A continued increase in pulmonary load (Ea) and quickly exhausts the capacity for homeometric adaptation to maintain Ees/Ea coupling. At this stage, the right ventricle begins to rely on heterometric adaptation, characterized by right ventricular dilation and increased right ventricular preload.  The result is increased sarcomere stretch and initial maintenance of right ventricular stroke volume via the Frank-Starling mechanism.  Because heterometric adaptation does not actually increase right ventricular contractility, (Ees is a "load independent" property) the slope of Ees is often unchanged or may even decrease slightly.  While stroke volume can be relatively preserved during heterometric adaptation, it comes at the cost of increased wall stress and reduced myocardial efficiency (more energy required for the same amount of stroke work). 

Sustained increases in Ea can also lead to more chronic structural adaptation, such as RV myocardial hypertrophy.  These changes complement, but are distinct from, both homeometric and heterometric mechanisms. Hypertrophy develops over weeks to months in response to persistent pressure overload, leading to increased wall thickness and partial normalization of wall stress. Functionally, this remodeling allows the RV to augment its contractile capacity and effectively raise baseline Ees over time, thereby helping to restore or preserve RV–PA coupling (Ees/Ea) despite elevated Ea. In this sense, hypertrophy can be viewed as a longer-term extension of the homeometric strategy, building the structural substrate needed to sustain higher contractility. However, this adaptation has limits: as afterload continues to rise or disease progresses, hypertrophy often becomes maladaptive, with fibrosis, ischemia, and impaired energetics leading to declining contractility and renewed uncoupling, at which point heterometric mechanisms (RV dilation and increased preload) predominate—again at the cost of increased wall stress and reduced efficiency.