Arrhythmia: Mechanism, Classification, ECG features

ARRHYTHMIA| farheen ansari
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ARRHYTHMIA
Heart arrhythmia (also known as arrhythmia, dysrhythmia, or irregular heartbeat) is a group of conditions in which
the heartbeat is irregular, too fast, or too slow. [Arrhythmia refers to any change from the normal sequence of
electrical impulses, causing abnormal heart rhythms.]
Many types of arrhythmia have no symptoms. While most types of arrhythmia are not serious, some predispose a
person to complications such as stroke or heart failure. Others may result in cardiac arrest.
There are four main types of arrhythmia:
 Extra beats [premature atrial contractions, premature ventricular contractions, and premature junctional
contractions],
 Supraventricular tachycardia [atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia],
 Ventricular arrhythmias [ventricular fibrillation and ventricular tachycardia] and
 Bradyarrhythmias.
NORMAL CARDIAC CELLULAR ELECTROPHYSIOLOGY:
Understanding the mechanisms of arrhythmias is helpful to the appropriate management and treatment of all
arrhythmia types. Since the mechanisms that lead to clinical arrhythmias are frequently due to abnormalities beyond
the tissue level, it is also essential to understand what occurs at the cellular level.
Cardiac myocytes are highly specialized cells responsible for both conduction of electrical impulses and mechanical
contraction. Some myocytes demonstrate automaticity, defined by the capability of cardiac cells to undergo
spontaneous diastolic depolarization and to initiate an electrical impulse in the absence of external electrical
stimulation.
Spontaneously originated action potentials (APs) are propagated through cardiac myocytes, which are excitable,
referring to their ability to respond to a stimulus with a regenerative AP. Successful propagation of the cardiac
impulse is enabled by gap junctions; specialized membrane structures composed of multiple intercellular ion
channels that facilitate electrical and chemical communication between cells. Cardiac APs are regionally distinct
(Figure 1) due to each cell type expressing different numbers and types of ion channels.
Under normal conditions, the sinoatrial node is the primary pacemaker of the heart, with a resting membrane
potential of approximately −60mV. Prior research has demonstrated that the If current plays a major role in the
initiation of diastolic depolarization. [This current is also referred to as a “funny” current because, unlike most
voltage-sensitive currents, it is activated by hyperpolarization rather than depolarization.]
At the end of the action potential, the If is activated and depolarizes the sarcolemmal membrane. If is a mixed Na-
K inward current modulated by the autonomic nervous system through cAMP. (Cyclic adenosine monophosphate
is a second messenger important in many biological processes. cAMP is a derivative of adenosine triphosphate and
used for intracellular signal transduction in many different organisms, conveying the cAMP-dependent pathway.)
In addition to If, multiple time- and voltage-dependent ionic currents have been identified in cardiac pacemaker
cells, which contribute to diastolic depolarization. These currents include (but are not limited to) ICa-L, ICa-T, IST, and
various types of delayed rectifier K currents. Many of these membrane currents are known to respond to β-
adrenergic stimulation. All these membrane ionic currents contribute to the regulation of SA node automaticity
by altering membrane potential.
Figure 1. The cardiac action potential. A: sinus node
action potential. B: muscle cell action potential.

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The aggregate activity of various currents results in a net inward flow of sodium (Na+
) and thus an increase in the
membrane potential. When it reaches −40mV, calcium (Ca2+
) currents (T-type ICa,T- and L-type ICa,L) are activated, and
serve as the predominant ion carriers during the AP upstroke of pacemaker cells (Ca2+
-dependent). Subsequently,
outward potassium (K+
) currents are activated and Ca2+
currents are inactivated. The membrane potential decreases
due to the outward flow of K+
, the major repolarizing ion of the heart. Upon reaching the resting membrane
potential, the cycle is ready to repeat itself.
 The resting membrane potential of muscle cells is −90mV. Inflow of positive charge (Ca2+
and Na+
) through the
gap junction increases the voltage towards threshold (approximately −65mV) initiating an AP. At this point,
Na+
channels are triggered to open, resulting in a large but transient inward Na+
current (phase 0).
 The Na+ current is quickly inactivated, followed by a subsequent
outward K+
current and thereby initiating repolarization (phase 1).
 The ICa,L plays an important role during the AP plateau (phase 2),
opposing the K+
current.
 The ICa,L is the main route for Ca2+
influx and triggers Ca2+
release
from the sarcoplasmic reticulum, initiating contraction of the
myocyte. Activation of delayed rectifier K+
channels and inactivation
of Ca2+
channels leads to termination of the plateau and initiates late
repolarization (phase 3).
 Finally, outward K+
channels mediate the final repolarization (phase
4).
Following contraction, the cardiac myocytes must enter a relaxation or
refractory phase during which they cannot be depolarized. The refractory
period is defined by the time interval following excitation during which the cell
remains unexcitable. This is due to the lack of availability of depolarizing
current (which is Na+
in muscle cells). It is classified as either absolute or relative (Figure 3), depending on whether it
is completely unexcitable or needs a greater stimulus than normal.
The depolarization activates ICa,L, which provides Ca to activate the cardiac ryanodine receptor (RyR2). The
activation of RyR2 initiates sarcoplasmic reticulum (SR) Ca release (Ca-induced Ca release), leading to contraction
of the heart, a process known as EC (excitation-contraction) coupling. Intracellular Ca (Cai) is then pumped back
into SR by the SR Ca-ATPase (SERCA2a) and completes this Ca cycle.
Na channel
blocked
Figure 3. Refractory periods, showing the
absolute and relative refractory periods
during the action potential.

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MECHANISMS OF CARDIAC ARRHYTHMIAS:
Cardiac arrhythmias are associated with abnormal initiation of a wave of cardiac excitation, abnormal propagation of
a wave of cardiac excitation, or some combination of the two. Cardiac arrhythmias can manifest themselves in many
different ways, and it is still not always possible to determine the mechanism of an arrhythmia.
SA NODE ACTION POTENTIAL:
Diastolic depolarization:
In mammals, cardiac electrical activity originates from specialized myocytes of the sinoatrial node (SAN) which
generate spontaneous and rhythmic action potentials (AP). The unique functional aspect of this type of myocyte
is the absence of a stable resting potential during diastole. Electrical discharge from this cardiomyocyte may be
characterized by a slow smooth transition from the Maximum Diastolic Potential (MDP, -70 mV) to the threshold
(-40 mV) for the initiation of a new AP event. The voltage region encompassed by this transition is commonly
known as pacemaker phase, or slow diastolic depolarization or phase 4.
The duration of this slow diastolic depolarization (pacemaker phase) thus governs the cardiac chronotropism. It is
also important to point out that the modulation of the cardiac rate by the autonomic nervous system also acts on
this phase. Sympathetic stimuli induce the acceleration of rate by increasing the slope of the pacemaker phase,
while parasympathetic activation exerts the opposite action.
The heart muscle itself is triggered to beat (systole) due to the accumulation of positive charges at the peak of
the pacemaker AP. The rest period between successive beats is called diastole; during this time the pacemaker
membrane potential is undergoing diastolic depolarization.
The section of the diagram shows the influx of sodium ions through the HCN channel.
The change in pacemaker membrane potential during this time is a slow, gradual upward slope
due to the influx of sodium ions through hyperpolarization-activated cyclic nucleotide-gated
channels (HCN).These channels were originally called 'funny' channels because they activate
during repolarization while other channels activate during depolarization. The influxing sodium
current competes with the effluxing potassium current and is responsible for the 'turnaround'
in the AP at the end of repolarization.
Hyperpolarization-activated Cyclic Nucleotide-gated Channels (HCN)
The 'hyperpolarization-activated' part of the channels' name indicates that they, unlike other channels, activate
during repolarization. These channels are additionally unique in that they do not have inactivation gates. They
are mixed channels that preferentially allow the influx of sodium ions but also allow some efflux of potassium
ions. They are often called 'pacemaker channels' because the autonomic nervous system can modify their gating
behavior thus changing the heart rate.
Figure 1: reaction of action potential from the various
cardiac regions to the body surface electrocardiogram
(ECG).

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DISORDERS OF IMPULSE
FORMATION
DISORDERS OF IMPULSE
CONDUCTION
Automaticity Reentry
Altered normal automaticity Anatomic reentry
Abnormal automaticity Functional reentry
Triggered activity
Delayed afterdepolarization
Early afterdepolarization

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1. DISORDER OF IMPULSEFORMATION:
Automaticity is the property of cardiac cells to generate spontaneous action potentials. Spontaneous activity is the
result of diastolic depolarization caused by a net inward current during phase 4 of the action potential, which
progressively brings the membrane potential to threshold. The sinoatrial (SA) node normally displays the highest
intrinsic rate. All other pacemakers are referred to as subsidiary or latent pacemakers because they take over the
function of initiating excitation of the heart only when the SA node is unable to generate impulses or when these
impulses fail to propagate.
1) Altered Normal Automaticity:
Some specialized heart cells, such as sinoatrial nodal cells, the atrioventricular (AV) node, and the His-Purkinje
system, as well as some cells in both atria, possess the property of pacemaker activity or automaticity. Suppression
or enhancement of this activity may lead to clinical arrhythmias.
Under normal conditions, the sinoatrial nodal cells have the fastest rate of firing and the so-called subsidiary
pacemaker cells fire at slower rates, so the normal hierarchy is maintained.
The firing rate is determined by the interaction of 3 factors:
- the maximum diastolic potential,
- the threshold potential at which the AP is initiated, and
- the rate or slope of phase 4 depolarization.
A change in any of these may alter the rate of impulse initiation.
Pacemaker activity is controlled by the autonomic nervous system and can be modulated by a variety of systemic
factors, including metabolic abnormalities and endogenous or pharmacologic substances.
Parasympathetic activity reduces the discharge rate of the pacemaker cells (Figure 4) by releasing acetylcholine (Ach)
and hyperpolarizing the cells by increasing conductance of the K+
channels. It may also decrease ICa-L and If activity,
which further slows the rate.
Figure 4. Parasympathetic effects on the action potential
(reduction of the heart rate).

