MANAGEMENT OF ATRIAL FIBRILLATION IN THE EMERGENCY DEPARTMENT Who Should Be Admitted?

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1 ATRIAL FIBRILLATION IN DAILY PRACTICE MANAGEMENT OF ATRIAL FIBRILLATION IN THE EMERGENCY DEPARTMENT Who Should Be Admitted? Wissam ELZEIN 1, Wael CHALAK 1, Charles JAZRA 2 Elzein W, Chalak W, Jazra C. Management of atrial fibrillation in the emergency department: Who should be admitted? J Med Liban 2013; 61 (2): INTRODUCTION Atrial fibrillation (AF) is the most common cardiac arrhythmia managed in the emergency department (ED). It is expected to be progressively more prevalent in the next decades with aging population. The management of new onset AF in ED is still controversial and despite the international guidelines the management of AF is heterogeneous in different EDs [1-2]. In some patients the AF can be managed, although differently, in the emergency ward without the need for hospital admission [3-4]. Several questions are to be answered in the setting of the management of AF in the ED: 1. What should be the initial workup: ECG, blood test, chest X-ray, echo? 2. What should be the medical therapy: anticoagulation, rate control strategy? 3. Should the patient be cardioverted? Which method should be used? 4. Should the patient be admitted to hospital? 5. Could we discharge the patient safely? 1. WORKUP Regardless of the type of atrial fibrillation, the first goals at the ED are identification of the type of AF (first detected, paroxysmal, persistent or permanent) treatment of precipitating or underlying causes clinical and electrical stabilization in addition to prevention of thromboembolic event. A first step management is to establish that the patient is hemodynamically stable by assessing his vital signs and whether he needs inpatient evaluation for an associated condition [5]. The initial workup must include a good history describing symptoms, tolerance, characteristics of AF (first episode, frequency, duration, precipitating factors, mode of termination and response to treatment), presence of underlying heart disease or reversible conditions either cardiac or noncardiac (electrolyte imbalance, thyrotoxicosis, fever, pneumonia, drug abuse and alcohol use). 1 Faculty of Medical Sciences, Lebanese University, Hadeth; 2 Saint Joseph Hospital, Bawchrieh, Lebanon. Correspondence : Elzein Wissam, MD. wiwati@hotmail.com Home medications should be documented along with complete physical examination to detect any sign of heart failure or any other organ failure [3-4]. ECG should be done to confirm AF and to describe ventricular rate, presence of left ventricular hypertrophy (LVH), left bundle branch block (LBBB), prior or recent myocardial infarction (MI) or pre-excitation syndrome, other atrial arrhythmia and evolution of RR, QT intervals and QRS duration. Initial blood tests include: Complete blood count, international normalized ratio (INR), serum levels of electrolytes, urea, creatinine, cardiac enzymes, liver function tests, blood glucose, arterial blood gas, thyroid function tests and serum toxicology [5]. Recent trials reported NT-proBNP was a remarkable predictor of incident AF, independent of any other previously described risk factor [6]. Initial management includes establishment of an intravenous line, oxygen supplement if needed and continuous ECG monitoring to detect silent episodes of AF and for assessment of rate control or bradycardia [5]. 2. MEDICAL THERAPY Except in specific cases (e.g. lone AF), the medical therapy of AF consists of anticoagulant drug administration (besides either rate or rhythm control management). It reduces significantly the risk of ischemic stroke in valvular and nonvalvular AF (NVAF) [7-8]. Although there is no survival benefit in rhythm control over the rate control strategy [9-10] the maintenance of sinus rhythm is relevant in patients with paroxysmal and persistent AF because the restoration of sinus rhythm maintains the atrial contribution to cardiac output and improves the clinical and hemodynamic status. The most studied anticoagulant drug is unfractioned heparin UFH and, less validated, subcutaneous enoxaparin. In symptomatic patients already taking antivitamin- K (warfarin), emergency management of acute atrial fibrillation depends on the INR [11-13]. Types of rate control drugs [3, 14-15] The rate-control agents act primarily by increasing atrioventricular (AR) nodal refractoriness by a variety of different mechanisms. Beta-blockers and calcium channel blockers are first-line agents for rate control in AF (class I); ß-blockers prolong AV refractoriness by targeting the adrenergic receptors. Calcium channel blockers target the L-type calcium. These drugs can be administrated either intravenously 96 Lebanese Medical Journal 2013 Volume 61 (2)

