Mechanisms, Classification, and Clinical Aspects of Arrhythmias

Chapter 14
Mechanisms, Classification, and Clinical Aspects of Arrhythmias


Arrhythmias are defined as any cardiac rhythms other than the normal sinus rhythm. Sinus rhythm originates in the sinus node. The ECG characteristics of normal sinus rhythm are as follows:

  • A sinus stimulus generated in a sinus node and subsequently is transmitted at appropriate rates of conduction transmitted through atria (P wave), the atrioventricular (AV) junction, and the intraventricular specific conduction system (ISCS). It initiates a positive P wave in I, II, aVF, V2–V6, and positive or + − in leads III and V1.
  • In adults, in the absence of pre‐excitation, the PR interval ranges from 0.12 to 0.20 sec.
  • At rest, the sinus node discharge cadence ranges from 60 to 80 beats per minute (bpm) and tends to be regular, although it shows generally slight variations, which are not evident by palpation or auscultation. Under normal conditions, however, and particularly in children, it may show slight to moderate changes depending on the phases of respiration, with the heart rate increasing with inspiration. Thus, the evidence of a completely fixed heart rate both during the day and at night is suggestive of alterations of the heart rhythm, usually associated to certain degree of autonomic nervous system (ANS) dysfunction.

It is important to remember that:

  • The term arrhythmia does not mean rhythm irregularity, as regular arrhythmias can occur, often with absolute stability (i.e. atrial flutter, paroxysmal atrial tachycardia, etc.), sometimes presenting with heart rates in the normal range, as is the case of atrial flutter with 4:1 AV conduction. On the other hand, some irregular rhythms should not be considered arrhythmias (mild to moderate irregularity in the sinus discharge, particularly when linked to respiration, as already stated, also known as sinus respiratory arrhythmia).
  • A diagnosis of arrhythmia in itself does not mean pathology. In fact, in healthy subjects, the sporadic presence of certain arrhythmias, both active (premature complexes) and passive (escape complexes, certain degree of AV block, sinus respiratory arrhythmia, etc.), is frequently observed.


There are various ways to classify cardiac arrhythmias.

  • According to the site of origin: Arrhythmias are divided into supraventricular (including those having their origin in the sinus node, the atria, and the AV junction), and ventricular arrhythmias.
  • According to the underlying mechanism: Arrhythmias may be explained by: (i) abnormal formation of impulses (increased automaticity and triggered activity); (ii) reentry of different types; (iii) decreased automaticity; and (iv) disturbances of conduction (see later).
  • From the clinical point of view: Arrhythmias may be paroxysmal, incessant, or permanent. The first occurs suddenly and usually disappears spontaneously (i.e. AV junctional reentrant paroxysmal tachycardia or paroxysmal AV block), permanent are always present (i.e. permanent atrial fibrillation), and incessant are characterized by intermittent but repetitive presence.
  • Finally, from an electrocardiographic point of view, arrhythmias may be divided into either active or passive (Table 14.1):

    1. Active arrhythmias, due to increased automaticity, reentry, or triggered electrical activity (see later and Table 14.2), generate isolated or repetitive premature complexes on the ECG, which occur before the cadence of the regular sinus rhythm. Premature complexes may be produced in a parasystolic or extrasystolic ectopic focus that may be supraventricular or ventricular. The extrasystolic mechanism has a fixed coupling interval, whereas the parasystolic has a varied coupling interval. Premature and repetitive complexes include all types of supraventricular or ventricular tachyarrhythmias (tachycardias, fibrillation, flutter). In active cardiac arrhythmias, due to classic reentrant mechanisms, a unidirectional block exists in some part of the circuit.

      Table 14.1 Classification of arrhythmias according to their electrocardiographical presentation

      Active arrhythmias Passive arrhythmias
      Supraventricular Escape complex
      Premature complexes Escape rhythm
      Tachyarrhythmias Sinus bradycardia
      Different types of tachycardia Sinoatrial block
      Atrial fibrillation Atrial block
      Atrial flutter Atrioventricular block
      Ventricular Ventricular block
      Premature complexes Aberrant conduction
      Different types of tachycardia Cardiac arrest
      Ventricular flutter
      Ventricular fibrillation

    2. Passive arrhythmias occur when cardiac stimuli formation and/or conduction are below the range of normality due to a depression of the automatism and/or a stimulus conduction block in the atria, the AV junction, or the specific intraventricular conduction systems (ICS).

