ECG Abnormalities
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This article “ECG Abnormalities” is part of the almostadoctor ECG series. It provides information about the interpretation of ECGs. For a quick view of common ECG abnormalities see Summary of ECG Abnormalities. To learn about the basic principle of an ECG, see Understanding ECGs

Conduction Abnormalities

Always remember the pattern of conduction:
SA node AV node His Bundle bundle branches
When looking at conduction abnormalities, you are best to look at whichever lead shows p waves most clearly. This is usually lead II or V1.

The PR interval the time taken for the depolarisation to spread from the SA node to the ventricular muscle. This should not be greater than 0.2s – i.e. 1 big square.

First degree Heart block

1st Degree Heart Block
1st Degree Heart Block

If the PR interval is greater than 0.2s, then we call it first degree AV node block. All the waves will still be present, however you will notice a larger gap (pause) between the p wave and QRS complex.
First degree heart block is not in itself very important – it can be a sign of coronary artery disease, acute rheumatic carditis, digoxin toxicity or electrolyte disturbance, but does not usually require treatment.

Second degree Heart block

This is where there is an intermittent absence of QRS complexes – and thus an indication that there is a blockage somewhere between the AV node and the ventricles.

There are three types:

  • Mobitz type 2 phenomenon – this is where there is a regular rhythm, and a fairly constant PR interval, but every now and again there is an absent QRS (pictured above). basically for every QRS, there are 2 or 3 p waves.
Mobitz Type II
Mobitz Type II
  • Wenckebach phenomenon (aka Mobitz type 1)progressive lengthening of the PR interval followed by an absence of the QRS, then a shortened PR interval and normal QRS, and the cycle begins again. The cycle is variable in length, and the R-R interval shortens with the lengthening of the PR interval

    Wenckebach phenomenon (aka Mobitz type I)
    Wenckebach phenomenon (aka Mobitz type I)
  • 2:1 and 3:1 conduction – there is one normal cycle, then one cycle with an absent QRS (2:1) or there is one normal cycle, then two cycles without a QRS (3:1) – pictured below
2:1 Conduction Block
2:1 Conduction Block



  • Acute – MI
  • Chronic – heart disease (CHD)


  • Mobitz type 2 and Weckenbech don’t require any specific treatment
  • X:1 block may require a pacemaker (temporary or permanent), especially if the ventricular rate is slow

Third degree Heart block – complete heart block

Complete Heart Block (Third degree heart block)
Complete Heart Block (Third degree heart block)

This occurs when atrial contraction is normal, but no beats are conducted to the ventricles.
The ventricles are still excited by their own internal ‘ectopic pacemaker’ system! Thus the definition of complete heart block is:

  • P wave ~90/min (more p waves than QRS complexes)
  • QRS ~36/min
  • Variable PR intervals
  • No relationship between P wave and QRS complexes, but both are present.
  • Abnormally shaped QRS due to abnormal spread of conduction throughout ventricles
    • QRS will generally be broad (~160ms – as opposed to a maximum of 120ms in a normal heart – 4 little squares as opposed to 3 little squares)
  • Right axis deviation
  • Escape rhythms present (more on these later)


  • MI – it will occur acutely, and is often transient
  • Chronic – often due to fibrosis around the Bundle of His, or bundle branch block of both branches
  • Always indicates underlying disease – more often fibrosis then ischaemia
    • Consider temporary or permanent pacemaker

More info about complete heart block:

  • Patients with AV block can be haemodynamically stable; however they should require an urgent pacemaker because this situation can change at any time
  • If the number of atrial and ventricular complexes is equal then we call it AV dissociation, and not AV block

Bundle Branch Block

If the wave of depolarisation can reach the intraventricular septum, then the PR interval will usually be normal. And in bundle branch block, this is still the case. However, the time taken for depolarisation to spread throughout the ventricles is altered because of the block, and thus the duration of the QRS is lengthened. So, in bundle branch block there is:

  • Normal PR interval
  • Lengthened QRS duration (greater than 120ms – >3 little squares)

The QRS complexes in bundle branch block are often distinctive shapes – helping to differentiate from other causes of widened QRS complexes.

