This document discusses various topics related to cerebral physiology: - Cerebral circulation involves blood flow to the brain through paired internal carotid and vertebral arteries. Cerebral blood flow is tightly regulated to maintain adequate oxygen and glucose delivery to brain tissue. - Cerebral metabolism relies heavily on glucose and oxygen to produce ATP and support neuronal activity, particularly in gray matter. Interruption of blood flow can cause rapid loss of consciousness and irreversible damage. - Factors like cerebral perfusion pressure, blood gas levels, temperature, and viscosity influence cerebral blood flow through mechanisms like autoregulation. The blood-brain barrier restricts passage of molecules into brain tissue. Cerebrospinal fluid protects the brain and helps regulate int

1. CEREBRAL PHYSIOLOGY
Speaker: Dr. Parul Sharma
Moderator: Dr. Virendra

2. CONTENTS
 Cerebral Circulation
 Cerebral Metabolism
 Cerebral Blood Flow
 Regulation of Cerebral Blood Flow
 Cerebral Perfusion Pressure
 Blood Brain Barrier
 Cerebrospinal Fluid
 Intracranial Pressure
 Cerebral Ischemia
 Strategies for Brain Protection

3. CEREBRAL CIRCULATION
 Arterial supply to brain  paired right and left
Internal Carotid Artery anterior circulation,
 And , paired right and left vertebral arteries
posterior circulation.
 3 paired arteries that originate from the circle of
Willis perfuse the brain anterior, middle and
posterior cerebral arteries.

4.  Posterior communicating arteries and the anterior
communicating artery complete the loop
 Anterior and posterior circulation equally.

6. CEREBRAL METABOLISM
 Brain normally consumes 20% of total body
oxygen.
 Most of this oxygen consumption (60%) is used to
generate ATP to support neuronal electrical activity.
 CMR, called the Cerebral Metabolic Rate, is
expressed in terms of oxygen consumption, and in
adults is 3-3.8 ml/100g/min or 50ml/min

7. CMR...
 Greatest in  gray matter of cerebral cortex 
parallels cortical electrical activity.
 Because of the relatively high oxygen consumption
and the absence of significant oxygen reserves 
interruption of cerebral perfusion 
unconsciousness within 10 sec.
 If not re-established within 3-8 minutes  ATP
stores depleted  irreversible cellular injury begins.

8.  Most sensitive to hypoxic injury  hippocampus
and cerebellum.
 Primary energy source for neurons  glucose.
Consumption  5mg/100g/min.
 Therefore, CMRO2 parallels glucose
concentration.
 During starvation, this relation not maintained as
ketone bodies also become major energy source.

9. CEREBRAL BLOOD FLOW
 Variety of methods available to measure
1) Positron emission tomography
2) Xenon enhanced CT
3) Single photon emission CT
4) CT perfusion scans

10.  Best described by Hagen Poiseuille equation for
laminar flow  direct relationship between flow,
CPP and calibre of vessels.

11.  CBF averages 50ml/100g/min.
 Grey matter  80ml/100g/min
 White matter  20ml/100g/min
 Total CBF  750ml/min i.e. 15-20% of cardiac
output
 Flow rates below  20-25ml/100g/min  cerebral
impairment  slowing on EEG

12.  15-20ml/100g/min  flat or isoelectric line on EEG
 <10ml/100g/min  irreversible brain damage.

13. REGULATION OF CEREBRAL BLOOD
FLOW
 1. Cerebral Perfusion Pressure
 2. Autoregulation
 3. Extrinsic mechanisms
 Respiratory gas tensions
 Temperature
 Viscosity

14. RESPIRATORY GAS TENSIONS
 Particularly PaCO2
 BF changes 1-2ml/100g/min/mmHg change in
PaCO2. immediate secondary to changes in
pH of CSF and cerebral tissue
 Acute changes in PaCO2, not HCO3- affects
CBF acute metabolic acidosis has little effect on
CBF H+ ions cant cross BBB

15.  Marked hyperventilation shifts ODC left  may
result in cerebral impairment even in normal
individuals
 Only marked changes in PaO2 alter CBF.

16. TEMPERATURE
 CBF changes 5-7%/1 degree change in
temperature
 Hypothermia both CMR and CBF
 Between 17-37 degree celcius, Q10 for humans
approx. 2 for every 10 degree increase in
temperature, CMR doubles.

