Atrial fibrillation (AF) is encountered with significant frequency in the Emergency Department (ED). In fact, atrial fibrillation is the single most common arrhythmia seen in the ED. As per the 2020 CCS review, AF resulted in 8815 same-day procedures, 76 964 ED visits, 25 892 acute care admissions in Canada in a given year.1 The CAEP 20212 guidelines were created in consensus with academic, community ED physicians and cardiologists from multiple sites across Canada. This post will review the literature leading to the new best practice guidelines and highlight major updates since the last management guidelines were posted in 2018 while identifying sources of practice variation.
This blog post will review the following and apply guidelines to common cases seen below:
- New safe rhythm control timelines
- Rate control and pitfalls
- Stroke prevention
Case 1: Ms. Rapide is a 63 yo female with hx of HTN, CAD with previous PCI (2014) and peripheral vascular disease. Her medications include amlodipine and ASA. She presents to your ED with a clear onset of palpitations 15 hours ago.
Case 2: Mr. Beaucoeur is a 50-year-old male with hx of EToH use disorder and hypothyroidism presenting to your ED with a first-time presentation of paroxysmal atrial fibrillation within 48 hours.
CAEP 2021 Atrial Fibrillation/Flutter Guidelines
Management of patients with atrial fibrillation / flutter can be broken down into four steps:
- Is this a primary or secondary arrhythmia?
- Is the patient stable or unstable?
- Has the patient been adequately anticoagulated?
- Select appropriate management
STEP 1 – PRIMARY VS SECONDARY ARRHYTHMIA
Acute, symptomatic atrial fibrillation / flutter is a complex condition that may be caused by an isolated electrophysiological disorder (primary arrhythmia) or is a symptom of an underlying disease process (secondary arrhythmia, note that this is less common). Some etiologies leading to secondary atrial fibrillation include: sepsis, hemorrhage, pulmonary embolism, heart failure, ACS, thyrotoxicosis, cardiac and non-cardiac surgery, acute infections, catecholamine excess and mitral valve disease.1 The treatment pathway for atrial fibrillation will vary depending on the presence of an underlying cause which can be identified on history and physical examination.
Complete a thorough history and physical exam to assess for the following underlying secondary condition1:
- Decompensated Heart Failure: increasing weight, orthopnea, dyspnea, pitting edema, adventitious lung sounds suggestive of pulmonary edema, jugular venous distension. Global decreased LV function and B lines on POCUS
- Hypovolemia: recent illness or decreased PO intake, dry mucous membranes, decrease urine output
- Pulmonary Embolism: VTE history or risk factors, dyspnea, clear lung sounds, enlarged RV on POCUS, septal flattening, McConnell’s sign
- ACS: Cardiac risk factors, Chest pain, diaphoresis, N/V
- Sepsis: Clinical Assessment
The following signs and symptoms may suggest that AF / AFL may more likely be secondary to underlying medical cause and therefore may require additional workup12:
- No palpitations reported
- Lack of sudden onset of symptoms
- Dyspnea present
- Persistent retrosternal chest pain
- No prior history of ED cardioversions
- Permanent atrial fibrillation on OACs
- HR < 150
Work-up / Investigations
Upon presentation to the ED, the workup required for patients with AF / AFL can be variable. CCS (2020) suggests that all initial evaluation of patient’s newly diagnosed with AF AFL include: ECG, TTE and basic laboratory investigations – but what about initial presentation to ED? Investigations in these patients is guided based on the potential for identifying a reversible cause and baseline to guide anticoagulation as required where it is suggested to complete CBC, electrolytes, extended electrolytes, creatinine / BUN, coagulation studies and TSH. In the setting where there is suspicion for cardiogenic shock, LFTs, VBG and lactate is recommended.
It is worth noting variation in guideline recommendations, as the CAEP 2021 best practice checklist does not suggest ordering coagulation studies, TSH or TEE.
There is much discussion to be had regarding troponin levels. In general, patients with AF / AFL can be expected to have an elevated troponin due to increased cardiac demand from the arrhythmia. An unpublished review of charts at the University Health Network in Toronto showed that 86% had their troponin drawn, 14% had a positive test and 5% were treated with ACS.4 Of note, most of those treated for ACS had hypotension, signs of heart failure or ECG changes after rhythm or rate control.5 Briefly, having a slightly positive troponin in an asymptomatic patient with AF/AFL can be problematic as it may lead to further delays to discharge and, potentially, unwarranted treatment of ACS. The bottom line is that routine testing for troponin is not recommended in these patients UNLESS there is a clinical suspicion for underlying ACS.
