Mechanisms of cardiac arrhythmias: from

automaticity to re-entry (reentry)

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reentry-triggered-activity/

1. Introduction to ECG Interpretation

1. Clinical electrocardiography and ECG interpretation
2. Cardiac electrophysiology: action potential,
automaticity and vectors
3. The ECG leads: electrodes, limb leads, chest
(precordial) leads, 12-Lead ECG (EKG)
4. The Cabrera format of the 12-lead ECG & lead –aVR
instead of aVR
5. ECG interpretation: Characteristics of the normal ECG
(P-wave, QRS complex, ST segment, T-wave)
6. How to interpret the ECG / EKG: A systematic approach
2. Arrhythmias and arrhythmology
1. Mechanisms of cardiac arrhythmias: from automaticity
to re-entry (reentry)
2 Ab t t i l d ti ( b
 2. Aberrant ventricular conduction (aberrancy,
aberration)
3. Premature ventricular contractions (premature
ventricular complex, premature ventricular beats)

4. Premature atrial contraction (premature atrial beat /

complex): ECG & clinical implications
5. Sinus rhythm: physiology, ECG criteria & clinical
implications
6. Sinus arrhythmia (respiratory sinus arrhythmia)
7. Sinus bradycardia: definitions, ECG, causes and
management
8. Chronotropic incompetence (inability to increase heart
rate)
9. Sinoatrial arrest & sinoatrial pause (sinus pause /
arrest)
10. Sinoatrial block (SA block): ECG criteria, causes and
clinical features
11. Sinus node dysfunction (SND) and sick sinus syndrome
(SSS)
12. Sinus tachycardia & Inappropriate sinus tachycardia
13. Atrial fibrillation: ECG, classification, causes, risk
factors & management
14. Atrial flutter: classification, causes, ECG diagnosis &
management
15 Ectopic atrial rhythm (EAT) atrial tachycardia (AT) &
 15. Ectopic atrial rhythm (EAT), atrial tachycardia (AT) &
multifocal atrial tachycardia (MAT)
16. Atrioventricular nodal reentry tachycardia (AVNRT):
ECG features & management

17. Pre-excitation, Atrioventricular Reentrant (Reentry)

Tachycardia (AVRT), Wolff-Parkinson-White (WPW
syndrome)
18. Junctional rhythm (escape rhythm) and junctional
tachycardia
19. Ventricular rhythm and accelerated ventricular
rhythm (idioventricular rhythm)
20. Ventricular tachycardia (VT): ECG criteria, causes,
classification, treatment (management)
21. Longt QT interval, long QT syndrome (LQTS) & torsades
de pointes
22. Ventricular fibrillation, pulseless electrical activity and
sudden cardiac arrest
23. Pacemaker mediated tachycardia (PMT): ECG and
management
24. Diagnosis and management of narrow and wide
complex tachycardia
3. Myocardial Ischemia & Infarction
1. Introduction to Coronary Artery Disease (Ischemic
Heart Disease) & Use of ECG
2. Classification of Acute Coronary Syndromes (ACS) &
 2. Classification of Acute Coronary Syndromes (ACS) &
Acute Myocardial Infarction (AMI)
3. Clinical application of ECG in chest pain & acute
myocardial infarction

4. Diagnostic Criteria for Acute Myocardial Infarction:

Cardiac troponins, ECG & Symptoms
5. Myocardial Ischemia & infarction: Reactions, ECG
Changes & Symptoms
6. The left ventricle in myocardial ischemia and
infarction
7. Factors that modify the natural course in acute
myocardial infarction (AMI)
8. ECG in myocardial ischemia: ischemic changes in the
ST segment & T-wave
9. ST segment depression in myocardial ischemia and
differential diagnoses
10. ST segment elevation in acute myocardial ischemia
and differential diagnoses
11. ST elevation myocardial infarction (STEMI) without ST
elevations on 12-lead ECG
12. T-waves in ischemia: hyperacute, inverted (negative),
Wellen's sign & de Winter's sign
13. ECG signs of myocardial infarction: pathological Q-
waves & pathological R-waves
14. Other ECG changes in ischemia and infarction
 14. Other ECG changes in ischemia and infarction
15. Supraventricular and intraventricular conduction
defects in myocardial ischemia and infarction
16. ECG localization of myocardial infarction / ischemia
and coronary artery occlusion (culprit)

