Af Akut

Acute atrial fibrillation
Highlights
Summary Overview
Basics
Definition Epidemiology Aetiology Pathophysiology Classification
Diagnosis
History & examination Tests Differential Step-by-step Criteria Guidelines Case history
Treatment
Details Step-by-step Emerging Guidelines Evidence
Follow Up
Recommendations Complications Prognosis
Resources
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History & exam

Key factors
presence of risk factors irregular pulse rate
Other diagnostic factors

palpitations
dizziness dyspnoea hypotension elevated jugular venous pressure added heart sounds rales evidence of stroke History & exam details
Diagnostic tests
1st tests to order
ECG serum electrolytes cardiac biomarkers thyroid function tests CXR transthoracic echocardiogram transoesophageal echocardiogram (TOE)
Tests to consider
electrophysiological study exercise stress tests
Diagnostic tests details
Treatment details
Presumptive
haemodynamically unstable direct current (DC) cardioversion
Acute
haemodynamically stable with left atrial thrombus o o o o without heart failure rate control with beta-blockers and/or calcium-channel blockers (CCBs) anticoagulation cardioversion following 3 to 4 weeks of anticoagulation with heart failure rate control with digoxin or amiodarone or dronedarone
o o
anticoagulation cardioversion following 3 to 4 weeks of anticoagulation haemodynamically stable without left atrial thrombus: symptom onset <48 hours
o o o o o o o o
without heart failure: low thromboembolic risk rate control with beta-blockers and/or calcium-channel blockers (CCBs) cardioversion without heart failure: high thromboembolic risk rate control with beta-blockers and/or calcium-channel blockers (CCBs) cardioversion + heparin anticoagulation with heart failure rate control with digoxin or amiodarone or dronedarone cardioversion + heparin anticoagulation haemodynamically stable without left atrial thrombus: symptom onset 48 hours
o o o o o o o o o o
without heart failure: low thromboembolic risk rate control with beta-blockers and/or calcium-channel blockers (CCBs) heparin cardioversion once heparin anticoagulation established long-term aspirin post-cardioversion without heart failure: high thromboembolic risk rate control with beta-blockers and/or calcium-channel blockers (CCBs) anticoagulation cardioversion following 3 to 4 weeks of anticoagulation with heart failure rate control with digoxin or amiodarone or dronedarone anticoagulation cardioversion following 3 to 4 weeks of anticoagulation haemodynamically stable without left atrial thrombus: asymptomatic
o o o
low thromboembolic risk observation rate control with beta-blockers and/or calcium-channel blockers (CCBs) cardioversion high thromboembolic risk
o o o o
anticoagulation observation rate control with beta-blockers and/or calcium-channel blockers (CCBs) cardioversion Treatment details
Summary
Chaotic and irregular atrial arrhythmia, the prevalence of which increases progressively with age and affects almost 5% of the population older than 69 years of age. Causes significant morbidity and mortality including palpitations, dyspnoea, angina, dizziness or syncope, and features of congestive heart failure (CHF), tachycardia-induced cardiomyopathy, stroke, and death. ECG shows absent P waves, presence of fibrillatory waves, and irregularly irregular QRS complexes. Most patients presenting with acute atrial fibrillation (AF) do not require immediate intervention. Most patients will require medical therapy to control ventricular rate. Patients who develop haemodynamic compromise should have immediate direct current cardioversion. If the precise timing of the onset of AF is unclear, a transoesophageal echocardiogram must be performed to exclude left atrial clots before cardioversion.
Definition
Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterised by unco-ordinated atrial activation and variable ventricular response. [1] Acute AF is defined as a new onset or a first detectable episode of AF, whether symptomatic or not.
Epidemiology
AF is considered to be the most common sustained cardiac arrhythmia; [3] however, the true prevalence is difficult to ascertain. The incidence of AF increases progressively with age, ranging from 2 to 3 new cases per 1000 population per year between the ages of 55 and 64 years, to 35 new cases per 1000 population per year between the ages of 85 and 94 years. [4]The overall prevalence among men and women is similar. [1] [5] [6] Moreover, AF is less common among black and Indo-Asian people than white people. [1] [7] In the UK, the prevalence of AF in general practice is around 2.5% to 5%, and among acute medical emergency admissions 3% to 6% of patients have AF. [8] Epidemiological data on acute (new-onset) AF are limited. Extrapolation from the Framingham study indicates the incidence of acute AF in middle-aged (age 55 years) women and men to be 0.2% and 0.3%, respectively. [9] In patients with a first-ever ischaemic stroke, there is a high prevalence (15% to 25%) of AF, and the incidence of acute AF is around 5%. [10] [11] New-onset AF occurs in approximately 10% of patients after acute MI and independently predicts a worse short- and long-term prognosis among patients with acute MI and heart failure. [12] [13]
Aetiology
Coronary artery disease (CAD), hypertension, heart failure, valvular disease, pericardial and pleural diseases, diabetes, thyroid disorders, disorders of the lung, and advanced age are known risk factors for the development of acute AF. [1] [3] [4] [8] [9] However, AF may occur in the absence of any underlying cardiac or non-cardiac diseases, for example, as a result of heavy alcohol intake. [4] [14]
Pathophysiology
Pathophysiology of AF involves multiple aetiologies and complex electrophysiological changes.[1] [3] [4] [8] [15] [16] [17] AF is usually associated with anatomically and histologically abnormal atria as a result of underlying heart disease. Dilation of the atria with fibrosis and inflammation causes a difference in refractory periods within the atrial tissue and promotes electrical re-entry that results in AF. The fractionation of a mother wave into multiple wavelets in the presence of enlarged atria in conjunction with the short refractory periods and slow conduction properties of the atria lead to sustained AF. The presence of rapidly firing foci, typically in the pulmonary veins, may trigger AF that is sustained by the first mechanism. [17]
Multiple wavelets of atrial fibrillation compete with each other in the atrium and bombard the AV node with many signalsFrom: Cox D, Dougall H. Student BMJ. 2001;09:399-442
AF may also result as degeneration of other rapid arrhythmias, such as atrial tachycardia, atrial flutter, or AV nodal re-entrant tachycardia and AV reentrant tachycardia. The latter occurs in the presence of either concealed or manifest accessory bypass tracts. [1] [3] [4] [8] [15] [16]Patients with WolffParkinson-White syndrome have a congenital accessory bypass tract that causes arrhythmias. Acute AF causes an increase in coronary flow. However, this is not adequate to compensate for the increased myocardial oxygen demand that occurs as a result of irregularity in the ventricular rhythm. [18] Cardiac ischaemia may develop even in patients without CAD, and this contributes to left ventricular
dysfunction and subsequent symptoms of chest discomfort, dizziness and shortness of breath. [18]
Classification
Classification of AF subtypes [2] AF may be classified into 5 patterns:
1. 2. 3. 4. Acute or a new-onset AF: the first detectable episode of AF whether symptomatic or not. Paroxysmal AF: terminates spontaneously within 7 days (usually within 48 hours of presentation). Persistent AF: lasts longer than 7 days or requires termination by cardioversion. Long-standing persistent AF: has lasted for 1 year when it is decided to adopt a rhythm control strategy. 5. Permanent AF: Sinus rhythm cannot be restored or maintained.
History & examination

Key diagnostic factorshide all
presence of risk factors (common)
Key risk factors include increasing age, diabetes mellitus, hypertension, CHF, valvular heart disease, CAD, other atrial arrhythmias, cardiac or thoracic surgery and hyperthyroidism.
irregular pulse rate (common)
Although a hallmark of AF, irregularity of the pulse rate may not be appreciated during very rapid pulse rate.
Other diagnostic factorshide all

palpitations (common) Palpitations are often described as a fluttering in the chest or a feeling of the heart 'galloping'. hypotension (common) AF with a rapid ventricular rate may cause haemodynamic instability. elevated jugular venous pressure (common) Acute AF may be associated with heart failure. added heart sounds (common)
Underlying valvular disease, such as mitral stenosis due to rheumatic heart disease, may be audible.
A gallop rhythm may be heard in heart failure. S3 is typically not heard because of an absence of atrial kick.
Pericardial rub may be heard in cases of pericarditis. dizziness (uncommon) Occurs as a result of rapid heart rate and hypotension. dyspnoea (uncommon)
A history of shortness of breath and orthopnoea suggests underlying heart failure. rales (uncommon) May be present in patients with heart failure. evidence of stroke (uncommon)
Risk
Signs of an acute stroke, such as hemiplegia or dysphasia, may be the first presentation of AF. factorshide all
Strong increasing age The odds ratio of AF for each decade of advancing age was 2.1 for men and 2.2 for women. [19] diabetes mellitus
Significantly associated with risk of AF in both sexes (odds ratio 1.4 for men and 1.6 for women). [19]
hypertension CHF
Significantly associated with risk of AF in both sexes (odds ratio 1.5 for men and 1.4 for women). [19] Significantly associated with risk of AF in both sexes (odds ratio 4.5 for men and 5.9 for women). [19]
valvular heart disease CAD
Significantly associated with risk of AF in both sexes (odds ratio 1.8 for men and 3.4 for women). [19] CAD and MI are significantly associated with risk of AF (odds ratio 1.4 for men and 1.2 for women ). [19]
other atrial arrhythmias
May be associated with atrial flutter, Wolff-Parkinson-White syndrome, or AV nodal re-entrant tachycardias. [1]
cardiac or thoracic surgery Common postoperative complication. [1] hyperthyroidism
About 10% to 15% of patients with untreated thyrotoxicosis develop AF. [20]
Weak hypoxic pulmonary conditions
Pulmonary embolism, pneumonia, COPD, or obstructive sleep apnoea may precipitate AF. [1] [3] [20] [21]
alcohol intoxication Consumption of 35 drinks per week among men was associated with a hazard ratio of 1.45. [14] obesity
Likely to be due to increase in left atrial size. [1] [21]
Diagnostic tests
1st tests to orderhide all
Test
ECG Should be the first test requested. View image
serum electrolytes and metabolic status. Also helpful in choosing anti-arrhythmic agents and their dosages. cardiac biomarkers Myocardial ischaemia may be a cause or consequence of AF. thyroid function tests Thyrotoxicosis may present with AF. CXR normal. Pneumonia, pericarditis, or heart failure may precipitate acute AF.
Routine biochemistry should be done to assess for the presence of other co-morbid conditions, and to assess ele
CXR in patients who are otherwise healthy and presenting with acute AF (e.g., secondary to alcohol ingestion) m
transthoracic echocardiogram stenotic or regurgitation abnormalities, cardiomyopathy with low LVEF, or pericardial disease. Echocardiogram in patients who are otherwise healthy and presenting with acute AF (e.g., secondary to alcohol ingestion) may be normal. transoesophageal echocardiogram (TOE) necessary to restore sinus rhythm.
May show abnormalities, such as LVH, left atrial enlargement, segmental or global wall motion abnormalities, va
TOE is necessary in patients presenting with acute AF, where the exact onset of AF is unclear, and cardioversion
The presence of atrial thrombus increases the risk of embolic stroke.
Tests to considerhide all

