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

The objective of this study was to assess ventilatory response to stimulation with CO2 in patients suffering obstructive sleep apnea syndrome (OSAS) but without chronic obstructive pulmonary disease (COPD), by examining differences between hyper- and normocapnic patients and comparing the results obtained with the usual techniques used to stimulate hypercapnia (rebreathing and stable-state). To this end, we studied 15 obese patients, all with an apnea-hypopnea index greater than 10 from a polysomnograph lasting a full night. The following lung function tests were performed: spirometry, air way resistance measures and static lung volumes by plethysmograph and arterial gasometry. We later analyzed ventilatory response by the stable-state method, with increasing CO2 concentrations (from 1 to 9%) and by the rebreathing method. Results from the two methods were similar for all patients: delta VE/delta PCO2 (0.64 +/- 0.35 vs 0.67 +/- 0.48 l/min/mmHg; p = 0.59), delta Vt/delta PCO2 (28.33 +/- 16.23 vs 26.42 +/- 16.94 ml/mmHg; p = 0.9), delta Vt/Ti/delta PCO2 (28.82 +/- 20.9 vs 29.41 +/- 23.78 ml/s/mmHg; p = 0.89) y delta P0.1/delta PCO2 (0.11 +/- 0.07 vs 0.117 +/- 0.05 cmH2O/mmHg; p = 0.58). We compared the results obtained by the two techniques by dividing the sample into two groups of 7 and 8 patients, respectively, depending on whether PaCO2 level before stimulation was higher or lower than 45 mmHg. The hypercapnic patients (group I) were older (61 +/- 3.5 vs 50 +/- 9 years; p = 0.04) but were not different with respect to body mass from the normocapnic patients (group II) (37.59 +/- 6.4 vs 34.56 +/- 4.75 kg/m2; p = 0.33). The results from the two techniques for stimulating hypercapnia were similar within each group, with a statistically significant decrease (p < 0.03) in patients with daytime hypercapnia in delta VE/delta PCO2 delta Vt/delta PCO2, delta Vt/Ti/delta PCO2 and delta P0.1/delta PCO2. We conclude that there are no differences in the results obtained with the rebreathing and stable state techniques. Likewise, ventilatory response to stimulation with CO2 in individuals with OSAS and daytime hypoventilation is less than of normocapnic patients.
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PMID:[Hypercapnic stimulation and ventilation response in the syndrome of sleep obstructive apnea. Comparison of reinhalation and steady state]. 896 13

We tested the hypothesis that the awake ventilatory response to hypoxia and hypercapnia may contribute to the variability of respiratory effort developed in response to upper airway obstruction in obstructive sleep apnea syndrome. The polygraphic recordings of 38 patients diagnosed as having obstructive sleep apnea on the basis of an apnea+hypopnea index greater than 10 were examined. All subjects received hypoxic and hypercapnic ventilatory tests the day before the nocturnal polysomnography. Thirty apneas during non-rapid eye movement (NREM) sleep and at least 10 apneas during rapid eye movement sleep were analyzed. For each considered apnea, we measured esophageal pressure (Pes) swings during the first three breaths preceding apnea and during the first three and last three occluded efforts occurring during the apnea. We considered as indices of respiratory effort the overall increase from the minimum to the maximum Pes (delta Pes), the rate of increase of Pes during apnea (RPes), and the maximal respiratory effort at the end of apnea (Pes max fin). In NREM sleep, all three indices of respiratory effort were correlated positively with the awake ventilatory response to hypoxia or hypercapnia and with the apnea index. No correlation was found between the indices of respiratory effort and body mass index, age, pulmonary function tests, awake blood gases, apnea duration, and apnea desaturation. In rapid eye movement sleep, none of the considered variables predicted the degree of respiratory effort. In conclusion, our results suggest that the degree of ventilatory response to upper airway occlusion in obstructive sleep apnea may be influenced by the sensitivity of central neural drive to chemical stimuli.
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PMID:Role of chemosensitivity in intrathoracic pressure changes during obstructive sleep apnea. 897 Mar 64

