| Cirrhosis is a diffuse process of fibrosis and conversion of normal liver parenchyma into abnormal regenerative nodules. The clinical features associated with chronic liver disease reflect the severity of its pathogenesis. Activation of the SNS, increases levels of norepinephrine, or increased cytokines from the portal venous bacteraemia and endotoxemia in cirrhotic patients might stimulate carbon monoxide production. Carbon monoxide reduces the contractility of cardiac myocytes through cyclic GMP and decreases the influx of calcium. Heme oxygenase messenger ribonucleic acid transcription, protein expression, and total hemeoxygenase activity were increased in cirrhotic hearts compared to sham-operated control rat hearts. The sodium overload causes an increase in end-systolic volume in cirrhotic subjects in a standard, resting hemodynamic set-up. In the presence of ascites in cirrhotic patients, contractile dysfunction is prominent despite an increase in both arterial vasodilation (after-load) and venous return (pre-load). Due to the lack of proper functioning of the pump, the cardiac index is decreased, and systemic vascular resistance is elevated in cirrhosis with compensation, which is not related to the patient's hypertensive status. The capacity of the heart to increase pulse rate or LV EF with heavy work or drug intake is dampened in cirrhotic patients. Thus results in a decrease in liver parenchymal mass, decrease in liver function and alters the blood flow. Fall in the heart rate and cardiac output due to a decline in cardiac response may be because of impaired sensitivity to activate SNS and cardiovascular reflex regulation, which add to the chronotropic in adaptiveness.ddd |
