Cardiac Arrythmias

Question 1

How is a Normal Sinus Rhythm characterized? (ECG)

Answer 1

Normal sinus rhythm is characterized by
P waves that are upright in leads I and II of the ECG (see Fig. 30.18)
but inverted in lead AVR.

Question 2

How does one recognize Sinus Arrhythmia?

Answer 2

During inspiration, parasympathetic tone falls and
the heart rate quickens; on expiration, the heart rate falls. This variation
is normal, particularly in children and young adults. Typically,
sinus arrhythmia results in predictable irregularities of the pulse.

Question 3

Extrinsic causes of Sinus Bradycardia

Answer 3

Common extrinsic causes of sinus bradycardia include:

• hypothermia, hypothyroidism, cholestatic jaundice and raised
intracranial pressure

• drug therapy with beta-blockers,
digitalis and other antiarrhythmic
drugs

• neurally mediated syndromes

Question 4

Intrinsic causes of Sinus Bradycardia

Answer 4

Common intrinsic causes include:

• acute ischaemia and infarction of the sinus node (as a complication
of acute myocardial infarction)

• chronic degenerative changes, such as fibrosis of the atrium and 
sinus node (sick sinus syndrome).

Question 5

What causes Sick Sinus Syndrome or Sinoatrial Disease?

Answer 5

Sick sinus syndrome or sinoatrial disease is usually caused
by idiopathic fibrosis of the sinus node.

Other causes of fibrosis,
such as ischaemic heart disease, cardiomyopathy or myocarditis,
can also cause the syndrome.

Question 6

Neurally mediated syndromes are caused by what? And what do they present as?

Answer 6

Neurally mediated syndromes are due to a reflex (Bezold–Jarisch)
that may result in both bradycardia (sinus bradycardia, sinus arrest
and AV block) and reflex peripheral vasodilation. These syndromes
usually present as syncope or pre-syncope
(dizzy spells).

Question 7

Carotid sinus syndrome occurs in which age group and leads to what?

Answer 7

Carotid sinus syndrome occurs in the elderly and mainly leads
to bradycardia. Syncope occurs

Question 8

Neurocardiogenic (vasovagal) syncope is presented in which age group?

Answer 8

Neurocardiogenic (vasovagal) syncope usually presents in
young adults but may present for the first time in elderly patients
(see p. 1029).

It results from a variety of situations (physical and
emotional) that affect the autonomic nervous system. The efferent
output may be predominantly bradycardic, predominantly
vasodilatory or mixed.

Question 9

What is Postural orthostatic tachycardia syndrome (POTS)?

Answer 9

Postural orthostatic tachycardia syndrome (POTS) is a sudden
and significant increase in heart rate associated with normal
or mildly reduced blood pressure and produced by standing.

The underlying mechanism is a failure of the peripheral vasculature
to constrict appropriately in response to orthostatic stress,
which is compensated by an excessive increase in heart rate.

Many medications, such as antihypertensives, tricyclic antidepressants
and neuroleptics, can be the cause of syncope,
particularly in the elderly.

Question 10

How to characterize First-degree AV block? (EKG)

Answer 10

This is simple prolongation of the PR interval to more than 0.20 sec.

Every atrial depolarization is followed by conduction to the ventricles
but with delay

Question 11

Second-degree AV block (1/5) - Mobitz I

Answer 11

• Mobitz I block (Wenckebach block phenomenon) is progressive
PR interval prolongation until a P wave fails to conduct. The PR
interval before the blocked P wave is much longer than the PR
interval after the blocked P wave.

Question 12

Second-degree AV block (2/5) - Mobitz II

Answer 12

• Mobitz II block occurs when a dropped QRS complex is not
preceded by progressive PR interval prolongation. Usually, the
QRS complex is wide (>0.12 sec).

Question 13

Second-degree AV block (3/5) - 2 : 1 or 3 : 1 (advanced) block

Answer 13

• 2 : 1 or 3 : 1 (advanced) block occurs when every second or third
P wave conducts to the ventricles. This form of second-degree
block is neither Mobitz I nor Mobitz II.

Question 14

Second-degree AV block (4/5) - Wenckebach AV block

Answer 14

Wenckebach AV block in general is due to block in the AV node,
whereas Mobitz II block signifies block at an infranodal level, such
as the His bundle. The risk of progression to complete heart block
is greater and reliability of the resultant escape rhythm is less with
Mobitz II block. Therefore, pacing is usually indicated in Mobitz II
block, whereas patients with Wenckebach AV block are usually
monitored.

Question 15

Second-degree AV block (5/5) - Acute myocardial infarction

Answer 15

Acute myocardial infarction may produce second-degree
heart block. In inferior myocardial infarction, close monitoring
and transcutaneous temporary back-up
pacing are all that
is required. In anterior myocardial infarction, second-degree heart block is associated with a high risk of progression to complete
heart block, and temporary pacing followed by permanent
pacemaker implantation is usually indicated. Block either
in the AV node or at an infranodal level may cause 2 : 1 heart
block. Management depends on the clinical setting in which it
occurs.

