Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypopneas or pauses in respiratory effort frequently precede episodes of obstructive sleep apnea resulting in mixed apneas. We studied five subjects after chronic tracheostomy for obstructive sleep apnea. During stable non-REM (NREM) sleep, subjects breathed entirely through the tracheostomy. Tracheostomy occlusion caused experimental obstructive apnea which lasted 13.9 +/- 4.7 sec and ended with transient arousal and pharyngeal opening. At the end of the apnea there was marked hyperventilation (inspired minute ventilation rose 21.6 +/- 3.5 L on the first breath) followed by hypocapnia, hypopnea, and pauses in inspiratory effort as the subjects resumed NREM sleep. Hypocapnia was greater before inspiratory pauses lasting at least 5 sec than before shorter pauses (PETco2, 4.2 +/- 1.8 mm Hg below baseline vs 1.2 +/- 2.5 mm Hg below baseline). In three patients, pauses in inspiratory effort following experimental obstructive apnea were prevented by administration of 4 percent CO2 and 40 percent O2 inspired gas. This study suggests that: hyperventilation with hypocapnia occurs at the termination of obstructive apneas, and hypocapnia may be responsible for the attenuation or cessation of respiratory effort initiating the subsequent cycle of obstruction.
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PMID:A possible mechanism for mixed apnea in obstructive sleep apnea. 308 45

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

Disagreement exists on the effect of sleep on hypoxic ventilatory responses. We hypothesized that these differences were due to variabilities in methodology of inducing hypoxia, specifically, as they pertained to the PCO2 level during the studies. We therefore measured ventilatory responses to hypoxia with (eucapnic) and without (hypocapnic) added CO2 during wakefulness and sleep in 7 goats. Eucapnic responses to hypoxia were significantly decreased during both slow wave (SWS) and REM sleep. This decrease was not apparent when hypocapnia was allowed to occur. In 4 goats also provided with electromagnetic flow probes for brain blood flow (BBF) measurements, hypocapnia significantly attenuated the increase in BBF induced by hypoxia during both the awake and SWS stages. Concomitantly measured cerebral venous blood also showed lower oxygen tension during hypocapnia. We postulate that under hypocapnic conditions, the depressant effects of brain hypoxia may contribute to the obscuring of differences in hypoxic responses during wakefulness and sleep.
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PMID:Determinants of the ventilatory responses to hypoxia during sleep. 643 57

1. The present study was designed to determine the effect of sleep on the tonic output to respiratory muscle and on the level of chemical respiratory stimulation required to produce rhythmic respiratory output. 2. Chronically implanted electrodes recorded expiratory (triangularis sterni) and inspiratory (diaphragm and parasternal intercostal) electromyographic (EMG) activities in three trained dogs during wakefulness and sleep. The dogs were mechanically hyperventilated via an endotracheal tube inserted into a permanent tracheostomy. During the studies, a cold block of the cervical vagus nerves was maintained to avoid the complicating effects of vagal inputs on respiratory drive and rhythm. 3. During wakefulness, steady-state hypocapnia (partial pressure of CO2, PCO2 = 30 mmHg) abolished inspiratory EMG activity, resulting in apnoea, but the expiratory muscle became tonically active. Compared to wakefulness, the level of the tonic expiratory EMG activity was decreased in non-REM (non-rapid eye movement) sleep (median decrease = 34%, P = 0.005) and was further decreased in REM sleep (median decrease = 78%, P < 0.0001). During REM sleep, the tonic expiratory EMG activity was highly variable (mean coefficient of variation = 39% compared to 7% awake, P < 0.0001) and in some periods of REM, bursts of inspiratory EMG activity and active breathing movements were observed despite the presence of hypocapnia. 4. During constant mechanical hyperventilation, progressive increases in arterial PCO2 (in hyperoxia) were produced by rebreathing. Measurement of the CO2 threshold for the onset of spontaneous breathing showed that this threshold was not different between wakefulness and non-REM sleep (mean difference = 0.1 mmHg from paired observations, 95% confidence interval for the difference = -1.0 to +1.1 mmHg, P = 0.898). 5. The results show that sleep reduces the tonic output to respiratory muscles but does not increase the CO2 threshold for the generation of rhythmic respiratory output. These observations suggest that changes in the tonic drives to the respiratory motoneurones may be a principal mechanism by which changes in sleep-wake states produce changes in respiratory output.
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PMID:Effects of sleep on the tonic drive to respiratory muscle and the threshold for rhythm generation in the dog. 801 11

