What Actually Causes POTS? A Mechanistic Reading of Postural Orthostatic Tachycardia Syndrome — Why the standard POTS model produces variable results

The diagnostic criterion for POTS is hemodynamic. The heart rate rises with posture. That is the definition. It is also as far as the diagnostic process usually goes. The patient is given the POTS label and the symptomatic-management toolkit. The mechanism that produced the hemodynamic finding is rarely investigated in detail because the clinical infrastructure for that investigation does not exist in most settings. This is why POTS patients often experience their care as "manage the symptoms and learn to live with it." The clinical mechanism is treated as essentially unknowable, and the focus shifts to making the patient functional within their constraint. For some patients this is sufficient. For many, the constraint is not a permanent feature of their physiology. It is the readout of a specific lesion that, if identified, can be addressed. The Host Capacity Model approach to POTS begins with the question of which lesion is producing the hemodynamic phenotype in the specific patient. Different patients have different lesions. The lesions are mechanistically distinguishable. They respond to different interventions. Stratifying the case is the precondition for moving beyond pure symptomatic management.