Conduction Defects

Chapter 1: Overview of atrioventricular (AV) blocks

This article covers the fundamental principles of atrioventricular (AV) blocks, which are classified into three types: first-degree, second-degree, and third-degree AV blocks. Readers already familiar with the basics of AV blocks can proceed directly to the subsequent chapters, which provide detailed discussions on each type.

First-degree AV block

Second-degree AV block

Third-degree AV block

The atrioventricular (AV) conduction system and AV blocks

The atrioventricular (AV) system is composed of the AV node and the His-Purkinje system, which transmit electrical impulses from the atria to the ventricles. Conduction through the AV node is intentionally slow (due to the low concentration of gap junctions in AV nodal cells), which allows for ventricular filling to complete prior to ventricular contraction. In contrast, contractile cells–and Purkinje fibers in particular–are rich in gap junctions, enabling rapid impulse conduction through the ventricles.

After passing the AV node, the electrical impulse travels through the His bundle, which bifurcates into the left and right bundle branches. The left bundle branch further subdivides into two fascicles. From these branches and fascicles, Purkinje fibers extend into the myocardium. Conduction through the Purkinje system is very rapid, due to the high density of gap junctions. This rapid transmission ensures that the majority of the ventricular myocardium depolarizes nearly simultaneously, which is crucial for maximizing the efficiency of ventricular contraction (Figure 1).

Figure 1. Components of the ventricular conduction system and the temporal association between the ECG waveforms and impulse transmission through the heart. Atrioventricular (AV) blocks occur due to dysfunction in the conduction system.

The atrioventricular (AV) node is densely innervated by both sympathetic and parasympathetic nerve fibers. Sympathetic stimulation enhances impulse conduction through the AV node, a phenomenon known as the bathmotropic effect. In contrast, parasympathetic stimulation increases resistance within the AV node, further slowing the transmission of impulses. Intense parasympathetic activity can result in a complete blockage of impulse conduction. If such blockage persists for 6 seconds or more, syncope occurs unless an escape rhythm arises.

Overview of AV blocks

Impulse conduction from the atria to the ventricles may be delayed or blocked. These conditions are referred to as atrioventricular (AV) blocks, subdivided according to the degree of block. First-, second- and third-degree AV block may all be diagnosed using the ECG.

First-degree AV block

Synonyms: AV block 1, AV block I

The term block is slightly misleading because first-degree AV block only implies that the conduction is abnormally slow. By definition, the PR interval is >0.22 s. However, all impulses are conducted to the ventricles. First-degree AV block is rarely serious and may be left untreated in the vast majority of cases (exceptions are discussed later).

Second-degree AV block

Synonyms: AV block 2, AV block II

In second-degree AV block, some impulses are completely blocked, such that not all P-waves are followed by QRS complexes. Second-degree AV block is subdivided into the following variants:

Second-degree AV block Mobitz type 1. May also be referred to as Wenckebach block.

Second-degree AV block Mobitz type 2.

Second-degree AV block (particularly Mobitz type 2) requires treatment.

Third-degree AV block

Synonyms: complete heart block, AV dissociation, AV block III, AV block 3

In third-degree AV block, no atrial impulses are conducted to the ventricles. The atria and the ventricles are electrically disconnected. This condition is referred to as AV dissociation. Importantly, for the ventricles to exhibit any electrical—and consequently mechanical—activity, an escape rhythm must originate from an ectopic focus located distal to the block. Third-degree AV block is a critical condition; as escape rhythms may fail to develop, be transient, or produce an insufficient heart rate. In the absence of an escape rhythm, cardiac arrest will ensue.

Symptoms caused by AV blocks

First-degree AV block is virtually always asymptomatic. It may cause symptoms if the delay is very long, because atrial and ventricular activity may become severely desynchronized.

Second-degree AV block is usually asymptomatic unless there is a high-degree block (i.e. many atrial impulses are blocked). The patient may experience irregular heart rate, palpitations, pre-syncope or even syncope. Syncope is more common in Mobitz type 2 blocks.

Third-degree AV block is mostly symptomatic because it causes a reduction of cardiac output due to bradycardia. Lightheadedness, dyspnea, angina, dizziness, pre-syncope, or syncope may occur. Cardiac arrest occurs if an escape rhythm is not established.

Causes of AV blocks

AV blocks occur due to functional or anatomical blocks in the AV system. The block may be located in the atrioventricular node, His bundle, bundle branches or fascicles. A wide range of conditions may cause AV blocks:

Idiopathic fibrosis of the conduction system: Roughly half of all AV blocks are due to fibrosis. This correlates strongly with age.

Ischemic heart disease: 35% of all AV blocks are due to acute or chronic ischemic heart disease (coronary artery disease). All types of AV block may occur due to ischemia/infarction. Note that inferior myocardial infarction usually causes transient AV blocks (which resolve within 7 days), whereas anterior wall infarction generally causes permanent AV blocks. AV block due to myocardial ischemia and infarction has been discussed in the chapter Supraventricular and Intraventricular Conduction Defects in Myocardial Infarction and Ischemia.

Vagal stimulation: The Vagus nerve slows the heart rate and conduction through the AV node. Vagal activity increases in the following situations: carotid sinus massage (intentional or not), Valsalva maneuver, acute pain, and hypersensitive carotid sinus reflex. Vagal fibers unload acetylcholine on AV nodal cells which slows conduction and may even block conduction with ensuing asystole. In the vast majority of cases, the asystole is transient.

Structural heart disease: aortic stenosis, aortic regurgitation, mitral valve stenosis, mitral valve regurgitation, myocarditis, perimyocarditis, myocardial infarction, heart surgery and cardiomyopathy may all bring about damage to the conduction system and cause AV blocks.

Congenital: Any degree of AV block may occur at birth.

Hyperkalemia, hypokalemia.

Digoxin: Recall that digoxin may cause all arrhythmias and conduction defects, including all degrees of AV block.

Verapamil, amiodarone, beta-blockers, and phenytoin may all cause AV block.

Hypothermia.

Borreliosis (Lyme disease, caused by Borrelia spp.).

Beta-blockers are not contraindicated in patients with first-degree or second-degree Mobitz type 1 AV block; however, these conditions necessitate ECG monitoring after initiating beta-blocker therapy to ensure the block does not worsen. In contrast, second-degree Mobitz type 2 and third-degree AV blocks are contraindications for beta-blocker use unless a permanent pacemaker has been implanted.

Localization of the level of the block

Localizing the level of the block is relevant as it has implications for the prognosis and treatment. The more distal (from the atrioventricular node) the block, the greater the risk of development of complete heart block (third-degree AV block). This is because automaticity diminishes gradually with the distance from the AV node. It is often difficult to localize the level of the block on the 12-lead ECG. There are, fortunately, some rules of thumb that should be used. The block in first-degree AV block is mostly located in the atrioventricular node. The block in second-degree AV block Mobitz type 1 is also mostly located in the atrioventricular node. These types of AV block are the most benign. The block in second-degree AV block Mobitz type 2 is mostly located in the bundle of His or distal to it. The block in third-degree AV block is mostly located in the atrioventricular node or the bundle of His.

QRS duration may be used to differentiate between blocks located in the AV node and the bundle of His (i.e. proximal to the bifurcation of the bundle of His). For the QRS duration to be normal (QRS duration <0.12 s) the impulse must pass through the bundle of His and be delivered to both bundle branches. Thus, normal QRS duration implies that the block is located proximal to the bifurcation of the bundle of His. Prolonged QRS duration (QRS duration ≥0.12 s) is less helpful, because it may be due to either (1) block located distal to the bifurcation, or (2) block located proximal to the bifurcation but with concomitant (separate) bundle branch block.

To conclude, if the QRS duration is <0.12 the block is most likely located in the AV node or bundle of His, which indicates a better prognosis than broad QRS complexes, which are much more likely to be due to blocks distal to the bifurcation of the bundle of His. An electrophysiological study is necessary to firmly establish the level of the block, but this is only rarely needed (because management is based primarily on the degree of the AV block).

Figure 2. Principles of AV blocks and the emergence of escape rhythms / beats.

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Chapter 2: First-degree AV block (AV block I, AV block 1)

First-degree AV block: ECG criteria, clinical characteristics & managementContents<span style="color: #000000;">ECG criteria for first-degree AV block</span>First-degree AV block with wide QRS complexPrognosis of first-degree AV blockTreatment of first-degree AV block

This chapter discusses first-degree atrioventricular (AV) block, also referred to as 1st-degree AV block, AV block I, or AV block 1. Before proceeding, it is recommended to review the basic concepts of AV blocks (refer to Introduction to AV Blocks). The term block is somewhat imprecise in the context of first-degree AV block, as it does not represent a true conduction block but rather a delay in the propagation of electrical impulses from the atria to the ventricles. This delay is characterized by a prolonged PR interval on the ECG, defined as a PR interval ≥0.22 seconds. Importantly, all P-waves are followed by QRS complexes. First-degree AV block is rarely of clinical significance and typically does not require intervention. In most cases, the conduction delay is localized to the atrioventricular node.