2 or orally. They are effective at rest and with exertion. They slow the heart rate and relax the blood vessels. The selection of a ß-blocker or calcium channel blocker should be based on the physician s experience and the patient s clinical condition. Different rate-slowing drugs are recommended in the ED setting by ACC/AHA/ESC guidelines, including, esmolol, an intravenous short acting ß-blocker (plasma half-life of 9 min) given usually at multiple infusion steps, at the dose of 500 mcg/kg/1 min (bolus dose) with mcg/kg/min for maintenance dose and metoprolol (2.5-5 mg/2 mn IV up to 3 doses) or propranolol (0.15 mg/kg IV). These agents should be used with caution in asthmatic patient and are the drugs of choice in the settings of ischemic heart disease. Verapamil ( mg/kg/2 mn) and diltiazem (0.25 mg/kg/2 mn IV & 5-15 mg/h IV) are the calcium channel blockers commonly used for rate control in AF, but the response is transient, and repeated doses or a continuous intravenous infusion may be required. They are contraindicated in patients with heart failure. Digoxin (0.25 mg IV Q 2 h up to total of 1.5 mg & mg/d), is a cardiac glycoside that improve the cardiac output favoring its use as a second line agent or reserved for those with heart failure or left ventricular dysfunction often in combination with ß-blocker [5]. It is used to slow AV node conduction mediated by enhanced vagal tone but it does little in acute setting to control the ventricular rate in active patients or in conditions of high sympathetic drive such as fever. Additionally digoxin may aggravate paroxysmal AF by shortening the atrial muscle refractory period and increasing the rate of fibrillation. There is little pharmacological advantage of the intravenous route over the oral route, except in patients in whom it cannot be administrated orally. Caution should be exercised in elderly patients and those with renal failure [3, 15]. Amiodarone (300 mg IV bolus then 0.5 mg/kg/min for 6 h then 1 mg/kg/min for 18 h) has a class IIa recommendation from the ACC/AHA/ESC-guidelines for use as a rate-controlling agent for patients who are intolerant or unresponsive to other agents. It has both sympatholytic and calcium antagonistic properties. Caution should be exercised in those who are not receiving anticoagulation, as amiodarone can promote cardioversion. It is considered as first line therapy in patient with heart failure and LVH. However, a combination of drugs, with careful dose titration, may be necessary to control the rate of ventricular response in patients with acute AF. Extreme care must be taken in patients with pre-excitation syndrome and AF. In such situation calcium channel blockers and ß-blockers are contraindicated for rate control because anterograde conduction along the accessory pathway is facilitated when these agents are administrated and this can result in ventricular fibrillation and hypotension. When acute AF is associated with hemodynamic compromise in Wolff-Parkinson-White patients, early direct current cardioversion should be performed. 3. CARDIOVERSION Cardioversion is used generally, in ED, in the presence of persistent AF to restore sinus rhythm or of acute AF that produces hemodynamic instability (signs of shock, signs of heart failure, worsening of angina or patient with rapid ventricular response). Whenever AF duration exceeds 48 hours, electrical cardioversion must be done under adequate anticoagulation for 3-4 weeks before procedure. Although the thromboembolic risk is low (0.8%) if atrial fibrillation duration is < 48 hours, ED patients should not be assumed to be free of left atrial thrombus [3-4, 11, 16]. However, a transesophageal echocardiography (TEE) before cardioversion should be done in stable patients to rule out occult left atrium (LA)/left atrial appendage (LAA) thrombi or other thrombotic features [17]. The role of TEE in ED remains a [much] debated issue. After successful cardioversion, it is necessary to start the patient on an antiarrhythmic drug to prevent AF recurrence if the patient has no identifiable reversible causes. Drugs of choice to prevent recurrent AF and maintain normal sinus rhythm include class I or class III antiarrhythmic agents [3, 16, 18]. These drugs are contra-indicated in the presence of heart failure (except amiodarone), coronary artery disease, potential arrhythmic effect and advanced sinus or atrio-ventricular node dysfunction [18]. Either pharmacological or electrical cardioversion may be applied depending on the patient medical history, the