MANAGEMENT OF CIRRHOTIC CARDIOMYOPATHY IN INTENSIVE CARE UNIT PATIENTS

Abstract

Cirrhosis has known effects on the cardiovascular system. These changes have been designated under the term cirrhotic cardiomyopathy. Half of cirrhotic patients may present this syndrome, which consists of structural, electrophysio-logical and functional alterations. Cirrhotic cardiomyopathy is defined as chronic cardiac dysfunction in patients with cirrhosis, characterized by blunted contractile responsiveness to stress and/or altered diastolic relaxation with electrophysio-logical abnormalities, in the absence of known cardiac disease. The main clinical features of CCM include attenuated systolic contractility in response to physiologic or pharmacologic strain, diastolic dysfunction, electrical conductance abnormalities and chronotropic incompetence. Particularly the diastolic dysfunction with impaired ventricular relaxation and ventricular filling is a prominent feature of CCM. The underlying mechanism of diastolic dysfunction in cirrhosis is likely due to the increased myocardial wall stiffness caused by myocardial hypertrophy, fibrosis and subendothelial edema, subsequently resulting in high filling pressures of the left ventricle and atrium. There are no strict diagnostic criteria but impaired cardiac response to stress, LV diastolic dysfunction and prolonged QT are the most prominent features. The clinical relevance of this syndrome is not well established yet, but these patients do not tolerate any conditions requiring a further increase of cardiac output. Therefore it is important for clinicians to be aware of this syndrome. Electrocardiogram, determination of natriuretic peptides, and echocardiography are the cornerstones of diagnosis. Increased cardiac output due to hyperdynamic circulation is a pathophysiological hallmark of the disease. The underlying mechanisms involved in pathogenesis of CCM are complex and involve various neurohumoral and cellular pathways, including the impaired β-receptor and calcium signaling, altered cardiomyocyte membrane physiology, elevated sympathetic nervous tone and increased activity of vasodilatory pathways predominantly through the actions of nitric oxide, carbon monoxide and endocannabinoids. The impact of cirrhotic cardiomyopathy in the overall prognosis of patients with cirrhosis is not well documented. Management consists mainly of diuretics to control volume overload since no specific therapy has proved effective yet. Cirrhotic cardiomyopathy is generally reversible after liver transplantation. The liver transplantation is the only established effective therapy for patients with end-stage liver disease and associated cardiac failure. Liver transplantation has been shown to reverse systolic and diastolic dysfunction and the prolonged QT interval after transplantation.