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

Our study aimed to assess the impact of acute respiratory failure (ARF) on survival of patients with chronic obstructive pulmonary disease (COPD) receiving long-term oxygen therapy (LTOT) plus nasal intermittent positive pressure ventilation (NIPPV). Survival was analysed retrospectively in 24 patients with severe COPD initiated to NIPPV in addition to LTOT. Fourteen patients were established on NIPPV following exacerbation of acute respiratory failure which has required mechanical ventilation (group 1). Ten patients (group 2) have never been hospitalized for ARF. Comparison of clinical details at baseline, 6 months, 1, 2, and 3 years for the two groups failed to reveal any difference with the exception of prior episodes of ARF. The probability of survival at 3 years was 65% (95% confidence interval [CI] 43-86) for the overall population, 46% (95% CI 15-77) in group 1, and 74% (95% CI 42-105) in group 2. The difference between the two groups was statistically significant. We show that ARF requiring mechanical ventilation appears to be a factor that is negatively correlated with survival for patients treated by LTOT plus NIPPV. This data suggests that NIPPV should be tried before ARF arising in COPD patients who present a deterioration in chronic respiratory failure with hypercapnia.
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PMID:[Impact of acute respiratory failure on survival of COPD patients managed with long-term non-invasive ventilation and oxygen therapy]. 1075 60

Acute Respiratory Failure (ARF) results in an inability to maintain gas exchange at a rate commensurate with the demands of the body and results in hypoxemia and/or hypercarbia, the mechanisms of which may be different. Hypoxemia commonly occurs due to Ventilation Perfusion (V/Q) mismatching, intrapulmonary shunt, diffusion defect or hypoventilation. Hypercarpnic respiratory failure may also be multifactorial but is usually due to inhibited central respiratory drive or inefficient respiratory muscle pump. Hypercapnia may occur in upper and lower airways obstruction, respiratory muscle fatigue and occasionally due to excess CO2 production (burns and excessive glucose administration). Issues in management centre around assessment of severity, determining the need for intervention, establishing diagnosis and etiology and institution of specific treatment. Diagnosis of respiratory failure may be made clinically and confirmed by blood gas analysis. Calculation of oxygenation indices will delineate extent of hypoxemia. When evaluating a child with respiratory failure, one should be aware that a child with prominent respiratory symptoms may have non-respiratory disease (i.e. metabolic acidosis, DKA) and conversely, advanced respiratory failure may be present in a child with no respiratory distress (central hypoventilation secondary to drugs, infection) careful assessment of history, complete physical examination and evaluation of lab parameters may clarify the diagnosis. Serial assessment of sensorium, respiratory symptoms, ABG and response to treatment will provide valuable clues to determine the need for intervention. Oxygen, like any drug, must be administered in a prescribed dose, only when indicated with the potential risks borne in mind. A variety of oxygen delivery devices are available; which ever device is used, the resulting FiO2 and devisable end points must be clearly determined. Hazards of oxygen therapy range from retinal damage in premature infants, damage to the alveolar capillary membrane with resultant hypoxemia) atelectasis and decreased mucociliary activity.
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PMID:Acute respiratory failure and oxygen therapy. 1133 23

The term permissive hypercapnia defines a ventilatory strategy for acute respiratory failure in which the lungs are ventilated with a low inspiratory volume and pressure. The aim of permissive hypercapnia is to minimize lung damage during mechanical ventilation; its limitation is the resulting hypoventilation and carbon dioxide (CO2) retention. In this article we discuss the rationale, physiologic implications, and implementation of permissive hypercapnia. We then review recent clinical studies that tested the effect of various approaches to permissive hypercapnia on the outcome of patients with acute respiratory failure.
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PMID:Permissive hypercapnia. 1137 9

Home mechanical ventilation improved with as non invasive mechanical ventilation, not using endotracheal connection, which supplanted home mechanical ventilation with tracheostomy. Its main indication is chronic restrictive ventilatory failure with hypoxia and hypercapnia, the severity of which is revealed during an acute respiratory failure episode or through the apparition of diurnal signs of nocturnal hypoventilation. Its other indications are more controversial in obstructive respiratory failure, where long term oxygen therapy remains the first choice treatment, and where home mechanical ventilation is proposed when the disease worsens, with recurrent episodes of hospitalisation for acute decompensation.
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PMID:[Modalities and indications for ventilation at home]. 1146 7

