NEUROSURGICAL ANAESTHESIA

Applied cerebral physiology

Christopher Taylor Nicholas Hirsch

Learning objectives
After reading this article, you should understand the: C importance of an uninterrupted supply of oxygen and glucose for normal cerebral metabolism C fundamentals of the regulation and measurement of cerebral blood ow C concept of intracranial pressure and how it affects cerebral perfusion pressure.

Abstract
The brain uses large amounts of glucose for its basal energy requirements, and these are further increased during cerebral activation. In order that glucose can provide this energy, a plentiful and uninterrupted supply of oxygen is necessary. Cerebral blood ow is therefore critical for normal cerebral function. Its control is dictated by local intrinsic metabolic needs as well as extraneous factors such as arterial blood pressure, arterial carbon dioxide and oxygen tension, temperature and neural factors. This article reviews cerebral metabolism and cerebral blood ow and techniques by which both can be monitored.

Keywords Cerebral autoregulation; cerebral blood ow; cerebral metabolism; intracranial pressure

Cerebral metabolism and blood ow

The primary function of the brain is the generation of nerve action potentials in response to stimulation, and this function is affected by the movement of ions against electrical gradients and the release and regeneration of neurotransmitters at synapses. These functions require a large amount of energy in the form of adenosine triphosphate (ATP). Under normal conditions, the metabolic fuel is almost exclusively glucose and an appropriate supply of oxygen is needed for the oxidative processes involved. This article outlines the mechanisms by which the brain receives its vital supply of glucose and oxygen and balances these against its demands (Table 1). Cerebral metabolism Mass for mass, the brain consumes more energy than any other tissue in the body. Under basal conditions, about 60% of this energy is used to fuel the Na/K-ATPase ion pumps, which maintain the ionic gradients across neuronal membranes. During increased neuronal activity, this demand is further

increased. Glucose is the major source of this energy and thus, under normal conditions the brains respiratory quotient is approximately 1. It enters the brain by active transport across the bloodebrain barrier via the transporter GLUT 1 in cerebral capillaries and is then distributed to the cells of the central nervous system (CNS) by various transporter molecules (i.e. GLUT 1 to astrocytes, GLUT 3 to neurones and GLUT 5 to microglial cells). These glucose transporters are up-regulated in hypoxic conditions. Glucose uptake is high in brain tissue and the cerebral metabolic rate for glucose (CMRGl) is about 30 mg/ 100 g/min, which represents approximately 25% of the bodys total glucose consumption. Whilst the level of the brains glucose requirement is impressive, its reserves are not. Hypoglycaemia soon results in cerebral cellular dysfunction, manifested as anxiety and confusion, which soon progresses to convulsions and coma. The symptoms seen reect the greater susceptibility of cortical structures to hypoglycaemia compared with the brainstem. Whilst cerebral cells do contain glycogen, this (and all available glucose) is exhausted within 2 min if cerebral blood ow (CBF) ceases. Following uptake into cerebral cells, about 70% of the glucose is oxidized to carbon dioxide and water in the glycolytic and tricarboxylic acid (TCA) pathways, and together with oxidative phosphorylation within mitochondria, provides the ATP necessary for energy supplies. The remainder is converted to amino acids, proteins and lipids. Under hypoxic conditions astrocytes metabolize glucose anaerobically by glycolysis to form lactate, generating enough

Normal cerebral physiological values

Christopher Taylor MRCP FRCA is a Consultant Neuroanaesthetist at the National Hospital for Neurology and Neurosurgery, London. He qualied from University College London medical school in 1996. He has a specialist interest in neuroanaesthesia and neurocritical care medicine. Conicts of interest: none declared. Nicholas Hirsch FRCA FRCP is a Consultant Neuroanaesthetist at the National Hospital for Neurology and Neurosurgery, London, and Honorary Lecturer at the Institute of Neurology. He qualied from Guys Hospital in 1978 and trained in anaesthesia in London and at Yale University. His research interests involve neuroanaesthesia and neurocritical care medicine. Conicts of interest: none declared. CBF CBF (global) Grey matter White matter CMRO2 (grey matter) CMRO2 (white matter) CMRGl (global) 750 ml/min or 15% of cardiac output 50 ml/100 g/min 90 ml/100 g/min 20 ml/100 g/min 3 ml/100 g/min 1 ml/100 g/min 30 mg/100 g/min or 25% of total body consumption

CBF, cerebral blood ow; CMRO2, cerebral metabolic rate for oxygen; CMRGl, cerebral metabolic rate for glucose.

