Atrial fibrillation and flutter

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ARRHYTHMIAS
Atrial fibrillation and flutter — epidemiology and
mechanisms
Atrial fibrillation
Atrial fibrillation is a supraventricular arrhythmia characterised
by rapid, chaotic depolarisation of the atria. The atrial rhythm
is irregular, with rate from 300–500 per minute. Although the
AV node limits the number of these impulses that reach the
ventricles, atrial fibrillation usually produces a rapid, irregular
ventricular rhythm (Fig. 1; Table 1). Since the AV node
determines heart rate, the ventricular rate tends to be slower in
elderly patients in whom the AV node conducts less well.
Epidemiology
Atrial fibrillation is the most common arrhythmia seen in
general practice and hospital medicine. It is especially
common in the elderly, with a prevalence of 0.5% in the
adult population, rising to 10% among individuals aged over
75 years. It is associated with a 5–6-fold increase in the
incidence of stroke. A 70-year-old with atrial fibrillation thus
has an annual risk of stroke or transient cerebral ischaemic
attack of 5%. Risk factors for atrial fibrillation consist mainly
of conditions that lead to increased atrial wall stress. These
are summarised in Table 2.
within the pulmonary vein orifices, are commonly responsible
for episodes of atrial fibrillation in patients with otherwise
apparently normal hearts (Fig. 3). Once initiated, the
arrhythmia is maintained by re-entry (pp. 98–99). Macro reentry occurs when a continuous loop of atrial depolarisation is
set up around an anatomical or functional conduction barrier
(e.g. vein orifice, zone of diseased atrial tissue). During atrial
fibrillation, multiple re-entry circuits are established in the
atria. These circuits tend to maintain themselves more readily
in diseased or enlarged atria. Once atrial fibrillation is
established, the chance of spontaneous return to sinus rhythm
diminishes because of maladaptive changes that occur in atrial
tissue. This includes shortening of the refractory period of
atrial myocytes, which encourages macro re-entry because
myocytes are excitable for a greater proportion of each cardiac
cycle. This process is known as electrical remodelling.
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Clinical manifestations
Atrial fibrillation can be paroxysmal, persistent or permanent.
Paroxysmal atrial fibrillation is characterised by intermittent,
self-terminating episodes of tachycardia. Sometimes this
progresses to persistent atrial fibrillation, in which an
intervention (such as direct current [DC] cardioversion, pp.
106–107) may restore sinus rhythm, or permanent atrial
fibrillation, which is resistant to such treatments.
Atrial fibrillation may not produce symptoms, especially if
the associated heart rate response is not rapid. If symptoms
occur, their severity is determined by the underlying condition
of the heart, and patients’ heart rate at rest and during exercise.
Patients may describe fatigue or reduced effort tolerance, or
more definite symptoms of palpitation, dyspnoea and
dizziness. If the heart rate is rapid, cardiac failure or angina may
develop in susceptible patients. It is rare for atrial fibrillation to
cause syncope, unless the patient has severe left ventricular
impairment or valvular stenosis. In some cases, the first clinical
manifestation of atrial fibrillation is stroke or systemic
embolism. This is caused by the development of thrombus in
the left atrial appendage (Fig. 2), due to loss of atrial mechanical
function and stasis, followed by embolisation.
Atrial flutter
Atrial flutter is a related arrhythmia that shares the same risk
factors as atrial fibrillation (with the exception of
thyrotoxicosis). The mechanisms that underlie these
arrhythmias are different, resulting in distinct clinical
manifestations, electrocardiographic characteristics and
treatment options.
Clinical manifestations
Atrial flutter can also present in paroxysms or as a persistent
arrhythmia. If 2:1 AV block occurs, the presentation may be
with regular, rapid palpitation. (Rarely, 1:1 AV conduction can
occur in young patients, and this may cause an extreme
tachycardia, presyncope or syncope.) Otherwise the clinical
features are similar to those of atrial fibrillation. Atrial stasis can
occur with atrial flutter (because of loss of atrial contraction)
Mechanisms
Atrial fibrillation is the result of substrate and trigger. The
substrate usually consists of a disease that affects the atria,
such as ischaemic heart disease (associated with atrial
ischaemia and infarction). The trigger often consists of a
rapidly discharging ectopic atrial focus. Although this focus
can arise anywhere in the atria, left atrial foci, occurring at or
V1
Fig. 1 Rhythm strip of atrial fibrillation.
Fig. 2 Transoesophageal echocardiogram showing thrombus in
the left atrial appendage caused by stasis. In atrial fibrillation,
atrial mechanical function is lost, predisposing to left atrial thrombus and
embolic events.