The pulmonary artery pressure (Ppa) responses to short runs of acute hypoxia at two different levels of end-tidal CO2 were measured in nine normal subjects and in 20 patients with moderate to severe obstructive sleep apnea (OSA). In normal subjects the mean increase in Ppa in response to eucapnic hypoxia was 8 +/- 2 mm Hg (SEM) and was not different from the response to hypercapnic hypoxia (9 +/- 2 mm Hg, p > 0.2). In patients with OSA, the mean increase of Ppa was 8 +/- 1 mm Hg to eucapnic hypoxia, and the response to hypercapnic hypoxia was higher at 10 +/- 1 mm Hg (p = 0.01). Pulmonary pressor response to hypoxia was augmented (> 10 mm Hg) by hypercapnia in four of 20 patients with OSA but in none of the normal subjects. Normoxic hypercapnia alone was a weak stimulus, increasing Ppa by > 5 mm Hg in only two of nine patients with OSA studied. In conclusion, Ppa increases in both normal subjects and patients with OSA exposed to a ramp of acute isocapnic hypoxia. There were clear interindividual differences in pulmonary artery response. Hypercapnia did not produce clinical significant changes in Ppa in either group.
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PMID:Pulmonary artery pressure response to hypoxia in sleep apnea. 900 11

Obstructive sleep apnea is a common breathing problem that results in recurrent episodes of nighttime hypoxemia, hypercapnia, bradytachycardia, and hypertension, as well as sleep disturbance and daytime hypersomnolence. The obstruction is located in the oropharynx and is caused by hypotonia of the pharyngeal dilator muscles. In this paper, the various mechanisms affecting motor output to the upper airway muscles are reviewed. In particular, the respiratory function of the pharyngeal dilator muscles, the various reflex mechanisms underlying their control, and the effects of sleep on these mechanisms are discussed. The literature relevant to the central neuronal circuits and neurotransmitters that may be involved in the state-dependent activity of the pharyngeal dilator muscles is also reviewed. In addition to an examination of these basic mechanisms, consideration is given throughout this review as to how these mechanisms may relate to the normal control of pharyngeal patency awake and asleep and how they may be involved in the pathogenesis of obstructive sleep apnea.
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PMID:Motor control of the pharyngeal musculature and implications for the pathogenesis of obstructive sleep apnea. 908 93

Episodes of sleep disordered breathing are surprisingly common in asymptomatic, middle-aged individuals. The majority of these events are hypopneas, rather than apneas. Even though these events cause rather modest decreases in arterial oxygen saturation, they evoke substantial increases in arterial pressure. In this population, mild to moderate sleep disordered breathing is associated with elevated daytime blood pressure. The mechanisms responsible for the acute and chronic cardiovascular effects of sleep disordered breathing are incompletely understood. Chemoreflex mechanisms appear to be more important than intrathoracic pressure changes in causing the acute elevation in arterial pressure that occurs after obstructive sleep apnea. Arousal from sleep may contribute to this pressor response, either in an additive or synergistic manner. Relatively brief exposure to combined hypoxia and hypercapnia during wakefulness can produce an increase in sympathetic outflow to skeletal muscle that persists after return to room air breathing. This lingering post-asphyxic effect on sympathetic outflow may be the basis of chronically elevated sympathetic nervous system activity which accompanies sleep apnea syndrome and may contribute to sustained hypertension in these individuals.
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PMID:Acute and chronic cardiovascular responses to sleep disordered breathing. 908 12

