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Intravenous induction

  1. Thiopentone or propofol are used for induction.

Inhalational agents

  1. Isoflurane is the volatile agent of choice for maintenance (AI 01) as it has the least effect on hepatic blood flow. Isoflurane in oxygen or oxygen-air mixture is used for maintenance. Desflurane and sevoflurane can also be used.
  2. Halothane should be avoided (PGI 01, AIIMS 03, Maharashlra 03). However, it should be kept in mind that halothane is not contraindicated in pre-existing liver disease. It should be avoided so as not to confuse the diagnosis if liver tests deteriorate post-operatively.

Muscle relaxants

  1. Cisatracurium and atracurium are the muscle relaxants of choice.
  2. Succinylcholine is not metabolized by liver, However the enzyme pseudocholinesterase is synthesized in liver.
    1. Therefore, there may be prolonged duration of action of Sch in liver disease. However, it is clinically insignificant.

Effect of anaesthesia on hepatic blood flow

  1. Hepatic blood flow usually decreases during regional and general anaesthesia. Multiple factors are probably reponsible including:-
    1. Direct and indirect effect of anaesthetic agent
    2. The type of ventilation employed
    3. Type of surgery being performed
  2. All anaesthetic agents indirectly reduce hepatic blood flow in proportion to any decrease in mean arterial blood pressure or cardiact output.
  3. Decrease in cardiac output reduces hepatic bloodflow via reflex sympathetic activation which vasoconstricts both, the arterial and splanchnic circulation.

Effect of different anaesthetic procedures on hepatic flood flow

  1. If an adequate intravascular volume is maintained, spinal and epidural anaesthesia decrease hepatic blood flow
  2. primarily by lowering arterial blood pressure. Where as general anaesthesia usually decreases it though
  3. reduction in blood pressure and cardiac output and sympathetic stimulation.

Effect of volatile anaesthetic agents on hepatic blood flows

  1. All volatile anaesthetic agents reduce portal hepatic blood flow "This decrease is greatest with halothane and least with isoflurane". (AIIMS-10)
  2. Isojlurane appears to be the only volatile agent causing significant direct arterial vasodilation that can increase hepatic arterial blood jlow.
  3. However even with isoflurane total hepatic blood flow decreases because the decrease in portal blood flow usually offsets any increase in hepatic artery flow.


Normal cerebral blood flow = 50 ml/100g/min
Determinants of cerebral blood flow:
  1. PaCO2
    • CBF increases by 1ml/min for every 1mm Hg rise in PaCO2 above 40 mm Hg and vice-versa
    • Ideal PaCO2 is 30mmHg
  2. PaO2:
    • Below a PaO2 of 50mm Hg there is sudden cerebral vasodilation & CBF increases
  3. Blood pressure:
    • In a normotensive patient autoregulation of CBF occurs between a MAP of 60-150mm Hg.
    • Above this pressure, there is cerebral edema
    • Below this pressure, the CBF decreases with fall in BP, thus reducing CPP.
Preoperative events that cause sudden increase in ICP:
  1. Anxiety
  2. Painful stimulation (stabilization pin insertion, skull retraction)
  3. Induction of anesthesia (Laryngoscopy response)
  4. Inadequate muscle relaxation.
Methods to Decrease ICP:
  1. Posture (avoid head low)
  2. Controlled Hyperventilation
    [PaCO2 ~ 30 mmHg in adults
    ~ 20-25 mmHg in children]
  3. CSF drainage
  4. Hyperosmotic drugs (mannitol 0.25 – 1 gm/kg iv)
  5. Diuretics – Frusemide 1 mg/kg iv
  6. Corticosteroids – Reduce edema around tumors / injured tissue
  7. Barbiturates – Reduce CBF

Drugs that ICP

Drugs that ICP



Volatil inhalationl Agents

Opioids, intravenous agents


Venous Air Embolism:
Potential hazard most commonly in sitting position
Veins in skull may not collapse due to attachment to bone
Doppler transducer (most sensitive)
Sudden drop in Et CO2
Appearance /increase in Et N2
Increase in RA pressure & PAP
Gasp reflex
Hypotension, arrhythmias & cyanosis [Late signs]
Occlude venous air entry site
Discontinue N2O
Aspirate air via central venous line
FiO2 = 100%
Sympathomimetics, ionotropes, β2 agonists

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