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SOE 407: Cerebral Blood Flow Physiology

Introduction

Regarding blood flow to the brain…

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Question No. 2

Q: How much oxygen does the brain consume?

Answer No. 2

  • Resting oxygen consumption of the brain is ~50 ml/minute
  • Consumes ~20% of total body oxygen requirements at rest

Question No. 3

Q: What is the cerebral blood flow rate and how does it vary between white and grey matter?

Answer No. 3

  • Global CBF is ~50ml / 100g brain tissue / minute
    • White matter: 20ml/100g/min
    • Grey matter: 70ml/100g/min
  • Receives ~15% of cardiac output at rest

Question No. 4

Q: What do you understand by the threshold values for cerebral ischaemia?

Answer No. 4

  • More sensitive to even short periods of reduced blood flow than other organs in the body
  • Clinically a reduction in CBF to 30 ml/100g/min for as little as 5 seconds can result in syncope and loss of consciousness as occurs during a vasovagal episode
  • Decreases in CBF lead to progressive cellular ischaemia:
Cerebral Blood Flow
Effect
<50 mL/100 g/min
Cellular acidosis
<40 mL/100 g/min
Impaired protein synthesis
<30 mL/100 g/min
Cellular oedema
<20 mL/100 g/min
Failure of cell membrane ion pumps, with loss of transmembrane electrochemical gradients
<10 mL/100 g/min
Cellular death

Question No. 5

Q: Define cerebral perfusion pressure?

Answer No. 5

  • The net pressure gradient driving blood flow through the cerebral circulation which results in cerebral blood flow
  • It depends upon the mean arterial pressure (MAP), the intracranial pressure (ICP) and the central venous pressure (CVP) - many exclude CVP from the equation as its effects are usually negligible:

CPP = MAP - (ICP + CVP)

  • The normal CPP is 70–80 mmHg
  • A CPP of 30-40 mmHg is the threshold for critical ischaemia

Question No. 6

Q: Which factors affect cerebral blood flow?

Answer No. 6

Affecting Cerebral Perfusion Pressure
  • Changes in mean arterial pressure (MAP)
  • Changes in intracranial pressure (ICP)
  • Changes in central venous pressure (CVP)
Affecting Radius of Cerebral Vessels
  • Myogenic control
  • Metabolic mediators:
    • pCO2
    • pO2
    • Cerebral metabolic rate
    • Temperature
  • Neurogenic mediators
  • Endothelial mediators
  • Chemical mediators:
    • Volatile anaesthetics
    • Intravenous anaesthetics
Affecting Blood Rheology
  • Haematocrit

Question No. 7

Q: What is autoregulation?

Answer No. 7

The ability of an organ to regulate its blood flow despite changes in its perfusion pressure

Question No. 8

Q: Draw a graph to demonstrate cerebral autoregulation? How does this change in hypertensive patients?

Answer No. 8

  • Cerebral blood flow is autoregulated between a MAP of 50 - 150 mmHg
    • Outside the autoregulatory range:
      • When MAP >150 mmHg CBF becomes directly proportional to CPP
      • When MAP falls <50 mmHg CBF falls proportionally below the ‘normal’ value of 50 mL/100 g/min, resulting in ischaemia
    • In hypertensive patients autoregulation occurs between a higher range of pressures (60 and 160 mmHg)
  • Can be displayed using an autoregulation curve:
    • Represents an oversimplification of the true relationship
    • In vivo changes in perfusion pressure may be regional and there is not a neat linear relationship at each end of the curve
Effects of cerebral autoregulation, demonstrating the relationship between cerebral perfusion pressure and cerebral blood flow

Question No. 9

Q: When does cerebral autoregulation become impaired and how does this affect cerebral blood flow?

Answer No. 9

  • Autoregulation becomes impaired in intracranial pathology (e.g. traumatic brain injury, infection and haemorrhage)
  • Leads to a more directly proportional relationship between CPP and cerebral blood flow
Loss of autoregulation and reliance upon CPP

Question No. 10

Q: What are the underlying mechanisms that maintain cerebral autoregulation?

