You are on page 1of 56

The Beginners

Essential Guide
Clinical
to theAnatomy
Surface ECG

By
Dr. Marc Barton
Contents
1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

2. Anatomy & Physiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

3. Rate, Rhythm & Axis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

4. Waves, Segments & Intervals . . . . . . . . . . . . . . . . . . . . . . . . . 14

5. Acute Coronary Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . 19

6. Bundle Branch Blocks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26

7. Fascicular Blocks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

8. Bradyarrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

9. Tachyarrhythmias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

10. Other Resources . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47


1
Introduction

The electrocardiogram, or ECG, is a simple diagnostic test which records


the electrical activity of the heart over a set time period via the process of
attaching a series of electrodes at particular points on a patient’s body.

Many medical students, and even some more experienced medical


professionals, struggle with ECG interpretation. If a stepwise, logical
approach is taken, interpreting the ECG should be a simple process and can
provide an immense amount of useful information, especially when used in
conjunction with a patient’s clinical presentation. The ECG is undoubtedly
one of the most useful investigations available to us in medicine.

1
2
Anatomy & Physiology

The Electrical Conduction System of the Heart

In order to be able to interpret an ECG, a basic understanding of the heart’s


electrical conduction system is required. The heart is often compared to
a pump that is made up of muscle. The pumping action of the heart is
controlled by the cardiac conduction system.

The sinoatrial node (SA node) is the pacemaker of the heart and is the point
of origin of the electrical impulses that are propagated through the heart.
The SA node is located in the right atrium and automatically generates
an electrical impulse 60-100 times per minute under normal conditions.
These electrical impulses stimulate the atria to contract and then travel
to the atrioventricular node (AV node), which is located in the inter-atrial
septum. Here the impulse is briefly slowed before continuing down the
conduction pathway to the bundle of His. The bundle of His divides in the
septum between the two ventricles into the left and right bundle branches,
which are situated in the left and right ventricular muscle respectively.
Conduction then spreads out via specialized tissue within the ventricular
walls known as Purkinje fibres.

Fig 1. The cardiac conduction system

2
Placement of Electrodes
The correct placement of electrodes is vitally important as misplacement
can result in misinterpretation and missed or incorrect diagnosis. Somewhat
confusingly a 12-lead ECG only has 10 electrodes. These 10 electrodes
allow the electrical activity of the heart to be looked at from 12 different
positions. There are 4 limb electrodes and 6 chest electrodes, and their
placement is as follows:

Chest electrodes:

• V1 – Right sternal edge, 4th intercostal space


• V2 – Left sternal edge, 4th intercostal space
• V3 – Midway between V2 and V4
• V4 – Left mid-clavicular line, 5th intercostal space
• V5 – Anterior axillary line, 5th intercostal space
• V6 – Left mid-axillary line, 5th intercostal space

Fig 2. Placement of chest electrodes.

Limb electrodes:

• LA – Left arm (between shoulder and elbow)


• RA – Right arm (between shoulder and elbow)

3
• LL – Left leg (above the ankle and below the torso)
• RL – Right leg (above the ankle and below the torso)

The lead attached to the right leg is a neutral lead and is solely present to
complete the electrical circuit. It plays no role in the formation of the ECG
itself.

Lead Groups
An ECG lead is not actually a physical lead but instead a view of the heart’s
electrical activity from a particular angle across the body. The 10 electrodes
provide 12 views, hence the term ’12-lead ECG’.

The ECG leads are grouped into two electrical planes, horizontal and
vertical. The chest leads view the heart from a horizontal plane whilst the
limb leads view the heart from a vertical plane.

The Chest Leads


There are six chest leads: V1, V2, V3, V4, V5 and V6. These are unipolar
leads as they only have one associated electrode. The positive pole is the
electrode itself and the negative pole is the centre of the heart. These leads
look at the heart in a horizontal plane from the front and left side. Leads V1
and V2 look at the right ventricle, leads V3 and V4 look at the septum and
leads V5 and V6 look at the anterior and lateral walls of the left ventricle.

The Limb Leads


The limb leads are leads AVR, AVL, AVF, I, II and III. Each of these leads
represents a measured voltage that also has a direction. By combining
the magnitude of the measured voltage and the direction of the voltage, a
vector is formed.

The limb leads AVR, AVL and AVF are also unipolar leads as they only
have one associated electrode. The voltages of these electrodes are very
small and have to be ‘augmented’ by built in amplifiers. The ‘AV’ used in

4
the terminology for these leads therefore stands for ‘Augmented Vector’.
For these leads the negative pole is once again the centre of the heart and
the three leads create a triangle with the heart in the middle. The vectors
created are shown below in figure 3:

Fig 3. Limb leads AVR, AVL and AVF.

The limb leads I, II and III are called bipolar leads because they have two
associated electrodes. AVR, AVL and AVF make up an equilateral triangle,
known as ‘Einthoven’s Triangle’.

Fig 4. Einthoven’s Triangle.

5
Information is gathered between these leads to create three more vectors:

• Lead I – information between AVR and AVL


• Lead II – information between AVR and AVF
• Lead III – information between AVL and AVF

The sum of these vectors is shown below in figure 5:

Fig 5. Limb leads I, II and III.

Finally by combining all 6 of these vectors together we create the ‘hexaxial


system’, which gives us a perspective of the view of all six of the limb leads.

Fig 6. The ‘hexaxial system’.

We will return to the concept of the ‘hexaxial system’ later when we consider
the calculation of the axis of the ECG.

6
3
Rate, Rhythm & Axis

The ECG Tracing


We have already learnt that the ECG is a simple diagnostic test that records
the electrical activity of the heart over a set time period.

