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Effect of anesthetic drugs and techniques on CBF and CMR . Dr Prashant Kumar. University College of Medical Sciences & GTB Hospital, Delhi. Rationale . Why should we know the effect of anesthetic agents on CBF & CMRO2? CBF - Continuous delivery of energy substrates is dependent on CBF. ↓
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Dr Prashant Kumar
University College of Medical Sciences & GTB Hospital, Delhi
Why should we know the effect of anesthetic agents on CBF & CMRO2?
- Continuous delivery of energy substrates is dependent on CBF.
can influence neuronal outcome (particularly during ischemia).
- CBF & CMR : important etiology of cerebral ischemia
All IV Induction Agents (except ketamine)
GABAA receptor agonist
Opening of Cl- channel
Inhibition neuronal transmission
► Deep Level: Burst suppression pattern
► Extremely deep level: Isoelectric pattern
►Reduction of CMR coupled with a decrease in CBF
►no increase in ICP (or even reduction in ICP)
► prevention of increase in CBV
►maintenance of cerebrovascular auto regulation
►maintenance of vasoreactivity to CO2
► Increase in CBF (but not when used with other sedatives or in a brain injured pts)
► Increase in ICP (but not when used with other sedatives or in a brain injured pts)
► Increase in CMR (particularly in Limbic structures)
► Cerebral protection via NMDA antagonism in animals
►(S) enantiomer → ↑ in CMR
►(R) enantiomer → ↓in CMR, particularly in temporomedial cortex & in cerebellum
Anesthetic drugs (diazepam, midazolam, propofol, isoflurane) have been shown to blunt or eliminate ↑ in ICP effect of ketamine.
►Limited use as induction agent
► Sedation in ICU (Head injury patients in whom hypothermia is being used)
► Modest decrease in CBF
► modest decrease in CMRO2
► modest decrease in ICP
► maintains autoregulation
► Preserves vasoreactivity to CO2
► Increases seizure threshold – used as antiepileptic
► Antidote (flumazenil) is available
Potentiates the cardiovascular effects of hypnotics (so, with moderate dose of opioids, reduce the dose of hypnotics)
Stable haemodynamics during induction
► Modest reduction in CBF & CMRO2
► No effect on ICP (if MAP is maintained)
► Autoregulation : maintained
► Cerebral vasoreactivity to CO2 maintained
► EEG changes depends on dose (small dose: minimal change)
► fear of sedation, pupillary changes, nausea, cough suppression
Inspite of studies showing that morphine does not ↑S/E
►No Change if MAP is maintained
►↑ 2º to autoregulatory vasodilatation after reduction in MAP
CBF unaltered or modest reduction
4-6μg/ml for induction
2-4μg/ml for maintenance
Although poor correlation between the occurrence of visible muscle fasciculation & ↑ in ICP is seen
Little reason to avoid SCh when rapid paralysis is required
►direct cerebral vasodilation
►2̊ (autoregulation) response to a reduction in MAP
↑ CBF, CMR, ICP.
↓CMR (reduced need for substrate)
associated vasoconstriction (which balances vasodilation)
Halothane > enflurane > desflurane= isoflurane > sevoflurane
So, CMR may ↑ or ↓ or no change
but data suggests a favorable profile for neuroanesthesia
Fluid from brain parenchyma
Renal excretion of fluid
↓ICP (onset 48-72 hours)
- Obtundation of vasopressor response during laryngoscopy, incision or during extubation
Why optimization of BP is must before neurosurgery?
Sudden hypertensive episode
↓(Disturbed cerebral autoregulation)
- Hypotension → ↓ CPP
compression of neck veins
↓ed cerebral venous drainage
( reduces venous return from head)
1. Hyperventilation Hypocapnia
Retraction of brain tissue ↓ CBF
Ischemia (more in pathological condition)
Case reports on immediate loss of hearing in the immediate post op are available.