Arrhythmias

Content
In this chapter we will discuss:
Mechanisms of arrhythmias
Tachycardias:
Supraventricular
Junctional
Ventricular
Ectopic beats

Introduction
Arrhythmias (non-normal heart rhythms) can be a challenge
to understand, but with a systematic approach, diagnosis is
often less difficult than it may appear at first.
Some definitions are useful when talking about arrhythmias:
Bradycardia < 60 bpm
Tachycardia > 100 bpm
Ectopic beats = extra beats (extrasystole)
Supraventricular = origin in atria or conduction system up to the
division of the His bundle
Ventricular = origin in ventricles
Wide QRS = > 0,12 seconds
Narrow QRS = < 0,12 seconds
AV dissocation = no relation between the contraction of atria and

A good stepwise approach to diagnose

tachycardia is to follow these steps:
1. What is the ventricular heart rate?
Some tachycardias have typical heart rates, e.g. a narrow complex
tachycardia of 150 beats per minute that is very regular is likely an atrial
flutter.
2. What is the QRS width?
If the QRS < 120 ms (i.e. a narrow complex), then it is either a sinus
arrhythmia, a supraventricular rhythm or a junctional tachycardia.
If the QRS > 120 ms, it is either a ventricular tachycardia or a
supraventricular rhythm with additional bundle branch block. This is a
challenging diagnosis. Therefore a flowchart should be used (discussed
later).
3. What is the heart axis and did it change?
If the heart axis turns significantly when compared to the heart axis
during sinus rhythm a ventricular origin of the rhythm is more likely.

A good stepwise approach to interpret the

heart rhythm is to follow these steps
4. 'Cherchez le P', French for find the P waves.
Do you see P waves? Leads II and V1 are often most suitable to find P waves.
What is the rate of the P waves?
What is the P wave morphology?
5. What is the relationship between P waves and QRS complexes?
Is there a 1:1 relation between P waves and QRS complexes? If not there may
be AV Dissociation due to a Ventricular Arrhythmias or AV Block
Is every P wave followed by a QRS complex? And every QRS preceded by a P
wave?
What is the PR interval and does it change?
6. What is the clinical setting?
A wide complex tachycardia in a hemodynamically unstable 70-year-old man
with previous myocardial infarction should be considered a ventricular
tachycardia until proven otherwise
A wide complex tachycardia in a 24-year-old woman with recurrent spells of
tachycardia that respond to vagal manoeuvres is most likely an AVNRT with
aberrant conduction

Mechanisms of Arrhythmias
Abnormal impulse formation
Abnormal impulse formation can result in abnormal frequency, as in symptomatic sinus
bradycardia. But often the problem is an abnormal location of impulse formation, as is the
cause in an ectopic pacemaker.
Abnormal automaticity
The sinus node contains pacemaker cells that have spontaneous firing capacity. This
is called normal automaticity. Abnormal automaticity occurs when other cells start
firing spontaneously, resulting in premature heartbeats. An example of rapid
autonomous firing is accelerated idioventricular rhythm.

Triggered activity
During triggered activity heart cells contract twice, although they only have been
activated once. This is often caused by so called afterdepolarizations (early or
delayed afterdepolarizations EADs / DADs) caused by electrical instability in the
myocardial cell membrane. A typical example of this is Torsade de pointes.

Mechanisms of Arrhythmias
Conduction delay:
Conduction delay can cause a slow heart rate, as happens during AV
conduction blocks. If conduction delay occurs more distally in the heart, i.e.
within the ventricles, the QRS complex will widen and a left or right bundle
branch block can be seen on the ECG. Conduction delay is discussed in
topic 2.

Re-entry:
Re-entry is a common cause of arrhythmias. Ventricular tachycardia and
AV-nodal re-entry are typical examples. Re-entry can occur when a
conduction path is partly slowed down, e.g. by scar tissue.

Supraventricular Tachycardias
Sinus Arrhythmia
Sinus Tachycardia
Atrial Fibrillation
Atrial Flutter
Atrial Tachycardia
AV-junctionele extrasystole
AV Nodal Re-entry
Tachycardia (AVNRT)
AV Re-entry Tachycardia (
AVRT)

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An overview of pathological supraventricular

arrhythmias and their origin

Atrial fibrillation can be coarse, making it difficult to differentiate from atrial flutter. However,
notice that the flutter waves are irregular: this is atrial fibrillation

Atrial Fibrillation

Regularity

Grossly irregular

Atrial frequency

400-600 BPM

Ventricular frequency

75-175 BPM

Origin

Atria (SVT)

