Model for a general mechanical blood damage prediction.
Knowledge of the correlation between mechanical loading of formed blood elements and the amount of their destruction is important for the prediction of blood trauma in artificial circulatory devices as well as in natural circulation. A hemodynamic assessment and optimization of artificial organs to minimize trauma could be undertaken in the design phase given a comprehensive mechanical blood damage model. A theory to determine blood trauma theoretically as a combination of a mechanical loading analysis and a phenomenological blood damage resistance hypothesis is presented. Arbitrary stress-time functions of blood particles predicted by flow analysis are reduced to a set of simple time functions for which the damage behavior may, in principle, be obtained from mechanical blood damage tests. A classification of those stress functions into damaging and nondamaging parts is followed by an overall trauma prediction considering cumulative effects by means of a damage accumulation hypothesis. Theoretical determination of blood destruction caused by mechanical stresses in a centrifugal pump is one possible application of the proposed theory. The strategy of hemolysis prediction is demonstrated for the Aries Medical Isoflow Pump. Irregular stress-time loading functions of particles passing the pump domain obtained by three-dimensional numerical flow simulations were reduced and classified into harmonic components. To relate these functions to their hemolytic response can only be done in a qualitative manner since blood damage behavior under transient stress loading has not been sufficiently investigated. Accurate prediction of blood trauma using the proposed theory will require detailed study of the influence of frequency and amplitude of harmonic stress loading on formed blood elements.
Bludszuweit
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University of Strathclyde, Bioengineering Unit, Glasgow, Scotland, U.K.
D001783:Blood Flow Velocity / Q000502:physiology; D004910:Erythrocyte Membrane / Q000473:pathology; D004912:Erythrocytes / Q000166:cytology / Q000473:pathology*; D006353:Heart-Assist Devices / Q000009:adverse effects*; D006461:Hemolysis / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D013314:Stress, Mechanical