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The hallmark of normal automaticity is overdrive suppression. Overdriving a latent pacemaker cell faster than its
intrinsic rate decreases the slope of phase 4, mediated mostly by enhanced activity of the Na/K exchange pump.
When overdrive stimulation has ended, there is a gradual return to the intrinsic firing rate called the ‘warm-up’
period (Figure 5). The degree of suppression and the recovery time are proportional to the rate and duration of the
applied stimulation.
This mechanism plays an important role in maintaining sinus rhythm, continuously inhibiting the activity of
subsidiary pacemaker cells. In patients with external pacemakers, the intrinsic rhythm is also suppressed by this
mechanism.
The absence of overdrive suppression may indicate that the arrhythmia is the result of a mechanism other than
enhanced normal automaticity. However, the reverse is not always true because enhanced normal automatic activity
may not respond to overdrive pacing or faster intrinsic rates due to entrance block.
Clinical examples: sinus tachycardia associated with exercise, fever, and thyrotoxicosis; atrial and ventricular
accelerated rhythms; inappropriate sinus tachycardia and AV junctional rhythms.
2) Abnormal automaticity:
Atrial and ventricular nonpacemaker myocardial cells, which in the normal heart typically do not exhibit spontaneous
activity, may exhibit automaticity properties. This can happen under conditions that drive the maximum diastolic
potential towards the threshold potential, which is explained by the interplay of numerous currents that together
result in a net inward depolarizing current associated with a decrease in potassium conductance.
The intrinsic rate of an automatic abnormal focus depends on the membrane potential; the more positive the
membrane potential, the faster the automatic rate. Abnormal automaticity is thought to play a role in cases of
elevated extracellular potassium, low intracellular pH, and catecholamine excess.
An important distinction between enhanced normal and abnormal induced automaticity is that the latter is less
sensitive to overdrive suppression, although there are situations where it may be observed. Under these
circumstances, an ectopic automatic focus displays characteristics of other arrhythmia mechanisms.
Abnormal automaticityoccurs when other cells start firing spontaneously, resulting in premature heartbeats. All
cardiac cells have spontaneous firing capacity, but only at a very slow heart rate. Therefore, during a normal heart
The suppressive effect of Ach is frequently used in practice for both diagnostic and therapeutic purposes.
Tachycardias resulting from enhanced normal automaticity are expected to respond to vagal maneuvers
(promoting Ach release) with a transient decrease in frequency, and a progressive return towards baseline after
transiently accelerating to a faster rate upon cessation of the maneuver (a phenomenon known as post-vagal
tachycardia).
Conversely, sympathetic activity increases the sinus rate. Catecholamines increase the permeability of Ica-L,
increasing the inward Ca2+
current. Sympathetic activity also results in enhancement of the If current, thereby
increasing the slope of phase 4 repolarization.
Metabolic abnormalities such as hypoxia and hypokalemia can lead to enhanced normal automatic activity as a
result of Na/K pump inhibition, thereby reducing the background repolarizing current and enhancing phase 4
diastolic repolarization.
In degenerative conditions that affect the cardiac conduction system, suppression of the sinus pacemaker cells
can be seen, resulting in sinus bradycardia or even sinus arrest. A subsidiary pacemaker may manifest as a result
of suppression of sinus automaticity.
Figure 5. Overdrive suppression in a Purkinje fiber and post-
suppression warm-up period.

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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.
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.
Clinical examples: premature beats, atrial tachycardia, accelerated idioventricular rhythm, ventricular tachycardia
(VT), particularly in the acute phase, associated with ischemia and reperfusion.
 Increased normal automaticity:
They are early impulses that appear before the basal rhythm and are originated in a supraventricular or
ventricular extrasystolic or parasystolic focus. May be isolated (extrasystoles and parasystoles) or repetitive
(automatic atrial and ventricular tachycardias, or triggers of reentrant supraventricular tachycardias and atrial or
ventricular flutter and fibrillation).
Extrasystoles are related to the preceding impulse and thus have a fixed coupling interval. The focus in which
the extrasystole originates remains depolarized after each impulse of the basal rhythm because this area is not
protected by an entry block, as happens with parasystoles. As a result, a new stimulus may arise depolarizing the
neighboring myocardium before the next stimulus of the basal rhythm arrives. This explains the fixed coupling
interval. By contrast, parasystoles have a variable coupling interval, because the focus automaticity is
independent of the preceding impulse.
A. EXTRASYSTOLIC IMPULSES:
(see PVC).
The ectopic, atrial, AV junction, or ventricular foci present a sharper increase in phase 4 (TDP), which
explains why the threshold potential is reached earlier originating an early impulse before the next basal
stimulus can depolarize the ectopic foci. The fact that the coupling interval of successive extrasystoles is
fixed is explained because the increase in the speed of phase 4 in all cases is related to the preceding
impulse.
Figure 6 explains the active arrhythmias (extrasystole) and passive (escapes) that are produced due to the
different changes in the slope of the curve of phase 4 of the sinus node or the ectopic foci.
B. PARASYSTOLIC IMPULSES:
Parasystole is a kind of arrhythmia caused by the presence and function of a secondary pacemaker in the
heart, which works in parallel with the SA node (figure 7). Parasystolic pacemakers are protected from
depolarization by the SA node by some kind of entrance block. This block can be complete or incomplete.
Parasystolic pacemakers can exist in both, the atrium or the ventricle. Atrial parasystolia are characterized by
narrow QRS complexes. Two forms of ventricular parasystole have been described in the literature, fixed
parasystole and modulated parasystole.

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Figure 6. Left: see the lines joining the TAPs of the sinus node, the AV junction, and the ventricular Purkinje system. This figure shows
the generation of active and passive arrhythmias due to disturbances of automaticity: (a) normal diastolic depolarization curve of the
sinus node; (b) diminished diastolic depolarization curve; (c) diastolic depolarization curve of sinus node with normal rate of rise but
starting at a lower level; (d) normal diastolic depolarization curve with a less negative TP; (e) normal diastolic depolarization curve of
the AV junction; note that before this curve is complete (i.e. before it reaches the TP), the sinus stimulus (arrow) initiates a new AP
(end of the continuous line in ‘3’); (f) normal diastolic depolarization curve of a ventricular Purkinje fiber (the same as in ‘e’ applies);
(g) marked decrease of the automaticity of the AV junction; (h) increase of automaticity of the AV junction; (i) increased automaticity
in ventricular Purkinje fibers. Therefore, under pathologic conditions, the increased automaticity of the AV junction (h) and the
ventricular Purkinje system (i) may be greater than that of the sinus node (active rhythms). Alternatively, the normal automaticity of
the AV junction (broken lines in ‘e’ and ‘g’) or the ventricle (broken line in ‘f’) may substitute the sinus depressed automaticity (b and
b′) (passive rhythms). Right: ECG examples of the different electrophysiologic situations commented on (normal sinus rhythm: 1-2;
sinus bradycardia:1-2b; junctional extrasystole: 1-2 h; junctional escape complex 1-2e; ventricular extrasystole: 1-2i and ventricular
escape complex: 1-2f).
Fixed ventricular parasystole occurs when an ectopic pacemaker is protected by entrance block, and thus its
activity is completely independent from the sinus pacemaker activity. Hence, the ectopic pacemaker is
expected to fire at a fixed rate. Therefore, on ECG, the coupling intervals of the manifest ectopic beats will
wander through the basic cycle of the sinus rhythm. Accordingly, the traditional electrocardiographic criteria
used to recognize the fixed form of parasystole are:
 the presence of variable coupling intervals of the manifest ectopic beats;
 inter-ectopic intervals that are simple multiples of a common denominator;
 fusion beats.
Modulated parasystole is a variant of the above. It results from incomplete entrance block of the ectopic
pacemaker. In this situation, the dominant pacemaker or other cardiac tissues can exert electrotonic (being
the spread of electrical activity through living tissue or cells in the absence of repeated action potentials.)
influences on the parasystolic focus. Electrotonic influences arriving early in the pacemaker cycle delay the
firing of the parasystolic focus, whereas those arriving late in the cycle accelerate its firing. A special case of
modulated parasystole occurs when the action potentials of the parasystolic focus exert electrotonic
influence on the focus itself. This is termed ‘automodulation’. As has been shown in the atria, a parasystolic
Fig. 7. Protected pacemaker. Entrance block of the dominant
pacemaker allows exit conduction of the subsidiary pacemaker,
which can generate action potentials that excite the rest of the
myocardium.

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impulse exerts electrotonic influences on the parasystolic focus itself during the supernormal phase, where
the focus accelerates rather than delaying its discharge. Repetition of this mechanism would then result in a
tachycardia.
Parasystolic impulses are not related to the preceding complexes and thus have a variable coupling interval.
Furthermore, they present an entry block that prevents it from being depolarized by the basal rhythm that is
usually sinus rhythm.
When the parasystolic impulses find the surrounding tissue outside the refractory period, an ectopic
complex with a variable coupling interval is recorded and fusion complexes often appear. Due to the
independence of the basal rhythm the parasystolic impulses are multiple among themselves.
3) Triggered activity:
Triggered activity (TA) is defined by impulse initiation caused by afterdepolarizations (membrane potential
oscillations that occur during or immediately following a preceding AP). Afterdepolarizations occur only in the
presence of a previous AP (the trigger), and when they reach the threshold potential, a new AP is generated. This
may be the source of a new triggered response, leading to self-sustaining TA.
Based on their temporal relationship, 2 types of afterdepolarizations are described: early afterdepolarizations (EADs)
– occur during phase 2 or 3 of the AP, and delayed afterdepolarizations (DADs) – occur after completion of the
repolarization phase (Figure 8).
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 afterdepolarizationsEADs / DADs) caused by electrical instability in
the myocardial cell membrane.
 Early afterdepolarization-induced triggered activity:
The EADs are oscillatory potentials that occur during the AP plateau (phase 2 EADs) or during the late
repolarization (phase 3 EADs) [before full repolarization]. Both types may appear during similar experimental
conditions, but they differ morphologically as well as in the underlying ionic mechanism. Phase 2 EADs appear to
be related to Ica-L current, while phase 3 EADs may be the result of electronic current across repolarization or the
result of low IK1.
A fundamental condition underlying the development of EADs is AP prolongation, which manifests on the
surface electrocardiogram (ECG) as QT prolongation. Some antiarrhythmic agents, principally class IA and III
drugs, may become pro-arrhythmic because of their therapeutic effect of prolonging the AP. Many other drugs
[Class IB antiarrhythmic drugs (flecainide, encainide, indecainide), Phenothiazines, Tricyclic and tetracyclic
antidepressants, Erythromycin, Antihistamines, Cesium, Amiloride, Barium] can predispose to the formation of
EADs, particularly when associated with hypokalemia and/or bradycardia or additional factors that result in
prolongation of the AP. Catecholamines may enhance EADs by augmenting Ca2+
current, however the resultant
increase in heart rate along with the increase in K+
current effectively reduces the APD and thus abolishes EADs.
Figure 8. Representation of triggered activity. A: phase 2
early afterdepolarization. B: phase 3 early
afterdepolarization. C: delayed afterdepolarization.
EADs are usually but not exclusively associated with prolonged action potential durations (APDs), which occur
when the inward current is greater in amplitude than the outward current. Several factors can tip the balance
towards the inward direction. These include increases in the late sodium current (INa), the calcium current
(ICa), or INCX (sodium-calcium exchanger), or decreases in the repolarizing potassium currents (IKr, IKs, IK1).
Two mechanisms have been proposed for the EADs that are associated with prolongations in APDs and occur
during phase 2 of the action potential.

