THE ELECTROCARDIOGRAM (ECG)

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THE ELECTROCARDIOGRAM (ECG)

Chapter objectives

After studying this chapter you should be able to:

1. Describe how the standard 12 lead ECG is recorded.

2. Explain the origin of the various elements of the ECG trace.

3. Enumerate the basic normal values in relation to aspects of the ECG and explain the relevance of values outside these ranges.

4. Discuss how pathology impacts on the characteristic patterns of the ECG.

5. Describe the effect of certain drugs on ECG traces and their clinical significance.

Introduction

It is as important to recognize what the electrocardiogram (ECG) is not, as much as what it is. The origin of the cardiac action potential and the structure of the specialized conducting system of the heart are described in Chapter 3. The ECG is not a recording of the electrical activity of individual cells; it does not look like the action potential but reflects the activity of large numbers of cells taken en masse. It is possible to measure this activity because the heart lies in a container, the human body, which is full of a salt solution capable of carrying electrical current. Thus electrodes placed on the skin at a distance from the heart can be affected by the electrical changes within the myocardium. At rest the electrical activity of the heart dominates that of other excitable tissues such as nerve or skeletal muscle because of its relatively large mass and the coordination of its activity. A recording of the electrical activity of the heart is called an electrocardiogram. The overall net direction of the spread of excitation through the muscle mass of the left ventricle is called the cardiac axis.

It is helpful to understand the characteristics of the ECG in terms of the underlying physical process. At rest the cardiac myocytes have a resting membrane potential around −85 mV (see Chapter 2). A group of cells undergoes depolarization; the membrane potential rises to around +30 mV before repolarization. Figure 7.1 shows a schematic ‘block’ of myocardial tissue that has groups of cells in all phases of polarization. The wavefront of depolarization is moving from left to right in the diagram from an area of tissue that has just been depolarized towards tissue which is about to be depolarized. If we consider electrodes applied to the left and right of our block of tissue we see that there is an electrical potential difference between the electrodes. It is this potential difference between the tissue in front of the wave of depolarization and the tissue behind it that we measure as an ECG. The flow of current is from behind the wavefront of depolarization to in front of it and this is by convention taken as ‘positive’ and produces an upward deflection of the recorder pen.

Fig. 7.1 Origin of the ECG signal.

The heart is a complex shape with depolarization spreading simultaneously in many different directions. At any one moment in time there will however be a dominant (net) direction of the spread of depolarization. By considering the heart as a battery lying in the direction of the spread of depolarization the sequential changes in deflection of the ECG pen can be more easily understood. This is equivalent to holding the battery at various orientations (Fig. 7.2). It is important to realize that it is not the heart that is changing orientation, only the direction of the wavefront of depolarization within the heart. The shape of the ECG waveform reflects the changing distribution of polarized and depolarized tissue within the heart with time.

Fig. 7.2 Variation of ECG with orientation.

The amplitude of the ECG deflection reflects the mass of tissue involved. Thus the atrial element of the ECG (P wave) is always smaller than the ventricular element (QRS complex), even though the change in membrane potential is the same in each case. Hypertrophied ventricles, for example, resulting from hypertension, will tend to give larger deflections than the average. The amplitude of the ECG deflection is also affected by other physical factors such as size, chest inflation and fat tissue.

To summarize:

• The ECG represents the spread of depolarization and repolarization through the myocardium.

• The pattern of the ECG is dependent on the net activity of the myocardium at any given instant.

• The pattern of the ECG is dependent on the relative orientation of the heart and the electrodes.

• Many pathological factors within the myocardium such as hypertrophy and ischaemic damage affect the pattern of the ECG.

• Many extracardiac factors such as posture and chest deformity may affect the ECG.

What information can be derived from an ECG recording?

• Heart rate: an ECG recording can trigger electronic ratemeters.

• Rhythm: normal and abnormal rhythms can be recorded.

• Conduction times through components of the heart can be evaluated from the duration of the components of an ECG trace.

• The direction of the mean cardiac axis of the heart in both vertical and horizontal planes can be determined.

• The extent and location of ischaemic damage.

• The effects of altered electrolyte concentration.

• The effects of drugs which affect the conducting system (antiarrhythmic drugs, digitalis glycosides, calcium channel blockers) can be monitored.

Interesting facts

British physiologist Augustus D. Waller published the first human electrocardiogram in 1887. It was recorded with a capillary electrometer from Thomas Goswell, a technician in the laboratory. Subsequently, Waller often demonstrated his technique using his dog ‘Jimmy’ who would patiently stand with paws in glass jars of saline.

Producing a 12-lead ECG

The electrical activity of the heart was first recorded in 1887 by A.D. Waller who concluded that such recordings would not be of clinical value. Willem Einthoven made his first recordings of the ECG in 1901. Identifying differences in the ECG made Einthoven believe that this was an investigation of value. He was awarded the Nobel Prize for his work in 1924.