Test
electrophysiological study May show accessory bypass tract that causes arrhythmias, such as in Wolff-Parkinson-White syndrome. exercise stress tests Exercise echocardiography and the exercise nuclear imaging stress test are both useful to determine structural use dependence pro-arrhythmic effect of class Ic anti-arrhythmic agents.
abnormalities of the heart and assess for CAD, for assessing adequate rate control, and to determine whether th
A treadmill exercise stress test may also be useful for risk stratification for risk of sudden cardiac death in patient
Wolff-Parkinson-White syndrome. The sudden loss of pre-excitation delta waves at faster heart rate during exerc cardiac death from AF is therefore lower.
test indicates that the antegrade conduction property of the accessory bypass tract is weaker, and the risk of sud
Differential diagnosis
Condition Differentiating signs/symptoms Differentiating tests
Atrial flutter
Clinical history and physical examination may not be useful to differentiate from AF.
ECG shows absence of P waves, presence of characteristic flutter wave 3:1, 4:1) irregular. View image
tooth appearance in the inferior limb leads, and QRS complexes that ar
Wolff-ParkinsonWhite syndrome
Usually presents at younger age (teens or early 20s).
Classic ECG has shortened PR interval and delta wave on the QRS com degenerate into AF. View image
An electrophysiological study with view to curative ablation procedure is rapid ventricular rate.
with ECG changes suggestive of Wolff-Parkinson-White syndrome who
Often precipitated
by exercise.
Atrial tachycardia
Clinical history and physical examination may not be useful to differentiate from AF. However, atrial tachycardia (in particular, multifocal atrial tachycardia) is more common in patients with severe COPD.
ECG shows abnormal P waves. In multifocal atrial tachycardia, there ar morphologies of P waves. View image
Step-by-step diagnostic approach

Most patients with acute AF present with rapid palpitations, fluttering in the chest, dizziness, or shortness of breath. Some patients may also present with stroke and embolic events. The onset of the first episode, its duration, and precipitating factors should be established.
History and examination

Most patients present with symptoms related to the arrhythmia, most of which occur as a result of a rapid ventricular rate. Typical symptoms include palpitations, a sense of the heart racing, dizziness and shortness of breath. Some patients may present with focal neurological deficits such as hemiplegia or dysphasia due to a stroke. The pulse should be assessed. An irregularly irregular pulse, both in the rhythm and volume, is characteristic. Signs of the underlying cause of AF,
such as elevated jugular venous pressure and bibasilar crepitations in heart failure or tremor, sweating, and goitre in hyperthyroidism, should be looked for.
ECG
An ECG should be the first test requested. Absent P waves that have been replaced by irregular fibrillatory waves, and irregularly irregular QRS complexes will confirm the diagnosis of AF.
Atrial fibrillationFrom the collections of Arti N. Shah and Bharat K. Kantharia
In contrast, P waves that have been replaced by a saw tooth appearance in the inferior limb leads, and QRS complexes that are regularly (typically 2:1, 3:1, 4:1) irregular are characteristic of atrial flutter. View image Abnormal and variable morphology P waves can occur in atrial tachycardia. View image The ECG may also show evidence of possible underlying causes, such as LVH or previous MI.
Investigation for causal factors

Blood biochemistry should be checked for abnormal potassium or magnesium levels. Cardiac biomarkers should be checked if chest pain is a feature. Thyroid function testing should be part of the initial assessment, particularly in older people, as classic signs of thyrotoxicosis may not be obvious. [20] Liver function tests (LFTs) are useful to determine presence of a multisystem disorder affecting the liver. Furthermore, LFTs are useful to choose appropriate anti-arrhythmic agents and to monitor anti-arrhythmic drug therapy. For example, amiodarone is contraindicated in the presence of liver dysfunction; and amiodarone treatment should be discontinued when LFTs show abnormalities.
A chest x-ray (CXR) should be performed to look for underlying structural heart disease, such as enlargement of the cardiac chambers or valvular calcification, and signs of heart failure. The CXR may also suggest a precipitating cause of AF, such as pneumonia. Following the initial assessment, patients should undergo echocardiography to evaluate cardiac chamber size and left ventricular function. This may also reveal an underlying cause such as valvular disease. A transesophageal echocardiogram (TEE) is essential in patients before cardioversion (unless they are already anticoagulated) to rule out left atrial clots. Electrophysiological studies may be required to identify arrhythmias such as Wolff-Parkinson-White syndrome, atrial flutter, or paroxysmal supraventricular tachycardia. [1] Exercise echocardiography and the exercise nuclear imaging stress test are both useful to identify structural abnormalities of the heart and assess for CAD. A stress test is also useful to assess adequate rate control when a rate control strategy is used. The exercise stress test also helps to determine whether there is a use dependence proarrhythmic effect of class Ic antiarrhythmic agents such as flecainide and propefanone. A treadmill exercise stress test may be useful for risk stratification for risk of sudden cardiac death in patients with Wolff-Parkinson-White syndrome. The sudden loss of preexcitation delta waves at a faster heart rate during exercise stress testing indicates that the antegrade conduction property of the accessory bypass tract is weaker, and the risk of sudden cardiac death from AF is therefore lower.
Click to view diagnostic guideline references.
Diagnostic criteria
Risk factors for thromboembolism in patients with AF [1]

Less validated or weaker risk factors
Female gender Age 65 to 74 years CAD Thyrotoxicosis.
Moderate risk factors
Age 75 years Hypertension Heart failure LV ejection fraction 35% Diabetes mellitus.
High risk factors

Previous stroke, transient ischaemic attack, or embolism Mitral stenosis Prosthetic heart valve.
CHADS2 scoring system for risk of thromboembolism [22] [2]

In patients with AF and non-valvular (particularly rheumatic) heart disease, the risk of thromboembolic stroke may be estimated by calculating the CHADS2 score. The variables are congestive heart failure (C), hypertension (H), age (A), diabetes mellitus (D), and a history of stroke (S). Each variable is given 1 point except the presence of a history of stroke or prior transient ischaemic attack, which is given 2 points. The validation of this scheme indicates low risk for a CHADS2 score of 0, moderate risk for a CHADS2 score of 1 to 2, and high risk for a CHADS2 score of >2 for future risk of thromboembolic stroke. The stroke rate per 100 patients-years without antithrombotic therapy according to CHADS2 score is as follows: Score 0: stroke risk 1.9% (95% CI 1.2-3.0) Score 1: stroke risk 2.8% (95% CI 2.0-3.8) Score 2: stroke risk 4.0% (95% CI 3.1-5.1) Score 3: stroke risk 5.9% (95% CI 4.6-7.3) Score 4: stroke risk 8.5% (95% CI 6.3-11.1)
Score 5: stroke risk 12.5% (95% CI 8.2-17.5) Score 6: stroke risk 18.2% (95% CI 10.5-27.4). The CHADS2 score system is useful and easy to remember. However, because the risk of thromboembolic events is a continuum, categorisation of the risks into low, moderate, and high is artificial, especially taking only a few risk factors into account. The recent 2010 European Society of Cardiology guidelines emphasise a risk factor-based approach using the CHA2DS2VASc score system. [2] In this system, 2 points are assigned for a history of stroke or transient ischaemic attack; 2 points for age 75 years; and 1 point each for age 65 to 74 years, a history of hypertension, diabetes, recent cardiac failure, vascular disease (MI, complex aortic plaque, and peripheral arterial disease [PAD], including prior revascularisation, amputation due to PAD, or angiographic evidence of PAD), and female sex. Based on the CHA2DS2-VASc score system, the adjusted stroke rate (% per year) is as follows: Score 0: stroke rate 0% Score 1: stroke rate 1.3% Score 2: stroke rate 2.2% Score 3: stroke rate 3.2% Score 4: stroke rate 4.0% Score 5: stroke rate 6.7% Score 6: stroke rate 9.8% Score 7: stroke rate 9.6% Score 8: stroke rate 6.7% Score 9: stroke rate 15.2%.
HEMORR2HAGES score system [23]

