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

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.

• 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

  

• 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

Causes

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

Management

• 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

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)

Causes

• 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)

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 MarroW – because 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)

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

Causes

• 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.

Treatment

• 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 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

Extrasystoles

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 2^nd degree heart block:
  • In 1^st and 2^nd 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

Fibrillation

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 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!

Wolff-Parkinson-White Syndrome (WPW syndrome)

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

Pacemakers

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

• 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

• 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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Indications

Various studies have shown that high and medium risk patients can benefit from CABG, but there is no benefit to low risk patients.

• The greatest degree of benefit is for those with LAD disease and 1/3 artery disease. Those with only one artery involved (and it is not the LAD) have less benefit
• The benefits are reduced the longer you leave it between identifying those who would benefit, and carrying out the surgery.

PCI or CABG?

• Single lesions in nice straight vessels – PCI
• Calcified lesion is tortuous vessels – CABG
• LAD – CABG
• Other single or double vessel involvement – PCI
• Strongly positive ETT – CABG

Single, double triple?

Procedure

Normally performed through a mid sternal inscision (medial sternotomy)
Veins are usually harvested from the saphenous vein of the legs – however, arteries may also be used, and arteries tend to give better results. This often occurs after the thorax has been opened and the surgeon has examined the arteries.

• Arteries that can be used include; internal thoracic arteries (internal mammary), gastro-epiploic, inferior epigastric, radial artery.
• Over 75% of patients have 3 grafts or more – at least one of these grafts is usually an artery
• After 10 years, 83% of internal thoracic grafts are still patent, but only 41% of saphenous grafts.

The arteries to be by-passed are reviewed an angiography by the surgeon before the procedure.
Most surgeons prefer to perform the operation with cardioplegia. This is where the heart is manually stopped during an operation. It usually involves cooling the heart to around 34’C (mild hypothermia), before injecting cold crystalloid cardioplegic solution into the coronary circulation. This induces asystole but it also protects the myocardium from damage.

• Antegrade cardioplegia – this is where the solution is introduced via the aortic root
• Retrograde cardioplegia – this is where the solution is introduced via the coronary sinus
• During cardioplegia, blood is diverted from the SVC and IVC via venous cannulae to a heart lung machine. This device both oxygenates and pumps the blood, as well as removing CO2.
• Many surgeons also use an aortic cross clamp. This is a device that goes across the aorta and limits the systemic circulation.
• During the operation the heart may be cooled to 15-20’. This slows down the metabolism of the heart and thus reduces the risk of damage to the myocardium.
• Blood may be injected into the coronary arteries in a bid to reduce myocardium damage if the surgery last longer than ½ hour.

Prognosis

• A successful graft lasts about 10-15 years.
• The surgery decreases the risk of death from CVD. However, 5 years after the surgery, the risk is about the same as somebody who has always been managed on drug treatments
• The age of the patients affects the prognosis – generally, the younger the patient the better the prognosis, and longer the graft will be viable for.
• The surgery significantly increases the quality of life, reduces symptoms, and increases exercise tolerance, as well as reducing the need for anti-anginal medications.
• 75% of patients are free of ischaemic events at 5 years. This is around 50% at 10 years
• At 10 years:
  • Those who had a saphenous graft have no benefit over those on medical therapy
  • Those who had an arterial graft do still have benefit
• The greatest benefit is to those with left main stem disease.
• Women, on average, have worse outcomes than men. This is thought to be the result of a combination of factors, including; smaller coronary arteries, higher age at operation.

Complications

Death – (1-3%) – the risk of this is increased in those that are:

• Smokers
• Overweight
• Obese
• Diabetic
• Female
• Older
• Short (height)
• Having an operation for an acute coronary syndrome

MI – 2%
Ventricular arrhythmias – such as broad complex tachycardia
Stroke – 2%. Reducing the amount of handling of the aorta can reduce the risk of embolism. The risk of stroke is also higher in those that have carotid artery stenosis.
Bleeding – clopidogrel and aspirin should be stopped 7 days before surgery. Note that in PCI, they are often actually used during and after surgery!
CABG seems to increase the resistance of patients to aspirin. Thus the drug is not as effective in these patients due to increased cell turnover.
Cognitive decline – has been reported in many patients but is difficult to measure. It is often mild and will reverse several months after treatment.

Long-term management

• Cessation of smoking
• Aspirin
• ACE inhibitor
• Beta-blocker
• Statin
• Control of BP
• Control of diabetes
• Weight and exercise management

References

Read more about our sources

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