Mechanical Events In Physiopathology Of Idiopathic PulmonaryEmphysema: A Theoretical Analysis

摘要

Lung volume reduction (LVR) surgery, now quitefrequently used as a therapeutic option in lung emphysema, is aimed atadvantageously interfering with the structural alterations ofbronchoalveolar architecture and the thoracic cage and diaphragm changescharacterizing the emphysema. All the changes of the emphysematousparenchyma are triggered by interalveolar septa rupture. The purpose of thisarticle is to analyze this main pathogenic event and its purely mechanicalconsequences, which are the only ones that can be expected to be modified byLVR, independently of the nature and extent of the etiopathogenic processthat brought the septa to the condition in which their rupture was possible. Introduction The etiopathogenesis of lung emphysema is quite complex and its details not yet completely clarified; in fact apart from forms in which it is possible to prove an alteration in the elastic properties of the lung caused by a genetically defined a-1 antitrypsin deficiency (1), in the majority of cases the origin is certainly related to prolonged action on the lung parenchyma of a variety of physical and chemical agents (cigarette smoke, toxic substances, etc.) which can produce the anatomopathological picture of emphysema (2,3).It has recently been proved, however, that simple lung volume reduction (LVR) has beneficial effects in selected patients, by causing a rearrangement of the residual lung and thoracic cage-diaphragm disposition. The purpose of this article is, therefore, to analyze the physiopathology of emphysema, confining this analysis to the mechanical events in the fine pulmonary architecture and thoracic cage-diaphragm disposition, that are the only factors that can be expected to be modifiable by LVR. Surgical Physiopathology Despite the fact that the nature, extent and severity of the alveolar membrane alterations probably differ according to the underlying pathogenic agent, a common element characterizes the final picture of emphysema due to any pathogenic agent, i.e. rupture of the interalveolar septa. This elementary injury triggers a series of consequences, essentially mechanico-structural, in the delicate and interconnected bronco-alveolar architecture whose final rearrangement conditions, at least in part, the clinical symptoms. The direct effects of this main event can be summarized in the following points. Intrapulmonary air collection- surrounding parenchymal collapse The alveolar sacs that form the acina, i.e. the lung functional unit, have an organized architectural structure that, chiefly because of the uniform and particular characteristics of elasticity of the alveolar walls, but also because of the complex interalveolar communication system (pores of Kohn) and surfactant, guarantees harmonious, uniform expansion and ventilation of the alveoli during the respiratory cycle. The simple rupture of a relatively small number of interalveolar septa through the immediately consequent redistribution of the elastic forces, causes an important alteration in lung architecture characterized essentially by the creation of intraparenchymal air spaces and by the collapse of adjacent healthy parenchyma. A useful and clarifying simulation of the mechanism of the lung structure disarrangement resulting from septa rupture is offered, in a two-dimensional model, by interrupting a series of threads in an elastic net, distended at moderate tension over a finite surface (Fig. 1). In this model, statically similar to lung structure, the interruption of an individual thread, simulating the rupture of an alveolar septum, generates a new structural arrangement in which at least four components can be recognized: the rupture of an alveolar septum puts two contiguous alveoli in wide communication, creating a bigger individual air space, with an air/alveolar wall ratio less favorable for gas exchange (Fig. 1); the contemporaneous redistribution of the net elastic forces in consequence of the lack of the balancing action of the interrupted