Cerebral blood flow
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Transcript of Cerebral blood flow
Cerebral blood flow and regulation
Tushar Kumar
INTRODUCTION
Brain is a closed structureMost of it is brain tissue
while some of it is blood and CSF
Brain comprises 80%Cerebral blood volume: 12%CSF contribute to 8% of the
space inside the skull vault
Monro – Kellie doctrine
Anatomy :• Circulation of brain
was first described by WILLIS in 1664
1. Anterior circulation and Posterior circulation via circle of Willis
2. Collateral arterial inflow channels
3. Leptomeningial collaterals- pial to pial anastomoses
Anatomy
Circulation via circle of Willis: anterior circulation: via 2 carotid arteries and their derivations
Posterior circulations: via 2 vertebral arteries joining to form basilar artery
It lies in subarachnoid space and encircles pituitary gland
Willisian channels: anterior communicating artery, posterior communicating artery and ophthalmic artery via external carotid artery
Circle of willis with its collaterals
Collateral circulation
In a normal individuals there is no net flow of blood across these communicating arteries
But to maintain patency and prevent thrombosis there is to an fro flow of blood
Their importance appears when a pressure gradient develops
Second collateral flow appears in surface connections that bridge pial arteries.
They bridge major arterial territories ( ACA – PCA, ACA- MCA, MCA – PCA)
They are called leptomeningial pathways or equal pressure path ways.
Cerebral microcirculation
Capillary density in grey matter is 3 times higher than white matter
Pre capillary vessels divide and reunite to form anastomotic circle called as circle of Duret
They are highly tortuous and irregularVelocity of RBC’s is higher in these capillaries To facilitate transfer of substrate and nutrients RBC’s
have to traverse longer distance via these capillaries
Cerebral microcirculation
Fast capillaries: These are the ones who do not take part in transfer of substrate
BUT
During cerebral hypoperfusion they have a decrease in blood velocity , diverting blood to slower functional capillaries.
Venous drainage
3 set of veins drain from brain
1. Superficial cortical vein2. Deep cortical veins3. Dural sinuses
All ultimately drain into right and left IJV
Cerebral blood supply:Physiological considerations:
Brain accounts for 2% of body weight yet requires 20% of resting oxygen consumption
O2 requirement of brain is 3 – 3.5 ml/100gm/min
And in children it goes higher up to 5 ml/100gm/min
Brain has high metabolic rate
That’s why brain requires higher blood supply
55ml/100gm/min is the rate of blood supply
requires more requires
more substratete
substrate
requires mlacks of storage of
energy substrate
Cerebral blood supply
Cortical grey matter 75 – 80 ml/100gm/min
Subcortical white matter 20ml/100gm/min
CMRO2 : 5.5 ml/100gm/minFunctional requirement is
3.3 ml/100gm/minIntegrity required 02 is
2.2 ml/100gm/min
60% functional
40 % integrity
Factors regulating cerebral blood flow
• Hemodynamic autoregulation• Metabolic mediators and chemoregulation• Neural control• Circulatory peptides
Cerebral blood flow regulation1. Flow metabolism coupling: Hemodynamic
regulationCerebral blood flow (CBF) closely follows cerebral
perfusion pressure (CPP)Within the range of 50 to 150 mm Hg of CPP , blood
flow remains constant.Where CPP = MAP – ICPMAP :Mean arterial pressure and ICP : Intracranial pressure.
Pure changes in perfusion pressure involve myogenic response in vascular smooth muscles (Bayliss effect)
Flow metabolism coupling:
Mechanism that CPP responds to: mean BP
pulsatile pressureMediators involved are: H+, K+, adenosine,
glycolytic intermediate and phospholipid metabolites
Nitric oxide controls the smooth muscles tone
Cerebral blood flow regulation
a. Pressure regulation: Ohm’s law: flow = Pi – Pf
RHagen poiseuille relation : R = 8L μ
r⁴where Pi – Pf is change in pressure,
R is resistance , L is the length of the tube , μ is coefficient of viscosity and r is radius of the tube.
So we derive that: R = Pi – Pf = 8L μ flow r⁴
Cerebral blood flow regulation
Arteriolar diameter as well as cerebral vascular resistance both vary with CPP but CBF remains constant in this range.
Cerebral blood flow regulation
2. Venous physiology:Venous system contains
most of the cerebral blood volume
Slight change in vessel diameter has profound effect on intracranial blood volume
But evidence of their role is less
Less smooth muscle content
Less innervations than arterial
system
Cerebral blood flow regulation
Pulsatile perfusion:Fast and slow components of myogenic response
bring a change in perfusion pressureCardiac output:Cardiac output may be responsible for improved
cerebral blood flowThey are indirectly related via central venous pressure and large cerebral vessel tone.
Cerebral blood flow regulation
Rheological factors:Related with blood viscosity.
Hematocrit has main influence on blood viscosity.
