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.
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.
Authors: Zachary M Smith; Erin Krizay; Rui Carlos Sá; Ethan T Li; Miriam Scadeng; Frank L Powell; David J Dubowitz Journal: J Appl Physiol (1985) Date: 2017-07-13
Authors: Edward A W Dyer; Susan R Hopkins; Joanna E Perthen; Richard B Buxton; David J Dubowitz Journal: Respir Physiol Neurobiol Date: 2007-10-26 Impact factor: 1.931
Authors: Mark H Wilson; Mark E G Edsell; Indran Davagnanam; Shashivadan P Hirani; Dan S Martin; Denny Z H Levett; John S Thornton; Xavier Golay; Lisa Strycharczuk; Stanton P Newman; Hugh E Montgomery; Mike P W Grocott; Christopher H E Imray Journal: J Cereb Blood Flow Metab Date: 2011-06-08 Impact factor: 6.200