Arrhythmias and arrhythmology

Chapter 1: Mechanisms of cardiac arrhythmias: from automaticity to re-entry (reentry)

This section introduces the most common arrhythmias encountered in clinical practice, beginning with a discussion of the underlying mechanisms of cardiac arrhythmias. While a detailed understanding of these mechanisms is not essential for all clinicians, it is reasonable to acquire an understanding of the overarching concepts. Arrhythmogenesis (mechanisms of arrhythmias) is presented in this chapter, followed by in-depth discussions of specific arrhythmias in subsequent chapters.

Cardiac arrhythmias can be subdivided into the following categories:

Bradyarrhythmias (bradycardia): arrhythmias commonly due to dysfunctional automaticity in pacemaker cells or blocking of impulses somewhere along the conduction system.

Supraventricular tachyarrhythmias (tachycardia): rapid arrhythmias due to impulses originating from the atria.

Ventricular tachyarrhythmias (tachycardia): rapid arrhythmias due to impulses originating from the ventricles.

This classification facilitates the differential diagnosis and management of arrhythmias. Since the management of arrhythmias, particularly tachyarrhythmias, is often considered challenging, separate chapters are dedicated to their diagnosis and management. The recommendations presented throughout this section align with the guidelines issued by the European Society of Cardiology (ESC), the American Heart Association (AHA), and the American College of Cardiology (ACC).

Definition of heart rhythm

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

An arrhythmia is defined as an abnormal heart rhythm or heart rate, which is not physiologically justified. The latter criterion is important because rhythms that are physiologically justified should not be considered abnormal. For example, sinus bradycardia (a slow rhythm directed by the sinoatrial node) is a common finding in athletes and during sleep; in these scenarios, it should not be considered abnormal. On the other hand, sinus bradycardia developing during physical exercise is considered abnormal, because heart rate must increase during exercise.

Mechanisms of cardiac arrhythmias

The mechanisms underlying cardiac arrhythmias are being unraveled at an accelerating pace, making arrhythmology a field of intense research activity. This is partly due to the rise of cardiac imaging and invasive electrophysiological methods which allow for detailed in vivo studies of arrhythmias. However, this chapter focuses on clinical aspects of arrhythmology to provide readers with a solid understanding of common arrhythmias. Readers seeking an in-depth discussion on mechanisms are referred to Zipes et al.

Main causes of cardiac arrhythmias

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

Abnormal impulse formation

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

Increased or abnormal automaticity

Triggered activity

Increased or abnormal automaticity

As discussed in Chapter 1, several structures in the heart possess automaticity (i.e. the ability to depolarize spontaneously). These structures are as follows:

The sinoatrial (SA) node: the sinoatrial node is the primary pacemaker of the heart. It directs the heart rhythm during normal circumstances and the rhythm is referred to as sinus rhythm.

Parts of the atrial myocardium: There are clusters of atrial myocardial cells located around the crista terminalis, the entrance of the coronary sinus and the inferior vena cava, as well as cells around the mitral and tricuspid valves, which possess automaticity. These cells are not conduction cells per se; they are contractile cells possessing automaticity. Thus, automaticity is not exclusive to cells of the conduction system.

Myocardium surrounding the atrioventricular (AV) node: It is a common misconception that the atrioventricular (AV) node possesses automaticity, as there is no compelling evidence to support this claim. There is, however, evidence indicating that cell clusters surrounding the AV node possess automaticity. For the sake of simplicity, this automaticity will still—despite the clarification provided—be referred to as the automaticity of the AV node.

The His-Purkinje network: The bundle of His and the entire Purkinje network possess automaticity.

These are the natural pacemakers of the heart because these structures possess automaticity, which is the intrinsic ability to depolarize spontaneously without previous stimulation. The intrinsic rate of spontaneous depolarization in these pacemaker structures follows:

Sinoatrial node: 70 depolarizations per minute.

Atrial myocardium: 60 depolarizations per minute.

Cells around the atrioventricular node: 40 depolarizations per minute.

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

The sinoatrial node serves as the primary pacemaker of the heart simply because it possesses the fastest automaticity. Heart rhythm is governed by the fastest pacemaker, as it depolarizes before competing pacemakers, resetting their “clocks” before they can generate an action potential. Furthermore, automaticity gradually decreases with increasing distance from the sinoatrial node. This stepwise decline in automaticity is referred to as pacemaker hierarchy.

The sinoatrial node may become dysfunctional and fail to depolarize. This could potentially result in cardiac arrest but it rarely does, because the absence of sinoatrial impulses will allow for one of the other pacemakers to take over the heart rhythm. This behavior is the reason why other pacemakers are referred to as latent pacemakers. Any rhythm that replaces the sinus rhythm is referred to as an escape rhythm. In case the sinoatrial node is dysfunctional, an escape rhythm will most likely come from atrial myocardium, because it has the second-highest rate of spontaneous depolarization. If the atrial myocardium also fails to generate action potentials, an escape rhythm will likely come from cells around the atrioventricular node, and so on. Note that the ventricular myocardium does not normally possess automaticity.

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

Automaticity in the sinoatrial node can increase without physiological motivation and cause sinus tachycardia at rest. This is called inappropriate sinus tachycardia.

The automaticity in latent pacemakers can increase, for example, during hypoxia, whereby they start discharging action potentials at a higher rate than the sinoatrial node and thus take over the heart rhythm.

Purkinje cells located around the ischemic zone during acute myocardial ischemia/infarction can increase their automaticity and initiate ventricular tachycardia.

As mentioned above, ventricular myocardium does not possess automaticity, and neither does the vast majority of atrial myocardium. However, during pathological circumstances, even these cells may start discharging action potentials.

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

Triggered activity (after-depolarizations)

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

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

Importantly, after-depolarizations may cause extrasystoles but they do not cause persistent arrhythmias. However, the extrasystoles might induce another arrhythmia mechanism (re-entry, see below) which may cause persistent arrhythmias.

Figure 1. Late and early depolarizations trigger action potentials.

Abnormal impulse conduction: re-entry (reentry)

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

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

Figure 2. Re-entry phenomenon.

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

The prerequisites for re-entry have been noted in Figure 2. A brief explanation is repeated:

A pathway of electrically connected myocardium must exist, forming a closed circuit through which an electrical impulse can propagate repeatedly. Any cardiac cell capable of generating an action potential may participate in this circuit, which can range in size from a few millimeters to several decimeters in diameter.

It is essential that the myocardial cells within the circuit exhibit varying capacities for conducting electrical impulses. This variability, arising from differences in refractoriness, conductivity, and/or excitability, results in a block of the incoming impulse.

The circuit must surround a central core of tissue that is incapable of being depolarized, creating a “central block.” This non-depolarizable core may consist of necrotic myocardium, fibrotic scar tissue, or anatomical structures such as the fibrous rings of the cardiac valves.

Re-entry is subdivided into functional and anatomical. Knowledge of this distinction is not crucial for clinical practice.

Anatomical re-entry

The explanations outlined above actually apply to anatomical re-entry. In this type of re-entry, the central blocking consists of distinct anatomical structures. For example, atrial flutter (a re-entry tachyarrhythmia) arises when the impulse circles around the tricuspid valve. In that scenario, the valve is the central blocking structure (valvular tissue cannot be depolarized) and the circuit incorporates myocardium surrounding the valve.

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

Functional re-entry

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

Functional re-entry circuits are small, unstable and may engender additional re-entry circuits. Functional re-entry is fundamental for the development of atrial and ventricular fibrillation.

Clinical significance

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

Termination of re-entry

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

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Chapter 2: Aberrant ventricular conduction (aberrancy, aberration)

Aberrant conduction is not a mechanism of arrhythmia; it is a ventricular conduction disturbance. It is discussed in this chapter because the phenomenon is frequently observed during arrhythmias. As previously discussed, all cardiac cells—both conduction and contractile cells—must undergo rapid repolarization to ensure they are excitable when the next action potential occurs. If any component of the ventricular conduction system has not fully repolarized by the time the next impulse reaches the ventricles, the impulse will be blocked at that point. The length of the refractory period (see Basic Cardiac Electrophysiology) varies with heart rate. The length is shortened as heart rate increases and vice versa. Thus, long cycles (i.e. long RR intervals) are associated with long refractory periods and short RR intervals have shorter refractory periods. Aberrant conduction occurs when the length of the cardiac cycle is changed without a compensatory change in the length of the refractory period. This is explained by the changes in the refractoriness in the His-Purkinje system related to changes in the RR interval.

Figure 1 shows a premature atrial beat causing aberrant ventricular conduction. A premature atrial beat is simply an extra (unexpected) beat discharged by an ectopic focus in the atria. The impulse from the premature beat reaches the His-Purkinje system early, while some fibers are still refractory. In this case (Figure 1) it encounters a refractory right bundle branch and therefore the impulse is conducted with right bundle branch block morphology. This is an example of how changes in the length of the cardiac cycle causes aberration.

Figure 1. The figure shows a supraventricular extrasystole (i.e a premature atrial complex/beat) which is conducted with aberration. The supraventricular impulse reaches the His-Purkinje system while the right bundle branch is still refractory and therefore blocks the impulse. The resulting QRS complex has a right bundle branch block morphology (rSR pattern), which is due to aberrant ventricular conduction (aberration, aberrancy).

In clinical practice aberration is commonly seen in patients with atrial fibrillation because these patients have rapid and irregular rhythms with frequently changing RR intervals. Refer to Figure 2.

Figure 2. Ashman’s phenomenon.

Aberrancy can occur in three different situations, all related to changes in cardiac cycle length. These situations are as follows:

Premature ventricular depolarization: As exemplified in Figure 1, if the atrial impulse reaches the ventricular His-Purkinje system too early – while conduction fibers are still refractory – the impulse might be blocked. This is a frequent finding among healthy individuals and in those with heart disease. If such aberration occurs at normal heart rate (<100 beats/min) it is most likely to have a right bundle branch block morphology. If the aberration occurs during higher heart rates, it is more likely that the QRS complex will have a left bundle branch block morphology. However, left bundle branch block morphology is more common (regardless of heart rate) among persons with heart disease. Alternating block (right and left bundle branch block alternating from one beat to another) is uncommon.

Ashman’s phenomenon: This type of aberration occurs when the RR interval is first prolonged and then shortened. The initial prolongation increases the length of the refractory period and the subsequent early impulse will therefore encounter refractory fibers. Thus, Ashman’s phenomenon requires a long RR interval followed by a short RR interval (Figure 2). These aberrantly conducted beats typically have right bundle branch block morphology.

Sudden acceleration in heart rate: If the heart rate accelerates suddenly, the bundle branches may not be able to accommodate (i.e shorten) their refractory periods appropriately. The aberration may persist if the heart rate stabilizes at a high rate, but it usually resolves as the His-Purkinje system manages to adapt its refractory period. If the acceleration occurs at low heart rates, the aberrantly conducted beat will exhibit right bundle branch morphology. If the rate accelerates at higher heart rates, it will typically exhibit a left bundle branch block morphology.

The majority of all aberrantly conducted beats have right bundle branch block morphology. This is due to the longer refractory period of the right bundle branch at normal heart rates. Aberration may also occur in either of the fascicles (anterior or posterior fascicle of the left bundle branch). Left bundle branch morphology at normal heart rate suggests underlying heart disease.

Differentiating aberration from premature ventricular complexes

Aberrantly conducted beats may be difficult to differentiate from premature ventricular beats but it is mostly possible to differentiate these entities. In Figure 1 a P-wave is visible before the aberrantly conducted beat and this assures a supraventricular origin of the impulse and the wide QRS complex is therefore due to aberration. Premature ventricular complexes are not preceded by P-waves (other than by randomness). Premature ventricular complexes are, however, more common than aberrantly conducted beats. Aberrantly conducted beats display typical bundle branch block morphology, which premature ventricular complexes do not. Aberrantly conducted beats are not followed by a full compensatory pause (discussed later), which premature ventricular beats are.

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Chapter 3: Premature ventricular contractions (premature ventricular complex, premature ventricular beats)

Premature ventricular complexes are also referred to as premature ventricular beats, premature ventricular contractions or just ventricular beats/contractions/complexes. These terms will be used interchangeably in this discussion.

A premature ventricular complex is recognized on the ECG as an abnormal and wide QRS complex occurring earlier than expected in the cardiac cycle. It is caused by an impulse discharged from an ectopic focus which may be located anywhere in the ventricles. The ectopic impulse depolarizes the ventricles; because the impulse is discharged in the ventricles it will spread partly or entirely outside of the conduction system and thus produce a wide QRS complex (QRS duration ≥0.12 s). Refer to Figure 1 for an example.

The premature ventricular impulse replaces a sinus beat and induces a delay to the next sinus beat (the RR interval is increased after a premature ventricular complex). This yields more time to fill the ventricles with blood (increased ventricular filling). The person with premature beats might perceive this as palpitations, because of the stronger ventricular contractions caused by the increased filling.

Ventricular premature complexes are not preceded by P-waves because the ectopic impulse originates in the ventricles and does not influence the atria (with exceptions discussed below).

Although premature ventricular contractions are mostly harmless, they may trigger sustained ventricular tachyarrhythmias. This will also be discussed later.

Figure 1. Premature ventricular contraction (complex/beat). Typical appearance. Note the paper speed 50 mm/s (1 large box equals 100 ms).

The impulse discharged from an ectopic focus in the ventricles will spread abnormally (because the impulse did not enter the ventricles through the bundle of His). Abnormal depolarization will consequently lead to abnormal repolarization. This explains the secondary ST-T changes seen on premature ventricular complexes; the ST-T vector will be directed oppositely to the QRS vector. As seen in Figure 1 the premature ventricular complex displays a positive QRS complex followed by a negative ST-T segment. Thus, the ST-T segment is directed oppositely to the QRS (this is called discordant ST-T segment).

Ventricular premature contractions and the complete compensatory pause

A premature ventricular contraction is followed by a complete compensatory pause which means that the next sinus beat will occur on schedule. The interval between the sinus beats occurring before and after the premature beat will be two sinus cycles (2 RR intervals). This is explained by the fact that the premature ventricular impulse does not discharge and reset the sinoatrial node, which will therefore continue on schedule. Refer to Figure 2.

Figure 2. The complete compensatory pause following a premature ventricular contraction.

Classification of premature ventricular contractions

When every other beat on the ECG is a premature ventricular complex (PVC), the rhythm is referred to as PVC in bigeminy (Figure 3). If every third beat is a PVC, it is referred to as PVC in trigeminy. Similarly, there can be quadrigeminy and so on.

Figure 3. Premature ventricular contractions in bigeminy.

Two consecutive premature ventricular contractions are referred to as a pair or couplet. If 3 to 30 premature ventricular contractions occur consecutively, it is referred to as non-sustained ventricular tachycardia (if the rate is >100 beats/min) or ventricular rhythm (if the rate is <100 beats/min). If more than 30 consecutive beats are premature ventricular contractions it is referred to as sustained ventricular tachycardia if the rate is >100 beats/min.

Premature ventricular complexes discharged by the same ectopic focus will typically have similar morphology (appearance) and constant timing. Such premature ventricular complexes are referred to as monomorphic (or unifocal). This is exemplified in Figure 3.

Polymorphic premature ventricular complexes display constant timing but varying morphology. These beats typically originate in the same ectopic focus but the spread of the impulse (from that ectopic focus) varies from one beat to another (Figure 4).

Figure 4. Polymorphic premature ventricular complexes (contractions).

Multifocal premature ventricular complexes have varying morphology and varying timing. These beats are discharged by several ectopic foci in the ventricles (Figure 5).

Figure 5. Multifocal premature ventricular contractions.

It is also possible to determine where the ectopic focus is located by assessing the morphology of the premature beat in lead V1. If the morphology in lead V1 is similar to a right bundle branch block (i.e predominantly positive), the ectopic focus is located in the left ventricles. If the morphology in lead V1 is similar to a left bundle branch block (i.e predominantly negative), the ectopic focus is located in the right ventricles.

Fusion beats

If a normal atrial impulse is conducted to the ventricles approximately simultaneously as a premature ventricular impulse is discharged, the ventricles might be depolarized by both these impulses. This typically occurs if the premature ventricular impulse is discharged late, around the time of the normal sinus impulse. The morphology resulting QRS complex will resemble a combination (a fusion) of the normal beat and the PVC. Refer to Figure 6.

Figure 6. Fusion beat.

Exceptions from complete compensatory pause

Although the complete compensatory pause is very typical of the premature ventricular complex (PVC), there are instances where it does not occur.

Interpolated PVC: If a PVC occurs early after a normal beat, the atrioventricular conduction system might have repolarized by the time the next sinus impulse is discharged (this impulse is usually not conducted to the ventricles due to refractoriness in the atrioventricular conduction system), whereby the atrial impulse will reach the ventricles and depolarize them. This is called an interpolated PVC and it appears on the ECG as a PVC occurring between two sinus beats and there are no beats replaced and no pause.

Retrograde atrial activation: Occasionally the ventricular impulse may be conducted backwards through the bundle of His into the atria and depolarize both the atria and the sinoatrial node. This resets the clock of the sinoatrial node. The next sinus beat will occur one sinus cycle after resetting the sinoatrial node. The pause will be less than compensatory and the retrograde P-wave is often visible on the ST-T-segment.

Ventricular echo: This is a rare phenomenon in which the impulse from the PVC is conducted through the atrioventricular node and there it circulates back to the ventricles which are activated again. This yields a couplet with less than compensatory pause.

Clinical relevance of premature ventricular contractions

Premature ventricular contractions are common among both healthy individuals and there is robust evidence that do not affect long-term cardiovascular prognosis among those individuals. Premature ventricular complexes are even more common among individuals with heart disease. Premature ventricular complexes can be debilitating, even for healthy individuals.

Healthy persons

Almost 30% of all healthy individuals display premature ventricular contractions during exercise stress testing. Male sex, stress, nervousness, tobacco, coffee, hypokalemia, infection, alcohol, sleep deprivation and certain drugs are associated with increased occurrence of premature ventricular beats. Moreover, the frequency of premature beats increases with age.

Healthy individuals might display premature ventricular complexes on ECG during screening. It may be symptomatic or asymptomatic. Palpitations and the feeling that the heart “skips a beat” are common symptoms. Chest or throat discomfort is less common.

A few premature ventricular contractions daily in otherwise healthy individuals are considered benign and do not affect cardiovascular prognosis. However, if ventricular premature beats make up a significant proportion of all heartbeats during the day, the situation is more problematic. If >15% of all beats are premature ventricular beats there is a risk of PVC-induced cardiomyopathy and left ventricular dysfunction. In such cases it is wise to refer to patient for invasive examination; it is often possible to eliminate the ectopic focus (foci) using ablation therapy. This can also reverse established cardiomyopathy.

Persons with heart disease

Premature ventricular beats are common among those with heart disease. The frequency of premature beats is increased in a wide range of conditions, such as ischemic (coronary) heart disease. These individuals are generally more affected by premature beats, as they already have compromised cardiac function. Because premature ventricular beats have ineffective ventricular contraction, it can reduce cardiac output and thus cause deterioration of ischemic heart disease and heart failure.

R-on-T phenomenon

R-on-T phenomenon has been discussed here.

Treatment of premature ventricular contractions

Underlying heart disease must be ruled out among persons without previously known heart disease. The procedure must be individualized and guided by ECG, anamnesis and findings from physical examination. Rather few otherwise healthy individuals necessitate treatment. Among those with heart disease, the proclivity to treat should be higher. Before treatment is instigated, it is important to analyze potassium and magnesium levels because hypokalemia and hypomagnesemia may cause PVCs and these causes are reversible.

Treatment is instigated if (1) symptoms are significant, (2) of PVCs make up a significant portion of all beats during the day (examined with Holter-ECG), or (3) if the PVCs have a negative hemodynamic effect. The first choice of drug is beta-blockers (bisoprolol 5–10 mg once daily or sustained-release metoprolol 50–100 mg once daily). However, beta-blockers are often insufficient and symptoms may persist. Class I antiarrhythmic drugs can be tried, as can amiodarone. One should have invasive treatment with ablation in mind.

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Chapter 4: Premature atrial contraction (premature atrial beat / complex): ECG and clinical implications

A premature atrial contraction is produced by an impulse discharged from an ectopic focus located anywhere in the atria. In most cases, the premature atrial impulse is conducted to the ventricles, which results in ventricular depolarization and the appearance of a QRS complex. Because the impulse originates in the atria it will pass through the bundle of His and therefore produce a normal QRS complex (provided that intraventricular conduction is normal).

A premature atrial contraction induces a delay to the next sinus beat (the RR interval is prolonged after a premature beat). This yields more time to fill the ventricles with blood (increased ventricular filling). Persons with premature beats might perceive this as palpitations, because of the stronger ventricular contractions caused by the increased filling. Frequent premature beats can also be perceived as having an irregular heart rhythm (despite the underlying sinus rhythm).

Although atrial premature beats are harmless, they can trigger sustained supraventricular tachyarrhythmias (e.g. atrial fibrillation, AVNRT, AVRT, etc.).

Premature atrial contraction on ECG

A premature atrial contraction occurs when an ectopic focus in the atria discharges before the next sinus impulse. The premature impulse may depolarize the atria and subsequently, the ventricles, provided that the myocardium and conduction system have repolarized. This appears as a P-wave and QRS complex occurring earlier than expected (Figure 1). The interval from the premature beat to the next sinus beat will be longer than one normal sinus interval.

The P-wave of a premature atrial contraction has the following characteristics (Figure 1):

A premature P-wave occurs earlier than the sinus P-wave was expected.

A premature P-wave has a different morphology (appearance), as compared with the sinus P-wave. The appearance depends on the location of the ectopic focus from which the impulse is discharged. If the impulse is discharged close to the sinoatrial node, the P-wave will be similar to the normal P-wave. If the impulse is discharged near the atrioventricular node, the atria will be depolarized in the opposite direction and thus generate a negative (retrograde) P-wave (Figure 2). Thus, the P-wave morphology of premature atrial beats differs from the sinus P-wave. Note that the P-wave might occur on the preceding T-wave if it is discharged very early.

The PR interval is normal in most cases but might be prolonged. Most premature atrial complexes are conducted through the atrioventricular node to the ventricles. The PR interval will typically be normal but can be prolonged if the premature beat reaches the atrioventricular node before it has repolarized completely. The earlier the impulse reaches the atrioventricular node (and bundle of His), the longer the PR interval (because more fibers will be refractory). If the premature atrial impulse reaches the atrioventricular node (or bundle of His) while it is completely refractory, the impulse will be blocked and no QRS complex appears.

Figure 1. Typical premature atrial contraction.

Figure 2. Atrial premature beat with retrograde P-wave.

The QRS complex appears if the atrial impulse is conducted to the ventricles. Because the impulse enters the ventricles through the bundle of His (which means that both bundle branches will conduct the impulse to each respective ventricle) the QRS complex is normal (i.e QRS duration <0.12 s). However, the QRS complex can be wide (QRS duration ≥0.12 s) if there is a left or right bundle branch block. Commonly, the premature atrial impulse arrives before one of the bundle branches has repolarized, which leads to a bundle branch block. This type of bundle branch block is termed aberration (or aberrant ventricular conduction), which was discussed previously. Figure 3 shows how a premature atrial contraction is conducted aberrantly.

Figure 3. Atrial premature beat conducted with right bundle branch block.

Incomplete compensatory pause

A premature atrial contraction will most likely also depolarize the sinoatrial node and reset its clock. It will usually take some time for the impulse to travel from the ectopic focus to the sinoatrial node. Once the impulse has reset the sinoatrial node, the next sinus impulse will be discharged one normal sinus period from that time point. Hence, the interval between the premature beat and the next sinus beat will be equal to the time it takes for the impulse to travel to the sinoatrial node plus one sinus period. As evident in Figure 4, this means that the sinus beat after the premature beat will also occur earlier than expected (because the sinus node was discharged earlier than expected). The term incomplete compensatory pause implies that the interval between the sinus beats before and after the premature beat is less than two sinus periods (Figure 4).

Figure 4. Premature atrial beat with incomplete compensatory pause.

A compensatory pause implies that the sinus beat after the premature beat occurs on schedule, such that there are two sinus cycles (2 RR intervals) between the beats before and after the premature beat. This is the hallmark of ventricular premature beats.

Variants of premature atrial contractions

Should the premature atrial impulse reach the atrioventricular node or bundle of His before these have repolarized sufficiently, the impulse will be blocked. Only the P-wave will appear on the ECG and it may be superimposed on the preceding T-wave (Figure 5).

Figure 5. Premature atrial beat blocked in the atrioventricular node or bundle of His.

Occasionally the premature atrial impulse affects the sinoatrial node such that it requires some additional time to recover. This prolongs the interval from the premature beat to the next sinus beat. The next sinus beat might actually occur where it would be expected (i.e after a compensatory pause) or even later.

Similarly, if the premature atrial impulse fails to reset the sinoatrial node, the next sinus impulse will occur on schedule and activate the atria (if the atria have repolarized after the premature contraction). Hence, the premature atrial contraction will occur between two sinus beats (1 RR interval between the sinus beats), and this is referred to as an interpolated premature atrial beat.

If every other beat is an atrial premature contraction, it is called atrial bigeminy (Figure 6). If every third beat is an atrial premature contraction it is called atrial trigeminy. Similarly, there is quadrigeminy and so forth.

Figure 6. Atrial premature contractions in bigeminy.

Clinical relevance

Premature atrial contractions are very common, both among healthy individuals and those with significant heart disease. The prevalence of premature atrial beats increases with age. It is considered normal to have a few premature atrial complexes per day. And the frequency increases during emotional stress, by drinking coffee and smoking. Premature atrial beats are more common among persons with heart disease, particularly conditions affecting the atria.

Note that if premature atrial beats are discharged frequently during rapid sinus rhythm or sinus tachycardia, it may resemble atrial fibrillation, which is why one should always look carefully for P-waves (which are not visible during atrial fibrillation).

Treatment of premature atrial contractions

Premature atrial contractions are only treated if the individual is symptomatic or if the beats precipitate tachyarrhythmias. Beta-blockers (usually bisoprolol tablets 5–10 mg once daily) or calcium channel blockers are the most effective alternatives.

Final note

A premature beat can also be referred to as an early beat, extrasystole, ectopic beat (because the impulse is discharged from an ectopic focus) or premature contraction. These terms are also used for premature impulses arising in the ventricles (discussed in the next article).

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Chapter 5: Sinus rhythm: physiology, ECG criteria & clinical implications

A rhythm is defined as three consecutive heartbeats with identical waveforms on the ECG. The similarity of the waveforms indicates that the origin of the impulse is the same. The sinoatrial (SA) node is the heart’s pacemaker under normal circumstances and the rhythm is referred to as sinus rhythm. Hence, sinus rhythm is the normal rhythm of the heart. The physiology of the SA node and pacemaker cells in the heart have been discussed previously.

Definition (criteria) for sinus rhythm

Regular rhythm with a ventricular rate between 50 and 100 beats/min.

P-wave with constant morphology preceding every QRS complex.

The P-wave is positive in lead II.

Figure 1 (below) shows normal sinus rhythm at a paper speed of 25 mm/s.

Figure 1. Sinus rhythm. Paper speed 25 mm/s.

Figure 2 (below) shows the same ECG at 50 mm/s.

Figure 2. Sinus rhythm. Paper speed 50 mm/s.

Manual calculation of heart rate

At 25 mm/s paper speed, the heart rate is equal to 300 divided by the number of large boxes between two beats (for simplicity, use the distance between two R waves). As seen in Figure 2, there are 5 large boxes between two R waves, hence the heart rate is:

300/5 = 60 beats/min

At 50 mm/s paper speed, the heart rate is equal to 600 divided by the number of large boxes between two beats. As seen in Figure 2, there are 10 large boxes between two R waves:

600/10 = 60 beats/min.

Refer to Figure 3 for clarification.

Figure 3. Manual calculation of heart rate.

