Normally the body is able to compensate for these changes through cerebral vascular autoregulation and autonomic reflexes. In one of the most well-known reflex
arcs, reduced cardiac output leads to decreased stimulation of carotid sinus and aortic arch baroreceptors, as well as mechanoreceptors in the left ventricle wall [4]. The resulting increase in sympathetic tone maintains blood pressure for adequate cerebral perfusion. However, in neurally mediated syncopes, there is acute and inappropriate hypotension and bradycardia exacerbating the reduction in cerebral perfusion, resulting in a transient loss of consciousness. It is hypothesized that increased ventricular contraction in response to reduced venous return stimulates the left ventricle mechanoreceptors to a degree that is able to override the baroreceptor reflex and cause an inappropriate increase in parasympathetic tone[4]. Aside from laughter-induced syncope, this mechanism is also thought to account for syncope secondary to coughing, sneezing and other Valsalva-related activities