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Cardiac arrest during pregnancy
Journal of Clinical Anesthesia (2005) 17, 229 – 234
Case Conference of the University of Florida Series Editors: A. Joseph Layon, MD ! Michael E. Mahla, MD Associate Series Editors: Lawrence Caruso, MD ! Andrea Gabrielli, MD
Cardiac arrest during pregnancyB Carl W. Peters MD (Associate Professor)a,*, Abraham J. Layon MD (Professor)a, Rodney K. Edwards MD (Assistant Professor)b a
Department of Anesthesiology, University of Florida College of Medicine, Gainesville, FL 32610-0254, USA Department of Obstetrics and Gynecology, University of Florida College of Medicine, Gainesville, FL 32610-0254, USA
b
Received 20 September 2004; accepted 20 September 2004
Comment by Rodney K. Edwards, MDb Keywords: Cardiac arrest; Pregnancy; HIV infection
Abstract This case involves cardiac arrest of a 29-week pregnant African American woman, occurring 2 days after surgical correction of an incarcerated ventral hernia with small bowel obstruction. The patient could not be resuscitated from the arrest. Details of the case are presented, and diagnostic and unique management considerations for this uncommon occurrence are set forth.
1. Introduction Cardiac arrest is an infrequent occurrence in pregnancy [1]. The causes generally fall into 1 of 2 categories [2]. The first category includes those conditions that affect only pregnant individuals. The other is a list of non– pregnancy- associated potentially deadly processes that can often be recognized and treated but are made more complex and difficult to manage by their appearance in the parturient. In the former group lie the familiar
B
Case conference presentations are selected and edited at the Department of Anesthesiology, University of Florida College of Medicine. T Corresponding author. ATTN: Editorial Office, Department of Anesthesiology, University of Florida College of Medicine, Box 100254, Gainesville, FL 32610-0254, USA. Tel.: +1 352 265 8012; fax: +1 352 265 8013. E-mail address: [email protected] (C.W. Peters). 0952-8180/$ – see front matter doi:10.1016/j.jclinane.2004.09.003
conditions associated with pregnancy, namely eclampsia and preeclampsia, HELLP syndrome, puerperal hemorrhage, peripartum cardiomyopathy, amniotic fluid embolism, and anesthetic catastrophe associated with labor and delivery. In the latter category are the traditional killers of nonpregnant individuals such as pulmonary thromboembolic events; heart disease, both congenital and acquired; rapidly progressive infection leading to sepsis; and endocrine and inflammatory disorders. We present a 29-week pregnant patient who died of an unknown event. She was a model for risk factors for several conditions mentioned in the next sections, but the specific cause of her death is unknown because no postmortem examination was allowed. The clinical picture was further clouded by the complication of HIV infection, although the patient’s blood cell counts at the time of her death were unknown. The case is presented in detail, including pertinent differential diagnostic considerations.
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2. Case report The patient was a 34-year-old African American woman who was positive for hepatitis C and HIV since 1998, and 29 weeks pregnant by ultrasound and by dates. She had undergone gastric bypass surgery in 1990, but she was morbidly obese at the time of this event. Two inguinal hernia repairs had been done since the gastric bypass surgery. The patient presented to labor and delivery triage with 1 day of abdominal pain. Physical examination findings were abdominal tenderness and reducible ventral hernia. An abdominal computed tomographic (CT) scan was performed, which showed findings consistent with a small bowel obstruction. The patient was evaluated by the general surgery service, which recommended conservative management. The patient was admitted to the hospital and followed closely. Twenty-four hours after the initial evaluation, a dilated small bowel loop was seen on plain abdominal film with an area of tenderness to the right of her gastric bypass incision. On the basis of these findings, the patient was taken to the operating room for surgical exploration and reduction of her small bowel obstruction. During the operative intervention, blood loss was 50 mL and urine output was 375 mL. She received 4000 mL of crystalloid (2 L of normal saline and 2 L of lactated Ringer’s solution) and 2 units of packed red blood cells. Vecuronium 10 mg was given for muscle relaxation during the case, and the patient’s trachea remained intubated in the recovery room for approximately 60 minutes postoperatively because of residual neuromuscular blockade. Extubation thereafter was successful, with subsequent vital signs of blood pressure of 128/57 mm Hg, heart rate (HR) 119 bpm, temperature 35.9 8C, respiratory rate (RR) of 17 breaths/min, and pulse oximetric saturation (Spo2) of 100% (inspired oxygen concentration [Fio2] not specified). She remained in the recovery room for part of the night. Early in the morning, approximately 36 hours after arrival at the hospital, the patient was transferred to the surgical intensive care unit (SICU) for persistent marginal Spo2 that had developed during her recovery room stay, namely 96% on an Fio2 of .5. Arterial blood gas (ABG) analysis on arrival at the SICU showed pH 7.43, Paco2 26 mm Hg, Pao2 59 mm Hg, and sodium bicarbonate (HCO3 )16 mM/L on oxygen 7 L by mask. One hour later, ABG showed pH 7.45, Paco2 24 mm Hg, Pao2 69 mm Hg, and HCO3 16 mM/L on 6 L O2 by mask. Serum electrolytes at that time were sodium 135 mEq/L, potassium 3.7 mEq/L, chloride 108 mEq/L, HCO3 20 mM/L, BUN 32 mg/dL, creatinine 0.5 mg/dL, glucose 133 mg/dL, total calcium 8.1 mg/dL, magnesium 1.4 mEq/L, and phosphate 3.2 mM/L. Hemoglobin was 10.1 gm/dL, hematocrit 32%, platelets 417 000 cells/lL, and white blood cell count 11 000 cells/lL. During morning rounds, the patient was found to have very small tidal volumes. A chest radiograph showed pulmonary edema, with the comment by the managing physician of bimpending respiratory failure.Q Dobutamine
C.W. Peters et al. was administered for inotropic support, and the patient was given aggressive pulmonary toilet with emphasis on full sitting position to assist in respiration. Diuretic medication was administered with a target of 1 to 1.5 L of urine production. An echocardiogram was ordered, but no record exists in the hospital computer records as to whether it was done. All electrolyte abnormalities were corrected during the day. By that evening, about 48 hours after arrival, the patient’s RR was 35 to 40 breaths/min and Spo2 was 93% on supplementary oxygen. At that point, the patient was started on full-face bilevel positive airway pressure, with an inspiratory pressure of 15 cm H2O, an expiratory pressure of 10 cm H2O, and Fio2 of 0.7. This treatment improved the patient’s Spo2 to between 95% and 97%. Lower extremity Doppler ultrasound studies performed to evaluate for a deep venous thrombosis (DVT) and were negative; the decision was then made not to obtain CT studies of the pelvis or chest. By the next morning, 60 hours after arrival in the hospital, the patient had diuresed 3 L of fluid. The chest radiograph, which was difficult to interpret because of the patient’s morbid obesity, showed a picture compatible with improving pulmonary edema. However, it did show possible air bronchograms, and on the basis of this finding, the original antibiotic treatment was changed to include coverage for aspiration pneumonia. Bilevel positive airway pressure respiratory support was increased to 23/20 cm H2O, the patient was continued in the full upright sitting position, and discussion was conducted about the indications for endotracheal intubation in this patient. By the next morning, about 84 hours after arrival in the hospital, the patient was noted to be extremely tachypneic, with RR as high as 47 breaths/min. Clinically, she was in extremis from a respiratory standpoint despite Spo2 of 100%. Her HR ranged from 120 to 145 bpm despite treatment with metoprolol. At that point, the decision was made to intubate the patient’s trachea. As she was being helped into the supine position for intubation, which was performed easily, she was noted to become bradycardic. The rhythm deteriorated into ventricular fibrillation within 3 minutes despite high-flow oxygen delivered by the bagvalve mask and the administration of atropine; advanced cardiac life support (ACLS) measures were begun. Simultaneously, the obstetric physicians were called to the bedside for an emergency cesarean section. The time interval between this call being placed and delivery of the fetus was 16 minutes. The ACLS measures that were used during this time were defibrillation (14 times with 360 joules), bilateral chest tube placement and pericardiocentesis for pulseless electrical activity, administration of epinephrine 29 mg in divided doses, vasopressin boluses of 40, 40, and 80 units, 2 g of calcium chloride, 150 meq of HCO3 in divided doses, and an epinephrine infusion. Transcutaneous cardiac pacing was attempted but was unsuccessful. The patient’s rhythm alternated between pulseless electrical activity and ventricular fibrillation, in spite of these measures and continuous cardiopulmonary resuscitation
Cardiac arrest during pregnancy (CPR). The rhythm eventually degenerated into asystole refractory to any measure, and the patient was declared dead. Unfortunately, the newly delivered infant had no signs of life, and could not be revived despite the heroic efforts of the neonatal critical care physicians. The family declined autopsy on both individuals.