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Clinical examples: torsades de pointes (twisting of the tips), the characteristic polymorphic VT seen in patients
with long QT syndrome.
 Delayed afterdepolarization-induced triggered activity:
A DAD is an oscillation in membrane voltage that occurs after completion of repolarization of the AP (during
phase 4). These oscillations are caused by a variety of conditions that raise the diastolic intracellular Ca2+
concentration [which can result from exposure to digitalis, catecholamines, hypokalemia, and hypercalcemia, and
in hypertrophy and heart failure], which cause Ca2+
mediated oscillations that can trigger a new AP if they reach
the stimulation threshold.
It is worth noting that DADs and late EADs are somewhat similar. Both occur under conditions of intracellular
calcium overload and involve spontaneous release of calcium from the sarcoplasmic reticulum. The difference
appears to be the timing of this release, which occurs during the repolarizing phase of the action potential in the
case of late EADs, and at the resting membrane potential for DADs. Indeed, for atrial fibrillation, both EADs and
DADs have been implicated as the mechanisms of arrhythmogenesis
Triggered arrhythmias induced by DADs may be terminated by single stimuli; therefore, other electrophysologic
features are needed to distinguish them from the reentrant tachycardias.
 Firstly, depolarizing shifts in the membrane potential can reactivate the L-type calcium channels,
resulting in increased ICa,L that further depolarizes the membrane. This sets up a positive feedback
loop, triggering an action potential.
 Secondly, at membrane potentials negative to the threshold of ICa,L activation (but before full
repolarization), spontaneous calcium release from the sarcoplasmic reticulum can activate INCX,
resulting in membrane depolarization.
An EAD-mediated TA appears to be the underlying cause of arrhythmias that develop in the setting of long QT
syndrome. While the true mechanism of these arrhythmias is still debated, it is accepted that enhanced
repolarization dispersion seen in the syndrome can create a pro-arrhythmic substrate. In such an
electrophysiologic milieu an EAD can initiate the tachycardia.
The intermittent nature of EADs has recently been examined, demonstrating that it is due to slow changes in
[Na+
]i and potentially explaining why arrhythmias do not occur all the time.
EADs have also been associated with shortening in APDs, occurring late in phase 3 of the action potential.
Here, an abbreviated APD permits normal calcium release from the sarcoplasmic reticulum. If the
intracellular calcium concentration ([Ca2+
]i) remains elevated when the membrane potential is negative to the
equilibrium potential for NCX, INCX can be activated, causing membrane depolarization. These late EADs are
clinically relevant, as they can occur immediately after termination of other types of tachycardia, such as
atrial flutter, AT, VT, and VF. In such instances, repolarization time is shortened and a transient increase in
sarcoplasmic calcium release can be induced when reverting to sinus rhythm.
Whatever be the underlying mechanism, if the change in membrane potential brought about by the EAD is
sufficiently large, it will activate INa, resulting in triggered activity. EADs and their resulting triggered activity
are thought to underlie the arrhythmogenesis observed in heart failure and long QT syndromes.
The proposed mechanism for the genesis of DADs is as follows: high levels of intracellular calcium induce
spontaneous calcium release from the sarcoplasmic reticulum, activating three calcium-sensitive currents—
the nonselective cationic current, INS, the sodium–calcium exchange current, INCX, and the calcium-activated
chloride current, ICl,Ca. Together, these constitute the transient inward current (ITI) that is responsible for
membrane depolarization. If the depolarization produced by the DAD is sufficiently large, INa is activated,
leading to triggered activity. DAD-induced triggered activity is thought to underlie the arrhythmogenesis
observed in catecholaminergic polymorphic ventricular tachycardia (CPVT).
A critical factor for the development of DADs is the duration of the AP. Longer APs are associated with more
Ca2+
overload and facilitate DADs. Therefore, drugs that prolong AP (e.g., Class IA antiarrhythmic agents) can
occasionally increase DAD amplitude.

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Adenosine has been used as a test for the diagnosis of DADs. Adenosine reduces the Ca2+
inward current indirectly
by inhibiting effects on adenylate cyclase and cyclic adenosine monophosphate. Thus, it may abolish DADs
induced by catecholamines, but does not alter DADs induced by Na+
/K+
pump inhibition. The interruption of VT by
adenosine points toward catecholamine-induced DADs as the underlying mechanism.
Clinical examples: atrial tachycardia, digitalis toxicity-induced tachycardia, accelerated ventricular rhythms in the
setting of acute myocardial infarction, some forms of repetitive monomorphic VT, reperfusion-induced
arrhythmias, right ventricular outflow tract VT, exercise-induced VT (e.g. catecholaminergic polymorphic VT).
2. DISORDERS OF IMPULSE CONDUCTION:
1) Block:
Conduction delay and block occurs when the propagating impulse fails to conduct. Various factors involving both
active and passive membrane properties determine the conduction velocity of an impulse and whether conduction is
successful, such as the stimulating efficacy of the impulse and the excitability of the tissue into which the impulse is
conducted. Gap junction coupling plays a crucial role for the velocity and safety of impulse propagation.

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Most commonly, impulses are blocked at high rates as a result of incomplete recovery of refractoriness. When an
impulse arrives at tissue that is still refractory, it will not be conducted or the impulse will be conducted with
aberration.
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.
Many factors can alter the conduction, including rate, autonomic tone, drugs (e.g., calcium channel blockers,
beta blockers, digitalis, adenosine/adenosine triphosphate), or degenerative processes (by altering the
physiology of the tissue and the capacity to conduct impulses).
2) Reentry:
Reentrant arrhythmias can be confined to a single chamber of the heart, or can involve several chambers. In some
instances, it is convenient to think of the underlying circuit for the reentrant excitation as a one-dimensional ring, as
was initially proposed by Mines (1913). In other cases, the reentrant circuit might be taking place in two dimensions
and the wave shape would be a rotating spiral wave. This notion was first made explicit by Wiener and Rosenblueth
(1948). However, since the heart is three-dimensional, in other situations it is necessary to think of the reentrant
circuit as a three-dimensional scroll wave as proposed by Winfree, who was the first to discover spiral waves
experimentally in the context of excitable systems (Winfree, 1972).
Re-entry occurs when an action potential fails to extinguish itself and reactivates a region that has recovered from
refractoriness. It can be divided into two types:
(i) reentry that occurs in the presence of an obstacle, around which an action potential can travel (circus-type);
(ii) reentry that occurs without an obstacle (reflection or phase 2).
Reentry can occur when a conduction path is partly slowed down. As a result of this, the signal is conducted by both a
fast and a slow pathway. During normal sinus rhythm this generally does not cause problems, but when an
extrasystole follows rapidly upon the previous beat, the fast pathway is sometimes still refractory and cannot
conduct the signal.
Prerequisites for reentry include:
 A substrate: the presence of joined myocardial tissue with different electrophysiological properties,
conduction, and refractoriness.
 An area of block (anatomical, functional, or both): an area of inexcitable tissue around which the wavefront
can circulate.
 A unidirectional conduction block.
 A path of slowed conduction that allows sufficient delay in the conduction of the circulating wavefront to
enable the recovery of the refractory tissue proximal to the site of unidirectional block.
 A critical tissue mass to sustain the circulating reentrant wavefronts.
 An initiating trigger.
 Reentry involving an obstacle (circus-type)
This occurs when an action potential travels around an anatomical or functional obstacle and re-excites its site of
origin.
TYPES OF CIRCUS-TYPE REENTRY:
A. Anatomic reentry – where the circuit is determined by anatomical structures,
B. Functional reentry – which in turn includes different mechanisms. . It is characterized by a lack of anatomic
boundaries.
 Leading circle
 Anisotropic reentry
Fig. 9. Circus-type reentry requires a structural or functional obstacle (gray center)
around which an action potential can circulate.

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 Figure of 8 reentry
 Spiral wave (rotor) reentry
Both forms can coexist in the same setting and share biophysical mechanisms. Reentry is the most common
arrhythmia mechanism seen in clinical arrhythmias, both in classical or variant forms.
 ANATOMICAL REENTRY/CLASSIC REENTRY:
Although the conceptualization of a wave traveling on a one-dimensional ring seems overly simplistic, from
perspectives of both mathematics and medicine there are several interesting consequences (Rudy, 1995).
Experimental systems, simulations, and theoretical analyses have demonstrated that waves circulating on
one-dimensional rings may experience an instability such that the circulation is not constant. Instead, there
can be a complex fluctuating propagation velocity that arises as a consequence of the interaction of the
wavefront with its own refractory tail (Frame and Simpson, 1988; Quan and Rudy, 1991; Courtemanche et al.,
1993; Vinet and Roberge, 1994).
The classic reentry mechanism is based on an inexcitable anatomical obstacle surrounded by a circular
pathway in which the wavefront can reenter, creating fixed and stable reentrant circuits. The anatomic
obstacle determines the presence of 2 pathways (Figure 10). When the wavefront encounters the obstacle, it
will travel down one pathway (unidirectional block), propagating until the point of block, thus initiating a
reentrant circuit.
The ring model was the first example of circus-type reentry involving an anatomical obstacle. It emerged
from experiments using disks made from sub-umbrella tissue of a jellyfish. Mayer made the following
observations. The disks were paralyzed when they were separated from their sense organs. They did not
pulsate in seawater, but did so when ring-like cuts were made on the tissue. Upon mechanical
stimulation, the disks then showed “rhythmical pulsations so regular and sustained as to recall the
movement of clockwork”.
The ring model was the first example of circus-type reentry involving an anatomical obstacle. It emerged
from experiments using disks made from sub-umbrella tissue of a jellyfish. Mayer made the following
observations.
The disks were paralyzed when they were separated from their sense organs. They did not pulsate in
seawater, but did so when ring-like cuts were made on the tissue. Upon mechanical stimulation, the
disks then showed “rhythmical pulsations so regular and sustained as to recall the movement of
clockwork”.
Later, Mines used a ring-like preparation of the tortoise heart, demonstrating that it was possible to
initiate circus-type reentry by electrical stimulation. If an excitation wave has a high propagation rate
and a long duration, the whole circuit would be excited at the same time, causing the excitation to die
out. In contrast, one with slower conduction and a shorter duration would permit the tissue ahead of the
excitation wave to recover from refractoriness, which can therefore be reexcited, resulting in circus-type
reentry.
Mines predicted, “A circulating excitation of this type may be responsible for some cases of paroxysmal
tachycardia as observed clinically.” He also proposed three criteria for this type of reentry:
(a) an area of unidirectional block must exist;
(b) the excitation wave propagates along a distinct pathway, returns to its point of origin, and starts
again; and
(c) interruption of the circuit at any point would terminate this circus movement.
Figure 10: Anatomic reentry: the central
obstacle creates 2 paths; when the impulse
arrives, unidirectional block occurs and
slow conduction through the other path
allows reentry.
Figure 11. Schematic
representation of an
excitable gap.