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Chapter 6: Sinus arrhythmia (respiratory sinus arrhythmia)

Sinus arrhythmia and respiratory sinus arrhythmia both refer to the same phenomenon. Sinus arrhythmia fulfill all criteria for sinus rhythm except from the fact that the rhythm is slightly irregular (Figure 1). This is mostly a normal (physiological) finding, particularly among young and healthy individuals. The phenomenon is explained by the heart rate variation caused by respiration. The heart rate increases during inspiration due to diminished vagal tone. And the opposite, i.e the heart rate decreases during expiration due to increased vagal tone. This causes the slightly irregular rhythm seen in Figure 1. The rhythm becomes completely regular if the person holds the breath.

However, sinus arrhythmia may be a pathological finding in some cases. Sinus arrhythmia is not a normal finding among older individuals. In that scenario it might be explained by myocardial ischemia (affecting the sinoatrial node), sinus node dysfunction or side effects of digoxin treatment. If the rhythm becomes completely regular when holding the breath, it is likely that the arrhythmia is benign; otherwise further examination is warranted.

Figure 1. Sinus arrhythmia (respiratory sinus arrhythmia).

Treatment of sinus arrhythmia

Sinus arrhythmia is a normal finding among young and healthy individuals. It is generally not a normal finding among older individuals and might necessitate further examination. If it is caused by underlying heart disease (e.g. myocardial ischemia), the treatment is directed at that process.

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Chapter 7: Sinus bradycardia: definitions, ECG, causes and management

Definition of sinus bradycardia

Sinus bradycardia fulfills the criteria for sinus rhythm but the heart rate is slower than 50 beats per minute. ECG criteria follow:

Regular rhythm with a ventricular rate slower than 50 beats per minute.

P-waves with constant morphology preceding every QRS complex.

P-wave is positive in limb lead II.

Normal (physiological) causes of sinus bradycardia

Sinus bradycardia (SB) is considered a normal finding in the following circumstances:

During sleep.

Well-trained individuals display SB at rest due to high vagal tone. These individuals have developed a highly efficient left ventricle, capable of generating sufficient cardiac output at low heart rates.

During vasovagal syncope (e.g during intense emotional stress)

During vagal maneuvers (Valsalva maneuver, carotid sinus [baroreceptor] stimulation).

It is common to discover SB in healthy young individuals who are not well-trained. This is also a normal finding.

Abnormal (pathological) causes of sinus bradycardia

In all other situations, sinus bradycardia should be regarded as a pathological finding. Numerous pathological conditions cause sinus bradycardia. The most important causes are as follows:

Myocardial ischemia/infarction – Particularly ischemia or infarction located to the inferior wall of the left ventricle. This type of bradycardia is due to diminished automaticity (pacemaker function) in the sinoatrial node or conduction defects (e.g. second-degree AV block) as a result of ischemia/infarction.

Sinus Node Dysfunction (SND) – Sinus node dysfunction implies that the cells of the sinoatrial node are defective and fail to generate electrical impulses.

Side effects of drugs (notably beta blockers, digitalis, verapamil, diltiazem, amiodarone, clonidine) – These drugs affect the pacemaker cells in the sinoatrial node. They may also induce conduction defects (e.g. AV block).

Increased intracranial pressure (manifests with sinus bradycardia and hypertension).

Hypothyroidism.

Hypothermia.

Hyperkalemia.

ECG example of sinus bradycardia

Figure 1 shows sinus bradycardia at a paper speed of 25 mm/s.

Figure 1. Sinus bradycardia. Paper speed 25 mm/s. Calculate the rate by dividing 300 by the number of large boxes between two cycles (e.g. between two R waves). As seen in the figure, there are approximately 6.5 large boxes between two R waves. 300/6.5 equals 46 beats/min. Click to zoom.

Figure 2. Sinus bradycardia, two premature ventricular contractions, incomplete right bundle branch block and ST-segment depressions in V2-V6. Click to zoom.

Figure 3. Sinus bradycardia. The small q-waves in inferior leads (II, aVF, III) are not significant. Low voltage in limb leads. Click to zoom.

Figure 4. Sinus bradycardia. Click to zoom.

Treatment of sinus bradycardia

Benign causes of sinus bradycardia (e.g. vasovagal reaction, well-trained athletes) do not require treatment. When benign causes are unlikely, it is necessary to identify reversible causes, to direct targeted interventions toward them. A permanent pacemaker is generally indicated when reversible causes are absent and the patient is symptomatic or at risk of developing symptoms.

The most common non-reversible causes of sinus bradycardia are sinus node dysfunction, side effects of medications and acute myocardial infarction.

Holter ECG is useful to determine the frequency, severity and situational dependence of sinus bradycardia. If sinus bradycardia is likely due to drug side effects, it is necessary to weigh the risk of terminating the medication as compared with implanting a permanent pacemaker and continuing the treatment. Commonly, patients with bradycardia have a strong indication for drugs that aggravate or cause bradycardia (e.g. beta-blockers in heart failure). In such scenarios, it is very common to provide the patient with a permanent pacemaker to continue optimal medical treatment.

Sick sinus syndrome (sinus node dysfunction), a common cause of bradycardia, is also discussed separately.

Algorithm for acute management of bradycardia

Treatment of acute bradycardia is discussed in the following chapter:

Management of bradycardia (bradyarrhythmia)

Please refer to the chapter referenced above for details. In summary, acute bradycardia is managed as follows:

Terminate or adjust any medications that cause or aggravate the bradycardia.

If bradycardia causes hemodynamic effects (reduced cardiac output or hypotension), the following algorithm is used:

Prepare an external pacing device (e.g. a defibrillator with a pacing function and position the electrodes in the anterior-posterior position. Prepare to administer a sedative (e.g. midazolam) or analgesic (e.g. morphine) during transcutaneous pacing.

Immediately give 1 mg atropine iv. Repeat up to 3 mg.

If atropine is insufficient, start infusion of isoproterenol. An ampoule with 5 ml (0,2 mg/ml) isoproterenol is mixed with 245 ml glucose (50 mg/ml) with a starting dose of 0,01 μg/kg/min. This is titrated until an adequate effect is achieved.

Transcutaneous pacing (external pacing) is started if atropine and isoproterenol fail. Transcutaneous pacing is indicated until a temporary transvenous pacemaker can be implanted.

Patients with bradycardia due to myocardial ischemia or infarction only require treatment if cardiac output is reduced or if the bradycardia predisposes to malign ventricular arrhythmias (the algorithm above applies to this situation as well). However, bradycardia due to inferior wall ischemia or infarction is mostly transient and rarely necessitates a permanent pacemaker. Bradycardia due to anterior wall infarction, however, is mostly permanent and requires a pacemaker.

Permanent (long-term) treatment of bradycardia

Permanent symptomatic bradycardias are treated with pacemakers.

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Chapter 8: Chronotropic incompetence (inability to increase heart rate)

Chronotropic incompetence is an independent predictor of overall and cardiovascular mortality. The condition is very common among individuals with heart failure. Notably, beta-blockers actually increase chronotropic competency in patients with heart failure, despite their negative chronotropic effect. Among persons who do not suffer from heart failure, chronotropic incompetence may be caused by beta-blockers, amiodarone or digitalis. Sinus node dysfunction (SND) is a common cause of chronotropic incompetence.

Definition of chronotropic incompetence: the age expected maximal heart rate

Chronotropic incompetence is defined as failure to reach 80% of the expected maximum heart rate (age-adjusted). To determine this it is necessary to perform an exercise stress test, during which it is fundamentally important that the patient performs maximally. Only two variables are needed to determine whether chronotropic incompetence exists, namely age and heart rate. The following equation is used:

Figure 1. Maximum heart rate equation.

The numerator is the achieved increase in heart rate and the denominator is the expected increase in heart rate (220 – age estimates the age-adjusted max heart). Thus, the formula yields how large (%) the increase in heart rate was in relation to the expected increase. The cut-off for chronotropic incompetence is 80% (i.e less than  80% diagnoses chronotropic incompetence)

Management of chronotropic incompetence

Treatment of chronotropic incompetence and other bradyarrhythmias are discussed in the chapter Treatment of bradyarrhythmias.

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Chapter 9: Sinoatrial arrest & sinoatrial pause (sinus pause / arrest)

A sinoatrial arrest occurs when the sinoatrial node does not discharge an impulse for ≥2 seconds. Failure to discharge an impulse within <2 seconds is defined as a sinoatrial pause. Refer to Figure 1.

Figure 1. Sinoatrial arrest. Also note the ST-segment elevations (which in this case have no relation to the sinoatrial arrest).

As discussed in Chapter 1, if the sinoatrial node fails to discharge an impulse, three latent pacemaker structures can discharge impulses that will salvage the situation. Latent pacemakers can continue discharging impulses until the sinoatrial node recovers and starts discharging. Less than 3 consecutive beats (or from a latent pacemaker (or any other ectopic focus) are referred to as escape beats. Three or more consecutive beats from a latent pacemaker (or other ectopic focus) are referred to as an escape rhythm.

In most cases, the escape rhythm originates in either of the following three structures (discussed in detail in Chapter 1):

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 atrioventricular node 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 a junctional rhythm.

The His-Purkinje network: All these fibers possess automaticity with an intrinsic rate of depolarization of around 20–40 beats/min. If the impulses are discharged 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 is 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.

Adam-Stokes attack

Syncope due to sinus arrest is referred to as Adam-Stokes attack.

Causes of sinoatrial arrest/pause

High vagal tone is benign and the most common cause of sinus arrest/pause. It commonly affects younger individuals who endure intense emotional stress, acute pain or other stimuli that increases vagal tone. In all other situations, sinus arrest/pause should be considered abnormal, and the following differential diagnoses are at hand:

Sinus node dysfunction.

Side effects of drugs (diltiazem, verapamil, beta-blockers, digitalis).

Hypoxia.

Myocardial ischemia/infarction.

Hyperkalemia.

Treatment of sinoatrial arrest/pause

Sinus arrest/pause due to increased vagal tone does not necessitate treatment but it might be wise to observe the patient for 24 hours (including ECG monitoring). In all other situations, the underlying condition should be targeted and, if necessary, bradycardia should be treated (treatment alternatives are discussed in the article on sinus node dysfunction).

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Chapter 10: Sinoatrial block (SA block): ECG criteria, causes and clinical features

Sinoatrial (SA) block implies that the impulses discharged in the sinoatrial node are either not conducted to the atria or are so with a delay. This manifests with loss of P-waves (loss of atrial activation) and consequently loss of QRS complexes (loss of ventricular depolarization).

Sinoatrial blocks are subdivided into three degrees according to the nature of the block. The nature of these blocks is very similar to the atrioventricular (AV) blocks. Importantly, first-degree sinoatrial block and third-degree sinoatrial block cannot be diagnosed using surface ECG (i.e. ECG recorded on the body surface). This is because the electrical potentials generated by the sinoatrial node are much too small to be detected on the surface ECG. Intracardiac electrodes – with the placement of electrodes against the sinoatrial node – are necessary to diagnose first- and third-degree sinoatrial block. However, a second-degree sinoatrial block may be diagnosed using conventional ECG.

Causes of sinoatrial (SA) block

The following conditions cause sinoatrial block:

Sinus node dysfunction (SND)

Perimyocarditis

Acute myocardial infarction (or ischemia)

Drug side effects (procainamide, digitalis)

Well-trained athletes display sinoatrial block as a physiological and normal finding.

First-degree sinoatrial (SA) block

First-degree sinoatrial block implies that the time interval from the discharge of the impulse in the sinoatrial node to the onset of atrial depolarization is prolonged. As seen in Figure 1 this merely entails that the distance between the sinus impulse and P-wave is increased and this cannot be discerned from the surface ECG (because discharge of the impulse in the sinoatrial node is not noticeable on surface ECG).

Figure 1. Upper tracing shows normal impulse conduction from the sinoatrial node to the atria. Atrial activation commences almost immediately after discharge of the impulse in the sinoatrial node. Lower tracing shows first-degree sinoatrial block, in which the time interval from impulse discharge to atrial activation is prolonged and this cannot be discerned on the surface ECG. As seen here, the rhythm is still regular and all complexes appear normal.

Second-degree sinoatrial (SA) block

Second-degree sinoatrial block is further subdivided into type 1 and type 2. The block, in both types, may be regular, temporary, or intermittent.

Second-degree sinoatrial (SA) block type 1 (Wenckebach block)

In type 1 second-degree sinoatrial block there is a delay in the conduction from the sinoatrial node to the atrium and this delay increases gradually until one impulse is completely blocked and a loss of P-wave occurs. The P-P interval is gradually decreased. The ensuing pause is twice as long as the cardiac cycle preceding the block. The P-P interval after the pause is longer than the P-P interval before the pause. Refer to Figure 2 (below). This type of block, where there is a gradual exhausting of the conduction before it is completely blocked, is referred to as Wenckebach phenomenon (also referred to as Wenckebach periodicity).

Figure 2. Type 1 second-degree sinoatrial block.

Second-degree sinoatrial (SA) block type 2

In type 2 second-degree sinoatrial block impulses are blocked sporadically (without any Wenckebach phenomenon). The pauses between the visible beats are always multiples of the normal P-P interval (Figure 3). Typically, there will be 2 to 4 P-P intervals between the beats (implying that one, two or three sinus impulses are blocked). This is illustrated in Figure 3 (below).

Figure 3. Several cases of type 2 second-degree sinoatrial block.

Third-degree sinoatrial (SA) block

Third-degree sinoatrial block implies that no impulses are conducted from the sinoatrial node to the atrium. Hence, the maintenance of cardiac rhythm (and thus life) will depend on the awakening of a latent pacemaker. Studies clearly show that a latent pacemaker will virtually always awake, such that the mortality in third-degree sinoatrial block is very low. The salvaging rhythm is referred to as an escape rhythm and it is likely to arise in the atrial myocardium (specific clusters of myocardium with automaticity), the junctional area (near the atrioventricular node), or in the His-Purkinje network (in that order). Refer to Figure 4. However, third-degree sinoatrial block cannot be discerned from surface ECG.

Figure 4. Third-degree sinoatrial block.

Management and treatment of sinoatrial (SA) block

Sinoatrial blocks may cause bradycardia. Evidence shows that the bradycardia and the sinoatrial block itself do not convey any significant increase in mortality. However, a sinoatrial block may compromise cardiac output and cause symptoms or worsen symptoms. Symptomatic sinoatrial block is therefore frequently treated with a permanent pacemaker. Treatment alternatives are discussed in the article on sinus node dysfunction.

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Chapter 11: Sinus node dysfunction (SND) and sick sinus syndrome (SSS)

Sinus node dysfunction and sick sinus syndrome

Sinus node dysfunction is an umbrella term for conditions that either affect the automaticity of the sinoatrial node or block the impulse from reaching the atria. Disturbed automaticity and blocked impulses lead to arrhythmias that characterize sinus node dysfunction. The conditions encircled by the term sinus node dysfunction are as follows:

Sinus bradycardia (which in its purest form means that the automaticity is diminished).

Chronotropic incompetence (inability of the sinoatrial node to adequately increase its automaticity during physical activity).

Sinus arrest & sinus pause (intermittent failures to discharge impulses).

Sinoatrial block (delayed or blocked impulse conduction between the sinoatrial node and the atrium).

All these conditions have been discussed in detail in the previous articles.

Hence, sinus node dysfunction may manifest with any of the four abovementioned conditions. The majority of patients will experience symptoms, although some cases are asymptomatic. Symptomatic patients typically experience fatigue, dizziness, dyspnea, presyncope/syncope, or diminished exercise tolerance. Whenever such symptoms are associated with ECG evidence of sinus node dysfunction, the condition is referred to as sick sinus syndrome.

Causes of sinus node dysfunction

The causes have been discussed in each respective article. A rehearsal follows.

Reversible causes of sinus node dysfunction

Age-related degenerative disease (development of fibrosis) of the sinoatrial node.

Myocardial ischemia/infarction.

Perimyocarditis.

Drug side effects (diltiazem, verapamil, beta-blockers, digitalis, amiodarone, clonidine, procainamide).

Hypoxia (hypoxemia)

Hyperkalemia.

Hyperthermia

Increased intracranial pressure

Irreversible causes of sinus node dysfunction

Age-related degenerative disease (fibrosis)

Myocardial ischemia/infarction

Lesions due to heart surgery

Myocarditis

Collagen disease

Amyloidosis

Risk of supraventricular tachyarrhythmia (tachycardia)

Sinus node dysfunction is also associated with a high risk of developing supraventricular tachyarrhythmias, especially atrial fibrillation and atrial flutter. The condition in which sinus node dysfunction is accompanied by supraventricular tachyarrhythmia is referred to as tachy-brady syndrome, because these individuals are affected by bradycardia as well as tachycardia.

Treatment of sick sinus syndrome and bradycardia in general

Sick sinus syndrome is, if caused by irreversible conditions, a progressive disease that necessitates treatment. Implementation of an external artificial pacemaker is an effective treatment. In cthe ase of concomitant tachyarrhythmia, the pacemaker allows for adequate (high) dosing of rate-controlling drugs (e.g beta-blockers) without the risk of worsening the bradycardia.

Persons with sick sinus syndrome should receive an artificial pacemaker to reduce symptoms and increase function. However, it should be noted that any bradycardia originating in the sinoatrial node is unlikely to lead to premature death. Moreover, it is still debated whether the transient periods of atrial standstill in sinus bradycardia are associated with an increased risk of thromboembolism.

Pacemaker treatment is discussed in a separate article.

Treatment of bradycardia (due to any cause)

Benign (physiological) causes of bradycardia (e.g. vasovagal reaction, well-trained athletes) need not be treated. When in doubt whether the bradycardia is physiological, it is useful to perform a Holter ECG (ambulatory recording). If drug side effects are believed to be the cause, it is fundamental to weigh the risk of terminating drug therapy as compared with implementing an artificial pacemaker in order to be able to continue drug therapy. It is very common that patients with bradycardia have a strong indication for drugs that aggravate or even cause the bradycardia; in such scenarios, it is generally considered to be evidence-based to implement an artificial pacemaker that will allow for drug therapy to continue.

Bradycardia (of any cause) may be treated according to the following algorithm:

Terminate or adjust any medications that cause or aggravate the bradycardia.

In case of acute bradycardia with circulatory compromise: (1) 1–2 ml of atropine 0.5 mg/ml is the first-line therapy. It can be repeated if necessary. (2) If atropine is insufficient or requires too frequent dosing, infusion isoproterenol should be given. An ampoule with 5 ml (0,2 mg/ml) isoproterenol is mixed with 245 ml glucose (50 mg/ml) with a starting dose of 0,01 μg/kg/min. This is titrated up until adequate effect is achieved. (3) If atropine and isoproterenol fail, it might be necessary to perform transcutaneous pacing (external pacing. Most modern defibrillators are equipped with the ability to perform transcutaneous pacing. Transcutaneous pacing is only indicated until a permanent pacemaker can be implemented. (4) An alternative to transcutaneous pacing is temporary transvenous pacing, which is also indicated until a permanent pacemaker can be implemented.

Permanent treatment: Permanent symptomatic bradycardias are treated with artificial pacemakers. Patients with chronotropic incompetence may require a pacemaker to increase exercise capacity and reduce symptoms. Patients with tachy-brady syndrome may also necessitate rate-controlling drugs (e.g. beta-blockers) and anticoagulation (if atrial fibrillation or flutter can be verified).

Patients with bradycardia due to myocardial ischemia/infarction only demand treatment if cardiac output is compromised or if the bradycardia predisposes to more malign arrhythmias (the algorithm above applies to this situation as well).

Note, however, that bradycardias due to inferior wall ischemia/infarction is transient in most cases and rarely necessitatesa permanent pacemaker. Anterior wall infarctions, on the other hand, generally leave permanent bradycardia and thus demand permanent pacemakers. Learn more about conduction defects caused by ischemia and infarction.

(none)

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Chapter 12: Sinus tachycardia & Inappropriate sinus tachycardia

Sinus tachycardia is the most common tachyarrhythmia (tachycardia). Sinus tachycardia is the result of an increased rate of depolarization (i.e increased automaticity) in the sinoatrial node. This simply means that the sinoatrial node discharges electrical impulses at a higher frequency than normal. Similar to sinus rhythm, the rhythm is regular with a positive P-wave in lead II, but the heart rate exceeds 100 beats per minute.

Although sinus tachycardia is the most common tachyarrhythmia, it may not always be straightforward to diagnose on the ECG. Moreover, many clinicians remain uncertain about the implications of sinus tachycardia. A crucial task is to distinguish three types of sinus tachycardia. These types differ fundamentally in terms of pathophysiology, prognosis, and treatment. The types of sinus tachycardia are as follows:

Normal (physiologic) sinus tachycardia: The automaticity (rate of spontaneous depolarization) in the sinoatrial node is increased during physical activity, stress, and nervousness. This is due to altered tone in the autonomic nervous system, with increased sympathetic input (leading to stimulation of beta-adrenergic receptors) and parasympathetic withdrawal.

Sinus tachycardia secondary to disease and medications: A wide range of diseases and medications may cause sinus tachycardia; e.g congestive heart failure, lung disease (e.g COPD), fever, infections, anemia, myocardial ischemia/infarction, pulmonary embolism, pheochromocytoma, hyperthyroidism, hypovolemia, pharmacological substances (alcohol, amphetamine, coffee, anticholinergic drugs, beta-adrenergic agonists). In all of these conditions, sinus tachycardia is merely an expression of an underlying disease or substance effect, which may require attention. Therefore, management of sinus tachycardia always requires that each of these causes be assessed thoroughly, as many of the causes require prompt treatment.

Inappropriate sinus tachycardia: When all the abovementioned causes have been ruled out and the sinus tachycardia persists without any known cause, it may be classified as inappropriate sinus tachycardia. This diagnosis can only be established after all other causes have been ruled out. Inappropriate sinus tachycardia is presumably more common than previously thought and the condition may hamper the quality of life substantially.

The management of sinus tachycardia is aimed at finding secondary causes that can be treated or, when no cause can be found, establishing a diagnosis of inappropriate sinus tachycardia. Although there are no evidence-based treatments for inappropriate sinus tachycardia, patients frequently benefit from obtaining a diagnosis, because it justifies their symptoms (treatment alternatives are discussed below).

ECG in sinus tachycardia

Sinus tachycardia fulfills all criteria for sinus rhythm but the heart rate is faster than 100 beats per minute. Thus, the ECG criteria for sinus tachycardia follow.

ECG criteria for sinus tachycardia

Regular rhythm with ventricular rate >100 beats per minute.

P-wave with constant morphology preceding every QRS complex.

The P-wave is positive in lead II.

Figure 1. ECG showing sinus tachycardia. Paper speed 25 mm/s. Calculate the heart rate by dividing 300 by the number of large boxes between R-waves. There are approximately 3 large boxes between the R-waves; 300/3 equals 100 beats per minute.

ECG characteristics of sinus tachycardia

Note that at heart rates above 140 beats per minute, it may be difficult to discern the P-waves from the previous T-wave, particularly if the paper speed is 25 mm/s (using 50 mm/s may be advised). Always search carefully for the P-wave as it may be very discrete and only cause an irregularity of the contour of the T-wave. Finding the P-wave is a requirement for establishing a diagnosis of sinus tachycardia.

On the contrary to many paroxysmal supraventricular tachyarrhythmias (e.g AVNRT, AVRT, or atrial tachycardia), sinus tachycardia has a gradual onset and the patient can often report that the palpitations accelerated gradually. Note that the mode of onset (abrupt vs. gradual) is an important piece in the puzzle to determine which type of arrhythmia a patient suffers from. Abrupt onset suggests that the tachyarrhythmia is AVNRT, AVRT, atrial tachycardia, atrial flutter or atrial fibrillation. It may, however, also be a special form of sinus tachycardia referred to as SANRT (discussed below).

Long-standing sinus tachycardia may lead to ST-segment depressions on the ECG. Such ST-segment depressions may be seen anywhere but most commonly in leads V3, V4, V5 and V6. The ST-segment tends to be either horizontal or upsloping. Long-standing sinus tachycardia may also cause diminished T-wave amplitude on the ECG. This occurs in the same leads that display ST-segment depressions. These ST-segment depressions and diminished T-wave amplitude should disappear rapidly (within minutes) after the sinus tachycardia has resolved. Otherwise, one must suspect other causes of ST-segment depression (e.g. acute myocardial ischemia).

Sinus tachycardia with strong sympathetic activation has a bathmotropic effect on the conduction system. This implies that the speed of impulse conduction is increased. Therefore, the PR interval may be slightly (but not significantly) reduced. Long-standing and rapid sinus tachycardia, on the other hand, may exhaust the atrioventricular node and bring about a slowing of conduction that prolongs the PR interval (again, not significantly).

Maximum heart rate

It is often difficult to differentiate sinus tachycardia from other supraventricular tachycardias (e.g. atrial flutter, AVNRT etc). Many of these tachycardias have a tendency to present themselves with a particular heart rate. There is an age-dependent upper limit for the impulse frequency of the sinoatrial node. The maximal discharge rate in the sinoatrial node diminishes with age (due to diminishing sensitivity to catecholamines). Hence, using the individual expected maximum sinus rate may help differentiate sinus tachycardia from other arrhythmias. Any tachycardia with a rate faster than the age-expected maximum rate is probably not sinus tachycardia.

The maximum discharge rate in the sinoatrial node is estimated using the following formulas:

Formula 1: Estimation of maximal heart rate in relation to age and sex.

Note that at maximal exercise capacity, the sinus rate may be somewhat higher than the formula estimate. Also note the third formula, which is necessary to estimate a maximum frequency in patients using beta-blockers (which diminish the discharge frequency of the sinoatrial node).

Normal range for sinus rhythm

The lower limit of sinus tachycardia is 100 beats per minute and this is an arbitrary and questioned figure. The main reason for this is that observational studies (both retrospective and prospective) and randomized controlled clinical trials have shown that the association between heart rate and mortality is linear, and mortality increases gradually at heart rates above 60 beats per minute. Moreover, studies in recent years show that resting heart rate is a strong predictor of overall and cardiovascular mortality.

Inappropriate sinus tachycardia

Inappropriate sinus tachycardia is a condition where sinus tachycardia is present at rest and the sinus rate is usually excessively high during physical activity. The condition has been recognized for more than seven decades but many clinicians are still unaware of it. A large body of science suggests that inappropriate sinus tachycardia is caused by increased automaticity in the sinoatrial node. The cause of the increased automaticity, however, remains elusive. Theories suggest hypersensitivity to catecholamines, disturbance in the autonomic nervous system, etc. Inappropriate sinus tachycardia may only be diagnosed when all other causes of sinus tachycardia have been ruled out.

Patients with sinus tachycardia present with a resting heart rate above 100 beats per minute. They also tend to have an excessive increase in heart rate during all sorts of physical activity. Their heart rate during sleep is higher than the average individual. For some unexplained reason women, particularly health care workers, are overrepresented. Pre-syncope, syncope, chest discomfort, dyspnea, anxiety and fatigue are also common symptoms.

No clear evidence points to any increased mortality in inappropriate sinus tachycardia. This is somewhat unexpected given that tachycardia is a well-known risk factor for cardiomyopathy (tachycardia-induced cardiomyopathy). It is not unlikely that individuals with inappropriate sinus tachycardia will be at greater risk of cardiovascular disease but the evidence is yet lacking.

Management of high resting heart rate and inappropriate sinus tachycardia (IST)

Non-pharmacological Interventions

First-line management includes lifestyle modifications:

Avoidance of stimulants (e.g., caffeine, nicotine, alcohol).

Regular aerobic exercise to improve autonomic balance.

Adequate hydration and increased salt intake to support plasma volume.

Use of compression garments and elevating the head of the bed to mitigate orthostatic symptoms .

Pharmacological therapy

Beta-blockers: Agents like bisoprolol (5–10 mg once daily) are commonly used but may have limited efficacy and tolerability due to side effects such as fatigue and hypotension.

Ivabradine: A selective If current inhibitor that reduces heart rate without affecting blood pressure or myocardial contractility. Studies have shown its effectiveness in IST patients, particularly those intolerant to beta-blockers.

Calcium channel blockers: Non-dihydropyridine agents (e.g., verapamil) may be considered, though evidence for their efficacy in IST is limited.

