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

We have previously described a canine model of obstructive sleep apnea (OSA) in which sleep-wake state is monitored continuously by a computer that produces tracheal occlusion when sleep occurs. Our aim was to assess the effects of long-term application of this model on resting ventilation and on the ventilatory and arousal responses to hypercapnia and hypoxia. Five dogs were maintained on the model for 15.5 +/- 1.7 (mean +/- SE) wk, with a mean apnea index of 57.5 +/- 4.5 occlusions/h of sleep. Resting ventilation and the ventilatory and arousal responses to progressive hypoxic and hypercapnic rebreathing were assessed during wakefulness (W) and both slow-wave (SWS) and rapid-eye-movement (REM) sleep at baseline prior to intervention, at the end of the OSA phase, and following a 1 to 3-mo recovery period. During the period of OSA there were small changes in respiratory timing at rest, but no significant changes in PCO2 or SaO2. As compared with baseline, the ventilatory response to hypoxia during OSA was strikingly reduced during W, and significantly although less markedly reduced during SWS and REM. The reduction was due to a decreased breathing frequency response to hypoxia. In addition, during OSA there was a significant decrease from baseline in SaO2 at arousal during hypoxic rebreathing in both SWS and REM. All responses returned to normal during recovery. In contrast to hypoxia, hypercapnic ventilatory responses during OSA were slightly increased over their baseline values both in W and SWS, owing to a leftward shift of the ventilation-versus-PCO2 relationship. During recovery, these responses reverted partly to baseline for W and reverted completely to baseline for SWS. There were no significant changes in arousal PCO2 during hypercapnic rebreathing in either SWS or REM across the pre-OSA baseline, OSA, and post-OSA recovery periods. We conclude that long-term application of the OSA model is associated with a selective, reversible decrease in ventilatory and arousal responses to hypoxia.
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PMID:Ventilatory and arousal responses to hypoxia and hypercapnia in a canine model of obstructive sleep apnea. 931 9

Sleep is characterized by many changes in the respiratory system, including a reduction in respiratory motor output associated with the loss of wakefulness, increased upper airway resistance, and blunted protective reflexes (such as load compensation), that result in reduced alveolar ventilation. The development of carbon dioxide retention appears to be linked to the exaggeration of sleep-related changes on ventilation by coexistent respiratory system disorders. Sleep-disordered breathing is becoming increasingly recognized in subjects with neuromuscular diseases, who may be prone to nocturnal respiratory events due to diaphragm and bulbar muscle weakness, abnormal central respiratory control, obesity, and sleep position restrictions. Nocturnal gas exchange deterioration may occur in patients with chronic obstructive pulmonary disease, particularly during rapid eye movement sleep when activity of the respiratory muscles other than the diaphragm is inhibited. Concurrent obstructive sleep apnea syndrome may further compromise nocturnal ventilation, thereby contributing to the development of acute or chronic respiratory failure. The use of noninvasive nocturnal ventilation at night has resulted in significant improvements in symptoms of hypoventilation and daytime carbon dioxide retention in various clinical settings, yet important questions remain about implementation of this modality.
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PMID:Sleep-wake cycles and the management of respiratory failure. 936 92

