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

The successful management of outpatients with COPD requires a multifaceted approach that includes prophylactic, palliative, and life-extending therapies. All patients should undergo smoking cessation, avoid potentially harmful environments, and receive influenza and pneumococcal vaccines at recommended intervals. Although medical therapy may yield only marginal benefits in patients with minimal airway responsiveness, even small improvements may translate into significant functional benefits and will be greatly appreciated. Therefore, every effort should be expended to optimize the patient's medical regimen and to ascertain that methods of delivery (such as use of spacers) are as recommended. Physical therapy measures may be useful in patients with copious sputum production, and pursed-lip and diaphragmatic breathing exercises may reduce dyspnea and lend a sense of control to patients with severe flow limitation. Oxygen therapy is the only modality demonstrated to improve survival in patients with severe COPD and may give symptomatic relief to some patients. Its use, however, is restricted to patients meeting guidelines for hypoxemia, and although dyspneic patients not meeting these guidelines may desire oxygen, insurers will decline coverage for them. Newer modalities, such as noninvasive ventilation, may improve gas exchange and quality of life in some patients with hypercapnia and nocturnal oxygen desaturations, but subgroups of COPD patients who benefit have not been well-defined, and pending further investigation, guidelines for use should be considered tentative. Patients should be encouraged to enter a comprehensive rehabilitation program, but if one is unavailable or the patient declines, a rehabilitation approach should be applied. Practitioners should attempt to educate patients at each visit, offering advice not only on medications, but also on regular exercise, good nutrition, and ways of coping psychologically with chronic illness. By taking such a comprehensive and caring approach, and being available to assist with problems and crises, the practitioner can help to enhance the quality and length of the COPD patient's life.
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PMID:Outpatient management. 977 Feb 59

In patients with obstructive lung disease, a strategy of mechanical ventilation that prolongs expiratory time and limits lung hyperinflation can decrease barotrauma. To prolong expiratory time, decrease minute ventilation and inspiratory time. Side effects of this strategy--high peak pressures and hypercapnia--are generally well tolerated. Additional goals for COPD patients include resting and strengthening respiratory muscles and decreasing load on the respiratory system. Short-acting benzodiazepines and morphine are effective for sedation and analgesia. Paralytic agents should be considered only if adequate control of the patient's cardiopulmonary status cannot be achieved by sedation alone.
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PMID:Techniques for ventilating patients with obstructive pulmonary disease. 1015 Jun 97

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

There is sufficient clinical evidence to justify the use of long-term NPPV in selected patients with COPD who have daytime hypercapnia complicated by nocturnal hypoventilation that can be reversed with NPPV. In those patients, NPPV can improve their arterial blood gases and symptoms, reduce their hospital stay, and increase their QOL. In selected COPD patients with acute exacerbation, NPPV can decrease rates of tracheal intubation leading to reduced mortality. For maximal effectiveness, NPPV must be used early in the course of the respiratory failure (less severe levels of acidosis).
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PMID:[Noninvasive positive pressure ventilation in patients with COPD]. 1049 9

The development of positive pressure ventilation delivered through a nasal or face mask has greatly expanded the use of non-invasive ventilation in patients with chronic respiratory insufficiency, particularly during sleep. Disorders ranging from neurologic and neuromuscular, such as polio and muscular dystrophy, central alveolar hypoventilation, thoracic cage disorders such as kyphoscoliosis, and pulmonary disorders such as COPD, particularly of the blue-bloater type. The relative hypoventilation that is common to each condition is due to varying combinations of an inadequate respiratory drive and an increase in the work of breathing. Previous studies have shown sustained reversal of awake hypercapnia in patients with alveolar hypoventilation syndrome using nocturnal NIPPV. We analysed 10 consecutive patients with chronic respiratory insufficiency due to diverse aetiologies over a period of time using long-term domiciliary nocturnal NIPPV. Awake hypercapnia and hypoxaemia improved in nine patients over time and deteriorated in one patient. There was no significant change in pulmonary function apart from one patient with progressive muscular dystrophy who deteriorated. A considerable reduction in the need for subsequent hospital admission was noted in the group as a whole following institution of NIPPV. We conclude that nocturnal NIPPV improves awake gas exchange in patients with chronic respiratory failure.
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PMID:Nocturnal nasal intermittent positive pressure ventilation (NIPPV) therapy for chronic respiratory failure: long-term effects. 1059 22

