FIGURE 5.

Potential mechanisms by which pubertal hormones exacerbate susceptibility to vasovagal syncope (VVS). The normal cardiovascular response to orthostatic stress is shown (black text). In patients with VVS, hypovolemia and excessive venous pooling, particularly in the splanchnic vascular bed, combine to produce particularly large orthostatic reductions in stroke volume and cardiac output. Impaired baroreflex responses, and blunted orthostatic increases in vascular resistance and vascular capacitance fail to appropriately compensate, and ultimately blood pressure and cardiac output fall dramatically, with cerebral hypoperfusion and subsequent presyncope or syncope. Impairments in cerebral autoregulatory control and excessive reductions in cerebral blood flow in response to the hypocapnia during orthostasis further contribute to the decline in cerebral perfusion (blue text). Hormones that potentially exacerbate the impaired cardiovascular responses to orthostatic stress in patients with VVS are indicated (orange text). GH, growth hormone; IGF-1, insulin-like growth factor-1.