The authors have studied chemical control of breathing in 37 normocapnic patients with OSA. These patients had increased apnea-hypopnea index (AHI = 51 +/- 22), obesity (BMI = 32.4 +/- 5.6 kg/m2) and normal lung function tests. Control group consisted of 20 healthy subjects with normal weight (BMI = 23.1 +/- 2.4 kg/m2). Respiratory responses (ventilatory and P0.1) to hypercapnic and hypoxic stimulation during rebreathing tests were measured with computerized methods. The obtained results in OSA patients were compared with the data of the control group. The results exceeding mean values of the control group above 1.64 SD were recognized as hyperreactive responses. The majority e.g. 26 patients (OSA-N) had normal respiratory responses during hypercapnic stimulation. delta V/delta PCO2 = 16.8 +/- 4.5 L/min/kPa, P0.1/delta PCO2 = 3.5 +/- 2.4 cm H2O/kPa/. In remaining 11 patients (OSA-H) respiratory responses were significantly increased delta V/delta PCO2 = 39.1 +/- 18.8 L/min/kPa, P0.1/delta PCO2 = 8.6 +/- 3.9 cm H20/kPa). During isocapnic hypoxic stimulation majority e.g. 25 patients (OSA-H) had significantly increased respiratory responses delta V/delta SaO2 = 3.28 +/- 1.63 L/min/%, delta P0.1/delta SaO2 = 0.54 +/- 0.43 cm H2O/%/. In remaining 12 patients (OSA-N) respiratory responses were within normal limits delta V/SaO2 = 1.2 +/- 0.28 L/min/%, delta P0.1/ delta SaO2 = 0.21 +/- 0.07 cm H2O/%/. The above results indicated, that majority OSA patients (67.5%) had increased ventilatory and P0.1 responses to hypoxic stimulation. Among them also 11 patients had increased respiratory responses to hypercapnia. It seems, that increased respiratory responses to hypoxic stimulus in OSA patients are symptoms of protective reaction to hypoxaemia occurring during repetitive sleep apnoea and reveals increased neuro-muscular output.
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PMID:[Chemical control of breathing in patients with obstructive sleep apnea]. 941 Feb 80

Patients with obstructive sleep apnea experience repetitive apneic events during sleep, with consequent hypoxia and hypercapnia. Hypoxia and hypercapnia, acting via the chemoreflexes, elicit increases in sympathetic nerve activity. The sympathetic responses to hypoxia and hypercapnia are potentiated during apnea, when the sympathetic inhibitory influence of the thoracic afferent nerves is eliminated. As a consequence of the sympathetic vasoconstrictor response to apneic events, patients with obstructive sleep apnea manifest marked increases in blood pressure during sleep, especially evident at the end of the apnea. The increases in sympathetic activity and blood pressure during sleep in these patients appear to carry over into the daytime such that patients with sleep apnea have an increased prevalence of hypertension and high levels of sympathetic nerve activity. Although the mechanism underlying the persistent elevation in sympathetic activity during the daytime is not known, it is likely that the increased sympathetic drive is implicated in the higher daytime blood pressures in these patients. Whereas patients with sleep apnea have an increased prevalence of hypertension, in those patients with sleep apnea who do have hypertension, the sympathetic response to apneic events may be potentiated. This may be secondary to impaired baroreflex sensitivity, since the baroreflexes exert an inhibitory influence on the chemoreflex responses to hypoxia. Treatment with continuous positive airway pressure results in an acute reduction in blood pressure and sympathetic activity during sleep. Prolonged effective treatment of sleep apnea may also reduce daytime blood pressure levels. This review examines the physiology of the chemoreflex responses to hypoxia, hypercapnia and apnea, as well as the physiologic responses to sleep in normal humans. These physiologic responses are compared with the pathophysiologic sympathetic and hemodynamic responses that characterize obstructive sleep apnea. Increases in sympathetic activity and blood pressure in patients with obstructive sleep apnea may play a role in linking sleep apnea to hypertension and cardiac and vascular events.
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PMID:The sympathetic nervous system and obstructive sleep apnea: implications for hypertension. 948 12

A two-year-old boy with a history of slow growth, snoring during sleep and adenoid hypertrophy underwent adenoidectomy and transtympanic drainage under general anesthesia. Immediately after extubation, severe inspiratory stridor and shallow labored breathing began and persisted over a period of two hours, in spite of corticoid administration and oxygen therapy. The signs receded partially when the patient was seated and with a mandibular traction maneuver. As symptoms persisted, foreign body obstruction was ruled out by examination of the cavum and upper airway under general anesthesia and with orotracheal intubation. The patient was transferred to the pediatric intensive care unit, where he remained intubated for 18 hours. After extubation, stridor and shallow labored breathing reappeared but gradually receded as the residual effects of sedation disappeared. The parents mentioned symptoms suggestive of obstructive sleep apnea syndrome (OSAS) occurring since the boy was 6 months old and that had worsened in recent months. OSAS in children is characterized by intermittent obstruction of the upper airway during sleep, causing snoring and periods of apnea/hypopnea that lead to hypoxemia and hypercapnia. The most frequent cause is hypertrophy of the adenoid and tonsils, and the treatment of choice is adenotonsillectomy, although the risk of postoperative respiratory distress in such children is high. It is important to rule out OSAS in children who are candidates for adenotonsillectomy so that such patients are not scheduled for ambulatory surgery, but rather given adequate postoperative monitoring and treatment.
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PMID:[Compromized postadenoidectomy respiration in a child with obstructive sleep apnea syndrome]. 949 65

