The COVID-19 pandemic has led to a significant increase in cases of Postural Orthostatic Tachycardia Syndrome (POTS), a condition that disrupts the body’s involuntary functions. Before the pandemic, POTS was considered a relatively rare disorder, but the incidence rate has risen dramatically following SARS-CoV-2 infections. For many people experiencing persistent symptoms after a COVID-19 infection, the underlying problem may be this form of autonomic dysfunction. This acceleration in diagnoses suggests a strong connection between the virus and this debilitating health issue.
Understanding Postural Orthostatic Tachycardia Syndrome
Postural Orthostatic Tachycardia Syndrome is a disorder of the autonomic nervous system, the body’s “autopilot” that controls involuntary functions like heart rate, breathing, and blood pressure. This malfunction of the autonomic nervous system is broadly termed dysautonomia. In a healthy person, shifting from lying down to standing automatically constricts blood vessels in the lower body to push blood back up toward the brain.
For an individual with POTS, this automatic response fails, causing blood to pool in the lower extremities. The heart attempts to compensate for the resulting drop in blood pressure and reduced blood return by beating much faster, which is the defining characteristic of the syndrome. Diagnosis requires an increase in heart rate of 30 beats per minute or more within ten minutes of standing, without a significant drop in blood pressure.
Symptoms of POTS fall under the umbrella of orthostatic intolerance. These include lightheadedness, dizziness, and near-fainting, which are usually relieved by lying down. Patients also report severe fatigue, cognitive difficulties often called “brain fog,” and heart palpitations. Before the rise in post-COVID cases, the exact cause of POTS was often unknown, categorized as a primary disorder without an identifiable trigger.
The Generalized Link Between Viral Illnesses and POTS
The association between POTS and infections is not a new phenomenon; medical experts have long recognized that severe illness can act as a trigger. Historically, viral infections like Epstein-Barr virus (mononucleosis), influenza, and Lyme disease have been documented as preceding events in a substantial number of POTS cases. A significant percentage of people diagnosed with POTS prior to the COVID-19 pandemic traced the onset of their symptoms back to an infection.
The biological theory behind this connection centers on the body’s immune response. When the immune system activates to fight off a pathogen, it sometimes produces antibodies that mistakenly target the body’s own tissues. This autoimmune response can inadvertently attack components of the autonomic nervous system responsible for regulating heart rate and blood vessel constriction.
The resulting inflammation or nerve damage prevents the nervous system from properly maintaining blood flow when a person is upright. The SARS-CoV-2 virus represents the latest and most widespread infectious trigger linked to this long-established post-viral pathway.
Specific Mechanisms of COVID-19 Induced POTS
The high volume of SARS-CoV-2 infections has led to a significant number of new POTS diagnoses, highlighting the virus’s capacity to initiate this condition. Data suggests a dramatic increase in incidence, with new cases rising from approximately 1.42 per million person-years before the pandemic to 20.3 per million person-years afterward. Researchers are investigating several mechanisms by which COVID-19 specifically induces POTS, often in people who experienced only mild initial infections.
One widely accepted theory involves an autoimmune reaction triggered by the viral infection. SARS-CoV-2 may cause the immune system to produce autoantibodies that target the adrenergic receptors on blood vessel walls and nerve endings. These receptors respond to adrenaline-like hormones, which usually tighten blood vessels upon standing. When these receptors are blocked or damaged, the blood vessels cannot constrict effectively, leading to blood pooling.
A second mechanism involves direct viral damage or persistence within the nervous system. The SARS-CoV-2 virus utilizes the ACE-2 receptor to enter cells, which are present in the central nervous system and on nerves that regulate autonomic functions. While the initial infection might clear, the virus could potentially persist in certain tissues, or its remnants could cause prolonged neurotoxicity and inflammation, injuring the nerve fibers of the autonomic system.
A third major theory focuses on inflammation and endothelial dysfunction. COVID-19 is known to cause widespread inflammation and damage to the endothelium, the inner lining of blood vessels. This damage can lead to microclot formation and impaired function, preventing the coordinated constriction needed to manage blood flow against gravity. The chronic inflammatory state can also lead to sympathetic nervous system overactivation, contributing to the rapid heart rate seen in POTS.
Clinical Management and Living with POTS
Diagnosis of POTS begins with objective testing to confirm the criteria. The active standing test or the tilt table test are the primary methods used to observe the sustained increase in heart rate upon changing posture. Once POTS is confirmed, management generally follows two main pillars: non-pharmacological lifestyle adjustments and targeted pharmacological interventions.
Non-pharmacological strategies focus on counteracting the primary physiological problems of low blood volume and venous pooling. Patients are advised to increase their fluid intake, aiming for two to three liters of water daily, and to increase salt intake, sometimes up to 10 to 12 grams per day, to help retain that fluid. This expansion of blood volume helps ensure more blood returns to the heart and brain.
Compression garments, such as medical-grade stockings that extend to the waist, are recommended to physically prevent blood from pooling in the legs and abdomen. Physical reconditioning through structured exercise is also an intervention, often starting with horizontal exercises like swimming or using a recumbent bicycle to build muscle strength without triggering orthostatic symptoms. The upright component of exercise is slowly introduced as tolerance improves.
For pharmacological management, medications are used to help control the heart rate or improve blood vessel constriction. Specific classes of drugs, such as beta-blockers, can help slow the heart rate and reduce the severity of the tachycardia. Vasoconstrictors are another class of medication prescribed to help narrow the blood vessels, improving the body’s ability to maintain blood pressure when standing. A personalized approach to both lifestyle and medication is necessary to manage symptoms and improve a person’s quality of life.