More Atrial Fibrillation Management Pearls in the ED
- May 5th, 2016
- Jennifer Robertson
Author: Jennifer Robertson, MD, MSEd // Edited by: Alex Koyfman, MD (@EMHighAK – EM Attending Physician, UTSW / Parkland Memorial Hospital) and Manpreet Singh, MD (@MPrizzleER – Clinical Instructor & Ultrasound/Med-Ed Fellow / Harbor-UCLA Medical Center)
Atrial fibrillation (AF) is the most common atrial arrhythmia worldwide and the overall incidence is expected to rise in the future (1, 2, 3). Overall, AF is responsible for up to one quarter of all embolic strokes and also may contribute to heart failure and even dementia (3, 4, 5, 6). AF is also the most frequently diagnosed arrhythmia in emergency departments (ED) (5, 6). ED visits for AF are rising, which emphasizes the need for ED providers to properly understand and manage the condition (7).
In the normal heart, impulses originate from the sinus node, followed by regular atrial and ventricular activation and contraction. In AF, the impulses are not regular and it is these irregular beats that cause ineffective atrial contraction, which can lead to clot formation in the left atrial appendage, causing potential for stroke (8). The irregular beats can also occasionally lead to dangerous tachycardias.
AF can be divided into five main categories based on its presentation and duration. This includes first diagnosis, paroxysmal, persistent, long-standing persistent, and permanent AF (9, 10). Paroxysmal AF usually terminates on its own within 48 hours but may continue up to seven days, while persistent AF is present for longer than 7 days and typically requires treatment. Long standing AF is defined as lasting longer than one year and permanent AF is defined as the presence of continuous AF that is accepted by both the patient and his or her physician.
Patients with AF usually present to the ED because of symptoms as a result of an irregular, rapid heart rate (8). These symptoms will vary, and some patients may even be asymptomatic (9). Typically, symptoms of AF include palpitations, chest pain, shortness of breath, lightheadedness, or syncope (8, 9). Some may be considered hemodynamically unstable, showing signs of shock, pulmonary edema, angina or myocardial infarction (10, 11). However, most patients who present to the ED with AF or AFL will be alert with a normal, perfusing blood pressure (11). However, as discussed in sections below, careful evaluation of both stable and unstable AF/AFL patients is critical, as treatment and disposition will depend on each patient’s diagnosis and hemodynamic stability (10, 12).
Emergency Department Evaluation
Although not specific to the ED, the American Heart Association (AHA) and American College of Cardiology (ACC) provide updated, evidence-based recommendations for evaluating patients with AF/AFL (12). According to the AHA/ACC, electrocardiography (ECG) is the primary method to initially diagnose AF or AFL. Patients should always be evaluated with a complete history and physical examination (H&P). The H&P should focus on onset, frequency and duration of symptoms. The H&P should also focus on associated symptoms, clinical type of AF such as paroxysmal or permanent, prior response to therapies, and presence of any underlying heart disease or reversible conditions. Reversible conditions may include drug or alcohol use, infection, or hyperthyroidism (12). Blood tests such as thyroid, renal and hepatic function should also be obtained, especially during a first episode of AF or AFL. Any other conditions associated with AF should always be considered, including evaluation for pulmonary embolism (PE), hypokalemia, obstructive sleep apnea, alcohol withdrawal, and acute myocardial infarction (MI) (12, 13, 14).
Many patients with AF or AFL also have underlying coronary artery disease (CAD) and patients with AF or AFL RVR commonly present with chest pain (11, 13, 15). Overall, clinical judgment is recommended to rule out AMI, including whether any chest pain started before or after the palpitations (16). ECG findings and clinical suspicion for AMI should also be used when determining whether workup for AMI should be included in patient assessment (16). Unless the history and ECG findings are suspicious for acute coronary syndrome, then workup for AMI can be eliminated (11, 15).
Emergency Department Treatment
While the ED workup of AF or AFL with RVR is quite standard, treatments tend to vary (8, 17). If no known reversible causes of the acute AF or AFL can be found, then treatment should be initiated. The main goals of AF treatment are to relieve symptoms, improve functional capacity, and possibly improve left ventricular function (10). This can be done via rhythm or rate control.
