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

An adequate analysis of the pathophysiology of the disease and of its ensuing type and degree of limitations is essential for evaluating the abilities for physical performance in patients with pulmonary diseases. Maximal exercise testing is an indispensable diagnostic tool in this respect. In light of moderate obstructive disease (FEV1 > approximately 60% pred), the exercise limitation comes from the cardio-circulatory system and/or peripheral muscle function. A rehabilitation program for these patients can be based on endurance training at high heart rate levels. Patients with a ventilatory limitation (FEV1 < 40%-60% pred.) show a failure of the respiratory pump, resulting in hypercapnia during exercise. Rehabilitation treatment will contain ergonomics, exercises for mobility and agility, breathing exercises with low-frequency breathing, relaxation exercises, and inspiratory muscle training. An oxygen-uptake limitation can be found in patients with a diffusion problem, severe ventilation-perfusion mismatch, or a reduced contact time between blood and alveolar gas. Such problems can often be seen in emphysema, and express themselves as isolated hypoxaemia during exercise. These patients benefit from a program consisting of ergonomics, exercises for mobilising the thoracic wall, low-frequency breathing, and exercising with additional oxygen. Many patients with chronic obstructive pulmonary disease (COPD) are limited for psychosocial reasons. The dyspnea is a negatively rewarding side effect of exercise in these patients. They tend to avoid all exertion, and thus get into a vicious circle of inactivity, low fitness, and unpleasant sensations during exercise. The inactivity often is also induced by the patient's family, since a 'patient-role' requires a quiet lifestyle.
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PMID:Exercise limitations in patients with pulmonary diseases. 800 21

To clarify effects of aging on the load compensation response and the sensation of dyspnea, we examined 28 healthy male volunteers for ventilatory and P0.1 responses to hyperoxic progressive hypercapnia with and without inspiratory flow-resistive loading (17 cm H2O/L/s) while the intensity of dyspnea was simultaneously assessed by visual analogue scaling every 15 s. Of the 28 subjects, 14 were 61 to 79 yr of age and were classified as the older group; the others, 19 to 48 yr of age, were classified as the control group. Neither delta VE/delta PETCO2 nor delta P0.1/delta PETCO2 was different between the two groups without loading. In the control group, the delta P0.1/delta PETCO2 increased with loading (p < 0.01) without a change in the delta VE/delta PETCO2. In the older group, the delta P0.1/delta PETCO2 did not change with loading so that the delta VE/delta PETCO2 decreased with loading (p < 0.01). In the 28 subjects as a whole, the percent change in delta P0.1/delta PETCO2 with loading was inversely correlated with age (r = -0.53, p < 0.01). At PETCO2 levels of 45, 50, and 55 mm Hg, irrespective of loading, the dyspnea intensity was greater in the older group than in the control group, whereas the P0.1 expressed as its ratio to the predicted maximal inspiratory mouth pressure was not different between the two groups. We conclude that aging attenuates the compensatory response to inspiratory flow-resistive loading and it increases the intensity of dyspnea for a given level of PETCO2.
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PMID:Effects of aging on respiratory load compensation and dyspnea sensation. 825 6