From an electrocardiographic point of view, many passive cardiac arrhythmias show a slower than expected heart rate (bradyarrhythmia). However, some type of conduction delay or block in some place of the specific conduction systems (SCS) may exist without slow rate, for example, first‐degree or some second‐degree sinoatrial or AV blocks. Thus, the electrocardiographic diagnosis of passive cardiac arrhythmia can be made because it may be demonstrated that the ECG changes are due to a depression of automatism and/or conduction in some part of the SCS, without this manifesting in the ECG as a premature complex, as it does in reentry. Therefore, atrial or ventricular blocks may be considered arrhythmias. In this book, we have discussed them as a separate entity in Chapters 9 and 10.

Clinical significance and symptoms

The incidence of the majority of arrhythmias increases progressively with age, and arrhythmias are less frequent in children (some exceptions apply like arrhythmias associated to congenital heart diseases and channelopathies (see Brugada syndrome). Data from Holter ECG recordings (see Chapter 25, Holter electrocardiographic monitoring and related techniques) have demonstrated that some isolated premature ventricular complexes (PVC) are present in about 10–20% of young people in 24‐hour recordings, and their presence is nearly a rule in the 80+ age group. Similarly, sustained chronic arrhythmias, such as atrial fibrillation, are exceptional in children but are present in about 10% of subjects over 80 years of age. However, there are arrhythmias that arise particularly in children, such as some paroxysmal AV junctional reentrant tachycardias using accessory pathways (AVRT), some ectopic junctional tachycardias, as well as some monomorphic ventricular tachycardias (idiopathic), and polymorphic ventricular tachycardias (catecholaminergic). Finally, there are also some cases of congenital AV block.

Table 14.2 Mechanisms involved in the main supraventricular and ventricular tachyarrhythmias

Arrhythmia Main mechanism Heart rate (bpm)
Sinus tachycardia  automaticity >90

Sinoatrial reentry 100–180
Monomorphic atrial tachycardia (Tables 15.415.6) Focus origin (micro‐reentry,  automaticity or triggered activity) 90–40 (incessant tachycardia)Till 200–220 (macro‐reentrant paroxysmal tachycardia)

Macro‐reentry If >220, it is considered an atypical flutter
Junctional ectopic tachycardia Abnormal generation of stimuli 100–180
Junctional reentrant tachycardia
140–200 (paroxysmal tachycardia)

  • Reentry only through AV junctional circuit
Reentry in circuit exclusively comprising the AV junction

  • Reentry circuit with anomalous pathway involvement
Reentry in circuit involving also an anomalous pathway (may be paroxysmal or incessant) Generally <140 (incessant tachycardia)
Chaotic atrial tachycardia Multiple atrial foci 100–200
Atrial fibrillation Micro‐reentry
Automatic focus with fibrillatory conduction
Rotors with fibrillatory conduction
350–700 (atrial waves)
Atrial flutter Macro‐reentry Generally, 240–300 with AV conduction mainly 2 × 1
Classic VT with structural heart disease Reentry with anatomical or functional circuit (rotors) From 110 to >200
VT/VF in channelopathies In most of the cases (long and short QT, and Brugada syndrome) due to differences in the duration and/or the morphology of AP at different myocardial areas From 140 to >200
Idioventricular rhythm Increase of automaticity 60–100
VT with narrow QRS Usually reentry (verapamil‐sensitive) 120–160
Parasystolic VT Protected automatic focus Generally <140
Torsades de pointes VT Post‐potentials and/or rotors 160–250
VT with no evident heart disease Triggered activity, reentry or automaticity increase 110–200
Ventricular flutter Macro‐reentry 250–350
Ventricular fibrillation Micro‐reentry with fibrillatory conduction
Automatic focus with fibrillatory conduction
Rotors with fibrillatory conduction

TAP: transmembrane action potential; VT: ventricular tachyarrhythmia.

The most important clinical significance of arrhythmias is related to an association with sudden cardiac death (Bayés de Luna and Baranchuk, 2017; Goldstein et al. 1994). It is also important to remember that frequently arrhythmias, especially atrial fibrillation, may lead to embolism, including cerebral embolism, sometimes with severe consequences. Also, fast arrhythmias may trigger or worsen heart failure. For further information, consult general references on Recommended Reading.

ECG diagnosis of arrhythmias: preliminary considerations

To make a valid ECG interpretation of an arrhythmia and understand the electrophysiologic mechanism that may explain its presence, it may be useful to consider the following tips and recommendations.

