Overview

Atrioventricular (AV) block describes impaired signalling from the sinoatrial node (SAN) to the atrioventricular node (AVN). The signalling may be delayed or completely blocked. Delayed signalling from the SAN to AVN manifests as PR interval prolongation.

If the signal is entirely blocked, the ventricles can still be activated through escape rhythms, which are where depolarisation is triggered by the AV node (junctional escape), fascicles (fascicular escape), or the ventricular cardiomyocytes themselves (ventricular escape). These escape rhythms occur in an attempt to maintain a heartbeat when the SAN is not functioning properly.

As a general rule of thumb, the ‘lower down’ a block is, the worse it is. For instance, a block at the level of the AVN is less severe than one that affects the bundle branches.

First-Degree Heart Block

Overview

First-degree atrioventricular (AV) block describes abnormally slow conduction through the AV node. Despite the slowing in conduction, every impulse that originates from the SAN is passed to the ventricles. This leads to PR interval prolongation.

On an ECG, a first-degree AV block is defined as a PR interval >0.20 seconds (>5 small squares).

Figure 1: an ECG showing first-degree heart block

First-degree heart block that is asymptomatic is relatively common and does not need treatment.

Causes

Second-Degree Heart Block

Overview

Second-degree atrioventricular (AV) block describes impaired conduction between the atria and ventricles leading to PR interval progression. More specifically, second-degree heart block describes when one or more (but not all) atrial impulses fail to pass to the ventricles.

Second-degree AV block can be divided into two subtypes:

  • Mobitz type I (Wenckebach)
  • Mobitz type II

Mobitz type I (Wenckebach)

In a Mobitz type I (Wenckebach) heart block, there is a progressive prolongation of the PR interval until a P wave is completely blocked (known as a dropped beat).

This occurs because each impulse leads to the prolongation of the refractory period of the AV node. When an impulse from the atria arrives at the AV node during the relative refractory period, it is conducted more slowly. As the refractory period gets longer with each impulse, an atrial impulse arrives at the AV node during its absolute refractory period and is not conducted. After this, the AV node resets and the cycle repeats.

On an ECG, this appears as progressive PR prolongation until a P-wave is dropped, resulting in a P-wave with no QRS complex following it.

Figure 2: An ECG showing a Mobitz type I heart block

Its causes include:

  • Normal variant in people with high vagal tone and no structural heart disease (e.g. athletes)
  • Inferior myocardial ischaemia
  • Hyperkalaemia
  • Some drugs (e.g. beta-blockers, calcium channel blockers, digoxin)

Mobitz type II

In a Mobitz type II heart block, the PR interval is constant, however, each P wave is associated with a QRS complex until one P wave arises that does not have a QRS complex. There is usually a fixed number of P-waves for every successful QRS complex. For example, if there are three P waves for every QRS complex, this is a 3:1 Mobitz II block.

This occurs because the block is lower down than Mobitz type I, below the AV node.

There is a high risk of asystole with Mobitz type 2 heart blocks. This is because dropped beats can happen suddenly and unexpectedly, and progress to third-degree (complete) heart block or asystole, resulting in sudden cardiac death.

Figure 3: An ECG showing a Mobitz type 2 heart block. It is a 4:1 block, one of the p waves is embedded within the T wave

Mobitz type II blocks are most commonly due to structural heart damage. It is rarely seen in patients without structural heart disease. Its causes include:

  • Anterior myocardial infarction
  • Myocardial fibrosis/sclerosis
  • Amyloidosis
  • Haemochromatosis
  • Rheumatic fever
  • Autoimmune disorders (e.g. systemic lupus erythematosus, systemic sclerosis)
  • Hyperkalaemia
  • Some drugs (e.g. beta-blockers, calcium channel blockers, digoxin, adenosine, amiodarone)

2:1 block

A 2:1 block describes the presence of two P waves for each QRS complex. Because Mobitz type I blocks occur in regular cycles, there is always a fixed number of P waves to QRS complexes. In general, in the P:QRS ratio, Mobitz type I blocks have one more P wave than QRS complex (e.g. 5 P waves and 4 QRS complexes per cycle are a 5:4 Mobitz Type I block). Mobitz type II blocks generally have a fixed ratio of P:QRS complexes and are generally X:1 (e.g. 3:1, 4:1, 5:1). Ratios of 3:1 and above are known as ‘high-grade AV blocks’. With 2:1 blocks, it is difficult to tell whether it is due to a Mobitz type I or type II block. 