1. To determine whether discomfort associated with breathing (dyspnoea) is related to the chemical drive to breath, three subjects were totally paralysed while fully conscious. Subjective responses to a rising CO2 stimulus were obtained during rebreathing, rebreathing with CO2 added, and breath holding. Dyspnoea was measured with a 10-point Borg scale. 2. Following nasotracheal intubation and ventilation (oxygen saturation, O2,Sat, 98-100% and end-tidal CO2, PET,CO2, 30-40 mmHg), total neuromuscular blockade was induced by a rapid injection of atracurium (> 2.5 mg kg-1) and complete paralysis was maintained with an infusion (5 mg (kg h)-1). Paralysis was confirmed by abolition of the compound muscle action potentials of both the diaphragm and abductor hallucis evoked by supramaximal electrical stimulation of the relevant nerves. Communication via finger movement was preserved for the first 20-30 min following paralysis by inflation of a sphygmomanometer cuff on one arm. 3. Before and during complete paralysis, dyspnoea increased progressively during hypercapnia produced by rebreathing (with or without CO2 added to the circuit at 250 ml min-1). The mean PET,CO2 eliciting 'severe' dyspnoea was 46 mmHg during rebreathing, 42 mmHg during 'breath holding', and 52 mmHg during rebreathing with added CO2. There were no significant differences between the values obtained during paralysis and in the control study immediately before paralysis. The duration of breath holding was not prolonged by paralysis and the PET,CO2 at the 'break point' was not altered by paralysis. 4. Thus, dyspnoea is preserved following total neuromuscular blockade. This suggests that chemoreceptor activity, via the central neuronal activity which it evokes, can lead to discomfort in the absence of any contraction of respiratory muscles. 5. During paralysis, attempted contraction of arm, leg and trunk muscles increased heart rate and blood pressure. For attempted handgrip contractions, the increases in heart rate (range, 7-15 beats min-1) and mean arterial pressure (range, 20-32 mmHg) were similar to those recorded with actual contractions in trials immediately before paralysis. In one subject, graded increases in heart rate and blood pressure occurred for attempted contractions of 45 s duration over a range of intensities (0-100% maximal effort). 6. During complete paralysis, transcranial electromagnetic stimulation of the motor cortex produced illusory twitch-like movements of the wrist and digits. This also occurred in separate studies during complete ischaemic paralysis and anaesthesia of the forearm and hand.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Respiratory sensations, cardiovascular control, kinaesthesia and transcranial stimulation during paralysis in humans. 830 55

1. A previous study showed that when combined with exercise in normal subjects, hypercapnic and hypoxic ventilatory stimuli did not have a specific effect on the intensity of the sensation of breathlessness in addition to their stimulation of ventilation. The aim of the present study was to assess the significance of another reflex ventilatory stimulus, metabolic acidosis, in the genesis of this sensation. 2. Six subjects performed progressive exercise tests (mean workload, 103 W; range, 88-125 W) with normal acid-base status. Following NH4Cl-induced metabolic acidosis (mean change in base excess, -3.6 mmol l-1; range, -0.3 to -6.8 mmol l-1) exercise was repeated (mean workload, 91 W; range, 53-116 W) such that the combined ventilatory stimulation resulted in levels of ventilation (mean maximum, 65 l min-1) 'matched' to those resulting from exercise alone. A third, 'matched ventilation', exercise test was performed during metabolic acidosis but with end-tidal PCO2 controlled to a normal level (mean workload, 56 W; range, 17-103 W). Breathlessness was assessed using a visual analogue scale (VAS). 3. Progressive hypercapnic ventilatory stimulation was given before (mean maximum end-tidal PCO2 (PET,CO2), 61 mmHg) and during metabolic acidosis (mean maximum PET,CO2, 57 mmHg) to achieve the same peak level of ventilation (mean maximum, 59 l min-1). Breathlessness was assessed with the VAS. 4. As ventilation increased during a test, there were no statistically significant differences in the increasing breathlessness scores with metabolic acidosis compared to control, for either exercise (mean VAS, 22 mm vs. 24 mm) or progressive hypercapnia (mean peak VAS, 31 mm vs. 32 mm). 5. These results do not support the idea that metabolic acidosis is associated with a change in the relationship between the intensity of breathlessness and ventilation; this is similar to results found with other reflex ventilatory stimuli. 6. These findings are consistent with the hypothesis that the degree of reflex ventilatory activation is an important determinant of the intensity of the sensation of breathlessness in healthy humans, irrespective of the exact nature of ventilatory stimulus.
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PMID:Metabolic acidosis and breathlessness during exercise and hypercapnia in man. 835 Feb 72

