Neurophysiology and Neuroanaesthesia

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

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