Background and aims Cardiovascular collapse due to Bezold-Jarisch Reflex (BJR) can occur unexpectedly in healthy patients under neuraxial anesthesia. BJR manifests as triad of bradycardia, hypotension, and peripheral vasodilation which is triggered by cardiac mechanoreceptor. We report successful resuscitation during combined spinal-epidural anesthesia.
Methods A 38-year-old male, 78 kg, was scheduled for interlocking nail operation for femur. PR was 64x/min and BP was 134/84 mmHg. Infusion of 500ml Ringer’s Lactate was administered. Epidural catheter was installed in right lateral decubitus posture. Subarachnoid block at level L4-L5 using 20mg 0,5% heavy bupivacain and 0,1mg morphine. T10 height sensory block was achieved, 15 min later, patient was suddenly unconscious and developed bradycardia 30x/min. BP was undetectable and accompanied by apnea. Atropine 0,5mg and facemask ventilation were immediately administered. Hypotension treated with ephedrine 10mg, 3 times. Bolus colloid and crystaloid fluid were given. Patient underwent intubation continued by general anesthesia. When stable (PR 120x/min, BP 110/65 mmHg), the surgery was started. No episode of cardiovascular collapse was noted throughout the rest of surgery.
Results Neuraxial anesthesia can increase cardiac vagal tone and decrease venous return. Reduced venous return stimulates cardiac sensory receptor that elicits increased parasympathetic activity and inhibition of sympathetic activity, which manifested as classical BJR triad of hypotension, bradycardia, and peripheral vasodilation. BJR activation can be prohibited by interventions like preventing decreased ventricular volume using intravenous fluid or inhibiting reflex’s afferent pathway using vagolytic drugs.
Conclusions BJR may be responsible to immediate cardiovascular collapse during neuraxial anesthesia and prompt intervention is the key to elude patient mortality.
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