The ECG machine does this by creating a trace in which voltage is plotted
on the vertical axis and time is plotted on the horizontal axis. The needle
moves across the graph paper that the ECG is recorded on and is deflected
a given distance depending upon the voltage that is measured. This tracing
is recorded on graph paper that is divided into 1 mm2 ‘small squares’ and
5 mm2 ‘large squares’.

The standard ECG paper speed is 25 mm/sec and therefore:

• 1 mm (1 ‘small square’) = 0.04 seconds


• 5 mm (1 ‘large square’) = 0.2 seconds

On the vertical axis 10 mm (10 ‘small squares’) is equal to 1 mV when


standard calibration is used.

7
Please refer to the ECG tracing below to familiarize yourself with the waves
of the ECG and how they are labeled:

Fig 7. ECG Waves

These correspond to the following events:

• P wave – atrial depolarization


• QRS complex – ventricular depolarization
• T wave – ventricular repolarisation

We will return to the concept of ECG waves in more detail in the next
chapter.

When interpreting an ECG the first three things that should be assessed
are:

1. The rate
2. The rhythm
3. The axis

8
ECG Rate
The heart rate can be calculated from the ECG using a number of different
methods and depending upon the circumstances.

In most circumstances when there is a regular rhythm the simplest way to


calculate the rate is by counting the number of ‘large squares’ between the
‘spike’ of each complex. These are the R waves and this is called the ‘R-R
interval’, this will be discussed in more detail later. By dividing 300 by this
number you will then have calculated the heart rate.

Fig 8. Calculating rate using the ‘R-R interval’.

In this case there are 5 ‘large squares’ between each R wave:

Rate = 300/5 = 60 beats per minute

If the rhythm is very fast and there is less than 1 ‘large square’ between
each R wave then an alternative method is to count the number of ‘small
squares’ between each consecutive R wave and then and then divide 1500
by this number.

9
Calculation of the rate becomes more difficult if there is an irregular rhythm,
such as in atrial fibrillation. Under these circumstances the rate can be
calculated by counting the number of complexes on the rhythm strip
provided across the bottom of the ECG and then multiplying this number
by 6. This will give the average rate over a 10 second period.

In order to interpret the rate and its relevance it is also important to know
what the rate means. In an adult the rate can be interpreted as follows:

• < 60 beats per minute = bradycardia


• 60-100 beats per minute = normal
• > 100 beats per minute = tachycardia

ECG Rhythm
The best way to assess the ECG rhythm is by inspecting the rhythm strip.
This is usually a 10 second recording from lead II.

The first thing to look at is whether or not the QRS rhythm is regular or
irregular. This can be done by inspecting the rhythm strip and looking at the
R-R interval. One approach is to place a piece of paper across the top of the
rhythm strip marking a small line next to the top of an R wave, then draw
another small line next to the top of the next R wave, and then slide the paper
along the rhythm strip. If the rhythm is regular you should see that your two
lines match the tops of the R waves throughout the entire rhythm strip.

If the rhythm is irregular the next thing to be determined is if it is regularly


irregular or irregularly irregular. An underlying regular rhythm can be made
irregular by the presence of extrasystoles (ectopic beats).

Once the regularity of the rhythm has been assessed, the QRS morphology
should be inspected. The QRS complex is less than 0.12 seconds in duration
(3 ‘small squares’) under normal circumstances. If the QRS duration is
less than this then the rhythm originates from above the bifurcation of the
bundle of His (i.e. it is ‘supraventricular’) and originates in the SA node,
atria or the AV node. If the QRS duration is greater than this, then the
rhythm is either coming from the ventricular myocardium or, alternatively,
is supraventricular with aberrant conduction.

10
Having assessed the QRS duration, the rhythm strip and ECG in general
should then be inspected carefully for the presence of atrial activity. As P
waves correspond with atrial depolarization, this can be done by looking for
the presence or absence of P waves. If there are no P waves present and
the baseline is irregular this is very suggestive of atrial fibrillation:

Fig 9. Rhythm strip demonstrating atrial fibrillation.

A ‘saw-toothed’ shaped baseline is suggestive of the flutter waves of atrial


flutter. An absence of P waves entirely is suggestive of sinoatrial arrest.

If the rhythm is regular, the QRS duration and morphology is normal, and
there is a P wave present before each QRS complex, then ‘normal sinus
rhythm’ is said to be present:

Fig 10. Rhythm strip demonstrating normal sinus rhythm.

The QRS Axis


The axis of the ECG is the average direction of the overall electrical activity
of the heart. When talking about the ECG axis, it is generally the QRS axis
that is being referred to. The QRS axis is the most important to determine
but it should be borne in mind that it is also possible to calculate the P
wave and T wave axes.

The normal QRS axis is between -30 and +90 degrees. Left axis deviation
is said to be present if the major QRS vector is between -30 and -90
degrees. Right axis deviation is said to be present if the major QRS vector

11
is between +90 and +180 degrees. If the QRS vector is between +/- 180
and -90 degrees the axis is referred to as either ‘extreme axis deviation’ or
‘indeterminate axis’.

Fig 11. The axis of the ECG.

Calculating the axis


There are several ways of calculating the QRS axis, but the most efficient
is the ‘quadrant method’.

The quadrant method works by looking at leads I and AVF. If we return


to the ‘hexaxial system’ we can see how this can be used to look at the
relationship between the QRS axis and these two leads:

Fig 12. The relationship between leads I and AVF and the QRS axis.