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Atrial fibrillation and flutter — epidemiology and mechanisms
Sino-atrial
node
Pulmonary
veins
5
SVC
4
F
TV
Eustachian
ridge
F
CS 3
F
F
F
F
6
2
LV
IVC
1
RV
Bundle
of His
Fig. 3 Ectopic beats can arise from sleeves
of conducting tissue within the
pulmonary veins. These can trigger episodes
of atrial fibrillation.
and thromboembolic complications do
occur, although the risk is not as high as
with atrial fibrillation.
Mechanisms
Fig. 4 Schematic of atrial flutter circuit. The
main structures in the right atrium are the
tricuspid valve (TV), coronary sinus (CS), superior
vena cava (SVC) and inferior vena cava (IVC). The
circuit itself runs around the tricuspid annulus.
Fig. 6 ECG leads showing atrial flutter
with 4:1 AV block. The flutter waves (F) occur
at a rate of 300 per minute.
Table 3 Key ECG features of atrial flutter
■ Consistent organised atrial activity
(pp. 116–117). The AV node limits the
ventricular response to atrial flutter.
Often 2:1 or 4:1 AV block occurs,
resulting in a regular ventricular
rhythm of 150 or 75 beats per minute
(Fig. 6). Variable AV block can also
occur, resulting in an irregular
ventricular rhythm as with atrial
fibrillation (Table 3).
■ Flutter waves prominent in inferior leads (II, III, aVF)
■ Regular or irregular ventricular rhythm may be seen
■ A regular, narrow complex tachycardia of 150 bpm
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Atrial flutter is usually the result of a
single, large re-entry circuit within the
right atrium (Figs 4 and 5). This circuit is
centred round the tricuspid valve ring
(annulus), and the left atrium is
activated passively from this circuit. In
most cases the atria depolarise at a rate
of around 300 beats per minute.
Importantly, the flutter circuit passes
through a narrow strip of tissue (known
as the ‘flutter isthmus’) in between the
tricuspid annulus and the inferior vena
cava. This strip of tissue can be targeted
for radiofrequency ablation, a potentially
curative treatment for this arrhythmia
Table 1 Key ECG features of atrial
fibrillation
is likely to be atrial flutter with 2:1 AV block. Flutter
waves may be masked by the QRS complexes and
T waves, but may be unmasked by i.v. adenosine
(pp. 110–111)
Atrial fibrillation and
flutter — epidemiology
and mechanisms
■
■ No consistent organised atrial activity
■ Unsteady baseline (fibrillation waves)
■ Irregular ventricular rhythm (unless third-degree
AV block also present)
■
Table 2 Risk factors for atrial fibrillation
■ Advanced age
■
■ Valvular heart disease (especially mitral valve disease)
■ Hypertension
■ Ischaemic heart disease (per se and with heart failure)
■ Cardiomyopathies
■
Atrial fibrillation is caused by multiple,
interlacing re-entry circuits involving
predominantly the left atrium.
Risk factors include age, hypertension,
mitral valve disease, cardiomyopathy and
coronary artery disease.
Atrial fibrillation affects around 10% of
people aged over 75 years.
Episodes of atrial fibrillation may be
triggered by ectopic beats originating in
the pulmonary veins.
■ Thyrotoxicosis
Fig. 5 Three-dimensional map of right atrial depolarisation obtained during electrophysiological study for atrial flutter. This is a map of
the right atrium viewed through the tricuspid annulus (red ring). The depolarisation wave (denoted by concentric colours) passes between the tricuspid annulus
(TV6) and the inferior vena cava (IVC).
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ARRHYTHMIAS
Atrial fibrillation and flutter — management
Persistent atrial flutter/fibrillation
Two types of management strategy can be adopted — rate
control and rhythm control. With rate control, the atrial
arrhythmia itself is not terminated and treatment is directed
at controlling the ventricular response and preventing
embolic complications. With rhythm control, treatment is
directed at restoring and maintaining sinus rhythm. Both
strategies have advantages and disadvantages. The choice is
governed by risk of thromboembolic complications, severity
of symptoms and an assessment of whether the patient is
likely to maintain sinus rhythm. Patients with long-standing
atrial fibrillation (especially if due to mitral valve disease,
hypertension or advanced LV dysfunction) are least likely to
maintain sinus rhythm after cardioversion. Recent evidence
(the AFFIRM trial) suggests that aggressive attempts to
restore sinus rhythm in asymptomatic patients may be
harmful and increase the risk of stroke.
digoxin are preferable in patients with significant
ventricular impairment. The target is a resting heart rate of
50–80 bpm.
