Reversal of electrical storm after intraaortic balloon pump counterpulsation in a patient with acute myocardial infarction
Electrical storm after intra”>Case report
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American Journal of Emergency Medicine
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American Journal of Emergency Medicine 33 (2015) 734.e1-734.e3
Reversal of electrical storm after intraaortic balloon pump counterpulsation in a patient with acute myocardial infarction?
Abstract
Electrical storm is the clustering of hemodynamically destabilizing ventricular tachycardia or ventricular fibrillation. effective management of electrical storm during acute myocardial infarction is a challenge. We report the case of a 53-year-old man who had a witnessed cardiac arrest with ventricular fibrillation in the emergency department. He required Continuous chest compressions, tracheal intubation, and emergency cardiac defibrillation. Although he was defibrillated 10 times and intravenous Antiarrhythmic drugs were administered, the ventricular arrhythmias were still not under control. In the setting of his hemody- namic collapse, an intraaortic balloon pump (IABP) was immediately inserted for hemodynamic support. The electrical storm was successful terminated under the IABP support. After successful resuscitation, electrocardiogram showed ST-segment elevation in leads II, III, and aVF as well as the Right precordial leads. With the IABP support for more than half an hour, the patient had spontaneous recanalization of the occluded infarct-related artery; and coronary angiography confirmed the entire coronary artery patency.
Electrical storm is a life-threatening syndrome that is defined as 2 or more sustained episodes of ventricular tachycardia and/or ventricular fibrillation in 24 hours [1]. The clinical presentation of electrical storm might be very dramatic with hemodynamic instability that involves cardiac arrest or multiple episodes of potentially fatal arrhythmias requiring multiple electrical cardioversions or defibrillations. Refractory ventricular tachycardia and/or ventricular fibrillation occurring as a storm after acute myocardial infarction has a poor prognosis [2]. Effective management of electrical storm during acute myocardial infarction is a challenge. Herein, we report a case of refractory elec- trical storm occurring after an acute myocardial infarction. Al- though the patient was defibrillated 10 times and intravenous antiarrhythmic drugs were administered, the ventricular arrhyth- mias were still not under control. In the setting of his Hemodynamic collapse, an intraaortic balloon pump (IABP) was immediately inserted. He underwent a successful reversal of the electrical storm under the IABP support.
A 53-year-old man was admitted to our hospital with a 3-hour history of chest pain. While in the emergency department, the pa- tient had a witnessed cardiac arrest with ventricular fibrillation. He required continuous chest compressions, tracheal intubation, and
? Disclosures: The authors have no conflicts of interest to disclose.
emergency cardiac defibrillation. The ventricular fibrillation was terminated with electrical defibrillation at first; but after a while, he developed repetitive prolonged phases of incessant pulseless Polymorphic ventricular tachycardia or ventricular fibrillation. Although the patient was defibrillated 10 times during the following minutes, the ventricular arrhythmias were still not under control (Fig. 1). intravenous amiodarone, lidocaine, and metoprolol were also ineffective to suppress Ventricular tachyarrhythmias. His hemo- dynamic status continued to worsen. An IABP was immediately inserted for hemodynamic support. The situation of his hemody- namic status was soon stabilized, and the electrical storm was suc- cessful terminated under the IABP support. After successful resuscitation, a 12-lead electrocardiogram showed junctional tachycardia with ST-segment elevation in leads II, III, and aVF as well as the right precordial leads (Fig. 2). Hypokinesia of the interior wall motion was detected by bedside transthoracic echocardiography, and left ventricular ejection fraction was 40%. Laboratory test re- vealed a leukocytosis of 14.64×109/L and serum levels of troponin I of 75.007 ng/mL (reference range, 0-0.04 ng/mL). On the basis of these findings, he was diagnosed with acute inferior wall infarction with right ventricular infarction.
With the IABP support for more than half an hour, a second 12-lead
ECG was performed that showed accelerated junctional rhythm with more than 50% resolution of the ST-segment elevation in leads II, III, and aVF (Fig. 3). The electrocardiographic ST-segment resolution strongly predicted spontaneous recanalization of the occluded infarct- related artery, and his hemodynamic status was relatively stable under the IABP assist. Therefore, we did not perform coronary angiogra- phy immediately. He was eventually extubated on the second day and weaned off the IABP on day 4 of admission because of his consciousness recovery and clinical condition improvement. On the seventh day of admission, coronary angiography was performed that revealed that the entire coronary artery appeared normal (Fig. 4). He was managed on oral aspirin, clopidogrel, atorvastatin, and metoprolol and discharged on day 12 without any complications and with close follow-up.
