Revisiting human cerebral blood flow responses to augmented blood pressure oscillations

Key points summary

Cerebral autoregulation is most effective in buffering against pressure fluctuations slower than 0.03 Hz (∼30 seconds). This suggests that frequency bands for characterizing cerebral autoregulation should be redefined Low cross‐spectral coherence below 0.03 Hz highlights the limitations of transfer function approaches Hemodynamic changes induced by lower body pressure could not fully explain the differences in autoregulation estimated from spontaneous vs augmented fluctuations and thus observations of spontaneous fluctuations should not be relied on whenever possible.

Abstract

There is currently little empirical basis for time scales that are thought to be most significant in cerebrovascular counter‐regulation of changes in arterial pressure. While it is well established that cerebral autoregulation behaves as a "high pass" filter, recommended frequency bands have been largely arbitrarily determined. To test effectiveness of cerebral autoregulation, we refined oscillatory lower body pressure (LBP) to augment resting pressure fluctuations below 0.1 Hz by a factor of two in thirteen young male volunteers, and thoroughly characterized the time and frequency responses of cerebral autoregulation. We observed that despite a threefold increase in arterial pressure power < 0.03 Hz with oscillatory LBP, we saw no change in cerebral blood flow power, indicating near perfect counter regulation. In contrast, in the range of 0.03–0.10 Hz, both cerebral blood flow and arterial pressure power more than doubled. Our data demonstrate that cerebral autoregulation is most effective in buffering against pressure fluctuations slower than 0.03 Hz (∼30 seconds). This suggests that frequency bands of interest should be redefined and recording length should be much increased to account for this. Furthermore, low cross‐spectral coherence below 0.03 Hz, even when pressure fluctuations were augmented, highlights the uncertainty in transfer function approaches and the need to either report precision or use nonlinear approaches. Finally, hemodynamic changes induced by LBP could not fully explain the differences in autoregulation estimated from spontaneous vs augmented fluctuations and thus observations of spontaneous fluctuations should not be relied on whenever possible.

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