Neurophysiology and

anaesthesia
 Peculiarities of brain

 Has a high metabolic rate

 Has no oxygen stores
 Unableto 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  Extrinsic factors

 Myogenic  Respiratory gas
Regulation  Arterial BP
 Metabolic  Hematocrit
Regulation  Temperature
 Neuronal
Regulation
 Hormonal
regulation
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

 ↑ CO2
 potassium
 ↑ H+
 adenosine

 prostanoids
 ↑ 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 DOCTRINE
The cranial vault is a rigid structure with fixed
volume
Brain 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.

Intracranialelastance 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 include

a)Displacement of CSF from cranial to spinal
compartment
b)An increase in CSF resorption
c)Decrease in CSF production
d)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  Isoflurane
 Has greatest effect on  CBF
CBF  Auto regulation
 Con.> 1% - abolishes maintained up to 1 MAC
auto regulation  is > in sub cortical than
 Generalized increase in neocortical areas
CBF  At equivalent MAC
 At equivalent MAC CBF CBF up to 20%
up to 200%
 Simultaneous
 Prior hyperventilation hyperventilation can
to be initiated 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
 Itis a direct acting and potent cerebral
vasodilator
IV induction agents

 Intravenousanesthetics 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. dilated
 Induced 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

normal ischemic
Thank you