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🦠 POTS Autonomic Dysfunction Simulator

The simulator models postural orthostatic tachycardia syndrome (POTS) with parameters of heart rate changes during transition to a vertical position, and the role of fludrocortisone/beta-blockers.

Long COVID / ME/CFS2DModerate60 FPS
pots-autonomic-dysfunction-simulator ↗ Open standalone

Supine Baseline — Normal Autonomic Regulation

Resting heart rate reflects balanced vagal and sympathetic tone.

  • 60–80: Typical supine HR (beats per minute)
  • <3 s: Baroreflex latency (normal reflex arc)
  • ~1–3M: POTS prevalence (US, mostly women 15–50)
  • ~30%: Long COVID link (report POTS-like symptoms)

Why baseline matters

Supine HR sets the reference point for diagnosing the standing HR increase.

Autonomic nervous system role

Sympathetic and parasympathetic branches jointly set resting cardiac tone.

Standing Up — Healthy Orthostatic Compensation

Gravity pools blood in the legs; healthy reflexes correct within seconds.

  • 10–20: Normal HR rise (bpm on standing)
  • ~500 mL: Venous pooling (shifts to legs/pelvis)
  • ~30 s: Compensation time (to stabilize)
  • minimal: BP change (in healthy adults)

Baroreceptor reflex

Falling venous return triggers vasoconstriction and a modest HR rise.

Vasoconstriction efficiency

Healthy vessels tighten quickly, limiting the compensatory HR need.

Impaired Compensation — Excessive Standing Tachycardia

In POTS, vasoconstriction is inadequate, so heart rate rises sharply instead.

  • ≥30 bpm: Diagnostic threshold (HR rise within 10 min)
  • ≥40 bpm: Adolescent threshold (age 12–19)
  • ≥120: Standing HR (often reached in POTS)
  • minimal: BP drop (distinguishes from hypotension)

Why heart rate substitutes

Weak vasoconstriction forces the heart to compensate via rate alone.

Not a blood pressure problem

Pressure stays relatively stable, unlike orthostatic hypotension.

Living the Tachycardic Response — Symptom Burden

Sustained excess heart rate produces disabling everyday symptoms.

  • common: Palpitations (racing/pounding heart)
  • common: Lightheadedness (near-syncope episodes)
  • frequent: Brain fog (reduced cerebral flow)
  • chronic: Fatigue (often disabling)

Cerebral perfusion effects

Reduced effective flow to the brain drives fog and lightheadedness.

Functional impact

Symptoms often limit standing time, exercise, and daily activity.

Fludrocortisone and Beta-Blockers — Restoring Orthostatic Tolerance

Volume expansion or direct rate control blunt the excessive HR spike.

  • volume↑: Fludrocortisone (reduces compensatory need)
  • HR↓: Beta-blocker (blunts rate response directly)
  • 10–20mg: Low-dose propranolol (common starting dose)
  • often marked: Symptom improvement (with combined therapy)

Volume expansion strategy

Fludrocortisone raises blood volume, easing venous pooling on standing.

Direct rate control

Beta-blockers cap the maximum HR response independent of volume.

⚙ Under the hood

The simulator models postural orthostatic tachycardia syndrome (POTS) with parameters of heart rate changes during transition to a vertical position, and the role of fludrocortisone/beta-blockers.

CanvasBiomedicine

2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install

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