Tachyarrhythmias

TACHYARRHYTHMIAS
SMITA JAIN
BANASTHALI VIDYAPITH

Introduction
A cardiac arrhythmia is an abnormality of initiation, timing, or sequence of
cardiac depolarization. It can result in either tachycardia or bradycardia.
What is Tachyarrhythmia?
Tachyarrhythmia's are cardiac rhythms associated with an elevated heart
rate, greater than 100 beats/min.

What Causes Tachyarrhythmia?
Tachyarrhythmia results from one of the three mechanisms discussed below:
I. Abnormal Automaticity:
 Automaticity is the ability of cardiac cells to initiate spontaneous action
potentials. In normal conditions, the sinus node has the fastest
spontaneous firing and it acts as a predominant pacemaker.
 AV node, His bundle, and Purkinje fibers fire an impulse at a
progressively slower rate and are usually suppressed by the activity of
the sinus node. When any of these cardiac cells start firing
spontaneously, they cause abnormal automaticity and result in premature
heartbeats.
 Abnormal automaticity or spontaneous impulse generation can develop
when pathologic conditions depolarize myocardial cells. For example, an
injury current can develop between a depolarized ischemic cell and
normal cells, leading to repetitive activity in the normal cells. Cellular
depolarization can result from medications, ischemia, metabolic
disturbance, or local trauma.

II. Triggered Activity:
Usually, the heart cells have to contract once for each impulse but during a
triggered activity the heart cells contract twice for each impulse. This is often
caused by after-depolarizations because of electrical instability in the
myocardial cell membrane. After-depolarizations can be either early or
delayed.
a. Early after-depolarizations (EADs):
 They are related to increased calcium ion and sodium ion currents that
maintain the plateau phase of the action potential.
 They are important in the genesis of Torsades de Pointes.
 They are facilitated by increased early repolarization.
b. Delayed after-depolarization (DADs):
 They arise from the repolarized membrane (phase 4).
 They occur in states of increased intracellular calcium ions. Excessive
intracellular calcium ions and generation of inward current by Na+/Ca+2
exchanger causes DAD.

III. Re-entry:
 It is the most common mechanism for the formation of arrhythmia. It
consists of an electrical pathway which causes an impulse to travel back
into the atrium immediately after it has been depolarized, thus,
depolarizing it again. This process will continue as long as the impulse
encounters the cells that are receptive to it.
 It occurs due to abnormal impulse conditions that result from anomalous
anatomic pathway or poor impulse propagation.
 Fibrotic changes in the heart associated with hypertrophy or injury can
lead to areas of slow conduction and provide micro and macro pathways
for re-entry.
The three conditions required for re-entry to occur are:
 Presence of two electrical pathways
 Presence of unidirectional block in one pathway
 Presence of slow conduction, which allows recovery of the excitability
in the previously blocked area

Classification of Tachyarrhythmia's
Tachyarrhythmia are classified based on their anatomic location of origin or
width of the QRS complex.
a. Based on Anatomical location:

b. Based on the width of the QRS complex:
Tachyarrhythmia is broadly classified into either narrow complex tachycardia
(NCT) or wide complex tachycardia (WCT) based on the width of the QRS
complexes.

Steps to Diagnose Tachyarrhythmia
from ECG Pattern
Step 1 - Analyze the heart rate:
 Tachyarrhythmia are associated with a heart rate greater than 100 bpm.
Therefore, you should first check the heart rate by using the 10-second rule
or by 300 rule, which was discussed in lesson 1 of the module.
 In a 10-second rule, you need to count the number of QRS complexes
present in a 10 second period and then multiply the number by 6.
Step 2 - Analyze the rhythm:
Tachyarrhythmia usually have an abnormal rhythm. Therefore, you should
check the RR interval in the given ECG strip to determine whether the patient
has a regular or irregular rhythm.

Step 3 - Check the width of the QRS complex:
The width of the normal QRS complex is 60 to 120 millisecond (ms).
Tachyarrhythmia is characterized by narrow or wide QRS complex.
A narrow QRS complex has a duration of 120 ms (three small boxes). It
indicates that the ventricles are depolarized through the His-Purkinje system.
A narrow complex tachyarrhythmia does not compromise the circulation of
blood and so they are easier to manage than a wide complex
tachyarrhythmia.
On the other hand, a wide QRS complex has an interval of greater than
120ms. It indicates that the ventricles are not depolarized normally. Any
impulse generated in the ventricles will result in wide QRS completely as
the impulse spreads completely or partially outside the conduction system.

Step 4 - Check the morphology of P wave:
While examining the P waves, you should check the following aspects:
 Are P waves present?
 Do P-waves precede each QRS complex?
 Do all the P waves have a uniform shape or have a varying shape?
 Does P wave have normal configuration?
The absence of P waves before a QRS complex indicates that the rhythm is
either atrial fibrillation or the impulse originates in AV node. P waves that
are present but not clearly associated with QRS complex are indicative of
heart block.
Step 5 - Determine PR interval and PR ratio:
The duration of the normal PR interval is 120 to 200 millisecond (or 3 to 5
small squares). You can measure the PR interval by counting the number of
small squares between the onset of the P wave and the beginning of the QRS
complex. Then multiply the number of squares by 0.04 second. Check if the
PR interval is within the normal range and if the PR interval constant
throughout the ECG strip. A long PR interval can be observed in patients
with atrial tachycardia and atypical AV nodal re-entry tachycardia.

