A. The brain uses more oxygen and glucose per 100 g of tissue than any large organ and is completely dependent on uninterrupted cerebral blood flow (CBF) (i.e., has no appreciable reserves of oxygen and glucose).

B. Clinical monitoring directed toward early detection and reversal of potentially dangerous conditions.

C. Neurologic monitoring falls into two distinct categories.

1. Electroencephalography (EEG) and evoked potentials (EPs): define a qualitative threshold consistent with the onset of cerebral ischemia.

2. Monitors of intracranial pressure (ICP), CBF, and cerebral metabolism: provide quantitative physiologic information.

D. Cerebral ischemia: defined as cerebral oxygen delivery (CdO₂) insufficient to meet metabolic needs.

E. CdO₂ components: CBF, hemoglobin concentration, arterial hemoglobin saturation (SaO₂).

A. Systemic monitoring.

1. Pulse oximetry (SpO₂) and blood pressure (BP) provide clues about the adequacy of global brain oxygenation.

2. Cerebral perfusion pressure (CPP = mean arterial pressure [MAP] − ICP) does not alter CBF over a range of pressures of approximately 50 to 150 mm Hg.

3. PaCO₂ regulates cerebral vascular resistance over a range of 20 to 80 mm Hg.

4. CBF is acutely halved if PaCO₂ is halved, and it is doubled if PaCO₂ is doubled.

5. A decreasing arterial O₂ content (CaO₂), resulting from a decrease in hemoglobin or in SaO₂, normally causes CBF to increase.

B. Neurologic examination.

1. Neurologic examination quantifies three key characteristics: level of consciousness, focal brain dysfunction, and trends in neurologic function.

2. The Glasgow Coma Scale (GCS), originally developed as a prognostic tool, has become a quick, reproducible estimate of level of consciousness (Table 15-1).