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

To investigate the severity of oxygen desaturation following voluntary hyperventilation (VHV) in normal subjects and its possible relation to chemoresponsiveness, we examined respiration following VHV in 16 normal male subjects. Monitoring was performed according to the standard polysomnography protocol including measurements of arterial oxygen saturation (SaO2) and transcutaneous PCO2 (PtcCO2). The subjects hyperventilated voluntarily for 3 min, and were then observed for more than 15 min. They hyperventilated again for another 3 min, and were followed again for more than 15 min. Eleven subjects fell into non-REM sleep after VHV, and their mean lowest SaO2 was 67.6 +/- 13.0% (n = 15 trials in 11 subjects, mean +/- SD). Falling asleep during hypocapnia caused desaturation, and periodic breathing was invariably observed soon after. The difference between the PtcCO2 during non-REM sleep with stable breathing and the PtcCO2 when the SaO2 was 90% following VHV was defined as the delta PtcCO2 (90). The delta PtcCO2 (90) and hypoxic ventilatory response (HVR) were positively and significantly correlated (r = 0.73, p < 0.01). While the subjects were awake, the mean lowest SaO2 was 73.5 +/- 17.4% (17 trials in 12 subjects). Remaining awake induced oxygen desaturation in some subjects but not in others. In one subject, desaturation during the waking state was caused by hypoventilation, not by central apnea. In the seven subjects whose respiration following VHV was monitored during the waking state in one trial and during the sleeping state in another trial, plots of the PtcCO2-SaO2 relationship for the waking state were generally positioned above those made for the sleeping state.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen desaturation following voluntary hyperventilation in normal subjects. 811 44

We present a view of the neuromechanical regulation of breathing and causes of breathing instability during sleep. First, we would expect transient increases in upper airway resistance to be a major cause of transient hypopnea. This occurs in sleep because a hypotonic upper airway is more susceptible to narrowing and because the immediate excitatory increase in respiratory motor output in response to increased loads is absent in non-REM sleep. Secondly, sleep predisposes to an increased occurrence of ventilatory "overshoots", in part because abruptly changing sleep states cause transient changes in upper airway resistance and in the gain of the respiratory controller. Following these ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include: a) hypocapnia-if transient, will inhibit carotid chemoreceptors and cause hypopnea, but if prolonged will inhibit medullary chemoreceptors and cause apnea; b) a persistent inhibitory effect from lung stretch; c) baroreceptor stimulation, from a transient rise in systemic blood pressure immediately following termination of apnea or hypopnea may partially suppress the accompanying hyperpnea; d) depression of central respiratory motor output via prolonged brain hypoxia. Once apneas are initiated, reinitiation of inspiration is delayed even though excitatory stimuli have risen well above their apneic thresholds, and these prolonged apneas are commonly accompanied by tonic EMG activation of expiratory muscles of the chest wall and upper airway.
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PMID:Sleep-induced breathing instability. University of Wisconsin-Madison Sleep and respiration Research Group. 872 83

Patients suffering from severe heart failure may develop breathing disorders during sleep. Results may be heavy disturbances in sleep architecture, worsening of haemodynamics and of the prognosis of these patients. Causes of breathing disorders are probably instability of breathing regulation caused by hypoxaemia, hypocapnia, and prolonged blood circulation time. This study examined the influence exercised by different concentrations of continuously applied oxygen during night time on breathing disorders, oxygen saturation and sleep architecture in patients with severe heart failure (NYHA III-IV). All patients showed an improvement in sleep architecture. Total sleeping time increased significantly. Fragmentations of sleep by arousal reactions decreased, time of REM-sleep and non-REM-sleep III and IV increased significantly.
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PMID:[Effect of long-term oxygen therapy on sleep architecture in patients with severe dilated cardiomyopathy and Cheyne-Stokes respiration]. 934 Jun 29

