EM guidemap - Atrial fibrillation

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Introduction and definitions

Clinical evaluation and diagnostic testing

Clinical management of AF in an ED setting

Appendix
Introduction and definitions

- this guidemap is primarily a distillation of the most essential information from the "ACC/AHA/ESC Guidelines for the Management of Patients with Atrial Fibrillation", which was published in 2001 - and this guidemap provides clinical information which is most likely to be useful to emergency physicians practicing medicine in a hospital-based ED setting

- the distilled information has been reduced to brief statements and multiple "quick-to-read" tables and algorithms, and the hyperlinks should help make the "memory-jogging" information more readily accessible

- this guidemap is mainly focused on issues that are relevant to a practicing emergency physician => consult the complete version of the ACC/AHA/ESC guidelines for further details regarding the long-term outpatient management of AF

Definitions from the ACC/AHA/ESC guidelines

Atrial fibrillation = A supraventricular tachyarrhythmia characterised by uncoordinated atrial activation, manifested on the ECG by rapid oscillations or fibrillatory waves that vary in size, shape and timing; and associated with an irregular, frequently rapid, ventricular response when AV function is intact

- a rapid, irregular, wide QRS complex tachycardia suggests AF conducted over an accessory pathway (especially if the ventricular rate is > 200 bpm) or associated bundle-branch block

Atrial flutter = A supraventricular tachyarrhythmia characterised by coordinated atrial activation, with saw - tooth flutter waves at a rate of 240 - 340 bpm and flutter (f) waves inverted in leads II, III and aVF and upright in V1 (occasionally the opposite pattern with upright f waves in the inferior leads and an inverted f wave in lead V1 is found)

- 2:1 block is often present in atrial flutter, and the ventricular rate is then usually 120 - 160 bpm

- atrial flutter can degenerate into AF, or alternate with AF

Lone atrial fibrillation = Variably defined as AF occurring in patients < 60 years of age in the absence of clinical or echocardiographic evidence of cardiopulmonary disease

(* in younger patients, approximately 30 - 45% of paroxysmal, and 20 - 25% of persistent AF cases occur as lone AF)

Idiopathic atrial fibrillation = Atrial fibrillation of uncertain etiology irrespective of the age of the patient or the presence of cardiopulmonary disease

Recurrent atrial fibrillation = Two-or-more episodes of AF

Paroxysmal atrial fibrillation = Recurrent AF which spontaneously resolves (self-terminating)

(* by definition - paroxysmal AF must terminate spontaneously within 7 days, but most resolve within 24 hours)

Persistent atrial fibrillation = First episode AF (or recurrent AF)  that requires termination by cardioversion

Permanent AF = AF that cannot be terminated by cardioversion, or maintained in sinus rhythm after cardioversion

(* the above definitions come from the ACC/AHA/ESC guidelines and apply to AF that lasts > 30 seconds + AF that is unrelated to a reversible precipitating cause [eg. recent alcohol intake, sympathomimetic drug intoxication, recent AMI, recent cardiac surgery, myocarditis, hyperthyroidism and acute pulmonary disease]; note that according to the ACC/AHA/ESC guidelines, AF is classified as persistent AF even if it has been present for > 1 year - if no attempt has been made to terminate the arrhythmia, and it becomes classified as permanent AF if cardioversion fails to convert the arrhythmia or if cardioversion is not attempted - ??? I regard the classification system as poorly defined, and it is not clear to me when persistent AF becomes permanent AF)

Acute atrial fibrillation = Atrial fibrillation < 48 hours in duration

Chronic atrial fibrillation = Atrial fibrillation > 48 hours in duration

(* note that these definitions are arbitrary, and note that there are many different definitions in the medical literature; from an emergency physician's perspective it is not possible to differentiate paroxysmal AF from persistent AF when a patient presents to the ED with new-onset AF => it may be better conceptually to divide patients into two groups - AF duration < 48 hours, and AF duration > 48 hours [which also includes patients with atrial fibrillation of unknown duration] - because it is acceptable to electively cardiovert patients with AF < 48 hours, while cardioversion needs to be delayed if the AF duration is unknown, or ill-defined, or > 48 hours unless a TEE is negative for left atrial thrombi)

- AF can negatively affect cardiac output by three mechanisms

- long lasting, persistently fast AF can adversely affect atrial function (tachycardia-induced atrial cardiomyopathy) and also produce a dilated ventricular cardiomyopathy; heart failure secondary to tachycardia-induced cardiomyopathy can also be the presenting feature of AF

- AF predisposes to systemic thromboembolism, and acute ischemic stroke is due to emboli arising within the left atrium in 65 - 75% of cases, while the other 25 - 35% of cases are due to associated co-morbid diseases eg. hypertension, carotid artery disease or atheromatous pathology in the proximal aorta