Abnormal central regulation of upper airway muscles may contribute to the pathophysiology of the childhood obstructive sleep apnea syndrome (OSAS). We hypothesized that this was secondary to global abnormalities of ventilatory control during sleep. We therefore compared the response to chemical stimuli during sleep between prepubertal children with OSAS and controls. Patients with OSAS aroused at a higher PCO2 (58 +/- 2 vs. 60 +/- 5 Torr, P < 0.05); those with the highest apnea index had the highest arousal threshold (r = 0.52, P < 0.05). The hypercapnic arousal threshold decreased after treatment. For all subjects, hypoxia was a poor stimulus to arousal, whereas hypercapnia and, particularly, hypoxic hypercapnia were potent stimuli to arousal. Hypercapnia resulted in decreased airway obstruction in OSAS. Ventilatory responses were similar between patients with OSAS and controls; however, the sample size was small. We conclude that children with OSAS have slightly blunted arousal responses to hypercapnia. However, the overall ventilatory and arousal responses are normal in children with OSAS, indicating that a global deficit in respiratory drive is not a major factor in the etiology of childhood OSAS. Nevertheless, subtle abnormalities in ventilatory control may exist.
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PMID:Arousal and ventilatory responses during sleep in children with obstructive sleep apnea. 960 86

The presence of abnormalities of the respiratory center in obstructive sleep apnea (OSA) patients and their correlation with polysomnographic data are still a matter of controversy. Moderately obese, sleep-deprived OSA patients presenting daytime hypersomnolence, with normocapnia and no clinical or spirometric evidence of pulmonary disease, were selected. We assessed the ventilatory control and correlated it with polysomnographic data. Ventilatory neuromuscular drive was evaluated in these patients by measuring the ventilatory response (VE), the inspiratory occlusion pressure (P.1) and the ventilatory pattern (VT/TI, TI/TTOT) at rest and during submaximal exercise, breathing room air. These analyses were also performed after inhalation of a hypercapnic mixture of CO2 (delta P.1/delta PETCO2, delta VE/delta PETCO2). Average rest and exercise ventilatory response (VE: 12.2 and 32.6 l/min, respectively), inspiratory occlusion pressure (P.1: 1.5 and 4.7 cmH2O, respectively), and ventilatory pattern (VT/TI: 0.42 and 1.09 l/s; TI/TTOT: 0.47 and 0.46 l/s, respectively) were within the normal range. In response to hypercapnia, the values of ventilatory response (delta VE/delta PETCO2: 1.51 l min-1 mmHg-1) and inspiratory occlusion pressure (delta P.1/delta PETCO2: 0.22 cmH2O) were normal or slightly reduced in the normocapnic OSA patients. No association or correlation between ventilatory neuromuscular drive and ventilatory pattern, hypersomnolence score and polysomnographic data was found; however a significant positive correlation was observed between P.1 and weight. Our results indicate the existence of a group of normocapnic OSA patients who have a normal awake neuromuscular ventilatory drive at rest or during exercise that is partially influenced by obesity.
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PMID:Assessment of ventilatory neuromuscular drive in patients with obstructive sleep apnea. 969 1

