Systemic arterial blood pressure during obstructive sleep apnoea.
The cardiovascular changes that accompany obstructive apnoeic events are now well recognized, but their relationship to other processes during the apnoea, whether mechanical, chemical or neurophysiological remains unclear. These relationships have been examined by focusing on arterial blood pressure measured non-invasively using the Finapres device, gas tensions (SaO2, ETCO2), intrathoracic effort (Ppl) and the median EEG frequency (derived from off-line FFT analysis). Eighteen patients with OSA were studied (mean age 43.7 y, BMI 31.2, A + HI 41.2) during 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 pressure initially fell with the onset of apnoea, remained stable until mid-apnoea but rose acutely with apnoea termination. The mean systolic and diastolic pressures were greater during inspiration for the initial and mid-apnoeic efforts, but this difference was reversed at apnoea termination, possibly reflecting the onset of the arousal response. The change in blood pressure over the apnoea was unrelated to apnoea duration 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 SaO2, but not to changes in ETCO2. There was no correlation between the change in EEG frequency and blood pressure over the apnoea as a whole but the increase in blood pressure from the final effort to the first breath correlated with the change in EEG frequency. These data suggest that the change in arterial pressure during an obstructive apnoea are only weakly dependent on the intensity of inspiratory effort made, but are modified by chemical factors and especially changes in sleep state. The close relationship between arousal and change in blood pressure in NREM events confirms the usefulness of cardiovascular markers of arousal responses in OSA.
Calverley
PM
Aintree Chest Centre, and University Department of Medicine, Liverpool, UK.
Rees
K