12
It can be seen that lead I cuts the hexaxial system in half horizontally (at
0 degrees) and lead AVF cuts the hexaxial system in half vertically (at +90
degrees). Therefore these two leads can be used to divide the hexaxial
system into four quadrants and the QRS axis can be placed in one of those
quadrants:

Interpretation Axis Quadrant Lead AVF Lead I


Normal 0 to +90 degrees Lower left Positive Positive
Possible left axis deviation 0 to -90 degrees Upper left Negative Positive
Right axis deviation +90 to 180 degrees Lower right Positive Negative
Extreme axis deviation -90 to 180 degrees Upper right Negative Negative

One limitation of this method is that the QRS axis can be up to -30 degrees into
the upper left quadrant and it still be considered as normal. When the QRS
axis is in this region (between 0 and -30 degrees) it is sometimes referred to as
physiological left axis deviation. One way around this problem is to look closely
at the QRS complex in lead II. When the QRS complex in lead II is positive the
axis is generally normal (physiological left axis deviation) but when the QRS
complex in lead II is negative there is left axis deviation present.

The QRS axis provides us with lots of useful information about the patient
and it is useful to know some causes of both left axis deviation and right
axis deviation when formulating a differential diagnosis based around the
ECG findings.

A list of a few of these causes is shown below:

Right axis deviation Left axis deviation


Right heart strain e.g. P.E. Normal (physiological axis deviation)
Right ventricular hypertrophy Left ventricular hypertrophy
Right bundle branch block Left bundle branch block
Left posterior fascicular block Left anterior fascicular block
Lateral wall myocardial infarction Inferior myocardial infarction
Wolff-Parkinson White syndrome Wolff-Parkinson-White syndrome
Ostium secundum ASD Ostium primum ASD

After calculating the rate, rhythm and axis, the next step in ECG interpretation
should be evaluation of the waves, segments and intervals.

13
4
Waves, Segments
& Intervals

Waves
As the ECG trace is recorded there are a series of upwards and downwards
deflections created that represent atrial and ventricular depolarization and
repolarization. These are known as the ECG waves.

The P wave is the first positive deflection on the ECG. It is a small smooth
contoured wave and represents atrial depolarization. Atrial repolarisation is
not visible as the amplitude is too small. The normal P wave is:

• < 120 ms in duration (3 ‘small squares’)


• < 2.5 mm in amplitude in the limb leads
• < 1.5 mm in amplitude in the chest leads
• Positive in lead II and negative in lead AVR

The second wave seen on the ECG is the QRS complex. The QRS complex
is a series of 3 deflections that represents ventricular depolarization. It
is less than 0.12 seconds in duration (3 ‘small squares’) under normal
circumstances.

By convention the first deflection in the complex, if it is negative, is called a


Q wave. A Q wave represents the normal left-to-right depolarization of the
interventricular septum. A normal Q wave is:

• < 40 ms wide (1 ‘small square’)


• < 2 mm in amplitude
• < 25% of the depth of the QRS complex

Small Q waves are usually normal, but if they exceed the normal criteria
listed above they are termed ‘pathological Q waves’ and can be indicative
of an evolving or past myocardial infarction.

14
The first positive deflection in the complex is called an R wave. This is the
largest wave in the QRS complex and represents depolarization of the thick
ventricular walls.

A negative deflection after an R wave is called an S wave. This small


wave represents depolarization of the Purkinje fibres. S waves travel in
the opposite direction to the R waves because the Purkinje fibres spread
throughout the ventricles from top to bottom and then back up though the
walls of the ventricles.

The positive deflection seen on the ECG tracing following the QRS complex
is called a T wave. T waves represent ventricular repolarization. A normal
T wave is:

• Positive in all leads except V1 and AVR


• < 5 mm in amplitude in the limb leads
• < 15 mm in amplitude in the chest leads

Fig 13. The ECG waves.

This ECG can be further divided into segments and intervals. These are
useful when assessing for certain types of pathology. It is important to
recognize that segments and intervals are different entities. Segments
should be examined to look for deviation from the isolectric line whilst
intervals should be analysed with reference to their duration.

15
Segments
The PR segment commences at the endpoint of the P wave and ends at the
start of the QRS complex. It represents the duration of the conduction of
electrical impulses from the AV node to the bundle branches and Purkinje
fibres. The PR segment is isoelectric under normal circumstances but
deviation can occur in the presence of pericarditis and atrial ischaemia.

The other major segment is the ST segment, which commences at the


end of the S wave (the J point) and ends at the beginning of the T wave.
The ST segment is also isoelectric under normal circumstances, as the
atria are relaxed and the ventricles contracted and there is therefore
no visible electrical activity. The most important causes of ST segment
deviation are myocardial ischaemia and infarction, with ischaemia causing
ST depression and infarction causing ST elevation.

The TP segment commences at the end of the T wave and ends at the
beginning of the P wave. This segment represents the isolectric line and
should always be the baseline point of reference when assessing the other
segments.

Fig 14. The ECG segments.

16
Intervals
The PR interval commences at the start of the P wave and ends at the
start of the QRS complex. It represents the time taken for the electrical
impulse to be conducted through the AV node. It is between 0.12 and
0.20 seconds (3-5 ‘small squares’) under normal circumstances. The PR
interval is prolonged (> 0.20 seconds) in the presence of 1st degree heart
block and is shortened (< 0.12 seconds) in the presence of certain pre-
excitation syndromes.

