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

The Division of Pulmonary and Critical Care Medicine, Edward Hines Jr. Veterans Administration Hospital, and Loyola University of Chicago Stritch School of Medicine, Hines, IL, USA

CORRESPONDENCE: F. Laghi, Division of Pulmonary and Critical Care Medicine, Edward Hines Jr. VA Hospital, 111N, 5th Avenue and Roosevelt Road, Hines, IL, 60141, USA. Fax: 1 7082027907

Keywords: airway occlusion pressure, control of breathing, diaphragmatic function, inspiratory muscle loading, respiratory centre drive, twitch interpolation

Received: February 17, 2000
Accepted February 7, 2001

This work was supported by grants from the Veterans Administration Research Service, the American Lung Association of Metropolitan Chicago, and the Gaylord and Dorothy Donnelley Foundation; A. Topeli was supported from Hacettepe University School of Medicine and Turkish Education Foundation, Ankara, Turkey.

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 (r²=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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