The cardiovascular changes that accompany obstructive apnoeic events a
re now well recognized, but their relationship to other processes duri
ng the apnoea, whether mechanical, chemical or neurophysiological rema
ins unclear. These relationships have been examined by focusing on art
erial blood pressure measured non-invasively using the Finapres device
, gas tensions (Sa(O)2, ETCO(2)), intrathoracic effort (Ppl) and the m
edian EEG frequency (derived from off-line FFT analysis). Eighteen pat
ients with OSA were studied (mean age 43.7 y, BMI 31.2, A + HI 41.2) d
uring stable NREM sleep. However, not all variables were measured for
each patient. Data were analysed for the breath before, at the start,
mid and end of the apnoea and immediately afterwards. Mean blood press
ure initially fell with the onset of apnoea, remained stable until mid
-apnoea but rose acutely with apnoea termination. The mean systolic an
d diastolic pressures were greater during inspiration for the initial
and mid-apnoeic efforts, but this difference was reversed at apnoea te
rmination, possibly reflecting the onset of the arousal response. The
change in blood pressure over the apnoea was unrelated to apnoea durat
ion and only weakly associated with the intensity of the peak pleural
pressure. The rise in blood pressure at end apnoea was related to the
fall in SaO(2), but not to changes in ETCO(2). There was no correlatio
n between the change in EEG frequency and blood pressure over the apno
ea as a whole but the increase in blood pressure from the final effort
to the first breath correlated with the change in EEG frequency. Thes
e data suggest that the change in arterial pressure during an obstruct
ive apnoea are only weakly dependent on the intensity of inspiratory e
ffort made, but are modified by chemical factors and especially change
s in sleep state. The close relationship between arousal and change in
blood pressure in NREM events confirms the usefulness of cardiovascul
ar markers of arousal responses in OSA.