The QT interval commences at the start of the QRS complex and ends at
the endpoint of the T wave. It represents the duration of time taken for the
ventricles to depolarize and repolarize. The normal QT interval is less than
440 ms under normal circumstances and tends to be longer in women.
There are numerous causes of a prolonged QT interval, including electrolyte
disturbance (hypokalaemia, hypocalcaemia and hypomagnesaemia),
hypothermia, drugs, congenital syndromes and myocardial ischaemia.

Fig 15. The ECG segments.

17
Summary
In summary the method we suggest for interpreting an ECG is as follows:

1. Measure the rate


2. Assess the rhythm
3. Calculate the QRS axis
4. Examine the waves
5. Examine the segments
6. Measure the intervals

If these 6 steps are followed methodically most abnormalities should


become apparent and you will be very unlikely to miss any significant
pathology.

18
5
Acute Coronary
Syndromes

The term ‘acute coronary syndromes’ describes a group of clinical


conditions, all of which usually present with chest pain as a consequence
of myocardial ischaemia or infarction.

The acute coronary syndromes comprise:

• Unstable angina
• Non-ST elevation myocardial infarction
• ST elevation myocardial infarction

Unstable angina is defined by one or more of:

1. Angina of effort occurring over a few days with increasing frequency


provoked by progressively less exertion (‘crescendo angina’)
2. Episodes of angina occurring recurrently and predictably, without
specific provocation by exercise
3. An unprovoked and prolonged episode of cardiac chest pain

The ECG in unstable angina may be normal or can show T wave or ST


segment changes. The cardiac enzymes are usually normal in unstable
angina.

Non-ST elevation myocardial infarction (NSTEMI) generally presents with


typical cardiac chest pain that is sustained for greater than 20 minutes. The
ECG usually shows T wave or ST segment changes and cardiac enzymes
are usually raised.

ST elevation myocardial infarction (STEMI) generally presents with


characteristic cardiac chest pain. The ECG shows ST segment elevation
and development of Q waves and cardiac enzymes are raised.

19
Pathogenesis
These clinical syndromes form part of a spectrum of the same disease
process. In the vast majority of cases this process is initiated by the fissuring
of an atheromatous plaque in a coronary artery causing:

• Haemorrhage into the plaque causing it to swell and restrict the


lumen of the artery
• Contraction of smooth muscle within the artery wall, causing further
constriction of the lumen
• Thrombus formation on the surface of the plaque, which may
cause partial or complete obstruction of the lumen of the artery, or
distal embolism

Laboratory tests
A number of markers of cardiac damage are available. The following table
is a guide to the timing of the initial rise, peak and return to normality:

Notes Normal at Peak Initial rise Marker


CK-MB = main cardiac 2-3 days 18 hours 4-8 hours Creatine kinase
isoenzyme
Low specificity from 24 hours 6-7 hours 1-4 hours Myoglobin
skeletal muscle damage
Appears to be most 3-10 days 24 hours 3-12 Troponin I
sensitive and specific hours
= heart fatty acid binding 24 hours 5-10 hours 1.5 hours HFABP
protein
Cardiac muscle mainly 14 days 24-48 hours 10 hours LDH
contains LDH

Troponin I and T
Troponin assays are now commonly used in the diagnostic and prognostic
assessment of patients presenting with acute coronary syndromes. Troponin
I and T are sub-units of the complex that is involved in the regulation of the
calcium-mediated contractile process of cardiac muscle. Troponin I takes

20
up to 10 days to return to normal and Troponin T may take as long as 14
days.

The British Cardiac Society definition and prognosis of ACS depending on


Troponin T at 12 hours is as follows:

Troponin T < 0.01 Troponin T > 0.01 Troponin T > 1.0


and < 1.0
BCS definition ACS with unstable ACS with myocyte ACS with clinical MI
angina necrosis
30 day mortality 4.5% 10.4% 12.9%
6 month mortality 8.6% 18.7% 19.2%

The ECG Changes Associated with STEMI


The earliest ECG change associated with a STEMI is an increase in the
ventricular activation time. Infarcting myocardium is slower to conduct
electrical impulses and, as a consequence, the interval between the start
of the QRS and the apex of the R wave may be prolonged (> 0.045 s). Tall,
positive, T waves can also be seen in the hyperacute phase of a myocardial
infarction.

As the MI progresses, an upward sloping ST segment develops. The


ST segment loses its normal upward concavity, straightens, then slopes
upwards, before becoming elevated. Reciprocal ST depression may also
be seen on the ‘opposite side’ of the heart. The ST segments then start to
return to normal and T wave inversion frequently develops as this occurs.

Pathological Q waves develop, which represent significant myocardial


necrosis and replacement by scar tissue, and reflect electrically inert
necrotic myocardium.

Q waves are considered pathological if:

• > 40 ms wide (1 ‘small square’)


• > 2 mm in amplitude
• > 25% of the depth of the QRS complex

21
With time the ST segments revert to become iso-electric, unless a ventricular
aneurysm develops. The T waves gradually become positive again but the
pathological Q waves usually remain.

Figure 16. The ECG changes associated with myocardial infarction.

The ECG criteria for a STEMI are as follows:

• ≥ 2 mm of ST segment elevation in 2 contiguous precordial leads


• ≥ 1mm in other leads (2 contiguous)
• An initial Q wave or abnormal R wave develops over a period of
several hours to days.

Localization of Myocardial Infarction


Being able to localize the coronary artery implicated in a myocardial
infarction provides valuable information for the clinician. The treatment and
complications vary depending upon its location. For example, an anterior
wall infarction can result in hypotension, tachycardia, shock and in the
long term chronic heart failure can develop. By contrast, an inferior wall
infarction is often accompanied by bradycardia because of involvement
of the sinus node. The long-term effects of an inferior wall infarction are

22
usually less severe than those of an anterior wall infarction. Having a good
understanding of coronary artery anatomy is essential for being able to
localize an MI.