We measured inspiratory resistance (R1), inspiratory occlusion pressure (P0.1), and the ventilatory responses to hypercapnia and isocapnic hypoxia during waking and during stage 2 non-rapid eye movement sleep in nine young men who were habitual snorers. They were studied on 2 nights during the 3 hours after receiving a bedtime drink containing either a placebo or 100-proof vodka (1.5 ml/kg) in orange juice. We compared the results with those we reported previously in 10 nonsnoring but otherwise similar men. Waking R1 was the same in nonsnorers and snorers, and it was not affected by ethanol. During sleep on the control night, R1 increased by 70% in nonsnorers and by 280% in snorers. On the ethanol night, the increase from waking to sleeping was more than doubled in both nonsnorers and snorers. P0.1 and the responses to hypercapnia and hypoxia showed no differences between nonsnorers and snorers, therefore the results from the two groups were pooled. Minute ventilation and the hypercapnic response decreased from waking to sleeping and P0.1 was more negative during sleep, but there was no significant effect of ethanol. There was a significant correlation between the changes from waking to sleeping in R1 and P0.1 on the ethanol night suggesting that inspiratory effort increased in response to the increased resistance. The response to isocapnic hypoxia showed no effect of either sleep state or drink. Inspiratory time did not change but mean inspiratory flow (VT/T1) was significantly reduced during sleep on both control and ethanol nights. The duty cycle ratio (T1/Ttot) was significantly increased during sleep on the ethanol night. Despite its great effect on inspiratory resistance, especially in snorers, ethanol, in the dose used in our study, does not augment the depression of minute ventilation or of the hypercapnic response that occur normally in stage 2 non-rapid eye movement sleep. After ethanol, our subjects showed the decreased VT/T1 and the increased T1/Ttot that occur normally during sleep in response to an inspiratory resistive load. However, they also showed increased inspiratory effort. The combination of increased inspiratory resistance and greater inspiratory effort would increase the tendency of an unstable upper airway to collapse and could account for the aggravation of obstructive sleep apnea by ethanol.
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PMID:Effect of bedtime alcohol on inspiratory resistance and respiratory drive in snoring and nonsnoring men. 911 50

Alcohol intake has been shown to worsen obstructive sleep apnea and increase nocturnal hypoxemia. The mechanisms of this action are unclear. Animal studies suggest that a reduction in chemoreflex sensitivity may be implicated. Using a double-blind, randomized, vehicle-controlled design, we tested the hypothesis that oral alcohol intake depresses chemoreflex sensitivity in humans. We examined the effects of oral alcohol intake (1.0 g/kg body wt) on blood pressure, heart rate, heart rate variability, muscle sympathetic nerve activity, forearm vascular resistance, and minute ventilation in 16 normal male subjects. Peripheral and central chemoreflex sensitivity were measured in response to hypoxia (n = 10) and hypercapnia (n = 6), respectively. Plasma alcohol increased from 0 to 23.2 +/- 1.5 mmol/L (107 +/- 7 mg/dL) at 60 minutes and 20.2 +/- 1 mmol/L (93 +/- 4 mg/dL) at 85 minutes after alcohol intake (P < .0001). Alcohol induced an increase in heart rate from 59 +/- 2 to 66 +/- 2 beats per minute (P < .01) and increased the ratio of low- to high-frequency variability of heart rate (P < .05). Although alcohol increased sympathetic nerve activity by up to 239 +/- 22% of baseline values (P < .01), forearm vascular resistance after alcohol was lower than that after vehicle (P < .05). Blood pressure did not increase compared with the vehicle session. Oxygen saturation during hypoxia after alcohol was 4 +/- 1% lower than it was during hypoxia after vehicle (P < .05) although arterial blood PO2 was unchanged. Alcohol did not affect the cardiovascular, sympathetic, or ventilatory responses to either hypoxia or hypercapnia. Acute increases in plasma alcohol increase heart rate and sympathetic nerve activity; blood pressure is not increased, probably because of vasodilator effects of alcohol. Alcohol does not alter chemoreflex responses to hypoxia or hypercapnia; thus, alterations in chemoreflex sensitivity are unlikely to explain the effects of alcohol on sleep apnea. Alcohol may reduce the affinity of hemoglobin for oxygen.
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PMID:Effects of alcohol on sympathetic activity, hemodynamics, and chemoreflex sensitivity. 918 Jun 29