The normal P: R ratio is 1:1. If the P: R ratio is 2:1,3:1, or greater, it
indicates that the patient has focal or macro reentrant atrial tachycardia with
AV nodal block.
Step 6 - Check if the onset of palpitations is gradual or abrupt:
A gradual onset suggests sinus tachycardia, whereas an abrupt onset
suggests an arrhythmia. Let us learn in detail about the ECG changes
associated with each type of tachyarrhythmia.
Ectopic Beats
Ectopic beats are the extra heartbeats that arise from the impulses generated
at points in the myocardium other than sinoatrial node (the physiological
pacemaker). Ectopic beats are the most common cause of irregular pulse.
They are also referred to as premature contractions or extra systoles. They
occur early in the cardiac cycle before the next sinus beat and are followed
by a gap in the pulse known as a compensatory pause. The compensatory
pause prevents the propagation of the next sinus beat.

Depending on the actual location, they are classified into two types:
I. Supraventricular ectopic beats
II. Ventricular ectopic beats
Supraventricular Ectopic Beats
(SVEBs)
A supraventricular ectopic beat is an early atrial depolarization, which
originates either in one of the atria or outside the sinoatrial node. It is
characterized by a premature QRS complex in the ECG.
SVEBs occur singly or in groups and indicate atrial irritability. An isolated
SVEB is not significant but a high frequency suggests a higher risk in the
patients. They are followed by an incomplete or non-compensatory pause,
which is caused due to SA node depolarization by ectopic impulse. It usually
lasts less than twice the duration of the normal P-P cycle. An increasing trend
in SVEBs may be an indicator or sign of atrial fibrillation, which may lead to
heart attack or stroke.

ECG Criteria of SVEBs:
Sample ECG Analysis

Ventricular Ectopic Beats (VEB)
Ventricular ectopic beats are early heartbeats that begin in the ventricles.
They are characterized by wide and bizarre QRS complex due to early
initiation of impulse in one of the ventricles, which spreads to the other
ventricle with some delay. This delay occurs due to slow conduction of an
impulse through the ventricles than through the normal conduction pathway.
The QRS complex tends to be followed by a compensatory pause. In VEB,
the QRS complex is not always preceded by a P wave.
The P wave may occur directly before or after the QRS complex but it does
not bear any relationship to it.
Ventricular ectopics may be isolated or may be few in a row, bigeminal or
trigeminal pattern, or in couplets or triplets (rapid succession of three or
more VEBs with a heart rate of more than 100bpm). If more than six
ventricular ectopics are present in a row, it indicates ventricular tachycardia.

Isolated VEBs have little effect on the pumping action of the heart and usually
do not cause symptoms unless they are frequent. The primary symptom
reported by patients with isolated VEBs is a feeling of the heart 'skipping a
beat. This symptom may not be dangerous for people who do not have a heart
disorder, but it may be followed by a life threatening arrhythmia such as
ventricular tachycardia or ventricular fibrillation in people with a structural
heart disorder.
Ventricular ectopics may be positive or negative complexes. To check if the
VEB is positive or negative, you need to view the ECG pattern of the patient
in lead V1. If the QRS complex in lead V1 is positive, it indicates that the
impulse is coming from the left and it is traveling towards the right. If the QRS
complex in lead V1 is negative, it indicates that the impulse is coming from the
right and it is traveling towards left.
If some ventricular ectopics on the rhythm strip are positive and some are
negative, they are collectively referred to as multifocal ectopics. If the
ventricular ectopic falls so early that it interrupts the T-wave of the preceding
complex, then it causes a high risk of ventricular tachycardia or fibrillation.

ECG Criteria of Ventricular Ectopic:

In the given ECG strip, lead II has premature ventricular contractions, which
are caused by an early ectopic impulse within the ventricles. They occur after
a sinus P wave before a normal QRS complex, below the bundle of His,
which extends depolarization resulting in a wider QRS complex that is often
bizarre in shape, or between two consecutive sinus beats.
The ECG strip has wide QRS complex (greater than 5 small squares) as the
impulses are generated from the ventricles, and action potentials travel
slowly from one myocyte to another. You can also find a compensatory pause
between two QRS complexes showing a PVC, and a duration twice the
distance of other R-R intervals.

Supraventricular Tachyarrhythmia's
Arrhythmias are categorized into supraventricular and ventricular depending on
their origin. Supraventricular arrhythmias originate in the atria or conducting
system not in the ventricle, whereas ventricular arrhythmias originate in the
ventricles.
Supraventricular tachyarrhythmias are relatively more common and occur in
patients of all ages, with or without structural heart disease. They can be further
divided into two categories- atrial and atrioventricular (AV) junction
tachyarrhythmia. Atrial tachyarrhythmias require only atrial tissue and AV
junctional tachyarrhythmia need AV junctional tissue.