We hypothesized that obese children with a history of breathing difficulty during sleep would demonstrate (1) evidence of complete and partial obstructive sleep apnea (OSA) with hypercarbia and/or hypoxemia; and (2) correlation between symptoms, degree of obesity, adenoid and tonsil size, and polysomnography (PSG) results. We evaluated 32 obese children [% ideal body weight (IBW), 196 +/- 45%] with a sleep history questionnaire, airway radiographs, electrocardiograms (ECG), and PSG. By history, we found snoring (100%), difficulty breathing (59%), sweating (44%), restlessness (53%), arousals (41%), apnea (50%), worsening with upper respiratory infection (URI) (81%), hypersomnolence (59%), and mouth breathing (59%). We found adenoid and/or tonsil enlargement on 75% of airway x-ray pictures. ECGs were abnormal in 5 patients. Among all patients, mean sleep study oxyhemoglobin saturation (SaO2) was 85 +/- 16% and mean end-tidal CO2 (PetCO2) was 51 +/- 7 torr; 84% had paradoxical inward movement of the chest on inspiration, 59% had OSA, and 66% had partial OSA. In those with > or = 200% IBW and adenotonsillar enlargement, elevated PetCO2 and the presence of hypoxemia (SaO2 < 90%) for > or = 5% of the total sleep time (TST) were correlated, unlike in patients of similar weight but without adenotonsillar enlargement. Individuals symptoms did not correlate with the severity of PSG abnormalities. By discriminant analysis, using three variables (IBW, presence of adenotonsillar tissue, and presence of > or = 5 symptoms), we could predict PSG abnormalities with up to 81% reliability. Our findings indicate that in obese children, particularly those with %IBW > or = 200 and adenotonsillar hypertrophy, with sleep-disordered breathing evaluation by polysomnography should be considered.
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PMID:Polysomnography in obese children with a history of sleep-associated breathing disorders. 836 18

1. Visual analogue scaling of breathlessness made at discrete intervals during ventilatory stimulation tests can provide useful information about the intensity of this sensation. The aim of the present study was to investigate the use of continuous visual analogue scaling as a means of improving the temporal resolution of this measurement. 2. Six normal naive subjects scaled breathlessness using a visual analogue scale, during steady-state exercise. Further changes in this sensation were induced by either sustained hypercapnia or acute hypoxia; these responses were assessed either continuously or at discrete 30 s intervals and the two scaling methods were compared. 3. The continuous method of assessing breathlessness compared favourably with that of the more established discrete method, providing reproducible measurements in repeated tests equivalent in intensity to those obtained every 30 s. 4. Transient changes in the sensation of breathlessness produced by acute episodes of hypoxia were identified using the continuous scaling method but not with discrete scaling. 5. The continuous method of scaling breathlessness should aid the investigation of the neurophysiological basis of this sensation by allowing temporal relationships between changes in respiratory variables and the sensory consequences to be more carefully defined.
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PMID:Comparison between continuous and discrete measurements of breathlessness during exercise in normal subjects using a visual analogue scale. 840 92

We describe the clinical, radiologic, functional, and pulmonary hemodynamic characteristics of a group of 30 nonsmoking patients with a lung disease that may be related to intense, long-standing indoor wood-smoke exposure. The endoscopic and some of the pathologic findings are also presented. Intense and prolonged wood-smoke inhalation may produce a chronic pulmonary disease that is similar in many aspects to other forms of inorganic dust-exposure interstitial lung disease. It affects mostly country women in their 60s, and severe dyspnea and cough are the outstanding complaints. The chest roentgenograms show a diffuse, bilateral, reticulonodular pattern, combined with normalized or hyperinflated lungs, as well as indirect signs of pulmonary arterial hypertension (PAH). On the pulmonary function test the patients show a mixed restrictive-obstructive pattern with severe hypoxemia and variable degrees of hypercapnia. Endoscopic findings are those of acute and chronic bronchitis and intense anthracotic staining of the airways appears to be quite characteristic. Fibrous and inflammatory focal thickening of the alveolar septa as well as diffuse parenchymal anthracotic deposits are the most prominent pathologic findings, although inflammatory changes of the bronchial epithelium are also present. The patients had severe PAH in which, as in other chronic lung diseases, chronic alveolar hypoxia may play the main pathogenetic role. However, PAH in wood-smoke inhalation-associated lung disease (WSIALD) appears to be more severe than in other forms of interstitial lung disease and tobacco-related COPD. The patients we studied are a selected group and they may represent one end of the spectrum of the WSIALD.
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PMID:Pulmonary arterial hypertension and cor pulmonale associated with chronic domestic woodsmoke inhalation. 841 64

