Postural Tachycardia Syndrome (POTS)

Patient O.T. is a 26-year-old white woman who works in the music industry. She was diagnosed with pneumonia and treated with inhalers. Shortly afterward, she developed spells of tachycardia. Her episodes of tachycardia were primarily associated with upright posture. In addition to rapid palpitations, she complained of lightheadedness and presyncope on standing, intermittent stabbing chest pains (typically on standing), mental clouding with an inability to concentrate, severe fatigue, and exercise intolerance. Orthostatic vital signs recorded a supine heart rate (HR) of 73 bpm with a blood pressure (BP) of 103/72 mm Hg. After standing for 1 minute, her HR increased to 106 bpm with a BP of 109/80 mm Hg, and after 5 minutes, her HR was 122 bpm with a BP of 118/75 mm Hg. She was diagnosed with postural tachycardia syndrome (POTS). Under normal conditions, the assumption of upright posture effects an instantaneous shift of ≈500 mL of blood from the thorax to the lower abdomen, buttocks, and legs. There is a secondary shift of plasma volume (10% to 25%) out of the vasculature and into the interstitial tissue, which decreases venous return to the heart (preload), resulting in a transient decline in cardiac filling and BP. This unloads the baroreceptors and triggers a compensatory decrease in parasympathetic tone and an increase in sympathetic activation, with a resultant increase in HR and systemic vasoconstriction (countering the initial decline in BP). The net hemodynamic effect of transition to upright posture is a 10- to 20-bpm increase in HR, a negligible change in systolic BP, and a ≈5-mm Hg increase in diastolic BP. Orthostatic dysregulation occurs when this gravitational regulatory mechanism does not respond properly. Patients can present with orthostatic hypotension (seen in autonomic nervous system failure) or with orthostatic tachycardia (seen in POTS). Patients with POTS typically maintain (or …