Atrial Tachyarrhythmias
SINUS TACHYCARDIA:
Sinus tachycardia (ST) is a dysrhythmia that originates in the sinus node and
follows the normal conduction pathways through the heart, producing normal
depolarization and a normal ECG pattern. It is associated with a higher heart
rate usually 100 to 180 beats/minute.
Cause:
The sinus node is innervated by the sympathetic and vagal nerve endings.
Sympathetic stimulation, as well as vagal withdrawal, increase the sinus rate.
Circulating catecholamines also affect the sinus rate.
Some of the common causes of ST are listed below:
Physiologic factors: Fever, hypoxia, hemorrhage, hypotension, anemia, pain,
anxiety and injury to any body part accelerates the heart rate and causes ST
 Medications: Atropine, quinidine sulfate, aminophylline, epinephrine,
dopamine, thyroid hormones, and glucagon can increase the heart rate and
general metabolism of the body.
 Damage to heart tissue: Acute injury as myocardial infarction, trauma,
infection, congestive heart failure or cor pulmonale can increase the heart
rate.

Symptoms:
 Dizziness
 Syncope
 Weakness
 Weak pulse
 Disorientation
 Chest tightness
 Shortness of breath
 Increased heart rate
 Occasional palpitations

Sample ECG Analysis:
 Heart rate: The heart rate can be calculated by using the 10-second rule
method. In lead II, there is 19 QRS complex in a 10 second period. So,
the heart rate is 19 x 6 = 114 beats/min.
 Rhythm: The R-R interval is same across the strip indicating that the
patient has a regular rhythm.
 QRS interval: Normal
 P wave: Normal, upright and consistent
 P: Q ratio: 1:1, Each P wave is followed by a QRS
Interpretation: The given ECG strip indicates that the patient has a normal
rhythm and a heart rate > 100 beats/min. The waveforms are normal with
upright P waves in the lead II recordings. Each P wave is followed by a
QRS complex indicating that the impulse is coming from the sinus node
and not from other regions of the heart. These findings suggest that the
patient has sinus tachycardia.

Atrial Tachycardia
Atrial tachycardia (AT) is formed by a rapid succession of three or more atrial
ectopic. It is characterized by an increased atrial rate (150 to 250 beats/minute)
and has similar features to the single atrial ectopic beat. It is usually faster than
sinus tachycardia. The rapid atrial heart rate shortens the diastole, resulting in
a loss of atrial kick, reduced cardiac output, reduced coronary perfusion, and
ischemic myocardial changes. As the tachycardia's do not involve the AV
node, vagal maneuvers or AV nodal blockers are ineffective in terminating the
tachycardia.
Causes:
One area in the atria becomes very irritable and initiates impulses rapidly one
after another, taking over the
pacemaker function from the SA node. All the impulses are conducted through
the atrioventricular node to the
ventricles through normal conduction pathways.

 MI
 Cardiomyopathy
 Congenital anomalies
 Wolff-Parkinson-White syndrome
 Valvular heart disease
Symptoms:
 Dizziness
 Syncope
 Weakness
 Weak pulse
 Disorientation
 Chest tightness
 Shortness of breath
 Increased heart rate
 Chest palpitations

 Heart rate: 120 beats /min
 Rhythm: Regular
 QRS Complex: Normal
 P wave: Abnormal; It is upright in lead V1 and inverted in leads II, III,
and aVF.
 P: Q ratio: 1:1; Each QRS complex is preceded by a P wave
 Interpretation: A heart rate of 120bpm and abnormal P wave indicates
that the patient has atrial tachycardia
Atrial tachycardia is sub classified based on the mechanism. Let us now
learn about the three forms of atrial tachycardia:
 Atrial tachycardia with block
 Multifocal atrial tachycardia
 Paroxysmal atrial tachycardia

Atrial Tachycardia with Block
It is caused due to increased automaticity of the atrial tissue. A 2:1 block occurs when
the atrial rate speeds up and the atrioventricular (AV) conduction becomes impaired.
The ECG characteristics of atrial tachycardia with a block are:

Multifocal Atrial Tachycardia
Multifocal atrial tachycardia is caused due to increased automaticity by an
intermittent firing of numerous atrial foci. It is characterized by a high atrial rate (100
to 130 bpm) and abnormal P wave morphology. It is most common in patients with
the chronic pulmonary disease. Most atrial tachycardias except multifocal atrial
tachycardia are treated using radiofrequency ablation. Treatment for multifocal atrial
tachycardia depends on the underlying pulmonary illness.
The ECG characteristics of multifocal atrial tachycardia are:

The ECG strip given above indicates that the patient has a rapid irregular rhythm
with a heart rate > 100 bpm. The arrow marks in the ECG points the P waves with
three distinctive morphologies, which is a characteristic feature of multifocal atrial
tachycardia.