emergency department facilities and the expertise or the physician experience. Both the pharmacological and electrical cardioversion have the same risk for thromboembolic events. The former is simpler but less effective than the latter and it is limited by drug related adverse events [19-21]. Electrical cardioversion Electrical cardioversion of AF is performed with the patient having fasted for at least six hours and under adequate anesthesia using mainly short-acting agents. The energy requirement is lower with devices delivering biphasic rather than monophasic waveforms and overall success is greater with the anterior-posterior (sternum and left scapular) than with the anterior-lateral (ventricular apex and right infraclavicular) alignment of paddle positions. An initial shock of 200 joules is recommended. Sinus rhythm can be restored, in general in up to 90% of patients, but the rate of relapse is high unless antiarrhythmic drug therapy is given concomitantly. Cardioversion of patients with implanted pacemaker and defibrillator devices is safe when appropriate precautions are taken. The device should be interrogated immediately before and after cardioversion to verify appropriate function. The paddles should be positioned as distant as possible from the device, preferably in the anterior-posterior configuration. The risks of electrical cardioversion are mainly related W. ELZEIN et al. Atrial fibrillation in ED Lebanese Medical Journal 2013 Volume 61 (2) 97

3 to embolic events and cardiac arrhythmias especially ventricular and supraventricular premature beats, bradycardia occurring mainly in case of a slow ventricular response to AF in the absence of drugs that slow AV nodal conduction, and short periods of sinus arrest [3-4, 22]. Pharmacological (chemical) cardioversion Despite the development of new antiarrhythmic drugs, some disadvantages still persist, particularly the proarrhythmic effect of many of these drugs. However, no sedation or anesthesia backup is required for successful pharmacological conversion [4]. Patients who undergo a failed attempt at chemical cardioversion can subsequently undergo successful electrical cardioversion [20]. Two different categories of agents are used for chemical cardioversion: Potassium channel blockers relax the heart muscle and slow the electrical signals that cause AF. Examples include amiodarone, ibutilide and sotalol. These agents increase the length of the interval between paroxysms but often do not totally abolish the arrhythmia. Nevertheless, existing data suggest ibutilide is probably the most effective agent for the chemical cardioversion of acute AF in the ED setting. Ibutilide has a rapid action (within one hour after administration) and is safe in patients with Wolff-Parkinson-White syndrome. The most important side effect is its ability to induce transient episodes of torsade de pointes which do not require any intervention in hemodynamically stable patients. [3-4]. Sodium channel blockers improve the rhythm by slowing the electrical conduction. Examples include flecaine, propafenone and quinidine. Atrium-selective or AF-selective Na + channel blockade that can suppress AF, while exerting little or no effect in the ventricle, is being studied and include two recently introduced agents: vernakalant and ranolazine [23]. Intravenous vernakalant (Brinavess ) is an atrialrepolarization-delaying agent that is currently approved in Europe (but not in the US) for the rapid conversion of new-onset AF to sinus rhythm. It blocks atrial-specific potassium and sodium ion channels but differs from typical class III agents by blocking the cardiac transient outward potassium current with increased potency as the heart rate increases. It also slightly blocks the herg potassium channel, leading to a prolonged QT interval. This may theoretically increase the risk of ventricular tachycardia, though this does not seem to be clinically relevant. In pivotal randomized, phase III trials, intravenous vernakalant 3 mg/kg administered as a 10-minute infusion, followed by a 2 mg/kg 10-minute infusion after 15 minutes if AF persisted, was effective in the rapid termination of new onset AF in nonsurgical patients (3 hours duration 7 days) and in those with postoperative AF (3 hours duration 72 hours) following cardiac surgery [24-25]. Ranolazine has been shown to produce atrial-selective depression of sodium channel-dependent parameters and suppress AF in a variety of experimental models [26]. 