Question 16

Third-degree (complete) AV block

Answer 16

Complete heart block occurs when all atrial activity fails to conduct
to the ventricles (Fig. 30.42). In patients with complete heart block,
the aetiology needs to be established (Box 30.13). In this situation,
life is maintained by a spontaneous escape rhythm.
A narrow-complex
escape rhythm (<0.12 sec QRS complex)
originates from the His bundle and therefore implies that the
region of block lies more proximally in the AV node. The escape
rhythm occurs with an adequate rate (50–60 b.p.m.) and is relatively
reliable. Treatment depends on the aetiology. Recent-onset,
narrow-complex
AV block that has transient causes may respond
to intravenous atropine but temporary pacing facilities should be
available for the management of these patients. Chronic narrow-complex
AV block requires permanent pacing (dual-chamber;
see
p. 1049) if it is symptomatic or associated with heart disease. Pacing
is also advocated for isolated, congenital AV block, even if
asymptomatic.
Broad-complex
escape rhythm (>0.12 sec) implies that the
escape rhythm originates below the His bundle and therefore that
the region of block lies more distally in the His–Purkinje system. The
resulting rhythm is slow (15–40 b.p.m.) and relatively unreliable. Dizziness
and blackouts (Stokes–Adams attacks) often occur. In the
elderly it is usually caused by degenerative fibrosis and calcification
of the distal conduction system (Lev’s disease). In younger individuals
a proximal progressive cardiac conduction disease due to
an inflammatory process is known as Lenegre’s disease. Sodium
channel abnormalities have been identified in both syndromes.
Broad-complex
AV block may also be caused by ischaemic heart
disease, myocarditis or cardiomyopathy. Permanent pacemaker
implantation (see p. 1049) is indicated, as pacing considerably
reduces the mortality. Because ventricular arrhythmias are not
uncommon, an implantable cardioverter–defibrillator (ICD) may be indicated in those with severe left ventricular dysfunction (>0.30 sec
duration).

Question 17

How may an incomplete bundle branch block look like on the ECG?

Answer 17

An incomplete bundle branch block produces slight widening of the QRS complex (up to 0.12 sec).

Question 18

Complete block of a bundle branch - Right [RBBB] and left bundle branch block [LBBB]

Answer 18

This is associated with a wider QRS complex (≥0.12 sec). The
shape of the QRS depends on whether the right or the left bundle
is blocked.

Right bundle branch block (Fig. 30.43A) produces late activation
of the right ventricle. This is seen as deep S waves in leads I
and V6, and as a tall late R wave in lead V1 (late activation moving
towards right-sided
leads and away from left-sided
leads).

Left bundle branch block (Fig. 30.44) produces the opposite:
a deep S wave in lead V1 and a tall late R wave in leads I and V6.
Because left bundle branch conduction is normally responsible for
the initial ventricular activation, left bundle branch block also produces
abnormal Q waves.

Question 19

What is Inapproriate sinus tachycardia?

Answer 19

Inappropriate sinus tachycardia is a persistent increase in resting heart
rate unrelated to, or out of proportion with, the level of physical or emotional
stress. It is found predominantly in young women. Sinus tachycardia
due to intrinsic sinus node abnormalities, such as enhanced
automaticity, or abnormal autonomic regulation of the heart with excess
sympathetic and reduced parasympathetic input, is extremely rare.

In general, sinus tachycardia is a secondary phenomenon and
the underlying causes need to be actively investigated. Depending on the clinical setting, acute causes include exercise, emotion, pain,
fever, infection, acute heart failure, acute pulmonary embolism and
hypovolaemia. Chronic causes include pregnancy, anaemia, hyperthyroidism
and catecholamine excess. The underlying cause should
be found and treated, rather than treating the compensatory physiological
response. If necessary, beta-blockers
may be used to slow
the sinus rate – in hyperthyroidism, for example (see Box 21.30);
ivabradine, an IF (pacemaker current) blocker, may be useful when
beta-blockade
cannot be tolerated

Question 20

Atrioventricular nodal re-entrant
tachycardia (AVNRT)

Answer 20

https://www.youtube.com/watch?v=j8pVU9snSH4

In AVNRT, there are two functionally and anatomically different
pathways predominantly within the AV node: one is characterized
by a short effective refractory period and slow conduction, and the
other has a longer effective refractory period and conducts faster. In
sinus rhythm the atrial impulse that depolarizes the ventricles usually
conducts through the fast pathway. If the atrial impulse (e.g.
an atrial premature beat) occurs early when the fast pathway is still
refractory, the slow pathway takes over in propagating the atrial
impulse to the ventricles. It then travels back through the fast pathway,
which has already recovered its excitability, thus initiating the
most common ‘slow–fast’, or typical, AVNRT.

