Exertional dyspnoea in patients with airway obstruction, with and without CO2 retention

Abstract

Background-Dyspnoea is a common and disabling symptom in patients with cardiopulmonary disease. Unfortunately the mechanisms that produce dyspnoea are still poorly understood. The relationship between dyspnoea and the load on the ventilatory muscles, chemical drive, and ventilatory indices was therefore assessed in patients with obstructive pulmonary disease during an incremental exercise test. Methods-Fifty patients with a wide range of obstructive pulmonary disease (mean forced expiratory volume in one second (FEV 1 ) 66.1 (28.8)% predicted) performed an incremental cycle ergometer test. A subdivision was made between subjects with CO 2 retention ( PaCO 2 >0, n = 22) and subjects without CO 2 retention ( PaCO 2 <0, n = 28) during exercise. During the test dyspnoea (Borg score), oesophageal pressures (mechanical load on the ventilatory muscles (time tension index (TTI)), blood gas tensions, and minute ventilation were measured. Correlations for changes in mechanical and chemical factors with changes in dyspnoea score were calculated to assess relevant factors. An analysis of covariance was used to examine whether there was a relationship between dyspnoea score and each of these factors and whether this relationship was diVerent between the subgroups with and without CO 2 retention. Multiple regression analysis was used to assess the independent eVect of each parameter on dyspnoea sensation. Furthermore, the amplitude of pleural pressure swing ((Pi + Pe)act) generated at maximal work load (Ptot, an indication of the load on all respiratory muscles) was calculated. Analysis of covariance was used to assess whether there was a relationship between tidal volume (VT) and Ptot and whether this relationship was diVerent between the groups (slopes are an expression of the length-tension inappropriateness, LTI). Results-In the total group and the group without CO 2 retention a significant correlation between dyspnoea and the increase in the inspiratory time tension index (TTIi) was present. In the group with CO 2 retention a significant correlation was seen between dyspnoea and PaCO 2 . The factors PaO 2 , VE%MVV and (VT/Ti) showed a correlation with a p value of <0.10 both in the total group and in those without CO 2 retention. In an analysis of covariance the relationship between dyspnoea score and PaCO 2 appeared to be significantly diVerent between the two subgroups, being more pronounced in the group with CO 2 retention. No other relationships with change in dyspnoea score were found. There was no significant relationship between VT and Ptot in the total group nor in the two subgroups, indicating some length-tension inappropriateness in both groups. Conclusion-In patients with distinctive pulmonary disease who are normocapnic or hypocapnic the mechanical load ( TTIi) and length-tension inappropriateness (LTI) on ventilatory muscles seem to be the main determinant of exertional dyspnoea. As soon as hypercapnia occurs, this seems to override all other inputs for dyspnoea. (Thorax 1998;53:768-774)

Breathing pattern and gas exchange at peak exercise in COPD patients with and without tidal flow limitation at rest

“…This unexpected finding could be explained by the higher intensity of exercise in the non-FL patients (table 3) and, consequently, the different ventilatory demand at which the two groups were compared (table 2). These data are also consistent with the results of KILLIAN et al [28] and CLOOSTERMAN et al [23] who found that many patients with very severe COPD stopped exercise primarily because of leg fatigue rather than dyspnoea. The higher leg fatigue Borg scores at peak exercise in the present FL patients probably reflect muscle weakness due to deconditioning and/or muscle dysfunction [29,30].…”

“…In patients with CO 2 retention, the changes in VT/tI from rest to peak exercise were smaller than in the subjects without CO 2 retention, but their concurrent increase in neuromuscular inspiratory drive was significantly greater. According to the present results, the COPD patients of CLOOSTERMAN et al [23] who exhibited CO 2 retention during peak exercise, should mainly represent individuals who exhibited FL at rest, supporting the notion that increased inspiratory load, rather than neuromuscular inspiratory drive, limits VT,max (and hence ventilation) in COPD patients who exhibited FL at rest. In fact, it is likely that during heavy exercise a ceiling effect occurs in patients with severe COPD, making the inspiratory reserve volume impossible to be lowered further.…”

“…However, this notion is controversial [26] and is not supported by the present results because at peak exercise no significant correlation between the Borg dyspnoea score and Pa,CO 2 was found either in the whole patient population (r~-0.01) or in the subgroup of patients who exhibited FL at rest (r~-0.10). Furthermore, like CLOOSTERMAN et al [23], this study also divided patients into those who did (n~33) and did not (n~19) increase their Pa,CO 2 during exercise, and found no significant correlations between the Borg dyspnoea score and the increase in Pa,CO 2 from rest to peak exercise, both in the whole population and in the subgroup of patients who exhibited FL at rest.…”

“…While the above analysis suggests that in COPD patients, CO 2 retention during peak exercise is due to increased inspiratory load and not decreased inspiratory drive, it has also been suggested that CO 2 retention during exercise may limit VT,max per se, through a dyspnogenic effect [23,25]. However, this notion is controversial [26] and is not supported by the present results because at peak exercise no significant correlation between the Borg dyspnoea score and Pa,CO 2 was found either in the whole patient population (r~-0.01) or in the subgroup of patients who exhibited FL at rest (r~-0.10).…”

“…The lower VT/tI in the FL patients could be due to smaller neuromuscular inspiratory drive and/or greater inspiratory impedance. Data from CLOOSTERMAN et al [23] suggest that inspiratory impedance limits VT/tI. They measured the neuromuscular inspiratory drive in terms of the inspiratory swing in pleural pressure divided by the time in which it was generated (PI/tI) in 50 COPD patients during an incremental exercise test.…”