(* the proportion of all strokes due to AF varies with age;  increasing from ~ 10% in the 60 - 70 year age group to ~ 30% in the 80 - 90 year age group)

- conversion of AF to sinus rhythm has the advantage that it decreases, or eliminates, the need for long-term oral anticoagulants, which is associated with bleeding complications in elderly patients

- acute temporary causes of AF include alcohol abuse, hyperadrenergic states or sympathomimetic drug intoxication, cardiac or non-cardiac surgery, electrocution, myocarditis, PE, chronic pulmonary disease, and hyperthyroidism

- 90% of AF is due to organic heart disease, non-valvular heart disease accounts for 50 - 80% of those cases

- some common cardiovascular causes of AF include valvular heart disease (especially mitral stensosis), coronary artery disease, cardiomyopathy, hypertensive heart disease and heart  failure

- neurogenic AF is rare, and can be vagal (suggested by a slow ventricular rate) or adrenergic (suggested by a fast ventricular rate > 150 bpm in the absence of pre-excitation) in origin

- symptoms of AF depend on the duration of AF, ventricular rate, underlying cardiac function and individual patient perception; common symptoms include palpitations, lightheadedness, fatigue, dyspnea, or syncope

(* syncope usually implies sinus node dysfunction, valvular aortic stenosis, HCM or an accessory pathway)

- the management of new-onset AF is primarily focused on rate control therapy; however, certain AF patients may require specific therapy

- the choice of rate controlling drugs depends on the presence, or absence, of LV dysfunction (* beta blockers are often the drugs of choice in patients with a hyperadrenergic state or with increased sympathetic tone eg. post CABG, hypoxia, PE, myo-pericarditis, thyrotoxicosis)

- anti-arrhythmic drugs are often used to prevent recurrences of AF

(* see the appendix for recommended ACC/ECC algorithms)
 
Clinical evaluation and diagnostic testing

- the physical examination may suggest AF on the basis of an irregular pulse, irregular jugular venous pulsations, and a variation in the loudness of the first heart sound

- the ACC/AHA/ESC guidelines recommend the following minimum clinical evaluation, and additional testing, of patients with AF
 

Minimum clinical evaluation

1. History and physical examination, to define 

  • The presence and nature of symptoms associated with AF
  • The clinical type of AF (first episode, paroxysmal, persistent, or permanent)
  • The onset of the first symptomatic attack or date of discovery of AF
  • The frequency, duration, precipitating factors, and modes of termination of AF
  • The response to any pharmacological agents that have been administered
  • The presence of any underlying heart disease or other reversible conditions (eg, hyperthyroidism or alcohol consumption)
2. Electrocardiogram, to identify 
  • Rhythm (verify AF)
  • LV hypertrophy
  • P-wave duration and morphology or fibrillatory waves
  • Preexcitation
  • Bundle-branch block
  • Prior MI
  • Other atrial arrhythmias
  • To measure and follow the RR, QRS, and QT intervals in conjunction with antiarrhythmic drug therapy
3. Chest radiograph, to evaluate 
  • The lung parenchyma, when clinical findings suggest an abnormality
  • The pulmonary vasculature, when clinical findings suggest an abnormality
4. Echocardiogram, to identify 
  • Valvular heart disease
  • Left and right atrial size
  • LV size and function
  • Peak RV pressure (pulmonary hypertension)
  • LV hypertrophy
  • LA thrombus (low sensitivity)
  • Pericardial disease
5. Blood tests of thyroid function
  • For a first episode of AF, when the ventricular rate is difficult to control, or when AF recurs unexpectedly after cardioversion
Additional diagnostic testing

One or several tests may be necessary 

1. Exercise testing

  • If the adequacy of rate control is in question (permanent AF)
  • To reproduce exercise-induced AF
  • To exclude ischemia before treatment of selected patients with a type IC antiarrhythmic drug
2. Holter monitoring or event recording
  • If diagnosis of the type of arrhythmia is in question
  • As a means of evaluating rate control
3. Transesophageal echocardiography
  • To identify LA thrombus (in the LA appendage)
  • To guide cardioversion
4. Electrophysiological study
  • To clarify the mechanism of wide-QRS-complex tachycardia
  • To identify a predisposing arrhythmia such as atrial flutter or paroxysmal supraventricular tachycardia
  • Seeking sites for curative ablation or AV conduction block/modification

 
Clinical management of AF in an ED setting

New-onset AF

- an emergency physician needs to be able to appropriately answer many important questions when dealing with a new-onset AF patient in the ED

1) Is the patient clinically stable, or is emergent electrical cardioversion indicated?
2) Does the patient need immediate rate control therapy to control the ventricular rate?
3) Does the patient have a reversible, or precipitating, cause of the AF?
4) Does the patient need to be admitted to hospital?
5) Is the patient a candidate for expedited elective cardioversion in the ED?
6) Does the patient need to be anticoagulated immediately +/- is long-term anticoagulation indicated?

