Physiology
Cerebral blood flow and intracranial pressure

https://doi.org/10.1016/j.mpaic.2011.02.010Get rights and content

Abstract

The Monro–Kellie 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 5–13 mmHg, with minor cyclical variations owing to the effects of the arterial pressure waveform and respiration. 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 pressure of carbon dioxide in arterial blood (PaCO2) and CBF is almost linear. CBF increases by 25% for each kPa increase in PaCO2. Hypoxia (PaO2 <6.7 kPa) is also a potent stimulus for increasing CBF. The brain is intolerant of hypo- or hyperperfusion and therefore requires a constant flow of blood over a range of pressures, which is achieved by autoregulation. Below the lower limit of autoregulation, CBF mirrors mean arterial pressure (MAP), and eventually a reduced flow causes cerebral ischaemia. Monitoring of the central nervous system, including measurements of neuronal function, ICP, CBF and cerebral oxygenation, can guide pharmacological and surgical treatment according to the individual status of the patient.

Section snippets

Brain

The brain has a mass of approximately 1400 g and consists of neural and supporting (glial) elements and intracellular and extracellular water. Tight junctions of the capillary endothelium and choroid plexus endothelium form the blood–brain barrier. In health, this maintains an environment suitable for nerve function and removes the need for lymphatic drainage of the brain. Pathological increases in brain tissue are the result of cell membrane failure with increased intracellular water

Cerebrospinal fluid

CSF is the clear fluid occupying the space between the arachnoid and pial layers of the meninges. CSF provides a constant supply of glucose, maintains a chemically stable environment, and supports the transport of metabolites and neurotransmitters. It bathes the spinal cord as well as the brain, which in effect floats within the CSF with a resultant effective weight reduction of approximately 97%. CSF reduces the effects of mechanical forces on the brain by displacing in response to linear and

Blood

The brain is supplied with blood via the internal carotid and vertebral arteries. Venous drainage is via the cerebral veins, sinuses and internal jugular veins. Under normal conditions there is approximately 150 ml of blood in the skull, most of which (about 100 ml) is within the venous system. Although cerebral blood volume (CBV) is small, cerebral blood flow (CBF) is relatively high compared with other organs. Normal global CBF is about 50 ml/100 g/minute, grey matter receiving 80 ml/100

Intracranial pressure

The relationship between the volumes of brain tissue, CSF and blood gives rise to the intracranial pressure (ICP). In the normal adult, the ICP is 5–13 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

Control of cerebral blood flow

Several protective mechanisms control CBF. The brain is intolerant 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

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 thought to be mediated by changes in hydrogen ion

Oxygen

Hypoxia (PaO2 <6.7 kPa) is a potent stimulus for increasing CBF. It causes a rapid increase in CBF secondary to the development of a metabolic acidosis. The effects of hyperoxia on CBF were classically described by Kety and Schmidt, who demonstrated a 13% decrease in CBF with FiO2 85–100% attributed to an increase in cerebral vascular resistance. More recent studies have confirmed a reduction in CBF by up to 30% with inspired oxygen concentrations of 100%.

Autoregulation

The effective perfusion pressure of the brain is the difference between the mean arterial pressure (MAP) and the ICP, termed the cerebral perfusion pressure (CPP). There is an additional component to the calculation, further subtracting the jugular bulb pressure (effective venous pressure) from the MAP, but this is usually omitted as being insignificant clinically.CPP=MAP−ICP

The brain is intolerant of hypo- or hyperperfusion, and therefore requires a constant flow of blood over a wide range of

Autonomic nervous system

The cerebral vasculature is innervated by the autonomic nervous system. The sympathetic supply to the extraparenchymal vessels 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

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 haematocrit 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 20–25 ml/100 g/minute, and this is accompanied by slowing of electrical activity on electroencephalography (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 measurements of neuronal function, CBF and cerebral oxygenation, can guide pharmacological and surgical treatment according to the individual status of the patient. Multimodality monitoring of more than one parameter can help overcome some of the limitations 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 and with two or more of the following risk factors is suggested:

  • •

    age over 40 years

  • •

    motor posturing

  • •

    systolic BP less than 90 mmHg.

Patients at risk of elevated ICP requiring general anaesthesia should also have ICP monitoring. Derived values from 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 spectrophotometric probe. This method uses the Fick principle to monitor regional 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.

References (0)

View full text
Copyright © 2011 Published by Elsevier Ltd.