Death from Circulatory Failure

As Ribbert (1916a) pointed out, it is fairly rare for the blood to remain liquid postmortem. When the body dies from circulatory failure, both the blood cells and the vessel walls continue to consume the residual oxygen in that blood. This progressive de-oxygenation gradually 'suffocates' both blood and tissues, so that, over the course of (say) 3-4 h, gross hypoxaemia ensues. The white cells of normally oxygenated blood would instigate the repair or removal of dead or dying vascular endothelium, but we may not expect suffocated blood cells to perform this (or any other) service.

The consequences of death by circulatory failure will depend on whether it is gradual, allowing (often massive) thrombi to form in the heart and major arteries, or sudden. If it is sudden, the vascular endothelium gradually dies, but only the leukocytes and platelets in its immediate vicinity will be available to congregate upon it; the circulation has ceased, so there is no further supply of 'fresh', still-living, blood cells. The extent of such coagulation will depend on the numbers of leukocytes/platelets in the immediate neighbourhood that remain viable when the endothelium has died. Any coagulum that forms will not have the layered structure of a thrombus; it will be clot-like.

However, if circulatory failure is gradual, the changes in endothelial cell pheno-type resulting from hypoxia will become generalised throughout the vascular system: the deterioration of cardiac output will mean that the mural endothelium cannot be adequately oxygenated via the vasa venarum. In other words, the mechanisms discussed in Chapter 12 will no longer be confined to the venous valve cusp parietalis; potentially, they could take effect in all vascular endothelia. Still-viable blood cells throughout the circulation will continue to circulate over the dead or dying endothelia, and leukocytes will congregate. This will apply particularly to the right heart and pulmonary arteries, which are relatively hypoxaemic during life and would be expected to suffer hypoxic endothelial death more quickly than the rest vascular system. In these or similar circumstances, one might expect sequestration of perhaps all the white cells in the body, as Ribbert (1916a) suggested. As the coagula become more extensive, circulation is further impaired, exacerbating the endothelial hypoxia. The 'thrombotic' process therefore accelerates quasi-exponentially in the final vicious cycle of death.

According to a recent paper by Porat et al. (2004), heart valve cusp endothelium shows a pro-coagulatory response to hypoxia. The mechanism underpinning the extensive agonal semi-solidification in the heart and major blood vessels described by Ribbert (1916a) may therefore be exactly analogous to that involved in venous valve pockets during the genesis of DVT; though the crucial receptor in the heart valves seems to be the receptor tyrosine kinase tie-1 (Porat et al. 2004), which has not been implicated in the venous endothelial response (Chapter 12). The particular tendency of agonal white thrombi to develop on the heart valves is consistent with these findings.

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