Prolonged upright posture results in some degree of pooling of blood in the lower extremities that can lead to diminished intracardiac volume. This phenomenon is exacerbated if the individual is dehydrated. The resultant arterial hypotension is sensed in the carotid sinus baroreceptors, and afferent nerve fibers from these receptors trigger autonomic signals that increase cardiac rate and contractility. However, pressure receptors in the wall and trabeculae of the underfilled left ventricle may then sense stimuli, activating high-pressure C-fiber afferent nerves from these receptors. They may respond by sending signals that trigger paradoxical bradycardia and decreased contractility, resulting in additional and relatively sudden arterial hypotension. The bradycardia reaction to acetic acid veratril in the cardiac pacemaker region was first described by von Bezold. Jarisch identified the reaction as chemoreceptor reflex via the vagus nerve, relayed in the nucleus tractus solitarii.
The Bezold–Jarisch reflex is responsible for the sinus bradycardia that commonly occurs within the first 60 minutes following an acute myocardial infarction, and explains the occurrence of AV node block in the context of acute posterior or inferior myocardial infarction. Bradycardia in this setting may be treated with atropine.
It usually occurs in nitrate therapy and use of serotonin agonists. The Bezold–Jarisch reflex has been suggested as a possible cause of profound bradycardia and circulatory collapse after spinal anesthesia. Also, it is one of the complications of interscalene brachial plexus block. The reflex occurs with several biologically active chemicals, like nicotine and capsaicin, when reaching sensitive areas.