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Cerebral blood flow andintracranial pressureEmily Shardlow

Alan Jackson

AbstractThe MonroeKellie hypothesis states that if the skull is intact, then the sum

of the volumes of the brain, cerebrospinal fluid (CSF) and intracranial blood

volume is constant. An increase in volume in one of the three components

within the skull must be compensated for by a decrease in the volume of

the other remaining components, otherwise the intracranial pressure (ICP)

will increase. Brain tissue is not easily displaced; therefore changes in

venous blood or CSF volumes initially act as the major buffers against

a rise in ICP. In the normal adult, the ICP is 5e13 mmHg, with minor cyclical

variations owing to the effects of the arterial pressure waveform and respi-

ration. Cerebral blood flow (CBF) is determined by a number of factors. It is

closely linked to the metabolic activity of the brain to ensure adequate

delivery of oxygen and substrates. The relationship between partial pres-

sure of carbon dioxide in arterial blood (PaCO2) and CBF is almost linear.

CBF increases by 25% for each kPa increase in PaCO2. Hypoxia (PaO2

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The homeostatic mechanism not only compensates for increased

intracranial systolic blood volume, but results in significant

smoothing of the systolic/diastolic pressure differences to which

the brain is exposed. Failure of this homeostasis has been impli-

cated in the pathogenesis of a wide range of cerebral disorders.

In health, systolic expansion of the basal cerebral arteries

producesa pressurewave within theCSF, causingan outflow of CSF

through the foramen magnum into the compliant spinal CSF space,equivalent to 50% of the increase in intracerebral volume. Simi-

larly, with diastolic relaxationof the artery, CSF flows back into the

cranium. The systolic CSF pressure wave is also transmitted to the

major dural venous sinuses by expansion of the arachnoid granu-

lations,therefore dissipating the systolic pressure wave. In addition,

the elastic arterial walls absorb part of the energy of the systolic

arterial pulse wave, which is then released during diastole to

maintain constant capillary flow (Windkessel effect). The combi-

nation of these processes maintains a constant perfusion pressure

and flow in the cerebral capillary bed despite the major changes in

arterial feeding pressure between diastole and systole.

Intracranial pressureThe relationship between the volumes of brain tissue, CSF and

blood gives rise to the intracranial pressure (ICP). In the normal

adult, the ICP is 5e13 mmHg, with minor cyclical variations

owing to the effects of the arterial pressure waveform and

respiration. ICP also varies with posture, coughing and straining.

A sustained increase in ICP to more than 15 mmHg is termed

intracranial hypertension. At an ICP of more than 20 mmHg,

areas of focal ischaemia appear, and at values of ICP more than

50 mmHg, global ischaemia supervenes.

As previously described by the MonroeKellie hypothesis, an

increase in volume in one of the three components within the skull

must be compensated for by a decrease in the volume of the other

remaining components. Brain tissue is not easily displaced; therefore

changes in venous blood or CSF volumes initially act as the major

buffers against a rise in ICP. The ability to compensate is influenced

by the time-scale involved, with slow-growing lesions better toler-

ated than acute insults. When compensatory mechanisms are no

longer sufficient the compliance (change in volume per unit change

in pressure, dV/dP) of the intracranial cavity is greatly reduced and

ICP rises. Within the skull, it is the change in ICP for unit change in

volumethat is of interest, or dP/dV,and theterm elastance should be

used. The pressureevolume curve is the traditional method of

expressing this relationship (Figure 1). This suggests that patholog-

ical increases in ICP occur as a result of continuing increase in

intracranialvolume. If we acceptthat the volumeof theskull is fixed,

it is therefore more accurate to regard the relationship as the force

required to displace volume from the cranium to accommodate the

new volume. As the force generated is difficult to measure, it is the

resultant pressure (ICP) that is normally measured (force pressure

area). The resultant curve is actually a composite of pressure

versus displaced volume curves for venous blood, CSF and arterial

blood, each of which is successively more difficult to displace.

Control of cerebral blood flow

Several protective mechanisms control CBF. The brain is intol-

erant of hypoxia and depends on oxidative phosphorylation of

glucose to generate ATP (adenosine triphosphate).