17. The ECG in assessment of myocardial reperfusion

18. Approach to patients with chest pain: differential
diagnoses, management & ECG
19. Stable Coronary Artery Disease (Angina Pectoris):
Diagnosis, Evaluation, Management
20. NSTEMI (Non ST Elevation Myocardial Infarction) &
Unstable Angina: Diagnosis, Criteria, ECG, Management
21. STEMI (ST Elevation Myocardial Infarction): diagnosis,
criteria, ECG & management
4. Conduction Defects
1. Overview of atrioventricular (AV) blocks
2. First-degree AV block (AV block I, AV block 1)
3. Second-degree AV block: Mobitz type 1 (Wenckebach) &
Mobitz type 2 block
4. Third-degree AV block (3rd degree AV block, AV block
3, AV block III)
5. Management and treatment of AV block
(atrioventricular blocks)
6. Intraventricular conduction delay: bundle branch
blocks & fascicular blocks
 7. Right bundle branch block (RBBB): ECG, criteria,
definitions, causes & treatment
8. Left bundle branch block (LBBB): ECG criteria, causes,
management

9. Left bundle branch block (LBBB) in acute myocardial

infarction: the Sgarbossa criteria
10. Fascicular block (hemiblock): left anterior & left
posterior fascicular block on ECG
11. Nonspecific intraventricular conduction delay (defect)
5. Cardiac Hypertrophy & Enlargement
1. Atrial and ventricular enlargement: hypertrophy and
dilatation on ECG
2. ECG in left ventricular hypertrophy (LVH): criteria and
implications
3. Right ventricular hypertrophy (RVH): ECG criteria &
clinical characteristics
4. Biventricular hypertrophy ECG and clinical
characteristics
5. Left atrial enlargement (P mitrale) & right atrial
enlargement (P pulmonale) on ECG
6. Drugs & Electrolyte Imbalance
1. Digoxin - ECG changes, arrhythmias, conduction
defects & treatment
2. ECG changes caused by antiarrhythmic drugs, beta
blockers & calcium channel blockers
 blockers & calcium channel blockers
3. ECG changes due to electrolyte imbalance (disorder)
7. Genetics, Syndromes & Miscellaneous
1. ECG J wave syndromes: hypothermia, early
repolarization, hypercalcemia & Brugada syndrome
2. Brugada syndrome: ECG, clinical features and
management
3. Early repolarization pattern on ECG (early
repolarization syndrome)
4. Takotsubo cardiomyopathy (broken heart syndrome,
stress induced cardiomyopathy)
5. Pericarditis, myocarditis & perimyocarditis: ECG,
criteria & treatment
6. Eletrical alternans: the ECG in pericardial effusion &
cardiac tamponade
7. Long QT Syndrome (LQTS)
8. Exercise Stress Testing (Exercise ECG)
1. Exercise stress test (treadmill test, exercise ECG):
Introduction
2. Exercise stress test (exercise ECG): Indications,
Contraindications, Preparation
3. Exercise stress test (exercise ECG): protocols,
evaluation & termination
4. Exercise stress testing in special patient populations
5. Exercise physiology: from normal response to
myocardial ischemia & chest pain
 myocardial ischemia & chest pain
6. Evaluation of exercise stress test: ECG, symptoms,
blood pressure, heart rate, performance

Clinical ECG Interpretation Arrhythmias and arrhythmology

Mechanisms of cardiac arrhythmias: from automaticity to
re-entry (reentry)
In Progress
Section 2, Chapter 1
In Progress
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Chapter contents Show

Definition of heart rhythm
Mechanisms of cardiac arrhythmias
Main causes of cardiac arrhythmias
Abnormal impulse formation
Increased or abnormal automaticity
Triggered activity (after depolarizations)
Abnormal impulse conduction: re-entry (reentry)
Anatomical re-entry
Functional re-entry
Clinical significance
Termination of re-entry
Next chapter
Related

Section Progress
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h i f di h h i f
Mechanisms of cardiac arrhythmias: from
automaticity to re-entry
The aim of this chapter is to present the most common
arrhythmias in clinical practice. The initial discussion will

focus on the mechanisms of cardiac arrhythmias. Although

a detailed understanding of the mechanisms underlying
cardiac arrhythmias is not necessary for all clinicians, it is
wise to invest time in grasping the concepts as it will
facilitate understanding of subsequent articles and chapters.
This chapter starts with a discussion on arrhythmogenesis
(mechanisms of arrhythmias) and thereafter each
arrhythmia is discussed separately.