Paroxysmal Atrial Tachycardia
(PAT)
The mechanism of paroxysmal atrial tachycardia (PAT) is similar to atrial tachycardia
expect that it starts suddenly and often ends suddenly as a result of the rapid firing of an
ectopic focus. PAT is sometimes faster than atrial tachycardia.
The ECG characteristics of atrial tachycardia with block are:

Atrial Fibrillation
Atrial Fibrillation (AF) is defined as chaotic, asynchronous, electrical activity
in atrial tissue. It results from the firing of multiple impulses from numerous
ectopic pacemakers in the atria. It is the most common sustained
tachyarrhythmia, which is characterized by the absence of P waves and an
irregularly irregular ventricular rhythm. The rate of atrial fibrillation cannot be
measured, as it often exceeds 300 to 600 beats/minute producing a chaotic
baseline.
The ECG contains uneven baseline fibrillatory waves, or f waves rather than
clear distinguishable P waves. The irregular fibrillatory waves are usually easy
to recognize and are referred to as coarse atrial fibrillation.

When some ectopic sites in the atria initiate impulses, depolarization cannot
spread in an organized manner. Small sections of the atria are depolarized
individually, resulting in the atrial muscle quivering, and there is no
organized atrial contraction. Mural thrombi are common consequences of
long-term atrial fibrillation.
In atrial fibrillation, the AV node is bombarded by hundreds of atrial
ectopics at varying rates and amplitudes. The AV node therapeutically and
randomly conducts impulses at a varying rate of speed, so the ventricular
response is irregular. When a patient first experiences atrial fibrillation, the
atrial rates are immeasurable, and the ventricular rhythm is irregular and
very rapid. The ventricles respond only to impulses conducted through the
AV node, hence the characteristic, wide variation in RR intervals can be
seen in patients with AF. A rapid ventricular rate may be life-threatening.
A normal ventricular response is defined as 60 to 100 beats /minute, so when
the ventricular response rate drops below 100, atrial fibrillation is considered
under control. A ventricular response rate of > 100 beats/minute indicates
fast or uncontrolled AF.

Characteristics of 'f Waves':
 f waves are often coarse (> 2 mm) in recent A.
 f waves are usually fine (< 1 mm) in AF of greater duration.
 f waves are of greater amplitude when there is hypertrophy or left atrial
myocardium and become smaller with increasing atrial scarring and fibrosis.
 The amplitude of f waves does not correlate with actual atrial size.

The given ECG strip consists of coarse fibrillatory waves in lead V1. The
heart rate is 132 beats/minute, which is an indication of rapid ventricular
response. The rhythm is irregularly irregular as two subsequent RR
intervals have the same duration. In lead V1- the QT interval cannot be
measured as the T waves are not clearly detectable. The duration of QRS
complex is less than 0.1 sec. Therefore, these findings suggest that the
patient has AF with a rapid ventricular response.
Atrial Flutter
Atrial flutter is characterized by an atrial microreentrant circuit (typically
in the right atrium) leading to regular atrial depolarizations at a rate of 250
to 350 beats/minute. There is typical 2:1 conduction through the
atrioventricular node, resulting in heart rates close to 150 beats/min.

Atrial flutter results from one of the two mechanisms:
 An atrial ectopic focus similar to atrial tachycardia but with a much faster atrial
rate
 A self-perpetuating circular path of atrial depolarization that typically forms a
continuous circuit between the inferior and superior vena cava within the right
atrium.
The atrial muscles respond to this rapid stimulation by producing
waveforms that resemble the teeth of a saw. The sawtooth deflections are
called flutter waves (F waves). The typical atrial flutter wave consists of an
initial negative component followed by a positive component producing a
V-shaped waveform with a sawtooth appearance. The sawtooth waves
affect the whole baseline to the extent that there is no isoelectric line
between the F waves, and the T wave is partially or completely eclipsed by
the flutter waves. Flutter waves in the lead V1 may resemble P waves.
Flutter waves can be best seen in leads II, III, aVF.You can easily identify
the F waves in an ECG strip by turning it upside down!

The QRS complexes are usually normal as long as conduction through the
ventricles is normal. In atrial flutter, the ventricular rate is slower than the atrial
rate. The ventricular the rate depends on the number of impulses conducted
through the AV node to the ventricles.
The ventricular rate is a fraction of the atrial rate, e.g.
 2:1 block = 150 bpm
 3:1 block = 100 bpm
 4:1 block = 75 bpm
During the early stages of atrial flutter, there is typically 2:1 conduction
through the atrioventricular node that results in a ventricular rate close to
150 beats/minutes. In other words, every other atrial impulse is
conducted through to the ventricles. If the AV conduction ration remains
constant (2:1), the ventricular rhythm will be regular, and the rhythm is
described as atrial flutter with 2:1 AV conduction. If the conduction ratio
varies from 4:1 to 2:1 to 6:1, the ventricular rhythm will be irregular and
the rhythm is described as atrial flutter with variable AV conduction.

