Computational models of cardiac electrophysiology, energetics, and contraction, applied to clinically relevant stressors: ischemia, hemorrhage, beta-adrenergic drive, mitochondrial dysfunction, and trauma.

• Cardiac cell models. Published myocyte models (ToR-ORd, Gauthier 2012, Colman 2019, …) reimplemented in Julia / SciML for composability and reuse.
• Excitation–contraction coupling and mitochondrial energetics. Coupled whole-cell models linking calcium handling, force generation, and ATP supply.
• Beta-adrenergic and signaling pathways. Upstream signaling layered onto the electrophysiology stack.
• Trauma and hemorrhage. Windkessel and 0D electromechanical models targeting battlefield-relevant physiology.
• Numerics and infrastructure. Rush–Larsen integrators, debugging tools, and shared tooling across the model packages.