severe fulminant biventricular failure resulting in cardiogenic shock, dramatically responded to medical therapy with full recovery of systolic function.
Presenter
Mohanad Shehadeh, M.D., Hamad Medical Corporation, Doha, Qatar
Mohanad Shehadeh, M.D., Hamad Medical Corporation, Doha, Qatar, Mohamed Salah Abdelghani, M.D., Hamad Medical Corporation, doha, doha, Qatar, Abdulrahman Arabi, M.D., HMC Heart Hospital, Doha, Qatar and Shabib Abdullah Al Aasmi, M.D., National Heart Center ,Oman, Muscat, Oman
Keywords: Cardiogenic Shock
Title : Severe fulminant biventricular failure resulting in cardiogenic shock, dramatically responded to medical therapy with full recovery of systolic function. Introduction : Cardiogenic shock in setting of acute biventricular failure is usually associated with high morbidity and risk of cardiac death. Full recovery of reversible causes of severe biventricular failure takes weeks to months. Here, we present a case of cardiogenic shock secondary to severe fulminant biventricular failure which recovered completely on medical therapy within one week. Clinical Case A 19-year-old female patient with no past medical history of chronic disease. She was brought to the Emergency Department complaining of epigastric pain and vomiting, systemic review was remarkable for recent stress due to entry exams. EKG showed sinus tachycardia with RBBB pattern and ST depression in leads I and AvL, Troponin levels were elevated. Chest XR was unremarkable and US abdomen showed evidence of hepatomegaly, TTE showed severe reduction in biventricular systolic function with EF of 25%. The Patient was admitted to CICU as case of cardiogenic shock SCAI stage C, evidenced by hypotension, tachycardia, and lactic acidosis. The patient was started on Dobutamine and furosemide infusion. Respiratory viral panel, Thyroid function test and autoimmune work up all came negative She underwent right heart catheterization which showed severe biventricular failure (with more affection of the RV, which explained her presentation with recurrent vomiting and hepatomegaly), she had severely reduced RV function with PAPI of 0.3, RA/LA 0.75. PAPI improved after NTG to 0.66. Cardiac output was 4.43 l/min (by fick) which increased to 6.07 l/min with NTG, these findings were suggestive of potential improvement to preload reduction. PVR was within normal. CAG ruled out CAD. The patient was kept on Dobutamine and furosemide infusion, Isosorbide dinitrate infusion was added. Her condition improved dramatically over 72 hours, her Cardiac Output improved and came back to normal values, Heart rate came down to normal limits and lactic acidosis resolved. Dobutamine was discontinued and she was started on guideline-directed medical therapy for management of HFrEF. The Patient was transferred to the ward. On day 6 of admission, the patient underwent cardiac MRI which surprisingly came completely normal. The LV EF was 57%, RV EF 49%, No myocardial infarction or myocardial fibrosis and no MRI findings of myocarditis. Discussion Acute severe biventricular failure usually results in cardiogenic shock which necessitates intensive care management with close clinical and hemodynamic monitoring. We would like to report a rare case of severe biventricular failure with unclear etiology, which responded to guideline-directed medical therapy with dramatic complete recovery and restoration of the biventricular function by day 6 of presentation. Though final diagnosis is unclear. Yet, the involvement of both ventricles, rapid recovery and restoration of the biventricular function and the absence of myocardial edema or fibrosis in cardiac MRI point toward a typical form of stress cardiomyopathy.