Right Bundle Branch Block (RBBB)

Right Bundle Branch Block (RBBB)
Right Bundle Branch Block (RBBB) – the basics
Right Bundle Branch Block (RBBB) with 1st degree AV block on a full ECG

In many people, this does not cause abnormalities of the ECG. It often indicates right sided heart disease.
In the normal heart, the depolarisation of the septum occurs from right to left. In RBBB this still happens, but because the RBB is blocked, then the right ventricle does not depolarise at the same time as the left. So, left ventricular depolarisation continues as normal, and produces a normal R and a normal S wave. But after this has happened, the right ventricle then depolarises, and causes a second R wave (R1). This creates a distinctive pattern on the ECG:

  • V1 – creates an ‘M’ shaped QRS – because the R wave is positive, S is negative (and R1 is also positive). This is also known as an ‘RSR’ pattern – there is an up (‘R’) then a down (‘S’), then another up (‘R’)
  • V6 – creates a ‘W’ shaped QRS – because the R wave is negative, and S is positive (and R1 is also negative)

You can try to remember this with the word MarroWbecause V1 can look like an “M”, and V6 makes a “W”
Important – the QRS complexes will also be wide – greater than 120ms
The axis of any BBB can be either normal, LAD or RAD. It is most commonly normal.
There is no specific treatment – and it may often be caused by an atrial septal defect

Left Bundle Branch Block (LBBB)

Left Bundle Branch Block (LBBB)
Left Bundle Branch Block (LBBB) – basic waveform
Left Bundle Branch Block (LBBB)
Left Bundle Branch Block (LBBB) on a full ECG

Usually indicates left sided heart disease. Can indicate an acute MI (if it is new onset).
The QRS sign, and physiology behind LBBB is pretty much the exact opposite of that in RBBB, so the sign is opposite.
You can use the word WillaM to try and remember this one!

But how do you know which side is which?! – well, William has “LL” in the middle for left, and Marrow has RR in the middle for right! You could also try the sentence – William left his Marrow

NB – the William and Marrow signs are not always that great;

  • RBBB – you may only see the ‘M’ in lead V1
  • LBBB – you may only see the ‘M’ in lead V6


  • Ischaemic disease – if the patient has had recent chest pain, LBBB is likely to indicated MI, and thus thrombolysis should be considered.
  • Aortic stenosis
  • If the patient is asymptomatic, then no treatment is needed

Bifascicular block

This refers to any situation in which two of the three main fascicles of the His/Purkinje system are blocked.
These three fascicles are;  the right fascicle, the left anterior fascicle and the left posterior fascicle. So there is one on the right and two on the left.

  • Usually it refers to RBBB with either left anterior fascicular block (LAFB, sometimes called LAH – left anterior hemiblock) or left posterior fascicular block (LPFB, sometimes called LPH – left posterior hemiblock).
  • Some people consider LBBB a bifascicular block because technically LBBB occurs above the bifurcation of the LAF and the LFP, and thus both are blocked.


  • A new bifascicular block in a patient with acute MI needs emergency pacemaker placement
  • A bifascicular block with RBBB and LAH is as stable condition that can go unchanged for years. You will need to look at old ECG’s to establish how long it has been there
  • A bifascicular block with RBBB and LPH should be considered for pacemaker therapy. If the pattern is new or old, the patient should be referred for emergency pacemaker.

Note – both LPH and LAH can cause left axis deviation

Rhythm Abnormalities

Rhythms can originate in 3 places in the heart – the SA node, the region around the AV node (known as nodal, or junctional rhythm), or the ventricular muscle

Sinus Rhythm

This means that the rhythm of the heart is being controlled by the SA node – i.e. this is the ‘normal’ rhythm of the heart.
It is possible have a sinus tachycardia, sinus bradycardia, and also sinus arrhythmias. The way to tell if it is ‘sinus’ or not is

  • There is one P wave per QRS
  • There is a constant PR interval

Sinus arrhythmia

Sinus Arrhythmia
Sinus Arrhythmia

Sinus tachycardia

Associated with; exercise, fear, pain, haemorrhage, thyrotoxicosis

Sinus bradycardia

Associated with; athletic training, fainting attacks, hypothermia, myxoedema, seen immediately after MI

Supraventricular rhythms

This is any rhythm that originates outside of the ventricles, and spreads to the ventricles in the normal manner; via the bundle of His, and left and right bundle branches. Thus, sinus rhythm is a supraventricular rhythm, as is junctional rhythm.

These will produce:

  • Normal QRS complexes – because the part of the heart producing the QRS is not in the ventricles – so the conduction will still pass through the ventricles as if it was produced normally, no matter if the producing part of the heart was the SA node, junctional region, or atrial muscle.
    • Unless! – there is also a right or left BBB, in which case the QRS may be wide

Ventricular rhythms – the bradycardias

The spread of the electrical charge in this case is abnormal, and thus the QRS us abnormal. Repolarisation is also abnormal, and so the T wave is an abnormal shape.
There will be:

  • Wide QRS complexes   

Atrial escape

This is a supraventricular rhythm. It occurs when the normal depolarisation of the SA node has not occurred, and some part of the atrium starts the depolarisation instead.