It is appropriate to subdivide cardiac arrhythmias into

the following groups:

Bradyarrhytmias (bradycardia): arrhythmias that are

typically due to dysfunctional automaticity in pacemaker
cells or blocking of impulses somewhere along the
conduction system.
Supraventricular tachyarrhythmias (tachycardia):
arrhythmias in which the impulses emanating from the
atria.
Ventricular
tachyarrhythmias (tachycardia): arrhythmias in which
the impulses emanating from the ventricles.

This classification is not flawless but it facilitates differential

diagnostics and management of arrhythmias. Because
management of arrhythmias, particularly tachyarrhythmias,
is often considered difficult, a special section is devoted to
diagnosis and management of arrhythmias. The
recommendations presented throughout this section is in

line with guidelines and recommendations issued by the

European Society for Cardiology (ESC), the American Heart
Association (AHA) and the American College of Cardiology
(ACC).

Definition of heart rhythm

A rhythm is defined as three consecutive heartbeats
displaying identical waveforms on the ECG. The similarity of
the waveforms indicates that the origin of the impulse is the
same. The sinoatrial (SA) node is the heart’s pacemaker
under normal circumstances and the rhythm is referred to
as sinus rhythm.

An arrhythmia is defined as an abnormal heart rhythm or

heart rate, which is not physiologically justified. The
latter criteria is important because rhythms which are
physiologically justified should not be considered abnormal.
For example, sinus bradycardia (a slow rhythm directed by
the sinoatrial node) is a common finding in athletes and
during sleep; in these scenarios, it should not be considered
abnormal. On the other hand, sinus bradycardia developing
during physical exercise is considered abnormal,
because heart rate must increase during exercise.
Mechanisms of cardiac arrhythmias
The mechanisms underlying cardiac arrhythmias are
being unraveled at an increasing pace. Arrhythmology is a
very exciting area with intense research activity. This is

partly due to the rise of cardiac imaging and invasive

electrophysiological methods which enable detailed in vivo
studies of arrhythmias. However, this chapter will not
elaborate on research in arrhythmology; the discussions will
be strictly clinical in order to provide the reader with robust
knowledge of common arrhythmias. Readers who are
interested in deeper studies are referred to Zipes et
al (Clinical Arrhythmology, Elsevier, 2015).

Main causes of cardiac arrhythmias

Arrhythmias arise if the impulse formation is abnormal, or
if the impulse transmission is abnormal, or if both these
are abnormal. These circumstances are now discussed in
detail.

Abnormal impulse formation

Abnormal impulse formation can cause arrhythmias by the
following two mechanisms:

Increased or abnormal automaticity

Triggered activity

Increased or abnormal automaticity

 y

As discussed in Chapter 1 there are several structures in the

heart that possess automaticity (i.e ability to depolarize
spontaneously). These structures are as follows:

The sinoatrial (SA) node: the sinoatrial node is the

primary pacemaker of the heart. It directs the heart
rhythm during normal circumstances and the rhythm is
referred to as sinus rhythm.
Parts of the atrial myocardium: There are clusters of
atrial myocardial cells located around the crista
terminalis, the entrance of the coronary sinus and the
inferior vena cava, as well as cells around the mitral and
tricuspid valves, which possess automaticity. These cells
are not conduction cells per se; they are actually
contractile cells that possess automaticity. Thus,
automaticity is not exclusive to cells of the conduction
system.

Myocardium surrounding the atrioventricular (AV)

node: It is a common misconception that the
atrioventricular (AV) node possess automaticity, because
there is no compelling evidence for that. There is,
however, evidence that cell clusters surrounding the
AV node possess automaticity. This automaticity will still –
despite what has just been stated – be referred to as
automaticity of the AV node in order to facilitate
understanding.
 The His-Purkinje network: The bundle of His and the
entire Purkinje network possess automaticity.

These are the natural pacemakers of the heart, because

these structures possess automaticity, which is the intrinsic

ability to depolarize spontaneously without previous

stimulation. The intrinsic rate of spontaneous
depolarization in these pacemaker structures follows:

Sinoatrial node: 70 depolarizations per minute.

Atrial myocardium: 60 depolarizations per minute.

Cells around the atrioventricular node: 40

depolarizations per minute.
His-Purkinje network: 20–40 depolarizations per
minute.