Answer No. 10

  • The autoregulatory vessel calibre changes are mediated by interplay between myogenic, neurogenic, metabolic and endothelial mechanisms:
Myogenic Tone
  • Thought to be the primary mechanism behind cerebral autoregulation
  • Cerebral vascular smooth muscle vasoconstricts in response to increased wall tension and vasodilates in response to decreased wall tension
  • Results in change of vessel calibre to maintain a constant cerebral blood flow
Metabolic Response
  • Decreased perfusion due to a fall in perfusion pressure can lead to accumulation of metabolic products in tissue (H+/K+/adenosine/nitric oxide/CO2)
  • Mediate cerebral vasodilatation and thus increased cerebral blood flow
  • Important mechanism in smaller vessels that are subject to changes in the local environment
Neurogenic Response
  • Vascular smooth muscle is under autonomic control and mediates vasoreactivity in small and medium sized vessels
  • Thought to play minor role in autoregulation in health
  • Differences in regional innervation in the brain may contribute to the pathophysiology of certain conditions such as PRES
Endothelial Response
  • Endothelial tissue secretes a number of vasodilators and vasoconstrictors in a paracrine manner
  • Thought to play a minor role in cerebral autoregulation

Question No. 11

Q: What effect does PaCO2 have on cerebral blood flow? Can you draw a graph to describe this?

Answer No. 11

  • Increases linearly between a PaCO2 range of 3-10 kPa:
    • Due to CO2 mediated vasodilatation
  • Below 3.5 kPa, cerebral vasoconstriction leads to tissue hypoxia with subsequent reflex vasodilatation and maintenance of blood flow
  • Above 10 kPa vasodilatation is maximal with no further increase in flow. Increased blood volume may lead to a rise in ICP
  • In chronic hypercapnia the curve is shifted to the right, with a higher kPa over which linear vasodilatation occurs
Relationship between PaCO2 (carbon dioxide) and cerebral blood flow

Question No. 12

Q: What effect does PaO2 have on cerebral blood flow? Can you draw a graph to describe this?

Answer No. 12

  • At 'normal' PaO2 of >8 kPa there is minimal effect on cerebral blood flow
  • As PaO2 falls below this level there is a rapid rise in cerebral blood flow:
    • Mediated by hypoxia-induced vasodilation
    • Results in a CBF of around 110ml/100g/min at a PaO2 of 4.0 kPa
    • May contribute to further rises in ICP in patients with head injury
Relationship between PaO2 (oxygen) and cerebral blood flow

Question No. 13

Q: How does cerebral blood flow change in response to cerebral metabolic rate?

Answer No. 13

  • There is a linear correlation between cerebral blood flow and CMR
    • Known as ‘flow–metabolism coupling’
    • Exact mechanisms are unclear but are likely due to accumulation of vasodilatory metabolic by-products (e.g. CO2, H+, K+ and adenosine
  • Occurs on a local level to match CBF to metabolically active areas of the brain:
    • Demonstrated by the higher blood flow to the more metabolically active grey matter (70ml/100g/min) than white matter (20ml/100g/min)
  • Also occurs on total brain level with CBF matched to total brain metabolism:
    • Increase in overall CMR (during pyrexia or seizures) results in increased CBF
    • Decreased CMR (during general anaesthesia or hypothermia) results in decreased CBF

Question No. 14

Q: What effects do commonly used anaesthetic drugs have on cerebral blood flow?

Answer No. 14

Intravenous Anaesthetic Agents

(excluding ketamine)

  • Propofol, thiopentone and etomidate all reduce CMR
  • As a result of flow–metabolism coupling they all result in a fall in cerebral blood flow
  • Autoregulation is not affected
Ketamine
  • Causes increased cerebral blood flow
    • Increases cardiac output and MAP
    • Increases CMR and dilates cerebral vasculature
  • Counteracts mild increase in ICP to maintain perfusion
Volatile Anaesthetic Agents

(excluding N2O)

  • Unique in their ability to uncouple CMR and CBF:
    • Cause a decrease in CMR
    • However, also abolish autoregulation and cause cerebral arteriolar vasodilatation, leading to increased CBF
  • The action is dose-dependent:
    • Below 1 MAC both effects are approximately equal and CBF is unchanged
    • Above 1 MAC the reduction in CMR is already maximal and CBF increases due to cerebral arteriolar vasodilatation
  • Sevoflurane has the lowest vasodilatory potential of the volatile agents
    • Order of vasodilating potency is halothane > enflurane > desflurane > isoflurane > sevoflurane
N2O
  • Both potently dilates cerebral arteries and increases CMR
  • As a result CBF significantly increases
Opioids
  • No significant effect on either CMR or CBF
  • CBF will rise in the setting of opioid induced CO2 retention
NMBA
  • No significant effect on either CMR or CBF

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