Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia

Scano, Giorgio; Spinelli, Andrea; Duranti, Roberto; Gorini, Massimo; Gigliotti, Francesco; Goti, P; Milic–Emili, J.

doi:10.1183/09031936.95.08010078

Cited by 59 publications

(46 citation statements)

References 34 publications

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“…Patients approaching the fatigue threshold usually adopt breathing strategies which reduce the chance of this highly deleterious state occurring. Initial observations in stable patients showed that their respiratory drive, as assessed by mouth occlusion pressure, was high but that there was a difference in the breathing pattern of patients who showed a high CO 2 tension when stable and those that did not [18]. The former tended to exhibit a more rapid shallow breathing pattern and this was investigated subsequently by workers in Italy who found that the tidal volume was inversely related to CO 2 tension as was the maximum pleural pressure that the subjects could develop [19].…”

Section: Physiological Basis Of Respiratory Therapy In Chronic Obstrumentioning

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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Section: Physiological Basis Of Respiratory Therapy In Chronic Obstrumentioning

confidence: 99%

Respiratory failure in chronic obstructive pulmonary disease

Calverley¹

2003

Eur Respir J

107

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“…The patient then underwent a carbon dioxide rebreathing test following standard technique [15]. During resting breathing and carbon dioxide (CO 2 ) rebreathing, P0.1 was recorded every 10 -20 s [5]. After a rest period of ¢20 min, CO 2 rebreathing was repeated.…”

Section: Study Protocolmentioning

confidence: 99%

“…An inability to maintain a normal respiratory motor response during an exacerbation of COPD could lead to critical hypoventilation, respiratory failure, and death. Unfortunately, investigations have yielded inconsistent results, with reports of increased [4], decreased [5,6], and equivalent [7,8] respiratory motor output in hypercapnic and normocapnic patients. These conflicting findings stem, in part, from limitations of techniques used to measure respiratory motor output, such as the diaphragmatic electromyogram and airway occlusion pressure [9].…”

mentioning

confidence: 99%

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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“…Surprisingly the authors do not discuss the findings of SCANO et al [2] in the same patients and address the very same problem, using the same CO 2 -rebreathing experiments. Their results showed that the response of the electrical activity in the diaphragm to hypercapnia was not significantly different in normocapnic and hypercapnic COPD patients or in control subjects.…”

mentioning

confidence: 88%

CO2-response in chronic obstructive pulmonary disease

Folgering¹

1999

Eur Respir J

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Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia

Cited by 59 publications

References 34 publications

Respiratory failure in chronic obstructive pulmonary disease

Respiratory failure in chronic obstructive pulmonary disease

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

CO2-response in chronic obstructive pulmonary disease

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