1141

Abstract

Case Reports: A 49 year old male was found unresponsive in the bathroom of a gas station with hypotension, bradycardia and hypoxia. He was intubated emergently with improvement in hemodynamics and oxygenation. Initial evaluation in the emergency room identified normal lab work other than an elevated troponin. Computer tomography angiography identified no abnormalities except for marked septal thickening and alveolar consolidation consistent with pulmonary edema. Upon admission to the intensive care unit, echocardiography showed a left ventricular (LV) ejection fraction of 35% with regional wall motion abnormalities. Cardiology review indicated that the wall motion abnormalities did not follow a coronary vascular territory distribution and therefore was consistent with stress-induced cardiomyopathy. Drug screen testing was negative for cocaine, opiates, and methamphetamines. Patient was awake and alert, on minimal ventilatory support, with normal hemodynamics and work of breathing. Chest x-ray showed resolution of pulmonary edema and the patient was asking to be extubated.Prior to extubation, patient’s family informed the staff that in the last two months patient had experienced recurrent choking episodes, falling to the ground with his hands around the neck. The patient was therefore extubated in the operating room where a large pedunculated mass was identified arising from the true vocal cords with complete occlusion of the glottic opening. Tracheostomy followed by debulking of the tumor was performed. Biopsy confirmed squamous cell carcinoma. Upon repeat echocardiography four days later, all wall motion abnormalities had resolved and LV ejection fraction was 66%. Teaching Point: Our patient experienced stress-induced cardiomyopathy after developing negative pressure pulmonary edema (NPPE) from an upper airway obstruction. Once the obstruction was relieved, both the pulmonary edema and the LV dysfunction resolved. Reports of cardiac dysfunction in the setting of NPPE from strangulation, hanging, and acute airway obstruction during anesthesia have been previously reported, but there is still debate as to the etiopathogenesis of the LV dysfunction in this setting.