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Cerebral blood flow and
regulation
Tushar Kumar
INTRODUCTION
Brain is a closed structure
Most 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 irregular
Velocity 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 vein
2. Deep cortical veins
3. 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/min
Functional requirement is
3.3 ml/100gm/min
Integrity 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 regulation
1. Flow metabolism coupling: Hemodynamic
regulation
Cerebral 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 – ICP
MAP :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 pressure
Mediators 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
R
Hagen poiseuille relation : R = 8L μ
r⁴
where 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 pressure
Cardiac output:
Cardiac output may be responsible for improved
cerebral blood flow
They 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
↑COX
endothelium
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
CBF
Hypoxia is a potent stimulus for arteriolar
dilatation
At 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 temperature
For 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 yes
propofol ↓ ↓ yes yes
etomidate ↓ ↓ yes ….
morphine ± ↓ …. yes
fentanyl ± ± yes yes
benzodiazepines ↓ ↓ yes …
ketamine ↑ ↑ yes yes
lignocaine ↓ ↓ … …
response
Pharmacology and autoregulation
Inhalational agents affecting CBF
volatile
anaesthetic CBF CMR
Preserve
response to
CO2
Preserve
autoragulation
Xenon ↓ ↓ yes yes
desflurane ↑ ↓ yes yes
sevoflurane ↑ ↓ yes yes
isoflurane ↑ ↓ yes yes
enflurane ↑ ↓ yes yes
halothane ↑↑↑ ↓ yes yes
nitrous oxide ↑ ↑ … …
Pharmacology and autoregulation
Vasoactive 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 vasodilators
Ions 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 molecules
Alteration to vasomotor function
Vascular 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 right
Protection from breakthrough but at the cost of
risk of ischemia
May suffer cerebral ischaemia during
hemorrhage, shock or hypotension
Clinical considerations
Elderly patients:
With age CBF decreases
Younger people have increased blood flow in
frontal areas…. Frontal hyperaemia
But with age this increased flow reduces
Flow in other areas are well maintained hence
blood is more uniformly distributed
Autoregulatory 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
Hyperperfusion
leads to circulatory
breakthrough
Fluid 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 considerations
Cerebral 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 viscosity
Autoregulation has failed and it behaves like
fluid in a rigid tube
Pressure gradient across the ends are now same
so distal area have the lowest flow
This makes watershed areas more vulnerable to
ischemic changes
Considerations for ischemia
Consideration relevant to
global ischemia
Prevent and treat
hypotension as well as
vasogenic & 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