P-wave

Absent

Effect of adenosine

Slows down rate, irregularity remains

Algorithm to diagnose SVTs

Supraventricular tachycardias
Small QRS(<0,12)
Sinustachycardia

Regular

HR
(bpm)

P-top

Yes

100-180 Preceds every QRS

complex

Therapy

None or cause
(fever, fear, anemia)

Atrial tachycardia

Yes

75-200

Precedes every QRS

complex but deviated
form

Atrial Fibrillation

No

60-175

absent

Atrial Flutter

Yes

75-150

Sawtooth in lead II

AVNRT

Yes

180-250 In or after QRS complex Sinus carotis

AVRT

Yes

150-250 RP<PR

Sinus carotis
massage,
betablocker,
amiodarone
Chemical/electrical
cardioversion or
rate control
Chemical/electrical
cardioversion or
rate control
massage,
adenosine
Chemical/electrical
cardioversion or

Supraventricular tachycardias
Regular

HR (bpm) P-top

SVT with block

Yes

75-200

absent

AVRT

Yes

150-250

RP<PR

Wide QRS(>0,12)

Therapy

Supraventricular
Sinus Node
Sinus Rhythm: Regularly, each P-wave precedes a QRS complex ( in I,II, AVF).
Normal: 60-100 bpm
Bradycardia: < 60 bpm (can be normal, e.g. during sleep or beta blocker use)
Tachycardia: > 100 bpm (can be normal, e.g. during exercise)

sinustachycardi
a

Sinusbradycardia

Sinus arrhythmia:
Normal P waves, normal PR-interval, irregular PP-interval with
variations > 0,16 seconds on a beat-to-beat basis.

Sinusarrest:
Sudden disappearing of P waves. Either the sinus node is not firing or
the signal is not conducted from the sinus node towards the atrium
(sinusarrest due to sino-atrial (SA) block). Often an ectopic pacemaker
takes over, but the new rate varies slightly from the old one.

Sinusarrest

Junctional Arrhythmias
AVNRT
AV junctional tachycardia
Nodal rhythm
Idioventriclar rhythm
Ventriculophasic reflex

AVNRT
AV Nodal Re-entry Tachycardia (AVNRT) or Atrial-Ventricular Nodal
Re-entry Tachycardia is a supraventricular arrhythmia. It is a nodal
arrhythmia.
Most frequently occuring form of regular tachycardia.
Females > males ( 3:1).
Symptoms: fast-paced heart rate.
Therapy: vagal stimulation (squat, massage of the Carotid sinuses),
medication (adenosine, verapamil), or electrocardioversion.
A regular rhythm with a rate of 180-250 beats / min.
Has a re-entry with a circuit in and around the AV node. A condition for
AVNRT to occur is that 2 electric pathways occur in and around the AV
node (a slow paced and a fast paced pathway). That gives way to the
occurrence of re-entry.

Typical and Atypical AVNRT

Typical AVNRT (also described as common AVNRT or slow-fast
AVNRT):
The impulse travels over the slow pathway towards the ventricles and
returns via the fast pathway to the atria. The retrograde P wave (or
Atrial echo) shows up at the end of the QRS. 90 % of all patients with
ANVRT are diagnosed with typical ANVRT.
Atypical AVNRT (also described as uncommon AVNRT or fastslow AVNRT):
The impulse travels via the fast pathway towards the ventricles and
returns via the slow pathway to the atria. The retrograde P wave
appears far behind the QRS. Only about 6% of all AVNRT patients are
diagnosed with atypical AVNRT.
The remaining cases of AVNRT patients are diagnosed with a form that
is even more rare. This form of AVNRT is slow/slow AVNRT (the

AVNRT on the ECG

Two sensitive characteristics to identify AVNRT on the ECG are:

R. This is a small secondary R wave. It resembles a RBBB, but the

QRS width stays < 120 ms.
RP << 100 ms. (The distance between the R and P waves is less
than 100 ms, so the P waves fuses with the QRS complex)

AV nodal re-entry
tachycardia

AV-Nodal Re-entry Tachycardie

Example

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AV re-entry tachycardia
In patients with an accessory AV connection a re-entry
tachycardia with a large loop can occur: AV re-entry
tachycardia. The loop can can have 2 directions:
Orthodromic tachycardia: from the atria through the AV
node - ventricles - accessory pathway - atria. As the
ventricles are depolarised through the normal conduction
system QRS complexes resemble QRS complexes during
sinus rhythm.
Antidromic tachycardia: atria - accessory pathway ventricles - retrograde through the AV node - atria.

AV re-entry tachycardia can only occur in patients with an

accessory AV connection.
Such a connection is clearly present in patients with WPW ,
in whom pre-exitation results in a delta wave on the
ECG (next slide)
In patients with a concealed bundle tract the accessory
bundle can only conduct from the ventricles to the atria, but
not in the other direction (unidirectional block). In these
patients only orthodromic AV re-entry tachycardia can occur.