Several societies, including the American Heart Association/American College of Cardiology (AHA/ACC), the Canadian Cardiovascular Society (CCS) and the European Society of Cardiology (ESC) all have guidelines for the management of acute AF with RVR (10, 12, 18). While most of the guidelines agree on managing these patients, there are some differences, including the use of cardioversion and anticoagulation (10, 12, 18).
Whether or not patients are acutely managed with rate or rhythm control, thromboembolic risk should always be considered (12). It should also be noted that patients with valvular atrial fibrillation are deemed high risk for stroke and should always be treated with warfarin. This is because none of the novel oral anticoagulants (NOACs) have been studied in patients with valvular atrial fibrillation (10, 12, 18).
All three societies recommend using the same risk scores of CHADS2 (Congestive Heart Failure, Hypertension, Age > 75 years, Diabetes Mellitus and Prior Stroke or transient ischemic attack (TIA)) and/or CHADS2-VASc (CHADS2 plus vascular disease, age 65-74 years and female gender) to determine if a patient is eligible for oral anticoagulation (10, 12, 18). The presence of each risk factor gives the patient with AF or AFL a point toward being eligible for oral anticoagulation. All three societies recommend that all patients with AF or atrial flutter (AFL), whether paroxysmal or persistent, or permanent should be risk stratified using a prediction model for stroke (10, 12, 18).
Each society does have slight variations in their recommendations on who should be anticoagulated and these recommendations can be viewed in each individual article cited in the reference section (10, 12, 18). The use of anticoagulation should always be kept in mind when treating patients with AF and AFL in the ED, whether the patient is stable or unstable or if rate or rhythm control is utilized. Patients who are high risk for stroke should be considered candidates for anticoagulation, even in emergent situations.
Rate versus Rhythm Control
The Unstable Patient
All three societies recommend urgent electrical cardioversion in any unstable patient who presents in AF or AFL with RVR (10, 12, 19). Instability includes AF or AFL causing hypotension, cardiac ischemia, or pulmonary edema (19). However, as previously mentioned, all causes of any hemodynamic instability, such as sepsis, should be considered when evaluating and treating these patients. Again, stroke risk should be considered and each society varies slightly in recommending anticoagulation in unstable patients. For example, the AHA/ACC recommends that any unstable patient with AF or AFL for > 48 hours or unknown duration be cardioverted and placed on anticoagulation immediately. If a patient is known to have the AFL or AF for < 48 hours but also has a high risk of stroke based on the recommendations in the previous section, then intravenous (IV) heparin, low molecular weight heparin (LMWH) or a NOAC should also be given before or immediately after cardioversion (12). Patients who are low risk for stroke and have known AF or AFL for less than 48 hours do not require anticoagulation (12).
The Stable Patient: Rate Control
Most patients with AF or AFL who present to the ED will be alert and have a normal perfusing blood pressure and thus will not require immediate cardioversion (16). Rate control in stable patients is recommended by all three societies as an option for stable patients with AF or AFL with RVR (10, 12, 18, 19). A rapid tachycardia can eventually lead to cardiomyopathy and heart failure. The goal of rate control is to reduce these risks as well as minimize symptoms associated with a rapid heart rate (20).
Rate control in stable ED patients usually comprises a rate control agent, an OAC if necessary and delayed cardioversion after 4 weeks of OAC in high risk stroke patients (19). All 3 societies recommend administering a beta blocker or non-dihydropyridine calcium channel blocker for initial rate control in patients with symptomatic rapid AF or AFL in the ED setting (10, 12, 18, 19). Both agents are used in the acute management of rapid AF or AFL by slowing atrioventricular (AV) node conduction and by prolonging the AV node refractory period (17). Clinicians should be conscious of patients with hypotension when giving calcium channel blockers and they should never be given in patients with AF with associated pre-excitation (12). Amiodarone or digoxin can be given if beta blockers or calcium channel blockers are unsuccessful or contraindicated, as in the setting of heart failure and/or hypotension (10, 12, 14). Additionally, in patients with pre-excitation and AF, IV amiodarone and digoxin and should never be administered as per the AHA/ACC (12). However, the EHC notes that amiodarone or a class I anti-arrhythmic drug can be given in patients AF and pre-excitation (10, 12). Of course, any high risk stroke patients, as per mentioned above, should be anticoagulated during and after the patient is rate controlled (10, 12, 19).
