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B,
Associate
Professor,
Dept of
Anaesthesia,
DrPSIMS & RF,
CHINOUTAPALLI.
Definition
The perfusion of brain insufficient to provide supply
gm / min)
gm / min)
Types
( 1 ) Global Cerebral ischemia
Complete No CBF
Seen in cardiac arrest
Most vulnerable regions of brain
-hippocampus , Cerebral cortex
- Incomplete - CBF
Seen in hypotension, shock
( 2 ) Focal Cerebral ischemia
occlusion of a single cerebral artery
ATP depletion
lactate
ischemic damage
free radical formation
immediate
NMDA
Cellular edema
Cell membrane lysis
Cell death
delayed( 24 72 hrs )
NMDA
Ca+2 influx
phospholipases
proteases
Cell death
Ca+2
phospholipases A,A2,C
mitochondrial Ca+2
proteases
(calpains)
Hydrolysis of membrane
mitochondrial dysfunction
Phospholipids
& damage
essential
protein
FFA release
breakdown
PG , LT cerebral edema
TxA2 platelet aggregation
ischemia
Free radicals lipid peroxidation
Mitochondrial & cell
membrane damage
damage
NECROSIS
APOPTOSIS
- Milder ischemia
- cell disintegration
- cant be reversed
reversed
arrest
minute
CEREBRAL PROTECTION
reperfusion Injury
Normalisation of ICP
RECOMBINANT TISSUE
PLASMINOGEN ACTIVATOR
The only recognised treatment to improve
neurologic deficit
The neurological signs shouldnt be minor &
(fracture) on examination
if anti coagulation is
taken, INR 1.7 for 3 hours window
deficits
irrespective of INR
Baseline NIH (National Institute of Health )
mg ) over 60 minutes
10% of the dose as bolus over 1 minute
every 15
severe headache
acute
hypertension
nausea / vomiting
and obtain an emergency
CT scan
Delay insertion of nasogastric tubes / indwelling
HYPOTHERMIA
Mild - 32C - 35C
Moderate - 26C - 32C
Deep - 18C 25C
Mechanism of neuroprotection
in CMRO2
Delayed ischemic / anoxic depolarisation
Metabolism downregulation
Preservation of ion homeostasis
Ca+2 influx
excitatory amino acid release
Preservation or reduction of damaging secondary
biochemical changes
Preservation of protein synthesis & blood brain
barrier
Prevention of lipid peroxidation
in edema formation
Neuroprotection of white matter
Modulation of inflammatory response & apoptotic
cell death
Complications of
Hypothermia
1.Cardiovascular
complications
3.Metabolism
-
myocardial depression
- dysrhythmia including
ventricular fibrillation
-hypotension
- inadequate tissue
perfusion
- ischemia
2.Coagulation
- thrombocytopenia
- fibrinolysis
- platelet dysfunction
- slowed metabolism of
anaesthetic agents
- neuromuscular
blockade
- protein catabolism
4.Shivering
-
O2 consumption
CO2 production
cardiac output
arterial O2
to other treatment
TPS
in CMRO2 upto 55% - 60%
CMRO2 more than CBF
Also CBV & ICP
preserves CO2 reactivity
Inverse Steal Phenomenon
dosage 3-5 mg/kg every 5-10 min
in animal models
Not shown to improve outcome after global
Protective mechanisms
GABA agonism
Free radical scavenging
membrane lipid peroxidation & damage
NMDA antagonism
Ca+2 channel blockade
Maintenance of protein synthesis
PROPOFOL
2,6 di iso propyl phenol
CBF more than CMRO2 (possible direct
barbiturates
So maintain MAP & CPP
electrophysiologic monitoring
( SSEP , MEP ,
BAEP )
So it is a favourable anaesthetic in neurosurgery
ETOMIDATE
Short acting imidazole
CMRO2 by 50%,CBF & ICP
CO2 reactivity preserved
Maintains cardiovascular stability and CPP
Causes adrenocortical suppression for upto 24
BENZODIAZEPINES
CMRO2 & CBF but slight in ICP
preserves CO2 reactivity
inhibitory GABA neurotransmission
also has anticonvulsant, amnestic & anxiolytic properties
Caution for avoiding excessive sedation in patients at
risk for ICP due to hypoventilation induced hypercapnia
DEXMEDETOMIDINE
Sedative, analgesic, anxiolytic, & sympatholytic
no respiratory depression
MAC for inhalational anesthetics
found to be neuroprotective in animal models of focal
ischemia
also found to CBF without altering CMRO2 ,which is not
observed in humans
KETAMINE
- a phencyclidine derivative
- CBF, thus ICP
But unchanged or slight in CMRO2
- abolishes autoregulation
- a non competitive NMDA receptor antagonist.
LIDOCAINE
INHALATIONAL ANESTHETICS
Cerebrovasodilators
Nitrous oxide
CBF, CMRO2 & ICP
cavities and
avoided in
- Pneumocephalus
- Any surgical procedure within 2 weeks of a
craniotomy in which N2O was used.
ANTICONVULSANT DRUGS
Seizures ischemic effects by in CBF, CMRO2 ,
Diazepam -2-20 mg
Midazolam - 1-5 mg
TPS - 25-100 mg
Pentobarbital - 100 mg
OTHER PHARMACOLOGICAL
APPROACHES
Calcium channel blockers
Nimodipine
the incidence & severity of vasospasm after
aneurysmal SAH
By blocking Ca+2 influx into vascular smooth muscle &
preventing its hypercontraction
oral route only 60 mg every 4 hours for 21 days
Caution against hypotension
i.v. route should not be given because of life threatening
adverse events & death
Nicardipine
i.v.form
ischemic damage in animal studies but not shown
benefit in clinical trials
Magnesium
Ca+2 influx into cells by blocking channels &
cerebral ischemia
Clinical trials are underway
- Dizocilpine
- Magnesium
- Xenon
Glycine binding site antagonism with
- HA-966
- 7- chlorokynurenic acid
AMPA receptor antagonism with
- Riluzole
- Lamotrigine
Both es glutamate release during ischemia
Clinical trials are underway
Tirilazad
- under investigation
Superoxide dismutase
Deferoxamine
Vitamin E
Mannitol
Glucocorticoids
Nitric oxide
Erythropoeitin
Thank you