Coronary Artery Anatomy


The left coronary artery arises from the aorta above the left cusp of the
aortic valve. It supplies the left atrium, left ventricle, intraventricular
septum and part of the left branch bundle of His. It is larger than the right
coronary artery. It passes between the left side of the pulmonary trunk and
the left auricle and then birfucates into the left anterior descending artery
(LAD), which is also called the anterior interventricular branch, and the
left circumflex artery (LCA). Sometimes an additional artery arises at the
bifurcation called the ramus or intermediate artery.

The LAD follows the anterior interventricular groove towards the apex
of the heart and then continues to the posterior surface of the heart to
anastamose with the posterior interventricular branch.

The LCA follows the anterior interventricular groove to the left border of the
heart and then proceeds to the posterior surface. It then gives rise to the
left marginal branch, which follows the left border of the heart.

The right coronary artery arises above the right cusp of the aortic valve. It
supplies the right atrium, the SA and AV nodes and the posterior part of
the interventricular septum. It runs along the right atrioventricular groove
before branching. The right marginal artery arises first and then the right
coronary artery continues on to the posterior surface of the heart, still
running in the right atrioventricular groove. The posterior descending artery
(PDA), which is also called the posterior interventricular artery, arises next
and then follows the posterior interventricular groove towards the apex of
the heart.

23
Figure 17. Coronary artery anatomy.

The following table summarizes the vessels involved in the various different
types of myocardial infarction:

Vessel involved Location of MI ECG Leads


Left anterior descending Anteroseptal V1-V3
Left anterior descending Anterior V3-V4
Left anterior descending / left circumflex artery Anterolateral V5-V6
Left anterior descending Extensive anterior V1-V6
Left circumflex artery Lateral I, II, aVL, V6
Right coronary artery (80%) Inferior II, III, aVF
Left circumflex artery (20%)
Right coronary artery Right ventricle V1, V4R
Right coronary artery Posterior V7-V9

24
This illustrated version superimposed on an ECG should make this very
clear:

Figure 18. Localization of myocardial infarctions.

25
6
Bundle Branch Blocks

A bundle branch block is a disorder in which there is an obstruction in the


heart’s electrical conduction system. These can be broadly divided into two
different types of block:

• Left bundle branch block (LBBB) – where the obstruction is in the


left bundle branch
• Right bundle branch block (RBBB) – where the obstruction is in
the right bundle branch

Fig 19. Anatomy of left and right bundle branch blocks

Left Bundle Branch Blocks


In left bundle branch block (LBBB) the left ventricle is not directly activated
by impulses travelling through the left bundle branch. The right ventricle,
however, is still activated as normal by the right bundle branch.

26
The left ventricle is activated by impulses travelling through the myocardium
across the septum. As this occurs more slowly than conduction through
the bundle of His the QRS complex becomes widened.

Normally the septum is activated from left to right, which produces small
Q waves in the lateral leads. In the presence of LBBB, however, this septal
activation is reversed, which eliminates these normal septal Q waves.

The right to left depolarization of the myocardium produces deep S waves


in the right praecordial leads (V1-V3) and tall R waves in the lateral leads
(I, V5 and V6). It also usually causes left axis deviation. As the ventricles
are activated sequentially from right to left, rather than simultaneously, the
R wave in the lateral leads is broad and notched (‘M’ shaped).

Secondary T wave changes are a normal finding in LBBB. T wave changes


are classed as secondary if the T wave is upright when the terminal portion
of the QRS complex is negative and the T wave is inverted when the
terminal portion of the QRS complex is positive. Primary T wave changes
occur when these rules are violated and are consistent with myocardial
ischaemia.

The diagnosis of ST-elevation myocardial infarction can be made in the


presence of LBBB by using the Sgarbossa ECG algorithm.

The diagnostic criteria for LBBB are:

• Broad QRS complex (> 120 ms)


• Dominant S wave in lead V1
• Broad, monophasic R wave in lateral leads (I, AVL, V5 and V6)
• Prolonged R wave peak time > 60 ms in left praecordial leads
(V5-V6)
• Absence of Q waves in lateral leads (I, V5 and V6)

27
Fig 20. ECG example demonstrating LBBB

Right Bundle Branch Blocks


In right bundle branch block (RBBB) the right ventricle is not directly
activated by impulses travelling through the right bundle branch. The left
ventricle, however, is still activated as normal by the left bundle branch.

The right ventricle is activated by impulses travelling through the myocardium


across the septum. As this occurs more slowly than conduction through
the bundle of His, the QRS complex becomes widened.

As the left ventricle is activated normally, the early part of the QRS complex
remains unchanged. The delayed activation of the right ventricle, however,
produces a secondary R wave (R’) in the right praecordial leads, and a wide,
slurred S wave in the lateral leads. It also causes secondary repolarisation
abnormalities, with T wave inversion and ST depression being seen in the
right praecordial leads.

Secondary T wave changes are also a normal finding in RBBB. T wave


changes are classed as secondary if the T wave is upright when the terminal
portion of the QRS complex is negative and the T wave is inverted when the
terminal portion of the QRS complex is positive. Primary T wave changes

28
occur when these rules are violated and are consistent with myocardial
ischaemia.

Unlike in the presence of LBBB, the changes of ST-elevation myocardial


infarction can usually be clearly seen in RBBB.

