Atrial fibrillation

Abhay Bajpai
Edward Rowland

Atrial fibrillation (AF) is the commonest car- Classification Key points

diac arrhythmia. The incidence increases with
Classification of AF has always been Atrial fibrillation (AF) is the
age and affects 5% of UK population above
controversial.3–5 The current classification is commonest cardiac
the age of 65 yr and 10% above 75 yr.1 2 In the arrhythmia; its incidence
based on two important elements: patterns

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United States, AF accounts for more than 35% increases with age.
of evolution of arrhythmia and the response
of all admissions for cardiac arrhythmias.3
to treatment. Diabetes mellitus,
Men are 1.5 times more likely to develop
First onset AF is the first clinical presenta- hypertension and ventricular
AF than women. AF is often associated hypertrophy are commonly
tion where the patient is still in AF and the
with structural heart disease, but in many associated with non-valvular
episode has been present for less than 48 h.
patients it can occur with no detectable disease atrial fibrillation.
Paroxysmal AF is the occurrence of recur-
(lone AF). Thromboembolic events and heart
rent episodes that typically last minutes to Primary aims of management
failure resulting from AF lead to significant of AF are conversion to sinus
hours, occasionally days, but eventually self-
morbidity, mortality and increased cost of rhythm, maintenance of sinus
terminate.
management. rhythm and prevention of
Persistent AF is present when arrhythmia is
thromboembolic
Definition and not self-terminating, but pharmacological or
complications.
electrocardiographic patterns electrical cardioversion is required to restore
sinus rhythm. In elderly patients who are
AF is a supraventricular arrhythmia charac- asymptomatic, adequate rate
AF is permanent when all attempts to
terised by complete absence of coordinated control of AF appears to offer
restore sinus rhythm have been abandoned
atrial contractions. On the electrocardiogram the same benefits as rhythm
because of physician or patient decision, fre-
there is consistent absence of P waves which control.
quent recurrence, or inability to cardiovert the
are replaced by fibrillatory waves. AF is Chronic AF carries a high risk
patient.
associated with an irregular and frequently of ischaemic stroke from
rapid ventricular response if atrioventricular thromboembolism; all
conduction is intact. Regular R-R intervals Pathophysiology and patients at risk must receive
are possible in the presence of atrioventricular mechanisms adequate anticoagulation.
block or interference by ventricular or junc- Anticoagulation should be
The mechanisms of AF are not fully clear, but
tional tachycardia.3 A wide QRS complex continued in patients with risk
at least three aspects seem to be important in
tachycardia that is rapid, irregular or sus- factors despite successful
its genesis and maintenance: conversion to sinus rhythm.
tained strongly suggests underlying bundle
branch block or conduction over an accessory  There may be enhanced automaticity
pathway (e.g. Wolf–Parkinson–White syn- within ‘sleeves’ of atrial tissue that extend
drome) especially if the ventricular rate is into the pulmonary veins or vena caval
extremely rapid (over 200 beats min 1). junctions.6 These foci can act as trigger
AF can be commonly associated with points to generate multiple atrial ectopics
other arrhythmias such as atrial flutter or leading to AF and their elimination by
atrial tachycardia. Atrial flutter is a more means of ablation may possibly provide Abhay Bajpai
organised and regular form of atrial activation a permanent cure, particularly in those Clinical Research Fellow
resulting in a saw-tooth pattern or flutter with structurally normal hearts. Cardiovascular Sciences
waves (f) on the electrocardiogram. Atrial flut-  In chronic AF, maintenance of arrhythmia St George’s
University of London
ter can arise during treatment of AF with is sustained by multiple re-entering and London
antiarrhythmic drugs. Atrial flutter itself can randomly circulating wavelets that collide UK
degenerate into AF, can be triggered by AF and divide into ‘daughter-wavelets’ thus Edward Rowland
or the pattern can alternate between AF and maintaining the chaotic electrical state.7 8 Consultant Cardiologist
flutter. Other atrial arrhythmias can also trig-  The longer the duration of AF, the more St George’s Hospital
ger AF and are identified by the presence of P difficult it is to restore sinus rhythm and London
UK
waves which are separated by an isoelectric prevent recurrences. This is due to electri- E-mail: erowland@sgul.ac.uk
baseline. cal and structural remodelling of atrial (for correspondence)

doi:10.1093/bjaceaccp/mkl051
Continuing Education in Anaesthesia, Critical Care & Pain | Volume 6 Number 6 2006 219
ª The Board of Management and Trustees of the British Journal of Anaesthesia [2006].
All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Atrial fibrillation

