Chemical control stability in patients with obstructive sleep apnea.

The role of chemical control instability in the pathogenesis of obstructive sleep apnea (OSA) is not clear. We studied 32 patients with OSA during sleep while their upper airway was stabilized with continuous positive airway pressure. Twelve patients had repetitive OSA whenever they were asleep, regardless of body position or sleep stage, and were classified as having severe OSA (apnea-hypopnea index [AHI] = 88 +/- 19). The remaining 20 patients had sporadic OSA or repetitive OSA for only part of the time (mild/moderate OSA; AHI = 27 +/- 16). Susceptibility to periodic breathing (PB) was assessed by gradually increasing controller gain, using proportional assist ventilation. The increase in loop gain (LG) at each assist level was quantified from the ratio of assisted tidal volume (VT) to the VT obtained during single-breath reloading tests (VT amplification factor [VTAF]). Nine of 12 patients with severe OSA developed PB, with recurrent central apneas, whereas only six of 20 patients in the mild/moderate group developed PB (p < 0.02). This difference was observed despite the subjection of the mild/moderate group to greater amplification of LG; the highest values of VTAF in the mild/moderate and severe groups were 2.7 +/- 1.0 and 1.9 +/- 0.7, respectively (p < 0.01). We conclude that the chemical control system is more unstable in patients with severe OSA than in patients with milder OSA. We speculate that this may contribute to the severity of OSA, at least in some patients.

[1]  A I Pack,et al.  Sleep-induced periodic breathing and apnea: a theoretical study. , 1991, Journal of applied physiology.

[2]  Phillipson Ea,et al.  Control of breathing during sleep. , 1978 .

[3]  D. Hudgel,et al.  Pattern of breathing and upper airway mechanics during wakefulness and sleep in healthy elderly humans. , 1993, Journal of applied physiology.

[4]  J. Dempsey,et al.  Effect of hypercapnia on total pulmonary resistance during wakefulness and during NREM sleep. , 1991, The American review of respiratory disease.

[5]  A. Rechtschaffen,et al.  A manual of standardized terminology, technique and scoring system for sleep stages of human subjects , 1968 .

[6]  J. Dempsey,et al.  Effect of chemoreceptor stimulation and inhibition on total pulmonary resistance in humans during NREM sleep. , 1994, Journal of applied physiology.

[7]  M. Younes,et al.  Control of breathing during sleep assessed by proportional assist ventilation. , 1998, Journal of applied physiology.

[8]  Ronald M. Gilgenbach,et al.  Gyrotron‐backward‐wave‐oscillator experiments utilizing a high current, high voltage, microsecond electron accelerator , 1992 .

[9]  N. Cherniack,et al.  Cheyne-Stokes breathing. An instability in physiologic control. , 1973, The New England journal of medicine.

[10]  J. Dempsey,et al.  Effects of sleep-induced increases in upper airway resistance on ventilation. , 1990, Journal of applied physiology.

[11]  M. Younes,et al.  Susceptibility to periodic breathing with assisted ventilation during sleep in normal subjects. , 1998, Journal of applied physiology.

[12]  I. Homma,et al.  Experimentally induced Cheyne-Stokes breathing. , 1979, Respiration physiology.

[13]  J A Dempsey,et al.  Effect of hypoxia-induced periodic breathing on upper airway obstruction during sleep. , 1987, Journal of applied physiology.

[14]  M. Younes,et al.  Proportional Assist Ventilation , 2003 .

[15]  S. Kuna,et al.  Response of genioglossus muscle activity to nasal airway occlusion in normal sleeping adults. , 1988, Journal of applied physiology.

[16]  J A Dempsey,et al.  Interaction of sleep state and chemical stimuli in sustaining rhythmic ventilation. , 1983, Journal of applied physiology: respiratory, environmental and exercise physiology.

[17]  J. Dempsey,et al.  Effect of mechanical loading on expiratory and inspiratory muscle activity during NREM sleep. , 1990, Journal of applied physiology.

[18]  M. Younes,et al.  Ventilatory stability during sleep studied with proportional assist ventilation (PAV). , 1996, Sleep.