On the ECG you can see atrial escape where there is:

  • An abnormal p wave – because the excitation has begun somewhere away from the SA node
  • Normal QRS
  • Normal beats after the abnormal one

Junctional escape

  • No p waves
  • Normal QRS
  • Slightly slower rate (~75bpm max)

Ventricular escape

Most commonly seen in complete heart block, although you may see it without complete heart block, and it may occur as a one off instance.

Note there is no wave before the escape in this instance – because in this case the escape is a result of the SA node failing to fire (and the junctional escape also failing to kick in), and not a result of a bundle block. Note that in this type of escape, normal rhythm is restored afterwards, whereas in branch block, normal rhythm is not restored.

Accelerated idioventricualr rhythm

Normally, the ventricular rhythm is slower than that of the SV node. However, in this particular instance, there is a rhythm of around 75pm, but it has been generated by the ventricles.
This is often benign and need not be treated (although it is also associated with MI).
You should not confuse it with ventricular tachycardia – which requires a heart rate of over 120bpm

  • There are widened QRS complexes, as well as abnormal T waves



These basically have the same appearance as their corresponding escape beats, except that where an escape beat occurs later than expected, an extrasystole occurs earlier than expected.

  • Junctional extrasystole – absent or misplaced P wave – because the depolarisation travels towards the atria and the ventricles, not just away from the atria and towards the ventricles like a normal beat. Normal QRS
  • Atrial extrasystole – Normal QRS, normal looking beat – apart from it occurred earlier than expected.

The Tachycardias

These are the result of foci either in the atria or in the junctional (AV node) region depolarising quickly. To identify the origin of the tachycardia you have to look at the p wave.

  • When tachycardias occur intermittently they are called ‘paroxysmal’.

Supraventricular Tachycardia

Atrial tachycardia

  • Atria depolarise >150bpm
  • P waves superimposed on the t wave of the preceding beat
  • QRS complexes are the same shape as normal
  • The AV node cannot conduct faster than 200bpm. if the rate of atrial depolarisation is faster than this, then atrioventricular block occurs, where there are some p waves, not followed by QRS complexes.
  • Differentiating from 2nd degree heart block:
    • In 1st and 2nd degree heart block, the rhythm is roughly sinus rhythm
    • In atrial tachycardia, the rhythm is fast

Atrial flutter

  • Rate >250bpm
  • No flat lines between P waves (‘saw tooth p waves’)
  • Often associated block – remember the AV node cannot pass on rhythms of greater than about 125bpm. thus if there is an atrial rate of 250, the ventricular rate will be 125, and 2:1 block will be present. If the rate ventricular rate is 100, and the atrial rate is 300, then it is 3:1 block.
  • P waves may be difficult to discern from T waves – however you can tell if they are p waves because they occur regularly, even if they look like T waves. In the example below you can’t see t waves – they are all p waves.

Junctional (nodal) tachycardia

  • Due to an area around the AV node causing depolarisation – results in p waves very close to the QRS, or no p waves visible.
  • QRS is normal – because like all supraventricular arrhythmias the ventricles are still activated in the normal way.
  • Basically – there are probably no p waves, but a normal, regular QRS

These are usually due to small re-entry circuits around the AV node- and are sometimes called atrioventricular nodal re-entry tachycardias (AVNRE).

Carotid sinus pressure
By applying pressure to the carotid sinus you can stimulate the AV and SA nodes via vagal stimulation. This will reduce the frequency of discharge of the SA node, and increase the time of conduction across the AV node.
Thus, by applying pressure to the carotid sinus you can:

  • Reduce the rate of some arrhythmias
  • Completely stop some arrhythmias
  • It will have NO EFFECT ON VENTRICULAR TACHYCARDIAS – thus is can help you differentiate from SVT (supra ventricular tachycardias)

Applying the pressure reduces the frequency of QRS complexes, and allows the underlying atrial arrhythmia to become more visible.

Ventricular Tachycardia

These are caused by a foci in the ventricles discharging at a high frequency. This causes an abnormal spread of charge through the ventricles, resulting in wide and abnormal QRS complexes.

  • QRS is broad
  • T waves difficult to identify
  • No p waves
  • Regular QRS (~200bpm)
  • REMEMBER – you also see wide and abnormal QRS complexes in bundle branch block


Differentiating BBB with supraventricular tachycardia, from VT

  • Remember the clinical state of the patient:
    • If they have just had an MI it is most likely to be VT
  • An isolated incidence of broad complex tachycardia is more difficult to differentiate:
    • Look very carefully for p waves (only present in BBB not VT)
    • Compare the tachycardia to the patient’s normal rhythm (if possible) – if the QRS is the same shape in both then it is BBB with supra-v tachycardia
    • If the QRS is >160ms (4 small squares) then it is most likely ventricular.
    • Left axis deviation normally means ventricular in origin
    • If the QRS’s are irregular, it is most likely AF with BBB


This occurs when individual muscle fibres contract of their own accord. So far all the rhythms we have looked at have involved synchronous muscle contraction.

