Ebook ECG workbook (3rd edition): Part 2

(BQ) Part 2 book ECG workbook presents the following contents: Axis deviation, ischaemia, injury and necrosis, sites of infarction, bundle branch blocks, chamber enlargement, hemiblocks, bifascicular blocks and trifascicular blocks, paced rhythms, a systematic approach to ECG interpretation.

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Chapter 8

Axis deviation

We have already learned about the normal pathway of the impulse as it travels through theconducting system We have also seen how the direction of this impulse and the position ofelectrodes around the heart affect the polarity of the limb leads

However, there may be times when the normal pathway of the impulse is disrupted, e.g by apiece of damaged tissue as the result of a heart attack Such a disruption may cause the pathway

of the impulse to deviate to the left or the right or in extreme cases back up to the direction from

which it came This is known as axis deviation

This disruption will affect the polarity of the limb leads If something is causing the impulse totravel back from where it came, the aVR may be positive on the ECG, rather than negative, becausethe impulse is now travelling towards the aVR Meanwhile Lead II may be negative, as the impulse

is now travelling away from the lead

One way of working out axis deviation is therefore by looking at the polarity of two of the limbleads This can be most easily done by assessing Lead I and the aVF

In a normal ECG, as we know, all the limb leads should be positive except aVR Therefore, if

the ECG shows a normal axis deviation (meaning that there is no disruption of the normal pathway of electrical activity) both Lead I and the aVF should look positive (see fig 8.1).

Figure 8.1: Normal cardiac axis demonstrated by both Lead I and the aVF being positive.

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If there is an extreme axis deviation (severe disruption of the electrical pathway) the opposite will occur – Lead I and the aVF will look negative (see fig 8.2).

Figure 8.2:

Extreme axis deviation Lead I and the aVF lead are negative Note that the aVR is positive; the electrical impulses are therefore moving in the opposite direction from normal.

If the impulse deviates to the left, there is left axis deviation, Lead I is positive and the aVF is

negative This can be easily remembered by thinking about the tips of the QRS complexes of these

two leads as leaving each other or leaving the page: LEFT and LEAVING (start with the same

letter!) (see fig 8.3)

Figure 8.3:

Left axis deviation Lead I is positive and the aVF is negative.

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In right axis deviation, Lead I is negative and the aVF is positive The tips of the QRS complexes reach for each other: RIGHT and REACHING (see fig 8.4).

Figure 8.4: Right axis deviation

Extreme axis deviation is the most worrying for a patient, then right axis deviation, and then left

In practice, axis deviation does not necessarily require any treatment in itself However, itraises the question of what has caused the axis deviation in the first place For the clinician, theaxis deviation will indicate how the patient’s condition may be affecting the pathway of the impulsethrough the conducting system, and thus how likely the patient is to become unstable and havearrhythmias Using the above method, axis deviation can be assessed at a glance as the ECG iscoming out of the ECG machine

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Axis deviation

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SUMMARY: Axis deviation

Left +ve -ve (leaving)

Right -ve +ve (reaching)

Extreme -ve -ve

Occasionally, in more advanced cardiology, it may be necessary to talk about axis deviation in terms ofdegrees of deviation, rather than just in terms of normal, left, right or extreme This can be done byplotting the axis on a graph called the Hexaxial Reference System (see fig 8.5) If an ECG shows a rightaxis deviation of +95 degrees, for example, it is not as serious as a right axis deviation of +170 degrees.The first method that we learned will be adequate for the majority of ECGs that you will encounter.However, calculating axis deviation using the Hexaxial Reference System is useful if you encounter aLead I and aVF that are equiphasic (equally positive and negative) In addition, some complexarrhythmias can be distinguished from one another by the degree of axis deviation that is present

Figure 8.5:

The Hexaxial Reference System.

The purpose of including the Hexaxial Reference System within this text is simply to help makesense of what looks like a complex diagram in many ECG books Such diagrams can make learnersthink they have reached their limit with ECG interpretation!