Case 7.1 The electrocardiogram: 1

A patient with exercise-induced angina

In Case 5.1:1 in Chapter 5, the case history of Colin Davis, a 50-year-old smoker, was described. He suffered from chest pain on exercise. He was referred to the local hospital where he was given an exercise test on a treadmill. He developed angina during the test and an ECG showed ST segment depression in the lateral leads V₄–V₆. These ST segment changes disappeared when the exercise test was terminated.

This case history raises the following questions.

1. Why does myocardial ischaemia lead to ST segment depression?

2. What do the leads showing ST segment changes tell us about the localization of ischaemia in the heart?

Answers to these questions are to be found in the text of this chapter and they are discussed in Case 7.1:2.

Recording a 12 lead ECG requires the connection of two groups of electrodes to the subject:

1. limb leads (I, II, III, aVR, aVL, aVF)

2. chest leads (generally V₁ to V₆).

The limb lead electrodes are the simplest set of electrodes and were used by Einthoven in his experiments. The basic electrode positions are on the right arm, left arm and left leg. By using the electrodes in pairs we generate sets of measurements with a specific axis or vector described as a ‘lead’. Lead I utilizes the right and left arms and the axis of measurement is from right to left directly through the chest (Fig. 7.3). Lead I is taken as 0° and angles are measured clockwise from lead I. Lead II utilizes the right arm and left leg giving an axis theoretically at +60° to lead I. Lead III utilizes the left arm and left leg giving an axis which lies at +120°. These axes are summarized in Figure 7.3. A further electrode is placed on the right leg. This is not used directly for recording but serves as a neutral reference for the other leads.

Fig. 7.3 Basic limb leads.

It is standard practice to use the wrists and ankles for the limb electrodes. This is convenient but not essential as the limbs effectively serve as ‘wires’ connected to the shoulders or hips which are the point of geometrical definition. In small children especially it is sometimes easier to use the shoulders and hips to site electrodes for leads I, II and III.

Augmented limb leads (aVR, aVL, aVF)

The augmented limb leads are produced by combining pairs of electrodes to produce ‘virtual’ electrodes which do not have direct physical existence. Thus, for example, by electronically combining the right arm and left arm electrodes we get a virtual electrode which appears to lie within the centre of the upper chest (Fig. 7.4). This virtual electrode can then be linked with the electrode on the left leg to give a new lead (aVF) with a new (vertical) axis. The complete set of augmented limb leads is produced by combining groups of three limb electrodes as shown in Table 7.1.

Table 7.1

A complete set of augmented limb leads produced by combining groups of three limb electrodes

Augmented limb lead	+ve electrode	−ve electrode
aVR	Right arm	Left arm + Left leg
aVL	Left arm	Right arm + Left leg
aVF	Left leg	Right arm + Left arm

Fig. 7.4 Combining electrodes. Adapted from Hampton 2003.

The geometry of the augmented leads is shown in Figure 7.5. The result is a new series of axes which complement the three basic limb leads. It is now possible to identify leads which come in pairs at right angles (orthogonal) to each other: lead I and aVF, lead II and aVL, lead III and aVR. This is of practical value in simplifying the analysis of the ECG (see later in this chapter).

Fig. 7.5 Augmented limb leads. Adapted from Hampton 2003.

Chest leads

The limb leads provide information about the depolarization wavefront in a coronal (vertical) plane. The chest leads give us information about the wavefront in a skewed transverse plane which approximates to the base–apex axis of the heart. The surface electrodes are applied as shown in Figure 7.6 A and as described below.

Fig. 7.6 Chest leads. (A) Position on chest. (B) Orientation in transverse plane. Adapted from Hampton 2003.

V₁: 4th intercostal space right sternal edge

V₂: 4th intercostal space left sternal edge

V₃: directly halfway between V₂ and V₄

V₄: 5th left intercostal space mid-clavicular line

V₅: anterior axillary line directly lateral to V₄

V₆: mid-axillary line directly lateral to V₄.

The limb leads are ‘combined’ electronically to create a virtual electrode over the spine. Thus leads V₁ to V₆ record the movement of the depolarization wavefront from the virtual electrode out in the direction of each of the chest electrodes as shown in Figure 7.6B.

12 lead ECG

We now have a total of 12 leads (I, II, III, aVR, aVL, aVF and V_1–6) derived from 10 electrodes. This is the standard ECG printout, an example of which is shown in Figure 7.7. Though more leads and different arrangements of presentation are possible this is the commonest form in which the ECG is presented. Note, the ‘V’ leads as described here may sometimes be shown as ‘C’ leads on a printout (see Figure 7.7).

Fig. 7.7 Standard 12-lead ECG.

The components of the ECG trace

A schematic ECG waveform recorded in lead II is shown in Figure 7.8. The standard nomenclature, P, QRS, T and U waves is arcane. Originally waveforms were labelled A, B, C and D. As the equipment developed the waveforms changed shape and needed new labels. It was decided to use the second half of the alphabet starting at O for the starting point of the recording. The next features were labelled P, Q, R, S and T respectively. The flat line which precedes the P wave is equivalent to ‘O’ but this labelling is not used.