ECG examples of first-degree atrioventricular block (AV block 1). Click to zoom.

ECG criteria for first-degree AV block

PR interval ≥0,22 s.

All P-waves are followed by QRS complexes.

First-degree AV block with wide QRS complex

First-degree AV block with normal QRS complex (QRS duration <0.12 s) is localized in the AV node in 90% of the cases and the bundle of His in 10% of cases. If the ECG displays first-degree AV block (PR interval ≥0,22 s) along with wide QRS complexes (QRS duration ≥0,12 s) there is a high probability that the block is located bilaterally in the bundle branches. This type of first-degree AV block often progresses to third-degree (complete) AV block, and therefore necessitates an artificial pacemaker.

Blocks located proximal to the AV node (prenodal blocks)

First-degree AV block may actually be due to the slowing of impulse conduction prior to the AV node. This is mostly due to fibrosis of atrial myocardium. The ECG shows, besides prolonged PR interval, wide P-waves with low amplitude. Prenodal block is, however, uncommon.

Prognosis of first-degree AV block

Isolated first-degree AV block with normal QRS complexes has very good prognosis and may even occur in otherwise healthy individuals. However, if the QRS complexes are wide there is a risk of distal block which may progress to more advanced block (second- or third-degree AV block). A pacemaker is often necessary in individuals with first-degree AV block and wide QRS complexes.

Treatment of first-degree AV block

Refer to Management of Atrioventricular (AV) Blocks

Management and treatment of AV block (atrioventricular blocks)

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Chapter 3: Second-degree AV block: Mobitz type 1 (Wenckebach) & Mobitz type 2 block

In this chapter, the focus will be on second-degree atrioventricular (AV) block. Before proceeding, it is advised to review the introductory chapter on AV blocks (refer to Introduction to AV Blocks). Second-degree AV block is defined by the intermittent failure of atrial impulses to conduct to the ventricles, resulting in some P-waves not being followed by QRS complexes. This condition is further categorized into two distinct subtypes: type 1 (also known as Mobitz type 1 or Wenckebach block) and type 2 (referred to as Mobitz type 2).

Second-degree AV block Mobitz type I exhibits the Wenckebach phenomenon, which is characterized by a progressive delay in impulse conduction, eventually leading to a blocked atrial impulse. On the ECG, this is observed as a gradual prolongation of the PR interval with each successive beat until a P-wave fails to conduct, resulting in a dropped QRS complex.

Second-degree AV block Mobitz type II is characterized by sporadically occurring blocks, without the Wenckebach phenomenon.

Second-degree AV block Mobitz type I (Wenckebach block)

Second-degree AV block Mobitz type 1 is sometimes referred to as Wenckebach block. However, the Wenckebach phenomenon may also occur in sinoatrial (SA) block which is why the term should not be used specifically for AV blocks.

Mobitz type 1 block is characterized by a gradual prolongation of the PR interval over a few heart cycles until an atrial impulse is completely blocked, which manifests on the ECG as a P-wave not followed by a QRS complex. This cycle repeats itself over and over again, such that every cycle ends with a blocked P-wave. Refer to Figure 1.

The degree of the block should be determined. It is denoted by counting the number of P-waves before each block. If every third P-wave is blocked, then there is 3-to-2 block (which is the most common). If every fourth P-wave is blocked, it is classified as 4-to-3 block, which is less common. 5-to-4 block is even more uncommon. Note that the higher the degree of block, the more difficult it may be to verify that the PR interval is being gradually prolonged. Indeed, in 2-to-1 block it may be impossible to observe a PR prolongation.

ECG examples of AV block II, Mobitz type II

Figure 1. Second-degree AV block Mobitz type 1, also known as Wenckebach block.

Clinicians frequently find it difficult to differentiate between Mobitz type 1 and Mobitz type 2. A very simple rule of thumb can be applied to do this: whenever there are varying PR intervals, the diagnosis is Mobitz type 1 (Wenckebach block).

Electrophysiology of second-degree AV block Mobitz type 1

The dysfunction in the AV node in Mobitz type 1 block can be viewed as a tendency to exhaust the conduction capacity. It starts with the successful conduction of an atrial impulse (either with normal or abnormal PR interval). The AV node is dysfunctional, such that it will not be able to repolarize adequately by the time the next impulse arrives, which is why the conduction will be slower than the previous and the PR interval becomes prolonged. The AV node becomes more and more exhausted (i.e more and more refractory) each time until it is completely refractory and blocks the atrial impulse. This manifests on the ECG with gradual prolongation of the PR interval until a P-wave is blocked and thus not followed by a QRS complex. The AV node then recovers (after the complete block), only to repeat the cycle again. These cycles are often referred to as Wenckebach periods.

Prognosis in second-degree AV block Mobitz type 1

Mobitz type I block may occur in younger healthy individuals (particularly during sleep). It is also common among athletes due to their high vagal tone. It is more common in older individuals. The prognosis is good, even in the elderly. Mobitz type 1 block generally does not progress to more advanced blocks. Should it progress to more advanced blocks, which typically is due to a more distal location of the block, an artificial pacemaker is needed.

Treatment of second-degree AV block Mobitz type 1

Refer to Management of Atrioventricular (AV) Blocks.

Second-degree AV block Mobitz type II

Mobitz type 2 block implies that some atrial impulses are blocked sporadically. The PR interval is constant (although it may be prolonged). Mobitz type 2 is more serious, because it is usually chronic and tends to progress to third-degree AV block. Moreover, cardiac output may be reduced if many impulses are blocked. Approximately 20% of patients have a block located in the bundle of His, and 80% have a block located in the bundle branches. Mobits type 2 block necessitates an artificial pacemaker. Refer to Figure 2 for ECG example.

Figure 2. Second-degree AV-block Mobitz type 2.

Differentiate Mobitz type 1 block from Mobitz type 2 block

Both Mobitz type 1 block and type 2 block result in blocked atrial impulses (ECG shows P-waves not followed by QRS complexes). The hallmark of Mobitz type 1 block is the gradual prolongation of PR intervals before a block occurs. Mobitz type 2 block has constant PR intervals before blocks occur. Thus, if one can spot the gradual prolongation of PR intervals, Mobitz type 1 block should be diagnosed. If it is difficult to discern the prolongation, but there are still varying PR intervals, one should still diagnose Mobitz type 1 block. The PR interval is constant in Mobitz type 2 block.

The following situations may pose a diagnostic challenge:

If the PR prolongation is minimal before a P-wave is blocked.

If many impulses are blocked (2-to-1 block), the PR prolongation becomes difficult to discern.

In these situations, there are additional tools to differentiate the two:

Atropine or physical activity: these two increase the heart rate which induces Wenckebach phenomenon in Mobitz type 1 block.

Vagal stimulation: this causes increased block if the block is located in the AV node, which suggests Mobitz type 1 block.

If the PR interval is prolonged, Mobitz type 1 block is more likely.

If the QRS complexes are abnormal, Mobitz type 2 block is more likely.

Treatment of second-degree AV block Mobitz type 2

Read: Management and treatment of AV block 1, 2 and 3.

Management and treatment of AV block (atrioventricular blocks)

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Chapter 4: Third-degree AV block (3rd degree AV block, AV block 3, AV block III)

This chapter discusses third-degree AV block, which is synonymous with AV dissociation, complete AV block, AV block III and AV block 3. In third-degree AV block, no atrial impulses are conducted to the ventricles. The atria and the ventricles are electrically dissociated from each other. This condition is referred to as atrioventricular (AV) dissociation. Importantly, for the ventricles to have any electrical (and thus pumping) activity at all, an escape rhythm must arise in an ectopic focus (located distal to the block). Third-degree AV block is a very serious condition because escape rhythms may (1) not occur, (2) occur transiently, or (3) occur but generate insufficient cardiac output. If no escape rhythm occurs, cardiac arrest will ensue.

Progression from first-degree AV block to third-degree AV block is rare. Progression from second-degree AV block Mobitz type 1 (Wenckebach block) is uncommon. However, second-degree AV block Mobitz type 2 frequently progresses to third-degree AV block.

ECG examples are given in Figure 1.

Figure 1. Third-degree AV block (complete heart block, AV dissociation).

Figure 2. Example of third-degree AV block. Click to zoom.

ECG features of third-degree AV block

On the ECG P-waves have no relation to the QRS complexes. The QRS complexes may be normal or wide. P-waves have constant PP interval and ride straight through the strip, without any relation to QRS complexes. P-waves may occur on the ST-T segment (Figure 1, upper panel). The atrial rate is typically faster than the ventricular rate.

It may be very difficult to establish a diagnosis of third-degree AV block if the atrial and ventricular rate is equal and the P-waves occur right before the QRS complexes. This scenario, which is referred to as isoarrhythmic AV block, may even simulate sinus rhythm.

