The Case
58 year-old man with history of mitral valve prolapse presents with 4 days of intermittent palpitations, lightheadedness, and shortness of breath. The symptoms resolve spontaneously. He denies any illicit substance use.
Vital signs on arrival: T 97.5F, HR 71, BP 140/89, RR 18, SpO2 100% on room air.
While in the ED, his palpitations return. ECG is shown below.
Rapid atrial flutter with rapid, variable AV conduction
After receiving 3 doses of adenosine (6mg, 12mg, 12mg), the HR and repeat ECG were unchanged. Two doses of diltiazem 20mg IVP were then given with an adequate response following the 2nd dose, resulting in the ECG:
Atrial flutter with more controlled ventricular rate
A dose of diltiazem 60mg PO was given following the above ECG. CXR was unremarkable and labs showed a troponin 0.034, lactate 2.7. Cardiology was consulted for a HR persistently >120. The patient was given aspirin, placed on a diltiazem and heparin infusions, and admitted to CCU.
TEE showed EF 55-60% with moderate-severe mitral valve prolapsed and mitral regurgitation and no atrial thrombus. Electrophysiology study on HD #2 showed atrial flutter with typical counterclockwise rotation at the cavo-tricuspid isthmus. Ablation at the isthmus terminated the macro-reentrant circuit and restored normal sinus rhythm. Stimulation testing afterwards confirmed successful bi-directional block at the cavo-tricuspid isthmus. The patient was discharged home on HD #3 on metoprolol, diltiazem, and warfarin with Cardio-Thoracic surgery follow-up for mitral valve repair.
Atrial Flutter
Atrial flutter occurs when atrial tissue is altered due to a number of structural and/or electrophysiological mechanisms. This results a reentry circuit that is usually located within the right atrium near to the tricuspid valve annulus. The atrial rate is usually 250-350/min with the ventricular rate dependent on the refractoriness of the AV node. What is usually observed is some degree of “block”, either fixed or variable, at the AV node. The ECG shows a typical sawtooth P’ pattern, in leads II, III, aVF, and V1 with narrow QRS-complexes unless aberrant conduction is also present.
Image taken from Atrial Flutter, Circulation, Nov 2005.
General Approach
When a patient is found to be in atrial flutter or fibrillation with a rapid ventricular rate, it’s important to identify any underlying illness that may be contributing to the tachycardia and try to determine whether or not this rhythm is new. Scheuermeyer et al, found that patients in rapid atrial flutter/fibrillation with an acute underlying illness had a nearly 6-fold increase in adverse events with early as opposed to delayed rate control. Patients that underwent delayed treatment with AV nodal agents (which may have allowed more time for IV crystalloid administration) also had more successful rate control. Successful rate control increased from 16.2% in the first hour to 25.0% in the fourth hour, whereas the adverse event rate decreased from 48.6% to 28.0% during the same time period. The majority of adverse events in the study were in patients presenting with rapid atrial flutter/fibrillation related to underlying sepsis or decompensated CHF.
Management
Rate Control
Let’s pass on the topic of rate vs rhythm control (hopefully this topic goes away in the near future). But for anyone interested, especially our medical students in the audience, see the AFFIRM trial referenced at the end.
A recent systematic review (Martindale JL, et al. 2015) reported that there isn’t great data out there comparing calcium-channel blockers to beta-blockers for acute rate control in the ED. Currently, the decision on which agent to use may depend on mostly physician preference, however, there is emerging evidence to show that calcium-channel blockers (i.e. diltiazem) may be superior in the acute care setting while beta-blockers (i.e. metoprolol) be superior in the outpatient setting.
When to Cardiovert?
According to guidelines, the time during which we should consider cardioversion is when the onset of atrial flutter/fibrillation is < 48 hours or the patient has been on anticoagulation with therapeutic levels for at least 3 weeks. In the Finnish CardioVersion (CV) study, patients presenting within 48 hours of symptom onset were cardioverted without peri-procedural or post-procedural anticoagulation. The risk of thromboembolic complications following cardioversion (88% of which were electrical cardioversion) was found to be 0.7% within 30-days, mainly due to cerebral infarction. This is comparable to the risk of thromboembolic complications following 3-weeks of anticoagulation, which is estimated to be 0.3-0.8%. However, particular patient characteristics were identified that substantially increased the risk for thromboembolism: Age > 60, female gender, and presence of heart failure or diabetes. In a patient with CHF, the risk of thromboembolism increased to 3.3% and if the same patient also has diabetes, the risk further increased to 9.8%!
A retrospective analysis of the Finnish CV study, showed that the overall risk of thromboembolism of 0.7% can be further broken down based on time to cardioversion. Those cardioverted within 12 hours had a risk of 0.3% and those cardioverted between 12-48 hours had a risk of 1.1%. We can interpret this as meaning the sooner, the better! Cardioversion within 12 hours has a low risk of stroke. Between 12-48 hours, we should consider discharging moderate-to-high risk patients with anticoagulation after cardioversion after weighing the risk vs benefit for each patient.
Note: The patient in the case presentation may not have been a good candidate for elective cardioversion as the history seems to suggest a paroxysmal nature. Atrial flutter/fibrillation in these patients will often resolve spontaneously.
Aggressive vs Conservative
The Ottawa Aggressive Protocol Study (Steill IG, et al. 2010) was designed to evaluate the effectiveness and safety of rapid cardioversion and discharge of patients with recent-onset atrial flutter/fibrillation. The goal was to discharge patients home within 1 hour of cardioversion. According to this protocol, the patients could be discharged home on anticoagulation if CHADS2 score > 1; those who present > 48 hours after symptom onset should receive TEE-guided cardioversion.
How to Cardiovert?
