🩸 Liver Blood Flow – Dual Supply and Hepatic Arterial Buffer Response (HABR)


🔹 Overview of Liver Blood Supply

The liver receives approximately 25–30% of cardiac output, which is ~1500 mL/min in an adult.

🔸 Dual Blood Supply

Source

Contribution

Nature of Blood

Oxygen Contribution

Portal vein

~75% (1100 mL/min)

Deoxygenated, nutrient-rich

~50–60% of hepatic O₂

Hepatic artery

~25% (400 mL/min)

Oxygenated, systemic arterial blood

~40–50% of hepatic O₂



🔹 Anatomy of Hepatic Blood Flow

  • Portal vein drains:
    • Gastrointestinal tract (excluding lower rectum)
    • Spleen
    • Pancreas
    • Gallbladder
  • Hepatic artery arises from the celiac trunk (common hepatic → proper hepatic artery), delivers oxygenated blood.
  • Both blood supplies mix in hepatic sinusoids before draining via:
    • Central veins → hepatic veins → IVC


🔹 Functional Zonation of Hepatic Lobule (Viva High-Yield)

Zone

Location

Characteristics

Zone 1

Periportal

Closest to blood inflow (O₂-rich) → active metabolism (gluconeogenesis, urea synthesis)

Zone 2

Mid-zonal

Intermediate

Zone 3

Centrilobular

Lowest O₂ → vulnerable to hypoxia and drug toxicity (e.g., acetaminophen injury)



🔹 Regulation of Hepatic Blood Flow

1. Intrinsic Regulation (Autoregulation)

  • Maintains constant hepatic blood flow across a wide MAP range (60–140 mmHg)
  • Mediated by:
    • Myogenic response
    • Metabolic vasodilators (adenosine, NO)

2. Extrinsic Factors

  • Sympathetic stimulation → constriction of hepatic artery (mainly)
  • Humoral control: vasopressin, angiotensin II


🔹 Hepatic Arterial Buffer Response (HABR)

🔸 Definition

The Hepatic Arterial Buffer Response (HABR) is a unique compensatory mechanism by which the hepatic artery adjusts its flow inversely in response to changes in portal vein flow, thus maintaining total hepatic blood flow relatively constant.

This phenomenon is unique to the liver.


🔹 Mechanism of HABR

🔸 Role of Adenosine

  • Adenosine is continuously produced by liver cells and washed away by flowing blood (especially portal blood).
  • ↓ Portal flow → ↓ adenosine washout → ↑ adenosine concentration → hepatic artery vasodilation
  • ↑ Portal flow → ↑ adenosine washout → ↓ adenosine → hepatic artery constriction

This inverse relationship ensures total liver perfusion stays stable, even when one source fluctuates.


🔹 Characteristics of HABR

Feature

Details

Time of onset

Within minutes (fast-acting)

Mediators

Adenosine, NO (secondary)

Location of action

Pre-sinusoidal hepatic arterioles

Effectiveness

Partial compensation (not 100%)

Occurs only in dual blood supply organs

Unique to liver (not seen in kidneys, lungs, etc.)



🔹 Physiological Significance

  1. Maintains constant hepatic oxygenation
  2. Buffers sudden drops in portal flow (e.g., during meal absorption, portal vein compression)
  3. Prevents hepatic ischemia during fluctuating GI blood flow


🔹 HABR and Oxygen Supply

  • Although portal vein contributes more volume, the hepatic artery is richer in Oâ‚‚.
  • HABR is essential for preserving oxygenation when portal blood is reduced (e.g., in splanchnic vasoconstriction).


🔹 Clinical Implications

1. Liver Transplantation

  • HABR is lost in transplanted livers → makes graft more vulnerable to hypoperfusion.

2. Liver Resection / Portal Vein Clamping

  • ↓ portal flow → HABR-mediated ↑ hepatic artery flow → protects remnant liver.

3. Shock States (e.g., Sepsis)

  • HABR may be overwhelmed → hepatic ischemia, especially in zone 3.

4. Volatile Anesthetics (e.g., Halothane)

  • Suppress HABR → risk of hepatic hypoxia

5. Portal Hypertension

  • Persistent portal flow abnormalities → long-term HABR activation may not be sufficient to prevent ischemic injury.

6. Pharmacological Agents

  • Adenosine antagonists (e.g., caffeine, theophylline) can impair HABR.


🔹 Anesthetic Considerations

Concern

Explanation

Volatile anesthetics

Halothane reduces hepatic arterial flow & blunts HABR

Propofol, etomidate

Relatively better hepatic perfusion

Hepatic ischemia risk

During hypotension, portal vein ligation, or CV instability

Liver failure cases

Already impaired HABR → monitor closely during anesthesia



🔹 Key Viva Points

  • Portal vein: High flow, low pressure, nutrient-rich
  • Hepatic artery: Low flow, high pressure, oxygen-rich
  • HABR mediator: Adenosine
  • Clinical loss of HABR: Liver transplant, volatile anesthetics
  • Functional unit of liver: Hepatic acinus (Zone 1–3)
  • Most vulnerable zone: Zone 3 (centrilobular)