Treatment of postural orthostatic tachycardia syndrome should be individualized based on the underlying pathophysiologic mechanism, such as autonomic neuropathy, hypovolemia, or hyperadrenergic state.
What are the pathophysiologic mechanisms and appropriate individualized treatments for Postural Orthostatic Tachycardia Syndrome (POTS)?
Treatment for POTS should be individualized based on the underlying pathophysiologic mechanism, which may include partial autonomic neuropathy, hypovolemia, or a hyperadrenergic state.
Postural orthostatic tachycardia syndrome (POTS) is a clinically heterogeneous disorder with multiple contributing pathophysiologic mechanisms manifesting as symptoms of orthostatic intolerance in the setting of orthostatic tachycardia (increase in heart rate by at least 30 beats per minute upon assuming an upright position) without orthostatic hypotension. The three major pathophysiologic mechanisms include partial autonomic neuropathy, hypovolemia, and hyperadrenergic state. Patients often will exhibit overlapping characteristics from more than one of these mechanisms. The approach to the treatment of POTS centers on treating the underlying pathophysiologic mechanism. Stockings, abdominal binders, and vasoconstrictors are used to enhance venous return in partial neuropathic POTS. Exercise and volume expansion are the main treatment strategies for hypo-volemic POTS. For hyperadrenergic POTS, beta-blockers and avoidance of norepinephrine reuptake inhibitors is important. Attempts should be made to discern which pathophysiologic mechanism(s) may be afflicting patients so that treatment regimens can be individualized.
Mar et al. (Wed,) conducted a review in Postural Orthostatic Tachycardia Syndrome (POTS). Individualized therapy (stockings, exercise, volume expansion, beta-blockers) was evaluated. Treatment of postural orthostatic tachycardia syndrome should be individualized based on the underlying pathophysiologic mechanism, such as autonomic neuropathy, hypovolemia, or hyperadrenergic state.