Fig. 7.8 Elements of the ECG waveform.

The P wave represents atrial depolarization. It has a relatively low amplitude because of the low muscle mass of the atrial myocardium.

There is a variable gap between the end of the P wave and the start of the QRS complex, the P–R interval. This interval represents the time taken for the atrial depolarization to reach the ventricular myocardium (see Chapter 2). It is a period of apparent inactivity but it in fact mainly represents the time needed for depolarization of the atrioventricular node (AV node) and the bundle of His. Since only a small amount of cardiac tissue is involved and this is surrounded by other, inactive, ventricular myocardium it does not produce a measurable deflection. However this region is extremely important as many clinically significant pathologies, such as heart block, have their origins in this region of the heart and cause characteristic changes in this part of the ECG.

It is crucial to remember that one of the major functions of the AV node is to control the rate of transmission of atrial impulses to the ventricles. It can only do this if there is complete insulation of the ventricles from the atria. This is achieved because the atrioventricular valve root tissue, of which the atrioventricular junction is composed, is fibrous and electrically inactive. It thus produces a natural barrier to the passage of electrical activity from the atria to the ventricles. The weakness of this control mechanism is that the heart is vulnerable to significant functional impairment if the AV node is compromised (see discussion of heart block below) or if there are breaks in this insulation (see discussion of Wolff–Parkinson–White syndrome below).

The QRS complex reflects the stages of mass ventricular depolarization. The initial deflection is produced by the posterior–anterior depolarization of the interventricular septum. In the normal heart the next stage is the depolarization of the bulk of the left ventricular apex and free wall. The final portion of the QRS complex is produced by the depolarization of the right ventricular free wall. The width of the QRS complex reflects the rate at which the wave of depolarization travels through the ventricles. This is largely determined by the Purkinje fibres of the specialized conducting system (see Chapter 2) which act as rapid distributors of the wave of depolarization through the myocardium.

The precise pattern of the QRS complex varies between individuals but most importantly it depends on the ECG lead being examined. For example leads V₁ and V₆ examine the heart from almost opposite directions and so usually approximate to an inverted image of each other, ventricular depolarization being dominantly negative in V₁ and positive in V₆.

During the QRS phase atrial re-polarization occurs. This is a diffuse process which lacks sufficient coherence to develop a significant waveform and is usually ‘drowned out’ by the QRS complex.

A further ‘quiet’ phase occurs: the ST segment. This phase represents the period when all of the ventricular muscle has been depolarized and myocardial contraction occurs. Myocardial contraction is not complete until the end of the T wave which represents the phase of ventricular repolarization.

Interesting facts

The Dutch physiologist Einthoven started transmitting electrocardiograms in 1905 from the hospital to his laboratory 1.5 km away via telephone cables. On March 22nd the first ‘telecardiogram’ was recorded from a healthy and vigorous man and the tall R waves were attributed to his cycling from laboratory to hospital for the recording.

The T wave

Why is the T wave generally an upwards deflection if it represents repolarization? Since this is the opposite process to depolarization we might expect the T wave to be a downwards deflection if repolarization spreads in the same direction as depolarization. However the wave of depolarization is distributed by specialized conducting tissues (Purkinje fibres) which have the characteristic of rapid conduction. Repolarization is not a process which can be transmitted from cell to cell but is determined by the innate electrical characteristics of the individual cells. This has the effect that the wavefront of repolarization tends to be more diffuse and travels broadly in the opposite direction to the wave of depolarization. A wavefront of the opposite polarity travelling in the opposite direction gives a deflection in the same direction on the ECG recording. The T wave is broader than the QRS complex because the process of repolarization is more diffuse and travels less rapidly.

Other elements of the ECG

U waves represent late depolarizations of the myocardium. They are often not visible on a normal trace but where they do occur they are normal features provided they are small. However they are also associated with some pathological states such as digoxin toxicity and hypokalaemia.

Practical use of the ECG

As has been discussed the ECG tracing reflects the movement of depolarization through the myocardium. By understanding the origin of its component parts we can infer a great deal of information about the structure and function of the underlying heart. The ECG is an extremely useful tool because it is quick and easy to produce at the bedside and is non-invasive.

The standard ECG is produced with a paper speed of 25 mm/s—thus each small 1 mm square corresponds to 0.04 s.

Heart rate

For the purpose of examining rate and rhythm the standard 12 lead ECG is printed with a particularly long recording of lead II (Fig. 7.7) which is referred to as the rhythm strip. Lead II is usually selected because it is one of the leads which gives particularly clear representations of the P wave. V₁ may be used for the same reason.

The heart rate may be determined by measuring the distance between R waves in successive complexes. By multiplying the distance in millimetres by 0.04 we obtain the number of seconds between complexes which may then be divided into 60 to give the number of complexes in a minute. A simpler method is to bear in mind that if there is one large square on the ECG paper between each QRS complex this is equivalent to a rate of 300 beats per minute (bpm). By dividing 300 by the number of large squares between R waves we may obtain the rate in bpm directly. A typical resting heart rate of 75 bpm would give four large squares (20 mm) between QRS complexes.

