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

Abstract

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.

B-Mode Ultrasound Assessment of Diaphragm Structure and Function in Patients With COPD

“…Contrary to our hypotheses, our results show that patients with COPD have comparable diaphragm thickness and contraction to that of normal subjects. Th is is consistent with the work of Topeli et al, 16 who reported normal diaphragm structure, diaphragm function, and respiratory drive in patients with COPD.…”

Increased injury and intramuscular collagen of the diaphragm in COPD: autopsy observations

“…The mean fibre area was not different, which suggests that hypertrophy did not compensate significantly. Further, the diaphragm may already be maximally activated during acute exacerbations in some individuals with COPD [8]. In this case, the areas of disrupted sarcoplasm and collagen accumulation observed in this study may have contributed to a peri mortem loss of inspiratory force.…”

“…It is likely that during repeated or prolonged exacerbations, the COPD diaphragm may experience maximal activation leading to injury and incomplete regeneration, as shown in animal models [8][9][10][11]. Although individuals with COPD show a high susceptibility to exertioninduced diaphragm injury following inspiratory resistive loading [12], the extent of injury has, to date, been examined only in stable COPD patients.…”

Blunted ventilatory response to hypoxia/hypercapnia in mice with cigarette smoke-induced emphysema

“…Second, as compared to FA-exposed mice, the greatest change of ventilation in CS-exposed mice was the rapid breathing, leading to an increase of V̇E. Actually, a rapid breathing rate has often been observed in hypercapnic COPD patients (Altose et al 1977;Fahey et al 1983;Gorini et al 1990;van de Ven et al 2002), although the baseline ventilation has been reported to be increased (Gorini et al 1990;Topeli et al 2001), decreased (Altose et al 1977), or unchanged (Sorli et al 1978;Montes de Oca et al 1998;van de Ven et al 2002). Additionally, we also found a slightly, but significantly higher HR in CSexposed mice as compared to FA-exposed mice (Fig.…”