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

Although negative pressure assisted ventilation with an assist-control mode may have a potential therapeutic role in the treatment of severe dyspnoea, the effects of negative pressure assisted ventilation with the assist-control mode on dyspnoea and breathing patterns have not been examined. We examined the effects of negative pressure assisted ventilation with the assist-control mode on dyspnoea and breathing patterns produced by a combination of resistive loading and hypercapnia in nine healthy subjects breathing spontaneously. Subjects were asked to rate their sensation of respiratory discomfort using a visual analogue scale. Negative pressure assisted ventilation caused a significant reduction in sensation of respiratory discomfort from a visual analogue scale score of 74 (55-91) (median (range)) before negative pressure assisted ventilation to 34 (15-53) during negative pressure assisted ventilation (p<0.01). During negative pressure assisted ventilation, there were significant changes in breathing patterns characterized by an increase in tidal volume and a decrease in respiratory frequency, while neither minute ventilation nor end-tidal carbon dioxide tension changed. Our results indicate that negative pressure assisted ventilation with the assist-control mode is effective in relief of dyspnoea and that negative pressure assisted ventilation influences the control of breathing to minimize respiratory discomfort.
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PMID:Effects of negative pressure assisted ventilation on dyspnoeic sensation and breathing pattern. 987 77

The role of non-invasive nocturnal domiciliary ventilation (NNV) in chronic obstructive pulmonary disease (COPD) patients with chronic hypercapnia is still discussed. The aims of this study were to evaluate the long-term survival, the clinical effectiveness and side-effects of NNV in these patients. Forty-nine stable hypercapnic COPD patients on long-term oxygen therapy (LTOT) were assigned to two groups: in Group 1, 28 patients performed NNV by pressure support modality in addition to LTOT; in Group 2, 21 patients continued their usual LTOT regimen. Treatment was assigned according to the compliance to NNV, after an in hospital period. Mortality rate, hospital stay (HS) and ICU admissions (IA) were recorded in the two groups. HS and IA were compared to those recorded in a similar period of follow-back. Lung and respiratory muscle function, dyspnoea, and exercise capacity (by 6-min walk test) were evaluated baseline and every 3-6 months up to 3 yr. Mean follow-up time was 35 +/- 7 months. Mortality rate was not different between the two groups: 16, 33, 46% and 13, 28, 50% at 1, 2 and 3 yr in Groups 1 and 2 respectively. Lung and respiratory muscle function did not significantly change over time. A significant increase in 6-min walk test (from 245 +/- 78 to 250 +/- 88, 291 +/- 75, 284 +/- 89 m after 1, 2 and 3 yr respectively, P < 0.01) was observed only in patients undergoing NNV. In comparison to the follow back HS significantly decreased in both groups (from 37 +/- 29 to 15 +/- 12 and from 32 +/- 18 to 17 +/- 11 days/pt/yr in Groups 1 and 2 respectively, P < 0.001) whereas IA significantly decreased only in patients performing also NNV (from 1.0 +/- 0.7 to 0.2 +/- 0.3/pt/yr, P < 0.0001). Addition of NNV by pressure support modality to LTOT does not improve long term survival but significantly reduces ICU admissions and improves exercise capacity in severe COPD with hypercapnia.
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PMID:Outcome of COPD patients performing nocturnal non-invasive mechanical ventilation. 992 52

We have measured how a low concentration of nitrous oxide affected respiratory sensation and ventilation. Severe dyspnoea was induced in nine normal subjects by a combination of hypercapnia and inspiratory elastic load (50 cm H2O litre-1). Subjects were asked to rate their sensation of respiratory discomfort using a visual analogue scale (VAS) while breathing either 20% nitrous oxide or 20% nitrogen gas mixture. We compared the effects of each gas mixture on respiratory sensation and ventilation using steady-state values of ventilatory variables and VAS scores obtained before, during and after inhalation of each gas mixture. Inhalation of 20% nitrous oxide reduced the sensation of respiratory discomfort from a median VAS score of 6.5 (range 5.0-8.1) before inhalation to 3.6 (2.4-5.9) during inhalation (P < 0.05). There was no significant change in minute ventilation but tidal volume increased during inhalation of 20% nitrogen did not alter VAS scores or ventilatory variables. We found that a low concentration of nitrous oxide greatly alleviated the intensity of dyspnoea without changing respiratory load compensation.
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PMID:A low concentration of nitrous oxide reduces dyspnoea produced by a combination of hypercapnia and severe elastic load. 1061 66