1) Is the patient clinically stable, or is emergent electrical cardioversion indicated?

Immediate electrical cardioversion is indicated for paroxysmal AF that is deemed unstable at the time of ED presentation - AF with a rapid ventricular response, which is primarily responsible for any symptomatic hypotension, angina or heart failure that is unresponsive to pharmacological measures

2) Does the patient need immediate rate control therapy to control the ventricular rate?

- rate control therapy is indicated if the patient remains in AF and the ventricular rate is  > 100 bpm

3) Does the patient have a reversible, or precipitating, cause of the AF?

- the patient should not be labelled as having paroxysmal AF or persistent AF without first excluding reversible, precipitating causes of the AF

An emergency physician should first consider, and exclude, precipitating or reversible causes of AF due to recent heavy alcohol intake, acute coronary ischemia, myo-pericardial inflammation, valvular heart disease, electrolyte imbalance, sympathomimetic drug abuse, adrenergic or vagal influences, recent surgery (especially cardiac surgery),  hyperthyroidism, acute pulmonary disease or PE - and manage the patients accordingly

(* see the appendix for a more comprehensive list of conditions associated with AF)

4) Does the patient need to be admitted to hospital?

- in the recent past, patients with new-onset AF were routinely admitted to hospital to r/o AMI or other serious pathology => however, further studies have demonstrated that the likelihood of an AMI is very small if there are no clinical or ECG signs of an AMI at the time of ED presentation

- routine hospital admission is often necessary if:-

- low risk criteria for admission include:- - a policy of using a 24 hour observation trial of rate control therapy in hospital before considering the use of expeditious elective cardioversion, has the advantage that 50 - 80% of paroxysmal AF resolves within 24 hours, and those patients will not require further therapy

- many cardiologists choose to discharge asymptomatic AF patients with well-controlled ventricular rates, on rate controlling drugs + oral anticoagulants, and arrange for outpatient follow-up => delayed elective cardioversion therapy is considered if the AF persists

5) Is the patient a candidate for expedited elective cardioversion in the ED?

- expedited elective cardioversion can be performed in the ED if the patient has new-onset AF of < 48 hours duration, and if a TEE is negative for left atrial thrombi in patients with AF > 48 hours duration

(*see the algorithm for the ED management of new-onset AF based on the duration of AF)

6) Does the patient need to be anticoagulated immediately +/- is long-term anticoagulation indicated?

- it is often recommended that heparin should be administered in the ED if a AF patient is going to be admitted to hospital for expedited elective cardioversion (AF duration < 48 hours, or AF duration > 48 hours with a negative TEE study)

(* it is unclear, from reading the EBM literature, for how long heparin should be used if the AF duration is < 48 hours and the patient is not going to require long-term anticoagulation [medical literature suggestions include: 1) a single IV dose of heparin just prior to cardioversion, 2) a few bolus doses of IV heparin every 4 - 6 hours, 3) continuous heparin infusion to maintain the PTT in the therapeutic range of aPTT = 1.5 - 2.5 and 4) a few days of LMWH  therapy]; for AF duration > 48 hours with a negative TEE study, heparin by infusion to achieve an aPTT of 1.5 - 2.5 should be continued until the INR is in the therapeutic range because oral anticoagulants should always be used for 4 weeks after cardioversion; standard heparin dose = 80mg/kg loading dose followed by 18mg/kg/hr maintenance dose => adjust dose q 6h based on the aPTT)

- it is often recommended that heparin should also be routinely used for AF patients (AF duration of < 48 hours), who are going to be cardioverted in the ED using either pharmacological or electrical cardioversion - irrespective of whether the cardioversion is emergent or early elective (expedited elective)

(* the ACC/AHA/ESC guidelines do not offer specific advice on whether heparin should be given in this situation - the guidelines merely state that short term anticoagulation is optional [level of evidence: C] ; many authors reviewing the subject of antithrombotic therapy in AF suggest that a single dose of heparin should be given before the cardioversion procedure; the Fifth ACCP Consensus Conference on antithrombotic therapy in AF also suggests that short term anticoagulation therapy should follow the single heparin bolus in the following situations: 1) patients who have been in AF for a few days but develop acute hemodynamic instability; 2) patients in whom recurrent AF is likely because of past experience or mitral valve disease; and 3) individuals who, following cardioversion, demonstrate spontaneous echo contrast in the left atrium or left atrial appendage)

- patients with AF duration > 48 hours, who are candidates for delayed elective cardioversion, should routinely be treated with oral anticoagulants for 3 weeks prior to elective cardioversion, and for 4 weeks after elective cardioversion; LMWH may be beneficial for the first few days of outpatient oral anticoagulant therapy until the INR is in the therapeutic range (especially recommended if the patient has a high risk of thromboembolism)