  • It is advisable to have a magnifying glass and a pair of compasses. They may be used to accurately measure the wave duration, the distance between P waves or QRS complexes, the differences in the coupling interval (distance between a premature P wave or QRS complex and the P wave or QRS complex of the preceding basal rhythm), etc. In the modern digital era, amplification of images is simply done using electronic tools. Semiautomatic calipers are also available and measurements are considered more reproducible.
  • It is helpful to take long strips of the ECG tracing (this is especially important in the case of possible parasystole) and to record 12‐lead ECGs. This will help to perform the differential diagnosis of ventricular versus supraventricular tachycardias with aberrancy, and it will also help to determine the site of origin and mechanisms of supraventricular and ventricular arrhythmias.
  • In the case of paroxysmal tachycardias, a long strip should be recorded during carotid sinus massage, and some maneuvers (deep inspiration and Valsalva, as well as other vagal maneuvers) performed for diagnostic and therapeutic purposes (Figure 14.1).
  • It is necessary to obtain ECG recordings during exercise testing, both in patients with premature complexes, in order to verify if they increase or decrease, and in patients with bradyarrhythmias, to identify an abrupt or gradual acceleration. If acceleration is abrupt, and the heart rate is doubled or even more, this indicates a 2:1 sinoatrial block. If acceleration is gradual, this indicates a bradycardia due to depression or automatism.
  • It is useful to have an overall patient history and previous ECGs, especially in patients with potential pre‐excitation syndrome or in patients with wide QRS complex tachycardias.

  • The “secret” to making a correct diagnosis of arrhythmia is to properly detect and analyze the atrial and ventricular activity and to look at the AV relationship. For this purpose, over 80 years ago Lewis created some diagrams that are still considered very useful today (Johnson and Denes 2008; Antiperovitch et al. 2019). In most cases, only three areas are required to explain the site of onset and the stimulus pathway: atria, AV junction, and ventricles (Figures 14.214.4).
  • It is convenient to determine the sensitivity, specificity, and predictive value of the different signs and diagnostic criteria. This is especially important when performing differential diagnosis in the case of wide QRS tachycardia, between ventricular tachycardia and supraventricular tachycardia with aberrancy (see Chapter 25).
  • As previously stated, it is often necessary to perform special techniques, such as exercise testing, Holter ECG recording, amplified waves, EPS, imaging techniques, etc., to better understand the prevalence of arrhythmias, the electrophysiologic mechanisms that may explain them, and the correct diagnosis, as well as for prognostic evaluation and the prescription of a particular treatment (see Chapter 25 and Bayés de Luna and Baranchuk, 2017).

Mechanisms responsible for active cardiac arrhythmias

Frequently, active arrhythmias are triggered by one mechanism and perpetuated by another. In addition, there are modulating factors (unbalanced ANS, ischemia, ionic and metabolic alterations, stress, alcohol and coffee consumption, etc.) that favor the appearance and maintenance of arrhythmias.

When analyzing tachyarrhythmias, we can use the analogy of a burning forest (see Table 14.1). The fire may be triggered by a match (premature impulse), but for the fire to perpetuate, the bushes and trees (i.e. substrate) must be dry enough. There are many modulating factors having an impact on whether the fire (arrhythmia) starts sooner and is perpetuated, such as wind or heat (equivalent to tachycardia, instability of the ANS, ischemia, etc.), or is extinguished early, such as rain or cold (equivalent to the stability of the ANS, sympathetic nervous system integrity, etc.).

Schematic illustration of the correct procedure for carotid sinus massage (CSM). The force applied with the fingers should be similar to that required to squeeze a tennis ball, during a short time period (10–15seconds), and the procedure should be repeated four to five times on either side, starting on the right side.

Figure 14.1 Note the correct procedure for carotid sinus massage (CSM). The force applied with the fingers should be similar to that required to squeeze a tennis ball, during a short time period (10–15seconds), and the procedure should be repeated four to five times on either side, starting on the right side. Never perform this procedure on both sides at the same time. It is advisable to auscultate the neck before proceeding with CSM. Caution should be taken in older people and in patients with a history of carotid sinus syndrome. The procedure must include continuous ECG recording and auscultation. A–E: examples of how different arrhythmias react to CSM.

Schematic illustration of several examples of Lewis (ladder) diagrams including: (A) the atrioventricular (AV) junction, (B) the AV and sinoatrial (SA) junctions, (C) a ventricular arrhythmogenic focus, and (D) a division of the AV junction in two parts (AH–HV).