3. Discussion Cardiac arrest is reported to occur in about 1 in every 30 000 pregnancies that are near term [1]. This fact seems surprising, in that pregnant women are usually in the prime of health, unfettered by the acute or chronic conditions that are the harbinger of what is usually a fatal occurrence in older populations (ie, those that are most often afflicted). The rate of occurrence is consistent, however, and is predictably due to events that fall into 2 general categories of pathology. These categories are (1) those conditions that impact the cardiovascular stability of the population in general but affect the pregnant patient more dramatically, and (2) those entities that are specifically related to pregnancy. Deep venous thrombosis and pulmonary embolism (PE) often intrude into what seems to be a stable uneventful pregnancy [3]. Pulmonary embolism is seen in 24% of parturients who develop DVT for which they are not appropriately treated, whereas only 4.5% of those treated develop a PE. In patients not treated, approximately 15% die, whereas less than 1% of treated patients die. The likelihood of occurrence of DVT and PE is increased in pregnant women by the presence of the 3 major risk factors: endothelial vascular injury, hypercoagulable state, and venous stasis [4]. The timely discovery and treatment of DVT and PE is frustratingly difficult. The signs and symptoms of PE are notoriously nonspecific, being seen in a host of cardiopulmonary conditions. Furthermore, reliance on the presence of certain findings as a signal that a DVT workup is warranted will leave one disappointed — DVT often remains clinically silent within the limb [5]. Laboratory or diagnostic studies to confirm or exclude DVT or PE may either clarify or confuse the physician. Suspicion of PE may be investigated in a number of ways. Ventilation-perfusion scintigraphy is considered the first-line tool by many clinicians. High probability scan gives positive predictive value of 97%. Up to 70% of scans warrant further investigation [6]. Continued suspicion of PE or pelvic DVT, despite a negative ventilationto-perfusion study, warrants further radiological studies such as CT pulmonary angiography, conventional pulmonary angiography, or magnetic resonance imaging for complete evaluation [7,8]. The implications of radiography for the pregnant patients are obvious, and must be scrutinized and evaluated meticulously before radiographic studies are used in the parturient. Primary heart disease can lead to cardiac arrest in gravid patients. Many women with congenital heart disease are now surviving into child-bearing years and becoming pregnant;
231 decompensation and arrest can thus occur during pregnancy. Coronary artery disease leading to myocardial infarction complicates 0.01% of pregnancies [9]. Myocardial infarction occurs more often in the obese, diabetic, hypertensive, or hyperlipidemic gravid patient. Furthermore, the pregnant woman is more likely to be older and a smoker now than in the past. When these facts are added to the aforementioned risk factors, management of heart disease in the pregnant patient becomes a genuine challenge. The combination of subtlety of ischemia-related symptoms, intolerance to fluid overload in those with borderline cardiovascular reserve, and difficulty in resuscitation of the pregnant woman make for a dismal outlook for the gravid patient with coronary artery disease who suffers a cardiac arrest. When it happens, infarction occurs most often in the third trimester, and mortality rates vary from 21% to 45% [10]. As to other forms of cardiac disease, valvular cardiac pathology is variably tolerated. Regurgitant lesions may be better handled by the parturient who is already vasodilated, and therefore, afterload reduced by virtue of her pregnant condition [11]. Pulmonary hypertension, primary and secondary, is particularly difficult to manage successfully, with death rates varying between 30% and 52%. Causes of secondary pulmonary hypertension include recurrent pulmonary thromboembolism, HIV, inflammatory conditions such as vasculitis and connective tissue disorders, and congenital heart disease. Management may include inhaled or intravenous vasodilators and employment of pulmonary artery catheterization in the peripartum period for early identification of increasing pulmonary artery pressure. Infections can complicate pregnancy and warrant aggressive intensive therapy to forestall the onset of septic shock, which occurs in 1 per 5000 pregnancies. Ninety-five percent of the bacterial causes of septic shock in pregnancy are gram-negative organisms [12]. The most common infectious entities that lead to septic shock are chorioamnionitis, pyelonephritis, endometritis, and toxic shock syndrome. Mortality for septic shock associated with pregnancy ranges from 33% to 66%. Hormonal disorders complicate pregnancy, occasionally with lethal results. Thyroid storm, pituitary apoplexy from enlarging prolactinoma leading to Sheehan’s syndrome (hypopituitarism from infarct of the pituitary gland from postpartum shock or hemorrhage), hypercalcemia from hyperparathyroidism, and cardiovascular decompensation from pheochromocytoma can cause maternal cardiac arrest and death. Diabetic ketoacidosis in pregnancy carries an estimated mortality rate of about 1%. At greatest risk is the undiagnosed woman with first manifestation of diabetes as diabetic ketoacidosis in pregnancy [13]. An uncommon event is the occurrence of pregnancy in a woman with one of the rheumatologic-autoimmune diseases. The paucity of experience hinders in-depth analysis of the impact of these diseases on the pregnancy, but a few observations are warranted. Systemic lupus erythematosus (SLE) occurs at a rate of 15 to 50 per 100 000 people in the
232 United States, and more than 90% of these affected individuals are women. Morbidity in the parturient is increased, related for the most part to the 15% to 25% incidence of preeclampsia in those with SLE. Further confounding the analytical picture is the difficulty in differentiating SLE-related preeclampsia from the signs and symptoms of lupus nephritis or lupus cerebritis. The appearance of these conditions can be quite similar, with severe hypertension and proteinuria, or mental status changes and seizures, but the treatment regimens are quite different, with the treatment of one condition being quite destructive to a patient with the other of these conditions. The complexity of the interactions of SLE and other collagen-vascular diseases such as polyarteritis nodosa and rheumatoid arthritis and their effect on pregnancy warrant specialty consultation [14]. From the standpoint of obstetric conditions that can lead to cardiac arrest, there is a host of repeat killers. Preeclampsia and eclampsia frequently evolve into lethal events such as intracerebral hemorrhage, cardiovascular instability, multiorgan system failure, and uncontrolled bleeding in other body sites from coagulopathy. The former condition is characterized by severe hypertension, abdominal pain, oliguria, deteriorating renal function, headache and visual changes, liver function test abnormalities, and pulmonary edema. The addition of seizures to this milieu of symptoms defines the onset of eclampsia, although up to 38% of eclamptic patients can experience seizures without any preeclamptic symptoms [15]. Two percent of those experiencing eclamptic seizures die as a result of the complications of these events. At highest risk are those with preexisting hypertension, multiple gestations, first pregnancy, those with a family history of preeclampsia, renal disease, and diabetes. A common companion to eclampsia is the HELLP syndrome, consisting of hemolysis, elevated liver enzymes, and low platelets. The rate of occurrence is less than 1% of pregnancies, occurs in late pregnancy (27-36 weeks’ gestation), and carries a mortality rate of 1% to 3% [16]. Up to one third of the fetuses delivered to women with this condition may die. Most frequent laboratory manifestations in this condition are a low platelet count (below 100 000 cells/lL) and serum transaminases that are slightly elevated. Hemorrhage, both prepartum (abruption and placenta previa) and associated with delivery itself (natural and surgical) and its immediate aftermath, can be massive and may lead to death from exsanguination [2]. The hemorrhage may be obvious or subtle. Massive hemorrhage occurs in pregnancy for a number of reasons. It can be surprisingly difficult to diagnose in timely fashion. Large vessels supplying and draining the uterus provide a conduit for major blood loss when pathological processes such as abruption, uterine rupture or atony, or placenta previa complicate the pregnancy or delivery. Uterine atony is the most common cause and is treated primarily with medications that constrict the uterine tissue and vessels. Late identification of massive hemorrhage can lead to cardiac arrest, which is particularly difficult to correct because of the blate startQ on
