cerebral blood flow & icp

7/29/2019 Cerebral Blood Flow & Icp

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CEREBRAL BLOOD FLOW &

ICP

Dr Gowri De Zylva


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CEREBRAL BLOOD FLOW & ICP

Arterial supply & Venous drainage

Cerebral metabolism

CBF measurement Regulation of CBF

BBB

CSF & ICP


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CEREBRAL CIRCULATION

Arterial supply 2/3 via two internal carotidarteries: 1/3 via two vertebral arteries

Circle of Willies

Anterior cerebral artery- superior & medialpart of cerebral hemisphere

Posterior cerebral artery- Occipital lobe &

medial side of the temporal lobe Middle cerebral artery- lateral side of the

hemisphere & internal capsule


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Venous drainage

Deep structures drain via internal cerebral

veins

Midline great cerebral vein inferior

sagital sinus in mid line

Transverse sinus- sigmoid sinus- jugular

vein


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CEREBRAL METABOLISM

Brain consumes 20% of total body oxygenconsumption

CMRo2- 3-3.5ml/100gm/min(50 ml/min) in

adult CMRo2 > Grey matter

High oxygen consumption & absence of

significant reserve, interruption of cerebralperfusion unconscious in 10 sec due todecrease in O2 tension < 30mm of Hg


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CMRo2

If no CBF 3-8min irreversible cellular injury

Hippocampus & cerebellum more sensitive to

hypoxic injury

Primary energy source is Glucose

Brain glucose consumption-5mg/100g/min

90-95% of glycolysis is aerobic

CMRo2 parallels glucose consumption Starvation ketone bodies,aminoacids & fat also

becomes major substrate


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CREBRAL BLOOD FLOW

MEASUREMENT

All methods used are based on the Fick

principle

Blood flow through any organ

=Amount of substance removed from the

blood by the organ per unit time/ A-V con

difference

= uptake (Qx)/ A-V diff


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Inhalation method

Kety method using nitrous oxide

Partition coefficient for N2O in BBB= 1

N2O equates between BBB in 10-11 min Uptake= amount in venous blood at

equilibrium/ partition coefficient

15% N2O+ 21%O2 is inhaled for 10 min &the conc. in venous jugular bulb & arterial

conc. measured at regular intervals


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Inhalation technique

Uptake of N2O= amount in venous blood

at equilibrium/ part coeffi- 1

= amount in venous blood at the end of 10

min/ mean A-V difference


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Limitations

N2o levels are not easy to measure

If prolonged circulation equilibrium will notbe reached within 10min

No indication of regional flow


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Intra Arterial method

Radio active kr/xe injected into carotid

artery

Clearance calculated using scintillation

counter

Processed by computer Display on the

screen


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Advantages

Change in regional flow with mental &

physical activity can be visualised

Diseased area of brain can be visualised

REGIONAL FLOW can be measured byDoppler Probes placed Extracranialy


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Values

Total CBF 50ml/100g/min

Total CBF 750ml/min (15-20% of COP)

Gray matter 80ml/100g/min White matter 20ml/100g/min

CBF < 20-25ml/100g/min- slow wave EEG

< 15- 20ml/100g/min-isoelectric EEG< 10ml/100g/min- irreversible

brain damage


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Regulation of CBF

Cerebral perfusion pressure(CPP)

Auto regulation

Extrinsic mechanisms- Respiratory gas tensions

- Temperature- Viscosity- Autonomic influences


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CEREBRAL PERFUSION

PRESSURE

CPP= MAP- (ICP+ VP)

CPP normal 100mm of Hg.(ICP=


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AUTOREGULATION

Wide swings in blood pressure within little

change in blood flow

CBF remains constant between 60-

160mm of Hg

Beyond this limit blood flow becomes

pressure dependant

MAP> 150-160mm of Hg- Disrupt BBB

results in cerebral edema & hemorrhage


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CEREBRAL AUTOREGULATION

CURVE

Shift to right in patients with chronic

arterial hypertension

Long term antihypertensive therapy can

restore cerebral auto regulation towards

normal

Two theories to explain auto regulation


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MYOGENIC & METABOLIC

Myogenic theory- Intrinsic response of smooth

muscle cell in cerebral arterioles to change in

MAP

Metabolic theory- cerebral metabolic demands

determine the arterial tone

Metabolites- H, NO, Adenosine, prostaglandins Auto regulation is lost in trauma, tumor, infection &

