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

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

The larynx has three functions: phonation, airway protection, and respiration. Few studies have dealt with laryngeal respiratory function. To elucidate respiratory regulation by the larynx, we studied the changes in the activity of the intrinsic laryngeal muscles during hypercapnia in decerebrated cats. The electromyographic activities of the posterior cricoarytenoid (PCA) and thyroarytenoid (TA) muscles were recorded simultaneously with an electromyogram of the diaphragm, endotracheal pressure, and concentrations of O2 and CO2. The activity of the intrinsic laryngeal muscles during hypercapnia (end-tidal CO2, 8% to 10%) was analyzed in comparison with that during eucapnia. In hypercapnia, both the PCA and TA muscles increased their activities, and the endotracheal pressure during expiration was elevated to a higher level than that in eucapnia. TA muscle activities returned to the level during eucapnia after ligation of the common carotid arteries. These findings suggest that hypercapnia causes a further widening of the glottis during inspiration to decrease inspiratory resistance and a further narrowing of the glottis during expiration to prevent alveolar collapse. Thus it may be concluded that the larynx actively participates in respiratory regulation under the control of the brain stem through a process of peripheral inputs from the carotid receptors.
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PMID:Changes in laryngeal muscle activities during hypercapnia in the cat. 1006 54

O-Isobutyl S-[2-(diethylamino)ethyl]methylphosphonothioate (VR) is a structural isomer of a more well-known chemical warefare agent, O-ethyl S-[2(diisopropylamino)ethyl]methylphosphonothioate (code designation VX). In this study, cardiorespiratory and central nervous system (CNS) effects of VR (2LD50 or 22.6 microg kg(-1); s.c.) were evaluated in urethane-anesthetized (Group 1) and unanesthetized (Group 2) guinea pigs instrumented for concurrent recordings of electrocorticogram (ECoG) and a variety of cardiorespiratory activities. The first sign of intoxication was a state of progressive bradycardia, vascular hypotension and arrhythmia (Group 1, approximately 13 min post-VR; Group 2, approximately 6 min post-VR). Bradypnea, excessive salivation and compensatory changes in blood pressure typically did not emerge until 3-5 min prior to apnea (Group 1, approximately 28 min post-VR; Group 2, approximately 15 min post-VR). An idioventricular rhythm, which signalled a failing myocardium, appeared at the same time or shortly after the development of a bradypneic profile. Another notable toxicity component of VR, based on arterial pH, pO2/pCO2 and bicarbonate (HCO3-) level data, was a state of combined hypercapnia, acidemia and hypoxemia during the development of bradypnea. Taken together, findings from this study indicated that changes in medullary respiratory unit activity and ECoG data displayed little, if any, notable signs of CNS perturbation prior to the terminal stage (approximately 1 min prior to respiratory failure). Thus, in addition to displaying a greater sensitivity to perturbation by VR, the peripheral cardiorespiratory system components also appeared to play a more important role in precipitating a progressively dysfunctional cardiorespiratory status that ultimately led to collapse of central respiratory mechanisms and death.
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PMID:Cardiorespiratory effects of O-isobutyl S-[2-(diethylamino)-ethyl] methylphosphonothioate -- a structural isomer of VX. 980 34