Table 1

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ATP to allow glutamate uptake. The lactate released into the extracellular space is actively taken up by neurones and converted to pyruvate, which then enters the tricarboxylic acid (TCA) cycle to generate more energy aerobically. This lactate is thought to be a vital energy substrate during neuronal activation and for recovery of synaptic function following hypoxic injury; it has a monocarboxylate transporter (similar to glucose), which allows active transport across the bloodebrain barrier. During prolonged fasting the brain uses ketone bodies (end products of fatty acid metabolism in the liver) as an alternative fuel. They are exported from the liver and actively taken up by the brain. There, they are broken down to acetyl coenzyme A (acetyl-CoA), which is oxidized via the TCA cycle to yield energy. Under such conditions the brain is capable of regenerating glucose (gluconeogenesis) from alternative substrates such as glycerol, glutamine and glycine. Cerebral blood ow Normal aerobic cerebral metabolism requires a plentiful and uninterrupted supply of oxygen. Blood reaches the brain via the anterior paired internal carotid arteries and posterior paired vertebral arteries. About 70% of the total CBF is supplied by the carotid arteries. These anterior and posterior circulations are joined at the circle of Willis in the base of the brain but it is important to note that this anastomosis is incomplete in 50% of individuals. Although the brain constitutes only 2% of the total body mass, it receives 15% of the cardiac output (750 ml/min in adults). Resting CBF is approximately 50 ml/100 g/min. The ow is not evenly distributed. Grey matter, which is metabolically more active, receives approximately 90 ml/100 g/min and in these regions the rate of oxygen consumption, termed the cerebral metabolic rate for oxygen (CMRO2), is about 3 ml/100 g/ min. White matter receives about 20 ml/100 g/min and its CMRO2 is approximately 1 ml/100 g/min. The level of CBF is critical. Complete interruption of CBF produces loss of consciousness within seconds as does a reduction of CBF to approximately 20 ml/100 g/min. Neuronal conversion to anaerobic metabolism occurs below 18 ml/100 g/min and the electroencephalogram becomes at. Brain cell death (infarction) takes place at about 3 h with ows of 10 ml/100 g/min and after 30 min at ows of 5 ml/100 g/min. Cerebral perfusion pressure (CPP) The perfusion pressure (i.e. the arteriovenous pressure gradient) in the brain is more complex than that of other organs because it is conned within an incompressible vault. It is dependent on the pressure difference between the mean arterial pressure (MAP) or the driving pressure (measured at brain level) and the intracranial pressure (ICP) or the pressure that needs to be overcome to supply adequate blood to the brain. This pressure difference is known as the CPP. A normal CPP is 70e80 mmHg; the threshold for critical ischaemia is 30e40 mmHg. As can be seen from the equation below, even at normal levels of MAP, an elevated ICP of more than 20 mmHg will compromise CPP and therefore reduce cerebral blood ow. This emphasizes the importance of maintaining an adequate MAP in circumstances such as head injury to ensure adequate perfusion.

Cerebral Perfusion Pressure Mean Arterial Pressure Intracranial Pressure

Intracranial pressure The contents of the skull are brain parenchyma (80%), blood (9%), CSF (6%) and interstitial uid (5%). After fusion of the cranial sutures, the brain becomes contained within a rigid bone box. Normal intracranial pressure is 7e12 mmHg and is determined by the balance between the rate of CSF formation and absorption (the latter depending on the venous sinus pressure and the resistance of the arachnoid villi). ICP is a dynamic pressure and uctuations occur with arterial pulsations, position, respiration, coughing and straining (Figure 1). The MonroeKellie doctrine states that because intracranial volume is xed, an increase in volume of one of the components contained within the skull, unless accompanied by a reduction in volume of the other components, will lead to a rise in ICP. Initially, as the brain volume increases, compensation occurs by movement of CSF into the spinal compartment, accompanied by an increase in absorption, a decrease in CSF production and a reduction in cerebral blood volume; this limits the rise in ICP. However, as these compensatory mechanisms are overwhelmed, intracranial compliance falls, and ICP rises dramatically with further small increases in intracranial volume (Figure 2). Eventually, if unchecked, rises in ICP will cause brainstem compression with hypertension, bradycardia and irregular respiration (Cushings reex). Anaesthetists institute various methods to reduce ICP acutely in high-risk patients with critically high ICPs. With the exception of