The Hexaxial Reference System is divided into 30-degree segments The numbers at thebottom of the Hexaxial Reference System are positive and those at the top half, negative

If you look at Figure 8.5 you will see which portion of the diagram represents which type of axisdeviation Here the heart is superimposed onto the Hexaxial Reference System In normalcircumstances, the pathway of the impulse would flow through the conducting system directlytowards Lead II This falls within the normal axis deviation quadrant of the Hexaxial ReferenceSystem Anything deviating between +90 degrees and -30 degrees is considered normal axisdeviation If the pathway of the impulse deviates to the patient’s left it would fall in the upper right-

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hand quadrant (as you look at the page) of the Hexaxial Reference System If deviation is to the right,

it would fall in the lower left-hand quadrant And if the pathway of the impulse goes back to where

it came from, it would travel towards the upper left quadrant, which represents extreme axis

deviation

Calculating axis deviation in degrees using the Hexaxial Reference System

Here is a step-by-step method to follow:

1 Look at the ECG and decide, by looking at Lead I and Lead aVF, if it is a normal, left, right or

extreme axis deviation If lead 1 is equiphasic (a complex that is as positive as it is negative), it is sufficient at this stage to say that it is either a left or a normal axis, for example

2 Now look at the Hexaxial Reference System and remind yourself in which quadrant of the

Reference System the axis will fall (For instance, if it is a normal axis deviation it will fall between +90 degrees and -30 degrees.)

3 Look back at the ECG and find the smallest, equiphasic complex (the smallest complex that is

both positive and negative) in the limb leads Remember: the smallest limb lead complex may not be equiphasic; you need to choose the lead that is both small and equiphasic

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Axis deviation

Figure 8.5a: Normal electrical conduction;

the impulses move towards Lead II.

Figure 8.5b: Left axis deviation; the impulses

move in the approximate direction of Lead aVL

Figure 8.5c: Right axis deviation; the impulses

now move in the direction of Lead III

Figure 8.5d: Extreme axis deviation; all electrical

activity is moving in the opposite direction to normal.

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4 Once you have found this lead, go to the Hexaxial Reference System and find the positive pole

of that electrode

5 From this electrode, move 90 degrees around the Hexaxial Reference System towards the

quadrant that you first decided your axis would fall in (see step 2 above)

6 Look at the lead that you have arrived at and the degree of axis deviation that it represents This

is the axis deviation of the ECG For example, Figure 8.1 shows a normal axis deviation of +60degrees Lead aVL is the smallest, equiphasic complex in the limb leads Moving 90 degrees towards the quadrant that represents normal axis deviation takes us to Lead II and +60 degrees

7 Why move 90 degrees? We have already learned that if an impulse travels towards an electrode

we get a positive deflection, and if it travels away from an electrode we get a negative deflection

If we travel at 90 degrees to an electrode, we get an equiphasic complex (see fig 8.6)

Figure 8.6: How the direction of the electrical current affects the shape of the QRS complex.

The equiphasic complex is recorded when the direction of the axis is around 90 degrees to the lead In effect, the current is moving towards and then away from the lead so it will be displayed on the ECG as being equally positive and negative.

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Chapter 8 activities

Measuring cardiac axis can be a tricky skill to learn at first, so don’t worry if you feel as though youhaven’t quite got the hang of it yet The good news is that, with a little practice, you will soon beable to estimate the cardiac axis on a 12 lead ECG quickly and easily The activity for this chapterwill give you more opportunity to practise this skill

When you have completed this activity you should be able to:

● recognise normal, left and right axis deviation;

● estimate the degrees of axis deviation on a 12 lead ECG

Activity 8.1: Measuring cardiac axis

Time required to complete this activity: 15 minutes Answers are provided on p 92.

Look at the three ECGs below and estimate the cardiac axis for each one

Use both the methods that you have been shown in this chapter This should enable you to fill in the boxesunder each ECG, choosing one of the words in brackets when they are given

Once you have done this, and have checked your answers, you should go and practise some more Youcould start by looking at the ECG that you recorded back in Chapter 1

Remember: the more you practise, the easier it will become!

Lead I is (positive or negative)

Lead aVF (positive or negative)

Therefore the axis is (left, right or normal)

Lead is the smallest equiphasic lead Lead is 90 degrees to the most equiphasic lead

Therefore, the cardiac axis is degrees

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Activities

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Lead I is (positive or negative)

Lead aVF (positive or negative)

Therefore the axis is (left, right or normal)

Lead is the smallest equiphasic lead Lead is 90 degrees to the most equiphasic lead.Therefore, the cardiac axis is degrees

Figure 8.8: ECG 2.