Atrial flutter with 2:1 block can be misdiagnosed as sinus tachycardia. Here
are some clues that will help you to distinguish 2:1 atrial flutter with sinus
tachycardia:
In sinus tachycardia, the P and T waves are usually distinctly different from
each other. Another clue to differentiate sinus tachycardia at 150 beats/min
from atrial flutter with 2:1 AV block is finding the P' midway between the
QRS complexes. Distortion of the QRS by suspected P' is called Ta
distortion. Further, the patient with atrial flutter may complain of a sudden
onset of rapid heart rate, feeling of weakness and dread. However, these
symptoms are less likely to occur in patients with sinus tachycardia.

Classification of Atrial Flutter:

The given ECG strip contains inverted flutter waves in leads II, III, and
aVF with an atrial rate nearly 300 bpm. The flutter waves present in lead
V1 resemble the upright P waves. The rhythm is regular. There is a 2:1 AV
block resulting in a ventricular rate of 150 bpm. Occasional irregularity
with a 3:1 cycle is seen in V1-3. It is an example of anticlockwise flutter.
Difference between atrial flutter and atrial fibrillation:

Supraventricular Tachycardia
Supraventricular tachycardias (SVT) involve at least some part of the atrium or
atrioventricular junction. SVT is a very common group of arrhythmias, which
develop as a result of abnormal automaticity, triggered activity or reentry
mechanism. It is characterized by a rapid heart rate (120-200bpm) and a rhythmic
succession of QRS complex. The QRS complex duration is typically narrow
(<120ms), reflecting conduction over the AV node and His-Purkinje system, but
sometimes can have a wide QRS complex due to pre-existent or rate-dependent
bundle branch blocks or other aberrant interventricular conduction disturbances.
Both atrial flutter and atrial fibrillation are supraventricular tachycardias but
because of the differences in their mechanisms and clinical manifestations, they
are grouped separately from other types of supraventricular tachycardias,
commonly referred to as paroxysmal supraventricular tachycardia (PSVT).

Classification:
Based on the ECG criteria supraventricular tachycardia can be classified
into the two types:
 Short RP/long PR interval tachycardia
 Long RP/Short PR interval tachycardia
Short RP/Long PR Interval
Tachycardia
A short RP tachycardia demonstrates a short RP pattern with P waves embedded
within or occurring closely after the preceding QRS complex. The RP interval
reflects the retrograde conduction time for an impulse to travel from ventricular
to atrial tissue. A short RP tachycardia occurs with reentrant supraventricular
tachycardia when the retrograde VA conduction time is shorter than the
anterograde AV conduction time. In general, atrioventricular nodal reentrant
tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT) are
short RP tachycardia.

Atrioventricular Nodal Reentrant
Tachycardia (AVNRT)
AVNRT is the most common paroxysmal supraventricular tachycardia in
adults. It is more common in women than in men. In patients with AVNRT, the
atrioventricular junction has two or more functionally discrete pathways – the
fast and slow pathway. The "fast pathway "conducts impulses rapidly but has a
relatively long effective refractory period. The "slow pathway" has a slower
conduction velocity but a shorter effective refractory period than the fast
pathway.
AVNRT is a reentrant tachycardia that involves the AV node. The retrograde
conduction typically occurs along the fast pathways. As a result, the atria are
reactivated during or shortly after ventricular activation. During typical
AVNRT, the P wave falls on the ST segment or within the terminal part of the
QRS complex. (In most cases, the interval between ventricular and atrial
activation—the V-A intervals thus < 70 ms)

Based on the contribution of the fast and slow pathways in the antegrade and
retrograde limbs of the tachycardia circuit, AVNRT is classified into typical and
atypical forms.
Typical AVNRT:
In typical AVNRT, a premature atrial depolarization (PAD) conducts to the
atrioventricular junction through the atrium. The PAD arrives at the AV node
when the fast pathway is in a refractory state. Therefore, the impulse conducts
antegradely via the slow pathway with a shorter refractory period. When the
impulse reaches the end of the slow pathway, the fast pathway is ready for
retrograde conduction. Therefore, typical AVNRT is also called "Slowfast“
AVNRT.
In typical AVNRT, the RP interval is very short, and the P wave is usually
hidden within the QRS complex or appears at the end of QRS complex because
of the simultaneous atrial and ventricular activation. It may be present as'
pseudo r' in leads V1 or aVR and as 'pseudo s' in inferior leads or notching at
the end of aVL.

Atypical AVNRT:
In atypical AVNRT, a premature atrial depolarization conducts to the
atrioventricular junction through the atrium. It occurs when the antegrade
conduction to the ventricle occurs via the fast pathway, while the retrograde
conduction to the atrium is through the slow pathway. Therefore, atypical AVNRT
is commonly called as "fast-slow" AVNRT. In atypical AVNRT, the RP interval is
longer, and P waves are manifested as negative deflections within the ST segment
or shortly before the next QRS complex in the inferior leads.
ECG Characteristics:
Typical and atypical AVNRTs usually have a narrow QRS complex, however
concomitant bundle branch block (BBB) can rarely create a wide QRS complex.
Several differences in ECG characteristics will help you to distinguish between
typical and atypical AVNRTs.

