Left ventricular pV loops showing the initial response (A–C) and 4 cycles (D–F) after applying a step change in loading conditions and contractility. (A) Altering afterload by increasing/decreasing the systemic vascular resistance, R
sys pivots arterial elastance E
a curve. Endsystolic elastance, E
es and intercept V
d characterizing the ESPVR was determined by linear regression of end-systolic data points V
es and p
es, marked by solid circles. (B) Increasing/decreasing preload shifts E
a curve and increases/decreases stroke volume via the Starling mechanism, mediated by the length-dependence of the active stress model. Determination of ESPVR was consistent with afterload protocol. (C) Increasing/decreasing contractility increases/decreases stroke volume, LV peak pressure and p
es. For each contractile state afterload was also perturbed to determine end-systolic elastance E
es and V
d.