C.W. Peters et al. resuscitation that causes the event in the first place. Treatment involves simultaneous pathways of employment of ACLS algorithms and repletion of intravascular blood volume. The astute clinician must remain alert to the signs and symptoms that are manifestations of bleeding and must provide hemodynamic support to the hemorrhaging patient. Peripartum cardiomyopathy affects about 1000 pregnant women each year in the United States. The condition is characterized by the onset of heart failure symptoms within 1 month before delivery to about 5 months after delivery. Peripartum cardiomyopathy is a diagnosis of exclusion, and all other etiologies of congestive heart failure must be ruled out before its being invoked as the cause. This condition is felt to be a form of infectious myocarditis, possibly viral in origin, or perhaps autoimmune or idiopathic in etiology. The clinical picture manifests typical features of heart failure: chest pain, orthopnea and paroxysmal nocturnal dyspnea, overt fluid overload with pedal edema, and shortness of breath with exertion. Sinus tachycardia and nonspecific ST-wave and T-wave changes are often seen. In about 50% of patients, the cardiomyopathy resolves after delivery; of those cases that do not resolve, most patients die [17]. Amniotic fluid embolism occurs infrequently in pregnancy but generates high rates of morbidity and mortality. The phenomenon was first described in 1926 by Meyer, as noted by R.G. Mason [18] and is characterized by respiratory distress, cardiovascular collapse, altered mental status, and alteration of coagulation parameters [19]. The presentation may masquerade as any of the other more common life-threatening conditions that may happen abruptly in the peripartum period. These conditions include eclampsia with status-epilepticus, acute thromboembolism, and anaphylaxis. Seventy percent of the cases of amniotic fluid embolism occur during labor and delivery, the majority within 5 minutes of delivery. A small percentage of cases occurs before delivery, and 19% of cases occur during cesarean section. A very broad estimate of overall occurrence is 3 per 100 000 pregnancies [20], and the fatality rate varies from 22% to 88%. Anesthetic complications such as an unmanageable airway and drug-induced hemodynamic instability are wellrecognized companions to obstetric anesthesia [21]. Vasodilator side effects of both regional and general anesthetic drugs can precipitate cardiac arrest in the parturient who already is in a barely compensated state of hypovolemia or who is dehydrated from preeclampsia. Deaths from the consequences of the difficult obstetric airway have decreased in frequency mainly because of greater clinician awareness and the invention of useful airway management adjuncts. This frequency, however, has not dropped to zero. If cardiac arrest does occur, a number of issues arise. All ACLS measures must begin immediately, as in any episode of cardiac arrest. The pregnant state, however, complicates matters. Airway management is complicated by the gastric hypokinesis of pregnancy; cricoid pressure should be
Cardiac arrest during pregnancy maintained until the airway is secured to prevent the higher risk of aspiration of gastric contents. Efficient ventilation and oxygenation are more difficult to accomplish because of the increased oxygen requirements and decreased chest wall compliance of pregnancy [1]. Venous return to the heart from the lower extremities will occur only when compression of the inferior vena cava is released by rolling the patient toward her left side with support from a wedge, an overturned chair, or the knees of an assistant kneeling on the floor on the patient’s right side. Cardiopulmonary resuscitation and mask ventilation can be efficiently accomplished when the patient is turned no more than 308 to the left. Cardiopulmonary resuscitation and ACLS measures are seldom needed on the labor and delivery ward, so frequent rehearsals of mock scenarios involving cardiac arrest will shorten the response times and heighten the awareness of correct ACLS procedures when these procedures are warranted. In addition, the literature is replete with guidance for successful perimortem and postmortem cesarean section for emergency delivery of an infant from a dying mother, both to save the infant or the mother [22 - 24]. In the case of maternal cardiac arrest and possible perimortem cesarean section (from the ancient Roman legal code known as Lex Caesare [25]), time obviously is the most crucial issue. For arrests that occur in the labor and delivery suite, the obstetrician is immediately at hand to perform the operation. At more distant sites, recognition of the potential need for surgical intervention for delivery of the fetus must be immediate so as to summon the appropriate individual for surgical assistance. In Great Britain, between 1972 and 1996, 56 postmortem cesarean sections yielded 6 neurologically normal children. A 10-year survey of perimortem cesarean sections yielded 25 healthy survivors from 40 deliveries. In the most comprehensive review of the literature on the subject, 93% of the surviving infants were born within 15 minutes of the maternal death, and only 2 had neurological defects; 70% of the survivors were delivered within 5 minutes [25]. One final consideration that fits into neither large category mentioned above, but that sits in the background of any analysis of this patient’s management and outcome, is the influence of her HIV infection on her cardiovascular condition. There is an evolving body of literature defining the influence of HIV infection on cardiovascular status. Eight to 10% of the new HIV patients develop symptomatic heart failure over a 2- to 5-year period. However, there is little information addressing HIV infection as a predictor of sudden cardiac decompensation and cardiac arrest, specifically in the parturient. It has been well demonstrated that HIV can profoundly affect cardiovascular integrity in a number of ways. These ways include the association of HIV infection with myocarditis, with nutritional deficiencies that affect contractility, and with side affects of medications used to treat HIV infection [26] All of these processes may lead to dilated cardiomyopathy. In addition, HIV infection is associated with pericardial effusions that may progress to tamponade, with
233 bacterial, fungal, and marantic endocarditis; with pulmonary hypertension; and with vasculitic, atheromatous, and hypertensive cardiac conditions. The mental jump from occult HIV-related cardiac pathology to the sudden pregnancyrelated cardiovascular decompensation of this unfortunate individual is easy to make, although we remain unsure of the precise cause of her death.
