271. Guidelines: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure Question #12 with Dr. Shashank Sinha

Published: March 8, 2023, 10:50 p.m.

The following question refers to Section 9.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.\xa0\nThe question is asked by Western Michigan University medical student & CardioNerds Intern Shivani Reddy, answered first by Brigham & Women\u2019s medicine resident and Director of CardioNerds Internship\xa0Dr. Gurleen Kaur, and then by expert faculty Dr. Shashank Sinha.\nDr. Sinha is an Assistant Professor of Medical Education at the University of Virginia School of Medicine and an advanced heart failure, MCS, and transplant cardiologist at Inova Fairfax Medical Campus. He currently serves as both the Director of the Cardiac Intensive Care Unit and Cardiovascular Critical Care Research Program at Inova Fairfax. He is also a Steering Committee member for the multicenter Cardiogenic Shock Working Group and Critical Care Cardiology Trials Network and an Associate Editor for the Journal of Cardiac Failure, the official Journal of the Heart Failure Society of America.\nThe\xa0Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure\xa0series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders\xa0Dr. Amit Goyal\xa0and\xa0Dr. Dan Ambinder, with mentorship from\xa0Dr. Anu Lala,\xa0Dr. Robert Mentz, and\xa0Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance.\nEnjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.\t\t\n\t\t\t\t\t\t\t\t\t\t\t\tQuestion #12\n\t\t\t\t\t\n\n\n\nMr. Shock is a 65-year-old man with a history of hypertension and non-ischemic cardiomyopathy (LVEF 25%) who is admitted with acute decompensated heart failure. He is currently being diuresed with a bumetanide drip, but is only making 20 cc/hour of urine. On exam, blood pressure is 85/68 mmHg and heart rate is 110 bpm. His JVP is at 12 cm and extremities are cool with thready pulses. Bloodwork is notable for a lactate of 3.5 mmol/L and creatinine of 2.5 mg/dL (baseline Cr 1.2 mg/dL). What is the most appropriate next step?\n\n\n\n\nA\n\n\nAugment diuresis with metolazone\n\n\n\n\nB\n\n\nStart sodium nitroprusside\n\n\n\n\nC\n\n\nStart dobutamine\n\n\n\n\nD\n\n\nStart oral metoprolol\n\n\n\n\nE\n\n\nNone of the above\n\n\n\n\n\t\t\t\t\t\t\t\t\t\t\t\tAnswer #12\n\t\t\t\t\t\n\n\n\nExplanation\n\n\nThe correct answer is C \u2013 start dobutamine.\n\xa0\nIn this scenario, the patient is in cardiogenic shock given hypotension and evidence of end-organ hypoperfusion on exam and labs. The patient\u2019s cool extremities, low urine output, elevated lactate, and elevated creatinine all point towards hypoperfusion.\n\xa0\nIn patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and preserve end-organ function (Class 1, LOE B-NR). Further, in patients with cardiogenic shock whose end-organ function cannot be maintained by pharmacologic means, temporary MCS is reasonable to support cardiac function (Class 2a, LOE B-NR).\n\xa0\nThe SCAI Cardiogenic Shock Criteria can be used to divide patients into stages. Stage A is a patient at risk for cardiogenic shock but currently not with any signs or symptoms, for example, a patient presenting with a myocardial infarction without present evidence of shock. Stage B is \u201cpre-shock\u201d \u2013 this may be a patient who has volume overload, tachycardia, and hypotension but does not have hypoperfusion based on exam and lab evaluation. Stage C is classic cardiogenic shock \u2013 the cold and wet profile. Bedside findings for Stage C shock include cool extremities, weak pulses, altered mental status, decreased urine output, and/or respiratory distress. Lab findings include impaired renal function, increased lactate, increased hepatic enzymes, and/or acidosis. Stage D is deteriorating with worsening hypotension and hypoperfusion with escalating use of pressors or mechanical circulatory support.