Interventional approaches

Catheter ablation targeting the sinus node has been attempted in refractory cases. However, this approach carries significant risks, including the potential need for permanent pacemaker implantation, and is generally reserved for patients with debilitating symptoms unresponsive to medical therapy.

Sinoatrial nodal re-entrant tachycardia (SANRT)

Sinoatrial nodal re-entrant tachycardia (SANRT) is caused by a re-entry circuit in or by the sinoatrial node. It is recognized on the ECG (typically requires ECG monitoring for a longer period) as abruptly starting sinus tachycardia. Normal sinus tachycardia does not start abruptly, but rather gradually. The P-wave in SANRT is identical to the sinus P-wave. Other terms used for this condition are sinus node reentry or sinus node reentrant tachycardia.

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Chapter 13: Atrial fibrillation: ECG, classification, causes, risk factors & management

Atrial fibrillation is the most common abnormal tachyarrhythmia (only sinus tachycardia is more common). The prevalence of atrial fibrillation correlates strongly with age. Approximately 10% of individuals aged 80 years and above have atrial fibrillation, whereas the arrhythmia is unusual among persons younger than 50 years of age. The overall prevalence in a Western population is 1.0% to 1.5%. The crude prevalence is lower in non-Western countries, primarily due to the younger age-composition in those countries (adjusted prevalence figures are scarce). Indeed, the strongest risk factor for developing atrial fibrillation is age. Other significant risk factors are as follows: male sex, hypertension, left ventricular hypertrophy, left ventricular dysfunction, valve disease, coronary artery disease, cardiomyopathy, congestive heart failure, congenital heart disease, diabetes mellitus (both type 1 and type 2), obesity, smoking, obstructive sleep apnea and chronic obstructive pulmonary disease (COPD). Moreover, certain other tachyarrhythmias predispose to developing atrial fibrillation: atrial flutter, AVNRT and AVRT (pre-excitation, WPW syndrome) being the most common.

Atrial fibrillation with onset during hyperthyroidism (thyrotoxicosis), alcohol overdose, thoracic surgery, acute myocardial infarction, pericarditis/myocarditis or pulmonary embolism is often a reversible arrhythmia with low risk of recurrence. Atrial fibrillation in other circumstances (particularly those listed above) is usually a progressive disease.

Complications of atrial fibrillation and available treatments

In multivariable models (i.e statistical models in which adjustment has been made for confounders) individuals with atrial fibrillation are at five times increased risk of stroke and two times increased mortality, as compared with individuals without atrial fibrillation. The increased risk of stroke is explained by formation of thrombi in the left atrial appendage. Such thrombi may leave the appendage and enter the systemic circulation which causes thromboembolic occlusions of arteries in the brain, limbs or other organs. However, the increased risk in mortality is not completely explained by the increased risk of stroke; people with atrial fibrillation are at increased risk of cardiovascular mortality in general. This is not surprising given the adverse effects of long periods of tachycardia and desynchronized atrial and ventricular activity.

Fortunately, the treatment of atrial fibrillation has come a long way. Treatment with anticoagulation is highly effective in reducing stroke risk. Wrfarin and novel oral anticoagulants can reduce the risk of stroke by 70%, as compared with placebo. Besides anticoagulation, atrial fibrillation is treated with rate and/or rhythm control. Rate control implies the use of medications that slow ventricular rate (beta-blockers being the mainstay of this therapy). Rate control does not affect the rhythm per se. Rhythm control, on the other hand, attempts to restore sinus rhythm by use of antiarrhythmic drugs. Randomized controlled trials have not demonstrated any clear difference in mortality when comparing rate and rhythm control. However, rhythm control conveys risks (most antiarrhythmic drugs have a pro-arrhythmic effect as well), which is why clinicians mostly choose rate control. Both rate and rhythm control reduce morbidity, and mortality and improve quality of life. These approaches are discussed further below.

Symptoms of atrial fibrillation

Approximately 25% of all individuals with atrial fibrillation are asymptomatic (they have no symptoms). In such individuals, screening with ECG may reveal atrial fibrillation. Unfortunately, atrial fibrillation is too often discovered first at hospital admission due to its complications (stroke, thromboembolism, heart failure, dyspnea). Most individuals, however, do experience symptoms and they do so before developing complications. Symptoms such as palpitations, dyspnea, fatigue, chest/throat discomfort, and impaired exercise capacity are common and may all coexist. Dizziness is also common. Syncope, however, is uncommon. If a patient with atrial fibrillation experiences episodes of syncope or even pre-syncope, one must suspect tachy-brady syndrome, which implies that there is concomitant sinus node dysfunction. Atrial fibrillation debuting with congestive heart failure is uncommon among persons with previously normal left ventricular function.

Note that the tachyarrhythmia symptoms of atrial fibrillation (palpitations, chest discomfort, etc) occur abruptly. and patients typically report that the palpitations started suddenly.

ECG in atrial fibrillation

Examples of atrial fibrillation. Click to zoom.

The hallmark of atrial fibrillation is the absence of P-waves and an irregularly irregular (i.e completely irregular) ventricular rate. The baseline (isoelectric line between QRS complexes) is characterized by either fibrillatory waves (f-waves) or just minute oscillations. Fibrillatory waves are small with varying morphology and high frequency (300 to 600 waves per minute). The amplitude of f-waves may vary from small to large. Large f-waves must not be mistaken for flutter waves (F-waves) which are seen in atrial flutter. It is, luckily, easy to distinguish these two because f-waves always show varying morphology whereas flutter waves are more or less identical (f-waves also have higher frequency than flutter waves). Figures 1 and 2 show ECG examples of atrial fibrillation.

Figure 2. Atrial fibrillation without visible f-waves. Instead, there are minute oscillations of the baseline.

The ventricular rate is completely irregular, typically in the range of 100 to 180 beats per minute. Patient age, current medications, and concomitant AV blocks modify the ventricular rate. Atrial fibrillation with very rapid ventricular rate may appear as a regular rhythm (which is yet another reason to switch from 25 mm/s to 50 mm/s paper speed), which is why it is important to carefully measure the regularity of the rhythm. Refer to ECG in Figure 3. When in doubt, it is generally safe to apply carotid massage, which increases vagal activity to the atrioventricular node and thus increases blocking in the atrioventricular node; this lowers the ventricular rate and makes the irregularity more clear.

Figure 3. Rapid atrial fibrillation.

Atrial fibrillation and Ashman’s phenomenon

Atrial fibrillation does not affect the morphology of the QRS complex, provided that intraventricular conduction is normal. However, Ashman’s phenomenon is frequently seen in atrial fibrillation. Ashman’s phenomenon is a special type of aberrant ventricular conduction, in which a bundle branch block occurs as a result of an abrupt change in the length of the cardiac cycle. The ECG below shows an example of Ashman’s phenomenon.

Figure 4. ECG showing Ashman’s phenomenon during atrial fibrillation.

Figure 5. Example of 12-lead ECG with atrial fibrillation. Paper speed: 25 mm/s.

Classification of atrial fibrillation

Atrial fibrillation is classified according to the duration of the arrhythmia.

First diagnosed atrial fibrillation: Atrial fibrillation that has not been diagnosed before, irrespective of its duration and symptoms.

Paroxysmal atrial fibrillation: Paroxysmal atrial fibrillation with duration less than 7 days. The arrhythmia is self-terminating in the vast majority of cases and it typically lasts less than 48 hours.

Persistent atrial fibrillation: lasts more than 7 days and generally requires intervention to be terminated.

Long-standing persistent atrial fibrillation: continuous atrial fibrillation lasting more than 12 months.

Permanent atrial fibrillation refers to a situation where both the patient and clinician have agreed to accept the condition, typically after numerous attempts to induce cardioversion, and have discontinued efforts to restore sinus rhythm. This decision may be revisited if the patient and clinician wish to make another attempt to restore sinus rhythm.

Whether the arrhythmia converts to sinus rhythm spontaneously or through cardioversion (electrical or pharmacological) does not affect the classification. However, electrical and pharmacological cardioversion does limit the natural duration of the arrhythmia and may therefore affect the classification.

Atrial fibrillation is typically a progressive disease that usually evolves towards permanent atrial fibrillation. This is generally a stepwise process in which persons with paroxysmal atrial fibrillation tend to have an increasing number of episodes until the arrhythmia is persistent. Once persistent, the number of episodes with persistent atrial fibrillation tends to increase until the arrhythmia is long-standing persistent. It should be noted, however, that some patients have paroxysmal or persistent atrial fibrillation throughout their disease course, while others never return to sinus rhythm after a first diagnosis.

Treatment with ablation is only meaningful in paroxysmal or persistent atrial fibrillation. Treatment with anticoagulants, rate control, or rhythm control should be considered in all types of atrial fibrillation.

Other types of atrial fibrillation

The term lone atrial fibrillation is used to describe a patient younger than 60 years of age, who does not have any other concomitant heart diseases or risk factors, and whose echocardiographic examination is normal. This type of atrial fibrillation has a good prognosis and generally does not require anticoagulation therapy.

The terms “valvular” and “non-valvular” atrial fibrillation are used to distinguish whether the atrial fibrillation is potentially secondary to valvular disease. This distinction has therapeutic implications, as valvular atrial fibrillation is significantly more challenging to convert to sinus rhythm. Attempting to cardiovert valvular atrial fibrillation is generally not considered effective, as most cases relapse into atrial fibrillation shortly after cardioversion, if the procedure is successful at all.

Arrhythmias associated with atrial fibrillation

Patients with atrial fibrillation frequently present with atrial flutter and/or atrial tachycardia. Individuals with pre-excitation (Wolff-Parkinson-White syndrome) are at high risk of developing atrial fibrillation. Some studies suggest that up to 30% of patients with clinically overt pre-excitation develop atrial fibrillation.

Mechanisms: atrial fibrillation begets atrial fibrillation

A large body of evidence demonstrates that atrial fibrillation in itself causes hemodynamic and electrophysiological changes in the myocardium which lead to increased susceptibility to new episodes of atrial fibrillation. Frequent and long-standing episodes of atrial fibrillation can thus create the prerequisites necessary for new episodes to emerge. These changes are illustrated in Figure 5. Ultimately, the anatomic and electrophysiological changes will lead to permanent atrial fibrillation (as explained below).

Figure 5. Flow chart showing the development of atrial fibrillation and how it promotes continued fibrillatory activity.

Electrophysiological mechanisms of atrial fibrillation

The short story

The anatomic and electrophysiological mechanisms causing atrial fibrillation are still under investigation. The underlying mechanisms are somewhat complicated (discussed in detail below). For those not interested in electrocardiology, it is sufficient to know that atrial fibrillation is caused by electrical chaos in the atria. The chaos is due to the simultaneous existence of multiple re-entry circuits that generate impulse waves that propagate through the atria. These impulse waves collide with each other and with refractory cells, which fragments the waves and causes additional chaos. Interested readers may continue to read the detailed explanation of this.

The long story

Atrial fibrillation is dependent on two mechanisms: a trigger and a driver. The trigger is the event that initiates the atrial fibrillation and the driver is the mechanism that will maintain the arrhythmia. The atria in individuals who develop atrial fibrillation display electrophysiological and anatomical properties that promote triggers and drivers. Aging, the strongest risk factor of atrial fibrillation, leads to degeneration of the myocardium and conduction cells. Other risk factors, such as structural heart disease (cardiomyopathy, heart failure, valvular disease), ischemic heart disease, pulmonary disease, genetic predisposition, autonomic dysfunction, etc, are other risk factors that promote triggers and drivers. Studies unambiguously show that most triggers and drivers arise from the pulmonary veins that empty oxygenated blood into the left atrium.

The transition between pulmonary veins and atrial myocardium appears to be electrically vulnerable and studies show that the majority of patients with paroxysmal atrial fibrillation have a trigger by a pulmonary vein. The trigger is composed of an ectopic focus which discharges impulses at a high rate. These impulses may induce short bursts of atrial fibrillation but unless a driver is established, the fibrillation will cease once the trigger stops discharging impulses. A driver may be established if the impulses spreading from the trigger encounter myocardium with varying conductivity or excitability. When the impulse encounters an area with varying conductivity/excitability, re-entry may arise due to blocking of the impulse. New impulse waves will spread from the re-entry and these waves may collide with other impulse waves and either be terminated or encounter new blocks which fragment the impulse. Fragmentation of the impulse will cause its remnants to spread in a random fashion through the atria. To sum up, paroxysmal atrial fibrillation is initiated by a trigger that discharges impulses at high frequency; impulses may encounter myocardium with heterogeneous or varying conductivity/excitability which may act as a block that gives rise to re-entry circuits. These re-entry circuits beget additional re-entry circuits.

Early phases of atrial fibrillation (i.e paroxysmal and newly diagnosed atrial fibrillation) are characterized by featuring one or a few ectopic foci. Such focus or foci can be localized and eliminated by means of ablation therapy. This is generally a cure for atrial fibrillation because elimination of the trigger will remove the initial cause. However, the number of ectopic foci and the number of generated re-entry circuits increase gradually as time goes and this correlates strongly with progression to persistent and long-standing persistent atrial fibrillation. For the same reason, ablation therapy is less effective in persons with persistent or long-standing persistent atrial fibrillation.

The explanation for the fact that the number of ectopic foci and re-entry circuits increase is because the atrial fibrillation (and the risk factors accompanying it) induce electrophysiological and anatomical changes in the atria and these changes promote triggers and drivers. This gradual evolution of atrial myocardium is referred to as atrial remodeling. The degree of atrial remodeling correlates strongly with the number of episodes of atrial fibrillation. Among the changes in the atria are, for example, changes in the expression and function of ion channels (particularly calcium channels) and the development of fibrosis. Ultimately the functional and anatomical structure of the atria becomes so remodeled that the atrial fibrillation becomes permanent.

Besides the pulmonary veins, ectopic foci may be located by the entry of the superior vena cava, inferior vena cava, the coronary sinus, and the attachment of Marshall’s vein.

The autonomic nervous system appears to have an important role in inducing paroxysmal atrial fibrillation. One-third of all individuals with paroxysmal atrial fibrillation experience their episodes in situations with high vagal activity (during sleep, at rest, or high sympathetic activity (during exercise, stress, etc). The autonomic nervous system modifies the action potentials in the atrial myocardium, particularly around the pulmonary veins. However, the autonomic innervation of the atria is not homogenous (the spread of autonomic fibers in the atria varies) which means that the effect on the action potentials is also not homogenous and this promotes atrial fibrillation.

Although atrial fibrillation is triggered by an ectopic focus in most cases, it may also be triggered by other arrhythmias such as AVRT or atrial flutter or even bradycardia. The latter (bradycardia) is believed to cause atrial fibrillation because at low heart rates, ectopic focuses may come to express themselves when they are not suppressed by the sinoatrial node.

Examination of atrial fibrillation

Atrial fibrillation is confirmed through various electrocardiographic methods, including resting ECG, Holter ECG, and event recorder. Holter ECG is particularly useful for assessing the frequency and duration of arrhythmia episodes, including asymptomatic episodes. The diagnostic criteria for atrial fibrillation based on electrocardiographic findings are as follows:

Atrial fibrillation present throughout the entire 12-lead resting ECG recording.

Atrial fibrillation lasting more than 30 seconds on Holter ECG or event recorder.

If coronary artery disease is suspected, myocardial perfusion imaging (SPECT or PET) or coronary CT angiography should be considered.

The following blood tests should be conducted for all patients: hemoglobin, sodium, potassium, creatinine, estimated glomerular filtration rate (eGFR), calcium, liver enzymes, PK-INR, APTT, lipid profile, glucose, HbA1c, thyroid-stimulating hormone (TSH), and T4 levels.

Echocardiography is recommended for all patients with newly diagnosed atrial fibrillation.

NT-pro-BNP levels may be measured if heart failure is suspected.

Management of atrial fibrillation

Treatment of acute atrial fibrillation

• Avoid attempting cardioversion in patients with severely compromised left ventricular ejection fraction. Converting to sinus rhythm in such patients can lead to a lower heart rate and a significant reduction in cardiac output, potentially resulting in cardiogenic shock.• For patients not on anticoagulants or those receiving sub-therapeutic doses, previous guidelines recommended a 48-hour window for attempting cardioversion. However, in 2024, the European Society of Cardiology (ESC) revised this recommendation, shortening the window to a maximum of 24 hours for attempting cardioversion.

Approximately 60% of cases of acute atrial fibrillation will convert spontaneously to sinus rhythm within 16 hours from the onset of symptoms. If there are no signs of circulatory compromise one may expect the situation for 24 hours (counting from symptom onset) until cardioversion is attempted. If one plans performing cardioversion it must be done within 24 hours from symptom onset. Cardioversion is contraindicated after 24 hours due to the high risk of thromboembolism (unless a transesophageal echocardiogram can be performed to rule out thrombus formation in the atria (left atrial appendage). Electrical cardioversion is the most effective method, yielding a success rate of >90% with biphasic shock ≥120 J. Pharmacological cardioversion (flecainide, propafenone, ibutilide, amiodarone, vernakalant) is less effective (approximately 75% success rate) and these antiarrhythmic drugs may cause arrhythmias as well as circulatory compromise due to negative inotropic effect. Nevertheless, in any arrhythmia, electrical cardioversion is the safest treatment alternative.

Repeated administration of intravenous beta-blockers, digoxin or calcium channel blockers may be needed to lower ventricular rate. It is wise to start with beta-blockers and then, if beta-blockers are insufficient, administer digoxin.

One must immediately address whether the patient is in need of anticoagulants, and most patients should be admitted with a dose of low-molecular-weight heparin (LMWH) until a decision has been made regarding anticoagulation.

Long-term treatment of atrial fibrillation

Rate control of atrial fibrillation (control of ventricular rate)

The rapid ventricular rate during atrial fibrillation is one of the main causes of the increased mortality observed in individuals with atrial fibrillation. Rate control implies that the ventricular rate is the treatment target. The aim is to slow the ventricular rate as much as possible without provoking excessive bradycardia. Rate control is accomplished with medications that affect the AV node; more specifically these drugs slow conduction through the AV node and this results in fewer atrial impulses being conducted to the ventricles. Beta-blockers (propranolol, metoprolol, atenolol, esmolol, nadolol), calcium channel blockers (diltiazem, verapamil) and digoxin (digitalis) are excellent choices to lower ventricular rate. Sotalol is reserved for cardiologists, as it has pro-arrhythmic effects as well. Rate control is not inferior to rhythm control in terms of survival. Aiming at a ventricular rate below 100 beats per minute can be recommended. Details on medications and dosages follow in Table 1.

Rate control of atrial fibrillation: medications that slow conduction through the AV node

MEDICATION	ADVANTAGES	DISADVANTAGES	DOSAGE	ONSET OF ACTION	ELIMINATION HALF-LIFE
BETA-BLOCKERS
Propranolol	Rapid onset of effect, short durations of effect for IV forms; heart rate control at rest and with activity; oral forms available with varying durations of effect	May worsen heart failure in decompensated patient; may exacerbate reactive airway diseases; may cause fatigue, depression; abrupt withdrawal may cause rebound tachycardia, hypertension	• IV: 1 mg given as bolus, repeat q5min as needed to achieve goal• Oral: 10-30 mg/dose q6-8hr	• IV: onset of action within 5 min• Oral: onset of action within 1-2 hr	• IV: duration of effect is 30-60 min• Oral: 3-5 hr
Metoprolol	Same as propranolol.	Same as propranolol.	• IV: 2.5-5 mg over 2-3 min, repeat q5min as needed to achieve goal• Oral: 12.5-100 mg/dose q6-8hr• Sustained-release preparations available for once-daily dosing	• IV: onset of action within 5 min• Oral: onset of action within 1-2 hr	• IV: duration of effect is 30-60 min• Oral: 3-6 hr
Atenolol	Same as propranolol.	Same as propranolol.	• IV: 5 mg over 5 min, repeat q10min to achieve goal• Oral: 25-100 mg/dose q8-12hr	• IV: onset of action within 5 min• Oral: onset of action within 1-2 hr	• IV: duration of effect is 30-60 min• Oral: 6-9 hr
Esmolol (intravenous only)	Same as propranolol.	Same as propranolol.	• IV: 500 µg/kg over 1 min, then maintenance dose of 25-300 µg/kg/min; titrate by 25-50 µg/kg/min q5-10min to achieve goal	• IV: onset of action within 5 min	N/A
Nadolol (oral only)	Same as propranolol.	Same as propranolol.	• Oral: 40-80 mg daily initially; increase to 240-320 mg daily as needed to achieve goal; can be given once daily	• Oral: onset of action within 1-2 hr	14-24 hr
CALCIUM CHANNEL BLOCKERS
Diltiazem	Same as for beta blockers	May worsen heart failure in decompensated patient; may cause fatigue; abrupt withdrawal may cause rebound tachycardia, hypertension	• IV: 0.25 mg/kg over 2 min, then infusion at 5-15 mg/hr for up to 24 hr; repeat bolus of 0.35 mg/kg may be necessary• Oral: 30-120 mg/dose q6-8hr; sustained-release preparations available as once- or twice-daily doses	• IV: onset of action within 5 min• Oral: onset of action of 1 hr	5-7 h
Verapamil	Same as for beta blockers	May worsen heart failure in decompensated patient; may cause fatigue; abrupt withdrawal may cause rebound tachycardia, hypertension	• IV: 5- to 10-mg bolus q15-30min to achieve goal• Oral: 80-120 mg dose q8-12hr; sustained-release preparations available as once- or twice-daily doses	• IV: onset of action within 5 min• Oral: onset of action of 1 hr	5-12 h
OTHER
Digoxin (digitalis)	Can be used in patients with heart failure	Slow onset of action; poor control of heart rate with activity; narrow therapeutic margin; long duration of effect	IV loading dose of up to 1.0 mg in first 24 hr, with bolus of 0.25-0.5 mg IV push; then remainder in divided doses 16-8hr; maintenance oral dose, 0.125-0.25 mg qd	• IV: up to 30 min• Oral: 2-4 hr	36 hr

Note that these medications may cause bradycardia, which may ultimately require consideration of other measures, such as catheter ablation of the AV node (discussed below).

Rhythm control of atrial fibrillation

Rhythm control means attempting to restore sinus rhythm. This is done by means of anti-arrhythmic drugs (sotalol, flecainide, propafenone, amiodarone, disopyramide, dronedarone). Rhythm control may be considered although most patients will relapse within one year and it does not provide a survival benefit as compared with rate control.

Catheter ablation

Ablation is a highly effective treatment for paroxysmal atrial fibrillation. There are usually one or a few ectopic foci that can be localized and eliminated with ablation therapy. Approximately 70% of paroxysmal atrial fibrillation cases may be cured with ablation therapy. Persistent atrial fibrillation has a more complex arrhythmia mechanism (more ectopic foci, more re-entry circuits spread throughout the atria, more atrial remodeling) and the effect of ablation is considerably poorer. Roughly 50% of cases with persistent atrial fibrillation are cured with ablation therapy. Lung vein isolation is part of the treatment and aims to create a scar around the lung veins so they become electrically isolated from the atrium.

Ablation therapy should be considered in all patients with symptomatic atrial fibrillation which is paroxysmal or persistent. The patient should have tried at least one anti-arrhythmic drug before ablation therapy.

Although ablation therapy is a proven effective method, there is always a risk of future relapse.

Anticoagulation as prophylaxis against thromboembolism

Stroke, transient ischemic attach and peripheral emboli are common in atrial fibrillation and must be addressed. The risk of thromboembolism is not, as previously believed, equal in all forms of atrial fibrillation. A recent meta-analysis by Ganesan et al. showed that paroxysmal atrial fibrillation is associated with a lower risk of stroke than persistent atrial fibrillation. However, the benefits of anticoagulation are equal in the two groups and both should be managed using the same treatment algorithms. Thus, current guidelines on anticoagulation in atrial fibrillation do not put forward any specific advice in relation to the type of atrial fibrillation.

Begin by judging the risk of thromboembolism by using CHADS score and/or CHADS-VA score. The risk of bleeding should be assessed using HAS-BLED score. Patients with a greater risk for thromboembolism than bleeding should be offered anticoagulation. The risk of stroke will be reduced by 70% using cheap anticoagulants such as warfarin. Newer options (dabigatran, apixaban, rivaroxaban) are more expensive, equally effective in reducing stroke events, do not require monitoring of PK/INR, and appear to cause fewer serious bleedings.

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Chapter 14: Atrial flutter: classification, causes, ECG criteria and management

Atrial flutter is the second most common pathological tachyarrhythmia. Only atrial fibrillation is more common. Atrial flutter occurs almost exclusively among persons with significant heart disease, predominantly ischemic heart disease. However, most cardiac conditions may be associated with atrial flutter. As compared with several other supraventricular tachyarrhythmias, atrial flutter does not occur among otherwise healthy individuals. Atrial flutter causes characteristic ECG changes, as discussed below.

Atrial flutter tends to accompany atrial fibrillation, although some individuals may only present with atrial flutter. Similar to atrial fibrillation, atrial flutter can be classified into the following types:

Acute atrial flutter (includes newly diagnosed cases).

Paroxysmal atrial flutter.

Chronic atrial flutter.

The observant will notice that the classification differs slightly from that of atrial fibrillation. Acute and paroxysmal cases are common in clinical practice. Chronic flutter is, however, very rare. Thus, as compared with atrial fibrillation, atrial flutter is not capable of persisting for longer periods of time. This is due to the fact that atrial flutter is caused by a macro re-entry circuit (a large re-entry circuit) and re-entry circuits are vulnerable processes that usually self-terminate within minutes, hours, or days. In the vast majority of cases, the re-entry circuit in atrial flutter is located in the right atrium and it typically loops around the tricuspid valve. Impulses spread rapidly through the atria from this re-entry circuit.

Examples of atrial flutter. Click to zoom.

ECG in atrial flutter

The ECG shows regular flutter waves (F-waves; not to be confused with f-waves seen in atrial fibrillation) which gives the baseline a saw-tooth appearance. Atrial flutter is the only diagnosis causing this baseline appearance, which is why it must be recognized on the ECG. The flutter waves (on the contrary to f-waves in atrial fibrillation) have identical morphology (in each ECG lead). Flutter waves are typically best seen in leads II, III aVF, V1, V2 and V3. The exact appearance of the flutter waves will depend on the location and direction of the re-entry circuit. In the most common type of atrial flutter, the re-entry loops around the tricuspid valve in a counter-clockwise direction. This yields negative flutter waves in II, III, and aVF and positive flutter waves in V1 (Figure 1). If the re-entry has a clockwise direction, the flutter waves are positive in lead II, III, aVF, and the P-waves typically have a notch on the apex. Please note that for most clinicians it is not necessary to be able to determine the direction of the re-entry loop.

Figure 1. Typical atrial flutter.

The atrial rate (i.e the rate measured between flutter waves) typically ranges between 250 and 350 beats per minute (which is slower than the atrial rate in atrial fibrillation). The atrioventricular node is not capable of conducting all impulses, which is why some impulses will be blocked. The degree of blocking in the atrioventricular node is specified by counting the number of flutter waves preceding each QRS complex. If 3 flutter waves occur before each QRS complex then it is 3:1 block. If there are 2 flutter waves before each QRS complex then it is 2:1 block.

In typical cases of atrial flutter, the atrial rate is around 300 beats per minute with a 2:1 block, which yields a ventricular rate of about 150 beats per minute. One should always consider atrial flutter when confronted with a regular tachyarrhythmia at 150 beats per minute. Note that with a paper speed of 25 mm/s, which is standard in the US and many other countries, a 2:1 block will be difficult to discern because the flutter wave may fuse with the preceding T-wave. Increasing the paper speed to 50 mm/s or applying carotid massage (which increases the atrioventricular block) will be helpful in such situations. Figure 2 shows another ECG with atrial flutter.

Figure 2. 3:1 conducted atrial flutter.

Note that the degree of block in the atrioventricular node may vary from one cardiac cycle to the next and this yields an irregular ventricular rate. As seen in Figure 3, however, it is usually simple to diagnose atrial flutter with irregular ventricular rate because the flutter waves become clear at longer RR intervals.

Figure 3. Atrial flutter with varying AV block.

