Doppler study of middle cerebral artery blood flow velocity and cerebral autoregulation during a simulated ascent of Mount Everest.

OBJECTIVE

To explore cerebral hemodynamics in 8 healthy volunteers in a hypobaric chamber up to the altitude of Mount Everest after a progressive stepwise decompression to 8,848 m.

METHODS

Physiological, clinical, and transcranial Doppler data were collected after at least 3 days at 5,000, 6,000, and 7,000 m and within 4 hours of reaching 8,000 m and returning to sea level.

RESULTS

Three subjects were excluded at 8,000 and 8,848 m because of acute neurological deficits. Heart rate increased; mean arterial pressure remained stable; PaO2 and PaCO2 decreased with altitude; hemoglobin (Hb) and hematocrit (Ht) increased; arterial O2 content decreased over 6,000 m; middle cerebral artery blood flow velocity (MCAv) increased only during acute exposure to 8,000 m; and the corresponding pulsatility (PI) and resistivity indices (RI) decreased over 5,000 m. PI and RI correlated with heart rate. The transient hyperemic response (THR) of MCAv to common carotid compression was depressed at 8,000 m.

CONCLUSIONS

At 8,000 m, the increase in MCAv seemed to reflect the normal hemodynamic response to acute hypoxia. The decrease of THR at this altitude could be an indication of impaired cerebral autoregulation. The role of impaired cerebral autoregulation in the genesis of acute neurologic deficits, observed at 8,000 m and above in 3 subjects, remains speculative.