Management of Secondary AF / AFL
In 2014, Scheuermeyer et al. published a retrospective study in ACEP comparing 416 patients with “complex” AF / AFL. What they found was that active management (cardioversion or rate control) produced major adverse events (13.1%, 95% CI 7.4%-20.3%) including intubation, CPR, death, stroke, and new hypotension requiring vasopressors in patients with secondary AF.9 This study has led to the primordiality of focusing on resuscitation and treatment of the acute illness rather than control of rate or rhythm. Ultimately, treatment for secondary AF / AFL is guided by the underlying cause that was identified given that their arrhythmia may be transient as a compensatory mechanism for their underlying condition. Cardioversion is therefore avoided in these patients due to the potential for harm. Furthermore, aggressive rate control is not recommended as this may compromise the patient’s compensatory abilities for increasing cardiac output.
STEP 2 – PATIENT STABILITY
The next step is to identify your unstable patients. Of note, instability due to primary atrial fibrillation and atrial flutter is uncommon except for AF with RV pre-excitation (WPW). Any patients identified to have any of the following signs of cardiovascular instability require urgent electrical cardioversion12:
- Hypotension (sBP <90mmHg) and Signs of shock (altered mental status); or
- Pulmonary edema (significant dyspnea, crackles and hypoxia; or
- Cardiac ischemia (severe chest pain, ST depression (<2mm) despite therapy.
It is important to note that ST depression in atrial fibrillation is common and often due to rate-related ischemia in the setting of CAD; however, this should not be considered unstable unless the patient has anginal chest pain or if the ST segments do not resolve once the patient is no longer in atrial fibrillation.
STEP 3 – SAFETY TO CARDIOVERT PRIMARY ARRHYTHMIA
Once a patient has been identified as more stable after assessing criteria from Step 2, an assessment should be performed to determine the safety of cardioverting a primary arrhythmia. The AFFIRM trial (2002) fathered the dogma of rate vs rhythm control having no significant difference in terms of morbidity and quality of life outcomes however, those who were unlikely to tolerate being in AF were excluded from the study.18 Furthermore, the RAFF 3 showed us that this method reduces length of stay in ED and utilizes less hospital resources.14 For this reason, unless there is a compelling reason to do so otherwise, rhythm control is the preferred method of treatment when safety is determined. Ultimately, when deciding to proceed with rate vs rhythm control, an assessment of your patient’s eligibility is necessary in preventing any risk of a serious embolic event (SEE). Generally, thromboembolic risk peri-cardioversion can be conceptualized by 2 mechanisms:
- Generation of thrombi during persistent AF with embolization after restoration of organized atrial contraction
- Atrial stunning which is responsible for thrombi post-cardioversion regardless of modality (pharmacological, electrical, spontaneous).2
Given the high risk of stroke in certain populations, the new CAEP 2021 Guidelines provide recommendations to guide safe cardioversion recommendations as outlined below2:
Finally, determination of adequate anticoagulation for 3 weeks is based on MD judgement but also confirmation of compliance on history for DOAC and INR > 2 on current or most recent test for Warfarin.12
STEP 4A – MANAGEMENT – RHYTHM CONTROL
Pharmacologic vs Electrical Cardioversion
For either method of cardioversion, chemical or electrical. The best practice checklist suggest that either is acceptable, if one does not work, simply try the other. They also suggest no rate control pre-treatment to rhythm control as this is ineffective and delays treatment.12 When considering chemical or electrical cardioversion, it is recommended to discuss the options with the patients and review previous visits outlining the most successful method if the patient has a history of paroxysmal AF. The RAFF2 trial suggests that a trial of chemical cardioversion (with procainamide) prior to electrical cardioversion worked in 52% of patients and can avoid a resource intensive procedural sedation. However, generally the drug-shock group vs the shock-only group had similar effective rates (96% vs 92%) (absolute difference 4%, 95% CI 0-9, p=0.07).10
To perform chemical cardioversion, Class I or III antiarrhythmics are commonly employed:
To perform chemical cardioversion, Class I or III antiarrhythmics are commonly employed:
To perform electrical cardioversion:
To perform electrical cardioversion:
STEP 4B – MANAGEMENT – RATE CONTROL
Rate control can be performed in the ED if cardioversion is deemed unsafe as per the above guidelines. Rate control may also be considered based on patient or physician preference in the stable and minimally symptomatic patient. Given the potential harm associated with rate control agents in patients with new or existing heart failure, one may enhance the sensitivity of their therapeutic approach by looking at a recent echocardiogram report, or performing bedside PoCUS to assess LV function. In patients with grossly reduced LV function, rate control should be approached cautiously.
When considering rate control, your target resting heart rate is <100 bpm and <110 bpm with walking.12 A study by Wong et al. sought to describe ED rate control management and outcomes in patients with AF who were not successfully managed by rhythm control or not attempted rhythm control. Of note, they found that only 59.0% of patients achieved a rate control with resting HR < 100 at ED discharge and 47% of patients were managed with unsuitable choice of agents (2.6%), route of administration (27.4%), underdoses (6.0%), overdosed (3.4%) or administered beyond recommended time frame (7.7%).17
Generally, calcium channel blockers (CCB) and beta blockers (BB) are first line therapies for rate control in the ED. Should the patient be on a home dose of CCB or BB prior to their ED visit, it is best to start with the medication from the same drug class initially. Ultimately, there is no evidence of superiority of either class and should there be challenges with achieving rate control with one class, the other class is a good substitute. An exception to this management algorithm is if the patient has HF where CCB and BB are contraindicated due to risk of myocardial suppression and subsequent cardiogenic shock. In such circumstances, the rate control medication of choice is digoxin.