Atypical atrial flutter

Atypical atrial flutter is a consequence of cardiac surgery or extensive ablation therapy. These interventions may cause atrial flutters with very varying ECG appearance. However, flutter waves can still be seen and a history of ablation therapy or cardiac surgery will be sufficient for diagnosing an atypical atrial flutter.

Treatment and management of atrial flutter

The probability of spontaneous conversion to sinus rhythm is low, as compared with atrial fibrillation. Moreover, pharmacological cardioversion is not particularly effective. Vagal stimulation can be attempted and it sometimes terminates the atrial flutter, or at least elucidates the flutter waves by increasing the RR interval (by increasing the AV block). Second to vagal stimulation, electrical cardioversion is the choice of therapy. A synchronized shock with 50–100 J energy is sufficient in the vast majority of cases. Should the atrial flutter convert to atrial fibrillation, another shock at 200 J is recommended.

If pharmacological cardioversion is considered, ibutilid might be the primary choice with up to 70% success rate. Procainamide is an alternative. As with all antiarrhythmic drugs, there is a significant risk of arrhythmias that are more malign than atrial flutter, which is why care and experience are needed.

The risk of systemic thromboembolism must also be considered. Although the risk of atrial flutter appears to be lower than atrial fibrillation, guidelines still advocate the use of the same algorithms for anticoagulants in both these arrhythmias. Rate control is difficult to achieve in atrial flutter.

Ablation therapy is a highly effective treatment that may cure the majority of patients referred to the intervention. It should be considered early in the disease course.

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Chapter 15: Ectopic atrial rhythm (EAT), atrial tachycardia (AT) & multifocal atrial tachycardia (MAT)

Ectopic atrial tachycardia (EAT, or atrial tachycardia) arises when an ectopic focus within the atria generates electrical impulses at a rate exceeding that of the sinoatrial (SA) node. This enhanced atrial activity is most commonly attributable to abnormal automaticity or re-entry mechanisms; triggered activity is a less frequent cause. The atrial rate typically ranges from 120 to 250 beats per minute. To fulfill the diagnostic criteria for EAT, the ventricular rate must exceed 100 beats per minute. When the ventricular rate remains below this threshold, the arrhythmia is classified instead as an ectopic atrial rhythm (EAR).

Ectopic atrial tachycardia (EAT) most commonly occurs in individuals with underlying structural or electrical heart disease. Less frequently, it may also present in individuals without identifiable cardiac disease. Contributing factors include pulmonary disorders, particularly obstructive pulmonary disease, the use of theophylline, and elevated catecholamine states. EAT typically has an abrupt onset, although a brief warm-up phase lasting approximately 5 to 10 seconds may precede the full tachycardia. It is characterized by short, rapid bursts of atrial activity. In the majority of cases, the arrhythmia is self-limiting; however, it may recur and, in some instances, persist for extended durations. As for any long-standing tachycardia, there is a risk of developing tachycardia-induced cardiomyopathy.

In pediatric populations, a distinct form of atrial tachycardia may occur due to embryological remnants within the atrial myocardium. These residual tissues, persisting from cardiac embryogenesis, are capable of exhibiting markedly increased automaticity, thereby serving as ectopic pacemaker foci.

The term “ectopic” is often omitted in clinical practice, and these arrhythmias are commonly referred to simply as atrial tachycardia or atrial rhythm, depending on the ventricular response.

The ECG in ectopic atrial rhythm and atrial tachycardia

A regular rhythm with P-waves that differ in contour from sinus P-waves. If the P-waves in lead II are retrograde (negative), the diagnosis is straightforward, as sinus P-waves are never negative in this lead. When P-waves are positive in lead II, comparison of P-wave morphology during tachycardia and sinus rhythm is typically required.

The isoelectric baseline lacks the saw-tooth pattern characteristic of atrial flutter.

Each P-wave is followed by a QRS complex; atrioventricular block is uncommon unless the patient is receiving digoxin.

The ventricular rate is regular, typically ranging from 100 to 250 beats per minute in atrial tachycardia and less than 100 beats per minute in atrial rhythm.

Refer to ECG examples in Figures 1, 2 and 3 below.

Figure 1. Atrial rhythm.

Figure 2. Atrial tachycardia.

Figure 3. Atrial tachycardia.

Causes of ectopic atrial tachycardia and ectopic atrial rhythm

Side effect of digoxin.

Heart failure.

Lung disease (COPD, pulmonary hypertension, etc).

Ischemic heart disease (coronary artery disease).

Structural heart disease, any.

Treatment of atrial tachycardia

Discontinuation of digoxin is typically sufficient in patients whose atrial tachycardia is induced by the drug. Management of all other cases aligns with the approach used for atrial fibrillation and atrial flutter. Beta-blockers, digoxin, and calcium channel blockers may be used to control the ventricular rate. If rate control is inadequate, the use of Class IA, IC, or III antiarrhythmic agents may be considered. Catheter ablation should be considered in patients with a high risk of recurrence. Electrical cardioversion is generally ineffective in the treatment of atrial tachycardia.

Multifocal atrial tachycardia

Figure 4. Multifocal atrial tachycardia

Multifocal atrial tachycardia is an uncommon variant of ectopic atrial tachycardia. As illustrated in Figure 4, it is characterized by an irregular rhythm with clearly discernible P-waves (unlike atrial fibrillation) while the morphology of the P-waves varies from beat to beat. This variability is due to the presence of multiple ectopic atrial foci generating impulses that activate the atria. The arrhythmia typically has a gradual onset. In most cases, there is a 1:1 atrioventricular conduction, meaning each atrial impulse is conducted to the ventricles. The ventricular rate usually ranges between 100 and 150 beats per minute.

Multifocal atrial tachycardia may be intermittent with intervening periods of sinus rhythm. The most common underlying causes are heart failure, atrial ischemia, increased atrial pressure, use of theophyllamine or chronic lung disease (particularly COPD). Multifocal atrial tachycardia may occur in children.

Note that if the atrial rhythm is below 100 beats per minute, it is referred to as multifocal atrial rhythm.

Treatment of multifocal atrial tachycardia

Treatment should be directed toward correcting the underlying cause, as resolution of the precipitating factor often leads to spontaneous termination of the arrhythmia. Electrical cardioversion is contraindicated as it is ineffective and may potentially exacerbate the arrhythmia. Beta-blockers are generally considered the first-line pharmacologic option, provided there are no contraindications such as significant pulmonary disease. The efficacy of conventional antiarrhythmic agents is limited, though diltiazem, verapamil, and amiodarone may be considered in selected cases. In addition, magnesium and potassium supplementation is recommended as part of supportive management.

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Chapter 16: Atrioventricular nodal reentry tachycardia (AVNRT): ECG features & management

Atrioventricular nodal reentrant tachycardia (AVNRT) is a common tachyarrhythmia observed across all age groups, from children to the elderly, and frequently occurs in otherwise healthy individuals. The arrhythmia is characterized by its abrupt onset and termination and typically presents with symptoms associated with supraventricular tachyarrhythmias, including palpitations, dyspnea, chest discomfort, and anxiety. As the tachyarrhythmia originates above the ventricles, ventricular depolarization proceeds normally via the His-Purkinje system, and in most cases, there is no significant hemodynamic compromise. However, in cases of rapid AVNRT or in patients with underlying structural heart disease, the arrhythmia may result in symptoms indicative of reduced cardiac output, such as pre-syncope or syncope.

Definition of Paroxysmal Supraventricular Tachyarrhythmia (PSVT)

The arrhythmias AVNRT, AVRT (Pre-excitation, Wolff-Parkinson-White syndrome) and ectopic atrial tachycardia have traditionally been referred to as paroxysmal supraventricular tachycardias, because these tachyarrhythmias originate in the atria (hence “supraventricular”) and they tend to be paroxysmal. However, the term PSVT does not have any clinical relevance and it may lead to misunderstanding. Use of the term PSVT is therefore not recommended.

Synonyms for AVNRT

Atrioventricular nodal reentrant tachycardia

Atrioventricular nodal reentry tachycardia

Atrioventricular nodal reentrant tachyarrhythmia

Atrioventricular nodal reentry tachyarrhythmia

Some textbooks use the term “node” instead of “nodal”. AVNRT should not be confused with AVRT, which is the result of pre-excitation (accessory pathway).

AVNRT is caused by reentry in the atrioventricular (AV) node

Atrioventricular nodal reentrant tachycardia (AVNRT) is caused by a re-entry within the atrioventricular node. In most cases, the re-entry is induced by a premature atrial beat reaching the atrioventricular node while some fibers are still refractory. If an atrial impulse reaches the atrioventricular node when there are two pathways, one being refractory and the other capable of conducting the impulse, re-entry may arise. This is illustrated in Figure 1 (study this figure carefully). The impulse will only be conducted through the excitable pathway whereas it will be blocked in the refractory pathway. If the refractory pathway has repolarized before the impulse has left the atrioventricular node, it may circulate back (upwards) through the previously refractory pathway, as shown in Figure 1. The impulse may subsequently circulate within the atrioventricular node, as long as it encounters excitable tissue. As it circulates within the node, it emits impulses both upwards to the atria and downwards (via His bundle) to the ventricles. Hence, the ventricles will be activated normally via the His-Purkinje system and therefore the QRS complexes are normal (QRS duration < 0.12 s), unless there is a intraventricular conduction defect. The ventricular rhythm is regular (as is the atrial) with a rate ranging between 150 and 250 beats per minute.

The P-wave is not visible in most cases, because it is hidden within the QRS complex (the atria and the ventricles are activated simultaneously, but ventricular potentials dominate the ECG). In some cases, however, the P-wave will be visible, either before or after the QRS complex. In either case it will be retrograde (in lead II, III and aVF) because of the direction of atrial activation. P-waves in AVNRT are discussed in detail below.

Figure 1. Mechanism leading to atrioventricular nodal reentrant tachycardia (AVNRT).

ECG features of Atrioventricular Nodal Reentrant Tachycardia (AVNRT).

There are three types of AVNRT and the difference between them lies in the configuration of the re-entry circuit. Virtually all cases of AVNRT are characterized by having one fast and one slow pathway. Findings on the ECG depend on which of these pathways that lead the impulse in antegrade direction (to the ventricles) and in the retrograde direction (to the atria). The three types of AVNRT are now discussed (illustrated in Figure 2).

Typical AVNRT (slow-fast): 90% of all cases of AVNRT

In typical AVNRT the pathway with antegrade conduction is the slow pathway, whereas retrograde conduction is fast (hence called slow-fast AVNRT). Typical AVNRT occurs when the atrial impulse (typically a premature atrial impulse) reaches the atrioventricular node when the fast pathway is refractory and the slow pathway is excitable (Figure 1 for the mechanism and Figure 2 for ECG example). The impulse is conducted through the slow pathway and before it leaves the atrioventricular node the fast pathway has recovered, such that the impulse may also travel up via the fast pathway. The impulse starts to circulate within the atrioventricular node and a re-entry circuit is established. The re-entry circuit will emit impulses up to the atria and down to the ventricles simultaneously, which is why the P-wave will be hidden within the QRS complex.

In roughly 25% of slow-fast AVNRT the atria will be activated slightly after the ventricles, which is why the P-wave can be seen right after the QRS complex (often fused with it). The P-wave will be retrograde in lead II, III and aVF; because it is (more or less) fused with the QRS, it will imitate an s-wave and therefore it has been termed pseudo s. The same P-wave is positive in lead V1, where it imitates an r-wave and therefore it has been termed pseudo r. In most cases, a previous ECG recording is needed to verify that these waves do not exist normally. If a previous ECG is not at hand, one could suspect such waves to be P-wave if the waves are smooth (as is the P-wave); ventricular deflections are sharp waves. Refer to Figure 2.

Figure 2. Types of atrioventricular nodal reentry tachycardia (AVNRT).

Atypical AVNRT (fast-slow): 10% of all cases of AVNRT

In atypical AVNRT the fast pathway conducts the impulse in antegrade direction while the slow pathway conducts it in the retrograde direction. The P-wave will be visible before the QRS complex. The P-wave will be retrograde in lead II, III and aVF and positive in lead V1. Refer to Figure 2, panel B.

Very atypical AVNRT (slow-slow): <1 % of all cases of AVNRT

In this case, both pathways are slow and the P-wave occurs somewhere on the ST-T-segment. Refer to Figure 2, panel C.

The ECG below shows a recording from a 20-year old male who arrived at the emergency room due to palpitations and dyspnea which started abruptly (Figure 3). The arrhythmia was terminated by administration of 5 mg adenosine i.v.

Figure 3. AVNRT in a 20-year old male suffering from palpitations.

RP interval (RP time)

The RP interval (i.e the time interval from R-wave to P-wave) is fundamental to assess when managing arrhythmias with visible P-waves. Typical AVNRT has a short RP interval (i.e shorter than half the RP interval). Atypical and very atypical AVNRT has a long RP interval (i.e longer than half the RP interval). Refer to this article to learn about RP interval.

Treatment of AVNRT

Treatment in the emergency setting

Always attempt to terminate the AVNRT by applying vagus stimulation (Valsalva maneuver, carotid massage, or, if the patient is a child, bringing ice-cold water to the face). If vagus stimulation is not successful, adenosine can be administered safely, starting at 5 mg iv. The handling and dosing of adenosine are discussed in a separate article. If adenosine is contraindicated or fails after 2 to 3 repeated administrations, it is reasonable to try verapamil 5–10 mg iv or diltiazem 0.25 mg/kg iv. Almost 90% of all cases of AVNRT will be terminated using this algorithm.

Synchronized electrical cardioversion may be preferred over verapamil and diltiazem. Importantly, electrical cardioversion is the first choice if there are signs of hemodynamic compromise. 10–100 J biphasic shock (synchronized) is usually adequate. Beta-blockers have no place in the acute treatment of AVNRT.

Long-term treatment and prophylaxis

Patients with recurring episodes of AVNRT should be considered for long-term/prophylactic treatment with beta-blockers, calcium channel blockers or digoxin. Radiofrequency ablation cures virtually all patients who are referred for intervention.

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Chapter 17: Pre-excitation, Atrioventricular Reentrant (Reentry) Tachycardia (AVRT), Wolff-Parkinson-White (WPW) syndrome

Pre-excitation

The atrioventricular node and bundle of His are normally the only communication between the atria and the ventricles. The atrial impulse must pass through the atrioventricular node, which delays the impulse due to its slow conduction, before the impulse may reach the ventricles. The physiological advantages of this configuration have been discussed in Chapter 1. Some individuals, however, possess an additional pathway between the atria and the ventricles. Such pathways may be conductive, such that they can transmit the atrial impulse to the ventricles directly. These pathways are termed accessory pathways (or bundle of Kent). They are remnants of the embryological development of the heart. Accessory pathways (Kent’s bundle) may be able to conduct the impulse from the atria to the ventricles (antegrade direction), from the ventricles to the atrial (retrograde direction) or both.

Accessory pathways do not display the slow conduction that the atrioventricular node does, and this means that any impulse reaching the accessory pathways may travel directly to the ventricles without any delay. Hence, the ventricle will be excited (depolarized) earlier than expected, which is referred to as pre-excitation. This manifests with three features on the ECG and the combination of these features are unique to pre-excitation:

ECG features of pre-excitation

Short PR interval: The PR interval is <0.12 seconds.

Delta wave: depolarization of ventricular myocardium will start where the accessory pathway inserts into the ventricle, and the impulse will spread slowly because it will propagate outside of the conduction system. This is reflected on the ECG as a slow start of the QRS complex and this part of the QRS complex is referred to as a delta wave.

QRS duration ≥0.12 s: Because the delta wave is included in the QRS duration, the total QRS duration will be prolonged.

Individuals with accessory pathways (Kent’s bundle) only display pre-excitation on the ECG when impulses are actually conducted over the accessory pathway. In most individuals with accessory pathways, the conduction over the pathway is intermittent, meaning that pre-excitation may not be seen at all times.

Figure 1 presents ECG findings during normal atrioventricular impulse transmission as well as ECG findings during pre-excitation.

Figure 1. Hallmarks of pre-excitation on the ECG.

Secondary ST-T changes during pre-excitation

As mentioned in Chapter 1, pre-excitation causes secondary ST-T changes. This is due to the fact that pre-excitation leads to abnormal depolarization of the ventricles and this leads to abnormal repolarization as well. The ST-T segment is directed oppositely to the delta wave, meaning that a positive delta wave will be followed by a negative ST-T segment (typically with ST-segment depression and T-wave inversion). ECG in Figure 2 exemplifies how delta waves are associated with secondary ST-T changes.

Figure 2. Pre-excitation in a 25 year old woman. There are numerous leads showing ST-segment depression and T-wave inversion. There is very short PR interval, wide QRS complexes and delta waves in numerous leads. Can you spot them?

Note that negative delta waves may simulate pathological Q-waves (and thus be confused with previous myocardial infarction).

ECG examples of pre-excitation (short PR interval, prolonged QRS duration, delta waves, secondary ST-T abnormalities). Click to zoom.

Atrioventricular reentrant (reentry) tachycardia (AVRT)

Individuals with accessory pathways are at risk of developing atrioventricular reentrant tachycardia (AVRT). This is a rapid tachyarrhythmia in which a macroscopic re-entry circuit involves the atria, atrioventricular node, accessory pathway and the ventricles. In most cases, the re-entry is induced by a premature atrial beat. Atrioventricular reentrant tachycardia (AVRT) occurs in two types: orthodromic and antidromic (illustrated in Figure 3). In orthodromic AVRT the re-entry impulse circulates in antegrade direction through the atrioventricular node. In antidromic AVRT the impulse travels in retrograde direction through the atrioventricular node.

Figure 3. Antidromic and orthodromic AVRT.

Wolff-Parkinson-White (WPW) syndrome

An individual with evidence of pre-excitation on resting ECG who also has recurring tachyarrhythmias is said to have Wolff-Parkinson-White syndrome. This is a rather common condition and some studies suggest that the prevalence is 1–2 in 1000 in the population. Wolff-Parkinson-White syndrome is more common in men.

As mentioned above the majority of individuals with accessory pathways only have intermittent conduction over the accessory pathway and the delta wave is only visible on those occasions. The following rules are important to note:

Pre-excitation can only occur if the accessory pathway is capable of antegrade conduction.

If the accessory pathway is capable of conducting the impulse in both directions (atria to ventricles as well as ventricles to atria) the individual will display pre-excitation during sinus rhythm and also be at risk of antidromic and orthodromic AVRT.

If the accessory pathway is only capable of conducting from the atria to the ventricles, there will be pre-excitation during sinus rhythm and risk of developing antidromic AVRT.

In one-third of all cases, the accessory pathway is only capable of conducting from the ventricles to the atria. In these cases, there can not be pre-excitation, but there is a risk of antidromic AVRT. This condition is referred to as concealed WPW syndrome (because the delta wave is not visible).

Figure 3 displayed the characteristics of orthodromic and antidromic AVRT.

Location of the accessory pathway

Being able to locate the accessory pathway is a task relevant to cardiologists. The location of the accessory pathway is as follows:

53% left free ventricular wall

36% posteroseptal

8% right free ventricular wall

3% anteroseptal

The 12-lead ECG is useful to determine the location of the accessory pathway. This is done by assessing which leads display the delta wave as well as the direction of the delta wave (negative vs positive). We recommend the use of the following algorithm (Figure 4) to determine the location of the accessory pathway in pre-excitation (Brugada et al.).

Figure 5. Algorithm for localization of the accessory pathway in pre-excitation.

ECG criteria pre-excitation

Short PR interval (<0,12 s).

Delta wave and prolonged QRS duration (≥0,12 s).

Frequently, secondary ST-T changes with the ST-T-segment being directed opposite to the delta wave.

Figure 5 (below) shows an example of pre-excitation during sinus rhythm.

Figure 5. Pre-excitation during sinus rhythm.

Figure 6. ECG recording with every other beat conducted through the accessory pathway, resulting in variations in QRS amplitude (electrical alternans).

Orthodromic AVRT

Orthodromic AVRT means that the ventricles are depolarized normally via the atrioventricular node and His-Purkinje system (Figure 3). Because the impulse reaches the ventricles through the His-Purkinje network the QRS complexes will appear normal (i.e QRS duration will be <0.12 s). Orthodromic AVRT represents approximately 95% of all cases of AVRT and it arises when a premature atrial beat encounters a refractory accessory pathway but excitable atrioventricular node. The impulse will then propagate normally through the His-Purkinje system, depolarize the ventricles and circulate back to the atria via the accessory pathway. A ventricular premature beat may induce orthodromic AVRT by the same principles.

ECG in orthodromic AVRT

Normal QRS complexes (QRS duration <012 s).

Regular ventricular rate 150-250 beats per minute.

P-wave is visible in most cases. It is retrograde in leads II, III and aVF and it occurs after the QRS complex (somewhere on the ST segment or early on the T-wave). The retrograde P-wave may simulate an ST-segment depression when it occurs early on the ST-segment.

RP interval (discussed in this article) is short but typically longer than 70 ms. RP interval may, however, be long if the accessory pathway is slow.

Orthodromic AVRT may be difficult to discern from AVNRT and it is often necessary to perform an invasive examination.

Antidromic AVRT

The re-entry impulse travels in retrograde direction through the atrioventricular node in antidromic AVRT. This variant arises when a premature atrial impulse is discharged near the atrioventricular node when it is refractory. The premature atrial impulse will then travel from the atria to the ventricles via the accessory pathway and subsequently back to the atria via the atrioventricular node.

Antidromic AVRT yields wide QRS complexes and delta waves. However, the delta waves may be difficult to discern and it is often difficult (sometimes impossible) to differentiate antidromic AVRT from ventricular tachycardia. Antidromic AVRT represents 5% of all cases of AVRT. It may reach very high heart rates and cause hemodynamic compromise.

The ECG in antidromic AVRT

Wide QRS complexes (≥0.12 s). The delta wave is visible in most cases.

Regular ventricular rate 150–250 beats per minute.

P-wave is generally not visible, but if it is, it is retrograde and occurs before the QRS complex (i.e the RP interval is long).

It is recommended to examine the first QRS complexes that follow the termination of an arrhythmia suspected to be antidromic AVRT; the chance of spotting delta waves is maximal on the first QRS complexes following the termination of the arrhythmia.

Pre-excitation and atrial fibrillation

Conduction from atria to ventricles via an accessory pathway during atrial fibrillation causes irregular tachycardia with wide QRS complexes. This is worrying because the accessory pathway does not exhibit the physiological impulse delay that characterizes the atrioventricular node. Hence, the conduction through the accessory pathway may be rapid, and the ensuing ventricular rate may cause hemodynamic compromise. It is contraindicated to administer adenosine (or other agents blocking conduction through the atrioventricular node) to patients with irregular wide QRS complex tachycardias because the arrhythmia may be a pre-excited atrial fibrillation. Blocking of conduction through the atrioventricular node may lead to accelerated impulse transmission through the accessory pathway, whereby atrial fibrillation may cause ventricular fibrillation and cardiac arrest.

Long-term prognosis of pre-excitation and WPW syndrome

The majority of all patients with pre-excitation will experience AVRT. The arrhythmia causes typical tachycardia symptoms (palpitations, dyspnea, anxiety, chest discomfort) but may also reduce cardiac output to the point of syncope or heart failure. Life-threatening cardiac arrhythmias are unusual, with the exception of pre-excited atrial fibrillation administered adenosine.

Atrial fibrillation is prevalent among people with pre-excitation. Up to 30% may develop atrial fibrillation. Some individuals with pre-excitation display multiple accessory pathways, which increase the risk of atrial fibrillation and complicate treatment.

Occasionally, the function in the accessory pathway ceases spontaneously and the risk of pre-excitation and arrhythmias is eliminated.

Management of pre-excitation, AVRT and WPW syndrome

Management in the emergency setting

Orthodromic AVRT

Orthodromic AVRT is treated the same way as AVNRT. Adenosine is generally safe and very effective in terms of terminating orthodromic AVRT. Note that administration of adenosine may induce atrial fibrillation and this may aggravate the arrhythmia. For the same reason agents that block atrioventricular transmission (beta-blockers, diltiazem, verapamil) should not be administered in patients with pre-excitation and concomitant atrial fibrillation, atrial flutter or atrial tachycardia. Procainamide is a better choice. If pharmacological therapy fails or the patient is hemodynamically affected, electrical cardioversion is warranted.

Antidromic AVRT

Antidromic AVRT is also treated with adenosine. If adenosine is unsuccessful, beta-blockers are tried (i.v. metoprolol 5 + 5 + 5 mg, with 10–15 minute intervals). As for orthodromic AVRT, electrical cardioversion is warranted if pharmacological therapy fails or if the patient is hemodynamically affected.

Pre-excited atrial fibrillation / flutter

Pre-excited atrial fibrillation/flutter: Electrical cardioversion is always the primary choice in pre-excited atrial fibrillation. Agents blocking transmission in the atrioventricular node (Adenosine, beta-blockers, calcium channel blockers, digoxin) are strictly contraindicated for reasons explained above. Pharmacological agents that may be tried are amiodarone, flekainid, propafenon, procainamide and sotalol. Experience suggests that procainamide is the best alternative. If the duration of arrhythmia is <48 hours, there is a significant probability that the arrhythmia will self-terminate and covert to sinus rhythm. If the duration of the arrhythmia is >48 hours the patient must be anticoagulated (as conventional in atrial fibrillation) before electrical cardioversion.

It can be recommended that calcium channel blockers and digoxin not be used in patients with pre-excitation because of the risk of atrial fibrillation in this population.

Long-term management

Patients with asymptomatic pre-excitation during sinus rhythm do not necessitate any treatment (although a discussion with a cardiologist may be warranted). Patients with WPW syndrome (i.e pre-excitation with episodes of tachyarrhythmias) should be referred for ablation. The vast majority of patients will be cured by ablation therapy. If medications are needed as a bridge to ablation, beta-blockers should be preferred.

Rare variants of pre-excitation

Lown-Ganong-Levine syndrome

LGL (Lown-Ganong-Levine) syndrome has traditionally been described as pre-excitation with an accessory pathway between the atria and His bundle (with antegrade conduction). This is considered to result in tachyarrhythmias with short PR intervals but no delta wave and normal QRS complexes. However, there is no evidence that such a syndrome actually exists and electrophysiological studies have consistently failed to verify the existence of such an accessory pathway in patients presenting with such arrhythmias. Therefore, the term LGL syndrome should not be used.

Mahaim fibers

Mahaim fibers are accessory pathways between the atria or the atrioventricular node and the bundle branches (left or right bundle branch). In most cases, the accessory pathway is connected to the right bundle branch which results in tachycardia with left bundle branch morphology on the ECG.

Permanent Junctional Reciprocating tachycardia (PJRT)

PJRT (Permanent Junctional Reciprocating tachycardia) is an incessant tachyarrhythmia caused by an accessory pathway. The RP interval is long and the accessory pathway is typically located posterolaterally and has slow retrograde conduction.

Figures

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Chapter 18: Junctional rhythm (escape rhythm) and junctional tachycardia

In this article, you will learn about rhythms arising in, or near,  the atrioventricular (AV) node. The most common rhythm arising in the AV node is junctional rhythm, which may also be referred to as junctional escape rhythm. Junctional tachycardia is less common. Basic knowledge of arrhythmias and cardiac automaticity will facilitate understanding of this article.

As discussed in Chapter 1 the atrioventricular node does not exhibit automaticity, meaning that it does not discharge spontaneous action potentials, at least not under normal circumstances. However, impulses are occasionally discharged in the atrioventricular node or by cells near the node. The following must be noted:

There are cells with pure automaticity around the atrioventricular node. These cells are capable of spontaneous depolarization (i.e they display automaticity) and can therefore act as latent pacemakers (which become active when atrial impulses do not reach the atrioventricular node).

The cells in the atrioventricular node itself may start discharging impulses under pathological circumstances, such as in ischemia.

In both cases listed above the impulse will originate in the junction between the atria and the ventricles, which is why ectopic beats and ectopic rhythms originating there are referred to as junctional beats and junctional rhythms. The atria will be activated in the opposite direction, which is why the P-wave will be retrograde. In most cases, the P-wave is not visible because when impulses are discharged from the junctional area, atria and ventricles are depolarized simultaneously and ventricular depolarization (QRS) dominates the ECG. If the atria are activated prior to the ventricles, a retrograde P-wave will be visible in leads II, III and aVF prior to the QRS complex. If the ventricles are activated prior to the atria, a retrograde P-wave (leads II, III and aVF) will be seen after the QRS complex.