P Wave: While analyzing the ECG of a patient with suspected AVNRT, you
should first check the P-wave morphology, width, location, and mechanism
of initiation. The P wave axis is similar for both typical and atypical AVNRT.
The P wave is inverted in inferior leads II, III, and aVF in both the types of
AVNRT as the activation of the atria occurs in an inferior-to-superior
direction. In lead V1 the P wave is upright as the AV node which is located
posteriorly causes posterior-to-anterior activation of the atria.
The width of the P wave is different in two forms of AVNRT. In typical
AVNRT, the P wave tends to be narrow, whereas in atypical AVNRT it is
wider because of the difference in anatomical location of the fast and slow
conducting pathways that activate the atria.
In typical AVNRT, P wave is rarely visible on the ECG due to simultaneous
conduction of the ventricles through the slow pathway anterogradely and
atria through the fast pathway retrogradely. Due to this, the P waves are
inscribed in the QRS complex or occur near the QRS creating a short RP
interval (RP interval is less than half the RR interval). This can sometimes
manifest as a "pseudo-S wave" in the inferior leads II, III, and aVF, and
"pseudo-R wave" in lead V1.

In atypical AVNRT, P waves are clearly visible. Due to retrograde conduction
through a slow pathway, the presence of the P wave occurs later than QRS
complex, resulting in an RP interval that is frequently longer than half the RR
interval.
The mode of initiation of the reentrant circuit is another ECG feature that
helps you to distinguish typical from atypical AVNRT. An initiating atrial
premature beat is commonly associated with typical AVNRT. On the other
hand, a ventricular premature beat is more likely to precipitate an atypical
AVNRT.

Atrioventricular Reentrant
Tachycardia (AVRT)
AVRT is the second most common form of paroxysmal supraventricular
tachycardia. AVRT is more common in males than in females. It is narrow
complex tachycardia with a short PR interval. An accessory pathway
connects the atria to the ventricles. The tachycardia is caused due to the
reentry of impulses from the ventricles back to the atria, creating a self-
sustained circuit. The accessory pathway forms one arm of the reentry circuit
and the usual AV nodal pathway forms the other arm of the circuit. The
reentry circuit of AVNRT is larger than ANRT as the accessory pathway is
located away from the AV node.
Delta waves are the pathological waves that can be seen as a slurred upstroke
at the beginning of the QRS complex. They are formed when the accessory
pathway conducts the atrial impulse to the ventricle.

Wolff-Parkinson-White (WPW)syndrome is a classic example of AVRT. WPW
syndrome is characterized by the presence of delta wave, short PR interval
(<120ms) and wide QRS complex. Delta waves are the slurred upstroke in the
QRS complex. They are often associated with a short PR interval. It is most
commonly associated with a preexcitation syndrome such as WPW.

The two types of AVRT are:
 Orthodromic AVRT
 Antidromic AVRT
Orthodromic AVRT:
It occurs when an impulse is conducted through the AV node and then through
the accessory pathway in a retrograde direction. In this condition, AVRT is
associated with narrow QRS complexes that have a normal morphology.
Sometimes a rate-related aberration may be present, during which the QRS
complexes will have a typical right or left bundle branch block (BBB)
morphology or an intraventricular conduction delay.
The ECG characteristics of orthodromic AVRT are:
 Presence of distinct P wave after the QRS complex, which allows us to
differentiate between AVRT and AVNRT (during AVNRT the P wave is
hidden within, partly merging with or close to the QRS complex).
 Presence of retrograde P wave, which is closer to the preceding QRS
complex than to the following QRS complex due to rapid conduction to
the atria.
 RP interval < PR interval

Antidromic AVRT:
It occurs when the impulse is conducted antegrade down the bypass tract.
A direction myocardial activation occurs in antidromic AVRT as
ventricular activation is done through the accessory pathway and the
normal His-Purkinje system. Therefore, wide and abnormal QRS
complexes that do not have either a typical right or left BBB morphology
are associated with antidromic AVRT. In this condition, the QRS
complexes resemble the pre-excited complexes during the sinus rhythm.
The ECG characteristics of antidromic AVRT are:
QRS complexes are usually broader than during sinus rhythm and may
resemble ventricular tachycardia due to slow conduction of impulse from
one fiber to another QRS complexes are followed by retrograde P-waves.

Long RP/Short PR Interval
Tachycardia
Long RP tachycardia is characterized by an RP interval, which is longer than the
next PR interval during tachycardia. This pattern occurs when the retrograde VA
conduction time in reentrant arrhythmias is long due to a slowly conducting
retrograde pathway during tachycardia. It consists of negative P waves in the
inferior leads. It consists of the permanent form of junctional reciprocating
tachycardia (PJRT).

Junctional Tachycardia
Junctional tachycardia is an ectopic beat which, begins in the pacemaker
cells found in the atrioventricular bundle (bundle of His). Junctional
tachycardias can be regular or irregular with variable conduction to the atria.
Types of Junctional tachycardia:
Permanent form of Junctional Reciprocating Tachycardia (PJRT):
A PJRT may start without any particular trigger, from sinus rhythm. It may
terminate and reinitiate, such that throughout the day the patient has
predominant PJRT rhythm, with brief, interspersed intervals of sinus beats. It
occurs mostly in infants and children. It is often incessant with occasional
interruptions by sinus beats. It does not require premature beats or PR
prolongation for its initiation and may be initiated by a modest increase in
sinus rate.

