Pathogenesis of apneas in hypersomnia-sleep apnea syndrome.

The American review of respiratory disease (Impact Factor: 10.19). 03/1982; 125(2):167-74.
Source: PubMed

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.

  • [Show abstract] [Hide abstract]
    ABSTRACT: In patients with heart failure (HF), altered breathing patterns, including periodic breathing, Cheyne-Stokes breathing, and oscillatory ventilation, are seen in several situations. Since all forms of altered breathing cause similar detrimental effects on clinical outcomes, they may be considered collectively as an “altered breathing syndrome.” Altered breathing syndrome should be recognized as a comorbid condition of HF and as a potential therapeutic target. In this review, we discuss mechanisms and therapeutic options of altered breathing while sleeping, while awake at rest, and during exercise.
    Current Heart Failure Reports 01/2015; 12(2). DOI:10.1007/s11897-014-0250-4
  • [Show abstract] [Hide abstract]
    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. DOI:10.1016/S1389-9457(03)00065-0 · 3.10 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: In an adult population, the prevalence of sleep apnea is 4% for men and 2% for women. Generally, nasal positive pressure ventilation is the best therapeutic option. To date, and in spite of the possible presence of marked brady-arrhythmias during sleep apnea, there is no recognised indication for Pacemaker implantation. However, recent data show the potential benefit of permanent cardiac stimulation in these patients. Increasing heart rate (using atrial pacing) improves cardiac output, and reduces pulmonary congestion and pulmonary vagal afferent nerves are no longer stimulated. The incidence of central sleep apnea is thereby reduced. Excessive nocturnal vagal tone increases snoring and sleep apnea, because of excessive relaxation of the oropharyngeal muscles. In patients with bradycardia, atrial stimulation may oppose increased vagal tone, by stimulating the sympathetic system or maintaining it at a minimal level. It is therefore possible that cardiac stimulation will become part of the treatment of sleep apnea in patients with documented bradycardia and/or heart failure.
    Annales de Cardiologie et d Angéiologie 08/2003; 52(4):239-245. DOI:10.1016/S0003-3928(03)00083-0 · 0.30 Impact Factor