The secondary pulmonary lobule forms the basic unit of lung structure and function (7). The normal roentgen anatomy of the secondary pulmonary lobule has been discussed previously (3). That report indicated that the elements forming the secondary pulmonary lobule could be divided into “core structures” and “septal structures.” The “core structures” of radiologic significance are the pulmonary arteriole and terminal bronchiole, while the “septal structures” of radiologic significance are the connective tissue, the pulmonary lymphatics, and the pulmonary veins. In order to emphasize the practical importance of considering the secondary pulmonary lobule when evaluating abnormal chest radiographs, examples of pathology involving each of these 5 structures will be illustrated and discussed. The usefulness of the concept, however, extends well beyond these examples into almost every aspect of pulmonary pathology. Pathology of the “Core Structures” Pulmonary Arteriole Since the lung can be considered an aggregate of secondary pulmonary lobules, a pulmonary infarct must represent a combination of infarcted secondary pulmonary lobules. Formalin fume-fixed lung specimens often show well established infarcts to be composed of secondary pulmonary lobules sharply demarcated from adjacent normal lobules by the interlobular septum (Fig. 1). Failure of infarcts to be truly cone-shaped is usually ascribed to the presence of an anastomotic circulation which keeps the apex viable. Such an anastomotic circulation cannot be between the pulmonary arteries because these vessels have been clearly shown to be true end arteries (6, 7). Anastomoses between bronchial arteries and pulmonary veins are, however, well documented (1). The role of the bronchial arterial circulation in pulmonary infarction is unclear, but it would appear that any communication between bronchial arteries and pulmonary veins, even if effective in supplying blood to a portion of lung distal to the pulmonary embolus, would still not afford a satisfactory anatomic explanation for the location of the viable lung-infarct interface seen on radiographs and gross specimens. It seems more reasonable to assume that the shape of infarcts is due to the anatomic configuration, in irregular layers, of the infarcted secondary lobules. Further confirmation that devitalized secondary pulmonary lobules represent the building blocks of which infarcts are constructed is afforded by Figure 2, which shows a secondary pulmonary lobule in an area of pulmonary infarction and yet still viable despite the fact that the surrounding lobules are devitalized. It is possible that this segment of viable lung within the infarct represents a portion of a secondary pulmonary lobule supplied by another pulmonary arteriole. A second theoretic possibility is that such a viable lobule was protected because it was not being perfused during the period of the embolic shower.
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