4. Comment by Rodney K. Edwards, MD, MS The authors provide an interesting case report and a thorough review of the potential causes of cardiac arrest during pregnancy. As stated, no postmortem examination was conducted, and this fact makes determination of the cause of this particular patient’s death impossible to ascertain. Fortunately, such an occurrence during pregnancy is quite uncommon. However, when pregnant women do suffer cardiac arrest, prompt action is needed from individuals skilled with the provision of CPR, knowledgeable about the physiologic changes associated with pregnancy, and experienced with emergent cesarean delivery. Otherwise, mortality for both mother and fetus is the likely outcome. The authors discuss the fact that the gravid uterus impairs venous return to the heart during CPR. However, left lateral tilt does not completely alleviate the problem. Tilting the patient helps to relieve this obstruction. However, it also decreases the effectiveness of chest compressions, because this lateral tilt causes the trunk to roll [27,28]. Because emptying the uterus will alleviate some of this obstruction to venous return, perimortem cesarean delivery has been advocated as a way not only to attempt to salvage a viable fetus but also to improve the effectiveness of CPR in pregnant women with cardiac arrest. In 1986, Katz et al [29] reviewed reports of successful results with perimortem cesarean delivery. They found that infant survival was most likely if delivery occurred within 5 minutes of cardiac arrest, and that infant survival without serious neurological impairment was unlikely if delivery occurred more than 15 minutes after cardiac arrest. Therefore, these authors and several texts recommend initiating delivery within 4 minutes of cardiac arrest. This recommendation — that delivery should be initiated within 4 minutes after cardiac arrest — assumes that delivery of the infant can be effected in approximately 1 minute. Because of several factors present in this patient, this interval may not have been achievable. Because of her morbid obesity and recent surgery, abdominal entry would require more time than for the usual emergent cesarean delivery. Furthermore, for obvious reasons, this patient’s hepatitis C and HIV infections would understandably result in care to avoid injury to the surgeon or any assistants. Another factor that could result in delay in initiating a perimortem cesarean delivery is the location of the patient at the time of arrest. This woman was located in the SICU at the
234 time of her cardiac arrest. It likely would require more time to summon obstetricians to this unit than to an emergent delivery in the labor and delivery unit. If a pregnant woman is critically ill, locating a pack containing the instruments necessary to perform a cesarean delivery at her bedside and notifying the obstetrics team of any deterioration in status before cardiac arrest would decrease the interval from cardiac arrest to delivery. In the case report, there is no mention of whether the fetal HR tracing was being monitored. The ABG reports indicate that maternal, and therefore fetal, oxygenation was marginal. Monitoring the fetal HR tracing can provide some insight as to the status of the fetus in a pregnant woman with respiratory distress. Oxygen delivery to the fetus is inadequate with maternal Po2 values at or below 60 mm Hg, and efforts to improve oxygenation of the mother are needed. Fetal HR tracing analysis may suggest a need for increased oxygen delivery to the pregnant woman, even if measures of her Spo2 are reassuring. Furthermore, fetal condition before maternal cardiac arrest can predict the likelihood of intact neonatal survival. As an example, unlike the case reported herein, if the etiology of cardiac arrest were massive hemorrhage, maternal circulation would be directed preferentially to the brain, heart, and adrenal glands. Therefore, the uteroplacental circulation would be diminished long before cardiac arrest, and intact neonatal survival would be unlikely, regardless of the time interval from cardiac arrest to delivery. In summary, cardiac arrest during pregnancy is an uncommon event. When it does occur during the latter part of pregnancy, perimortem cesarean delivery may improve the outcome for both the fetus/neonate and the pregnant woman. Provision of care by a multidisciplinary health care team and optimal communication between the members of this team will maximize the likelihood of survival for both patients. Beyond 24 weeks’ gestation, the standard ABCs of CPR (airway, breathing, and circulation) should also include a bDQ — for delivery [30]. Unfortunately, even under ideal circumstances, mortality is the usual outcome for both the pregnant woman who experiences cardiac arrest and her fetus.
References [1] Morris S, Stacey M. Resuscitation in pregnancy. BMJ 2003; 327(7426):1277 - 9. [2] Whitty JE. Maternal cardiac arrest in pregnancy. Clin Obstet Gynecol 2002;45:377 - 92. [3] Andres RL, Miles A. Venous thromboembolism and pregnancy. Obstet Gynecol Clin 2001;28:613 - 30. [4] Phelan JP. Thromboembolic disease. In: Clark SL, Cotton DB, Hankins GD, et al, editors. Critical care obstetrics, 3rd ed. Malden (Mass)7 Blackwell Science; 1997. p. 369 - 98.
