Case Reports  |   December 2002
Management of Unexplained Antepartum Circulatory Collapse Directed by Transesophageal Echocardiography Findings
Author Notes
  • Acting Assistant Professor.
  • Received from the Department of Anesthesiology, University of Washington, Seattle, Washington.
Article Information
Case Reports
Case Reports   |   December 2002
Management of Unexplained Antepartum Circulatory Collapse Directed by Transesophageal Echocardiography Findings
Anesthesiology 12 2002, Vol.97, 1630-1631. doi:
Anesthesiology 12 2002, Vol.97, 1630-1631. doi:
PRIMARY nontraumatic spontaneous coronary artery dissection (SCAD) is a rare cause of myocardial infarction that occurs predominantly in young women. Although myocardial infarction in pregnancy itself is rare, and the etiology of SCAD is uncertain, approximately one-third of reported SCAD in women occurs between the third trimester of pregnancy and 4 months postpartum. 1 
We report a previously healthy 19-yr-old woman being treated for premature labor who presented with acute circulatory collapse at 32 weeks gestation. After resuscitation and emergency Cesarean section, the use of transeophageal echocardiography (TEE) excluded the diagnosis of pulmonary embolism or aortic dissection as possible causes of her collapse. Instead, the finding on TEE of left ventricular akinesis in the distribution of the left main coronary artery prompted urgent angiography to delineate the etiology.
Case Report
A healthy 19-yr-old G1P0 female was admitted to the labor service at 31 weeks gestation for premature labor. She was managed with, and responded to, magnesium tocolysis and antibiotic therapy. After several days of observation without magnesium therapy, she resumed uterine contractions and intravenous magnesium was restarted. Again, she responded to treatment and the magnesium infusion was decreased incrementally. Her blood pressure was stable at 100–115/70 mmHg.
On the eighth day after admission, she complained of sudden onset of chest pressure and shortness of breath. She also complained of nausea and became diaphoretic. The first recorded blood pressure after the onset of distress was 60/49 mmHg at which time the patient was minimally responsive to commands. She rapidly became unconscious and cyanotic with poor peripheral pulses and was immediately taken to the operating room for advanced resuscitation and simultaneous emergency Caesarean section.
The airway was secured and the presence of bilateral breath sounds was confirmed with the end-tidal carbon dioxide recorded as 35 mmHg. Surgical incision followed instantly while the patient was ventilated with 100% oxygen and anesthesia was maintained with boluses of intravenous fentanyl. The systemic blood pressure was restored with administration of crystalloid, and supported with continued administration of intravenous fluids, boluses of ephedrine, and a titrated phenylephrine infusion. A Swan Ganz catheter was inserted into the right internal jugular vein. The initial pulmonary artery pressure recorded was 36/16 mmHg. The electrocardiogram showed a sinus tachycardia of 120 beats/min with a slightly widened QRS complex.
A viable infant was delivered promptly but during subsequent closure of the surgical incision, 30 min after initial collapse, the maternal condition deteriorated. The patient rapidly became cyanotic and hypotensive. The cardiac rhythm changed to a wide complex tachycardia followed by a bradycardia at a rate of 30–40 beats/min and the systolic blood pressure dropped to 60 mmHg. The central venous pressure was 20 mmHg and the pulmonary artery pressure was 32/18 mmHg.
Resuscitative measures continued with the presumed diagnosis of pulmonary embolism. Amniotic fluid embolism was ruled out because of the absence of signs of coagulopathy or hemolysis. Wound closure was achieved 67 min after incision, after which the patient was transferred urgently to the cardiac operating room for possible pulmonary embolectomy after TEE.
The TEE showed akinesis of the entire left ventricle in the distribution of the left main coronary artery and associated moderate to severe mitral regurgitation. The left atrium was dilated. The right ventricle was of normal size and the free wall was functioning normally. There was no evidence of thrombus in the main or right pulmonary arteries. The aortic valve was morphologically normal and competent. There was no dissection in the ascending aorta and color Doppler imaging of blood flow demonstrated patency of the left main coronary ostium, although distal flow was not well seen. A twelve-lead electrocardiogram was performed simultaneously and was consistent with an acute anterolateral infarct. The diagnosis of an acute coronary syndrome was made and pulmonary embolism excluded. The patient was transferred to the cardiac catheterization laboratory for angiography and possible percutaneous intervention.
