Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six young male patients with grade I (mild) myotonic dystrophy and a complaint of excessive daytime sleepiness were studied during wakefulness and sleep. Pulmonary function tests during wakefulness showed evidence of mild abnormality related to respiratory muscle weakness. During sleep, some patients developed a sleep apnea syndrome with high sleep Apnea Indices. There was no relation between hypoxic and hypercapnic ventilatory responses during wakefulness and sleep Apnea Indices. But hypoxemia and hypercapnia worsened considerably during REM sleep. Myotonic dystrophy patients with sleep apnea presented increased pulmonary and systemic arterial pressures during sleep. It was also during sleep that arrhythmias were observed.
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PMID:Respiratory and hemodynamic study during wakefulness and sleep in myotonic dystrophy. 22 21

36 night sleep recordings were carried out on 15 patients suffering from myotonia dystrophica. 9 of these patients complained of diurnal hypersomnia. 10 patients had a disturbance of night sleep with a reduction of REM sleep sometimes associated with interruption of the recording with an increase in the light stages of sleep or alternatively with an increase of REM sleep with a reduction in the latency period of the first paradoxical sleep or with narcoleptic elements. 13 patients had abnormally early abolition of chin EMG activity, almost on falling asleep. 11 cases had pathological apnoeic episodes during sleep and in 9 of the 10 patients who underwent respiratory function studies there was a restrictive airways defect. In addition 9 had frank hypoxia without hypercapnia and 4 a right to left shunt. 3 clinically unaffected patients but with affected relatives were also investigated, 2 were found to have sleep disturbances 1 of which was associated with early abolition of tone.
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PMID:[Disturbances of wakefulness, sleep and respiratory function in Steinert's disease]. 92 30

We have examined the respiratory changes that occur during physiological sleep in three dogs with exteriorized cervical vagal loops. Sleep stage was determined by behavioral and EEG criteria. During non-REM (NREM) sleep breathing was slower (mean change, 23%),deeper (mean change, 18%), and less variable (coefficients of variation, 0.05-0.10) than during wakefulness (W); minute volume of ventilation (Ve) decreased (mean change, 14%) and alveolar CO2 pressure (PAco2) increased slightly (mean change, 1.3 mmHg). In addition, the rate of O2 consumption and ventilatory response to hypercapnia were decreased. In contrast, REM sleep was characterized by rapid, shallow, and considerably more irregular (coefficients of variation, 0.18-0.30) breathing; Ve increased markedly and PAco2 decreased (mean change, 5.2 mmHg). Blockade of both cervical vagus nerves produced comparable changes in each stage of sleep (W, NREM, REM): breathing became slower and deeper, but the differences between stages and the marked irregularity in REM sleep persisted. In contrast, the Hering-Breuer inflation reflex (HBIR) was strong in W and NREM sleep, but weak in REM sleep. The results indicate that changes in respiratory control and stability during sleep are not due to fluctuations in vagal influence despite the fact that one vagal reflex (HBIR) was sleep-state dependent.
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PMID:Regulation of respiration in sleeping dogs. 93 95

As sleep apnea is more prevalent in men and testosterone has known effects on sleep apnea and chemosensitivity, reduction of androgen activity may influence sleep-disordered breathing and respiratory control. We studied the effect of 1 wk of treatment with flutamide, a nonsteroidal antiandrogen, on sleep, respiration, and ventilatory control in eight men with sleep apnea. Results on flutamide were compared with two baseline studies performed before and after the drug treatment period. Although effective androgen blockade was achieved as evidenced by increased hormone levels, flutamide had no effect on sleep architecture or chemoresponsiveness to hypoxia and hypercapnia. There was a trend towards a reduction in respiratory disturbance index in both NREM and REM sleep (41 +/- 4 baseline versus 34 +/- 3 flutamide, p = 0.09 NREM; 53 +/- 4 baseline versus 48 +/- 3 flutamide, p = 0.16 REM), but this was not significant. Our results indicate that androgen blockade had no clinically significant effect on sleep, sleep-disordered breathing, or chemosensitivity in patients with moderate to severe sleep apnea. More specific blockers such as gonadotrophin-releasing hormone analogs may have more clinical effect or, alternatively, androgen blockade may be more beneficial in patients with milder sleep apnea.
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PMID:Androgen blockade does not affect sleep-disordered breathing or chemosensitivity in men with obstructive sleep apnea. 145 53