The rhythm is recognized on ECG from normal regular QRS complexes,
usually at a rate of 140–240/min (Fig. 30.45A). Sometimes,
the QRS complexes will show typical bundle branch block. P waves
either are not visible or are seen immediately before or after the
QRS complex because of simultaneous atrial and ventricular activation.
It is less common (5–10%) to observe a tachycardia when
the atrial impulse conducts anterogradely through the fast pathway
and returns through the slow pathway, producing a long RP′ interval
(‘fast–slow’ or long RP′ tachycardia).

Question 21

Atrioventricular re-entrant
tachycardia

Answer 21

https://www.youtube.com/watch?v=j8pVU9snSH4

This large circuit comprises the AV node, the His bundle, the ventricle
and an abnormal connection of myocardial fibres from the
ventricle back to the atrium. It is called an accessory pathway or
bypass tract and results from an incomplete separation of the atria
and the ventricles during fetal development.

In contrast to AVNRT, atrioventricular re-entrant
tachycardia
(AVRT) is due to a macro re-entry
circuit and each part of the circuit
is activated sequentially. As a result, atrial activation occurs after
ventricular activation and the P wave is usually seen clearly between
the QRS and T waves (Fig. 30.45B).

Accessory pathways are most commonly situated on the left
but may occur anywhere around the AV groove. The most common
accessory pathways, known as Kent bundles, are in the free wall or
septum. In about 10% of cases, multiple pathways occur. Mahaim
fibres are atriofascicular or nodofascicular fibres that enter the ventricular
myocardium in the region of the right bundle branch. Accessory
pathways that conduct from the ventricles to the atria only are
not visible on the surface ECG during sinus rhythm and are therefore
‘concealed’. Accessory pathways that conduct bidirectionally usually
are manifest on the surface ECG. If the accessory pathway conducts
from the atrium to the ventricle during sinus rhythm, the electrical
impulse can conduct quickly over this abnormal connection to depolarize
part of the ventricles abnormally (pre-excitation).
A pre-excited
ECG is characterized by a short PR interval and a wide QRS complex
that begins as a slurred part known as the δ wave (Fig. 30.45C).
Patients with a history of palpitations and a pre-excited
ECG have a
condition known as Wolff–Parkinson–White (WPW) syndrome.

During AVRT, the AV node and ventricles are activated normally
(orthodromic AVRT), usually resulting in a narrow QRS complex.

Less commonly, the tachycardia circuit can be reversed, with activation
of the ventricles via the accessory pathway, and atrial activation
via retrograde conduction through the AV node (antidromic
AVRT). This results in a broad-complex
tachycardia. These patients
are also prone to atrial fibrillation.

During atrial fibrillation, the ventricles may be depolarized by
impulses travelling over both the abnormal and the normal pathways.
This results in pre-excited
atrial fibrillation, a characteristic
tachycardia that is typified by irregularly irregular broad QRS complexes
(Fig. 30.45D). If an accessory pathway has a short antegrade
effective refractory period (<250 ms), it may conduct to the ventricles
at an extremely high rate and may cause ventricular fibrillation.
The incidence of sudden death is 0.15–0.39% per patient-year
and
it may be a first manifestation of the disease in younger individuals.
Verapamil and digoxin may allow a higher rate of conduction over
the abnormal pathway and precipitate ventricular fibrillation. Therefore,
neither verapamil nor digoxin should be used to treat atrial
fibrillation associated with the WPW syndrome.

Question 22

Acute management of AVNRT and AVRT

Answer 22

In an emergency, distinguishing between AVNRT and AVRT may
be difficult but is usually not critical, as both tachycardias respond
to the same treatment. Patients presenting with SVTs and haemodynamic
instability (e.g. hypotension, pulmonary oedema) require
emergency cardioversion. If the patient is haemodynamically stable,
vagal manoeuvres, including right carotid massage (see Box 30.10),
the Valsalva manoeuvre and facial immersion in cold water, can be
successfully employed.

If physical manoeuvres have not been successful, intravenous
adenosine (initially 6 mg by i.v. push, followed by 12 mg if needed)
should be tried. Adenosine is a very short-acting
(half-life
<10 sec),
naturally occurring purine nucleoside that causes complete heart
block for a fraction of a second following intravenous administration.
It is highly effective at terminating AVNRT and AVRT or unmasking underlying atrial activity, but rarely affects ventricular
tachycardia. The side-effects
of adenosine are very brief but may
include chest pain, sense of impending doom, bronchospasm,
flushing or heaviness of the limbs. Adenosine should be used with
caution in patients with a history of asthma. An alternative treatment
is verapamil 5–10 mg i.v. over 5–10 min or beta-blockers
(esmolol,
propranolol, metoprolol). Verapamil must not be given after beta-blockers
or if the tachycardia presents with broad (>0.12 sec) QRS
complexes.

Question 23

Long-term management of AVNRT and AVRT

Answer 23

Patients with suspected cardiac arrhythmias should always be
referred to a cardiologist for electrophysiological evaluation and
long-term
management, as both pharmacological and non-pharmacological
treatments, including ablation of an accessory
pathway, are readily available. Verapamil, diltiazem and beta-blockers
have proven efficacy in 60–80% of patients. Sodium-channel
blockers (flecainide and propafenone), potassium
repolarization current blockers (sotalol, dofetilide, azimilide) and the
multichannel blocker amiodarone may also prevent the occurrence
of tachycardia.