Although midazolam has been proposed for the treatment of a variety of conditions such as anxiety, dyspnoea, hiccups and status epilepticus, terminal agitation is the only condition where its use is based on a reasonably large number of published clinical studies. A causal approach is generally recommended. Whenever possible, the aetiological condition (pain, fever, constipation, etc.) should be corrected. Such general measures as ensuring a peaceful, familiar environment, and the use of a night light, fluid therapy to counteract dehydration, and antipyretics for fever are beneficial. When symptomatic treatment is needed, drugs with little anticholinergic effect are to be recommended. The use of benzodiazepines as single drug treatment may exacerbate the condition. Haloperidol or risperidone (which has fewer side effects) are recommended. If the agitation is marked, a common strategy is to add lorazepam. Chlormethiazole is an alternative. Subcutaneous midazolam should be reserved for refractory cases. Attention should be paid to dosage, reduced doses being given to the elderly, patients on opioid medication, and patients with impaired liver or renal function. Overdosage may induce deep sedation, and result in carbon dioxide retention and subsequently heart failure and pulmonary oedema which may be fatal.
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PMID:[Midazolam (Dormicum) in terminal anxiety and agitation. The last choice alternative in palliative care]. 1035 70

The effects of noninvasive positive pressure ventilation (NIPPV) in COPD patients (pts) with hypercapnic respiratory failure were evaluated. The study group consisted of 19 COPD pts (16M, 3F, mean age 60 +/- 8 years) on LTOT for at least 6 month before study. Patients were enrolled in random order to group I, which continued LTOT and to group II, which started nocturnal NIPPV and continued LTOT. There were 12 pts in group 1 and 7 pts in group II. Two pts from the group did not tolerate NIPPV and were transferred to group I. To ventilate the pts we used portable, volume ventilators. Mean time of follow-up in group I was 23 +/- 13 months and 16 +/- 10 months in group II. During that time died 5 pts from 1 and 4 pts from group II. Differences between functional variables (FEV1, FVC, FEV1/VC, PaO2, PaCO2, pH, PEmax, 6MWD), dyspnea, number of hospitalizations and mortality in both groups were not statistically significant. In both groups progression of the disease (decrease of FEV1, worsening of hypoxaemia and increase of hypercapnia) was observed. NIPPV did not slow down progression of the disease.
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PMID:[Noninvasive positive pressure ventilation in COPD patients with hypercapnic respiratory failure]. 1048 24

The ventilatory drive is affected by several factors such as chemosensitivity, basal arterial oxygen or carbon dioxide tension, mechanical impedance, and respiratory muscle dysfunction. Blunted ventilatory drive or a decrease in the perception of dyspnea in bronchial asthma and chronic obstructive pulmonary disease (COPD) could lead to a decrease in the alarm reaction to dangerous situations such as severe airway obstruction, severe hypoxemia, or severe hypercapnia. This could delay management and treatment, causing an increase in the morbidity and mortality of patients with bronchial asthma and COPD. The ventilatory drive to chemical stimuli can be altered by a beta-2-agonist, oxygen administration; and lung volume reduction, and an increased dyspnea sensation may be improved by corticosteroid, chest wall vibration, or lung volume reduction. The ventilatory drive has been found to play a key role in determining the severity of asthma and COPD.
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PMID:Role of ventilatory drive in asthma and chronic obstructive pulmonary disease. 1057 Jul 33

Alveolar hypoventilation associated with neuromuscular disease can occur in acute and chronic forms. In the acute form, progressive weakness of respiratory muscles leads to rapid reduction in vital capacity followed by respiratory failure with hypoxemia and hypercarbia. Symptoms are those of acute respiratory failure, including dyspnea, tachypnea, and tachycardia. In the chronic form, impairment of the respiratory muscles affects mechanical properties of the lungs and chest wall, decreases the ability to clear secretions, and eventually may alter the function of the central respiratory centers. Symptoms include orthopnea, fatigue, disturbed sleep, and hypersomnolence. Treatment and outcome of the disease's chronic form are dependent on the underlying clinical cause of the alveolar hypoventilation. For chronic but stable diseases such as old polio, quadriplegia, or kyposcoliosis, mechanical support of minute ventilation can reverse symptoms. For chronic and progressive disease such as muscular dystrophy and amyotrophic lateral sclerosis, mechanical support of minute ventilation provides only symptomatic relief and is usually associated with deterioration to the point of complete ventilator dependency for survival. For the chronic progressive forms of alveolar hypoventilation, there is currently a need for quality randomized controlled clinical trials to define physiologic indicators and appropriate timing for mechanical support of minute ventilation.
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PMID:Neuromuscular disease and hypoventilation. 1057 Jul 36

