RESPIRATORY FUNCTION IN PULMONARY THROMBOEMBOLIC DISEASE

This is a correlative study of the clinical, electrocardiographic and respiratory function data in twenty-one subjects with respiratory symptoms and abnormal pulmonary perfusion scans as a result of pulmonary thromboembolic disease; sixteen subjects had subsequent functional studies and the duration of observation was up to three years. Two causal factors in the production of arterial hypoxaemia were recognized: ventilation-perfusion ratio nonhomogeneity and pulmonary arteriovenous shunting. Ventilation-perfusion ratio nonhomogeneity was the most important factor. In more than half of the patients reversible regional pulmonary vasoconstriction was demonstrated by a rise in the VD:VT ratio on breathing oxygen. The range of the steady state pulmonary diffusion capacity (DLCO) and the fractional carbon monoxide (CO) uptake was wide, but in the absence of other cardiovascular or respiratory diseases a reduction in the DLCO and fractional carbon monoxide uptake was unusual. The DLCO in pulmonary thromboembolic disease was usually normal, but there were unreal high and negative values. The vital capacity was reduced in about half of the patients, but the clinical and spirometric evidence of airways obstruction was infrequent. © 1969.