Because of the oscillatory pattern of upper airway resistance and breathing during sleep in patients with obstructive sleep apnea (OSA), we hypothesized that OSA patients have an underlying instability of ventilatory drive to inspiratory muscles. To assess the stability of ventilatory drive in OSA patients and controls, we used the pseudorandom binary stimulation (PRBS) test and examined the closed- and open-loop responses to hyperoxic hypercapnia. The closed-loop response is produced by interactions of dynamic gain in controller, plant, and ventilatory feedback. The open-loop response reflects controller dynamic gain or frequency-dependent chemosensitivity. As compared with 16 nonapneic, nonobese control subjects, a group of nine obese OSA patients had a higher peak response and a more rapid and irregular recovery phase of the closed-loop CO2 response in the PRBS test. The two groups had similar open-loop responses in the PRBS test, suggesting that central dynamic CO2 chemosensitivity was not abnormal in OSA. We conclude that the differences between OSA patients and controls in the closed-loop response in the PRBS test are not due to differences in dynamic controller gain, but are related to differences in dynamic plant gain and/or negative ventilatory feedback. In addition to OSA, obesity may affect these variables and may have been responsible for our findings.
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PMID:Instability of ventilatory control in patients with obstructive sleep apnea. 976 73

Several studies have demonstrated a clear association between snoring, sleep apnoea and increased risk of stroke. However, the possible role of sleep apnoea in the pathophysiogenetic mechanisms of cerebrovascular disease is still unknown. Our aim in this study was to investigate cerebral haemodynamic changes during the waking state in eight patients with sleep apnoea syndrome (OSAS) by means of transcranial Doppler (TCD). In particular, we studied cerebral vascular reactivity (CVR) to hypercapnia calculated by means of the breath holding index (BHI). The investigation was performed in the early morning, soon after awakening, and in the late afternoon. Data were compared with those of eight healthy subjects matched for age and vascular risk factors. OSAS patients showed significantly lower BHI values with respect to controls both in the morning (0.56 vs. 1.36; P < 0.0001) and in the afternoon (1.12 vs. 1.53; P < 0.0001). In patients, BHI values in the afternoon were significantly higher than in the morning (P < 0.0001). These data demonstrate a diminished vasodilator reserve in OSAS patients, particularly evident in the morning. This reduction of the possibility of cerebral vessels to adapt functionally in response to stimulation could be linked to hyposensitivity of cerebrovascular chemoreceptors after the continuous stress caused by nocturnal hypercapnia.
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PMID:Impairment of daytime cerebrovascular reactivity in patients with obstructive sleep apnoea syndrome. 984 56

In the present study, respiratory drives to chemical stimuli and peripheral chemosensitivity were evaluated in patients with obstructive sleep apnoea (OSAS). The effects of oral administration of domperidone, a selective dopamine D2-receptor antagonist, were also examined, to study the respiratory effects of endogenous dopamine on peripheral chemoreceptors. Sixteen patients with OSAS and nine normal control subjects were studied. Respiratory responses to hypercapnia and hypoxia were measured using the rebreathing method and isocapnic progressive hypoxia method, respectively. The hypoxic withdrawal test, which measures the decrease in ventilation caused by two breaths of 100% O2 under mild hypercapnic hypoxic conditions (end-tidal oxygen and carbon dioxide tensions approximately 8.0 kPa and 5.3-6.7 kPa, respectively), was used to evaluate peripheral chemosensitivity. In the patients with OSAS, ventilatory responses to hypercapnia and hypoxia were significantly decreased compared with those of control subjects. Hypoxic withdrawal tests showed that peripheral chemosensitivity was significantly lower in patients with OSAS than in normal subjects. Hypercapnic ventilatory response and peripheral chemosensitivity were enhanced by administration of domperidone in the patients with OSAS, although no changes in either of these were observed in the control subjects. The hypoxic ventilatory response and peripheral chemosensitivity in the patients with OSAS were each significantly correlated with severity of hypoxia during sleep. These findings suggest that peripheral chemosensitivity in patients with obstructive sleep apnoea syndrome may be decreased as a result of abnormality in dopaminergic mechanisms and that the reduced chemosensitivity observed in patients with obstructive sleep apnoea syndrome may affect the severity of hypoxia during sleep.
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PMID:Depression of peripheral chemosensitivity by a dopaminergic mechanism in patients with obstructive sleep apnoea syndrome. 1006 91


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