Av blockI44.3

Marcus Gerbezius described the symptoms of complete AV block as early as 1717. However, the anatomist Giovanni Battista Morgagni, who described the clinical picture 44 years later, is considered the first person to describe it in the literature (Lüderitz 2013).

The Dublin physicians Robert Adams and William Stokes described the Adam- Stokes seizures named after them in 1827 and 1846, respectively (Lüderitz 2013).

In 1903, after the introduction of polygraphic methods, Wenckebach recognized the 2nd-degree AV block type Wenckebach (type I), named after him. Mobitz, after whom AV- block 2nd degree type II was named, additionally elaborated important distinguishing features of the different block types in 1924 (Lüderitz 1983).

Congenital AV block 3 was first described by Morquio in 1901 (Ebert 2009).

Historically, AV block was the first indication for pacemaker therapy (Fröhlig 2006).

AV block refers to impaired conduction of the electrical impulse between the atrial and ventricular myocardium (Buchta 2019).

AV block is one of the bradyarrhythmias (Kasper 2015) and is divided according to severity into:

• 1st degree AV block:

This is a so-called "delayed conduction of excitation" (Herold 2022). All atrial actions are still conducted to the ventricles (Fröhlig 2006).

The path taken by the electrical impulse from the sinus node to travel through the atria to the AV node and into the His-Purkinje system to cause ventricular contraction is called the PR interval (Mangi 2022). This is prolonged in AV block and is > 200 ms. The site of the delay is typically in the AV- node. However, it can also be located in the atria, in the His bundle or in the His Purkinje system (Kasper 2015 / Erdmann 2009).

• 2nd degree AV block:

This is also referred to as "intermittent conduction interruption" (Herold 2022).

The AV block of the 2nd degree is subdivided into

- Mobitz type I or also called Wenckebach type and

- Mobitz type II (Kasper 2015).

- Mobitz type I:

The block is found above the His bundle in approximately > 70% of cases (Herold 2022). There is an increasing prolongation of PQ- time until atrial action is no longer transmitted to the ventricles (Spes 2022).

- Mobitz type II:

Here, the block is within or below the His bundle. After a preceding P wave, there is a sudden failure of a QRS complex. The PQ time is constant (normal or prolonged). Mobitz type II is always due to organic heart disease (Herold 2022).

• AV block of the 3rd degree:

In type 3, there is no conduction of atrial actions to the ventricles at all. This may occur intermittently or permanently (Spes 2022).

The ventricles are excited from a subordinate center, recognizable by a QRS- duration < 120 ms, provided that the substitute center is located in the AV- node or His- bundle. The replacement rhythm is slower the deeper the excitation center is localized (Spes 2022).

Other classifications include:

- Location of block (Kasper 2015).

- permanent / intermittent / paroxysmal

- acute AV block / chronic AV block

- congenital / acquired AV block (Fröhlig 2006)

For acquired and persistent AV conduction disorders, the incidence is 200 / 1 million inhabitants / a (Kasper 2015).

In young people, transient AV block is not uncommon. This is most likely caused by high vagal tone, which occurs in about 10% of all young adults (Kasper 2015).

In Europe, approximately 70-80% of permanent pacemakers are implanted due to AV conduction disorders (Kasper 2015).

The indication for pacemaker implantation in 2002 is AV block grade 3 in 22% and AV block grade 2 in 12% (Fröhlig 2006).

The causes of AV block are manifold. They can be functional (and thus reversible) or structural (and thus irreversible). They are partly analogous to extrinsic and intrinsic causes underlying AV- node dysfunction (Kasper 2015).

2nd degree AV- block type Mobitz I need not always be pathological. It is also found in patients with increased vagal tone without evidence of structural heart disease. On the other hand, 2nd degree AV block type Mobitz II rarely occurs in patients without structural heart disease. It occurs preferentially in myocardial ischemia, fibrosis, or sclerosis of the myocardium (Mangi 2022).

Autonomous due to, for example:

- Hypersensitivity of the carotid sinus (Kasper 2015).

- Increased vagotonus (occurs e.g. in athletes as 1st degree AV- block, which disappears under exercise (Herold 2022).

Metabolic or endocrine due to e.g.:

- hyperkalemia

- hypermagnesemia

- hypothyroidism

- Adrenal insufficiency (Kasper 2015)

Drug related due to e.g.:

- beta blockers

- calcium channel blockers

- digitalis

- Antiarrhythmics class I and III

- lithium

- Adenosine (Kasper 2015)

- Chemotherapeutic agents such as cyclophosphamide, arsenic trioxide, bortezomib (Glikson 2021).

