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Cardiovasc Toxicol (2012) 12:263–265 DOI 10.1007/s12012-012-9165-z

Case Report: An Unusual Heart Rhythm Associated with Organophosphate Poisoning Enes Elvin Gul • Ilknur Can • Fred M. Kusumoto

Published online: 24 April 2012 Ó Springer Science+Business Media, LLC 2012

Abstract Organophosphate pesticides have emerged as a common cause of poisoning, particularly in developing countries. The most common electrocardiographic abnormalities observed in organophosphate poisoning are sinus tachycardia, QT interval prolongation, and, very rarely, ventricular arrhythmias. We report a case of organophosphate poisoning associated with atrial fibrillation, right bundle branch block, QT interval prolongation, and intermittent narrow QRS complexes that were most likely due to automaticity from the region of the left posterior fascicle. Keywords Organophosphate intoxication  Electrocardiogram  Arrhythmia

Case Presentation A-59-year-old man was brought to the emergency department due to altered mental status. In an attempted suicide, 5 h earlier, he had ingested an unknown quantity of an organophosphate insecticide solution. On admission, the patient was semicomatose. Physical examination was unremarkable other than a rapid irregular heart rhythm. Complete blood count showed leukocytosis (white blood cell count, 23,100 cells/lL). Blood chemistry was within normal limits. The blood level of buteryl-choline-esterase E. E. Gul (&)  I. Can Department of Cardiology, Meram School of Medicine, Konya University, 42090 Konya, Turkey e-mail: [email protected] F. M. Kusumoto Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Jacksonville, FL, USA

level was tested and was found to be 1.05 units/L (normal reference values 3.4–7.1 units/L). The patient was treated with an intravenous bolus of atropine 2 mg and a slow infusion of pralidoxime. On admission, 12-lead ECG revealed a rapid irregular heart rate of approximately 155 beats per minute due to atrial fibrillation (Fig. 1). The QRS complexes varied, with a baseline right bundle branch block pattern, interspersed with relatively narrow QRS complexes with left axis deviation that were immediately followed by QRS complexes with a right bundle branch block associated with a more prominent terminal S wave in lead V1 despite a relatively long R–R interval. In addition, the QTc was markedly prolonged, approximately 0.54–0.56 s. Since the narrow QRS complexes occurred at relatively constant intervals and had a left anterior fascicular block morphology, we believe that they were generated by a parasystolic focus within or near the posterior fascicle. In support of this interpretation is the observation that a wider QRS complex with a more prominent S0 wave is present immediately after several of the narrow QRS beats. This observation would be unlikely in the presence of variable conduction in the right bundle branch, but could be explained by retrograde penetration of the proximal right bundle branch from a site of left ventricular automaticity. After 3 days of pralidoxime treatment, ECG revealed normal sinus rhythm with 0.5-mm ST-segment elevation in inferior leads, shortening of the QTc (0.49 s), and normalization of ventricular depolarization (Fig. 2).

Discussion Organophosphate (OP) compounds are widely used in the world as agriculture insecticides [1] and are one of the most

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common causes of intentional poisoning in Turkey [2]. Organophosphate compounds cause irreversible inhibition of acetylcholinesterase that is associated with increased muscarinic receptor and nicotinic receptor activity in the

Fig. 1 ECG on admission shows atrial fibrillation with an incomplete right bundle branch block. Narrow QRS complexes (asterisk) at relatively fixed intervals are observed (double headed arrows). In addition, QRS complexes with a more complete right bundle branch block pattern (arrowheads) are observed after the narrow QRS complexes. The QT interval is prolonged even in the presence of right bundle branch block. Typical ST-segment and T-wave changes associated with right bundle branch block are observed

Fig. 2 Follow-up ECG on day 3 shows resolution of atrial fibrillation and right bundle branch block. The QT interval has shortened but remains prolonged. ST-segment elevation is observed in the inferior leads