Heart rate may vary considerably from beat to beat (beat-to-beat variation). This may result from normal physiological variation or irregularity. Cardiac monitors will usually display the heart rate in bpm averaged over a number of beats. The wise, but busy, clinician will take a pulse for at least 15 s to avoid wrongly estimating the minute rate; standard textbook teaching is to count the pulse for a whole minute. The more irregular the pulse the longer it must be recorded to achieve a representative average.

Rhythm

Rhythm, as opposed to rate, is an analysis of the regularity of heart activity. The normal state of the heart is sinus rhythm, which is usually regular although the rate may vary by a factor of four even in a healthy individual. Trained athletes may have resting heart rates in the region of 40 bpm but achieve maximum heart rates of around 180 bpm depending on physiological demand and age. The criteria used to define sinus rhythm are as follows:

• single P wave precedes every QRS complex

• P–R interval is constant and within normal range for duration

• P wave axis is normal

• P–P interval is constant.

In some individuals a marked sensitivity of the sinus node to vagal tone produces a regular variation in heart rate with respiration. The heart rate increases on inspiration. This is known as sinus arrhythmia and is illustrated in Figure 7.9. It is more common in children and tends to disappear as they get older.

Fig. 7.9 Sinus arrhythmia. (Source: Adapted from Hampton JR, 2008.)

Normal intervals on the ECG

The definition and normal ranges for various ECG intervals are shown in Figure 7.10 and Table 7.2. Most pathologies increase the length of intervals by damaging the conduction tissue. For example surgery on the right ventricle may damage the Purkinje fibres which distribute electrical activity throughout the right ventricle. This leads to delayed depolarization of the right ventricle when compared with the left ventricle. The QRS complex is slurred, with particular broadening of the latter part of the complex.

Table 7.2

Normal ranges for ECG intervals and some pathologies

Fig. 7.10 ECG intervals.

Axis

We have discussed the speed (rate) and coordination (rhythm) of electrical activity shown by the ECG. We now come to how the ECG can be used to identify the direction of travel of the wavefront of depolarization through the heart. Figure 7.2 shows how the orientation of the wavefront of depolarization with respect to the electrodes gives a different signal depending on the lead examined. Of course the heart is not a simple block of tissue but a complex tubular structure. However we can use the basic principle of Figure 7.2 to derive the following rules which allow us to define the direction of travel of depolarization;

• deflections are greatest and positive in the leads falling along the line of travel

• deflections are minimal in leads at right angles (orthogonal) to the line of travel

• the greater the amount of tissue involved the greater the deflection.

Case 7.1 The electrocardiogram: 2

Colin’s ECG changes

In Colin’s case he develops chest pain and ST segment depression in the lateral leads. The ST segment depression actually represents a failure of the TP segment to return to the isoelectric state because the underlying portion of myocardium is unable to achieve full repolarization under conditions of ischaemia. ST segment depression of over 2 mm is considered significant.

As a simple rule of thumb the leads nearest the area of ischaemic change are most affected and so indicate the underlying affected myocardium. In this case the changes are likely to reflect underperfusion of the apex and posterior wall of the left ventricle. The left ventricle is the dominant oxygen consumer of the heart and stenosis in either of the coronary systems may induce ischaemia in portions of the left ventricle, particularly under circumstances of increased demand. The more proximal the stenoses the greater the volume of myocardium affected.

Thus by examining the deflection in various leads it is possible to identify the depolarization vector, a concept which tells us in what direction the wavefront is travelling, and to some extent the amount of tissue involved. There are two main forms of the depolarization vector: instantaneous and average or mean. The difference between these two is shown in Figure 7.11A. The instantaneous vector involves measurements taken at a single point in time. From the shape of the QRS complex it can be inferred that this vector varies with the cardiac cycle. The mean vector is derived from the average deflection in a lead. Thus the mean vector gives an average over the whole of the cardiac cycle.

Fig. 7.11 Estimating the axis—instantaneous and mean.

Measuring the axis: Einthoven’s triangle

In Einthoven’s original work he used the geometry of the limb leads to construct an equilateral triangle (Fig. 7.11B). To estimate the axis of any part of the ECG we must measure the deflection in a given lead and by adding these components together in line with their respective leads we generate a vector which represents the direction of depolarization (Fig. 7.11B). By using the limb leads we assess the vertical (frontal) plane vector.

Einthoven’s triangle has confused and intimidated many generations of students. However the concept is similar to that of vectors in mathematics. A vector in any two-dimensional plane may be described by the sum of its orthogonal components (Fig. 7.11C). The fact that the three limb leads describe a triangle makes the summation more difficult. In practice the same result can be obtained from two leads at right angles. Since the three basic limb leads are not orthogonal we must use the augmented limb leads.

To identify the depolarization vector it is only necessary to use one orthogonal pair. The simplest are I and aVF as these lie parallel to what would be natural axes for any two-dimensional plane. However it is crucial to remember that aVF points down (towards the feet) and so the frontal plane vector is positive in aVF when pointing down.