C.W. Peters et al. [5] Hull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation, lung scanning and venography for clinically suspected pulmonary embolism with abnormal lung perfusion scan. Ann Intern Med 1983;98:891 - 9. [6] Value of the ventilation/perfusion scan in acute pulmonary embolism: results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). The PIOPED Investigators. JAMA 1990; 263:2753 - 9. [7] Greer IA, Barry J, Mackon N, Allan PL. Diagnosis of deep venous thrombosis in pregnancy: a new role for diagnostic ultrasound. BJOG 1990;97:53 - 7. [8] Weinmann EE, Salzman EW. Deep-vein thrombosis. N Engl J Med 1994;331:1630 - 41. [9] Mabie WC, Freire CM. Sudden chest pain and cardiac emergencies in the obstetric patient. Obstet Gynecol Clin North Am 1995;22:19 - 37. [10] Ramsey PS, Ramin KD, Ramin SM. Cardiac disease in pregnancy. Am J Perinatol 2001;18:245 - 66. [11] Lupton M, Oteng-Ntim E, Ayida G, Steer PJ. Cardiac disease in pregnancy. Curr Opin Obstet Gynecol 2002;14:137 - 43. [12] Lee W, Clark SL, Cotton DB, et al. Septic shock in pregnancy. Am J Obstet Gynecol 1988;159:410 - 6. [13] Lucas MJ. Diabetes complicating pregnancy. Obstet Gynecol Clin North Am 2001;28:513 - 36. [14] Friedman SA, Bernstein MS, Kitzmiller JL. Pregnancy complicated by collagen vascular disease. Obstet Gynecol Clin North Am 1991;18:213 - 36. [15] Lipstein H, Lee CC, Crupi RS. A current concept of eclampsia. Am J Emerg Med 2003;21:223 - 6. [16] Doshi S, Zucker SD. Liver emergencies during pregnancy. Gastroenterol Clin North Am 2003;32:1213 - 27. [17] Brown CS, Bertolet BD. Peripartum cardiomyopathy: a comprehensive review. Am J Obstet Gynecol 1998;178:409 - 14. [18] Masson RG. Amniotic fluid embolism. Clin Chest Med 1992; 13:657 - 65. [19] Fletcher SJ, Parr MJ. Amniotic fluid embolism: a case report and review. Resuscitation 2000;43:141 - 6. [20] Davies S. Amniotic fluid embolus: a review of the literature. Can J Anaesth 2001;48:88 - 98. [21] Kuczkowski KM, Reisner LS, Benumof JL. Airway problems and new solutions for the obstetric patient. J Clin Anesth 2003;15:552 - 63. [22] Esposito MA, DeLony R, Goldstein PJ. Postmortem cesarean section with infant survival: a case report of an HIV-infected patient. Md Med J 1997;46:467 - 70. [23] Parker J, Balis N, Chester S, Adey D. Cardiopulmonary arrest in pregnancy: successful resuscitation of mother and infant following immediate caesarean section in labour ward. Aust N Z J Obstet Gynaecol 1996;36:207 - 10. [24] Finegold H, Darwich A, Romeo R, Vallejo M, Ramanathan S. Successful resuscitation after maternal cardiac arrest by immediate cesarean section in the labor room [Letter]. Anesthesiology 2002; 96:1278. [25] Whitten M, Irvine LM. Postmortem and perimortem cesarean section: what are the indications? J R Soc Med 2000;93:6 - 9. [26] Barbaro G. Cardiovascular manifestations of HIV infection. Circulation 2002;106:1420 - 5. [27] Kuhlmann RS, Cruikshank DP. Maternal trauma during pregnancy. Clin Obstet Gynecol 1994;37:274 - 93. [28] Moise Jr KJ, Belfort MA. Damage control for the obstetric patient. Surg Clin North Am 1997;77:835 - 52. [29] Katz VL, Dotters DJ, Droegemueller W. Perimortem cesarean delivery. Obstet Gynecol 1986;68:571 - 6. [30] Phelan JP, Kirkendall C, Shah SS. Fetal considerations in the critically ill gravida. In: Dildy II GA, editor. Critical care obstetrics, 4th ed. Malden (Mass)7 Blackwell Science; 2004. p. 593 - 611.
Case Conference of the University of Florida Series Editors: A. Joseph Layon, MD ! Michael E. Mahla, MD Associate Series Editors: Lawrence Caruso, MD ! Andrea Gabrielli, MD
Cardiac arrest during pregnancyB Carl W. Peters MD (Associate Professor)a,*, Abraham J. Layon MD (Professor)a, Rodney K. Edwards MD (Assistant Professor)b a
Department of Anesthesiology, University of Florida College of Medicine, Gainesville, FL 32610-0254, USA Department of Obstetrics and Gynecology, University of Florida College of Medicine, Gainesville, FL 32610-0254, USA
b
Received 20 September 2004; accepted 20 September 2004
Comment by Rodney K. Edwards, MDb Keywords: Cardiac arrest; Pregnancy; HIV infection
Abstract This case involves cardiac arrest of a 29-week pregnant African American woman, occurring 2 days after surgical correction of an incarcerated ventral hernia with small bowel obstruction. The patient could not be resuscitated from the arrest. Details of the case are presented, and diagnostic and unique management considerations for this uncommon occurrence are set forth.
1. Introduction Cardiac arrest is an infrequent occurrence in pregnancy [1]. The causes generally fall into 1 of 2 categories [2]. The first category includes those conditions that affect only pregnant individuals. The other is a list of non– pregnancy- associated potentially deadly processes that can often be recognized and treated but are made more complex and difficult to manage by their appearance in the parturient. In the former group lie the familiar
B
Case conference presentations are selected and edited at the Department of Anesthesiology, University of Florida College of Medicine. T Corresponding author. ATTN: Editorial Office, Department of Anesthesiology, University of Florida College of Medicine, Box 100254, Gainesville, FL 32610-0254, USA. Tel.: +1 352 265 8012; fax: +1 352 265 8013. E-mail address: [email protected] (C.W. Peters). 0952-8180/$ – see front matter doi:10.1016/j.jclinane.2004.09.003
conditions associated with pregnancy, namely eclampsia and preeclampsia, HELLP syndrome, puerperal hemorrhage, peripartum cardiomyopathy, amniotic fluid embolism, and anesthetic catastrophe associated with labor and delivery. In the latter category are the traditional killers of nonpregnant individuals such as pulmonary thromboembolic events; heart disease, both congenital and acquired; rapidly progressive infection leading to sepsis; and endocrine and inflammatory disorders. We present a 29-week pregnant patient who died of an unknown event. She was a model for risk factors for several conditions mentioned in the next sections, but the specific cause of her death is unknown because no postmortem examination was allowed. The clinical picture was further clouded by the complication of HIV infection, although the patient’s blood cell counts at the time of her death were unknown. The case is presented in detail, including pertinent differential diagnostic considerations.