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Chapter 9

Ischaemia, injury and necrosis

Animal experiments have played a major part in the development of ECG knowledge over theyears Fye (1994) describes how, as far back as 1790, Luigi Galvani used electrical stimulation tomake a dead frog’s leg dance This was the first step in making a connection between electricalstimulation and the heart’s contraction and it led on to the discovery of links between the heart’sconducting system and myocardial contraction

Ischaemia

Much later, Bayley (1944) identified ECG changes by means of experiments performed on dogs If

a tourniquet is tied around a dog’s coronary artery while it is connected to an ECG, and the

coronary artery is occluded for a few minutes, a startling change occurs on the ECG trace The T

waves turn upside down (T wave inversion) This is known as an ischaemic change The term

ischaemia refers to a condition where there is insufficient oxygenated blood reaching the

myocardium (heart muscle) When the tourniquet is released the T waves turn upright again

Ischaemia is therefore a reversible change

We can relate this to patients with angina Angina is a condition in which the supply of blood

to the myocardium does not match its demand for oxygen The process may be reversed by givingthe patient a tablet of Glyceryl trinitrate (GTN) GTN reduces the amount of blood flowing into theheart (its preload) and therefore lowers the heart’s workload, reducing the myocardial need foroxygen – a similar effect to that gained by releasing the tourniquet

There are two other ischaemic changes that we may see on an ECG: ST depression (where the second part of the QRS complex and the T wave are depressed below the baseline); and T wave

flattening.

Figure 9.1: ST depression The amount of ST depression is measured from between the J point (the end

of the S wave) and the isoelectric line.

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Figure 9.2: T wave inversion.

It is useful to record an ECG when a patient is experiencing chest pain Often one of theseischaemic changes will be present and this may confirm that the patient’s pain is cardiac in origin

An exercise treadmill test is sometimes used to quantify a patient’s symptoms during aerobicexercise As the patient exerts themselves on the treadmill, the myocardium demands moreoxygen and the patient may show symptoms The development of ST depression on the ECGrecorded during this procedure may indicate that the heart is becoming ischaemic, as the demandfor oxygen increases with exercise ST depression is measured from the bottom of the ECG’sbaseline to the ST segment

Injury

Following the Bayley experiment, scientists examined what would happen if the tourniquet was left onthe dog’s coronary artery a little longer When this was tried, another startling change occurred The

second half of the QRS complex became elevated above the baseline Known as ST elevation, this is

the change that is often seen when the patient is having a heart attack (acute myocardial infarction)

This is known as the injury stage and it can still be reversed if it is treated early enough The

supply of oxygen to the myocardium has been occluded and the occlusion therefore needs to beremoved in order to reinstate the blood supply – again, like releasing the tourniquet This is done

by mechanically opening the vessel in a procedure called primary angioplasty and then inserting

a coronary stent This procedure is carried out in a specialist Angiography Suite It is performed byintroducing a catheter up through the femoral artery to the heart This enables a balloon to beinflated in order to open up the artery Alternatively, a metal structure (a stent) can be used to keepthe artery open The criteria for primary angioplasty are that the patient’s ECG should show:

● 2 mm or more ST elevation in at least two chest leads;

● or 1 mm or more ST elevation in two or more of the limb leads (Springings et al 1995);

● or have a posterior myocardial infarction (see Chapter 10);

● or new left bundle branch block (see Chapter 11)

The longer the treatment is delayed, the more likely the myocardium is to die from lack of oxygen.This is why the public are being educated to report symptoms of chest pain and seek help early Oncethey have called for help, the patient’s transfer to hospital for primary angioplasty should be as quick

as possible (the ‘call-to-balloon’ time) The time between their arrival at hospital and the time theyreceive their primary angioplasty should also be as quick as possible (the ‘door-to-balloon’ time)

In order to try to reduce deaths from coronary heart disease, current guidelines for thetreatment of ST-segment elevation myocardial infarction recommend a door-to-balloon time of 90minutes or less for patients undergoing primary percutaneous coronary intervention (Menees 2013)

Necrosis

To continue with the Bayley experiment, our experimenters then wondered what would happen ifthe tourniquet was left on the dog’s coronary artery for even longer? What happened was that afterabout six hours of occluding the blood supply to the myocardium, the myocardium started to die

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This is the necrosis (death) stage and manifests itself on the ECG by the development of deep

Q waves (see fig 9.3)

Figure 9.3: Large Q waves on the ECG of a post-myocardial infarction patient.