The reason that the sinoatrial node is the primary

pacemaker is simply that it has the fastest automaticity.
Heart rhythm is directed by the fastest pacemaker because
that pacemaker will depolarize before the competing
pacemakers and reset their “clocks” before they
discharge an action potential. The list also indicates that
automaticity diminishes gradually with the distance from
the sinoatrial node. This stepwise decline in automaticity is
referred to as the pacemaker hierarchy of the heart.

The sinoatrial node may become dysfunctional and fail to

depolarize. This could potentially result in cardiac arrest but
it rarely does because the absence of sinoatrial impulses
it rarely does, because the absence of sinoatrial impulses
will allow for one of the other pacemakers to take over
the heart rhythm. This behavior is the reason why the other
pacemakers are often referred to as latent
pacemakers. Any rhythm that replaces the sinus rhythm is

referred to as an escape rhythm. In case the sinoatrial node

is dysfunctional, an escape rhythm will most likely come
from atrial myocardium, because it has the second-highest
rate of spontaneous depolarization. If the atrial myocardium
also fails to generate action potentials, it is likely that
an escape rhythm will come from cells around the
atrioventricular node and so on. Note that ventricular
myocardium does not possess automaticity.

The automaticity in the sinoatrial node increases during

physical exercise. The increased automaticity is a normal
reaction since the cardiac output must increase during
exercise. This is an example of normal (physiological)
increase in automaticity. However, in certain circumstances,
the automaticity in the sinoatrial node and the other latent
pacemakers can increase without physiological motivation.
Some examples follow:

Automaticity in the sinoatrial node can increase without

physiological motivation and cause sinus tachycardia at
rest. This is called inappropriate sinus tachycardia.

The automaticity in latent pacemakers can increase, for

example, during hypoxia, whereby they start
discharging action potentials at a higher rate than the
 discharging action potentials at a higher rate than the
sinoatrial node and thus take over the heart rhythm.
Purkinje cells located around the ischemic zone during
acute myocardial ischemia/infarction can increase their
automaticity and initiate ventricular tachycardia.

As mentioned above, ventricular myocardium does not

possess automaticity, and neither does the vast majority of
atrial myocardium. However, during pathological
circumstances, even these cells may start discharging action
potentials.

In other words, any cell may acquire abnormal automaticity

and cause extrasystoles (extra beats) and arrhythmias. A
wide range of conditions may cause abnormal automaticity;
for example myocardial ischemia, hypokalemia, digoxin,
hypoxia, lung disease, disturbances in the autonomic
nervous system etc. These conditions cause abnormal
automaticity by changing the resting membrane potential of
the cell, bringing it closer to the threshold for
depolarization.

Triggered activity (after depolarizations)

An action potential may induce an after depolarization,

which is a depolarization occurring either during or after
the repolarization phase. An after depolarization occurring
during repolarization is referred to as an early
depolarization, whereas after depolarizations occurring
after the repolarization are referred to as late
depolarizations (Figure 1). Early and late depolarizations
 p ( g ) y p
may be strong enough to reach the threshold for eliciting
another depolarization. In other words, after
depolarizations may trigger action potentials. An action
potential which is engendered by an after depolarization is
referred to as a triggered action potential. Such action
potentials cause extrasystoles (extra heartbeats that fall in
between the normal beats).

Early depolarizations are typically seen during bradycardia,

hypokalemia, hypoxia, acidosis, hypocalcemia and in drug
side effects. Late depolarizations are seen in
digoxin overdosing and during sympathetic stimulation.

Importantly, after depolarizations may cause

extrasystoles but they do not cause persistent
arrhythmias. However, the extrasystoles might induce
another arrhythmia mechanism (re-entry, see below) which
may cause persistent arrhythmias.
Figure 1. Late and early depolarizations triggering action
potentials.

Abnormal impulse conduction: re-entry

(reentry)
Normal impulse transmission implies that the depolarizing
wave spreads rapidly, uniformly and unhindered through
the myocardium. This requires that all cells ahead of the
impulse wave are excitable and offer equal capacity to
transmit the impulse. Only under such circumstances can
the depolarization (the impulse) spread through the
myocardium like a wavefront in water. Should the impulse
encounter cells that are not excitable or areas where the
conductivity is heterogeneous, re-entry might occur.

It is fundamental to understand how re-entry occurs, as this

mechanism is responsible for the majority of arrhythmias
requiring treatment. The mechanism is somewhat intricate,
but it can easily be understood with an illustration. Refer to
Figure 2 and study it carefully. As seen in Figure 2, re-entry
means that the depolarizing wavefront moves around itself
in a circle. It is simply an electrical circle loop. This circular
movement of the depolarizing wave is referred to as circus
t
movement.
Figure 2. Re-entry phenomenon.

