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Journal of the Accident and Medical Practitioners Association (JAMPA) 2004; Vol. 1 (No. 1)
 Accident and Medical Practitioners Association, New Zealand
___________________________________________________________________________
Acute Atrial Fibrillation:
Key Issues in Emergency Management
Etienne de Beer, MBChB, FAMPA
Emergency Care Centre, North Shore Hospital, Takapuna, North Shore City
About the author
Dr Etienne de Beer, MBChB, FAMPA is a Medical Officer Special Scale (MOSS) working
in the Emergency Care Centre at North Shore Hospital, Takapuna. He has a special interest in
the management of medical emergencies, particularly acute arrhythmias.
Address for correspondence: Dr Etienne de Beer, MBChB, FAMPA, Emergency Care
Centre, North Shore Hospital, Private Bag, Takapuna.
E-mail: [email protected]
Issues this article will address

Incidence and significance of atrial fibrillation

Rhythm control in atrial fibrillation

Rate control in atrial fibrillation

Prevention of thromboembolic complications
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Salient Points

Presentation to an emergency department due to acute onset of atrial fibrillation (AF)
is a common occurrence.

In most cases, a decision has to be made between aiming for conversion to sinus
rhythm or accepting the arrhythmia and controlling the ventricular rate. In the absence
of clear guidance from clinical trials, this choice needs to be individualised for each
patient.

The need for anticoagulant therapy should be assessed in each case.
Key words: Atrial fibrillation · Thromboembolism · Cardioversion · Ventricular rate control
· Anticoagulant therapy
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Introduction: Incidence and Significance of Atrial Fibrillation
Acute atrial fibrillation (AF) is the most common form of paroxysmal tachycardia in patients
presenting to emergency departments.[1] The incidence of AF steadily increases with age
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 85 and 94 years.[2] Symptoms of
uncontrolled AF vary from palpitations to poor cardiac performance, resulting in decreased
effort tolerance, worsening manifestations of coronary artery disease, congestive heart failure
(CHF), and possible sudden cardiac death. Sustained AF is associated with a five-fold
increase in the risk of thromboembolic events, especially stroke.[1] The presence of AF
increases mortality and is associated with a relative risk of death of about 1.5 for males and
1.9 for females.[2]
The challenge of AF has aptly been termed “the last big hurdle in treating supraventricular
tachycardia”.[2] The past decade has witnessed extraordinary growth in all areas of
knowledge regarding AF, but important questions remain unanswered largely because of the
absence of definitive clinical trials.[3,4]
Illustrative Case History
The following case history illustrates some key points regarding the management of patients
presenting with acute AF.
CASE DESCRIPTION
DW, a 62-year-old female, presented to an emergency department because of palpitations,
dyspnoea on exertion, and generalised weakness. The palpitations were rapid and irregular,
and had commenced abruptly at rest 2 hours earlier. There was no associated chest pain or
light-headedness.
There was a history of hypertension for which the patient took enalapril 5 mg daily, and
type 2 (non-insulin-dependent) diabetes mellitus which was controlled by diet. There was
no previous history of palpitations, syncope, chest pain, transient ischaemic attacks (TIAs),
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or cerebrovascular accident (CVA).
The patient was undistressed and her colour and perfusion were normal. Her pulse was 130
beats/min and irregularly irregular, BP 150/92 mm Hg, and respiratory rate 14/min. There
was no oedema, jugular venous pressure (JVP) was not raised, and lung fields were clear.
The heart sounds were dual and there were no murmurs. The abdomen was normal. An
ECG showed AF with a ventricular rate of 140 beats/min, and left ventricular hypertrophy
(LVH) by voltage criteria with lateral repolarisation changes unchanged from a previous
ECG. A chest x-ray showed borderline cardiomegaly and no signs of left ventricular failure.
The patient was assessed as having haemodynamically stable acute AF with no evidence of
CHF or acute ischaemia. Oxygen was administered and cardiac monitoring was begun. An
intravenous line was established, and blood drawn for a full blood count, urea and
electrolyte determinations, and thyroid function tests. An infusion of 150 mg amiodarone
over 30 minutes was commenced.
On completion of the amiodarone infusion, the patient remained in AF with a ventricular
rate of 100-110 beats/min and BP 130/78 mm Hg. A further infusion of amiodarone 150 mg
over 30 minutes was administered. Shortly after completion of this infusion, the patient
reverted to sinus rhythm with a heart rate of 60 beats/min and BP 120/74 mm Hg.
The blood count and urea and electrolyte levels were found to be normal, and the patient
was discharged with a referral for an outpatient echocardiograph and follow-up by her
general practitioner. She was advised of the possibility of recurrences of the arrhythmia,
and advised to seek medical attention promptly if she had further palpitations.
Emergency Management Considerations
When assessing a patient with newly diagnosed AF, the clinical significance of the
arrhythmia needs to be determined and associated conditions identified. Potentially harmful
effects of antiarrhythmic treatment on underlying cardiac conditions should be taken into
account.
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Major issues to consider are:

