Observe the Atrioventricular (AV) Node in the upper-mid portion of the heart, and the Left and Right Bundle Branches at the intraventricular septum

Introduction to Atrioventricular (AV) Blocks

Heart block type that originate from a group of arrythmias  raised from failed or delayed transmission above the atrioventricular (AV) node to the ventricles - Classified into 1st, 2nd & 3rd degree AV blocks.

  • If QRS is < 0.12s then the AV block is located in AV node or Bundle of His (better prognosis)
  • Broad QRS indicates distal blocks (further than bifurcation of Bundle of His)
AV Block Causes:
  • Conduction system degrading or ischemia
  • Idiopathic Fibrosis of conduction system
  • Vagal stimulation
  • Hyperkalaemia
  • Medications (Beta Blockers, Digoxin, Amiodarone, Verapamil etc.)
  • Lyme Disease (Borreliosis)
  • Hypothermia
Type of AV blockDefinitionClinical Features
1st Degree AV blockDifficulty transmitting impulse through AV node (where SA node is normal).
Due to this delay, the PR interval is longer – Once this travels through AV node, the impulse travels normally.
2nd Degree AV Block / Mobitz-Type I (Wenchkebach) Represents a delayed transmission impulse through the AV node – However the time it takes to reach the ventricles increase for every impulse.

This results in gradual PR interval increase. This continues until SA node intervenes with a sinus beats which resets the cycle again to prevent a fall in blood pressure.

The RR interval shortens with each beat of the cycle.

The P-P interval remains constant

2nd Degree AV block / Mobitz-Type IISevere 2nd degree block resulting in a dropped beat, due to SA node impulse not being transmitted to the ventricles.

If 2 or more impulses are blocked at the AV node before reaching the ventricles, it is called 2:1 or 3:2 block.

Can develop into 3rd degree AV block or ventricular standstill.

3rd Degree AV block / Complete Heart BlockNo communication through AV node resulting in separate atrial & ventricle transmission by their own branches. The SA node fires at 60-100 where the ventricles are at about 20-40bpm from nearby impulses from AV node or; within the ventricles.

Perfusion is through junctional or ventricular escape rhythm – Can result to ventricle standstill.

Hypotension is displayed due to inability of atria to intervene resulting in diminished cardiac output.


Introduction to Bundle Branch Blocks

Normal PQRST wave means good normal conduction – Conduction is initiated by the sinoatrial node (SA node) in the right atrium.

  1. Impulse spread to left atrium via Bachmann Bundles and towards ventricles via AV node
  2. In the ventricles, impulse travel along Bundle of His then
  3. The impulse then bifurcates (divide) into left & right bundle branches
  4. These branches terminate in a network of conduction tissues (Purkinje Fibres)

Conduction is very fast – In event where conduction branch is impaired, the impulse finds a way past the obstruction by transmitting impulses from cell-to-cell until it can re-join the fast conduction system again. Hence the process is delayed (due to added time due to added distance as result of the blockage) reflected by a wider QRS complex.

Examine QRS width & configuration for right (V1 / V2) & left (V5 / V6) ventricles


Non-Specific Intraventricular Conduction Delay
  • When there is a conduction delay (widened QRS) without LBBB or RBBB – Can be observed after a large MI event where necrotic areas can cause conduction disturbances – Some other changes can be due to myocardial fibrosis, amyloidosis, cardiomyopathy or hypertrophy.
QRS Complex criteria for intraventricular conduction delay:
  1. 1. > 110 ms (2.5 to 3 small boxes or more) in adults OR;
  2. 2. > 90ms (2 to 2.5 small boxes or more) in children 8 to 16 years OR;
  3. 3. > 80ms (2 small boxes or more) in children < 8 years AND;
  4. 4. Do not met criteria for RBBB or LBBB.
Right Bundle Branch Block (RBBB)
  • When the conduction through the right bundle is obstructed (delaying right ventricular depolarisation) – Depolarisation of right ventricle will rely on the impulse from the left ventricle.
ECG Behaviour in RBBB:
  • QRS complex > 0.10 (wide)
  • rSR’ / rsr’ / rsR’ complex pattern in V1 & V2
    • Second R-wave (R’) is larger than 1st R-wave and S-waves does not reach the baseline – Basically QRS displays “M” shape.
  • ST depression & T-wave inversion in V1 & V2
  • Deep & Broad S-Wave in Lead I, aVL, V5-V6
  • Secondary ST-T changes (ST-T segment opposite to QRS)

TIP: Compare V1 & V6


  • V1 produces an “M” shape pattern
  • V6 has a broad & deeper S wave

Example 1:


Example 2:


The impulse from left ventricle will be slow as it needs to travel partly or entirely outside of the conduction system resulting in slow & abnormal activation of right ventricles creating an abnormal and prolonged QRS complex. Therefore, the left ventricle will activate before the right ventricle; therefore, displaying its own vector.