Junctional beats and junctional rhythm

Junctional rhythm may arise in the following situations:

If the normal sinus impulse disappears (e.g sinus arrest) cells around the atrioventricular node may discharge impulses. Less than three consecutive beats are referred to as junctional beats (also called junctional escape beats). Three or more consecutive junctional beats are referred to as junctional rhythm (also called junctional escape rhythm). Junctional escape rhythm is a regular rhythm with a frequency of around 40–60 beats per minute. In case of sinus arrest (or any scenario in which atrial impulses do not reach the atrioventricular node), junctional escape rhythm may be life-saving.

During complete heart block (third-degree AV-block) the block may be located anywhere between the atrioventricular node and the bifurcation of the bundle of His. If there are cells (with automaticity) distal to the block, an escape rhythm may arise in those cells. For example, consider a complete block located in the atrioventricular node. In such scenarios, cells in the bundle of His (which possess automaticity) will not be reached by the atrial impulse and hence start discharging action potentials and an escape rhythm. This will also manifest as a junctional escape rhythm on the ECG. Indeed, the surface ECG frequency cannot differentiate escape rhythms originating near the atrioventricular node from those originating in the bundle of His.

Well-trained athletes may have very high Vagal tone which lowers the automaticity in the sinoatrial node to the point where cells in the AV-junction establish an escape rhythm. This is asymptomatic and benign.

ECG criteria for junctional rhythm

Regular ventricular rhythm with rate 40–60 beats per minute.

Retrograde P-wave before or after the QRS, or no visible P-wave.

The QRS complex is generally normal, unless there is concomitant intraventricular conduction disturbance.

Figure 1 (below) displays two ECGs with a junctional escape rhythm.

Figure 1. Two types of junctional (escape) rhythm.

Treatment of junctional beats and rhythm

Symptomatic junctional rhythm is treated with atropine. Doses and alternatives are similar to management of bradycardia in general.

Junctional tachycardia

Junctional tachycardia is caused by abnormal automaticity in the atrioventricular node, cells near the atrioventricular node, or cells in the bundle of His. It is very rare among adults and elderly, but is relatively common in children. When occurring in adults and the elderly it is referred to as nonparoxysmal junctional tachycardia (NPJT) whereas it is referred to as junctional ectopic tachycardia (JET) in children.

NPJT is caused by ischemia, digoxin overdose, theophylline overdose, catecholamines, electrolyte disorders and perimyocarditis.

As true for the other junctional beats and rhythms, the P-wave is retrograde (or invisible). However, if the junctional impulse is not conducted retrogradely the atria may run an independent rhythm; this is called atrioventricular dissociation (AV dissociation) because the atrial and ventricular rhythms are dissociated from each other. This type of AV dissociation is easy to differentiate from AV dissociation due to third-degree AV-block, because in third-degree AV-block the atrial rhythm is higher than the ventricular; the opposite is true in this scenario.

It may be very difficult to differentiate junctional tachycardia from AVNRT.

Treatment of junctional tachycardia

The primary objective is to treat the underlying cause and/or eliminate provocative medications. Electrical cardioversion is ineffective and should be avoided (electrical cardioversion may be pro-arrhythmogenic in patients on digoxin). If the genesis of the arrhythmia is unknown or if the arrhythmia persists after removing medications, it is recommended that amiodarone, beta-blockers or calcium channel blockers are tried, in that order.

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Chapter 19: Ventricular rhythm and accelerated ventricular rhythm (idioventricular rhythm)

This article provides an overview of ventricular rhythm and accelerated ventricular rhythm, the latter also known as idioventricular rhythm. Recognizing these arrhythmias on the electrocardiogram (ECG) is of clinical importance. Diagnosis and management of ventricular tachycardia will be addressed in a separate chapter. The following arrhythmias are discussed in this chapter:

Ventricular rhythm

Accelerated ventricular rhythm, which is also called idioventricular rhythm.

The hallmark of all ventricular rhythms is the wide QRS complex (QRS duration ≥0.12 seconds). The QRS complex is wide simply because the ectopic impulses that cause these rhythms spread partially or entirely outside of the ventricular conduction system, and thus the ventricular depolarization is slow (yielding a wide QRS complex).

Because the ventricular depolarization is abnormal, the repolarization will also be abnormal (read about secondary ST-T changes on ECG). Hence, all beats and rhythms arising in the ventricles will display discordant ST-T segments, meaning that the QRS complex and the ST-T segment will have opposite directions. Figure 1 provides an example.

Figure 1. Ventricular rhythm.

One exception to the rule above should be noted. If an ectopic focus arises in or near the bundle of His, the impulse may be delivered to both bundle branches and subsequently the entire ventricular myocardium normally. This may yield a ventricular rhythm with narrow QRS complexes. However, this is very uncommon and of little clinical significance.

Causes of ventricular rhythm and idioventricular rhythm

The usual mechanisms are responsible for all ventricular rhythms. Increased automaticity (in His-Purkinje fibers), abnormal automaticity (in contractile myocardium), re-entry (anywhere) or triggered activity (anywhere) may all cause ventricular arrhythmias. Indeed, any cell type in the ventricles may cause ventricular arrhythmias.

Definitions and ECG criteria for ventricular rhythm and idioventricular rhythm

Ventricular rhythm exists if 3 or more consecutive beats have a ventricular origin. The ventricular rate is between 20 to 40 beats per minute and the rhythm is regular. There is always secondary ST-T changes, meaning that the ST-T segment is discordant (Figure 1). Ventricular rhythm typically occurs during complete heart block (third-degree AV block). Importantly, ventricular rhythm is not a reliable rhythm as it may cease working. Figure 1 exemplifies a ventricular rhythm.

Accelerated ventricular rhythm (idioventricular rhythm) is a rhythm with rate at 60–100 beats per minute. As in ventricular rhythm the QRS complex is wide with discordant ST-T segment and the rhythm is regular (in most cases). Idioventricular rhythm starts and terminates gradually. It occurs in other situations than does ventricular rhythm; idioventricular rhythm is primarily seen after reperfusion in an occluded coronary artery. It also occurs as side effect of drugs, hypoxia, myocarditis and electrolyte disorders. Because the rate (60–100 beats per minute) is on a par with the rate in sinus rhythm and there is atrioventricular conduction, these rhythms typically compete which is seen on the ECG with sinus rhythm alternating with accelerated ventricular rhythm.

As mentioned in the previous paragraph, idioventricular rhythm is very typical during reperfusion and in that scenario it is a good prognostic marker because it signals that coronary blood flow has been restored. Note that in that setting the idioventricular rhythm may appear with varying QRS morphologies (i.e multifocal ventricular complexes). In virtually all cases (particularly in myocardial ischemia) idioventricular rhythm is benign and does not demand treatment. It does not progress to ventricular tachycardia or ventricular fibrillation and it does not affect cardiac output to the point of hemodynamic compromise.

Figure 2. Idioventricular rhythm (accelerated ventricular rhythm).

ECG Example: Idioventricular rhythm (accelerated ventricular rhythm) – Accelerated ventricular rhythm at a rate of 56 for the first 5 beats followed by 2 fusion beats; the last 2 beats are normal sinus rhythm. Source: 10.1371/journal.pone.0110274 | License

Management and treatment of ventricular rhythms

Asymptomatic patients need no treatment. Idioventricular rhythm is virtually always transient and returns to sinus rhythm spontaneously. Patients with ventricular rhythm with inadequate cardiac output are managed as patients with bradycardia. By administering atropine, the supraventricular impulse rate may increase which may take over the ventricular rhythm as well.

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Chapter 20: Ventricular tachycardia (VT): ECG criteria, causes, classification, treatment

This chapter deals with ventricular tachycardia from a clinical perspective, with emphasis on ECG diagnosis, definitions, management, and clinical characteristics. Ventricular tachycardia is a highly nuanced arrhythmia that originates in the ventricles. A wide range of conditions may cause ventricular tachycardia and the ECG is as nuanced as are those conditions. Regardless of etiology and ECG, ventricular tachycardia is always a potentially life-threatening arrhythmia that requires immediate attention. The ventricular rate is typically very high (100–250 beats per minute) and cardiac output is affected (i.e reduced) in virtually all cases. Ventricular tachycardia causes immense strain on the ventricular myocardium, simultaneously as the cause of the arrhythmia already affects cellular function. This results in electrical instability which explains why ventricular tachycardia may progress to ventricular fibrillation. Left untreated, ventricular fibrillation leads to asystole and cardiac arrest. All healthcare providers, regardless of profession, must be able to diagnose ventricular tachycardia.

Causes of ventricular tachycardia

Patients with ventricular tachycardia almost invariably have significant underlying heart disease. The most common causes are coronary heart disease (acute coronary syndromes or ischemic heart disease), heart failure, cardiomyopathy (dilated cardiomyopathy, hypertrophic obstructive cardiomyopathy), valvular disease. Less common causes are arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/ARVD), Brugada syndrome, long QT syndrome, sarcoidosis, Prinzmetal’s angina (coronary vasospasm), electrolyte disorders, congenital heart disease and catecholamine-induced ventricular tachycardia.

The vast majority of patients with ventricular tachycardia either have coronary artery disease (ischemic heart disease), heart failure, cardiomyopathy or valvular heart disease. In these populations, one of the strongest predictors of sudden cardiac death is left ventricular function. Individuals with reduced left ventricular function (e.g. defined as ejection fraction <40 %) are at high risk of sudden cardiac arrest.

Idiopathic ventricular tachycardia (IVT)

Ventricular tachycardia may be classified as idiopathic if no cause can be identified. Idiopathic ventricular tachycardia has a more favorable prognosis, as compared with other forms of ventricular tachycardia.

Mechanisms of ventricular tachycardia

Ventricular tachycardia (VT) may emerge due to increased/abnormal automaticity, re-entry or triggered activity. All types of myocardial cells may be engaged in initiation and maintenance of this arrhythmia. As mentioned above VT causes hemodynamic compromise. The rapid ventricular rate, which may be accompanied by already impaired ventricular function, does not allow for adequate filling of the ventricles, which results in reduced stroke volume and reduced cardiac output.

Most patients experience presyncope or syncope if the arrhythmia is sustained. In its fulminant course, VT degenerates to ventricular fibrillation, which then degenerates into asystole and cardiac arrest. Importantly, the progress from VT to cardiac arrest may be aborted either spontaneously or by means of treatment. Interestingly, treatment of VT is considered one of the greatest advances in cardiology. Until 1961, patients with acute myocardial infarction were placed in beds located far away from physicians’ and nurses’ stations in order to not disturb the patients’ rest. It was believed that the mere presence of physicians and nurses caused harmful stress. Approximately 30% of patients died in the hospital and fatal tachyarrhythmias was presumably the leading cause. Animal studies conducted in the late 1950s, 1960 and 1961 showed that VT could be terminated by delivering an electrical shock. This prompted physicians to construct coronary care units, in which all patients with acute myocardial infarction were monitored with continuous ECG and ventricular tachyarrhythmias were handled by means of immediate resuscitation and defibrillation.

Ventricular tachycardia in acute coronary syndromes (myocardial infarction)

Acute coronary syndromes are subdivided into unstable angina (UA), ST-elevation myocardial infarction (STEMI) and non-ST elevation myocardial infarction (NSTEMI). The risk of VT is high in these conditions. Moreover, the risk is highly time-dependent, being highest in the hyperacute phase (the first minutes to hours after symptom onset). The vast majority of individuals who die in the acute phase of myocardial infarction die from ventricular tachyarrhythmias. Death due to pumping failure (i.e cardiogenic shock) is less common. Because the risk is highest in the first minutes to hours, most deaths occur outside of the hospital. The risk of VT (and thus ventricular fibrillation) diminishes gradually as time elapses. In addition to time, the major determinant of VT is the extent of the ischemia/infarction. The larger the ischemic are the greater the risk of arrhythmias.

ECG criteria for ventricular tachycardia

ECG features of ventricular tachycardia

≥3 consecutive ventricular beats with rate 100–250 beats per minute (in most cases >120 beats per minute). Ventricular tachycardia with rate 100 to 120 beats per minute is referred to as slow ventricular tachycardia.  Ventricular tachycardia with rate >250 beats per minute is referred to as ventricular flutter.

Wide QRS complexes (QRS duration ≥0,12 s).

Types of ventricular tachycardia

The ECG allows for subclassification of ventricular tachycardia. The discussion below may be perceived as advanced, but the reader should know that it is not required that all clinicians be able to classify ventricular tachycardias; merely being able to recognize it is sufficient. Therefore, the purpose of the discussion below is to present the reader with several types of ventricular tachycardia just for reference.

Sustained vs. Non-sustained ventricular tachycardia

Ventricular tachycardia with duration <30 seconds is classified as non-sustained ventricular tachycardia. Sustained ventricular tachycardia has duration >30 seconds.

Monomorphic ventricular tachycardia

In monomorphic ventricular tachycardia, all QRS complexes display the same morphology (minor differences are allowed). This indicates that the impulses originate in the same ectopic focus. In structural heart disease (coronary heart disease, heart failure, cardiomyopathy, valvular disease, etc) monomorphic ventricular tachycardia is typically caused by re-entry. Refer to Figure 1.

Figure 1. Monomorphic ventricular tachycardia (VT, VTach). P-waves are visible but they do not have any relation to the QRS complexes. This situation is referred to as “AV dissociation” and indicates that atrial and ventricular activity and independent. AV dissociation confirms that the arrhythmia is ventricular tachycardia. However, AV dissociation is frequently difficult to spot.

The Purkinje fibers in the interventricular septum appear to have an important role in ventricular tachycardia among patients with coronary heart disease. These Purkinje fibers appear to be highly arrhythmogenic in the setting of myocardial ischemia, particularly re-ischemia. Because any impulse arising in the interventricular septum will enter the Purkinje network (to some degree) the QRS complexes tend to be shorter than arrhythmias originating in the free ventricular walls. QRS duration is generally 120 to 145 ms in ventricular tachycardias arising in the septum.

Fascicular ventricular tachycardia is an idiopathic form of VT. It is caused by re-entry in the fascicles of the left bundle branch (i.e in the Purkinje fibers). Fascicular ventricular tachycardia occurs in people aged less than 50 years of age, and predominantly in males. The QRS complexes display morphology similar to right bundle branch block and there is left axis deviation.

Right ventricular outflow tract (RVOT) ventricular tachycardia is a monomorphic VT originating in the outflow tract of the right ventricle. The arrhythmia is mostly idiopathic but some patients may have ARVC (arrhythmogenic right ventricular cardiomyopathy). Because the impulses originate in the right ventricle, the QRS complexes have left bundle branch appearance and the electrical axis is around 90°. Refer to Figure 2.

Figure 2. Ventricular tachycardia (VT) originating in the right ventricular outflow tract (RVOT).

Polymorphic ventricular tachycardia

A ventricular tachycardia with varying QRS morphology or varying electrical axis is classified as polymorphic. The rhythm may be irregular. Polymorphic ventricular tachycardia is typically very fast (100–320 beats per minute) and unstable. There are several types of polymorphic ventricular tachycardia. The most common cause is myocardial ischemia. The second most common cause is prolonged QTc interval (Long QT syndrome).

Familial catecholaminergic polymorphic ventricular tachycardia (CPVT) is a hereditary ventricular tachycardia in which emotional or physical stress induces the arrhythmia, which may lead to circulatory collapse and cardiac arrest. This type of ventricular tachycardia may be bidirectional (see below). The diagnosis is established using exercise stress testing, since the sympathetic activity induces the arrhythmia.

Brugada syndrome causes polymorphic VT (mostly during sleep or fever).

Early repolarization and hypertrophic obstructive cardiomyopathy also causes polymorphic VT.

Bidirectional ventricular tachycardia means that the QRS morphology alternates from one ebat to another. In most cases it alternates between two variants of the QRS complex.  Bidirectional ventricular tachycardia is seen in familial CPVT, digoxin overdoes and long QT syndrome. Refer to Figure 3.

Figure 3. Bidirectional ventricular tachycardia.

Ventricular tachycardia in ischemic heart disease

Coronary artery disease (ischemic heart disease) is by far the most common cause of ventricular tachycardia and the mechanism is mostly re-entry. As mentioned earlier in this chapter, re-entry occurs when there is a central block ahead of the depolarizing impulse and the cells surrounding the block has varying conductivity. In ischemic heart disease, the central block is typically ischemic/necrotic myocardium (which do not conduct any impulses) while the surrounding cells have dysfunctional conduction due to ischemia. Ventricular tachycardia due to ischemia poses a high risk of degenerating into ventricular fibrillation and cardiac arrest.

Hence, ventricular tachycardia in coronary artery disease is mostly monomorphic. It may be polymorphic, if there are several ectopic foci or if the impulse from one foci spreads varyingly.

Locating the ectopic foci causing ventricular tachycardia

The ECG provides valuable information regarding the location of the ectopic foci causing the tachycardia. This is done by classifying ventricular tachycardias broadly as either “left bundle branch appearance” or “right bundle branch appearance”. Ventricular tachycardias with ECG waveforms reminding of a left bundle branch block (dominant S-wave in V1) originate in the right ventricle. The opposite is also true, namely that ventricular tachycardias reminding of right bundle branch block (dominant R-wave in V1) originates in the left ventricle. This might be useful in trying to decipher what the cause of the ventricular tachycardia may be. Figure 4 and Figure 5 below shows examples.

Figure 4. Ventricular tachycardia with right bundle branch block (RBBB) morphology. However, the first R-wave is larger than the second R-wave, which is not the case in RBBB. This suggests that the rhythm is not a supraventricular tachycardia conducted with RBBB, but rather ventricular tachycardia (VT).

Figure 5. Ventricular tachycardia with left bundle branch block morphology.

Distinguishing ventricular tachycardia from supraventricular tachycardias with wide QRS complexes

Occasionally supraventricular tachycardias (which mostly have normal QRS complexes, i.e QRS duration <0.12 seconds) may display wide QRS complexes. This might be due to concomitant bundle branch block, aberration, hyperkalemia, pre-excitation or side effect of drugs (tricyclic antidepressants, antiarrhythmic drugs class I). It is fundamental to be able to differentiate supraventricular tachycardias with wide QRS from VT and the reason for this is simple: VT is potentially life-threatening, whereas supraventricular arrhythmias rarely are. Hence, wide QRS complexes do not guarantee that the rhythm is ventricular in origin.

Fortunately, there are several characteristics that separate ventricular tachycardia from supraventricular tachycardias (SVT). These characteristics can be used separately or in algorithms (which are easy to use) to determine whether a tachycardia with wide QRS complexes (often called wide complex tachycardia) is a ventricular tachycardia or an SVT. Before dwelling into these characteristics and algorithm it should be noted that 90% of all wide complex tachycardias are ventricular tachycardias! If the patient suffers from any of the conditions stated above as risk factors for ventricular tachycardia, one should be very prone to assume that it is ventricular tachycardia.

Characteristics of ventricular tachycardia are now discussed.

Atrioventricular (AV) dissociation

AV dissociation means that atria and ventricles function independently of each other. On the ECG this manifests as P-waves having no relation to QRS complexes (P-P intervals are different from R-R intervals, PR intervals vary and there is no relation between P and QRS). Note that it is often difficult to discern P-waves during VT (esophagus ECG may be very helpful). If AV dissociation can be verified, VT is very likely to be the cause of the arrhythmia. However, occasionally the ventricular impulses may be conducted retrogradely through the His bundle and AV node to the atria and depolarize the atria synchronously with the ventricles; thus VT may actually display synchronized P-waves.  The following ECG shows VT with AV dissociation (the arrows point at P-waves).

Figure 1 (repeated). Monomorphic ventricular tachycardia (VT, VTach). P-waves are visible but they do not have any relation to the QRS complexes. This situation is referred to as “AV dissociation” and indicates that atrial and ventricular activity and independent. AV dissociation confirms that the arrhythmia is ventricular tachycardia. However, AV dissociation is frequently difficult to spot.

Initiation of the tachyarrhythmia

If the start of the tachycardia is recorded it is valuable to assess the initial beats. If the R-R intervals during the start of the tachycardia were irregular, it suggests ventricular tachycardia. This is called warm-up phenomenon and is characteristic of ventricular tachycardia. Supraventricular tachycardias do not display warm-up phenomenon (with the exception of atrial tachycardia).

Initiation by premature atrial beats

Ventricular tachycardia is not induced by premature atrial beats, but supraventricular tachycardias typically do. If the start of the tachycardia is recorded, one must examine whether it was preceded by a premature atrial beat.

Fusion beats & capture beats

If a ventricular impulse is discharged simultaneously as the atrial impulse enters the His-Purkinje system, the ventricles will be depolarized by both. The resulting QRS complex will have an appearance resembling both a normal QRS and a wide QRS. Such beats are called fusion beats, and such beats are diagnostic of ventricular tachycardia. Figure 6 shows an example.

Occasionally during a ventricular tachycardia, the atrial impulse will break through and manage to depolarize the ventricles. This is seen as the occurrence of a normal beat in the midst of the tachycardia. Such beats are called capture beats and they are also diagnostic of ventricular tachycardia.

Figure 6. Capture beats and fusion beats seen during ventricular tachycardia.

Regularity

Ventricular tachycardia is mostly regular, although the R-R intervals may vary somewhat. Discrete variability in R-R intervals actually suggest ventricular tachycardia. However, polymorphic ventricular tachycardia may be irregular. Supraventricular tachycardias may also be irregular; the most common being atrial fibrillation. Note that pre-excitation during atrial fibrillation causes an irregular wide complex tachcyardia, with heart rate >190 beats per minute in most cases.

Previously existing bundle branch block

Individuals with previously existing conduction defects (right or left bundle branch block) or other causes of wide QRS complexes (pre-excitation, drugs, hyperkalemia) should have their ECGs during tachyarrhythmia compared with the ECG during sinus rhythm (or any earlier ECG). If the QRS morphology during the tachyarrhythmia is similar to the QRS complex in sinus rhythm, it is likely to be an SVT. Moreover, if the patient has recently had premature ventricular complexes, and the QRS during tachyarrhythmia resembles that of the premature ventricular complexes, then it is likely to be ventricular tachycardia.

Electrical axis

Electrical axis between –90° and –180° strongly suggests ventricular tachycardia (although antidromic AVRT is a differential diagnosis). If the electrical axis during tachycardia differs >40° from the electrical axis during sinus rhythm, it also suggests ventricular tachycardia. If the tachyarrhythmia has a right bundle branch block pattern but the electrical axis is more negative than –30° it suggests ventricular tachycardia. If the tachyarrhythmia has a left bundle branch block pattern but the electrical axis is more positive than 90° it suggests ventricular tachycardia. In general, left axis deviation suggests ventricular tachycardia.

QRS duration

QRS duration >0.14 s suggest ventricular tachycardia. QRS duration >0.16 s strongly suggest ventricular tachycardia. Note that ventricular tachycardia originating in the interventricular septum may have a relatively narrow QRS complex (0.120–0.145 s). Antidromic AVRT may also have >0.16 s. Class I antiarrhythmic drugs, tricyclic antidepressants and hyperkalemia may also cause very wide QRS complexes.

Concordance in V1–V6

Concordance means that all QRS complexes from lead V1 to lead V6 head in the same direction; all are either positive or negative. If any lead displays biphasic QRS complexes (e.g qR complex or RS complex) there cannot be concordance. Negative concordance (all QRS complexes being negative) strongly suggest ventricular tachycardia). Positive concordance (all QRS complexes being positive) are mostly due to ventricular tachycardia but may be caused by antidromic AVRT. The following figure presents concordance. To conclude, concordance is strongly suggestive of ventricular tachycardia.

Figure 7. Concordance in QRS complexes from V1 to V6 in ventricular tachycardia.

Figure 8. Lead I, II, III, V1 aVR, aVL and aVF. As seen in the beginning of the recording, the patient has an underlying rhythm of atrial fibrillation. The atrial fibrillation is interrupted by a rapid and regular tachycardia with wide QRS complex. The 4th beat from the end is a premature ventricular beat and its QRS morphology is identical to the QRS seen during the tachycardia. Hence, the tachycardia also originates from the ventricles, which implies that it is ventricular tachycardia (VT). Source | License

Absence of RS complexes

If there is no QRS complex from lead V1 to lead V6 which is an RS complex (i.e consists of an R wave and an S wave), then ventricular tachycardia is very likely.

Adenosine

It is not recommended that adenosine be administered when ventricular tachycardia is suspected, because adenosine may accelerate the frequency and aggravate the arrhythmia. Occasionally adenosine is still administered (when suspecting that the arrhythmia is actually a SVT with wide QRS complexes). If adenosine do not have any effect or if it accelerates the tachycardia, it is likely to be ventricular tachycardia.

In addition to these characteristics, researchers have developed several algorithms to differentiate ventricular tachycardia from SVTs. These algorithms are briefly outlined below (refer to Management and Diagnosis of Tachyarrhythmias for details)

Brugada’s algorithm

This is the most used algorithm. If any of the five criteria below are fulfilled, a diagnosis of ventricular tachycardia can be made.

Brugada’s algorithm

If there is no RS complex in any chest lead (V1–V6) a diagnosis of ventricular tachycardia can be made. Otherwise, continue to next criteria.

Assess the RS interval (interval from start of the R-wave to the nadir of the S-wave). If any RS interval is >100 ms and the R-wave is wider than the S-wave, a diagnosis of ventricular tachycardia can be made. Otherwise, continue to next criteria.

If there is AV dissociation, a diagnosis of ventricular tachycardia can be made. Otherwise, continue to next criteria.

Assess the QRS morphology in V1, V2, V5 and V6 (see below). If the QRS morphology is compatible with ventricular tachycardia, then the diagnosis is ventricular tachycardia.

If no criteria have been fulfilled, a diagnosis of supraventricular tachycardia can be made.

Judging the QRS morphology (criteria #4 in Brugada’s algorithm)

If the QRS complex in V1–V2 resembles a right bundle branch block (i.e positive QRS)

V1:

Monophasic R complex suggests ventricular tachycardia.

qR complex suggests ventricular tachycardia.

if R is taller than R’, ventricular tachycardia is suggested.

Triphasic complexes (rSr’, rsr’, rSR’, rsR’) suggests SVT

V6:

rS, QS, R or Rs complex suggests VT.

If the QRS complex in V1–V2 resembles a left bundle branch block (i.e negative QRS)

V1:

The initial portion of the QRS complex is smooth in ventricular tachycardia. SVT has a sharp start of the QRS complex.

R-wave duration ≥40 ms suggest ventricular tachycardia.

Duration from start of QRS complex to nadir of S-wave ≥60 ms suggests ventricular tachycardia.

V6:

QR or QS complex suggest ventricular tachycardia.

R or RR complex without initial q-wave suggests SVT.

All in all, Brugada’s criteria have very high sensitivity (90%) and specificity (60–90%) for diagnosing ventricular tachycardia.

Brugada’s algorithm for differentiating ventricular tachycardia from antidromic AVRT

The algorithm above frequently fails to differentiate ventricular tachycardia from antidromic AVRT. Although antidromic AVRT is an uncommon cause of ventricular tachycardia, it is important to be able to differentiate these entities. The older the patient and the more significant the heart disease, the more likely is ventricular tachycardia. The Brugada group has also developed an algorithm to differentiate antidromic AVRT from ventricular tachycardia. The algorithm follows:

Brugada’s algorithm for differentiating ventricular tachycardia and antidromic AVRT

If the QRS complex is net negative in V4–V6, ventricular tachycardia is more likely.

If the QRS complex is net positive in V4–V6 and any of the leads V2–V6 display a qR complex, ventricular tachycardia is very likely.

If there is AV dissociation, ventricular tachycardia is very likely.

If there are no signs of ventricular tachycardia, antidromic AVRT should be strongly considered.

