The liver is the largest solid organ in the body (the skin is overall the largest organ) and receives a large volume of blood. At rest, the liver receives around 25% of the cardiac output (approximately 1500 mL/min). Unlike other organs, the liver receives a dual blood supply.
The liver is the largest solid organ in the body (the skin is overall the largest organ) and receives a large volume of blood. At rest, the liver receives around 25% of the cardiac output (approximately 1500 mL/min). Unlike other organs, the liver receives a dual blood supply:
The right and left hepatic arteries contribute approximately a third of the liver’s blood supply (500 mL/min) and half of its O2 requirements.
The portal vein1 accounts for the majority of blood supplied to the liver (1000 mL/min). Because the blood has already passed through the abdominal organs, it has a lower oxygen saturation (SaO2):
– In the fasting state, portal blood has an SaO2 saturation of approximately 85%.
– In the fed state, portal blood has an SaO2 saturation of approximately 70%.
Because of its dual blood supply, regulation of hepatic blood flow is more complicated than that of other organs. Hepatic blood flow is regulated by intrinsic and extrinsic mechanisms:
Intrinsic mechanisms. In common with other arterial systems, hepatic arterial blood flow remains relatively constant despite changes in arterial pressure as a result of autoregulation (see Chapter 34). Below a mean arterial pressure of 60 mmHg, autoregulation fails and blood flow becomes pressure dependent.
In contrast, the portal vein has very little smooth muscle, so it cannot regulate blood flow in the same way. Instead, blood flow is proportional to the pressure gradient in the portal vein.
The two different sources of hepatic blood have a semi-reciprocal relationship, referred to as the ‘hepatic arterial buffer response’. If portal vein blood flow falls, the hepatic arteries maintain overall liver blood flow through a vasodilatation response involving adenosine as the chemical mediator. However, if hepatic arterial blood flow falls, the portal vein cannot compensate (this is why the relationship is semi-reciprocal).
Extrinsic mechanisms. The hepatic vessels are innervated by the sympathetic nervous system:
– In the hepatic artery, increased sympathetic activity causes vasoconstriction.
– More important is the effect of sympathetic nervous activity on the portal vein, portal venules and hepatic veins. Around 500 mL of blood is stored within these capacitance vessels. Sympathetic stimulation increases the tone of the vessels, resulting in around 250 mL of blood being returned to the circulation. Together with the splanchnic capacitance vessels, around 1000 mL of blood can be mobilised at times of physiological stress.
During spontaneous breathing, hepatic venous blood flow is increased during inspiration as a result of negative intrathoracic pressure. During expiration, the opposite occurs.
In contrast, positive-pressure ventilation causes a decrease in hepatic venous blood flow as a result of positive intrathoracic pressure. Likewise, positive end-expiratory pressure (PEEP) increases intrathoracic pressure, which results in a reduced hepatic venous blood flow.
Intraoperatively, liver blood flow is altered by both anaesthetic and surgical factors:
– Positive-pressure ventilation and PEEP: as discussed above.
– Drugs: volatile agents and vasopressors reduce hepatic arterial blood flow.
– Minute ventilation: hypocapnoea reduces portal vein blood flow whilst hypercapnoea increases blood flow.
– Regional anaesthesia: neuraxial blockade reduces hepatic blood flow to a similar extent as general anaesthesia.