Third-degree AV block causes cardiac arrest unless an escape rhythm emerges. The escape rhythm may have narrow or wide QRS complexes, depending on where the impulses are discharged and whether there is a concomitant bundle branch block. Escape rhythms with narrow QRS complexes indicate that the block and the ectopic focus (which generates the escape rhythm) are located proximal to the bifurcation of the His bundle. This rhythm is often referred to as a junctional escape rhythm. The junctional escape rhythm is regular, with a frequency of roughly 40 beats per minute. If the escape rhythm has wide QRS complexes and a frequency of 20–40 it is most likely a ventricular escape rhythm. Ventricular escape rhythms are unreliable, such that they may cease and thus cause cardiac arrest. Junctional escape rhythm is more reliable (the risk of cardiac arrest is considerably lower). Moreover, ventricular escape rhythms are slow, resulting in reduced cardiac output and risk of hypoperfusion.

Distinguishing AV block 2 and AV block 3

In case the distinction between second-degree AV block and third-degree AV block is difficult, the following rules may be helpful.

Irregular ventricular rhythm suggests second-degree AV block because escape rhythms in third-degree AV block are regular.

Regular ventricular rhythm with association between P and QRS and constant PR interval suggests second-degree AV block.

Regular ventricular rhythm and varying PR interval suggest third-degree AV block because atrial and ventricular rates are most often not equal (which makes the PR interval appear as varying).

Management of third-degree AV block

Please refer to Management of AV Blocks.

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Chapter 5: Management and treatment of AV block (atrioventricular blocks)

Evaluation of patients with suspected AV blocks requires a thorough medical history (with emphasis on causes of AV blocks; please refer to the Causes of AV blocks) and physical examination. It is also reasonable to analyze cardiac troponins if there is any probability of myocardial ischemia as the underlying cause. Holter ECG may be valuable if the diagnosis is uncertain. Echocardiography is generally performed in order to evaluate ventricular function, since it may affect the choice of device therapy and also suggest whether other interventions (e.g. heart failure management, evaluation for coronary artery disease, etc.) are warranted. Management of AV blocks aims to restore atrioventricular conduction either pharmacologically or by means of artificial pacemakers. Both methods may be used in the acute setting, whereas long-term management only includes pacemaker therapy.

Treatment of AV block in the acute setting

Treatment in the acute setting is directed at managing bradycardia and reduced cardiac output. Bradycardia causing hemodynamic instability is a potentially life-threatening condition and should be managed urgently. The risk of cardiogenic shock is high and pharmacological interventions are often futile. A transcutaneous pacemaker is often necessary in the acute setting and is currently the only treatment with class I recommendation according to European (ESC) and North American (AHA, ACC) guidelines. For details regarding the management of bradycardia, please refer to Management of acute bradycardia. A summary of the treatments is provided below.

Figure 1. Management of acute bradycardia in the emergency setting.

In the event of manifest or impending circulatory collapse, transcutaneous pacing must be started immediately. The risk of circulatory collapse is highest with AV block 2 Mobitz type 2 and AV block 3. The only treatment with a class I recommendation for the management of acute bradycardia is transcutaneous pacing. Pharmacological interventions (Table 4) should be considered temporary, often insufficient, treatments that can be attempted until a pacemaker is established.

Drug	Effect	Dose, kinetics	Comment
Atropine	Acetylcholine receptor antagonist	1 mg IV every 3-5 minutes, maximum 3 mg IV.T½ 3 h.50% renal elimination.	• Typically the first choice of drug.• Effective in sinus bradycardia or AV node block.• Dose <0.5 mg may worsen bradycardia and should not be given.• Relative contraindications are ileus, glaucoma.
Isoprenaline /Isoproterenol	α-1, α-2, β-1, β-2 agonist	Start infusion at 4 μg/min and titrate to desired resultT½ 1 min	• May cause ventricular arrhythmias (dose-dependent).• Prolonged use often causes headaches, tremors.• Effective if bradycardia is caused by beta blockers.
Adrenaline (Epinephrine)	α and β agonist	Infusion of 2–10 μg/min (titrate as needed).T½ 5 min.	• Effective if hypotension is present.• Can be given as a bolus.• Effective if bradycardia is caused by beta blockers.
Dopamine	Dopamine receptor agonist, α- and β-agonist	Infusion of 5−20 μg/kg/minT½ 2 min	• Avoid boluses.• Effective if bradycardia is caused by beta blockers.
Dobutamine	β-1 agonist	Infusion of 3−10 μg/kg/min.T½ 2 min	Effective if inotropic effect is required.
Theophylline / theophyllamine / aminophylline	Adenosine receptor antagonist, phosphodiesterase inhibitor. Exact mechanism is unknown.	100−200 mg slow iv injection.	Rarely used.
Glucagon	Counteracts beta blockers. An antidote to beta blockers.	2–10 mg bolus followed by 2–5 mg/h infusion	Antidote to beta blockers.
Calcium	Counteracts calcium channel blockers (CCB). Antidote to CCBs.	10 ml calcium 0.2 mmol/ml iv.	Antidote to CCBs.
Digoxin antibodies	Binds to digoxin.	Digitalis antidote (anti-digoxin, Fab fragment).	Given in case of suspected digoxin intoxication.

Atropine

Evidence: Class IIa recommendation

Atropine is the first choice for the pharmacological treatment of acute bradycardia.

Dosage: 1 mg iv, every 3-5 minutes, to a maximum of 3 mg.

Doses lower than 0.5 mg IV may worsen bradycardia and should never be given.

The effect of atropine is temporary.

If atropine is ineffective, isoprenaline, adrenaline (epinephrine) or dopamine can be tried.

Atropine counteracts acetylcholine-mediated bradycardia by inhibiting the effect of acetylcholine on the sinus node and AV node. Atropine is effective in sinus bradycardia and AV block located in the AV node.

Atropine is typically ineffective in complete AV block and Mobitz type 2 second-degree AV block.

Atropine is not used in patients with heart transplantation.

Isoprenaline (isoproterenol)

Evidence: Class IIa recommendation

Isoprenaline is a second-line pharmacological treatment for acute bradycardia.

Dosage: Start infusion at 4 μg/min and titrate to the desired result.

Half-life: 5 minutes.

Isoprenaline enhances AV conduction in nodal blocks. In infranodal blocks, isoprenaline is effective only if it induces an escape rhythm, or enhances the automaticity of an existing escape rhythm.

Adrenaline (epinephrine)

Evidence: Class IIb recommendation

Effective in hypotension and when an inotropic effect is required.

Dosage: Infusion of 2–10 μg/min (titrate as needed).

Can be added to dopamine.

Dopamine

Evidence: Class IIb recommendation

Effective in hypotension and when an inotropic effect is required.

Dosage: Infusion 5−20 μg/kg/min.

Can be added to adrenaline.

Temporary pacemaker

Transcutaneous pacemaker

Evidence: Class I recommendation

Most defibrillators have a pacemaker function, allowing the device to operate as an external pacemaker. (Video 1, Figure 2, Figure 3).

A pacemaker is the safest treatment for acute bradycardia.

A transcutaneous pacemaker should be established immediately if there is a risk of hemodynamic collapse.

AV block 2 Mobitz type 2 and AV block 3 are strong indications for a transcutaneous pacemaker.

Figure 2. Example showing Zoll R Series defibrillator. Note that the Mode Selector is set to Pacer to activate the pacemaker settings.

Video 1. Example of transcutaneous pacemaker with Zoll R Series. The function looks similar for other manufacturers.

Pain and discomfort during transcutaneous pacing

Although transcutaneous pacing can be unpleasant or somewhat painful, all patients tolerate the procedure. Pain is caused by muscle contractions. Administration of sedatives (midazolam) or analgesics (morphine) is recommended, using the following doses:

Midazolam: 1–3 mg initial dose. Total dose 4-8 mg. Lower dose range in cases aged >60 years.

Morphine: 2.5 mg IV.

Figure 4. Placement of electrode pads in the anteroposterior direction for transcutaneous pacing.

How to perform transcutaneous pacing

Explain to the patient the purpose of the procedure.

Administer sedatives / analgesics.

Position electrode pads in anteroposterior direction (Figure 4).

If there is time, trim chest/back hair (do not shave). Dry the skin if wet.

Do not relocate already attached pads (the adhesive becomes poor).

Activate the pacemaker function (Video 1, Figure 2, Figure 3).

Set the pacing rate to 50 beats/min.

Gradually increase the current (start with 20 mA).

Identify the pacemaker spikes (stimulation artifacts) on the ECG recording.

Determine if pacemaker spikes are followed by QRS complexes (indicating electrical capture).

If electrical capture is visible, palpate the femoral artery to examine whether there is mechanical capture (i.e. ventricular contractions).

Monitor blood pressure and pulse oximetry.

When the threshold for capture (lowest current producing mechanical capture) is identified, the output (current) is increased by 10% (in order to provide stimulations with a safety margin).

Most patients require a current in the range of 20 to 140 mA

Avoid unnecessary pacing by using a low base frequency (e.g. 30–40 beats/min).