Select the below tabs for dosing and indications of each medication.
Calcium channel blocker
It is important to monitor for patients who may have diagnosed or undiagnosed WPW, pre-excitation. When evaluating an ECG, assess for a wide QRS which may either be secondary to either 1) AF with aberrancy (+RBBB or LBBB) with classic morphological QRS, or 2) AF with pre-excitation (WPW). WPW should also be considered when the QRS morphology is bizarre, polymorphic or much faster than typical AF (HR approaching 300).12 In the event that WPW is identified the following management changes should be considered:
- Do not give any of the ABCD drugs (adenosine, beta blocker, calcium channel blocker or digoxin)
- This will block the AV node thereby sending impulses down the accessory bypass tract which has no slowing mechanism resulting in V. tachycardia
- Electrical cardioversion is usually required
- Procainamide IV can be considered if stable12
Stroke prevention is guided with consideration of the patients CHADS-65 score: CHF history, Hypertension history, Age ≥ 65, Diabetes mellitus history and Stroke / previous TIA symptoms. Both the CCS and CAEP guidelines recommend that an oral anticoagulant be started by the Emergency Physician.
Clare et al. (2019) highlighted the necessity of discharge prescriptions for anticoagulation where 67.8% of patients who had a Rx leaving the ED had a filled a prescription vs 37.2% of those leaving the ED without an initial prescription.3 Looking a little closer to home, Wong et al. (2020) demonstrated that 11.5% of CHADS-65 positive patients left the ED without a OAC prescription.16
There are 3 major groups to review in regards to stroke prevention or SEE risk reduction for atrial fibrillation patients upon discharge from the ED:
If CHADS-65 Positive (> 1 criteria)
- Full anticoagulation prior to discharge is required.
- DOACs preferred over warfarin
- Warfarin required if mechanical valve, rheumatic mitral stenosis, severe renal impairment (CrCl <30ml/min)12
- If patient is CHADS-65 positive with CAD:
- If stable CAD, discontinue ASA and start OAC only
- If other anti-platelet or recent PCI <12 months and still on DAPT:
- Discuss with cardiology on call
- Typical management includes keeping the P2Y12 and starting a OAC while discontinuing the ASA.
If CHADS-65 Negative with CAD / vascular / aortic disease
- Thrombosis Canada guidelines suggest starting patient on ASA 81mg PO daily
- These individuals have increased stroke risk that warrants prevention (RR 22% vs placebo)12
If CHADS-65 Negative
- There is some controversy of managing patients with anticoagulation post-cardioversion if they are CHADS-65 negative.
- Generally, CHADS-65 negative patients carry a very low stroke risk and there is no evidence for or against anticoagulation.13
- The CCS updated their guidelines suggesting that unless there is a strong contraindication, all patients undergoing cardioversion in the ED should be anticoagulated for 4 weeks on OAC or warfarin (weak recommendation, low quality).13
- The CAEP 2021 guideline highlights that 4 weeks of anticoagulation is based on low quality evidence, and instead recommend shared decision making with your patient.
- Bottom line recommendations:
- Consider anticoagulation for 4 weeks post-cardioversion for CHADS-65 negative after consideration of risks vs benefits with patient.
- The risk of bleeding and stroke is low in CHADS-65 negative patients on short course of OAC.12
- Particular consideration for OAC x 4 weeks post-cardioversion should be made for those with vascular disease or aortic disease who we know have an increased risk of SSE as per the FinCV trial. We may suggest they start the OAC and then transition to ASA the following month.\
The following anticoagulation medications can be used on discharge in the ED setting:
- DOACs are the preferred anticoagulant:
- Dabigatran 150mg BID
- Dose change to 110mg BID for age >80 yo or 75yo with bleeding risk
- Rivaroxaban 20mg daily
- Dose change to 15mg daily if CrCl 30-49ml/min
- Apixaban 5mg BID
- Dose change to 2.5mg BID if >2 of 1) Cr >133umol/L, 2) Age>80 yo, or 3)BW <60kg
- Edoxaban 60mg daily
- Dose change to 30mg daily if CrCl 30-50ml/min or body weight <60kg
- Dabigatran 150mg BID
- Starting dose 5mg daily (or 1-2mg if frail, low weight or Asian descent)
- Remember to arrange for INR testing after 3-4 doses of warfarin as an outpatient
- Subsequent dosing needs to be communicated with the patient on day of INR test 12