Reference

Anatomy & Physiology

The mechanisms underneath the monitoring. Each section explains what is physically happening, then what it means for a decision at the bedside.

The Monro–Kellie doctrine

The adult skull is a closed box of fixed volume. Inside it sit three things: brain tissue (roughly 80% of the volume), blood (about 10%) and cerebrospinal fluid (about 10%). Because the container cannot expand, the sum of those three volumes is constant.

The consequence is the whole of neurocritical care in one sentence: anything that adds volume must be matched by something else giving way, or the pressure rises. A growing haematoma is accommodated first by squeezing CSF out into the spinal subarachnoid space, then by reducing cerebral venous blood volume. Both buffers are small, and once they are spent the pressure climbs steeply.

Intracranial compliance

Compliance is the change in volume tolerated per unit change in pressure. Plotted out, the intracranial pressure–volume relationship is not a straight line but a hockey stick: nearly flat while the buffers hold, then turning sharply upward once they are exhausted.

This explains an otherwise puzzling bedside observation — a patient can sit at an unremarkable pressure for hours and then deteriorate over minutes. Nothing about the rate of the underlying process changed. The patient simply moved from the flat part of the curve to the steep part.

Cerebral perfusion pressure

Perfusion of the brain depends on the pressure gradient across it, not on systemic blood pressure alone:

CPP = MAP − ICP

A patient with a MAP of 80 and an ICP of 25 has a CPP of 55, despite a blood pressure that looks entirely reasonable. Raising the MAP and lowering the ICP are the only two levers available, and in most situations both are worth pulling.

Measurement technique matters more than it is usually given credit for. The arterial transducer should be levelled at the tragus (approximating the foramen of Monro) rather than the phlebostatic axis; levelling at the heart instead overstates CPP by roughly 10 mmHg in a head-up patient.

Cerebral autoregulation

A healthy brain holds cerebral blood flow roughly constant across a wide range of perfusion pressures — conventionally quoted as about 50 to 150 mmHg — by constricting and dilating its arterioles. Outside that range, flow follows pressure passively: too little and the tissue is ischaemic, too much and you get hyperaemia, oedema and haemorrhage.

Two important qualifications:

• The curve shifts. Chronic hypertension moves it to the right, so a "normal" pressure may be inadequate for that patient.
• Injury impairs it. After traumatic brain injury, subarachnoid haemorrhage or hypoxic injury, autoregulation may be regionally or globally lost — leaving flow directly pressure-dependent in exactly the patients in whom that is most dangerous.

Determinants of cerebral blood flow

Four factors dominate, and three are directly manipulable:

Venous drainage

Outflow obstruction is the most easily missed cause of a rising ICP, and the cheapest to fix. Cerebral venous blood leaves via the jugular system, and anything that impedes it raises intracranial volume directly.

• Head-up positioning of about 30° aids drainage.
• Keep the head midline; neck rotation kinks jugular outflow.
• Check that collars and tube ties are not compressing the neck.
• High intrathoracic pressure — coughing, ventilator dyssynchrony, high PEEP in a hypovolaemic patient — transmits backward and impedes drainage.

Before escalating to osmotherapy, it is worth confirming that none of these is the actual problem.

Herniation syndromes

When pressure gradients develop between compartments, brain tissue is displaced across the fixed dural and bony boundaries. Recognising the pattern localises the lesion:

• Uncal (transtentorial): the medial temporal lobe compresses the third cranial nerve and midbrain — a fixed, dilated pupil on the side of the lesion, then contralateral weakness and falling consciousness.
• Central: downward displacement of the diencephalon, producing a rostral-to-caudal deterioration in consciousness, pupils and breathing pattern.
• Subfalcine: the cingulate gyrus passes under the falx, which may compress the anterior cerebral artery and cause leg-predominant weakness.
• Tonsillar: the cerebellar tonsils descend through the foramen magnum onto the medulla — Cushing's triad (hypertension, bradycardia, irregular respiration) and respiratory arrest.