The necrosis stage is irreversible and this is what we want to avoid for our patients Oncemyocardium is dead, it cannot be salvaged The more necrosis occurs, the poorer the prognosis for

the patient This is why early reperfusion is vital Once Q waves develop on an ECG, they stay

there Therefore, it is sometimes difficult, without an old ECG, or a sound patient history, toascertain whether a patient’s infarction is six hours old or considerably older!

We have already learned that it is normal to have Q waves in some leads For Q waves to indicatenecrosis (or be pathological), they have to be 25% of the height of the R wave or 2 mm in depth

In time, T wave inversion then occurs in the leads with the Q waves and the ST elevationreturns to baseline, leaving the T wave inverted This is often referred to as the evolving pattern ofmyocardial infarction (see fig 9.4)

Figure 9.4: The evolution of an acute myocardial infarction In the early stages there is no Q wave but

there is ST elevation In the first few hours the Q wave develops and the T wave becomes inverted If reperfusion of the affected artery does not take place then the myocardium becomes irreversibly damaged and this is shown as a large Q wave At this stage the T wave is still inverted because the area around the necrosed myocardium is ischaemic Over the coming weeks and months the necrosed tissue solidifies into scar tissue and the ischaemic zone around it develops new blood vessels; the Q wave remains a permanent feature of the ECG but the T wave will become positive again.

Non ST segment elevation myocardial infarction

Infarction may be limited to the inner part of the ventricular walls rather than the full thickness ofthe myocardium, or it can simply result in microscopic myocardial damage In this case

repolarisation is affected but not depolarisation; and the ECG will show deep, symmetrical T wave

inversion or ST depression, rather than ST elevation and Q waves Therefore, these types of infarcts

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Ischaemia, injury and necrosis

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are often referred to as non ST elevation infarcts (see fig 9.5) The difference between the T wave

inversion in ischaemia and T wave inversion in the non Q wave myocardial infarction is that the Twaves stay inverted rather than reverting to normal when the patient’s symptoms improve

Figure 9.5: The effects of ST and non ST elevation myocardial infarction (MI) on the ECG complex The

ST elevation MI is associated with myocardial injury that extends from the endocardium to the epicardium The ECG shows ST elevation from the injured tissue and a large Q wave as a result of the developing necrosis The non ST elevation MI only affects a portion of the endocardium and the ECG shows the ischaemic changes (T wave inversion) from the surrounding tissue.

Patient risk stratification

The term acute coronary syndrome is used to refer to several conditions within a spectrum of the

same disease process The extent to which these physical changes reduce the flow of blood throughthe coronary artery determines the exact nature of the clinical acute coronary syndrome thatensues Acute coronary syndrome comprises:

● unstable angina;

● non ST segment elevation myocardial infarction (NSTEMI);

● Q wave myocardial infarction

In the last few years much has changed in Cardiology in terms of how patients are risk

stratified An example of this is the use of troponin testing as a biochemical marker of myocardial

damage The presence of ST elevation in acute myocardial infarction is only about 50% sensitive

(Menown et al., 2000) Not all patients who develop myocardial necrosis exhibit ECG changes Thus,

a normal ECG does not rule out a diagnosis of myocardial infarction

Troponins are contractile proteins that are present in heart muscle cells and leak into thepatient’s bloodstream during even minor myocardial injury In addition, they may predict cardiac

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events in patients with acute coronary syndromes It is now clear that any amount of myocardialdamage, as detected by cardiac troponins, implies an impaired clinical outcome for the patient,

whatever the ECG reading (Mingels et al., 2000)

Increasing acute chest pain admissions to hospital in the UK continue to stretch limitedresources in Coronary Care units There is therefore an urgent need to discriminate rapidly betweenhigh-risk and low-risk patients

Differential diagnosis

Differential diagnosis is made more difficult because many ECG changes sometimes, but do not

always, indicate acute coronary syndrome Here are some examples:

● QS complexes occasionally occur in V1 and V2 as a normal variant in tall, thin individuals because of the positional changes of the electrodes relative to the heart

● Persistent ST elevation in the chest leads often indicates formation of a ventricular aneurysm.

