Cerebral blood flow is regulated by several factors including cerebral metabolic rate, cerebral perfusion pressure, arterial carbon dioxide and oxygen levels, drugs, and intracranial pathology. The brain consumes a high amount of oxygen given its metabolic rate, receiving 12-15% of cardiac output despite being only 2% of body weight. Oxygen requirement and factors affecting cerebral circulation were presented, covering topics such as vascular supply, autoregulation, perfusion pressure, extrinsic mechanisms, and effects of anesthetic agents.

1. OXYGEN REQUREMENT CMR
AND FACTOR EFFECTING
CEREBRAL CIRCULATION
CO-ORDINATOR: DR.S.PANDEY (MD)
PRESENTED BY: DR.BRAJENDRA(JR-2)

2. CEREBRAL BLOOD FLOW
Cerebral blood flow (CBF) is governed by :
*cerebral metabolic rate
* cerebral perfusion pressure
(CPP = MAP- ICP)
* arterial blood carbon dioxide (PaCO2)
*oxygen (PaO2) tensions
*various drugs, and intracranial pathology

3. • The adult human brain weight approximately 1350 g
(represents about 2% percent of total-body weight)
• It receives 12% to 15% of cardiac output.
(reflect brain's high metabolic rate)
• At rest, the brain consumes oxygen at an average
rate of approximately 3.5 mL of oxygen per 100 g of
brain tissue per minute.
• Whole-brain O2 consumption (50 mL/min)
represents about 20% of total-body oxygen
utilization.

4. VASCULAR SUPPLY OF BRAIN
Arterial supply
• Arterial supply to the brain comes
from four arteries:
the paired internal carotid arteries.
the paired vertebral arteries.
• These form the circle of Willis from
which the anterior, middle and
posterior cerebral arteries arise.
Venous drainage
• venous drainage of the brain is via
the numerous dural venous
sinuses, which drain into the
internal jugular vein

6. Physical Principle
• Blood flow is dependent on blood pressure and
vascular resistance i.e.flow = pressure/ resistance.
CBF= CPP/CVR
CPP = MABP –CVP
CBF = MABP - CVP / CVR
• As cerebral venous pressure is only slightly
more(nearly equal) to ICP, we assume for clinical
purposes that
CBF = MABP-ICP / CVR

7. Cerebral Metabolism
The brain normally consumes 20% of total body
O2.Most cerebral 02(60%)is used to grnerate ATP to
support neuronal electrical activites.
The cerebral metabolic rate (CMR) is usually experessed
in terms of 02 consumption(CMRo2)-50ml/min
CMRo2 is greatest in gray matter of the cerebral cortex
bcz of relatively high o2 consumption and the absence
of segnificant reserves,interruption of cerebral
perfusion usually result in unconsciousness with in 10
sec as o2 tension rapidly drops below 30 mm Hg.
Hippocampus and cerebellum seem to be most sensitive
to hypoxic injury.

8. Glucose as primary energy source for neuronal
cells.Brain glucose consumption is approx
5mg/100mg/min.CMRo2 normally parallels glucose
consumption.this relationship not maintained
during starvation when ketone bodies also become
mejor energy substrates.
Cerebral function is normally dependent on a
continuous supply of glucose.
Acute sustained hypoglycemia is injurious to the
brain.

9. CBF Regulation
• The flow-metabolism coupling is critical during times of stress
or extreme conditions such as hypotension or hypoxia. These
processes involve following regulatory mechanisms to maintain
flow at required levels:
1. Cerebral Auto-regulation
2. Cerebral perfusion pressure
3. Extrinsic Mechanism
a).Respiratory gas tension
b).Temperature
c).Viscosity
d).Autonomic Influences
4. Circulatory Peptides

10. Cerebral Auto-regulation
The brain normally tolerates a wide range of blood
pressure ,with little change in blood flow.
The cerebral vasculature rapidely(10-60s)adapts to
changes in CPP.Decreases CPP result in cerebral
vasodilation ,whereas elevations induce
vasoconstriction.
In normal individuals CBF nearly constant b/w MAP abt
60-160 mm Hg.
Beyond these limits blood flow become pressure
dependent .pressure above 150-160 mm Hg can
disrupt the BBB and may result in cerebral edema and
hemorrhage