4. WHICH SUBSETS OF AF PATIENTS NEED HOSPITAL ADMISSION? Hospitalization can be limited to highly symptomatic patients, those with structural heart disease, those who have had an embolic event or are at high risk of thromboembolism, those of non-cardiac causes of AF especially chronic obstructive pulmonary disease exacerbation and patients with failure of rate control in the ED. 5. WHICH SUBSETS OF AF PATIENTS CAN BE SAFELY DISCHARGED FROM THE ED? Many patients may be safely discharged from the ED; patients with no structural heart disease or with a controlled ventricular rate, as well as those under 60 years of age with lone AF. This leads to reduction of costs and increases the number of available beds in the ED. Patients with persistent AF whose rhythm is converted to normal sinus rhythm by cardioversion can be discharged home after initiation of an appropriate oral antiarrhythmic treatment to prevent recurrence. Patients started on amiodarone may be safe for discharge after emergency cardioversion because of its minimal depression of myocardial function and low proarrhythmic potential. Amiodarone is currently the only agent for which there is substantial data to support initiation of outpatient treatment for AF. All patients discharged home should be closely monitored, and both patient and physician should be on alert to possible adverse drug effects. CONCLUSION AF is the most common arrhythmias worldwide; there are disparities in management of atrial fibrillation in EDs despite adherence to the current guidelines. We recommend anticoagulation as mainstay of therapy, except in specific cases, in addition to rate or rhythm control. Cardioversion is used in case of hemodynamic instability or persistence of AF despite medical therapy. Many patients can be discharged safely through rapid assessment and effective treatment of AF in the ED which lead to cost reduction and increase in available beds in hospitals. REFERENCES 1. Buccelletti F, Di Somma S, Galante A et al. Disparities in management of new-onset atrial fibrillation in the emergency department despite adherence to the current guidelines. Intern Emerg Med 2011; 6: Del Arco C, Martin A, Laguna P, Gargantilla P. Analysis of current management of atrial fibrillation in the acute setting: GEFAUR-1 study. Ann Emerg Med 2005; 46: Fuster V, Ryden LE, Cannom DS et al Guidelines for the management of patients with atrial fibrillation- Executive summary. A report of the American College of 98 Lebanese Medical Journal 2013 Volume 61 (2) W. ELZEIN et al. Atrial fibrillation in ED

4 Cardiology, American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines. (ACC/AHA/ ESC-2006) Circulation 2006; 114: Wakai A, O Neill JO. Emergency management of atrial fibrillation. Postgraduate Medicine Journal 2003; 79: Ezekovitz MD, Aikens TH, Nagarakanti R et al. Atrial fibrillation. Outpatient presentation and management. Circulation 2011; 124: Patton K, Ellinor P, Heckbert S et al. N-Terminal Pro-B- Type Natriuretic Peptide is a major predictor of the development of atrial fibrillation: The Cardiovascular Health Study (CHS). Circulation 2009; 120: Estes NAM 3 rd, Halperin JL, Calkins H et al. ACC/AHA/ Physician consortium Clinical performance measures for adults with nonvalvular atrial fibrillation or atrial flutter. A report of the American College of Cardiology/ American Heart Association Task Force on Performance Measures and the Physician Consortium for Performance Improvement. Circulation 2008; 171: Connolly SJ, Pogue J, Eikelboom J et al. On behalf of the ACTIVE W investigators. Benefit of oral anticoagulation over antiplatelet therapy in atrial fibrillation depends on the quality of international normalized ratio control achieved by centers and countries as measured by time in therapeutic range. Circulation 2008; 118: Wise DG, Waldo AL, DiMarco JP et al. Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002; 347: Van Gelder IC, Hagens VE, Bosker HA et al. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. New Engl J Med 2002; 347: Ederhy S, Di Angelantonio E, Meuleman C et al. Low molecular weight heparin and nonvalvular in atrial fibrillation. Archive des Maladies du Cœur et des Vaisseaux 2006; 99: Steinberg JS, Sadaniantz A, Kron J et al. Analysis of cause-specific mortality in the atrial fibrillation follow-up investigation of rhythm management (AFFIRM) study. Circulation 2004; 109: Camm AJ, Kirchhok P, Lip GH. Guidelines for the management of atrial fibrillation. European Heart Journal 2010; 31: Wyse DG, Gersh BJ. Atrial fibrillation: Perspective thinking inside and outside the box. Circulation 2004; 109: Pages RL. Newly diagnosed atrial fibrillation. New Engl J Med 2004; 351: Wyse G l. Cardioversion of atrial fibrillation for maintenance of sinus rhythm, a road to nowhere. Circulation 2009; 120: Illien S, Maroto-Jarvinen S, von der Recke