Dynamic intracranial pressure (ICP) trace

15

10

ICP (mmHg)

Cardiac pulsation Respiratory variation

Time (seconds)
Figure 1

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Intracranial pressure-volume curve

30

ICP (mmHg)

P2
20

P1
10

V2

V1

Intracranial volume (arbitrary units)

ICP, intracranial pressure; P, pressure; V, volume

Figure 2

surgical CSF drainage or decompression, methods for the control of ICP depend on either reducing intracranial blood volume or reducing interstitial uid volume. Reduction of intracranial blood volume can be achieved by reducing arterial carbon dioxide tension (PaCO2), which promotes cerebral vessel vasoconstriction, or by increasing venous drainage with a head-up position and providing adequate sedation and muscular relaxation, which reduce intrathoracic pressure. Interstitial uid volume reduction can be achieved by uid restriction or by the administration of diuretics (e.g. mannitol and furosemide) or corticosteroids. Conversely, poor anaesthetic technique may result in a dramatic rise in ICP in patients with existing raised ICP. CSF CSF is an ultraltrate of plasma that circulates freely throughout the cerebral ventricles and the central canal of the spinal cord. It is formed (and reabsorbed) at the rate of about 500 ml/day by energy-dependent and perfusion-related processes in the choroid plexuses and the cerebral ventricles. CSF then ows through the foramen of Monro to the third ventricle, into the fourth ventricle via the aqueduct of Sylvius and then into the cisterna magna and subarachnoid spaces via the medial foramen of Magendie and the lateral foramen of Luschka. Ultimately CSF is reabsorbed through the subarachnoid villi into the cerebral venous sinuses as a result of the pressure gradient between CSF and sinus (see article on Cerebrospinal Fluid and its Circulation, pp 355e356 of this issue). If the rate of formation of CSF exceeds the rate of reabsorption (e.g. if blockage of the CSF circulation is present) hydrocephalus occurs and results in increased ICP. The bloodebrain barrier exists between the bloodstream and the CNS and prevents transfer of potentially harmful substances

reaching the brain. This semi-permeable barrier consists of three cellular layers: the vascular endothelium and its basement membrane, the astrocytes and pericytes. The endothelial cells have very few pinocytic vesicles and are sealed by tight junctions (zona occludens) with no anatomical gaps. This provides a high electrical resistance barrier. The existence of the bloodebrain barrier explains the difference between the constituents of plasma and CSF. CSF protein content is very low compared with plasma (0.2 versus 60 g/litre), and increased levels in CSF indicate disruption to the barrier. Similarly, concentrations of potassium, calcium, glucose, urea and lymphocytes are lower in CSF. The passage of substances across the bloodebrain barrier is directly proportional to their lipid solubility and is facilitated by active transport mechanisms but is inversely proportional to molecular weight, ionic charge and degree of plasmaeprotein binding. Lipophilic substances (carbon dioxide, oxygen, volatile anaesthetic agents) pass freely, unlike large-molecular-weight molecules (e.g. proteins) and highly charged moieties (e.g. sodium ions). Proteins and drugs (e.g. penicillin) cannot cross the barrier unless it is inamed (e.g. in meningitis). The integrity of the barrier can be examined by the intravenous injection of radioactive isotopes bound to protein; scanning techniques can then be used to determine whether the radioactive label is escaping from cerebral vessels. Ruptured aneurysms and increased permeability at tumour sites may be detected using such techniques. Water moves freely across the bloodebrain barrier, depending on osmotic gradients. Sudden changes in plasma osmolality secondary to changes in electrolyte or glucose concentrations can therefore lead to potentially problematic uid shifts in the brain. This emphasizes the importance of correcting sodium and glucose abnormalities slowly. The bloodebrain barrier is disrupted by a number of processes, including hypertension, stroke, trauma, status epilepticus, hypercarbia, hypoxia, and especially inammation (chemical, infective or autoimmune). When disruption occurs, uid movement becomes largely dependent on hydrostatic gradients.

Control of cerebral blood ow

Various mechanisms exist that allow an adequate basal CBF to supply the substrate demands of the brain. However, in addition, local regulatory mechanisms direct blood ow to regions of the brain that are particularly active (i.e. blood ow is coupled to local metabolic needs). Furthermore, other physiological variables inuence CBF (Box 1). Flowemetabolism coupling and local chemical regulators Local neuronal activity causes an increase in CMRO2 and CMRGl and is accompanied by an increased regional CBF to match glucose and oxygen use with delivery. The parallel change in CBF with CMRO2 and CMRGl is known as owemetabolism coupling. There is evidence to suggest that CBF may be modulated by changes in glucose consumption rather than oxygen consumption under hypoxic conditions. The regulatory changes involved in owemetabolism coupling have a short latency (about 1 second), where transient changes in the concentration of local metabolic mediators seem to determine the ne control of regional CBF by affecting vascular tone.

