ATRIAL FLUTTER

Atrial flutter is characterised by a large (macro) re-entry circuit,

usually within the right atrium encircling the tricuspid annulus.
The atrial rate is approximately 300/min, and is usually
associated
with 2 : 1, 3 : 1 or 4 : 1 AV block (with corresponding heart rates
of 150, 100 or 75/min). Rarely, in young patients, every flutter
wave is conducted, producing a rate of 300/min and, potentially,
haemodynamic compromise. The ECG shows saw-tooth flutter
waves (Fig. 16.34). When there is regular 2 : 1 AV block, it may
be
difficult to identify flutter waves that are buried in QRS
complexes
and T waves. Atrial flutter should always be suspected when
there is a narrow-complex tachycardia of 150/min. Carotid
sinus pressure or intravenous adenosine may help to establish
the diagnosis by temporarily increasing the degree of AV block
and revealing flutter waves (Fig. 16.35
Management
Medical management with digoxin, β-blockers or verapamil is •
often successful in controlling the ventricular rate (p. 479). In •
many cases, however, it may be preferable to try to restore •
sinus rhythm by direct current (DC) cardioversion. Following •
cardioversion, β-blockers or amiodarone can be used to prevent •
recurrent episodes of atrial flutter. Class Ic anti-arrhythmic drugs •
such as flecainide are contraindicated because there is a risk of •
slowing the flutter circuit, facilitating 1 : 1 AV nodal conduction and •
producing a paradoxical extreme tachycardia and haemodynamic •
compromise. Catheter ablation is a highly effective treatment, •
offering a greater than 90% chance of complete cure, and is •
the treatment of choice for patients with persistent symptoms. •
Anticoagulant management in patients with atrial flutter, including •
management around cardioversion, is identical to that of patients •
with atrial fibrillation (p. 471 •
Atrial fibrillation
Atrial fibrillation (AF) is the most common sustained cardiac •
arrhythmia, with an overall prevalence of 0.5% in the adult •
population of the UK. The prevalence rises with age, affecting •
1% of those aged 60–64 years, increasing to 9% of those aged •
over 80 years. It is associated with significant morbidity and •
a twofold increase in mortality. This is mainly because of its •
association with underlying heart disease but also because of •
its association with systemic embolism and stroke •
Pathogenesis
AF is a complex arrhythmia characterised by both abnormal •
automatic firing and the presence of multiple interacting re-entry •
circuits looping around the atria. Episodes of AF are initiated by •
rapid bursts of ectopic beats arising from conducting tissue in •
the pulmonary veins or from diseased atrial tissue. It becomes •
sustained because of re-entrant conduction within the atria or •
sometimes because of continuous ectopic firing (Fig. 16.36). •
Re-entry is more likely to occur in atria that are enlarged or in •
which conduction is slow, as is the case in many forms of heart •
disease. During episodes of AF, the atria beat rapidly but in an •
uncoordinated and ineffective manner. The ventricles are activated •
irregularly at a rate determined by conduction through the AV •
node. This produces the characteristic ‘irregularly irregular’ pulse. •
The ECG (Fig. 16.37) shows normal but irregular QRS complexes; •
there are no P waves but the baseline may show irregular •
fibrillation waves. Commonly, AF is classified as paroxysmal •
(intermittent episodes that self-terminate within 7 days), persistent •
(prolonged episodes that can be terminated by electrical or •
pharmacological cardioversion) or permanent. It can be difficult •
to identify what type of AF patients have at first presentation but •
this usually becomes clearer as time progresses. Unfortunately •
for many patients, paroxysmal AF becomes permanent as the •
underlying disease process progresses. This is partly because of •
electrophysiological changes that occur in the atria within a few •
hours of the onset of AF and which tend to maintain fibrillation: •
a process called electrical remodelling. When AF persists for a •
period of months, structural remodelling also occurs, leading to •
atrial fibrosis and dilatation that predispose to chronicity of the •
AF. Early treatment of AF can sometimes prevent the arrhythmia •
from becoming persistent •
Clinical features
The typical presentation is with palpitation, •
breathlessness
and fatigue. In patients with poor ventricular function or •
valve
disease, AF may precipitate or aggravate cardiac failure •
because
16.21 Common causes of atrial fibrillation •
• Coronary artery disease •
(including acute MI) •
• Valvular heart disease, •
especially rheumatic mitral •
valve disease •
• Hypertension •
