthesia-related maternal mortality is often related to an airway management catastrophe encountered in the course of general anesthesia for cesarean, including Mendelson syndrome. Regional anesthesia can cause arrest secondary to excessively high regional block or systemic toxicity of local anesthesia; both should be considered in the differential diagnosis of any patient who arrests during administration of spinal/epidural anesthesia. Unintentional cephalad progression of spinal block can result in sympathectomy-related vasodilation, inhibition of compensatory tachycardia, diaphragmatic paralysis, and aspiration. Pregnant patients are particularly prone to systemic toxicity from local anesthetics, which may be due to inadvertent intravascular administration of drug through an epidural catheter. This is more likely to occur when higher doses of the drug are administered during cesarean birth. Systemic toxicity manifests as seizures, coma, severe myocardial depression, and ventricular arrhythmias.

If you suspect local anesthetic systemic toxicity related to lipophilic local anesthetics (eg, bupivacaine, ropivacaine), administer 1.5 mL/kg ideal body weight of 20% intralipid solution as an intravenous bolus, followed by an infusion at 0.25 mL/kg/min (~100 mL bolus, infusion at 15 mL/min). Additional boluses can be given if needed. Amiodarone is the preferred antidysrhythmic. In some cases, cardiopulmonary bypass has been used to maintain life until the drug dissociates from cardiac tissue.

Other causes of maternal death that do not easily fit into the Hs and Ts memory aid that should nevertheless be remembered include intracranial hemorrhage related to preeclampsia/eclampsia, septic shock, congenital or acquired heart disease, and aortic dissection.

At the end of the code, the team should conduct a debriefing. Concerns or suggestions about improving the code process should be recorded for later discussion. In many critically ill obstetrical patients, a fine, somewhat artificial line exists between arrest resuscitation and postcode resuscitation. The code “ends” when a pulse is detected, allowing CPR to cease. However, the underlying cause of the arrest often persists and requires ongoing therapy. The following describes postarrest management. Remarkable neurologic recovery has been observed in pregnant patients who have survived prolonged cardiopulmonary arrest. Therefore, we advocate an aggressive approach in the hours and days following cardiac arrest.

Considerations for the hour after the code

• If cesarean was performed, leaving the abdominal incision open can facilitate direct access for ligation of maternal vessels, if necessary, and allows for cross-clamping vascular structures in extreme cases. This also ameliorates the possibility of abdominal compartment syndrome.

• Resuscitated patients who have suffered massive hemorrhage or amniotic fluid embolism are likely to develop consumptive and dilutional coagulopathies. They will likely require additional platelets, fresh frozen plasma, and/or cryoprecipitate. Rewarming the hypothermic patient may also improve hemostasis. Activated factor VII (45-90 μg/kg) is currently unproven to improve clinical outcomes in this situation, but may be considered when standard hemostatic therapies have failed. Interventional radiology can often provide hemostasis via embolization for hemorrhage originating from the uterine arteries.

• Massive transfusions may be associated with hydrostatic pulmonary edema and transfusion-related lung injury. Hypocalcemia can develop from citrate toxicity, and may precipitate hypotension; calcium replacement alleviates this quickly.

• Intra-abdominal hemorrhage can lead to abdominal compartment syndrome, wherein elevated intra-abdominal pressure is transmitted to the chest, thereby tamponading the heart and restricting the lungs. This typically results in shock, hypoxemia with high ventilator airway pressures, and oliguria/anuria. Bladder pressure will typically exceed 25 cm H₂O. Abdominal compartment syndrome is treated by laparotomy.

• Many important causes of maternal arrest and death are not included in the Hs and Ts. Sepsis and preeclampsia are examples that do not have specific ACLS interventions, but may still require emergent postresuscitative treatment. In particular, patients with severe preeclampsia/eclampsia may suffer from posterior reversible encephalopathy syndrome, requiring emergent intravenous antihypertensive therapy.

Therapeutic Hypothermia

Two randomized controlled trials demonstrate improved neurologic outcomes in comatose patients treated with 24 hours of mild hypothermia (32-34°C) after cardiac arrest secondary to ventricular fibrillation. Subsequent observational studies of therapeutic hypothermia included survivors of PEA/asystole arrest. Case reports have demonstrated good maternal and perinatal outcome after therapeutic hypothermia in pregnancy.

Therapeutic hypothermia is recommended in those (including gravid patients) who do not demonstrate purposeful movements or obey commands after cardiac arrest, regardless of cause. The main relative contraindication is life-threatening bleeding, as hypothermia induces a mild coagulopathy. This might be managed by radiologic or surgical intervention in those with uterine bleeding, but it is likely too risky in patients with intracranial hemorrhage related to preeclampsia/eclampsia. Hypothermia should be achieved as quickly as possible (≤6 hours), maintained for 24 hours, then withdrawn slowly. Cardiac complications range from benign maternal (and fetal) sinus bradycardia to fatal atrial or ventricular arrhythmias if severe hypothermia unintentionally results from poorly monitored cooling procedures. Therefore, institutional and personal preparedness is essential in postresuscitative care. Fetal heart rate monitoring is recommended during therapeutic hypothermia. Full details of how to safely administer therapeutic hypothermia are beyond the scope of this chapter.

Achieving Fetal Viability: Somatic Support of the Brain Dead Mother

A pregnant woman rarely suffers brain death in the first or second trimester, although intracranial hemorrhage, brain trauma, or intracranial malignancy is known to cause it. Postmortem neurogenic hemodynamic instability is common in this situation, but circulation may sometimes be sustained by aggressive supportive measures. Multiple reports have described somatic support of the brain dead mother so as to achieve fetal viability and maturity. One example from our institution was that of a gravida who suffered brain death at 23 weeks’ gestation: the fetus achieved a gestational age of 30 weeks in utero before delivery was affected. The child survived without long-term morbidity. Homeostasis of cardiopulmonary, endocrine, and other somatic systems requires a committed critical care team, but can yield a bright outcome amidst tragedy.

An obstetric code is a situation in which a physician is called upon to save 2 lives in less than 5 minutes. Although it is fortunate that obstetric arrests are rare, their infrequency degrades our ability to study them and our readiness to deal with them when the need suddenly arises. Understanding the pathophysiology and preparing ahead at an individual and institutional level are key to providing the best chance for maternal and fetal survival. If you are ever called upon to manage an obstetric code, the following are key: start and maintain high-quality CPR with displacement of the uterus to the left, intubate early, remember the 4-minute rule, and identify the etiology of the arrest quickly.