Two physiological concepts explaining the detrimental effects of excessive volume loading. (a) Normal ventricle: at end-systole (ES), the right ventricular (RV) free wall moves toward the septum. (b) Pericardial restraining effects (above, before volume loading; below, after excessive volume loading): RV dilatation, as a result of excessive volume loading, can lead to the elevation of intrapericardial pressure, increase in pericardial constraint (red arrow), and change of geometry due to interventricular septum shift. These changes contribute to the low-output state by decreasing left ventricular (LV) distensibility, preload, and ventricular elastance. (c, d) Role of the interventricular septum (c, pure RV infarction; d, RV infarction with septal ischaemia). (c) At ES, the RV free wall moves toward the septum. At end-diastole (ED), the RV dilates during diastole and the septum reverse curves toward the volume-reduced LV. At ES, the septum thickens but moves paradoxically into the RV, displacing the RV volume despite RV free wall dyskinesis. (d) Septal ischaemia depresses septal contraction and global LV function, resulting in LV dilatation. The septum stops thickening and there is increased systolic septal displacement into the RV. Pansystolic septal thinning and more extensive paradoxical displacement are associated with further depression of RV performance.