The diagnostic criteria for RBBB are:

• Broad QRS complex (> 120 ms)


• RSR’ pattern in leads V1-V3 (‘M’ shaped QRS complex)
• Wide, slurred S wave in the lateral leads – I, AVL, V5 and V6 (‘W’
shaped QRS complex)

Fig 21. ECG example demonstrating RBBB

‘William Marrow’
A useful mnemonic for distinguishing between the ECG patterns of left
bundle branch block (LBBB) and RBBB is ‘WiLLiaM MaRRoW’:

• WiLLiaM – in LBBB there is a ‘W’ in lead V1 and an ‘M’ wave in


lead V6
• MaRRoW – in RBBB there is an ‘M’ wave in lead V1 and a ‘W’ wave
in lead V6

29
Fig 22. The characteristics of LBBB and RBBB

Causes of Bundle Branch Blocks


There are numerous potential causes of bundle branch blocks. RBBB can
be a normal finding in young, healthy people. LBBB, unlike right bundle
branch block, is almost always an indication of heart disease.

The commonest pathological causes are summarized in the table below:

Right bundle branch block Left bundle branch block


Ischaemic heart disease Ischaemic heart disease
Rheumatic heart disease Anterior myocardial infarction
Right ventricular hypertrophy Hypertension
(cor pulmonale) Aortic stenosis
Pulmonary embolus Dilated cardiomyopathy
Cardiomyopathy Primary fibrosis of the conducting system
Myocarditis (Lenegre disease)
Congenital heart disease (e.g. ASD) Hyperkalaemia
Degenerative disease of the conduction Digoxin toxicity
system

30
7
Fascicular Blocks

In the last chapter we learnt about left and right bundle branch blocks.
Left bundle branch blocks can be further sub-classified into left anterior
fascicular blocks and left posterior fascicular blocks if the obstruction is
limited to one fascicle only.

Under normal circumstances the left bundle branch consists of three


fascicles:

• The left anterior fascicle, which supplies the upper and anterior
parts of the left ventricle
• The left posterior fascicle, which supplies the posterior and infero-
posterior parts of the left ventricle, and;
• The septal fascicle, which supplies the septal wall

Left Anterior Fascicular Block


In left anterior fascicular block (LAFB) the anterior portion of the left bundle
branch is defective. In LAFB the cardiac impulses are therefore conducted
to the left ventricle via the left posterior fascicle first, which creates a delay
in the activation of the anterior and upper parts of the left ventricle.

The diagnostic criteria for LAFB are:

• Left axis deviation (axis usually between -45 and -90 degrees)
• Small Q waves with tall R waves in leads I and AVL (‘qR complexes)
• Small R waves with deep S waves in leads II, III and AVF (‘rS’
complexes)
• QRS duration normal or slightly prolonged (80-110 ms)
• Prolonged R wave peak time in AVL > 45 ms
• Increased QRS voltage in limb leads

31
Fig 23. ECG example of LAFB

Left Posterior Fascicular Block


In left posterior fascicular block (LPFB) the posterior portion of the left
bundle branch is defective. In LPFB the cardiac impulses are therefore
conducted to the left ventricle via the left anterior fascicle first, which
creates a delay in the activation of the posterior and infero-posterior parts
of the left ventricle.

The diagnostic criteria for LPFB are:

• Right axis deviation (> +90 degrees)


• Small R waves with deep S waves in leads I and AVL (‘rS’ complexes)
• Small Q waves with tall R waves in leads II, III and AVF (‘qR’
complexes)
• QRS duration normal or slightly prolonged (80-110 ms)
• Prolonged R wave peak time in AVF > 45 ms
• Increased QRS voltage in limb leads
• No evidence of right ventricular hypertrophy
• No evidence of any other cause of right axis deviation

32
Fig 24. ECG example of LPFB

Bifascicular Block
Bifascicular block is a conduction abnormality of the heart in which two of
the three main fascicles of the His-Pukinje system are blocked.

This can be either:

• Right bundle branch block and left anterior fascicular block (the
most common pattern) or;
• Right bundle branch block and left posterior fascicular block

Although it is a sign of extensive conducting system disease, the risk of


progression to complete heart block is relatively low (approximately 1%
per year)

No treatment is usually required for asymptomatic patients but a pacemaker


is recommended for those suffering syncope.

33
Fig 25. ECG example of bifascicular block (RBBB & LAFB)

Trifascicular Block
Trifascicular block is a conduction abnormality of the heart in which
two of the three main fascicles of the His-Pukinje system are blocked
in combination with a first-degree atrioventricular (AV) block. The term
‘trifascicular block’ is something of a misnomer as the AV node is not a
fascicle.

Trifascicular block can therefore be either:

• Right bundle branch block, left anterior fascicular block and first
degree AV block, or;
• Right bundle branch block, left posterior fascicular block and first
degree AV block

Trifascicular block is considered to be a precursor to complete heart block


and it is estimated that there is a 50% lifetime need for the insertion of a
permanent pacemaker in patients with trifascicular block.

34
Fig 26. ECG example of trifascicular block (RBBB, LAFB and 1st degree AV block)

35
8
Bradyarrhythmias

A bradycardia is defined as being present when the ventricular rate is less


than 60 per minute. It can be normal during sleep or in very fit athletes, or
can be pathological secondary to drug treatment (e.g. beta-blockade) or
due to problems with SA node or AV conduction.

The causes of heart block include:

• Increased vagal tone


• Inferior myocardial infarction
• Myocarditis
• Electrolyte disturbance (e.g. hyperkalaemia)
• AV nodal blocking drugs (e.g. beta-blockers, digoxin)
• Cardiac surgery
In severe cases treatment with an implantable pacemaker may be
necessary.

