Cardiac considerations in liver transplantation

Abstract

A ttention to the heart before, during, and after liver transplantation can pay off in terms of better outcomes. This, even though today's liver transplant patients are older than those in the past and more likely to have fatty liver disease as the cause of their liver failure, and even though liver failure, the transplant procedure, and the posttransplant regimen can all predispose to heart disease.The changing demographics of patients receiving liver transplants and the unique cardiac pathophysiology of patients with advanced liver disease pose signifi cant challenges in managing these patients perioperatively, as we will discuss in the following sections.

Hemodynamic monitoring in liver transplantation ‘the hemodynamic system’

“…Hemodynamic instability (HDI) is universal in almost every liver transplantation [1 ▪▪ ,30,50,59,63,74]. Prolonged hypotension is associated with impaired perfusion of vital organs and vital organ injury [11,18,25,32,85].…”

“…Prolonged hypotension is associated with impaired perfusion of vital organs and vital organ injury [11,18,25,32,85]. HDI in liver transplantation is multifactorial and can be caused by massive fluid shifts, clamping, and unclamping of the inferior vena cava, surgical bleeding, coagulopathy, myocardial dysfunction, dynamic left ventricular outflow tract obstruction (LVOTO), severe vasodilation, and postreperfusion syndrome (PRS) [1 63,66,67,74]. The prevalence of cirrhotic cardiomyopathy (CCM) ranges from 17.5 to 78.6% according to which diagnostic criteria are used [14].…”

“…The prevalence of cirrhotic cardiomyopathy (CCM) ranges from 17.5 to 78.6% according to which diagnostic criteria are used [14]. Blunted chronotropic and inotropic response to stress with sudden circulatory decompensation on exposure to stress are characteristic of CCM and contribute to perioperative morbidity and mortality [14,58,59,74]. Intraoperative stresses in the form of sudden hypovolemia, hypervolemia, use of vasopressors and inotropes can trigger decompensation of the cirrhotic heart during liver transplantation [14,58,59,74].…”

“…Blunted chronotropic and inotropic response to stress with sudden circulatory decompensation on exposure to stress are characteristic of CCM and contribute to perioperative morbidity and mortality [14,58,59,74]. Intraoperative stresses in the form of sudden hypovolemia, hypervolemia, use of vasopressors and inotropes can trigger decompensation of the cirrhotic heart during liver transplantation [14,58,59,74]. The incidence of intracardiac thrombi (ICT) and pulmonary embolism is 1-6% with an intraoperative mortality of 30-55% [63,74].…”

“…Intraoperative stresses in the form of sudden hypovolemia, hypervolemia, use of vasopressors and inotropes can trigger decompensation of the cirrhotic heart during liver transplantation [14,58,59,74]. The incidence of intracardiac thrombi (ICT) and pulmonary embolism is 1-6% with an intraoperative mortality of 30-55% [63,74]. Intraoperative cardiac arrest occurs in 3-5% of liver transplantation with a mortality of about 31.6%.…”