Gas exchange abnormalities after pneumonectomy in conditioned foxhounds

Loss of a major portion of lung tissue has been associated with impaired exercise capacity, but the underlying mechanisms are not well defined. We studied the alterations in gas exchange during exercise before and after left pneumonectomy in three conditioned foxhounds. After pneumonectomy, minute ventilation and O₂ consumption at comparable submaximal work loads were unchanged but arterial PCO₂ at any work load was higher, implying that ventilatory response to CO₂ was impaired. Arterial hypoxemia and an elevated alveolar-arterial O₂ tension difference (AaDO₂) developed during heavy exercise. Using the multiple inert gas elimination technique, we determined the distributions of ventilation-perfusion (V̇A/Q̇) ratios postpneumonectomy. Significant increase in V̇A/Q̇ inequality developed during exercise while the foxhounds were breathing room air, accounting for an average of 42% of the total increase in AaDO₂ while diffusion limitation accounted for 58%. While the animals were breathing hypoxic gas mixture, diffusion limitation accounted for an average of 88% of the total increase AaDO₂. Cardiac output and O₂ delivery were reduced at a given O₂ consumption after pneumonectomy. After pneumonectomy, the animals reached O₂ consumptions close to the maximum expected for normal dogs. Compensation for the impairment in O₂ delivery post-pneumonectomy occurred mainly by an increase in hemoglobin concentration. Training probably played an important role in returning exercise capacity toward prepneumonectomy levels. We conclude that significant abnormalities in gas exchange develop during exercise after loss of 42% of lung tissue, but the animals demonstrate a remarkable ability to compensate for these changes.