Arterial PCO2 as an index of activity in fibrosing alveolitis.
Alveolar hyperventilation is a characteristic feature of the interstitial lung diseases, yet its pathogenesis remains unknown. We examined the relationship between inflammatory alveolar acinar cell counts and the steady state, resting arterial PCO2 in patients with fibrosing alveolitis. To eliminate the influence of overwhelming mechanical lung restriction or resting hypoxemia, we studied 20 patients who, despite having clinicopathologically confirmed fibrosing alveolitis, had vital capacities exceeding 50 percent of predicted, and arterial O2 saturations above 90 percent. There was a significant inverse relationship between the proportion of polymorphonuclear leukocytes (PMNs) in the recovered BAL fluid and the arterial PCO2 (r = -0.67; p less than 0.01). When PCO2 was above 35 mm Hg, the BAL PMN count was 8 percent or less (mean = 3.4; SD = 2.5), while the mean BAL PMN count among those patients whose PCO2 was less than 35 mm Hg was significantly higher (mean = 11.7; SD = 3.7; p less than 0.01). PCO2 levels were unrelated to arterial O2 saturation or PaO2. No relationship was found between the PCO2 and BAL lymphocyte counts. The findings suggest that in fibrosing alveolitis, the arterial PCO2 may be used as an indicator of the state of the inflammatory component of the alveolitis.
D002245:Carbon Dioxide / Q000097:blood*; D005260:Female; D006801:Humans; D007249:Inflammation; D007958:Leukocyte Count; D008171:Lung Diseases / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009504:Neutrophils; D010313:Partial Pressure; D012119:Respiration
D002245:Carbon Dioxide