Cerebral Blood Flow & Icp
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Transcript of 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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