The breaking of the interalveolar septa represents, in the pathogenetic mechanism of emphysema, a final event, common to the different etiologic agents. This elementary injury causes a series of consequences, essentially of mechanic-structural type (intrapulmonary aerial spaces-confining parenchyma collapse, bronchial obstruction, dead space augmentation) on the thin and articulate bronchoalveolar architecture, whose final rearrangement determines, at least in part, the clinical picture. In short, the break of alveolar septa involves the formation of intraparenchymal aerial spaces with collapse of the confining lung; the compensatory mechanism to this situation, involves the hyperexpansion of the thoracic cage and flattening of the diaphragm, with the aim of allowing ventilation of the healthy residual parenchyma. Because of the finite capability of expansion of the thoracic cage and of the diaphragm in respect to the theoretical capability of the lung of large intraparenchymal aerial spaces formation, it is easy to imagine that emphysema can cause a serious functional respiratory deficit even before a significant quantity of pulmonary parenchyma is destroyed by the pathogenic process. It may then be hypothesized that a simple reduction of the volume of the lung, even sacrificing a part of "working" parenchyma, might allow the residual lung to come back to a normal ventilation, wholly ameliorating the respiratory exchanges. The clinically more remarkable consequence of lung volume reduction is the amelioration of ventilation mechanics with a decreased respiratory work due to the shift of the tidal volume toward values less proximal to the maximal expandability of the thoracic wall and of the diaphragm. On the other end, it is possible to anticipate an equally significant effect on bronchial obstruction, due to the more favorable matching of the compliance of the thoracic wall and that of the lung. LVRS has significant effect on the TV sharing ratio between emphysematous spaces and residual healthy parenchyma; the hyperexpansion of the residual lung in fact causes the distension of the emphysematous spaces, continuing in the natural compensatory mechanism of the emphysema. The decreased ventilation and thus re-breathing of the residual emphysematous spaces, together with the improved ventilation may ameliorate hypercapnia. Obviously no direct effects can be expected from LVRS on the conditions of the alveolar membrane and thus on gas diffusion capacity through it. The time duration of the amelioration achieved with the lung volume reduction is still to be demonstrated.
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PMID:[The surgical physiopathology of essential pulmonary emphysema and volume-reduction intervention]. 997 94

Obstructive sleep apnoea (OSA) is a potentially life-threatening breathing disorder characterized by repeated collapse of the upper airway during sleep, with cessation for breathing. Patients with OSA are at risk of severe cardiovascular and respiratory complications secondary to recurrent hypoxia and hypercapnia in addition to an overall reduced quality of life for sufferers and their families. An overview of the aetiology including pathophysiology, clinical signs and symptoms and diagnosis was presented in the first article in this series. In this article the management of OSA is presented, with particular emphasis on the role of dentistry in contemporary management.
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PMID:The relationship between obstructive sleep apnoea and dentistry: 2. Management. 1047 9

Obstructive sleep apnoea is a potentially life-threatening breathing disorder characterized by repeated collapse of the upper airway during sleep, with cessation of breathing. Patients are at risk of severe cardiovascular and respiratory complications secondary to recurrent hypoxia and hypercapnia and the overall quality of life for sufferers and their families may be reduced. This article gives an overview of the aetiology (including pathophysiology), clinical signs and symptoms, diagnosis and treatment. The role dentistry can play in contemporary management of the disorder will be discussed in a second article.
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PMID:The relationship between obstructive sleep apnoea and dentistry: 1. Aetiology and diagnosis. 1047 30

To elucidate the role of serotonin in the maintenance of normal breathing and upper airway (UA) patency in obesity, we studied the effects of systemic administration of ritanserin, a serotonin (5-HT) 2A and 2C receptor antagonist, on ventilation (V E) during room air breathing and during hypoxic (10% O2) and hypercapnic (4% CO2) ventilatory challenges in awake young (6-8 wk) and older (7-8 mo) obese and lean Zucker (Z) rats. Older obese Z rats adopted a more rapid shallow breathing pattern compared with older lean rats. The administration of ritanserin (1 mg/kg intraperitoneally) to older obese rats resulted in a reduction in V E (439 +/- 35 [SD] to 386 +/- 41 ml/kg/min, p < 0.01), a decrease in respiratory rate, a prolongation of inspiratory time, and an increase in V O2 (16.4 +/- 1.7 to 18.2 +/- 1.9 ml/kg(0.75)/min, p < 0.05) during room air breathing. By comparison, it had little effect on ventilation in young lean and obese Z or older lean Z rats. Ritanserin also had no effect on ventilatory responses to either hypoxia or hypercapnia in young or older lean and obese Z rats. The collapsibility of the isolated UA was examined in older Z rats. The pharyngeal critical pressure (Pcrit) of older obese rats was significantly greater than that of lean rats (p < 0.05), indicating that obese rats have more collapsible UA than lean rats. The administration of ritanserin significantly increased Pcrit in older obese rats (-1.6 +/- 0.3 to -0.8 +/- 0.2 cm H2O, p < 0.01) and in lean rats (-3.1 +/- 1.0 to -2.4 +/- 0.6 cm H2O, p < 0.05). We suggest that the 5-HT(2A/2C) receptor subtype plays an important role in the maintenance of UA stability and normal breathing in obesity, and we speculate that older obese Z rats may have augmented serotonergic control of UA dilator muscles as a mechanism to prevent pharyngeal collapse.
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PMID:Serotonergic modulation of ventilation and upper airway stability in obese Zucker rats. 1131 30