Flow-metabolic coupling

The cerebral blood flow is normally closely matched to the cerebral

metabolic rate for oxygen (CMRO2). The flow-metabolic coupling

was described by Roy and Sherrington in 1890 and stated that the

brain possesses an intrinsic mechanism by which vascular supply

can be varied locally or globally in correspondence with local

variations in functional activity. The mediator of this coupling is

subject to continuing research. At present nitric oxide (NO) is being

investigated as a possible mediator which may be modifiedwith NO

synthetase inhibitors to alter pathophysiological responses to braininjury. CMRO2 under normal conditions is 3.5 ml/100 g/minute. It

accounts for20% of the totalbodyoxygen consumption and25% of

basal glucose utilization. CBF is closely linked to the metabolic

activity of the brain to ensure adequate delivery of oxygen and

substrates. At any time, some regions may haverelatively increased

activity and blood flow, while other areas are less active. Any

condition that reduces global metabolic activity will reduce CMRO2and CBF. At a brain temperature of 27C, CMRO2 and CBF are

approximately halved, and CBF is about 10% at 20C, as neuronal

activity virtually ceases at this temperature.

There is evidence of benefits of hypothermia in preventing

secondary brain injury after a primaryinsult. However, as moderate

and severe hypothermia can be detrimental to outcome, only mildhypothermia has been accepted as a therapeutic manoeuvre.

Controversy lies in the fact that the results of studies using hypo-

thermia are conflicting. Such studies include the National Acute

Brain Injury Study trial, which concluded that mild hypothermia

after headinjurydoes not reducemortalityor brain dysfunction; but

studies of head-injured patients with severe intracranial hyperten-

sion have demonstrated a beneficial effect and improved outcome.

Conversely, hyperthermia and seizures increase CMRO2 and CBF.

Hyperglycaemia is associated with an increase in cerebral metab-

olism. Reduced CBF subsequent to an acute head injury results in

additional anaerobic metabolism, and therefore blood glucose

should be tightly controlled.

Reproduced with permission from Rosner M J. Pathophysiology and

management of increased intracranial pressure. In: Andrews BT, ed.

Neurosurgical intensive care. New York: McGraw-Hill, 1993

Pressurevolume curve

Pressuregene

rated

Displaced volume

Arterial

CSF

Venous

Composite curve

Figure 1

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Carbon dioxide

The relationship between partial pressure of carbon dioxide in

arterial blood (PaCO2) and CBF is almost linear. CBF changes by

25% for each kPa change in PaCO2. At a PaCO2 of 10.6 kPa, CBF is

approximately doubled. Beyond this, there is no further increase

in flow because the cerebral resistance vessels are maximally

vasodilated. Conversely, at a PaCO2 of 2.7 kPa flow is halved and

plateaus as a result of maximum vasoconstriction. This is thoughtto be mediated by changes in hydrogen ion concentration in the

extracellular fluid surrounding the vascular smooth muscle.

The response of cerebral vasculature to changes in PaCO2 can be

used therapeutically in patients with raised ICP. Hyperventilation

causes vasoconstriction with a reduction in CBV and ICP. Extreme

hypocarbia (PaCO2

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arises from the cervical ganglia and the supply to the parenchymal

microvasculature from the locus ceruleus. Their main action is

vasoconstriction, which probably serves to protect the brain by

shifting the autoregulation curve to the right in hypertension. The

parasympathetic nerves arise from the pterygopalatine and otic

ganglia and contribute to cerebral vasodilatation. This is most

apparent in conditions such as hypotension and post-ischaemia

reperfusion. It is also thought that initial changes in CBF to meetmetabolic demands are initiated via neurogenic mechanisms and

then sustained by local chemical factors.

Blood viscosity

Blood viscosity is directly related to the haematocrit. Reductions

in haematocrit improve flow, but this is offset by a reduction in

the oxygen-carrying capacity of the blood. The optimum hae-

matocrit at which there is a balance between flow and oxygen

capacity is approximately 30%.

