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 2015 guidelines for full details (see suggested readings). Figure 17.4 illustrates the general approach to the pulseless patient.
Adult cardiac arrest algorithm—2015 update. Reproduced with permission from © 2015 American Heart Association. American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2015;132:S444-S464.
A simplified overview of how the code leader should run an obstetric code in a patient at more than 20 weeks gestation is provided in Fig. 17-5 with a detailed description to follow.
General approach to running an obstetric code.
The following five things should be accomplished as quickly as possible upon entering the patient’s room:
Assess the pulse and start CPR if pulseless. Assign a team member to provide manual leftward uterine displacement.
Assess the airway and breathing. Instruct airway team to give 100% oxygen and proceed with intubation.
Assess 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 17-6, 17-7, 17-8 will assist in rhythm interpretation.
If the rhythm is pulseless VF or VT, remove the fetal monitor and immediately shock the patient (Fig. 17-9).
If the rhythm is not VF or VT, give epinephrine 1 mg intravenously or down the endotracheal tube.
Assign support staff to mobilize personnel and equipment necessary to perform cesarean delivery and to resuscitate the neonate, in case emergent delivery is indicated.
Allocate a team member to establish venous access above the diaphragm, if it is not already available. A humeral intraosseous catheter is useful for this purpose if available.
BRIEF INTERLUDE: Take a deep breath. You have rapidly implemented the initial “CABD” (Circulation, Airway, Breathing, Defibrillation) approach to ACLS and have gathered resources you might soon need.
Make sure everyone else is doing their jobs. Be sure someone is manually displacing the uterus to the left while chest compressions are properly performed. Compressions should be hard and fast—100 to 120 per minute. Have a ready supply of CPR personnel waiting in line to relieve one another. Each CPR cycle should last 2 minutes, but you might have to order a new CPR provider to take over sooner if the current provider is unable to provide adequate compressions for the full 2 minutes. If waveform capnography is used to monitor CPR effectiveness, the partial pressure of end-tidal CO2 should exceed 10 mm Hg. The person bag-ventilating the patient via and an advanced airway should be providing breaths at a rate of 10/min (once every 6 seconds). If onlookers are detracting from the code-team’s performance by increasing the ambient noise and stress of the code, assign a capable team member to clear the room of nonessential personnel.
Initiate cesarean delivery if no pulse after 4 minutes (two CPR cycles). In our experience, a midline abdominal and uterine incision provides easier access for the operator to deliver baby and placenta and may facilitate maternal resuscitation by allowing access to the abdominal aorta. However, the best surgical approach for the individual obstetrician is the one that they are personally most comfortable in performing. If accessible, compression of the aorta may assist with resuscitation by facilitating the delivery of cardiac output and drugs primarily to the heart and brain as opposed to the lower extremities. The surgeon should 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 briskly resume upon return of spontaneous circulation (ROSC).
Support the circulation. Continue giving epinephrine 1 mg intravenously every 3 to 5 minutes (approximately every other CPR cycle). Volume resuscitate if appropriate.
Determine and treat the cause of arrest. The mother is unlikely to survive unless the underlying cause of arrest is identified and specifically treated. Cardiovascular diseases, hemorrhage, and pulmonary embolism (PE) are the most common reported causes of maternal arrest. The cause in an individual patient might be obvious as in the case of massive bleeding, or occult as in the case of amniotic fluid embolism (AFE). Sudden death in a previously apparently normal patient suggests PE or AFE. Iatrogenic causes such as systemic toxicity of local anesthetics or magnesium should be considered. There is not enough time in a code to perform laboratory or radiographic studies, requiring the code leader to rely on bedside diagnosis based on targeted history and physical examination.
Ventricular tachycardia (monomorphic).
Ventricular tachycardia (polymorphic).
Algorithm for pulseless VF/VT.
The “Hs and Ts” is a memory aid to assist code leaders in determining the cause of an arrest. I have taken the liberty of modifying them for application in obstetrical arrest (see Table 17-3). I personally find it helpful to actually write these out at the bedside during the code in order to verify that I have considered all the most common etiologies. 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 during the code.
TABLE 17-3Differential Obstetric Arrest: the Hs and Ts |Favorite Table|Download (.pdf) TABLE 17-3 Differential Obstetric Arrest: the Hs and Ts
|Hs ||Ts |
[H+] ↑ (acidosis)
Hypertension-related complications of eclampsia/-preeclampsia
Hypovolemia causing pulselessness equates with massive acute hemorrhage. This diagnosis may initially be occult since 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 [hemolysis, elevated liver enzymes, and low platelet count]), sometimes associated with right upper quadrant or epigastric pain.
If you think the patient is bleeding to death, optimalize intravenous access by placing multiple large gauge (>18 gauge) peripheral IVs, a low-resistance central venous catheter such as a 9-French introducer, or an intraosseous line. Rapid administration of intravenous fluids can be augmented by using low-resistance IV tubing (blood transfusion tubing) and by manually pumping the fluid/blood in. A liter of fluid can be given in less than 5 minutes with the appropriate equipment. Standard infusion pumps deliver inadequate rates for code 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 (PRBCs), fresh frozen plasma, and platelets, so it is imperative that the blood bank is immediately notified of the emergent clinical situation. A reasonable balance in massive transfusion is to order PRBC, fresh frozen plasma, and single donor platelets in a ratio of 6:6:1. Uterine massage, uterotonic medications, and uterine balloon tamponade should be rapidly employed, if appropriate. Hemostasis may require surgical and/or radiologic intervention, if the patient survives the code.