14
Initiation and maintenance of reentry will depend on the conduction velocity and refractory period of each
pathway, which determines the wavelength (wavelength=conduction velocity × refractory period). For
reentry to occur, the wavelength must be shorter than the length of the pathway. Conditions that decrease
conduction velocity or shorten the refractory period will allow the creation of smaller circuits, facilitating the
initiation and maintenance of reentry.
The excitable gap is a key concept essential to understanding the mechanism of reentry (Figure 11). The
excitable gap refers to the excitable myocardium that exists between the head of the reentrant wavefront
and the tail of the preceding wavefront. This gap allows the reentrant wavefront to continue propagation
around the circuit. The presence of an excitable gap also makes it possible to enter in the reentrant circuit
using external pacing and explains the phenomena of resetting, entrainment, and termination of the
tachycardia with electrical stimulation.
Clinical examples: AV reentrant tachycardia associated with a bypass tract, AV nodal reentrant tachycardia,
atrial flutter, bundle branch reentry VT, post-infarction VT.
Using the accompanying applet, it is possible to decrease the size of the ring (which decreases the period
of rotation) and thus observe the initiation of the primary wavelength mode, which is discordant
alternans with one node.
In addition, if a single stimulus is delivered to the medium during the course of the reentrant
propagation (by clicking in the applet window), the propagating wave will either be reset or annihilated
(Quan and Rudy, 1991; Glass and Josephson, 1995; Sinha et al., 2002; Comtois and Vinet, 2002). Further,
periodic stimulation can lead to the entrainment or annihilation of the propagating wave (Glass et al.,
2002; Sinha et al., 2002; Comtois and Vinet, 2002).
Finally, a sequence of premature stimuli delivered to the heart during normal sinus rhythm can often
lead to the initiation of tachycardia. In some clinical settings, analysis of the resetting, entrainment, and
initiation of tachycardias offers clinicians important clues about the arrhythmia mechanism, and
consequently can help the cardiologist choose an appropriate therapy (Stevenson and Delacretaz, 2000;
Josephson, 2002).
The ability to induce monomorphic ventricular tachycardia using a sequence of up to three premature
stimuli is often taken as an indication of anatomical reentry as a mechanism for the tachycardia. Since at
least part of the reentrant circuit is assumed to be one-dimensional, this can provide a target for ablation
therapy.
Several types of reentrant arrhythmias can be explained clearly using one-dimensional rings and cables.
One example is AV nodal reentrant tachycardia (AVNRT).
When this arrhythmia is present, the AV node has two distinct pathways, one fast, with a rapid velocity
but relatively long refractory period, and the other slow, with a slower velocity but shorter refractory
period. Normally, an impulse from the atria comes from a common pathway and is conducted by both
pathways. However, while the impulse from the fast pathway reaches the His-Purkinje system, the
impulse in the slow pathway takes longer to propagate and finds the common pathway in the His-
Purkinje system refractory from the fast pathway impulse.
Certain circumstances (such as an atrial premature beat) may produce an impulse that arrives at the AV
node while the fast pathway is still refractory, so that only the slow pathway conducts the impulse.
However, upon reaching the common pathway at the His-Purkinje system, the fast pathway may no
longer be refractory, and the impulse may propagate retrogradely back to the atria.
In turn, this impulse may propagate to the slow pathway, setting up a reentrant ring in the AV node.
A similar phenomenon occurs in preexcitation syndrome (Wolff-Parkinson-White Syndrome). In this
arrhythmia, an abnormal accessory pathway provides a secondary means for impulses to propagate from
the atria to the ventricles. An impulse that travels along this accessory pathway avoids the AV nodal
delay and therefore reaches the ventricles before the impulse that travels through the AV node and His-
Purkinje system, leading to ECG abnormalities during normal sinus rhythm including a shortened PR
interval, a widened QRS complex and a broader QRS upstroke (called the delta wave) that arises because

15
 FUNCTIONAL REENTRY:
The possibility of circus-type reentry occurring without an anatomical obstacle was later suggested. In
functional reentry, the circuit is not determined by anatomic obstacles; it is defined by dynamic
heterogeneities in the electrophysiologic properties of the involving tissue. The location and size of
functional reentrant circuits can vary, but they are usually small and unstable. As previously stated,
functionally determined reentrant circuits can occur due to different mechanisms:
1. Leading circle reentry.
In 1976, Allesie et al. described a reentrant mechanism in the absence of an anatomical boundary. They
postulated that the impulse circulates around a central core that is maintained in a refractory state
because it is constantly bombarded by impulses and travels through partially refractory tissue. Leading
circle was defined as “the smallest possible pathway in which the impulse can continue to circulate.
The leading circle, as the smallest pathway that can support reentry, is shown as a bold black arrow.
Inside the leading circle, centripetal wavelets (small arrows) emanating from it constantly maintain the
central core in a refractory state.
This type of reentry is less susceptible to resetting, entrainment, and termination by pacing maneuvers
because there is not a fully excitable gap.
2. Anisotropic reentry.
In this, both anatomic and functional properties participate in determining the path taken by the
circulating wavefront.
the impulse begins to propagate slowly through the ventricles before the specialized conduction system
is invoked and initiates rapid conduction. The presence of this pathway can lead to a reentrant loop.
Another anatomically based reentrant tachycardia is atrial flutter. This rhythm is characterized by
circulating waves, most usually confined to the right atrium.
During atrial flutter, the excitation typically passes through a narrow isthmus between the tricuspid valve
and the coronary sinus. Atrial flutter is usually associated with a regular conduction pattern through the
AV node, most usually 2:1 or 4:1 conduction, although in some instances there are fluctuations in the
conduction ratio.

16
Anisotropic conduction relates to directionally dependent conduction velocity in cardiac muscle and
depends on the structure and organization of myocytes within cardiac tissue. These include the
orientation of fibers and non-uniform distribution of gap junctions, with a larger number of channels
poised to propagate the impulse longitudinally rather than transversely. The heterogeneity in
conduction velocities and repolarization properties of the anisotropic tissue can result in blocked
impulses and slowed conduction that allows reentry even in small anatomical circuits.
Clinical examples: anisotropic reentry in atrial and ventricular muscle, which may be responsible in the
setting of VT originating in surviving myocardial infarction.
3. Figure of eight reentry.
This type of reentry consists of 2 concomitant wavefronts circulating in opposite directions (clockwise
and counterclockwise) around 2 functional or fixed arcs of block (representing the ischemic zone) that
merge into a central common pathway.
Clinical example: this type of reentry may be seen in the setting of infarction-related VT.
4. Spiral wave (rotor) reentry.
A variation of functional reentry termed spiral wave reentry was later described. A spiral wave is a two-
dimensional wave of excitation emitted by a self-organizing source of functional reentrant activity,
termed a rotor. The three-dimensional equivalent of a spiral wave is a scroll wave. One may encounter
other terms for this phenomenon in the literature, such as “vortices” or “reverberators.”
Spiral wave activation is organized around a core, which remains unstimulated because of the
pronounced curvature of the spiral. This curvature also limits the spiral propagation velocity, resulting in
slow conduction and block.
Single or double spiral waves or scroll waves are often generated in excitable cardiac tissue or models of
cardiac tissue by a single impulse delivered in the wake of a propagating wave during the vulnerable
period, as show in figure 13, 14. These reentries do not rotate around obstacles; instead, they are called
functional as they rotate around a "functional" obstacle called the core of the spiral or scroll wave.
A single spiral or scroll wave with a fixed repetitious motion (which may be anchored to some
anatomical feature such as a blood vessel or scar) likely would lead to a monomorphic tachycardia.
A meandering spiral or scroll wave likely would be associated with a polymorphic tachycardia or perhaps
fibrillation.
Polymorphic tachycardias and fibrillation also may be associated with "fibrillatory" conduction, in which
a rotating spiral or scroll wave fractionates as it propagates throughout the cardiac tissue, or with
Figure 12. Schematic representation of Figure of eight reentry
Figure 13. Initiation, development, and rotation of
single spiral wave re-entry in square block of
cardiac muscle tissue

17
multiple spiral or scroll waves. In the latter case, the spiral and scroll waves may not be located around
stationary cores, but may migrate. Spirals and scrolls may disappear by collision with boundaries or by
collision with rotating waves of opposite chirality, and they may be regenerated as a consequence of
fibrillatory conduction.
In contrast to the leading circle model, there is a fully excitable gap. The tip of the wave moves along a
complex trajectory and can radiate waves into the surrounding medium (known as “break-up” of a
mother wave). Spirals may have completely different dynamics and can circulate with different patterns,
change one to another, become stationary or continuously drift or migrate. These characteristics result
in both monomorphic and polymorphic patterns.
Spiral waves are not fixed in space but can drift through the tissue. This drift phenomenon is
accompanied by a Doppler effect, in which the frequency of excitation at a given measurement site
depends on the location of this site relative to the drifting spiral wave. Thus, the sites in front of the
wave are excited faster than those behind the wave. This may be the underlying mechanism of torsade
Figure 14. Initiation, development, and rotation of
double spiral wave re-entry in square block of
cardiac muscle tissue.
The mathematics underlying the generation, stabilization, migration, and destruction of spiral and
scroll waves is a rich topic and has been subject to extensive investigation.
If an initiated spiral wave is itself unstable, it may quickly break up into multiple waves. Clinical
evidence exists for this, especially in the case of ventricular fibrillation, which is usually preceded by a
short-lived ventricular tachycardia. The transition from tachycardia to fibrillation can occur either by a
single relatively stable wave with breakup far from the core, or by waves that continually form and
annihilate.
Many different mechanisms have been proposed to explain the transition from a single spiral wave to
multiple waves (Bar and Eiswirth, 1993; Biktashev et al., 1994; Fenton and Karma, 1998; Fenton et al.,
2002; Bernus et al., 2003).
Since real hearts are three-dimensional, and there is still no good technology to image excitation
throughout the heart depth (as opposed to the surface), the actual geometry of excitation waves in
cardiac tissue associated with some arrhythmias is not as well understood and is now the subject of
intense study.
From an operational point of view, it seems likely that any arrhythmia that cannot be cured by a small
localized lesion in the heart will best be described by rotating spiral or scroll waves. Such rhythms
include atrial and ventricular fibrillation. In these rhythms, there is evidence for strong fractionation
(breakup) of excitation waves giving rise to multiple small spiral waves and patterns of shifting blocks
(Fenton et al., 2002).
Ventricular tachycardias also can occur in patients other than those who have experienced a previous
heart attack, and perhaps even in hearts with completely normal anatomy. In these individuals, it is
likely that spiral and scroll waves are the underlying geometries of the excitation.
A particularly dangerous arrhythmia, polymorphic ventricular tachycardia (in which there is a
continually changing morphology of the electrocardiogram complexes), is probably associated with
meandering spiral and scroll waves (Gray et al., 1995).