Infectious due to e.g.:

- Endocarditis

- Lyme disease (affects the heart in up to 50 %, of which about 10 % develop AV block)

- syphillis

- diphtheria

- tuberculosis

- Toxoplasmosis (Kasper 2015)

Congenital due to e.g.:

- congenital heart disease

- myotonic dystrophy (Kasper 2015)

Inflammatory due to e.g:

- Systemic lupus erythematosus

- scleroderma

- rheumatoid arthritis (Kasper 2015)

Infiltrative by e.g.:

- amyloidosis

- Sarcoidosis (Kasper 2015)

Traumatic / neoplastic due to e.g:

- Lymphomas

- mesotheliomas

- melanomas

- Radiatio (Kasper 2015)

Degenerative due to e.g.:

- Lenègre disease

- M Lev (Kasper 2015)

Diseases of the coronary vessels such as:

- acute myocardial infarction (Kasper 2015).

Preferably, AV- block occurs in patients with:

- myocardial ischemia

- aging or fibrosis of the myocardium

- cardiac infiltration diseases (Kasper 2015)

SA activation functions normally during AV block, and atrial systole shows a normal or accelerated rate. In contrast, ventricular activation is slowed or absent (Kasper 2015), recognizable by the prolonged PR interval (Mangi 2022).

The decrease in heart rate causes a drop in cardiac output and blood pressure. This drop is registered by the baroreceptors in the aortic arch and carotid sinus and leads to a central stimulation of the sympathetic nervous system (Siegenthaler 2006).

In 1st degree AV block there are usually no symptoms (Herold 2022).

Only with increasing disturbance of the excitation conduction can it come to:

- dizziness

- drowsiness

- Dyspnea under stress

- Signs of cardiac insufficiency

- confusion due to reduced cerebral blood flow (Sunjeet Siidhu 2020)

- fatigue

- syncope

- Death (Kasper 2015)

Syncope caused by bradycardia or asystole is also known as "(Morgagni) Adam Stokes seizure" (Fröhlig 2006).

The diagnosis of AV block is made electrocardiographically and can be performed with a long-term ECG, stress EC G, and His-bundle ECG (Herold 2022).The severity of the conduction disturbance can be determined, as well as the location of the blockage (Kasper 2015).

In 40-60% of patients, it is not possible to attribute the AV block to a known underlying disease (Fröhlig 2006).

ECG

Basically, the PR interval (the time required for the electrical impulse of the sinus node to pass through the atria to the AV node and into the His-Purkinje system to cause ventricular contraction) is prolonged in AV block (Mangi 2022).

- 1st-degree AV- block:

- PQ- time prolonged to > 0.20 sec.

- P- wave may fall into the repolarization wave of the preceding beat if PQ- time is greatly prolonged (Herold 2022).

- 2nd degree AV- block:

- Mobitz I:

- constant PP- time

- with each beat prolongation of the PQ interval until there is no transition (Herold 2022)

- the resulting pause is shorter than a double PP interval (Herold 2022)

- Mobitz II:

- after a preceding P-wave a QRS-complex suddenly fails

- the pause corresponds to a double PP interval

- PQ time is normal or constantly prolonged.

- The AV block can occur sporadically or regularly. In case of regular occurrence, if only 1 of 2 sinus excitations is transmitted, it is called a 2: 1 block; if only 1 of 3 excitations is transmitted, it is called a 3: 1 block (Herold 2022).

- 3rd degree AV block:

- complete dissociation of atrial and ventricular actions

- normal-frequency P waves without relation to the slowed QRS complexes (Herold 2022)

- secondary stimulation centers are AV- nodes and His- bundles, frequency is > 40 / min, ventricular complexes appear narrow

- tertiary stimulation centers of the ventricular myocardium with a frequency < 40 min and ventricular complexes deformed like a leg block (Herold 2022)

Exercise ECG

To distinguish between AV block 2 Mobitz II with a 2: 1 conduction and AV block 2 Mobitz I with failure of every 2nd conduction, the stress ECG is suitable.

In AV block 2 Mobitz I the conduction improves, in AV block 2 Mobitz II the AV conduction worsens in the form of a 3: 1 or 4: 1 block (Herold 2022).

Electrophysiological examination (EPU)

The EPU represents an invasive examination procedure, which also includes the His bundle ECG (HBE) (Haas 2011). The HBE is particularly indicated for further clarification in patients with syncope, v. a. a higher-grade blockage and additionally existing structural heart diseases (Kasper 2015).

His-bundle ECG (HBE):

In HBE, an electrode catheter is placed transvenously directly to the His- bundle (Klinge 2002).

This allows the PQ- time of the conventional ECG to be divided into one before and after the His- bundle:

- 1. supra- His- block (also called intranodal block):

In this case, there is a prolonged AH- interval (time from atrial [A] to His- potential [H]) or failure of H- potential.

- 2. infra- or intra- His- block (infranodal block):

The HV- interval (the time from deflection of the His- bundle potential to the earliest excitation of the ventricular complex [Scriba 2000] is prolonged or there is a total failure of the V- potential (Herold 2022).

- 2nd degree AV block:

- Mobitz I: In the His-bundle ECG, a supra-His conduction delay with increasing prolongation of the AH time leads to a (periodic) failure of a His potential. The standard value of the AH time is 60 - 120 msec (Herold 2022).