Pregnancy poses a 5- to 10-fold increased risk for venous thromboembolism. PE is the most common cause of death in pregnancy in many series, accounting for up to 30% of maternal mortality. Some patients with PE present with syncope or sudden death without prominent dyspnea or hypoxemia. Observation of asymmetric lower extremity edema, typically affecting the left leg, can be a clue to underlying deep venous thrombosis during the code. Although bedside echocardiogram is not sensitive for the diagnosis of PE in a hemodynamically stable patient, it is sensitive during a code because acute right ventricular failure is the mechanism by which PE causes arrest. The code team leader might reasonably suspect PE based on clinical grounds and need to proceed with treatment without the benefit of customary confirmatory radiological tests.
If you suspect PE, a conservative amount of intravenous fluids (500-1000 mL) can be considered to optimize preload of the right ventricle. Norepinephrine infusion (eg, 5-50 μg/min) can be used to maintain mean arterial pressure more than 60 mm Hg in order to ameliorate threatened right coronary perfusion. If the patient is pulseless and the baby is viable, emergent cesarean delivery should be performed. If delivery does not restore maternal circulation, the situation is nearly hopeless, but several desperate measures can be considered. Tissue plasminogen activator (tPA), 50 to 100 mg, may be given as an intravenous bolus. We try to obtain a bedside echocardiogram to confirm right ventricular dilation and hypocontractility before giving tPA, but have proceeded without it in grave situations in which the ultrasound machine was not immediately available. Thrombolysis may dramatically restore maternal circulation, but hemorrhage from the C-section wound and all venipuncture and arterial puncture sites will likely ensue. The obstetricians at our facility have achieved reasonable surgical hemostasis during a perimortem cesarean delivery in a patient receiving tPA. The operative team, including a skilled general or vascular surgeon, should 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. Another option to treat an arrest due to PE is emergent veno-arterial extracorporeal membrane oxygenation—unfortunately, so-called “eCPR” (extracorporeal cardiopulmonary resuscitation) is not available at most institutions.
If a pulse can be recovered and sustained by resuscitative measures, other options become feasible. Surgical or interventional thrombectomy may be considered. 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 PE in some patients. Definitive treatment should be initiated, such as intravenous unfractionated heparin (80 U/kg bolus, 18 U/kg/min initial infusion rate) after taking into account overlap with thrombolytic agents.
AFE is an unpredictable and unpreventable event that can occur anytime during pregnancy but should particularly be suspected when a pregnant patient suddenly experiences cardiorespiratory collapse during labor or in the immediate postpartum period. Patients usually present with shock, severe hypoxemia, coma, seizures, and disseminated intravascular coagulation (DIC). The diagnosis is clinically-based, since there is no available validated diagnostic test. The pathophysiology of AFE is complex. Studies suggest that early pulmonary hypertension and right heart failure are followed by left heart failure as well as vascular dilation and increased permeability akin to that seen in anaphylaxis.
If you think the patient has AFE, fluids should be given with caution since hypovolemia is not typical, and most patients with AFE quickly develop pulmonary edema. Echocardiography might be helpful, as acute pulmonary hypertension and right heart failure have been treated successfully in some cases with iNO (20-40 ppm) and left heart failure might improve with a dobutamine infusion (beginning at 5 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 maternal mortality is often related to an airway management catastrophe encountered in the course of preparation for cesarean section. Regional anesthesia can cause arrest secondary to excessively high spinal 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 in some cases. This is more likely to occur when higher doses of the drug are administered during cesarean delivery. 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.
Severe hypermagnesemia more than 10 mg/dL can occur in patients receiving intravenous magnesium for preterm labor or preeclampsia, especially in the presence of renal insufficiency. Weakness and hyporeflexia/areflexia are usually clinically apparent in the prearrest phase. 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 similar to that seen with severe hyperkalemia. Myocardial and respiratory muscle failure and life-threatening ventricular arrhythmias lead to arrest. If the patient was receiving intravenous magnesium before coding, stop it and give intravenous/intraosseous (IV/IO) calcium chloride ~300 milligrams or calcium gluconate 1 gram (10 mL of 10% solution).
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.
Bedside echocardiography can be helpful in considering the etiology of arrest so long as it does not interrupt CPR or ACLS. A cardiac echo probe positioned in the subxyphoid location during CPR can provide a quick cardiac evaluation when CPR is briefly discontinued for rhythm determination. A dilated, hypocontractile right ventricle is consistent with pulmonary or amniotic embolism, a hyperdynamic, underfilled left ventricle with hemorrhagic shock. A hypocontractile left ventricle is often seen in peripartum cardiomyopathy, acute myocardial infarction, local anesthetic toxicity, and in some cases of AFE.