When the heart is stopped for good: hypotension-bradycardia paradox revisited

In vasovagal syncope, occurrence of bradycardia/asystole in the wake of hypotension has often been considered paradoxical. The major objective of this teaching module is to critically examine the pathophysiological mechanism and significance of the hypotension-bradycardia paradox unique to this condition. We narrate here how we discussed the pathophysiology of vasovagal syncope in a large classroom session attended by 275 doctors and medical students. A case study was used to describe the typical clinical presentation of vasovagal syncope. The pathophysiological mechanisms involved were then discussed systematically using a series of open-ended questions. We made it clear 1) that the occurrence of bradycardia or asystole in the face of acute severe hypotension is a mechanism to possibly minimize further blood loss, prevent myocardial damage, and increase ventricular filling; and 2) that fainting, which occurs as a consequence of this, is a homeostatic mechanism that serves to restore venous return and cerebral blood flow before blood pressure is normalized by neural reflex mechanisms. Eighty-four percent of participants reported that they were satisfied with the session. The information contained herein could be used to explain to any suitable audience the neural regulation of blood pressure in the face of acute severe hypotension and the pathophysiology of vasovagal syncope.