● Peaked T waves are characteristic of hyperkalaemia and flat T waves of hypokalaemia.

● T wave inversion is a normal variant in leads V1, V2, and V3 in Afro-Caribbean individuals

● Concave ST elevation, with widespread T wave inversion occurs with pericarditis.

● Deep, inverted T waves are sometimes found after intracerebral bleeds

● Similar T wave changes are often seen after tachyarrhythmias or Stokes–Adams attacks.

SUMMARY:

● Ischaemia – T wave inversion, ST depression, T wave flattening

● Injury – ST elevation

● Necrosis – Q waves

Caution: It is possible for the ECG to be normal during a myocardial infarction or for other

conditions to cause these changes Therefore the ECG should never be used in isolation.

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Ischaemia, injury and necrosis

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● and myocardial necrosis.

Activity 9.1: Recognising abnormalities associated with

acute coronary syndrome

Approximate time required to complete this activity: 15 minutes

Answers are provided on p 93.

Look at Figure 9.6 (opposite), which shows a 12 lead ECG with a number of abnormal changes on it Then complete the following table:

ECG N for ‘no’ or Y for ‘yes’, as appropriate

waves? elevation? depression? inversion? flattening? (ischaemia, injury, necrosis)I

IIIIIaVR

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Figure

9.6:A

12 lead ECG with

a number

of abnormal ECG changes

on it.

Activities 9

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Figure 10.1: The leads of the 12 lead ECG and the surfaces of the heart These are the four regions in

which damage most commonly occurs during myocardial infarction They can be recognised on the ECG

by ST elevation in the leads that are closest to these regions

Inferior myocardial infarction

ST elevation in leads:

IIIIIaVF

Anterior myocardial infarction

aVL

Septal myocardial infarction

ST elevation in leads:

V3–V4ECG 3 chapters 8–11:Layout 1 10/09/2014 11:06 Page 63

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Looking at the left ventricle, we can label the different walls of this chamber: anterior, posterior,inferior and lateral.

● The front surface of the left ventricle is referred to as the anterior surface.

● The bottom part of the left ventricle is the inferior surface.

● The back of the left ventricle is the posterior surface.

● The side of the left ventricle is the lateral surface.

The changes described in Chapter 9 will appear in those ECG leads facing the area of ischaemia,injury or necrosis

Anterior leads

V1 to V6 are generally known as the anterior leads You can remember this by reminding yourself that

the V leads are the ones you put across the front (or anterior aspect) of the chest when you take an ECGrecording ST elevation in these leads would be called an acute anterior myocardial infarction (see fig

10.2) To be more specific, V1 and V2 look at the right ventricle; and V3 and V4 look at the septum.

Figure 10.2: Acute anterior myocardial infarction.

Inferior leads

Leads II, III and aVF are the inferior leads ST elevation in these leads would therefore be called

an acute inferior myocardial infarction (see fig 10.3).

Lateral leads

The lateral leads are V5 and V6, I and aVL (the latter two are often referred to as high lateral

leads) If ST elevation occurs in these leads it is called an acute lateral myocardial infarction.

Sometimes combinations of leads are affected For instance, ST elevation in II, III, aVF, V5 and

V6 would be called an acute inferior-lateral myocardial infarction.

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In most people, the right coronary artery supplies the right atrium, the right ventricle and theinferior part of the left ventricle Therefore, occlusion of the right coronary artery can produce aninferior myocardial infarction As blood supply to the right atrium is affected, ischaemia to the SA

and AV nodes explains why bradyarrhythmias and heart blocks are often associated with inferior

myocardial infarctions

The left anterior descending coronary artery, in the majority of the population, supplies blood tothe front of the left ventricular wall and the septum If this artery is occluded, an anterior myocardialinfarction usually results and is often complicated by impairment of the left ventricular function

As you can see, having a knowledge of the ECG and the coronary circulation can often helpyou to predict the complications that might accompany the infarction and enable you to takepreventative measures

Sites of infarction

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Figure 10.4: Reciprocal changes; ST elevations in II, III and aVF indicate an acute inferior MI Leads V2 and V3 are mirroring these changes in the inferior wall

of the left ventricle.