Cardiac catheterization demonstrated an occluded left main coronary artery attributed to spontaneous dissection that could not be opened by percutaneous transluminal angioplasty or stent placement. She was transported emergently back to the operating room for coronary artery bypass grafting of the left anterior descending artery and the circumflex artery. Due to extensive myocardial injury and severe left ventricular failure the patient required a ventricular assist device to be weaned from cardiopulmonary bypass before being taken to the intensive care unit.
The patient recovered to her normal neurologic status after surgery. The baby progressed well and remained healthy. The patient required ongoing in-hospital support from the ventricular assist device over the next 6 months, which was finally withdrawn after she suffered an intracranial hemorrhage resulting in significant neurologic compromise.
The pattern and severity of presentation of SCAD are variable and relate to the extent of the dissection, its rate of development, and the vessel involved. 2 The left main coronary artery is affected in less than 1% of cases, with the left anterior descending artery being the most common (75%) followed by the right main coronary artery (20%). 3 The prognosis is poor because of the resultant large area of threatened or infarcted myocardium associated with pump failure, malignant arrhythmias, and sudden death. 2 
A high index of suspicion and prompt diagnosis is critical for optimizing the chances of survival and facilitating the choice of intervention in a patient with SCAD. Treatment options at the time of clinical diagnosis of SCAD are controversial and include thrombolysis, percutaneous transluminal coronary angioplasty or stent placement, and acute coronary artery bypass surgery. The choice of intervention is dependent on the patient's clinical condition and associated angiographic findings such as coexisting coronary spasm, atherosclerosis, or the presence of intracoronary thrombosis. 1,2,3 
TEE is recommended to diagnose and direct further investigation or treatment in hemodynamically unstable patients presenting with cardiogenic shock or cardiac arrest. Treatment of these patients has been demonstrated to change after TEE diagnosis. 4,5 The anatomic and hemodynamic information obtained by TEE may be sufficient to prompt a major surgical intervention without confirmatory tests in cases of massive pulmonary embolism, pericardial tamponade, papillary muscle rupture, and aortic dissection. 4,5,6 TEE can reliably establish the cause of a circulatory arrest during resuscitation with a sensitivity of 93%, specificity of 50%, and positive predictive value of 87%. 5 
The diagnosis of pulmonary embolism by direct visualization of thrombus on TEE occurs in less than 10% of patients with pulmonary emboli. 6 The indirect findings include a dilated right atrium and right ventricle and tricuspid regurgitation. 5,6 
In the presented case, the preliminary diagnosis of pulmonary embolism was ruled out by TEE. The TEE demonstrated an extensive and severe wall motion abnormality indicating an acute coronary syndrome in the distribution of the left main coronary artery. Specific findings can suggest the etiology of a coronary occlusion but delineation of the nature and extent of pathology in most cases requires angiography to direct further treatment.
Detection by TEE of extension of an aortic dissection through the ostium and into the left main coronary artery has been reported in a patient with thoracic pain and no evidence of myocardial ischemia or infarction. 7 In that patient, the dissection flap was clearly seen to enter the ostium and color Doppler imaging demonstrated the distinction between the true and false lumen of the left coronary main stem. The left ventricle showed concentric hypertrophy without impaired systolic function. The patient was treated surgically with a supracoronary aortic graft.
Dissection of the proximal left anterior descending artery was suggested by TEE and confirmed angiographically in a young male patient who presented with electrocardiogram evidence of an acute myocardial infarct following blunt chest trauma in a motorcycle accident. 8 Transthoracic echocardiography revealed poor left ventricular contractility with septal and apical akinesis. The subsequent TEE identified a short intimal flap located at the proximal left anterior descending artery, which was slightly thickened and pointed to the orifice of the left main coronary artery. The patient was treated medically.
A previously healthy 40-yr-old woman, with no cardiac risk factors, was reported to have presented 1 week postpartum following successful resuscitation after cardiac arrest. 9 Her electrocardiogram was consistent with acute anterior infarction. A TEE was performed to exclude aortic dissection. The TEE showed severe hypokinesis of the anteroseptal wall. The proximal left anterior descending artery was thickened, with a linear density in the wall, suggestive of SCAD without intimal flap. Coronary angiography confirmed a luminal irregularity and the patient was treated medically, but subsequently required stent placement.
SCAD and associated myocardial infarction is a rare but important etiology of peripartum circulatory collapse. Early diagnosis is critical for the survival of these patients. TEE has been demonstrated to suggest the diagnosis of SCAD and distinguish it from other causes of coronary artery dissection. 7,8,9 Features on two-dimensional imaging may include a visible flap or thickening of the coronary artery wall. Color Doppler imaging may show a disturbance of, or obstruction to, blood flow. SCAD can subsequently be confirmed with coronary angiography.
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