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

• Published in: The European respiratory journal Vol. 18; no. 1; pp. 53 - 60
• Main Authors: Topeli, A, Laghi, F, Tobin, M.J
• Format: Journal Article
• Language: English
• Published: Leeds Eur Respiratory Soc 01.07.2001; Maney
• Subjects: Aged; Biological and medical sciences; Chronic obstructive pulmonary disease, asthma; Diaphragm - physiopathology; Female; Humans; Hypercapnia - physiopathology; Lung Volume Measurements; Male; Medical sciences; Middle Aged; Pneumology; Pulmonary Disease, Chronic Obstructive - physiopathology; Respiratory Center - physiopathology; Respiratory Muscles - physiopathology; Spirometry; Work of Breathing - physiology; Human; Lung disease; Respiratory disease; Carbon dioxide; Exploration; Hypercapnia; Chronic; Lung function; Treatment; Mechanic of breathing; Rehabilitation(human); Bronchus disease; Obstructive pulmonary disease; Diaphragm; Technique
• ISSN: 0903-1936; 1399-3003
• DOI: 10.1183/09031936.01.00014101

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.