The typical ECG characteristics of PJRT are:
 It has a long RP interval with negative wave in leads II, III, and aVF.
 The rhythm is typically very regular.
 The QRS complex is narrow.
 The heart rate is 90 to 250 bpm
Nonparoxysmal junctional tachycardia:
Nonparoxysmal (i.e., gradual onset) junctional tachycardia is a benign
dysrhythmia that is usually associated with a gradual increase in rate to more
than 100 beats/min. It rarely exceeds 120 beats/min. It is a marker for
potentially serious heart disease or digitalis intoxication. It may be due to
enhanced automaticity or triggered activity. It may show AV dissociation or
retrograde ventricular conduction.

Paroxysmal junctional tachycardia:
Paroxysmaljunctional tachycardia, also known as focal or automatic
junctional tachycardia, is an uncommon dysrhythmia. As it has a sudden
onset and ends abruptly it is called as paroxysmal junctional tachycardia. It is
often precipitated by a PJC. The ventricular rate for paroxysmal junctional
tachycardia is generally faster, at a rate of 140 beats/min or more. When the
ventricular rate is > 150 beats/min, it is difficult to distinguish junctional
tachycardia from other supraventricular tachycardias. AV dissociation is
common but there may be retrograde ventriculoatrial conduction with
varying degree of retrograde block. The tachycardia does not require the
atrium or the ventricle for its prorogation. When incessant it can cause a
tachycardia dependent cardiomyopathy with heart failure.

The ECG characteristics of junctional tachycardia include the following:
 Rhythm: Ventricular rhythm may be regular or irregular
 Heart rate: 101 to 180 beats/min
 P waves: Occurs before, during, or after QRS complex
P wave is inverted in leads II, III, and aVF
 PR interval: 0.12 sec or less; if P wave does not occur before the QRS
complex then you cannot measure PR interval
 QRS duration: 0.11 sec or less

Differential Diagnosis of the
Narrow-QRSComplex Tachycardias
An essential component in the differential diagnosis of tachycardias is to
distinguish between tachycardias with normal QRS complex and abnormal QRS
complex. The first step to distinguishing narrow-complex tachycardias from one
another is to assess the R-R interval to check the rhythm. If the rhythm is irregular,
then it may be atrial fibrillation or atrial flutter. If the rhythm is regular, then you
should check the P waves.
The next step is to check the morphology and position of P waves about the QRS
complex. It helps to determine the relationship between the atrial and ventricular
activity. A P wave morphologically identical to that seen in sinus rhythm probably
means that the tachycardia is originating somewhere near the SA node, regardless
of the mechanism. When the QRS complexes are preceded by P waves, which have
a different configuration from sinus P wave, and have a longer or equal PR interval
than sinus P wave, it indicates that the atrial tachycardia is arising from an ectopic
focus. Check if the atrial rate and ventricular rate. If the atrial rate is greater than
the ventricular rate, it indicates atrial flutter or atrial tachycardia. If not, then check
RP interval.

The third step is to analyze the RP interval, if the RP interval is longer than PR
interval, it indicates atrial tachycardia, PJRT, or Atypical AVNRT. If the RP is
shortened than PR interval, then check if the RP interval is shortened than 0.07
sec which indicates AVNRT. If the RP interval is longer than 0.07sec, then it
indicates AVRT, AVNRT, and atrial tachycardia.
The flow chart given below depicts the procedure of differential diagnosis
of the narrow-QRS-complex tachycardias:

Ventricular Arrhythmia
Ventricular arrhythmias originate in the ventricles below the bifurcation of the
bundle of His. These arrhythmias occur when electrical impulses depolarize the
myocardium using a different pathway from normal impulse conduction.
The ECG characteristics of ventricular arrhythmia are:
The QRS complex is wider than normal due to prolonged conduction time
through the ventricles and abnormal depolarization of the ventricles.
 The deflection of the T wave and QRS complex are in opposite
directions due to abnormal ventricular repolarization and depolarization
 The P wave is absent in most of the ventricular arrhythmias because
atrial depolarization doesn't occur. If a P wave is present, it originates in
the sinus node, causing it to be dissociated from the ventricular rhythm.
 The atrial rate is usually slower than the ventricular rate, as it originates
at the sinus node

Fusion and capture beats may be present, which helps in distinguishing
ventricular tachycardia from other broadcomplex tachycardia.
Fusion beats: They occur when a normal supraventricular stimulus causes
ventricular activation which fuses with the complex originating in the ventricle
and produces a hybrid complex. The resulting hybrid QRS complex looks
partly like a normal QRS complex and partly like a ventricular ectopic beat.
Capture beats: They occur when an atrial stimulus arrives at a non-refractory
AV node and is conducted normally in the ventricles. This results in a normal
P wave followed by a normal QRS complex in the middle of a series of wide
QRS complexes.

