Pathogenesis of apneas in hypersomnia-sleep apnea syndrome.
ABSTRACT To define the pathogenesis of apneas, eight patients with hypersomnia-sleep apnea syndrome were studied during nocturnal sleep. Diaphragmatic and genioglossal electromyograms quantitated as moving time average activity showed parallel periodic fluctuations resembling the pattern of Cheyne-Stokes breathing. Hypopneas and occlusive apneas occurred at the nadir of these cyclic changes, and mixed apneas represented an extreme of this periodicity with no inspiratory activity at the nadir of the cycle. Tracings of central apneas were compatible with an extremely prolonged expiratory phase. Electromyogram activity of both muscles showed an inversely linear relationship with oxygen saturation but genioglossal activity at the resolution of upper airway occlusion was increased out of proportion to the increase in diaphragmatic activity and the degree of oxygen desaturation. These results indicated that occlusive and mixed apneas result from an instability of ventilatory control during sleep, which seems to be an exaggeration of periodic breathing observed at sleep onset.
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ABSTRACT: We describe the respiratory, cardiac, and sleep-related characteristics of two types of sleep-related respiratory pauses in children that can fulfill current criteria of pathological apnea, but often seem to be benign: prolonged expiratory apnea (PEA) and post-sigh central apnea (PSCA). All outpatient comprehensive overnight polysomnography completed on children without significant underlying medical conditions completed during an 18-month period were retrospectively reviewed for the presence of augmented breaths followed by a respiratory pause. Events were identified as a PEA or PSCA based on characteristic features. Physiologic parameters associated with the respiratory events were recorded and compared. Fifty-seven (29 PEA and 28 PEA) events were identified in 17 patients (8.5 ± 3.5 years old). Median durations of PEA and PSCA were not significantly different. For both PEA and PSCA, average heart rate (HR) during the augmented breath before the respiratory pause differed from lowest instantaneous HR during the first half of the pause. When compared to each other, the lowest instantaneous HR recorded in the first half of PEA was lower than that for PSCA (63.9 [59.41-68.3] vs 66.75 [61.7-80.75]) beats per min, p = 0.03. No PEA or PSCA event was associated with an oxygen desaturation more than 3% from baseline. PEA and PSCA have stereotypic HR changes and resemble pathologic apneas but appear to be benign. Clinical significance of PEA and PSCA is yet to be determined. Consistent recognition of the events is required, given their frequency of occurrence and potential for misclassification. CITATION: Haupt ME; Goodman DM; Sheldon SH. Sleep related expiratory obstructive apnea in children. J Clin Sleep Med 2012;8(6):673-679.Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine 05/2012; 8(6):673-9. · 2.93 Impact Factor
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ABSTRACT: The pathophysiology of obstructive sleep apnoea (OSA) is complex and incompletely understood. A narrowed upper airway is very common among OSA patients, and is usually in adults due to nonspecific factors such as fat depo- sition in the neck, or abnormal bony morphology of the upper airway. Functional impairment of the upper airway dilating muscles is particularly impor- tant in the development of OSA, and patients have a reduction both in tonic and phasic contraction of these muscles during sleep when compared to normals. A variety of defective respiratory control mechanisms are found in OSA, including impaired chemical drive, defective inspiratory load responses, and abnormal upper airway protective reflexes. These defects may play an important role in the abnor- mal upper airway muscle responses found among patients with OSA. Local upper airway reflexes mediated by surface receptors sensitive to intrapharyngeal pressure changes appear to be important in this respect. Arousal plays an important role in the termination of each apnoea, but may also contribute to the development of further apnoea, because of a reduction in respi- ratory drive related to the hypocapnia which results from postapnoeic hyperventi- lation. A cyclical pattern of repetitive obstructive apnoeas may result. A better understanding of the integrated pathophysiology of OSA should help in the development of new therapeutic techniques.
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ABSTRACT: Objectives: To determine the effect of atrial overdrive pacing on sleep apnea severity in patients with sinus node dysfunction.Study design: Unblinded, cross-over study of the effect of atrial pacing on sleep apnea–hypopnea, with randomized order of study conditions (paced versus unpaced).Study population: Fifteen patients (11 men, 4 women), mean age 69 (SD 9) years, with sinus node dysfunction and permanent dual-chamber pacemakers, with polysomnographic evidence of either central or obstructive sleep apnea–hypopnea (mean apnea–hypopnea index (AHI) 27 (SD 16)). None had symptomatic heart failure, but 11 (73%) had mildly reduced left ventricular ejection fraction (40–56%).Methods: One hundred and fifty-two patients with pacemakers implanted at least one year previously for symptomatic sinus node dysfunction (including tachycardia–bradycardia syndrome) were screened for symptoms of sleep apnea. Of 47 patients identified, 26 underwent polysomnography and 15 had an apnea index >5/h and an AHI >15/h. Following the baseline polysomnogram, subjects underwent polysomnography on the subsequent two nights under the following conditions, in random order: (1) pacemaker set at a rate 15beats/min higher than the mean heart rate of the diagnostic study (overdrive pacing phase); and (2) pacemaker rate reduced to 40beats/min (no-pacing phase). The main outcome measure was the difference in AHI between the two pacing modes.Results: Mean nocturnal heart rate during the pacing phase was 72/min, versus 51/min during the no-pacing phase. During the no-pacing phase, AHI was unchanged from the baseline night at 28/h (SD 22). During overdrive pacing, however, the AHI was 61% lower at 11/h (SD 14). The AHI was lower on the pacing than the no-pacing night in all 15 subjects, regardless of whether the predominant type of apnea was central or obstructive. The mean central apnea index fell from 13 (SD 17) to 6 (SD 7), and the obstructive apnea index from 6 (SD 4) to 3 (SD 1). Both lowest oxyhemoglobin saturation and the percent time at saturation below 90% also improved on the pacing night. There was little difference in total sleep time between pacing and no-pacing nights; other measures of sleep quality were not reported.Conclusions: The authors conclude that atrial overdrive pacing at a relatively modest rate causes a substantial improvement in both central and obstructive sleep apnea, by mechanisms that are uncertain.Sleep Medicine 05/2003; 4(3):259-260. · 3.10 Impact Factor