MECHANISM OF SLEEP-INDUCED PERIODIC BREATHING IN CONVALESCING STROKE PATIENTS AND HEALTHY ELDERLY SUBJECTS

Citation
Dw. Hudgel et al., MECHANISM OF SLEEP-INDUCED PERIODIC BREATHING IN CONVALESCING STROKE PATIENTS AND HEALTHY ELDERLY SUBJECTS, Chest, 104(5), 1993, pp. 1503-1510
Citations number
38
Categorie Soggetti
Respiratory System
Journal title
ChestACNP
ISSN journal
00123692
Volume
104
Issue
5
Year of publication
1993
Pages
1503 - 1510
Database
ISI
SICI code
0012-3692(1993)104:5<1503:MOSPBI>2.0.ZU;2-V
Abstract
Cerebral vascular ischemic strokes are known to precipitate Cheyne-Sto kes periodic breathing. Interestingly, Cheyne-Stokes-like breathing du ring sleep may be associated with obstructive sleep apnea (OSA) in som e individuals. Therefore, it was reasoned that stroke patients with pe riodic breathing in sleep would be susceptible to OSA. Because oscilla tions in upper airway resistance can occur as a component of sleep-ind uced periodic breathing, we hypothesized that stroke patients with sle ep-induced periodic breathing would have oscillations in upper airway resistance. These oscillations, in resistance would be expected to con tribute to OSA. We studied stroke patients with sleep-induced periodic breathing and control subjects to evaluate the relationship between u pper airway resistance and ventilation in periodic breathing in sleep. Ventilation and upper airway resistance were measured in presleep wak efulness and in stage 2 NREM sleep. Mean tidal volume, minute ventilat ion, respiratory cycle timing variables, and upper airway resistance w ere not different between stroke and control subjects, either awake or asleep. Upper airway resistance increased and ventilation volume decr eased from wakefulness to sleep in both groups. In an equivalent numbe r of subjects from each group, reciprocal patterned oscillations in ti dal volume and upper airway resistance were present at a 5 to 12.5 bre ath frequency during sleep. As upper airway resistance increased, tida l volume decreased. Stroke patients had wider fluctuations in upper ai rway resistance than control subjects, likely contributing to the high er number of sleep-disordered breathing events observed in the stroke patients.