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Figure 10.5: Posterior and inferior myocardial infarction Note that there is ST depression in leads V1–V3 There are tall R waves in V1–V3 There are ST

elevations in Leads II, III and aVF, which show the inferior MI We can therefore conclude that there is posterior involvement in this inferior MI.

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The ECG workbook

Posterior myocardial infarction

We have not yet talked about posterior myocardial infarctions and we have used up all the leads

from our 12 lead ECG! Posterior myocardial infarction is usually recognised when there is a reciprocal change in V1 and V2 (see fig 10.5) For example, ST depression in these leads reflects posterior ST elevation and the development of an abnormally tall R wave in V1 and V2 reflects

posterior Q waves The right coronary artery also supplies the blood to the posterior of the leftventricle A posterior infarction can therefore be caused by an occlusion of the right coronary arteryand is often accompanied by an inferior myocardial infarction Posterior myocardial infarctions areslightly more difficult to recognise, and if they are overlooked the patient can miss out on the

benefits of revascularisation

SUMMARY:

V1–V4 Anterior leads

II, III and aVF Inferior leads

V5 , V6, I and aVL Lateral leads

Always suspect a posterior infarct if the ECG shows tall R waves or ST depression in V1 and V2, especially if accompanied by an inferior myocardial infarction.

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It is very important to be familiar with the different surfaces of the heart when you are looking atischaemia and infarction The ECG changes associated with these conditions occur in very specificregions and these should be remembered The activities for this chapter will reinforce yourknowledge of how the ECG leads represent the different regions of the myocardium

When you have completed these two activities, you should be able to:

● identify the ECG lead that shows each surface of the myocardium;

● recognise patterns of infarction and ischaemia on an ECG

Activity 10.1: The surfaces of the myocardium

Approximate time needed to complete this activity: 5 minutes Answers are provided on p 93.

Draw a line linking each box on the left with the appropriate box on the right

Myocardial region ECG leads

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Activities

Activity 10.2: Recognising infarction on the 12 lead ECG

Look at the two 12 lead ECGs shown in Figures 10.6 and 10.7 (pages 71 and 72) Can you identify thelocation of the infarction in both cases?

Make a note of any other abnormalities that you can see

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Chapter 11

Bundle branch blocks

Delay or blockage of conduction of the electrical impulse in the bundle branches is called a bundle

branch block

Bundle branch blocks are frequently found in patients with cardiac disease but areoccasionally found in the normal heart (Kourtesis, 1976) Their presence alone does not requiretreatment The ultimate prognosis depends on the condition that is causing it, rather than theconduction defect itself Right bundle branch block is of minor clinical significance, except as anindicator of possible coronary heart disease Left bundle branch block is rare in the otherwisenormal individual and is most commonly seen in ischaemic heart disease It therefore carries a

more severe prognosis than right bundle branch block (Eriksson et al., 2005).

Left bundle branch block

In left bundle branch block there is a delay or blockage of conduction in the main left bundlebranch This affects the normal depolarisation in the ventricles

In left bundle branch block, the impulse begins in the SA node and depolarises the atria, thentravels through the AV node to the left and right bundle branches On finding the left bundle branchblocked, the impulse travels down the right bundle branch The septum is unable to depolarisefrom left to right as normal and instead depolarises from right to left If V1 is our electrode, theimpulse will initially be travelling away from it, as the septum depolarises This causes a negativedeflection (Q wave) to be inscribed However, this is often not visible Right ventriculardepolarisation follows If VI is our electrode, the impulse would now travel towards the electrode so

a small positive deflection (R wave) would be inscribed The left ventricle is then depolarised Theimpulse is now travelling away from V1 and so a negative deflection (S wave) would be inscribed(see fig 11.1) Thus, the pattern of left bundle branch block in V1 is negative

Figure 11.1: The conduction sequence of left bundle branch block.

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V6V1

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workbook Figure 11.2: Left bundle branch block ECG.

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As V6 sits opposite V1, it will be affected in the opposite way Therefore the small Q wavesthat are usually seen in the lateral leads will not be evident The entire QRS complex in left bundlebranch block will be widened (greater than 0.12 seconds) owing to the conduction delay (see fig11.2, page 62).