Patients with pre-exitation during sinus rhythm are at risk of

developing an AV re-entry tachycardia

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AV-rentry tachycardia on the left, sinus rhythm on the right. Polymorphic VT and
VPB's in the middle (induced by adenosine). Note the absence of pre-exitation
during orthodromic tachycardia with the P wave halfway between QRS complexes.
Also note the clear delta wave during sinus beats on the right.

Nodal rhythm
During nodal rhythm the ventricular rate is 40-50 bpm and oftenwise
the QRS complexes are narrow as they are conducted by the bundle
branches.

Idioventricular rhythm
Rate is 30-45 bpm. The QRS complexes are wide (> 0.12 sec, often >
0.16 sec) because the ventricular signal is transmitted by cell-to-cell
conduction between cardiomyocytes and not by the conduction system.
Accelerated idioventricular rhythm is a rapid form (60-120 bpm) of
idioventricular rhythm associated with reperfusion during myocardial
infarction.

Idioventricular rhythm

Ventricular arrhythmias
Ventricular

Ventricular Tachycardia
Ventricular Flutter
Ventricular Fibrillation
Torsades de pointes
(Idio)ventricular Escape
Rhythm
Accelerated
Idioventricular Rhythm (A.
I.V.R.)

Ventricular Tachycardia

Regularity

(Mostly) Regular

Atrial frequency

60-100 bpm

Ventricular frequency

110-250 bpm

Origin (SVT/ VT)

ventricle

P wave

AV dissociation

Effect of adenosine

No rate reduction (sometimes accelerations)

Ventricular Tachycardia

Accelerated idioventricular rhythm

Regularity

Regular (mostly)

Atrial frequency

60 - 100 bpm

Ventricular frequency

50 - 110 bpm

Origin (SVT/ VT)

Ventricle

P wave

AV dissociation

Effect of adenosine

No rate reduction (sometimes accelerations)

Accelerated idioventricular rhythm

AIVR is a rhythm that results from increased automaticity of

ventricular cardiomyocytes, often in the setting of reperfusion
after a myocardial infarction. It is a relatively benign form of
ventricular tachycardia.

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AIVR

AIVR
2 sinus beats

Ventricular Fibrillation

Regularity

Irregular

Atrial frequency

60 - 100 bpm

Ventricular frequency

400 - 600 bpm

Origin (SVT/ VT)

Ventricle

P wave

AV dissociation

Effect of adenosine

None

Ventricular fibrillation
Ventricular fibrillation is chaotic depolarisation of the ventricles.
Mechanically this results in an arrested cardiac pump function
and immediate death. VF can only be treated by immediate
defibrillation.

Ventricular fibrillation
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VF on a heart rate monitor

Ventricular Flutter

Regularity

Regular

Atrial frequency

60 - 100 bpm

Ventricular frequency

150 - 300 bpm

Origin (SVT/ VT)

Ventricle

P wave

AV dissociation

Effect of adenosine

None

Ventricular flutter
Ventricular flutter is mostly caused by re-entry with a frequency of
300 bpm.
The ECG shows a typical sinusoidal pattern. During ventricular
flutter the ventricles depolarize in a circular pattern, which prevents
good function.

Ventricular flutter

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Torsades de pointes

Regularity

Regular

Atrial frequency
Ventricular frequency

150 - 300 bpm

Origin (SVT/ VT)

Ventricle

P wave

AV dissociation

Effect of adenosine

No rate reduction (sometimes accelerations)

Torsade de Pointes is typically initiated with a short-longshort sequence. The beat following the long RR interval
has an extra long QT interval and therefore greatly
increased the chance of R- on-T phenomenon resulting in
Torsade de Pointes.

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A twelve lead registration of Torsade de pointes. Copyright 2001

Texas Heart Institute

Approach to the wide complex

tachycardia
Differentiating a supraventricular tachycardia with concomitant
bundle branch block from a ventricular tachycardia can be quite
challenging. It is however a clinically important difference as
treatment and prognosis can differ widely between the two
diagnoses.
On the next slide you will see a flowchart that will lead you to
the right diagnosis. Important questions in this flowchart are:
Is the rhythm regular or irregular?
What is the atrial - ventricular relationship?
How does the QRS complex look like in the
precordial
leads?
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Ectopic beats
The pacemaker cells in the sinus node are not the only cells in
the heart that can depolarize spontaneously. Actually all
cardiomyoctyes have this capacity. The only reason why the
sinus node 'rules' is that it is the fastest pacemaker of the
heart. All healthy cardiomyocytes from the sinus node to the
ventricles can function as ectopic pacemakers.
Ectopic pacemaker activity can originate from the atria (60-80
bpm), AV-node (40-60 bpm) and the ventricles (20-40 bpm).
So, if the sinus rate drops (e.g. during atrial infarction), other
cells can take over. The configuration of ectopic complexes, or
extrasystoles, as seen on the ECG reveals its origin, whether
they are atrial, nodal or ventrical.