The prognostic value of hypercapnia and/or pulmonary hypertension differs in patients with sequela of pulmonary tuberculosis (TBseq) and those with chronic obstructive pulmonary disease (COPD) who are receiving home oxygen therapy (HOT). In an attempt to identify the factors, if any, that might explain this difference, we first compared nutritional status, respiratory function test results, dyspnea indexes, and other data for hypercapnic patients (PaCO2 > or = 45 Torr) and normocapnic patients (PaCO2 < 45 Torr) receiving HOT. Second, we examined the relationship between the degree of pulmonary hypertension and several respiratory function parameters for patients in each disease category. In 44 patients with TBseq, nutritional status estimated by body mass index and serum albumin was significantly better in the hypercapnic patients than in the normocapnic patients. However, this difference was not observed in 37 patients with COPD. In 30 patients with TBseq, the degree of pulmonary hypertension correlated significantly only with PaO2; in 32 patients with COPD, however, significant correlations were observed not only with PaO2 but also with PaCO2, %VC, and FEV1. These differences distinguishing groups of patients with the 2 diseases may provide an explanatory basis for the difference in prognostic value of hypercapnia and/or pulmonary hypertension in patients receiving HOT.
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PMID:[An analysis of nutritional status and pulmonary hypertension in patients with sequela of pulmonary tuberculosis and chronic obstructive pulmonary disease]. 1058 88

Lung disease affects exercise performance through a number of mechanisms, including hypoxemia, abnormal ventilatory mechanics, abnormal ventilatory muscles, abnormal ventilatory patterns, abnormal right heart function and subjective dyspnea. Supplemental oxygen improves hypoxemia and thus improves exercise impairment resulting from hypoxemia-related reductions in oxygen delivery. Supplemental oxygen also reduces exercise ventilation. This, in turn, reduces ventilatory muscle work, and the concomitant permissive hypercapnia may have beneficial effects at the cellular level. Additionally, in obstructive disease patients, an improved ventilatory pattern may reduce air trapping. Supplemental oxygen may also improve right ventricular dysfunction in patients with underlying right ventricular dysfunction. Finally, supplemental oxygen may reduce dyspnea caused by oxygen-related carotid body activity. Important questions remain. First, is long-term oxygen use of benefit in patients with only exercise hypoxemia? Second, is exercise conditioning possible in patients with exercise hypoxemia? Third, does supplemental oxygen enhance exercise conditioning efforts in those patients with CLD but without exercise hypoxemia? If the answer to this last question is yes, what selection criteria should be used to identify those who would benefit? The answers to all of these questions will have enormous impact on our approach to the optimal management of CLD patients.
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PMID:Oxygen therapy and exercise response in lung disease. 1077 91

Furosemide is known to influence the activity of vagally mediated mechanoreceptors in the airways. Because vagal afferent fibers may play an important role in modulation of the sensation of dyspnea, it is possible that inhaled furosemide may modify the sensation of dyspnea. In a double-blind, randomized, crossover study, we compared the effect of inhaled furosemide on dyspneic sensation with that of placebo. Severe dyspneic sensation was induced in 12 healthy subjects in two ways: (1) breathholding and (2) loaded breathing with a combination of inspiratory resistive load (240 cm H(2)O/L/s) and hypercapnia induced by extra mechanical dead space (0.26 L). Subjects were asked to rate their sensation of respiratory discomfort using a visual analogue scale (dyspneic VAS). Breathholding times and changes in dyspneic VAS score during a 5-min period of loaded breathing were measured after inhalation of placebo and furosemide (40 mg). Total breathholding time after inhalation of furosemide (median, 93 [interquartile range, 78 to 112]s) was prolonged compared with the total breathholding time after placebo inhalation (67 [47-74]s). We also found that respiratory discomfort during loaded breathing after inhalation of furosemide develops more slowly and is less than that observed after inhalation of placebo. Our findings indicate that inhaled furosemide greatly alleviates the sensation of dyspnea induced experimentally by breathholding and by a combination of resistive loading and hypercapnia.
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PMID:Inhaled furosemide greatly alleviates the sensation of experimentally induced dyspnea. 1085 74


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