Table 1 Causes and risk factors for AF Cardioversion by either means carries a risk of thromboem-
Acute causes AF associated with cardiovascular disease bolism, particularly when the arrhythmia has been present
Alcohol binge drinking Following myocardial infarction
for longer than 48 h; anticoagulation prophylaxis must be
Cardiac and non-cardiac surgery Hypertension, especially if left initiated before the procedure. In the long-run, it may become
Myocarditis/pericarditis ventricular hypertrophy appropriate to accept the arrhythmia as permanent. Recent
Pulmonary embolism Valvular heart disease (often mitral)
Pulmonary hypertension Congenital heart disease, mainly atrial
studies have pointed out that rate controlling the AF could be
Chest infections septal defects (ASD) at least as effective as restoration of sinus rhythm in terms of
Hyperthyroidism Sick sinus syndrome symptom control and survival, particularly in stable patients aged
Diabetes mellitus
approximately 60 years old.
Neurogenic AF Familial AF

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High vagal tone (nocturnal episodes) Identified in a small group of patients11
High sympathetic tone (daytime
episodes; associated with
ischaemic heart disease,
stress, excessive caffeine,
alcohol)
tissue resulting in shortening of effective refractory periods,
thereby maintaining and increasing the duration of AF.9 10
Causes and risk factors
As described above, the risk of developing AF increases with age.
Whilst rheumatic valvular disease remains the most common
cause for AF in developing countries, most patients develop
AF on the basis of coronary artery disease and systemic hyper-
tension. Clinically important causes and risk factors for AF are
summarised in Table 1. Echocardiographic predictors include
large atria, diminished ventricular function and increased left
ventricular wall thickness. When AF occurs in normal hearts
without signs of any demonstrable cardiovascular disease, it is
termed ‘lone atrial fibrillation’
Principles of management
The management of AF still represents one of the major thera-
peutic challenges in medicine. Based on current evidence and
guidelines, there are four main principles3:
(i) Restoration of sinus rhythm by pharmacological or electri-
cal means.
(ii) Control of ventricular rate during paroxysmal or persistent
AF, and chronically in those with permanent AF.
(iii) Prevention of recurrence of paroxysmal or persistent AF
following successful restoration of sinus rhythm.
(iv) Prevention of thromboembolic phenomena.
When a patient is seen in the emergency setting, the main
priority is to control the fast ventricular response and, depending
on the haemodynamic status of patient, this can be achieved
either by urgently restoring sinus rhythm or by controlling the
ventricular rate. Immediate electrical cardioversion is indicated in
patients with a rapid ventricular rate who are either haemody-
namically unstable or have evidence of acute myocardial
ischaemia or heart failure that do not respond promptly to phar-
macological measures. In less acute situations, pharmacological
cardioversion can be attempted, thereby avoiding the require-
ment for general anaesthesia.
Restoration of sinus rhythm
Direct current cardioversion
Direct current cardioversion (DCC) involves a synchronised
direct current electrical shock delivered across the chest wall.
Sinus rhythm can be restored in a significant proportion of
patients with success rates varying between 65% and 90%. The
success of DCC appears to be greater with anterior-posterior
positioning of paddles (sternum and left scapular) than with
anterior-lateral (ventricular apex and right infraclavicular).
Other factors include nature of heart disease, transthoracic resis-
tance and output waveform (monophasic or biphasic).1 3
Elective DCC is performed under adequate short-acting
anaesthesia. In an emergency situation, the need for anaesthesia
depends on the nature of the emergency and conscious level of the
patient; it is reasonable to perform DCC under conscious seda-
tion if the urgency of the situation is such that there can be no
delay. In a recent report, elective DCC performed under con-
scious sedation was also shown to be safe and not associated
with any intolerable discomfort to the patient.12
Devices that deliver a monophasic waveform of current
have been conventionally used for cardioversion. Initial shock
energy of 200 J is recommended for cardioversion of AF using
a monophasic device. The sequence of energy commonly used is:
200 J; 200 J; 300 J; and 360 J.3 Biphasic machines achieve car-
dioversion at much lower energy levels and are increasingly
replacing monophasic devices.
It is safe to cardiovert patients with implanted devices such
as permanent pacemaker or internal defibrillator provided the
implanted device is interrogated immediately before and
after cardioversion to assess any malfunction. The paddles
used for cardioversion should be placed as far as possible from
the implanted device, preferably in the anterior-posterior
position.
Brief arrhythmias can arise immediately following DCC.
These are mainly ventricular and supraventricular premature
beats, bradycardia and short periods of sinus arrest. Ventricular
tachycardia or fibrillation can be precipitated in patients with
hypokalaemia and digitalis intoxication. Patients with underlying
conduction defects are at risk of developing profound brady-
cardia, complete heart block or asystolic periods following
cardioversion. These patients are identified by having a slow
ventricular response to AF in the absence of rate-reducing