Flow is inversely related with hematocrit.In small vessels cells move faster than plasma.This reduces microvascular hematocrit and
viscosity FAHRAEUS LINDQVIST EFFECT
Metabolic and chemical regulation
1. Carbon dioxide
coupler between flow and metabolism
At normal conditions CBF has linear relationship with CO2 between 20 – 80 mm Hg
For every mm Hg change of PaCO2 CBF changes by 2 – 4 %
CO2 induced vasodilatation
Mechanism by which CO2 produces vasodilatation
CARBON DIOXIDE : How it works
ADULT↑CO2
↑H+ ions
NO
↑nNOS
C GMP
K+ Channel
Ca2+ Channel
↓Ca2+
↓Ca2+
Smooth Ms Relaxation
↑K+
CARBON DIOXIDE : How it works
Neonates ↑CO2
↑H+ ions
PG
↑COXendothelium
C AMP
K+ Channel
Ca 2+ Channel
↓Ca2+
↓Ca2+
Smooth Ms Relaxation
↑K+
Metabolic and chemical regulation
Oxygen:Within physiological range PaO2 has no effect on
CBFHypoxia is a potent stimulus for arteriolar
dilatationAt PaO2 50 mmHg CBF starts to increase and at
PaO2 30 mm Hg it doubles
CO2 and Oxygen
Metabolic and chemical regulation
Temperature:Like other organs cerebral metabolism
decreases with temperatureFor every 1˚C fall in core body temperature
CMRO2 decreases by 7 %At temperature < 18 ˚C EEG activity ceases
Temperature
Pharmacology and autoregulation
Anaesthetic drugs can alter autoregulatory responses as seen with blood pressure and CO2 drug
CBF CMR
Preserve response to CO2
Preserve autoregulation
barbiturates ↓ ↓ yes yespropofol ↓ ↓ yes yesetomidate ↓ ↓ yes ….morphine ± ↓ …. yesfentanyl ± ± yes yesbenzodiazepines ↓ ↓ yes …ketamine ↑ ↑ yes yeslignocaine ↓ ↓ … …
response
Pharmacology and autoregulation
Inhalational agents affecting CBF
volatile anaesthetic CBF CMR
Preserve response to CO2
Preserve autoragulation
Xenon ↓ ↓ yes yesdesflurane ↑ ↓ yes yessevoflurane ↑ ↓ yes yesisoflurane ↑ ↓ yes yesenflurane ↑ ↓ yes yeshalothane ↑↑↑ ↓ yes yesnitrous oxide ↑ ↑ … …
Pharmacology and autoregulationVasoactive agents:
Drugs that do not cross blood brain barrier do not affect CBF
Pharmacology and autoregulation
Dexmedetomidine: Causes 25% reduction in CBF primarily by
reducing CMR
ACE inhibitors, Angiotensin receptor antagonists, β blockers…….. Do not reduce CBF or alter autoregulation
Metabolic mediators and chemoregulation
Control CBF by acting as local vasodilatorsIons and chemicals
H+, K+, adenosine and phospholipid metabolites
Final common pathway is via NO
Neurogenic effects
Neurogenic effects: sympathetic tone shift the curve to right
Circulatory peptides:
Vasoactive peptides like angiotensin II do affect CBF.
Reactive oxygen moleculesAlteration to vasomotor functionVascular remodeling
De silva et al: effects of angiotensin II on cerebral circulation: role of oxidative stress; review article – front physiology ; jan 2013
To summarize
Clinical considerations
Hypertensive patients:Autoregulatory curve shifts to rightProtection from breakthrough but at the cost of
risk of ischemiaMay suffer cerebral ischaemia during
hemorrhage, shock or hypotension
Clinical considerations
Elderly patients:With age CBF decreasesYounger people have increased blood flow in
frontal areas…. Frontal hyperaemiaBut with age this increased flow reducesFlow in other areas are well maintained hence
blood is more uniformly distributedAutoregulatory failure occurs in morel elderly
Auto regulatory failure
For auto regulatory failure to occur vasomotor paralysis is the end point
• Acute ischemia• Mass lesions all lead to • Inflammation vasomotor• Prematurity paralysis• Neonatal asphyxia• Diabetes mellitus
Autoregulatory failure
Right sided failure
Hyperperfusionleads to circulatory
breakthroughFluid from capillaries seep
into the extracellular space leading to edema
e.g. AVM
Left sided failure
Hypoperfusion Ischemia Na˖ and Ca 2˖ influx with
water and K+ efflux leads to cytotoxic edema and infarction
e.g. ischemic stroke
Autoregulatory failure
Two stages before infarction:
a. Penlucida at flow 18 – 23 ml/100gm/min brain becomes inactive but function can be restored at any time by reperfusion
b. Penumbra at lower flow rates brain function can be restored by reperfusion but only within a time limit
Hemodynamic considerationsCerebral steal: it means blood is diverted from
one area to another if pressure gradient exists between the two circulatory beds
Vasodilatation in ischemic brain takes blood from ischemic areas to normal areas causing more ischemia
Vasoconstriction results in redistribution of blood from normal to ischemic areas leading to inverse steal or ROBIN HOOD EFFECT
Hemodynamic considerations
Vessel length and viscosity At breakthrough point flow depends on vessel
length and viscosityAutoregulation has failed and it behaves like
fluid in a rigid tubePressure gradient across the ends are now same
so distal area have the lowest flowThis makes watershed areas more vulnerable to
ischemic changes
Considerations for ischemia
Consideration relevant to global ischemia
Prevent and treat hypotension as well asvasogenic & cytotoxic
edema
Induction of mild hypothermia for 24 hrs
Consideration relevant to focal ischemia
Barbiturate coma, volatile anesthetics (xenon),
calcium channel antagonists
PaCO2 and temperature
Therapies for enhancing perfusion
• Induced hypertension• Inverse steal• Hypocapnea• Hemodilution• Pharmacological agents
• Barbiturates, propofol
• Intra arterial delivery of drugs. Like mannitol and vasodilators
References:
1. Mishra L D; cerebral blood flow and anaesthesia; Indian J. Anaesth. 2002; 46 (2) : 87-95
2. Joshi et al; cerebral and spinal cord blood flow; Cottrell and Young’s Neuroanesthesia; 5th ed, 2010: 17 – 59
3. Patel et at; Cerebral physiology and effect of anesthetic drugs; Miller’s anesthesia 8th ed : 387 – 423
4. De silva et al: Effects of angiotensin II on cerebral circulation: role of oxidative stress; review article – front physiology ; jan 2013
Thank you