Refinement of catheter ablation techniques has rendered many
AV junctional tachycardias entirely curable. Modification of the slow
pathway is successful in 96% of patients with AVNRT, although a
1% risk of AV block is present. In AVRT, the target for catheter ablation
is the accessory pathway(s). The success rate of ablation of a
single accessory pathway is approximately 95%, with a recurrence
rate of 5%, requiring a repeat procedure.

Question 24

Causes of Atrial fibrillation

Answer 24

Although rheumatic heart disease, alcohol intoxication and thyrotoxicosis
are the ‘classic’ causes of atrial fibrillation, hypertension
and heart failure are the most common causes in the developed
world. Hyperthyroidism may provoke atrial fibrillation, sometimes as
virtually the only feature of the disease, and thyroid function tests
are mandatory in any patient with atrial fibrillation that is unaccounted
for. Atrial fibrillation occurs in one-third
of patients after
cardiac surgery.

Question 25

Familial Atrial fibrillation is linked to which chromosomal gene defects?

Answer 25

Gene defects linked to chromosomes 10,
6, 5 and 4 have been associated with familial atrial fibrillation.

Question 26

ECG of Atrial fibrillation

Answer 26

The ECG shows fine oscillations of the baseline (so-called
fibrillation
or f waves) and no clear P waves (Fig. 30.46A). The QRS
rhythm is rapid and irregular. Untreated, the ventricular rate is usually
120–180/min but it slows with treatment.

Question 27

The clinical classification of atrial fibrillation

Answer 27

The clinical classification of atrial fibrillation includes:
• first detected – irrespective of duration or severity of symptoms
• paroxysmal – stops spontaneously within 7 days
• persistent – continuous >7 days
• longstanding persistent – continuous >1 year
• permanent – continuous, with a joint decision between the patient
and the physician to cease further attempts to regain sinus
rhythm.

The classification is helpful in choosing between rhythm restoration
and rate control. Atrial fibrillation may be asymptomatic and the
‘first detected episode’ should not necessarily be regarded as the
true onset.

Question 28

What is the acute management of Atrial fibrillation

Answer 28

When atrial fibrillation is due to an acute precipitating event, such
as alcohol toxicity, chest infection or hyperthyroidism, the provoking
cause should be treated. Strategies for the acute management of
atrial fibrillation are:
• Ventricular rate control, achieved by drugs that block the AV
node (see later).
• Cardioversion, achieved electrically by DC shock (see p. 1048),
or medically by intravenous infusion of an antiarrhythmic drug
such as flecainide, propafenone, vernakalant or amiodarone.
Cardioversion can also be achieved by giving an oral agent (flecainide
or propafenone) previously tested in hospital and found
to be safe in a particular patient (‘pill-in-
pocket’
approach).
The choice depends on:
• how well the arrhythmia is tolerated (is cardioversion urgent?)
• whether anticoagulation is required before considering elective
cardioversion
• whether spontaneous cardioversion is likely (previous history?
reversible cause?).

Question 29

What is the procedure on Cardioversion for Atrial fibrillation

Answer 29

Conversion to sinus rhythm can be achieved by electrical DC cardioversion
in about 80% of patients. Biphasic waveform defibrillation
is more effective than conventional (monophasic) defibrillation, and
biphasic defibrillators are now standard. To minimize the risk of thromboembolism
associated with cardioversion, patients are fully anticoagulated
with warfarin (International Normalized Ratio (INR) 2.0–3.0) or
with a direct acting oral anticoagulant agent (DOAC) for 3 weeks before
cardioversion (unless atrial fibrillation is of less than 48 hours’ duration)
and at least 4 weeks after the procedure. The patient is then assessed
for the necessity for long-term
anticoagulation based on their thromboembolic
risk score (see later). If cardioversion is urgent and the patient
is not on any anticoagulation, transoesophageal echocardiography is
used to exclude the presence of atrial thrombus.

Question 30

Long-term management of Atrial fibrillation (1/4) - The 2 main strategies

Answer 30

Two strategies are available:
• ‘rate control’ (AV nodal slowing agents plus oral anticoagulation)
• ‘rhythm control’ (antiarrhythmic drugs plus DC cardioversion
plus oral anticoagulation).
Major randomized studies in patients predominantly over the
age of 65 years (AFFIRM) or in patients with heart failure (AF-CHF)
have shown that there is no net mortality or symptom benefit to be
gained from one strategy compared with the other. Which strategy
to adopt needs to be assessed for each individual patient. Factors
to consider include the likelihood of maintaining sinus rhythm
and the safety/tolerability of antiarrhythmic drugs in a particular
patient.

