Deterioration of cerebral autoregulation during orthostatic stress: insights from the frequency domain

Abstract

To determine whether dynamic cerebral autoregulation is impaired during orthostatic stress, cerebral blood flow (CBF) velocity in the middle cerebral artery (transcranial Doppler) and mean arterial pressure (MAP; Finapres) were measured continuously in 12 healthy subjects during ramped maximal lower body negative pressure (LBNP) to presyncope. Velocity and pressure were averaged over 6-min periods of stable data at rest and during LBNP to examine steady-state cerebral hemodynamics. Beat-to-beat variability of velocity and pressure were quantified by a “variation index” (oscillatory amplitude/steady-state mean value) and by power spectral analysis. The dynamic relationship between changes in pressure and velocity was evaluated by the estimates of transfer and coherence function. The results of the study were as follows. Steady-state MAP remained relatively constant during LBNP, whereas CBF velocity decreased progressively by 6, 15, and 21% at −30, −40, and −50 mmHg LBNP, respectively ( P < 0.05 compared with baseline). At the maximal level of LBNP (30 s before presyncope) MAP decreased by 9.4% in association with a prominent reduction in velocity by 24% ( P < 0.05 compared with baseline). The variation index of pressure increased significantly from 3.8 ± 0.3% at baseline to 4.5 ± 0.6% at −50 mmHg LBNP in association with an increase in the variation index of velocity from 6.0 ± 0.6 to 8.4 ± 0.7% ( P < 0.05). Consistently, the low- (0.07–0.20 Hz) and high-frequency (0.20–0.30 Hz) power of variations in pressure and velocity increased significantly at high levels of LBNP ( P < 0.05) in association with an increase in transfer function gain (24% at −50 mmHg, P < 0.05). We conclude that the damping effects of autoregulation on variations in CBF velocity are diminished during orthostatic stress in association with substantial falls in steady-state CBF velocity. We suggest that these changes may contribute in part to the development of presyncope.