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.