- long-term anticoagulation is recommended for patients with permanent AF, or recurrent paroxysmal/persistent AF, because the risk of thromboembolism is similar

- long-term anticoagulation is usually not necessary for first-episode paroxysmal AF patients, who spontaneously convert to sinus rhythm within hours of AF onset, or first-episode persistent AF patients who are cardioverted in the ED (if the AF duration is < 48 hours) - unless the intrinsic risk of thromboembolism is very great (multiple high risk factors for thromboembolism are present)

Cardioversion

Emergent cardioversion

Immediate electrical cardioversion is indicated for patients with paroxysmal AF + rapid ventricular response + evidence of angina/AMI or heart failure or hypotension, which does not respond promptly to pharmacologic measures - starting with a synchronized DC shock of 200J (appropriately smaller doses for biphasic waveform defibrillators) => 360J if no response to the first shock, and repeated prn => ibutilide (1mg) may be used to decrease the defibrillatory threshold in patients not responding to high dose synchronised DC shocks

Elective cardioversion

- reasons for elective cardioversion of persistent AF to sinus rhythm include:-

(* it is questionable whether long-term use of anti-arrhythmic drugs is warranted to maintain sinus rhythm for the sole purpose of preventing atrial remodelling if the patient's heart rate can be effectively controlled by rate-controlling drugs; it is still uncertain to what degree restoration of sinus rhythm decreases the long-term risk of thromboembolism if all other thromboembolism risk factors remain present)

- elective cardioversion is usually indicated if the symptoms of AF are unacceptable, although some cardiologists routinely use cardioversion to accelerate the restoration of sinus rhythm in all patients with a first-episode of AF (irrespective of the presence and/or degree of disabling symptoms) - because those cardiologists believe that "AF begets AF", and they believe that the longer the patient remains in AF, the more difficult it will be to convert the AF to sinus rhythm as a result of the electrophysiological remodelling process

(* the evidence is still not compelling that patients who are cardioverted to sinus rhythm do better over the long-term than asymptomatic AF patients,  who are easily, safely and adequately anticoagulated and who have well controlled ventricular rates -- because AF patients converted to sinus rhythm frequently relapse into AF and they may require serial electrical cardioversion procedures and aggressive anti-arrhythmic therapy to maintain sinus rhythm => further studies may help clarify this therapeutic dilemma)

- electrical cardioversion is the "gold standard" approach to cardioversion and has a success rate of ~ 80 - 90% if the AF is acute

Expedited elective electrical cardioversion can be performed in the ED by an emergency physician if the duration of AF is < 48 hours, and there are no contraindications (eg. left ventricular dysfunction, mitral valve disease, previous history of thromboembolism, or high risk of thromboembolism)

- electrical cardioversion is not indicated for patients who alternate between sinus rhythm and AF over short periods of time, and multiple cardioversion attempts should be avoided if the patient relapses to AF after a short period of sinus rhythm following temporarily successful electrical cardioversion

- electrical cardioversion usually requires an initial DC shock of 200J or greater; the standard ACLS-recommended dose of 100J is often insufficient

- the serum electrolytes, serum magnesium and serum digoxin level should be checked prior to electrical cardioversion => electrical cardioversion can precipitate VT/VF in patients with hypokalemia and/or digoxin-toxicity, and lower DC energy levels should be used in digitalized patients

- electrical cardioversion is safe in patients with implanted pacemakers or defibrillators if the paddles are placed as distant from the device as possible => the device should be interrogated immediately before and after cardioversion to verify appropriate function

- transient ST-segment elevation can occur after electrical cardioversion and does not imply cardiac ischemia

- a rise in cardiac marker levels does not imply cardiac muscle damage

- failure of electrical cardioversion occurs in 10 - 25% of cases when used without prior phamacological anti-arrhythmia therapy, that is specifically intended to decrease the electrical defibrillatory threshold

- starting pharmacological anti-arrhythmia therapy before electrical cardioversion can enhance cardioversion by DC shock and reduce the rate of immediate AF recurrence => it may therefore be appropriate to first establish therapeutic plasma concentrations of the chosen anti-arrhythmic drug at the time of cardioversion, and also maintain the plasma levels for a few weeks thereafter to help decrease the rate of subacute (within two weeks) AF recurrence

(* pretreatment with pharmacological agents is most appropriate in patients who have previously failed to respond to electrical cardioversion, and in those who developed immediate or subacute recurrence of AF)

- drugs that enhance DC cardioversion and prevent immediate recurrence of AF include:-

(* after conversion to sinus rhythm, patients receiving drugs that prolong the QT interval should probably be observed in the hospital for 24 - 48 hours to evaluate the effects of heart rate slowing and to detect and promptly treat torsade des pointes - as recommended by the ACC/AHA/ESC guidelines)

