Brain and muscle oxygen saturation during head-up-tilt-induced central hypovolaemia in humans.

Near-infrared spectrophotometry-determined cerebral (ScO2) and muscle oxygen saturations (SmO2) were followed in 15 volunteers during passive 50 degrees head-up-tilt-induced central hypovolaemia, and in nine volunteers during ventilatory manoeuvres affecting arterial carbon dioxide tension. During head-up tilt, mean arterial pressure [MAP, 88 (77-118) to 97 (80-136) mmHg, median and range] and heart rate [HR; 66 (49-77) to 87 (42-132) beats min-1 P < 0.01] increased, but after 22 (1-45) min they declined [to 61 (40-91) mmHg and 69 (38-109) beats min-1, respectively, P = 0.001] and pre-syncopal symptoms developed. Central hypovolaemia was indicated by an increased thoracic electrical impedance, and a decreased cardiac output and central venous oxygen saturation. The arterial oxygen saturation, pulmonal oxygen uptake and skin temperatures remained constant. The ScO2 remained stable at 72 (62-77)% until the pre-syncopal incidence, when it decreased to 62 (31-73)% (P = 0.001), and tilt down made it increase to 75 (36-87)% (P < 0.05) before the recovery value was established. In contrast, SmO2 decreased during tilting [75(70-87) to 65 (53-70)%], and recovered to 70 (53-83)%, P < 0.01) during the hypotensive episode. The end-tidal CO2 tension decreased only during tilt-up. The ScO2 decreased, and SmO2 increased during hyperventilation, and ScO2 increased during breathing of 5% carbon dioxide. Rebreathing from a bag made SmO2 decrease and resulted in a biphasic ScO2 response: it first increased and subsequently decreased. Cardiovascular changes during tilt were not reflected in skin temperature. The ScO2 reflected the maintained autoregulation of cerebral blood flow until the perfusion pressure decreased markedly. In contrast, SmO2 mirrored muscle vasoconstriction early during tilt, and vasodilatation when pre-syncopal symptoms appeared.