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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have emphasized the mechanisms and consequences of sleep state effects on the manifestation of a sensitive apneic threshold. In the absence of the stabilizing influences of wakefulness, even the healthy person is vulnerable to instabilities and ventilatory control as maintenance of a rhythmic breathing pattern becomes overwhelmingly dependent on CO2. This sleep-induced unmasking of the depressant effects of hypocapnia contrasts with the relatively minor effects of sleep on the ventilatory response to a wide variety of other acute or chronic ventilatory stimuli or inhibitors. This combination of an apneic threshold with a maintained hypoxic (and asphyxic) responsiveness during non-REM sleep probably explains much of the periodic breathing in hypoxic sleep in adults and in newborns. Furthermore, applying acute hypoxia to persons with upper airways that are susceptible to collapse, i.e., snorers, showed that fluctuating chemical stimuli and the accompanying instability in ventilatory control during sleep can cause obstructive apnea, at least under conditions where chemoreceptor stimuli are sufficient to initiate some inspiratory effort but insufficient to insure a completely patent upper airway. We emphasize that chemoreceptor-induced instability and/or apnea probably plays little or no role in the induction of many other varieties of sleep apnea including most obstructive sleep apneas and perhaps even in some types of nonobstructive apnea. The consequences of these chemoreceptor-induced instabilities are, of course, substantial in terms of impairment of pulmonary gas exchange and the precipitation of events that contribute significantly to the development of chronic cor pulmonale.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A sleep-induced apneic threshold and its consequences. 371 65

Central sleep apnea is a disorder characterized by apneic episodes during sleep with no associated ventilatory effort. More commonly than not these apneas are seen in patients who also have obstructive and mixed events. Although patients with this disorder frequently complain of insomnia and depression, frank hypersomnolence is rarely encountered. As these complaints are common ones seen in numerous clinical situations, and since sleep studies are rarely conducted to investigate their etiology, the true incidence of central sleep apnea has not been determined. The etiology of central apnea remains unknown, although the association between these breathing events and a number of other disease processes has increased our understanding of the disorder. Central apneas during sleep commonly occur after hyperventilation with the associated hypocapnic alkalosis. This occurs at high altitude when hyperventilation is induced by hypoxia and at sea level when spontaneous nocturnal hyperventilation occurs. This suggests that PCO2 is the primary stimulus to ventilation during sleep and that loss of this drive, as occurs with hypocapnia, may produce dysrhythmic breathing. Patients with complete absence of ventilatory chemosensitivity such as occurs with Ondine's curse (central alveolar hypoventilation) or the obesity-hypoventilation syndrome may also have central apneas. For reasons that remain unexplained, central sleep apnea is commonly seen in patients with congestive heart failure, nasal obstruction, and certain neurologic disorders. However, in most patients with central sleep apnea no obvious cause or association can be found. The treatment of this disorder is not entirely satisfactory. If it is severe, mechanical ventilation during sleep can be provided by any one of a number of techniques. However, for the patient who simply complains of insomnia and is found to have a moderate number of central apneas, the treatment choices are limited. Acetazolamide has been shown to decrease central apneas during short-term use, but results have been variable with prolonged administration. Other ventilatory stimulants seem to have little efficacy. Interestingly, oxygen administration has been shown to reduce central apneas considerably in a number of studies, although the explanation for its success is unknown. Central sleep apnea therefore remains a relatively rare disorder whose etiology is not fully understood and whose treatment is not completely satisfactory.
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PMID:Central sleep apnea. 393 82

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 deposition in the neck, or abnormal bony morphology of the upper airway. Functional impairment of the upper airway dilating muscles is particularly important 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 abnormal 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 reduction in respiratory drive related to the hypocapnia which results from postapnoeic hyperventilation. 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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PMID:Pathophysiology of obstructive sleep apnoea. 758 88

