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Rapid Onset of Broken Heart Syndrome and Cardiogenic Shock Following Cesarean Section
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A3503 - Rapid Onset of Broken Heart Syndrome and Cardiogenic Shock Following Cesarean Section
Author Block: L. Yadav1, G. S. Thind1, S. Edward2; 1WMU School of Medicine, Kalamazoo, MI, United States, 2Bronson Methodist Hospital, Novi, MI, United States.
Introduction Takotsubo cardiomyopathy (TCM) or broken heart syndrome is a transient cardiac syndrome that involves left ventricular (LV) apical akinesis and basal hypercontraction that may symptomatically mimic acute coronary syndrome (ACS). A significant emotional or physical stressor typically precedes the presentation. There have been reports of TCM after cesarean section but the rapidity of onset and reversal makes our case unique. Case A 33 year old African American woman was admitted to ICU after Cesarean section for concern for respiratory distress. The delivery had been uneventful. She had been diagnosed with Cryptococcal lymphadenitis in the neck in her third trimester at which time she had a normal cardiac echocardiogram. She was placed on noninvasive positive pressure ventilation overnight. In the morning, she was placed on room air and was oxygenating well. Over the next hour, she became severely tachypnic and desaturated. She was emergently. Chest xray revealed massive pulmonary edema. She was given a dose of intravenous Lasix without improvement in symptoms. Lactic acid was 2.9 and later increased to 5.3. Pro-BNP was 4251. EKG showed ST elevation in V1 - V3 and Troponin was elevated to 1.1. A beside TTE was performed which revealed EF of 25% and dilatation and hypokinesis of the left ventricle apex. After intubation, she was started on Milrinone infusion to improve cardiac output. Flotrac device showed severely decreased cardiac output with an improvement in stroke volume with a minibolus of crystalloid. She was fluid resuscitated. Impella device was considered but cardiac output and hemodynamics improved. Milrinone was stopped after 6 hours. She was extubated after 24 hours. A repeat bedside echocardiogram showed an EF of 40%. Discussion Post partum cardiomyopathy was kept in the differential diagnosis but the rapidity of onset and reversal along with typical echocardiogram appearance of the LV point toward the diagnosis of TCM. A cardiac angiogram was not performed due to absence of risk factors and rapid reversal. Early recognition and good critical care support was essential to save this patient’s life. Catecholaminergic inotrops should be avoided due to the role of endogenous catecholamines in causation of this condition. Mechanical LV support should be instituted early in case of cardiogenic shock if needed. Rate of recurrence is not well defined in this patient population.
Author Block: L. Yadav1, G. S. Thind1, S. Edward2; 1WMU School of Medicine, Kalamazoo, MI, United States, 2Bronson Methodist Hospital, Novi, MI, United States.
Introduction Takotsubo cardiomyopathy (TCM) or broken heart syndrome is a transient cardiac syndrome that involves left ventricular (LV) apical akinesis and basal hypercontraction that may symptomatically mimic acute coronary syndrome (ACS). A significant emotional or physical stressor typically precedes the presentation. There have been reports of TCM after cesarean section but the rapidity of onset and reversal makes our case unique. Case A 33 year old African American woman was admitted to ICU after Cesarean section for concern for respiratory distress. The delivery had been uneventful. She had been diagnosed with Cryptococcal lymphadenitis in the neck in her third trimester at which time she had a normal cardiac echocardiogram. She was placed on noninvasive positive pressure ventilation overnight. In the morning, she was placed on room air and was oxygenating well. Over the next hour, she became severely tachypnic and desaturated. She was emergently. Chest xray revealed massive pulmonary edema. She was given a dose of intravenous Lasix without improvement in symptoms. Lactic acid was 2.9 and later increased to 5.3. Pro-BNP was 4251. EKG showed ST elevation in V1 - V3 and Troponin was elevated to 1.1. A beside TTE was performed which revealed EF of 25% and dilatation and hypokinesis of the left ventricle apex. After intubation, she was started on Milrinone infusion to improve cardiac output. Flotrac device showed severely decreased cardiac output with an improvement in stroke volume with a minibolus of crystalloid. She was fluid resuscitated. Impella device was considered but cardiac output and hemodynamics improved. Milrinone was stopped after 6 hours. She was extubated after 24 hours. A repeat bedside echocardiogram showed an EF of 40%. Discussion Post partum cardiomyopathy was kept in the differential diagnosis but the rapidity of onset and reversal along with typical echocardiogram appearance of the LV point toward the diagnosis of TCM. A cardiac angiogram was not performed due to absence of risk factors and rapid reversal. Early recognition and good critical care support was essential to save this patient’s life. Catecholaminergic inotrops should be avoided due to the role of endogenous catecholamines in causation of this condition. Mechanical LV support should be instituted early in case of cardiogenic shock if needed. Rate of recurrence is not well defined in this patient population.
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