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Year : 2011  |  Volume : 55  |  Issue : 6  |  Page : 627-628  

Catastrophic complication - Bezold-Jarisch reflex: Case series

Departments of Anaesthesiology and Intensive Care, Postgraduate Institute of Medical Education and Research and Dr. Ram Manohar Lohia Hospital, New Delhi, India

Date of Web Publication5-Dec-2011

Correspondence Address:
Ajay Goila
Departments of Anaesthesiology and Intensive Care, Postgraduate Institute of Medical Education and Research and Dr. Ram Manohar Lohia Hospital, New Delhi 110 001
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0019-5049.90627

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How to cite this article:
Garg R, Goila A, Pawar M. Catastrophic complication - Bezold-Jarisch reflex: Case series. Indian J Anaesth 2011;55:627-8

How to cite this URL:
Garg R, Goila A, Pawar M. Catastrophic complication - Bezold-Jarisch reflex: Case series. Indian J Anaesth [serial online] 2011 [cited 2020 Oct 30];55:627-8. Available from: https://www.ijaweb.org/text.asp?2011/55/6/627/90627


The episodes of haemodynamic disturbances may lead to activation of various protective physiological reflexes. Clinical occurrences of Bezold-Jarisch reflex (BJR) is not much reported. Haemodynamic disturbances associated with BJR may be misconstrued as some adverse cardiac event. Being a reflex, it is immediate in onset and leads to severe bradyarrhythmia with hypotension and asystole. [1],[2]

A 62-year-old female was scheduled for total abdominal hysterectomy. She was a known hypertensive and diabetic on oral losartan, amlodepine, metoprolol and gliclazide. There were no symptoms suggestive of snoring, obstructive sleep apnoea, orthostatic hypotension or autonomic disturbances. Her pulse rate (PR) was 72/min and blood pressure (BP) 118/74 mmHg. Her cardiac, respiratory and central nervous system examination was normal. Hydration status was satisfactory. Investigations including haemogram, renal and liver function tests, electrocardiogram (ECG), chest X-ray and echocardiography were within normal limits. Perioperatively ECG, pulse oximeter (SpO 2 ), noninvasive automated blood pressure were monitored. Anaesthesia was induced with fentanyl (50 mg), thiopentone (350 mg) and lungs were ventilated with isoflurane (1%) in oxygen (100%). After intravenous atracurium besylate (50 mg), trachea was intubated. Intraoperative fluid administration was guided by the clinical parameters. After surgery, the incision site was infiltrated with 20 mL of 0.125% bupivacaine. Patient remained haemodynamically stable. Residual neuromuscular blockade was reversed and trachea was extubated after patient was fully conscious, moving her limbs and head lift was present. After extubation, head end of the operating table was raised by about 30΀ to facilitate spontaneous respiration. Within a minute, PR decreased from 88/min to 22/min. The BP also decreased from 128/78 mmHg to 60 mmHg systolic. Patient stopped breathing and oxygen saturation started falling (SpO 2 - 50-60%). Trachea was reintubated and intravenous atropine (0.6 mg) was administered. Lungs were ventilated with 100% oxygen and reverse trendelenberg position was given. Five hundred millilitres of ringer lactate was administered fast. Vitals became normal within next 1-2 minutes. Arterial blood gas analysis, serum electrolytes and blood sugar was within normal limits. Patient was shifted to intensive care unit (ICU) for further management. Twelve lead ECG and cardiac enzymes were normal. Patient remained haemodynamically stable and was fully conscious. Forty-five minutes later trachea was extubated. Next day, patient was shifted to high dependency unit and had an uneventful recovery.

The BJR is characterized by sudden bradycardia associated with hypotension, decreased inotropy, and coronary vasodilation resulting from stimulation of cardiac receptors. [1],[2] BJR is elicited by activation of certain inhibitory reflexes, which have origin with cardiac sensory receptors and that leads to increases parasympathetic nervous system activity and inhibits sympathetic activity. [1] Another physiological reflex, baroreceptor reflex gets activated by pressure receptors in the walls of the carotid sinuses and aorta due to arterial pressure changes in the circulation. [1] In humans these two reflexes acts complimentary to each other and control the blood pressure. The baroreceptor reflex appears to be the dominant regulator of blood pressure. [1] This relationship can be uncoupled by certain stimulus like severe volume loss, and the BJR activity can become dominant. The mechanism of the BJR is thought to be peripheral venous blood pooling and a heightened cardiac contractile state which result in reflex arterial vasodilation and a subsequent vagally mediated bradycardia. [3] The BJR overlaps with vasovagal syncope but it is not synonymous with it. [1] The activation of BJR can be prevented by interventions like preventing the decrease in ventricular volume using intravenous fluids, preventing ventricular hypercontractility by using b-adrenergic blocking drugs, or inhibiting the afferent limb of the reflex using a vagolytic drug. [1],[2],[4] We should manage it with the shortest possible turn-around time (STAT) with vagolytics, epinephrine or fluid infusion. We should avoid any event that may lead to a state of relative hypovolemia like sudden change in position of the patient.

   References Top

1.Campagna JA, Carter C. Clinical relevance of the Bezold Jarisch reflex. Anesthesiology 2003;98:1250-60.  Back to cited text no. 1
2.Chiladakis JA, Patsouras N, Manolis AS. The Bezold Jarisch reflex in acute inferior myocardial infarction: Clinical and sympathovagal spectral correlates. Clin Cardiol 2003;26:323-8.  Back to cited text no. 2
3.D'Alessio JG, Weller RS, Rosenblum M. Activation of the Bezold-Jarisch reflex in the sitting position for shoulder arthroscopy using interscalene block. Anesth Analg 1995;80:1158-62.  Back to cited text no. 3
4.Turker G, Demirag B, Ozturk C, Uckunkaya N. Cardiac arrest after interscalene brachial plexus block in the sitting position for shoulder arthroscopy: A case report. Acta Orthop Belg 2004;70:84-6.  Back to cited text no. 4

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Phillip Yen,Lenny Naftalin
Anesthesia Progress. 2015; 62(1): 40
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