The effect of a COPD crisis on arterial blood gases, heart rate, lactate and indices of oxidative stress were investigated before, during and 1 h after a 'run up to fatigue' in 6 COPD horses. They were investigated twice, randomly: once in acute crisis (C) and once in clinical remission (R). Arterial and mixed venous blood samples were collected and analysed for partial pressures in O2 and CO2. The mixed venous blood was also analysed for plasma lactate (LA) and packed cell volume (PCV), as well as for indices of oxidative stress, i.e. reduced glutathione, glutathione disulphide, glutathione redox ratio (GRR) and lipid hydroperoxides (LPH). The exercise test was an effort of increasing intensity on a treadmill at 0% slope, which was stopped when the horses showed signs of exhaustion. Their performance was evaluated by the number of steps and the running time in the last step. Heart rate was monitored continuously during the test. Blood sampling was performed before, just after and 1 h after the end of the test. The COPD crisis significantly reduced the time to fatigue. However, despite the fact that the exercise intensity and length were lower, peak HR and peak LA were similar in C and R, while arterial hypoxaemia and hypercapnia, and PCV were significantly higher in C, indicating a higher physiological stress in this condition. By contrast, the oxidative stress seemed to be higher in R than in C as suggested by the fact that, 1 h after exercise, GRR and LPH were significantly increased with regards to their pre-exercise values in R and not in C. The fact that exercise did not induce an oxidative stress in C could be partly related to (1) the lower exercise intensity reached by the horses, and (2) to the more severe hypoxaemia experienced in this condition. In conclusion, COPD horses in acute crisis show a significant decrease in performance. The reasons for this exercise intolerance remain unclear, but do not appear to be related to any increase of the oxidative stress in C.
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PMID:Cardiorespiratory measurements and indices of oxidative stress in exercising COPD horses. 1065 28

Sleep has well-recognized effects on breathing, including changes in central respiratory control, airways resistance, and muscular contractility, which do not have an adverse effect in healthy individuals but may cause problems in patients with COPD. Sleep-related hypoxemia and hypercapnia are well recognized in COPD and are most pronounced in rapid eye movement sleep. However, sleep studies are usually only indicated in patients with COPD when there is a possibility of sleep apnea or when cor pulmonale and/or polycythemia are not explained by the awake PaO(2) level. Management options for patients with sleep-related respiratory failure include general measures such as optimizing therapy of the underlying condition; physiotherapy and prompt treatment of infective exacerbations; supplemental oxygen; pharmacologic treatments such as bronchodilators, particularly ipratropium bromide, theophylline, and almitrine; and noninvasive positive pressure ventilation.
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PMID:Impact of sleep in COPD. 1067 75

