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LETTER TO EDITOR
Year : 2013  |  Volume : 29  |  Issue : 4  |  Page : 563-564

Cardiac arrest associated with ranitidine and ondansetron combination in day care gynecologic surgery


1 Department of Anaesthesia, Apollo Hospitals Bilaspur, Chhattisgarh, India
2 Department of Anaesthesia,Himalayan Institute of Medical Sciences, Dehradun, Uttarakhand, India

Date of Web Publication1-Oct-2013

Correspondence Address:
Vinit K Srivastava
Department of Anaesthesia, Apollo Hospitals Bilaspur, Chhattisgarh 495 006
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-9185.119136

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How to cite this article:
Srivastava VK, Jaisawal P, Agrawal S, Kumar D. Cardiac arrest associated with ranitidine and ondansetron combination in day care gynecologic surgery . J Anaesthesiol Clin Pharmacol 2013;29:563-4

How to cite this URL:
Srivastava VK, Jaisawal P, Agrawal S, Kumar D. Cardiac arrest associated with ranitidine and ondansetron combination in day care gynecologic surgery . J Anaesthesiol Clin Pharmacol [serial online] 2013 [cited 2019 Apr 20];29:563-4. Available from: http://www.joacp.org/text.asp?2013/29/4/563/119136

Sir,

Day care surgery has become increasingly popular because of its cost-saving potential. However, the occurrence of post-operative nausea and vomiting (PONV) can delay patient discharge. Ranitidine and ondansetron are commonly used as a premedication to reduce the chances of PONV. Herein, we present a case to emphasize a rare but serious cardiovascular side-effect probably caused by ranitidine and ondansetron combination.

A 38-year-old female patient was admitted for medical termination of pregnancy and laparoscopic tubal ligation in day care surgery unit. Her pre-anesthetic check-up was normal. All routine investigations were in normal limits and electrocardiography (ECG) showed a sinus rhythm. Pre-operatively her heart rate was 82 beats/min and blood pressure 120/76 mmHg. Patient was pre-medicated with ranitidine 50 mg intramuscularly 45 min before surgery. In operating room, all standard monitoring were attached. Before administration of ondansetron, heart rate and blood pressure were 76/min and 116/80 mmHg. She was given ondansetron 4 mg intravenously, slowly over 30 s. However within 30 s of administering the drug, she became unresponsive to stimuli, apneic and ECG showed flat line and no peripheral or central pulse could be palpated. Cardio pulmonary resuscitation (CPR) was started. Immediately, we intubated the trachea with 7.5 mmID cuffed endotracheal tube. Within 2 min of CPR and administration of atropine 0.6 mg, there was return of spontaneous circulation and the monitor showed a normal sinus rhythm with a heart rate of 96/min and blood pressure 132/80 mmHg. Subsequently, spontaneous respiratory efforts returned in the next 2 min. After observing her for another 5 min and ascertaining that she had adequate spontaneous respiratory efforts and oxygen saturation, trachea was extubated. She was awake, oriented, with no neurological deficit and had stable hemodynamics. Surgery was performed after 48 h and was uneventful. This time however she was pre-medicated with i.v. metoclopramide 10 mg 1 h prior to the procedure.

The maximum effect of intramuscularly ranitidine occurs approximately after 45 min and this is the time when we administered ondansetron i.v., so it is presumed that it may be due to combined effect or ondansetron alone. Ondansetron has rare cardiovascular adverse effects such as atrial fibrillation, bigeminy, sinus bradycardia, ventricular tachycardia, QT prolongation, cardiac arrest. [1],[2] Bradycardia and cardiac arrest (asystole) [3] is also reported with ranitidine.

The adverse cardiac effects of ranitidine may be due to H 2 receptor antagonism in coronary smooth muscle, through vasoconstriction or a rise in plasma histamine levels. [4] Other mechanisms may include a cholinergic action mediated by cholinesterase inhibition.

Ondansetron has submicromolecular affinity for K + channels encoded by "human ether-a go-go related gene," which is possibly responsible for the prolongation of cardiac repolarization, thus resulting in conduction disturbances like QT/QTc interval prolongation. [5] Presence of 5- hydroxytryptamine (5-HT) receptors in left ventricle usually precipitate the von Bezold Jarisch reflex and use of 5-HT 3 antagonist usually block this effect. However, the cardiovascular effect of ondansetron will depend on pre-existing serotonergic activity in both arms of the autonomic nervous system. The additional finding that this hemodynamic response was reversed by atropine emphasizes its likely parasympathomimetic origin.

The mechanism of cardiac arrest in this case is not clear either it is due to the combination of drug or ondensetron alone. Ondansetron and ranitidine both can cause bradycardia and cardiac arrest, so one should be careful when using the combination of two drugs.

 
  References Top

1.Havrilla PL, Kane-Gill SL, Verrico MM, Seybert AL, Reis SE. Coronary vasospasm and atrial fibrillation associated with ondansetron therapy. Ann Pharmacother 2009;43:532-6.  Back to cited text no. 1
    
2.Moazzam MS, Nasreen F, Bano S, Amir SH. Symptomatic sinus bradycardia: A rare adverse effect of intravenous ondansetron. Saudi J Anaesth 2011;5:96-7.  Back to cited text no. 2
[PUBMED]  Medknow Journal  
3.Hart AM. Cardiac arrest associated with ranitidine. BMJ 1989;299:519.  Back to cited text no. 3
    
4.Parkin JV, Ackroyd EB, Glickman S, Hobsley M, Lorenz W. Release of histamine by H2-receptor antagonists. Lancet 1982;2:938-9.  Back to cited text no. 4
    
5.Weissenburger J, Funck-Brentano C, Jaillon P, Charbit B. Droperidol and ondansetron in vitro electrophysiological drug interaction study. Fundam Clin Pharmacol 2009;23:719-26.  Back to cited text no. 5
    




 

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