Time-varying characterization of the cardiovascular response to arousal from sleep
 
 Anna Blasi, Ph.D., Consultant, BME Department, USC
 
  Abstract:
 
 Obstructive Sleep Apnea Syndrome (OSAS) patients are subject to periodic
 episodes of upper airway collapse for over 10 seconds. Each apnea episode
 causes a drop in blood oxygen saturation (hypoxia), accumulation of carbon
 dioxide (hypercapnia) and a drop in Heart Rate and Blood Pressure.
 Usually, the resumption of normal respiration is either preceded or
 followed by a transient arousal from sleep. These episodes can occur at a
 considerable rate per night (easily reaching the higher hundreds). We
 hypothesize that long-term accumulation of sympathoexcitation following
 arousal may be a factor in the development of systemic hypertension
 observed in OSAS. In our work we examine the effects of arousals alone on
 the autonomic control of the cardiovascular function with the aim to help
 better describe the chain of events that take place at and after arousal,
 and to establish how the long-term effects of OSAS could arise from the
 repetitive occurrence apneas. Through recursive autoregressive spectral
 analysis of cardiovascular and respiratory signals, we track the changes
 that acoustically-induced sleep interruption cause on the autonomic
 influence to the cardiovascular control of healthy subjects. The results
 point towards an increase in sympathetic activity, measured by a rise in
 Low Frequency oscillations of cardiovascular variability signals. This
 alteration seems to be lasting longer than the immediate changes in Blood
 Pressure, Heart Rate and EEG-induced arousal. Comparisons between healthy
 controls and OSAS show that, in this group, the pressor response to NREM
 arousal remains unchanged whereas the heart rate response is severely
 attenuated suggesting that long-term exposure to OSAS could impair the
 normal cardiac sympathoexcitatory reaction associated with NREM arousal.
 Moreover, in REM sleep, a stage with a generalized increase in sympathetic
 tone, healthy controls and OSAS patients show a similar impairment of the
 arousal response. With the help of a model in which we update recursively
 the kernel coefficients, we study the mechanisms involved in the
 cardiovascular control. We aim to show how the autonomic influences may be
 translated into actual changes of the cardiovascular function. The
 Arterial Baroreflex (ABR) seems to be one of the mechanisms involved
 directly in the changes observed in both Blood Pressure and peripheral
 sympathoexcitation.

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