Changes in regional ventilation after autologous blood clot pulmonary embolism

Background: Previous studies have suggested that pulmonary embolism (PE) and pulmonary artery occlusion result in a shift in alveolar ventilation away from unperfused regions. This study aimed to directly assess changes in regional specific ventilation (SV̇ _A) due to autologous blood clot PE using positron emission tomography. Methods: Pulmonary embolism was created in six anesthetized, paralyzed, and mechanically ventilated sheep by injecting cylindrical clots of autologous blood (7 mm in diameter and height). Clots were progressively infused into a central vein until a stable mean pulmonary artery pressure between 30 and 40 mmHg was achieved. A multislice positron emission tomography camera was used to image 15 contiguous, 6.5-mm-thick transverse cross-sections of the chest beginning just above the diaphragm. SV̇ _A from perfused regions (SV̇ _A,p was assessed as the ventilatory turnover rate of the tracer ¹³NN after central venous injection of ¹³NN-labeled saline. Results: Pulmonary embolism obstructed flow to 64% of imaged areas. Before PE, SV̇ _A,p was equivalent in areas that would remain perfused and those that would become embolized after PE (0.021 ± 0.007 vs. 0.021 ± 0.006 s ^-1; P = nonsignificant). After PE, SV̇ _A,p of areas remaining perfused increased to 0.033 ± 0.011 s ^-1 (P < 0.005). This effect on regional SV _A,p could have been caused by active redistribution of SV̇ _A,p or by a reduction in tracer concentration of perfused areas due to the dead space common to perfused and embolized regions. Model simulations indicated that the common dead-space effect could only explain a small part of the SV̇ _A,p increase. Conclusions: An increase in SV̇ _A of perfused regions occurs following PE with 7-mm autologous blood clots. This increase is most likely caused by a shift in ventilation away from embolized areas mediated by hypocapnic pneumoconstriction.