How to perform transcutaneous pacing during asystole

Follow the same procedure as above but start with maximum current strength (output) and gradually reduce the current until stimulation fails to produce capture. Then increase the current until capture is obtained, and another 10% output as a safety margin.

Checking transcutaneous pacing

Mechanical capture is confirmed by palpating a peripheral pulse (femoral artery) or assessing pulse oximetry. Avoid evaluating the pulse in the carotid artery (pectoral muscle contractions may be mistaken as arterial pulsations).

Muscle contractions are not equivalent to mechanical capture.

If the pacemaker stimulates more than necessary, there is undersensing, which means that the pacemaker does not detect the ventricular complexes (and therefore continues to pace). This is resolved by relocating the ECG leads so that they detect larger QRS amplitudes or increasing the gain on the defibrillator.

If the pacemaker does not stimulate due to artifacts there is oversensing, which can be resolved by eliminating the artifacts or relocating the leads.

Transvenous pacing

A transvenous pacemaker should be established if transcutaneous pacing is ineffective.

Transvenous pacemaker requires higher competence to establish and also entails a risk of infection, perforation and tamponade.

Access can be obtained via the jugular vein or the femoral vein. The introduction of a pacemaker lead via the jugular vein carries a risk of local thrombosis or infection, which complicates later pacemaker implantation. Pacing via the femoral vein requires immobilization of the patient since movements can cause dislocation of the lead.

A transvenous pacemaker can use a screw electrode, which can remain for up to 6 weeks and carries a significantly lower risk of lead dislocation.

Long-term treatment

First-degree AV block and second-degree AV block Mobitz type I: These AV blocks rarely require therapy, unless the patient is symptomatic. A pacemaker is indicated in patients who are clearly symptomatic, particularly if they display a wide QRS complex.

Second-degree AV block Mobitz type II and third-degree AV block: These cases should almost invariably receive a pacemaker. In the case of Mobitz type 2 with wide QRS complexes, a pacemaker is indicated even in the absence of symptoms. All cases of third-degree AV block necessitate a pacemaker.

Related articles

Overview of AV (atrioventricular blocks)

First-degree AV block (AV block 1)

Second-degree AV block (AV block 2)

Third-degree AV block (AV block 3)

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Chapter 6: Intraventricular conduction delay: bundle branch blocks & fascicular blocks

This chapter discusses intraventricular conduction delays (defects), which are caused by functional or anatomical defects in the components of the intraventricular conduction system. Because the conduction system is crucial for rapid and synchronized activation of the ventricles, conduction defects will typically cause abnormal ventricular activation (i.e. contraction). The significance of this will depend on the severity of the conduction defect and the affected ventricle. In general, a conduction defect in the left ventricle is more significant, as compared with a defect affecting the right ventricle. This is due to the fact that the left ventricle pumps against greater resistance and any disturbance in ventricular activation will reduce the efficiency of the pumping function. The primary ECG manifestations of conduction defects are prolonged QRS complexes and altered QRS appearance. These concepts will be discussed in detail in this and the subsequent articles. Note that the terms intraventricular conduction delay and intraventricular conduction defect are used interchangeably.

Normal and abnormal intraventricular impulse conduction

The intraventricular conduction system is composed of the His-Purkinje system. More precisely this system consists of the bundle of His, the left and right bundle branches and the fascicles of the left bundle branch (Figure 1). The interventricular septum obtains Purkinje fibers from the left bundle branch. The right bundle branch does not give off any Purkinje fibers during its passage through the septum. Purkinje fibers are branched off from the right bundle branch at the level of the origin of the anterior papillary muscle. A network of Purkinje fibers sprouts out from the bundle branches and fascicles and spread through the ventricular endocardium. Impulse conduction through the Purkinje network is very fast (4 m/s) which enables the vast majority of ventricular myocardium to be depolarized approximately simultaneously.

Figure 1 shows the components of the conduction system. Note that conduction defects in the atrioventricular (AV) node and the bundle of His have been discussed in the previous chapter. The current chapters discuss conduction defects located in the bundle branches and in the fascicles.

Figure 1. Components of the ventricular conduction system and the temporal association between the ECG and impulse transmission through the heart. An intraventricular conduction delay may occur whenever any of the main components of the conduction system is dysfunctional.

Conduction defects in the bundle branches and/or fascicles cause characteristic ECG changes. The type of ECG changes that occur are as follows:

Widening of the QRS complex – Anatomical or functional blocks in bundle branches or fascicles may block the impulse completely. Such a block in the left bundle branch is simply referred to as left bundle branch block. The consequence of left bundle branch block is that the left ventricle will be depolarized by impulses spreading from the right ventricle. Those impulses will spread through the right ventricle partly or entirely outside of the conduction system which will be slow and therefore cause a wide QRS complex. Similarly, a block in the right bundle branch causes right bundle branch block, in which the right ventricle will be depolarized by impulses spreading from the left ventricle. This will also yield a wide QRS complex.

Altered QRS morphology – Because the normal sequence of depolarization is altered in bundle branch blocks and fascicular blocks, the QRS morphology will also be altered. In each of these blocks, the QRS morphology will have a characteristic appearance which makes it fairly easy to diagnose them.

Altered electrical axis – Changes in the depolarization sequence may also alter the electrical vectors and thus the electrical axis.

Overview of bundle branch blocks and fascicular blocks

Bundle branch blocks (right and left bundle branch block)

An anatomical or functional block in the left bundle branch causes left bundle branch block (LBBB). Similarly, a block in the right bundle branch causes right bundle branch block (RBBB). The ventricles whose bundle branch is defective will be depolarized from impulses spreading from the opposite ventricle. This results in characteristic ECG changes depicted in Figure 2.

Figure 2. Characteristics of bundle branch blocks. (A): ECG features of right bundle branch block (RBBB). (B): ECG features of left bundle branch block (LBBB).

ECG changes in right bundle branch block (RBBB) and left bundle branch block (LBBB)

Right bundle branch block (Figure 2, panel A) is characterized by a second R wave (denoted R’) in V1, which gives lead V1 an rSR’ complex. In lead V6 a broad and deep S wave is noted. In left bundle branch block lead V1 shows a deep S-wave and in V6 a broad and clumsy R-wave is noted (Figure 2, panel B). Importantly, in both bundle branch blocks, the QRS duration is at least 0.12 seconds. Moreover, there are always secondary ST-T changes in these leads, such that the ST-T segment is discordant to the QRS complex (QRS and ST-T have opposite directions). Consequently, ST-segment elevations and ST-segment depressions are expected in bundle branch blocks.

Complete vs. incomplete bundle branch blocks

Complete bundle branch blocks have QRS duration ≥0,12 seconds, while incomplete bundle branch blocks are QRS duration <0.12 seconds. However, incomplete bundle branch blocks are of significance because they tend to progress to complete blocks.

Prognosis of bundle branch blocks

Right bundle branch block in asymptomatic individuals is not correlated with adverse outcomes. On the other hand, new right bundle branch block in patients with chest pain may indicate occlusion in the left anterior descending artery. Finally, new right bundle branch block in patients experiencing dyspnea (particularly if acute) may indicate pulmonary embolism. In the vast majority of cases, however, right bundle branch block is a benign finding with little if any impact of cardiovascular prognosis.

Left bundle branch block is always pathological and typically a consequence of ischemia or structural heart disease.

Figure 3 gives a detailed ECG comparison of the bundle branch blocks and fascicular blocks. This image should be memorized.

Figure 3. Overview of criteria and ECG changes in bundle branch blocks and fascicular blocks. All these intraventricular conduction delays are common and therefore important to recognize.

Fascicular block (hemiblock)

An anatomical or functional block in a fascicle causes a fascicular block. This was previously termed hemiblock. Block in the anterior fascicle is termed left anterior fascicular block (LAFB), and block in the posterior fascicle is termed left posterior fascicular block (LPFB).

Fascicular blocks may exist isolated or concomitant with right bundle branch block. Isolated LAFB is common, whereas isolated LPFB is very uncommon.

On the contrary to bundle branch blocks, fascicular blocks only cause slight prolongation of the QRS duration; it does not, however, reach ≥0,12 seconds. In other words, QRS duration in fascicular blocks is always <0.12 s unless there is a concomitant bundle branch block.

Bifascicular block

As mentioned above, a fascicular block may be accompanied by a right bundle branch block. This combination is termed bifascicular block. The most common bifascicular block is right bundle branch block with left anterior fascicular block (RBBB + LAFB). Left bundle branch block with simultaneous left posterior fascicular block (RBBB + LPFB) is uncommon. Simultaneous block in both fascicles (LPFB + LAFB) is equal to left bundle branch block (LBBB).

RBBB + LAFB

This combination is rather common and it is recognized through typical RBBB pattern in V1 and V6, along with LAFB pattern in lead II, III and aVF. QRS duration is ≥0,12 seconds. The electrical axis is –45° to –120° (left axis deviation).