Figure 14.2 Several examples of Lewis (ladder) diagrams including: (A) the atrioventricular (AV) junction, (B) the AV and sinoatrial (SA) junctions, (C) a ventricular arrhythmogenic focus, and (D) a division of the AV junction in two parts (AH–HV).

Image described in caption.

Figure 14.3 (A) (1) Normal atrioventricular (AV) conduction, (2) premature atrial impulse (complex) with aberrant conduction; (3) premature atrial impulse blocked at the AV junction; (4) sinus impulse with slow AV conduction that initiates an AV junctional reentrant tachycardia. (B) (1) Premature junctional impulse with an anterograde conduction slower than the retrograde; (2) premature junctional impulse sharing atrial depolarization with a sinus impulse (atrial fusion complex); (3) premature junctional impulse with exclusive anterograde conduction and, in this case, with aberrancy (see the two lines in the ventricular space); (4) premature junctional impulse concealed anterogradely and retrogradely; (5) premature atrial impulse leading to AV junctional reentrant tachycardia. (C) (1) Sinus impulse and premature ventricular impulse that cancel mutually at the AV junction; (2) premature ventricular impulse with retrograde conduction to the atria; (3) sinus impulse sharing ventricular depolarization with a premature ventricular impulse (ventricular fusion beat); (4) premature ventricular impulse triggering an AV junctional reentrant tachycardia. (D) Shows the way of the stimulus through the AV junction as per the diagram shown in Figure 14.2 A. The solid line shows the real way of the stimulus across the heart. In general, the dashed line is used instead, because it is the place at which the atrial and ventricular activity starts. Thus, the time that the stimulus spends to cross the AV junction, the most important information, is more visible. EF: ectopic focus.

We will now look at the specific mechanisms that initiate and perpetuate different arrhythmias. We will further discuss the triggering and/or modulating factors when we examine each particular arrhythmia in the following chapters.

Active arrhythmias may be related to the basal rhythm or occur independently. In the first case, the premature isolated P′ or QRS complex, or the first P′ wave or QRS complex in rapid rhythms, displays a fixed or nearly fixed coupling interval in the ECG. This is because the arrhythmia is initiated by a mechanism that depends on the previous basal rhythm. The coupling interval is defined as the time from the onset of the preceding QRS complex (if the active arrhythmia is a ventricular arrhythmia), or the P′ wave (if it is an atrial arrhythmia), to the beginning of the ectopic P′ or QRS complex (Figure 14.5A,B).

The active arrhythmias independent of the baseline rhythm are much less frequent. Usually they are isolated complexes of parasystolic origin and nearly always have a remarkable variable coupling interval (Figure 14.5C,D). These arrhythmias rarely occur as sustained tachycardias (see Chapter 16). We will now discuss the ECG features of these two types of active arrhythmias.

The different mechanisms of active arrhythmias are shown in Table 14.2.

Active arrhythmias with fixed coupling interval

Active arrhythmias appearing as isolated complexes or repetitive runs of several complexes (non‐sustained tachycardia) usually show a fixed coupling interval of the first complex (Figure 14.5A,B). Parasystolic active arrhythmias have a variable coupling interval of the first complex (see Active arrhythmias with variable coupling interval: the parasystole, below) (Figure 14.5C,D).

Abnormal generation of stimulus

Increased automaticity

Automaticity is the capacity of some cardiac cells (the automatic slow response cells present in the sinus node and to a lesser degree in the AV node) to not only excite themselves but also to produce stimuli that can propagate (Figure 14.6). Therefore, automatic cells excite themselves and produce stimuli that may propagate, whereas contractile cells are only excited by a stimulus from a neighboring cell, transmitting it to the nearest cell (domino effect theory) (see Figure 5.26). Under normal conditions, contractile cells are not automatic cells because they do not excite themselves.

Certain electrophysiologic characteristics of the automatic cells derive from the ionic currents responsible for the ascending slope of transmembrane diastolic potential (DP) (phase 4). In particular, the rapid inactivation during diastole of the outward K (Ip) current by the inward diastolic current If has an impact on heart rate (see Chapter 5). The most important characteristics are as follows:

Image described in caption.