18
de pointes, in which the periodic torsion of the QRS axis has been attributed to two widely separated
foci discharging at different frequencies.
Two counter-rotating spiral waves separated by a small distance can produce reentry in a figure-of-eight
configuration, which was first demonstrated in the canine heart using a healed myocardial infarction
mode.
Clinical examples: atrial and ventricular fibrillation, polymorphic VT
 Reentry not involving an obstacle:
Reentry can also occur without circus movement. This can be divided into reflection and phase 2 reentry.
 REFLECTION.
Reflection is a unique subclass of reentry that occurs in a linear segment of tissue, where the impulse travels
in both directions over the same pathway in the presence of severely impaired conduction.
 PHASE-2 REENTRY:
Phase 2 reentry is another mechanism that does not depend on circus-type movement. Its concept emerged
from experiments that introduced pinacidil, an activator of the ATP-regulated potassium current, IK,ATP, to
canine ventricular tissues. The canine ventricular action potentials have a “spike and dome” morphology.
Pinacidil increases IK,ATP, resulting in the shortening of APDs and thus loss of the action potential dome.
However, this effect is much more prominent in the epicardium than in the endocardium, possibly because
of a smaller endocardial Ito, and any changes produced there by pinacidil would be less dramatic.
Propagation of the action potential dome from sites where it is maintained to sites where it is abolished can
then result in an extrasystole. This mechanism, termed phase 2 reentry, produces closely coupled
The possibility of reflection was first suggested by a report that investigated the role of slowed action
potential conduction in reentrant excitation using excised canine Purkinje fibers. Depressed excitability in
discrete segments of the fibers was produced by increasing the extracellular potassium concentrations.
The authors made the following observations. An action potential traveling in the forward direction was
sometimes followed by a return extrasystole that traveled in the backward direction through the original
route. This only occurred when the initiating impulse reached an area of depressed excitability. It was
noted that the return extrasystole could arise from circus movement within the depressed segment, a
mechanism proposed earlier.
Later, reflection was demonstrated as a mechanism of reentrant arrhythmogenesis using the sucrose gap
model. Experiments used ion-free isotonic sucrose solution to create a central inexcitable gap in canine
Purkinje fibers, thereby dividing them into three segments (fig. 15). Electrical stimulation at the proximal
segment elicits an action potential. This excitation is transmitted across the gap to the distal segment
after a delay. However, this cannot be active in the form of action potentials because the extracellular
space is ion-free, but instead involves passive spread of the local current (electrotonic current) across the
low-resistance intracellular pathway.
When depolarization reaches threshold, an action potential is initiated in the distal segment. This in turn
generates electrotonic currents in the retrograde direction. With a further delay, the proximal region can
be reexcited when it has recovered from refractoriness, resulting in a return extrasystole, completing
reflection. Successful segment-type reflection requires a balance between the conduction delay and the
cellular membrane excitability.
Fig. 15. Reflection. Stimulation of the proximal segment elicits an action potential. Its
conduction across the middle segment cannot take place actively as the extracellular
region is ion-free. Instead, it involves electrotonic current spread intracellularly. After a
delay, when the membrane potential reaches threshold at the distal segment, another
action potential is generated.

19
extrasystolic beats capable of initiating circus movement reentry. It is termed phase 2 reentry because phase
2 (dome) of the action potential reenters to reexcite the myocardium.
Phase 2 reentry has been proposed as the mechanism responsible for the closely coupled extrasystole that
precipitates ventricular tachycardia/ventricular fibrillation (VT/VF) associated with Brugada and early
repolarization syndromes.
Figure 16. Example of phase 2 reentry due to heterogeneous dispersion of repolarization (HDR). According to Antzelevitch, dispersion
takes place at a transmural level and the AP of M cells is the longest compared with the AP of the rest of the wall areas. This HDR
produces a ventricular gradient (VG) between the areas with longer AP and the area with shortest AP and accounts for the possible
occurrence of VT/VF in patients with long QT syndrome (2) and short QT syndrome (3). In the Brugada syndrome (4) the HDR takes
places between the endocardium and the epicardium of the RV at the beginning of phase 2 (VG), because of the transient
predominance of outward Ito current. Epi: Epicardium; M: M cells.
Figure 17. J wave and ventricular fibrillation (VF) via phase 2 reentry. (a) VF in a patient with J wave in lead II, note the larger
amplitude of J wave in the beat preceding VF, following a longer R-R interval; (b) phase 2 reentry predisposing to VF in a canine right
ventricular wedge preparation in the presence of the K + channel opener pinacidil. Loss of action potential dome in Epi1 but not Epi2
caused propagation of the dome at Epi2 to Epi1, that is, phase 2 reentry (solid arrows), which manifested a short-coupled R-on-T
beats (open arrows) capable of triggering VF.
Electrotonic currents can flow from sites with longer APDs to sites with shorter APDs, and can cause
reexcitation when the latter sites have recovered from refractoriness. The arrhythmogenesis in Brugada
syndrome is thought to involve phase 2 reentry, where the resulting premature beat initiates spontaneous
polymorphic VT.

20
The concept of “prolonged repolarization-dependent reexcitation (PRDR)” proposed earlier is also similar to
that of phase 2 reentry. PRDR requires an area of myocardium with prolonged repolarization connected to
another area with a normal repolarization time-course. For example, EADs can prolong repolarization and
the resulting triggered activity in Purkinje fibers can conduct to the connecting ventricular muscle. However,
in PRDR, prolonged APDs per se do not cause reexcitation of the regions with shorter APDs, as they do in
phase 2 reentry. Rather, secondary depolarizations such as EADs or their resulting triggered activity in the
affected region provide an additional current source. Together, the local circuit currents generated by the
APD difference and by the EAD provide the necessary depolarizing currents for an extrasystole in the
affected region.
Furthermore, in PRDR, the interaction is between sites with prolonged and normal APDs, whereas in phase 2
reentry, it is between sites with normal and shortened APDs. Nevertheless, both mechanisms require an
increased transmural heterogeneity in the time courses of repolarization.
The presence of a prominent notch in the action potential of ventricular epicardium but not
endocardium gives rise to a transmural voltage gradient during ventricular activation that manifests as a
late delta wave following the QRS or what is commonly referred to as a J wave or Osborn wave. In
humans, the appearance of a prominent J wave on the ECG is considered pathognomonic of
hypothermia, hypercalcemia, or sudden death syndromes, including idiopathic ventricular fibrillation
(VF), ischemia/reperfusion-induced VF, and the Brugada syndrome.
[Brugada syndrome (BrS) is a genetic disorder in which the electrical activity within the heart is abnormal. Those
affected may have episodes of passing out. The abnormal heart rhythms seen in those with Brugada syndrome
often occur at rest and may be triggered by a fever.
There is no cure for Brugada syndrome. Those at higher risk of sudden cardiac death may be treated using an
implantable cardioverter defibrillator (ICD). In those without symptoms the risk of death is much lower, and how to
treat this group is less clear. Isoproterenol may be used in the short term for those who have frequent life-
threatening abnormal heart rhythms, while quinidine may be used longer term.
Brugada syndrome is diagnosed by identifying the pattern seen on the ECG which includes ST elevation in leads V1-
V3 with a right bundle branch block (RBBB) appearance. There may be evidence of a slowing of electrical conduction
within the heart, as shown by a prolonged PR interval. These patterns may be present all the time, but may appear
only in response to particular drugs (see below), when the person has a fever, during exercise, or as a result of other
triggers.
Three forms of the Brugada ECG pattern have been described:
 Type 1 has a coved type ST elevation with at least 2 mm (0.2 mV) J-point elevation and a gradually
descending ST segment followed by a negative T-wave.
 Type 2 has a saddle-back pattern with a least 2 mm J-point elevation and at least 1 mm ST elevation with a
positive or biphasic T-wave. Type 2 pattern can occasionally be seen in healthy subjects.
 Type 3 has either a coved (type 1 like) or a saddle-back (type 2 like) pattern, with less than 2 mm J-point
elevation and less than 1 mm ST elevation. Type 3 pattern is not rare in healthy subjects.
Fig. 18: ECG pattern in Brugada syndrome. According to a recent
consensus document, Type 1 ST segment elevation, either
spontaneously present or induced with the sodium channel-blocker
challenge test, is considered diagnostic. Type 2 and 3 may lead to
suspicion, but provocation testing is required for diagnosis. The ECGs in
the right and left panels are from the same patient before (right panel,
type 3) and after (left panel, type 1) administration of Ajmaline.

21
 RESETTING AND ENTRAINMENT OF REENTRANT ARRHYTHMIAS:
Over three decades of research and clinical applications, these phenomena have demonstrated that they stay as a
main tool for an intellectual understanding of reentry and to base strategies for localization of critical areas for
ablative therapies.
 RESETTING:
Resetting is the act of advancing a tachycardia impulse by timed premature electrical stimuli. The first
tachycardia complex in return should have the same morphological feature and cycle length as before the
extrastimulus, and the pause to this first tachycardia complex should be “reset” and therefore less than twice
the tachycardia cycle length.
The placement of a single pacing impulse into a tachycardia circuit that does not terminate it, but effects the
tachycardia in some fashion is called resetting or advancing the tachycardia. This maneuver is dependent on the
impulse travelling in the same direction as the tachycardia wavefront.
To reset a tachycardia the stimulated wavefront must reach the tachycardia circuit from the pacing site and
enter the excitable gap. Once it has entered the circuit, it will propagate in both directions, colliding in the
retrograde direction with the previous tachycardia impulse (antidromically) while in the anterograde direction it
will propagate and occur earlier than expected in time.
The degree of advancement depends on the prematurity of the extrastimulus and its conduction within the
circuit (i.e., the stimulus will propagate slower if the gap is only partially excitable).
If the stimulus enters the circuit during the relative refractory period, it can block in the anterograde direction
(because it is absolutely refractory) and collide antidromically with the previous beat, thus terminating the
tachycardia.
According to current recommendations, only a Type 1 ECG pattern, occurring either spontaneously or in response to
medication, can be used to confirm the diagnosis of Brugada syndrome as Type 2 and 3 patterns are not infrequently
seen in persons without the disease.]
A transmural gradient in the contribution of transient outward current (Ito) is responsible for the
transmural gradient in the magnitude of phase 1 and action potential notch, which in turn inscribes the J-
wave or J-point elevation in the ECG.
The presence of a prominent Ito-mediated notch predisposes canine ventricular epicardium to all-or-none
repolarization and phase 2 reentry. Under pathophysiologic conditions (e.g., ischemia, metabolic
inhibition, genetic defects in SCN5A) and with some pharmacologic interventions (e.g., INa or ICa blockers
or IK-ATP activators), canine ventricular epicardium exhibits an accentuation of the notch leading to loss of
the action potential dome secondary to a rebalancing of currents flowing at the end of phase 1 of the
action potential. The dome fails to develop when the outward currents (principally Ito) overwhelm the
inward currents (chiefly ICa), resulting in a remarkable (40–70%) abbreviation of the action potential. Loss
of the action potential dome is seldom homogeneous. The action potential dome usually is abolished at
some epicardial sites but not others, causing a marked dispersion of repolarization within the epicardium.
Electrical heterogeneity has been shown to give rise to phase 2 reentry in canine epicardium exposed to:
(1) K+
channel openers such as pinacidil;
(2) sodium channel blockers such as flecainide;
(3) combined sodium and calcium channel block, as with terfenadine;
(4) increased [Ca2
+]o;
(5) metabolic inhibition; and
(6) ischemic conditions.
Phase 2 reentry, e.g., from ischemia, can also initiate circus-type reentry. Block of Ito restores the action
potential dome, thus restoring electrical homogeneity and abolishing reentrant activity in all cases.
Accentuation of the epicardial action potential notch and/or loss of the action potential dome can appear
in the ECG as an elevated J point, accentuated J wave, or ST-segment elevation, all manifestations of the
pronounced transmural voltage gradient.

