Authors: Jerome H Check, Diane Check, Brooke Neumann.
Rationale: There are data supporting the concept that the etiology of idiopathic orthostatic edema is related to a delayed response by the sympathetic nervous system to secrete more dopamine from sympathetic nerve fibers to diminish cellular permeability of the capillaries in humans when changing from supime to an erect position to inhibit transudation of intravascular fluid to the extravascular space. This physiologic change is related to the increased hydrostatic pressure that occurs by standing. Evidence supporting this theory is that this clinical entity, manifested by edema of unknown origin and weight gain, is usually ameliorated by treatment with the sympathomimetic amine dextroamphetamine, which is known to increase dopamine release. We hypothesized that postural orthostatic tachycardia syndrome (POTS) may be caused by a more severe transudation of fluid from intravascular to extravascular space which results in light headedness and/or symptoms from hypovolemia related to transient inadequate blood supply to the brain, before compulsory mechanisms are triggered by the renin-angiotensin-aldosterone axis. Tachycardia is related to the need to increase the heart rate to allow the required 5 liters of blood per minute.
Objective: To determine if dextroamphetamine could improve a severe case of POTS.
Findings: A woman with severe treatment resistant POTS, with multiple syncopal episodes, had a great response to 60mg dextroamphetamine sulfate, which completely eradicated her POTS.
Conclusion: At least one form of POTS can have a good response to dopaminergic drugs e.g., dextroamphetamine, which also corrected other associated conditions e.g., dysmenorrhea, dyspnea on exertion, chest pain, headaches, chronic fatigue, brain fog, depression, and fibromyalgia.
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