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Neurophysiology and anaesthesia
Peculiarities of brain
Has a high metabolic rate Has no oxygen stores Unable to maintain its integrity
through anaerobic metabolism Neurons don’t require insulin for
transport of glucose across cell
membrane
Neurophysiology
2% of body weight
17%-20% of Cardiac output consumption at rest
20% of inspired oxygen
60% - for neuronal activity
40% - to maintain cellular integrity
CMR / CMRO2 - 3-3.8ml/100g/min 50ml/min
Cerebral glucose consumption - 5mg/100g/min
cerebral blood flow
80% - Internal carotid arteries 20% - Vertebral arteries Anterior n posterior communicating
arteries Circle of Willis Communication between exl & int
carotids – opthalmic arteries
Circle of willis
Physiology of CBF
Parallels with metabolic activity
Can vary from 10 – 300 ml/100g/min
Average – 50ml/100g/min
Gray matter – 80ml/100g/min
White matter- 20ml/100g/min
Total CBF- averages 750ml/min
< 20-25ml/100g/min- ischemia
Cerebral blood flow
Flow rates below 20-25ml/100g/min slowing of EEG.
Flow rates between 15-20ml/100g/min flattening of EEG.
Flow rates below 10ml/100g/min irreversible brain damage.
FACTORS CONTROLLING CBF
Cerebral perfusion pressure
CPP is the difference between Mean arterial pressure and intracranial pressure (or cerebral venous pressure, which ever is greater)
CPP = MAP – ICP
CPP = MAP - ICP
Normal CPP – 80 to 100mmHg More dependent on MAP ICP > 30mmHg compromise CPP CPP
< 50mmHg – slowing of EEG 25 – 40 mmHg – flat EEG < 25 mmHg – irreversible brain damage
Cerebral auto regulation
Ability of the cerebral blood vessels to alter their caliber in order to maintain a constant flow in face of variations in blood pressure
Cerebral auto regulation
CBF is kept constant over a wide range of
MAP ( 60 – 160 mm Hg )
CPP = MAP – Ven Press = MAP - ICP
↑ MAP Cerebral vasoconstriction
↓ MAP Cerebral vasodilatation
Constant CBF is maintained
Cerebral auto regulation
graph Pressures above 160mmHg Disrupts BBB Cerebral
edema Haemorrhage
Auto regulation……
The cerebral vasculature rapidly adapts to change in CPP. (10 - 60 sec)
In Hypertensive persons cerebral autoregulation curve shifts to higher pressure levels : 180 – 200mm Hg and towards right.
Changes in autoregulation
Absent ( Vasomotor paralysis ) brain trauma surgical retraction high ICP brain tumor seizures
Shift to right Systemic hypertension States of sympathetic activation
Shift to left Volatile anesthetic agents
FACTORS CONTROLLING CBF
Intrinsic factors Myogenic
Regulation Metabolic
Regulation Neuronal
Regulation Hormonal
regulation
Extrinsic factors Respiratory gas Arterial BP Hematocrit Temperature
Myogenic factors
Is the intrinsic response of smooth muscle cells in cerebral arterioles to changes in MAP
Protective mechanism against excessive pressure fluctuation at capillary level
Metabolic regulation
Hydrogen ions
potassium
adenosine
prostanoids
↑ CO2
↑ H+
↑ K+
↑ Adenosine
EDRF / Nitric Oxide
Innervation
The sympathetic fibers arise mainly from the superior cervical ganglion
The parasympathetic from the sphenopalatine and otic ganglia
Sensory fibers from the trigeminal ganglion
Neuronal regulation
α-Adrenergic receptors in arterial smooth muscle
Postganglionic sympathetic fibers release noradrenaline
Causes smooth muscle contraction and
arterial constriction Sympathetic innervation is responsible for
vascular tone
Sympathetic
Large & Medium sized arteries
normally overridden by autoregulation Historically thought to have no role in cerebral
circulation Comes into play in states of excessive circulatory
activity / pathologic states Role in prevention of cerebral haemorrhage –
cerebral vasospasm
Hormonal regulation
Adrenaline Vasopressin Angiotensin II
Effect of CO2 on CBF
CBF œ PaCO2 between 20 – 80 mmHg
1mmHg ↑↓ PaCO2-↑↓ CBF by 1-2ml/100g/min
After 24 – 48 hrs CSF HCO3- compensation limits the effects of hypocapnia/ hypercapnia
Persistent hyperventilation Leftward shift of oxy-Hb dissociation curve and marked changes in CBF cerebral impairment
Hypercarbia - CBF
The relationship between PaCO2 and CBF is sigmoid
with plateaus below 25 mmHg and above 75 mmHg.