If chronic hypercapnia in patients with severe COPD occurs as a consequence of respiratory muscle (RM) weakness or fatigue, we would expect that ventilatory muscle recruitment (VMR) and exercise performance in stable hypercapnic patients would differ from those in eucapnic patients. We evaluated exercise performance and RM function at rest and during exercise in 19 eucapnic (PCO(2) 40 +/- 3 mm Hg), and 13 hypercapnic (PCO(2) 52 +/- 10 mm Hg) patients with severe COPD. A metabolic cart was used to determine V E, V O(2), V CO(2), and HR. Gastric (Pg) and esophageal (Ppl) balloons were used to measure Pg, Ppl, and Pdi. Ventilatory muscle recruitment pattern (VMR) was partitioned using end-inspiratory and end-expiratory Pg and Ppl. Hypercapnic patients had lower FEV(1) (0.60 +/- 0.24 versus 0.95 +/- 0.31 L, p < 0.001), MVV (28 +/- 11 versus 41 +/- 13 L, p < 0.001), resting PO(2) (61 +/- 11 versus 70 +/- 11 mm Hg, p < 0.001), peak PO(2) (60 +/- 20 versus 75 +/- 22 mm Hg, p < 0.005), and V E(max) (24 +/- 10 versus 32 +/- 12 L/min, p < 0.001). Patients in both groups had similar FRC (5.7 +/- 1.6 versus 5.0 +/- 1.5 L), V O(2)max (0.58 +/- 0.30 versus 0.76 +/- 0.32 L/min), Watts (45 +/- 48 versus 71 +/- 59), V E/MVV (88 +/- 33 versus 79 +/- 14), and HRmax (117 +/- 17 versus 128 +/- 18 beats/min). PI(max) (67 +/- 28 versus 65 +/- 32 cm H(2)O) and PE(max) (98 +/- 34 versus 96 +/- 40 cm H(2)O) were also similar in both groups. VMR (DeltaPg/DeltaPpl) at rest (-0.28 +/- 0.51 versus 0 +/- 0.35) and during exercise (0.4 +/- 0.2 versus 0.39 +/- 0.15) was equally affected in both groups. We conclude that exercise capacity and ventilatory muscle recruitment are similarly impaired in eucapnic and hypercapnic patients with severe COPD. These findings make inability of the lung to increase ventilation and not respiratory muscle dysfunction a more attractive explanation for CO(2) retention in stable hypercapnic patients.
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PMID:Respiratory muscle recruitment and exercise performance in eucapnic and hypercapnic severe chronic obstructive pulmonary disease. 1071 37

Numerous epidemiologic studies have indicated that there is a genetic basis to COPD. This result suggests that COPD develops in genetically susceptible individuals after sufficient exposure to cigarette smoke. At present, most of the genes that contribute to the genetic component to COPD are unknown. alpha 1-Antitrypsin deficiency is clearly a risk factor for COPD, but the other genetic associations with this disease must be considered as tentative. The key to establishing that a gene modifies the risk for a disease is replication of the association in different populations. This is a difficult task, however, because different genetic risk factors may be present in different populations. In addition, these genetic factors may interact with each other and with environmental risk factors, obscuring the effect of the gene on the phenotype. Apart from alpha 1-AT only the GST-M1, VDBP and CFTR genes have been implicated as risk factors in more than one population. Identification of other candidate genes awaits further understanding of the pathogenesis of COPD at the molecular level. There is good evidence that the propensity to smoke cigarettes and the likelihood of quitting smoking are influenced by genetic factors. This information may be useful in efforts directed toward cessation; however, most of the genetic studies so far have shown a rather small effect. The responses to hypoxia and hypercapnia also seem to be influenced by genetic factors. Identification of the genes involved could yield important insights into the pathogenesis of COPD and may highlight new targets for therapeutic intervention for this debilitating disease.
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PMID:Genetic risk factors for chronic obstructive pulmonary disease. 1119 75

Respiratory, and particularly inspiratory, muscle function is altered in COPD. Many of these alterations are secondary to a mechanical disadvantage related to hyperinflation. Other factors, including corticosteroid therapy and nutritional depletion, are also deleterious to muscle function. In addition, the load imposed on the respiratory muscles is increased in COPD. Combined with the altered respiratory muscle function, this increase induces important changes in respiratory muscle drive and recruitment. Moreover, the imbalance between respiratory muscle function and load is an important determinant of dyspnea and hypercapnia. Because much of the lung and airway derangements are irreversible in COPD, the respiratory muscles appear to be an attractive target for therapeutic interventions.
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PMID:Respiratory muscle function and drive in chronic obstructive pulmonary disease. 1119 79


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