The normal range for the mean frontal QRS vector is −30° to +90° in the adult. In children the normal range is taken to be 0° to +180°. The variation in childhood is discussed in Chapter 12 but reflects the greater right ventricle workload before birth. Postnatally the left ventricle comes to dominate the right and so the axis swings from right to left.

At a more practical level we can identify four quadrants into which the mean frontal plane vector will fall by assessing leads I and aVF (Fig. 7.12). The net deflection in each lead is estimated as positive (upward) or negative (downward).

Fig. 7.12 Establishing the approximate axis—which quadrant?

The +/+ quadrant is within the normal range for all ages. The −/+ quadrant is normal for children but unusual for adults. The +/− quadrant is common in adults but very unusual in children and −/− is rare at any age though may be normal in children. More simply a −ve vector in lead aVF is generally pathological unless there is evidence to the contrary.

The concept of an axis can be applied separately to all parts of the ECG waveform; P wave, QRS complex and T wave. The P wave axis is frequently overlooked in the routine ECG analysis; however, it is a useful check on the function of the sinoatrial (SA) node. Since this is at the top right hand side of the heart a sinus P wave should spread to the left and down giving a P wave which is positive in leads I and II. Occasionally a second atrial focus may take over, particularly from the region of the coronary sinus (called a low atrial rhythm). Since this lies in the floor of the right atrium the P wave tends to be inverted in leads I and II. Retrograde P waves may occur in a variety of abnormal rhythms in which electrical activity is driven from ‘below’ the atria, e.g., ‘nodal’ rhythm with increased AV node automaticity or ventricular tachycardia. So long as retrograde conduction is possible the fastest initiator will drive the atrial rate. However, P waves may be difficult to discern.

The T wave axis is seldom assessed formally. However T wave inversion is a well-recognized sign of ischaemic heart disease. This is equivalent to displacement of the T wave axis from its normal alignment with the QRS axis.

The ECG and rhythm disturbances

An example of the macroscopic type of accessory pathway is the Wolff–Parkinson–White syndrome (WPW syndrome). In WPW there is myocardial bridging of the ring of fibrous tissue which acts as an insulator at the atrioventricular junction (see Chapter 2). In sinus rhythm the ECG typically shows a short P–R interval with slurring and broadening of the initial part of the QRS complex (so called Δ wave); an example is shown in Figure 7.13. In sinus rhythm the atrial depolarization is conducted to the ventricular myocardium via the normal AV nodal route but also, simultaneously, over the accessory pathway. The apparent shortening of the P–R interval occurs because the AV node slows conduction to the ventricles as normal but the accessory pathway conducts relatively rapidly initiating ventricular depolarization early with respect to the normal conducting system. Whilst the AV node is conducting it produces no obvious deflection on the ECG but the prematurely activated myocardium does. This premature activation spreads slowly through the ventricular myocardium producing the initial slurred portion of the QRS complex. However after the normal P–R interval, activation of the ventricles occurs as usual via the conducting system. Because this normal activation is distributed rapidly throughout the conducting system it overtakes the early activation of the ventricle and so ‘normalizes’ the QRS pattern. This is a good illustration of how the ECG may reflect simultaneous but separate events and how interpreting the ECG in the light of multiple processes aids understanding of the underlying electrical activity.

Fig. 7.13 Origin of the Δ wave in Wolff–Parkinson–White syndrome. Myocardial bridging of the AV junction allows pre-excitation (pale line) to activate ventricular myocardium ahead of depolarization through the AV node (dark line). (Source: Adapted from Hampton JR, 2008.)

A further group of arrhythmias are the broad complex tachycardias. The broadening of the QRS complexes implies delayed conduction through the ventricular myocardium.

Ventricular fibrillation

Using the criteria outlined above ventricular fibrillation is associated with:

Thomas Lewis of University College Hospital, London bought a string galvanometer (invented by Einthoven) in 1909. He published a paper detailing his careful clinical and electrocardiographic observations of atrial fibrillation. Lewis identified a fibrillating horse using the string galvanometer’s electrocardiogram recording. He then followed the horse to the slaughterhouse where he could visually confirm the fibrillating atrium.

Abnormalities of conduction

Abnormalities of conduction, as opposed to rhythm, apply to pathologies of the special conducting system of the heart and include heart block and bundle branch block. The term heart block refers to conditions in which the pattern of conduction through the heart is abnormal. Heart block can be divided into two major groups; pathologies affecting the AV node and proximal bundle of His (first, second and third degree heart blocks) and pathologies affecting the distributive conducting systems (intraventricular conduction disturbance, e.g. right and left bundle branch blocks). These topics are well covered in standard texts on the clinical interpretation of the ECG and have been referred to in Chapter 2. Here we shall confine ourselves to a brief overview.