220 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 6 Number 6 2006
 Atrial fibrillation

medications and facilities for temporary external or endocardial
pacing must be made available prior to attempting cardioversion.
Electrical cardioversion can also lead to transient ST segment
elevation with a rise in blood concentrations of cardiac troponins
and CK-MB, even without cardiac damage. The rate of relapse
after DCC is high unless anti-arrhythmic drug therapy to main-
tain sinus rhythm is given concomitantly. However, prophylactic
therapy to prevent recurrences following DCC should be consid-
ered individually for each patient.
treatment; however, it should be used with caution in patients
with acute ischaemia or myocardial dysfunction, as profound
hypotension may be induced by i.v. or high-dose oral loading.
There is emerging evidence that i.v. and oral amiodarone have
different electrophysiological properties and it may be possible to
administer i.v. amiodarone to cardiovert AF in patients who are
already on chronic oral treatment.14
Maintenance of sinus rhythm

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The relapse rate of AF following initial cardioversion is high
Pharmacological restoration of sinus rhythm (25–50% at 1 month). Maintenance of sinus rhythm after success-
ful cardioversion is achieved by continuation of oral therapy with
Prior to considering any anti-arrhythmic therapy, it is important
class I or III anti-arrhythmic drugs. Pre-treatment with these
to realise that up to 60% of patients with recent onset AF spon-
drugs also improves success rates of repeated DCC. Sotalol
taneously revert to sinus rhythm within 24 h to a few days.13
is useful for preventing recurrences of paroxysmal AF. However,
Pharmacological cardioversion is considered in patients who
it is vital to be aware of the pro-arrhythmic effects of these agents;
are haemodynamically stable; it is often successful in AF of
they can prolong the QT interval and lead to dangerous ventri-
<48 h.
cular arrhythmias. Thus, regular monitoring of corrected QT
Anti-arrhythmic drugs are classified according to the
interval (QTc) and QRS duration is important during outpatient
Vaughan Williams classification (Table 2). Current guidelines
reviews. Renal insufficiency and electrolyte imbalance also
on the management of AF3 recommend use of propafenone,
predispose to polymorphic ventricular tachycardia.
flecainide, ibutilide or dofetilide as first choice for pharmacologi-
cal cardioversion of AF of <7 days duration (conversion rates
of up to 90%).3 Flecainide and propafenone are safe in patients Rate control of atrial fibrillation
who do not have evidence of ischaemic heart disease or myocar- It is necessary to control the ventricular rate in persistent AF.
dial dysfunction. Dofetilide and ibutilide are relatively new Also, rate control may be a preferred strategy in patients with
