What Actually Causes POTS? A Mechanistic Reading of Postural Orthostatic Tachycardia Syndrome — The clinical pattern that defines POTS

A patient presents with lightheadedness on standing, palpitations that worsen with posture change, exercise intolerance, post-exertional crashes, brain fog that intensifies when upright, headaches that improve when lying down, and a sense that their body cannot regulate itself the way it used to. The diagnostic criterion is straightforward: a heart rate increase of 30 beats per minute or more (40 in adolescents) within 10 minutes of standing or upright tilt, in the absence of orthostatic hypotension, with chronic symptoms for at least three months. A tilt-table test confirms the diagnosis. The standard treatment that follows is symptomatic. Compression garments. Increased salt and fluid intake. Beta blockers for the tachycardia. Midodrine for the venous pooling. Fludrocortisone for the volume expansion. Ivabradine for selective heart-rate control without affecting blood pressure. Mestinon (pyridostigmine) for the cholinergic axis. Exercise programs like the Levine protocol for graded reconditioning. Some patients respond well to this approach. Many respond partially. A substantial fraction respond minimally despite carefully managed medications. The literature documents wide heterogeneity in response, similar to the heterogeneity seen in MCAS and chronic fatigue. The interpretation that this represents inadequate medication or insufficient adherence is partially correct. The mo