Changes in Regional Ventilation after Autologous Blood Clot Pulmonary Embolism

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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 (sV̇A) due to autologous blood clot PE using positron emission tomography.


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. sV̇A from perfused regions (sV̇A,p) was assessed as the ventilatory turnover rate of the tracer 13NN after central venous injection of 13NN-labeled saline.


Pulmonary embolism obstructed flow to 64% of imaged areas. Before PE, sV̇A,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, sV̇A,p of areas remaining perfused increased to 0.033 ± 0.011 s−1 (P < 0.005). This effect on regional sV̇A,p could have been caused by active redistribution of sV̇A,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 sV̇A,p increase.


An increase in sV̇A 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.

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