© 2002 American Thoracic Society
Exercise Carbon Dioxide Retention in Chronic Obstructive Pulmonary DiseaseA Case for Ventilation/Perfusion Mismatch Combined with HyperinflationJohn Rankin Laboratory of Pulmonary Medicine Department of Population Health Sciences University of Wisconsin Madison, Wisconsin
In health and, more often than not, even in moderate to severe chronic airway obstruction, arterial PCO2 in the resting awake state is usually guarded within very narrow limits. This precise control is attributable to the vigilance of sensitive chemoreceptors, a respiratory musculature with huge reserves for force development and increasing tidal volume, and the linear shape of the carbon dioxide (CO2) dissociation curve that allows for ventilatory correction of increased PaCO2 even in the face of nonuniform ventilation/perfusion (
In this issue of AJRCCM, O'Donnell and associates (pp. 663–668) remind us that severe CO2 retention often occurs during exercise in severe COPD, even when it is not present at rest (3). These authors identified patients with COPD who did and did not retain significant amounts of CO2 (more than 5 torr above resting levels) during heavy intensity exercise and used a correlative approach to identify potential independent causative factors. Most of the routine resting airway function measurements, including PaCO2, were not predictive of the increase in PaCO2 with exercise. Rather, a key predictor was the degree of There are analogies in healthy persons to the ventilatory limitation experienced in these exercising patients with COPD. For example, older nonsmoking fit subjects with normal age-related loss of lung elastic recoil have a high dead space-to-tidal volume ratio and undergo significant expiratory flow limitation at a lower minute ventilation during exercise than do younger subjects. Thus, although older subjects maintain an isocapnic hyperpneic response to exercise similar to that in the younger subjects, they must produce a greater overall ventilation at a higher end-expiratory lung volume and therefore experience shorter inspiratory muscle length and increased elastic work at any given exercise work rate. Even in young adults, expiratory flow limitation is sometimes achieved at the extraordinarily high work rates achieved in very fit subjects during heavy and maximum exercise; although this does not cause absolute CO2 retention (greater than the resting value) in these fit subjects, it limits the degree of compensatory hyperventilation normally experienced in less fit healthy subjects during heavy intensity exercise (9–11). It is important to emphasize that these mechanisms of ventilatory limitation and CO2 retention during exercise in COPD are proposed solely on the basis of statistical correlation. None of the key independent correlations in the study of O'Donnell and coworkers, although significant, account for more than 40% of the total variance in the amount of CO2 retention during exercise, although it does appear as though a combination of the resting end-expiratory lung volume plus its further change with exercise will enhance the prediction of exercise CO2 retention. Furthermore, correlative analysis only considers the variables that were measured, and important potential determinants of the ventilatory response, which were not determined in this study, include individual variations in central respiratory motor output and in the force output of the respiratory muscles during exercise. Both of these important determinants of the ventilatory response would likely be affected, and to a varying extent among individuals, in the presence of hyperinflation combined with the potent stimuli that drive exercise hyperpnea (8). It is imperative then that these postulated mechanisms for CO2 retention be tested experimentally. For example, in healthy fit subjects, inhalation of low-density helium–oxygen mixture improves the maximum flow-volume loop and reduces tidal expiratory flow limitation and minimizes increases in end-expiratory lung volume during heavy intensity exercise; a helium-oxygen mixture was also shown to augment the tidal volume and hyperventilatory response to both exercise and dead space breathing (10). Furthermore, in COPD with high dead space-to-tidal volume ratio and CO2 retention at rest, administration of a chronic ventilatory stimulant was successful in increasing alveolar ventilation sufficiently to reduce PaCO2 only in those instances where increased ventilatory drive resulted in an increased tidal volume (4). A limited inspiratory reserve volume (even at rest) was likely a key mechanical determinant of these patients' ventilatory responsiveness to treatment, just as it was during exercise in the study of O'Donnell and coworkers (3). Methods for experimentally reducing flow limitation and/or changing central respiratory motor output or even respiratory muscle maximum force output could similarly be applied to the exercising patient with COPD who has CO2 retention.
In summary, O'Donnell and associates have used a comprehensive approach and propose some insightful postulates to explain the complex problem of exercise-induced CO2 retention in COPD. They make a strong case for the importance of REFERENCES
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) distribution. In chronic obstructive pulmonary disease (COPD), this precise control of PaCO2 is not always as prevalent in other physiologic states, such as sleep (