11. Cerebral auto regulation curve
 graph
 Pressures above
160mmHg
 Disrupts BBB
 Cerebral
edema
 Haemorrhage

12. Myogenic and Metabolic mechanisms may explain
cerebral autoregulation.
Myogenic mechanisms involve an intrinsic response of
smooth muscles cells in cerebral arterioles to
changes in MAP.
Metabolic mechanisms indicate that cerebral
metabolic demands determine arteriolar tone.
Thus ,when tissue demand exceeds blood flow, the
release of tissue metabolits cause vasodilation and
increases flow.

13. Cerebral Perfusion Pressure
Cerebral Persusion Pressure(CPP)=MAP-ICP
CPP is normally 80-100 mm Hg.Moreover ICP is normally
less than 10 mm Hg,CPP is primarily dependent on
MAP.
Moderate to severe increases in ICP(>30mm Hg)can
compromise CPP &CBF even in the presence of normal
MAP
If CPP
<50mm Hg-slowing on EEG
25-40mm Hg-flat EEG
<25mm Hg-irreversible brain damage

14. Extrinsic Mechanisms
A.Respiratory gas tension
• Carbon dioxide is a powerful modulator of cerebrovascular
resistance, and perhaps clinically most accessible one.
• Any change in arteriolar PaCO2 within the range of 20 to 80 torr
has a direct effect on cerebral vessels except in neonates, in
whom the response to PaCO2 below 30 mmHg may be blunted.
• The CBF changes 1-2ml/ 100g/ min for every 1mmHg change in
PaCO2 within physiological ranges.
• On the other hand, PaO2 does not affect CBF and only a
reduction of PaO2 to <50 torr has a significant effect, by
stimulating arteriolar dilation.

16. B.Temperature
CBF changes 5% to7% per 1 ‘c.
Hypothermia decreases both CMR and
CBF,whereas hyperthermia has the reverse
effect.
B/W 17 to 37 ‘c ,the Q10 for humans ia approx
2 that is every 10 degree increase in
temperature the CMR double.

17. C).Blood viscosity on CBF
Hematocrit is the single most important determinant
of blood viscosity.
Decrease in hematocrit decrease viscosity and can
improve CBF ,unfortunately a reduction in
hematocrit also decrease the o2 carrying capacity
and thus can potentially impair o2 delivery.

18. D.Autonomic Influences
• Intracranial vessels are innervated by
sympathetic(vasoconstrictive) &
parasympathetic
(vasodilatory)system.Autonomic innervation
may also play an important role in cerebral
vasospasm in following brain injury and
stroke.
Circulatory Peptides
• The circulatory vasoactive substances such as
adrenaline,vasopressin and angiotensin II may
also have influence on CBF.

19. The CBF and its control mechanisms
Cerebral vasodilation

20. Effect of Anaesthetic Agents on CBF
Inhalational Agents
Nitrous Oxide :
• If used alone (in oxygen), the N2O is a potent
cerebral vasodilator and may also increase the
ICP but without any appreciable change in
CMRO2.
• When combined with barbiturates, narcotics,
volatile agents or hypocarbia, the effects on
CBF and ICP are attenuated or abolished.

21. Volatile Anaesthetics
• All the volatile anaesthetics cause dose related increase in
CBF and a decrease in CMRO2.
• Isoflurane is preferred over halothane in patients with
increased ICP, as it does not increase the CBF at doses less
than 1-1.5 MAC, whereas, the halothane consistently
increases CBF.
• The enflurane increases ICP significantly in patients with
space occupying lesions and has epileptogenic properties.
• Desflurane and Sevoflurane have a special role in
neuroanaesthesia as they ensure a rapid onset of and
emergence from anaesthesia.
• They cause a dose related rise in both CBF and ICP and a fall
in CMRO2, at least upto 2 MAC.
• The cerebral auto-regulation is preserved at 1 MAC
concentration of almost all the volatile anaesthetics.

