Recovery following SARS-CoV-2 infection (COVID-19) is not always linear. While many people return to baseline health within weeks, a substantial number experience persistent and debilitating symptoms lasting months or years. These lingering health issues are grouped under the term “Long COVID” or post-acute sequelae of SARS-CoV-2 infection. This phenomenon has revealed new patterns of chronic illness following an acute viral episode, affecting individuals regardless of initial disease severity.
Understanding Postural Orthostatic Tachycardia Syndrome
Postural Orthostatic Tachycardia Syndrome (POTS) is a chronic disorder of the autonomic nervous system, the body’s involuntary control center for functions like heart rate, blood pressure, and temperature regulation. POTS impairs the body’s ability to properly adjust to gravity when standing upright. The primary diagnostic feature is an excessive, sustained increase in heart rate upon standing.
For an adult, a diagnosis is established when the heart rate increases by at least 30 beats per minute within the first ten minutes of standing, or exceeds 120 beats per minute, without a significant drop in blood pressure. This distinguishes POTS from conventional orthostatic hypotension, where standing causes a measurable and sustained blood pressure drop. The sustained high heart rate is the body’s attempt to compensate for the pooling of blood in the lower extremities that occurs when upright.
The resulting symptoms are known as orthostatic intolerance, meaning they occur in an upright position and often improve when the person lies down. Patients frequently report lightheadedness, chronic fatigue, heart palpitations, and exercise intolerance. A common complaint is “brain fog,” referring to difficulty with concentration, memory, and mental clarity. These symptoms must be present for at least three months and cannot be explained by any other medical condition to meet the diagnostic criteria.
Establishing the Connection Between COVID-19 and POTS
Viral infections have long been recognized as potential triggers for POTS, and the COVID-19 pandemic has significantly accelerated the recognition of this connection. Numerous observational studies and clinical reports have documented a distinct increase in POTS diagnoses following SARS-CoV-2 infection. This has led many clinicians to consider POTS a specific, identifiable phenotype within the broader spectrum of Long COVID.
Epidemiological data suggest that a measurable percentage of COVID-19 survivors develop POTS, with estimates ranging from 2% to 14% of those infected meeting the full diagnostic criteria. A much larger proportion, potentially up to 61% in some cohorts, report experiencing POTS-like symptoms such as persistent tachycardia and orthostatic intolerance within several months of their acute illness. This association points to a clear temporal relationship between the viral infection and the onset of autonomic dysfunction.
The timeline for symptom emergence typically involves POTS symptoms appearing weeks to months after the initial infection, often between six to eight months post-recovery. The severity of the acute COVID-19 illness does not appear to correlate directly with the risk of developing post-COVID POTS. Many individuals who experience this syndrome had only mild or moderate initial COVID-19 symptoms.
Proposed Biological Mechanisms of Action
The exact processes by which the SARS-CoV-2 virus can trigger POTS are still under investigation, but several leading hypotheses center on the body’s immune and inflammatory responses. One prominent theory involves autoimmunity, where the viral infection mistakenly prompts the immune system to attack the body’s own tissues. This is thought to occur through a process called molecular mimicry, where viral components resemble proteins in the autonomic nervous system.
This autoimmune reaction may lead to the production of autoantibodies that target and interfere with autonomic receptors, such as adrenergic receptors, which are responsible for regulating heart rate and blood vessel constriction. Interference with these receptors can disrupt the signaling pathways that control heart rate and blood pressure when standing, resulting in the characteristic orthostatic tachycardia. The presence of these autoantibodies has been identified in some patients with post-COVID POTS, supporting this mechanistic link.
Another potential mechanism involves viral persistence, where remnants of the SARS-CoV-2 virus or its proteins remain in the body’s tissues. These viral reservoirs can cause chronic low-grade inflammation and immune activation. This sustained inflammatory state, known as neuroinflammation, can directly or indirectly impair the function of the peripheral and central nervous systems, including the autonomic nerves.
The involvement of Mast Cell Activation Syndrome (MCAS) is also being explored as a contributing factor. Mast cells are immune cells that release inflammatory mediators, and the SARS-CoV-2 virus may trigger an abnormal or exaggerated mast cell response. This excessive release of inflammatory chemicals could contribute to the systemic inflammation and dysautonomia observed in patients with post-COVID POTS.
Diagnosis and Management Approaches
Diagnosing POTS typically involves objective testing to confirm the diagnostic criteria of orthostatic tachycardia. The gold standard for this is the head-up tilt table test, which involves monitoring a patient’s heart rate and blood pressure while they are tilted upright on a specialized table. If a tilt table is not available, a simpler active standing test performed in a clinic can also be used to measure the change in heart rate over ten minutes of standing.
Management of post-COVID POTS focuses on alleviating symptoms and improving quality of life, and the approach is generally the same as for non-viral-triggered POTS. Non-pharmacological interventions are the initial step, aiming to increase blood volume and improve venous return. These strategies often include a significant increase in daily fluid intake, along with a high-salt diet to help the body retain that fluid.
Patients are advised to wear medical-grade compression stockings or abdominal binders to reduce blood pooling in the lower body. A structured, graded exercise program focusing on non-upright activities, such as rowing or recumbent cycling, is recommended to improve cardiovascular conditioning. For more severe symptoms, pharmacological treatments may be introduced, including beta-blockers or ivabradine to lower the heart rate, or fludrocortisone or midodrine to help regulate blood pressure and volume.