In addition to consideration of the risk of stroke and benefit of anticoagulation therapy, the risk of haemorrhage (particularly intracranial) has to be considered. For patients taking warfarin, several scoring systems aim to stratify this risk of bleeding. In the HEMORR2HAGES score, points are
assigned for each risk factor: hepatic or renal disease (H), ethanol abuse (E), malignancy (M), older age (>75 years) (O), reduced platelet count or function (R), rebleeding risk (R), uncontrolled hypertension (H), anaemia (A), genetic factor (G), excessive fall risk (E), and stroke (S). One point is awarded for each risk factor, except for a prior bleed (rebleeding risk), which is given 2 points. Using this system, the risk of major bleeding in National Registry of Atrial Fibrillation participants prescribed warfarin, stratified by HEMORR2HAGES score, was as follows: Score 0: 1.9 (0.6-4.4) bleeds per 100 point-years warfarin (95% CI) Score 1: 2.5 (1.3-4.3) bleeds per 100 point-years warfarin (95% CI) Score 2: 5.3 (3.4-8.1) bleeds per 100 point-years warfarin (95% CI) Score 3: 8.4 (4.9-13.6) bleeds per 100 point-years warfarin (95% CI) Score 4: 10.4 (5.1-18.9) bleeds per 100 point-years warfarin (95% CI) Score 5: 12.3 (5.8-23.1) bleeds per 100 point-years warfarin (95% CI)
HAS-BLED [24]
HAS-BLED is a scoring system in which the clinical characteristics of hypertension (H), abnormal renal or hepatic function (A), stroke (S), bleeding or its risks (B), labile INRs (L), elderly age group (>65 years) (E), and drugs/alcohol (drugs such as antiplatelets) (D) are given 1 point each. Based on this scoring system, the risk of bleeding is significantly higher for scores of 3.
Case history #1
A 65-year-old man with a history of hypertension, diabetes mellitus, and hyperlipidaemia presents to the emergency department with the first episode of rapid palpitations, shortness of breath, and discomfort in his chest. These symptoms started acutely and have been present for 4 hours. Physical examination shows an irregularly irregular radial pulse at rate between 90 and 110 bpm, BP 110/70 mmHg, and respiratory rate of 20 breaths per minute. Heart sounds are irregular, but no S3 or S4 gallop or murmurs are audible. There are no other abnormalities on examination.
Case history #2
A 56-year-old woman with a 6- week history of weight loss, anxiety, and insomnia presents with palpitation and dyspnoea. Her pulse rate is irregular at 140 to 150 bpm. Her BP is 95/55 mmHg. She looks thin, frail, and rather anxious and jittery. Her palms are sweaty and have fine tremors. She has a palpable smooth goitre. Examination of the eyes shows bilateral exophthalmoses.
Treatment Options
Treatment Patient group haemodynamically unstable line 1st Treatmenthide all
direct current (DC) cardioversion
Used immediately if the patient is haemodynamically unstable with chest pain, shortness of breath, dizziness or syncope, hypotension, and rapid heart rate.
DC cardioversion is performed under adequate short-acting general anaesthesia and involves delivery of an electrical shock synchronised with the intrinsic activity of the heart by sensing the R wave of the ECG (i.e., synchronised). The energy output for successful termination of acute AF varies from 200 J to a maximum of 400 J depending on the body size and the presence of other co-morbid conditions. Lower energy of 100 J may be used as the starting level when biphasic energy is used.
Presumptive
Treatment Patient group haemodynamically stable with left atrial thrombus without heart failure 1st line Treatmenthide all
rate control with beta-blockers and/or calcium-channel blockers (CCBs)
Rate-control therapy is required until cardioversion is successful.
Presumptive
Treatment Patient group line Treatmenthide all
Beta-blockers and CCBs slow AV nodal conduction of cardiac impulses and subsequently reduce ventricular rate.
Beta-blockers are particularly useful when acute AF is associated with an acute MI or angina, and when acute AF is precipitated after exercise.
Esmolol is useful in patients at risk of complications from beta-blockade, particularly those with reactive airway disease, left ventricular dysfunction, and/or peripheral vascular disease.
CCBs are preferred in patients with chronic lung disease where bronchospasm may occur with betablockers.
Both groups of medications may cause severe bradycardia, heart block, asystole, heart failure, or
Presumptive
hypotension.
If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used. Primary Options metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily OR esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes, repeat loading dose and increase infusion, consult specialist for further guidance on dose OR
Presumptive
diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion OR verapamil : 2.5 to 10 mg intravenous bolus, may give second bolus of 5-10 mg after 30 minutes if necessary Secondary Options metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily or esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes,
Presumptive
repeat loading dose and increase infusion, consult specialist for further guidance on dose -- AND -diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion or verapamil : 2.5 to 10 mg intravenous bolus, may give second bolus of 5-10 mg after 30 minutes if necessary plus [?] anticoagulation
Concomitant heparin and warfarin therapy should be started, and heparin continued until the warfarin levels are therapeutic (INR 2 to 3). Anticoagulation with warfarin at the target INR should be established
Presumptive
for 3 to 4 weeks before cardioversion is attempted. In selected patients warfarin may be substituted with dabigatran. Dabigatran should not be used in patients with marked renal insufficiency or those who have mechanical prosthetic valves. Warfarin may also be substituted with rivaroxaban or apixaban. [36] [37]
Anticoagulation is continued for at least 4 weeks after cardioversion, and may be required for longer in some patients. [1] Primary Options heparin : see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds or
Presumptive
enoxaparin : 1 mg/kg subcutaneously every 12 hours -- AND -warfarin : 5-10 mg orally once daily initially, adjust dose according to INR (target 2 to 3) or dabigatran : 150 mg orally twice daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation or rivaroxaban : 20 mg orally once daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation or apixaban : 5 mg orally twice daily; consult specialist
Presumptive
for guidance on when to start this drug and when to cease parenteral anticoagulation plus [?] cardioversion following 3 to 4 weeks of anticoagulation
Cardioversion should only be attempted once the patient has been established on anticoagulation with a target INR of 2 to 3 for 3 to 4 weeks.
DC cardioversion is fast, safe, and efficient. Class IC agents (flecainide, propafenone) have a higher mortality in patients with CAD and are contraindicated in patients with CAD and cardiac dysfunction. AF may convert to atrial flutter that may conduct with rapid ventricular rate.
Flecainide has strong evidence of efficacy for pharmacological conversion (odds ratio [OR], 24.7; CI, 9.0 to 68.3). High conversion rate of about 70%
Presumptive
at 3 hours after treatment and up to 90% at 8 hours. [47]
Propafenone also has strong evidence of efficacy for pharmacological conversion (OR, 4.6; CI, 2.6 to 8.2). High conversion rates of up to 76% at 8 hours after treatment. [47]
Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents in conversion to sinus rhythm.
Dronedarone is a multichannel blocker that inhibits the sodium, potassium, and calcium channels and has non-competitive anti-adrenergic activity similar to sotalol, propafenone, and flecainide, but has lower efficacy than amiodarone to maintain sinus rhythm. [28] [29] [30] [31] Additionally, although dronedarone can be safely administered in patients
Presumptive
with stable New York Heart Association (NYHA) class I-II heart failure, it is contraindicated in patients with NYHA class IV heart failure or NYHA class II or III heart failure with a recent (within the previous 4 weeks) decompensation requiring hospitalisation or referral to a specialised heart failure clinic. [48] [49]Dronedarone is also contraindicated in patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent AF) as a safety review showed that dronedarone doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, dronedarone is indicated for the maintenance of sinus rhythm after successful cardioversion in adult clinically stable patients with paroxysmal or persistent AF. Use of
Presumptive
dronedarone may be associated with an elevated risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing.

Amiodarone provides additional benefit of improved rate control in patients with acute AF. Ibutilide prolongs repolarisation of the atrial tissue by enhancing the slow inward depolarising Na+ current in the plateau phase of repolarisation. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacological conversion (OR, 29.1; CI, 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3 to 6
Presumptive
hours, a prolonged observation period is recommended in patients who have received ibutilide. [47]
Anticoagulation is continued for at least 4 weeks after cardioversion. [1] Primary Options direct current cardioversion OR flecainide : 200-300 mg orally as a single dose OR propafenone : 600 mg orally as a single dose OR amiodarone : 150 mg intravenously initially, followed
Presumptive
by 0.5 to 1 mg/min infusion for 24-48 hours OR dronedarone : 400 mg orally twice daily with meals OR ibutilide : 0.01 mg/kg (maximum 1 mg/dose) intravenously initially, may repeat 10 minutes after initial dose if no response
with heart failure 1st
rate control with digoxin or amiodarone or dronedarone

Digoxin is the preferred drug in patients with AF and heart failure. [1] [3] Amiodarone has multiclass (I to IV) anti-arrhythmic properties. It is used for rate control only if the other therapies are contraindicated.
Dronedarone can be safely administered in patients
Presumptive
with stable New York Heart Association (NYHA) class I-II heart failure, but it is contraindicated in patients with NYHA class IV heart failure or NYHA class II or III heart failure with a recent (within the previous 4 weeks) decompensation requiring hospitalisation or referral to a specialised heart failure clinic. [48] [49]Dronedarone is also contraindicated in patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent AF) as a safety review showed that dronedarone doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, dronedarone is indicated for the maintenance of sinus rhythm after successful cardioversion in adult clinically stable patients with paroxysmal or
Presumptive
persistent AF. Use of dronedarone may be associated with an elevated risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing. Primary Options digoxin : 0.75 to 1.5 mg orally as a loading dose given in divided doses on first day, followed by maintenance dose of 0.125 to 0.5 mg once daily Secondary Options amiodarone : 150 mg intravenously initially, followed by 0.5 to 1 mg/min infusion for 24-48 hours OR
Presumptive
dronedarone : 400 mg orally twice daily with meals plus [?] anticoagulation
Concomitant heparin and warfarin therapy should be started, and heparin continued until the warfarin levels are therapeutic (INR 2 to 3). Anticoagulation with warfarin at the target INR should be established for 3 to 4 weeks before cardioversion is attempted. In selected patients warfarin may be substituted with dabigatran. Dabigatran should not be used in patients with marked renal insufficiency or those who have mechanical prosthetic valves. Warfarin may also be substituted with rivaroxaban or apixaban. [36] [37]
Anticoagulation is continued for at least 4 weeks after cardioversion, and may be required for longer in
Presumptive
some patients. [1] Primary Options heparin : see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds or enoxaparin : 1 mg/kg subcutaneously every 12 hours -- AND -warfarin : 5-10 mg orally once daily initially, adjust dose according to INR (target 2 to 3) or dabigatran : 150 mg orally twice daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation or
Presumptive
rivaroxaban : 20 mg orally once daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation or apixaban : 5 mg orally twice daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation
1st
cardioversion following 3 to 4 weeks of anticoagulation
DC cardioversion is fast, safe, and efficient. Class III agents (including amiodarone and ibutilide)
Presumptive
are less efficacious than class IC agents in conversion to sinus rhythm.

