Cerebral Physiology

1. AUTO-REGULATION OF
CEREBRAL BLOOD FLOW
OBJECTIVES :
• Normal Rate of Cerebral Blood Flow
• a) Cerebral autoregulation and mechanisms bringing it about
• b) Effect of PaCO2 changes on CBF
• c) Effect of PaO2 changes on CBF
• d) Coupling of CBF with CMRO2
• e) Effects of anaesthetic agents on regulation of CBF
Presented By: Dr.Vrinda C

2. CEREBRAL BLOOD FLOW
CBF is tightly regulated to meet the brain's metabolic demands
Brain: 1350 gm; 2% of Total Body Weight
Normal blood flow through the brain of the adult person average
45 to 55 ml/ 100 grams of brain tissue/ minute.
For entire brain: 750 to 900 ml/min, 15 percent of the resting cardiac
output.

3. 1. It is important to maintain BF within narrow limits because too
much blood can raise intracranial pressure(ICP) which can
compress and damage delicate brain tissue.
2. Too little blood flow causes ischemia.
3. Ischemia results if blood flow to the brain is below 18 to 20 ml
/ 100 g / min Tissue death occurs if flow drops below 8 to 10
ml / 100 g /min

4. 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
60% of energy used for synaptic transmission.
40% used for maintaining cellular integrity.
Substrate requirement Lacks of storage of energy

7. 1. Myogenic/Pressure Autoregulation:
Myogenic theory: The vascular smooth muscles are highly
responsive to changes in pressure, that contributes to auto-
regulation of cerebral blood flow.
Arterioles dilate or constrict to maintain a constant CBF
Cerebral blood flow is well extremely "auto- regulated" between
mean arterial pressure limits of 70 and 150 mm Hg.

8. Cerebral perfusion pressure(CPP)
Cerebral perfusion pressure CPP:-
The net pressure of blood flow to the brain.
CPP can be defined as:
CPP = MAP – ICP
CPP is regulated by two balanced, opposing forces:
1. Mean Arterial pressure (MAP) is the force that pushes blood into the brain
2. intracranial pressure (ICP) force that pushes out.
• CPP is normally between 70 - 90 mmHg in adult human.
CPP = MAP – ICP

9. Hypertension, auto-regulation of cerebral blood flow occurs even when the
MAP rises to as high as 160 to 180 mmHg. If MAP falls below 60 mmHg,
cerebral blood flow become severely decreased.
But above and below the autoregulatory plateau, CBF is pressure
dependent and linearly varies with CPP.

11. 2. Metabolic Autoregulation
Increased local brain metabolism via increased neuronal activity
is associated with a proportional change in CBF called as
neurovascular coupling. Which is basically a feed-forward
mechanism.
Three metabolic factors have potent effects in controlling the
cerebral blood flow.
(1) Carbon dioxide concentration, (2) Hydrogen ion concentration,
(3)Oxygen concentration

12. Synaptic activity leads to glutamate release.
1. Activates glutamatergic receptors.
2. Metabotropic glutamate receptors in astrocytes.

13. Carbon dioxide concentration
CO2 is a potent vasodilator
CBF changes 1-2 ml/100g/min for each 1mmHg change in
PaCO2.
As the arterial tension of CO2 rises, CBV and CBF increases
When it is decreased vasoconstriction is induced
70% increase in arterial PCO2, approximately doubles the
cerebral blood flow

14. CBF increases linearly with increase in
PaCO2.
PaCO2 < 25mmHg -NO further reduction
in CBF
PaCO2 > 80mmHg –NO further increase
in CBF
Mod hypotension- response to changes
in PaCO2 attenuated
Severe hypotension-response is
abolished.

15. Hydrogen ion concentration
Carbon dioxide increase cerebral blood flow by combining first
with water in the body fluids to form carbonic acid, with
subsequent dissociation of this acid to form hydrogen ions.
The vasodilation is directly proportional to the increase in
hydrogen ion concentration.
Increased hydrogen ion depresses neuronal activity. It is
fortunate that it causes an increase in blood flow, which in turn
carries hydrogen ions, carbon dioxide, and other acid forming
substances away from the brain tissues.

16. Oxygen concentration.
If blood flow to the brain is insufficient to supply the needed
amount of oxygen,due to:
1. Reduction in Pa02 below 60mmHg
2. Reduction in Hb concentation
Immediate increase in cerebral blood flow.
Rostral ventrolateral medulla serves as oxygen sensor.
Stimulation of RVM by hypoxia leads to ATP dependent K+
channel opening ,hyperpolarisation and vasodilation in
vascular smooth muscles.

17. Impact of reduction in cerebral oxygen delivery either by hypoxemic hypoxia or
hemodilution is depicted.
CBF response in much greater with hypoxia.
Therefore, total cerebral oxygen delivery is better maintained by hypoxia than
hemodilution at a comparable level of arterial oxygen content.

18. 3. Neurogenic Autoregulation
The cerebral circulatory system has strong extra axial
sympathetic innervation that passes upward from the superior
cervical ganglia and intaaxial pathways from several nuclei.
ANS and Neurochemical control has minor role, MAP and
Metabolic Autoregulation is most important
During acute hypertension, sympathetic system attenuates
increase in BF
The sympathetic nervous system normally constricts the
large and intermediate-sized brain arteries enough to
prevent the high pressure from reaching the smaller brain
blood vessels. This is important in preventing vascular
hemorrhages, preventing the occurrence of "cerebral stroke.

19. EFFECTS OF ANESTHETICS ON CBF AND
CMR
The effect of volatile anaesthetic's on CBF is a balance between
1)reduction in CBF caused by CMR suppression and 2)augmentation
of CBF caused by direct cerebral vasodilation.
1. At .5 MAC –CMR suppression induced reduction in CBF predominates
2. At 1 MAC – CMR suppression and vasodilation gets balanced, CBF
unchanged
Higher MAC levels causes luxury perfusion.
Order of vasodilating potency
Halothane>enflurane>desflurane=isoflurane>sevoflurane

20. Dose dependent cerebral vasodilation
results in attenuation of autoregulatory
response to increasing MAP.

21. IV Anaesthetics
1.Barbiturates
With onset of anaesthesia, both CBF and CMRO2 are reduced
by approximately 30%. At larger doses of thiopentone it reduces
to 50-60%.
Nontoxic doses of depressant anaesthetic's causes reduction in
component of cerebral metabolism linked to electrical brain
function with minimal effect on cellular homeostasis.
Tolerance to CBF and CMR effects barbiturates quickly.

22. 2. PROPOFOL
Effects of propofol on CBF and CMR are similar to those of
barbiturates.
Both CBF and CMR decreases after administration of propofol
The combination of propofol and fentanyl anaesthesia
decreases subdural pressure in patients with intracranial
tumours.
Indicated that propofol effects reduction in CMR,CBF, and ICP.

23. Factors disturbing the Autoregulation
Noxious stimuli Stroke Cerebral perfusion pressure
Noxious stimuli such as :
1.Hypoxia due to occlusive cerebro-vascular disease
2. Trauma from head injury
3. Brain compression from tumours, cerebral edema. These factors
Results in the loss of normal cerebral blood flow (CBF) auto regulation.

24. THANK YOU.