ACUTE RIGHT VENTRICULAR DYSFUNCTION FIXED IN A HEARTBEAT

Abstract

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Acute right ventricular (RV) dilation is often associated with acute pulmonary embolism (PE) or right-sided myocardial ischemia. Acute RV dilation can lead to RV failure, in which the RV doesn't maintain sufficient blood flow through the pulmonary circulation. Common causes of RV failure include pulmonary arterial hypertension (PAH), COPD, and massive PE. In the ICU, pulmonary vascular disease complicated by insufficient myocardial contractility as well as derangements in excessive preload or afterload can result in changes in cardiopulmonary physiology. Determining the cause of RV decompensation and reversing it is integral in the initial management of RV failure. CASE PRESENTATION: 82-year-old female with no known medical history was admitted to medical service for sepsis secondary to cholecystitis requiring percutaneous cholecystectomy tube placement. She received IV fluids and appropriate antibiotics. On day two of hospitalization, a rapid response was called due to hypoxemia and increased work of breathing. Vital signs were afebrile, BP 88/56, HR 110, RR 26. She was placed on BIPAP and transferred to the ICU. Physical examination findings were significant for decreased breath sounds and 2+ edema in both lower extremities. Laboratory values were significant for elevated troponin 0.242 and BNP 1,000. No evidence of ischemia on EKG. CT angiography (CTA) showed bilateral pleural effusions but did not show evidence of PE. Bedside transthoracic echocardiogram (TTE) showed septal bounce and mild left atrial dilation and hypokinesis. Repeat TTE two days later showed a newly developed severely dilated RV with a severe reduction in systolic function, severely dilated right atrium and dyssynergic ventricular septal motion. Right heart cardiac catheterization confirmed elevated pulmonary artery pressures to 60-65 mmHg. Fluids were stopped, Lasix was given and sepsis was treated. TTE two days later showed marked improvement and near normalization of the RV systolic function. DISCUSSION: The patient's first TTE showed septal bounce consistent with pre-existing RV pressure overload. Acute severe RV dilation combined with hypotension likely represented an acute pulmonary hypertension crisis. The lack of a large PE on CTA ruled out thromboembolic disease for the cause of the acute dilation. RV infarct was unlikely as this would not cause elevated pulmonary artery pressures and elevated pulmonary vascular resistance. RV systolic function was restored once her sepsis was treated and fluids were stopped. It is likely that she had pre-existing primary pathology, such as chronic PAH, which was tipped over by her sepsis. CONCLUSIONS: Our patient manifested with acute RV failure in the setting of her septic physiology. Most cases of RV failure have gradual recovery; however, our case demonstrates an instance of varying RV function with significant rapid improvement in cardiac function. REFERENCE #1: Ventetuolo CE, Klinger JR. Management of acute right ventricular failure in the intensive care unit. Ann Am Thorac Soc. 2014;11(5):811-822. doi:10.1513/AnnalsATS.201312-446FR REFERENCE #2: Acute decompensated pulmonary hypertensionLaurent Savale, Jason Weatherald, Xavier Jaïs, Constance Vuillard, Athénaïs Boucly, Mitja Jevnikar, David Montani, Olaf Mercier, Gerald Simonneau, Elie Fadel, Olivier Sitbon, Marc HumbertEuropean Respiratory Review Dec 2017, 26 (146) 170092; DOI: 10.1183/16000617.0092-2017 REFERENCE #3: Matthews JC, McLaughlin V. Acute right ventricular failure in the setting of acute pulmonary embolism or chronic pulmonary hypertension: a detailed review of the pathophysiology, diagnosis, and management. Curr Cardiol Rev. 2008;4(1):49-59. doi:10.2174/157340308783565384 DISCLOSURES: No relevant relationships by Joseph Bahgat, source=Web Response No relevant relationships by Frantz Hastrup, source=Web Response