class III agents and are most useful for cardioverting atrial flutter. paroxysmal AF who are stable at presentation, as 60% of these
However, there is an increased incidence of torsade de points or patients can spontaneously revert to sinus rhythm within 24 h.
polymorphic ventricular tachycardia with use of these drugs. The aim of rate control in AF is to improve symptoms and
In clinical practice, amiodarone is a reasonable alternative prevent worsening of ventricular dysfunction. Recent evidence
to class Ic agents and is the drug of choice in patients with vent- from randomised trials (AFFIRM,15 PIAF,16 RACE,17
ricular dysfunction and ischaemic heart disease. Amiodarone STAF18) has shown that rate control is at least as effective as
also has an added advantage of providing prompt rate control rhythm control in improving symptoms and functional capacity,
in addition to its anti-arrhythmic effect. This rate controlling particularly in those over 65 yr of age. What is considered
effect (beta blockade and calcium channel blockade properties) adequate rate control remains controversial. Heart rate should
is observed early following i.v. loading; the class III anti- neither be too high (leads to tachycardia induced cardiomyopa-
arrhythmic properties take effect at 8–24 h. Most of the toxicity thy) or too low (facilitates heart failure); it is considered to
of amiodarone is dose-dependent and related to chronic be controlled when the ventricular rate is 60–80 bpm at rest
and 90–115 bpm during exercise.
Table 2 Vaughan Williams Classification of Antiarrhythmic Drugs
Rate control is achieved by drugs which predominantly affect
Class Action Drugs conduction through the AV node. Commonly used agents
I Sodium channel blockade are digoxin, beta-blockers (atenolol, propranolol, metoprolol,
IA Prolong repolarisation Quinidine, procainamide, esmolol) and non-dihydropyridine calcium channel blockers
disopyramide
IB Shorten repolarisation Lidocaine, mexiletine, (verapamil and diltiazem). In permanent AF, digoxin can usually
tocainide, phenytoin provide adequate rate control. However, digoxin does not pre-
IC Little effect on Encainide, flecainide, vent excessive heart rates during exercise and combination ther-
repolarisation propafenone
II Beta-adrenergic blockade Propanolol, esmolol, apy with beta-blockers or calcium antagonists may be necessary,
acebutolol, l-sotalol especially in younger active individuals. In stable patients with
III Prolong repolarisation Amiodarone, bretylium, acute AF, calcium antagonists or beta-blockers (oral or i.v.) are
(potassium channel d,l-sotalol, ibutilide
blockade; other) preferred to digoxin due to their rapid onset of action (3–7 min).
IV Calcium channel blockade Verapamil, diltiazem, bepridil Digoxin is the drug of choice for rate control in patients with
Miscellaneous Miscellaneous Actions Adenosine, digitalis, heart failure, though there is emerging evidence in support of
magnesium
beta-blockers.