Critical cerebral blood flow

Below the lower limit of autoregulation, CBF mirrors MAP, and

eventually a reduced flow causes cerebral ischaemia. At a CPP of

approximately 25 mmHg, CBF is 20e25 ml/100 g/minute, and this

is accompanied by slowing of electrical activity on electroen-

cephalography (EEG). When perfusion pressure reaches 15 mmHg

(CBF 15 ml/100g/minute), electrical activity ceases, and below 10

mmHg, cellular integrity is lost with a massive efflux of potassium

and eventually cell death.

Monitoring

Monitoring of the central nervous system, including measure-

ments of neuronal function, CBF and cerebral oxygenation, can

guide pharmacological and surgical treatment according to the

individual status of the patient. Multimodality monitoring ofmore than one parameter can help overcome some of the limi-

tations of each method used.

Intracranial pressure monitoring

The guidelines for the Management of Severe Head Injury suggest

that ICP monitoring is indicated in head-injury patients with

a Glasgow Coma Scale (GCS) score between 3 and 8 and with an

abnormal CT scan. ICP monitoring in patients with a normal CT

scan andwithtwo or more of thefollowing risk factors is suggested:

age over 40 years

motor posturing

systolic BP less than 90 mmHg.

Patients at risk of elevated ICP requiring general anaesthesiashould also have ICP monitoring. Derived values from ICP and its

waveform give useful information.

Estimation of the pressureevolume compensatory reserve of

the brain can be calculated by correlating the amplitude of the

ICP pulse waveform with the mean ICP; and

The cerebrovascular pressureereactivity index is calculated

by correlation of the ICP response to slow spontaneous changes

in arterial blood pressure. This can be used to assess distur-

bances of cerebral autoregulation.

There are four main anatomical sites used in the measurement of

ICP: intraventricular, intraparenchymal, subarachnoid and

epidural. Non-invasive and metabolic monitoring of ICP has also

been studied, but the clinical value of these methods is currently

unclear. Each technique has advantages and disadvantages and

requires a unique monitoring system. Intraventricular monitors

are considered the gold standard of invasive ICP monitoring

catheters.A number of non-invasive devices to record ICP have been

studied, but none have demonstrated reproducible clinical success.

However, tissue resonance analysis (TRA), an ultrasound-based

method, has shown good correlation with invasive techniques.

Other non-invasive techniques include transcranial Doppler, which

estimates ICP from changes in the waveform that occur in response

to increased resistance to CBF. Intraocular pressure and tympanic

membrane displacement may also prove valuable in monitoring

ICP.

Cerebral haemodynamics

Transcranial Doppler ultrasonography measures blood flow

velocity (cm/second) in the cerebral arterial system both non-invasively and continuously. It allows discrimination of changes

in CBF and has several uses in anaesthesia and critical care. It

determines the quality of collateral circulation and detects

microemboli in carotid surgery. It can also differentiate between

vasospasm and hyperaemia in brain injury and subarachnoid

haemorrhage.

Cerebral oxygenation and metabolism

The metabolic state of the brain can be assessed using jugular

venous oxygen saturation (SjvO2) monitoring by cannulating the

internal jugular vein in a retrograde direction with a spectrophoto-

metric probe. This method uses the Fick principle to monitorregional oxygen consumption. Low SjvO2 may be due to increased

oxygen extraction or increased oxygen demand. High SjvO2 may

occur with abnormally high CBF due to loss of autoregulation or

high ICP causing shunting of blood past capillary beds. Normal

SjvO2 ranges from 55% to 71%.

Near-infrared spectroscopy is also used as a non-invasive

monitor of brain oxygenation. A forehead sensor shines

infrared light through the surface layers of the brain and the

light that re-emerges is sensed by a detector system. A

computer algorithm based upon the BeereLambert law is used

to display concentrations of oxygenated and deoxygenated

blood.

Invasive brain tissue oximetry is available to measure brainoxygen levels directly. Thistechnique uses a polarographic or fibre-

optic probe to measure local changes in regional oxygenation.

Microdialysis can also be used to assess cerebral oxygenation.

It is achieved via a catheter inserted into the brain. The catheter

has a dialysis membrane on the outside and low flow rates of

dialysis fluid are passed through the catheter using a pump

mechanism. The concentration of any substance passing across

the dialysis membrane can be measured. This technique currently

remains a research tool. A

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