230
2. Case report The patient was a 34-year-old African American woman who was positive for hepatitis C and HIV since 1998, and 29 weeks pregnant by ultrasound and by dates. She had undergone gastric bypass surgery in 1990, but she was morbidly obese at the time of this event. Two inguinal hernia repairs had been done since the gastric bypass surgery. The patient presented to labor and delivery triage with 1 day of abdominal pain. Physical examination findings were abdominal tenderness and reducible ventral hernia. An abdominal computed tomographic (CT) scan was performed, which showed findings consistent with a small bowel obstruction. The patient was evaluated by the general surgery service, which recommended conservative management. The patient was admitted to the hospital and followed closely. Twenty-four hours after the initial evaluation, a dilated small bowel loop was seen on plain abdominal film with an area of tenderness to the right of her gastric bypass incision. On the basis of these findings, the patient was taken to the operating room for surgical exploration and reduction of her small bowel obstruction. During the operative intervention, blood loss was 50 mL and urine output was 375 mL. She received 4000 mL of crystalloid (2 L of normal saline and 2 L of lactated Ringer’s solution) and 2 units of packed red blood cells. Vecuronium 10 mg was given for muscle relaxation during the case, and the patient’s trachea remained intubated in the recovery room for approximately 60 minutes postoperatively because of residual neuromuscular blockade. Extubation thereafter was successful, with subsequent vital signs of blood pressure of 128/57 mm Hg, heart rate (HR) 119 bpm, temperature 35.9 8C, respiratory rate (RR) of 17 breaths/min, and pulse oximetric saturation (Spo2) of 100% (inspired oxygen concentration [Fio2] not specified). She remained in the recovery room for part of the night. Early in the morning, approximately 36 hours after arrival at the hospital, the patient was transferred to the surgical intensive care unit (SICU) for persistent marginal Spo2 that had developed during her recovery room stay, namely 96% on an Fio2 of .5. Arterial blood gas (ABG) analysis on arrival at the SICU showed pH 7.43, Paco2 26 mm Hg, Pao2 59 mm Hg, and sodium bicarbonate (HCO3 )16 mM/L on oxygen 7 L by mask. One hour later, ABG showed pH 7.45, Paco2 24 mm Hg, Pao2 69 mm Hg, and HCO3 16 mM/L on 6 L O2 by mask. Serum electrolytes at that time were sodium 135 mEq/L, potassium 3.7 mEq/L, chloride 108 mEq/L, HCO3 20 mM/L, BUN 32 mg/dL, creatinine 0.5 mg/dL, glucose 133 mg/dL, total calcium 8.1 mg/dL, magnesium 1.4 mEq/L, and phosphate 3.2 mM/L. Hemoglobin was 10.1 gm/dL, hematocrit 32%, platelets 417 000 cells/lL, and white blood cell count 11 000 cells/lL. During morning rounds, the patient was found to have very small tidal volumes. A chest radiograph showed pulmonary edema, with the comment by the managing physician of bimpending respiratory failure.Q Dobutamine
C.W. Peters et al. was administered for inotropic support, and the patient was given aggressive pulmonary toilet with emphasis on full sitting position to assist in respiration. Diuretic medication was administered with a target of 1 to 1.5 L of urine production. An echocardiogram was ordered, but no record exists in the hospital computer records as to whether it was done. All electrolyte abnormalities were corrected during the day. By that evening, about 48 hours after arrival, the patient’s RR was 35 to 40 breaths/min and Spo2 was 93% on supplementary oxygen. At that point, the patient was started on full-face bilevel positive airway pressure, with an inspiratory pressure of 15 cm H2O, an expiratory pressure of 10 cm H2O, and Fio2 of 0.7. This treatment improved the patient’s Spo2 to between 95% and 97%. Lower extremity Doppler ultrasound studies performed to evaluate for a deep venous thrombosis (DVT) and were negative; the decision was then made not to obtain CT studies of the pelvis or chest. By the next morning, 60 hours after arrival in the hospital, the patient had diuresed 3 L of fluid. The chest radiograph, which was difficult to interpret because of the patient’s morbid obesity, showed a picture compatible with improving pulmonary edema. However, it did show possible air bronchograms, and on the basis of this finding, the original antibiotic treatment was changed to include coverage for aspiration pneumonia. Bilevel positive airway pressure respiratory support was increased to 23/20 cm H2O, the patient was continued in the full upright sitting position, and discussion was conducted about the indications for endotracheal intubation in this patient. By the next morning, about 84 hours after arrival in the hospital, the patient was noted to be extremely tachypneic, with RR as high as 47 breaths/min. Clinically, she was in extremis from a respiratory standpoint despite Spo2 of 100%. Her HR ranged from 120 to 145 bpm despite treatment with metoprolol. At that point, the decision was made to intubate the patient’s trachea. As she was being helped into the supine position for intubation, which was performed easily, she was noted to become bradycardic. The rhythm deteriorated into ventricular fibrillation within 3 minutes despite high-flow oxygen delivered by the bagvalve mask and the administration of atropine; advanced cardiac life support (ACLS) measures were begun. Simultaneously, the obstetric physicians were called to the bedside for an emergency cesarean section. The time interval between this call being placed and delivery of the fetus was 16 minutes. The ACLS measures that were used during this time were defibrillation (14 times with 360 joules), bilateral chest tube placement and pericardiocentesis for pulseless electrical activity, administration of epinephrine 29 mg in divided doses, vasopressin boluses of 40, 40, and 80 units, 2 g of calcium chloride, 150 meq of HCO3 in divided doses, and an epinephrine infusion. Transcutaneous cardiac pacing was attempted but was unsuccessful. The patient’s rhythm alternated between pulseless electrical activity and ventricular fibrillation, in spite of these measures and continuous cardiopulmonary resuscitation
Cardiac arrest during pregnancy (CPR). The rhythm eventually degenerated into asystole refractory to any measure, and the patient was declared dead. Unfortunately, the newly delivered infant had no signs of life, and could not be revived despite the heroic efforts of the neonatal critical care physicians. The family declined autopsy on both individuals.
3. Discussion Cardiac arrest is reported to occur in about 1 in every 30 000 pregnancies that are near term [1]. This fact seems surprising, in that pregnant women are usually in the prime of health, unfettered by the acute or chronic conditions that are the harbinger of what is usually a fatal occurrence in older populations (ie, those that are most often afflicted). The rate of occurrence is consistent, however, and is predictably due to events that fall into 2 general categories of pathology. These categories are (1) those conditions that impact the cardiovascular stability of the population in general but affect the pregnant patient more dramatically, and (2) those entities that are specifically related to pregnancy. Deep venous thrombosis and pulmonary embolism (PE) often intrude into what seems to be a stable uneventful pregnancy [3]. Pulmonary embolism is seen in 24% of parturients who develop DVT for which they are not appropriately treated, whereas only 4.5% of those treated develop a PE. In patients not treated, approximately 15% die, whereas less than 1% of treated patients die. The likelihood of occurrence of DVT and PE is increased in pregnant women by the presence of the 3 major risk factors: endothelial vascular injury, hypercoagulable state, and venous stasis [4]. The timely discovery and treatment of DVT and PE is frustratingly difficult. The signs and symptoms of PE are notoriously nonspecific, being seen in a host of cardiopulmonary conditions. Furthermore, reliance on the presence of certain findings as a signal that a DVT workup is warranted will leave one disappointed — DVT often remains clinically silent within the limb [5]. Laboratory or diagnostic studies to confirm or exclude DVT or PE may either clarify or confuse the physician. Suspicion of PE may be investigated in a number of ways. Ventilation-perfusion scintigraphy is considered the first-line tool by many clinicians. High probability scan gives positive predictive value of 97%. Up to 70% of scans warrant further investigation [6]. Continued suspicion of PE or pelvic DVT, despite a negative ventilationto-perfusion study, warrants further radiological studies such as CT pulmonary angiography, conventional pulmonary angiography, or magnetic resonance imaging for complete evaluation [7,8]. The implications of radiography for the pregnant patients are obvious, and must be scrutinized and evaluated meticulously before radiographic studies are used in the parturient. Primary heart disease can lead to cardiac arrest in gravid patients. Many women with congenital heart disease are now surviving into child-bearing years and becoming pregnant;
