Vasoplegia in Heart, Lung, or Liver Transplantation: A Narrative Review.

Abstract

Vasoplegia is a pathophysiologic state of hypotension in the setting of normal or high cardiac output and low systemic vascular resistance despite euvolemia and high-dose vasoconstrictors. Vasoplegia in heart, lung, or liver transplantation is of particular interest because it is common (approximately 29%, 28%, and 11%, respectively), is associated with adverse outcomes, and because the agents used to treat vasoplegia can affect immunosuppressive and other drug metabolism. This narrative review discusses the pathophysiology, risk factors, and treatment of vasoplegia in patients undergoing heart, lung, and liver transplantation. Vasoplegia in this patient population is associated with acute kidney injury, hospital length of stay, and even survival. The mechanisms of vasoplegia in this patient population likely involve multiple pathways, including nitric oxide synthase, cyclic guanylate cyclase, cytokine release, hydrogen sulfide, adrenal axis abnormalities, and vasopressin deficiency. Contributors to vasoplegia in this population include mechanical circulatory support such as extracorporeal membrane oxygenation and cardiopulmonary bypass, organ ischemia time, preexisting infection, and medications such as angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and excessive sedation. Treatment of vasoplegia in this population begins with conventional catecholamines and vasopressin analogs. Occasionally, agents, including methylene blue, hydroxocobalamin, and angiotensin II, are administered. Though retrospective literature suggests a hemodynamic response to these agents in the transplant population, minimal evidence is available to guide management. In what follows, we discuss the treatment of vasoplegia in the heart, lung, and liver transplant populations based on patient characteristics and potential risk factors associated with non-catecholamine agents.