Obstructive sleep apnoea is a disease of increasing importance because of its neurocognitive and cardiovascular sequelae. Abnormalities in the anatomy of the pharynx, the physiology of the upper airway muscle dilator, and the stability of ventilatory control are important causes of repetitive pharyngeal collapse during sleep. Obstructive sleep apnoea can be diagnosed on the basis of characteristic history (snoring, daytime sleepiness) and physical examination (increased neck circumference), but overnight polysomnography is needed to confirm presence of the disorder. Repetitive pharyngeal collapse causes recurrent arousals from sleep, leading to sleepiness and increased risk of motor vehicle and occupational accidents. The surges in hypoxaemia, hypercapnia, and catecholamine associated with this disorder have now been implicated in development of hypertension, but the association between obstructive sleep apnoea and myocardial infarction, stroke, and congestive heart failure is not proven. Continuous positive airway pressure, the treatment of choice for obstructive sleep apnoea, reduces sleepiness and improves hypertension.
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PMID:Obstructive sleep apnoea. 1250 19

Non-invasive positive pressure ventilation (NIPPV) has been discussed comprehensively in the last years, but usage of non-invasive ventilation in Intensive Care Units is rare. The reasons may be uncertainty in indications and difficulties in handling the masks and ventilators. In the last years the introduction of full face masks and respiratory helmets has made it possible to ventilate patients with unusual facial forms and to avoid problems of pressure necrosis. Software components designed for NIPPV are available for standard respirators. Indications for NIPPV (neuromuscular diseases, spinal abnormalities, chest wall malformations, COPD, cardiogenic pulmonary edema) have been ensured in clinical trials. No sufficient data are available for the application of NIPPV in weaning and respiratory failure following extubation. Indication for NIPPV becomes apparent when therapy starts in early stage with sufficient ventilation pressure. Compared to standard therapy, no reliable advantage has been seen for NIPPV in hypoxic hypercapnia respiratory failure except for malignant diseases. However, prophylactic use in patients with high risk might be conceivable. For these patients strict criteria of termination are required to avoid missing the time point for intubation. Gas exchange disturbances in advanced lung fibrosis, pneumonia and ARDS are not amenable to NIPPV. Contraindications for NIPPV are non-compliant patients, absence of cough- and pharyngeal reflexes as well as retention of secretions and malignant ventricular arrhythmia. Relative contraindications are catecholamine-dependent circulatory collapse and acute myocardial infarction, since sufficient data for NIPPV are missing.
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PMID:[Noninvasive ventilation in the intensive care unit -- is it still negligible?]. 1267 84

Normal children have a less collapsible upper airway in response to subatmospheric pressure administration (P(NEG)) during sleep than normal adults do, and this upper airway response appears to be modulated by the central ventilatory drive. Children have a greater ventilatory drive than adults. We, therefore, hypothesized that children have increased neuromotor activation of their pharyngeal airway during sleep compared with adults. As infants have few obstructive apneas during sleep, we hypothesized that infants would have an upper airway that was resistant to collapse. We, therefore, compared the upper airway pressure-flow (V) relationship during sleep between normal infants, prepubertal children, and adults. We evaluated the upper airway response to 1). intermittent, acute P(NEG) (infants, children, and adults), and 2). hypercapnia (children and adults). We found that adults had a more collapsible upper airway during sleep than either infants or children. The children exhibited a vigorous response to both P(NEG) and hypercapnia during sleep (P < 0.01), whereas adults had no significant change. Infants had an airway that was resistant to collapse and showed a very rapid response to P(NEG). We conclude that the upper airway is resistant to collapse during sleep in infants and children. Normal children have preservation of upper airway responses to P(NEG) and hypercapnia during sleep, whereas responses are diminished in adults. Infants appear to have a different pattern of upper airway activation than older children. We speculate that the pharyngeal airway responses present in normal children are a compensatory response for a relatively narrow upper airway.
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PMID:Developmental changes in upper airway dynamics. 1499 May 59


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