Cardiovascular Physiology/Circulation | Respiratory Physiology | Pulmonary Vascular Diseases | Vascular Diseases (Non-Coronary)
Predicting perfusion deficit and redistribution in pulmonary embolism
KS Burrowes*, AR Clark, MH Tawhai
*Corresponding author: KS Burrowes
Oxford University Computing Laboratory, University of Oxford, , UK
F1000Posters 2010, 1: 548 (poster) [ENGLISH]
Poster [1.48 MB]
European Respiratory Society Annual Congress 2010, 18 - 22 Sep 2010, P1037
Pulmonary embolism is a major cause of morbidity and mortality. Little is known about the exact relationships between clinical embolism and patient characteristics and outcome. To understand how blood flow redistributes in the lung in the presence of an inert embolus, we applied a physiologically-validated, anatomically-based multi-scale model of blood flow within the full pulmonary blood flow circuit, to investigate alterations of flow characteristics and the redistribution of blood flow post-occlusion.
We aim to address the following points:
- In the absence of vasoactive signalling, is vascular occlusion sufficient to increase pulmonary arterial pressure (PAP) to pulmonary hypertension (PH) levels?
- How is cardiac output accommodated post-occlusion?
Model predictions indicated ~55% of lung tissue needed to be occluded before mean pulmonary arterial pressure exceeded hypertensive levels. This is higher than patient measurements and may be due to the absence of vasoconstriction in the model. Blood flow in non-occluded tissue was found to preferentially redistribute to non-dependent regions.
Further investigation of the impact of various factors occurring during pulmonary embolism on patient outcomes – with a focus on marrying computational modelling and patient data – are being conducted.
No relevant conflicts of interest declared.
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