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: Obstructive sleep disorders develop when the normal reduction in pharyngeal dilator activity at sleep onset occurs in an individual whose pharynx requires a relatively high level of dilator activity to remain sufficiently open. They range from steady snoring, to slowly evolving hypopneas, to fast-recurring obstructive hypopneas and apneas. A fundamental observation is that the polysomnographic picture differs substantially among subjects with the same pharyngeal collapsibility, and even in the same subject at different times, indicating that the type and severity of the disorder is determined to a large extent by the individual's response to the obstruction. The present report reviews the various mechanisms involved in the response to sleep-induced obstructive events. When the obstructive event takes the form of mild-moderate flow limitation, compensation can take place through an increase in the fraction of time spent in inspiration (Ti/Ttot) without any increase in maximum flow (V(MAX)). With more severe obstructions, V(MAX) must increase. Recent data indicate that the obstructed upper airway can reopen reflexly, without arousal, if chemical drive is allowed to reach a threshold (T(ER)) but that this is often preempted by a low arousal threshold. The relation between T(ER) and arousal threshold, as well as the lung-to-carotid circulation time and the rate of rise of chemical drive during the obstructive event, determine the magnitude of ventilatory overshoot at the end of an event and, by extension, whether initial obstructive events will be followed by stable breathing, slow evolving hypopneas with occasional arousals, or repetitive events.Journal of Applied Physiology 10/2008; 105(5):1389-405. DOI:10.1152/japplphysiol.90408.2008 · 3.43 Impact Factor
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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
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ABSTRACT: We studied the effects of alcohol ingestion on the response of upper airway resistance (UAR) to changing respiratory motor output in 9 normal subjects. Nasal and pharyngeal pressures were measured with two low bias flow catheters placed at the tip of the epiglottis and in the posterior nasopharynx. Respiratory flow was measured with a Fleisch no. 3 pneumotachograph connected to a tightly fitting mask. Breath-by-breath inspiratory upper airway resistances were calculated at isoflow during 1) a CO2 rebreathing (increase in drive), 2) 2 min following five slow vital capacities of 100% O2 (decrease in drive) (Post-O2 period), and 3) 1 min before each procedure (baseline measurements). The respiratory motor output was estimated by the pressure developed 0.1 sec after the onset of inspiration (P0.1) during rebreathing and by the mean inspiratory flow (VT/TI) during the post-O2 period. Measurements were performed before and after the ingestion of 1.5 ml/kg of 40% alcohol. Blood alcohol level rose from 0 to 14.9 +/- 1.8 mmol.L-1 (Mean +/- SD) and total supralaryngeal resistance increased from 2.8 +/- 1.8 cm H2O.L-1.sec to 4.2 +/- 1.8 cm H2O.L-1.sec (P less than 0.001, Student's paired t-test). During CO2 rebreathing UAR decreased exponentially as P0.1 increased both before and after alcohol intake. The slope of the plot Log (pharyngeal resistance) against P0.1 decreased from -17.0 x 10(-3) +/- 9.3 x 10(-3) before alcohol to -11.0 x 10(-3) +/- 6.6 x 10(-3) after alcohol intake (P = 0.03). The slope of the decrease in nasal resistance remained unchanged. A decrease in VT/TI occurred during the Post-O2 period and was accompanied by an exponential increase in UAR at each experiment. The slope of Log (pharyngeal resistance) over VT/TI was significantly higher after (-27.0 x 10(-3) +/- 7.1 x 10(-3)) than before alcohol (-12.0 x 10(-3) +/- 4.2 x 10(-3), P less than 0.001). The slope of the increase in nasal resistance with decreasing VT/TI rose from -8.4 x 10(-3) +/- 6.5 x 10(-3) to -13.0 x 10(-3) +/- 7.4 x 10(-3) after alcohol ingestion (P = 0.06). We conclude that alcohol ingestion depresses the pharyngeal responses to changing central drive in normal subjects.Respiration Physiology 09/1990; 81(2):153-63. DOI:10.1016/0034-5687(90)90042-W