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Factors inuencing cerebral blood ow

Local neuronal activity Autoregulation Raised intracranial pressure Arterial carbon dioxide tension (PaCO2) Arterial oxygen tension (PaO2) Haematocrit Temperature Autonomic nervous system regulation

Autoregulation
Vessel diameter

CVR

CBF (ml/100 g/min)

CBF
50 4.0

CBV (ml/100 g)

Box 1

Vasoconstriction occurs by the action of free calcium ions, thromboxane (a product of arachidonic acid/endoperoxidase metabolism) and endothelin (secreted by endothelial cells by endothelin-converting enzyme acting on endothelinA receptors in vascular smooth muscle). Some calcium-channel blockers blunt hypoxic vasodilatation and prevent adenosine release. Potent vasodilators include perivascular potassium (released in high concentrations during seizures, hypoxia, and electrical stimulation), adenosine, an ATP metabolite (in response to arterial hypotension and hypoxia), as well as prostaglandins (e.g. PGE2 and prostacyclin (PGI2)), lactate, acetylcholine, serotonin, substance P and nitric oxide. Nitric oxide is synthesized by endothelial cells and then diffuses into the smooth muscle layer inducing cyclic guanosine monophosphate (GMP) production, leading to smooth muscle relaxation and hence cerebral vessel vasodilatation. There is evidence to suggest that it is released in response to excitatory amino acid release, hypercapnoea, ischaemia, subarachnoid haemorrhage and volatile anaesthetic agents. Autoregulation Autoregulation is the maintenance of a constant CBF despite variations in CPP. Under normal conditions when both ICP and cerebral venous pressure are low, systemic arterial perfusion pressure (i.e. MAP) becomes the primary determinant of CPP. Between a MAP of 50 mmHg and 150 mmHg the mean CBF remains constant at 50 ml/ 100 g/min. However, autoregulation has its physiological limits, above and below which CBF is directly related to perfusion pressure (Figure 3). Autoregulation is achieved by alterations in cerebrovascular resistance (CVR) (occurring over 10e60 seconds) caused by myogenic reexes to transmural tension in the resistance vessels; thus, as CPP increases from 50 to 150 mmHg, cerebral arterioles constrict and therefore restrict increases in CBF. Autoregulation may be modied by sympathetic nervous system activity. Thus, chronic hypertension or sympathetic stimulation shifts the autoregulatory curve to the right, whilst sympathetic blockade or cervical sympathectomy shifts the curve to the left. Symptoms of ischaemia occur only when the MAP falls below 60% of the lower autoregulatory limit. Above the upper autoregulatory limit, mechanisms such as forced cerebral arteriolar dilatation, reversal of hydrostatic gradients and cerebral oedema result in increases of cerebral blood volume and ICP. Autoregulation is disrupted in the presence of intracranial pathology, hypoxaemia, hypercarbia, xed vascular obstructions (e.g. carotid atheroma), and volatile anaesthetic agents.

CBV

0 0 50 100 150

CPP (mm Hg)

CBF, cerebral blood flow; CBV, cerebral blood volume; CPP, cerebral perfusion pressure; CVR, cerebrovascular resistance

Figure 3

Raised cerebral venous pressure An elevated cerebral venous pressure reduces cerebral venous drainage, expands cerebral blood volume, disrupts capillary Starlings forces leading to cerebral oedema, raises intracranial pressure and therefore reduces CBF. It may be caused by obstruction of venous drainage by neck compression from neck collars or tracheal tube ties, from head-down positioning (e.g. during central line insertion) or from increased intrathoracic pressure (e.g. from coughing, straining, incomplete muscle relaxation and the application of positive end-expiratory pressure during positive pressure ventilation). Arterial carbon dioxide tension Carbon dioxide is a potent vasodilator of cerebral blood vessels. As PaCO2 rises between 3.5 kPa (26 mmHg) and 8 kPa (60 mmHg) there is a linear increase in CBF (Figure 4). Above a PaCO2 of 8 kPa cerebral vessels are maximally dilated and no further increase in vessel diameter is possible; conversely, at a PaCO2 of 3 kPa cerebral vessels are maximally constricted. The effect of hypocarbia on cerebral vasculature is achieved by an increase in brain hydrogen ion (H) concentration, which takes place in minutes, reecting the time taken for the conversion of in the perivascular space. The vasoCO2 to HCO 3 and H constricting effect of a low PaCO2 is progressively attenuated by a fall in the brains bicarbonate level, which normalizes the pH. The opposite is true for prolonged hypercarbia. Arterial oxygen tension and oxygen content CBF is directly responsive to changes in oxygen delivery and remains unaltered until a threshold of an arterial oxygen tension (PaO2) of 6.8 kPa (50 mmHg) is reached. Below this threshold
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Effect of PaCO2 on cerebral blood flow