Right bundle branch block

A delay or blockage of the conduction in the right bundle branch is called right bundle branchblock A normal impulse is initiated in the SA node and causes the atria to depolarise The impulsethen travels through the AV node and reaches the bundle branches If the right bundle branch isblocked, the impulse will go down the left bundle branch The initial activation in the ventriclesremains the same as that in normal depolarisation (i.e from left to right) Lead V1 will have aninitial R wave inscribed, as the initial impulse is travelling towards that electrode The left ventricledepolarises first and inscribes an S wave in V1, as the forces of depolarisation are now travellingaway from V1 The right ventricle then depolarises As the wave of depolarisation moves towardsV1, an R’ is inscribed Again, the opposite pattern will be inscribed in V6 (see fig 11.3)

The entire QRS complex will be widened (greater than 0.12 seconds) owing to the conductiondelay Thus, the pattern of right bundle branch block is a broad positive complex in V1 (see fig 11.4,page 64)

A simple way of reminding yourself what left and right bundle branch block look like on anECG is by remembering two words:

WILLIAM MARROW

The letter ‘L’ in William represents left bundle branch block and the letter ‘R’ in Marrowrepresents right bundle branch block The first letter of each word will tell you what V1 should looklike on the ECG, i.e in the left bundle branch block V1 should be broad and negative (like the Wshape in William) Likewise, in the right bundle branch block V1 should be narrow and positive (likethe M shape in Marrow)

Clinical significance

In right bundle branch block the initial depolarisation pathway of the impulse is not altered, so theECG signs of myocardial infarction are not obscured However, this is not the case with left bundlebranch block This is another item that we could add to our list of factors that can mimic myocardialinfarction on the ECG

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Bundle branch blocks

V6V1

Figure 11.3: The sequence of conduction in right bundle branch block.

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Figure 11.4: Right bundle branch block ECG.

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Bundle branch blocks

If we now have Q waves in the anterior leads (due to the altered depolarisation pattern), theECG in left bundle branch block could easily be mistaken for an ECG showing necrosis in theanterior leads The conduction defect also alters the polarity of the QRS complex and T waves, in

as much as the T wave is now directed opposite to the QRS complex This opposite polarity is theresult of the depolarisation-repolarisation disturbance produced by the block To the untrained eye,however, inverted T waves can be mistaken for signs of ischaemia, and T waves that are upright(when QRS complexes are negative) can be mistaken for ST elevation Left bundle branch blocktherefore renders the ECG impossible to interpret

So what happens if a patient is admitted to hospital with an acute onset of cardiac soundingchest pain and the ECG shows left bundle branch block? How do we know if the patient is infarcting

so that we can give them thrombolysis, bearing in mind that blood tests performed this early maygive us false positive results?

This problem needs to be handled by proving that it is new left bundle branch block This can

be done by reviewing old ECGs from the patient’s previous admission where possible If the oldECG shows narrow complexes, bundle branch block was not present before

We know that a common cause of left bundle branch block is an acute cardiac event In such

a case the patient would have an angiogram to assess whether their coronary arteries wereoccluded and if so an angioplasty would be performed The site of infarction will not be determined

by the ECG This highlights the importance of copying and keeping patients’ discharge ECGs

SUMMARY: Bundle branch blocks

● Assess rhythm strip – are the QRS complexes wider than 0.12 seconds?

● If yes, it is either a ventricular rhythm or a bundle branch block.

● Go to V1 on the ECG – is it broad and positive or broad and negative?

● Is it a WILLIAM or MARROW pattern?!

● Left bundle branch block renders the ECG impossible to interpret However if you can prove that the left bundle branch block is new (by looking at an old ECG), the patient may benefit from primary angioplasty

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In Chapter 11 you have seen that there are ECG patterns that indicate a conduction block in thebundle branches These patterns can vary quite a lot and do not always look as you would expect.The following activity will give you an opportunity to examine some bundle branch block patternsthat vary considerably from each other

When you have completed this activity, you should be able to:

● recognise RSR and QRS patterns in a variety of ECG complexes;

● differentiate between right and left bundle branch block on a 12 lead ECG

Activity 11.1: Recognising RSR and QRS patterns

Look at the ECG rhythm strips in Figure 11.5 and label the complexes on each: R, S, R1 or S1 In the boxesbelow the rhythm strips make notes about the complex (its width, whether it is positive or negative, etc.),then identify whether it is right or left bundle branch block

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