22
 ENTRAINMENT:
Entrainment is the continuous resetting of a tachycardia circuit (Figure 20). During overdrive pacing all
myocardial tissue will maintain the pacing rate, with resumption of the intrinsic morphology and rate upon
either abrupt cessation of pacing or slowing of the pacing rate below the intrinsic rate.
Let us imagine that in the situation represented in Figure 19 (panel B), after the orthodromic wavefront has
traveled a good way along the reentrant circuit, for example when it is reaching the exit site, a second paced
stimulus is delivered at the pacing site; similar phenomena will take place and the previously reset circuit will be
Figure 19. Schematic diagram illustrating the mechanism of resetting in reentrant arrhythmias. Panel A represents a circular reentrant
circuit. Most of it is surrounded by a black circumferential barrier that is, interrupted on its right side. The black area inside the circuit
represents unexcitable tissue. The white area around the circuit would be the remaining of the heart (the cardiac chamber). Inside the
circuit electrical activation is taking place, represented by the blue arrowhead that is followed by a tail of refractoriness (blue area). So
all the blue area is not excitable at this precise moment. The tissue in the circuit that is excitable, usually referred to as excitable gap,
is depicted in light gray. As the activation inside the circuit proceeds, it is expected that it will be confined in the circuit only as long as
a barrier exists, so it will exit to the surrounding myocardium as soon as there is no barrier (exit site, "exit" in the figure). If activation
wavefronts generated outside the circuit approach it, they would activate the tissue inside the circuit if there is no barrier and if the
tissue is excitable. So the entry site would be the closest site to the external activation wavefront that is not surrounded by barrier and
that is excitable. Considering the situation in panel B, where the wavefront is generated geometrically closer to the upper boundary of
the barrier, the entry site would be its most superior end, as represented in panel A ("entry"). Panel B represents the situation several
milliseconds later. An extrastimulus has been delivered at a site away from the circuit. The corresponding wavefront has reached the
reentrant circuit at a time the tissue was excitable (small red arrow). Activation inside the circuit proceeds both in the direction of
activation during tachycardia (orthodromic wavefront, "ortho" in the figure) and in the opposite direction (antidromic wavefront,
"antidromic" in the figure). Since the antidromic wavefront collides with the activation wavefront inside the circuit, the final result is
that the activation jumps from site 1 to site 2, thus short-circuiting the circuit (see text for further explanations).
In the case of reentrant circuits the phenomena underlining resetting are more complex, as schematically
presented in Figure 19. If an extrastimulus is delivered at an adequate site and with an adequate timing, the
resultant wavefront (Fig. 19, panel B) may access and penetrate the circuit. As a result, two wavefronts are
generated usually called orthodromic and antidromic, according to whether they proceed in the same or the
opposite direction as during tachycardia.
As can be appreciated in Figure 19, the antidromic wavefront is necessarily destined to collide with the
activation wavefront from the tachycardia (blue arrowhead), and both wavefronts will extinguish. So the only
wavefront that will keep proceeding is the orthodromic wavefront.
The final result, as depicted in Figure 19, is that when the activation inside the circuit is at site 1, in reality it is
at site 2, so the activation has "jumped" over a certain distance (distance between site 1 and site 2) inside
the circuit, so it will take less time to arrive to the exit site of the circuit next time, so the activation will be
advanced (reset, the tachycardia clock will be advanced) for just one beat. Since the circuit has not changed,
if no more external perturbations occur, the following beats will appear with intervals identical to the
tachycardia cycle length (TCL) but having now the reset beat as the time reference.
From the above discussion, it becomes clear that for resetting to occur there has to be an interaction
between the basic rhythm (tachycardia) and an external perturbation (either artificially generated, such as
programmed extrastimuli, or naturally occurring such as a premature atrial or ventricular contraction), and
that resetting results from a peculiar type of interaction: change in the tachycardia clock but maintenance of
the tachycardia circuit.

23
reset again. If pacing continues at the pacing site at a constant rate, a little faster than the tachycardia rate, each
pacing stimulus could arrive at the entry site of the circuit a little earlier than the activation wavefront of the
tachycardia itself (in reality the orthodromic wavefront of the previous paced beat).
What is unique to this situation is that each paced beat interacts with the tachycardia wavefront and resets the
circuit. By virtue of this interaction, all the tissue of the chamber where the circuit is located (including the tissue
of the reentrant circuit itself) is activated at the pacing rate, either by the antidromic wavefront of the paced
beat, the orthodromic wavefront of the paced beat, or by the orthodromic wavefront of the preceding beat
(after having proceeded along the tachycardia circuit). This is schematically shown in Figure 21A, that depicts
activation in a ladder diagram format to include time as the X-axis. But also unique to this situation is that the
tachycardia somehow remains "alive" so that if pacing is stopped at any moment the tachycardia will continue
unaltered.
It is interesting to note that, despite all the tissue in the chamber undergoing a higher number of electrical
activations per minute (is accelerated), conduction velocity does not increase in any part of the chamber (it
could even decrease). This apparent paradox, particularly in relation to the reentrant circuit, is explained
because part of the tissue in the reentrant circuit is occupied in a different way as during tachycardia, as
depicted in Figure 21; the area of the reentrant circuit occupied by the antidromic wavefront occupies the circuit
Figure 21B. Activation during tachycardia and during pacing is
schematically depicted in a ladder diagram format with time as the X-
axis. The tissue is schematically divided into the reentrant circuit
("circuit") and the remaining of the chamber ("chamber"). Panel A
represents activation during tachycardia (left) and during the last two
beats (n – 1 and n beats) of a pacing train, introduced at a distance
from the chamber, producing entrainment (right). Blue arrows
represent activation during tachycardia in an ondulating format to
represent circular continuous activation. During entrainment, each
paced wavefront (St) propagates through the intervening tissue (red
arrow in chamber). As it enters the circuit, it generates an orthodromic
wavefront (red arrows in the circuit) and an antidromic wavefront
(green arrows in the circuit); the latter collides with the activation
resulting from the orthodromic wavefront of the previous paced beat
("n green" collides with "n – 1 red"). Please note that, during
entrainment, all the tissue within the reentrant circuit is accelerated at
the pacing cycle length despite conduction velocity being the same as
during tachycardia (See text for further discussion). Panel B represents
pacing-induced tachycardia termination and reinitiation. Tachycardia
terminates in the second beat due to block of the orthodromic
wavefront inside the circuit. The fourth paced impulse blocks in the
antidromic direction so tachycardia reinitiates. If pacing would have
been stopped after the second or third paced impulse, the tachycardia
would have been terminated, but as it is stopped after the fourth beat,
the tachycardia continues. Please note that despite activation of the
intervening tissue ("chamber") at the pacing rate, some areas of the
reentrant circuit are not activated at that rate.
Figure 20. A: reentrant circuit. B: a timed premature stimulus can enter the circuit,
collide in a retrograde fashion with the previous impulse while in the anterograde
direction exiting earlier than expected. C: termination occurs if the stimulus enters
during the relative refractory period (anterograde block and retrograde collision).
Stim, stimulus.

24
in a different way (a different direction) but at the same time as other parts of the circuit are being activated (by
the orthodromic wavefront, in fact by two orthodromic wavefronts, that are generated by the present paced
beat [n beat] and by the previous paced beat [n – 1 beat] after it has proceeded along the reentrant circuit,
Figure 3A). The fact that several parts of the reentrant circuit are activated at the same time by different
wavefronts explains the apparent paradox of acceleration in depolarization rate but not in conduction velocity.
Summary:
 Waldo et al observed that a critical rate of pacing was required to terminate atrial flutter.
 At lower rates of pacing, continuation of the arrhythmia occurred immediately after cessation of pacing.
 It led to the recommendation of prophylactic implantation of electrodes to terminate arrhythmias by
rapid pacing impulse.
 The stimuli can enter the circuit and propagate in an antidromic and orthodromic direction.
 Entrainment can occur during pacing at sites that are within or outside the circuit.
 Entrainment alone does not indicate that the location of the pacing site is relative to the circuit.
 FUSION:
A fused beat possesses intermediate morphology between a fully stimulated complex and the tachycardia
complex. It can be observed on the surface ECG (if a significant amount of myocardium is depolarized) or
intracardiac recordings. For fusion to occur, the tachycardia wavefront must exit the circuit and collide with the
pacing stimulus before depolarization of the surrounding myocardium (Figure 22). This requires a circuit with
distinct entry and exit sites supporting a reentrant mechanism. Resetting and entrainment with fusion are
specific to reentrant arrhythmias, but since they are sometimes challenging to identify, failure to detect them
does not invalidate reentry as the arrhythmia mechanism.
Waldo et al. made the seminal observation that continuous pacing during reentrant tachycardia followed by
persistence of the tachycardia was sometimes associated with the phenomenon of constant fusion as recognized
in the surface ECG. They proposed that this observation could demonstrate entrainment and was formulated as
two criteria for the recognition of entrainment (they also proposed two additional entrainment criteria):
(1) "when pacing at a constant rate that is faster than the rate of the tachycardia and which fails to interrupt
it, there is the demonstration of constant fusion beats in the ECG except for the last captured beat,
which is not fused";
(2) "during a tachycardia, when pacing at two or more constant rates that are faster than the rate of the
tachycardia but which fails to interrupt it, there is the demonstration of constant fusion beats in the ECG
at each rate, but different degrees of constant fusion at each rate"(Fig. 23).
Figure 23.Example of constant and progressive fusion. Both panels illustrate entrainment of an accessory pathway-mediated tachycardia by
right apical ventricular pacing at two constant pacing rates (330 ms on the left and 300 ms on the right panel). In both panels the first four QRS
complexes are paced and show a constant morphology. In the left panel the paced QRS morphology is totally unexpected for an apical paced
site, and the QRS is narrower than in the right panel, because the paced QRS are fused (constant fusion). Please note a dramatic difference in
the morphology of the paced QRS complex in relation to pacing rate (progressive fusion).
Figure 22. Schematic representation of a fused beat. Stim, stimulus.