Amiodarone provides additional benefit of improved rate control in patients with acute AF. Ibutilide prolongs repolarisation of the atrial tissue by enhancing the slow inward depolarising Na+ current in the plateau phase of repolarisation. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacological conversion (OR, 29.1; CI, 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3 to 6 hours, a prolonged observation period is recommended in patients who have received ibutilide. [47]
Presumptive
Anticoagulation is continued for at least 4 weeks after cardioversion. [1] Primary Options direct current cardioversion OR amiodarone : 150 mg intravenously initially, followed by 0.5 to 1 mg/min infusion for 24-48 hours OR ibutilide : 0.01 mg/kg (maximum 1 mg/dose) intravenously initially, may repeat 10 minutes after initial dose if no response
Presumptive
Treatment Patient group haemodynamically stable without left atrial thrombus: symptom onset <48 hours without heart failure: low thromboembolic risk 1st line Treatmenthide all
Patients are considered at low risk of thromboembolic disease if their age is <75 years and there is no structural heart disease, diabetes, hypertension, rheumatic heart disease, prosthetic heart valves, or history of prior thromboembolism, and the left ventricular (LV) ejection fraction is >35%.
Rate-control therapy is required until cardioversion is successful. Beta-blockers and CCBs slow AV nodal conduction of cardiac impulses and subsequently reduce ventricular rate.
Presumptive
Esmolol is useful in patients at risk of complications from beta-blockade, particularly those with reactive airway disease, LV dysfunction, and/or peripheral vascular disease.
Both groups of medications may cause severe bradycardia, heart block, asystole, heart failure, or hypotension.
If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be
Presumptive
used. Primary Options metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily OR esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes, repeat loading dose and increase infusion, consult specialist for further guidance on dose OR diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion
Presumptive
OR verapamil : 2.5 to 10 mg intravenous bolus, may give second bolus of 5-10 mg after 30 minutes if necessary Secondary Options metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily or esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes, repeat loading dose and increase infusion, consult specialist for further guidance on dose -- AND --
Presumptive
diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion or verapamil : 2.5 to 10 mg intravenous bolus, may give second bolus of 5-10 mg after 30 minutes if necessary plus [?] cardioversion
Patients with low thromboembolic risk presenting with new-onset AF within 48 hours can undergo immediate cardioversion without the need for anticoagulation.
DC cardioversion is fast, safe, and efficient. Class IC agents (flecainide, propafenone) have a
Presumptive
higher mortality in patients with CAD and are contraindicated in patients with CAD and cardiac dysfunction. AF may convert to atrial flutter that may conduct with rapid ventricular rate.
Flecainide has strong evidence of efficacy for pharmacological conversion (odds ratio [OR], 24.7; CI, 9.0 to 68.3). High conversion rate of about 70% at 3 hours after treatment and up to 90% at 8 hours. [47]
Presumptive
Amiodarone provides additional benefit of improved rate control in patients with acute AF. Dronedarone is a multichannel blocker that inhibits the sodium, potassium, and calcium channels and has non-competitive anti-adrenergic activity similar to sotalol, propafenone, and flecainide, but has lower efficacy than amiodarone to maintain sinus rhythm. [28] [29] [30] [31] Additionally, although dronedarone can be safely administered in patients with stable New York Heart Association (NYHA) class I-II heart failure, it is contraindicated in patients with NYHA class IV heart failure or NYHA class II or III heart failure with a recent (within the previous 4 weeks) decompensation requiring hospitalisation or referral to a specialised heart failure clinic. [48] [49]Dronedarone is also contraindicated in
Presumptive
patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent AF) as a safety review showed that dronedarone doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, dronedarone is indicated for the maintenance of sinus rhythm after successful cardioversion in adult clinically stable patients with paroxysmal or persistent AF. Use of dronedarone may be associated with an elevated risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing.
Ibutilide prolongs repolarisation of the atrial tissue by
Presumptive
enhancing the slow inward depolarising Na+ current in the plateau phase of repolarisation. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacological conversion (OR, 29.1; CI, 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3 to 6 hours, prolonged observation period is recommended in patients who have received ibutilide. [47]
Vernakalant, a sodium- and ultrarapid potassiumchannel blocker with atrial selective effects, has been recommended for approval by the European Medicines Agency for rapid cardioversion of recentonset AF to sinus rhythm in adults (7 days for nonsurgical patients; 3 days for surgical patients). [38]
Presumptive
[39] [40] Before its use, contraindications should be checked, the patient should be adequately hydrated, and ECG and haemodynamic monitoring should be used. The infusion can be followed by DC cardioversion if necessary. Primary Options direct current cardioversion OR flecainide : 200-300 mg orally as a single dose OR propafenone : 600 mg orally as a single dose OR amiodarone : 150 mg intravenously initially, followed
Presumptive
by 0.5 to 1 mg/min infusion for 24-48 hours OR dronedarone : 400 mg orally twice daily with meals OR ibutilide : 0.01 mg/kg (maximum 1 mg/dose) intravenously initially, may repeat 10 minutes after initial dose if no response OR vernakalant : 3 mg/kg intravenous infusion over 10 min initially, followed by 15 min of observation, followed by 2 mg/kg intravenous infusion over 10 min if necessary
without heart failure: high thromboembolic risk 1st
Patients are considered at high risk of
Presumptive
thromboembolic disease if their age is 75 years and/or 1 of the following risk factors are present: structural heart disease, diabetes, hypertension, rheumatic heart disease, prosthetic heart valves, history of prior thromboembolism, or left ventricular (LV) ejection fraction 35%.

Esmolol is useful in patients at risk of complications
Presumptive
from beta-blockade, particularly those with reactive airway disease, LV dysfunction, and/or peripheral vascular disease.
If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used. Primary Options metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses;
Presumptive
200 mg orally twice daily OR esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes, repeat loading dose and increase infusion, consult specialist for further guidance on dose OR diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion OR verapamil : 2.5 to 10 mg intravenous bolus, may give second bolus of 5-10 mg after 30 minutes if necessary
Presumptive
Secondary Options metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily or esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes, repeat loading dose and increase infusion, consult specialist for further guidance on dose -- AND -diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion or
Presumptive
verapamil : 2.5 to 10 mg intravenous bolus, may give second bolus of 5-10 mg after 30 minutes if necessary plus [?] cardioversion + heparin
IV heparin (activated partial thromboplastin time (aPTT) of 45 to 60 seconds) or subcutaneous low molecular weight heparin should be started before cardioversion.
Flecainide has strong evidence of efficacy for
Presumptive
pharmacological conversion (odds ratio [OR], 24.7; CI, 9.0 to 68.3). High conversion rate of about 70% at 3 hours after treatment and up to 90% at 8 hours. [47]
Dronedarone is a multichannel blocker that inhibits the sodium, potassium, and calcium channels and has non-competitive anti-adrenergic activity similar to sotalol, propafenone, and flecainide, but has lower efficacy than amiodarone to maintain sinus
Presumptive
rhythm. [28] [29] [30] [31] Additionally, although dronedarone can be safely administered in patients with stable New York Heart Association (NYHA) class I-II heart failure, it is contraindicated in patients with NYHA class IV heart failure or NYHA class II or III heart failure with a recent (within the previous 4 weeks) decompensation requiring hospitalisation or referral to a specialised heart failure clinic. [48] [49]Dronedarone is also contraindicated in patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent AF) as a safety review showed that dronedarone doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, dronedarone is indicated for the maintenance of sinus rhythm after
Presumptive
successful cardioversion in adult clinically stable patients with paroxysmal or persistent AF. Use of dronedarone may be associated with an elevated risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing.

Amiodarone provides additional benefit of improved rate control in patients with acute AF. Ibutilide prolongs repolarisation of the atrial tissue by enhancing the slow inward depolarising Na+ current in the plateau phase of repolarisation. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacological conversion (OR, 29.1; CI, 9.8 to 86.1). Conversion
Presumptive
rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3 to 6 hours, prolonged observation period is recommended in patients who have received ibutilide. [47] Primary Options direct current cardioversion or flecainide : 200-300 mg orally as a single dose or propafenone : 600 mg orally as a single dose or amiodarone : 150 mg intravenously initially, followed
Presumptive
by 0.5 to 1 mg/min infusion for 24-48 hours or dronedarone : 400 mg orally twice daily with meals or ibutilide : 0.01 mg/kg (maximum 1 mg/dose) intravenously initially, may repeat 10 minutes after initial dose if no response -- AND -heparin : see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds or enoxaparin : 1 mg/kg subcutaneously every 12 hours plus anticoagulation
Presumptive
[?]
Anticoagulation with warfarin is required for patients at high risk for thromboembolism after sinus rhythm has been restored. IV or subcutaneous heparin is started before cardioversion and should be continued until the warfarin levels are therapeutic (INR 2 to 3). In selected patients warfarin may be substituted with dabigatran. Dabigatran should not be used in patients with marked renal insufficiency or those who have mechanical prosthetic valves. Warfarin may also be substituted with rivaroxaban or apixaban. [36] [37]
Anticoagulation is continued for at least 4 weeks after cardioversion. Primary Options warfarin : 5-10 mg orally once daily initially, adjust
Presumptive
dose according to INR or dabigatran : 150 mg orally twice daily OR rivaroxaban : 20 mg orally once daily OR apixaban : 5 mg orally twice daily
Patients with heart failure are considered at high risk of thromboembolism. Additional risk factors may also be present, including age 75 years, structural heart disease, diabetes, hypertension, rheumatic heart disease, prosthetic heart valves, or history of prior thromboembolism, and left ventricular ejection
Presumptive
fraction is 35%.

