Abstract

Postural orthostatic tachycardia syndrome (POTS) is defined as the development of orthostatic symptoms associated with a rapid (within 10 minutes) increase in heart rate by more than 30 beats per minute or to a heart rate that exceeds 120 beats per minute without orthostatic hypotension. The symptoms of orthostatic intolerance are due to brain hypoper fusion and sympathetic overaction. Patients are usually female and aged 15 to 50 years. POTS represents a category of disease rather than a single distinct illness. Patients with POTS can experience difficulty with daily routines including housework, shopping, eating, and attending work or school. Reports of patients with “POTS-like symptoms” have been made for over 100 years. The pathophysiologic mechanisms of POTS include peripheral denervation, β-receptor supersensitivity, hypovolemia and impaired cerebral auto regulation. Prolonged deconditioning may also interact with these mechanisms to exacerbate symptoms. Although 3 types of POTS (low-flow, normal-flow, and high-flow POTS) have been distinguished based on differences in peripheral blood flow and peripheral arterial resistance, thoracic hypovolemia is the common final pathophysiologic mechanism. Therapies are directed at relieving the central hypovolemia or at compensating for the circulatory dysfunctions. Treatments include use of water, saline infusion, α-agonists, β-antagonists, and other agents that may correct the central hypovolemia. These have resulted in varying degrees of success, and they are often used in combination.

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