Postural Orthostatic Tachycardia Syndrome (POTS) is a medical condition defined by an abnormal response of the body to an upright posture. It is a disorder of the autonomic nervous system, which controls involuntary functions like heart rate, blood pressure, and digestion. The syndrome is characterized by orthostatic intolerance, meaning symptoms worsen significantly upon standing and improve when lying down. Exploring its history helps understand how this complex disorder transitioned into a distinct, medically recognized diagnosis.
Early Recognition of Dysautonomia
Long before the specific term POTS existed, physicians observed symptom clusters resembling the disorder’s core features. The earliest formal descriptions date back to the American Civil War, where surgeon Jacob Mendes Da Costa detailed a condition he termed “irritable heart” in 1871. This syndrome, later known as Da Costa’s Syndrome, was characterized by palpitations, fatigue, shortness of breath, and chest pain, particularly following physical exertion or illness.
Over the following decades, this constellation of symptoms was reclassified multiple times, often grouped under names like “soldier’s heart,” “effort syndrome,” or “neurocirculatory asthenia.” These early labels reflected a lack of understanding regarding the underlying physiological mechanism, sometimes leading clinicians to suggest the condition was psychosomatic. While these historical syndromes captured the disabling symptoms of orthostatic intolerance, they lacked the precise physiological measurement that would later define modern POTS.
Formal Definition of Postural Orthostatic Tachycardia Syndrome
The shift from ambiguous symptom clusters to a defined physiological disorder occurred in the 1990s. The term “Postural Orthostatic Tachycardia Syndrome” was formally coined in 1993 by researchers, including Dr. Philip Low and Ronald Schondorf, at the Mayo Clinic. This naming established POTS as a distinct clinical entity separate from other forms of orthostatic intolerance, such as neurally mediated syncope. This definition provided the medical community with the first objective, measurable criteria for diagnosis.
The physiological measurement defining the syndrome was a sustained increase in heart rate upon standing, without a significant drop in blood pressure. The criteria required an increase of 30 beats per minute (bpm) or more within the first 10 minutes of moving from lying to an upright position. For adolescents aged 12 to 19, the required increase was set slightly higher at 40 bpm. This elevated heart rate is the body’s compensatory attempt to maintain blood flow to the brain when the autonomic nervous system fails to constrict blood vessels adequately.
Evolution of Diagnostic Criteria
Following the formal naming in 1993, the medical understanding of POTS deepened, leading to the refinement of diagnostic criteria and the classification of subtypes. Current diagnostic consensus specifies that the symptoms and the sustained heart rate increase must be present for at least three months to confirm a chronic condition. This duration requirement helps distinguish chronic POTS from temporary orthostatic responses often triggered by acute illness or dehydration.
Research has since identified that POTS is not a single disease but a syndrome with multiple underlying causes, leading to the classification of several distinct subtypes. The three most commonly described variants are neuropathic POTS, hyperadrenergic POTS, and hypovolemic POTS. Neuropathic POTS is associated with damage to the small fiber nerves that constrict blood vessels in the lower limbs, leading to blood pooling. Hyperadrenergic POTS involves an excessive release of the stress hormone norepinephrine upon standing, causing an exaggerated heart rate and blood pressure response.