• Sinoatrial disease •
• Hyperthyroidism •
• Alcohol •
• Cardiomyopathy •
• Congenital heart disease •
• Chest infection •
• Pulmonary embolism •
• Pericardial disease •
• Idiopathic (lone atrial •
fibrillation) •
of loss of atrial function and heart rate control. A fall in BP •
may cause lightheadedness, and chest pain may occur •
with
underlying coronary artery disease. In older patients, AF •
may
not be associated with a rapid ventricular rate and may be •
asymptomatic, only to be discovered as a result of a •
routine
examination or an ECG. Asymptomatic AF may also •
present with
systemic embolism and is a major cause of stroke in the •
elderly
Investigations
Assessment of patients with newly diagnosed AF should •
include a
full history, physical examination, a 12-lead ECG, •
echocardiogram
and thyroid function tests to exclude thyrotoxicosis. This is •
an unusual but potentially treatable cause of AF. Additional •
investigations may be needed to determine the nature and •
extent
of any underlying heart disease. In particular •
echocardiographic
assessment is useful to identify any structural heart disease, •
particularly mitral valve disease. •
Management
Paroxysmal atrial fibrillationd •
Occasional attacks of AF that are well tolerated do not necessarily •
require treatment. Beta-blockers are normally used as first-line •
therapy if symptoms are troublesome, since they reduce the •
ectopic firing that normally initiates the arrhythmia. They are •
particularly useful for treating patients with AF associated with •
coronary artery disease, hypertension and cardiac failure. Class •
Ic drugs (see Box 16.30), such as propafenone or flecainide, are •
also effective at preventing episodes but should not be given to •
patients with coronary artery disease or left ventricular dysfunction. •
Flecainide is seldom used alone, since it can precipitate atrial •
flutter, and is usually prescribed with a rate-limiting β-blocker •
Class III drugs can also be used; amiodarone is the most •
effective
agent for preventing AF but side-effects restrict its use to when •
other measures fail. Dronedarone is an effective alternative but •
is contraindicated in patients with heart failure or significant left •
ventricular impairment. Digoxin and verapamil are not effective •
for the prevention of AF but can help with rate control by •
slowing
conduction through the AV node. Catheter ablation can be •
considered where anti-arrhythmic drug therapy is ineffective •
or causes side-effects. Ablation can disconnect the pulmonary •
veins from the LA electrically, preventing ectopic triggering •
of AF. In addition, lines of conduction block can be created •
within the atria to prevent re-entry. Ablation prevents AF in •
approximately 75% of patients with prior drug-resistant •
episodes,
although a repeat procedure is sometimes required before •
this is
achieved. Ablation for AF is an attractive treatment when •
drugs are
ineffective or poorly tolerated but may be complicated by •
cardiac
tamponade, stroke, phrenic nerve injury and, rarely, •
pulmonary
vein stenosis. •
Rate control If sinus rhythm cannot be restored, treatment •
should be directed at maintaining an appropriate heart rate. •
Digoxin, β-blockers and rate-limiting calcium antagonists, such •
as verapamil or diltiazem (p. 479), reduce the ventricular rate •
by slowing AV conduction. This alone may produce a striking •
improvement in cardiac function, particularly in patients with mitral •
stenosis. Beta-blockers and rate-limiting calcium antagonists are •
more effective than digoxin at controlling the heart rate during •
exercise and have additional benefits in patients with •
hypertension
or structural heart disease. Combination therapy with digoxin •
and a β-blocker can help with rate control but calcium channel •
antagonists should not be used with β-blockers because of the •
risk of bradycardia. •
In exceptional cases, poorly controlled and symptomatic •
AF
can be treated by implanting a permanent pacemaker and •
then
deliberately inducing complete AV nodal block with •
catheter
ablation. This is known as the ‘pace and ablate’ strategy. •
Thromboprophylaxis Loss of atrial contraction and left atrial •
dilatation cause stasis of blood in the LA and may lead to •
thrombus formation in the left atrial appendage. This predisposes •
patients to stroke and other forms of systemic embolism. •
and permanent AF. •
Several agents can be used to reduce stroke risk in AF. •
Warfarin therapy adjusted to a target INR of 2.0–3.0 reduces •
the risk of stroke by about two-thirds at the cost of an annual •
risk of bleeding of 1–1.5% and is indicated for patients with a •
CHA D -VASc score of 2 or more, unless there are coexisting •
2 S