To investigate the relationship between hypercapnia during sleep and its influence on the PaCO2 during the morning after sleep in patients with obstructive sleep apnea syndrome (OSAS), the transcutaneous PCO2 (PtcCO2) was measured throughout the night, and the arterial blood gases (ABG) were also measured while awake before and after polysomnography in 30 OSAS patients with (n=13, hypercapnic group: HC) and without (n=17, normocapnic group: NC) hypercapnia. Significant differences were observed in the body mass index (p=0.03), the difference between the highest PtcCO2 during sleep and the PtcCO2 during awake before sleep (D-PtcCO2), (HC: 11.l+/-1.7 mmHg; NC: 6.3+/-0.5 mmHg; p=0.0057) and the lowest SaO2 during sleep (p=0.0007). In the HC, the PaCO2 on the morning after sleep (50.0+/-0.14 mmHg) was significantly increased (p=0.0029) compared with the PaCO2 on the night before sleep (47.4+/-1.1 mmHg). In the NC, this phenomenon was not observed. Severe hypercapnia (high D-PtcCO2) during a single night's sleep has a significant effect on the waking PaCO2 immediately following sleep in the HC.
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PMID:Changes in the arterial PCO2 during a single night's sleep in patients with obstructive sleep apnea. 924 Apr 92

Even if different mechanisms of various interactions during sleep are known, it is still unsolved by which mechanisms physiological reactions during sleep may start a pathophysiological course. Hypoxia, Hypercapnia and repetitive sympathetic elevations are well known elements in the control of the arterial resistance. Furthermore investigations in patients with sleep apnea showed changes of the pulsatile secretion pattern within the renin-angiotensin-system and the antinatriuretic peptides. These changes were reversible under nasal CPAP-therapy, nycturia as a frequent symptom disappeared. Nevertheless neither hypoxia nor intrathoracic pressure changes nor the arousals can assert the longterm influence on the blood pressure alone, a multifactorial confluence must be assumed. Further it is unclear how a tonic increase of the arterial blood pressure may occur in dependence of the REM- and NREM-sleep cycle changes as well as during daytime. First investigations in sleeping man seem to indicate, that a disturbance of the physiological coupling of breathing and circulation may present a pathogenetic element. Finally it remains open, whether the changes of the cardiorespiratory coupling during sleep of control persons and of patients with OSA are comparable, and whether they may be procured for an explanation of the pathogenesis of arterial and pulmonary hypertension. Further investigations in the control mechanisms of breathing and circulation related to the circuits of chemo- and baroreception, thresholds during wakefulness and sleep may be of decisive help to process the question, to what extent clinical states find a correlate in a disturbed cardiorespiratory coupling and, much more significantly, whether a disturbance in the physiological cardiorespiratory coupling appears already in early states of a disease. Sleep with ist complex physiology as well as with its characteristic pathophysiological phenomenon of sleep related breathing disorders has opened a new interdisciplinary field where tools like the polysomnography and electronic data analysis are used by physiologists, pathophysiologists as well as by physicians.
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PMID:[Cardiorespiratory coupling in obstructive sleep apnea (OSA)]. 924 90

We studied 20 patients with obstructive sleep apnea syndrome (OSAS) prospectively, before and after administering continuous positive airway pressure through a nasal mask (CPAPn) at night for 10 months, with the aim of determining the effects of ventilatory pattern of long-term treatment with CPAPn in OSAS patients. The following data were collected for all patients: anthropometric variables, lung function test results, arterial gasometric readings at rest, oxygen alveolar-arterial differential [Dif(A-a)O2)], central respiratory function variables at rest and during hypercapnic stimulus. Mean duration (range) of treatment with CPAPn was 12.5 (10-18) months. We observed a significant increase in PaO2 (p = 0.01) and a decrease in PaCO2 (p = 0.02) with slight variations in body weight and no changes in lung mechanics or in Dif(A-a)O2. The ventilatory pattern at rest showed an increased in VE and in respiratory frequency (p = 0.0003 and p = 0.033, respectively) with non significant changes in VT. The VT/Ti ratio increased (p = 0.015) and P0.1 decreased slightly (p = 0.025). We found no significant changes in the CO2 response slopes of VE or P0.1. In conclusion, CPAPn improves hypoxemia and hypercapnia in OSAS patients, above all by increasing baseline basal ventilation. The exact mechanisms implicated are poorly understood, but our data suggest a certain direct or indirect effect on respiratory muscles, reducing muscle fatigue, thus favoring greater availability during sleep.
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PMID:[Long-term effects of nasal continuous positive airway pressure on ventilatory patterns of patients with obstructive sleep apnea syndrome]. 928 May 59


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