Hepatic Blood Flow

Describe the distribution of blood volume and flow in the various regional circulations and explain the factors that influence them, including autoregulation. These include, but not limited to, the cerebral and spinal cord, hepatic and splanchnic, coronary, renal and utero-placental circulations

The liver serves as a blood reservoir (30ml per 100g, half of which may be mobilised in hypovolaemia), and receives 25% of cardiac output from a unique dual blood supply:

• Hepatic arterial system, which supplies about one-third of blood, but 40-50% of O₂
  Hepatic arterial blood has an SpO₂ of ~98%, as would be expected. It is a high-pressure, high-resistance, high-flow system (average velocity 18cm.s^-1), with the capacity to autoregulate.

• Portal venous system, which supplies the remaining two-thirds of blood.
  It is a low-resistance, low-pressure, low-velocity system (average flow 9cm.s^-1), with no capacity to autoregulate.
  The SpO₂ of portal venous blood varies depending on gut activity:
  • In the resting gut, SpO₂ is ~85%
  • In the active gut, SpO₂ is ~75%

Regulation of Flow

As with other organs, blood flow is autoregulated via intrinsic and extrinsic mechanisms, and may be affected by external factors.

Intrinsic Autoregulation

• Myogenic autoregulation
• Hepatic arterial buffer response
  This is also known as the "hepatic artery-portal venous semi-reciprocal interrelationship".
  • Hepatic arterial resistance is proportional to portal venous blood flow, such that a reduction in portal venous flow causes a decrease in hepatic arterial resistance and increases hepatic arterial flow
    This is probably mediated by adenosine.

Extrinsic Autoregulation

• Autonomic Nervous System
  Both the hepatic and portal vasculature have sympathetic innervation:
  • The hepatic artery has dopamine receptors, as well as β- and α-adrenoreceptors
  • The portal vein has only α-adrenoreceptors
    Activation of these receptors causes venoconstriction, reducing the compliance of the hepatic vasculature and mobilising up to 250ml of blood in times of sympathetic stress.

• Endocrine and hormonal effects
  A number of substances affect portal flow:

External Factors

Flow in the hepatic vein is dependent on venous return:

• Increased venous return (e.g. negative-intrathoracic pressure) increases hepatic flow

• Decreased venous return (e.g. positive-pressure ventilation, tamponade, haemorrhage), reduces hepatic flow, and in extreme cases flow may only occur intermittently throughout the cardiac cycle

• Exercise reduces both portal vein and hepatic arterial flow

Microvasculature

Hepatic arterioles and portal venules form the hepatic triad with a bile canaliculi. Hepatic arterioles and venules anastomose to form sinusoids, which create a specialised low-pressure (~2mmHg) capillary system which drains into the central veins of the hepatic acinus.

This arrangement:

• Optimises hepatic O₂ extraction
  Increased hepatic O₂ demand is met by increasing O₂ extraction, rather than by increasing flow (as occurs in the heart).
• Prevents shunting and retrograde flow

References

1. CICM March/May 2013
2. Leslie RA, Johnson EK, Goodwin APL. Dr Podcast Scripts for the Primary FRCA. Cambridge University Press. 2011.
3. Kam P, Power I. Principles of Physiology for the Anaesthetist. 3rd Ed. Hodder Education. 2012.
4. Kogire M, Inoue K, Sumi S, Doi R, Yun M, Kaji H, Tobe T. Effects of gastric inhibitory polypeptide and glucagon on portal venous and hepatic arterial flow in conscious dogs. Dig Dis Sci. 1992 Nov;37(11):1666-70.