CEREBRAL BLOOD FLOW & ICP

Dr Gowri De Zylva

CEREBRAL BLOOD FLOW & ICP

Arterial supply & Venous drainage Cerebral metabolism CBF measurement Regulation of CBF BBB CSF & ICP

CEREBRAL CIRCULATION
Arterial supply 2/3 via two internal carotid arteries: 1/3 via two vertebral arteries Circle of Willies Anterior cerebral artery- superior & medial part of cerebral hemisphere Posterior cerebral artery- Occipital lobe & medial side of the temporal lobe Middle cerebral artery- lateral side of the hemisphere & internal capsule

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

CEREBRAL METABOLISM
Brain consumes 20% of total body oxygen consumption CMRo2- 3-3.5ml/100gm/min(50 ml/min) in adult CMRo2 > Grey matter High oxygen consumption & absence of significant reserve, interruption of cerebral perfusion unconscious in 10 sec due to decrease in O2 tension < 30mm of Hg

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

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

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

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

Limitations
N2o levels are not easy to measure If prolonged circulation equilibrium will not be reached within 10min No indication of regional flow

Intra Arterial method

Radio active kr/xe injected into carotid artery Clearance calculated using scintillation counter

Processed by computer Display on the screen

Advantages
Change in regional flow with mental & physical activity can be visualised Diseased area of brain can be visualised REGIONAL FLOW can be measured by Doppler Probes placed Extracranialy

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

Regulation of CBF
Cerebral perfusion pressure(CPP) Auto regulation Extrinsic mechanisms - Respiratory gas tensions - Temperature - Viscosity - Autonomic influences

CEREBRAL PERFUSION PRESSURE

CPP= MAP- (ICP+ VP) CPP normal 100mm of Hg.(ICP=<10) CPP primarily depends on MAP CPP(40)= MAP(70) + ICP(30) CPP < 50mm of Hg- slowing of EEG < 25-40mm of Hg - Flat EEG <25mm of Hg- irreversible damage

AUTOREGULATION
Wide swings in blood pressure within little change in blood flow CBF remains constant between 60160mm of Hg Beyond this limit blood flow becomes pressure dependant MAP> 150-160mm of Hg- Disrupt BBB results in cerebral edema & hemorrhage

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

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

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

Respiratory Gas Tensions

Acute acidosis has little effect on CBF because H cannot cross the BBB readily PaCo2 < 20mm of Hg EEG changes in normal individuals Disease vessels cannot responds to Co2 Hypoventilation- Increase PaCo2-steel phenomenon Hyperventilation decrease PaCo2-Robin Hood effect- inverse steel phenomenon Po2<50mm of Hg(6.7kpa)- increase CBF

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

VISCOSITY
Decrease in Hematocrit decreases viscosity; increases CBF;decreases oxygen carrying capacity Optimal cerebral oxygen delivery = 30-35% hematocrit

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

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

BBB
Manitol (osmoticaly active)- normally does not cross BBB. BBB is disrupted by-tumor, truma,seizure infection,hypoxia,hypercarbia,^Bp. At this point fluid movement across BBB depends on hydrostatic pressure rather than osmotic gradient.

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.

Normal constituents of CSF

Na-135mmol/l, Cl-115-125mmol/l,Ca11.5mmol/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

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

INTRA CRANIAL PRESSURE

Monro- Kellie Doctrine The cranial cavity is a rigid closed container.Thus any change in intracranial blood volume is accompanied by the opposite change in CSF volume if ICP is maintained. Brain 80-85%;blood5-7%;CSF-5-12%

ICP
Normal ICP = 7-17mm of Hg(1-2kpa) Intracranial compliance is determined by change in ICP in response to a change in intra cranial volume.

Initial increase in volume is well compensated.

Compensatory Mechanisms
Displacement of CSF to spinal compartment. Increase CSF absorption Decreased CSF production Decrease in cerebral blood volume As point eventually reaches at which further increase production precipitates rise in ICP(curve).

Factors raise ICP

BLOOD - increased CBF -impaired venous drainage(cough),kinked jugular vein,Head down position BRAIN -tumor,abcess,hematoma,cerebral oedema CSF- hydrocephalus Benign intracranial hypertensions

ICP monitoring
Types of monitoring- Extra dural fiber optic probe;Intracerebral transducer Waves obtained resemble the arterial wave form. 3variations in ICP wave forms A waves cerebral vasodilatation B waves- changes with respiration C waves-relates to systemic vasomotor tone