• P T Macklem and D Eidelman.
• Meakins-Christie Laboratories, McGill University Clinic, Royal Victoria Hospital, Montreal, Canada.
• Respiration. 1990 Jan 1;57(3):187-92.

AbstractWe calculated specific lung elastance (Es,L) as the change of lung elastic recoil pressure (Pel,L) required to produce a given fractional change in lung volume (delta VL/VL,0) as a function of transpulmonary pressure (PL) from published data in normal lungs, and in patients with chronic obstructive pulmonary disease (COPD) or alpha 1-antitrypsin deficiency (alpha 1-AD). Es,L, in normal lungs, is the bulk modulus, and was systematically greater than PL.dEs,L/dPL increased with VL.PL at Es,L = 30 cm H2O decreased with age in normal lungs, but Es,L at PL = 8 cm H2O showed no age relationship. In both COPD and alpha 1-AD Es,L and dEs,L/dPL were increased compared to normal lungs. We conclude that Es,L is a curvilinear function of PL in normal lungs, COPD and alpha 1-AD, and is systematically greater than PL. The increase in Es,L and dEs,L/dPL in COPD and alpha 1-AD compared to normals probably represents two distinct abnormalities in the elastic properties of emphysematous lungs: (1) an increase in resting length of alveolar walls accounting for hyperinflation, and (2) a decrease in extensibility of alveolar walls once they become stressed. Using total lung capacity (TLC) as an index of the former and Es,L as an index of the latter, we showed no correlation between either and FEV1. Thus abnormalities in lung elastic properties in emphysema do not account for chronic expiratory flow limitation in emphysema. Furthermore, the increased values of Es,L in emphysema suggest that emphysematous airspaces are poorly ventilated. As they are presumably poorly perfused, emphysema per se may not disturb ventilation perfusion ratios seriously.

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