Atrial fibrillation

  • No p waves – just an irregular baseline
  • Irregular QRS – between 75-190bpm
  • Normal shape QRS – because conduction through the AV node is normal            
  • In V1 the trace resembles atrial flutter
  • Normal T waves
Atrial Fibrillation (AF)
Atrial Fibrillation (AF)


Atrial fibrillation is a particularly common arrhythmia, and is discussed in more detail in the Atrial Fibrillation article

Ventricular fibrillation

  • No discernable pattern – no QRS, no P, no T
  • Patient is very likely to lose consciousness – thus the diagnosis is easy!
  • Not compatible with life for any sustainable period of time – patient needs urgent defibrillation!
Ventricular Fibrillation (VF)
Ventricular Fibrillation (VF)

Wolff-Parkinson-White Syndrome (WPW syndrome)

Wolff-Parkinson-White Syndrome (WPW)
Wolff-Parkinson-White Syndrome (WPW)

In the normal heart the only route from the atria to the ventricles is through the AV bundle. However, in some individuals there exists an accessory pathway through which conduction is able to travel. This is usually on the left side of the heart. Conduction is able to travel through this accessory pathway, and is not delayed by the AV node, and thus there is pre-excitation of the ventricles.

  • The accessory pathway is known as the bundle of kent.
  • The incidence of WPW syndrome is between 1-3% of the general population (i.e. very high!)
  • The vast majority of patients will be asymptomatic, but there is a risk of sudden death. This occurs in about 0.6% of those with WPW.  
  • This sudden death can occur when there isparoxysmal tachycardia. When this occurs, the signal from the atria, travels down through the accessory pathway, and then back up the bundle of His, and back into the atria. This sets of a loop of depolarisation, sometimes called a re-entry circuit.

Findings in an asymptomatic individual:

  • Sinus rhythm
  • Right axis deviation
  • Short PR interval
  • Short QRS complex
  • Delta wave – this is a short upstroke that occurs just before the QRS. It basically looks like the upstroke of the R wave is a bit bent – it starts off with a low gradient, and then increases to its normal gradient.

Findings during re-entry tachycardia:

  • No p waves
  • tachycardia
  • Often indistinguishable from other forms of SVT on the acute ECG


Example of ventricular pacing
Example of ventricular pacing

When an artificial pacemaker is present:

  • There may be occasional P waves, not related to QRS
  • QRS is preceded by a spike – which is the pacemaker stimulus.
  • QRS complexes are broad – because pacemakers usually stimulate the right ventricle – and thus the depolarisation is ventricular in origin.

Q waves – these show the spread of depolarisation of the ventricles travelling in the horizontal plane, thus they are often not present, because the charge travels equally in both directions and cancels itself out overall. Lead III is a good one to look at Q waves, and they are often normally present here.
When pathological Q waves are present (basically big Q waves – see MI notes for definition), then this is basically a sign that part of the heart tissue is dead – because it is no longer ‘cancelling out’ the opposite side of the heart.

Ectopic Beats

An ‘ectopic’ is an unexpected event that occurs out of sequence. Atrial and ventricular ectopics occur when p waves (atrial) or QRS complexes (ventricular) occur out of sync with the rest of the ECG. They are typically single events and can occur anywhere from once every few seconds (or less), to only very occasionally.

Atrial Ectopics

Arial Ectopic (Premature Atrial Complex - PAC)
Arial Ectopic (Premature Atrial Complex – PAC)
  • Often referred to as a Premature Atrial Complex (PAC)
  • An abnormal p wave, followed by a normal QRS. Often no p wave is visible as it is hidden in the preceding T wave
  • Results from abnormal pacemaker stimulus from somewhere in the atria
  • Benign
  • Often symptomatic
  • Pulse may be irregularly irregular (mimicking AF)
  • Associated with:
    • Lack of sleep
    • Stress / anxiety
    • Caffeine
    • Large amounts of exercise
    • Hypokalaemia
    • Hypomagnesia
    • Beta-blockers
  • Slight increased risk of AF to the affected patient

Ventricular Ectopics

Ventricular Ectopic Beat (VEB)
Ventricular Ectopic Beat (VEB)
  • Sometimes called VEBs (ventricular ectopics beats)
  • The abnormal QRS complex is normally widened because the conduction does not follow the normal pathways
  • Pulse may be irregularly irregular (mimicking AF)
  • Common with age
  • Usually benign
  • Can predispose to VT (more than 4 consecutive VEBS is considered a ‘run’ of VT
  • Usually asymptomatic
  • Do not usually require any treatment

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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