Neurocritical Care Fundamentals and Neurophysiology
Core physiology to master
Monro-Kellie doctrine governs everything intracranial: brain, blood, and CSF share a fixed volume, so any added volume (edema, hematoma, hydrocephalus) must displace another or raise ICP. Understand the pressure-volume curve - compliance falls steeply as ICP rises, so small volume changes near the steep portion cause large ICP swings. Cerebral perfusion pressure (CPP) = MAP − ICP; remember MAP is the driver and ICP is the back-pressure.
Cerebral autoregulation normally maintains constant CBF across MAP ~60–150 mmHg but is impaired in acute injury, making perfusion pressure-dependent. Know that hyperventilation lowers PaCO2, causing cerebral vasoconstriction and reduced CBF - a temporizing, not therapeutic, maneuver because it risks ischemia. CO2 reactivity, the CBF response to PaCO2 (~3% per mmHg), is a favorite question target.
Traps
- Confusing ICP waveform components (P1 arterial, P2 compliance, P3 venous); a rising P2 relative to P1 signals poor compliance.
- Assuming a normal CPP means adequate perfusion - in impaired autoregulation, local ischemia can occur despite normal global numbers.
- Forgetting that the brain relies on continuous glucose and oxygen delivery; hypoxia and hypoglycemia both cause secondary injury.
Rule of thumb
If MAP falls or ICP rises, CPP falls - always recalculate rather than eyeballing. A MAP of 80 with ICP 25 gives CPP 55, below typical targets of 60–70.
Worked example
MAP 70, ICP 20 → CPP 50. Raising MAP to 90 (e.g., vasopressor) restores CPP to 70 without touching ICP - the preferred first move when ICP is not critically elevated.