Principal considerations on the stroke volume-heart size relationship based on different heart models.

The aim of the present study was to show by hemodynamic investigations in a rat heart and by theoretical considerations based on different heart models that a chronic enlargement of the heart does not necessarily lead to an impairment of the stroke volume. In the experiments performed on rat hearts of various sizes, in situ pressure-volume diagrams were obtained which clearly demonstrate that, in principle, larger hearts are able to eject larger stroke volumes despite the fact that for geometrical reasons, they have to develop higher wall stress. These findings are supported by calculations of stroke volume-heart size relations being based on the assumption of different geometrical models for the left ventricle. By means of these relations, when applying them to pressure-volume data of a dilated or failing heart, it is in principle possible to differentiate between effects of altered geometry and of altered contractility. A simple lever-pump system is introduced which is appropriate to simulate transmission aspects in the transformation of myocardial shortening into ventricular ejection for hearts of variable size.