Re-entry occurs if the depolarizing impulse encounters a

blocked area (“Central blocking” in Figure 2) that can only

be passed on one side. The impulse manages to get around

the central blocking on one side, circulates around it and
travels back. If the previously blocked area (blue area in
Figure 2) has become excitable by the time the impulse
arrives there, it will pass it. The depolarizing wavefront will
then be able to continue this looping for as long as it
encounters excitable tissue. This circus movement is
typically very fast and it emits depolarizing impulses to the
surrounding myocardium. Hence, the re-entry circuit
generates impulses that activate the myocardium at a very
high rate.

The prerequisites for re-entry have been noted in Figure 2.

A brief explanation is repeated:

There must exist a path of electrically connected

myocardium. This path should form a circuit, around
which the impulse can loop. Any cardiac cell that can
carry out an action potential may be part of the circuit.
The circuit may vary from a few millimeters to a
decimeter in diameter.
It is crucial that the cells included in the circuit have
varying ability to conduct the impulse. This variation is
due to differences in refractoriness, conductivity and/or
 excitability, and it will lead to blocking of the arriving
impulse.
The circuit must surround a core of tissue that cannot be
depolarized (central blocking). This core can consist of

necrotic myocardium, scar tissue or even valves (the

valves have a fibrous ring).

Re-entry is subdivided into functional and anatomical.

Knowledge of this distinction is not crucial for clinical
practice.

Anatomical re-entry

The explanations outlined above actually apply to

anatomical re-entry. In this type of re-entry the central
blocking consists of distinct anatomical structures. For
example, atrial flutter (which is a re-entry tachyarrhythmia)
arises when the impulse starts to circle around the tricuspid
valve. In that scenario, the valve is the central blocking
(valvular tissue cannot be depolarized) and the circuit is
composed of the myocardial fibers surrounding the valve.

Anatomical re-entry is fixed, which means that the location

of the re-entry and the speed by which it circulates is
constant. It is also a stable re-entry; episodes of atrial flutter
may persist for hours or even days. AVNRT (atrioventricular
node re-entrant tachycardia), AVRT (atrioventricular re-
entrant tachycardia), most cases of ventricular tachycardia
(particularly those originating in the His-Purkinje network,
ll i f i ) l d i l
as well as post-infarction cases) are also due to anatomical
re-entry.

Functional re-entry

Functional re-rentry is somewhat more difficult to grasp

because the central blocking and the circuit around is more
difficult to define anatomically. The central blocking and the
circuit arise due to electrophysiological heterogeneity
(variation) in the myocardium. Such heterogeneity includes
varying refractoriness, conductivity and/or excitability. An
impulse traveling through an area with such heterogeneity
might encounter a functional block, circulate around it and
during its first lap the wavefront will emit impulses both
outwards and inwards (towards the core of the circuit). The
core becomes bombarded with impulses and thus becomes
refractory.

Functional re-entry circuits are small, unstable and may

engender additional re-entry circuits (this is explained in
the article on atrial fibrillation). Functional re-entry is
fundamental for the development of atrial and ventricular
fibrillation.

Clinical significance

Re-entry is the most common cause of supraventricular and

ventricular arrhythmias that require treatment. Most cases
of atrial flutter are due to re-entry and re-entry has a
fundamental role in the development of atrial fibrillation.
 p
Re-entry can also occur in the sinoatrial node and
atrioventricular node. Notably, ventricular tachycardia
in persons with ischemic heart disease is caused by re-entry.

Termination of re-entry

The re-entry circuit will die out if the wavefront encounters

tissue that cannot be excited (depolarized). The wavefront
must continuously encounter excitable tissue in order to
continue its movement. If it encounters non-excitable tissue
it will be terminated. The purpose of delivering an electrical
shock through the heart (for example during ventricular
tachycardia) is to depolarize all excitable cells in the heart,
including those involved in the re-entry, whereby the re-
entry is terminated (the wavefront will encounter refractory
cells).

Next chapter

Aberrant ventricular conduction (aberration, aberrancy)

Related

Normal Sinus Rhythm

Sinus Arrhtyhmia (Respiratory Sinus Arrhythmia)

Sinus Tachycardia

Sinus bradycardia

Ventricular tachycardia (VT)