- drugs with uncertain effect on electrical cardioversion rates include:-

Pharmacological cardioversion in the ED is an alternative to electrical cardioversion for stable patients

- pharmacological cardioversion avoids the need to use deep sedation, which is required for electrical cardioversion, but it has the potential disadvantage of precipitating torsade des pointes VT or other serious arrhythmias in a small percentage of cases => the patient therefore has to be monitored for 6 - 8 hours after cardioversion, while electrically cardioverted patients can be safely discharged after 1 hour if they are stable

- pharmacological cardioversion is most likely to be effective within 7 days of AF onset, and the success rate varies between ~ 40 - 70%; the actual success rate depends on the particular drug used and the duration of AF; all the recommended drugs are much more effective for AF of recent onset

(* there are few head-to-head studies comparing different cardioverting drugs, and variability in the duration of AF +/- types of underlying cardiac disease makes accurate comparisons of "drug effectiveness" difficult; also, the use of pharmacological cardioversion in the ED for patients with AF duration < 48 hours obviously "pre-selects" a group of AF patients, who have a high incidence of paroxysmal AF, which may have a rate of spontaneous termination of  > 50% without the use of cardioverting drugs)

The choice of pharmacological cardioversion should primarily be based on safety concerns, and treatment of precipitating or reversible causes of AF should precede the initiation of pharmacological cardioversion

- anticoagulation and rate control should be established before initiating pharmacological cardioversion

- there is no single drug that is regarded as the drug-of-choice for pharmacological cardioversion in the ED =>  ibutilide is a frequent choice in the EDs of the USA, although oral propafenone is steadily gaining favor in the USA
 

Drugs used for pharmacological cardioversion in-hospital
Drug Route of adminstration Dosage Potential adverse effects
 Amiodarone Oral  Inpatient - 1.2 - 1.8g /day in divided dose until 10g total, then 200 - 400mg/day maintenance or 30mg/kg as single dose Hypotension, bradycardia, QT prolongation, torsade des pointes, GI upset, phlebitis, constipation
  IV 5 - 7mg/kg over 30 - 60 min, then 1.2 - 1.8g per day by continuous IV infusion or in divided oral doses until 10g total, then 200 - 400mg/day maintenance  
 Dofetilide Oral 500mcg bid if Cr clearance > 60ml/min 
250mcg bid if Cr clearance 40-60ml/min 
125 mcg bid if Cr clearance 20-40ml/min 
dofetilide is contraindicated if Cr clearance < 20ml/min		 QT prologation, torsade des pointes
 Flecainide* Oral 200 - 300mg Hypotension, rapidly conducting atrial flutter
  IV 1.5 - 3mg/kg over 15 min  
 Ibutilide IV 1mg over 10 min, repeat 1mg after 10 min if necessary QT prolongation, torsade des pointes 

(serum magnesium and potassium must be in the upper normal range + corrected baselineQT interval must be > 450msec prior to ibutilide therapy; 2g of magnesium IV can be given as a prophylactic preload bolus)
 Propafenone* Oral 450 - 600mg Hypotension, rapidly conducting atrial flutter
  IV 1.5 - 2mg/kg over 15 min  

* These drugs should be used cautiously, or not at all, in patients with cardiac ischemia or impaired left ventricular function; dofetilide and amiodarone are recommended for patients with left ventricular dysfunction

(* emergency physicians often choose a drug based on personal familiarity and personal experience, and they do not always consider the alternative choices  => see an excellent online article at emed.home or the textbook chapter on AF at emedicine.com for more information on drugs used in the pharmacological cardioversion of AF; Vaughan-Williams type 1a or 1c drugs can facilitate the organization of AF into atrial flutter and also produce 1:1 AV conduction => AV nodal drugs should always be administered before using those cardioverting drugs)

- there are few prospective data on the safety of outpatient initiation of anti-arrhythmic therapy for pharmacological cardioversion of AF; the complication of proarrhythmia is rare in patients with normal ventricular function and normal baseline QT intervals without profound bradycardia

- propafenone or flecainide may be initiated out-of-hospital if sinus node or AV node disease is not suspected => however, some physicians only recommend out-of-hospital use of propafenone or flecainide for infrequent paroxysmal AF recurrences that are well tolerated (using a "pill-in-the-pocket" for occasional use on an "as needed" basis) if initial therapy in-hospital was shown to be safe for the first episode of paroxysmal AF (no evidence of bradyarrhythmias due to occult sinus node or AV node disease)

(* out-of-hospital drug termination of AF should be avoided in patients with symptomatic sick sinus syndrome, AV conduction disturbances, or bundle-branch block)

- sotalol may be used for outpatient therapy in patients with little-or-no heart disease, if  the baseline uncorrected QT interval is < 450 msecs, serum electrolytes are normal and none of type III drug-related proarrhythmia risk factors are present

