Decreased Cerebral Autoregulation during Syncope in the Young

Cerebral blood flow (CBF) is reduced  prior to syncope in part due to hyperpnea and hypocapnia, which is known to cause  cerebral vasoconstriction. However, close observation of blood pressure and cerebral blood flow oscillations (measured by transcranial Doppler ultrasound) suggest a close phasic relation of arterial pressure and cerebral blood flow occurs near the end of upright tilt in episodic fainters. This was measured using techniques of "phase synchronization in which the timing of fluctuations in arterial pressure (AP) and cerebral blood flow (CBF) are quantitatively compared. Under normal operating conditions cerebral autoregulation prevails, meaning that CBF is nearly independent of AP. However, a high degree of phase synchronization implies that AP and CBF oscillate in synchrony and are therefore interdependent, implying loss of autoregulation.

Arterial pressure (AP) and cerebral blood flow velocity (CBFV) from a representative fainter. A: AP during tilt. B: CBFV during tilt. C: magnified AP between the marker lines in A before faint. D: magnified CBFV between the marker lines in B before faint. Immediately before faint, AP and CBFV become synchronized, and oscillations in AP are transferred to oscillations in CBFV.

Time intervals for 10-min head-up tilt (HUT) table testing. Note that time 0 is the beginning of HUT. A: set of time intervals for a representative fainting subject. Time intervals for the syncope group were as follows: baseline (supine conditions before being tilted upright), early (from the time of tilt until 1 min later), middle (from the previous point until 1 min before the faint), prefaint 1 min (1 min before the faint), faint [the time of faint until the return to the supine position (mean time of 16 s)], early recovery (ER; from the return to the supine position until 1 min later), and late recovery (LR; from the previous point until 2 min later). B: set of time intervals for a representative control subject. For the control group, the baseline, early, and middle time intervals were the same as in the syncope group. Preend 1 min, 1 min before returning to the supine position; late, the final 16 s of tilt until the return to the supine position. ER and LR time intervals were the same as in the syncope group.

Clearly oscillations in blood pressure are present and rendered most obvious during upright tilt during thoracic volume unloading. Equally clear is that such fluctuations may begin dissipating prior to faint. This goes along with measurements of low frequency (i.e. 0.1Hz, Mayer waves) blood pressure oscillations which are reduced as fainting approaches. 

Using narrow bandpass filtering and Hilbert transform methods we derived phases for AP and CBF and their phase difference, which were then used to compute the  phase synchronization index:

A: Phase synchronization for a representative control subject during resting supine conditions. B: Phase synchronization for a representative syncopal subject during resting supine conditions. C: synchronization for a representative control subject during 70° HUT. D: synchronization for a representative syncopal subject during 70° HUT. Note that in C and D, time 0 is defined as the beginning of HUT. During resting supine conditions, the control and syncope groups did not differ. During HUT, control subjects had oscillations in phase synchronization similar to baseline. In the syncope group, fainters demonstrated a prefaint drop in synchronization followed by a steady increase to maximum synchronization at faint (as noted by the arrows in D). This maximum synchronization was stable and maintained after fainters returned to the supine position. “Down” denotes the return to supine conditions.

The presence of complete phase synchronization between AP and CBF implies the absence of cerebral autoregulation. Our data demonstrate a rapid biphasic change of autoregulation, which is induced by and temporally related to vasovagal syncope. Approximately 2 min before fainting, syncopal subjects have a sudden rapid decrease in phase synchronization between AP and CBF followed by a prolonged increase in phase synchronization linking AP and mean CBF. The 2-min period corresponds to a period of increased cerebral autoregulation, which is followed by a virtual loss of autoregulation during the faint and into recovery. During this period of autoregulatory failure, CBFV appears to be linked to blood pressure as if a linear passive resistance relationship existed between the two. This fulfills criteria for phase synchronization. Cerebral autoregulation in fainters does not recover immediately upon becoming supine and roughly parallels the time course of clinical recovery, which can be prolonged after fainting. Our data also show that phase synchronization is a dynamic quantity even under resting conditions. At rest, autoregulation is not a constant but is intermittent and variable, as suggested by Giller and Mueller and Latka et al. We postulate that during the period of AP-CBF asynchrony, CBF is tightly controlled by neuronal activities and brain metabolism and unrelated to AP, whereas during the period of synchronization, CBF is determined by AP alone. Thus, synchronization unlinks CBF from cerebral metabolic control. Strictly speaking, phase synchronization, as measured here, is related to dynamic autoregulation. The change in ETCO2 during tilt cannot account for all of the reduction in CBFV during the prefaint 1 min and faint intervals when synchronization is maximum, although the effects of CO2 are still important and may account for a portion.

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Splanchnic pooling in syncope
Hyperpnea and Biphasic Peripheral Resistance Changes Characterize Vasovagal Syncope in the Young
Decreased Cerebral Autoregulation during Syncope in the Young