We report 16 adult men (age, 41 to 75 yr) with neuralgic amyotrophy (NA) who presented with dyspnea due to involvement of the diaphragm. All patients developed breathlessness after a prodrome of acute severe neck and shoulder pain. Bilateral diaphragm paralysis (BDP) was confirmed in 12 patients and unilateral diaphragm paralysis (UDP) in four by the absence of electrical and mechanical responses to percutaneous phrenic nerve stimulation. Global expiratory muscle strength was well preserved in all patients, but inspiratory muscle strength was reduced in proportion to the extent of diaphragmatic involvement. Lung function showed low lung volumes with preservation of carbon monoxide transfer coefficient in all patients. Two BDP patients were hypoxic (PaO2 = 67 and 54 mm Hg, respectively) on daytime arterial blood gas analysis; the latter patient with pre-existing chronic obstructive pulmonary disease and marked obesity also had borderline hypercapnia (PaO2 = 49 mm Hg). Overnight sleep studies in three BDP and two UDP patients showed frequent intermittent arterial oxygen desaturations apparently caused by obstructive sleep apneas, but there was no evidence of alveolar hypoventilation. Follow-up muscle studies in five BDP and four UDP patients between 2 and 4 yr after initial referral showed complete recovery of diaphragmatic function in only two UDP patients, one of whom relapsed a year later. We postulate that NA may be an important but underrecognized cause of diaphragmatic paralysis in otherwise normal patients. Diaphragmatic strength returns very slowly, if at all.
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PMID:Diaphragmatic dysfunction in neuralgic amyotrophy: an electrophysiologic evaluation of 16 patients presenting with dyspnea. 842 Apr 34

To clarify whether endogenous opioids modulate the dyspnea intensity and, if so, by what mechanism they act on it, we examined 12 healthy male volunteers aged 19-27 yr for ventilatory and peak mouth pressure (Pm) responses to hypoxic progressive hypercapnia with inspiratory flow-resistive loading after the intravenous infusion of 3 mg of naloxone or saline. The intensity of dyspnea was simultaneously assessed by visual analogue scaling every 15 s. Naloxone administration increased both ventilatory and Pm responses to hypoxic progressive hypercapnia (P < 0.05 for both). The increase in dyspnea intensity for a given increase in end-tidal PCO2 was significantly greater after naloxone infusion than after saline (P < 0.05). However, there were no differences in the increase in dyspnea intensity for a given increase in minute ventilation or Pm. These results suggest that the endogenous opioid system suppresses the respiratory output under a strong, acute respiratory stress in normal adults and that this system may relieve the dyspnea sensation secondary to the suppression of the brain stem respiratory center without specific effects on the processing of respiratory sensations in the higher brain.
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PMID:Effects of naloxone on the sensation of dyspnea during acute respiratory stress in normal adults. 845 74

To examine possible genetic influence on the sensation of dyspnea and on load compensation, we conducted a twin study using healthy adult pairs (10 monozygotes, MZ, and 9 dizygotes, DZ). The ventilatory response to progressive hypercapnia (HCVR) was examined under three different conditions: hyperoxia (PETO2 > 150 mm Hg), hypoxia (PETO2 maintained at 50 to 55 mm Hg), and hyperoxia with an inspiratory flow-resistive load (17 mm H2O/L/s), with simultaneous assessment of the dyspnea sensation by visual analog scale (VAS). Although the VDZ/VMZ ratio (VMZ and VDZ are within-pair variances in MZ and DZ, respectively) for the slope value of the minute ventilation-PETCO2 regression line was not different from 1 in hyperoxia either with or without an inspiratory load, it was significantly larger than 1 in hypoxia (F = 5.17, p < 0.05), suggesting that a genetic influence on HCVR existed only in the presence of hypoxia. During 3% CO2 inhalation, the VDZ/VMZ ratio for the tidal volume (VT) was larger than 1 in hyperoxic HCVR with loading (F = 7.89, p < 0.01), and that for respiratory frequency (f) was larger than 1 only in hypoxic HCVR (F = 3.59, p < 0.05). At a PETCO2 of 55 mm Hg, the VT ratio was larger than 1 under all conditions (F = 5.91, p < 0.05; F = 6.99, p < 0.05; F = 3.75, p < 0.05; respectively), and the f ratio was significantly larger than 1 again only in hypoxic HCVR (F = 3.48, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dyspnea sensation and chemical control of breathing in adult twins. 848 30


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