Dronedarone is a multichannel blocker that inhibits the sodium, potassium, and calcium channels and has non-competitive anti-adrenergic activity similar to sotalol, propafenone, and flecainide, but has lower efficacy than amiodarone to maintain sinus rhythm. [28] [29] [30] [31] Additionally, although dronedarone can be safely administered in patients with stable New York Heart Association (NYHA) class I-II heart failure, it is contraindicated in patients with NYHA class IV heart failure or NYHA class II or
Presumptive
III heart failure with a recent (within the previous 4 weeks) decompensation requiring hospitalisation or referral to a specialised heart failure clinic. [48] [49]Dronedarone is also contraindicated in patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent AF) as a safety review showed that dronedarone doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, dronedarone is indicated for the maintenance of sinus rhythm after successful cardioversion in adult clinically stable patients with paroxysmal or persistent AF. Use of dronedarone may be associated with an elevated risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for
Presumptive
the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing. Primary Options digoxin : 0.75 to 1.5 mg orally as a loading dose given in divided doses on first day, followed by maintenance dose of 0.125 to 0.5 mg once daily OR dronedarone : 400 mg orally twice daily with meals Secondary Options amiodarone : 150 mg intravenously initially, followed by 0.5 to 1 mg/min infusion for 24-48 hours plus cardioversion + heparin
Presumptive
[?]
IV heparin (activated partial thromboplastin time (aPTT) of 45 to 60 seconds) or subcutaneous low molecular weight heparin should be started before cardioversion.
DC cardioversion is fast, safe, and efficient. Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents in conversion to sinus rhythm.
Amiodarone provides additional benefit of improved rate control in patients with acute AF. Dronedarone is a multichannel blocker that inhibits the sodium, potassium, and calcium channels and has non-competitive anti-adrenergic activity similar to sotalol, propafenone, and flecainide, but has lower efficacy than amiodarone to maintain sinus
Presumptive
rhythm. [28] [29] [30] [31] Additionally, although dronedarone can be safely administered in patients with stable New York Heart Association (NYHA) class I-II heart failure, it is contraindicated in patients with NYHA class IV heart failure or NYHA class II or III heart failure with a recent (within the previous 4 weeks) decompensation requiring hospitalisation or referral to a specialised heart failure clinic. [48] [49]Dronedarone is also contraindicated in patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent AF) as a safety review showed that dronedarone doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, dronedarone is indicated for the maintenance of sinus rhythm after
Presumptive
successful cardioversion in adult clinically stable patients with paroxysmal or persistent AF. Use of dronedarone may be associated with an elevated risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing.
Ibutilide prolongs repolarisation of the atrial tissue by enhancing the slow inward depolarising Na+ current in the plateau phase of repolarisation. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacological conversion (OR, 29.1; CI, 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3 to 6
Presumptive
hours, prolonged observation period is recommended in patients who have received ibutilide. [47] Primary Options direct current cardioversion or flecainide : 200-300 mg orally as a single dose or propafenone : 600 mg orally as a single dose or amiodarone : 150 mg intravenously initially, followed by 0.5 to 1 mg/min infusion for 24-48 hours or
Presumptive
dronedarone : 400 mg orally twice daily with meals or ibutilide : 0.01 mg/kg (maximum 1 mg/dose) intravenously initially, may repeat 10 minutes after initial dose if no response -- AND -heparin : see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds or enoxaparin : 1 mg/kg subcutaneously every 12 hours plus [?] anticoagulation
Anticoagulation with warfarin is required for patients
Presumptive
at high risk for thromboembolism after sinus rhythm has been restored. IV or subcutaneous heparin is started before cardioversion and should be continued until the warfarin levels are therapeutic (INR 2 to 3). In selected patients warfarin may be substituted with dabigatran. Dabigatran should not be used in patients with marked renal insufficiency or those who have mechanical prosthetic valves. Warfarin may also be substituted with rivaroxaban or apixaban. [36] [37]
Anticoagulation is continued for at least 4 weeks after cardioversion. Primary Options warfarin : 5-10 mg orally once daily initially, adjust
Presumptive
dose according to INR OR dabigatran : 150 mg orally twice daily OR rivaroxaban : 20 mg orally once daily OR apixaban : 5 mg orally twice daily
haemodynamically stable without left atrial thrombus: symptom onset 48 hours without heart failure: low thromboembolic risk 1st
Patients are considered at low risk of
Presumptive
thromboembolic disease if their age is <75 years and there is no structural heart disease, diabetes, hypertension, rheumatic heart disease, prosthetic heart valves, or history of prior thromboembolism, and left ventricular (LV) ejection fraction is >35%.

Esmolol is useful in patients at risk of complications from beta-blockade, particularly those with reactive
Presumptive
airway disease, LV dysfunction, and/or peripheral vascular disease.
If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used. Primary Options metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily
Presumptive
OR esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes, repeat loading dose and increase infusion, consult specialist for further guidance on dose OR diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion OR verapamil : 2.5 to 10 mg intravenous bolus, may give second bolus of 5-10 mg after 30 minutes if necessary Secondary Options
Presumptive
metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily or esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes, repeat loading dose and increase infusion, consult specialist for further guidance on dose -- AND -diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion or verapamil : 2.5 to 10 mg intravenous bolus, may give
Presumptive
second bolus of 5-10 mg after 30 minutes if necessary plus [?] heparin
Heparin should be started, and cardioversion should be delayed until the patient is established on heparin with a target activated partial thromboplastin time of 45 to 60 seconds. Primary Options heparin : see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds OR enoxaparin : 1 mg/kg subcutaneously every 12 hours
Presumptive
plus [?]
cardioversion once heparin anticoagulation established
Cardioversion may be carried out once heparin is established provided the transoesophageal echocardiogram is negative.
Propafenone also has strong evidence of efficacy for
Presumptive
pharmacological conversion (OR, 4.6; CI, 2.6 to 8.2). High conversion rates of up to 76% at 8 hours after treatment. [47]
Amiodarone provides additional benefit of improved rate control in patients with acute AF. Dronedarone is a multichannel blocker that inhibits the sodium, potassium, and calcium channels and has non-competitive anti-adrenergic activity similar to sotalol, propafenone, and flecainide, but has lower efficacy than amiodarone to maintain sinus rhythm. [28] [29] [30] [31] Additionally, although dronedarone can be safely administered in patients with stable New York Heart Association (NYHA)
Presumptive
class I-II heart failure, it is contraindicated in patients with NYHA class IV heart failure or NYHA class II or III heart failure with a recent (within the previous 4 weeks) decompensation requiring hospitalisation or referral to a specialised heart failure clinic. [48] [49]Dronedarone is also contraindicated in patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent AF) as a safety review showed that dronedarone doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, dronedarone is indicated for the maintenance of sinus rhythm after successful cardioversion in adult clinically stable patients with paroxysmal or persistent AF. Use of dronedarone may be associated with an elevated
Presumptive
risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing.
Ibutilide prolongs repolarisation of the atrial tissue by enhancing the slow inward depolarising Na+ current in the plateau phase of repolarisation. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacological conversion (OR, 29.1; CI, 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3 to 6 hours, prolonged observation period is recommended in patients who have received ibutilide. [47]
Presumptive
Primary Options direct current cardioversion OR flecainide : 200-300 mg orally as a single dose OR propafenone : 600 mg orally as a single dose OR amiodarone : 150 mg intravenously initially, followed by 0.5 to 1 mg/min infusion for 24-48 hours OR dronedarone : 400 mg orally twice daily with meals OR
Presumptive
ibutilide : 0.01 mg/kg (maximum 1 mg/dose) intravenously initially, may repeat 10 minutes after initial dose if no response plus [?] long-term aspirin post-cardioversion
Following successful cardioversion, heparin can be discontinued and the patient started on long-term aspirin therapy. Primary Options aspirin : 300 mg orally once daily
without heart failure: high thromboembolic risk
1st
Patients are considered at high risk of thromboembolic disease if their age is 75 years
Presumptive
and/or 1 of the following risk factors are present: structural heart disease, diabetes, hypertension, rheumatic heart disease, prosthetic heart valves, history of prior thromboembolism, or left ventricular (LV) ejection fraction 35%.

Esmolol is useful in patients at risk of complications from beta-blockade, particularly those with reactive
Presumptive
airway disease, LV dysfunction, and/or peripheral vascular disease.
If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used. Primary Options metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily
Presumptive
OR esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes, repeat loading dose and increase infusion, consult specialist for further guidance on dose OR diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion OR verapamil : 2.5 to 10 mg intravenous bolus, may give second bolus of 5-10 mg after 30 minutes if necessary Secondary Options
Presumptive
metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily or esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes, repeat loading dose and increase infusion, consult specialist for further guidance on dose -- AND -diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion or verapamil : 2.5 to 10 mg intravenous bolus, may give
Presumptive
second bolus of 5-10 mg after 30 minutes if necessary plus [?] anticoagulation
Concomitant heparin and warfarin therapy should be started, and heparin continued until the warfarin levels are therapeutic (INR 2 to 3). Anticoagulation with warfarin at the target INR should be established for 3 to 4 weeks before cardioversion is attempted. In selected patients warfarin may be substituted with dabigatran.Dabigatran should not be used in patients with marked renal insufficiency or those who have mechanical prosthetic valves. Warfarin may also be substituted with rivaroxaban or apixaban. [36] [37]
Anticoagulation is continued for at least 4 weeks after cardioversion. [1]
Presumptive
Primary Options heparin : see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds or enoxaparin : 1 mg/kg subcutaneously every 12 hours -- AND -warfarin : 5-10 mg orally once daily initially, adjust dose according to INR (target 2 to 3) or dabigatran : 150 mg orally twice daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation or rivaroxaban : 20 mg orally once daily; consult
Presumptive
specialist for guidance on when to start this drug and when to cease parenteral anticoagulation or apixaban : 5 mg orally twice daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation plus [?] cardioversion following 3 to 4 weeks of anticoagulation
DC cardioversion is fast, safe, and efficient. Class IC agents (flecainide, propafenone) have a higher mortality in patients with CAD and are contraindicated in patients with CAD and cardiac
Presumptive
dysfunction. AF may convert to atrial flutter that may conduct with rapid ventricular rate.
Amiodarone provides additional benefit of improved rate control in patients with acute AF.
Presumptive
Dronedarone is a multichannel blocker that inhibits the sodium, potassium, and calcium channels and has non-competitive anti-adrenergic activity similar to sotalol, propafenone, and flecainide, but has lower efficacy than amiodarone to maintain sinus rhythm. [28] [29] [30] [31] Additionally, although dronedarone can be safely administered in patients with stable New York Heart Associaion (NYHA) class I-II heart failure, it is contraindicated in patients with NYHA class IV heart failure or NYHA class II or III heart failure with a recent (within the previous 4 weeks) decompensation requiring hospitalisation or referral to a specialised heart failure clinic. [48] [49]Dronedarone is also contraindicated in patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent
Presumptive
AF) as a safety review showed that dronedarone doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, dronedarone is indicated for the maintenance of sinus rhythm after successful cardioversion in adult clinically stable patients with paroxysmal or persistent AF. Use of dronedarone may be associated with an elevated risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing.
Ibutilide prolongs repolarisation of the atrial tissue by enhancing the slow inward depolarising Na+ current in the plateau phase of repolarisation. Up to 70% of
Presumptive
all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacological conversion (OR, 29.1; CI, 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3 to 6 hours, a prolonged observation period is recommended in patients who have received ibutilide. [47]
Anticoagulation is continued for at least 4 weeks after cardioversion. [1] Primary Options direct current cardioversion OR flecainide : 200-300 mg orally as a single dose
Presumptive
OR propafenone : 600 mg orally as a single dose OR amiodarone : 150 mg intravenously initially, followed by 0.5 to 1 mg/min infusion for 24-48 hours OR dronedarone : 400 mg orally twice daily with meals OR ibutilide : 0.01 mg/kg (maximum 1 mg/dose) intravenously initially, may repeat 10 minutes after initial dose if no response
Patients with heart failure are considered at high risk of thromboembolism. Additional risk factors may also
Presumptive
be present, including age 75 years, structural heart disease, diabetes, hypertension, rheumatic heart disease, prosthetic heart valves, or history of prior thromboembolism, and left ventricular ejection fraction is 35%.