RBBB + LPFB

This combination is uncommon. It may only be diagnosed in the absence of right ventricular hypertrophy.

Lead V1 shows RBBB pattern while lead aVL and I display LPFB pattern.

QRS duration is ≥0,12 seconds.

There is right axis deviation.

Trifascicular block

A trifascicular block is defined as the presence of a bifascicular block with a simultaneous first- or second-degree AV block. However, the term trifascicular block may cause confusion, and it is therefore recommended that each defect be stated separately.

Bilateral bundle branch block

The term bilateral bundle branch block has also caused some confusion in the literature. The term is most commonly used to describe a complete bundle branch block (RBBB or LBBB) with simultaneous first- or second-degree AV block. As for trifascicular block, this term should be avoided. Instead, each defect should be described separately.

Alternating bundle branch block

The ECG may alternate between LBBB and RBBB. This carries a poor prognosis because the risk of developing a third-degree AV block is high, particularly if there is a simultaneous first-degree AV block.

Intermittent bundle branch block

Sporadically occurring bundle branch block is common, particularly during tachycardia (refer to Abberant ventricular conduction).

This was a brief overview of the intraventricular conduction delays. Each of these will be discussed in separate chapters:

Left bundle branch block (LBBB)

Right bundle branch block (RBBB)

Fascicular blocks (hemiblocks)

Non-specific intraventricular conduction defect

Left bundle branch block (LBBB) in the diagnosis of acute myocardial infarction is discussed in a separate chapter:

Left bundle branch block (LBBB) and acute myocardial infarction (AMI).

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Chapter 7: Right bundle branch block (RBBB): ECG, criteria, definitions, causes & treatment

Right bundle branch block (RBBB) is due to an anatomical or functional dysfunction in the right bundle branch, such that the electrical impulse is blocked. Figure 1 illustrates the components of the ventricular conduction system, including the right bundle branch (RBBB). In the presence of right bundle branch block, depolarization of the right ventricle relies on electrical impulses originating from the left ventricle. However, these impulses propagate slowly as they travel partially or entirely outside the specialized conduction system. This slow propagation leads to a delayed and abnormal activation sequence of the right ventricle, resulting in a prolonged and abnormal QRS complex on the ECG. The hallmark of right bundle branch block is QRS duration ≥0,12 seconds, large R’-wave in V1/V2 and a broad and deep S-wave in V5/V6.

Figure 1. The sinoatrial (SA) node and atrioventricular (AV) node are located in the atria and are not part of the ventricular conduction system. The AV node transitions into the bundle of His, which bifurcates into the right and left bundle branches. The left bundle branch further divides into the anterior and posterior fascicles. Both the right bundle branch and the fascicles extend into the fine Purkinje network, which spreads throughout the myocardium.

Figure 2 illustrates a normal ECG, a left bundle branch block (LBBB) and a right bundle branch block (RBBB).

Figure 2. Left bundle branch block (LBBB) and right bundle branch block (RBBB). The paper speed is 25 mm/s (1 large box equals 200 ms). The hallmark of both RBBB and LBBB is the QRS duration which is by definition 120 ms or longer.

ECG criteria for right bundle branch block (RBBB)

QRS duration ≥0,12 seconds.

Leads V1-V2: The QRS complex resembling the letter M. More specifically, the QRS complex displays rsr’, rsR’ or rSR’ pattern (rSR’ is the most common; Figure 2). Occasionally the S-wave does not reach the baseline. The second R-wave (denoted R’) is virtually always larger than the first R-wave.

Leads V5, V6, I, aVL: Broad S-wave. S-wave duration is greater than R-wave duration, or S-wave duration is greater than 40 ms in V6 and I.

ST-T changes: V1-V2 shows downsloping ST-segments and inverted T-waves. Leads V5, V6, I and aVL show positive T-waves.

If QRS duration is between ≥0,110 seconds and <0,12 seconds, the right bundle branch block is said to be incomplete. Note that a second r-wave (r’) may occur as a normal variant in lead V1 (the normal variant has a normal QRS duration). Moreover, the normal septal q-waves (seen in V5, V6) are not affected by the right bundle branch block. Occasionally, right bundle branch block only displays a broad and notched R-wave in V1 (instead of two R-waves); in that scenario, the R-wave peak time should be >0.05 seconds.

Figure 3 shows the distinguishing features of right and left bundle branch block in the precordial (chest) leads.

Figure 3. Characteristics of right and left bundle branch block in leads V1/V2 and V5/V6.

Figure 4 shows morphological differences between LBBB and RBBB on 12-lead-ECG at paper speed 50 mm/s.

Figure 4. RBBB and LBBB.

Electrophysiology of right bundle branch block (RBBB)

Under normal conditions, both ventricles depolarize simultaneously. However, the QRS morphology is dominated by electrical vectors from the left ventricle due to its significantly larger mass compared to the right ventricle. In right bundle branch block (RBBB), the right ventricle depolarizes after the left ventricle, allowing its electrical vectors to become evident. These vectors manifest in the later part of the QRS complex as an R’ wave (pronounced “R prime”), which is directed anteriorly and rightward.

Due to the abnormal depolarization sequence of the right ventricle in RBBB, repolarization is also abnormal, leading to secondary ST-T changes, which appear on the ECG as discordant ST-T segments. These ST-T segments are directed opposite to the QRS complex. As illustrated in Figure 3, a positive QRS complex in lead V1 is accompanied by a negative ST-T segment, defined by ST-segment depression and T-wave inversion. Similar patterns are typically observed in lead V2 as well. However, RBBB does not cause secondary ST-T changes in V5-V6.

The electrical axis in right bundle branch block (RBBB)

Right bundle branch block does not affect the electrical axis of the heart. Axis deviation indicates that there is a concomitant fascicular block, or other abnormality. Left axis deviation suggests concomitant left anterior fascicular block. Right axis deviation suggests concomitant left posterior fascicular block.

Clinical significance of right bundle branch block

Prevalence of RBBB

The prevalence of right bundle branch block (RBBB) in healthy individuals varies by age, gender, and diagnostic criteria, ranging from 0.2% to 8% in the general population. Specifically, complete RBBB is observed in approximately 3.2%, while incomplete RBBB (iRBBB) accounts for 4.6%, leading to a combined prevalence of 8% for all forms of RBBB (Alventosa-Zaidin et al.). RBBB is more common in men than women; one study reported complete RBBB in 1.4% of men compared to 0.5% of women (Bussink et al.). The prevalence of complete RBBB increases with advancing age, reaching up to 11.3% in individuals aged 80 years or older.

Long-term prognostic implications of RBBB

While traditionally considered benign in asymptomatic individuals, recent evidence suggests that RBBB may be linked to an increased cardiovascular risk. The Copenhagen City Heart Study (1976–2003) analyzed 18,441 participants who were free from prior myocardial infarction, heart failure, or left bundle branch block, following them through 2009 for all-cause mortality and cardiovascular outcomes. The study found that right bundle branch block (RBBB) and incomplete RBBB (iRBBB) were more prevalent in men than women (1.4%/4.7% in men vs. 0.5%/2.3% in women). Key predictors of incident RBBB included male sex, older age, high systolic blood pressure, and the presence of incomplete RBBB. Complete RBBB was associated with increased all-cause mortality (1.3-fold higher relative risk) and cardiovascular mortality (1.9-fold higher relative risk), as well as an elevated risk of myocardial infarction (1.7-fold higher relative risk) and pacemaker implantation (2.2-fold higher relative risk). However, it was not associated with heart failure or atrial fibrillation. In contrast, incomplete RBBB was not associated with any adverse outcomes. The findings suggest that RBBB in asymptomatic individuals may signal increased cardiovascular risk, challenging the perception of its benign nature (Bussink et al.).

Important differential diagnoses in the emergency setting

New onset right bundle branch block in patients with chest pain may indicate occlusion in the left anterior descending (LAD) artery. These cases will most likely exhibit anterior ST-segment elevations. Moreover, new onset right bundle branch block in patients presenting with dyspnea (particularly if onset is acute) suggests pulmonary embolism.

Causes of right bundle branch block (RBBB)

Idiopathic fibrosis or degeneration in the right bundle branch

Congenital heart disease

Ischemic heart disease (coronary artery disease)

Acute cor pulmonale (pulmonary embolism)

Chronic obstructive pulmonary disease

Cardiac surgery may cause permanent or transient RBBB

PCI may cause transient RBBB

Cardiomyopathy (particularly hypertrophic obstructive cardiomyopathy)

Aberrant ventricular conduction (aberrancy)

Diagnosis of ischemia and infarction in the setting of RBBB

The right bundle branch block does not interfere with the diagnosis of ischemia/infarction. It is possible to diagnose pathological Q-waves (because the initial part of the QRS is not affected by the RBBB). Acute ischemia (ST-T changes) may also be judged as usual, despite the bundle branch block. Note that acute cor pulmonale with RBBB may cause large Q-waves in V1–V3, II, III and/or aVF.

