Figure 1.

Possible mechanisms contributing to POTS. The underlying mechanisms are likely related to excessive venous pooling on orthostasis which is caused by excessive venous distension. In response to this reduction in cardiac venous return, increased SNS output occurs, increasing venoconstriction which may be impaired if small fibre neuropathy is present. Additionally, autoantibody-mediated impairment of peripheral vasoconstriction may occur. Tachycardia occurs in response to reduced venous return, in order to maintain cardiac output. Deconditioning can result in smaller left ventricular mass, requiring higher heart rate to maintain cardiac output. Possible reasons for the higher prevalence in women could be smaller heart mass, smaller muscle pump and an overlap with autoimmunity. Figure adapted with permission from www.stopfainting.com