- Mobitz II: This is an infra-His conduction delay with a prolonged HV interval. To transfer the excitation to the His bundle, the AV area needs more than 1 impulse, i.e. several P waves can precede the QRS complex (Michels 2010). The AH interval is normal (Herold 2022).

- Thyroid levels

- Lyme antibodies

- Hyperkalemia

- hypercalcemia

- Digitalis level (Glikson 2021)

- Epilepsy

Seizures may occur in the setting of Morgagni- Adam- Stokes seizures (Herold 2022). See also Complications

- The differential diagnoses of syncope are numerous (Herold 2022)

- Heart failure:

This may develop due to severe bradycardia (< 40 / min) (Herold 2022).

- Morgagni- Adams- Stoke- seizure (MAS- seizure):

If there is prolonged asystole or if the ventricular rhythm does not start immediately after the onset of total block (preautonomic pause), these MAS- seizures may occur. During the seizure the pupils are wide (!), reflexes may be weakened or not triggerable at all (Herold 2022).

- Asystole of 3 - 5 sec. leads to pallor and dizziness.

- Asystole of 10 - 15 sec leads to loss of consciousness

- Asystole of 20 - 30 sec leading to seizure

- Asystole of 30 - 60 sec leads to respiratory arrest

- Asystole > 3 min to irreversible brain damage and exitus lethalis (Herold 2022)

- Progression of AV- block to higher degrees with danger of sudden cardiac death:

The danger exists as soon as a prolongation of excitation by the His- Purkinje- system, i.e. a prolongation of the HV- interval (norm time between 35 - 55 msec [Herold 2022]) is electrophysiologically recognizable. In patients with a prolongation of the HV interval of > 100 ms, the risk of complete AV block increases to 10% per year (Kasper 2015).

- Causal therapy

Any triggering underlying diseases should be taken care of therapeutically accordingly, medications possibly changed, electrolytes balanced, etc.

Therapeutic measures can improve symptoms in patients with AV block and, in particular, prevent sudden cardiac death (SCD) (Glikson 2021).

- Symptomatic therapy

- AV- block I. Grade:

In asymptomatic patients, a wait-and-see approach is recommended initially (Buchta 2019).

The indication for pacemaker implantation exists only if there is a proven correlation between symptoms and AV block (Glikson 2021).

It should be considered in these patients that although increased RV- pacing with optimal AV- delay can increase stroke volume, in some patients RV- pacing induces heart failure (Aizawa 2022).

- AV- block 2nd degree Mobitz type 1:

Patients with AV- block II Mobitz type 1 often do not require therapy. Occasionally, however, bradycardia with subsequent hypotension occurs. These patients usually respond well to atropine (Mangi 2022).

Pacemaker implantation is given if symptoms are present or if there is proven block at the intra- or infra-His level (Glikson 2021).

- 2nd degree AV block Mobitz type II:

Since there is a risk of total AV block in this case, a pacemaker indication is given. In addition, all conduction-delaying drugs such as digitalis, antiarrhythmics, etc. should be discontinued. Atropine should not be given at this stage as it may lead to worsening of the block pattern (Herold 2022).

- 3rd degree AV block:

In this case, there is always an indication for pacing therapy, even if the AV- block is intermittent and asymptomatic (Buchta 2019).

- Selection of pacing:

In patients with persistent AV- block:

- plus atrial fibrillation, the standard therapeutic option is: a VVIR- pacemaker (ventricular unicameral perception / pacing with rate adaptation)

- plus sick sinus syndrome: a DDD(R) pacemaker (dual chamber perception / pacing with rate adaptation)

- without sick sinus syndrome: one DDD pacemaker (dual chamber perception / pacing) [Glikson 2021])

- plus heart failure with a HFrEF (heart failure with reduced ejection fraction) of < 40 %, cardiac rechronization therapy (CRT) is recommended (Glikson 2021).

If the AV block is paroxysmal, a DDD is recommended in case of

- sinus rhythm, a DDD pacemaker plus AVM (atrial management = AV delay programming with avoidance of values > 230 ms)

- Atrial fibrillation a VVI- pacemaker plus frequency hysteresis (Glikson 2021)

The prognosis for patients with AV- Block 2 Mobitz Type I is very good. In most cases, they do not even require therapy (Mangi 2022).

In AV- block 2 Mobitz type II, the prognosis depends on the etiology of the block pattern (Mangi 2022).

Among junctional blocks, those located more proximally have a better prognosis than subjunctional blocks located more distally:

- Supra- His blocks are:

- reversible

- lead less often to Morgagni Adam Stokes seizures

- often show a replacement rhythm from the His bundle (Herold 2022)

- Infra- His- blocks:

- here a ventricular replacement rhythm is found

- the replacement rhythm is often delayed

- the risk for Morgagni Adam Stokes seizures is very high (Herold 2022)

Patients with AV- block should receive lifelong follow-up (Mangi 2022).

For patients with 1st- and 2nd-degree AV block, digitalis is contraindicated because digitalis can lead to complete block (Buchta 2019).

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