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Chapter 8: Left bundle branch block (LBBB): ECG criteria, causes, management

Left bundle branch block (LBBB) results from anatomical or functional impairment of the left bundle branch (LBB), leading to a blockage of electrical impulse conduction through this bundle. Consequently, depolarization of the left ventricle is achieved by impulses spreading from the right ventricle. The electrical impulse will propagate through the left ventricle partially or entirely outside the specialized conduction system. This slower conduction results in a prolonged QRS duration. The defining features of LBBB include a QRS duration of ≥0.12 seconds, a deep and broad S-wave in leads V1 and V2, and a wide, notched R-wave in leads V5 and V6. Figure 1 (25 mm/s) illustrates the differences between normal conduction, left bundle branch block (LBBB) and right bundle branch block (RBBB).

Figure 1. 25 mm/s. Normal QRS (A), left bundle branch block (B) and right bundle branch block (C). One large box equals 100 ms at paperspeed 25 mm/s.

Figure 2 shows 12-lead-ECGs demonstrating right and left bundle branch blocks.

Figure 2. 50 mm/s. ECG examples of right bundle branch block (RBBB) and left bundle branch block (LBBB).

The cardiac conduction system

The cardiac conduction system ensures rapid and synchronized spread of depolarization, which is essential for coordinated and efficient atrial and ventricular activity. The conduction system includes the sinoatrial (SA) node, atrioventricular (AV) node, Bundle of His, bundle branches (left and right bundle branch), and Purkinje fibers. The conduction system allows for rapid spread of the depolarization to the contractile cells. Figure 3 illustrates the components of the conduction system and its temporal relationship to the ECG waveforms. The cardiac cycle begins in the sinus node (sinoatrial node), where depolarization occurs through automaticity (refer to Cardiac Electrophysiology). The electrical impulse propagates through the atria via the internodal pathways and Bachmann’s bundle, eventually reaching the atrioventricular (AV) node. Here, conduction is briefly delayed to allow adequate ventricular filling. The impulse then travels through the Bundle of His, which bifurcates into the left bundle branch (LBB) and the right bundle branch (RBB). The left bundle branch further divides into the anterior and posterior fascicles. The bundle branches and fascicles play a critical role in disseminating the impulse throughout the ventricles. Dysfunction in the bundle branches or fascicles will result in characteristic ECG changes.

Figure 3. The cardiac conduction system.

ECG criteria for left bundle branch block (LBBB)

Diagnosing left bundle branch block is relatively straightforward. The hallmark of LBBB is the prolonged QRS duration. A QRS duration of 120 ms (0.12 s) or more is required to diagnose a complete left bundle branch block. In addition to prolonged QRS duration, LBBB is characterized by deep and broad S-waves in leads V1 and V2 and broad, frequently nothed, R-wave in V5 and V6. Secondary ST-T changes occur invariably in the presence of LBBB. The following ECG criteria and characteristics are used to diagnose LBBB:

QRS duration ≥0,12 seconds.

Leads V1-V2: deep and broad S-wave. The small r-wave is missing or smaller than normal; if missing, a QS complex appears in V1 and occasionally V2, but rarely in V3. The S-wave in V1 may be notched and resemble the letter W.

Leads V5-V6: Broad, completely positive and often notched R-wave.

Leads I and aVL: Similar to V5 and V6.

ST-T changes: Left-sided leads (V5, V6, I and aVL) show T-wave inversions and ST segment depressions. V1–V3 shows ST-segment elevation and positive T-waves. The ST-segment elevation rarely exceeds 5 mm.

Figure 4 illustrates the distinguishing features of RBBB and LBBB.

Figure 4. ECG patterns in LBBB and RBBB. LBBB is characterized by deep and broad S-waves in V1/V2 and broad and notched R-waves in V5/V6. RBBB is characterized by rSR’ complex in V1/V2 (i.e. there are two R-waves and a large S-wave). The S-wave in V5/V6 is broad in the presence of RBBB.

Electrophysiology of left bundle branch block (LBBB)

Ventricular depolarization normally begins in the interventricular septum, which receives Purkinje fibers from the left bundle branch. Therefore, depolarization of the septum begins in its left aspect and progresses toward its right aspect. Depolarization of the septum generates the small r-waves observed in leads V1 and V2, as well as the small q-waves seen in leads V5 and V6, commonly referred to as “septal q-waves”. These normal patterns are illustrated in Figure 5.

Figure 5. Electrical vectors in the horizontal plane, and the corresponding ECG waveforms.

In left bundle branch block, depolarization of the septum occurs via impulses spreading from the right ventricle. Consequently, the small r-waves in V1–V2 and small q-waves in V5–V6 are either diminished or disappeared. Depolarization continues slowly towards the left ventricular free wall, and the vector is continuously directed leftward. This causes a wide S-wave in V1–V2 (referred to as QS complex if the r-wave is absent) and a broad and notched R-wave in V5–V6.

Due to the abnormal left ventricular depolarization sequence in LBBB, the repolarization process is also abnormal, leading to secondary ST-T changes that become apparent. In LBBB, it is expected that ST segment depressions and T-wave inversions exist in left-sided leads (V5, V6, I and aVL). Simultaneously, V1–V3 typically display ST-segment elevation and large S-waves.

Electrical axis in left bundle branch block (LBBB)

The electrical axis may be unaltered or deviate to the left or (rarely) to the right. Left axis deviation suggests a pronounced left bundle branch block.

Clinical implications of left bundle branch block (LBBB)

Left bundle branch block is always a pathological finding. It affects left ventricular contractility (systolic function) and is associated with adverse cardiovascular outcomes. LBBB is strongly associated with hypertension, left ventricular hypertrophy, aortic stenosis, aortic regurgitation, myocarditis, ischemic heart disease, heart failure, and cardiomyopathies. The Framingham Heart Study showed that left bundle branch block was associated with seven times as great a risk of heart failure, two times as great a risk of coronary artery disease and a significantly higher risk of developing right ventricular hypertrophy (Schneider et al.). Left bundle branch block is rare in younger individuals.

Diagnosis of acute myocardial ischemia and infarction in patients with left bundle branch block (LBBB)

In LBBB, activation of the left ventricle relies on electrical impulses spreading from the right ventricle, leading to slow and abnormal depolarization of the left ventricle. This abnormal depolarization produces an atypical QRS complex (discussed earlier). Additionally, the abnormal repolarization results in secondary ST-T changes, including ST-elevations in leads V1–V3, ST-depressions in leads V4, V5, V6, aVL, and I, as well as inverted T-waves in leads showing ST depressions. These ST-T changes are normal and expected findings in the presence of LBBB. However, the underlying electrical disturbance and associated secondary ST-T changes cause a significant challenge in diagnosing acute ischemia. Current guidelines from the European Society of Cardiology (ESC), the American Heart Association (AHA) and the American College of Cardiology (ACC) advise against using standard ECG criteria for diagnosing acute myocardial infarction in the presence of LBBB. Figure 6 shows typical ST-segment elevations and ST-segment depressions, observed in an asymptomatic patient with LBBB.

Figure 6. Left bundle branch block (LBBB) at two different paper speeds. Note the ST elevations and ST depressions.

There are three reasons why LBBB complicates the assessment of patients with suspected acute myocardial infarction:

Left bundle branch block (LBBB) can mimic acute STEMI, as it often presents with similar ECG changes, including ST-segment elevations, ST-segment depressions, and T-wave inversions. These overlapping features frequently lead to confusion between LBBB and acute STEMI.

LBBB may mask (conceal) ongoing myocardial ischemia: LBBB causes pronounced disturbance of ventricular repolarization, which usually prevents other ST-T changes (such as those arising from ischemia) from coming to expression on ECG. Therefore, ischemic ST-T changes (ST elevations, ST depressions, T-wave changes) are typically concealed in the setting of LBBB. A patient with acute STEMI may therefore display a normal LBBB pattern.

LBBB may be caused by ischemia/infarction: An acute myocardial infarction (particularly anterior STEMI) may cause LBBB. Hence, an acute myocardial infarction may result in LBBB, which then conceals the ischemic ST-T changes on ECG.

In summary, LBBB can arise from, mimic, or conceal acute myocardial ischemia and infarction, posing considerable diagnostic challenges. This prompted researchers to investigate patients with LBBB and suspected acute myocardial infarction (AMI) by referring them for urgent reperfusion therapy, which equaled fibrinolysis at the time (Wilner et al.). Their findings showed that a significant proportion of these patients had complete coronary artery occlusions and experienced better outcomes when managed as acute STEMI cases.