CBF becomes pressure dependant


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Extrinsic Mechanisms

Respiratory gas tensions

CBF is directly proportional to PaCo2 of

20-80mm of Hg

1mm of Hg change in PaCo2 = Blood flow

change 1-2ml/100g/min

Reduction of PaCo2 40 to 30(5.3to 4kpa)

reduces CBF 30%

It is an immediate effect due to changes in

CSF PH


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Respiratory Gas Tensions

Acute acidosis has little effect on CBF becauseH cannot cross the BBB readily

PaCo2 < 20mm of Hg EEG changes in normal

individuals Disease vessels cannot responds to Co2

Hypoventilation- Increase PaCo2-steelphenomenon

Hyperventilation decrease PaCo2-Robin Hoodeffect- inverse steel phenomenon

Po2


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TEMPERATURE

CBF changes 5-7% per degree C

Hypothermia reduces CBF,CMRo2;

Pyrexia increases CBF

20 degree C EEG is isoelectric

>42 degree C oxygen activity decreases

causing cell damage


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VISCOSITY

Decrease in Hematocrit decreases

viscosity; increases CBF;decreases

oxygen carrying capacity

Optimal cerebral oxygen delivery

= 30-35% hematocrit


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Autonomic Influences

Intense sympathetic stimulation causes

marked vaso constriction in large cerebral

vessels and decreases cerebral blood flow

Autonomic innervations also plays a role in

cerebral vasospasm following brain injury

& stroke


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BBB

Junction between vascular endothelial

cells are fused.

Lipid barrier allows lipid soluble drugs but

restrict ionised or large MW.

Acute hyper tonicity of plasma- net

movement of H2O out of brain.

Hypo tonicity vise versa


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BBB

Manitol (osmoticaly active)- normally doesnot cross BBB.

BBB is disrupted by-tumor, truma,seizureinfection,hypoxia,hypercarbia,^Bp.

At this point fluid movement across BBBdepends on hydrostatic pressure ratherthan osmotic gradient.


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CEREBRO SPINAL FLUID

Major function is to protect the CNS

against trauma.

Formed by choroid plexus

Absorbed by arachnoid granulation

CSF production is

21ml/Hr(500ml/d);0.3ml/min

It is isotonic with plasma; Active secretion

of Na in the choroid plexus.


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Normal constituents of CSF

Na-135mmol/l, Cl-115-125mmol/l,Ca1-

1.5mmol/l,K2.5-3.5mmol/l

Glucose 2-5mmol/l(if BS normal)

pH 7.3-7.5

Protein-0.2-0.4g/l

Urea-1.5-6mmol/l Lymphocytes 0-5


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CSF

CSF absorption is directly proportional to

ICP inversely proportional to CVP

CSF production is decrease by-carbonic

anhydrase inhibitor,

corticosteroids,spironolactones,

frusemide,isoflurane & vasoconstrictors

Brain & spinal cord lack lymphatic


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INTRA CRANIAL PRESSURE

Monro- Kellie Doctrine

The cranial cavity is a rigid closed

container.Thus any change in intracranial

blood volume is accompanied by theopposite change in CSF volume if ICP is

maintained.

Brain 80-85%;blood5-7%;CSF-5-12%


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ICP

Normal ICP = 7-17mm of Hg(1-2kpa)

Intracranial compliance is determined bychange in ICP in response to a change in

intra cranial volume.

Initial increase in volume is well

compensated.


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Compensatory Mechanisms

Displacement of CSF to spinal

compartment.

Increase CSF absorption

Decreased CSF production

Decrease in cerebral blood volume

As point eventually reaches at whichfurther increase production precipitates

rise in ICP(curve).


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Factors raise ICP

BLOOD- increased CBF-impaired venous drainage(cough),kinked

jugular vein,Head down position BRAIN

-tumor,abcess,hematoma,cerebraloedema

CSF- hydrocephalus

Benign intracranial hypertensions


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cerebral blood flow & icp

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