We have previously shown that hypocapnia triggers Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with congestive heart failure (CHF). Nasal continuous positive airway pressure (NCPAP) may attenuate CSR-CSA in patients with CHF and CSR-CSA. Accordingly, we hypothesized that attenuation of CSR-CSA by NCPAP would be related to an increase in PCO2. Therefore, we examined the effect of NCPAP on the frequency of apneas and hypopneas, transcutaneous PCO2 (PtcCO2), and minute volume of ventilation (VI) in 12 consecutive patients with CHF and CSR-CSA during stage 2 sleep. A control group of six patients, who did not receive NCPAP, was also studied. In the control group, there were no changes from baseline to 1 mo in the frequency of central apneas and hypopneas, mean PtcCO2, mean VI, or mean SaO2 during stage 2 sleep. In contrast, from baseline to 1 mo the NCPAP group experienced a decrease in the frequency of apneas and hypopneas (58.7 +/- 5.2 to 23.2 +/- 6.0/h of sleep, p < 0.001), an increase in mean PtcCO2 (34.6 +/- 1.4 to 40.8 +/- 1.1 mm Hg, p < 0.001), a reduction in mean VI (8.1 +/- 1.0 to 5.2 +/- 0.5 L/min, p < 0.01) and an increase in mean SaO2 (91.6 +/- 1.1 to 95.0 +/- 0.5%, p < 0.025) during stage 2 sleep while on 10.2 +/- 0.5 cm H2O nasal CPAP. We conclude that likely mechanisms through which NCPAP reduces CSR-CSA are by increasing SaO2 and raising PaCO2 during sleep toward or above the apneic threshold.
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PMID:Effect of continuous positive airway pressure on central sleep apnea and nocturnal PCO2 in heart failure. 795 21

Central apneas during sleep may arise as a result of reduction in PaCO2 below the apnea threshold. We therefore hypothesized that hyperventilation and arousals from sleep interact to cause hypocapnia and subsequent central apneas in patients with idiopathic central sleep apnea (ICSA). Accordingly, the relationships among preapneic ventilation, arousal from sleep, and the onset and duration of subsequent central apneas were examined during Stage 2 non-REM sleep in eight patients with ICSA (mean +/- SEM, 45.4 +/- 4.7 central apneas and hypopneas/h of sleep). During Stage 2 sleep, all episodes of periodic breathing with central apneas were triggered by hyperventilation. Minute ventilation (VI) was greater (6.3 +/- 0.7 versus 5.4 +/- 0.8 L/min, p < 0.05) and mean transcutaneous PCO2 (PtcCO2) was lower (37.8 +/- 1.3 versus 38.9 +/- 1.6 mm Hg, p < 0.05) during periodic breathing than during stable breathing. VI during the ventilatory phase of the periodic breathing cycle increased progressively with increasing grades of associated arousals from Grade 0 (no arousal) (10.3 +/- 1.4 L/min) to Grade 1 (EEG arousal) (12.6 +/- 1.6 L/min) to Grade 2 (movement arousal) (14.1 +/- 1.6 L/min, p < 0.01). There was a corresponding progressive increase in central apnea length following the ventilatory period from no arousal (14.1 +/- 2.0) to EEG arousal (16.4 +/- 1.8) to movement arousal (18.1 +/- 2.0 s, p < 0.01). We conclude that arousals and hyperventilation interact to trigger hypocapnia and central apneas in ICSA.
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PMID:Interaction of hyperventilation and arousal in the pathogenesis of idiopathic central sleep apnea. 804 35

A 63-year-old man with severe non-obstructive sleep apnoea (apnoea index 28; apnoea duration 45-60s; O2 saturation between 72% and 98%), who did not respond to common modes of treatment, was successfully treated with CO2. A tent was perfused with compressed air (6 1/min) and increasing amounts of CO2. A concentration of 3% CO2 (180 ml/min) was sufficient to raise the PaCO2 above apnoea threshold and to suppress apnoeas completely. As a result, O2 saturation remained normal throughout the whole night and the symptoms of sleep apnoea disappeared. We hypothesize that the PCO2 ventilatory drive was intact in our patient and that hypocapnia was the major factor causing the non-obstructive sleep apnoea syndrome. Administration of CO2 with a constant flow system could be a safe and easy alternative for patients with non-obstructive sleep apnoea syndrome who present with hypocapnia and an intact respiratory feedback control system.
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PMID:Beneficial effect of inhaled CO2 in a patient with non-obstructive sleep apnoea. 813 21

Periodic breathing with central apneas during sleep is typically triggered by hypocapnia resulting from hyperventilation. We therefore hypothesized that hypocapnia would be an important determinant of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with congestive heart failure (CHF). To test this hypothesis, 24 male patients with CHF underwent overnight polysomnography during which transcutaneous PCO2 (PtcCO2) was measured. Lung to ear circulation time (LECT), derived from an ear oximeter as an estimate of circulatory delay, and CSR-CSA cycle length were determined. Patients were divided into a CSR-CSA group (n = 12, mean +/- SEM of 49.2 +/- 6.3 central apneas and hypopneas per h sleep) and a control group without CSR-CSA (n = 12, 4.9 +/- 0.8 central apneas and hypopneas per h sleep). There were no significant differences in left ventricular ejection fraction, awake PaO2, mean nocturnal SaO2, or LECT between the two groups. In contrast, the awake PaCO2 and mean sleep PtcCO2 were significantly lower in the CSR-CSA group than in the control group (33.0 +/- 1.2 versus 37.5 +/- 1.0 mm Hg, p < 0.01, and 33.2 +/- 1.2 versus 42.5 +/- 1.2 mm Hg, p < 0.0001, respectively). Neither group had significant awake or sleep-related hypoxemia. In addition, CSR-CSA cycle length correlated with LECT (r = 0.939, p < 0.001). We conclude that (1) hypocapnia is an important determinant of CSR-CSA in CHF and (2) circulatory delay plays an important role in determining CSR-CSA cycle length.
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PMID:Role of hyperventilation in the pathogenesis of central sleep apneas in patients with congestive heart failure. 814 43

