Brain and muscle oxygen saturation during head‐up‐tilt‐induced central hypovolemia in humans

Summary. Near‐infrared spectrophotometry‐determined cerebral (ScO₂) and muscle oxygen saturations (SmO₂) were followed in 15 volunteers during passive 50° 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.