The key role of noninvasive positive pressure ventilation (NPPV) is well documented in chronic obstructive pulmonary disease (COPD) patients with acute respiratory failure (ARF) since it may avoid endotrachal intubation in >50% of cases when used as the initial treatment. However, currently only minimal data is available to assess usefulness of NPPV in COPD patients on a long-term basis. Even if such studies are difficult to manage, there is clearly a need for prospective studies comparing long-term oxygen therapy (LTOT) and NPPV in the most severe COPD in a large amount of patients and on a real long-term basis of several years. Two randomized prospective studies are being completed in Europe and the first preliminary results show that NPPV is associated with a reduction of hospitalization for chronic respiratory failure decompensation. The main beneficial effect of long-term mechanical ventilation in COPD patients with chronic respiratory failure implies a correction of nocturnal hypoventilation that could persist beyond the ventilation period because of a temporary improvement in carbon dioxide sensitivity that is often blunted in these patients. A synthesis from the literature suggest to consider NPPV for severe COPD patients who present with chronic hypoxia and hypercapnia and develop an unstable respiratory condition. Instability may be appreciated on a clinical basis and confirmed by a progressive worsening of arterial blood gas tensions, leading to frequent cardiorespiratory decompensations with ominous ARF episodes. NPPV should also be considered after an ARF episode successfully treated by noninvasive ventilation but with the impossibility to wean the patient from the ventilator. Thus, noninvasive positive pressure ventilation could be proposed as a preventive treatment in severe chronic obstructive pulmonary disease patients with unstable respiratory condition associated with fluctuating hypercapnia before, during and after an acute respiratory failure episode, avoiding the need for a tracheotomy. Adjunction of noninvasive ventilation to exercise rehabilitation is under evaluation.
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PMID:Noninvasive ventilation and obstructive lung diseases. 1149 Nov 76

Recourse to mechanical ventilation may prove necessary in adult patients with cystic fibrosis who have reached the stage of severe respiratory insufficiency. We report the experience of an intensive care service using non-invasive ventilation (NIV) as the first step in the management of acute respiratory failure in these patients. The records of 16 patients with cystic fibrosis presenting with acute respiratory failure and treated with NIV were analysed retrospectively. The characteristics of the group were: mean age 26.9 +/- 9.5 years; mean FEV1 21.5 +/- 10.4% predicted; mean body mass index 16.8 +/- 2.1; mean Pa CO(2) on admission 66 +/- 15 mm Hg. The mean duration of NIV in the ICU was 10 +/- 7 days. Eight patients (50%) died after having been intubated on account of failure of NIV. The eight survivors were discharged home with long-term NIV (mean duration 235 +/- 158 days). Six of them have received a lung transplant. The mode of onset of respiratory failure was an important prognostic factor: a rapid onset (<7 days) was invariably associated with death, on the other hand a gradual deterioration (> 7 days) was noted in the eight patients able to leave the ICU. In conclusion NIV may be regarded as the treatment of choice in patients with cystic fibrosis admitted to ICU with respiratory failure. In the case of persistent hypercapnia after the acute episode long-term NIV may keep them stable while awaiting lung transplantation.
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PMID:[Outcome of adult patients with cystic fibrosis admitted to intensive care with respiratory failure: the role of non-invasive ventilation]. 1241 58

Noninvasive mechanical ventilation using bilevel positive pressure ventilation (BiPAP) has not been studied in acute respiratory failure caused by MG. Eleven episodes in nine patients were initially managed with BiPAP, and endotracheal intubation was avoided in seven of these trials. Presence of hypercapnia (PaCO2 greater than 50 mm Hg) at onset predicted BiPAP failure and subsequent intubation. Results of this preliminary study suggest that a trial of BiPAP may prevent intubation in patients with myasthenic crisis without overt hypercapnia.
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PMID:BiPAP in acute respiratory failure due to myasthenic crisis may prevent intubation. 1284 84