231 decompensation and arrest can thus occur during pregnancy. Coronary artery disease leading to myocardial infarction complicates 0.01% of pregnancies [9]. Myocardial infarction occurs more often in the obese, diabetic, hypertensive, or hyperlipidemic gravid patient. Furthermore, the pregnant woman is more likely to be older and a smoker now than in the past. When these facts are added to the aforementioned risk factors, management of heart disease in the pregnant patient becomes a genuine challenge. The combination of subtlety of ischemia-related symptoms, intolerance to fluid overload in those with borderline cardiovascular reserve, and difficulty in resuscitation of the pregnant woman make for a dismal outlook for the gravid patient with coronary artery disease who suffers a cardiac arrest. When it happens, infarction occurs most often in the third trimester, and mortality rates vary from 21% to 45% [10]. As to other forms of cardiac disease, valvular cardiac pathology is variably tolerated. Regurgitant lesions may be better handled by the parturient who is already vasodilated, and therefore, afterload reduced by virtue of her pregnant condition [11]. Pulmonary hypertension, primary and secondary, is particularly difficult to manage successfully, with death rates varying between 30% and 52%. Causes of secondary pulmonary hypertension include recurrent pulmonary thromboembolism, HIV, inflammatory conditions such as vasculitis and connective tissue disorders, and congenital heart disease. Management may include inhaled or intravenous vasodilators and employment of pulmonary artery catheterization in the peripartum period for early identification of increasing pulmonary artery pressure. Infections can complicate pregnancy and warrant aggressive intensive therapy to forestall the onset of septic shock, which occurs in 1 per 5000 pregnancies. Ninety-five percent of the bacterial causes of septic shock in pregnancy are gram-negative organisms [12]. The most common infectious entities that lead to septic shock are chorioamnionitis, pyelonephritis, endometritis, and toxic shock syndrome. Mortality for septic shock associated with pregnancy ranges from 33% to 66%. Hormonal disorders complicate pregnancy, occasionally with lethal results. Thyroid storm, pituitary apoplexy from enlarging prolactinoma leading to Sheehan’s syndrome (hypopituitarism from infarct of the pituitary gland from postpartum shock or hemorrhage), hypercalcemia from hyperparathyroidism, and cardiovascular decompensation from pheochromocytoma can cause maternal cardiac arrest and death. Diabetic ketoacidosis in pregnancy carries an estimated mortality rate of about 1%. At greatest risk is the undiagnosed woman with first manifestation of diabetes as diabetic ketoacidosis in pregnancy [13]. An uncommon event is the occurrence of pregnancy in a woman with one of the rheumatologic-autoimmune diseases. The paucity of experience hinders in-depth analysis of the impact of these diseases on the pregnancy, but a few observations are warranted. Systemic lupus erythematosus (SLE) occurs at a rate of 15 to 50 per 100 000 people in the
232 United States, and more than 90% of these affected individuals are women. Morbidity in the parturient is increased, related for the most part to the 15% to 25% incidence of preeclampsia in those with SLE. Further confounding the analytical picture is the difficulty in differentiating SLE-related preeclampsia from the signs and symptoms of lupus nephritis or lupus cerebritis. The appearance of these conditions can be quite similar, with severe hypertension and proteinuria, or mental status changes and seizures, but the treatment regimens are quite different, with the treatment of one condition being quite destructive to a patient with the other of these conditions. The complexity of the interactions of SLE and other collagen-vascular diseases such as polyarteritis nodosa and rheumatoid arthritis and their effect on pregnancy warrant specialty consultation [14]. From the standpoint of obstetric conditions that can lead to cardiac arrest, there is a host of repeat killers. Preeclampsia and eclampsia frequently evolve into lethal events such as intracerebral hemorrhage, cardiovascular instability, multiorgan system failure, and uncontrolled bleeding in other body sites from coagulopathy. The former condition is characterized by severe hypertension, abdominal pain, oliguria, deteriorating renal function, headache and visual changes, liver function test abnormalities, and pulmonary edema. The addition of seizures to this milieu of symptoms defines the onset of eclampsia, although up to 38% of eclamptic patients can experience seizures without any preeclamptic symptoms [15]. Two percent of those experiencing eclamptic seizures die as a result of the complications of these events. At highest risk are those with preexisting hypertension, multiple gestations, first pregnancy, those with a family history of preeclampsia, renal disease, and diabetes. A common companion to eclampsia is the HELLP syndrome, consisting of hemolysis, elevated liver enzymes, and low platelets. The rate of occurrence is less than 1% of pregnancies, occurs in late pregnancy (27-36 weeks’ gestation), and carries a mortality rate of 1% to 3% [16]. Up to one third of the fetuses delivered to women with this condition may die. Most frequent laboratory manifestations in this condition are a low platelet count (below 100 000 cells/lL) and serum transaminases that are slightly elevated. Hemorrhage, both prepartum (abruption and placenta previa) and associated with delivery itself (natural and surgical) and its immediate aftermath, can be massive and may lead to death from exsanguination [2]. The hemorrhage may be obvious or subtle. Massive hemorrhage occurs in pregnancy for a number of reasons. It can be surprisingly difficult to diagnose in timely fashion. Large vessels supplying and draining the uterus provide a conduit for major blood loss when pathological processes such as abruption, uterine rupture or atony, or placenta previa complicate the pregnancy or delivery. Uterine atony is the most common cause and is treated primarily with medications that constrict the uterine tissue and vessels. Late identification of massive hemorrhage can lead to cardiac arrest, which is particularly difficult to correct because of the blate startQ on
C.W. Peters et al. resuscitation that causes the event in the first place. Treatment involves simultaneous pathways of employment of ACLS algorithms and repletion of intravascular blood volume. The astute clinician must remain alert to the signs and symptoms that are manifestations of bleeding and must provide hemodynamic support to the hemorrhaging patient. Peripartum cardiomyopathy affects about 1000 pregnant women each year in the United States. The condition is characterized by the onset of heart failure symptoms within 1 month before delivery to about 5 months after delivery. Peripartum cardiomyopathy is a diagnosis of exclusion, and all other etiologies of congestive heart failure must be ruled out before its being invoked as the cause. This condition is felt to be a form of infectious myocarditis, possibly viral in origin, or perhaps autoimmune or idiopathic in etiology. The clinical picture manifests typical features of heart failure: chest pain, orthopnea and paroxysmal nocturnal dyspnea, overt fluid overload with pedal edema, and shortness of breath with exertion. Sinus tachycardia and nonspecific ST-wave and T-wave changes are often seen. In about 50% of patients, the cardiomyopathy resolves after delivery; of those cases that do not resolve, most patients die [17]. Amniotic fluid embolism occurs infrequently in pregnancy but generates high rates of morbidity and mortality. The phenomenon was first described in 1926 by Meyer, as noted by R.G. Mason [18] and is characterized by respiratory distress, cardiovascular collapse, altered mental status, and alteration of coagulation parameters [19]. The presentation may masquerade as any of the other more common life-threatening conditions that may happen abruptly in the peripartum period. These conditions include eclampsia with status-epilepticus, acute thromboembolism, and anaphylaxis. Seventy percent of the cases of amniotic fluid embolism occur during labor and delivery, the majority within 5 minutes of delivery. A small percentage of cases occurs before delivery, and 19% of cases occur during cesarean section. A very broad estimate of overall occurrence is 3 per 100 000 pregnancies [20], and the fatality rate varies from 22% to 88%. Anesthetic complications such as an unmanageable airway and drug-induced hemodynamic instability are wellrecognized companions to obstetric anesthesia [21]. Vasodilator side effects of both regional and general anesthetic drugs can precipitate cardiac arrest in the parturient who already is in a barely compensated state of hypovolemia or who is dehydrated from preeclampsia. Deaths from the consequences of the difficult obstetric airway have decreased in frequency mainly because of greater clinician awareness and the invention of useful airway management adjuncts. This frequency, however, has not dropped to zero. If cardiac arrest does occur, a number of issues arise. All ACLS measures must begin immediately, as in any episode of cardiac arrest. The pregnant state, however, complicates matters. Airway management is complicated by the gastric hypokinesis of pregnancy; cricoid pressure should be