Atrial premature complexes

Premature atrial complexes origin from an ectopic pacing region
in the atria. They are an example of ectopic beats. The result is
a P-wave with often a different morphology from the preceding
ones.
A premature atrial complex is usually followed by a noncompensatory pause caused by the fact that atrial depolarization
enters the sinus node and resets the sinus rhythm.
Premature atrial complexes are common and usually benign.
In this example the extra P-wave is difficult to discern, but is
fused with the previous T wave.

PAC (premature atrial

complex)

Ventricular Premature Beats

A VPB is an ectopic beat that originates from the ventricles. VPBs are

conducted by the specialized conduction system and are therefore

broad. The QRS width is at least > 0.12 seconds, but often very broad
at around 0.16 - 0.20 seconds. The VPB is usually followed by a
compensatory pause, however this can be absent in the presence of
retrograde conduction through the AV-node.
Causes:
Ischemia, hypoxia, old scar tissue, idiopathic.
50% of healthy men have sporadic VPBs. The origin of the VPB can be
derived from its form. An LBTB-configured VPB originate in the right
ventricle. An RBTB-configured VPB comes from the left ventricle.
A sequence of three or more extrasystoles is called a non-sustained

If more than one VPB is present on the ECG, it can

be:
monomorphic: all VPBs have the same configuration and thus have
a mutual focus of origin.
multiformic: the complexes have different configurations.
bigemini: every sinus beat is followed by a ventricular extrasystole.
trigemini: every second sinus beat is followed by a ventricular
extrasystole.
doublet: a sequence of two VPB's.
triplet: a sequence of three VPB's. Three or more VPB's are often
a non-sustained ventricular tachycardia.

Bigemin
i

VPBs are associated with numerous cardiac diseases (e.g.

structural heart disease, ischemia, congenital arrhythmias,
pulmonary disease). However, VPBs are also relatively
common in patients without known heart disease. The
importance of VPBs for the prognosis is controversial.
Probably sporadic VPBs are relatively benign, whereas
frequent and complex VPBs are reason for further
examination.

Ventricular premature beat

Ventricular extrasystoles on an
ECG heart rate monitor

Non-compensatory pause
Non-compensatory pause, following an atrial premature complex
If a sinus complex is followed by an atrial premature complex, the electrical activity of
the atrial premature complex can enter the sinus node and reset its timing. If the sinus
rate were, for example, 60/min, the reset pacemaker cells will restart firing after 1 full
second had passed. The time from the extra complex to the next QRS complex in this
example is thus 1 second. The sequence "normal sinus complex" - "atrial premature
complex" - "normal sinus complex" will therefore be shorter than the 3 seconds it would
have taken if the premature complex had not occurred. This is called a non (fully)
compensatory pause. Sometimes the electrical activity of the atrial premature complex
cannot enter the sinus node due to refractoriness of the sinus node (if the interval
between previous sinus complex and atrial premature complex is short) or due to
electrical block to enter the sinus node (as in sinus nodal disease).

Compensatory pause
Fully compensatory pause, following a Ventricular premature
complex
The electrical activity of a ventricular premature complex is usually not
conducted through the AV node towards the atria. The sinus node will not be
reset. If the next sinus complex finds the AV nodal tissue still refractory (and
thus not conducting,) there will be a pause until the next sinus complex follows.
The interval between the premature ventricular complex and the next sinus
complex will be longer (longer than 1 second in the above example of a heart
rate of 60/min). This is called a fully compensatory pause. With the use of a
caliper (an instrument for measuring external or internal dimensions), the
preceding sinus rate can be tracked beyond the ventricular premature complex.
This is a telltale sign of a ventricular premature complex without retrograde
conduction.

Ventricular premature beat

Escape rhythms
All cardiac cells have spontaneous firing capacity, but aonly at
a very slow heart rate. Therefore, during a normal heart rate,
they will never have the chance to show off their firing capacity.
However, in pathologic conditions, such as during extreme
bradycardia, other cells can take over and cause for example
an AV-nodal heart rate.

Idioventricular escape rhythm

The last resort of automaticity are the ventricular cells which can
generate an idioventricular rhythm with a slow heart rate and very wide
QRS complexes.