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A Journal on Nuclear Medicine and Molecular Imaging
Affiliated to the and to the International Research Group of Immunoscintigraphy
Indexed/Abstracted in: Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index (SciSearch), Scopus
Impact Factor 2,413
Online ISSN 1827-1936
Guest Editors: Pistolesi M. and Pupi A.
From the Cardiac and Thoracic Department University of Pisa, Pisa, Italy
Institute of Clinical Physiology National Research Council, Pisa, Italy
The diagnostic strategy for pulmonary embolism, based on the mismatch of the ventilation/perfusion scan, was developed some 30 years ago on the following assumption: since the disorder involves the pulmonary vessels, it was surmised that in the embolized regions lung alveoli are unperfused or poorly perfused but well ventilated. Hence, it was inferred that this disorder was characterized, unlike parenchymal disease, by ventilation/perfusion mismatch in the affected lung zones and by an obvious increase of wasted ventilation, i.e., dead space. As matter of fact, experimental evidence on the redistribution of ventilation away from the vascular occluded lung had been already obtained in the early 60s of the last century. More recently, the behavior of regional pulmonary ventilation (V.A) and blood flow (Q.) in patients with acute pulmonary embolism (APE) has been studied by applying the multiple inert gas elimination technique (MIGET). It has been shown that the development of lung units with high V.A/Q. ratio (those with relative prevalence of perfusion obstruction) is accompanied by substantial redistribution of ventilation away from these units. Furthermore, radioisotopic techniques, used to visualize the topographic distributions of V.A and Q. in the same patients studied by MIGET, have shown reduced or absent V.A in the embolized regions. This may occur by different mechanisms in the various stages of APE: bronchoconstriction mediated by local hypocapnia, atelectasis (occasionally hemorrhagic) related to alteration of surfactant production, bronchiolar obstruction and pulmonary infarction ascribed to degenerative and/or necrotic changes secondary to insufficient blood flow. In dogs and humans alike, the dead space measured by MIGET does not increase and that obtained from CO2 increases far less than the amount of unperfused lung in APE thus confirming a substantial redistribution of ventilation away from the embolized lung zones. Taken together, all these observations provide the pathophysiological explanation of the unacceptedly low level of sensitivity for the diagnostic strategy of APE based on the mismatch of the ventilation/perfusion scan.