Figure 14.4 Placement of atrial and ventricular waves within the atrial and ventricular spaces, as seen at first glance (A). Although at first glance we do not see two atrial P waves for each QRS, we presume that atrial waves are ectopic (negative in V4 and very fast) (see arrows), and double than the QRS complexes, one visible and the other hidden within the QRS. This is confirmed when we carefully check the bigeminal rhythm. Later on we joined the atrial and ventricular waves through the AV junction (B). These data come from a patient with cardiomyopathy and digitalis intoxication, showing an atrial rate of 150 bpm and a first ventricular rate of 75 bpm. Later on, they are shown as coupled bigeminal complexes. This is an example of ectopic atrial tachycardia with 2 × 1 AV block and later Wenckebach 3 × 2 AV block. The atrial waves are ectopic because their morphology differs from sinus P waves seen in previous ECG, and because there are very narrow (50 ms) and negative in V4. The digitalis intoxication explains the presence of AV block. The first, third, fifth, seventh, and ninth P′ waves conduct with long PR interval. The seventh QRS complex (7) is premature and starts a series of coupled complexes (bigeminal rhythm). This complex is probably not caused by the eleventh atrial wave, as the corresponding P′R lasts only 180 ms, whereas the other conducted atrial waves (P′), with the same coupling interval, show a P′R of 400 ms. Instead, the tenth atrial wave (P′) may be conducted with a P′R of 0,56; and therefore the eleventh P′ is not conducted. The sequence: P′R = 400 ms, P′R = 560 ms, P′ not conducted is afterward repeated, perpetuating the Wenckebach sequence where the twelfth and thirteenth P′ waves are conducted, whereas the fourteenth is not, etc.

Schematic illustrations of (A) ventricular extrasystole; (B) atrial extrasystole; (C) ventricular parasystole; (D) atrial parasystole.

Figure 14.5 (A) Ventricular extrasystole; (B) atrial extrasystole; (C) ventricular parasystole; (D) atrial parasystole (see text). All numbers are expressed in milliseconds.

Schematic illustration of sinus node transmembrane action potential (TAP) (A) transmitted to the atrioventricular (AV) junction (B), the ventricular Purkinje (C), and ventricular muscle (D).

Figure 14.6 Sinus node transmembrane action potential (TAP) (A) transmitted to the atrioventricular (AV) junction (B), the ventricular Purkinje (C), and ventricular muscle (D).

  • The rate of rise of DP (phase 4): the faster the rise, the faster the heart rate and vice versa (Figure 14.7A).
  • The level or threshold potential (TP): the lower heart (further from 0), the faster the heart rate and vice versa (Figure 14.7B).
  • The baseline level of the previous DP: the more negative (further from 0), the lower the heart rate and vice versa (Figure 14.7C).

The modifications of these three factors account, in general, for the increase or decrease of the heart automaticity (Figure 14.8). Under normal conditions, the sinus automaticity is transmitted to the AV node and then to the ventricle (see arrows in Figure 14.8), immediately after which these two structures depolarize.

Schematic illustration of factors influencing the increase of automaticity (broken lines). (A) Faster diastolic depolarization. (B) Threshold potential (TP) decrease. (C) Transmembrane diastolic potential (DP) less negative than normal.

Figure 14.7 Factors influencing the increase of automaticity (broken lines). (A) Faster diastolic depolarization. (B) Threshold potential (TP) decrease. (C) Transmembrane diastolic potential (DP) less negative than normal.

The top part of Figure 14.8 shows how the normal sinus automaticity (1 and 2) produces a transmembrane action potential (AP) capable of propagating itself (B1 and C1). If for any of the reasons previously mentioned, such as reduced rate of the DP rise (b and b′), a lower baseline DP level (c), or a TP level nearer 0 (d), the normal sinus automaticity (a) decreases, the AP curve will not form in time (Figure 14.8: continuous line 2) but later, decreasing the sinus automaticity (A: broken line 2b). On the other hand, through an opposite mechanism, the sinus automaticity will increase and AP generation will take less time. This happens in the case of increase of the phase 4 slope of the AV node or ventricular cells (Figure 14.8 Bh and Ci). The decrease of level of TP or an increase in baseline level of the previous DP, explains the occurrence of active arrhythmias due to an increased automaticity (Figures 14.7 and 14.8). The effect of all these phenomena on the ECG becomes evident with the presence of heart rate variations under sinus rhythm (sinus bradycardia and tachycardia) and the presence of premature or late supraventricular and ventricular QRS complexes (see right side of Figure 14.8, and legend).

At least 10% of paroxysmal supraventricular tachycardias, as well as some ventricular tachycardias and supraventricular and ventricular premature complexes (extrasystoles) with fixed or nearly fixed coupling intervals, are caused by increased automaticity. It has been found (Haïssaguerre et al

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Oct 9, 2021 | Posted by in CARDIOLOGY | Comments Off on Mechanisms, Classification, and Clinical Aspects of Arrhythmias

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