Circulatory Disorders and Vascular Disease Affecting the Liver

Abstract

Cirrhosis is associated with a hyperdynamic circulatory state. This is manifested by increased cardiac output with a decreased arterial blood pressure and peripheral vascular resistance. Cirrhotic patients tend to have faster heart rates and lower blood pressures than controls and in general have warm, vasodilated peripheries [1]. The cardiac output is related to the severity of the liver disease [2]. As liver function and clinical status improve, the cardiac output returns towards normal. It is now believed that peripheral arterial vasodilatation, particularly in the splanchnic circulation, is the initiating factor in these haemodynamic disturbances [3]. The mechanisms causing this arterial vasodilatation are not clearly understood. It has been suggested that hyperglucagonaemia is an important cause but this is still controversial. Peripheral arterial vasodilatation is believed to lead to a reduction in “central blood volume”, causing functional hypovolaemia [4, although in cirrhosis total plasma volume is increased. Vasoconstrictor hormones such as renin, angiotensin, catecholamines, and antidiuretic hormone are secreted in response to this functional hypovolaemia and the sympathetico-adrenal axis is activated, causing renal salt and water retention and ultimately leading to the formation of ascites [3]. There are also abnormalities in regional haemodynamics: renal (discussed in Chap. 12), hepatic and splanchnic (discussed in Chap.11) and in the pulmonary circuit.