Question 31

Long-term management of Atrial fibrillation (2/4) - Rhythm control

Answer 31

This is advocated for younger, symptomatic and physically active
patients. Recurrent paroxysms may be prevented with oral medication. In general, patients with no significant heart disease
can be treated with any class Ia, Ic or III antiarrhythmic drug,
although it is recommended that amiodarone (because of its substantial
extracardiac adverse effect profile) should be reserved until
other drugs have failed.

For patients with heart failure or left ventricular
hypertrophy only amiodarone is recommended. Patients
with coronary artery disease may be treated with sotalol or amiodarone.
Patients with paroxysmal atrial fibrillation or with early
persistent atrial fibrillation (little left atrial dilation) may be treated
with left atrial ablation.

Question 32

Long-term management of Atrial fibrillation (3/4) - Rate control

Answer 32

As a primary strategy, this is appropriate in patients who:

• have the permanent form of the arrhythmia associated with
symptoms that can be further improved by slowing heart rate,
or are older than 65 years with recurrent atrial tachyarrhythmias
(‘accepted’ atrial fibrillation)

• have persistent tachyarrhythmias and have failed cardioversion(s)
and serial prophylactic antiarrhythmic drug therapy, and in whom
the risk/benefit ratio from using specific antiarrhythmic agents is
shifted towards increased risk.

Rate control is usually achieved with a combination of digoxin,
beta-blockers
or non-dihydropyridine
calcium-channel
blockers
(verapamil or diltiazem).

Digoxin monotherapy may be sufficient for elderly, non-ambulant patients. In younger patients the effect of catecholamines easily overwhelms the vagotonic effect of digoxin and additional AV nodal slowing agents are needed.

The ventricular rate response is generally considered to be controlled
if the resting heart rate is below 110 b.p.m. but stricter control,
between 60 and 80 b.p.m. at rest and below 110 b.p.m. during
moderate exercise, may be needed if symptoms persist.

To assess
the adequacy of rate control, an ECG rhythm strip may be sufficient
in an elderly patient but ambulatory 24-hour
Holter monitoring
and an exercise stress test (treadmill) are needed in younger
individuals.

Older patients with poor rate control despite optimal
medical therapy should be considered for AV node ablation and
pacemaker implantation (‘ablate and pace’ strategy). These
patients usually experience a marked symptomatic improvement
but require life-long
anticoagulation because of the on-going
risk
of thromboembolism.

Question 33

Long-term management of Atrial fibrillation (4/4) - Anticoagulation

Answer 33

A scoring system known as CHA2DS2VASc is used (Box 30.15) as
the first step in determining the need for anticoagulation.
Long-term
prophylaxis against ischaemic stroke with oral anticoagulation
must be balanced against the risk of haemorrhage. The
HAS-BLED
score is recommended by European, Canadian and UK
(NICE) guidelines. A high HAS-BLED
score identifies patients with
a high risk of bleeding (Box 30.16 and Fig. 30.47), and where risk
factors exist, attempts may be made to modify them for instance by
controlling hypertension and minimising alcohol intake.

When oral anticoagulation is required, either warfarin (dose
adjusted to maintain an INR between 2.0 and 3.0) or one of the direct
oral anticoagulants (the DOACs) can be used. These latter agents fall
into two classes: direct thrombin inhibitors (e.g. dabigatran) and oral
direct factor Xa inhibitors (e.g. rivaroxaban and apixaban). DOACs specifically
block a single step in the coagulation cascade, in contrast to
warfarin, which blocks several vitamin K-dependent
factors (II, VII, IX
and X). In comparison with warfarin, the DOACs have a rapid onset
of action, shorter half-life
and fewer food and drug interactions, and
do not require INR testing. Trial data have shown them to be equally
effective as, and maybe safer than, warfarin. Antiplatelet agents should
not be used to reduce stroke risk. Percutaneous left atrial appendage
occlusion (LAAO) may be offered where anticoagulation is contraindicated
or not tolerated.

Question 34

What is the atrial rate in Atrial Flutter?

&

How does the re-entrant process circulate in the heart?

Answer 34

Atrial flutter is usually
an organized atrial rhythm with an atrial rate typically between 250 and 350 b.p.m.

Typical, or isthmus-dependent,
atrial flutter involves a
macro re-entrant
right atrial circuit around the tricuspid annulus. The
wavefront circulates down the lateral wall of the right atrium, through
the Eustachian ridge between the tricuspid annulus and the inferior
vena cava, and up the interatrial septum, giving rise to the most frequent
pattern, referred to as counter-clockwise
flutter. Re-entry
can
also occur in the opposite direction (clockwise or reverse flutter).

Question 35

What are the ECG signs of Atrial Flutter?

Answer 35

The ECG shows regular sawtooth-like
atrial flutter waves (F
waves) between QRS complexes (see Fig. 30.46B). In typical
counter-clockwise
atrial flutter the F waves are negative in the inferior
leads and positive in leads V1 and V2. In clockwise atrial flutter
the deflection of the F waves is the opposite. If F waves are
not clearly visible, it is worth trying to reveal them by slowing AV
conduction by carotid sinus massage or by administering AV nodal
blocking drugs such as adenosine or verapamil.