The slope is approximately linear
Mechanism of CO2 on CBF
The mechanism of CO2 induced changes in vessel caliber
An increase in perivascular H+ concentration
Associated NOS activation
An increase in intracellular cGMP
K+ efflux
A reduction in intracellular Ca + + resulting in dilation
NOS inhibition attenuates the
Cyclooxygenase inhibition CBF response to CO2
Effect of oxygen
Hyperoxia – minimal decrease in CBF
10%
Severe hypoxia – PaO2 < 50mmHg
Increases CBF
Haematocrit
in haematocrit viscosity CBF
O2 carrying
capacity
haematocrit viscosity CBF
Optimal haematocrit – 30% to 34%
Temperature
CBF changes 5- 7% per OC
Hypothermia CBF & CMR
Pyrexia has reverse effect
Intracranial pressure
“ICP means supra tentorial CSF pressure measured in the lateral ventricles or over the cerebral cortex and is normally less
than 10mmHg.”
Minor variations may occur depending on site measurement but, in lateral recumbent position, lumbar CSFpressure normally approximates supratentorial pressure.
Intracranial pressure
MONRO-KELLIE DOCTRINEMONRO-KELLIE DOCTRINEThe cranial vault is a rigid structure with fixed volumeBrain 80%Blood 12%CSF 8%
Any increase in one component must be offset by an equivalent decrease in another to prevent rise in ICP
Intracranial pressure
ICP normally 10mmHg and less.
Intracranial elastance determined by measuring the change in ICP in response to change in intracranial volume
Initially increases in volume are initially well compensated until it reaches a point which further increase can cause rise in ICP
Intracranial elastance
Intracranial pressure
Major compensatory mechanisms includea)Displacement of CSF from cranial to spinal compartmentb)An increase in CSF resorptionc)Decrease in CSF productiond)Decrease in total cerebral blood volume
Applied aspects
Effects of anesthetic drugs on CBF Volatile anesthetics
Induction agents
Anesthetic adjuncts
Vasopressors
Vasodilators
Neuromuscular blocking agents
Volatile agents
Volatile agents – dose dependent dilatation of cerebral vessels
Impair auto regulation Response to CO2 retained May increase cerebral blood volume May result in elevated ICP
Halothane Has greatest effect
on CBF Con.> 1% -
abolishes auto regulation
Generalized increase in CBF
At equivalent MAC CBF up to 200%
Prior hyperventilation to be initiated
Isoflurane CBF Auto regulation
maintained up to 1 MAC
is > in sub cortical than neocortical areas
At equivalent MAC CBF up to 20% Simultaneous
hyperventilation can prevent in ICP
Sevoflurane: CBF effects similar to isoflurane Produce slightly less vasodilation Auto regulation maintained up to 1.5 MAC
Desflurane: CBF similar to isoflurane Autoregulation progressively abolished as dose
increases
Nitrous Oxide: When administered on its own- increases both
CBF and metabolism.
when added to a background of another anesthetic, it increases CBF without changing metabolism
It is a direct acting and potent cerebral vasodilator
IV induction agents
Intravenous anesthetics reduce CBF in a dose dependent fashion
coupled to the reduction in metabolism
Once maximal suppression of metabolism occurs, no further reduction in CBF occurs
Barbiturates
Barbiturates maximal 50% reduction in CBF and metabolism
CO2 reactivity is maintained but is quantitatively reduced compared to the awake response
Cerebral auto regulation maintained
intact
Propofol
Propofol produces a coupled dose dependent reduction in CMRO2 and CBF
High doses vasodilator effect overcomes the coupling & CBF increases
Both CO2 responses and auto regulation are maintained intact in the normal brain
In head injured patients static auto regulation may be impaired by high propofol infusion rates
Ketamine
Dilates the cerebral vasculature and increases CBF ( 50 – 60%)
Increases in CBF, CBV, CSF volume can increase ICP markedly in patients with decreased IC compliance
Opioids
Opioids at low doses produce very little effect on CBF (provided CO2 is not allowed to rise)
Auto regulation remains intact
Some opioids in ICP
BP vasodilatation to maintain CBF
cerebral blood volume
increase intracranial pressure.
Vasopressors
With intact auto regulation & BBB
in CBF occurs when
MAP<50 -60mmHg
MAP>150 – 160mmHg
In the absence of auto regulation, vasopressors CBF by direct effect on CPP.
Vasodilators
In the absence of hypotension
Cerebral vasodilatation
CBF
With Hypotension
CBF is maintained or increased
CBV & ICP in patients with IC compliance
NMBD
No direct effect on CBF
Histamine releasing agents can cause hypotension , CPP
What is Luxury perfusion ? Intra cerebral steal ? Reverse steal phenomenon ?
Luxury perfusion
The combination of a decrease in CMRO2 and increase in CBF has
been termed luxury perfusion met. Demand met. Supply
Luxury perfusion…
Seen in Acute cerebral infarction
Vessels – max. dilatedInduced hypotension with isoflurane
Intracerebral Steal
In a setting of focal ischemia , vasodilatation in a normal area would shunt blood away from the diseased area.
ischemic normal
Steal
Seen in
in PaCO2 in cerebral ischemia
Volatile anesthetic agents
Results in vasodilatation in normal areas not in ischemic areas
Reverse Steal phenomenon
Diversion or redistribution of blood flow from normal to ischemic areas in the brain is termed Reverse Steal / Robin Hood phenomenon
ischemicnormal
Thank you
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