Case 1: Ventricular arrhythmias during sudden cardiac arrest

Below is a Holter recording from a 62-year-old male with a history of coronary artery disease. The initial rhythm is sinus rhythm, interrupted by polymorphic VT which progresses to coarse ventricular fibrillation and subsequently fine ventricular fibrillation.

ECG 1. Sinus rhythm interrupted by ventricular tachycardia (VT).

ECG 3. Ventricular fibrillation (VF).

ECG 4. Ventricular fibrillation (VF).

ECG 5. Ventricular fibrillation (VF).

ECG 6. Delivery of shock, followed by asystole.

ECG 7. Asystole after shock.

ECG 8. Recurrence of supraventricular rhythm.

ECG 9. Supraventricular rhythm.

Management of ventricular tachycardia

General principles

The risk of degeneration to ventricular fibrillation (VF) is substantially higher in polymorphic VT, as compared with monomorphic VT. Ongoing myocardial ischemia is the most common cause of polymorphic VT.

Always search for and correct reversible causes of ventricular arrhythmias. These should be treated simultaneously with the administration of antiarrhythmic agents. Acute decompensated heart failure, acute myocardial ischemia, electrolyte disturbances (hypokalemia, hypomagnesemia), etc, are such causes.

In the context of antiarrhythmic drugs, structural heart disease (SHD) is defined as ischemic heart disease, valvular heart disease, congenital heart disease, ventricular hypertrophy or myocardial disease. Structural heart disease confers a substantial risk of ventricular arrhythmias and a significant risk of proarrhythmic effects of antiarrhythmic drugs. While several antiarrhythmic drug classes are available for emergency treatment of VT/VF in these patients, long-term treatment is limited mostly to amiodarone, beta-blockers or sotalol. In patients with structural heart disease, only amiodarone and beta-blockers are considered safe (with regards to proarrhythmic effects) for long-term use without the implantation of an ICD.

Amiodarone is safe and effective in the presence of significant structural heart disease (including severely reduced ejection fraction), with the exception of patients with ventricular tachycardia or ventricular fibrillation caused by QT-prolongation (long QT-syndrome). Amiodarone is unlikely to induce hazardous QT-prolongation in patients with normal QT-interval. Amiodarone may, however, induce lethal arrhythmias in patients with preexisting QT prolongation (congenital or acquired). Lidocaine is safe and effective in ventricular arrhythmias caused by QT prolongation (long QT syndrome).

It is important to distinguish polymorphic VT from torsade de pointes, since amiodarone (the most common first-line therapy) is contraindicated in torsade de pointes due to the fact that additional QT prolongation (induced by amiodarone) may cause degeneration into ventricular fibrillation and asystole. However, a polymorphic VT may exhibit the characteristic twisting of the points seen in torsade de pointes. A diagnosis of TdP should be made if a polymorphic VT occurs in a patient with a QTc interval >480 ms (QTc >500 ms in most patients).

Class III agents (amiodarone, dronedarone, dofetilide, ibutilide, sotalol) should be avoided in individuals at high risk of QT prolongation. QT prolongation >60 ms from baseline or QTc >500 ms, T-wave alternans, pronounced T–U wave distortion after a pause, and new ventricular ectopy are risk factors for torsade de pointes after the instigation of Class III agents (Dan et al).

Among the antiarrhythmic agents, only beta-blockers have been demonstrated to provide long-term protection for sudden cardiac arrest (SCA) and sudden cardiac death (SCD). Other antiarrhythmic drugs have failed to show efficacy in the prevention of SCD in randomized controlled trials. ICDs are effective for long-term prevention of SCD (Zipes et al, Priori et al). Beta-blockers are also effective in treating acute ventricular tachycardia, irrespective of type.

If antiarrhythmic agents fail to treat monomorphic VT, catheter ablation should be considered as an effective alternative (Tung et al).

Acute coronary angiography should be considered in all patients with ventricular arrhythmias potentially caused by myocardial ischemia. Coronary angiography should also be considered in the following scenarios:

New-onset ventricular arrhythmia in the absence of a clear (non-ischemic) cause.

In patients developing ventricular arrhythmias after recently undergoing a coronary intervention (stent thrombosis is highly likely in these scenarios).

Administration of prophylactic lidocaine upon return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest (OHCA) is associated with less recurrent VF/VT arrest. Thus, lidocaine may be used as prophylaxis after OHCA. Whether the same holds true for amiodarone remains unknown (Kudenchuck et al).

Non-sustained ventricular tachycardia (NSVT)

Patients without structural heart disease:

First-line therapy: beta-blockers or verapamil are usually effective.

Second-line therapy: amiodarone or sotalol.

Patients with structural heart disease:

First-line therapy: beta-blockers, verapamil and amiodarone.

Sotalol may be given to patients with moderate structural heart disease, including ischemic heart disease. Consider implantation of an ICD if sotalol is required for prophylaxis.

Class IC drugs (flecainide, propafenone) are only used in the absence of ischemia, previous myocardial infarction, and structural myocardial disease.

Sustained ventricular tachycardia

First-line therapy: beta-blockers, amiodarone, lidocaine, procainamide.

Second-line therapy: Sotalol.

Idiopathic ventricular tachycardia

Idiopathic ventricular tachycardia is defined as ventricular tachycardia in the absence of structural heart disease, genetic forms of ventricular tachycardia, including channelopathies. These arrhythmias mostly originate in the right ventricular outflow tract (RVOT), the left ventricular fascicular system (LVFS) or the mitral annulus.

First-line therapy: Beta-blockers are usually effective in treating idiopathic VT. Beta-blockers should be titrated to maximally tolerated dose.

Second-line therapy: Class IV agents (verapamil).

Third-line therapy: amiodarone, sotalol, flecainide, mexiletine, or propafenone are available as third-line alternatives.

Catheter ablation should be considered if beta-blockers fail.

Ventricular tachycardia in structural heart disease

First-line therapy: Beta-blockers.

Second-line therapy: Beta-blockers are frequently insufficient and may therefore require combination therapy with amiodarone.

Third-line therapy: Monotherapy with sotalol.

Monotherapy with beta-blocker is inferior to monotherapy with sotalol or combination therapy with amiodarone and beta-blocker (Connolly et al).

Polymorphic ventricular tachycardia and fibrillation in structural heart disease with normal QT interval

First-line therapy: Beta-blockers, amiodarone (150–300 mg i.v. bolus over 10 minutes), or lidocaine (1 mg/kg i.v bolus over 5 minutes). Immediate coronary angiography is indicated when ischemia is a likely cause.

Additional therapies:

Amiodarone or lidocaine.

Deep sedation and mechanical ventilation

Catheter ablation

Neuraxial modulation (Tung et al).

Catecholaminergic polymorphic VT (CPVT) typically responds to beta-blockers. Flecainide can be considered if beta-blockers fail. An ICD must be considered if beta-blockers fail.

Brugada syndrome causes polymorphic VT that responds to quinidine and isoproterenol.

Polymorphic ventricular tachycardia in patients with QT prolongation

Polymorphic ventricular tachycardia occurring during QT prolongation, with the characteristic twisting of the points, is referred to as torsade de pointes (TdP). The risk of degeneration into ventricular fibrillation and cardiac arrest is high. Torsade de pointes is treated as follows:

Magnesium sulfate 2 g i.v, regardless of serum magnesium level. Magnesium injections may be repeated and an infusion should be started.

Replenish serum potassium to levels around 4.5 to 5.0 mmol/L.

Torsade de pointes occurring during bradycardia or long pauses can be counteracted by increasing the heart rate (>70 beats per minute [bpm]):

If the patient has a pacemaker, increase the pacing rate.

In the absence of a pacemaker, start infusion isoproterenol.

Temporary pacing may be required until isoproterenol can be started.

Lidocaine 1 mg/kg i.v should be considered in all patients with torsade de pointes.

Ventricular arrhythmias in acute coronary syndromes (unstable angina, NSTEMI, STEMI)

The use of beta-blockers in acute coronary syndromes is still debated. Early studies suggested that beta-blockers may limit infarct size and prevent sudden cardiac death (Braunwald et al). Beta-blockers are considered safe in the early phase of acute coronary syndromes (in the absence of acute heart failure), and are likely to reduce the incidence of ventricular arrhythmias (VT, VF) and cardiac arrest. Short-acting beta-blockers can be initiated early (within 48 hours).

Beta-blockers are efficient for the treatment of monomorphic and polymorphic VT.

Revascularization is very important to prevent recurrent ventricular arrhythmias (VT, VF) and sudden cardiac death.

Amiodarone should be considered if beta-blockers and revascularization are insufficient to eliminate the arrhythmias.

Lidocaine is as effective as amiodarone and should be preferred in patients with hypotension (amiodarone may aggravate hypotension and cause cardiogenic shock).

Left ventricular dysfunction

Beta-blockers reduce the risk of sudden cardiac arrest in individuals with heart failure (Packer et al).

Randomized trials have demonstrated that an ICD increases survival in patients with heart failure. Amiodarone is the first-line therapy only if an ICD is not available.

Optimizing heart failure therapy with evidence-based drugs (beta-blockers, ARNI, ACEi/ARB, MRA, SGLT2-inhibitors) is presumably the most effective means for reducing the incidence of ventricular arrhythmias.

Antiarrhythmic drug therapy in inherited cardiomyopathies and channelopathies

Ventricular arrhythmias in arrhythmogenic cardiomyopathies and channelopathies are mostly treated with antiarrhythmic agents.

ARVC (Arrhythmogenic Right Ventricular Cardiomoypathy): ARVC typically causes monomorphic VT. These arrhythmias can be controlled with amiodarone or sotalol.

HCM (Hypertrophic Cardiomoypathy): HCM typically causes atrial fibrillation, atrial flutter and ventricular fibrillation (VF). Ventricular fibrillation is managed with amiodarone.

LQTS (Long QT Syndrome): Several beta-blockers are highly effective; e.g. propranolol, nadolol, metoprolol, and bisoprolol. Mexiletine, flecainide, and ranolazine are used in LQT3 syndrome.

Brugada syndrome: ventricular arrhythmias (polymorphic VT) are prevented and treated with quinidine. Acute therapy includes infusion of isoproterenol. An ICD may be warranted.

CPVT (Catecholaminergic polymorphic VT): beta-blockade (preferably nadolol) is first-line therapy and flecainide can be added.

Early repolarization syndrome, short-QT syndrome: quinidine is the first-line therapy.

Treatment of proarrhythmic effects: arrhythmias caused by antiarrhythmic agents

Risk factors: high drug dose, combination therapy with multiple antiarrhythmics, structural heart disease (ischemic heart disease, heart failure, etc), female sex, advanced age, renal failure, liver failure. Antiarrhythmic drugs may unmask underlying genetic arrhythmias (e.g flecainide and Brugada syndrome).

Monitor the heart rhythm, QRS duration and QTc interval when starting antiarrhythmic therapy (compare several 12-lead ECGs before and after administration of the drug). For Class III agents, QT prolongation >60 ms from baseline or QTc >500 ms, T-wave alternans, pronounced T–U wave distortion after a pause, and new ventricular ectopy are risk factors for torsade de pointes (Dan et al). Class IA agents (ajmaline, cibenzoline, disopyramide, pilsicainide, procainamide, quinidine) and Class III agents (amiodarone, dronedarone, dofetilide, ibutilide, sotalol) are most likely to cause torsade de pointes.

Flecainide, propafenone, mexiletine, disopyramide and quinidine are contraindicated in patients with a history of myocardial infarction.

Amiodarone rarely causes TdP.

Digitalis may cause most bradyarrhythmias and tachyarrhythmias, including VT.

Management

Discontinue the offending agent.

Search for and correct ongoing myocardial ischemia, hypokalaemia, hypomagnesemia, bradycardia, QT prolongation.

Treatment of drug-induced TdP:

Magnesium sulfate 2 g i.v, regardless of serum magnesium level. Magnesium injections may be repeated and an infusion should be started.

Replenish serum potassium to levels around 4.5 to 5.0 mmol/L.

Torsade de pointes occurring during bradycardia or long pauses can be counteracted by increasing the heart rate (>70 beats per minute [bpm]):

If the patient has a pacemaker, increase the pacing rate.

In the absence of a pacemaker, start infusion isoproterenol.

Temporary pacing may be required until isoproterenol can be started.

Lidocaine 1 mg/kg i.v should be considered in all patients with torsade de pointes.

Treatment of arrhythmias caused by class I agents:

First-line therapy: beta-blockers or calcium antagonists (IV) to control ventricular rate. Infusion of sodium bicarbonate may terminate the VT.

Treatment of arrhythmias caused by flecainide:

First-line therapy: beta-blockers.

Arrhythmias due to digitalis toxicity:Administer potassium, aim for high-normal potassium (4.5–5.0 mEq/L).

Administer beta-blockers, lidocaine and/or digitalis-specific antibodies.

Isoproterenol infusion or cardiac pacing is effective when digitalis causes bradyarrhythmias.

Drug manual

Class III antiarrhythmic drugs

Amiodarone

Drug	Amiodarone
Brand names	Nexterone, Pacerone, Cordarone
Indications	Ventricular tachycardia (VT)Ventricular fibrillation (VF)Premature ventricular beats (PVB)Atrial tachyarrhythmias (atrial fibrillation)Cardiopulmonary resuscitation (CPR)
Mechanism of action	Amiodarone is a class III antiarrhythmic agent and prolongs phase 3 of the cardiac action potential.
Receptor targets	INa, ICa, IKr, IK1, IKs, Ito, Beta receptor, Alpha receptor, nuclear T3 receptor
ECG effects	Sinus rate slowedPR prolongedQRS prolongedQTc prolongedAV nodal refractoriness increased
Delivery	IV, PO
Dose	VF/pulseless VT (cardiac arrest): 300 mg IV bolus in 20 ml glucose. May be repeated.Stable VT: 150 mg bolus over 10 minutes, then 1 mg/min over 6 hours, then 0.5 mg/min over 18 hours. The maintenance dose is 0.5 mg/min IV.Daily infusion dose: 1200 mg per 24 hours.Switch to oral regime when ventricular arrhythmias are controlled: 400 mg every 8 to 12 hours for 1–2 weeks, then 300–400 mg daily. If possible, use 200 mg daily PO dose for long-term use. Acquire thyroid function studies if long-term therapy may be needed.
T1/2	Amiodarone has a very long half-life (26-107 days) and persists in the body for months.
Contraindications	Pre-excitation (WPW syndrome)Long QT syndrome (congenital or acquired)
Adverse effects	Cardiac: Bradycardia. Hypotension. Thyreotoxic (hypothyreosis). QT prolongation (torsade de pointes, TdP). AV blocks. Amiodarone may slow VT rate below the programmed ICD detection rate. Amiodarone increases DFT (defibrillation threshold).Other: Corneal microdeposits, thyroid abnormalities, ataxia, nausea, emesis, constipation, photosensitivity, skin discoloration, ataxia, dizziness, peripheral neuropathy, tremor, hepatitis, cirrhosis, pulmonary fibrosis or pneumonitis.
Comparison	Amiodarone resulted in substantially higher rates of survival to hospital admission in a randomized trial comparing amiodarone to lidocaine for shock-resistant out-of-hospital ventricular fibrillation (Dorian et al, NEJM, 2002).

Sotalol

Drug	Sotalol
Brand names	Betapace, Sorine, Sotylize, Sotacor
Indications	VT (ventricular tachycardia)PVC (premature ventricular complexes)VF (ventricular fibrillation)
Mechanism of action	Class III antiarrhythmic agent with beta blocking activity.
Receptor targets	IKr, Beta 1 and 2 receptor
ECG effects	Sinus rate slowedQTc prolongedAV nodal refractoriness increased
Delivery	IV, PO
Dose	IV: 75 mg every 12 hPO: 40–120 mg every 12 h. May increase dose every third day to a maximum of 320 mg/d
T1/2	12 h
Adverse effects	Cardiac: Bradycardia, hypotension, HF, syncope, TdP Other: Fatigue, dizziness, weakness, dyspnea, bronchitis, depression, nausea, diarrheaSotalol decreases defibrillatory threshold.

Beta-blockers

Metoprolol

Drug	Metoprolol
Brand names	Dutoprol, Kapspargo, Lopressor, Lopressor Hct, Toprol, Toprol XL, Seloken
Indications	VT (ventricular tachycardia)PVC (premature ventricular complexes)
Mechanism of action	Lowers blood pressure, reduces heart rate, myocardial oxygen consumption and myocardial contractility. Blocks proarrhythmic sympathetic activity.
Receptor targets	Beta 1 adrenergic receptor blocker.
ECG effects	Sinus rate slowedAV nodal refractoriness increased
Delivery	IV or PO
Dose	IV (emergency): 5 mg every 5 min up to 15 mg.PO (stable patients): 25–200 mg daily of extended release.
T1/2	3–4 h (immediate release).8 hours (extended release).
Adverse effects	Cardiac: Bradycardia, hypotension, AV-block.Other: Dizziness, fatigue, diarrhea, depression, dyspnea.

Nadolol

Drug	Nadolol
Brand names	Corgard
Indications	VT (ventricular tachycardia)PVC (premature ventricular complexes)LQTS (Long QT Syndrome)CPVT (Catecholaminergic Polymorphic VT)
Mechanism of action	Beta 1 and 2 adrenergic blocker. Lowers blood pressure, reduces heart rate, myocardial oxygen consumption and myocardial contractility. Blocks proarrhythmic sympathetic activity.
Receptor targets	Beta 1 and 2 receptors
ECG effects	Sinus rate slowedAV nodal refractoriness increased
Delivery	IV, PO
Dose	PO: 40–320 mg daily
T1/2	20–24 h
Adverse effects	Cardiac: Bradycardia, hypotension, HF, AV-block.Other: Edema, dizziness, cold extremities, bronchospasm.

Esmolol

Drug	Esmolol
Brand names	Brevibloc
Indications	VT (ventricular tachycardia)
Mechanism of action	Beta 1 adrenergic blocker. Lowers blood pressure, reduces heart rate, myocardial oxygen consumption and myocardial contractility. Blocks proarrhythmic sympathetic activity.
Molecular targets	Beta 1 receptors
ECG effects	Sinus rate slowedAV nodal refractoriness increased
Delivery	IV, PO
Dose	IV: 0.5 mg/kg bolus, then 0.05 mg/kg/min infusion.
T1/2	9 minutes
Adverse effects	Bradycardia, hypotension, heart failure, AV-block. Dizziness, nausea.

Bisoprolol

Drug	Bisoprolol
Brand names	Ziac, Zebeta, Emconcor, Bisomyl
Indications	VT (ventricular tachycardia)PVC (premature ventricular complexes)
Mechanism of action	Beta 1 adrenergic blocker. Lowers blood pressure, reduces heart rate, myocardial oxygen consumption and myocardial contractility. Blocks proarrhythmic sympathetic activity.
Molecular targets	Beta 1 receptors
ECG effects	Sinus rate slowedAV nodal refractoriness increased
Delivery	IV, PO
Dose	PO: 2.5–10 mg once daily
T1/2	9–12 h
Adverse effects	Cardiac: Chest pain, bradycardia, AV-block.Other: Fatigue, insomnia, diarrhea

Carvedilol

Drug	Carvedilol
Brand names	Coreg
Indications	VT (ventricular tachycardia)PVC (premature ventricular complexes)LQTS (Long QT Syndrome)
Mechanism of action	Blocks beta 1 and beta 2 adrenergic receptors, and alpha adrenergic receptors. Lowers blood pressure, reduces contractility and blocks the proarrhythmic sympathetic activity.
Molecular targets	Beta 1, beta 2 receptors, alpha receptor.
ECG effects	Sinus rate slowedAV nodal refractoriness increased
Delivery	IV, PO
Dose	PO: 3.125–25 mg every 12 h
T1/2	7–10 h
Adverse effects	Cardiac: Bradycardia, hypotension, AV-block.Other: Edema, syncope, hyperglycemia, dizziness, fatigue, diarrhea

Propranolol

Drug	Propranolol
Brand names	Hemangeol, Hemangiol, Inderal, Innopran
Indications	VT (ventricular tachycardia)PVC (premature ventricular complexes)LQTS (Long QT Syndrome)
Mechanism of action	Blocks beta 1, beta 2 and alpha adrenergic receptors. Lowers blood pressure, reduces contractility and blocks proarrhythmic sympathetic activity. Blocks cardiac sodium channels.
Molecular targets	Beta 1 and 2 receptors, INa
ECG effects	Sinus rate slowedAV nodal refractoriness increased
Delivery	IV, PO
Dose	IV: 1–3 mg q 5 min to a total of 5 mgPO, immediate release: 10–40 mg q 6 hPO, extended release: 60–160 mg q 12 h
T1/2	Immediate release: 3–6 hExtended release: 8–10 h
Adverse effects	Cardiac: Bradycardia, hypotension, heart failure, AV-block.Other: Sleep disorder, dizziness, nightmares, hyperglycemia, diarrhea, bronchospasm.

Acebutolol

Drug	Acebutolol
Brand names	Sectral
Indications	VT (ventricular tachycardia)PVC (premature ventricular complexes)
Mechanism of action	Beta 1 receptor antagonist. Mild intrinsic sympathomimetic activity.
Molecular targets	Beta 1 and 2 receptors, Alpha receptor.
ECG effects	Sinus rate slowed AV nodal refractoriness increased
Delivery	IV, PO
Dose	PO: 200–1200 mg daily or up to 600 mg bid.
T1/2	Active metabolite: 8–13 h. Prolonged in renal impairment.Metabolised in liver. Excreted in feces (60%) and urine (40%).
Adverse effects	Cardiac: Bradycardia, hypotension, HF, AV-blocks.Other: Dizziness, fatigue, anxiety, impotence, hyper/ hypoesthesia

Class IC agents

Lidocaine

Drug	Lidocaine
Synonyms	Lidocaína, Lidocaina, Lidocaine, Lidocainum, Lignocaine
Brand names	Xylocard
Indications	Any VT (ventricular tachycardia), including torsade de pointes (long QT syndrome).Digitalis induced VT.Ventricular fibrillation (VF).
Mechanism of action	Class I-B antiarrhythmic.
Receptor targets	INa
ECG effects	QTc can slightly shorten
Effects	Potent terminator of ventricular arrhythmias.
Delivery	IV
Dose	Loading dose: 1-1.5 mg/kg IV bolus over 2-3 min.Infusion dose: 2 to 4 mg/min.Additional boluses may be given: 0.5 mg/kg repeated every 5-10 minutes.Max cumulative dose: 3 mg/kg
Adverse effects	Lidocaine toxicity: drowsiness; disorientation, paresthesia, twitching, seizures. Toxicity is managed by decreasing dose by 50% (same bolus then infusion 1 mg/min).Cardiac: Bradycardia, hemodynamic collapse, AVB, sinus arrest.Other: Delirium, psychosis, seizure, nausea, tinnitus, dyspnea, bronchospasm

Mexilitine

Drug	Mexilitine
Indications	VT (ventricular tachycardia)PVC (premature ventricular complexes)VT in long QT syndrome (LQT3)Ventricular fibrillation (VF)
Molecular targets	INa
ECG effects	QTc can slightly shorten
T1/2	10–14 h. Metabolized in liver. Excreted in urine.
Delivery	IV
Dose	PO: 150–300 mg q 8 h or q 12 h
Adverse effects	Cardiac: heart failure, AV-blocks.Other: Lightheaded, tremor, ataxia, paresthesias, nausea, blood dyscrasias

Class IC agents

Flecainide

Drug	Flecainide
Brand names	Tambocor
Indications	VT (ventricular tachycardia)PVC (premature ventricular complexes), in the absence of structural heart disease.(CPVT)
Receptor targets	INa, IKr, IKur
ECG effects	PR prolongedQRS prolonged
Delivery	IV, PO
Dose	PO: 50–200 mg q 12 h.
T1/2	7–22 h Metab: H Excr: U
Adverse effects	Cardiac: Sinus node dysfunction, AVB, drug-induced Brugada syndrome, monomorphic VT in patients with a myocardial scar, exacerbation of HFrEF. Flecainide causes increased defibrillation threshold.Other: Dizziness, tremor, vision disturbance, dyspnea, nausea

Propafenone

Drug	Propafenone
Brand names	Rythmol
Indications	VT (ventricular tachycardia)PVC (premature ventricular complexes), in the absence of structural heart disease.
Mechanism of action	Propafenone inhibits sodium channels (INa) to restrict the entry of sodium into cardiac cells, resulting in reduced excitation.
Molecular target	INa, IKr, IKur, Beta receptor, Alpha receptor
ECG effects	PR prolonged QRS prolonged; increased DFT
T1/2	Extensive metabolizers: 2–10 h.Poor metabolizers: 10–32 h.Metabolized in liver. Excreted in urine.
Delivery	IV
Dose	PO:Immediate release: 150–300 mg q 8 hExtended release: 225-425 mg q 12 h
Adverse effects	Cardiac: HF, AVB, drug-induced Brugada syndromeOther: Dizziness, fatigue, nausea, diarrhea, xerostomia, tremor, blurred vision

Class IV agents (Calcium channel blockers)

Diltiazem

Drug	Diltiazem
Synonyms	Diltiazemum
Brand names	Cardizem, Cartia, Matzim, Taztia, Tiadylt, Tiazac
Indications	VT specifically RVOT, idiopathic LVT
Mechanism of action	Diltiazem inhibits the calcium influx into cardiac and vascular smooth muscle during depolarization. Compared to dihydropyridine drugs, such as nifedipine, that preferentially act on vascular smooth muscle and verapamil that directly acts on the heart muscle, diltiazem displays an intermediate specificity to target both the cardiac and vascular smooth muscle. Diltiazem is used as an antihypertensive, antiarrhythmic, and as an antianginal agent.
Molecular targets	INa, IKr, IKur
ECG effects	Sinus rate slowedPR prolongedAV nodal conduction slowed
Delivery	IV, PO
Dose	IV: 5–10 mg every 15–30 min.Extended release, PO: 120–360 mg/day.
T1/2	Injection 2–5 h.Immediate release 4.5 hExtended release 12 hSevere hepatic impairment 14–16 h.Metabolized in liver. Excreted in urine.
Adverse effects	Cardiac: Hypotension, edema, heart failure, AV-blocks, bradycardia, exacerbation of HFrEF.Other: Headache, rash, constipation

Verapamil

Drug	Verapamil
Synonyms	Iproveratril, Vérapamil, Verapamilo, Verapamilum
Brand names	Calan, Isoptin, Isoptin Retard, Tarka, Verelan
Indications	VT (specifically RVOT, verapamilsensitive idiopathic LVT)
Mechanism of action	Verapamil is an L-type calcium channel blocker with antiarrhythmic, antianginal, and antihypertensive effect. Verapamil has a negative inotropic effect and should be avoided in HCM and severe HFrEF. L-type calcium channels are expressed in vascular smooth muscle (affecting vascular resistance) and myocardial tissue (affecting contractility). Verapamil lowers systemic vascular resistance and thus blood pressure. Verapamil also increases the refractory period in the AV node, thereby reducing AV nodal conduction.
Receptor targets	Cardiac L-type calcium channels.
ECG effects	Sinus rate slowed PR prolonged AV nodal conduction slowed
Delivery	IV, PO
Dose	IV: 2.5–5 mg q 15–30 min Sustained release PO: 240–480 mg/d
T1/2	3–7 hMetaoblized in liver. Excreted in urine.
Adverse effects	Cardiac: Hypotension, edema, HF, AVB, bradycardia, exacerbation of HFrEFOther: Headache, rash, gingival hyperplasia, constipation, dyspepsia

Class IA agents

Procainamide

Drug	Procainamide
Synonyms	Procainamida, Procainamide, Procaïnamide, Procainamidum
Brand names	Procan
Indications	VT (ventricular tachycardia), including digitalis induced VT.VF (Ventricular fibrillation)
Receptor targets	INa, IKr
Effects	Procainamide is a sodium channel blocker.
Delivery	IV
Dose	IV, loading dose: 10–17 mg/kg at 20–50 mg/minMaintenance dose: 1–4 mg/minPO (SR preparation): 500–1250 mg q 6 h
T1/2	2–5 h.Prolonged in renal dysfunction.
Adverse effects	Cardiac: TdP; AVB, hypotension and exacerbation of HFrEFOther: Lupus symptoms, diarrhea, nausea, blood dyscrasias

Other agents

Magnesium

Drug	Magnesium
Indications	VF (ventricular fibrillation)VT (ventricular tachycardia)Should be used in most patients with long QT syndrome (LQTS) with ventricular arrhythmias.
Mechanism of action	Electrolyte with antiarrhythmic effects, regardless of blood magnesium levels.
Effects	Membrane stabilization.
Delivery	IV
Dose	20 mmol IV over 20 min, then 20 mmol every 20 hour.