Question 36

Management of Atrial Flutter

Answer 36

Management of a symptomatic acute paroxysm is by electrical cardioversion.
Patients who have been in atrial flutter for more than
1–2 days should be treated in a similar manner to those with atrial
fibrillation and anticoagulated for 3 weeks prior to cardioversion.
Acute pharmacological cardioversion can be achieved using class Ic (flecainide, propafenone) or certain class III antiarrhythmic agents
(dofetilide, ibutilide; these have better efficacy than in atrial fibrillation
but are not available in many countries)

Recurrent paroxysms may be prevented by class III antiarrhythmic
agents (sotalol, amiodarone). AV nodal blocking agents may
be used to control the ventricular rate if the arrhythmia persists.
However, the treatment of choice for patients with recurrent atrial
flutter is catheter ablation (see p. 1059), which permanently interrupts
re-entry
by creating a line of conduction block within the isthmus
between the inferior vena cava and the tricuspid valve ring.
This technique offers patients whose only arrhythmia is typical atrial
flutter an almost certain chance of a cure, although the later occurrence
of atrial fibrillation is not uncommon.

Question 37

What is Atrial Tachycardia?
Mechanism?
Rate?
ECG?
Cause?

Answer 37

This is an uncommon arrhythmia. Its prevalence is believed to be
less than 1% in patients with arrhythmias. It is usually associated
with structural heart disease but in many cases it is referred to as
idiopathic. Macro re-entrant
tachycardia often occurs after surgery
for congenital heart disease. Atrial tachycardia with block is often a
result of digitalis poisoning.

The mechanisms of atrial tachycardia are attributed to enhanced
automaticity, triggered activity or intra-atrial
re-entry.
Atrial re-entrant
tachycardia is usually relatively slow (125–150 b.p.m.) and
can be initiated and terminated by atrial premature beats. The P′P′
intervals are regular. The PR interval depends on the rate of tachycardia
and is longer than in sinus rhythm at the same rate.

Atrial tachycardia
is typically caused by a focus that is frequently located along the
crista terminalis in the right atrium, adjacent to a pulmonary vein in
the left atrium, or around one of the atrial appendages. Short runs of atrial tachycardia
may provoke more sustained episodes of atrial fibrillation.

Question 38

Diagnosis of Atrial Tachycardia

Answer 38

Carotid sinus massage may increase AV block during tachycardia,
thereby facilitating the diagnosis, but does not usually terminate
the arrhythmia.

Question 39

Management of Atrial Tachycardia

Answer 39

Management options include cardioversion,
antiarrhythmic drug therapy to maintain sinus rhythm, AV nodal
slowing agents to control rate and, in selected cases, radiofrequency
catheter ablation.

Question 40

Sustained ventricular tachycardia

• Symptoms
• Rate

Answer 40

Sustained ventricular tachycardia (>30 sec) often results in pre-syncope
(dizziness), syncope, hypotension and cardiac arrest,
although it may be remarkably well tolerated in some patients.
Examination reveals a pulse rate typically between 120 and
220 b.p.m. Usually, there are clinical signs of atrioventricular dissociation
(i.e. intermittent cannon ‘a’ waves in the neck and variable
intensity of the first heart sound).

Question 41

Sustained ventricular tachycardia - ECG

Answer 41

The ECG shows a rapid ventricular rhythm with broad (often
≥0.14 sec), abnormal QRS complexes. AV dissociation may result
in visible P waves, which appear to march through the tachycardia,
capture beats (an intermittent narrow QRS complex owing to normal
ventricular activation via the AV node and conducting system)
and fusion beats (intermediate between ventricular tachycardia beat
and capture beat).

Question 42

Treatment/Management of Sustained ventricular tachycardia

Answer 42

Treatment may be urgent, depending on the haemodynamic situation.
If the patient is haemodynamically compromised (e.g. hypotensive
or pulmonary oedema), emergency DC cardioversion may
be required. On the other hand, if the blood pressure and cardiac
output are well maintained, intravenous therapy with beta-blockers
(esmolol), class I drugs or amiodarone is usually used. DC cardioversion
is necessary if medical therapy is unsuccessful.

Question 43

What is Ventricular fibrillation?
&
What are the signs/symptoms?

Answer 43

This involves very rapid and irregular ventricular activation with no
mechanical effect. The patient is pulseless and becomes rapidly
unconscious; respiration ceases (cardiac arrest).

Question 44

Ventricular fibrillation - ECG

Answer 44

The ECG shows
shapeless, rapid oscillations and there is no hint of organized complexes.

Question 45

Treatment/Management of Ventricular fibrillation

Answer 45

The only
effective treatment is electrical defibrillation. Basic and advanced
cardiac life support is needed.

Question 46

What is Brugada’s syndrome?

• Diagnosis
• Symptoms/Presentation
• Treatment/Management

Answer 46

This inheritable condition accounts for part of a group of patients
with idiopathic ventricular fibrillation who have no evidence of causative
structural cardiac disease. It is more common in young male
adults and in South-east
Asia.

