1Clinical Physiology Laboratory, Division of Pulmonary Medicine, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, Canada. These findings show the potential for V(D)alv/V(T)alv to quantify the embolic burden of PE. The V(D)alv/V(T)alv correlates with the lung perfusion defect and the pulmonary artery pressures in subjects with PE. Regression of V(D)alv/V(T)alv vs pulmonary artery pressures yielded r2 = 0.59. Regression of V(D)alv/V(T)alv vs perfusion defect yielded r2 = 0.41. Regression analysis was performed to show correlation between V(D)alv/V(T)alv and defect on V/Q scan or systolic pulmonary arterial pressure (SPAP).įor subjects with PE, the mean perfusion defect on lung scan was 38 +/- 22% the mean V(D)alv = 208 +/- 115 mL, V(T)alv = 452 +/- 251 mL, and V(D)alv/V(T)alv = 43 +/- 18%. Percentage perfusion defect was determined from V/Q scans by a radiologist blinded to other data. 
Airway dead space (V(D)aw) was subtracted to yield the alveolar dead space the percentage of alveolar volume occupied by alveolar dead space per breath = V(D)alv/V(T)alv x 100%. The V(D)alv/V(T)alv was determined from volumetric capnography and arterial blood gas analysis, which permits measurement of the physiologic dead space, V(D)phys (mL) =. Pulmonary embolism was excluded by PAG in 20 subjects.
Pulmonary embolism was diagnosed in 33 by high-probability ventilation/perfusion (V/Q) scan (n = 19) or by pulmonary arteriography (PAG, n = 14). To determine whether the alveolar dead space volume (V(D)alv), expressed as a percentage of the alveolar tidal volume (V(D)alv/V(T)alv), can predict the degree of vascular occlusion caused by pulmonary embolism (PE).įifty-three subjects with suspected PE were prospectively studied.
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