For almost two decades, European and North American guidelines recommended treating patients with symptoms of myocardial ischemia and new (or presumed new) LBBB as having acute STEMI. However, a growing body of evidence demonstrated that this approach resulted in an unacceptably high rate of unnecessary angiographies. Therefore, guidelines now advise that new (or presumed new) LBBB should not be used in isolation as a diagnostic criterion for acute myocardial infarction (O’Gara et al.). Instead, patients with a strong clinical suspicion of ongoing myocardial ischemia—regardless of ECG—should receive treatment similar to those with clear STEMI. This approach applies particularly to patients who remain symptomatic despite initial medical therapy, are hemodynamically unstable, or develop sustained ventricular arrhythmias. Similarly, the 2023 European Society of Cardiology (ESC) guidelines recommend treating patients with LBBB or RBBB and signs or symptoms strongly indicative of ongoing myocardial ischemia as having definitive STEMI, regardless of whether the bundle branch block was previously documented (Byrne et al.).

Sgarbossa criteria for diagnosing acute ischemia in the setting of LBBB

Several ECG criteria have been proposed to diagnose acute myocardial ischemia and infarction in the setting of LBBB. The most useful criteria are the Sgarbossa criteria (Neeland et al.). These criteria are summarized in Figure 7. For a detailed discussion, refer to LBBB and Acute Myocardial Infarction. In summary, no existing criteria demonstrate sufficient sensitivity to reliably detect acute myocardial infarction. Evaluating symptoms, hemodynamic status, and other signs of ischemia provides significantly greater value in guiding treatment decisions.

Figure 7. ECG criteria (Sgarbossa criteria) for acute STEMI in the setting of LBBB. Each criterion gives 2 to 5 points. Studies show that a cut-off of ≥3 points yields a sensitivity of 20–36% and specificity of 90–98% for acute STEMI in the setting of LBBB.

Left ventricular hypertrophy and left bundle branch block

Left ventricular hypertrophy (LVH) is characterized by an increase in left ventricular mass. This increased muscle mass can result in slightly prolonged depolarization and repolarization, leading to a mildly increased QRS duration; however, it typically does not reach or exceed 0.12 seconds. Moreover, the QRS morphology in left ventricular hypertrophy may also resemble that of left bundle branch block (particularly incomplete left bundle branch block). It is usually easy to separate the two. In hypertrophy, the septal q-waves (V5, V6, aVL and I) are preserved (or amplified), and the QRS complex has a very large amplitude. In left bundle branch block, the QRS duration is at least 0.12 seconds. Of course, LBBB and LVH may accompany each other.

Incomplete left bundle branch block (LBBB)

Incomplete left bundle branch block is less common than the complete form. In this condition, conduction through the left bundle branch is preserved but occurs at a reduced capacity compared to a normal bundle branch. Thus, the initial depolarization of the left ventricle occurs via impulses spreading from the right ventricle, but after a while, the impulse passes the block in the left bundle branch and executes the remained of ventricular depolarization normally. Hence, the initial QRS complex resembles left bundle branch block but QRS duration is <0.12 seconds. Incomplete left bundle branch blocks tend to progress to complete bundle branch blocks.

QRS duration >0,10 and < 0,12 seconds.

R-wave peak time ≥0,06 seconds in i V5, V6.

Absence of normal septal q-wave in V5, V6, I and aVL.

Notched ascending limb of R-wave in V5, V6, aVL and I.

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Chapter 9: Left bundle branch block (LBBB) in acute myocardial infarction: the Sgarbossa criteria

Contrary to right bundle branch block, left bundle branch block is always a pathological finding that affects cardiovascular and total mortality. Left bundle branch block is more common in individuals with structural and ischemic heart disease. Assessment of ischemia on ECG is difficult in the presence of left bundle branch block. This is because left bundle branch block causes substantial changes in left ventricular depolarization and repolarization, which result in secondary ST-T changes. Such ST-T changes may mimic (simulate) or mask ischemia.

Simulation of ischemia manifests as ST segment elevations in leads V1–V3, accompanied by ST segment depressions in leads V5, V6, I and aVL. Clinicians frequently confuse these elevations and depressions with those caused by STEMI (STE-ACS). Indeed, several studies have shown that the majority of patients inappropriately referred to the catheterization laboratory with suspicion of STEMI (STE-ACS) have left bundle branch block.

Masking of ischemia occurs because the ST-T changes induced by a left bundle branch block are more pronounced than those caused by ischemia. As a result, the ischemic changes are obscured and do not become apparent. However, there are exceptions to this rule, which will be discussed below. To address these challenges, researchers have developed ECG criteria designed to identify ischemia in the presence of left bundle branch block. The most widely recognized criteria to date were developed by Sgarbossa and colleagues and are therefore referred to as the Sgarbossa criteria. However, all such criteria remain, at best, suboptimal. Clinical judgment remains a more reliable tool for evaluating ischemia in these cases, a point emphasized in recent guidelines.

Implications of left bundle branch block in myocardial ischemia and infarction

A summary of the issues that arise when facing a patient with left bundle branch block (LBBB) and symptoms of ischemia follows:

Left bundle branch block (LBBB) can mimic acute STEMI, as it often presents with similar ECG changes, including ST-segment elevations, ST-segment depressions, and T-wave inversions. These overlapping features frequently lead to confusion between LBBB and acute STEMI. In fact, studies have shown that LBBB is the most common cause of false activations of the catheterization laboratory.

LBBB may mask (conceal) ongoing ischemia: LBBB causes severe disturbance of ventricular repolarization, which usually prevents other ST-T changes (such as those arising from ischemia) to come to expression on ECG. Therefore, ischemic ST-T changes (ST elevations, ST depressions, T-wave changes) are typically concealed in the setting of LBBB. A patient with acute STEMI may therefore display a normal LBBB pattern.

LBBB may be caused by ischemia/infarction: There are numerous causes of LBBB, such as heart failure, structural heart disease, fibrosis of the conduction system and acute myocardial infarction (particularly anterior STEMI). Hence, an acute myocardial infarction may actually result in LBBB which then masks the ischemic ST-T changes on ECG.

In summary, left bundle branch block (LBBB) can result from, mimic, or obscure acute myocardial ischemia and infarction, creating significant diagnostic challenges. These complexities led researchers to study patients presenting with LBBB and suspected acute myocardial infarction (AMI) by referring them for urgent reperfusion therapy, which at the time was primarily fibrinolysis (Wilner et al.). Their findings revealed that a substantial number of these patients had complete coronary artery occlusions, and outcomes improved when they were treated as acute STEMI cases.

Management of left bundle branch block (LBBB) in patients with acute coronary syndromes (ACS)

For many years, European and North American guidelines recommended managing patients with symptoms of myocardial ischemia and new (or presumed new) LBBB as acute STEMI. However, subsequent studies found that this approach led to an unacceptably high rate of unnecessary catheterization laboratory activations. In response, the most recent North American guidelines (O’Gara et al.) advise that new (or presumed new) LBBB should not be considered diagnostic of AMI in isolation. Instead, patients with a high clinical suspicion of ongoing myocardial ischemia, regardless of ECG or biomarker findings, should be treated similarly to those with clear STEMI. Particularly, patients who remain symptomatic despite initial medical therapy, are hemodynamically unstable, or develop sustained ventricular arrhythmias. Similarly, the 2023 European Society of Cardiology (ESC) guidelines were updated to recommend that patients presenting with LBBB or RBBB and signs or symptoms strongly indicative of ongoing myocardial ischemia should be treated as having definitive STEMI, irrespective of whether the bundle branch block is previously documented (Byrne et al.).

Sgarbossa’s ECG criteria for detecting ischemia in the presence of left bundle branch block (LBBB)

It is evident why researchers have faced challenges establishing ECG criteria for diagnosing acute STEMI in the presence of left bundle branch block (LBBB). Among the most useful and well-validated criteria are those developed by Sgarbossa and colleagues (Neeland et al.). These criteria, known as the Sgarbossa criteria, are summarized in Figure 1A. Each criterion gives 2 to 5 points. Studies show that a cut-off of ≥3 points yields a sensitivity of 20–36% and a specificity of 90–98%. Thus, while the Sgarbossa criteria demonstrate high specificity for detecting acute myocardial infarction, the sensitivity is notably low, making the criteria unreliable for the identification of acute STEMI.

Figur 1. (A) ECG criteria (Sgarbossa criteria) for acute STEMI in the setting of LBBB. Each criterion gives 2 to 5 points. Studies show that a cut-off of ≥3 points yields a sensitivity of 20–36% and specificity of 90–98% for acute STEMI in the setting of LBBB. (B) Smith-modified Sgarbossa criteria.

Modified Sgarbossa criteria

The modified Sgarbossa criteria, introduced by Smith et al (2012), replaces the third of the original Sgarbossa criteria (i.e the absolute 5 mm ST elevation) with an ST/S ratio less than -0.25. Measurement of the ST/S ratio is depicted in Figure 1B. Using this criterion improves the accuracy of the Sgarbossa criteria. Furthermore, the modified Sgarbossa criteria do not utilize a point system; instead, it only requires 1 of 3 criteria to be considered positive (i.e acute ischemia is strongly suggested).