The diagnosis is made by identifying
the classic ECG changes that may be present spontaneously or
may be provoked by the administration of a class I antiarrhythmic
(flecainide or ajmaline – principally used as a diagnostic agent in
suspected Brugada patients): right bundle branch block with coved
ST elevation in leads V1–V3 (Fig. 30.49). Atrial fibrillation may occur.

It can present with sudden death during sleep, resuscitated
cardiac arrest and syncope, or the patient may be asymptomatic
and diagnosed incidentally or during familial assessment.

The only successful
treatment is an ICD. Beta-blockade
is not helpful and may
be harmful.

Question 47

Which two major congenital long QT syndromes exist?

(Which is associated with congenital deafness?)

Answer 47

Two major syndromes have been described, one that is (Jervell–
Lange-Nielsen
syndrome) and one that is not (Romano–Ward syndrome)
associated with congenital deafness.

• Jervell–Lange-Nielsen
syndrome (autosomal recessive)
• Romano–Ward syndrome
(autosomal dominant)

Question 48

To date, thirteen long QT (LQT) subtypes have been identified but
three major ones account for the majority of cases.

Which three major subtypes is it and what provokes/associates/occurs in each of them?

Answer 48

• LQT1 (KCNQ1 gene mutation affecting the Iksα subunit), in
which the arrhythmia is usually provoked by exercise, particularly
swimming

• LQT2 (KCNH2 gene mutation affecting the Ikrα subunit), in which
arrhythmia provocation is associated with emotion and acoustic
stimuli

• LQT3 (SCN5A gene mutation affecting the INaα subunit), in
which the arrhythmias occur during rest or when asleep.

Question 49

What is acquired long QT syndrome provoked by (also for torsades de pointes)?

Answer 49

QT prolongation and torsades de pointes are usually provoked by
bradycardia.

Question 50

Clinical features of Long QT syndrome

Answer 50

Patients with a long QT develop syncope and palpitations as a result
of polymorphic ventricular tachycardia (torsades de pointes). They
usually terminate spontaneously but may degenerate to ventricular
fibrillation, resulting in sudden death.

Question 51

Torsades de pointes - ECG characteristics

Answer 51

Torsades de pointes is characterized on the ECG by rapid,
irregular, sharp complexes that continuously change from an upright
to an inverted position (Fig. 30.50B).
Between spells of tachycardia, or immediately preceding the
onset of tachycardia, the ECG shows a prolonged QT interval; the
corrected QT (see Box 30.9) is usually over 0.50 sec.

Question 52

Management of Acute (acquired) and Congenital long QT syndrome

Answer 52

Acute (acquired) long QT syndrome is treated as follows:
• Any electrolyte disturbance is corrected.
• Causative drugs are stopped.
• The heart rate is maintained with atrial or ventricular pacing.
• Magnesium sulphate 8 mmol (Mg2+) is given over 10–15 min for
acquired long QT.
• Intravenous isoprenaline may be effective when QT prolongation
is acquired (isoprenaline is contraindicated for congenital long
QT syndrome).

Long-term,
congenital long QT syndrome is generally treated
by beta-blockade,
pacemaker therapy and, occasionally, left cardiac
sympathetic denervation. LQT1 patients seem to respond
well to beta-blockade
while LQT3 patients are better treated with
sodium-channel
blockers. All long QT patients should avoid drugs
known to prolong the QT interval. Patients who remain symptomatic
despite conventional therapy, and those with marked QT prolongation
or a strong family history of sudden death, usually need
ICD therapy.

Question 53

Short QT syndrome

• MoA
• Symptoms/Presentation
• Treatment

Answer 53

Five types have been described; they are caused by genetic
abnormalities that lead to faster repolarization. Ventricular
arrhythmias and sudden death may occur and an ICD is the best
treatment.

Question 54

Monomorphic ventricular tachycardia
/Normal heart ventricular tachycardia

If left untreated, may lead to what?

Precisely where may this condition arise from the heart?

Treatment?

Answer 54

Monomorphic ventricular tachycardia in patients with structurally 
normal hearts (idiopathic ventricular tachycardia) is usually a benign 
condition with an excellent long-term 
prognosis. 

Occasionally, it
is incessant (so called Gallavardin’s tachycardia) and, if untreated,
may lead to cardiomyopathy.

Normal heart ventricular tachycardia arises from a focus in
either the right ventricular outflow tract or the left ventricular septum.

Treatment of symptoms is usually with beta-blockers.
There
is a special form of verapamil-sensitive
tachycardia that responds
well to non-dihydropyridine
calcium antagonists. In symptomatic
patients, radiofrequency catheter ablation is highly effective, resulting
in a cure in over 90% of cases. It is sometimes difficult to distinguish
arrhythmogenic right ventricular hypertrophy (see p. 1121)
from this seemingly benign disorder.

Question 55

Non-sustained ventricular tachycardia

• Defined as…
• Treatment?
• What can improve quality of life in symptomatic individuals?