Central sleep apnoea (CSA) in congestive heart failure is sleep state dependent and occurs typically in stages I and II of non-REM sleep. The pre-requisites are hypocapnia and some prolongation of the circulation time. It is not certain whether abnormalities in after-discharge activity in the brainstem are also important. The presence of CSA in patients with left ventricular dysfunction is a poor prognostic sign and associated with a higher mortality in that group compared to age, sex and ejection fraction matched patients with congestive cardiac failure alone. It is reasonable to speculate that the CSA causes an increase in sympathetic nervous system activity which would maintain afterload at a high level or tend to increase it with time. The application of a high afterload to an impaired left ventricle leads over time to a further reduction in ejection fraction. From other studies, particularly ACE inhibitor studies, it is known that ejection fraction and prognosis are almost linearly related. It could therefore be said that once CSA has developed it may lead to a vicious circle of increasing afterload and further reduction in ejection fraction, causing worsening CSA and further increases in afterload. A number of treatments have been shown to be of benefit: supplemental nocturnal oxygen therapy, acetazolamide and nasal CPAP therapy have all been shown to reduce CSA. In addition nasal continuous positive airways pressure (CPAP) has been shown by two groups in Canada to also improve ejection fraction. The beneficial effects on ejection fraction in particular, persist after the treatment has been withdrawn, which suggests either remodelling of the left ventricular musculature or a resetting of the baseline sympathetic nervous system activity. The impressive increase in ejection fraction due to three months nasal CPAP therapy in one study (an average 35% increase) is both dramatic and exciting for the future. It is reasonable to expect improvement in prognosis for patients with CCF whose ejection fraction rises with CPAP treatment. Finally, only a limited number of studies have been published. Unfortunately the impressive results from Canada have not yet been reproduced in other centres around the world.
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PMID:Central sleep apnoea and heart failure (Part I). 952 93

Central sleep apnoea (CSA) in congestive heart failure is sleep state dependent and occurs typically in stages I and II of non-REM sleep. The pre-requisites are hypocapnia and some prolongation of the circulation time. It is not certain whether abnormalities in after-discharge activity in the brainstem are also important. The presence of CSA in patients with left ventricular dysfunction is a poor prognostic sign and associated with a higher mortality in that group compared to age, sex and ejection fraction matched patients with congestive cardiac failure alone. It is reasonable to speculate that the CSA causes an increase in sympathetic nervous system activity which would maintain afterload at a high level or tend to increase it with time. The application of a high afterload to an impaired left ventricle leads over time to a further reduction in ejection fraction. From other studies, particularly ACE inhibitor studies, it is known that ejection fraction and prognosis are almost linearly related. It could therefore be said that once CSA has developed it may lead to a vicious circle of increasing afterload and further reduction in ejection fraction, causing worsening CSA and further increases in afterload. A number of treatments have been shown to be of benefit: supplemental nocturnal oxygen therapy, acetazolamide and nasal CPAP therapy have all been shown to reduce CSA. In addition nasal continuous positive airways pressure (CPAP) has been shown by two groups in Canada to also improve ejection fraction. The beneficial effects on ejection fraction in particular, persist after the treatment has been withdrawn, which suggests either remodelling of the left ventricular musculature or a resetting of the baseline sympathetic nervous system activity. The impressive increase in ejection fraction due to three months nasal CPAP therapy in one study (an average 35% increase) is both dramatic and exciting for the future. It is reasonable to expect improvement in prognosis for patients with CCF whose ejection fraction rises with CPAP treatment. Finally, only a limited number of studies have been published. Unfortunately the impressive results from Canada have not yet been reproduced in other centres around the world.
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PMID:Central sleep apnoea and heart failure (part II). 965 53


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