Atrioventricular conduction disturbance

First degree heart block is present when the P–R interval is greater than the normal range (Table 7.2). Since conduction through the atrium is only rarely significantly prolonged an increase in the P–R interval is usually attributable to a delay in conduction through the AV node. This is occasionally found in asymptomatic individuals with normal hearts and is not of clinical significance. However some drugs such as verapamil slow AV nodal conduction and may cause first degree block.

Second degree heart block occurs in two types. Mobitz type I is also known as the Wenckebach phenomenon in which the P–R interval increases steadily over a number of beats until a P wave occurs without being followed by a QRS complex. Again the significance of this finding is determined very much by the clinical context. Mobitz type II second degree block occurs when there are more P waves than QRS complexes but the relationship between P wave and QRS complex is fixed. The degree of block is described by the ratio of the number of P waves to each QRS complex, for example 2:1 block or 3:1 block.

Third degree or complete heart block occurs when there is no relationship between the atrial and ventricular rates. Third degree block only occurs where there is loss of conduction through the AV node or proximal bundle of His and usually reflects significant damage to the conducting system which is either iatrogenic (e.g. surgical) or pathological (e.g. infarction or infection). It is possible to recover from transient third degree heart block but frequently the individual is at risk of late recurrence, particularly if there is an associated bundle branch block. In complete heart block the ventricular rate is determined by the intrinsic rate of the ventricular muscle (see Chapter 2). In most cases the ventricular rate (30–40 bpm) is insufficient to maintain an adequate cardiac output. In this case emergency pacing is required until a permanent pacing system can be implanted. Emergency pacing may be achieved either using external pads on the chest or by placing a pacing wire into the right ventricle via the subclavian, femoral or jugular vein. Permanent pacing is achieved using a battery-powered generator connected to leads which activate the right atrium and right ventricle in synchrony. Modern pacing systems are extremely sophisticated and may even involve pacing both ventricles separately.

In congenital complete heart block the damage to the AV node occurs in utero. This is associated with a wide spectrum of outcomes from fetal death due to hydrops fetalis (fetal cardiac failure) to asymptomatic individuals who may manage many years without artificial pacing.

The term AV dissociation is frequently used as if it is synonymous with complete heart block. This term describes the condition in which there is no consistent relationship between P waves and QRS complexes. However, though the term AV dissociation includes complete heart block it also applies to conditions in which AV node conduction is intact. The crucial distinction with complete heart block is that AV dissociation occurs when the ventricular rate is greater than the atrial rate, but usually only slightly faster. This may be identified by measuring the P-P and R–R intervals and comparing them. This usually happens when damage has occurred to the sinoatrial node reducing its inherent rate. The AV node or bundle of His take over as the pacemaker and generate QRS complexes which are of normal width and morphology. The atrial rate is stable but slower than the ventricular rate.

Intraventricular conduction disturbances

The width of the QRS complex is largely determined by the time taken to distribute the wavefront of depolarization through the ventricular myocardium. The structure of the conducting system is discussed in Chapter 2. The bundle of His gives rise to left and right branches which supply the left and right ventricles respectively. These fibres follow the inner surface of their respective ventricle and so normal depolarization takes place from inside (endocardium) to outside (epicardium). The earliest ventricular myocardial activation occurs in the interventricular septum and is dominantly from left ventricle to right, producing a positive deflection in V₁ on the standard adult ECG. The depolarization of the left ventricular muscle mass proceeds next leading to a negative deflection in V₁ and positive deflection in V₆. Finally the anterior free wall of the right ventricle depolarizes producing a positive deflection in V₁ and negative deflection in V₆. When conduction is normal elements may be fused to give a single deflection which is dominated by the left ventricular components producing only a large negative deflection in V₁ and positive deflection in V₆. Figure 7.14A shows schematic patterns from V₁ and V₆.

Fig. 7.14 Bundle branch block patterns. (A) Normal. (B) Right bundle branch block. (C) Left bundle branch block.

Where damage occurs to the conducting system the distribution of activity through the ventricle is slowed and the different elements may become more obvious. The QRS complex also becomes wider as distribution throughout the ventricles takes longer.

One example of damage to the conducting system is the result of surgery on the right ventricle. Frequently this may damage the right bundle branch and leads to a typical pattern in the chest leads. Since the initial postero-anterior depolarization of the septum is enhanced the initial deflection in V₁ is positive, followed by a negative deflection arising from the depolarization of the left ventricle. However the right ventricular depolarization is delayed and so the complex is typically completed with a slurred positive deflection. This typical positive, negative, positive pattern (RSr′) in V₁ occurs with a complementary negative, positive, negative (QRS) in V₆ (Fig. 7.14B). This pattern is called right bundle branch block. It is important to note that the QRS complex is wider than normal, being especially broad in the latter part of the deflection. Partial right bundle branch block is a normal childhood variant in which the RSr′ pattern occurs without broadening of the QRS width. A typical ECG recording from V₁ is shown in Figure 7.15.

Fig. 7.15 Right bundle branch block pattern in V₁.

