Blood Flow Redistribution and Ventilation‐Perfusion Mismatch During Embolic Pulmonary Arterial Occlusion

Abstract

Acute pulmonary embolism causes redistribution of blood in the lung, which impairs ventilation/perfusion matching and gas exchange and can elevate pulmonary arterial pressure (PAP) by increasing pulmonary vascular resistance (PVR). An anatomically-based multi-scale model of the human pulmonary circulation was used to simulate pre- and post-occlusion flow, to study blood flow redistribution in the presence of an embolus, and to evaluate whether reduction in perfused vascular bed is sufficient to increase PAP to hypertensive levels, or whether other vasoconstrictive mechanisms are necessary. A model of oxygen transfer from air to blood was included to assess the impact of vascular occlusion on oxygen exchange. Emboli of 5, 7, and 10 mm radius were introduced to occlude increasing proportions of the vasculature. Blood flow redistribution was calculated after arterial occlusion, giving predictions of PAP, PVR, flow redistribution, and micro-circulatory flow dynamics. Because of the large flow reserve capacity (via both capillary recruitment and distension), approximately 55% of the vasculature was occluded before PAP reached clinically significant levels indicative of hypertension. In contrast, model predictions showed that even relatively low levels of occlusion could cause localized oxygen deficit. Flow preferentially redistributed to gravitationally non-dependent regions regardless of occlusion location, due to the greater potential for capillary recruitment in this region. Red blood cell transit times decreased below the minimum time for oxygen saturation (<0.25 s) and capillary pressures became high enough to initiate cell damage (which may result in edema) only after ~80% of the lung was occluded.

Comparison of generic and subject-specific models for simulation of pulmonary perfusion and forced expiration

“…The under-prediction of mPAP increase suggests that capillaries were more readily recruited in the generic model during arterial occlusion. Capillaries recruit in a gravitational pattern (greater recruitment in non-dependent tissue) [2]. A difference in the tissue distribution along the gravitational (cranio-caudal) axis could cause a different pattern of recruitment, and this would depend on the location of emboli.…”

“…Systemic oxygen demand was assumed the same pre-and post-occlusion, and ventilation was assumed to remain at baseline conditions post-occlusion. The perfusion simulation predicts the distribution of vessel and capillary distension and capillary recruitment, and the post-occlusion redistribution of flow which has a gravitational preference [2]. Mean pulmonary artery pressure (mPAP) is predicted as a consequence of the distribution of vessel size.…”

“…Multiscale models of lung structure and function are becoming more sophisticated, for example now including mechanotransduction across the cellular to whole organ scales [1], coupling of microcirculatory and large vessel fluid dynamics [2,3] and all simulated within subject-specific imaging-based model geometries. Three-dimensional computational fluid dynamics (CFD) is now used routinely to study complex flow phenomena in the central airways [4,5] and pulmonary blood vessels [6], with some emerging model linkages to tissue or cellular-scale function [7].…”

Pulmonary embolism: clinical guidelines of European Society of Cardiology (2014).The Task Force of the European Society of Cardiology for diagnosis and management of pulmonary embolism

“…Дыхательная недостаточность при ТЭЛА являет ся следствием преимущественно гемодинамических нарушений [79]. Низкий сердечный выброс приво дит к десатурации смешанной венозной крови.…”

Impact of tenecteplase in intermediate and high risk pulmonary embolism

“…Respiratory failure in PE is predominantly a consequence of haemodynamic disturbances. 17 Low cardiac output results in desaturation of the mixed venous blood. In addition, zones of reduced flow in obstructed vessels, combined with zones of overflow in the capillary bed served by non-obstructed vessels, result in ventilation-perfusion mismatch, which contributes to hypoxaemia.…”