Structure, mechanical properties, and modeling of cyclically compressed pulmonary emboli.

Pulmonary embolism occurs when blood flow to a part of the lungs is blocked by a venous thrombus that has traveled from the lower limbs. Little is known about the mechanical behavior of emboli under compressive forces from the surrounding musculature and blood pressure. We measured the stress-strain responses of human pulmonary emboli under cyclic compression, and showed that emboli exhibit a hysteretic stress-strain curve. The fibrin fibers and red blood cells (RBCs) are damaged during the compression process, causing irreversible changes in the structure of the emboli. We showed using electron and confocal microscopy that bundling of fibrin fibers occurs due to compression, and damage is accumulated as more cycles are applied. The stress-strain curves depend on embolus structure, such that variations in composition give quantitatively different responses. Emboli with a high fibrin component demonstrate higher normal stress compared to emboli that have a high RBC component. We compared the compression response of emboli to that of whole blood clots containing various volume fractions of RBCs, and found that RBCs rupture at a certain critical stress. We describe the hysteretic response characteristic of foams, using a model of phase transitions in which the compressed foam is segregated into coexisting rarefied and densified phases whose fractions change during compression. Our model takes account of the rupture of RBCs in the compressed emboli and stresses due to fluid flow through their small pores. Our results can help in classifying emboli as rich in fibrin or rich in red blood cells, and can help in understanding what responses to expect when stresses are applied to thrombi in vivo.