Damage to the anterior or posterior fascicles of the left bundle branches also gives typical ECG patterns. These are commonly seen after infarction of the respective portions of the left ventricle. Theoretically the left bundle branch is a more diffuse system consisting of multiple fibres. These have been simplified to anterior and posterior fascicles. If the left bundle is interrupted early in its course then several predictable results occur. The first is that the normal postero-anterior depolarization of the septum is reversed; followed by depolarization of the right ventricle giving a QR pattern in the anterior chest leads with a mirror image in the lateral leads (Fig. 7.14C). The late depolarization of the left ventricle gives a large terminal negative deflection in the anterior leads. This results in a broad QRS pattern in V₁ with an RSr′ in V₆.

Though bundle branch block may have little functional significance there are two key points to remember. Firstly, in general it is impossible to interpret the ECG in terms of acute ischaemic changes in the presence of bundle branch block. Secondly, very long prolongation of the QRS complex after surgery is associated with a significant risk of late fatal ventricular arrhythmias.

Cardiac structure and the ECG

The pattern of ECG complexes provides a variety of information about the structure of the heart. Right atrial hypertrophy is associated with tall, peaked P waves with an amplitude of more than 5 mm with standard ECG settings. Left atrial hypertrophy is characterized by a twin-peaked P wave known as P mitrale because this is most commonly associated with mitral stenosis.

Why is there this difference in the form of the P wave with hypertrophy of the different atria? This comes back to a complete understanding of the interaction between time and space which produces the ECG. Right atrial depolarization precedes left atrial depolarization because the sinus node lies in the right atrium. The right atrium is nearer the front of the chest and so, particularly in the anterior chest leads, produces a dominant deflection. Since the periods of depolarization overlap the P wave takes on a single hump, though in fact there are two separate events within it. If one or other waveform is changed the overall waveform is altered; if the right atrium is hypertrophied then the whole waveform becomes more peaked; if the left atrium is hypertrophied then the left atrial component of the P wave becomes more apparent and generates a second peak in the P wave, slightly later than that of the right atrial waveform. This is illustrated in Figure 7.16. This variation in P wave morphology emphasizes the complex interaction between cardiac morphology and function and the simplified tracing produced in the standard ECG.

Fig. 7.16 Interaction of right and left atrial waveforms. (A) Normal P wave. (B) Right atrial hypertrophy. (C) Left atrial hypertrophy.

As has been alluded to previously this summation of signals from different parts of the heart is important because it affects the way the ECG waveform appears and also how it changes in pathological conditions. For example, in the adult the QRS complex is dominated by the signals from the left ventricle which is much greater in mass than the right ventricle. In newborn babies this is not the case, with the right ventricle having similar mass to the left ventricle. Thus the complexes in the anterior chest leads (V₁, V₂) are very different in newborns and adults; in newborns they are dominantly positive whilst in adults they are dominantly negative (see Chapter 12). The right ventricle may be virtually ignored in interpreting the normal adult ECG.

Since the amplitude of ECG waveforms is affected by many factors, muscle mass, posture, lung volume, etc., interpreting ECG amplitudes in terms of underlying pathology is difficult. Hypertrophy of the left ventricle will tend to give increased amplitude of the S wave in V₁ and the R wave in V₆. This is essentially the same signal seen from the opposite direction. This may be increased in patients with severe hypertension or aortic stenosis where the workload of the left ventricle is significantly increased. Hypertrophic cardiomyopathy will also increase the amplitude of these voltages. The mean frontal QRS vector may also be skewed to the left by the excess signal from the left ventricle, though it is unusual for it to fall outside the normal range.

Interesting facts

In 1906, Einthoven published the first organized presentation of normal and abnormal electrocardiograms recorded with a string galvanometer. Left and right ventricular hypertrophy, left and right atrial hypertrophy, the U wave (for the first time), notching of the QRS, ventricular premature beats, ventricular bigeminy, atrial flutter and complete heart block were all described.

Ischaemia and the ECG

One of the common uses of the ECG is in acute assessment of chest pain. This may be caused by the restriction of blood flow to the myocardium, either reversible—angina pectoris—or irreversible—myocardial infarction. These two conditions produce rather different changes in the ECG which can be understood by considering the underlying processes.

Reversible ischaemia

Returning to the concept of the battery (see p. 72) the degree of deflection of the ECG signal is a function of the potential difference between the ends of the battery and the orientation of the battery with respect to the electrodes. Generally the maximum potential difference occurs when one end of the battery is fully depolarized (+30 mV) and the other is fully polarized (−85 mV) giving a total voltage of around 115 mV. If both ends of the battery are depolarized or both ends are polarized then there will be no potential difference and no net deflection. This is the condition which gives the isoelectric line on the ECG, i.e. zero displacement of the trace. Between the T and the Q wave the ventricular muscle cells are polarized. During the ST segment the ventricle is depolarized. The heart is in different states of polarization but the appearance of the ECG, a flat line, is the same.

