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Biomedical subjects

P Devadatta

Publications and source records attributed to P Devadatta.

3 recordsLinked to original sources

Pattern of breathing and upper airway mechanics during wakefulness and sleep in healthy elderly humans.

Elderly subjects are known to be prone to periodic breathing in sleep. Because periodic breathing may be associated with changes in upper airway caliber, we hypothesized that oscillations in upper airway caliber contribute to the increased prevalence of sleep-related periodic breathing in the elderly. We tested this hypothesis by measuring upper airway resistance, ventilatory variables, and the pattern of variation of these variables in groups of body size-matched young and elderly healthy individuals during wakefulness and stage 2 non-rapid-eye-movement sleep. No major differences existed between the two groups during either wakefulness or sleep in mean upper airway resistance or ventilation values. However, ventilation was more variable during sleep in the elderly; this variability was oscillatory in the majority of elderly subjects at an average rate of 0.04 breaths/cycle or one cycle approximately every 24 s. Oscillations in upper airway resistance during sleep were associated with reciprocal oscillations in tidal volume and/or minute ventilation at the same frequency. Those subjects who had significant oscillations in upper airway resistance had more apneas and hypopneas than those subjects without such oscillations. Oscillations in resistance and ventilation occurred in the supine but not in the lateral body position. We conclude that the wide oscillations in upper airway resistance present during sleep in supine healthy elderly subjects produce a fluctuating mechanical limitation of ventilation, which may contribute to periodic breathing.

Adult

Mechanism of sleep-induced periodic breathing in convalescing stroke patients and healthy elderly subjects.

Cerebral vascular ischemic strokes are known to precipitate Cheyne-Stokes periodic breathing. Interestingly, Cheyne-Stokes-like breathing during sleep may be associated with obstructive sleep apnea (OSA) in some individuals. Therefore, it was reasoned that stroke patients with periodic breathing in sleep would be susceptible to OSA. Because oscillations in upper airway resistance can occur as a component of sleep-induced periodic breathing, we hypothesized that stroke patients with sleep-induced periodic breathing would have oscillations in upper airway resistance. These oscillations in resistance would be expected to contribute to OSA. We studied stroke patients with sleep-induced periodic breathing and control subjects to evaluate the relationship between upper airway resistance and ventilation in periodic breathing in sleep. Ventilation and upper airway resistance were measured in presleep wakefulness and in stage 2 NREM sleep. Mean tidal volume, minute ventilation, respiratory cycle timing variables, and upper airway resistance were not different between stroke and control subjects, either awake or asleep. Upper airway resistance increased and ventilation volume decreased from wakefulness to sleep in both groups. In an equivalent number of subjects from each group, reciprocal patterned oscillations in tidal volume and upper airway resistance were present at a 5 to 12.5 breath frequency during sleep. As upper airway resistance increased, tidal volume decreased. Stroke patients had wider fluctuations in upper airway resistance than control subjects, likely contributing to the higher number of sleep-disordered breathing events observed in the stroke patients.

Aged

Decrease in functional residual capacity during sleep in normal humans.

A decrease in functional residual capacity (FRC) during sleep could result in worsening of ventilation distribution contributing to sleep hypoxemia. Therefore the purpose of this study was to determine whether FRC does decrease and to what extent it decreases in normal humans during sleep. Using helium dilution in a closed system we measured FRC in 10 healthy males during wakefulness, stage 2, stages 3-4, and rapid-eye-movement (REM) sleep. Mean FRC decreased from 3.14 +/- 0.01 (SE) liters during wakefulness to 2.95 +/- 0.01 liters in stage 2 sleep. Lowest sleep values were 2.86 +/- 0.01 liters in stages 3-4 and 2.83 +/- 0.01 liters in REM sleep (P less than 0.05 from wakefulness). Although the amount of the decrease in FRC identified during sleep was surely not large enough to impair ventilation distribution in normal humans, this degree of decrease might contribute to the hypoxemia seen in patients with severe airflow limitation.

Adult