The mechanism for arousal from sleep resulting from respiratory stimuli is unclear. We hypothesized that arousal is a result of increasing ventilation during sleep. To determine if this is true we compared minute ventilation at the point of arousal from non-REM sleep produced by the respiratory stimulant adenosine to that resulting from progressive hypercapnic stimulation. If this hypothesis is correct, the quantity of breathing immediately preceding arousal from sleep should be similar for each stimulus. We monitored electroencephalogram (EEG), electromyogram (EMG), end-tidal CO2, and inspired minute ventilation (VI) in five healthy young men during full-night sleep studies. Sleep state was monitored during the baseline state, during an intravenous infusion of 80 micrograms/kg/min of adenosine, and during multiple trials of progressive hyperoxic hypercapnia. Arousal from sleep occurred in association with increased breathing 4.2 +/- 1.1 times during adenosine infusion, 2.0 +/- 0 times during hypercapnic stimulation, and 4.0 +/- 0.6 times in the absence of stimulated breathing (spontaneously) per subject. Minute ventilation for the breath preceding arousal associated with adenosine stimulation (13.0 +/- 1.4 L/min) was similar to that preceding arousal caused by hypercapnia (12.9 +/- 1.1 L/min). In each case this level of breathing was greater than that preceding spontaneously occurring arousals (8.2 +/- 1.1 L/min), p less than 0.05). Although variable between subjects, there was a high correlation for these two variables within subjects (R = 0.96, p = 0.01). These data support the hypothesis that increasing ventilation induces arousal from sleep when ventilation is increased regardless of the stimulus producing this rising drive to breathe.
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PMID:Adenosine stimulation, ventilation, and arousal from sleep. 173 56

The percentage of the patients with PaCO2 more than 60 Torr and PaO2 more than 50 Torr were 13% in the patients with tuberculosis sequela (N = 502) and 4% in the patients with chronic obstructive lung disease (COLD, N = 727), who were treated with home oxygen therapy in the western region of Japan. Patients with chronic respiratory failure caused by tuberculosis sequela have higher PaCO2 than patients with COLD. Although the prognosis of patients with hypercapnia and moderate hypoxemia is not necessarily poor, some patients may need treatment for severe hypoventilation to prevent respiratory muscle fatigue and abnormal breathing during sleep. In this study, nine patients with hypercapnic chronic respiratory failure caused by tuberculosis sequela were ventilated by Chest Negative Pressure Ventilation (CNPV). The patients were monitored as in polysomnography by transcutaneous PCO2 (PtcCO2) electrode and Respiratory Inductance Plethysmography (RIP). Tidal volume induced by CNPV was larger during mouth breathing (504 +/- 128 ml, mean +/- s.d.) than during nose breathing (438 +/- 109 ml) calculated from RIP in awake state (N = 7). Oxygen saturation measured by ear oximeter and PtcCO2 were 94.4 +/- 2.9% and 57.8 +/- 12.2 Torr in awake state. Following CNPV SaO2 and PtcCO2 were 95.7 +/- 3.0%, 42.7 +/- 12.1 Torr in awake state (N = 9) and 93.0 +/- 4.4%, 57.0 +/- 15.7 Torr in Non-REM sleep (N = 5), respectively. CNPV is effective in these patients in awake state. During Non-REM sleep, CNPV maintains the PtcCO2 level only in awake state.
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PMID:[Tuberculosis sequelae: pathophysiological aspect (ventilation)]. 207 61

Arousal from sleep in response to asphyxia can be a lifesaving event. However, the mechanisms responsible for this important arousal response are uncertain. A unifying hypothesis is that arousal results from the increased respiratory effort that occurs as a result of ventilatory stimulation. If this is true, the magnitude of this effort during the breaths immediately preceding arousal from sleep should be similar regardless of the stimulus. Therefore, the negative inspiratory pleural pressure during the breaths preceding arousal would be similar, whether stimulated by added inspiratory resistive load, hypoxia, or hypercapnia. To test this hypothesis, we studied eight young, healthy men during full-night sleep studies. We measured their electroencephalography (EEG), electromyography (EMG), electrooculography (EOG), inspired ventilation (VI), end tidal PCO2 (PETCO2), O2 saturation, and esophageal pressure (esophageal balloon) while inducing arousal from non-REM sleep using (1) a 30-cm H2O/L/s added resistive load, (2) progressive hypoxia, and (3) progressive hyperoxic hypercapnia. All subjects were eventually aroused following the addition of the 30-cm H2O/L/s added load and during progressive hypercapnia. However, only six of the eight men were aroused when the O2 saturation was reduced to a minimum of 70%. For each stimulus, arousal occurred at very different levels of ventilation and arterial chemistry (SaO2 and CO2). However, ventilatory effort for each subject was similar at the point of arousal regardless of the stimulus. The peak-negative esophageal pressure for the single inspiration preceding arousal (for the six subjects arousing with all three stimuli) was 16.8 +/- 1.4 cm H2O for added resistive load, 15.0 +/- 2.4 cm H2O for hypoxia, and 14.7 +/- 2.1 cm H2O for hypercapnia. We conclude that increasing ventilatory effort may be the stimulus to arousal from sleep independent of the source of this rising drive to breathe.
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PMID:The influence of increasing ventilatory effort on arousal from sleep. 238 92

