At variance with Pa02st and Ve, which tended to return toward normal as a consequence of the progressive recovery of perfusion during the first week or the first month, the P(A-a)02, P(a-A)C02, and Vd/ Vt%, even after appropriate treatment, showed the persistence of some abnormalities six months later.
The incomplete recovery of perfusion and of some parameters of gas exchange in pulmonary embolism 180 days later may be due in part to the intrinsically sluggish recovery process and in part to the presence of preexisting conditions such as underlying cardiac or pulmonary diseases. In fact, it is known that the response of the pulmonary vascular system to severe pulmonary emboli with time may differ among individuals in relation to age, smoking habit, history of respiratory symptoms, or the presence of respiratory disease.
In the clinical evaluation of patients with pulmonary embolism, it may be important to follow closely the appearance and the changes in roentgenographic signs with time and their relationships to gas exchange parameters and ULSs. Previous observations have suggested the importance of considering the enlargement of descending pulmonary arteries in screening patients for pulmonary embolism. It has also been suggested to follow the resolution of pulmonary embolism from the progressive reduction of the enlargement of the right descending pulmonary artery. In our study, this finding, mainly if the characteristic “sausage” appearance is evident, and the Westermark sign were significantly associated with a more severe impairment of gas exchange, suggesting that these signs may identify patients with a more severe embolization.
Areas of atelectasis, which are evident as densities on the chest x-ray film in pulmonary embolism, have been hypothesized to be the morphologic evidence of intrapulmonary shunt. In our study, the occurrence of lung densities was more frequent after one week than at diagnosis, and over one-third of the patients still had densities at one month. We found that patients with lung densities had less impairment of pulmonary gas exchange and fewer ULSs than the other patients at diagnosis. The explanation of this finding could be that the zones of densities may represent areas where both perfusion and ventilation are absent, and thus, they are functionally silent.
In our study the presence of detectable chest x-ray abnormalities was appreciable at up to 30 days of treatment. Thus, the chest roentgenogram appears to be a good tool in giving anatomic information that may be useful for interpreting and, if necessary, in the absence of more specific techniques, substituting perfusion lung scintigraphy and gas exchange measurements during the first month of treatment.
In conclusion, perfusion impairment due to pulmonary embolism and its recovery after treatment may be appropriately evaluated by the combined use of perfusion lung scintigraphy, pulmonary gas exchange, and the chest roentgenogram. In the acute phase of embolization, perfusion lung scintigraphy gives information about the extent of obstruction of the pulmonary vascular bed. This can also be evaluated with other simple measurements, such as gas exchange parameters. For the follow-up of these patients, Pa02st and roentgenographic findings, in addition to perfusion lung scintigraphy, provide all of the anatomic and functional information necessary to evaluate the extent of recovery from pulmonary embolism under treatment. Therefore, the three examinations should be obtained in all patients during acute embolization and at 7 and 30 days later. suhagra 100