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

We report two cases of patients with Von Recklinghausen disease. They exhibited typical cutaneous and diffuse intrapulmonary lesions accompanied by effort dyspnea. Multiple radiological abnormalities were noticed and the pictures showed nodular and interstitial lesions as well as emphysematous areas. Pulmonary function tests revealed more or less marked hypoxemia without hypercapnia, and decreased maximal expiratory flows due, at least in part, to a loss of elastic recoil.
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PMID:[Von Recklinghausen's disease: functional pulmonary changes. 2 case reports]. 9 31

We have described a patient with paralysis of the diaphragm, in whom dyspnea, hypoxemia, and hypercapnia increased when he changed from the upright to the supine position. Ventilation (V) and perfusion (P) images of the right lung appeared to be normal and remained nearly the same in the upright and supine positions. In contrast, V and P images of the left lung were smaller than those of the right lung in the upright position and decreased further in the supine position. In addition, the ventilation image of the left lung was much smaller than the perfusion image in both positions.
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PMID:Ventilation-perfusion lung imaging in diaphragmatic paralysis. 42 31

A 38-year-old patient with effort dyspnea, somnolence, cianosis and cor pulmonale is presented. Chest roentgenograms and lung function studies suggested the diagnosis of pulmonary fibrosis. The patient showed also severe hypercapnia with normal resting ventilation and ventilatory response to exercise lower than usual for this condition. Autopsy confirmed the clinical diagnosis. This subject may belong to the growing group of patients where CO2 retention is not explained by their pulmonary pathology.
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PMID:Idiopathic interstitial pulmonary fibrosis with hypercapnia. 117 39

In a series of 102 patients with multiple injury including a blunt lesion of the chest treated in 1970 through 1973 the mortality rate could be reduced to 17 per cent. This compares favourably with a mortality of about 34 per cent in a similar group of patients treated in the same hospital during 1965 through 1969. The improvement is partly due to increasing experience of the surgical and anaesthesiological teams and especially to a better appreciation of the importance of ventilatory pulmonary insufficiency and acute respiratory distress syndrome which are frequent in these patients. Early respiratory assistance is indicated in all cases with an instability of the chest wall. The imminence of a respiratory distress syndrome may announce itself by the classical symptoms of an increased breathing rate with hypocarbia before hypoxia becomes manifest. In the majority of patients with a thoracic lesion however the syndrome starts with a combination of increasing dyspnoea and normo- or even hypercarbia. This should be recognized and promptly treated by artificial respiration before acidosis and hypoxia with cardiac arrest can occur.
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PMID:Blunt thoracic trauma in multiple injury. 124 43

Respiration is automatically regulated via chemo- and mechanoreceptors existing in and outside the lungs, but it is also controlled voluntarily by behavioral factors. Voluntary increase in ventilation accentuates dyspnea and the sensory intensity at a given ventilation does not differ from that of exercise-induced hyperventilation, but it is significantly smaller than that during hypercapnia or hypoxia. Voluntary constraint of ventilation augments dyspnea in proportion to the degree of constraint even under isocapnic hyperoxia, and the respiratory sensation during constrained breathing is qualitatively more discomfortable than that during hyperventilation. Changes in the level and pattern of breathing under constant levels of chemical stimuli increase respiratory sensations and the intensity of dyspnea is minimal near the spontaneous levels, which supports the hypothesis that breathing is behaviorally regulated in part to minimize dyspnea. The system of behavioral control of breathing appears to be involved in the maintenance of body homeostasis by modifying the respiratory output through respiratory sensations.
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PMID:[Dyspnea and behavioral control]. 140 64

To determine whether personality is related to dyspnea sensation, 19 healthy males and 17 male patients with pulmonary emphysema were tested for modified visual analog scale (VAS) during hypoxic and hypercapnic interventions. Personality was tested by both Yatabe-Guillford test and manifest anxiety scale. VAS score correlated positively with anxiety score during hypercapnia and inspiratory resistive loading under hypercapnia in healthy subjects. In patients, anxiety score correlated positively with VAS scores during hypoxia, hypercapnia, and resistive loading under hypercapnia. Scores for nervousness and cyclic tendency correlated with VAS scores during hypoxia and hypercapnia in patients. These results indicate close relation between anxiety and dyspnea in healthy as well as emphysematous subjects. In emphysema, nervousness and cyclic tendency are the additional determinants for dyspnea.
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PMID:[Relation between dyspnea and personality in patients with pulmonary emphysema and healthy subjects]. 140 68