Causes of RBBB:
  • Idiopathic fibrosis or RBB degeneration
  • Heart disease
  • Coronary Artery Disease
  • Pulmonary Embolism
  • COPD
  • Cardiac surgery or PCI may cause RBBB
  • Cardiomyopathy
Left Bundle Branch Block (LBBB)
  • When the conduction through the left bundle is obstructed (delaying left ventricular depolarisation) – Depolarisation of left ventricle will rely on the impulse from the right ventricle.
ECG Behaviour in LBBB:
  • QRS complex > 0.10 (wide)
  • Lateral QRS has a broad / notched R-wave with prolonged upstroke in Lead I, aVL, V5-V6
  • ST depression & T-wave inversion in Lead I, aVL, V5-V6
  • V1 & V2 has asymmetrical, broad, & deep QS complexes.
  • V1-V3 may have ST elevation (< 5mm) & positive T-waves  
  • Left axis deviation may be present (due to dominant ventricle)

TIP: Compare V1 & V6


  • V1 produces rS wave (V-shape QRS)  
  • V6 mini ‘M’ on the peak of QRS

Example 1:


Example 2:


The impulse from right ventricle will be slow as it needs to travel partly or entirely outside of the conduction system resulting in slow & abnormal activation of left ventricles creating an abnormal and prolonged QRS complex.

Causes of LBBB:
  • Ischemia & infarction (may be masked by LBBB)
  • Idiopathic fibrosis or LBB degeneration
  • Heart disease
  • Coronary Artery Disease
  • Cardiomyopathy
Fascicular Branch Block (Hemiblock)

Left bundle branch contains three (3) fascicular left, right and septal branch – Hemiblock is a block to one (1) fascicular branch only, therefore is not a complete LBBB. A normal conduction is when the impulse move down AV node to left bundle, then split into both fascicles where the Purkinje fibres merge - A hemiblock rely on impulses from other parts of the ventricles where fascicle is intact.

Left Anterior Fascicular Block (LAFB)
  • Can occur in healthy individuals, or those suffering from conditions such as LBBB related symptoms, or ventricle hypertrophy, & medications. Can be progressive to other blocks but rare.

Due to the block, the impulse backtracks and move down to the left posterior fascicle (LPF) causing left axis deviation.

  • Can mask symptoms of anteroseptal infarction
  • rS complex in Lead II, III, & aVF can mask Q-wave from prior inferior infarction
  • QRS 0.10 – 0.12s in V5 & V6
  • Left axis deviation (-60°)
  • No other cause of LBBB
Left Posterior Fascicular Block (LPFB)
  • Larger branch (greater blood supply); due to the block, the impulse backtracks and move down to the left anterior fascicle causing right axis deviation – similar causes as left anterior fascicular block (LAFB; unusual in healthy people, and overall rare)
  • Can mask inferior & lateral infarction
  • T-wave inversion may occur in inferior leads showing similar to post-ischemic T-wave
  • QRS 0.10 – 0.12s in V5 & V6
  • Left axis deviation (+120°)
  • No other cause of LBBB
  • No right ventricle hypertrophy

    Bifascicular Block

    Combination of either left anterior or left posterior hemiblock with RBBB – Dangerous condition as only one fascicle of left bundle branch is supplying the heart with electrical activity.

    • RBBB present
    • Left axis deviation or right axis deviation present


    College of Pre-Hospital Care. (2015). 12-Lead ECG Analysis: Self-Directed Learning Package. Version 3. St John Ambulance Ltd.  

    Curtis, K., & Ramsden, C. (2016). Emergency and trauma care for Nurses and Paramedics (2nd ed.). Elsevier Australia.

    DeLaune, S. C., Ladner, P. K., McTier, L., Tollefson, J., & Lawrence, J. (2016). Australian and New Zealand fundamentals of nursing (1st ed.). Cengage Learning Australia Pty Limited.

    ECG & ECHO Learning. (2020). Clinical ECG Interpretation. https://ecgwaves.com/topic/ecg-normal-p-wave-qrs-complex-st-segment-t-wave-j-point/

    Life in the Fast Lane. (2020). ECG Library. https://litfl.com/ecg-library/

    St John WA Ltd. (2017). Electrocardiography (ECG). Clinical Resources. https://clinical.stjohnwa.com.au/clinical-skills/assessment/vital-signs/electrocardiography-(ecg)

    WikiEM. 2020. The Global Emergency Medicine Wiki. https://www.wikem.org

    Page contributors:

    60825Thanh Bui, AP60825
    Event Medic, Emergency Medical Technician &
    Volunteer Development Officer



    Andrew Moffat, AP16790
    Volunteer Training Manager & Volunteer Development Officer

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