Cardiohepatic Interactions in Heart Failure an Overview
In the setting of cardiogenic shock complicated by ACLI, the aim of therapy is to restore cardiac output and simultaneously reduce right-side filling pressures. Monitoring for recovery of liver function should be a priority, with appropriate modification in doses of drugs that undergo hepatic metabolism while function normalizes.
Treatment of the underlying cardiac condition remains the primary approach to restoring normal liver function in congestive hepatopathy. This typically entails aggressive measures to decrease intracardiac filling pressures. Hepatic congestion, ascites, and jaundice may all respond to diuresis, but for patients with severe HF, augmentation of cardiac output may also be required to prevent further deterioration of liver function. In truly refractory cases, patients may undergo therapeutic paracentesis to relieve ascites or ultrafiltration to remove edema/ascites that is no longer responsive to diuretic therapy. The impact of these strategies on hepatic function and HF outcomes remains undefined. Furthermore, the physiologic similarities between congestive hepatopathy and intrinsic liver disease may allow translation of proven therapies used in cirrhosis (such as aldosterone antagonism) to play a greater role in the management of patients with severe congestive hepatopathy.
Management of Cardiogenic Liver Injury
In the setting of cardiogenic shock complicated by ACLI, the aim of therapy is to restore cardiac output and simultaneously reduce right-side filling pressures. Monitoring for recovery of liver function should be a priority, with appropriate modification in doses of drugs that undergo hepatic metabolism while function normalizes.
Treatment of the underlying cardiac condition remains the primary approach to restoring normal liver function in congestive hepatopathy. This typically entails aggressive measures to decrease intracardiac filling pressures. Hepatic congestion, ascites, and jaundice may all respond to diuresis, but for patients with severe HF, augmentation of cardiac output may also be required to prevent further deterioration of liver function. In truly refractory cases, patients may undergo therapeutic paracentesis to relieve ascites or ultrafiltration to remove edema/ascites that is no longer responsive to diuretic therapy. The impact of these strategies on hepatic function and HF outcomes remains undefined. Furthermore, the physiologic similarities between congestive hepatopathy and intrinsic liver disease may allow translation of proven therapies used in cirrhosis (such as aldosterone antagonism) to play a greater role in the management of patients with severe congestive hepatopathy.
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