25
How to detect fusion? A deeper discussion on fusion follows but let us mention by now that a mere change in
the QRS/P-wave contour during pacing is not enough. Pacing will always change the QRS/P-wave morphology
as long as it captures the myocardium and the pacing site is located away from the circuit.
The way to detect fusion is by comparing the QRS/P-wave contour during pacing when the tachycardia is
present with the QRS/P-wave contour during pacing at identical site and rate but in the absence of
tachycardia. Since this is not always easy to obtain, the second criterion formulated by Waldo et al is useful
because if progressive fusion can be demonstrated this obviates the need for stimulation in the absence of
tachycardia.
Figure 24. Schematic representation of entrainment with
electrocardiographic fusion in a ladder diagram. The format in both
panels is similar to that of Figure3A, but the exit from the tachycardia is
now depicted as a "tunnel-like" structure from the circuit, to allow the
representation of fusion in a 1-dimensional scheme (in the right panel).
Note that fusion in the activation of the chamber occurs because
activation resultant from the "n – 1" paced wavefront, as it exits
orthodromically from the circuit, is coincidental in time with the "n"
paced wavefront. The comparison of panel A with panel B illustrates
progressive fusion. As the pacing rate increases (panel B), since each
paced wavefront is generated sooner after the previous impulse, more
myocardial mass of the chamber will be activated by the paced
wavefront and less due to the exiting wavefront from the tachycardia, so
the degree of fusion will change, and this will be reflected in the
electrocardiogram. Please also note that the antidromic wavefront in
the circuit will also invade a greater proportion of the tissue in the
circuit.

26
From the above discussion it is clear that resetting and entrainment can occur both in the presence and in the
absence of electrocardiographic fusion.
DIFFERENCES BETWEEN RESETTING AND ENTRAINMENT:
As discussed above, the two phenomena are essentially similar in their mechanisms and implications. However,
they differ in several theoretical and practical aspects.
 The resetting phenomenon can easily be recognized by comparing the intervals encompassing the
extrastimuli with the TCL (tachycardia cycle length) (Fig. 1). As discussed above, the situation is different
for the entrainment response, we cannot use intervals, and thus other criteria are needed, which are
more difficult to observe and demonstrate.
 Resetting may be more limited than entrainment when there is a long conduction time between the
stimulation site and the circuit.
 The resetting response induces less modification in the dynamics of circuit. And this is so for two
reasons:
(1) It interacts with the circuit only once, so the interaction takes place with the "original reentrant
wavefront." In contrast, during entrainment there is repetitive resetting, so the interaction of each
wavefront occurs with the previously reset circuit.
(2) It interacts with the circuit with the lowest possible prematurity; using a strict protocol, the latest
coupled extrastimulus that resets the circuit will enter the circuit with the minimum possible degree
of prematurity, and so will advance the activation as little as possible, inducing the least possible
modification in the reentrant pathway. In contrast, by continuous pacing at a rate somehow faster
than the tachycardia rate, the degree of prematurity of the first beat that interacts (and resets) with
the circuit will be unknown (a value in between the difference between the tachycardia and the
PCL).
ELECTROCARDIOGRAPHIC FUSION AND ITS POTENTIAL LIMITATIONS FOR THE DETECTION OF TRANSIENT
ENTRAINMENT:
Electrocardiographic fusion is a phenomenon known for almost 100 years: a fusion complex reflects
"simultaneous activation of the atria or ventricles by two, or rarely more, impulses originating in the same or,
more often, in different chambers of the heart." However, for the practical application of the concept,
probably the word "impulses" could be substituted for "wavefronts" or, to be more precise, "large
wavefronts." For example, most people would agree that an example of a fused QRS complex is that
observed in ventricular preexcitation, where a single impulse (a sinus beat) results in two separate (large)
wavefronts that arrive in the ventricles at a similar time, so each QRS results from activation by the accessory
pathway and the normal conduction system. Although fusion can also occur at the atrial level it is generally
easier to observe it in the QRS complex than in the P wave. Fusion is so frequent that even the normal QRS is,
to some extent, a fusion between activation due to the left and the right bundles, but since this is a normal
situation, it is not usually considered under the heading of fused beats. Fused beats may occur in relation to
late-coupled extrasystoles, in rhythms of ventricular origin when sinus beats capture part of the ventricles or
when paced beats occur at a time when the heart has already been normally activated.
What is specific to fusion when pacing results in resetting or entrainment, is that the second wavefront is an
exiting wavefront from the tachycardia circuit and that it collides with the paced wavefront.
Another possible mechanism of fusion unrelated to entrainment may take place if conduction in the cardiac
chamber is slow enough and the pacing rate is fast enough for the activation wavefront of each beat to end
after initiation of the following beat. This mechanism is more frequently detected with intracardiac
recordings.
When two focal rhythms at similar rate compete for the activation of a chamber (for example, a VVI
pacemaker programmed at a rate similar to the sinus rate in a patient with intact conduction), there may be
fused beats with beat-to-beat variation in the degree of fusion. This is usually called variable fusion and
should be distinguished from constant and particularly from progressive fusion. In the latter, fusion is
constant at each rate but different at different pacing rates, whereas in the former the degree of fusion
varies beat-to-beat in the presence of a constant pacing rate.

27
FEATURES OF ARRHYTHMIA MECHANISMS:
We now present an approach to the differential diagnosis of arrhythmia mechanisms. Table 1 is a schematic diagram
of useful maneuvers (explained above) for distinguishing between the different arrhythmia mechanisms.
It is important to note that sometimes it may be very difficult to identify the mechanism responsible for the
arrhythmia, and even more challenging if we take into account that an arrhythmia can be initiated by one
mechanism but perpetuated by others (e.g. AF).
As shown in Table 1, automatic arrhythmias cannot be reproducibly initiated or terminated by programmed electric
stimulation. They can be reset, and rapid pacing can result in overdrive suppression or produce no effect. The
initiation may be facilitated by isoproterenol, in which the arrhythmia will typically start with a warm-up period with
the first tachycardia beat being identical to the next one. Adenosine can slow but usually does not terminate the
tachycardia.
Although TA can be initiated with pacing, initiation frequently requires isoproterenol. Arrhythmias due to TA can be
reset and usually pacing can terminate a TA tachycardia. The first beat is usually the extrastimulus or premature
beat, and therefore different from the subsequent one. These arrhythmias terminate in response to adenosine.
Reentrant tachycardias respond to pacing and demonstrate the hallmark features of resetting and entrainment with
fusion. Adenosine can terminate a reentrant tachycardia involving the AV node, but will not affect sodium-
dependent cells in the atria and ventricles.
Table 1. Maneuvers for Distinguishing Between the Different Arrhythmia Mechanisms.
AUTOMATICITY TRIGGERED ACTIVITY REENTRY
INITIATION BY PES (Programmed
Electric Stimulation)
No Yes (continuous
stimulation)
Yes
TERMINATION BY PES No Some times Yes
FIRST INTERVAL AT INITITATING Long, warm-up Short (same as or shorter
than rest)
Long (longer than
subsequent)
MORPHOLOGY OF FIRST BEAT Identical to
subsequent
Different from
subsequent
Different from
subsequent
ADENOSINE Transient slowing or
no response
Termination No response or AV block
CATECHOLAMINES Increase Increase (DAD) Increase/decrease
RESPONSE TO PES DURING
TACHYCARDIA
Reset or
compensatory pause
Reset or termination Reset or termination
RESET WITH FUSION No No Yes
RESPONSE TO CONTINUOUS
STIMULATION DURING
TACHYCARDIA
Overdrive suppression
if enhanced normal
automaticity
Acceleration or
termination
Entrainment or
termination
ENTRAINMENT WITH FUSION No No Yes
Furthermore, other noninvasive tools such as surface ECG should always be considered. The surface ECG may not
confirm a particular mechanism, but it can provide important clues. The sinus rhythm ECG may reveal disease
processes known to be associated with specific types of arrhythmias: a) Q waves consistent with prior myocardial
infarction suggest the substrate for reentry; b) a long QT interval raises suspicion for afterdepolarizations; c) a “delta
wave” makes reentry over an accessory pathway a plausible mechanism, and d) epsilon waves or Brugada pattern
ECGs suggest reentrant mechanisms.

28
CLASSIFICATION:
Arrhythmia may be classified by:
 rate (tachycardia, bradycardia),
 mechanism (automaticity, re-entry, triggered) or
 duration (isolated premature beats; couplets; runs, that is 3 or more beats; non-sustained= less than 30
seconds or sustained= over 30 seconds)
It may also be classified by site of origin:
1. Sinus Node dysfunction (SSS):
1) Sinus bradycardia
2) Sinus pause/ arrest
3) SA exit Block
4) Tachy- Brady Syndrome
5) Chronotropic incompetence
3. Disturbances of atrial impulse formation:
1) Premature Atrial Contractions
2) Atrial tachycardia:
i. Multifocal atrial tachycardia (MAT) or
Chaotic AT
3) Atrial flutter
4) Atrial fibrillation
5) Wandering Pacemaker
6) Atrial standstill
7) Supraventricular tachycardia:
i. Sinus tachycardia
ii. Atrial flutter
iii. Atrial fibrillation
iv. Junctional tachycardia
v. PSVT:
 Atrial tachycardia
 AVNRT
 AVRT (Atrioventricular reentrant
tachycardia or atrioventricular
reciprocating tachycardia)
- Wolff-Parkinson-White Syndrome
2. AV Junctional Abnormalities:
1) Atrioventricularnodal reentrant (AVNRT)
2) AVRT:
i. WPW syndrome
3) Premature Junctional Rhythm
4) Junctional rhythm (escape):
5) Accelerated Junctional Rhythm
6) Junctional Tachycardia
4. Disturbances of ventricular impulse formation:
1) Premature ventricular contractions
(extrasystole) sometimes called ventricular
extra beats (VEBs)
2) Ventricular tachycardia:
i. Monomorphic ventricular tachycardia
ii. Polymorphic ventricular tachycardia:
 Torsades de’ Pointes
3) Ventricular flutter
4) Ventricular fibrillation
5) Idioventricular Rhythm
6) Asystole (Ventricular standstill)
i. Agonal rhythms