17.  Conversely, CMR by 50% if temperature of brain
falls by 10%, and another 50% if temperature falls
from 27 to 17 degree Celsius
 At 20 degrees isoelectric EEG
 Hyperthermia above 42 degrees neuronal cell
injury

18. VISCOSITY
 Most important determinant hematocrit
 hematocrit viscosity  improves CBF
 But, reduction in hematocrit decreases oxygen
carrying capacity impair oxygen delivery
 Polycythemia  CBF

19.  Optimal cerebral oxygen delivery  hematocrit of
30%

21. CEREBRAL PERFUSION PRESSURE
 Difference in the pressures between the
arterial and venous circulation  dictates
the blood flow to the organ.
 CPP = MAP- ICP/CVP (whichever if greater)
 80-100mm Hg (or 70-90mm Hg)

22.  Because ICP is normally <15 mm Hg (5-15 mmHg)
 CPP primarily dependent  MAP
 The cerebrovascular resistance (CVR) is the
hindrance to the CBF predominantly by the calibre
of the vessels.

23.  Moderate to severe increases in ICP 
compromise CPP and CBF, even with normal MAP.
 CPP <50mm Hg slowing on EEG
 CPP 40-25mm Hg flat EEG
 Sustained pressure <25mm Hg irreversible brain
damage

24.  Cerebral vasculature rapidly adapts to changes in
CPP  10-60 sec
 in CPP  cerebral vasodilation
 in CPP  cerebral vasoconstriction
 CBF nearly constant between MAP 60-160mm Hg.
 Above these pressures  disrupts BBB  cerebral
edema and haemorrhage

26.  This curve is shifted to right in patients with chronic
arterial HTN.
 Directly proportional to PaCO2 between 20-80mm
Hg.
 Ions do not, but CO2 readily crosses BBB and
directly affects CBF.

27.  Intense sympathetic stimulation
vasoconstriction limits CBF
 Following brain injury or stroke vasospasm

28. BLOOD BRAIN BARRIER
 Cerebral vessels unique endothelial cells are
nearly fused
 The paucity of pores  BBB
 Lipid barrier allows passage of lipid soluble
substances, restricting those with high molecular
weight and ionized substances.
 Therefore, movement governed by size, lipid
solubility, and degree of protein binding in blood.

29.  Freely permeable CO2, O2, lipid soluble
molecules
 Poorly permeable  most ions, proteins, large
substances like mannitol.
 Acute hypertonicity  movement of water out of
brain parenchyma
 Acute hypotonicity water into the brain

30.  BBB disrupted by  severe HTN, tumours, trauma,
stroke, infection, marked hypercapnia, hypoxia, and
sustained seizures

31. CEREBROSPINAL FLUID
 Found in ventricles, cisterns, subarachnoid space
surrounding the brain and spinal cord.
 Function protect CNS against trauma as brain
floats in CSF (bouyancy)
 Formation  choroid plexus, minimal amount by
fluid leaking into perivascular spaces surrounding
cerebral vessels.

32.  Normal total CSF production 0.3-0.4 ml/min OR
21ml/hr OR 500ml/day
 Yet total CSF is only  150 ml

34.  Absorbed  arachnoid granulations over cerebral
hemispheres
 Active secretion of sodium in the choroid plexus
 Resulting fluid hypotonic, with lower potassium,
bicarbonate and glucose concentration
 Absorption translocation from arachnoid
granulations to ceberal venous sinuses.

36. INTRACRANIAL PRESSURE
 Cranial vault  rigid  fixed total volume of brain
(80%), blood (12%), and CSF (8%).
 Any increase in one component equivalent
decrease in another to prevent rise in ICP. 
Monroe Kellie Hypothesis / Doctrine
 Normal values 5-15mm Hg

37.  Major compensatory mechanisms for in ICP
 Initial displacement of CSF into spinal compartment
 absorption
o Sustained increase in ICP herniation

38. CEREBRAL ISCHEMIA
 Interruption of cerebral perfusion, metabolic
substrates (glucose) or severe hypoxemia
functional impairment.
 perfusion impairs clearance of potentially toxic
metabolites
 During ischemia, intracellular K+ , and intracellular
Na+ due to failure of ATP dependent pumps

39.  Sustained increase in intracellular Ca2+ activates
lipases and proteases structural damage to
neurons
 FFA , cyclooxygenase and lipoxygenase activity
formation of PG and LT cellular injury
 Lactic acid cellular function impaired with
defective repair mechanisms

40. STRATEGIES FOR BRAIN PROTECTION
 Ischemic brain injury focal (incomplete) or global
(complete)
 Global total circulatory arrest and global hypoxia
 Focal embolism, haemorrhage, atherosclerosis,
stroke as well as blunt, penetrating and surgical
trauma

41.  HYPOTHERMIA
 Decreases both basal and electrical metabolic
requirements
 Reduces free radicals and other mediators of cellular
injury

42.  OTHER GENERAL MEASURES
 Maintaining satisfactory CPP
 Oxygen carrying capacity
 Normal arterial oxygen tension
 Hyperglycemia avoided
 Normocarbia

43. Thank you 