Dronedarone is a multichannel blocker that inhibits the sodium, potassium, and calcium channels and has non-competitive anti-adrenergic activity similar to sotalol, propafenone, and flecainide, but has lower efficacy than amiodarone to maintain sinus rhythm. [28] [29] [30] [31] Additionally, although
Presumptive
dronedarone can be safely administered in patients with stable New York Heart Association (NYHA) class I-II heart failure, it is contraindicated in patients with NYHA class IV heart failure or NYHA class II or III heart failure with a recent (within the previous 4 weeks) decompensation requiring hospitalisation or referral to a specialised heart failure clinic. [48] [49]Dronedarone is also contraindicated in patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent AF) as a safety review showed that dronedarone doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, dronedarone is indicated for the maintenance of sinus rhythm after successful cardioversion in adult clinically stable
Presumptive
patients with paroxysmal or persistent AF. Use of dronedarone may be associated with an elevated risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing. Primary Options digoxin : 0.75 to 1.5 mg orally as a loading dose given in divided doses on first day, followed by maintenance dose of 0.125 to 0.5 mg once daily Secondary Options amiodarone : 150 mg intravenously initially, followed by 0.5 to 1 mg/min infusion for 24-48 hours
Presumptive
OR dronedarone : 400 mg orally twice daily with meals plus [?] anticoagulation
Concomitant heparin and warfarin therapy should be started, and heparin continued until the warfarin levels are therapeutic (INR 2 to 3). Anticoagulation with warfarin at the target INR should be established for 3 to 4 weeks before cardioversion is attempted. In selected patients warfarin may be substituted with dabigatran. Dabigatran should not be used in patients with marked renal insufficiency or those who have mechanical prosthetic valves. Warfarin may also be substituted with rivaroxaban or apixaban. [36] [37]
Anticoagulation is continued for at least 4 weeks
Presumptive
after cardioversion. [1] Primary Options heparin : see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds or enoxaparin : 1 mg/kg subcutaneously every 12 hours -- AND -warfarin : 5-10 mg orally once daily initially, adjust dose according to INR (target 2 to 3) or dabigatran : 150 mg orally twice daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation or
Presumptive
rivaroxaban : 20 mg orally once daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation or apixaban : 5 mg orally twice daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation plus [?] cardioversion following 3 to 4 weeks of anticoagulation
DC cardioversion is fast, safe, and efficient. Class III agents (including amiodarone and ibutilide)
Presumptive
are less efficacious than class IC agents in conversion to sinus rhythm.

Amiodarone provides additional benefit of improved rate control in patients with acute AF. Dronedarone is a multichannel blocker that inhibits the sodium, potassium, and calcium channels and has non-competitive anti-adrenergic activity similar to sotalol, propafenone, and flecainide, but has lower efficacy than amiodarone to maintain sinus rhythm. [28] [29] [30] [31] Additionally, although dronedarone can be safely administered in patients with stable New York Heart Association (NYHA) class I-II heart failure, it is contraindicated in patients with NYHA class IV heart failure or NYHA class II or III heart failure with a recent (within the previous 4
Presumptive
weeks) decompensation requiring hospitalisation or referral to a specialised heart failure clinic. [48] [49]Dronedarone is also contraindicated in patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent AF) as a safety review showed that dronedarone doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, dronedarone is indicated for the maintenance of sinus rhythm after successful cardioversion in adult clinically stable patients with paroxysmal or persistent AF. Use of dronedarone may be associated with an elevated risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for
Presumptive
the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing.
Ibutilide prolongs repolarisation of the atrial tissue by enhancing the slow inward depolarising Na+ current in the plateau phase of repolarisation. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacological conversion (OR, 29.1; CI, 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3 to 6 hours, a prolonged observation period is recommended in patients who have received ibutilide.
Anticoagulation is continued for at least 4 weeks
Presumptive
after cardioversion. [1] Primary Options direct current cardioversion OR amiodarone : 150 mg intravenously initially, followed by 0.5 to 1 mg/min infusion for 24-48 hours OR dronedarone : 400 mg orally twice daily with meals OR ibutilide : 0.01 mg/kg (maximum 1 mg/dose) intravenously initially, may repeat 10 minutes after initial dose if no response
Presumptive
Treatment Patient group haemodynamically stable without left atrial thrombus: asymptomatic low thromboembolic risk 1st line Treatmenthide all
observation
Most cases of acute AF revert to sinus rhythm spontaneously. Cases that revert spontaneously usually do so in the first 24 hours. [3]
Patients are considered at low risk of thromboembolic disease if their age is <75 years and there is no structural heart disease, diabetes, hypertension, rheumatic heart disease, prosthetic heart valves, or history of prior thromboembolism, and left ventricular ejection fraction is >35%.
Patients should be observed to see whether AF resolves spontaneously.
Presumptive
Treatment Patient group line 2nd Treatmenthide all

If AF does not resolve spontaneously, rate-control therapy is required until cardioversion is successful. Beta-blockers and CCBs slow AV nodal conduction of cardiac impulses and subsequently reduce ventricular rate.
CCBs are preferred in patients with chronic lung disease where bronchospasm may occur with beta-
Presumptive
blockers.
If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used. Primary Options metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily OR esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes,
Presumptive
repeat loading dose and increase infusion, consult specialist for further guidance on dose OR diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion OR verapamil : 2.5 to 10 mg intravenous bolus, may give second bolus of 5-10 mg after 30 minutes if necessary Secondary Options metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily or
Presumptive
esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes, repeat loading dose and increase infusion, consult specialist for further guidance on dose -- AND -diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion or verapamil : 2.5 to 10 mg intravenous bolus, may give second bolus of 5-10 mg after 30 minutes if necessary plus [?] cardioversion
Presumptive
If AF does not resolve spontaneously, cardioversion can be attempted. DC cardioversion is fast, safe, and efficient. Class IC agents (flecainide, propafenone) have a higher mortality in patients with CAD and are contraindicated in patients with CAD and cardiac dysfunction. AF may convert to atrial flutter that may conduct with rapid ventricular rate.
Propafenone also has strong evidence of efficacy for pharmacological conversion (OR, 4.6; CI, 2.6 to 8.2). High conversion rates of up to 76% at 8 hours after
Presumptive
treatment. [47]
Amiodarone provides additional benefit of improved rate control in patients with acute AF. Dronedarone is a multichannel blocker that inhibits the sodium, potassium, and calcium channels and has non-competitive anti-adrenergic activity similar to sotalol, propafenone, and flecainide, but has lower efficacy than amiodarone to maintain sinus rhythm. [28] [29] [30] [31] Additionally, although dronedarone can be safely administered in patients with stable New York Heart Association (NYHA) class I-II heart failure, it is contraindicated in patients with NYHA class IV heart failure or NYHA class II or
Presumptive
III heart failure with a recent (within the previous 4 weeks) decompensation requiring hospitalisation or referral to a specialised heart failure clinic. [48] [49]Dronedarone is also contraindicated in patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent AF) as a safety review showed that dronedarone doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, dronedarone is indicated for the maintenance of sinus rhythm after successful cardioversion in adult clinically stable patients with paroxysmal or persistent AF. Use of dronedarone may be associated with an elevated risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for
Presumptive
the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing.
Ibutilide prolongs repolarisation of the atrial tissue by enhancing the slow inward depolarising Na+ current in the plateau phase of repolarisation. Up to 70% of all conversions occur within 20 minutes of infusion. It has strong evidence of efficacy for pharmacological conversion (OR, 29.1; CI, 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3 to 6 hours, prolonged observation period is recommended in patients who have received ibutilide. [47] Primary Options
Presumptive
direct current cardioversion OR flecainide : 200-300 mg orally as a single dose OR propafenone : 600 mg orally as a single dose OR amiodarone : 150 mg intravenously initially, followed by 0.5 to 1 mg/min infusion for 24-48 hours OR dronedarone : 400 mg orally twice daily with meals OR ibutilide : 0.01 mg/kg (maximum 1 mg/dose) intravenously initially, may repeat 10 minutes after
Presumptive
initial dose if no response

high thromboembolic risk 1st
anticoagulation
Patients are considered at high risk of thromboembolic disease if their age is 75 years and/or 1 of the following risk factors are present: structural heart disease, diabetes, hypertension, rheumatic heart disease, prosthetic heart valves, history of prior thromboembolism, or left ventricular ejection fraction 35%.
Concomitant heparin and warfarin therapy should be started, and heparin continued until the warfarin levels are therapeutic (INR 2 to 3). Most cases of AF resolve spontaneously, but if cardioversion is required, anticoagulation with warfarin at the target INR should be established for 3 to 4 weeks before
Presumptive
cardioversion is attempted. In selected patients warfarin may be substituted with dabigatran. Dabigatran should not be used in patients with marked renal insufficiency or those who have mechanical prosthetic valves. Warfarin may also be substituted with rivaroxaban or apixaban. [36] [37]
Anticoagulation is continued for at least 4 weeks after cardioversion. [1] Primary Options heparin : see local protocol for dosing guidelines, maintain activated partial thromboplastin time (aPTT) at 45-60 seconds or enoxaparin : 1 mg/kg subcutaneously every 12 hours -- AND --
Presumptive
warfarin : 5-10 mg orally once daily initially, adjust dose according to INR (target 2 to 3) or dabigatran : 150 mg orally twice daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation or rivaroxaban : 20 mg orally once daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation or apixaban : 5 mg orally twice daily; consult specialist for guidance on when to start this drug and when to cease parenteral anticoagulation
Presumptive
plus [?]
observation
Most cases of acute AF revert to sinus rhythm spontaneously. Cases that revert spontaneously usually do so in the first 24 hours. [3]
Patients should be observed to see whether AF resolves spontaneously.
adjunct [?]