100

Haematocrit Haematocrit is the main determinant of blood viscosity and of oxygen content (and therefore oxygen delivery). CBF changes inversely with whole blood viscosity. Within the normal range of haematocrit, this has a minimal effect on CBF. However, in certain situations when CBF is pathologically decreased (e.g. cerebral vasospasm following subarachnoid haemorrhage), a decrease in haematocrit by haemodilution may improve CBF. Temperature Hypothermia (body temperature of less than 35  C) reduces CMRO2 and CMRGl, and as a result of owemetabolism coupling CBF decreases. The converse is true for hyperthermia up to a body temperature of 42  C, above which neuronal damage occurs as well as a corresponding reduction of oxygen uptake. For every 1  C change in body temperature CBF changes by 5%. At 18  C, the cerebral metabolic rate is so low that safe circulatory arrest (e.g. during cardiac surgery) is possible without causing ischaemic cerebral damage. This effect forms the basis of clinical trials of hypothermia in head injury and cerebrovascular surgery. Autonomic nervous system regulation Cerebrovascular vessels have a rich innervation. Large intracranial and pial vessels have a nerve supply originating from autonomic and sensory ganglia. These contain many vasoactive transmitters, which seem to have a role in the regulation of CBF. Although the exact function of the various neurones is difcult to dene, it seems that parasympathetic stimulation produces cerebral vasodilation and sympathetic stimulation produces vasoconstriction. Similarly, smaller intracerebral arterioles have rich innervation with many neurotransmitters.

CBF (ml/100 g/min)

50

20

0 0 3 kPa 8 kPa

PaCO2 (kPA)
CBF, cerebral blood flow; PaCO2, arterial carbon dioxide tension

Figure 4

CBF dramatically rises (Figure 5). This corresponds to the steep part of the oxyhaemoglobin dissociation curve (i.e. CBF is responsive not to PaO2 but to oxygen content). This effect explains the modest increase in CBF (an increase of 10%) when breathing 100% oxygen.

Measurement of cerebral blood ow

Effect of PaO2 on cerebral blood flow

100

A number of techniques for the measurement of CBF have emerged since the pioneering method of Kety and Schmidt in 1945. Many techniques now allow measurement of regional blood ow, giving useful information about changes in blood ow in diseased parts of the brain. KetyeSchmidt technique The Fick principle states that the blood ow through an organ can be measured by determining the amount of an inert substance (Q) removed from the bloodstream by the organ per unit time, and dividing that value by the difference between the concentration of the substance in arterial blood [A] and the concentration in the venous blood [V] from the organ. CBF Q A V

CBF (ml/100 g/min)

50

20

0 0 6.6

PaO2 (kPA)
CBF, cerebral metabolism blood flow; PaO2, arterial oxygen tension

Figure 5

Kety and Schmidt used nitrous oxide (N2O) as the inert substance. Patients breathed 15% N2O for 10 min whilst serial samples were taken from a peripheral artery and the jugular venous bulb and analysed for N2O content until equilibrium was reached. The total value of N2O taken up was determined by calculating the N2O content of jugular venous blood at equilibrium. This technique has a number of disadvantages: the N2O assay is time consuming and tedious and, when low CBF exists, the