Chemical Cardioversion
2014 AHA/ACC/EHR Guidelines recommend flecainide, dofetilide, propafenone, or ibutilide (Class I) with Level A evidence for pharmacologic cardioversion of atrial fibrillation. Previously, flecainide (Class IC antidysrhythmic) was thought to have the greatest efficacy of the agents above until ibutilide (Class III antidysrhythmic) came along. There appears to be no significant difference between the efficacy and rate of adverse events between these two agents. However, the risk of Torsades de Pointes with ibutilide is 7-8%. Magnesium levels should be measured and repleted prior to ibutilide administration. Lastly, as this is a fairly new drug, the cost is significantly higher (approx 30 times more) than flecainide. Flecainide does not increase the risk of Torsades de Pointes, however, it has been shown to have supraventricular pro-dysrhythmogenic properties. This may include conversion of atrial fibrillation to atrial flutter with 1:1 conduction.
Electrical Cardioversion
For patients presenting in atrial flutter < 48 hours, biphasic waveform cardioversion can be attempted at 100J. Cardioversion should be performed under procedural sedation with anterior & lateral electrode placement.* If initial attempt is unsuccessful, subsequent attempts should be increased by 50J, up to a maximum of 200J. If one or two shocks at 200J fails to cardiovert, consider compression of the electrodes to decrease impedance (or consider using handheld paddles), administering an antidyshythmic agent prior to the next shock, or “double shocking”. Ibutilide infusion prior to shock delivery has been shown to increase the chance of successful cardioversion while decreasing the mean amount of energy required.
*Most studies show that anterior-posterior electrode placement yields higher success when performed for atrial fibrillation. In these cases, a large amount of myocardium must be shocked for successful cardioversion. In atrial flutter, our target is the tricuspid valve annulus and anterior-lateral electrode placement has been shown to be superior for this specific dysrhythmia (Risuis T, et al. 2009).
Take Home Points
- Be thorough and identify any acute underlying illness that may be responsible for atrial fibrillation/flutter
- Prioritize fluid resuscitation (if indicated) over rate control
- There is a low risk of stroke if cardioversion is performed < 12 hours from symptom onset and there are no contraindications
- Electrical cardioversion is much more successful than pharmacologic cardioversion
- Have a back-up plan if your 1st attempt at electrical cardioversion is unsuccessful
Blog post by: Dr. Yonatan Yohannes
Case presentation by: Dr. Guy Carmelli on Feb. 3, 2016
Editing by: Dr. Ian deSouza
References
Boyer, M, Koplan BA. Atrial Flutter. Circulation. 2005;112:e334-e336.
Scheuermeyer, FX, Pourvali R, Rowe BH, et al. Emergency Department Patients With Atrial Fibrillation or Flutter and an Acute Underlying Medical Illness May Not Benefit From Attempts to Control Rate or Rhythm. Ann Emerg Med. 2015. 65;5:511-522.e2.
The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. A Comparison of Rate Control and Rhythm Control in Patients with Atrial Fibirllation. N Engl J Med. 2002;347:1825-1833.
Martindale JL, deSouza IS, Silverberg M, et al. Beta-blockers Versus Calcium Channel Blockers for Acute Rate Control of Atrial Fibrillation With Rapid Ventricular Response: A Systematic Review. Eur J Emerg Med. 2015;22(3):150-154.
2014 AHA/ACC/HRS Guideline for the Management of Patients with Atrial Fibrillation: Executive Summary. Circulation. 2014;130:2071-2104.
Airaksinen KE, Gronberg T, Nuotio I, et al. Thromboembolic Complications After Cardioversion of Acute Atrial Fibrillation: The FinCV (Finish CardioVersion) Study. J Am Coll Cardiol. 2013;62:1187-1192.
Airaksinen KE, Gronberg T, Nuotio I, et al. Time to Cardioversion for Acute Atrial Fibrillation and Thromboembolic Complications. JAMA. 2014;312:647-648.
Steill IG, Clement CM, Perry JJ, et al. Association of the Ottawa Aggressive Protocol with Rapid Discharge of Emergency Department Patients with Recent-Onset Atrial Fibrillation or Flutter. CJEM. 2010;12(3):181-191.
Volgman AS, Carberry PA, Stambler B, et al. Conversion Efficacy and Safety of Intravenous Ibutilide Compared with Intravenous Procainamide in Patients with Atrial Flutter or Fibrillation. J Am Coll Cardiol. 1998;31:1414-1419.
Domanovits H, Schillinger M, Thoennissen J, et al. Termination of Recent-Onset Atrial Fibrillation/Flutter in the Emergency Department: A Sequential Approach with Intravenous Ibutilide and External Electrical Cardioversion. Resuscitation. 2000:45:181-187.
Reisinger J, Gatterer E, Lang W. Flecainide Versus Ibutilide for Immediate Cardioversion of Atrial Fibrillation of Recent Onset. Eur Heart J. 2004;25:1318-1324.
Khan, IA. Pharmacologic Cardioversion of Recent Onset Atrial Fibrillation. Editorial. Eur Heart J. 2004;25:1274-1276.
Risuis T, Mortenses K, Schwemer TF, et al. Comparison of Antero-Lateral Versus Antero-Posterior Electrode Position for Biphasic External Cardioverson of Atrial Flutter. Am J Cardiol. 2009;104(11):1547-1550.
Viktorsdottir O, Henriksdottir A, Arnar DO. Ibutilide for Treatment of Atrial Fibrillation in the Emergency Department. Emerg Med J. 2006;23:133-134.
Page RL, Kerber RE, Russell JK, et al. Biphasic Versus Monophasic Shock Waveform for Conversion of Atrial Fibrillation: The Results of an International Randomized, Double-Blind Multicenter Trial. J Am Coll Cardiol. 2002;39:1956-1963.
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