Biomedical Engineering Reference
In-Depth Information
At the smallest spatial scale, micro-emboli (\170 lm in diameter) occluding
small pulmonary arteries appear to produce a larger PAP response, for the same
theoretical level of capillary bed occlusion, than their larger counterparts [ 92 ].
Small emboli are often used to induce PH and edema in animal models; compu-
tational modeling provides a means to properly interpret these experimental
models by providing an understanding of the implications of micro-embolus
occlusion. Under the hypothesis proposed by Read in 1969 [ 78 ] that occlusion to
proximal (high flow) capillary beds may account for the relative severity of micro-
emboli, Clark et al. [ 32 ] constructed an asymmetrically branching model of the
blood vessels in the acinus to investigate the effect of occlusion in this structure.
The idealized, symmetric ladder-like acinar structure described in Sect. 4 , while
useful in bridging the spatial scales in models of the full pulmonary circulation,
was inappropriate for this study as it could not capture the effect of a single
occlusion at the micro-scale. A multibranching geometry for pre-capillary acinar
vessels was therefore constructed [ 93 ], based on morphometric data regarding
acinar structure [ 94 ]. Aside from asymmetry in pre-capillary vessels, the model
retained the ladder-like structure of its symmetric counterpart, with capillary
connections at each level in the acinar tree. The model confirmed the hypothesis
that proximal micro-emboli have a greater impact on PVR than distal emboli.
However, although the blockage of normally high flow capillary beds—and so a
reduction in capillary surface area—increases PVR, the model predicted a sig-
nificant capacity for redistribution of blood flow through unblocked capillary beds.
It suggested that a major reason for a large increase in PVR with proximal
occlusions might be a result of the fact that blood must now travel through several
high resistance blood vessels before reaching the pulmonary capillaries. This again
highlighted the importance of a serial-parallel acinar structure being crucial to the
lung's ability to carry a high volume of blood at low pressures.
Subsequent modeling studies investigated the impact of larger (mm in diame-
ter) emboli in the anatomically-based full lung geometry of a single individual [ 33 ,
34 ]. Both studies simulated embolism by reducing the radius of an occluded vessel
to a percentage of its original (baseline) radius, depending on the level of occlu-
sion. Vessels were occluded based on locations determined from MDCT data in
patients presenting clinically with acute PE [ 33 ], and in a probabilistic manner by
occluding vessels based on their baseline blood flow rates [ 34 ]. Both studies
suggested that mechanical occlusion in the absence of any response to hypoxia,
vasoactive signaling, or prior pathology, was not sufficient to raise PAP to PH
levels, even with 70-80 % of the capillary bed occluded. Clinically, PH is seen in
some patients with far lower occlusion levels; for example McIntyre and Sasahara
observed PH in some patients with\30 % estimated capillary bed occlusion in the
absence of prior pulmonary disease [ 89 , 90 ]. The reason for the low impact of
mechanical occlusion on PAP in modeling studies is the capacity for the lung to
'recruit' capillary and large blood vessel volume in non-occluded regions, either
via distension of elastic vessels (because of increased blood pressures), or in the
case of the capillary bed by the direct recruitment of capillary vessels that may
ordinarily be unperfused. The redistribution of blood flow post-occlusion is more
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