- amiodarone can be used for outpatient therapy, even in patients with persistent AF, but in-hospital loading therapy may be better for AF patients with heart failure because earlier restoration of sinus rhythm is usually required

- the current standards for approval of dofetilide do not permit out-of-hospital iniation of therapy

- quinidine, procainamide and disopyramide should not be started out-of-hospital, and some physicians recommend avoiding these drugs in patients with ischemic heart disease, severe left ventricular hypertrophy, and all types of cardiomyopathy

Maintenance of sinus rhythm with anti-arrhythmic drugs (as an outpatient)

- recurrent paroxysmal/persistent AF is usually a chronic disorder => prophylactic anti-arrhythmic drug therapy is often recommended to maintain sinus rhythm unless the potential toxicity of the anti-arrhythmic drugs outweigh the benefits of restoration of sinus rhythm

- a low risk of AF recurrence is associated with a left atrial size < 4.5cm, recent onset AF, little or no heart failure, and no hypertensive heart disease

- a higher risk of AF recurrence (> one episode/month) is associated with female sex, underlying cardiac disease and heart failure, hypertension with LVH, age > 55 years and persistent AF > 3 months

- reversible cardiovascular and non-cardiovascular precipitants of AF should be corrected prior to considering long-term anti-arrhythmic therapy to maintain sinus rhythm

Long-term anti-arrhythmic drug therapy is often not indicated for a first-detected episode of AF, and can often be avoided in patients with infrequent and well tolerated paroxysmal AF

Basis for choosing a particular long-term anti-arrhythmic drug for maintenance of sinus rhythm

Selection of long term anti-arrhythmic agents for recurrent paroxysmal/persistent AF should be based on the absence, or presence, of specific underlying cardiovascular diseases

(* emergency physicians do not usually make decisions about long-term anti-arrhythmic drug therapy for the maintenance of sinus rhythm => therefore, detailed information about these drugs, their indications and contra-indications, have not been provided => consult the ACC/AHA/ESC guideline and other texts for detailed information before prescribing these dangerous drugs)

The choice of anti-arrhythmic medication may also depend on the likely inciting cause of the AF in patients without underlying heart disease

Lone AF

- beta blocker => flecainide, or propafenone, or sotalol => amiodarone or dofetilide

- quinidine, procainamide or disopyramide are only indicated when amiodarone fails or is contra-indicated

Adrenergically-mediated AF

- beta-blockers are a first choice

Vagally-mediated AF

- disopyramide is a first choice

(* digoxin may increase the rate of paroxysmal AF recurrences because of its vagotonic effect)

In general, only 30 - 50% of first-episode AF patients who are successfully cardioverted to sinus rhythm remain in sinus rhythm at the end of one year; long-term anti-arrhythmic drug therapy may increase that figure to 50 - 70%

- recurrence of AF in patients on chronic anti-arrhythmic drug therapy does not necessarily represent treatment failure, and continued use of anti-arrhythmic treatment may decrease the total arrhythmia burden over the long term

- similarly, when AF recurrences in patients on chronic anti-arrhythmic drug therapy are infrequent and well tolerated, a change in anti-arrhythmic therapy is not necessarily indicated

- multiple anti-arrhythmic drugs can be used if single anti-arrhythmic drug treatment fails eg. beta blocker, sotalol, or amiodarone + type 1C agent

- non-pharmacological correction of AF using surgical ablation techniques, or catheter ablation strategies, are promising techniques suitable for consideration by the patient's cardiologist if the patient does not respond to anti-arrhythmic drug therapy

- certain elderly patients may be better suited to remaining in permanent AF, and should not be too aggressively managed with anti-arrhythmic drugs, which have pro-arrhythmic and "nuisance" side-effects

Rate control during AF

- the rate is generally considered controlled when the resting heart rate is between 60 - 80 bpm and the exercise heart rate is between 90 - 115 bpm

- rate control therapy is primarily based on drugs that decrease conduction through the AV node

(* bradyarrhythmias may occur as a side-effect in elderly patients treated with digoxin, beta-blockers and calcium channel blockers if occult conducting system disease is present)

For AF patients presenting to the ED with a rapid ventricular rate, the primary focus of ED therapy should be directed at controlling the ventricular response rate

- US emergency physicians frequently choose diltiazem as the drug-of-choice to control the ventricular rate (although it has not been proven to have better efficacy than verapamil); beta-blockers may be a better choice in patients with cardiac ischemia, hyperadrenergic states or thyrotoxicosis
 

IV drugs for heart rate control of atrial fibrillation in the ED
Drug Loading dose Onset Maintenance dose Major side-effects
 Diltiazem  0.25mg/kg over 2 min => 0.35mg/kg over 2 min after 15 min if rate control still inadequate 2 - 7 min 5 - 15mg per hour by infusion Hypotension, heart block, heart failure 