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technique underestimates CBF. Most importantly, it gives a value for global CBF but not regional CBF. A variation of the KetyeSchmidt technique substitutes heat for the inert substance allowing a thermodilution principle to assess CBF. Xenon-133 wash-out Regional cortical blood ow can be measured by monitoring the decay of inhaled radioactive isotope xenon-133 using a battery of scintillation counters positioned over the head. The slope of the wash-out curve of the radioactive tracer is proportional to the CBF under the detector. The technique provides a two-dimensional analysis of regional CBF but primarily evaluates cortical blood ow. Three-dimensional resolution can be achieved using CT reconstruction in a technique called single-photon emission computed tomography (SPECT). Other imaging techniques Since metabolism is so tightly coupled to blood ow, the uptake of 2-deoxyglucose can be used to estimate regional blood ow. If 2-deoxyglucose is labelled with a positron emitter (e.g. oxygen-15, uorine-18, carbon-11), its uptake can be followed using positron emission tomography (PET) scanning and CBF can be estimated. Functional MRI (fMRI) can produce brain function maps, where changes in brain neuronal activity are reected in changes in regional CBF. Tomographic images can also be produced without the use of external contrast agents by a technique called blood oxygen-level dependent (BOLD) fMRI. Regional neuronal activation, especially in the cerebral cortex, triggers an inux of oxygenated haemoglobin that decreases the regional deoxyhaemoglobin levels, causing an increased MRI signal intensity. Transcranial Doppler ultrasonography (TCD) Transcranial Doppler ultrasonography (TCD) involves the application of a low-frequency (2 MHz) pulse range-gated ultrasound beam to the thin-boned transtemporal window, allowing assessment of the middle and anterior cerebral arteries. Flow velocities within these vessels can be determined using the Doppler effect. If the angle of the ultrasound beam and the diameter of the vessel remain constant, relative changes in ow velocity correlate closely with changes in CBF.

Intracerebral microdialysis This technique involves the insertion of a ne catheter, containing a dialysis membrane perfused with Ringers solution, into brain parenchyma. It enables molecules involved in cerebral metabolic pathways to be directly monitored and this can reveal information regarding the adequacy of cerebral oxygenation and blood ow. Metabolites such as glucose, pyruvate, lactate, glutamate and glycerol or drugs (e.g. phenytoin) diffuse into the solution of the probe from the interstitial uid (extracellular space) across the membrane and are analysed. The lactate:pyruvate ratio reects regional cerebral oxygen availability, and has been used clinically in the investigation of head injury and subarachnoid haemorrhage. A rise in the ratio suggests that anaerobic metabolism due to insufcient regional cerebral blood ow is occurring (secondary to hypoxia); treatment may then be taken to correct this impaired physiology. Cerebral oxygen partial pressure Sensors can be inserted into the brain parenchyma to measure the partial pressure of oxygen in the extra-cellular uid of the brain ( pBRO2); this reects the availability of oxygen for oxidative metabolism. Values obtained generally reect the balance between oxygen delivery and consumption. This technique is being used in research to optimize the treatment of subarachnoid haemorrhage and traumatic brain injury. Near infra-red spectroscopy This monitoring technique is based on the principle that light with wavelengths in the near infra-red region (650e900 mm) transmits through biological tissues, and is becoming increasingly used to image biological events in the cerebral cortex. Photons produced by a laser photodiode are directed into the skull, and whilst many are reected and dispersed, some are transmitted. Certain coloured compounds within the tissues (chromophores), especially oxyhaemoglobin, deoxyhaemoglobin and oxidized cytochrome oxidase, have characteristic absorption spectra. The emergent light intensity is detected and a computer converts the changes in light intensity into changes in chromophore concentration. Clinical applications of this technique include monitoring of cerebral oxygenation, CBF and volume. A

Measurement of cerebral oxygenation

Jugular bulb oximetry The jugular bulb is a dilatation of the internal jugular vein just below the base of the skull and may be catheterized using a Seldinger technique. Blood may be sampled for oxygen tension and saturation, giving an indication of CBF (lower values reecting greater uptake by the brain and therefore less blood ow, assuming O2 consumption remains constant). The major disadvantage of this technique is that only global CBF can be estimated and not regional changes. In addition, if CBF and oxygen consumption both decrease (e.g. in severe brain injury), jugular venous saturation may be unchanged.

FURTHER READING Barrett KE, Barman SM, Boitano S, Brooks H. Ganongs review of medical physiology. 23rd edn. New York: McGraw Hill Medical, 2009. Edvinsson L, Krause DN, eds. Cerebral blood ow and metabolism. Philadelphia: Lippincott, Williams and Wilkins, 2002. Matta BF, Menon DK, Turner JM, eds. Textbook of neuroanaesthesia and critical care. London: Greenwich Medical Media, 2000. Tisdall MM, Smith M. Multimodal monitoring in traumatic brain injury: current status and future directions. Br J Anaesth 2007; 99: 61e7.

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