Conversion to sinus rhythm

Slowing the ventricular rate

Preventing thromboembolic events.
In some patients, such as those with pulmonary oedema, acute myocardial infarction, or
unstable angina, urgent direct current (DC) cardioversion may be necessary.[2]
Rate Control or Restoration of Sinus Rhythm?
In the absence of an urgent need for cardioversion, the immediate choice is between
ventricular rate control and prompt restoration of sinus rhythm. The debate over which of
these two approaches to use is largely theoretical, with very little evidence from definitive
clinical trials available. Experimental studies suggest that remodelling of the atria during AF
can lead to persistent morphological changes that may develop within a relatively short
period, and tachycardia-induced electrical changes that may be more easily reversible. This
finding suggests that cardioversion should be performed as early as possible after the onset of
arrhythmia. Prompt treatment may result in a higher success rate in restoring sinus rhythm
and may prevent recurrences of AF. Potential benefits of this strategy include relief of
symptoms, prevention of tachycardia-induced dysfunction, improved exercise capacity and
quality-of-life, and possibly a reduction in the risk of thromboembolism and improved
survival.[5]
Because of factors such as these, supporters of rhythm control believe that patients who are
converted to sinus rhythm have a better outcome than those who remain in AF. Proponents of
rate control argue that rate control is achievable in most patients, that avoidance of potentially
toxic class I and III antiarrhythmic drugs improves outcome, and that the risk of
thromboembolism can be decreased with anticoagulants.
Two recent studies [6,7] reported the outcomes in more than 4500 older, high-risk patients
with AF who were randomly assigned to rhythm control or rate control. Rhythm control was
not associated with improved survival in either study. Rate control can thus be considered a
primary approach to the treatment of AF. When rhythm control is used, it can be discontinued
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early if it is not entirely satisfactory, e.g. due to lack of efficacy or adverse effects of
medications. Undoubtedly, cardioversion and maintenance of sinus rhythm will still be the
preferred approach in some patients, particularly where this leads to a marked improvement
in symptoms,[8] and where recurrences of AF while on antiarrhythmic therapy are not
troublesome.
Self-termination of acute AF occurs in up to two-thirds of cases within 24 hours. However,
the longer the AF persists, the less likely it is to revert spontaneously, and after one week
self-termination is rare.[2] In patients presenting with acute AF, a period of rate control only
may therefore be followed by spontaneous conversion to sinus rhythm. If spontaneous
conversion to sinus rhythm fails to occur, elective electrical cardioversion could still be
considered.
Pharmacological Control of the Ventricular Rate
Digoxin, which is often used in patients with impaired left ventricular function, does slow the
ventricular rate at rest, but has a slow onset of action and is relatively ineffective in patients
with activation of the sympathetic nervous system, e.g. with exertion. In patients with
preserved left ventricular function, an intravenous beta-blocker or calcium channel blocker
have a more rapid onset of action and slow the ventricular rate whether or not there is
sympathetic activation.[2] Dosages of commonly used agents are shown in Table 1. The
combination of a beta-blocker or calcium channel blocker with digoxin provides a synergistic
effect, and a beta-blocker plus digoxin is probably the most effective way to control the
ventricular rate pharmacologically in AF.[9]
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Table 1. Dosages of pharmacological agents commonly used for controlling the
ventricular rate (NB. the rate is usually considered controlled when the ventricular response
is 60-80/min at rest and 90-115/min during moderate exercise [17])
Agent/route of administration
IV administration:
 Beta-blocker – metoprolol
 Calcium channel blocker – verapamil
 Digoxin
Oral administration:
 Digoxin
 Beta-blockers:
Metoprolol
Propranolol
 Calcium channel blockers:
Diltiazem
Verapamil
Dosage
2.5-5 mg bolus over 2 min; can be repeated
twice (onset 5 min)
0.075-0.15 mg/kg over 2 min loading dose
(onset 3-5 min)
0.25 mg every 2 hours up to 1.5 mg (onset 2