The CSF pressure was measured continuously at the lumbar level during nocturnal sleep in 3 patients with sleep apnea hypersomnia syndrome. Nocturnal sleep was very unstable with frequent episodes of obstructive sleep apnea. When the patients were awake and relaxed in the supine position, their CSF pressure was stable and within the normal range. Episodic marked elevations of CSF pressure occurred frequently during sleep, and each elevation was preceded and accompanied by an episode of sleep apnea or hypopnea. Significant correlations were found between the duration of apneic episodes and increase of CSF pressure, and between decrease of SaO2 or TcPO2 and increase of CSF pressure. The duration of sleep apnea was longer, increase of CSF pressure was greater, and decreases of SaO2 and TcPO2 were more marked during REM sleep than during NREM sleep. It is suggested that the frequent marked episodic elevations of CSF pressure are caused by an increase in the intracranial vascular volume occurring mainly in response to transient hypercapnia and hypoxia, which are induced by pulmonary hypoventilation during the episodes of sleep apnea.
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PMID:Marked episodic elevation of cerebrospinal fluid pressure during nocturnal sleep in patients with sleep apnea hypersomnia syndrome. 257 29

Patients with IPD often develop oxygen desaturation during sleep. We investigated whether or not the degree of falls in SaO2 during sleep were correlated with the daytime data of pulmonary function tests, arterial blood gas tensions, or ventilatory responses to chemical stimuli. Fourteen patients with IPD who had restrictive ventilatory impairment were studied to evaluate these relationships. The magnitude of SaO2 depression from awake to REM sleep was inversely correlated with the level of baseline SaO2. Hypercapnic ventilatory response was inversely related to the amount of maximal desaturation in both REM and NREM sleep. These results indicate that patients with IPD who have insufficient ventilatory response to hypercapnia reveal larger falls in SaO2 during sleep, particularly if they have lower baseline SaO2.
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PMID:Arterial oxygen desaturation during sleep in interstitial pulmonary disease. Correlation with chemical control of breathing during wakefulness. 270 87

Administration of nocturnal oxygen for 1 night to patients with obstructive sleep apnea (OSA) causes a moderate reduction in apnea frequency without improving hypersomnolence. Therefore, we administered oxygen chronically to patients with OSA to determine: whether apnea frequency would be further reduced, whether the effect of oxygen upon apnea frequency is correlated with an increased ventilatory response to hypoxia and hypercapnia, and whether hypersomnolence improves with more prolonged oxygen administration. In a single-blinded, nonrandomized trial, we compared the effects of 1 month of oxygen (4 L/min by nasal cannula) with room air (4 L/min by nasal cannula) placebo during sleep in 7 men and 1 woman with obstructive sleep apnea. During non-REM sleep, acute oxygen administration elevated the average low oxy-hemoglobin saturation during apneic events and decreased apnea frequency. These acute effects persisted during chronic oxygen administration but reverted to the preoxygen effects immediately upon discontinuing oxygen. One month of oxygen did not affect the waking ventilatory response to hypoxia or hypercapnia; however, waking PaCO2 increased from 40 +/- 1 mm Hg (mean +/- SE) after placebo to 43 +/- 1 mm Hg after oxygen (p less than 0.01). Neither subjective nor objective hypersomnolence consistently improved after 1 month of oxygen administration. We conclude that: first, oxygen has no effect upon apnea frequency beyond the period of administration, and the reduction of apnea frequency is not correlated with an increased sensitivity to chemical ventilatory stimuli. The reduced apnea frequency may be related to an increased PaCO2 stimulating ventilation during sleep.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of chronic nocturnal oxygen administration upon sleep apnea. 309 78


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