The trigeminocardiac reflex (TCR) is defined as the sudden onset of parasympathetic dysrhythmia, sympathetic hypotension, apnea, or gastric hyper-motility during stimulation of any of the sensory branches of the trigeminal nerve. The proposed mechanism for the development of TCR is--the sensory nerve endings of the trigeminal nerve send neuronal signals via the Gasserian ganglion to the sensory nucleus of the trigeminal nerve, forming the afferent pathway of the reflex arc. It has been demonstrated that the TCR may occur with mechanical stimulation of all the branches of the trigeminal nerve anywhere along its course (central or peripheral). The reaction subsides with cessation of the stimulus. But, some patients may develop severe bradycardia, asystole, and arterial hypotension which require intervention. The risk factors already known to increase the incidence of TCR include: Hypercapnia; hypoxemia; light general anesthesia; age (more pronounced in children); the nature of the provoking stimulus (stimulus strength and duration); and drugs: Potent narcotic agents (sufentanil and alfentanil); beta-blockers; and calcium channel blockers. Because of the lack of full understanding of the TCR physiology, the current treatment options for patients with TCR include: (i) risk factor identification and modification; (ii) prophylactic measures; and (iii) administration of vagolytic agents or sympathomimetics.