Cardiac arrest during pregnancy maintained until the airway is secured to prevent the higher risk of aspiration of gastric contents. Efficient ventilation and oxygenation are more difficult to accomplish because of the increased oxygen requirements and decreased chest wall compliance of pregnancy [1]. Venous return to the heart from the lower extremities will occur only when compression of the inferior vena cava is released by rolling the patient toward her left side with support from a wedge, an overturned chair, or the knees of an assistant kneeling on the floor on the patient’s right side. Cardiopulmonary resuscitation and mask ventilation can be efficiently accomplished when the patient is turned no more than 308 to the left. Cardiopulmonary resuscitation and ACLS measures are seldom needed on the labor and delivery ward, so frequent rehearsals of mock scenarios involving cardiac arrest will shorten the response times and heighten the awareness of correct ACLS procedures when these procedures are warranted. In addition, the literature is replete with guidance for successful perimortem and postmortem cesarean section for emergency delivery of an infant from a dying mother, both to save the infant or the mother [22 - 24]. In the case of maternal cardiac arrest and possible perimortem cesarean section (from the ancient Roman legal code known as Lex Caesare [25]), time obviously is the most crucial issue. For arrests that occur in the labor and delivery suite, the obstetrician is immediately at hand to perform the operation. At more distant sites, recognition of the potential need for surgical intervention for delivery of the fetus must be immediate so as to summon the appropriate individual for surgical assistance. In Great Britain, between 1972 and 1996, 56 postmortem cesarean sections yielded 6 neurologically normal children. A 10-year survey of perimortem cesarean sections yielded 25 healthy survivors from 40 deliveries. In the most comprehensive review of the literature on the subject, 93% of the surviving infants were born within 15 minutes of the maternal death, and only 2 had neurological defects; 70% of the survivors were delivered within 5 minutes [25]. One final consideration that fits into neither large category mentioned above, but that sits in the background of any analysis of this patient’s management and outcome, is the influence of her HIV infection on her cardiovascular condition. There is an evolving body of literature defining the influence of HIV infection on cardiovascular status. Eight to 10% of the new HIV patients develop symptomatic heart failure over a 2- to 5-year period. However, there is little information addressing HIV infection as a predictor of sudden cardiac decompensation and cardiac arrest, specifically in the parturient. It has been well demonstrated that HIV can profoundly affect cardiovascular integrity in a number of ways. These ways include the association of HIV infection with myocarditis, with nutritional deficiencies that affect contractility, and with side affects of medications used to treat HIV infection [26] All of these processes may lead to dilated cardiomyopathy. In addition, HIV infection is associated with pericardial effusions that may progress to tamponade, with
233 bacterial, fungal, and marantic endocarditis; with pulmonary hypertension; and with vasculitic, atheromatous, and hypertensive cardiac conditions. The mental jump from occult HIV-related cardiac pathology to the sudden pregnancyrelated cardiovascular decompensation of this unfortunate individual is easy to make, although we remain unsure of the precise cause of her death.
4. Comment by Rodney K. Edwards, MD, MS The authors provide an interesting case report and a thorough review of the potential causes of cardiac arrest during pregnancy. As stated, no postmortem examination was conducted, and this fact makes determination of the cause of this particular patient’s death impossible to ascertain. Fortunately, such an occurrence during pregnancy is quite uncommon. However, when pregnant women do suffer cardiac arrest, prompt action is needed from individuals skilled with the provision of CPR, knowledgeable about the physiologic changes associated with pregnancy, and experienced with emergent cesarean delivery. Otherwise, mortality for both mother and fetus is the likely outcome. The authors discuss the fact that the gravid uterus impairs venous return to the heart during CPR. However, left lateral tilt does not completely alleviate the problem. Tilting the patient helps to relieve this obstruction. However, it also decreases the effectiveness of chest compressions, because this lateral tilt causes the trunk to roll [27,28]. Because emptying the uterus will alleviate some of this obstruction to venous return, perimortem cesarean delivery has been advocated as a way not only to attempt to salvage a viable fetus but also to improve the effectiveness of CPR in pregnant women with cardiac arrest. In 1986, Katz et al [29] reviewed reports of successful results with perimortem cesarean delivery. They found that infant survival was most likely if delivery occurred within 5 minutes of cardiac arrest, and that infant survival without serious neurological impairment was unlikely if delivery occurred more than 15 minutes after cardiac arrest. Therefore, these authors and several texts recommend initiating delivery within 4 minutes of cardiac arrest. This recommendation — that delivery should be initiated within 4 minutes after cardiac arrest — assumes that delivery of the infant can be effected in approximately 1 minute. Because of several factors present in this patient, this interval may not have been achievable. Because of her morbid obesity and recent surgery, abdominal entry would require more time than for the usual emergent cesarean delivery. Furthermore, for obvious reasons, this patient’s hepatitis C and HIV infections would understandably result in care to avoid injury to the surgeon or any assistants. Another factor that could result in delay in initiating a perimortem cesarean delivery is the location of the patient at the time of arrest. This woman was located in the SICU at the
234 time of her cardiac arrest. It likely would require more time to summon obstetricians to this unit than to an emergent delivery in the labor and delivery unit. If a pregnant woman is critically ill, locating a pack containing the instruments necessary to perform a cesarean delivery at her bedside and notifying the obstetrics team of any deterioration in status before cardiac arrest would decrease the interval from cardiac arrest to delivery. In the case report, there is no mention of whether the fetal HR tracing was being monitored. The ABG reports indicate that maternal, and therefore fetal, oxygenation was marginal. Monitoring the fetal HR tracing can provide some insight as to the status of the fetus in a pregnant woman with respiratory distress. Oxygen delivery to the fetus is inadequate with maternal Po2 values at or below 60 mm Hg, and efforts to improve oxygenation of the mother are needed. Fetal HR tracing analysis may suggest a need for increased oxygen delivery to the pregnant woman, even if measures of her Spo2 are reassuring. Furthermore, fetal condition before maternal cardiac arrest can predict the likelihood of intact neonatal survival. As an example, unlike the case reported herein, if the etiology of cardiac arrest were massive hemorrhage, maternal circulation would be directed preferentially to the brain, heart, and adrenal glands. Therefore, the uteroplacental circulation would be diminished long before cardiac arrest, and intact neonatal survival would be unlikely, regardless of the time interval from cardiac arrest to delivery. In summary, cardiac arrest during pregnancy is an uncommon event. When it does occur during the latter part of pregnancy, perimortem cesarean delivery may improve the outcome for both the fetus/neonate and the pregnant woman. Provision of care by a multidisciplinary health care team and optimal communication between the members of this team will maximize the likelihood of survival for both patients. Beyond 24 weeks’ gestation, the standard ABCs of CPR (airway, breathing, and circulation) should also include a bDQ — for delivery [30]. Unfortunately, even under ideal circumstances, mortality is the usual outcome for both the pregnant woman who experiences cardiac arrest and her fetus.
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