Cerebral Physiology — CBF, CMRO2, Autoregulation, CO2 Reactivity, Monro-Kellie

Brain receives ~15% of cardiac output (~750 mL/min in a 70 kg adult).

Cerebral metabolic rate of oxygen consumption (CMRO2) = 3.5 mL O2/100 g/min (~20% of total body O2 consumption despite being 2% of body weight).

60% of CMRO2 is electrical activity (suppressible by anesthetics); 40% is cellular maintenance (NOT suppressible — irreducible floor).

Flow-metabolism coupling: under physiologic conditions, CBF tracks CMRO2 closely via local metabolic regulation (CO2, H+, adenosine, NO, K+).

Anesthetics that suppress CMRO2 (propofol, barbiturates, etomidate) also reduce CBF proportionally — useful for neuroprotection at intentional EEG burst suppression.

Cerebral autoregulation maintains CBF nearly constant across mean arterial pressure (MAP) 50-150 mmHg via myogenic + metabolic + neurogenic mechanisms — arterioles constrict at high MAP, dilate at low MAP.

Above 150 or below 50, autoregulation fails + CBF becomes pressure-passive.

Chronic hypertension RIGHT-SHIFTS the curve to ~70-170 — these patients become symptomatic at MAP 60-70 even though that's 'normal,' and tolerate higher pressures without symptoms.

Acute treatment of severe HTN should not drop MAP >25% in first hour — risk of border-zone ischemia.

With impaired autoregulation, CBF becomes pressure-passive → tight MAP control matters more.

Mechanism: extracellular [H+] in brain ECF, mediated via perivascular arteriolar smooth muscle.

Acute hyperventilation to PaCO2 30-35 reduces CBF + ICP within minutes — useful for transient herniation rescue.

Effect WANES over 6-12 hours as bicarbonate is buffered out of CSF; sustained hyperventilation no longer reduces ICP + can cause rebound vasodilation when CO2 normalizes.

Avoid prophylactic hyperventilation <30 mmHg in TBI (Brain Trauma Foundation 4e) — risk of ischemia.

PaO2 reactivity: CBF rises only when PaO2 falls <50 mmHg (steep rise below that); within-normal-range O2 has minimal effect on CBF.

CPP <50 risks ischemia; CPP >70 may worsen ARDS-like cerebral edema.

ICP measurement gold standard: intraventricular catheter (also therapeutic — can drain CSF).

Total volume is fixed; an increase in one component (mass, edema, hemorrhage, CSF) must be compensated by reduction of another or ICP rises.

Once compensatory reserve exhausted, small further volume increases cause STEEP nonlinear ICP rises (intracranial pressure-volume curve). 'Tight brain' or 'full brain' in OR signals exhausted compensation; immediate interventions: head elevation 30°, neck neutral (jugular outflow), hyperventilation to PaCO2 30-35 (temporizing), mannitol 0.25-1 g/kg or hypertonic saline 3% 250 mL or 23.4% 30 mL, deepen anesthesia, drain CSF if EVD present, surgical decompression.

The ischemic penumbra is tissue between 10 and 22 — viable if reperfused, dead if not.

Time-is-brain — every minute of LAO stroke loses ~1.9 million neurons.

Neuroprotection during temporary aneurysm clipping or carotid clamping: maintain MAP at high-normal or 20% above baseline (collateral flow), mild hypothermia 33-34°C is controversial (IHAST trial showed no benefit in aneurysm surgery), propofol burst suppression (reduces CMRO2 ~50% — questionable clinical benefit), avoid hyperglycemia (target 140-180), avoid hyperthermia, supplemental O2.

Uncal (transtentorial) herniation: medial temporal lobe pushed through tentorial notch → ipsilateral CN III compression (blown pupil), contralateral hemiparesis, then contralateral pupil + decerebrate posturing.

Subfalcine: cingulate gyrus under falx → contralateral leg weakness, less acute but signals mass effect.

Emergency response to acute herniation: head up 30°, hyperventilate to PaCO2 30, hypertonic saline 23.4% 30 mL IV bolus or mannitol 1 g/kg, call neurosurgery for emergent decompression, deepen anesthesia, paralyze, ensure MAP supports CPP 60-70.