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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We compared the effects of a placebo with 0.125 and 0.25 mg of triazolam (Halcion) on sleep quality, oximetry, and respiratory events during sleep in ten stable outpatients with chronic obstructive pulmonary disease. The subjects had a forced expiratory volume in 1 s ranging from 17% to 76% of the predicted value (mean +/- SD, 38.1% +/- 19%) and a waking arterial oxygen pressure from 46 to 84 mm Hg (mean +/- SD, 67 +/- 12 mm Hg). Polysomnography was done on three nights within a two-week period after the patients received on a "blinded" basis either placebo or 0.125 or 0.25 mg of triazolam. Triazolam produced improvements in total sleep duration, time spent in stage 2 nonrapid eye movement (NREM) sleep, and subjective of sleep quality. For most patients, there was a nighttime drop in arterial oxygen percentage of saturation (SaO2) in the placebo condition, but triazolam did not cause a significant worsening, of the mean SaO2, minimum SaO2, or the number of apneic and hypopneic events. Across all experimental conditions, we documented little desaturation during wakefulness (mean low, 87.2% +/- 10.2%), more during NREM sleep (mean low, 83.2% +/- 12.6%), and most desaturation in REM sleep (mean low, 80.1% +/- 15.7%). We conclude that single-night use of triazolam improved the quality and duration of sleep in patients with chronic obstructive pulmonary disease. In patients without severe waking hypoxemia and without carbon dioxide retention, triazolam did not increase either nocturnal hypoxemia or respiratory events during sleep.
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PMID:Effect of triazolam on sleep and arterial oxygen saturation in patients with chronic obstructive pulmonary disease. 317 73

Snoring usually is trivial and unimportant, but it can turn into a social or medical problem. Obesity, hypertension and heart disease are more frequent among snorers than among nonsnorers, and especially snorers with hypersomnia during the day are at risk. Hypersomnia in association with snoring usually signifies obstructive sleep apnea. Increased resistance in the upper airways, together with negative inspiratory pharyngeal pressure and muscular hypotonia during deep non-REM and REM sleep, lead to collapse of the pharynx, hypoxia and hypercapnia. Only after arousal from sleep does muscle tone return, pharyngeal obstruction reopen and airflow resume. Since this process can occur 300 or 400 times a night, repetitive alveolar hypoventilation leads to pulmonary-arterial hypertension and cor pulmonale, and the repetitive sympathetic activations can cause systemic hypertension or serious cardiac arrhythmias. The countless arousals deprive the sufferer of deep non-REM and REM sleep and their consequence is sleep fragmentation. The symptoms are excessive daytime sleepiness, intellectual deterioration and personality and behavioral changes. Oronasomaxillofacial, endocrine and neuromuscular anomalies and diseases predispose to sleep apnea, and alcohol or CNS-depressant drugs can favour its occurrence. Diagnosis is made by nighttime oxymetry, and if this is abnormal, by polysomnography. After polysomnography it is possible to distinguish between obstructive and nonobstructive sleep apnea, and the decisions for an adequate treatment can be made.
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PMID:[Dangerous snoring. Sleep-apnea syndrome]. 331 92

Severe nocturnal hypoxemia may occur in patients with respiratory muscle weakness caused by neuromuscular disorders. Negative pressure ventilators may be partially effective in these patients but can cause upper airway obstructive apneas. We examined the effectiveness of positive pressure ventilation through a nose mask in preventing nocturnal hypoxemia and compared it with negative pressure systems. We reasoned that nasal positive pressure would provide stability for the upper airway. Five patients with neuromuscular disorders underwent a series of all-night sleep studies under control conditions, negative pressure ventilation, and positive pressure ventilation through a comfortable nose mask. Sleep staging and respiratory variables were monitored during all studies. Daytime awake lung function, respiratory muscle strength, and arterial blood gases were also measured. The severe hypoxemia and hypercapnia that occurred under control conditions were prevented by positive pressure ventilation through a nose mask. Negative pressure ventilation improved NREM ventilation in all patients, but did not prevent severe oxyhemoglobin desaturation, which occurred during REM sleep. Negative pressure ventilation appears to contribute to upper airways obstruction during REM sleep as evidenced by cessation of air flow, reduced chest wall movements, falls in arterial oxyhemoglobin saturation, and hypercapnia. With treatment, daytime PaO2 improved from a mean of 70 to 83 mm Hg, and PaCO2 decreased from a mean of 61 to 46 mm Hg. We conclude that nasally applied positive pressure ventilation is a highly effective method of providing nocturnal assisted ventilation because it stabilizes the oropharyngeal airway.
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PMID:Treatment of respiratory failure during sleep in patients with neuromuscular disease. Positive-pressure ventilation through a nose mask. 354 13

