Increased phase synchronization and decreased cerebral autoregulation during fainting in the young

Abstract

Vasovagal syncope may be due to a transient cerebral hypoperfusion that accompanies frequency entrainment between arterial pressure (AP) and cerebral blood flow velocity (CBFV). We hypothesized that cerebral autoregulation fails during fainting; a phase synchronization index (PhSI) between AP and CBFV was used as a nonlinear, nonstationary, time-dependent measurement of cerebral autoregulation. Twelve healthy control subjects and twelve subjects with a history of vasovagal syncope underwent 10-min tilt table testing with the continuous measurement of AP, CBFV, heart rate (HR), end-tidal CO2 (ETCO2), and respiratory frequency. Time intervals were defined to compare physiologically equivalent periods in fainters and control subjects. A PhSI value of 0 corresponds to an absence of phase synchronization and efficient cerebral autoregulation, whereas a PhSI value of 1 corresponds to complete phase synchronization and inefficient cerebral autoregulation. During supine baseline conditions, both control and syncope groups demonstrated similar oscillatory changes in phase, with mean PhSI values of 0.58+/-0.04 and 0.54+/-0.02, respectively. Throughout tilt, control subjects demonstrated similar PhSI values compared with supine conditions. Approximately 2 min before fainting, syncopal subjects demonstrated a sharp decrease in PhSI (0.23+/-0.06), representing efficient cerebral autoregulation. Immediately after this period, PhSI increased sharply, suggesting inefficient cerebral autoregulation, and remained elevated at the time of faint (0.92+/-0.02) and during the early recovery period (0.79+/-0.04) immediately after the return to the supine position. Our data demonstrate rapid, biphasic changes in cerebral autoregulation, which are temporally related to vasovagal syncope. Thus, a sudden period of highly efficient cerebral autoregulation precedes the virtual loss of autoregulation, which continued during and after the faint.

Dynamic Cerebral Autoregulation Is Acutely Impaired During Maximal Apnoea In Trained Divers

“…First, PhSI had increased above resting values by the breakpoint of maximal apnoea. The rise in phase-coupling strength between MAP and CBFV indicates a progressive weakening of the autoregulatory response over time [22,23]. Second, not only had DW decreased during maximal apnoea, but its value approached zero by the breakpoint.…”

“…Two oscillators are said to be 'synchronised' or 'phase-locked' when the difference in their phases remain constant over a given length of time [22,23,28,29]. In the present study, the strength of phase synchronisation between MAP and CBFV was used to assess the effectiveness of dCA during maximal apnoea.…”

“…That is, MAP and CBFV were considered to act as two autonomous oscillators, weakly-coupled in their phases through the action of the effector, dCA. According to this paradigm, dCA is intact when the oscillators CBFV and MAP are not synchronised in their phase dynamics [22,23]; i.e., the oscillator CBFV operates nearindependently of MAP. Conversely, when the dynamics of MAP and CBFV are tuned such that their phases become synchronised, fluctuations in arterial pressure are ''passively'' transmitted through the cerebral vasculature unabated, portending autoregulatory failure.…”

“…This filtering approach also had the effect of removing variability in each time-series due to respiration and the cardiac cycle. The intrinsic phases of the filtered MAP and CBFV time series, W MAP (t) and W CBFV (t), were extracted using the Hilbert transform [23,30]. The distribution of phase differences between MAP and CBFV was then determined as: DW(t)~W MAP (t){W CBFV (t).…”

“…Moreover, it is well-established that arterial O 2 tension exerts a modulatory effect on dCA, wherein arterial hypoxaemia seemingly impairs the autoregulatory response [19][20][21]. Consequently, dCA was assessed using phase synchronisation analysis [22,23] on spontaneous, beatto-beat values of mean arterial blood pressure (MAP) and middle cerebral artery blood flow-velocity (CBFV) during maximal apnoea. It was hypothesised that trained divers would display signs of impaired dCA by the breakpoint of apnoea, evidenced by a significant increase in the strength of phase synchronisation between arterial pressure and cerebral blood flow-velocity.…”