Answer 55

Non-sustained
ventricular tachycardia (NSVT) is defined as ventricular
tachycardia that is 5 consecutive beats or more but lasts
for less than 30 seconds (Fig. 30.51A).

NSVT can be found in 6% of
patients with normal hearts and usually does not require treatment.

It is documented in up to 60–80% of patients with heart disease.

There is insufficient evidence on prognosis but an ICD has been
shown to improve survival of patients with particularly poor left ventricular
function (ejection fraction ≤30%) by preventing arrhythmic
death.

Antiarrhythmic suppression of NSVT is not usually advocated
but beta-blockers
may improve quality of life in symptomatic
individuals.

Question 56

Ventricular premature beats (ectopics)

• Treatment
• ECG

Answer 56

These may be uncomfortable, especially when frequent. The patient
complains of extra beats, missed beats or heavy beats because
it may be the premature beat, the post-ectopic
pause or the next
sinus beat that is noticed. The pulse is irregular owing to the premature
beats. Some early beats may not be felt at the wrist. When
a premature beat occurs regularly after every normal beat, ‘pulsus
bigeminus’ may occur.

If premature ventricular beats are highly
symptomatic, treatment with beta-blockade
may be helpful. If the
ectopics are very frequent, left ventricular dysfunction may develop;
if the ectopics stem from a single focus, especially when in the right
ventricle, catheter ablation can be very effective.

These premature beats (Fig. 30.51B–D) have a broad (>0.12 sec) and
bizarre QRS complex because they arise from an abnormal (ectopic) site
in the ventricular myocardium. Following a premature beat, there is usually
a complete compensatory pause because the AV node or ventricle
is refractory to the next sinus impulse. Early ‘R-on-
T’
ventricular premature
beats (occurring simultaneously with the upstroke or peak of the T
wave of the previous beat) may induce ventricular fibrillation in patients
with heart disease, particularly following myocardial infarction.

Ventricular premature beats are usually treated only if symptomatic.
Simple measures, such as reassurance and beta-blocker
therapy, are normally all that is required.

Question 57

Class I drugs

Answer 57

These are membrane-depressant
drugs that reduce the rate of entry
of sodium into the cell (sodium-channel
blockers). They may slow
conduction, delay recovery or reduce the spontaneous discharge rate
of myocardial cells. Class I agents have been found to increase mortality
compared to placebo in post-myocardial
infarction patients with
ventricular ectopy (Cardiac Arrhythmia Suppression Trial (CAST) trials
– class Ic agents) and in patients treated for atrial fibrillation (class Ia
agent, quinidine). In view of this, class Ic agents, such as flecainide,
and all other class I drugs should be reserved for patients who do not
have significant coronary artery disease, left ventricular dysfunction
or other forms of significant structural heart disease.

Question 58

Class II drugs

Answer 58

These antisympathetic drugs prevent the effects of catecholamines
on the action potential. Most are β-adrenoceptor
antagonists.
Cardioselective
beta-blockers
(β1) include metoprolol, bisoprolol,
atenolol and acebutolol. Beta-blockers
suppress AV node conduction,
which may be effective in preventing attacks of junctional tachycardia,
and may help to control the ventricular rate during paroxysms
of other forms of SVT (e.g. atrial fibrillation). In general, beta-blockers
are anti-ischaemic
and anti-adrenergic,
and have proven beneficial
effects in patients post myocardial infarction (by preventing ventricular
fibrillation) and in those with congestive heart failure. It is therefore
advisable to use beta-blocker
therapy either alone or in combination
with other antiarrhythmic drugs in patients with symptomatic tachyarrhythmias,
particularly those with coronary artery disease.

Question 59

Class III drugs

Answer 59

These prolong the action potential, usually by blocking the rapid
component of the delayed rectifier potassium current (IKr), and do
not affect sodium transport through the membrane. The drugs in
this class are amiodarone and sotalol. Sotalol is also a beta-blocker.
Sotalol may result in acquired long QT syndrome and torsades
de pointes. The risk of torsades is increased in the setting of hypokalaemia,
and particular care should be taken in patients taking diuretic therapy. Amiodarone therapy, in contrast to most other
antiarrhythmic drugs, carries a low risk of proarrhythmia in patients
with significant structural heart disease, but its use may be limited
due to toxic and potentially serious side-effects.
Dronedarone is a
multichannel-blocking
drug that suppresses the recurrence of atrial
fibrillation and reduces hospital admissions in patients with cardiovascular
risk. However, it has proven harmful in patients with left
ventricular dysfunction and is contraindicated in heart failure.
Vernakalant is a multichannel blocker that is approved for
the rapid intravenous medical cardioversion of new-onset
atrial
fibrillation.

Question 60

Class IV drugs

Answer 60

The non-dihydropyridine
calcium-channel
blockers are particularly
effective at slowing conduction in nodal tissue. These drugs can
prevent attacks of junctional tachycardia (AVNRT and AVRT) and
may help to control ventricular rates during paroxysms of other
forms of SVT (e.g. atrial fibrillation).