Ventilatory and mouth occlusion pressure (P0.1) responses to progressive isocapnic-hypoxia and hyperoxic-hypercapnia were compared in eleven healthy sleeping men during the same night. Hypoxic and hypercapnic responses were determined during wakefulness, non-rapid and rapid-eye-movement sleep. The following parameters were measured: minute ventilation (VE), tidal volume (VT), 'duty cycle' (TI/TT), mean inspiratory flow rate (VT/TI) and P0.1, an index of the neuromuscular inspiratory drive. To allow a direct comparison between the two types of chemostimuli, responses were characterized by the value of the different parameters at 'equivalent' levels of hypoxia and hypercapnia, i.e., at levels which produced the same P0.1 during wakefulness: an oxyhaemoglobin saturation (Sao2) of 94% during the isocapnic-hypoxic tests (PETCO2 = 42.5 +/- 1.2 mmHg) was found to be equivalent to a PETCO2 of 47.4 +/- 3.7 mmHg during hypoxic-hypercapnic tests. For both tests, the arousal levels of the stimulus and of P0.1 were similar in all sleep stages. Sleep did not significantly modify P0.1 or breathing pattern responses to hypoxia (Sao2 = 94%). In contrast, at the 'equivalent' level of hypercapnic stimulation, P0.1 (P less than 0.05) and VE (P less than 0.01) responses were significantly impaired, particularly in REM sleep, with a decrease in VT (P less than 0.01) and VT/TI (P less than 0.05) responses. The results suggest that CO2 intracranial receptor mechanisms are more affected by sleep than the O2 peripheral receptor activity.
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PMID:Comparison between ventilatory and mouth occlusion pressure responses to hypoxia and hypercapnia in healthy sleeping man. 379 94

The heart rate in normal humans is determined by many factors. Assuming a normal hemoglobin concentration, left ventricular function, and metabolic rate, respiration, and its effects, along with autonomic nervous activity, appear to influence heart rate the most. Hypoxia and hypercapnia both increase heart rate during wakefulness and probably do the same during sleep. The hypoxic response is dependent on information from lung inflation and the carotid bodies. Respiratory rate, within limits, will determine the amplitude of the well-known (respiratory) sinus arrhythmia. During sleep, a distinct pattern of heart rate response and its respiratory arrhythmia are seen for each stage of sleep and are related to the level of autonomic nervous system activity during wakefulness. Blood pressure follows the same trend as heart rate during sleep, and changes in cardiac output and total peripheral vascular resistance are variable during sleep, but there is no consensus of opinion about the direction of these changes. Rhythm disturbances are predominantly those of bradyarrhythmias, exaggerated sinus arrhythmias, and transient AV block, which are probably occurring in REM sleep.
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PMID:Sleep and control of heart rate. 385 78

We determined the effect of nocturnal low-flow oxygen (NLFO) on arterial oxygen saturation (SaO2), transcutaneous PCO2 (TcPCO2), and sleep quality in 10 patients with cystic fibrosis (CF) and severe stable chronic obstructive pulmonary disease (COPD). The patients were studied on 2 nights, 1 with oxygen and 1 with air at 2 L/min. The NLFO had no effect upon sleep quality in our patients. The minimal SaO2 occurred during REM sleep and averaged 79.4%. With NLFO, this improved to 92.7%. The average maximal rise in TcPCO2 was 5.6 mmHg on falling asleep while breathing air; this increased a further 5.1 mmHg with NLFO. Two patients also had obstructive sleep apnea. Their SaO2 improved dramatically with NLFO, with no deterioration of ventilation. In 4 patients, ventilation was measured quantitatively. The only consistent changes during air were an increase in abdominal contribution to tidal volume and a drop in minute ventilation from Stage 3-4 to REM sleep of 26%, almost entirely caused by a drop in breathing frequency. The same changes occurred with NLFO. We conclude that NLFO is effective in alleviating the nocturnal hypoxemia of patients with CF with stable COPD and does not cause clinically important hypercapnia.
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PMID:The effect of oxygen on sleep, blood gases, and ventilation in cystic fibrosis. 642 55