Measuring ST/S ratio

Measure the amplitude of the R or S wave, whichever is most prominent, and ST segments (relative to the PR segment), to the nearest 0.5 mm. The ST/S ratio is calculated for each lead with a discordant ST deviation of ≥1 mm. Hence, whereas the original Sgarbossa criteria utilize an absolute ST-elevation measurement, the modified criteria suggest using a rule of proportionality; the amplitude of the ST deviation is compared to the amplitude of the R or S wave, which increases both sensitivity and specificity for acute myocardial infarction.

Figure 1B: Criteria 1 and 2 of the original Sgarbossa criteria are unchanged. The R or S wave, whichever is most prominent, and ST segments (relative to the PR segment), is measured to the nearest 0.5 mm. The ST/S ratio is calculated for each lead that has both discordant ST deviation ≥1 mm.

Infarction criteria in patients with left bundle branch block (LBBB), left ventricular hypertrophy (LVH) and pacemaker rhythms

European and North American guidelines recommend against applying standard ECG criteria for ischemia or infarction in the presence of left bundle branch block (LBBB), left ventricular hypertrophy (LVH), or ventricular pacemaker rhythm. These conditions significantly alter the QRS complex and ST-T waveforms, potentially mimicking or concealing signs of ischemia. However, it is reasonable to assess for abnormal waveforms within the specific context of LBBB, LVH, or paced rhythms. Examples of such abnormalities are outlined in the Sgarbossa criteria. Furthermore, some general recommendations can be provided:

Always compare the current ECG waveforms with previous recordings to identify any differences. Variations in the ST-T segment may indicate ischemia.

Ensure the ECG waveforms align with the expected patterns for the underlying condition. For instance, T-wave inversions in leads V5, V6, aVL, and I are typical in left bundle branch block; their absence may suggest ischemia.

Look for pseudonormalization of T-waves, as this can also be a marker of ischemia.

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Chapter 10: Fascicular block (hemiblock): Left anterior & left posterior fascicular block

Fascicular blocks were previously referred to as hemiblocks, but the latter term has been deprecated. The left bundle branch is subdivided into the following two fascicles: (1) the anterior (anterosuperior) fascicle, which delivers the electrical impulse to the anterior wall of the left ventricle; (2) the posterior (posteroinferior) fascicle, which delivers the electrical impulse to the posterior and inferior walls of the left ventricle. Anatomical or functional block in the anterior fascicle leads to left anterior fascicular block. Similarly, left posterior fascicular block is due to block in the posterior fascicle. Approximately 5–10% of all individuals have a third fascicle – the median or centroseptal fascicle – which gives off Purkinje fibers to the interventricular septum.

Fascicular blocks occur due to anatomical or functional blocks in a fascicle. This alters the ECG curve in a characteristic fashion which is rather easy to spot. The hallmark of fascicular blocks is the deviation of the electrical axis. The QRS duration is slightly prolonged but does not reach 0.12 s.

Block in the anterior fascicle causes left anterior fascicular block (LAFB). Block in the posterior fascicle causes left posterior fascicular block (LPFB). In a fascicular block, the myocardium without fascicular supply will depend on impulses spreading from other parts of the ventricle (where the fascicle is intact).

Figure 1. Left anterior fascicular block (anterior hemiblock) and left posterior fascicular block (posterior hemiblock).

Left anterior fascicular block (LAFB)

Left anterior fascicular block is due to anatomical or functional block in the anterior fascicle. Depolarization of the left ventricle will depend entirely on the posterior fascicle. The initial vector will be directed inferiorly (Figure 1, panel A), yielding a small r-wave in inferior leads (II, III and aVF) and small q-wave in lateral leads (aVL, I and -aVR). The second vector, which is considerably stronger, is directed to the left, back and upwards; this results in a deep S-wave in inferior leads and large R-wave in left lateral leads. Hence, inferior leads show rS complex and lateral leads show qR complex. Occasionally the T-wave in lead aVL will be inverted and in some cases lead I will display a monophasic R-wave instead of qR complex. The electrical axis will be shifted to the left (left axis deviation), ranging between -45° and -90°. The QRS duration will be slightly prolonged (the prolongation ranges between 0.01 to 0.04 seconds).

ECG criteria for left anterior fascicular block (LAFB)

Electrical axis between -45° to -90°. If the electrical axis is -30° to -45, probable LAFB may be diagnosed.

QRS duration <0,12 seconds but slightly prolonged.

aVL shows qR complex. V5–V6 usually also shows qR complexes.

Leads II, III and aVF display rS complexes.

Causes of left anterior fascicular block (LAFB)

LAFB may occur in persons who are otherwise healthy. The majority of those with LAFB, however, have significant heart disease. Myocardial infarction, coronary artery disease, left ventricular hypertrophy, dilated cardiomyopathy, hypertrophic cardiomyopathy, degenerative disease, hypertension, hyperkalemia, myocarditis, and amyloidosis may all cause LAFB.

Prognosis of left anterior fascicular block (LAFB)

Isolated LAFB is considered a benign conduction defect. Roughly 7% of cases progress to bifascicular block (which means that the LAFB is accompanied by a right bundle branch block), while 3% progress to third-degree AV block (complete heart block).

Noteworthy about left anterior fascicular block (LAFB)

LAFB may imitate anteroseptal infarction.

rS complexes in leads II, III and aVF may mask Q-waves from a prior inferior infarction.

Left posterior fascicular block (LPFB)

Left posterior fascicular block is much less common than LAFB. This is due to the fact that the posterior fascicle is larger and it has a greater arterial supply. Depolarization of the left ventricle will depend entirely on impulses from the anterior fascicle if the posterior one is defective. The vector is initially directed upwards and to the left, which yields a q-wave in lead aVF and R-wave in lead I. The second vector is directed downwards and to the right, which results in a prominent R-wave in lead aVF and an equally prominent S-wave in lead I. The electrical axis will be more positive than 90° (right axis deviation). As in LAFB, the QRS duration will be prolonged by approximately 0.01 to 0.04 s, but the total QRS duration will not reach 0.12 seconds. Refer to Figure 1.

ECG criteria for left posterior fascicular block (LPFB)

Electrical axis +90° to +180°.

rS complexes in leads I and aVL.

qR complexes in inferior leads (II, III and aVF).

Q-wave is mandatory in leads III and aVF.

QRS duration <0,12 seconds.

Causes of left posterior fascicular block (LPFB)

Degenerative processes, ischemic heart disease, hyperkalemia, myocarditis, amyloidosis and acute cor pulmonale may all cause LPFB. Importantly, LPFB is highly unusual in otherwise healthy individuals.

Noteworthy

Establishing a diagnosis of LPFB requires that there are no clinical or ECG criteria of right ventricular hypertrophy present. Right ventricular hypertrophy is more common than LPFB and may cause ECG findings similar to LPFB.

LPFB may imitate inferior infarction.

LPFB may mask lateral infarction.

T-wave inversion may occur in inferior leads and simulate post-ischemic T-waves.

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Chapter 11: Nonspecific intraventricular conduction delay (defect)

A nonspecific intraventricular conduction delay exists if the ECG displays a widened QRS appearance that is neither a left bundle branch block (LBBB) nor a right bundle branch block (RBBB). The QRS morphology of nonspecific intraventricular conduction delays may vary substantially.

Definition and causes of nonspecific intraventricular conduction delay

According to the American Heart Association/American College of Cardiology and the Heart Rhythm Society (AHA/ACCF/HRS) recommendations, a nonspecific intraventricular conduction delay is defined as “a QRS duration greater than 110 ms in adults, greater than 90 ms in children 8 to 16 years of age, and greater than 80 ms in children less than 8 years of age without meeting the criteria for RBBB or LBBB.”

These conduction delays may be observed after large myocardial infarctions, in which the large necrotic area may cause nonspecific conduction disturbances. Such conduction disturbances may also be superimposed on existing bundle branch blocks and alter their appearance.

Some patients develop nonspecific intraventricular conduction defects without any change in their QRS appearance. Such conduction delays may be due to myocardial fibrosis, amyloidosis, cardiomyopathy or hypertrophy.

Prognosis of nonspecific intraventricular conduction delay

Patients with nonspecific intraventricular conduction delays are at twice as great a risk of all-cause death and cardiovascular death, compared to patients without such disturbances, including those with RBBB and LBBB. This was reported in the Coronary Heart Disease Study,1 which enrolled 10,899 participants with baseline ECG examinations. Individuals with nonspecific intraventricular conduction delays were at particularly high risk of death due to arrhythmias.

Note that other causes of wide QRS complex must always be considered. For example, Wolff-Parkinson-White syndrome (WPW), pacemaker-stimulated beats, electrolyte imbalance and medications may prolong the QRS complex.

References

Aro AL, Anttonen O, Tikkanen JT, et al. Intraventricular conduction delay in a standard 12-lead electrocardiogram as a predictor of mortality in the general population. Circ Arrhythm Electrophysiol 2011;4:704–710.

Eschalier R et al. Heart Rhythm. 2015 May;12(5):1071-9. Nonspecific intraventricular conduction delay: Definitions, prognosis, and implications for cardiac resynchronization therapy.

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