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Syncope from sustained orthostasis results from cerebral hypoperfusion associated with reductions in arterial pressure at the level of the brain (BPMCA) and reductions in arterial CO2 as reflected by end-tidal values (PetCO2). It was hypothesized that reductions in PetCO2 increase cerebrovascular tone before a drop in BPMCA that ultimately leads to syncope. Twelve men (21-42 yr of age) completed an orthostatic tolerance test consisting of head-up tilt and progressive lower body negative pressure to presyncope, before and after completing 5 days of continuous head-down bed rest (HDBR). Cerebral blood velocity (CBFV), BPMCA, and PetCO2 were continuously recorded throughout the test. Cerebrovascular indicators, cerebrovascular resistance, critical closing pressure (CrCP), and resistance area product (RAP), were calculated. Comparing from supine baseline to 6-10 min after the start of tilt, there were reductions in CBFV, PetCO2, BPMCA, and CrCP, an increase in RAP, and no change in cerebrovascular resistance index. Over the final 15 min before syncope in the pre-HDBR tests, CBFV and CrCP were significantly related to changes in PetCO2 (r = 0.69 ± 0.17 and r = 0.63 ± 0.20, respectively), and BPMCA, which was not reduced until the last minute of the test, was correlated with a reduction in RAP (r = 0.91 ± 0.09). Post-HDBR, tilt tolerance was markedly reduced, and changes in CBFV were dominated by a greater reduction in BPMCA with no relationships to PetCO2. Therefore, pre-HDBR, changes in PetCO2 with orthostasis contributed to increases in cerebrovascular tone and reductions in CBFV during the progression toward syncope, whereas, after 5 days of HDBR, orthostatic responses were dominated by changes in BPMCA. [ABSTRACT FROM AUTHOR]

Reductions in end-tidal PCO2 (PETCO2) during upright posture have been suggested to be the result of hyperventilation and the cause of decreases in cerebral blood flow (CBF). The goal of this study was to determine whether decreases in PETCO2 reflected decreases in arterial PCO2 (PaCO2) and their relation to increases in alveolar ventilation (VA) and decreases in CBF. Fifteen healthy subjects (10 women and S men) were subjected to a 10-mm head-up tilt (HUT) protocol. PaCO2, VA, and cerebral flow velocity (CFV) in the middle and anterior cerebral arteries were examined. In 12 subjects who completed the protocol, reductions in PETCO2 and PaCO2 (-1.7 ± 0.5 and -1.1 ± 0.4 mmHg, P < 0.05) during minute 1 of HUT were associated with a significant increase in VA (+0.7 ± 0.3 1/mm, P < 0.05). However, further decreases in PaCO2 (-0.5 ± 0.5 mmHg, P < 0.05), from minute 1 to the last minute of HUT, occurred even though VA did not change significantly (-0.2 ± 0.3 1/mm, P = not significant). Similarly, CFV in the middle and anterior cerebral arteries decreased (-7 ± 2 and -8 ± 2%, P < 0.05) from minute 1 to the last minute of HUT, despite minimal changes in PaCO2. These data suggest that decreases in PIETCO2, and PaCO2 during upright posture are not solely due to increased VA but could be due to ventilation-perfusion mismatch or a redistribution of CO2 stores. Furthermore, the reduction in PaCO2 did not fully explain the decrease in CFV throughout HUT. These data suggest that factors in addition to a reduction in PaCO2 play a role in the CBF response to orthostatic stress. [ABSTRACT FROM AUTHOR]

Reductions in end-tidal PCO2 (PETCO2) during upright posture have been suggested to be the result of hyperventilation and the cause of decreases in cerebral blood flow (CBF). The goal of this study was to determine whether decreases in PETCO2 reflected decreases in arterial PCO2 (PaCO2) and their relation to increases in alveolar ventilation (VA) and decreases in CBF. Fifteen healthy subjects (10 women and S men) were subjected to a 10-mm head-up tilt (HUT) protocol. PaCO2, VA, and cerebral flow velocity (CFV) in the middle and anterior cerebral arteries were examined. In 12 subjects who completed the protocol, reductions in PETCO2 and PaCO2 (-1.7 ± 0.5 and -1.1 ± 0.4 mmHg, P < 0.05) during minute 1 of HUT were associated with a significant increase in VA (+0.7 ± 0.3 1/mm, P < 0.05). However, further decreases in PaCO2 (-0.5 ± 0.5 mmHg, P < 0.05), from minute 1 to the last minute of HUT, occurred even though VA did not change significantly (-0.2 ± 0.3 1/mm, P = not significant). Similarly, CFV in the middle and anterior cerebral arteries decreased (-7 ± 2 and -8 ± 2%, P < 0.05) from minute 1 to the last minute of HUT, despite minimal changes in PaCO2. These data suggest that decreases in PIETCO2, and PaCO2 during upright posture are not solely due to increased VA but could be due to ventilation-perfusion mismatch or a redistribution of CO2 stores. Furthermore, the reduction in PaCO2 did not fully explain the decrease in CFV throughout HUT. These data suggest that factors in addition to a reduction in PaCO2 play a role in the CBF response to orthostatic stress. [ABSTRACT FROM AUTHOR]