Mechanics of cardiac edema

Although heart tissue is normally 80% water by weight, the fluid component becomes mechanically apparent only when it deviates from normal. Cardiac edema (increased tissue fluid content), which occurs during ischemia or reperfusion following cardiopulmonary bypass, causes increased left ventricular passive stiffness. This work investigates how the interaction between edema and myocardial microstructure determines ventricular passive stiffness. A combination of experimental and theoretical studies examines the significance of deformation history and myocardial fluid content on heart muscle and the left ventricle. Pressure-volume (PV) curves were measured in the left ventricle (LV) of an excised potassium-arrested rabbit heart by inflation of an intraventricular balloon. Tissue fluid content was changed by coronary perfusion with osmotically active perfusates while heart weight was measured. Direct mechanical testing of excised myocardial specimens both biaxially (in the plane of the ventricular wall) and transmurally (through the thickness of the wall) was also performed. Load-history dependent mechanical properties in both preparations were evaluated. A doubling of heart weight (increase of water content to 90%) caused a nearly threefold increase in LV pressure at maximum balloon volume. Reversal of edema caused a reduction in pressure to near normal levels. However, this reduction occurred even though edema reversal was incomplete (water content remained above normal); suggesting edematous swelling caused inelastic deformation. A separate set of experiments showed a relation between distension and the zero-pressure volume of the ventricle; increased distension amplitude caused increased cavity volume. Similarly, in muscle samples increased stretch increased the unstressed reference length. A final set of experiments manipulated fluid content and balloon inflation to demonstrate that induction and reversal of edema itself causes inelastic deformation in the intact ventricle. These results indicate that increased myocardial water content is associated with increased LV passive stiffness and that reversal of edema causes a reduction of stiffness. Edema reversal is accompanied by increased cavity size because induction and reversal of edema causes inelastic deformation in the excised heart. Furthermore, both the intact heart and excised tissue specimens exhibit load-history dependent mechanical behavior