First-degree Heart Block


A first-degree heart block is present when the PR interval is prolonged
(greater than 0.20 seconds). It is a very common finding and represents a
delay in conduction across the atrio-ventricular junction (AV node and/or
the bundle of His).

Fig 27. First-degree heart block

36
Second-degree Heart Block
A second-degree heart block is present when some, but not all, P waves
are conducted to the ventricles, resulting in the absence of a QRS complex
after some P waves. There are two types:

• Mobitz Type I AV block


• Mobitz Type II AV block

Mobitz Type I AV Block


Mobitz type 1 AV block (also known as Wenkebach block) is a disease of the
AV node. It is characterised by a progressive prolongation of the PR interval
until, ultimately, the atrial impulse fails to conduct and a QRS complex is not
generated. The PR interval is shortest in the first beat of the cycle.

Mobitz type 1 AV block is generally considered to be a benign rhythm


that infrequently causes haemodynamic disturbance and has a low risk
of progression to complete heart block. Asymptomatic patients require
no treatment and those that are symptomatic usually respond to the
administration of atropine. Permanent pacing is rarely required.

Fig 28. Mobitz type I AV block

Mobitz Type II AV Block


Mobitz type II AV block is a disease of the His-Purkinje system below the
AV node. It is characterised by the presence of intermittent non-conducted
P waves without progressive prolongation of the PR interval. There is a
constant, often prolonged, PR interval in the conducted beats but some of
the P waves are not followed by QRS complexes. This may occur randomly,
without any constant pattern.

37
Patient with Mobitz type II AV block have an increased risk of progression
to complete heart block and asystole and frequently require treatment with
a permanent implantable pacemaker.

Fig 29. Mobitz type II AV block

Fixed Ratio Blocks


Fixed ratio blocks can be due to either Mobitz type I or Mobitz type II
atrioventricular block. It is not always easy to determine which of these is
the underlying cause of the fixed ratio block but the QRS complex provides
important clues.

Generally speaking:

• Mobitz type I conduction usually produces narrow QRS complexes


as the block is located at the level of the AV node. Mobitz type I
blocks tend to improve with atropine and have an overall more
benign prognosis.
• Mobitz type II conduction usually produces broad QRS complexes
(often in the context of a pre-existing LBBB). These tend to be
unresponsive to atropine and are more likely to progress to
complete heart block or asystole.

Fig 30. Mobitz type I 2:1 fixed ratio block

38
Third-degree Heart Block
A third-degree heart block (complete heart block) is present when there
is no relationship between the P waves and the QRS complexes. In third-
degree heart block atrial and ventricular depolarization arise completely
independently and there is a complete absence of atrioventricular
conduction. The perfusing rhythm is maintained by a junctional or
ventricular escape rhythm.

The patient typically has a severe bradycardia with independent atrial and
ventricular rates. There is a very high risk of ventricular standstill, resulting
in syncope if self-terminating, or asystole and sudden cardiac death if
prolonged. Patients with third-degree heart block require treatment with a
permanent implantable pacemaker.

Fig 31. Third-degree block

39
9
Tachyarrhythmias

A tachycardia is defined as being present when the ventricular rate is greater


than 100 per minute. A pathological tachyarrhythmia may arise from the
atrial myocardium, the AV junction, or from the ventricular myocardium.

When a tachycardia arises from tissue situated above the bundle of His,
it is described as being ‘supraventricular’. There will be narrow QRS
complexes if ventricular depolarization occurs normally, but broad QRS
complexes if a bundle branch block is also present.

When a tachycardia arises from tissue in the ventricle, below the bifurcation
of the bundle of His, it is described as being ‘ventricular’, and will always
be broad-complex.

Supraventricular Tachyarrhythmias
Broadly speaking supraventricular tachyarrhythmias can be subdivided
into several different types, including:

• Atrial fibrillation
• Atrial flutter
• Atrioventricular tachycardias

Atrial Fibrillation
Atrial fibrillation (AF) is the most common sustained arrhythmia
encountered in clinical practice. The lifetime risk over the age of 40 years
is approximately 25%.

AF is characterized by an irregularly irregular rhythm with an absence of


P waves and an isoelectric baseline on the ECG. The ventricular rate is
variable and the QRS complexes are usually narrow unless there is a co-

40
existing bundle branch block or accessory pathway. Fibrillatory waves may
be present and can be fine (amplitude < 0.5 mm), or coarse (amplitude
> 0.5 mm).

Fig 32. Atrial fibrillation

There are many potential causes of atrial fibrillation including:

• Ischaemic heart disease


• Hypertension
• Valvular heart disease
• Electrolyte disturbance (e.g. hypokalaemia)
• Thyrotoxicosis
• Drugs (e.g. sympathomimetics)
• Sepsis
• Alcohol excess

Atrial Flutter
Atrial flutter is a supraventricular tachyarrhythmia caused by a re-entry
circuit within the right atrium. Atrial activity is seen on the ECG as ‘flutter
waves’, which occur at a rate of approximately 300 per minute. These
flutter waves have a ‘saw-tooth’ appearance and are usually best seen in
the inferior leads (II, III, and aVF).

The ventricular rate is determined by the AV conduction ratio, the


commonest being a 2:1 block, which results in a ventricular rate of around
150 per minute. Higher-degree AV blocks can occur (e.g. 3:1 or 4:1 block)
and result in lower rate of ventricular conduction. A variable block may also
occur, which results in a variable rate.

