Reversible hypercapnia in chronic obstructive pulmonary disease: A distinct pattern of respiratory failure with a favorable prognosis

Costello, Richard W.; Deegan, Paul; Fitzpatrick, Michael; McNicholas, Walter T.

doi:10.1016/s0002-9343(97)00017-x

Cited by 133 publications

(109 citation statements)

References 14 publications

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“…This observation suggests that the respiratory controller recruits the inspiratory muscles to a lesser extent in patients who were normocapnic than in those who were hypercapnic (when both were clinically stable). Secondly, hypoxaemia at the time of hospital admission for an exacerbation was less severe in patients who were normocapnic when clinically stable than in patients who were hypercapnic when clinically stable [36]. This observation supports the notion that gas exchange is more severely compromised in patients who are hypercapnic than in those who are normocapnic.…”

Section: Discussionsupporting

confidence: 68%

“…Firstly, an increase in Pa,CO 2 during an exacerbation of COPD has been found to be greater in patients who were normocapnic when clinically stable than in patients who were hypercapnic when clinically stable [36]. This observation suggests that the respiratory controller recruits the inspiratory muscles to a lesser extent in patients who were normocapnic than in those who were hypercapnic (when both were clinically stable).…”

Section: Discussionmentioning

confidence: 99%

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The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD

2001

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The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD. A. Topeli, F. Laghi, M.J. Tobin. #ERS Journals Ltd 2001. ABSTRACT: How do the respiratory centres of patients with chronic obstructive pulmonary disease (COPD) and hypercapnia respond to acute increases in inspiratory load? A depressed respiratory motor output has long been postulated, but studies on this issue have yielded inconsistent results, partly due to limitations of investigative techniques. Many of these limitations can be overcome by the twitch interpolation technique, which is capable of accurately quantifying the degree of diaphragmatic activation, termed the voluntary drive to breathe. The hypothesis that patients with COPD and hypercapnia compensate for an acute increase in mechanical load on the inspiratory muscles with a lower voluntary drive to breathe than is the case with normocapnic patients was tested.Measurements were obtained in 15 patients with COPD, six of whom displayed hypercapnia and nine normocapnia. The maximum degree of diaphragmatic activation, expressed as a voluntary activation index (mean¡SEM), was higher in hypercapnic than in normocapnic patients (98.7¡0.7 versus 94.5¡0.9% (p~0.006)), as was the mean value (94.5¡0.7 versus 88.5¡1.9% (p~0.01)). Within-patient values of the index were also less variable in the hypercapnic patients (coefficients of variation, 3.4¡0.3 versus 6.1¡0.9%, p~0.01). Multiple regression analysis revealed the ratio of dynamic elastance to maximum transdiaphragmatic pressure, an index of inspiratory muscle loading, and pH as the only variables that correlated with maximum voluntary activation index (r 2~0 .69, p~0.02 for each variable). Contrary to the hypothesis, it was concluded that voluntary activation of the diaphragm was greater and less variable in hypercapnic patients than normocapnic patients with severe chronic obstructive pulmonary disease during an acute increase in inspiratory mechanical load. Whether greater diaphragmatic recruitment during episodes of a severe exacerbation of chronic obstructive pulmonary disease provides a survival advantage for hypercapnic patients with chronic obstructive pulmonary disease remains to be determined.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 99%

The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD

2001

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“…This occurs over many years; thus, it is probably constant enough to guide decision making on treatment such as chronic bronchitis. Longitudinal blood gas studies have not been commonly carried out in COPD, although type 2 failure does develop over time, occurring in 24% of patients who have had an acidotic hypercapnic exacerbation 5 years after the first event [101]. Predictors of hypoxia and hypercapnia include lung function and body composition [102].…”

Section: Constancy Of Copd Subgroupsmentioning

confidence: 99%

Clinically relevant subgroups in COPD and asthma

Turner

Tamási

Schleich³

et al. 2015

Eur Respir Rev

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As knowledge of airways disease has grown, it has become apparent that neither chronic obstructive pulmonary disease (COPD) nor asthma is a simple, easily defined disease. In the past, treatment options for both diseases were limited; thus, there was less need to define subgroups. As treatment options have grown, so has our need to predict who will respond to new drugs. To date, identifying subgroups has been largely reported by detailed clinical characterisation or differences in pathobiology. These subgroups are commonly called "phenotypes"; however, the problem of defining what constitutes a phenotype, whether this should include comorbid diseases and how to handle changes over time has led to the term being used loosely.In this review, we describe subgroups of COPD and asthma patients whose clinical characteristics we believe have therapeutic or major prognostic implications specific to the lung, and whether these subgroups are constant over time. Finally, we will discuss whether the subgroups we describe are common to both asthma and COPD, and give some examples of how treatment might be tailored in patients where the subgroup is clear, but the label of asthma or COPD is not. @ERSpublications Summary of subgroups of airways disease that can be found in COPD and asthma, and their management

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“…Many patients who present with respiratory failure are subsequently readmitted, sometimes at quite frequent intervals, and, to date, only one study has investigated the consistency of arterial blood gas tensions at presentation in such patients [8]. In that study, subjects were divided into those who presented with hypoxaemia without hypercapnia (type 1), those who presented with hypoxaemia with hypercapnia but only for the duration of the admission (type 2.1) and those in whom the hypercapnia was persistent (type 2.2).…”

mentioning

confidence: 99%

Respiratory failure in chronic obstructive pulmonary disease

Calverley¹

2003

Eur Respir J

107

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Respiratory failure in chronic obstructive pulmonary disease. P.M.A. Calverley. #ERS Journals Ltd 2003. ABSTRACT: 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. Eur Respir J 2003; 22: Suppl. 47, 26s-30s.

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Reversible hypercapnia in chronic obstructive pulmonary disease: A distinct pattern of respiratory failure with a favorable prognosis

Cited by 133 publications

References 14 publications

The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD

The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD

Clinically relevant subgroups in COPD and asthma

Respiratory failure in chronic obstructive pulmonary disease

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