The present report describes a case of refractory electrical storm associated with acute inferior wall infarction with right ventricular infarction. When the recurrent incessant ventricular tachyarrhythmias could not be controlled by electrical defibrillation and conventional antiarrhythmic drugs, IABP finally as a temporary mechanical circulato- ry support for improving hemodynamic status and termination of the electrical storm played an important role.
Electrical storm can manifest itself during acute myocardial infarction and in patients who have structural heart disease, an implant- able cardioverter-defibrillator, or an inherited arrhythmic syndrome [3]. Electrical storm occurring during acute myocardial infarction is
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Fig. 1. This patient presented early in the course of an acute myocardial infarction on admission. Electrocardiograph monitoring showed incessant polymorphic ventricular tachycardia or ventricular fibrillation. He had to be defibrillated 10 times during the following minutes.
Fig. 2. After successfully converting ventricular arrhythmias, ECG showed junctional tachycardia with ST-segment elevation in leads II, III, and aVF as well as the right precordial leads. He was diagnosed with acute inferior wall infarction with right ventricular infarction.
Fig. 3. With the IABP support for more than half an hour, a 12-lead ECG change showed accelerated junctional rhythm with more than 50% resolution of the ST-segment elevation in leads II, III, and aVF, which predicted spontaneous recanalization of the occluded infarct-related artery.
clinically increasingly common. The mechanism of ventricular arrhyth- mias occurring in the setting of acute myocardial infarction is relatively complex. The metabolic sequelae of ischemia, including intracellular hypercalcemia and acidosis, anaerobic lipid metabolism, and free- radical production, may contribute to arrhythmogenesis during acute
myocardial infarction [4]. Increased sympathetic tone augments electrical instability; and rapid efflux of intracellular potassium, leading to membrane depolarization, may be the most important of these effects. malignant ventricular arrhythmias complicate acute myocardial infarction, presenting in a trimodal temporal pattern: during acute
Z.-P. Zhang et al. / American Journal of Emergency Medicine 33 (2015) 734.e1-734.e3 734.e3
Fig. 4. Coronary angiography on day 7 of admission demonstrated that the entire right (A) and left coronary artery (B) systems appeared normal, which suggested spontaneous recanalization of the occluded right coronary artery.
coronary occlusion, abruptly after reperfusion, or developing after reperfusion [2]. Ventricular arrhythmias occurring during the early phase of acute myocardial infarction, most notably ventricular fibrilla- tion, probably result from chaotic reentry arising in the region of infarc- tion. However, when progressive myocardial damage compromises intramyocardial conduction after several hours, these chaotic reentrant arrhythmias occur less frequently; and Purkinje fibers in the infarct zone may develop abnormal automaticity, leading to the second phase of arrhythmogenesis [1, 5]. Late ventricular arrhythmias occurring more than 24 to 48 hours into the infarct may reflect the development of an anatomic substrate (scar) that supports reentry [6, 7].
Understanding the mechanism of ventricular arrhythmias is advan- tageous to the effective management of electrical storm. In our case, he had chest pain and refractory electrical storm with hemodynamic col- lapse, suggesting larger infarct size or ischemia and a trend toward more depressed global ventricular function. When myocardial ischemia resulted in the Hemodynamic deterioration, converting electrical storm became very difficult. In this case, IABP provided hemodynamic support and was beneficial to the electrical stability. The electrical storm finally was successfully under control with the IABP support. According to the electrocardiographic ST-segment elevation in the inferior wall and right precordial leads after converting ventricular arrhythmias, it was consistent with proximal to middle occlusion of the right coronary artery. Fortunately, under the IABP suport, the patient had spontaneous recanalization of the occluded infarct-related artery; and subsequent coronary angiography confirmed the right coronary artery patency.
This case demonstrates that acute myocardial infarction or Ischemia-reperfusion injury may be responsible for the electrical storm and, thus, IABP could be an effective therapeutic option in the critical setting of hemodynamic and electrical instability caused by acute myocardial infarction.
Zhi-Ping Zhang, MD
Xi Su, MD
Hua Yan, MD Dan Song, MD Cheng-Wei Liu, MD
Bo Liu, MD Ming-Xiang Wu, MD Yu-Chun Yang, MD
Cardiac Care Unit,Wuhan Asia Heart Hospital, Wuhan 430022, China Corresponding author: Zhi-Ping Zhang Cardiac Care Unit Wuhan Asia Heart Hospital No.753 jinghan avenue,hankou Wuhan, 430022, China Tel: +0118602765796870 Fax: +0118602785854036
E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2014.10.038
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