29
5. Heart blocks:
1) Conduction Abnormalities/Block, AV Block:
i. 1st
degree;
ii. 2nd
degree: Mobitz Type I and Mobitz type II;
iii. 3rd
degree.
2) IntraventricularConduction defect; BBB:
i. Right Bundle Branch Block;
ii. Left Bundle Branch Block; LAFB; LPFB;
iii. Bifascicular Block;
iv. Trifascicular Block
6. Sudden cardiac death syndromes:
1) Cardiac arrest:
 Brady-asystolic pattern
 Pulseless VT, VF
 Ventricular asystole (standstill)
 Pulseless electrical activity (PEA)
Fig. Four “look-alike” narrow complex tachycardias recorded in lead II. (A) Sinus tachycardia. (B) Atrial fibrillation. (C) Paroxysmal
supraventricular tachycardia (PSVT) resulting from atrioventricular nodal reentrant tachycardia (AVNRT). (D) Atrial flutter with 2:1 AV block
(conduction). When the ventricular rate is about 150 beats/min, these four arrhythmias may be difficult, if not impossible, to tell apart on the
standard ECG, particularly from a single lead. In the example of sinus tachycardia the P waves can barely be seen in this case. Next, notice that
the irregularity of the atrial fibrillation here is very subtle. In the example of PSVT, the rate is quite regular without evident P waves. In the atrial
flutter tracing, the flutter waves cannot be seen clearly in this lead.
DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIAS (WCTS):
A tachycardia with widened (broad) QRS complexes (i.e., 120 msec or more in duration) raises two major diagnostic
considerations:
1. The first, and most clinically important, is VT, a potentially life-threatening arrhythmia. As noted, VT is a
consecutive run of three or more ventricular premature complexes (PVCs) at a rate generally between 100
and 225 beats/min or more. It is usually, but not always, very regular, especially sustained monomorphic VT
at higher rates.
2. The second possible cause of a tachycardia with widened QRS complexes is termed SVT with aberration or
aberrancy (sometimes termed anomalous conduction and includes preexcitation).

30
1. SINUSNODEDYSFUNCTION(SND OR SSS):
Sick sinus syndrome (SSS), also called sinus dysfunction, or sinoatrial node disease ("SND"), is a group of abnormal
atrial rhythms presumablycaused by a malfunction of the sinus node, the heart’s primary pacemaker.
Sick sinus syndrome is the leading indication for permanent pacemaker implantation. The actual cause of sick sinus
syndrome is related to replacement of the sinus node with fibrinous tissue. This usually occurs concomitantly with
similar changes throughout the entire conduction system including the AV node and increases with age. On rare
occasions, ischemia to the SA node or other infiltrative disease can cause SSS.
Signs and symptoms:
Even though many types of sick sinus syndrome produce no symptoms, a person may present with one or more of
the following signs and symptoms:
 Stokes-Adams attacks – fainting due to asystole or ventricular fibrillation
 Dizziness or light-headedness
 Palpitations
 Chest pain or angina
 Shortness of breath
 Fatigue
 Headache
 Nausea
1) Sinus Bradycardia:
Sinus rhythm with a resting heart rate of < 60 bpm in adults, or below the normal range for age in children. It happens
when the electrical impulse that signals the heart to contract is not formed in heart’s natural pacemaker, the SA
node, or is not sent to the ventricles through the proper channels.
 Causes:
NON- PHARMACOLOGICAL PHARMACOLOGICAL
 Normal during sleep (young adults) [even of less
than 30 bpm]
 Increased vagal tone (e.g. athletes)
 Vagal stimulation (e.g. pain)
 Inferior myocardial infarction
 Sinus node disease
 Hypothyroidism
 Hypothermia
 Anorexia nervosa
 Electrolyte abnormalities – hyperkalaemia,
hypermagnesaemia
 Brainstem herniation (the Cushing reflex)
 Myocarditis
 Trained Athletes
 Beta-blockers
 Calcium-channelblockers (verapamil & diltiazem)
 Digoxin
 Central alpha-2 agonists (clonidine &
dexmedetomidine)
 Amiodarone
 Opiates
 GABA-ergic agents (barbiturates,
benzodiazepines,baclofen, GHB)
 Organophosphatepoisoning
Bradycardia most often affects elderly people, but it may affect even the very young. It may be caused by one of two
sources: The central nervous system does not signal that the heart needs to pump more, or the SA node may be
damaged.
 ECG criteria:
▫ Rate: 40-59 bpm
▫ P wave: sinus
▫ QRS: Normal (0.06-0.12)
▫ Conduction: P-R normal or slightly prolonged at slower rates
▫ Rhythm: regular or slightly irregular
▫ If bradycardia becomes slower than SAN, a junctional rhythm may occur.
Normal heart rates in children:
Newborn: 110 – 150 bpm
2 years: 85 – 125 bpm
4 years: 75 – 115 bpm
6 years+: 60 – 100 bpm

31
Characteristics:
▫ Longer R-R interval duration.
▫ P waves become less frequent.
Treatment: treat the underlying cause, atropine, isuprel, or artificial pacing if patient is hemodynamically
compromised.
2) Sinus Pause/ Arrest:
Sinoatrial arrest (also known as sinus arrest or sinus pause) is a medical condition wherein the sinoatrial node of
the heart transiently ceases to generate the electrical impulses that normally stimulate the myocardial tissues to
contract and thus the heart to beat. It is defined as lasting from 2.0 seconds to several minutes
Since the heart contains multiple pacemakers, this interruption of the cardiac cycle generally lasts only a few
seconds before another part of the heart (preserving heart rate and function), such as the atrio-ventricular junction
or the ventricles, begins pacing and restores the heart action.
- If a pacemaker other than the sinoatrial node is pacing the heart, this condition is known as an escape rhythm.
- If no other pacemaker begins pacing during an episode of sinus arrest it becomes a cardiac arrest.
This condition is sometimes confused with ‘sinoatrial block’, a condition in which the pacing impulse is generated,
but fails to conduct through the myocardium. Differential diagnosis of the two conditions is possible by examining
the exact length of the interruption of cardiac activity. Failure to discharge an impulse within < 2s is defined as
sinoatrial pause. Sinoatrial arrest occurs when the SAN does not discharge an impulse for > 2s.
If the next available pacemaker takes over, it is in the following order:
1. Atrial escape (rate 60–80): originates within atria, not sinus node (normal P morphology is lost).
2. Junctional escape (rate 40–60): originates near the AV node; a normal P wave is not seen, may occasionally
see a retrograde P wave.
3. Ventricular escape (rate 20–40): originates in ventricular conduction system; no P wave, wide, abnormal
QRS.
In most cases, the escape rhythm originates in either of the following three structures:
 Specific clusters of atrial myocardium: There are clusters of atrial myocardium that possess automaticity and
thus pacemaker function. The intrinsic rate of depolarization in these cells is 60 beats per minute. The
resulting P-wave is morphologically different from the sinus P-wave, but the QRS complex is normal (provided
that Intraventricular conduction is normal). This rhythm may be referred to as atrial rhythm.
 Cells near the atrioventricular node: The AVN does not possess automaticity, but cells surrounding it do.
These cells are capable of generating an escape rhythm with a rate of 40 beats per minute. QRS complexes
are normal (provided that intraventricular conduction is normal). If the P-wave is visible, it is retrograde in
lead II (because of the reversed direction of atrial activation) and may be located before or after the QRS
complex. This rhythm is referred to as junctional rhythm.
 The His-Purkinje network: All these fibers possess automaticity with an intrinsic rate of depolarization around
20-40 beats/min. If the impulses are discharge from fibers proximal to the bifurcation of the bundle of His,
QRS complexes will be normal (QRS duration <0.12 s), because both bundle branches receive the impulse
and spread it. If the impulse is discharged distal to the bifurcation of the bundle of His, the QRS complexes
will be wide (QRS duration > 0.12 s). The escape rhythm with wide QRS complexes are referred to as
ventricular rhythm.
All these rhythms are regular. Since there is competition between these latent pacemakers, the one with the fastest
intrinsic rate of depolarization will be the pacemaker, which means that it usually is atrial myocardium.
Asystole occurs if no escape rhythm awakes. It is uncommon that sinus arrest leads to persistent asystole; latent
pacemakers virtually always awake and salvage the rhythm.

32
 Causes:
▫ High vagal tone
▫ Hypoxia
▫ Myocardial ischemia/ infarction
▫ Hyperkalemia
▫ Side effects of drugs (Ex: Ca2+
channel blockers, β blockers, digitalis)
Treatment includes stop medications that suppress the sinus node (beta blocker, Calcium channel blocker,
digitalis, etc.); may need pacing.
 ECG criteria:
▫ Rate: normal
▫ P wave: those that are present are normal
▫ QRS: normal
▫ Conduction: normal
▫ Rhythm: The basic rhythm is regular. The length of the pause is not a multiple of the sinus interval.
3) SA Exit Block:
SA Block is a disorder in the normal rhythm of the heart, known as a heart block that is initiated in the sinoatrial
node which implies that the impulses discharged in the SAN are either not conducted to the atria or are so with a
delay (An AV block, occurs in the AV node and delays ventricular depolarization).
Emergency treatment consists of administration of atropine sulfate or transcutaneous pacing.
 Types:
SA blocks are categorized into three classes based on the length of the delay.
 FIRST DEGREE SINOATRIAL BLOCK:
 In a first degree sinoatrial block, there is a lag between the time that the SA node fires and actual
depolarization of the atria. This rhythm is not recognizable on an ECG strip because a strip does not
denote when the SA node fires.
 The ECG may simply show sinus rhythm or sinus bradycardia. This is different than a first-degree
atrioventricular, or AV, block, which shows a prolonged PR interval.
 It can be detected only during an electrophysiology study when a small wire is placed against the SA
node from within the heart and the electrical impulses can be recorded as they leave the p-cells in the
centre of the node followed by observing a delay in the onset of the p wave on the ECG.

33
 SECOND DEGREE SA BLOCK:
 Second degree SA block are broken down into two subcategories just like AV blocks are:
▫ The first is a second degree type I, or Wenckebach block.
- This rhythm is irregular, and demonstrates progressive shortening of the RR or PP intervals until
a P wave is blocked in the SA node, which would not appear on the ECG. [Note that this is quite
different from the Wenckebach AV block, in which the PR interval gets progressively longer,
before the dropped QRS segment.] A “sinus pause” ensues afterward and would be shorter than
two of the preceding RR intervals. Here is an example:
- ECG changes:
 PP cycle becomes progressively shorter
 No P waves & QRS complexes
 Pause is less than twice the preceding PP cycle
▫ Second-degree SA exit block type II occurs when there are consistent RR and PP intervals, then a P
wave is blocked in the SA node, also not seen on the ECG. The subsequent sinus pause here is an
exact interval of the preceding RR intervals, usually two times.
Fig. several cases of type 2
second-degree sinoatrial block

Arrhythmia: Mechanism, Classification, ECG features

Arrhythmia: Mechanism, Classification, ECG features

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