Immunology · Year 2 · from Immunology
Case 6: Long COVID with Postural Orthostatic Tachycardia Syndrome (POTS)
Clinical Image
Source: Wikipedia - Postural orthostatic tachycardia syndrome - CC BY-SA 4.0
Case Presentation
A 29-year-old previously healthy female graduate student presents to an autonomic disorders clinic 4 months after a mild COVID-19 infection that did not require hospitalization. She reports persistent debilitating fatigue, brain fog with impaired concentration, exercise intolerance with post-exertional malaise lasting 24-48 hours after minimal activity, palpitations, lightheadedness upon standing, and intermittent pre-syncope. She has been unable to attend classes or perform her research duties. She denies chest pain, weight loss, or joint symptoms. On examination, supine HR is 68 bpm and BP is 118/72 mmHg. Upon active standing, HR increases to 112 bpm within 3 minutes (delta HR +44 bpm) with BP 114/78 mmHg (no orthostatic hypotension). She becomes visibly diaphoretic and reports lightheadedness. A 10-minute active standing test confirms sustained tachycardia with HR peaking at 126 bpm. Head-up tilt table testing reproduces symptoms with HR increase from 64 to 118 bpm within 5 minutes without significant blood pressure drop. Norepinephrine levels drawn supine (280 pg/mL) and upright (890 pg/mL; elevated) suggest a hyperadrenergic component. Autoimmune panel reveals positive anti-ganglionic acetylcholine receptor antibodies at low titer. CBC, TSH, cortisol, echocardiography, and Holter monitoring are unremarkable. She is started on oral salt supplementation (6-8 g sodium/day), compression stockings (30-40 mmHg), a graduated recumbent exercise program, and propranolol 10 mg three times daily, with significant symptomatic improvement over 3 months.
Key Learning Points
- Post-acute sequelae of SARS-CoV-2 (PASC/Long COVID) affects 10-30% of patients regardless of acute disease severity; dysautonomia (particularly POTS) is a common manifestation, defined as a sustained HR increase of 30 or more bpm within 10 minutes of standing (or HR >120 bpm) without orthostatic hypotension
- Proposed mechanisms for post-COVID POTS include autoantibody-mediated autonomic neuropathy (anti-ganglionic AChR, anti-adrenergic receptor antibodies), persistent viral-induced small fiber neuropathy affecting sympathetic postganglionic fibers, brainstem neuroinflammation, and hypovolemia from impaired renin-angiotensin-aldosterone signaling
- Post-exertional malaise (PEM) in Long COVID shares pathophysiological features with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), potentially driven by mitochondrial dysfunction, impaired oxygen extraction, and microclot-mediated perfusion deficits
- Management is multimodal: volume expansion (salt, fluids), physical counter-maneuvers, graduated recumbent exercise (avoiding upright exertion initially), and pharmacotherapy tailored to the subtype -- beta-blockers for hyperadrenergic POTS, midodrine or fludrocortisone for neuropathic/hypovolemic subtypes