[19]  W. Riddle,et al.  A model for the relation between respiratory neural and mechanical outputs. I. Theory. , 1981, Journal of applied physiology: respiratory, environmental and exercise physiology.

[20]  E. Onal,et al.  Periodic breathing and the pathogenesis of occlusive sleep apneas. , 2015, The American review of respiratory disease.

[21]  M. Cosio,et al.  Mechanisms of apnea termination in obstructive sleep apnea. Role of chemoreceptor and mechanoreceptor stimuli. , 1994, American journal of respiratory and critical care medicine.

[22]  Michael R. Pinsky Heart–lung interactions , 1998 .

[23]  Remmers Je,et al.  Pathogenesis of upper airway occlusion during sleep , 1978 .

[24]  N. Anthonisen,et al.  Respiratory short-term poststimulus potentiation (after-discharge) in patients with obstructive sleep apnea. , 1992, The American review of respiratory disease.

[25]  C. Pollak,et al.  Quantitative analysis of sleep and sleep apnea before and after tracheostomy in patients with the hypersomnia-sleep apnea syndrome. , 1980, Sleep.

[26]  D. Roberts,et al.  Response of ventilator-dependent patients to different levels of proportional assist. , 1996, Journal of applied physiology.

[27]  A S Slutsky,et al.  Factors inducing periodic breathing in humans: a general model. , 1982, Journal of applied physiology: respiratory, environmental and exercise physiology.

[28]  D. Roberts,et al.  Response of ventilator-dependent patients to different levels of pressure support and proportional assist. , 1999, American journal of respiratory and critical care medicine.

[29]  E. Phillipson,et al.  Control of breathing during sleep. , 1978, The American review of respiratory disease.

[30]  S. Redline,et al.  Recognition and consequences of obstructive sleep apnea hypopnea syndrome. , 1999, Clinics in chest medicine.

[31]  W P Santamore,et al.  Mechanism of reduced cardiac output during positive end-expiratory pressure in the dog. , 1989, The American review of respiratory disease.

[32]  C Hendricks,et al.  Changes in inspiratory muscle electrical activity and upper airway resistance during periodic breathing induced by hypoxia during sleep. , 1987, The American review of respiratory disease.

[33]  A. Rechtschaffen A manual of standardized terminology, techniques and scoring system for sleep of human subjects , 1968 .

[34]  Lindell K. Weaver,et al.  Principles and Practice of Mechanical Ventilation , 1994 .

[35]  D. Hudgel,et al.  Instability of ventilatory control in patients with obstructive sleep apnea. , 1998, American journal of respiratory and critical care medicine.

[36]  P. McHale,et al.  The Effects of Airway Pressure on Cardiac Function in Intact Dogs and Man , 1982, Circulation.

[37]  J. Remmers,et al.  Pathogenesis of upper airway occlusion during sleep. , 1978, Journal of applied physiology: respiratory, environmental and exercise physiology.

[38]  E. Wolpert A Manual of Standardized Terminology, Techniques and Scoring System for Sleep Stages of Human Subjects. , 1969 .

[39]  M. Mathru,et al.  Hemodynamic response to changes in ventilatory patterns in patients with normal and poor left ventricular reserve , 1982, Critical care medicine.

[40]  J. Dempsey,et al.  Load compensation and respiratory muscle function during sleep. , 1992, Journal of applied physiology.

[41]  D. Hudgel,et al.  Neuromuscular and mechanical responses to inspiratory resistive loading during sleep. , 1987, Journal of applied physiology.

[42]  R. Hyatt,et al.  Static Behavior of the Respiratory System , 1987 .

[43]  F. Eldridge,et al.  Relationship of thoracic volume and airway occlusion pressure: muscular effects. , 1977, Journal of applied physiology: respiratory, environmental and exercise physiology.

[44]  M. Younes Proportional assist ventilation, a new approach to ventilatory support. Theory. , 1992, The American review of respiratory disease.

[45]  E. Onal,et al.  Induction of periodic breathing during sleep causes upper airway obstruction in humans. , 1986, Journal of applied physiology.