If AF does not resolve spontaneously, rate-control therapy is required until cardioversion is successful. Beta-blockers and CCBs slow AV nodal conduction of cardiac impulses and subsequently reduce ventricular rate.
Presumptive
If rate control is inadequate with monotherapy, a combination of a beta-blocker and CCB may be used. Primary Options metoprolol : 2.5 to 5 mg intravenous bolus initially,
Presumptive
may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily OR esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes, repeat loading dose and increase infusion, consult specialist for further guidance on dose OR diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion OR verapamil : 2.5 to 10 mg intravenous bolus, may give second bolus of 5-10 mg after 30 minutes if
Presumptive
necessary Secondary Options metoprolol : 2.5 to 5 mg intravenous bolus initially, may repeat every 5 minutes to a total of 3 doses; 200 mg orally twice daily or esmolol : 500 micrograms/kg intravenously as a loading dose, followed by 50 micrograms/kg/min infusion for 4 minutes, if no response after 5 minutes, repeat loading dose and increase infusion, consult specialist for further guidance on dose -- AND -diltiazem : 0.25 mg/kg/dose intravenous bolus, may give second bolus of 0.35 mg/kg if necessary, followed by 5-15 mg/hour infusion
Presumptive
or verapamil : 2.5 to 10 mg intravenous bolus, may give second bolus of 5-10 mg after 30 minutes if necessary adjunct [?] cardioversion
If AF does not resolve spontaneously, cardioversion should only be attempted once the patient has been established on anticoagulation with a target INR of 2 to 3 for 3 to 4 weeks.
DC cardioversion is fast, safe, and efficient. Class IC agents (flecainide, propafenone) have a higher mortality in patients with CAD and are contraindicated in patients with CAD and cardiac dysfunction. AF may convert to atrial flutter that may
Presumptive
conduct with rapid ventricular rate.
Flecainide has strong evidence of efficacy for pharmacological conversion (odds ratio (OR), 24.7; CI, 9.0 to 68.3). High conversion rate of about 70% at 3 hours after treatment and up to 90% at 8 hours. [47]
Amiodarone provides additional benefit of improved rate control in patients with acute AF. Dronedarone is a multichannel blocker that inhibits
Presumptive
the sodium, potassium, and calcium channels and has non-competitive anti-adrenergic activity similar to sotalol, propafenone, and flecainide, but has lower efficacy than amiodarone to maintain sinus rhythm. [28] [29] [30] [31] Additionally, although dronedarone can be safely administered in patients with stable New York Heart Association (NYHA) class I-II heart failure, it is contraindicated in patients with NYHA class IV heart failure or NYHA class II or III heart failure with a recent (within the previous 4 weeks) decompensation requiring hospitalisation or referral to a specialised heart failure clinic. [48] [49]Dronedarone is also contraindicated in patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent AF) as a safety review showed that dronedarone
Presumptive
doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, dronedarone is indicated for the maintenance of sinus rhythm after successful cardioversion in adult clinically stable patients with paroxysmal or persistent AF. Use of dronedarone may be associated with an elevated risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing.
Ibutilide prolongs repolarisation of the atrial tissue by enhancing the slow inward depolarising Na+ current in the plateau phase of repolarisation. Up to 70% of all conversions occur within 20 minutes of infusion. It
Presumptive
has strong evidence of efficacy for pharmacological conversion (OR, 29.1; CI, 9.8 to 86.1). Conversion rates are between 33% and 45% within the first 70 minutes. Because the half-life of ibutilide is 3 to 6 hours, prolonged observation period is recommended in patients who have received ibutilide. [47] Primary Options direct current cardioversion OR flecainide : 200-300 mg orally as a single dose OR propafenone : 600 mg orally as a single dose
Presumptive
OR amiodarone : 150 mg intravenously initially, followed by 0.5 to 1 mg/min infusion for 24-48 hours OR dronedarone : 400 mg orally twice daily with meals OR ibutilide : 0.01 mg/kg (maximum 1 mg/dose) intravenously initially, may repeat 10 minutes after initial dose if no response
Acute
Treatment approach
The 3 elements in the management of acute AF are:
1. 2. 3.
Ventricular rate control Restoration and maintenance of sinus rhythm Prevention of thromboembolic events. [1] [25] [26] [27]
Management of acute AF depends on the nature of its presentation, so the urgency of the treatment required should be assessed. Most cases of acute AF revert to sinus rhythm spontaneously, but do require adequate ventricular rate control with drugs such as beta-blockers, calcium-channel blockers, and occasionally digoxin. Cases that revert spontaneously usually do so in the first 24 hours. [3] Those patients who do not revert may require either direct current (DC) cardioversion or pharmacological cardioversion. Depending on further risks for AF, patients may require treatment with various antiarrhythmic agents to prevent AF. Among the newly available anti-arrhythmic agents, dronedarone, a multichannel blocker that inhibits the sodium, potassium, and calcium channels and has non-competitive anti-adrenergic activity similar to sotalol, propafenone, and flecainide, has lower efficacy than amiodarone to maintain sinus rhythm. [28] [29] [30] [31] Acute AF may be the first symptomatic presentation of paroxysmal AF, and it is necessary to perform transoesophageal echocardiography (TOE) to rule out left atrial (LA) clots before cardioversion. Many patients require anticoagulation before, during, and after cardioversion to prevent thromboembolic events. Because commonly used oral anticoagulants (vitamin K antagonists) take several days to have therapeutic effect, patients presenting with acute AF are treated with IV heparin (activated partial thromboplastin time [aPTT] of 45-60 seconds) or subcutaneous low molecular weight heparin while they are awaiting cardioversion and being evaluated for long-term anticoagulation. Dabigatran, a direct thrombin inhibitor, has been released after its comparison with warfarin in a large randomised trial, the RE-LY trial. As compared with warfarin, dabigatran was associated with lower rates of stroke and systemic embolism but similar rates of major haemorrhage. At a lower dose of dabigatran, the rates of stroke and systemic embolism were similar to those for warfarin. The rate of MI was higher with both doses of dabigatran than with warfarin. [27] [32] [33] Dabigatran may be associated with an increased risk of stroke, heart attack, and blood clot in patients with mechanical prosthetic valves and, therefore, should not be used in these patients. [FDA: dabigatran safety alert] (external link) Based on the current evidence, it is reasonable to use dabigatran as a first-line agent or subsequent replacement for warfarin in suitable patients who do not have marked renal insufficiency,
and who do not have mechanical prosthetic valves. [32] [33] [34] Another reasonable alternative to warfarin is the direct factor Xa inhibitor rivaroxaban. [32] [33] [35] The ROCKET AF trial compared rivaroxaban with warfarin in patients with non-valvular AF who were at increased risk for stroke. Rivaroxaban was found to be non-inferior to warfarin for the prevention of stroke or systemic embolism. The risk of major bleeding with rivaroxaban was similar to that of warfarin. [32] [33] [36] Apixaban is another direct factor Xa inhibitor that has been shown to be at least as efficacious as warfarin. [32] [33] Following favourable results from the ARISTOTLE trial, apixaban has now been approved to prevent stroke in patients with nonvalvular AF in some countries. [37] The choice of anticoagulation strategy depends on the presentation. Factors in the patient's presentation and diagnostic assessment which guide appropriate treatment include the following:
Whether the patient is haemodynamically stable or unstable If haemodynamically stable, whether the patient is symptomatic or asymptomatic If symptomatic, the onset of the symptoms (<48 hours, 48 hours, or unknown) The presence of associated heart failure The presence of a thrombus on TOE If a thrombus is absent on TOE, whether the patient has a high or low thromboembolic risk. Patients are considered at high risk of thromboembolic disease if their age is 75 years and/or 1 of the following risk factors are present: structural heart disease, diabetes, hypertension, rheumatic heart disease, prosthetic heart valves, history of prior thromboembolism, or left ventricular ejection fraction 35%.
Need for hospital admission

Patients who present with new-onset AF who are at low risk for major clinical consequences (young patients with no structural heart diseases, no major cardiac symptoms, or haemodynamic compromise) may be discharged directly from the emergency department after stable sinus rhythm is restored. Admission to hospital is indicated for the following patient groups:
Patients with underlying heart disease who have haemodynamic consequences or symptoms of angina, heart failure, or syncope or who are at risk for a complication resulting from therapy of the arrhythmia Older patients
Associated or precipitant medical conditions that require further treatment, such as heart failure, pulmonary problems (e.g., pneumonia, pulmonary embolism), hypertension, or hyperthyroidism.
Haemodynamically unstable AF
AF with a rapid ventricular rate causing ongoing chest pain, hypotension, shortness of breath, dizziness, or syncope requires immediate DC cardioversion. This is performed under adequate short-acting general anaesthesia and involves delivery of an electrical shock synchronised with the intrinsic activity of the heart by sensing the R wave of the ECG (i.e., synchronised). The energy output for successful termination of acute AF varies from 200 J to a maximum of 400 J depending on the body size and the presence of other co-morbid conditions. Lower energy of 100 J may be used as the starting level when biphasic energy is used.
Haemodynamically stable AF: symptomatic