Bretylium

Drug	Bretylium
Brand names	VF (ventricular fibrillation)VT (ventricular tachycardia)
Mechanism of action	Bretylium inhibits the release of norepinephrine. Bretylium is used for the prophylaxis and therapy of ventricular fibrillation (VF) and ventricular tachycardia (VT).
Effects	Bretylium blocks the release of noradrenaline from the peripheral sympathetic nervous system by inhibiting voltage-gated K+ channels and, possibly, the Na-K-ATPase.
Delivery	IV
Dose	Injection (undiluted): 5 mg/kg by rapid injection; if arrhythmia persists, may increase dose to 10 mg/kg and repeat as necessary.Infusion (diluted): 1-2 mg/min; alternatively, 5-10 mg/kg IV over at least 8 min repeated every 6 hour.

Referenser

Schleifer JW, Sorajja D, Shen W. Advances in the pharmacologic treatment of ventricular arrhythmias. Expert Opin Pharmacother 2015;16:2637–51.

Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Com. Europace 2006;8:746–837.

Priori SG, Blomstro ̈ m-Lundqvist C, Mazzanti A, Blom N, Borggrefe M, Camm J. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Europace 2015;17:1601–87.

Tung R, Vaseghi M, Frankel DS, Vergara P, Di Biase L, Nagashima K et al. Freedom from recurrent ventricular tachycardia after catheter ablation is associated with improved survival in patients with structural heart disease: an International VT Ablation Center Collaborative Group Study. Heart Rhythm 2015;12:1997–2007.

Connolly SJ, Dorian P, Roberts RS, Gent M, Bailin S, Fain ES et al. Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: the OPTIC Study: a randomized trial. JAMA 2006;295:165–71.

Kudenchuk PJ, Newell C, White L, Fahrenbruch C, Rea T, Eisenberg M. Prophylactic lidocaine for post resuscitation care of patients with out-ofhospital ventricular fibrillation cardiac arrest. Resuscitation 2013;84:1512–8.

Eugene Braunwald, Robert A Kloner.. Intravenous Beta-Blockade for Limiting Myocardial Infarct Size: Rejuvenation of a Concept. J Am Coll Cardiol. 2016 May 10;67(18):2105-2107.

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Chapter 21: Long QT (QTc) interval, long QT syndrome (LQTS) & torsades de pointes

The QT interval is the time interval from the beginning of the QRS complex to the end of the T-wave. This interval represents the total time taken to depolarize and repolarize the ventricles (Figure 1). The length of the QT interval correlates strongly with the risk of potentially life-threatening ventricular arrhythmias. Therefore, the QT interval must always be assessed when interpreting the ECG. Long QT syndrome (LQTS) is manifest when a long QT interval induces ventricular arrhythmias.

Figure 1. The QT interval on the ECG.

The QT interval is inversely related to heart rate. As the heart rate increases, the QT interval decreases and vice versa. The physiological purpose of this phenomenon is to allow for faster cardiac cycles during tachycardia (e.g during physical exertion). Therefore, to judge whether the QT interval is normal or not, one must adjust for the current heart rate. This is done by adjusting the QT interval for the heart rate, and the resulting QT interval is referred to as corrected QT interval, or simply QTc interval. The primary hazard lies in long QTc intervals because they induce a very unstable polymorphic ventricular tachycardia referred to as torsade de pointes. Abnormally short QTc interval is also arrhythmogenic but it is a very rare condition.

Several formulas have been suggested to calculate corrected QT intervals. Some of these formulas follow:

Bazett’s formula for calculating corrected QT duration (QTc).

Bazett Formula: QTc = QT interval / √(RR interval)

Fridericia Formula: QTc = QT interval / (RR interval)1/3

Framingham Formula: QTc = QT interval + 154 x (1 – RR interval)

Hodges Formula: QTc = QT interval + 1.75 x [(60 / RR interval) − 60]

RR interval = 60 / HR

Calculate corrected QTc interval

QTc Interval calculator

Bazett’s formula is the most commonly used formula. However, all above-listed formulas were developed many decades ago and they have multiple drawbacks. For example, Bazett’s formula is only suitable in adults with a heart rate between 60 and 90 beats per minute. Bazett’s formula over-adjusts at higher heart rates and under-adjusts at lower heart rates.

	1 to 15 years, male and female	Adult, male	Adult, female
Normal	<440 ms	<430 ms	<450 ms
Upper limit	440–460 ms	430–450 ms	450–470 ms
Prolonged	>460 ms	>450 ms	>470 ms

It is recommended that the automatic (machine) calculation of the corrected QT interval be used. Such QTc intervals are derived by all modern ECG machines and the formulas used are more precise than those listed above. It is recommended that whenever the QTc interval is prolonged, it should be verified manually.

How to measure the QT interval

Expert opinion suggests that QT intervals should be measured as follows (Anderson et al):

The QT interval should be measured manually, from the beginning of the QRS complex to the end of the T wave.

The QT interval should be measured in 3 to 5 consecutive beats in leads II, V5 and V6. Leads without U waves are preferred.

Calculate the mean QT interval for each lead and use the longest QT interval obtained.

Large U waves that are fused with the T wave should be included in the measurement. This may result in an overestimation of the QT interval.

If the patient uses QT-prolonging drugs, the QT interval should be measured during peak plasma concentrations of that drug.

The QT interval should be adjusted for heart rate.

Long QT interval causes long QT syndrome

An abnormally prolonged QTc interval is referred to as long QT interval. The upper reference limit for QTc interval is 460 ms in males and 470 ms in females. QTc intervals exceeding these limits may cause torsade de pointes. If this occurs, i.e if a person with a long QT interval experiences such ventricular arrhythmias, the condition is referred to as long QT syndrome (LQTS).

Causes of long QT interval

A long QT interval is either congenital (genetic) or acquired.

Congenital long QT syndrome is caused by mutations in cardiac ion channels. More than 10 types of congenital prolongation of the QT interval have been discovered. Congenital QT prolongation is a very serious condition with high mortality. Among untreated patients who have experienced one episode of syncope, 20% die within 1 year. Fortunately, this mortality figure may be reduced to 1% over 15 years of follow-up with the use of evidence-based treatments. Three types of LQTS (LQT1, LQT2 and LQT3) represent roughly 90% of all cases of congenital LQTS. It is estimated that the prevalence of congenital QT prolongation is 1 per 2000 individuals in the population (prevalence figures from Italy). Importantly, individuals with congenital QT prolongation frequently report occurrences of unexplained syncope or cardiac arrest in the family. Such hereditary information is a strong predictor of sudden cardiac death.

Acquired long QT syndrome is caused by medications (amiodarone, sotalol, procainamide), hypokalemia, hypomagnesaemia and pronounced bradycardia. Because each of these factors (medications, electrolyte disorders and bradycardia) are all common, but only appear to cause QT prolongation in some individuals, it is thought that there has to be an underlying genetic susceptibility to develop acquired long QT syndrome.

The risk of developing torsade de pointes (polymorphic ventricular tachycardia) is evident in both congenital and acquired QT prolongation. The longer the QT interval the greater the risk of developing torsade de pointes. In general, torsade de pointes develops at QTc intervals greater than 490 milliseconds.

Torsade de pointes is usually induced by a premature ventricular beat occurring early in the cardiac cycle. The risk of torsade de pointes increases during bradycardia. Torsade de pointes causes syncope (or pre-syncope) but the arrhythmia is usually self-terminating (within 30 seconds). A minority of cases of torsade de pointes progress to ventricular fibrillation, which is fatal unless treatment is given promptly. Figure 2 shows torsade de pointed.

Figure 2. Torsade de pointes (polymorphic ventricular tachycardia) caused by long QT syndrome.

Besides the QT interval itself, the T-wave may provide valuable information regarding the type of long QT syndrome; particularly it may differentiate between type 1 LQTS, type 2 LQTS and type 3 LQTS. The T-wave should be assessed in the chest leads. Refer to Figure 3. Occasionally persons with LQTS display T-wave alternans, meaning that the amplitude or direction of the T-wave alternates from one beat to the next. T-wave alternans is an indicator of very high risk of torsade de pointes. Sinus pauses may also occur in congenital LQTS.

Figure 3. Characteristics of T-waves in different types of LQTS (long QT syndrome).

ECG criteria for torsade de pointes

Prolonged QTc interval before the appearance of torsade de pointes.

Twisting of the QRS complexes around the isoelectric baseline (polymorphic ventricular tachycardia).

ECG showing an episode of sinus rhythm (with multiple ventricular premature beats) spontaneously converting to Torsade de Pointes ventricular tachycardia. Notice how arterial blood pressure (ABP) drops at the onset of TdP. ECG by Nakstad et al (Scand J Trauma Resusc Emerg Med. 2010; 18: 7)

Torsade de Pointes ventricular tachycardia degenerating into ventricular fibrillation. ECG by Nakstad et al (Scand J Trauma Resusc Emerg Med. 2010; 18: 7)

Congenital long QT syndrome (LQTS)

At least 13 variants of congenital LQTS have been described. The mutations have autosomal inheritance with reduced penetrance. LQTS type 1, type 2 and type 3 (called LQT1, LQT2 and LQT3) represent 90% of all cases of long QT syndrome. LQT1 and LQT2 each represent roughly 40% of all cases.

Long QT syndrome type 1 (LQT1) is caused by a mutation in the potassium channel KCNQ1 (loss of function mutation). The arrhythmias usually occur during physical activity (for some reason swimming appears to be highly arrhythmogenic) and other situations with high sympathetic activity.  LQT1 is characterized by T-wave with a broad base (Figure 3). LQT1 is the most common type of congenital LQTS.

Long QT syndrome type 2 (LQT2) is caused by a mutation in the potassium channel KCNH2 (loss of function mutation). The arrhythmias typically occur at sudden surprises (sudden sounds, fear or other situations with abrupt and sudden stress),  stress, physical activity or during sleep. The T-wave has low amplitude with an additional hump or notch (Figure 3). Women with LQT2 who are in the postpartum period have very high risk of developing torsade de pointes.

Long QT syndrome type 3 (LQT3): is caused by a mutation in the sodium channel SCN5A (leads to increased sodium flows). The risk of arrhythmia is highest during sleep. Bradycardia is also highly arrhytmogenic in these patients. The ST-segment is stretched out, the T-wave occurs late and is pointed (Figure 3).

Long QT syndrome type 4 (LQT4): is rare and represents 1% of all cases. The mutation occurs in the ANKB gene which produces a protein that anchors membrane proteins to the cytoskeleton. LQT3 can cause multiple arrhythmias, such as familial catecholamine ventricular tachycardia, atrial fibrillation, conduction defects, sinus node dysfunction and bradycardia.

The other variants of LQTS are extremely rare and usually part of more severe syndromes which engage multiple organ systems. These types are not discussed here.

Schwartz criteria for diagnosis of congenital LQTS

Schwartz criteria are used to diagnose congenital LQTS. These criteria are presented in Table 1.

Table 1. Long QT syndrome diagnostic criteria (Schwartz et al):

ECG findings	CRITERIA	POINTS
QTc interval	≥480 ms	3
	460–479 ms	2
	450–459 ms (male)	1
QTc during 4th minute of recovery from exercise stress test ≥480 ms		1
Torsade de pointes		2
T-wave alternans		1
Low heart rate for age (resting heart rate below the 2nd percentile)		0.5
Clinical History
Syncope with stress		2
Syncope without stress		1
Congenital deafness		0.5
Family history
Family members with definite LQTS		1
Unexplained sudden cardiac death below age 30 among immediate family members		0.5

Evaluation of risk

≤1 point: low probability of LQTS.

1.5 – 3 points: intermediate probability of LQTS.

≥3.5 points: high probability.

Notes

ECG findings are only valid in the absence of medications or disorders known to affect these electrocardiographic features.

QTc is calculated by Bazett’s formula where QTc = QT/√RR.

Only one of syncope and torsade de pointes can count.

The same family member cannot be counted in both criteria under Family history.

Long QT syndrome induced by medications and drugs

Long QT syndrome caused by medications is much more common than congenital variants. Medications that may induce or aggravate long QT syndrome include adrenaline, certain antihistamines, erythromycine, trimetoprime, sulfa, pentamidine, kinidine, procainamide, disopyramide, sotalol, probukol, bepridil, difetilid, ibutilid, cisaprid, ketokonazol, itrakonazol, tricyclic antidepressants, fenotiazines, haloperidol, indapimid, certain antiviral drugs, etc (Table 2). The list of drugs that cause LQTS is very long and updated continuously. The complete list is provided by CredibleMeds (www.crediblemeds.com) which is supported by the FDA.

Table 2. Drugs causing or aggravating long QT syndrome.

CLASS	DRUG	ASSOCIATION	RISK OF TORSADE DE POINTES	EFFECT	COMMENTS
Anesthetics	Enflurane	Probable			Drug-drug interactions lead to QT prolongation
	Halothane	Probable			Nonspecific arrhythmias reported in package insert.
	Isoflurane	Probable
Antiarrhythmics	Amiodarone	Certain	High	QT interval prolongation, Torsade de pointes	i.v. affects QTc less than oral; proarrhythmia infrequent.
	Adenosine	Proposed
	Disopyramide	Certain		QT interval prolongation, Torsade de pointes	Rate appears lower than that of quinidine
	Dofetilide	Certain	High	QT interval prolongation, Torsade de pointes	Proarrhythmia 0.8%.
	Flecainide	Certain	High	QT interval prolongation, Torsade de pointes	Proarrhythmia “rare.”
	Ibutilide	Certain	High	QT interval prolongation, Torsade de pointes	Proarrhythmia 1.7%.
	Procainamide	Certain	High	QT interval prolongation, Torsade de pointes	Rate appears lower than that of quinidine.
	Propafenone	Certain	Moderate	QT interval prolongation, Torsade de pointes	Proarrhythmia “rare.”
	Quinidine	Certain	High	QT interval prolongation, Torsade de pointes	“Quinidine syncope” in 2–6% of patients.
	Sotalol	Certain	High	QT interval prolongation, Torsade de pointes	Proarrhythmia ~2%.
Anticonvulsants	Felbamate	Proposed		Torsade de pointes, according to manufacturer.
	Fosphenytoin	Proposed		QT interval prolongation according to manufacturer.
Antidepressants	Amitriptyline	Certain	Moderate		Nonspecific ECG changes reported in package insert.
	Citalopram	Probable
	Desipramine	Certain		QT interval prolongation	VF, sudden death reported by manufacturer.
	Doxepin	Certain	Moderate
	Fluoxetine	Probable		QT interval prolongation, Torsade de pointes	1 in 10,000 ventricular arrhythmias reported by manufacturer.
	Imipramine	Certain	Moderate		Nonspecific arrhythmias reported in package insert.
	Maprotiline	Certain			ECG changes; QRS reported in package insert.
	Nortriptyline	Certain			Nonspecific arrhythmias reported in package insert.
	Paroxetine	Probable		Torsade de pointes	Lower risk than that of TCAs.
	Sertraline	Probable		QT interval prolongation, Torsade de pointes	Lower risk than that of TCAs.
	Venlafaxine	Proposed		QT interval prolongation	1:1000 risk of arrhythmia reported in package insert.
Antihistamines	Astemizole	Certain	Moderate	Not applicable
	Clemastine	Proposed
	Diphenhydramine	Proposed
	Loratadine	Proposed	Unknown		Prolongation appears unlikely.
	Terfenadine	Certain	Moderate
Antiinfectives	Clarithromycin	Probable	Moderate	QT interval prolongation, Torsade de pointes
	Erythromycin	Certain	Medium high	QT interval prolongation, Torsade de pointes	Known drug-drug interactions with other agents (e.g., terfenadine).
	Fluconazole	Probable			Risk may be higher with i.v. dosing.
	Foscarnet	Proposed		QT interval prolongation
	Ganciclovir	Proposed
	Gatifloxacin	Probable		QT interval prolongation
	Grepafloxacin	Certain
	Halofantrine	Certain	Moderate
	Ketoconazole	Probable		QT interval prolongation, Torsade de pointes	Known drug-drug interactions with other agents (e.g., cisapride).
	Levofloxacin	Proposed		Torsade de pointes	Lower risk than that of similar agents.
	Mefloquine	Proposed			QT with halofantrine.
	Moxifloxacin	Probable		QT interval prolongation	Lower risk than that of similar agents.
	Pentamidine	Certain	Moderate	QT interval prolongation, Torsade de pointes
	Quinine	Probable	Moderate
	Sparfloxacin	Certain
	Trimethoprim-sulfamethoxazole	Proposed	Low
Antipsychotics	Chlorpromazine	Probable			Nonspecific ECG changes and sudden death reported by manufacturer.
	Clozapine	Proposed
	Haloperidol	Certain	Moderate	QT interval prolongation, Torsade de pointes
	Mesoridazine	Certain		QT interval prolongation, Torsade de pointes
	Pimozide	Certain		QT interval prolongation, Torsade de pointes	Drug-drug interactions also lead to QT prolongation.
	Quetiapine	Proposed		QT interval prolongation
	Risperidone	Proposed		QT interval prolongation	Sudden death reported by manufacturer.
	Sertindole	Proposed	Moderate
	Thioridazine	Certain	Moderate	QT interval prolongation, Torsade de pointes
	Ziprasidone	Certain		QT interval prolongation
Cancer drugs	Arsenictrioxide	Certain		QT interval prolongation, Torsade de pointes
	Tamoxifen	Probable		QT interval prolongation	Overdose situations.
Cardiovascular agents	Bepridil	Certain	Moderate	QT interval prolongation, Torsade de pointes	QTc increases by ~8%.
	Indapamide	Proposed		QT interval prolongation
	Isradipine	Proposed		QT interval prolongation according to manufacturer.	QTc increases by ~3%.
	Mibefradil	Proposed
	Moexipril hydrochlorothiazide	Proposed		QT interval prolongation according to manufacturer.
	Nicardipine	Proposed		QT interval prolongation according to manufacturer.
	Probucol	Certain
Gatrointestinal agents	Cisapride	Certain	Moderate	QT interval prolongation, Torsade de pointes
	Octreotide	Proposed		QT interval prolongation
	Droperidol	Certain	Certain	QT interval prolongation, Torsade de pointes
	Dolasetron	Proposed		QT interval prolongation according to manufacturer.
Migraine agents	Naratriptan	Probable		QT interval prolongation
	Sumatriptan	Probable		QT interval prolongation
	Rizatriptan	Probable			1:1000 risk of arrhythmia.
	Zolmitriptan	Probable		QT interval prolongation
Miscellaneous agents	Amantadine	Low
	Epinephrine	Proposed
	Levomethadyl	Probable		QT interval prolongation, Torsade de pointes
	Methadone	Probable			Syncope according to manufacturer.
	Salmeterol	Proposed		QT interval prolongation according to manufacturer.
	Tacrolimus	Proposed
	Tizanidine	Probable		QT interval prolongation	1:1000 risk of arrhythmia.

Management of long QT syndrome (LQTS)

Torsade de pointes with hemodynamic compromise

Torsade de pointes causing syncope is treated with defibrillation. Start with 150 J (biphasic shock) and increase by 50 J for each shock. Ventricular fibrillation and cardiac arrest are treated with conventional resuscitation.

Hemodynamically stable torsade de pointes

Treatment of torsade de pointes is similar in congenital and acquired LQTS. Torsade de pointes is paroxysmal, which means that the arrhythmia occurs intermittently and self-terminates. It tends to recur, even after successful defibrillation. There is always risk of ventricular fibrillation which is why a defibrillator must be close at hand and readiness to perform resuscitation is necessary.

Treatment algorithm

All medications/drugs that may cause or aggravate the arrhythmia must immediately be stopped.

Magnesium infusion (regardless of blood magnesium levels): 1 gram of magnesium is administered intravenously for 60 seconds. This may be repeated after 5–10 minutes. If a continuous infusion is necessary, the dose is 5–10 mg/min.

Potassium infusion: only necessary if the patient has hypokalemia.

Bradycardia must be corrected: bradycardia may induce and aggravate torsade de pointes. To correct bradycardia, the following options are at hand:

atropine i.v 1–2 ml 0.5 mg/ml.

isoprenaline (isoproterenol) 0.01 μg/kg/min, which is titrated up until bradycardia resolves. Note that isoprenaline must be administered carefully because it activates beta-adrenergic receptors which is why it may aggravate the arrhythmia. In congenital LQTS isoprenaline is contraindicated because the risk of ventricular fibrillation is high. Therefore, isoprenaline may only be used in acquired LQTS and temporarily until a pacemaker can be established.

temporary transcutaneous/transvenous pacemaker. The pacemaker electrode should be placed in the atria and the rate should be set to 90 beats per minute. The rate may be increased gradually until the arrhythmia resolves.

The rationale behind atropine, isoprenaline and pacemaker therapy is simple: these three interventions all increase the heart rate, which decreases the QTc interval and thus terminates the torsade de pointes.

Long-term treatment for acquired long QT syndrome

No treatment is necessary after the removal of the medications causing the syndrome.

Long-term treatment for congenital long QT syndrome

Beta-blockers are very effective in congenital LQTS. Mortality is reduced dramatically if the right drug and right dose is given. Propranolol (usually sufficient with 3 mg/kg/day) and nadolol (usually sufficient with 1 mg/kg/day) are the most effective drugs. Metoprolol has a proven effect but is less effective than propranolol and nadolol. There are no studies available on atenolol, which therefore cannot be recommended. Patients with pronounced bradycardia should not be given beta-blockers due to the risk of provoking torsade de pointes.

Artifical pacemaker may be necessary if the maximal dose of beta-blockers is insufficient. If pacemaker is also insufficient, sympathectomy may be considered. Sympathectomy means that sympathetic nerve ganglia (thoracic) are removed surgically, which leads to the elimination of adrenergic stimulation to the heart. This is an effective method but requires surgery.

ICD (Intracardial Cardiac Defibrillator) is used in the following cases:

Patients who have experienced cardiac arrest.

Patients who have experienced syncope despite optimal treatment (maximal dose beta blocker, pacemaker and possibly sympathectomy).

If the anamnesis is very worrying and the QTc interval is >550 ms. T-wave alternans and sinus pause corroborates this further.

Short QT syndrome (SQTS)

Short QT syndrome is extremely rare but may cause polymorphic ventricular tachycardia. It is defined as QTc interval <0.35 s. Note that hypercalcemia and digoxin which may also shorten the QTc interval.

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Chapter 22: Ventricular fibrillation, pulseless electrical activity and sudden cardiac arrest

Ventricular fibrillation, pulseless electrical activity (PEA) and sudden cardiac arrest

This chapter will focus on ventricular fibrillation and pulseless electrical activity (PEA). These are highly lethal arrhythmias that lead to death if cardiopulmonary resuscitation is not started immediately. Ventricular fibrillation is the result of numerous re-entry circuits, causing rapid and chaotic ventricular depolarizations, rendering the left ventricle incapable of generating effective contractions. This results in circulatory collapse, loss of consciousness, and sudden cardiac arrest. Unlike ventricular tachycardia, ventricular fibrillation seldom self-terminates and death is imminent without immediate and resuscitative efforts.

Sudden Cardiac Arrest and Cardiopulmonary Resuscitation (CPR)

Approximately 80% of individuals who suffer a sudden cardiac arrest have ventricular fibrillation prior to the cardiac arrest. Most of these have atherosclerotic heart disease (coronary artery disease) as the underlying cause. Other common causes are cardiomyopathy (hypertrophic or dilated), arrhythmogenic right ventricular cardiomyopathy, Brugada syndrome, early repolarization. Electrolyte disorders, acidosis, hypoxemia and ischemia all aggravate the risk of developing ventricular fibrillation, in any situation.

ECG features of ventricular fibrillation

The ECG shows irregular waves with varying morphology and amplitude. No P-wave, QRS complex or T-wave can be seen. This is pathognomonic (unique) to ventricular fibrillation and must not be confused with any other arrhythmia.

Figure 1. Ventricular fibrillation and asystole.

ECG Case 1: Ventricular tachycardia progressing to ventricular fibrillation

Below are sequential ECG recordings during a sudden cardiac arrest in a 43-year-old male. Each ECG presents two leads recorded simultaneously.

ECG 1. Sinus rhythm interrupted by ventricular fibrillation (VF).

ECG 2. Ventricular fibrillation.

ECG 3. Ventricular fibrillation, coarse (large amplitudes).

ECG 4. Ventricular fibrillation.

ECG 5. Ventricular fibrillation, fine (low amplitudes).

ECG 6. Ventricular fibrillation, coarse.

ECG 7. Ventricular fibrillation, coarse.

ECG 8. Ventricular fibrillation.

ECG 9. Delivery of shock (red arrow), with subsequent asystole.

ECG 10. Recurrence of supraventricular complexes (red arrows).

ECG 11. Relapse of VF and new shock.

ECG 12. Sinus rhythm.

ECG 13. Ventricular tachycardia.

ECG 14. Sinus rhythm, with ST-segment elevations not seen previously.

ECG Case 2: Ventricular tachycardia progressing to ventricular fibrillation

Below are sequential ECG recordings during a sudden cardiac arrest in a 62-year-old male. Each ECG presents two leads recorded simultaneously.

ECG 1. Sinus rhythm interrupted by ventricular tachycardia (VT).

ECG 3. Ventricular fibrillation (VF).

ECG 4. Ventricular fibrillation (VF).

ECG 5. Ventricular fibrillation (VF).

ECG 6. Delivery of shock, followed by asystole.

ECG 7. Asystole after shock.

ECG 8. Recurrence of supraventricular rhythm.

ECG 9. Supraventricular rhythm.

Treatment of ventricular fibrillation

Ventricular fibrillation is treated according to the resuscitation algorithm.

Cardiac arrest and sudden cardiac death

For details regarding sudden cardiac arrest and death, please refer to Sudden Cardiac Arrest and Cardiopulmonary Resuscitation (CPR).

Cardiac arrest ensues when ventricular contractions cease or are meaningless. This immediately leads to syncope and soon death, unless resuscitation is attempted. Sudden cardiac death is defined as an unexpected death due to cardiac causes that occur within 1 hour of symptom onset. The person may or may not have known cardiac disease. Moreover, the time limit (1 hour) is not absolute. Sudden cardiac death causes 7 million deaths annually worldwide. The most common cause of sudden cardiac death is acute or chronic coronary artery disease (ischemic heart disease). Cardiomyopathies (dilated or hypertrophic), valvular disease, genetic mutations (LQTS, Brugada syndrome, early repolarization), etc, are much less common than ischemic heart disease.

The death mechanism is usually the same regardless of the underlying disease: electrical instability triggers ventricular tachycardia which degenerates into ventricular fibrillation which leads to asystole. The latter, asystole, means that there is no electrical activity in the heart and the ECG shows a flat line (Figure 1). Sudden cardiac death due to bradycardia or pulseless electrical activity is much less common.

Underlying causes

Acute or chronic ischemic heart disease causes 80% of all sudden cardiac deaths – Ventricular arrhythmias may arise during acute ischemia as well as in chronic ischemia.

Dilated or hypertrophic cardiomyopathy – Causes 10-15 % of all cases.

Less common causes (5% of all cases) – Atrial fibrillation with pre-excitation, arrhythmogenic right ventricular cardiomyopathy (ARVC), long QT syndrome (LQTS), Brugada syndrome, aortic stenosis, amyloidosis, third-degree AV-block III without escape rhythm.

Metabolic derangements, electrolyte disorders and exogenous substances, ischemia, etc, may precipitate ventricular arrhythmias in all these patient groups.

Asystole and brady-asystole

As seen in Figure 1, asystole occurs when there is no electrical activity in the heart. The heart is completely still during asystole; i.e. there are no atrial or ventricular depolarizations.