The EHC and Canadian guidelines both recommend keeping a heart rate (HR) of < 100bpm (10, 14). However, the AHA/ACC recommends that as long as patients remain asymptomatic and maintain preserved left ventricular (LV) function, then a lenient rate control strategy of a HR < 110 can be employed (12).
The ACC/AHA, Canadian, and EHC guidelines on the rate control of rapid AF or AFL recommend either beta blockers or calcium channel blockers as first line agents in controlling ventricular rate and do not favor one over the other (10, 12, 19). Recent studies have been conducted on the efficacy of beta blockers versus calcium channel blockers but unfortunately, there is still insufficient and limited evidence to recommend one agent over the other (16, 21-23).
Finally, while it is generally recommended to avoid administering both IV beta blockers and calcium channel blockers to the same patient in the same time period (16), no studies could be found on using one IV agent if the patient takes a different oral agent at home.
The Stable Patient: Rhythm Control
With the rhythm control approach, attempts are made to cardiovert patients to sinus rhythm in the ED, either pharmacologically or electrically. All three societies have very similar protocols for rhythm management in stable patients, however the Canadian guidelines tend to favor earlier cardioversion in the ED in the appropriate patients (19).
The AHA/ACC recommends that patients with AF or AFL of unknown duration or > 48 hours be anticoagulated for at least 3 weeks before any electrical or pharmacologic cardioversion, regardless of the CHADS2-VASc score (12). However, if patients have AF or AFL of less than 48 hours duration and have a low thromboembolic risk, then anticoagulation or no anticoagulation may be considered. Long term anticoagulation therapy should be based on each patient’s stroke risk profile (12).
In the past several years, clinicians in Ottawa, Canada coined the term the “Ottawa Aggressive Protocol”, which consists of acute rhythm control and discharge home for hemodynamically stable patients with recent onset (<48 hours) rapid AF or AFL (24). Stiell and colleagues evaluated this protocol in 660 patient visits. Mean age of the patients was 64.5 years, 92.5% had AF and 4.9% had AFL. Using IV procainamide and/or electrical cardioversion, 96.8% of patients were discharged home and 93.3% remained in normal sinus rhythm. No anticoagulation was provided upon discharge for most patients (42). There were few adverse effects, including hypotension in 6.7%, bradycardia in 0.3%, and a 7 day relapse of 8.6%. There were no strokes and no deaths. The limitation to this study is that there was no long term follow up for patients. The authors also mention that further studies are needed to evaluate the risk of thromboembolism and the role of heparin and/or OAC in the setting of recent onset AF and AFL in the ED (24).
Additional studies have since evaluated the safety of urgent cardioversion without anticoagulation in patients with acute onset AF or AFL (25, 26). Overall, there is still a slight stroke risk and thus, anticoagulation should still be considered in high risk stroke patients with hemodynamically stable AF or AFL with RVR. These risk factors include diabetes, older age, heart failure, and female gender (27). Until further research is conducted, high risk patients should be anticoagulated as per society guidelines, regardless of the onset of AF or AFL.
Rate versus Rhythm Control
Several studies conducted in the last several years sought to determine if rate control or rhythm control is the better option for survival and quality of life. Overall, no significant differences in terms of quality of life, morbidity or mortality could be found between the two strategies (28-32). However, many patients are very symptomatic in AF or AFL and thus, both the AHA/ACC and EHC suggest that ultimately patients should be cardioverted in the long run (10,12). However, in terms of ED management, it is up to the clinician when determining whether patients should be rate controlled or cardioverted to normal sinus rhythm. The AHA/ACC, EHC and Canadian guidelines all provide excellent recommendations and should be referred to when managing the patient with AF or AFL with RVR in the ED.
