1. Pulmonary Function Testing in Interstitial Pulmonary Disease
Brendan A. Keogh, M.D., Ronald G. Crystal, M.D. 
CHEST 
Volume 78, Issue 6, Pages (December 1980)
DOI: /chest
Copyright © 1980 The American College of Chest Physicians Terms and Conditions

2. Figure 1
Pathogenesis of most interstitial pulmonary disorders. Independent of whether or not cause is known, first manifestation of disease is alveolitis (accumulation of inflammatory and immune effector cells within alveolar structures). Although alveolitis differs among various interstitial disorders, it is these effector cells which cause derangements of alveolar capillary units such as interstitial fibrosis and changes in populations of parenchymal cells. Eventually, these changes are sufficient to cause loss of alveolar capillary unit as effective mediator of gas exchange. When enough alveolar capillary units are lost, “end-stage” lung results.
CHEST  , DOI: ( /chest )
Copyright © 1980 The American College of Chest Physicians Terms and Conditions

3. Figure 2
Gas exchange in patients with idiopathic pulmonary fibrosis. A (top), Changes in PaO2 with increasing Vo2. In normal individuals in steady state, change in PaO2 per unit change in V ˙ o2 (ΔPaO2/ΔVo2) is never less than —3 mm Hg/L/min. In typical patient with idiopathic pulmonary fibrosis, ΔPaO2/ V ˙ o2 is —17 mm Hg/L/min. B (bottom left), Pulmonary biopsy in 46-year-old man with idiopathic pulmonary fibrosis, showing predominantly alveolitis, with little fibrosis. When exercised, this patient showed ΔPaO2/Δ V ˙ o2 of —16 mm Hg/L/min (hematoxylin-eosin, original magnification × 220). C (bottom right), pulmonary biopsy in 31-year-old man with idiopathic pulmonary fibrosis, showing predominantly fibrosis, with little alveolitis. When exercised, this patient also demonstrated ΔPaO2/Δ V ˙ o2 of —17 mm Hg/L/min (hematoxylin-eosin, original magnification × 220). Thus, patients in B and C cannot be distinguished by studies of gas exchange. Although both have abnormal gas exchange with exercise, fact that B has predominantly alveolitis and C has predominantly fibrosis cannot be assessed by such testing.
CHEST  , DOI: ( /chest )
Copyright © 1980 The American College of Chest Physicians Terms and Conditions

4. Figure 3
Relationships of static deflation volume and pressure in patients with idiopathic pulmonary fibrosis. A (top), Percent predicted TLC plotted against transpulmonary pressure (Pst) for two patients with idiopathic pulmonary fibrosis. B (bottom left), Patient, 46-year-old man, had mild fibrosis on open lung biopsy (hematoxylin and eosin, original magnification × 220). C (bottom right). Patient, 55-year-old man, had severe fibrosis (hematoxylin and eosin, original magnification × 220). Compliance, maximum Pst, and coefficient of retraction (maximum Pst/TLC) for two patients correlated well with extent of fibrosis observed in biopsies. In contrast, there is little correlation between these volume-pressure relationships and extent of alveolitis.
CHEST  , DOI: ( /chest )
Copyright © 1980 The American College of Chest Physicians Terms and Conditions