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heart. Classically, three phases of cardiac toxicity due to OP poisoning have been described: first, a brief period of increased sympathetic tone due to nicotinic receptor activity, characterized with sinus tachycardia and hypertension, that

Cardiovasc Toxicol (2012) 12:263–265

is followed by prolonged and increased activity of parasympathetic tone mediated predominantly by muscarinic effects characterized by sinus bradycardia and hypotension, and finally, a period of QT interval prolongation that may be associated with polymorphic ventricular tachycardia [3]. Several studies have evaluated the electrocardiographic findings associated with organophosphate poisoning. In a group of 36 patients with organophosphate poisoning, a variety of ECG abnormalities were identified [4]: sinus tachycardia (72 %), sinus bradycardia (11 %), 1st-degree AV block (6 %), right bundle branch block (6 %), ST–T changes (19 %), and prolongation of the QT interval (19 %). Similarly, in another cohort of 85 patients who presented with OP poisoning, QT interval prolongation was observed in 56 % of patients and ST-segment elevation or low amplitude T waves in 18 % [5]. The most common rhythm disturbance was sinus tachycardia (32 %), and no other atrial or ventricular arrhythmias were observed [5]. In this case, dramatic prolongation of the QT interval was observed although no other repolarization abnormalities such as ST-segment or T-wave changes were observed. However, unusual variations in ventricular depolarization were observed. Variable conduction of the right bundle or concealed retrograde penetration of the right bundle is the most commonly observed reason for varying degrees of right bundle branch block in atrial fibrillation, particularly since the narrow QRS complexes have relatively long coupling intervals from the preceding QRS complex. However, if this were the mechanism, once a narrow QRS complex was observed, subsequent QRS complexes generally remain narrow. Enhanced ventricular automaticity is another potential mechanism of the present ECG finding in this patient. Automaticity refers to a cardiac muscle cell firing off an impulse on its own. All of the cells in the heart have the ability to initiate an action potential; however, only some of these cells are designed to routinely trigger

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heart beats. These cells are found in the conduction system of the heart and include the SA node, AV node, bundle of His, and Purkinje fibers. We postulate that increased nicotinic and muscarinic activity as a result of OP poisoning could contribute to the development of atrial fibrillation. Enhanced nicotinic activity stimulates postganglionic sympathetic terminals and produces a dramatic release of norepinephrine. Norepinephrine mediates its arrhythmogenic effects by increasing automaticity of cardiac cells and by decreasing the ventricular fibrillatory threshold. With the treatment for the organophosphate poisoning, atrial fibrillation and right bundle branch block resolved, and the QT interval prolongation improved. This case report illustrates the variety of ECG abnormalities that can be observed with organophosphate poisoning.

References 1. Kwong, T. C. (2002). Organophosphate pesticides: Biochemistry and clinical toxicology. Therapeutic Drug Monitoring, 24(1), 144–149. 2. Ozturk, M. A., Kelestimur, F., Kurtoglu, S., Guven, K., & Arslan, D. (1990). Anticholinesterase poisoning in Turkey—clinical, laboratory and radiologic evaluation of 269 cases. Human and Experimental Toxicology, 9(5), 273–279. 3. Ludomirsky, A., Klein, H. O., Sarelli, P., Becker, B., Hoffman, S., Taitelman, U., et al. (1982). Q-T prolongation and polymorphous (‘‘torsade de pointes’’) ventricular arrhythmias associated with organophosphorus insecticide poisoning. American Journal of Cardiology, 49(7), 1654–1658. 4. Anand, S., Singh, S., Saikia, U. N., Bhalla, A., Sharma, Y. P., & Singh, D. (2009). Cardiac abnormalities in acute organophosphate poisoning. Clinical Toxicology, 47, 230–235. 5. Yurumez, Y., Yavuz, Y., Saglam, H., Durkan, P., Ozan, S., Akdur, O., et al. (2009). Electrocardiographic findings of acute organophosphate poisoning. Journal of Emergency Medicine, 36, 39–42.

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