Key result
Sympathetic nervous system dysfunction, including ineffective adrenergic vasoconstriction, underlies various forms of orthostatic intolerance such as postural tachycardia syndrome and vasovagal syncope.
This review outlines the pathophysiological mechanisms underlying orthostatic intolerance, focusing on sympathetic nervous system dysregulation.
Hypothesis-generating for sympathetic-targeted therapies in orthostatic intolerance; leaves open prospective validation before clinical adoption.
Sympathetic circulatory control is key to the rapid cardiovascular adjustments that occur within seconds of standing upright (orthostasis) and which are required for bipedal stance. Indeed, patients with ineffective sympathetic adrenergic vasoconstriction rapidly develop orthostatic hypotension, prohibiting effective upright activities. One speaks of orthostatic intolerance (OI) when signs, such as hypotension, and symptoms, such as lightheadedness, occur when upright and are relieved by recumbence. The experience of transient mild OI is part of daily life. However, many people experience episodic acute OI as postural faint or chronic OI in the form of orthostatic tachycardia and orthostatic hypotension that significantly reduce the quality of life. Potential mechanisms for OI are discussed including forms of sympathetic hypofunction, forms of sympathetic hyperfunction, and OI that results from regional blood volume redistribution attributable to regional adrenergic hypofunction.
No takes yet. Share an insight, caveat, or question.
Julian M. Stewart (2012) conducted a review in Orthostatic intolerance. Sympathetic regulation was evaluated. Sympathetic nervous system dysfunction, including ineffective adrenergic vasoconstriction, underlies various forms of orthostatic intolerance such as postural tachycardia syndrome and vasovagal syncope.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: