Postural Orthostatic Tachycardia Syndrome (POTS) is a form of dysautonomia, meaning the autonomic nervous system incorrectly regulates involuntary body functions like heart rate, blood pressure, and body temperature. For many people with POTS, exposure to heat is a major trigger that causes a significant worsening of their symptoms. Understanding this phenomenon requires examining the body’s natural response to heat and how the underlying cardiovascular dysfunction in POTS interferes with that response. The exacerbation of symptoms is a direct result of how heat challenges the body’s delicate control over blood volume and circulation.
How the Body Uses Vasodilation to Cool Down
A healthy body manages heat stress through vasodilation, where blood vessels near the skin’s surface widen significantly. This widening allows a massive increase in blood flow to the periphery, which facilitates the transfer of heat from the body’s core to the environment. The skin’s circulation is highly compliant, meaning it can hold a substantial amount of blood, effectively turning the skin into a radiator for cooling the body down. This physiological adjustment is remarkably powerful, capable of diverting up to 60% of the heart’s output to the skin during severe heat stress. While this mechanism is effective for maintaining core body temperature, it inherently requires shifting a large volume of blood away from the central circulation.
Exacerbated Blood Pooling and Reduced Circulating Volume
Heat-induced vasodilation becomes problematic when combined with the specific pathology of POTS. The autonomic nervous system already struggles to maintain proper peripheral blood vessel tone, especially in the lower half of the body. When heat forces a massive, widespread dilation of these vessels, the impaired ability to constrict them means blood pools excessively in the lower extremities and the splanchnic circulation (abdomen). This pooling causes a severe reduction in the effective circulating volume. Since many POTS patients also experience chronic hypovolemia, heat further shifts this already-low circulating volume downward, severely diminishing the venous return of blood to the heart and reducing blood flow to the brain.
The Resulting Symptoms and Autonomic Compensation
When the effective circulating blood volume drops due to excessive pooling, the body senses hypovolemia and reflexively attempts to restore cerebral blood flow. The primary compensatory mechanism is an immediate, aggressive increase in heart rate, known as compensatory overdrive. This dramatic increase in heartbeats is an attempt to maintain cardiac output despite the significantly reduced volume of blood returning to the heart. This compensatory tachycardia is responsible for the palpitations and chest discomfort often felt by patients in the heat. However, the rapidly beating heart cannot fully overcome the massive pooling, leading to hypoperfusion symptoms such as dizziness, lightheadedness, pre-syncope, and “brain fog.”