In atrial flutter, rate control is difficult because the AV node
blocking response is not linear, and is usually a whole
fraction of an atrial rate of around 300 min –1. Thus, a
therapeutic dose of digoxin may not reduce heart rate from
150 bpm (2:1 AV block), but an additional agent may cause it
to fall abruptly to 75 bpm (4:1 block) or lower.
Table 1 Rhythm control strategy
Advantages
■ Restoration of atrial contraction
Disadvantages
■ General anaesthetic risk (not a major concern
— ↑ cardiac output with exercise
— appropriate rate response to
for most patients)
■ Drugs used to maintain sinus rhythm generally
exercise
have more proarrhythmic potential than do the
AV node blocking drugs used for rate control.
■ Recent evidence suggests embolic risk may be
increased
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Rhythm control strategy
Table 2 DC cardioversion protocol
The rhythm control strategy (Table 1) uses cardioversion to
restore sinus rhythm. Cardioversion is most often achieved
using a synchronised direct current (DC) shock applied to
the chest with paddles placed over the apex and base of the
heart. This procedure is performed under general
anaesthesia. Cardioversion can also be achieved using
antiarrhythmic drugs such as flecainide or amiodarone; this
pharmacological cardioversion is normally used to restore
sinus rhythm in patients with acute atrial fibrillation (of less
than 48 hours duration). For patients with established atrial
fibrillation, four weeks of prior anticoagulation (target INR
2.0 to 3.5) is mandatory. Here, cardioversion is dangerous
without prior anticoagulation. Restoration of atrial
mechanical function can cause ejection of clot from the left
atrial appendage in the days following the procedure.
Warfarin should be continued for at least 12 weeks after
cardioversion, and only stopped if sinus rhythm is still
maintained and likelihood of recurrence considered low.
■ Ensure patient has had at least three weeks of effective (INR>2) anticoagulation
■ Check serum K+ (success greater if > 4.0 mmol. L1 1)
■ Patient fasting > 6 hours
■ i.v. access
■ General anaesthesia with short-acting induction agent
■ Cardiovert using following protocol (start at 200 J for atrial fibrillation):
— 100 J synchronised shock (or 50 J biphasic)
if fails →
— 200 J synchronised shock (or 100 J biphasic)
if fails →
— 360 J synchronised shock (or 150 J biphasic)
if fails →
— 360 J anteroposterior shock
— [lower shock energies used (up to 150 J) with biphasic shock defibrillator]
■ Continue warfarin for at least 3 months if cardioversion successful
■ If cardioversion unsuccessful, consider repeating at later date after pre-treatment with
antiarrhythmic agent (e.g. amiodarone)
Table 3 Drugs to maintain sinus rhythm
Class Ic drugs (sodium channel blockers)
These agents should be avoided in patients with IHD or heart failure. In patients with
structurally normal hearts, the incidence of proarrhythmia is around 1%
■ flecainide 50–100 mg BD
■ propafenone 150 mg BD to 300 mg TID
DC cardioversion
Long-term success rates are disappointing with cardioversion
(< 50% of patients maintain sinus rhythm at six months)
(Table 2). Concomitant use of antiarrhythmic drugs increases
the proportion of patients that maintain sinus rhythm.
Amiodarone, sotalol, propafenone and flecainide are effective
but can be proarrhythmic and have other significant side
effects (Table 3). Therefore, unless the patient has a history of
intermittent atrial fibrillation progressing to chronic atrial
fibrillation or has had a previous cardioversion with
recurrence, antiarrhythmic drugs are not normally given.
Rate control strategy
Recent trials suggest that the rate control strategy (Table 4) is
at least as safe as rhythm control, and is especially
appropriate in asymptomatic patients — it avoids the hazards
of cardioversion and antiarrhythmic drugs.
Drugs for rate control
AV node blocking drugs are used to control heart rate. A
hierarchy of drugs is given in Table 5. β-blockers and
Class II drugs (β-blockers)
These have little proarrhythmic effect, and are a sensible first-line agent, especially when
ischaemia or heart failure is implicated as a cause
■ atenolol 25–100 mg D
■ metoprolol 25–100 mg BD
Class III drugs (potassium channel blockers)
Sotalol has combined β-blocking and class III activity. It causes proarrhythmia by causing
abnormal ventricular repolarisation (seen as QT interval prolongation). This can lead to
polymorphic ventricular tachycardia/sudden death. Proarrhythmia with sotalol is more
common in women and in patients with LVH. Amiodarone is the safest agent in patients with
significant LV compromise. It has many side effects (see pp 104–105, Fig. 4) and should be
avoided in young patients unless no effective alternative is found
■ sotalol 60–120 mg BD
■ amiodarone 100–400 mg D (usual dose 200 mg D)
For all of the above agents, except β-blockers, ambulatory monitoring within the first five
days of treatment is sensible to identify proarrhythmia
Table 4 Rate control strategy
Advantages
■ More appropriate for patients with valve
Disadvantages
■
Loss of atrial contribution to
■
Risk of embolic complications
disease or previous failed cardioversions
■ Less proarrhythmic potential from rate
cardiac output
controlling drugs
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Atrial fibrillation and flutter — management
I
III
aVF
V1
RA 1,2
RA 3,4
RA 5,6
RA 7,8
RA 9,10
RA 11,12
RA 13,14
Fig. 2 Surface (ECG (top four traces) and intracardiac electrograms
from right atrium, (RA) during successful ablation of atrial flutter.