22. Intravenous Agents
Barbiturates
• The barbiturates decrease both CBF and CMRO2 .
• Barbiturates does not prevent CBF auto -regulation, however,
the response to hypoxia and hypercapnia is attenuated
because of metabolic depression.
• Barbiturates may have direct effects on vascular tone causing
cerebral vasoconstriction hence a decrease in CBF and ICP.
Propofol
• The propofol decreases CBF and CMRO2 and may also
decrease the ICP particularly when combined with
hyperventilation.

23. Etomidate
• The etomidate resembles thiopental in terms of effects
on CBF and CMRO2.
• Compared to thiopental, there is only minimal
haemodynamic suppression even in high doses.
• The etomidate is rarely used in neuroanaesthesia and
intensive care due to high incidence of myoclonus and
adrenal cortical suppression.
Benzodiazepines
• They all cause a reduction in CBF due to a
decrease in both CVR and CMRO2.
• The reduction in CBF and CMRO2 appears to be
less than that observed with other intravenous
anaesthetics.

24. Ketamine
• It causes a significant increase in CBF and ICP but has
lesser effect on CMRO2.
• ketamine may emerge as an useful drug in cerebral
ischemia due to its NMDA antagonist property.
Narcotics
• The opioids provide potent analgesia associated with
a stable heamodynamics with low sympathetic tone
and a relaxed brain.
• They have a minimal to modest depressive effects on
CBF and CMRO2.

25. Local Anaesthetics
• The local anaesthetics (LA) rapidly cross the blood
brain barrier and because of their membrane
stabilizing effects, exert and effect on cerebral
function, CBF and CMRO2.
• In subtoxic doses, LA causes a modest and transient
decrease in CMRO2 and CBF(coupled with an
increase in CVR).
Muscle Relaxants
• Although muscle relaxants do not cross the blood-
brain barrier, secondary effect are possible mainly
due to histamine release, systemic haemodynamic
effects and altered afferent inputs from muscle
spindles.

26. • The succinylcholine can cause impressive increases in
CBF and ICP, which is secondary to increased muscle
spindle activity.
• d-Tubocurarine (dTC) is known to release histamine
and cause a modest rise in CBF and CSF pressures after
a bolus dose.
• Atracurium causes less concern, as it is associated with
less degree of histamine release. One of its
metabolites, laudanosine readily crosses the blood
brain barrier and may cause seizures in large doses.
• Pancuronium,in patients with intracranial pathology
and defective auto-regulation induces increases in CBF
and ICP.
• Vecuronium has no effect on ICP and is most
commonly used relaxant in neurosurgical patients.

27. Reversal / Prevention of Ischemia &
Enhancing CBF
• The cerebral ischemia may be prevented or reversed
by avoiding hypovolemia and maintaining adequate
intravascular volume, thereby an adequate CBF.

28. Intracranial Pressure
Intracranial Contents
• Brain tissue 1400g 85%
• CSF 70ml 5%
• Blood 130ml 10%
Cerebrospinal Fluid
• Total Volume of CSF 100-160 ml
• Rate of Formation of CSF 0.35-0.4 ml/min or
500-600 ml/day
• Therefore turnover rate = 4 times per day

29. Intracranial hypertension
• Defined as sustained ICP >15 mmHg
• Blood and CSF communicate with extracranial
compartments and allow a degree of adaptability
• Three compensatory mechanisms-
*Translocation of intracranial CSF through
foramen magnum to subarachnoid space around
spinal cord
*Increased CSF absorption by arachnoid villi
*Translocation of blood out of cranium
• Once these methods are exhausted there is an
abrupt rise in ICP with small increase in cerebral
volume ,Cerebral compliance and capacitance

30. CAUSES OF RAISED ICP
• Increased brain bulk-space occupying lesion,
cerebral oedema.
• Increased CSF volume-benign intracranial
hypertension, hydrocephalus.
• Increased cerebral blood flow.
• Increased arterial blood - hypoxia, hypercarbia,
halogenated inhalational agents.
• Increased venous blood –coughing, straining,
increased intrathoracic or intra-abdominal
pressure,obstruction to venous drainage in neck,
head down position.

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