G et al. Atrial fibrillation: Relation between clinical risk factors and transoesophageal echocardiography risk factors for thromboembolism. Heart 2003; 89: Blaauw Y, Van Gelder IC, Crijns HJGM. Treatment of atrial fibrillation. Heart 2002; 88: Bertaglia E, Zerbo F, Zoppo F et al. Success of serial external electrical cardioversion of persistent atrial fibrillation in maintaining sinus rhythm. A randomized study: European Heart Journal 2002; 23 (19): Michel JA, Stiell IG, Agarwal S et al. Cardioversion of paroxysmal atrial fibrillation in the emergency department. Annals of Emergency Medicine 1999; 33: Koenig BO, Ross MA, Jackson RE et al. An emergency department observation unit protocol for acute onset atrial fibrillation is feasible? Annals of Emergency Medicine 2002; 39: Sbragia P, Arques S, Franceschi F et al. Cardioversion by external electrical chock of AF: Does age affect immediate results. Archives des Maladies du Cœur et des Vaisseaux 2002; 95: Dobrev D, Nattel S. New antiarrhythmic drugs for treatment of atrial fibrillation. Lancet 2010; 375: Duggan ST, Scott LJ. Intravenous vernakalant: a review of its use in the management of recent-onset atrial fibrillation. Drugs 2011 Feb 12; 71 (3): Finnin M. Vernakalant: A novel agent for the termination of atrial fibrillation. Pharmacology, Medscape 12 October Burashnikov A, Di Diego JM, Zygmunt AC, Belardinelli L, Antzelevitch C. Atrium selective sodium channel block as a strategy for suppression of atrial fibrillation: differences in sodium channel inactivation between atria and ventricles and the role of ranolazine Circulation 2007 Sep 25; 116 (13): Heilbron B, Klein GJ, Talajic M, Guerra PC. Management of atrial fibrillation in the emergency department and following acute myocardial infarction. Can J Cardiol 2005; 21 (Suppl B): 61B-66B. APPENDIX 2004 CANADIAN CARDIAC SOCIETY CONSENSUS CONFERENCE RECOMMENDATIONS FOR THE MANAGEMENT OF ATRIAL FIBRILLATION IN THE EMERGENCY DEPARTMENT [27] CLASS I 1. In stable patients with duration of AF greater than 48 h or of uncertain duration in whom a decision has been made to attempt cardioversion, optimize rate control and anticoagulate to INR of 2.0 to 3.0 for 3 weeks before cardioversion (level of evidence C). 2. In patients with duration of AF greater than 48 h or of uncertain duration who are highly symptomatic after efforts to achieve adequate rate control, TEE to exclude atrial thrombus can be considered before cardioversion (level of evidence B). 3. Select a strategy of rate control or rhythm control based on symptoms and clinical variables (level of evidence B). >>>> W. ELZEIN et al. Atrial fibrillation in ED Lebanese Medical Journal 2013 Volume 61 (2) 99

5 4. When a decision is made to cardiovert patients with AF duration of less than 48 h, synchronized electrical cardioversion or pharmacological cardioversion may be used (level of evidence C). 5. When electrical cardioversion is chosen, use biphasic waveform when available to increase success and reduce cardioversion energy (level of evidence B). 6. After acute conversion of an episode of AF, long-term antithrombotic therapy should be prescribed based on thromboembolic risk and bleeding risk from antithrombotic therapy (level of evidence A). 7. In patients with AF and pre-excitation, perform urgent cardioversion if the patient is hemodynamically unstable. If stable, consider using class I or class III antiarrhythmic agents (level of evidence C). 8. Hospital admission can be limited to highly symptomatic patients, those with structural heart disease, those who have had an embolic event or those at high risk for thromboembolism, and those with failure of rate control in the ED (level of evidence C). CLASS IIA 1. Anticoagulation therapy with either unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) should be considered for most patients presenting to the ED with AF. Exceptions include those already on warfarin with an INR greater than 2.0, or those in whom the short-term risk of bleeding on anticoagulation therapy is thought to exceed the risk of thromboembolism (level of evidence C). 2. After conversion to sinus rhythm has been achieved, decide whether antiarrhythmic drug therapy is indicated based on the estimated probability of recurrence and the symptoms during AF (level of evidence C). CLASS III 1. Do not administer digoxin, calcium channel blocking agents or beta-blocking agents alone to patients with pre-excitation during AF (level of evidence B). 2. Do not administer adenosine to attempt rate control or cardioversion during AF (level of evidence B). 100 Lebanese Medical Journal 2013 Volume 61 (2) W. ELZEIN et al. Atrial fibrillation in ED