Titrate lower loading doses of 2.5 - 5mg every few mins in frail elderly patients 

Calcium can be used to prevent/reverse hypotension +/- bradyarrhythmias
 Esmolol 0.5mg/kg over 1 min 5 min 0.05 - 0.2 mg/kg/min Hypotension, bradycardia, heart block, heart failure, asthma
 Metoprolol 2.5 - 5mg bolus over 2 min; up to 3 doses q 5 min 5 min NA Hypotension, bradycardia, heart block, heart failure, asthma
 Verapamil 0.075 - 0.15mg/kg over 2 min 3 - 5 min NA Hypotension, heart block, heart failure
 Digoxin* 0.25 mg each 2 h, up to 1.5mg 2h 0.125 - 0.25mg daily Digitalis toxicity, heart block, bradycardia

(* digoxin is unsuitable for ED use because of its slow onset of action, and some physicians suggest that digoxin should never be used in the acute management of AF because it has not been shown to be better than placebo during the first few hours of therapy; digoxin works via a secondary vagotonic action on the AV node and digoxin does little to control the ventricular rate in hyperadrenergic states and active, exercising patients; digoxin may actually increase the incidence of paroxysmal AF in susceptible patients by shortening the atrial refractory period; digoxin may be a suitable choice for chronic therapy in permanent AF patients with systolic dysfunction and heart failure)

- chronic AF patients who have an excessive heart rate long-term despite appropriate therapy, and who develop evidence of a tachycardia-mediated decline in systolic function, are candidates for AV nodal ablation therapy

Preventing thrombo-embolism

- the 15 year cumulative incidence of embolic stroke in lone AF patients (patients < 60 years of age with no structural heart disease) is 1.3%/year, which is not significantly greater than the incidence in the age-matched population with normal sinus rhythm => routine antithrombotic therapy is therefore not warranted

- the annualized rate of stroke in non-valvular AF patients averages 5%/year, which is 2 - 7x the rate of the age-matched population without AF

(* as an overall group, patients with non-valvular AF have a 6x greater risk of thromboembolism compared to the age-matched population in normal sinus rhythm)

- studies suggest that there is no significant difference in annual stroke rates between patients with paroxysmal and chronic AF => recommendations for anticoagulation are the same for paroxysmal AF as for chronic AF

- valvular heart disease markedly increases the yearly rate of thromboembolism and patients with mitral stenosis may have an annualized thromboembolic stroke rate exceeding 15 - 20%/year

- patients with a previous history of TIA or stroke have an annualized incidence of stroke of 10 - 12%/year despite aspirin therapy, and they greatly benefit from long-term oral anticoagulant therapy

(* aspirin has only modest protection against cardioembolic strokes and decreases the risk by only 1 - 2% on average, and aspirin may have more protection against non-cardioembolic strokes)

High risk factors for thromboembolic stroke include prior TIA/stroke or systemic embolus, hypertensive heart disease, poor LV systolic function, age > 75 years (especially females), rheumatic mitral valve disease and prosthetic heart valves

Moderate risk factors for thromboembolic stroke include age 65 - 75 years, diabetes mellitus, and CAD with preserved LV function

One system of estimating stroke risk

Highest stroke risk = 10 - 12%/year

High stroke risk = 7 - 8%/year Moderate stroke risk = 2.5 - 3.5%/year - although moderate to severe left ventricular dysfunction is an independent echocardiographic risk factor for stroke, LA diameter is not necessarily an useful predictor of embolic stroke

Oral anticoagulants may be contra-indicated if bleeding risks outweight benefits

One system of estimating bleeding risks

Minor risk

Potentially reversible bleeding risks Increased risk of bleeding and/or decreased benefit of anticoagulation - in general, patients with a high risk of stroke should be treated with oral anticoagulants to achieve a target INR of 2 - 3 unless oral anticoagulants are contraindicated => the yearly rate of thromboembolism may be decreased to 1 - 2%/year with effective oral anticoagulation

-  the rate of decrease in stroke risk using oral anticoagulants depends on the stroke risk category

- the target intensity for oral anticoagulation is based on an attempt to balance the risk of major bleeding complications against the likely protection against future strokes => a target INR of 2 - 3 is usually the desired endpoint for non-valvular AF patients; an INR < 1.6 is associated with a very significant risk of future embolic strokes and an INR > 4 is associated with a significant risk of major bleeding

- a lower INR target of 2.0 (range 1.6 - 2.5) is appropriate in elderly patients > 75 years of age, who are deemed to be at increased risk of bleeding complications, but who do not have frank contraindications to the use of anticoagulant therapy

AF patients with rheumatic valvular disease, or prosthetic valves, require a higher level of oral anticoagulation => a minimum target INR of 2 - 3 may be acceptable, but a target INR of 2.5 - 3.5 may be optimum depending on the type of prosthetic valve
 