Just as there are variations in ED management of AF, there are also regional variations in dispositioning patients with AF or AFL with RVR from the emergency department (33, 34). As previously mentioned, it has been popular in Canada to cardiovert and discharge stable patients home (42). Studies have shown that discharge from the ED is safe for most patients (7, 24). It has been suggested that patients should be admitted if they have another ED diagnosis such as pneumonia, CAD, heart failure, or failure to achieve rate or rhythm control (11, 16). Otherwise, patients are likely safe to be discharged home with close outpatient follow up (35).
AF and AFL with RVR are common ED diagnoses that require prompt evaluation and treatment as uncontrolled AF and AFL may ultimately lead to stroke, heart failure, and premature death (10). Emergency physicians are not only in the unique position to make the initial diagnosis, but also provide patients with treatments that may prevent stroke, heart failure and death.
Emergency providers should initially assess stability and evaluate and treat any reversible causes such as sepsis or hyperthyroidism. Workup for ACS may or may not be necessary and should be considered on a case by case basis. If eligible, unstable patients should be cardioverted and anticoagulated as per protocols mentioned above. There have been no clear studies demonstrating long-term differences between rate and rhythm control in stable patients and thus, emergency providers can consider either option. However, stroke risk should always be kept in mind with both the rate and rhythm approaches and the AHA/ACC, EHC or Canadian guidelines should be referred to when determining anticoagulation needs. Patients with preserved LV function should be rate controlled to at least < 110 bpm or < 100 bpm in all others. Data on beta blockers versus calcium channel blockers remains limited and therefore, either medication may be chosen based on a case by case basis. Currently, there is no validated data on patients who may be discharged home versus admitted, but certain patients may be candidates for discharge if they are hemodynamically stable and have no comorbid conditions. Clinicians should continue to use clinical judgement regarding disposition.
In conclusion, while the research on the management of AF and AFL is quite extensive, there are areas that still require further study, such as managing rate versus rhythm, anticoagulation needs, and disposition decisions. Future studies will need to be conducted, but in the meantime, the most recent society guidelines provide useful recommendations on the management of these difficult patients.
References / Further Reading
1. McCartney DE, Lomas O, Cahill TJ. Atrial fibrillation. InnovAiT 2015; 8 (8): 485-92.
2. Wolf, PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham study. Stroke 1991; 2: 983-88.
3. Hobbs FR, Taylor CJ, Geersing GJ, et al. European primary care cardiovascular society (EPCCS) consensus guidance on stroke prevention in atrial fibrillation (SPAF) in primary care. Eur J Prev Cardiol 2015; 2047487315571890.
4. Albers GW, Amarenco P, Easton JD, et al. Antithrombotic and thrombolytic therapy for ischemic stroke. The seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest 2004; 126: 483S-S128.
5. Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics-2014 update: a report from the American Heart Association. Circulation 2014: 129 (3): e28.
6. Al-Zaiti SS. Inflammation-induced atrial fibrillation: Pathophysiological perspectives and clinical implications. Heart Lung 2015; 44(1): 59-62.
7. Atzema CL, Austin Pc, Miller E, et al. A population-based description of atrial fibrillation in the emergency department, 2002 to 2010. Ann Emerg Med 2013; 62: 570-77.
8. Hamilton A, Clark D, Gray A, et al. The epidemiology and management of recent-onset atrial fibrillation and flutter presenting to the emergency department. Eur J Emerg Med 2015; 22 (3): 155-61.
9. Shenasa M, Shenasa H, Soleimanieh M. Update on atrial fibrillation. The Egyptian Heart Journal 2014; 66 (3): 193-216.
10. Camm AJ, Kirchhof P, Lip GY, et al. Guidelines for the management of atrial fibrillation. Eur Heart J 2010; ehq278.
11. Stiell IG, Clement CM, Brison RJ, et al. Variation in management of recent-onset atrial fibrillation and flutter among academic hospital emergency departments. Ann Emerg Med 2011; 57 (1): 13-21.
12. January C, Wann S, Joseph S, et al. 2014 AHA/ACC/HRS guidelines for the management of patients with atrial fibrillation: executive summary. J Am College Cardiol 2014.
13. Kuipers S, Klouwenberg PMK, Cremer OL. Incidence, risk factors and outcomes of new onset atrial fibrillation in patients with sepsis: a systematic review. Crit Care 2014; 18: 688.