Third-Degree Heart Block

Overview

Also known as complete heart block, third-degree heart block is where no impulses from the SAN are conduced to the ventricles. The SAN continues sending impulses and ventricles activate via escape rhythms (discussed above). This leads to bradycardia (around 45-50 bpm) and haemodynamic instability.

On an ECG, there is no association between the P waves and QRS complexes. There may be a regular P-P interval and regular R-R interval, but the P-R interval may vary.

There is a high risk of asystole with third-degree heart blocks.

Figure 4: An ECG showing a third-degree heart block

The causes of a third-degree heart block are the same as Mobitz I and II, such as:

  • Inferior myocardial infarction
  • Drugs (beta-blockers, calcium channel blockers, amiodarone, adenosine, digoxin)

Bundle Branch Block

Overview

The left and right bundle branches emerge from the bundle of His in the heart. They transmit impulses from the bundle of His to the Purkinje fibres. The bundle branches are found along the interventricular septum and each bundle branch depolarises their respective ventricles. The interventricular septum itself is depolarised by the left bundle branch and is depolarised from left to right. The ventricles contract simultaneously.

Left Bundle Branch Block

Overview

Left bundle branch block (LBBB) describes slowed or absent conduction through the left bundle branch. This leads to delayed depolarisation of the left ventricle. This results in the left ventricle being depolarised via the right bundle branch, whose impulses travel through the right ventricle, and then to the left ventricle via the septum.

This leads to:

  • Prolonged, positive R waves in the left ventricular leads (I, V5-6)
    • These are usually negative, but since depolarisation is happening in the opposite direction,
  • Secondary R waves in the left ventricular leads (I, V5-6) giving “M-shaped” R waves
    • This is due to delayed activation between the right ventricle and left ventricle
  • QRS prolongation
    • Due to delayed conduction as the left ventricle now needs to be depolarised via the right ventricle through a slower and less efficient pathway

A quick and easy way to remember this is WiLLiaM:

  • There is a ‘W’ in V1 and an ‘M’ in V6

Figure 5: left bundle branch block

Causes

A new LBBB is always pathological. Causes include:

  • Myocardial infarction (MI)
    • This can make it difficult to diagnose an MI in a patient with a pre-existing LBBB.
    • The Sgarbossa criteria can help with this
  • Aortic stenosis
  • Hypertension
  • Cardiomyopathy

Right Bundle Branch Block

Overview

Right bundle branch block (LBBB) describes slowed or absent conduction through the right bundle branch. This leads to delayed depolarisation of the right ventricle. This results in the right ventricle being depolarised via the left bundle branch, whose impulses travel through the left ventricle first, then to the right ventricle via a slower and less efficient pathway.

This leads to:

  • Secondary R waves in the right ventricular leads (V1 and V2) giving “M-shaped” R waves
    • This is due to delayed activation between the left ventricle and right ventricle
  • QRS prolongation
    • Due to delayed conduction as the right ventricle now needs to be depolarised via the left ventricle through a slower and less efficient pathway
  • Wide, slurred S waves in leads I and V6

A quick and easy way to remember this is MaRROW:

  • There is an ‘M’ in V1 and a ‘W’ in V6

Figure 6: right bundle branch block

Causes

  • RBBB can be a normal variant
  • Ischaemic heart disease
  • Pulmonary disorders (e.g. COPD)
  • Right ventricular hypertrophy
  • Pulmonary embolism

Other Blocks

Overview

Other types of block include:

  • Bifascicular block:
    • RBBB and blockage of one of the fascicles of the left bundle branch
  • Trifascicular block:
    • Bifascicular block and third-degree heart block

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