Rapid, regular atrial depolarisation is seen to proceed around the right atrium
until sinus rhythm is restored by blocking the flutter circuit (see pp. 116–117).
Fig. 1 Computer-generated map of the left atrium in a patient
with atrial fibrillation due to pulmonary vein ectopy. The red dots
around the right upper pulmonary vein (RUPV) denote ablation lesions
delivered during the procedure. (RLPV, right lower pulmonary vein.)
104–105 is targeted. Current success rates are 80–90%.
Ablation can also be used to treat atrial fibrillation, by
targeting triggering foci in the pulmonary veins (Figs 1 and
2). This evolving treatment has a success rate of around 65%
in patients with otherwise normal hearts. ‘Dynamic overdrive’
pacemakers have recently been developed to suppress rate
changes and ectopic activity that may trigger atrial fibrillation
(Fig. 3). The pace and ablate strategy is used as a last resort for
symptomatic patients in whom drug treatment is ineffective
or poorly tolerated. Rate control is achieved by ablation of the
AV node and implantation of a permanent pacemaker.
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Table 5 Oral drugs for rate control in atrial fibrillation
Fig. 3 AF suppression pacemaker. This device paces the atria slightly
faster than the sinus rate, preventing bradycardia and atrial ectopy that
otherwise trigger atrial fibrillation.
Anticoagulation
Most patients with chronic atrial flutter/fibrillation require
long-term anticoagulation with warfarin. Exceptions are
patients who, from anticoagulation trials, are considered low
risk. In these cases, low-dose aspirin 75–300 mg daily is
sufficient prophylaxis. The European Society of Cardiology
has produced anticoagulation guidelines which are
summarised in Table 6.
First line
Digoxin 250 µg D (after leading with 600–1200 mg for one week)
OR
Verapamil 240 to 480 mg D
OR
Diltiazem 200 to 500 mg D
β-blocker (e.g. atenolol 50 to 100 mg D)
OR
If digoxin ineffective, ensure blood level therapeutic before adding a second agent
Second line
Combination of digoxin and either verapamil or β-blocker
Third line
Amiodarone 100 to 400 mg daily (after loading ⊗)
Table 6 ESC guidelines for anticoagulation in atrial fibrillation
■ Age > 60 years with diabetes or CAD
■ Age > 75 years (esp. women)
Intermittent atrial flutter/fibrillation
Intermittent atrial flutter/fibrillation may be a prelude to
chronic atrial fibrillation, but can exist as a separate entity.
The need for antiarrhythmic drugs is dictated by the severity
of symptoms. Anticoagulation may be needed if prolonged
(> 24 hours) episodes occur. Ambulatory ECG monitoring
helps guide treatment. Identification and treatment of
potential precipitants (e.g. hypertension, alcohol, valve
disease) should be done before committing to long-term
antiarrhythmic treatment.
■ Current or prior hypertension
■ Heart failure
■ History of TIA, stroke or other embolic event*
■ Rheumatic heart disease or prosthetic valve*
Warfarinise, INR range 2.0–3.0 except highest risk cases (*) where target range is 2.5–3.5.
Atrial fibrillation and flutter — management
■
■
Non-pharmacological treatments
Radiofrequency ablation
Radiofrequency ablation can be used to treat intermittent or
persistent atrial flutter; the isthmus zone described on pages
■
■
The rate control strategy is directed at limiting the ventricular response
to atrial fibrillation by using AV node blocking drugs such as digoxin,
ß-adrenoceptor antagonists and verapamil.
The rhythm control strategy uses cardioversion and antiarrhythmic
drugs to restore and maintain sinus rhythm.
Anticoagulation with warfarin should be considered for patients with
atrial fibrillation and risk factors for stroke.
Pacemaker implantation and AV nodal ablation can be used to control
heart rate in patients for whom drugs fail or are not tolerated.
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