Emergency (2013); 1 (1): ***-*** This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Copyright © 2014 Shahid Beheshti University of Medical Sciences. All rights reserved. Downloaded from: www.jemerg.com 147 Emergency (2014); 2 (3): 147-149 PHOTO QUIZ Worsened Dysrhythmia after Chemical Cardioversion with Digoxin; a Case of Malpractice Behrooz Hashemi1, Mehdi Pishgahi2, Marzieh Maleki1* 1. Department of Emergency Medicine, Shohadaye Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran 2. Department of cardiology, Shohadaye Tajrish Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran Figure 1  Figure 2  Cite this article as: Kashani P, Mirbaha S. Confusing hypoxia in a 21-year-old intubated multiple trauma patient. Emer- gency. 2014;2 (3): 147-9. Case presentation:1 The patient was a 23-year-old man referred to the emergency department (ED) with the chief com- plaint of palpitation. The patient experienced dizzi- ness, cold sweating, and lightheadedness after get- ting up which started spontaneously. He had four episodes of the same problems in seven months ago that felt better after taking 10 mg propranolol. However, in the current episode his problem was not solved by the same medication. He had no histo- ry of smoking, substance abuse, medication use, congenital heart disease, syncope, previous surgery, chest trauma, or any other known medical prob- lems. As well, he had no any positive history of the same problems in his family. The patients’ on- arrival vital signs were as follow: systolic blood pressure (SBP): 90 mmHg, pulse rate (PR): *Corresponding Author: Sahar Mirbaha; Department of Emergency Medicine, Shohadaye Tajrish Hospital, Tajrish Square, Tehran, Iran. Mobile phone: +989121549405; phone/fax: +982122721155. Email: mirsa317@yahoo.com Received: 1 April 2014; Accepted: 9 April 2014 150/minute, respiratory rate (RR): 14/minute, oral temperature: 37◦C, oxygen saturation 96% with nasal cannula and 100% oxygen, Glasgow coma scale (GCS) 15/15. He was not experienced any oth- er concomitant problems such as ischemic chest discomfort, shortness of breathing, or sign of circu- latory shock such as paleness, mottling, etc. On gen- eral physical examination the patients’ lung and heart sounds, four limbs pulses, and capillary refile were normal. As well, focused neurological and ab- dominal examinations did not have any positive finding. The patient underwent close cardiac, vital sign monitoring and electrocardiography (ECG). Figure 1 shows the on-arrival patients’ ECG. Atrial fibrillation (AF) was diagnosed by the correspond- ing physician and digoxin (!?) prescribed that led to severe lethargy, weakness, sweating, and bradycar- dia. Figure 2 shows the post mediation ECG of pa- tient. What is your diagnosis? This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Copyright © 2014 Shahid Beheshti University of Medical Sciences. All rights reserved. Downloaded from: www.jemerg.com 148 Kashani, Mirbaha Diagnosis: Wolff-Parkinson-White (WPW) syndrome + Atrial Fibrillation (AF) Case fate: The patient was admitted to CCU and after admin- istration of Procainamide, his symptoms revealed (Figure 3) and he was sent for catheter ablation. Discussion: According to American Heart Association (AHA) 2010 guideline for cardiopulmonary resuscitation (CPR), if the patient who manifested by tachycardia is presented with sever signs and symptoms includ- ing ischemic chest discomfort, acute heart failure, acute altered mental status, sustain hypotension or other signs of shock, considered as unstable case and needs immediate cardioversion. However, in other symptomatic stable ones the subject present- ed with irregular wide complex tachycardia, then avoiding atrioventricular (AV) nodal blocking agent is crucial. These agents such as β-adrenergic block- ers, calcium channel blockers, and Digitalis (sum- marized as BCD drugs) will not be effective, cannot block the conduction over the accessory pathway, and may even enhance conduction in hypotension or other dangerous outcomes such as ventricular fibrillation (VF) and cardiac arrest. Consequently, these drugs are contraindicated in such situations. Lidocaine is not useful for this purpose and may rarely exacerbate the conduction. Intravenous Pro- cainamide is the treatment of choice and amioda- rone may be a favorable second option in spite of some opposite literatures. Patients, who are hemo- dynamically unstable, clearly require electrical car- dioversion following current instructions (1-3). Wolff-Parkinson-White (WPW) syndrome is used for pre-excitation on ECG accompanied by paroxys- mal tachycardia that may be conducted antegrade over the normal AV system or retrograde through the accessory pathway (AP). Antegrade type is char- acterized by normal and narrow QRS complexes, regular rhythm, ventricular rate of 150-250 beats/minutes, and sudden onset and abrupt termi- nation. The classic electrocardiographic presenta- tion of WPW syndrome consists of short PR interval, slurred and thickened initial upstroke of the QRS complex which is termed as delta wave, relatively normal-narrow terminal QRS defluxion which some- times referred as the main QRS defluxion, Slight widening of the QRS defluxion, and secondary ST segment and T wave changes (4, 5). Although the incidence of dysrhythmias in WPW cases is rare, approximately 80% of dysrhythmias are AV reentrant tachycardia, 15-30% atrial fibrilla- tion (AF), and 5% atrial flutter. AF is considered as an emergent situation when rapid antegrade con- duction over an AP occurs in WPW syndrome. Clues in the ECG that may help suggesting WPW+AF in- clude rhythm irregularity, a rapid ventricular re- sponse (often with R-R intervals approaching 300 beats/minutes), wide, and bizarre QRS complexes (6, 7). Szumowski et al. found that age, gender, and the history of syncope are independent risk factors of AF in patients with WPW syndrome and also men- tioned that antegrade conduction via AP has a major importance in the development of AF (8). Hamada et al. mentioned that there are two mechanisms of paroxysmal AF in patients with WPW syndrome: one mechanism is reversible and AP-dependent atrial vulnerability, and the other one is intrinsic and AP-independent atrial vulnerability (9). During AF developing, the custom rate-limiting im- pression of the AV node will be bypassed, and the consecutive excessive ventricular rates (even 200- 240 beats/minutes) may lead to disastrous conse- quences such as ventricular fibrillation (VF), synco- pe, and sudden death. Those who have survived from VF dysrhythmia, presented a rapid pre-excited ventricular response as it was demonstrated during the induction of AF in electrophysiological study (2). Sudden cardiac death and other possible dangerous outcomes in patients suffer from symptomatic ar- rhythmias can be preventable. If they are enable to tolerate a rapid pre-excited ventricular response during AF (shortest pre-excited RR interval is less than 260 ms), accessory pathway catheter ablation or administration of antiarrhythmic drugs should be considered instead of such an invasive method to prevent conduction over the accessory pathway (2, 3). It could be concluded that sometimes no cure is bet- Figure 3  This open-access article distributed under the terms of the Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0). Copyright © 2014 Shahid Beheshti University of Medical Sciences. All rights reserved. Downloaded from: www.jemerg.com 149 Emergency (2014); 2 (3): 147-149 ter than wrong treatment. Without hurry, consult- ant with other colleagues and adhering to present guidelines in approach to dysrhythmias can be help- ful and even lifesaving. Acknowledgment: We would like to express our special thanks from emergency department staffs. Conflict of interest: There was no conflict of interest. Author’s contribution: All authors contributed in drafting/revising the manuscript, study concept or design, and interpre- tation of data. References: 1. Neumar RW, Otto CW, Link MS, et al. Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 suppl 3):S729-S67. 2. Hurst JW, Paulk Jr EA, Proctor HD, Schlant RC. Management of patients with atrial fibrillation. Am J Med. 1996;37(5):728-41. 3. Simonian SM, Lotfipour S, Wall C, Langdorf MI. Challenging the superiority of amiodarone for rate control in Wolff-Parkinson-White and atrial fibrillation. Intern Emerg Med. 2010;5(5):421-6. 4. Kaushik M, Sharma M, Ganju N. Wolff-Parkinson-White syndrome presenting as atrial fibrillation with wide-QRS complexes. J Indian Acad Clin Med. 2003;4:152-55. 5. Değirmencioğu A, Karakuş G, Baysal E, Zencirci E, Çakmak N. A rare manifestation of atrial fibrillation in the presence of Wolff-Parkinson-White syndrome: tachycardia-induced cardiomyopathy. Turk Kardiyol Dern Ars. 2014;42(2):178-81. 6. Szumowski L, Orczykowski M, Derejko P, et al. Predictors of the atrial fibrillation occurrence in patients with Wolff-Parkinson-White syndrome. Kardiol Pol. 2009;67(9):973-8. 7. Levis J, Garmel G. Atrial fibrillation with Wolff- Parkinson-White syndrome. Internet J Emerg Med. 2008;5(1):1-3. 8. Szumowski Ł, Walczak F, Urbanek P, et al. Risk factors of atrial fibrillation in patients with Wolff-Parkinson- White syndrome. Kardiol Pol. 2004;60(3):206-16. 9. Hamada T, Hiraki T, Ikeda H, et al. Mechanisms for Atrial Fibrillation in Patients with Wolff‐Parkinson‐White Syndrome. J Cardiovasc Electrophysiol. 2002;13(3):223-9.