Although lifesaving, mechanical ventilation can result in lung injury and contribute to the development of bronchopulmonary dysplasia. The most critical determinants of lung injury are tidal volume and end-inspiratory lung volume. Permissive hypercapnia offers to maintain gas exchange with lower tidal volumes and thus decrease lung injury. Further physiologic benefits include improved oxygen delivery and neuroprotection, the latter through both avoidance of accidental hypocapnia, which is associated with a poor neurologic outcome, and direct cellular effects. Clinical trials in adults with acute respiratory failure indicated improved survival and reduced incidence of organ failure in subjects managed with low tidal volumes and permissive hypercapnia. Retrospective studies in low birth weight infants found an association of bronchopulmonary dysplasia with low PaCO(2). Randomized clinical trials of low birth weight infants did not achieve sufficient statistical power to demonstrate a reduction of BPD by permissive hypercapnia, but strong trends indicated the possibility of important benefits without increased adverse events. Herein, we review the mechanisms leading to lung injury, the physiologic effects of hypercapnia, the dangers of hypocapnia, and the available clinical data.
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PMID:Permissive hypercapnia. 1246 3

Respiratory failure is still an important complication of chronic obstructive pulmonary disease (COPD) and hospitalisation with an acute episode being a poor prognostic marker. However, other comorbid conditions, especially cardiovascular disease, are equally powerful predictors of mortality. The physiological basis of acute respiratory failure in COPD is now clear. Significant ventilation/perfusion mismatching with a relative increase in the physiological dead space leads to hypercapnia and hence acidosis. This is largely the result of a shift to a rapid shallow breathing pattern and a rise in the dead space/tidal volume ratio of each breath. This breathing pattern results from adaptive physiological responses which lessen the risk of respiratory muscle fatigue and minimise breathlessness. Treatment is directed at reducing the mechanical load applied to each breath, correcting specific precipitating factors, e.g. bacterial infection, and maintaining gas exchange. Both bronchodilators and oral corticosteroids can improve spirometric results in exacerbations of COPD and should be routinely offered to patients with respiratory failure. Controlled oxygen is still not always prescribed appropriately and high inspired oxygen concentrations can lead to severe acidosis by either worsening ventilation/perfusion mismatching and/or inducing a degree of hypoventilation. Ventilatory support using noninvasive ventilation has revolutionised the approach to these patients. Acute respiratory failure due to chronic obstructive pulmonary disease remains a common medical emergency that can be effectively managed. More attention should be focused on the prevention of these episodes and identifying the factors which cause early relapse.
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PMID:Respiratory failure in chronic obstructive pulmonary disease. 1462 Nov 14

This study describes the blood gases features and short-term outcomes with noninvasive positive pressure ventilation (NPPV) treatment in the management of acute respiratory failure (ARF) during a severe acute respiratory syndrome (SARS) epidemic. Between April 22 and May 1, 2003, 120 patients meeting clinical criteria for SARS were admitted to a hospital for infectious diseases in Beijing, China. At 6 weeks after onset, 25% of patients (30/120) had experienced ARF. Of interest, 16 of these patients (53%) exhibited hypercapnia (PaCO (2) > 45 mm Hg), and 10 hypercapnic events occurred within 1 week of admission. The occurence of hypencapnia or CO (2) retention and was accompanied by myalgias. NPPV was instituted in 28 patients; one was intolerant of NPPV. In the remaining 27 patients, NPPV was initiated 1.2 +/- 1.6 days after ARF onset. An hour of NPPV therapy led to significant increases in PaO (2) and PaO (2)/FiO (2) and a decrease in respiratory rate ( p < 0.01). Endotracheal intubation was required in one third of the patients (9 of 27) who initially had a favorable response to NPPV. Remarkable pulmonary barotrauma was noticed in 7 of all 120 patients (5.8%) and in 6 of those (22%) on NPPV. The overall fatality rate at 13 weeks was 6.7% (8/120); it was higher (26.7%) in those needing NPPV. No caregiver contracted SARS. We conclude that NPPV is a feasible and appropriate treatment for ARF occurring as a result of a SARS infection.
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PMID:Noninvasive positive pressure ventilation treatment for acute respiratory failure in SARS. 1521 94


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