14. Goralnick E, Bontempo LJ. Atrial fibrillation. Emerg Med Clin N Am 2015; 33: 597–612
15. Brown AM, Sease KL, Robey JL, et al. The risk for acute coronary syndrome associated with atrial fibrillation among ED patients with chest pain syndromes. Am J Emerg Med 25(5): 523-28.
16. Atzema CL, Barrett TW. Managing atrial fibrillation. Ann Emerg Med 2015; 65: 532-39.
17. Fromm C, Suau SJ, Cohen V, et al. Diltiazem vs Metoprolol in the management of atrial fibrillation or flutter with rapid ventricular rate in the emergency department. J Emerg Med 2015; 49 (2): 175-82.
18. Cairns JA, Connolly S, McMurtry S, et al. Canadian Cardiovascular Society atrial fibrillation guidelines 2010: prevention of stroke and systemic thromboembolism in atrial fibrillation and flutter. Can J Cardiol 2011; 27 (1): 74-90.
19. Verma A, Cairns JA, Mitchell LB, et al. 2014 focused update of the Canadian Cardiovascular Society guidelines for the management of atrial fibrillation. Can J Cardiol 2014; 30(10), 1114-30.
20. Camm AJ, Savelieva I, Lip GY. Rate control in the medical management of atrial fibrillation. Heart 2007; 93 (1): 35-38.
21. Scheumeyer FX, Grafstein E, Stenstrom R, et al. Safety and efficiency of calcium channel blockers versus beta blockers for rate control in patients with atrial fibrillation and no acute underlying medical illness. Acad Emerg Med 2013; 20 (3): 222-30.
22. Martindale JL, Silverberg M, Freedman J, et al. β-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): 150-54.
23. Katchi F, Nagabandi S, Shuster J, et al. Treating rapid atrial fibrillation in decompensated heart failure: metoprolol is superior to diltiazem. Cardiology 2014; 128: 466.
24. Stiell 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): 181-91.
25. Airaksinen KE, Gronberg T, Nuotio I, et al. Thromboembolic complications after cardioversion of acute atrial fibrillation: the FinCV (FinnishCardioVersion) study. J Am Coll Cardiol 2013; 62 (13): 1187-92.
26. Nuotio I, Hartikainen JE, Gronberg T, et al. Time to cardioversion for acute atrial fibrillation and thromboembolic complications. JAMA 2014; 312 (6): 647-49.
27. Stiell IG, Healey JS, Cairns JA. Safety of urgent cardioversion for patients with recent-onset atrial fibrillation and flutter. Can J Cardiol 2015; 31 (23): 9e241.
28. Wyse DG, Waldo AL, DiMarco JP, et al. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002; 347 (23): 1825-33.
29. AFFIRM investigators. Clinical Factors that influence response to treatment strategies in atrial fibrillation: the atrial fibrillation follow-up investigation of rhythm management (AFFIRM) study. Am Heart J 2005; 149 (4): 645-49.
30. Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med 2002; 347 (23): 1834-40.
31. Roy D, Talajic M, Nattel S, et al. Rhythm control versus rate control for atrial fibrillation and heart failure. N Engl J Med 2008; 358 (25): 2667-77.
32. de Denus S, Sanoski CA, Carlsson J, et al. Rate vs rhythm control in patients with atrial fibrillation: a meta-analysis. Arch Intern Med 2005; 165 (3): 258-62.
33. Barrett TW, Jenkins CA, Self WH. Validation of the Risk Estimator Decision Aid for Atrial Fibrillation (RED-AF) for predicting 30-day adverse events in emergency department patients with atrial fibrillation. Ann Emerg Med 2015; 65 (1): 13-21.
34. Barrett TW, Self WH, Jenkins CA, et al. Predictors of regional variations in hospitalizations following emergency department visits for atrial fibrillation. Am J Cardiol 2013; 112(9): 1410–16.
35. Atzema CL, Austin PC, Chong AS, et al. Factors associated with 90 day death after emergency department discharge for atrial fibrillation. Ann Emerg Med 2013; 61 (5): 539-48.
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