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Cerebral blood flow

  • 1. Cerebral blood flow and regulation Tushar Kumar
  • 2. INTRODUCTION Brain is a closed structure Most 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
  • 3. 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
  • 4. 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
  • 5. Circle of willis with its collaterals
  • 6. 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.
  • 7. 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 irregular Velocity 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
  • 8. 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.
  • 9. Venous drainage 3 set of veins drain from brain 1. Superficial cortical vein 2. Deep cortical veins 3. Dural sinuses All ultimately drain into right and left IJV
  • 10. 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
  • 11. Cerebral blood supply Cortical grey matter 75 – 80 ml/100gm/min Subcortical white matter 20ml/100gm/min CMRO2 : 5.5 ml/100gm/min Functional requirement is 3.3 ml/100gm/min Integrity required 02 is 2.2 ml/100gm/min 60% functional 40 % integrity
  • 12. Factors regulating cerebral blood flow • Hemodynamic autoregulation • Metabolic mediators and chemoregulation • Neural control • Circulatory peptides
  • 13. Cerebral blood flow regulation 1. Flow metabolism coupling: Hemodynamic regulation Cerebral 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 – ICP MAP :Mean arterial pressure and ICP : Intracranial pressure. Pure changes in perfusion pressure involve myogenic response in vascular smooth muscles (Bayliss effect)
  • 14. Flow metabolism coupling: Mechanism that CPP responds to: mean BP pulsatile pressure Mediators involved are: H+, K+, adenosine, glycolytic intermediate and phospholipid metabolites Nitric oxide controls the smooth muscles tone
  • 15. Cerebral blood flow regulation a. Pressure regulation: Ohm’s law: flow = Pi – Pf R Hagen poiseuille relation : R = 8L μ r⁴ where 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
  • 16. Cerebral blood flow regulation Arteriolar diameter as well as cerebral vascular resistance both vary with CPP but CBF remains constant in this range.
  • 17. 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
  • 18. Cerebral blood flow regulation Pulsatile perfusion: Fast and slow components of myogenic response bring a change in perfusion pressure Cardiac output: Cardiac output may be responsible for improved cerebral blood flow They are indirectly related via central venous pressure and large cerebral vessel tone.
  • 19. 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
  • 20. 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 %
  • 21. CO2 induced vasodilatation Mechanism by which CO2 produces vasodilatation
  • 22. CARBON DIOXIDE : How it works ADULT ↑CO2 ↑H+ ions NO ↑nNOS C GMP K+ Channel Ca2+ Channel ↓Ca2+ ↓Ca2+ Smooth Ms Relaxation ↑K+
  • 23. CARBON DIOXIDE : How it works Neonates ↑CO2 ↑H+ ions PG ↑COX endothelium C AMP K+ Channel Ca 2+ Channel ↓Ca2+ ↓Ca2+ Smooth Ms Relaxation ↑K+
  • 24. Metabolic and chemical regulation Oxygen: Within physiological range PaO2 has no effect on CBF Hypoxia is a potent stimulus for arteriolar dilatation At PaO2 50 mmHg CBF starts to increase and at PaO2 30 mm Hg it doubles
  • 26. Metabolic and chemical regulation Temperature: Like other organs cerebral metabolism decreases with temperature For every 1˚C fall in core body temperature CMRO2 decreases by 7 % At temperature < 18 ˚C EEG activity ceases
  • 28. 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 yes propofol ↓ ↓ yes yes etomidate ↓ ↓ yes …. morphine ± ↓ …. yes fentanyl ± ± yes yes benzodiazepines ↓ ↓ yes … ketamine ↑ ↑ yes yes lignocaine ↓ ↓ … … response
  • 29. Pharmacology and autoregulation Inhalational agents affecting CBF volatile anaesthetic CBF CMR Preserve response to CO2 Preserve autoragulation Xenon ↓ ↓ yes yes desflurane ↑ ↓ yes yes sevoflurane ↑ ↓ yes yes isoflurane ↑ ↓ yes yes enflurane ↑ ↓ yes yes halothane ↑↑↑ ↓ yes yes nitrous oxide ↑ ↑ … …
  • 30. Pharmacology and autoregulation Vasoactive agents: Drugs that do not cross blood brain barrier do not affect CBF
  • 31. 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
  • 32. Metabolic mediators and chemoregulation Control CBF by acting as local vasodilators Ions and chemicals H+, K+, adenosine and phospholipid metabolites Final common pathway is via NO
  • 33. Neurogenic effects Neurogenic effects: sympathetic tone shift the curve to right
  • 34. Circulatory peptides: Vasoactive peptides like angiotensin II do affect CBF. Reactive oxygen molecules Alteration to vasomotor function Vascular remodeling De silva et al: effects of angiotensin II on cerebral circulation: role of oxidative stress; review article – front physiology ; jan 2013
  • 36. Clinical considerations Hypertensive patients: Autoregulatory curve shifts to right Protection from breakthrough but at the cost of risk of ischemia May suffer cerebral ischaemia during hemorrhage, shock or hypotension
  • 37. Clinical considerations Elderly patients: With age CBF decreases Younger people have increased blood flow in frontal areas…. Frontal hyperaemia But with age this increased flow reduces Flow in other areas are well maintained hence blood is more uniformly distributed Autoregulatory failure occurs in morel elderly
  • 38. 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
  • 39. Autoregulatory failure Right sided failure Hyperperfusion leads to circulatory breakthrough Fluid 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
  • 40. 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
  • 41. Hemodynamic considerations Cerebral 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
  • 42. Hemodynamic considerations Vessel length and viscosity At breakthrough point flow depends on vessel length and viscosity Autoregulation has failed and it behaves like fluid in a rigid tube Pressure gradient across the ends are now same so distal area have the lowest flow This makes watershed areas more vulnerable to ischemic changes
  • 43. Considerations for ischemia Consideration relevant to global ischemia Prevent and treat hypotension as well as vasogenic & 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
  • 44. Therapies for enhancing perfusion • Induced hypertension • Inverse steal • Hypocapnea • Hemodilution • Pharmacological agents • Barbiturates, propofol • Intra arterial delivery of drugs. Like mannitol and vasodilators
  • 45. 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

Editor's Notes

  1. Beyond the limits CBF is compromised and causes ischemia or circulatory breakthrough. Bayliss: 1902 neural innervation to vessels.
  2. There was a time when co2 was thought to be coupler between flow and metabolism.
  3. Proximal resistors in arteriolar bed.