Breathlessness induced by hypercapnia may be related to the sensation of respiratory effort or to the central or peripheral effects of CO2. To examine the relationship among breathlessness, respiratory effort, and hypercapnia, we studied eight normal naive subjects. By using a visual feedback system, subjects maintained a constant ventilation of 50-60 L/min. PETCO2 was held at 40 mm Hg during the first 2 min of each trial (control period), then for 4 min (test period) was either kept at 40 mm Hg or elevated to 50 mm Hg. At the end of each control and test period, subjects were asked to give separate ratings for dyspnea (an unpleasant urge to breathe) and for the sense of respiratory effort (analogous to lifting a weight) on a 50-cm visual analog scale. Hypercapnia was associated with a significant reduction in effort ratings (-7.3 +/- 6.4, mean +/- SD, p < 0.05) and a concomitant increase in dyspnea (+6.6 +/- 6.0, p < 0.05). We conclude that dyspnea associated with hypercapnia is dissociated from changes in respiratory effort, and that CO2 has a direct central effect that leads to breathlessness. Our data also suggest that the sense of effort at a given level of ventilation is less when the ventilation is the result of "reflex" stimuli to breathe rather than "voluntary" signals to the respiratory muscles.
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PMID:Dissociation between dyspnea and respiratory effort. 144 74

We recorded phrenic nerve activity and thalamic single unit firing in unanesthetized, suprathalamically decerebrated, paralyzed and ventilated cats, in which vagi and carotid sinus nerves (CSN) had been ablated. Seventy-six (14%) of 545 neurons in regions of the thalamus related to the ascending reticular system, which had been tonically firing at low respiratory drives, developed rhythmic increases of firing associated with each respiration when drive had been increased by CSN stimulation or hypercapnia. The increases of neuronal firing occurred in late inspiration/post-inspiration but sometimes lasted into expiration; the magnitude of change was graded according to the magnitude of respiratory activity. Thalamic neurons also fired with a rhythm related to ventilator-induced chest expansion, some units showing both the respiratory-associated and the ventilator-related rhythms. Simultaneously recorded mesencephalic and thalamic neurons developed similar rhythms when drive was increased. We suggest that these neuronal activities reflect the conveyance of information about respiration to the cortex, where it may lead to the sensation of dyspnea and perhaps to arousal.
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PMID:Respiratory-associated thalamic activity is related to level of respiratory drive. 145 2

To clarify whether endogenous opioids play modulatory roles in control of breathing and have any specific effects on the intensity of dyspnea, healthy volunteers were examined for two protocols of ventilatory response tests. 1) The ventilatory response to hypercapnic progressive hypoxia and the withdrawal response to assess peripheral chemoreceptor activity were compared before and after intravenous infusion of 3 mg naloxone in 21 healthy adults. The average ventilatory response increased significantly after naloxone infusion (p less than 0.05), whereas there were no significant changes between two tests with normal saline in the control study (n = 7). Because there was considerable interindividual variation in the response to naloxone administration, "high responders" (n = 8) who showed larger increases with naloxone than the upper limit of the 95% confidence interval for the change with the second saline in the control study were selected. They showed greater ventilatory responses before naloxone infusion than did the other subjects (p less than 0.01). There was no significant change in the withdrawal response before and after naloxone infusion, even in such high responders. 2) The ventilatory and peak mouth pressure responses to hypoxic progressive hypercapnia with inspiratory flow-resistive loading were measured after the intravenous infusion of 3 mg naloxone or saline in 11 male volunteers, while the intensity of dyspnea was simultaneously assessed. Naloxone administration increased the peak mouth pressure response (p less than 0.05) although the increase in ventilatory response did not reach statistical significance. The intensity of dyspnea tended to be greater after naloxone infusion than after saline infusion at end-tidal PCO2 levels of 55 Torr and 60 Torr (p = 0.06 and 0.09, respectively). However, the intensity of dyspnea was quite similar between trials with and without naloxone when compared at equivalent levels of either minute ventilation or peak mouth pressure. These findings suggest that endogenous opioids suppress respiratory outputs under a strong, acute respiratory stress in normal humans. This may be particularly true for those subjects who have greater chemosensitivity. Endogenous opioids appear to act centrally rather than peripherally, but do not have any specific modulatory role on the sensation of dyspnea.
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PMID:[Role of endogenous opioids in respiratory control system and dyspnea sensation in healthy adult humans]. 155 57

Problems facing a patient with severe dyspnea secondary to diaphragmatic herniation are hypoxia, hypercarbia and respiratory acidosis, and cardiovascular instability. It is easy to precipitate a crisis in these patients during anesthetic induction as a result of stress, bad positioning, induction of pneumothorax, or inappropriate anesthetic technique. These patients require a smooth, stress-free perianesthetic period with preoxygenation, positioning with the affected side down, rapid intravenous induction, endotracheal intubation, and mechanical ventilation. Maintenance with isoflurane is preferred, and nitrous oxide should be avoided. Close monitoring of the cardiovascular and pulmonary systems is essential. Recovery from anesthesia should include oxygen supplementation, pleural drainage, and local analgesia if required.
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PMID:Anesthesia for patients with diaphragmatic hernia and severe dyspnea. 158 3


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