Patients require rate-control therapy until cardioversion is successful. If there is no evidence of heart failure, beta-blockers or calcium-channel blockers are the preferred choice. If rate control is inadequate with monotherapy, a combination of a beta-blocker and calcium-channel blocker may be used. Patient should be carefully monitored to prevent excess AV nodal blockade. [1] If there is evidence of heart failure, digoxin[B Evidence] or amiodarone[C Evidence] should be used. Patients presenting with acute AF of <48 hours' duration and no evidence of LA thrombus on TOE should have DC[C Evidence] or pharmacological cardioversion. DC cardioversion is fast, safe, and efficient. Pharmacological cardioversion is accomplished with the use of anti-arrhythmic agents. However, these must be used with caution as they may cause bradycardia or tachyarrhythmias. Anti-arrhythmic agents with variable, but demonstrated, efficacy for cardioversion of acute AF include flecainide,[B Evidence] propafenone,[A Evidence] ibutilide, vernakalant, [38] [39] [40] dronedarone, [28] [29] [30] [31] and amiodarone.[C Evidence][B Evidence] Class III agents (including amiodarone and ibutilide) are less efficacious than class IC agents (flecainide and propafenone) in conversion to sinus rhythm. [1] [41] [42] [43]Intravenous vernakalant has demonstrated superior efficacy to amiodarone for acute conversion of recentonset AF. [40] Oral vernakalant appears to be effective in preventing AF recurrence post-cardioversion. [44] Dronedarone is a multiclass anti-arrhythmic agent. It is approved in Europe for the maintenance of sinus rhythm after successful cardioversion in adult
clinically stable patients with paroxysmal or persistent AF and associated cardiovascular risk factors (i.e., age >70 years, hypertension, diabetes, prior cerebrovascular accident, left atrial diameter 50 mm, or left ventricular ejection fraction <40%). Dronedarone is contraindicated in patients with NYHA class IV heart failure, or NYHA class II-III heart failure with a recent decompensation requiring admission to hospital or referral to a specialised heart failure clinic. Dronedarone is also contraindicated in patients with AF who cannot, or will not, be converted into normal sinus rhythm (i.e., permanent AF) as a safety review showed that dronedarone doubles the risk of serious cardiovascular events including stroke, heart failure, and death in patients with permanent AF. In Europe, it is indicated for the maintenance of sinus rhythm after successful cardioversion in adult clinically stable patients with paroxysmal or persistent AF. Although dronedarone is less effective than amiodarone for the maintenance of sinus rhythm, dronedarone has fewer adverse effects. [28] [45] However, use of dronedarone may be associated with an elevated risk of worsening, or new-onset, heart failure or liver toxicity. Patients should be asked to be vigilant for the symptoms of heart failure or liver toxicity during treatment, and should undergo regular liver function testing. The strategy for managing anticoagulation in these patients is as follows:
If the thromboembolic risk is low, no anticoagulation is required. If the thromboembolic risk is high, IV heparin (aPTT of 45-60 seconds) or subcutaneous low molecular weight heparin should be started before cardioversion. Once sinus rhythm is restored, the patients should be started on warfarin and heparin continued until the the warfarin levels are therapeutic (INR 2-3). Anticoagulation is continued for at least 4 weeks after cardioversion. [1] [46]
If the onset of symptoms is >48 hours or unknown and there is no evidence of LA thrombus on TOE, patients should have DC[C Evidence] or pharmacological cardioversion, but the cardioversion should not be attempted until the patient is established on anticoagulation. The strategy for managing anticoagulation in these patients is as follows:
If the thromboembolic risk is low, heparin should be started, and cardioversion should be delayed until the patient is established on heparin with a target activated partial thromboplastin time of 45 to 60 seconds. Following successful cardioversion, heparin can be discontinued and the patient started on long-term aspirin therapy. If the thromboembolic risk is high, concomitant heparin and warfarin therapy should be started, and heparin continued until the warfarin levels are therapeutic (INR 2-3). [1] [15]Anticoagulation with warfarin at the
target INR should be established for 3 to 4 weeks before cardioversion is attempted. [15] Anticoagulation is continued for at least 4 weeks after cardioversion. [1] [46]
If there is evidence of LA thrombus on TOE, concomitant heparin and warfarin therapy should be started, and heparin continued until the warfarin levels are therapeutic (INR 2-3). Anticoagulation with warfarin at the target INR should be established for 3 to 4 weeks before cardioversion is attempted. Anticoagulation is continued for at least 4 weeks after cardioversion, and may be required for longer in some patients. [1] [46]
Haemodynamically stable AF: asymptomatic

Patients with low thromboembolic risk can be observed. Most cases of acute AF revert to sinus rhythm spontaneously, usually in the first 24 hours. If AF does not resolve spontaneously, rate-control therapy is required until cardioversion is successful. Cardioversion can be attempted without the need for anticoagulation. Patients with high thromboembolic risk require immediate anticoagulation. Concomitant heparin and warfarin therapy should be started, and heparin continued until the warfarin levels are therapeutic (INR 2-3). Patients should be observed to see whether AF resolves spontaneously. If the AF does not resolve, anticoagulation with warfarin at the target INR should be established for 3 to 4 weeks before cardioversion is attempted. Rate-control therapy is required until cardioversion is performed. Anticoagulation is continued for at least 4 weeks after cardioversion.
Post-cardioversion management
Patients with a newly detected first episode of acute AF converted to sinus rhythm are not continued on rhythm maintenance therapy as the risks outweigh the benefits. Low thromboembolic-risk patients presenting within 48 hours of the onset of symptoms do not require long-term aspirin or anticoagulation. Low thromboembolic-risk patients presenting after this time should be continued on long-term aspirin therapy. Long-term anticoagulation is required for patients with identified high risk for thromboembolism even after sinus rhythm has been restored. [1] [46]
Emerging treatments
Azimilide Blocks both the rapid (Ikr) and slow (Iks) components of the delayed rectifier potassium current and possesses anti-arrhythmic activity at faster heart rates.
Several clinical studies have demonstrated the safety and efficacy of azimilide in the management of ventricular as well as supraventricular arrhythmias. [50] Tedisamil A class III anti-arrhythmic agent that has been reported to block several potassium currents. At higher concentrations, tedisamil inhibits the rapid inward sodium current as well as the chloride channel. Tedisamil is being investigated for acute termination of AF and atrial flutter.[51] [52] Trecetilide Trecetilide, a congener of ibutilide, is being evaluated in both IV and oral preparations for the termination and prevention of AF. [53] ACE inhibitors and angiotensin receptor blockers The renin-angiotensin-aldosterone system has emerged as an important hormonal system in the initiation and pathogenesis of AF. Therefore, ACE inhibitors and angiotensin receptor blockers are emerging as upstream therapy for the prevention of AF. However, they may not be used as primary or sole anti-arrhythmic therapy in patients with AF. [54] [55] Statins Statins have demonstrated some diverse pleiotropic properties, which include their influence on endothelial function, inflammation, plaque stability, thrombosis, angiogenesis, apoptosis, and gene expression. It is by modulating these factors that lipid-lowering drugs are considered to exhibit their anti-arrhythmic properties. Many clinical trials and their meta-analyses indicate that the use of statins significantly decreases the risk of incidence or recurrence of AF in patients in sinus rhythm with a history of previous AF or undergoing cardiac surgery or after acute coronary syndrome. [56] [57] Magnesium Many clinical trials and their meta-analyses indicate that intravenous magnesium is not very effective in converting acute-onset AF to sinus rhythm when compared with placebo or an alternative anti-arrhythmic drug. However, as a rate-control regimen, adding intravenous magnesium to digoxin reduces fast ventricular response in acute-onset AF. [58] [59]
Monitoring
Patients presenting with acute AF who have paroxysmal, persistent, or permanent AF need long-term follow-up. Depending on the nature of the underlying cause of AF (i.e., CAD, valvular heart disease, or heart failure), patients should have regular (minimum 6 to 12 months) echocardiograms and consideration of exercise stress testing. Patients who are taking anti-arrhythmic agents need follow-up for ECG monitoring. Exercise stress testing is recommended to assess for usedependence pro-arrhythmia of ventricular tachycardia in patients taking flecainide and propafenone. A regular follow-up to check and monitor INR is mandatory for those patients who are taking warfarin for anticoagulation. Routine monitoring of digoxin levels is not required but levels can be checked if toxicity or inadequate dosing is suspected.
Patient Instructions
Patients who have identifiable and known triggers to AF, such as alcohol, stimulants, caffeine, or nicotine, should be advised to avoid such triggers to help prevent recurrence.
Complications
Complicationhide all
acute stroke see our comprehensive coverage of Overview of stroke Patients usually have paroxysmal to persistent AF with risk factors to thromboembolic events, such as left atrial dilation, CHF, hypertension, diabetes, hyperlipidaemia, and advanced age. Controversy exists as regards treatment of established embolic acute stroke in the presence of acute AF. Anticoagulation in this setting may cause haemorrhagic stroke. Consultation with a consultant (neurologist) is highly recommended. Novel approaches to interrupt thrombus propagation by intravascular devices are being studied. MI see our comprehensive coverage of Overview of acute coronary syndrome Rapid ventricular rate and increased myocardial demand may lead to acute MI in people with CAD. CHF see our comprehensive coverage of Acute exacerbation of congestive heart failure
Rapid ventricular rate, increased myocardial demand, and unfavourable haemodynamics may lead to acute heart failure in people with CAD, left ventricular dysfunction, and valvular pathology.
Last updated: Jan 28, 2
Prognosis
The prognosis of acute AF depends on several factors, such as the precipitating event, underlying cardiac status, risk of thromboembolism, and whether the nature of the AF is paroxysmal, persistent, or permanent. In young patients with no structural cardiac abnormalities who have an episode of acute AF as a result of alcohol bingeing, prognosis is excellent with avoidance of alcohol. In contrast, short- and long-term prognosis for patients presenting with new onset of AF with heart failure following MI is poor. Furthermore, a meta-analysis has shown that there is an increased risk of mortality with the presence of AF in the setting of MI, which persists regardless of the timing of AF. [60] Patients with prior AF or new-onset AF following MI need close clinical follow-up.

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Acute atrial fibrillation

History & exam

Other diagnostic factors

Diagnostic tests details

History & examination

irregular pulse rate (common)

Other diagnostic factorshide all

valvular heart disease CAD

other atrial arrhythmias

cardiac or thoracic surgery Common postoperative complication. [1] hyperthyroidism

Weak hypoxic pulmonary conditions

Likely to be due to increase in left atrial size. [1] [21]

ECG Should be the first test requested. View image

The presence of atrial thrombus increases the risk of embolic stroke.

Tests to considerhide all

Usually presents at younger age (teens or early 20s).

with ECG changes suggestive of Wolff-Parkinson-White syndrome who

Step-by-step diagnostic approach

History and examination

Atrial fibrillationFrom the collections of Arti N. Shah and Bharat K. Kantharia

Investigation for causal factors

Risk factors for thromboembolism in patients with AF [1]

Moderate risk factors

High risk factors

CHADS2 scoring system for risk of thromboembolism [22] [2]

HEMORR2HAGES score system [23]

direct current (DC) cardioversion

rate control with beta-blockers and/or calcium-channel blockers (CCBs)

Rate-control therapy is required until cardioversion is successful.

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

at 3 hours after treatment and up to 90% at 8 hours. [47]

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

rate control with digoxin or amiodarone or dronedarone

Dronedarone can be safely administered in patients

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all

direct current (DC) cardioversion

Treatment Patient group haemodynamically unstable line 1st Treatmenthide all