We have carried out sequential studies of respiration and sleep state, from two weeks to two years of age in a girl with congenital central hypoventilation. When awake her minute ventilation (VE) and blood gases are normal, and when asleep she shows hypoventilation, with progressive hypoxia, hypercarbia and respiratory acidosis, most marked in NREM sleep. There has been no consistent change in VE (expressed as ml/kg/min) with age, awake or asleep, and she remains ventilator dependent when asleep. Growth and development are normal. We report a trial of almitrine bismesylate at the age of 21 months. A dose of 1.5 mg/kg/day orally for eight days produced minimal changes in VE, but when given 2.6 mg/kg/day for a further seven days there was a significant increase in VE in both NREM (27% increase) and in REM sleep (30% increase). These changes were accompanied by substantial improvements in blood gases, with PaCO2 less than 50 mmHg and PaO2 greater than 60 mmHg throughout a four hour study period asleep, off the ventilator, in air. After stopping almitrine bismesylate VE and blood gas values returned to pretreatment values. Almitrine bismesylate may be of value as an alternative to artificial ventilation in this condition.
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PMID:Almitrine bismesylate in congenital central hypoventilation. 642 94

Mild hypercapnia in the adult animal does not affect sleep pattern but more severe hypercapnia in the fetus increases the duration of REM sleep. Adult male rats were exposed daily for 2-3 h sessions at random to 6, 7, and 8% CO2 or room air. Breathing CO2 caused a 60% increase in sleep onset latency, a 28% decrease in sleep duration, but no change in percent time spent in REM. However, the duration of REM sleep episodes increased by 30%. Thus, in both fetal and adult animals severe hypercapnia appears to have a similar effect on sleep pattern.
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PMID:Hypercapnia alters sleep state pattern. 648 26

The effect of chloral hydrate (CH)-induced sleep on inspiratory drive has not been systematically assessed. To determine the effects of CH on the ventilatory responses to hypercarbia and to hypoxia, nine unanesthetized adult rabbit with chronic tracheostomy were studied. We compared awake ventilatory measurements before CH to non-REM sleep assessments at 30, 60, 90, and 120 min after administration of 250 mg/kg of CH. There were no significant differences between any of these assessment intervals for respiratory rate, PACO2, PAO2, tidal volume (VT), minute volume, Ti/Ttot, or VT/Ti. Hypercarbic ventilatory response to slopes were not diminished at any of the CH-sleep intervals compared to the awake mean slope. In addition, the ventilatory response to hypoxia at PAO2=70 mm Hg (V70) and the hypoxic response slope demonstrated no significant decrease at any of the CH-sleep intervals. In summary, absence of any significant decrease in either hypercarbic or hypoxic ventilatory response after CH administration indicates absence of any CH effect on chemical inspiratory drive.
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PMID:Experimental effects of chloral hydrate in ventilatory response to hypoxia and hypercarbia. 680 22

We studied the effects of hyperoxia and hypercapnia on obstructive apneic episodes (OAE) in a 39-year-old male with the sleep apnea and hypersomnolence syndrome (SAHS). While inspiring room air, our patient spent approximately 50% of his non-REM sleep time in OAE. When the inspired gas was changed to 100% oxygen, the frequency of the OAE decreased slightly, but a statistically significant increase in the duration of each episode was noted. Additionally, a CO2 rebreathe under hyperoxic conditions was carried out during non-REM sleep; no OAE were noted during this rebreathe. Therefore, this latter observation suggests that hypercapnia under hyperoxic conditions may reduce the frequency of OAE in patients with the SAHS.
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PMID:Effects of respiratory gases on the frequency and duration of obstructive apneic episodes in a patient with the sleep apnea-hypersomnolence syndrome. 680 21


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