Continuing Education in Anaesthesia, Critical Care & Pain | Volume 6 Number 6 2006 221
Atrial fibrillation
Table 3 Non-pharmacological management of AF
Rhythm control Rate control
Device therapy
 Atrial pacing (single or multisite)  Transcatheter AV junctional ablation and permanent  Percutaneous left atrial appendage transcatheter
pacemaker implantation
 Atrial defibrillators (stand-alone or with  Radiofrequency transcatheter AV junction
pacemaker function) modification
Ablation therapy
 Operative (Maze procedure, Pulmonary vein
isolation, His bundle ablation)
 Percutaneous transcatheter techniques
(pulmonary vein isolation, radiofrequency ablation
of triggers or substrate)
Patients with sick sinus syndrome with AF and present with
episodes of bradycardia, usually require the support of a perma-
nent pacemaker to allow the use of rate controlling medications.
Drugs acting on the AV node are contraindicated in patients with
accessory conduction pathways (e.g. Wolf–Parkinson–White
syndrome) as they can result in dangerously fast ventricular
rates by increasing the conduction via the accessory pathway.
In these situations amiodarone, flecainide or procainamide are
drugs of choice.
Prevention of thromboembolism
Chronic AF is associated with a 3–7% annual risk of ischaemic
stroke from thromboembolism. Guidelines 3 recommend admin-
istration of heparin prior to, or concurrently during, immediate
electrical or pharmacological cardioversion. If AF has been pre-
sent for longer than 48 h or the duration is unknown, warfarin
should be given for 3–4 weeks following successful cardioversion.
Patients admitted for elective cardioversion require adequate
anticoagulation with warfarin 3–4 weeks before and after the
procedure (INR 2–3). Those patients who cannot be anticoagu-
lated due to contraindications prior to cardioversion should
undergo transoesophageal echocardiographic examination to
exclude the presence of thrombus.
In chronic AF, the risks and benefits of antithrombotic ther-
apy (aspirin, warfarin) must be considered in each individual
patient. Chronic hypertension, age >65 yr, diabetes mellitus, pre-
vious ischaemic stroke, ventricular dysfunction and co-existent
ischaemic or valvular heart disease are considered as high risk
factors for thromboembolism in AF. All such high risk patients
must receive warfarin unless contraindicated. In the absence of
these factors (low risk patients) or when warfarin cannot be
given, aspirin 300 mg daily is an alternative. Young patients
with AF who do not have any clinical or echocardiographic
evidence of heart disease (‘lone AF’) are also at low risk of throm-
boembolism. Anticoagulation can be interrupted for a period of
up to 1 week for surgical and diagnostic procedures that carry a
risk of bleeding. However, these patients must receive heparin if
they are at high risk of thromboembolism or have mechanical
prosthetic valves.
222 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 6 Number 6 2006
Stroke prevention
occlusion (PLAATO)
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Principles of prevention of thromboembolism in patients with
atrial flutter are the same as those for AF. New anticoagulants
and thrombin inhibitors which do not require regular monitoring
and blood tests are currently being compared with warfarin in
various trials.
Non-pharmacological management
A wide variety of non-pharmacological approaches now exist
for managing AF and provide rhythm or rate control when
drug treatment has failed. Commonly used strategies are outlined
in Table 3.
Significant effort is currently being devoted to percutaneous
catheter based ablation of the triggers of AF (atrial premature
beats, monomorphic atrial tachycardias, atrial flutter). The vast
majority (>90%) of these triggers are now known to arise from
‘sleeves’ of atrial tissue with abnormal automaticity present
within the pulmonary veins. The procedure involves isolation
of pulmonary veins and radiofrequency ablation of the triggers
of AF. Although the technique can provide long-term mainte-
nance of sinus rhythm in a majority of patients, it can lead to
systemic embolism and pulmonary vein stenosis, especially if
multiple trigger areas are present. Methods using other energy
sources, such a cryotherapy and ultrasound, are currently being
evaluated and may minimise such complications.
Management in special situations
Cardiac surgery
The incidence of AF after cardiac surgery is high; 27–37% of
patients undergoing coronary artery bypass grafting and 50%
of those following valvular surgery will develop AF in the
post-operative period. The majority of AF episodes occur within
first 4 days of cardiac surgery with a peak incidence on the second
post-operative day. Whilst it is still unclear why some patients
develop AF post-operatively, certain factors have shown a
statistical relationship with AF (Table 4).19
There is clear evidence that C-reactive protein, a marker of
inflammation, peaks on the second post-operative day coinciding
with the peak incidence of AF. This suggests a unique role of