When the electrical impulses come from the ventricles instead of the atria, the atrial
kick is lost, and the cardiac output decreases as much as 30%. As a result, the patient
with ventricular arrhythmia may show signs and symptoms of reduced cardiac
output, including:
 Hypotension
 Agina
 Syncope
 Respiratory distress

Although ventricular arrhythmias may be benign, they may also be life-
treating as the ventricles are mainly responsible for cardiac output. Early
recognition and treatment of ventricular arrhythmias will increase the
chances of survival.
Ventricular arrhythmias are classified into the following types based on the
tachycardia morphology:
 Monomorphic ventricular tachycardia
 Polymorphic ventricular tachycardia
 Ventricular fibrillation
 Accelerated idio-ventricular tachycardia
 Ventricular Flutter

Monomorphic Ventricular
Tachycardia
It is the most common form of ventricular tachycardia. The ventricular
complexes have a uniform appearance (monomorphic), and each episode of
ventricular tachycardia continues for a variable time, usually terminating in a
long pause before sinus rhythm returns. Each paroxysm of tachycardia starts
with a ventricular ectopic beat, which occurs at the same fixed interval from the
previous QRS complex.

Polymorphic Ventricular
Tachycardia (PVT)
It consists of polymorphic QRS complexes which undulate around the isoelectric
line, with a marked change of amplitude occurring every 5 to 30 beats, changing
from one direction to another and back again.

Torsades-de-pointes
Torsades-de-pointes (turning of points) is a dangerous form of polymorphic
ventricular tachycardia characterized by paroxysms of ventricular tachycardia
when the QT interval is prolonged during sinus rhythm, and prominent U
waves may be seen. Prolongation of the QT interval implies prolongation of
repolarization. While this may affect the whole myocardium, polymorphic
ventricular tachycardia is more likely to occur when different regions of the
myocardium repolarise at different rates. Transient prolongation of the QT
interval may occur in the acute phase of myocardial infarction but, more
commonly, this is due to the administration of drugs that prolong the QT
interval such as class 1 antidysrhythmic agents or electrolyte imbalance.

Episodes of torsades-de-pointes usually terminate spontaneously but may
precede ventricular fibrillation. Antidysrhythmic drugs should be stopped, and
it may be necessary to increase the heart rate to over 100 beats/minute by
pacing to prevent recurrence until the precipitating drugs are metabolized or
electrolyte imbalance
has been corrected.
PVT unassociated with QT prolongation are uncommon but have the ECG
characteristics of torsades-de-pointes. If the QT interval in the sinus is
normal, management is that of monomorphic ventricular tachycardia.

Ventricular Fibrillation
Ventricular fibrillation is a disorganized, chaotic, electrical focus in the
ventricles that take over control of the heart. The ventricles do not beat in a
coordinated fashion but, instead, quiver asynchronously and ineffectively, just
as the atria respond in atrial fibrillation. The ECG tracings show an
undulating, wavy baseline composed of irregular waveforms that vary in
amplitude and morphology. The ventricular waves represent chaotic,
incomplete, and haphazard depolarization of small groups of muscle fibers in
the ventricles. P waves and QRS complexes are absent due to lack of
organized depolarization of atria and ventricles.
Coarse ventricular fibrillations indicate a more recent onset and are more
likely to be reversed by defibrillation alone. Whereas, fine ventricular
fibrillation indicates that the arrhythmia has been present longer and may
require therapy first, then defibrillation. If defibrillations do not restore the
cardiac rhythm, then the fine ventricular fibrillation progresses to ventricular
asystole.

Accelerated Idio-ventricular
Tachycardia
When escape rhythms arise in the ventricles or His-Purkinje system, they are
called idio-ventricular rhythms. They often occur in association with successful
thrombolysis. It is benign and requires no treatment. The rate is usually slow, at
about 60 beats/minute. Sometimes referred to as 'slow VT'. After about 30 beats,
sinus rhythm often takes over. Occasionally, the rhythm accelerates but the rate
does not exceed 120 beats/minute. Rarely, sustained ventricular tachycardia or
ventricular fibrillation may be replaced by idio-ventricular tachycardia.

Ventricular Flutter
It is characterized by a rapid ventricular rate of 180-250 beats/minute, in which
it is not possible to differentiate the QRS complexes from the ST segment or T
waves. It appears on the ECG as rows of hairpins or as a sine wave which, is
characterized by regular, large oscillations. It often precedes ventricular
fibrillation.

References
 Hatfield, A. (2014). The complete recovery room book. OUP Oxford.
 Heidbuchel, H. (2002). Management of cardiac arrhythmias, edited by
Leonard I. Ganz. ACTA CARDIOLOGICA, 57(4), 315-315.
 Lewis, K. M. (2000). Sensible Analysis of the 12-lead ECG. Cengage
Learning.
 Lilly, L. S. (2012). Pathophysiology of heart disease: a collaborative
project of medical students and faculty. Lippincott Williams & Wilkins
 Model, D. (2006). Making Sense of Clinical Examination of the Adult
Patient: Hands-on Guide. CRC Press.

Tachyarrhythmias

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