Recommendations for antithrombotic therapy based on the patient's thromboembolic risk stratification - one approach
Patient features Antithrombotic therapy
Age < 60 years 
No heart disease		  Aspirin (325mg/day) or no therapy
 Age < 60 years, but heart disease, but no risk factors present (heart failure, LV ejection < 0.35, hypertension) Aspirin (325mg/day)
Age > 60 years, but no risk factors present (heart failure, LV ejection < 0.35, hypertension) Aspirin (325mg/day)
Age > 60 years, with diabetes mellitus or CAD Oral anticoagulation (INR = 2-3) 
Addition of aspirin (81-162mg/day) optional
Age > 75 years, especially females Oral anticoagulation (INR = 2)
Heart failure, ejection fraction < 0.35, thyrotoxicosis, hypertension Oral anticoagulation (INR = 2-3)
Rheumatic heart disease (mitral stenosis), prosthetic heart valves, prior thromboembolism, persistent atrial thrombus on TEE Oral anticoagulation (INR = 2.5-3.5 or higher)

- in permanent AF patients without mechanical valves, anticoagulation can be stopped for up to one week for procedures that carry a substantial risk of bleeding, without substituting heparin during the interim period

Anticoagulation to prevent embolic stroke in patients undergoing cardioversion

- the thromboembolic rate for chronic AF (> 48 hours duration) patients undergoing elective cardioversion is similar for electrical and pharmacological cardioversion (~ 5%) => anticoagulation is therefore routinely recommended for 3 weeks prior to elective cardioversion, and for 4 weeks after cardioversion of chronic AF (thromboembolic risk decreases to 0.5%)

- a TEE-guided strategy for elective cardioversion in patients with AF > 48 hour duration has the same thromboembolism outcome results as the conventional empirical strategy of using oral anticoagulation for 3 weeks before, and 4 weeks after, cardioversion => the sole advantage of the TEE-guided strategy is limited to saving time, and allowing for expedited elective cardioversion if the TEE study is negative (which may be advantageous if the patient is not tolerating the AF symptoms well, or if adequate rate control is difficult to achieve)

- detection of LA/LAA thrombus is a contra-indication to expedited elective cardioversion of AF => delay cardioversion for 3 weeks while anticoagulating the patient

- transient mechanical dysfunction of the LA/LAA occurs after successful conversion of AF to sinus rhythm (whether spontaneous or electrical or mechanical cardioversion) => atrial stunning is associated with a significant risk of thrombus formation, especially in patients with chronic AF => anticoagulation is therefore routinely necessary for 4 weeks after cardioversion of chronic AF > 48 hours duration (even if the TEE is negative for atrial thrombi)

The ACC/AHA/ESC guidelines do not not specifically recommmended heparin anticoagulation when cardioversion is performed for AF < 48 hours duration; however, not all cardiologists agree - some cardiologists routinely recommend heparin anticoagulation at the time of ED presentation and during the peri-cardioversion period in high risk patients with AF duration < 48 hours (patients with a previous history of thromboembolic stroke or severe left ventricular dysfunction), while other cardiologists recommend heparin loading in all AF patients - just in case cardioversion therapy has to be delayed

(* although some TEE studies have shown asymptomatic atrial thrombi in a small percentage of patients with AF duration < 48 hours, which suggests that it would be prudent to empirically use heparin for all patients with AF duration < 48 hours undergoing cardioversion, it still remains controversial whether short-term anticoagulation is required before, or after, cardioversion for AF < 48 hours duration -- it is regarded as optional by the ACC/AHA/ESC guidelines and is given a class IIb recommendation in the ACC/AHA/ESC guidelines, which is defined as "usefulness/efficacy is less well established by evidence or opinion")

- it is unclear whether patients with self-limited episodes of paroxysmal AF require long-term or even short-term anticoagulation, and the decision to anticoagulate must be individualized, and based on the intrinsic risk of thromboembolism

(* see the ACLS guidemap for a summary of the ACLS-recommended treatment of stable atrial fibrillation in patients with normal and impaired left ventricular function, or WPW syndrome)
 
Appendix

Some conditions associated with atrial fibrillation

Cardiovascular conditions

Pulmonary conditions Non-cardiac conditions Vaughan Williams classification of anti-arrhythmic drug actions

Type 1A

Type 1B Type 1C Type II Type III Type IV Types of proarrhythmia during drug treatment of AF

Ventricular proarrhythmia

Atrial proarrhythmia Abnormalities of conduction or impulse formation
ACC/AHA/ESC algoritm for newly discovered AF

ED management of new-onset AF based on the duration of AF


ACC/AHA/ESC algorithm for recurrent paroxysmal AF


ACC/AHA/ESC algorithm for recurrent persistent AF

Disclaimer: My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use.