clinical risk factors that increase the risk of bleeding. These include •
peptic ulcer, uncontrolled hypertension, alcohol misuse, frequent •
falls, poor adherence and the use of other drugs that might •
interact with warfarin. If bleeding does occur in warfarin-treated •
patients, anticoagulation can be reversed by administering vitamin •
K or clotting factors. •
The factor Xa inhibitors rivaroxaban, apixaban and edoxaban, •
and the direct thrombin inhibitor dabigatran (collectively referred •
CHA2DS2-VASc stroke risk scoring system for •
non-valvular atrial fibrillation •
Parameter Score •
C Congestive heart failure 1 point •
H Hypertension history 1 point •
A2 Age ≥ 75 years 2 points •
D Diabetes mellitus 1 point •
S2 Previous stroke or transient ischemic attack (TIA) 2 points •
V Vascular disease 1 point •
A Age 65–74 years 1 point •
Sc Sex category female 1 point •
Maximum total score 9 points •
Annual stroke risk •
0 points = 0% (no prophylaxis required) •
1 point = 1.3% (oral anticoagulant recommended in males only) •
2+ points = > 2.2% (oral anticoagulant recommended) •
Supraventricular tachycardia
These are usually narrow-complex •
tachycardias and are characterised by a re-entry circuit or •
automatic focus involving the atria. The three principal •
types
are atrioventricular nodal re-entrant tachycardia (AVNRT), •
atrioventricular re-entrant tachycardia (AVRT) and atrial •
tachycardia. The term SVT is technically incorrect as, in •
many
cases, the ventricles also form part of the re-entry circuit. •
Atrioventricular nodal re-entrant tachycardia

AVNRT is a type of SVT caused by re-entry in a circuit involving •

the
AV node and its two right atrial input pathways: a superior ‘fast’ •
pathway and an inferior ‘slow’ pathway (see Fig. 16.39A •
below).
This produces a regular tachycardia with a rate of 120–240/ •
min. It tends to occur in the absence of structural heart disease •
and episodes may last from a few seconds to many hours. The •
patient is usually aware of a rapid, very forceful, regular heart •
beat and may experience chest discomfort, lightheadedness •
or breathlessness. Polyuria, mainly due to the release of ANP, •
is sometimes a feature. The ECG (Fig. 16.38) usually shows a •
tachycardia with normal QRS complexes but occasionally there •
may be rate-dependent bundle branch block. •
Management

Treatment is not always necessary. However, an acute episode •

may be terminated by carotid sinus pressure or by the Valsalva •
manoeuvre. Adenosine (3–12 mg rapidly IV in incremental doses •
until tachycardia stops) or verapamil (5 mg IV over 1 min) will •
restore sinus rhythm in most cases. Intravenous β-blocker or •
flecainide can also be used. In rare cases, when there is severe •
haemodynamic compromise, the tachycardia should be terminated •
by DC cardioversion (p. 482). •
In patients with recurrent SVT, catheter ablation (p. 484) is •
the most effective therapy and will permanently prevent SVT •
in more than 90% of cases. Alternatively, prophylaxis with oral •
β-blocker, verapamil or flecainide may be used but commits •
predominantly young patients to long-term drug therapy and can •
create difficulty in female patients, as these drugs are normally •
avoided during pregnancy. •