Table 4 Factors related to development of post-operative AF
Advanced age Prolonged P waves on ECG
Males Atrial dilatation
Previous AF High left ventricular end-diastolic pressure
Cardiac failure Cardiomegaly on chest X-ray
Hypertension Right coronary artery grafting
Chronic obstructive airway Prolonged bypass time
disease Inadequate cardioprotection and hypothermia
Chronic renal failure
Previous cardiac surgery
inflammation during the post-operative period in about 40% of
patients, particularly when it involves the pericardium or the
heart muscle.20
Post-operative AF is associated with increased morbidity and
mortality, largely due to heart failure, stroke and prolonged
hospital stay.
Various therapies have been investigated for prophylaxis
of post-operative AF.21 22 Guidelines3 recommend use of beta-
blockers in patients undergoing cardiac surgery. Once a common
practice to discontinue beta-blockers prior to surgery, these
agents have now been shown to reduce the risk of post-operative
AF by about 60%. No major differences exist between different
beta-blockers (sotalol, metoprolol, propranolol) in preventing
post-operative AF. Pre-operative use of amiodarone also appears
to be equally effective.
Haemodynamically unstable patients with AF should be
cardioverted urgently, either by direct current or pharmacologi-
cally using amiodarone. Ibutilide is particularly useful in patients
with atrial flutter. It is recommended that, following successful
DCC, patients should receive oral amiodarone for 6–8 weeks. The
vast majority of post-operative AF spontaneously reverts to sinus
rhythm within 2 weeks. Thus, haemodynamically stable patients
can be commenced on beta-blockers, provided these are not con-
traindicated, to achieve a rate control of <100 beats min 1. The
treatment can be supplemented or substituted with i.v. digoxin
and/or calcium channel blockers (verapamil or Diltiazem).
All patients who develop AF post-operatively must be
anticoagulated with heparin and warfarin as soon as it is deemed
safe. Anticoagulation should be continued for 4 weeks after dis-
continuing amiodarone or documentation of spontaneous return
of sinus rhythm.
Left, right or bi-atrial pacing have also shown to reduce the
occurrence of AF by 30–60%. Other therapies including use of
magnesium and inflammatory agents have been incompletely
evaluated.
Acute myocardial infarction
Intractable ischaemia or haemodynamic instability requires
urgent electrical cardioversion. In patients with heart failure,
i.v. digoxin or amiodarone is given to slow the ventricular
response and improve left ventricular function. I.V. beta-blockers
can be prescribed for rate control to patients who do not have
evidence of clinical left ventricular dysfunction, bronchospasm or
Continuing Education in Anaesthesia, Critical Care & Pain | Volume 6 Number 6 2006
Atrial fibrillation
atrio-ventricular block. In the setting of acute myocardial isch-
aemia, administration of class Ic antiarrhythmic drugs can be
harmful and these agents are best avoided.
Pregnancy
Digoxin, beta-blockers or calcium channel antagonists can be
used for rate control of AF during pregnancy. Haemodynami-
cally unstable patients should be electrically cardioverted.
Current guidelines 3 recommend use of antithrombotic therapy
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(anticoagulant or aspirin) throughout the duration of pregnancy
in all patients with AF, except those with ‘lone AF’. Oral anti-
coagulants carry a risk of teratogenicity and should be avoided if
possible, especially in the first and third trimesters of pregnancy.
Ventricular pre-excitation
In patients with Wolf–Parkinson–White syndrome, AF can lead
to extremely rapid ventricular rates. Unstable patients require
urgent DCC to prevent ventricular fibrillation. I.V. flecainide
or ibutilide should be given to restore sinus rhythm if there is
no haemodynamic compromise. Drugs acting on the AV node
(beta-blockers, digitalis glycosides, calcium channel antagonists,
adenosine) are contraindicated since these can increase the con-
duction of electrical activity through the accessory pathway.
Hyperthyroidism
During the hyperthyroid state, beta-blockers are necessary to
control the ventricular response, unless contraindicated when
diltiazem or verapamil can be given. Anticoagulation is recom-
mended if there are risk factors for stroke. Once patients are
rendered euthyroid, antithrombotic prophylaxis is the same as
for those without hyperthyroidism.
Pulmonary disease
It is once again important to realise that the vast majority of these
patients will spontaneously revert to sinus rhythm and unless
there is haemodynamic compromise, all that may be needed is
rate control with adequate anticoagulation. Correction of hypox-
aemia and acidosis are primary measures in patients who develop
AF during acute pulmonary illness or exacerbation of obstructive
airway disease. Calcium channel antagonists, verapamil or dilti-
azem, are preferred agents for rate control. Theophylline can
sustain AF, whilst beta-blockers, sotalol, propafenone and aden-
osine are contraindicated in patients with bronchospastic lung
disease. The long-term use of amiodarone can lead to pulmonary
fibrosis and is best avoided.
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Please see multiple choice questions 4–8.