The Liver β Structure, Dual Blood Supply & Functions
Functions of the liver (why losing it hurts everywhere)
π¬ Carbohydrate metabolism
Glycogenesis, glycogenolysis and gluconeogenesis β the liver buffers blood glucose. Loss β hypoglycaemia (also β insulin degradation).
π§ Fat metabolism
Fatty-acid oxidation (β acetoacetate), and synthesis of lipoproteins & cholesterol.
𧬠Protein metabolism
- Amino acids β glucose / lipids
- Synthesis of urea, plasma proteins (albumin) and clotting factors
π Secretory / excretory
Bile (β 400β800 mL/day); excretion of bilirubin, drugs & toxins.
π©Έ Vascular & reticulo-endothelial
Sinusoids lined by endothelial + Kupffer cells (phagocytic); a major blood reservoir; forms hepatic lymph (portal HTN β β sinusoidal pressure β β lymph β ascites).
βοΈ Endocrine / metabolic
- Metabolises IGF-1
- Converts T4 β T3
- Activates vitamin D
- Metabolises drugs & hormones
Dual blood supply
Hepatic blood flow β 25% of cardiac output
Total Hepatic Blood Flow~1500 mL/min Β· the liver is a major vascular reservoir
Hepatic artery20β30% of flowHigh Oβ content Β· supplies ~50% of Oβ Β· autoregulated
Portal vein70β80% of flowLower Oβ content but supplies ~50% of Oβ Β· NOT autoregulated Β· flow set by splanchnic bed
Delivered together to the hepatic sinusoids (perfused at low pressure)
π Hepatic Arterial Buffer Response (HABR) β the exam favourite
- The hepatic artery compensates for changes in portal flow to keep total hepatic flow (and Oβ delivery) constant. Mediated by adenosine washout:
- β Portal flow β adenosine is not washed away β accumulates around the arterioles β hepatic artery dilates (buffers the fall).
- β Portal flow β adenosine washed out β hepatic artery constricts.
- Anaesthetic relevance: the portal vein cannot autoregulate, so hepatic Oβ delivery depends heavily on the HABR β and the HABR is impaired by anaesthesia, hypotension, hypocapnia and surgical traction. Volatiles (esp. halothane) and low CO reduce hepatic flow β the diseased liver becomes ischaemic. Isoflurane best preserves hepatic flow among the older volatiles.
Regulation of hepatic blood flow (HBF)
Intrinsic: HABR (adenosine) + pressureβflow autoregulation (hepatic artery only) + transmural pressure (β β vasoconstriction).
Extrinsic: Neural β sympathetic stimulation β Ξ±-mediated portal venous & arterial vasoconstriction; Humoral β glucagon, secretin (vasodilate), catecholamines, angiotensin, vasopressin (vasoconstrict).
Extrinsic: Neural β sympathetic stimulation β Ξ±-mediated portal venous & arterial vasoconstriction; Humoral β glucagon, secretin (vasodilate), catecholamines, angiotensin, vasopressin (vasoconstrict).
π§ͺ Liver function tests β read them like an anaesthetist
- Hepatocellular injury: ALT, AST.
- Cholestasis: ALP, 5β²-nucleotidase, GGT.
- Detoxification / excretory: total & direct bilirubin, serum ammonia.
- Synthetic function: serum albumin, globulin, and the coagulation profile / PT.
- PT/INR is the single best acute marker of synthetic function β clotting-factor half-lives are short (~1β12 h) so PT rises quickly, whereas albumin (tΒ½ 18β20 days) reflects chronic synthetic capacity.
- All coagulation factors are made in the liver except von Willebrand factor and factor VIII (endothelium / megakaryocytes) β hence factor VIII can be normal or high even in advanced disease. Vitamin-K-dependent factors = II, VII, IX, X and proteins C, S, Z.