Postural Orthostatic Tachycardia Syndrome (POTS) is a complex condition involving the autonomic nervous system (ANS), the body’s involuntary control center. The ANS regulates functions like heart rate, blood pressure, digestion, and body temperature. For people with POTS, this system malfunctions, particularly when transitioning from lying down to standing upright. A persistent symptom is the feeling of chronic dehydration or perpetually low blood volume. This is rooted in a measurable physiological deficit that affects the body’s ability to circulate fluid effectively.
Understanding the Autonomic Dysfunction in POTS
The autonomic nervous system, which operates without conscious thought, is divided into the sympathetic (“fight or flight”) and parasympathetic (“rest and digest”) branches. When a healthy person stands up, gravity pulls blood downward, and the sympathetic nervous system immediately signals the small blood vessels in the lower body and abdomen to constrict. This action, known as vasoconstriction, ensures blood pressure remains stable and enough blood returns to the heart and brain.
In many cases of POTS, this nervous system response is faulty, a condition known as autonomic dysfunction. For example, in neuropathic POTS, the small nerve fibers in the lower limbs are damaged. These nerves transmit the signal for vasoconstriction, and when the signals are not properly transmitted, the blood vessels remain too relaxed and dilated.
The body fails to maintain vascular tone, which is the slight, continuous constriction that keeps blood flowing efficiently. Without the nervous system properly initiating vasoconstriction, the circulatory system cannot efficiently fight the pull of gravity. The underlying issue is not simply a lack of water intake, but a failure in the system designed to manage and distribute existing fluid volume.
The Role of Blood Pooling and Reduced Circulation
The immediate physical consequence of autonomic failure is the phenomenon of blood pooling. When an individual with POTS stands up, the slack, unconstricted blood vessels in the lower body, including the legs and abdomen, allow blood to accumulate. Gravity exacerbates this, causing a significant volume of blood to shift rapidly downward. This pooling can sequester an estimated 500 milliliters of blood in the lower extremities.
This shift means less blood is returning to the heart, a condition known as reduced venous return. The heart receives less blood to pump out, which reduces the amount of blood reaching the upper body, including the brain. The body senses a drop in the effective circulating volume, triggering the hallmark symptoms of POTS.
To compensate, the heart reflexively speeds up, leading to the excessive tachycardia that defines the syndrome. This rapid heart rate attempts to circulate the limited blood volume more quickly, trying to restore adequate flow to the brain. However, the underlying mechanical issue of blood pooling remains unresolved.
Plasma Volume Reduction and Fluid Imbalance
Blood pooling initiates a chain reaction that causes systemic fluid loss and dehydration. When blood pools in the lower extremities, the increased volume causes the pressure inside the vessels to rise significantly. This elevated pressure forces plasma, the liquid component of the blood, to leak out of the vessels and into the surrounding tissues. The plasma moves into the interstitial space, which is the area between the cells, causing swelling or edema often noticeable in the feet and lower legs.
This fluid shift reduces the effective circulating blood volume, creating a state of hypovolemia. Many people with POTS have a measurable plasma volume deficit, sometimes reduced by 10% to 25% compared to healthy individuals. This volume depletion causes the body to register a chronic state of dehydration, even with typical water consumption. The issue is the body’s inability to keep water within the circulatory system where it is needed.
Furthermore, some patients exhibit a paradox in the renin-angiotensin-aldosterone system (RAAS), which regulates blood volume and blood pressure. Despite low blood volume, which should trigger the RAAS to conserve sodium and water, these patients often have inappropriately low levels of plasma renin activity and aldosterone. This lack of a proper hormonal response means the kidneys do not receive the signal to retain sodium and water efficiently. Consequently, the body tends to excrete more fluid than it should, contributing to a persistent volume deficit.
Why Increased Fluid and Salt Intake is Necessary
Addressing the chronic volume deficit caused by blood pooling and fluid loss is the primary non-pharmacological strategy for managing POTS. The goal is to artificially expand the circulating plasma volume to compensate for fluid lost to the interstitial space and fluid inappropriately excreted by the kidneys. This requires increasing both fluid and sodium intake.
Salt is a powerful osmotic agent that helps the body retain water within the bloodstream. When sodium is consumed in higher quantities, it increases the concentration of electrolytes in the blood. This higher concentration draws water into the blood vessels and keeps it there, expanding blood volume.
Medical recommendations often involve consuming 3,000 to 10,000 milligrams of sodium daily, alongside two to three liters of water. This intentional volume expansion helps stabilize blood pressure and reduces the burden on the heart. Expanding the volume provides more fluid to circulate, mitigating symptoms like dizziness and excessive heart rate.