Brady-asystole is defined as asystole interrupted by occasional QRS complexes, but no rhythm capable of producing a noteworthy cardiac output.

Treatment of asystole and brady-asystole

Asystole and brady-asystole are treated according to the resuscitation algorithm.

Pulseless electrical activity (PEA)

Synonym: electromechanical dissociation (EMD)

Pulseless electrical activity is a term applied to any rhythm that is not accompanied by a detectable pulse. It may display complete P, QRS, and T waveforms but no pulse is palpable. This means that the heart’s electrical activity has been dissociated from mechanical contractions, which is why the synonym electromechanical dissociation is often used.

Causes of pulseless electrical activity

The following conditions may cause pulseless electrical activity: hypovolemia, hypoxia, cardiac tamponade, pressure pneumothorax, hypothermia, massive pulmonary embolism, drug overdose, and massive myocardial infarction. The most common of these is myocardial infarction. Massive myocardial infarctions may leave too little viable myocardium to generate stroke volumes that are palpable.

Treatment of pulseless electrical activity

Pulseless electrical activity is treated according to the resuscitation algorithm.

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Chapter 23: Pacemaker-mediated tachycardia (PMT): ECG and management

Pacemaker-mediated tachycardia may arise if the pacemaker records a rapid atrial rate (e.g. during a supraventricular tachycardia) and stimulates the ventricles with the same rate. This occurs if ventricular stimulation is set to be triggered by the atrial impulse. Another cause of pacemaker-mediated tachycardia is endless loop tachycardia, which also depends on the ventricular stimulation being triggered by atrial activity. In endless loop tachycardia, the ventricular impulse manages to propagate to the atria where the atrial electrode records the impulse (and assumes that it represents an atrial activation) and thus triggers another ventricular stimulation. This cycle may repeat itself so that a tachyarrhythmia is established.

Pacemaker mediated tachycardia on ECG

Pacemaker beats are mostly easy to recognize on the ECG. Pacemaker stimulation generates a stimulation artifact (“pacemaker spike”). Older pacemakers generate large and visible spikes, whereas newer models may generate very minute or even invisible spikes (at least in some leads). Pacemaker-stimulated beats display wide QRS complexes and a left bundle branch block pattern on ECG; this is explained by the fact that the pacemaker electrode is placed and stimulates the right ventricle. Hence, whenever a patient with a pacemaker presents with tachyarrhythmia and the QRS complexes appear with a left bundle branch block pattern, always suspect pacemaker-mediated tachycardia.

CRT devices (cardiac resynchronization therapy) may also cause tachycardias, and these devices produce slightly narrower QRS complexes (because they stimulate both ventricles simultaneously). A tachycardia with Q-wave or QS complex in lead I suggest that the tachycardia is caused by the CRT device.

(none)

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Chapter 24: Diagnosis and management of supraventricular and ventricular tachyarrhythmias: Narrow complex tachycardia & wide complex tachycardia

All clinically significant supraventricular and ventricular tachyarrhythmias have been reviewed in previous sections. However, given that each arrhythmia has been addressed in isolation, distinguishing between them in clinical scenarios may remain challenging. Effective management of tachycardia requires a comprehensive understanding of differential diagnoses, therapeutic strategies, and evidence-based interventions. Many tachyarrhythmias carry a potential risk of serious morbidity or mortality, underscoring the need for a structured and guideline-directed approach. This chapter focuses on practical diagnostic and therapeutic considerations, with recommendations aligned with current guidelines from both the American Heart Association (AHA) and American College of Cardiology (ACC), as well as the European Society of Cardiology (ESC). The classification of tachyarrhythmias into narrow complex (NCT) and wide complex tachycardia (WCT) will be emphasized, as this distinction significantly informs both diagnostic reasoning and treatment decisions in clinical practice.

Note that the terms tachycardia and tachyarrhythmia will be used interchangeably throughout this chapter. For sake of clarity, however, tachyarrhythmia is defined as an abnormal and rapid heart rate, whereas tachycardia is defined as the subjective perception of a rapid heart rate. These terms are often used interchangeably both in clinical practice and in the literature.

Tachyarrhythmias: causes, differential diagnoses, treatment and management

Any heart rate faster than 100 beats per minute is defined as tachycardia, which is synonymous with tachyarrhythmia. Except for sinus tachycardia during physical activity, all tachycardias should be considered pathological and the task is to clarify the cause of the tachycardia. The cause may range from benign to highly malignant, which is why expeditious management is warranted.

Initial management includes assessing the patient’s clinical status (symptoms, hemodynamics), ECG and risk factors (age, previous disease, medications, laboratory results, etc). Considering the ECG, which is fundamental in all arrhythmias, the first task is to determine whether the arrhythmia is a wide complex tachycardia (WCT) or a narrow complex tachycardia (NCT). This is done by simply judging the QRS duration. If the QRS duration is normal (<0.12 seconds), the arrhythmia is said to be a narrow complex tachycardia (NCT). If the QRS duration is prolonged (≥0.12 seconds), the arrhythmia is a wide complex tachycardia (WCT). This initial distinction will guide the rest of the thinking needed to arrive at a final diagnosis.

Narrow (normal) QRS complexes indicate that the ventricles are depolarized normally; this can only be the case if the impulse (which depolarizes the ventricles) passes through the bundle of His, and hence it originates in the atria. In other words: tachycardias with narrow QRS complexes originate in the atria. the term supraventricular tachycardia is often used to refer to tachycardias originating in the atria.

The significance of QRS duration in judging arrhythmias can be summarised as follows:

NCT – Narrow complex tachycardias (QRS duration <0,12 seconds) indicate the ventricles are depolarized via the His-Purkinje system and thus the impulse originates in the atria (i.e the arrhythmia is supraventricular).

WCT – Wide complex tachycardias (QRS duration ≥0,12 seconds) indicates the ventricles are not depolarized normally. The vast majority of WCTs originate from impulses generated in the ventricles (ventricular tachycardia being the most common arrhythmia). Any impulses generated in the ventricles will result in wide QRS complexes because the impulse will spread entirely or partly outside of the conduction system (which is slow). However, WCTs may be supraventricular, if the tachycardia is accompanied by one of the following conditions: bundle branch block, aberrant ventricular conduction (or simply aberration), hyperkalemia, pre-excitation, certain medications that prolong QRS duration.

Narrow complex tachycardias generally do not cause circulatory compromise and are therefore easier to manage than wide complex tachycardias. The latter (WCT) is in the vast majority of cases caused by ventricular tachycardia (or other ventricular arrhythmias) and may be potentially life-threatening. As always, there are exceptions to these rules. For example, a narrow complex tachycardia may cause circulatory compromise, or even collapse, in an individual with heart failure or ischemic heart disease. For this reason, management of tachycardias actually does not start with judging the ECG, it starts with judging the patient’s symptoms and hemodynamic status. Tachyarrhythmias typically causes one or more of the following symptoms:

Palpitations

Dyspnea

Chest discomfort

Hypotension

Syncope/presyncope

Lightheadedness

Heart failure

Renal failure

Pulmonary edema

Decreased consciousness

Shock

Myocardial infarction

Cardiac arrest

If the patient displays one or more of the first three symptoms (palpitations, dyspnea, chest discomfort) it is considered safe to take time to judge the ECG and additional information. All other symptoms listed above (highlighted in red) are signs of instability and thus indications for treatment. For clarity, in case of hemodynamic instability (ongoing or impending), the patient must be treated even though a definite diagnosis has not been established. The rationale behind this procedure is simple: treatment with electrical cardioversion is highly effective and terminates most arrhythmias (particularly the life-threatening ones) and early therapy may be life-saving. This is the consensus in North America as well as Europe.

The figure below sums up the discussion so far.

Figure 1. Overview of tachyarrhythmia (tachycardia).

Tachycardia: the value of anamnesis

Anamnesis is as always important. Many tachycardias have a triggering factor, such as physical or emotional stress, coffee consumption, etc. It is always useful to assess whether the tachycardia started abruptly or gradually. This may differentiate several tachycardias. Sinus tachycardia, for example, always starts gradually, whereas AVNRT always starts very abruptly. The patient can determine (as judged by symptoms) the start of the arrhythmia in most cases.

Previous medications, comorbidities and precious ECG tracings should all be assessed. The value of this lies in the fact that if there is any precipitating factor, the arrhythmia is likely to be related to that factor. For example, patients on sotalol medication (which may cause QT prolongation) are likely to have ventricular tachycardia; patients with previous myocardial infarction are very likely to have ventricular tachycardia if they present with a wide complex tachycardia; patients with previous atrial fibrillation are likely to have another episode if they present with an irregular tachycardia and so on.

ECG in tachycardia

The ECG is invaluable in the setting of tachycardia. Although it is often difficult to arrive at a definitive diagnosis, the ECG will allow for a more or less certain diagnosis in most cases. ECG interpretation must, as always, proceed systematically in order to avoid blunders. The following procedure is often used:

Assess QRS duration to determine whether the tachycardia is a wide complex tachycardia or narrow complex tachycardia.

Assess ventricular rate and regularity:

What is the ventricular rate (beats per minute)?

Is it regular? Is it irregular (but with repeated patterns) or even irregularly irregular (no patterns)?

Assess electrical axis

P-waves are extremely important to search for. They are, however, often difficult to spot. If P-waves are invisible, one may try relocating the arm electrodes to various locations on the chest wall. The purpose of this is to simply catch the P-waves and their relation to the QRS complex. Vagus stimulation, adenosine and esophagus ECG may also help reveal the P-waves.

Are P-waves retrograde in lead II, III and aVF?

What is the relation, on the ECG, between P-waves and QRS complexes?

Are P-P intervals regular?

Is the number of P-waves equal to the number of QRS complexes?

Because the etiology and management of narrow complex tachycardias and wide complex tachycardias differ, these two entities are now discussed separately.

Narrow complex tachycardia (NCT)

Narrow QRS complexes, defined as QRS duration <0.12 seconds, can only be achieved if the ventricles are depolarized via the His-Purkinje system; this allows the impulse to spread rapidly through both ventricles. With very few exceptions, all narrow complex tachycardias (NCT) originate in the atria, hence they are referred to as supraventricular tachycardias. In the vast majority of cases, narrow complex tachycardias do not cause hemodynamic compromise. However, older patients and patients with significant heart disease (particularly with reduced left ventricular function) may develop circulatory compromise. Younger patients and healthy patients generally have no problems enduring tachycardias at rates below 200 beats per minute; higher rates may cause circulatory effects due to reduced stroke volume (shortened diastole means reduced time to fill the ventricles with blood).

Causes of narrow complex tachycardia (NCT)

All differential diagnoses have been discussed in detail in the previous articles. Sinus tachycardia is by far the most common tachycardia. Note that there are no normal causes of sinus tachycardia; there is always a pathological condition (e.g. anemia, heart failure, etc) explaining its existence and that condition must be identified and targeted. Note that sinus tachycardia may be accompanied by frequent premature atrial beats (atrial ectopic beats), which may give the sinus rhythm an irregular ventricular rhythm that may be confused with atrial fibrillation. Also recall inappropriate sinus tachycardia, which is a condition with increased automaticity in the sinoatrial node without any known cause. The last tachycardia arising in the sinoatrial node is sinoatrial nodal reentry tachycardia (SANRT), which is characterized by abrupt onset of sinus tachycardia occurring paroxysmally. It may be difficult, or even impossible, to separate these types of sinus tachycardia. Moreover, atrial tachycardia (also known as ectopic atrial tachycardia) may mimic sinus tachycardia if the P-waves are similar to the sinus P-waves.

Atrioventricular nodal reentry tachycardia (AVNRT), atrioventricular reentry tachycardia (AVRT) and ectopic atrial tachycardia are all caused by reentry (note that 20% of ectopic atrial tachycardias are caused by increased automaticity). These tachycardias arise very abruptly and have a short duration. In most cases, they self-terminate within 30 minutes. All age-groups are at risk of developing these arrhythmias.

Atrial fibrillation and atrial flutter occur in older individuals. Atrial fibrillation must always be the primary suspect if the ECG shows irregular tachycardia without visible P-waves. Atrial flutter is generally regular, characterized by a baseline resembling sawteeth. Atrial flutter may be irregular if there is varying AV-block.

Junctional tachycardia is rare and difficult to discern from AVNRT.

Importantly, all supraventricular tachycardias may display wide QRS complexes if they are accompanied by one of the following conditions/defects:

Aberrancy (aberration): Aberration (aberrant ventricular conduction) means that a rate-dependent block appears in one of the bundle branches. This typically occurs in the right bundle branch, which has a longer refractory period than the left bundle. It is typical that aberration occurs in the right bundle branch block during rapid acceleration of the heart rate, or if the heart rate is very irregular (refer to Aberrancy / aberrant ventricular conduction).

Previously existing bundle branch block: Left and right bundle branch block cause wide QRS complexes. Access to earlier ECG tracings (preferably in sinus rhythm) is necessary to verify this.

Antidromic AVRT: Antidromic AVRT affects individuals with pre-excitation. The re-entry circuit travels from the atria to the ventricles via the accessory pathway and from the ventricles to the atria via the His bundle and atrioventricular node. The QRS complex is wide because ventricular depolarization starts where the accessory pathway inserts in the ventricular myocardium and the impulse spreads from there, entirely or partly outside of the conduction system (which is slow).

Pacemaker-mediated tachycardia: Pacemakers that stimulate in the ventricle as a response to sensing atrial impulses may cause tachycardia by two mechanisms: (1) an atrial tachyarrhythmia (e.g atrial fibrillation) may be transferred to the ventricles by the pacemaker; (2) the pacemaker impulse may propagate from the ventricles backward to the atria, where the pacemaker electrodes sense the impulse and as a response stimulates again in the ventricles; this cycle repeats itself. Pacemaker beats have wide QRS complexes if the pacemaker stimulates the ventricular myocardium directly (which is very common). Read more in Pacemaker Mediated Tachycardia.

Hyperkalemia and class I antiarrhythmics: both may prolong the QRS duration. Refer to Beta-blockers and Antiarrhythmic Drugs.

Adenosine for diagnosis and treatment of tachycardia

Adenosine is an endogenous purine nucleoside that modulates many physiological processes in the body. Adenosine acts as a prominent vasodilator in the heart and thus causes increased blood flow in the microcirculation. Adenosine also acts in the atrioventricular node where it slows conduction. The slowing of conduction through the atrioventricular (AV) node is what makes adenosine useful in diagnosing and treating supraventricular tachycardias. Slowing of AV nodal conduction will lead to an increased block of impulses in the AV node and this terminates arrhythmias whose re-entrant pathway involves the AV node. Adenosine will simply render the AV node refractory; when the re-entry impulse encounters the refractory tissue, it is terminated. The arrhythmias are AVNRT and AVRT. Adenosine will also terminate ectopic atrial tachycardias caused by re-entry (which constitutes 80% of atrial tachycardias). Adenosine does not terminate sinus tachycardia, atrial flutter, atrial fibrillation or the remaining ectopic atrial tachycardias. However, in these cases, adenosine will lower the ventricular rate (by increasing the block in the AV node) which may be helpful, as explained below.

Safety of adenosine in the treatment of tachycardia

Adenosine can be administered safely to all individuals with narrow complex tachycardia. It may also be administered, with care, to persons with regular wide complex tachycardias if it is likely that the tachycardia is not a ventricular tachycardia. Adenosine must not be administered during ventricular tachycardia because it may accelerate the ventricular tachycardia and cause hypotension. It is potentially lethal to administer adenosine to patients with irregular wide complex tachycardias because these arrhythmias may be rendered malignant. Irregular wide complex tachycardias may be caused by atrial fibrillation with pre-excitation (i.e atrial fibrillation in a person with accessory pathway). Administration of adenosine may cause AV-block that causes increased impulse conduction over the accessory pathway, by which the atrial fibrillation may propagate to ventricular fibrillation.

Adenosine may induce atrial fibrillation (in up to 12% of patients) and in rare cases even ventricular tachycardia.

To conclude, adenosine can be administered safely to all narrow complex tachycardias. Guidelines recommend the use of adenosine as an initial therapy choice. One should be careful when administering adenosine to regular wide complex tachycardias. Adenosine should never be administered in case of irregular wide complex tachycardias.

Doses and handling of adenosine

Adenosine is injected rapidly in a peripheral venous catheter (6 mg) or central venous catheter (3 mg) followed by flushing with 20 ml saline. The injection may be repeated with a doubled dose (12 mg in peripheral venous catheter, 6 mg in central venous catheter). Heart transplanted individuals are particularly sensitive and should therefore receive only half the dose in a peripheral venous catheter.

Adenosine is only given during continuous ECG monitoring and a defibrillator must be close at hand. Adenosine is contraindicated in high-degree AV block (second-degree and third-degree AV block), sick sinus syndrome (unless the patient has a pacemaker), pronounced hypotension, unstable angina pectoris and decompensated heart failure.

Most patients experience chest discomfort during adenosine administration. Anxiety and flushing are also common. Obstructive pulmonary disease is a relative contraindication to adenosine. Theophylline and caffeine reduce sensitivity to adenosine. Heart transplanted patients, and those on dipyramidole, have increased sensitivity. Adenosine dose in the pediatric population is weight-based.

Recall that in case of hemodynamic instability, electrical cardioversion is always the first choice.

Vagal stimulation for diagnosis and treatment of tachycardia

One may always try vagal stimulation before administration of adenosine. Commonly used methods are carotid massage, Valsalva maneuver, and splashing cold water on the face (only done in children). Carotid massage is performed with the patient in the supine position and head rotated slightly away from the side being massaged. The carotid artery is massaged, at the level of the larynx, with two fingers. The massage is best performed with a circulating movement for 10 to 20 seconds. It may be repeated on the opposite side. Correctly performed, this induces a baroreceptor reflex which increases vagal stimulation to the heart and thus increases the block in the AV node. This may terminate 5 to 20% of AVNRT and AVRT.

Vagal stimulation may be used as a diagnostic tool as well. Because of the increased AV nodal block, the ventricular rate is lowered and this may clarify the irregularity of atrial fibrillation; it may demask the characteristics sawtooth-formed baseline in atrial flutter as well. Note that some individuals have very sensitive baroreceptors in the carotid artery and these individuals may be affected by bradycardia or hypotension upon stimulation.

It is extremely rare that atherosclerotic material comes loose and causes stroke during carotid massage. There are, however, some case reports. One should always auscultate the carotid artery before massage and perform it restrictively in persons with known or presumed carotid artery stenosis. In case auscultation reveals murmurs, one should not perform carotid massage.

Analysis of atrial activity (P waves)

Analyzing atrial activity during tachyarrhythmias is crucial but difficult. P-waves may be invisible (hidden in other waveforms) or visible and in the latter case, they may have an abnormal appearance. If the ventricles and the atria are activated simultaneously, the P-wave will be hidden in the QRS complex. If atria and ventricles are not activated simultaneously, but separately, the P-wave may be visible. The direction of the P-wave (positive vs retrograde) depends on the origin of the impulse. If the impulse is discharged near the atrioventricular (AV) node, atrial activation will proceed in the opposite direction and the P-wave will be retrograde in leads normally showing a positive P-wave. If the atrial impulse originates near the sinoatrial (SA) node, the P-wave will appear normal (i.e it will be positive in leads normally showing a positive P-wave).

If P-waves are not clearly visible, one should always compare the ECG waveforms during the tachyarrhythmia with the waveforms durign sinus rhythm (if ECGs are available). Any small waves or deflection that are visible during the tachyarrhythmia, but not during sinus rhythm, may actually represent atrial activity (P-waves). Esophagus ECG, vagal stimulation and adenosine may all facilitate identification of atrial activity.

If no P-waves are visible, the primary suspect is AVNRT. If P-waves are visible, the following must be judged:

Are P-waves positive or retrograde?

How fast is the atrial rate?

Where do P-waves occur, in relation to the QRS complexes?

Are P-P intervals regular? Completely irregular? Irregular but with a repeating pattern?

Is the number of P-waves equal to the number of QRS complexes?

At very high atrial rates (>250 atrial beats per minute) one should suspect atrial flutter or atrial tachycardia. Besides this, the atrial rate is of little help.

Positive P-waves in leads II, aVF and III indicate that the impulse originates near the sinoatrial node. If the P-wave during tachycardia is identical to the P-wave during sinus rhythm, the tachycardia originates from the sinoatrial node (differential diagnoses: sinus tachycardia, inappropriate sinus tachycardia, SANRT) or near the sinoatrial node (differential diagnosis: ectopic atrial tachycardia located near the sinoatrial node). If the P-wave is positive but differs morphologically from the sinus P-wave, it is likely to be atrial tachycardia located elsewhere.

Retrograde P-waves are negative in leads II, aVF and III. This indicates that atrial activation is directed oppositely. This suggests AVRT, AVNRT, junctional tachycardia or atrial tachycardia (with ectopic focus near the AV node). Retrograde P-waves are usually associated with short RP intervals (discussed below). Indeed, the RP interval may be so short that the retrograde P-wave is fused with the terminal portion of the QRS complex. The retrograde P-wave will therefore imitate an s-wave in lead II (called “pseudo s”) and an r-wave in V1 (called “pseudo r”). In order to verify pseudo s and pseudo r, one must have a previous ECG recording at hand (and compare the waveforms).

RP interval

Figure 2. Differential diagnoses based on RP interval.

The RP interval must be assessed if there is one P-wave per QRS complex (i.e the ratio of P to QRS is 1:1). The RP interval is the interval from the beginning of the QRS complex to the beginning of the P-wave (Figure 2). The RP interval is either short or long.

A short RP interval is defined as an RP interval being less than half the RR interval (the interval between two R-waves). Short RP interval with retrograde P-wave indicates typical AVNRT or AVRT (rarely ectopic atrial tachycardia located near the AV node). Short RP interval that is <70 milliseconds strongly suggests typical AVNRT. Short RP interval that is >70 ms suggests AVRT. Short RP interval with positive P-wave suggests ectopic atrial tachycardia with first-degree AV-block. Refer to Figure 2.

A long RP interval means that the RP interval is longer than half the RR interval. If the P-wave is retrograde, it is usually ectopic atrial tachycardia with focus near the AV node); it may be atypical AVNRT, orthodromic AVRT with slow accessory pathway (also referred to as PJRT, permanent junctional reciprocating tachycardia). Positive P-waves with long RP interval suggest ectopic atrial tachycardia or sinus tachycardia.

Arrhythmia substrates on the resting ECG

In patients with tachycardia, it is extremely valuable to assess a previous resting ECG (ideally recorded during sinus rhythm). The resting ECG may reveal a wide range of abnormalities that indicate what the etiology of the tachycardia may be. These ECG changes on the resting ECG and their associated arrhythmias are presented in Figure 3.

Figure 3. Changes on resting ECG that may reveal cause of arrhythmias (arrhythmia substrates).

Algorithm for diagnosis and management of narrow complex tachycardia (NCT)

The clinical handling of narrow complex tachycardia is facilitated by using a flow-chart for diagnosis. The flow chart below (Figure 4) is adapted from European and North American guidelines. The corresponding flow chart is later presented for wide complex tachyarrhythmias.

Figure 4. Management and diagnosis of narrow complex tachycardia.

Wide complex tachycardia (WCT)

Tachyarrhythmias with wide (broad) QRS complexes, defined as QRS duration ≥0.12 seconds, are generally more alarming than narrow complex tachycardias. Roughly 80% of all wide complex tachycardias are caused by ventricular tachycardia, and this figure rises to 90% among patients with ischemic heart disease (coronary artery disease). However, approximately 10% of all wide complex tachycardias are actually supraventricular tachycardias accompanied by a factor disturbing ventricular depolarization. Those factors are as follows:

Existing right bundle branch block or left bundle branch block.

Aberrant ventricular conduction, i.e bundle branch block occurring due to acceleration of heart rate. (Aberration may occur in other instances, discussed in this article).

Hyperkalemia

Class I antiarrhythmic drugs.

Pacemaker-induced tachycardia.

Antidromic AVRT.

Nevertheless, the majority of wide complex tachycardias are ventricular tachycardias, which also means that the majority of patients presenting with wide complex tachycardias are at risk of developing unstable hemodynamics and even more malignant arrhythmias (ventricular fibrillation and asystole).

It is crucial to compare the ECG during tachycardia with the ECG during sinus rhythm if such is available. If earlier ECG reveals intraventricular conduction defects (left bundle branch block, right bundle branch block, or any other unspecified conduction defect that prolongs the QRS duration), one must compare the waveforms with those seen during tachycardia. IF the waveforms (QRS-ST-T) are similar during sinus rhythm and tachycardia, it is likely that the tachycardia is supraventricular in origin.

Pacemaker-mediated tachycardia must always be suspected in patients with artificial pacemakers. The pacemaker spike (stimulation artifact) reveals the pacemaker. Modern pacemakers (bipolar pacemakers) may produce a very minute pacemaker spike. In case the pacemaker spikes are not clearly visible, the following suggest pacemaker mediated tachycardia:

Left bundle branch block pattern (pacemaker stimulate in the right ventricle, which yields QRS with left bundle branch block pattern)

Wide R-wave in lead I.

Supraventricular tachycardias with wide QRS due to hyperkalemia are uncommon and easy to diagnose with blood analyze of potassium levels.

Aberrant ventricular conduction is fairly common and may be difficult to distinguish from ventricular tachycardia. The same is true for antidromic AVRT, which actually may be impossible to differentiate from ventricular tachycardia. However, antidromic AVRT constitutes <5% of all wide complex tachycardias.

Initial management of wide complex tachycardias (WCT)

Hemodynamic status must be assessed immediately because it may be unstable. If there are signs of compromised hemodynamics (hypotension, angina, chest discomfort, heart failure, lightheadedness etc) the patient should be treated with synchronized electrical cardioversion, even before a diagnosis has been established. A wide complex tachycardia is considered as a ventricular tachycardia until proven otherwise, and in the case of affected circulation it is highly likely that the arrhythmia is ventricular tachycardia. Note that some patients with ventricular tachycardia may be hemodynamically stable initially; sustained ventricular tachycardias, however, always cause circulatory symptoms. The greater the cardiac function, the less pronounced the symptoms.

Unconscious and pulselss patients are managed with advanced cardiac life support.

If the patient is hemodynamically stable, one may study the ECG carefully and attempt treating the arrhythmia pharmacologically. Pharmacological treatment alternatives have been discussed previously. A flow-chart with treatment and management is presented in Figure 5.

Characteristics of patients with wide complex tachycardia (WCT)

Medical history and use of medications must be assessed. Older age and the presence of structural heart disease increase the probability of ventricular tachycardia. Individuals presenting with wide complex tachycardia after recent myocardial infarction virtually always have ventricular tachycardia. All medications are of interest, including medications that prolong the QT interval, because this predisposes for polymorphic ventricular tachycardia. Class I antiarrhythmics may cause both aberrant conduction and ventricular tachycardia. Digoxin may also cause ventricular tachycardia (of all types), but it may also cause all supraventricular tachycardias. Digoxin is particularly arrhythmogenic during hypokalemia. Diuretics predispose to ventricular tachycardia due to side effects (hypokalemia, hypomagnesemia); torsade de pointes is not too uncommon.

Diagnostic maneuvers in wide complex tachycardia (WCT)

Vagal stimulation rarely terminates ventricular tachycardia. It may, however, increase blocking in the AV node, which may (if the arrhythmia is supraventricular) increase RR intervals and reveal AV dissociation. Verapamil, adenosine and beta-blockers are all hazardous in case of ventricular tachycardia (risk of developing hypotension and cardiac arrest). These drugs may be used if one is certain that the wide complex tachycardia is a supraventricular arrhythmia. If the arrhythmia is terminated by adenosine, digoxin, verapamil or diltiazem, one can be virtually certain that it had a supraventricular origin. Termination by means of lidocaine suggests ventricular tachycardia, although AVRT may also be terminated by lidocaine. Termination by means of procainamide or amiodarone does not differentiate ventricular from supraventricular origin.

The following algorithm, which should be at hand always, presents diagnosis and management of wide complex tachycardia.

Figure 5. Management and ECG diagnosis of wide complex tachycardias.

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