Similarly to atrial fibrillation, atrial flutter is frequently caused by underlying


disease. As it originates in the right atrium it is most strongly associated

41
with pathology of the right atrium, such as COPD, pulmonary embolus, and
congenital cardiac conditions.

Fig 33. Atrial flutter with 4:1 block

Atrioventricular Tachycardia
There are two main types of atrioventricular tachycardia:

• Atrioventricular nodal re-entrant tachycardia (AVNRT)


• Atrioventricular re-entry tachycardia (AVRT).

1. Atrioventricular Nodal Re-entrant Tachycardia (AVNRT)


AVNRTs originate above the level of the bundle of His and involve a re-
entrant circuit in or around the AV node. They are the most common cause
of palpitations in patients with hearts exhibiting no structural abnormality
and are more common in women than men (~75% of cases occurring in
women). They are typically paroxysmal and may occur spontaneously or
upon provocation with alcohol, stimulants, or exercise.

The ECG typically shows a tachycardia with a rate of between 140 and 280
per minute. The QRS complexes are usually normal and P waves may be
present (immediately before or after the QRS complex), or can be hidden
within the QRS complex.

Fig 34. AV nodal re-entrant tachycardia

42
2. Atrioventricular Re-entrant Tachycardia (AVRT)
Atrioventricular re-entrant tachycardias (AVRTs) result from the presence
of two conducting pathways creating a re-entry circuit very similar to AV
nodal re-entrant tachycardia (AVNRT). A very well known example is Wolff-
Parkinson-White (WPW) syndrome.

WPW syndrome is a disorder of the electrical conducting system of the


heart. It is caused by the presence of an abnormal electrical conduction
pathway, called the bundle of Kent, between the atria and the ventricles.
This bundle of Kent acts as a pre-excitation pathway. Electrical signals
travelling down the bundle of Kent can stimulate the ventricles, causing
premature contraction. This results in the generation of the AVRT.

Fig 35. The bundle of Kent (courtesy of Tom Luck via Wikimedia commons CC 3.0)

The typical ECG features of WPW in sinus rhythm are:

• Shortened PR (< 120 ms)


• Delta wave (slurring of the initial rise in the QRS complex)
• Widening of the QRS complex (> 110 ms)

43
In addition there are two distinct recognizable types of WPW:

• Type A – the delta waves and QRS complexes are predominantly


positive in the praecordial leads with a dominant R wave in V1. The
dominant R wave in V1 can be mistaken for RBBB
• Type B – The delta wave and QRS complex are predominantly
negative in leads V1 and V2 and positive in the other praecordial
leads, resembling LBBB

Fig 36. WPW rhythm strip demonstrating shortened PR interval and delta wave

Ventricular Tachyarrhythmias
Ventricular tachycardia (VT) refers to any rhythm faster than 100 beats
per minute arising distal to the bundle of His. The rhythm may arise from
working ventricular myocardium and/or the distal conduction system. VT
is associated with increased risk of sudden death.

Monomorphic Ventricular Tachycardia


When the ventricular activation sequence is constant, the ECG pattern
remains the same, and the rhythm is called monomorphic VT.

Monomorphic VT is most commonly seen in patients with underlying


structural heart disease. There is typically a zone of slow conduction, most
commonly due to scarring and/or fibrillar disarray.

There are numerous causes of monomorphic VT, including:

• Myocardial infarction
• Cardiomyopathy
• Surgical scar

44
• Heart muscle degeneration
• Occasionally observed in patients with structurally normal hearts

Fig 37. Monomorphic VT

Polymorphic Ventricular Tachycardia


Polymorphic VT occurs when the ventricular activation sequence varies. It
can be observed with or without structural heart disease.

‘Torsades de pointes’ is a specific form of polymorphic ventricular


tachycardia that occurs in the presence of prolongation of the QT interval.
It has a very characteristic appearance in which the QRS complex appears
to twist around the isoelectric baseline.

Fig 38. Torsades de pointes

A prolonged QT interval reflects prolonged myocyte repolarisation due to


ion channel malfunction and also gives rise to early after-depolarisations
(EADs). EADs can manifest as tall U waves, which can cause premature
ventricular contractions (PVCs). Torsades de pointes is initiated when a
PVC occurs during the preceding T wave (‘R on T’ phenomenon)

It can be caused by any cause of prolongation of the QT interval:

• Myocardial infarction
• Electrolyte disturbance e.g. hypokalaemia, hypomagnesaemia and
hypocalcaemia
45
• Congenital e.g. Romano-ward syndrome and Jervell-Lange-Neilsen
syndrome
• Drugs e.g. disopyramide, amiodarone, sotalol, terfenadine

Torsades de pointes can degenerate into ventricular fibrillation and result


in sudden cardiac death.

Ventricular Fibrillation
Ventricular fibrillation (VF) is the most serious of all the disturbances of
cardiac rhythm. The electrical activity of the heart becomes completely
disordered and the ventricles contract is a rapid, unsynchronized manner.
The heart can pump little or no blood and collapse and cardiac arrest
occurs rapidly.

Fig 39. Ventricular fibrillation

46
10
Other Resources

How to Pass Medical Exams – A Survival Guide for Medical Students and
Doctors

http://howtopassmedicalexams.com

47
Evidence-Based Medicine & Statistics for Medical Exams

https://statsprep.co.uk/

48
FRCEM Exam Prep

http://frcemexamprep.co.uk

49
MRCGP Exam Prep

http://mrcgpexamprep.co.uk

50
PLAB PREP

https://www.plabprep.co.uk

51
Top 10 Tips for Passing Medical Exams

https://www.medicalexamprep.co.uk/top-10-exam-tips

52