hours)
0.25 mg every 2 hours up to 1.5 mg (onset 2
hours), then 0.125-0.25 mg daily
25-100 mg twice daily (onset 4-6 hours)
80-240 mg daily in divided doses (onset 60-90
min)
120-360 mg daily in divided doses (onset 2-4
hours)
120-360 mg daily in divided doses (onset 1-2
hours)
Cardioversion
DC cardioversion is fast, safe, and efficient. Its major drawbacks are the need for conscious
sedation or anaesthesia and the possibility of early recurrence of the arrhythmia.
Pharmacological cardioversion may be superior to electrical cardioversion if it is associated
with earlier restoration of atrial mechanical function, a higher rate of conversion to sinus
rhythm, lower costs, or improved patient acceptance.[3] However, many of these issues
require further investigation and remain to be firmly established.
Early drug therapy to restore sinus rhythm can be considered in patients in whom the
arrhythmia has lasted less than 48 hours or who are on warfarin. Appropriate drug therapy
restores acute AF to sinus rhythm in up to 90% of cases.[2] Drugs with proven efficacy for
the conversion of recent-onset AF include flecainide, propafenone, procainamide, quinidine,
disopyramide, sotalol, amiodarone, dofetilide, and ibutilide. Flecainide (for dosage refer
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Table 2) is probably the most effective agent,[10] but is associated with significant
proarrhythmic effects and is therefore contraindicated in patients with structural and/or
ischaemic heart disease or major conduction disturbances.
Amiodarone is an effective (overall conversion rate greater than 90%) and safe agent for the
treatment of AF, provided rapid conversion is not required.[11-14] Although amiodarone has
many cardiac and non-cardiac adverse effects, the majority are related to the dose and
duration of treatment [12] and are therefore not a consideration when the drug is used for
cardioversion. The IV dosage of amiodarone is shown in Table 2.
Table 2. Dosages of pharmacological agents commonly used
for conversion of AF to sinus rhythm
Agent
Dosage
 Flecainide
2 mg/kg IV over 20 min
 Amiodarone
5 mg/kg IV over 60 min followed
by 50 mg/hour (up to total of 1.21.8 g in first 24 hours)
5-13 mg/kg IV at rate of 0.2-0.5
mg/kg/min (maximum advisable
dose 1000 mg)
 Procainamide
Efforts to convert AF to sinus rhythm or slow the ventricular rate can lead to profound
bradycardia and even asystole, especially in patients with underlying conduction system
disease or sinus node dysfunction. Consequently it is advisable to have temporary pacing
capability (transcutaneous or transvenous) or pharmacological support (IV dopamine,
isoprenaline, or atropine) available.[15]
Preventing Thromboembolic Events
When the duration of AF is unknown, it is necessary to give an anticoagulant before
cardioversion to prevent thromboembolic complications. In this situation, the options are as
follows:[2]

Warfarin for a minimum of 3 weeks before cardioversion (aiming for an INR
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[international normalized ratio] of 2 to 3); or

Transoesophageal echocardiography with immediate cardioversion in the absence of
evidence of thromboembolism. Short-term anticoagulant therapy before and during the
procedure is required.[16]
In both instances, anticoagulant therapy should be continued for at least 3 to 4 weeks after
cardioversion.
It has been shown that most patients with new-onset AF need not be admitted to hospital, and
that appropriately experienced emergency physicians can achieve safe cardioversion in lowrisk patients (exclusion criteria: unstable condition, complicated diagnosis requiring
admission, primary presentation not one of AF) before discharge – either with electrical
cardioversion or pharmacologically where the antiarrhythmic drug is discontinued once
cardioversion has been achieved.[1] Therefore, in the case of the patient discussed above
(DW), it was elected to attempt cardioversion with amiodarone, which ultimately proved
successful.
The need for anticoagulant therapy in a patient with an acute episode of AF that has
terminated is not clear, and should be individualised for each patient based on the intrinsic
risk of thromboembolism. Antiarrhythmic drugs to prevent recurrences of AF are usually
unnecessary, unless the AF is associated with severe symptoms related to hypotension,
myocardial ischaemia, or heart failure.
References
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