During ischaemia, maintenance of the myocardium in its fully polarized state is compromised as it requires substantial ATP generation to maintain ionic gradients (see Chapter 1). Thus for portions of the myocardium the resting potential is not as negative as normal. This means that in the fully polarized state there can be a current between different parts of the myocardium. However, because the depolarized state is less energy demanding, as entry of Na⁺ and Ca⁺⁺ ions are passive processes down concentration gradients, it is still possible for all myocardial cells to depolarize fully. The T–Q isoelectric line is displaced upwards by the residual flow of current between fully and partially polarized myocardium but during ventricular depolarization this is abolished. The ST segment alone therefore appears to be displaced.

Case 7.1 The electrocardiogram: 3

Unwelcome developments

Colin subsequently suffered a myocardial infarction (Chapter 5, Case 5.1:3). What are the specific ECG changes which are associated with myocardial infarction and how do they progress over time?

Initially downward curving ST segment elevation reflecting an area of myocardium that is no longer electrically active. T wave inversion occurs next. This may be seen as a deviation of the T wave axis away from tissue which no longer takes part in the repolarization process.

The appearance of Q waves is the last change which takes place in the ECG and is the change which remains longest. Q waves reflect the complete loss of myocardium in one portion of the left ventricle wall resulting in a signal being recorded which is actually from the opposite wall of the ventricle. Q waves greater than 3 mm are likely to be pathological. Q waves are frequently permanent as the myocardial tissue, once killed, cannot regenerate.

Infarction

Complete loss of blood supply to the myocardium produces a typical sequence of changes. Initially there is ST segment elevation over the area which undergoes infarction. Some 24–48 hours later T wave inversion occurs along with the development of Q waves (deep negative deflections in the leads closest to the area of infarction). The specific leads involved give an indication of the location and extent of the injury.

Q waves may be understood in the context of complete loss of electrically active tissue. Since, for practical purposes, the right ventricle may be ignored in the adult because the muscle mass is swamped by that of the left ventricle the ECG can be viewed as examining the left ventricle from the outside. The conducting tissue is located on the endocardial surface of the left ventricle and thus depolarization takes place from inside to outside (Fig. 7.17). Where a portion of the ventricle is damaged and becomes fibrosed, i.e. electrically inert then it becomes electrically ‘transparent’ forming an electrical ‘window’. Thus rather than producing a positive deflection as the near wall of the ventricle depolarizes from inside to outside, a negative deflection is produced as the lead records the activity in the opposite wall of the ventricle.

Fig. 7.17 Origin of Q waves on the ECG.

The change in the T wave reflects the overall change in the pattern of repolarization. This may be seen as a deviation of the T wave axis away from the region of infarction which now has a lower muscle mass analogous to the swing of the QRS axis towards areas of greater muscle mass.

Interesting facts

Cremer (1906) recorded the first oesophageal electrocardiogram which he achieved with the help of a professional sword swallower. Oesophageal electrocardiography later developed in the 1970s to help differentiate atrial arrhythmias. He also recorded the first fetal electrocardiogram from the abdominal surface of a pregnant woman.

Potassium and the ECG

Considering that potassium fluxes are so key to the membrane potential of myocardial cells (see Chapter 2), it is not surprising that the ECG may be altered by changes in plasma [K⁺].

With hypokalaemia the dominant effect is flattening of the T wave and may include ST segment depression and the development of prominent U waves. ECG changes associated with hypokalaemia are not clinically significant nor do they have any particular prognostic significance. An ECG may be considered a useful adjunct but is no substitute for monitoring of plasma [K⁺]. Hypokalaemia promotes the pro-arrhythmic effect of digoxin which acts to block the pumped inflow of K⁺ in exchange for Na⁺ (see Chapters 2 and 4).

As one might expect the effect of hyperkalaemia on the ECG is the opposite of hypokalaemia. The earliest feature is tall, peaked T waves. Higher levels of potassium produce P wave flattening, P-R elongation and eventually slurring of the QRS complex may occur. At high concentrations of potassium the differentiation of QRS and T wave may disappear as the ECG becomes sinusoidal in nature before sliding into ventricular fibrillation.

Case 7.1 The electrocardiogram: 4

An overweight patient with hypertension

In Case 10.1:1 in Chapter 10 the case history of 45-year-old John Ames is described. During an insurance medical he is found to be both obese and hypertensive. How might these two factors affect his ECG?

Increasing body size tends to reduce ECG voltages, particularly in the chest leads as they are most affected by distance from the heart. Hyperinflation of the chest, such as occurs in emphysema, may also reduce chest lead voltages. Conversely slim people may have large voltages in the chest leads even with a normal heart.

Chronic hypertension increases the workload of the heart and leads to left ventricular hypertrophy. The increased muscle mass generates greater ECG deflections. Various criteria are used for diagnosing left ventricular hypertrophy. The simplest is that the sum of the S wave in V₁ and R wave in V₆ are >40 mm with standard gain settings.

ECG monitoring in hyperkalaemia is clinically useful and indeed essential. The first evidence of hyperkalaemia may be sudden and refractory ventricular fibrillation even if there is little in the way of symptoms. For this reason continuous ECG monitoring is mandatory during IV infusions of potassium salts.