COVID and POTS: New Developments in Autonomic Dysfunctions

Some individuals recovering from COVID-19 have reported lingering symptoms resembling postural orthostatic tachycardia syndrome (POTS), a condition affecting the autonomic nervous system. This has raised concerns about whether COVID-19 could be triggering or worsening autonomic dysfunction in certain patients.

Understanding how COVID-19 contributes to POTS-like symptoms is crucial for diagnosis and treatment. Researchers are investigating potential mechanisms, including immune responses, neurological involvement, and cardiovascular changes.

Autonomic Nervous System Basics

The autonomic nervous system (ANS) regulates involuntary physiological functions, ensuring the body maintains homeostasis. It consists of two primary branches: the sympathetic and parasympathetic nervous systems. The sympathetic division prepares the body for stress, increasing heart rate, dilating airways, and redirecting blood flow to muscles. The parasympathetic system promotes recovery, slowing heart rate, stimulating digestion, and restoring balance after stress.

Dysfunction in this system can lead to disorders like POTS, where blood flow and pressure regulation upon standing become impaired. Normally, the ANS ensures adequate circulation by constricting blood vessels and slightly increasing heart rate. In POTS, this regulation fails, causing excessive heart rate elevation, dizziness, and fatigue. Possible underlying mechanisms include abnormalities in neurotransmitter signaling, vascular tone regulation, and baroreceptor sensitivity.

Core POTS Features

POTS is primarily characterized by an excessive heart rate increase upon standing—exceeding 30 beats per minute (bpm) in adults or 40 bpm in adolescents within 10 minutes—without a corresponding drop in blood pressure. This leads to dizziness, palpitations, and near-fainting episodes, significantly impacting daily life. Unlike orthostatic hypotension, where blood pressure drops upon standing, POTS is defined by heart rate abnormalities.

Beyond cardiovascular symptoms, POTS often presents with fatigue, brain fog, and exercise intolerance, resembling chronic fatigue syndrome or fibromyalgia. Gastrointestinal issues such as nausea and bloating, as well as temperature dysregulation and excessive sweating, suggest broader autonomic impairment. Symptoms fluctuate in severity, complicating diagnosis and management.

The condition has multiple subtypes, requiring different treatment approaches. Hyperadrenergic POTS involves excessive sympathetic activation, leading to high norepinephrine levels and symptoms such as tremors, anxiety, and hypertension. Hypovolemic POTS results from low blood volume, impairing circulation upon standing. Neuropathic POTS stems from small fiber nerve damage, reducing vascular constriction and causing excessive blood pooling.

Potential Links Between COVID And POTS

Cases of POTS-like symptoms emerging after COVID-19 have led researchers to explore links between the virus and autonomic dysfunction. Some individuals with no prior autonomic issues now experience persistent tachycardia, dizziness, and exercise intolerance long after recovering from the acute infection. Since POTS is associated with viral infections, autoimmune disorders, and neuropathic damage, SARS-CoV-2 may be acting as a trigger for dysautonomia.

A study in Nature Cardiovascular Research found that some post-COVID patients met the diagnostic criteria for POTS, with heart rate increases upon standing mirroring idiopathic cases. This suggests the virus may disrupt autonomic regulation, impair vascular control, or alter neurocirculatory responses. Many report worsening symptoms after minimal exertion, a hallmark of POTS.

Symptoms often appear weeks or months after the initial infection, aligning with other post-viral dysautonomias. Some individuals with pre-existing mild autonomic dysfunction report worsening symptoms post-COVID, suggesting the virus may not only trigger new cases but also exacerbate existing ones. This has significant implications for long-term management, as post-COVID POTS may require tailored interventions.

Immune Response And Inflammation

SARS-CoV-2 provokes a strong immune response, which in some individuals leads to prolonged inflammation contributing to POTS. The immune system’s reaction involves cytokines and inflammatory mediators that can persist beyond the acute infection. Prolonged immune activation has been observed in several post-viral syndromes and is increasingly recognized in post-COVID autonomic dysfunction.

Elevated levels of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) have been detected in individuals with lingering post-COVID symptoms, suggesting systemic inflammation disrupts autonomic regulation. Persistent inflammation can also impair vascular function, leading to endothelial dysfunction, which has been documented in post-COVID patients with POTS-like symptoms.

The endothelium, which regulates vascular tone, becomes compromised when exposed to chronic inflammation, reducing nitric oxide availability and affecting blood vessel dilation. This can lead to excessive blood pooling in the lower extremities upon standing, contributing to tachycardia and dizziness. Studies show markers of endothelial dysfunction remain elevated in post-COVID patients for months, reinforcing the role of unresolved inflammation in autonomic instability.

Neurological Involvement

COVID-19’s effects on the nervous system have raised concerns about its role in triggering POTS. Many recovering individuals report persistent neurological symptoms such as brain fog, headaches, and sensory disturbances, which overlap with POTS. These disruptions suggest the virus may interfere with autonomic regulation at a neural level, either through direct viral impact or dysfunction in neural signaling pathways.

Neuroinflammation and altered autonomic reflexes have been observed in post-COVID individuals through functional imaging and cerebrospinal fluid analysis. Some researchers propose that SARS-CoV-2 disrupts the vagus nerve, which regulates heart rate, digestion, and vascular tone. Damage to this nerve could explain persistent tachycardia, gastrointestinal symptoms, and blood pressure irregularities.

Cases of small fiber neuropathy, affecting nerves responsible for autonomic control, have been documented in post-COVID patients with POTS-like symptoms. These findings suggest neurological impairment is a significant factor in post-COVID autonomic dysfunction.

Cardiovascular Changes

The cardiovascular system relies on autonomic control to maintain stable circulation, particularly during postural changes. In post-COVID individuals with POTS-like symptoms, exaggerated heart rate responses upon standing suggest the virus may alter cardiovascular regulation. Some exhibit heart rate increases exceeding 40 bpm, characteristic of POTS, indicating imbalances in autonomic signaling.

Endothelial dysfunction may be a key factor, as impaired blood vessel regulation can lead to excessive blood pooling in the lower extremities, forcing the heart to compensate by increasing its rate. Studies indicate post-COVID individuals with dysautonomia show reduced vasoconstriction capacity, supporting the idea of vascular instability.

Abnormalities in blood volume regulation have also been observed, with some patients exhibiting signs of hypovolemia, exacerbating orthostatic intolerance. These cardiovascular disturbances highlight the complex interplay between autonomic dysfunction and circulatory control in post-COVID POTS cases.