We report on an 83 yr old man with hypersomnia and central sleep apnoea (CSA). He had several possible causes for CSA, including a central nervous system lesion, hypocapnia and anatomical narrowing of the airway at the hypopharyngeal level. We postulate that reduced central respiratory drive occurring in conjunction with upper airway narrowing may have led to central apnoeas. These in turn could have facilitated a complete passive hypopharyngeal collapse at the end of each apnoea, as visualized by somnofluoroscopy. The CSA could also have been favoured by respiratory instability due to chronic hypocapnia.
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PMID:Central sleep apnoea syndrome with upper airway collapse. 849 10

We wished to determine the effect of reduced ventilatory drive (hypopnea) on upper airway patency in humans during non-rapid-eye-movement (NREM) sleep. We studied nine subjects (58 trials) spanning the spectrum of susceptibility to upper airway collapse including normals, snorers and patients with mild sleep apnea. Hypocapnic hypopnea was induced by abrupt cessation of brief (1 min) nasal mechanical hyperventilation. Surface inspiratory EMG (EMGinsp) was used as an index of drive. Upper airway resistance and supraglottic pressure-flow plots were used as indexes of upper airway patency. Termination of nasal mechanical ventilation resulted in reduced VE to 4904 of pre-mechanical ventilation eupneic control. Upper airway resistance at a fixed flow did not change significantly in inspiration or expiration. Likewise, pressure-flow plots showed no increase in upper airway resistance except in one subject. However, maximum flow (Vmax) decreased during hypopnea in four subjects who demonstrated inspiratory flow-limitation (IFL) during eupneic control. In contrast, no IFL was noted in subjects who showed no evidence of IFL during eupnea. We concluded: (1) Reduced ventilatory drive does not compromise upper airway patency in normal subjects during NREM sleep; (2) the reduction in Vmax during hypopnea in subjects with IFL during eupneic control, suggests that reduced drive is associated with increased upper airway compliance in these subjects; and (3) upper airway susceptibility to narrowing/closure is an important determinant of the response to induced hypopnea during NREM sleep.
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PMID:Effect of induced hypocapnic hypopnea on upper airway patency in humans during NREM sleep. 936 Nov 50

In patients with congestive heart failure (CHF), elevated, left ventricular (LV) volume might lead to pulmonary congestion and hypocapnia, which would create a predisposition to the development of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). In addition, because LV volume affects cardiac output, it should influence the lengths of hyperpneas. We therefore evaluated LV volumes and transcutaneous PCO2 (PtcCO2) during wakefulness and stage 2 sleep in 16 patients with CHF due to nonischemic dilated cardiomyopathy (NIDC). Data were then compared between those with (n = 7) and those without CSR-CSA (n = 9). LV end-diastolic volume (LVEDV) was significantly higher in patients with than those without CSR-CSA (585 +/- 118 versus 312 +/- 41 ml, p < 0.05). Compared with patients without CSR-CSA, those with CSR-CSA had lower mean stage 2 sleep PtcCO2 (36.3 +/- 2.2 versus 41.2 +/- 1.2 mm Hg, p < 0.05) and a lesser change in PtcCO2 from wakefulness to stage 2 sleep (-0.4 +/- 0.3 versus 2.0 +/- 0.4 mm Hg, p < 0.001). Among patients with CSR-CSA, hyperpnea length was inversely related to LVEDV (R = 0.769, p = 0.043) owing to the direct relationship of cardiac output to LVEDV (R = 0.791, p = 0.034). We conclude that CSR-CSA in patients with CHF due to NIDC is associated with increased LV volumes possibly through the direct or indirect influence of LV volume on PaCO2 and cardiac output.
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PMID:Left ventricular volume in patients with heart failure and Cheyne-Stokes respiration during sleep. 937 74


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