THE NORMAL CARDIAC RHYTHM

Sinus rhythm is the only normal sustained rhythm. In young people the R-R interval is reduced (i.e. the heartrate is increased) during inspiration, and this is called sinus arrhythmia ( Fig. 1.1). When sinus arrhythmia is marked, it may mimic an atrial arrhythmia. However, in sinus arrhythmia each P-QRS-T complex is normal, and it is only the interval between them that changes.

Sinus arrhythmia becomes less marked with increasing age of the subject, and is lost in conditions such as diabetic autonomic neuropathy due to impairment of the vagus nerve function.

THE HEART RATE

There is no such thing as a normal heart rate, and the terms ‘tachycardia’ and ‘bradycardia’ should be used with care. There is no point at which a high heart rate in sinus rhythm has to be called ‘sinus tachycardia’ and there is no upper limit for ‘sinus bradycardia’. Nevertheless, unexpectedly fast or slow rates do need an explanation.

EXTRASYSTOLES

Supraventricular extrasystoles, either atrial or junctional (AV nodal), occur commonly in normal people and are of no significance. Atrial extrasystoles ( Fig. 1.4) have an abnormal P wave; in junctional extra-systoles either there is no P wave or the P wave may follow the QRS complex.

Ventricular extrasystoles are also commonly seen in normal ECGs ( Fig. 1.5).

In healthy people, normal sinus rhythm may be replaced by what are, in effect, repeated atrial extra-systoles. This is sometimes called an ‘ectopic atrial rhythm’ and it is of no particular significance ( Fig. 1.6).

THE P WAVE

In sinus rhythm, the P wave is normally upright in all leads except VR. When the QRS complex is predominantly downward in lead VL, the P wave may also be inverted ( Fig. 1.7).

In patients with dextrocardia the P wave is inverted in lead I ( Fig. 1.8). In practice this is more often seen if the limb leads have been wrongly attached, but dextrocardia can be recognized if leads V₅ and V₆, which normally ‘look at’ the left ventricle, show a predominantly downward QRS complex.

If the ECG of a patient with dextrocardia is repeated with the limb leads reversed, and the chest leads are placed on the right side of the chest instead of the left, in corresponding positions, the ECG becomes like that of a normal patient ( Fig. 1.9).

A notched or bifid P wave is the hallmark of left atrial hypertrophy, and peaked P waves indicate right atrial hypertrophy – but bifid or peaked P waves can also be seen with normal hearts ( Fig. 1.10).

THE PR INTERVAL

In sinus rhythm, the PR interval is constant and its normal range is 120-200 ms (3-5 small squares of ECG paper) ( Fig. 1.11). In atrial extrasystoles, or ectopic atrial rhythms, the PR interval may be short, and a PR interval of less than 120 ms suggests pre-excitation.

A PR interval of longer than 220 ms may be due to first degree block, but the ECGs of healthy individuals, especially athletes, may have PR intervals of slightly longer than 220 ms – which can be ignored in the absence of any other indication of heart disease.

PR interval ‘abnormalities’ will be discussed further in the context of normal people in Chapter 2.

THE QRS COMPLE

THE ST SEGMENT

The ST segment (the part of the ECG between the S wave and the T wave) should be horizontal and ‘isoelectric’, which means that it should be at the same level as the baseline of the record between the end of the T wave and the next P wave. However, in the chest leads the ST segment often slopes upwards and is not easy to define ( Fig. 1.29).

An elevation of the ST segment is the hallmark of an acute myocardial infarction (see Ch. 5), and depression of the ST segment can indicate ischaemia or the effect of digoxin. However, it is perfectly normal for the ST segment to be elevated following an S wave in leads V₂-V₅. This is sometimes called a ‘high take-off ST segment’. The ECGs in Figures 1.30 and 1.31 were recorded from perfectly healthy young men.

The ST segment is apparently raised when there is ‘early repolarization’, which causes the ST segment to be arched, and is usually only seen in the anterior leads, not the limb leads (see Fig. 1.39).

Box 1.3 shows the possible causes of ST segment elevation, other than myocardial infarction.

ST segment depression is measured relative to the baseline (between the T and P waves), 60-80 ms after the ‘J’ point, which is the point of inflection at the junction of the S wave and the ST segment. Minor depression of the ST segment is not uncommon in normal people, and is then called ‘nonspecific’; theadvantage of using this word is that it leaves the way open for a later change of diagnosis. ST segment depression in lead III but not VF is likely to be nonspecific ( Fig. 1.32). Nonspecific ST segment depression should not be more than 2 mm ( Fig. 1.33), and the segment often slopes upwards. Horizontal ST segment depression of more than 2 mm indicates ischaemia (see Ch. 5).

THE T WAVE

In a normal ECG the T wave is always inverted in lead VR, and often in lead V₁, but is usually upright in all the other leads ( Fig. 1.34).

The T wave is also often inverted in lead III but not VF. However, its inversion in lead III may be reversed on deep inspiration ( Figs 1.35 and 1.36).

T wave inversion in lead VL as well as in VR can be normal, particularly if the P wave in lead VL is inverted. The ECG in Figure 1.37 was recorded from a completely healthy young woman.

T wave inversion in leads V₂-V₃ as well as in V₁ occurs in pulmonary embolism and in right ventricular hypertrophy (see Chs 5 and 6) but it can be a normal variant. This is particularly true in black people. The ECG in Figure 1.38 was recorded from a healthy young white man, and that shown in Figure 1.39 from a young black professional footballer. The ECG in Figure 1.40 was recorded from a middle-aged black woman with rather nonspecific chest pain, whose coronary arteries and left ventricle were shown to be entirely normal on catheterization.

Box 1.4 summarizes the situations in which T wave inversion is seen.

Generalized flattening of the T waves with a normal QT interval is best described as ‘nonspecific’. In a patient without symptoms and whose heart is clinically normal, the finding has little prognostic significance. This was the case with the patient whose ECG is shown in Figure 1.41. In patients with symptoms suggestive of cardiovascular disease, however, such an ECG would require further investigation.

Peaked T waves are one of the features of hyper-kalaemia, but they can also be very prominent in healthy people ( Fig. 1.42). Tall and peaked T waves are sometimes seen in the early stages of a myocardial infarction, when they are described as ‘hyperacute’. They are, however, an extremely unreliable sign of infarction.

The T wave is the most variable part of the ECG. It may become inverted in some leads simply by hyperventilation associated with anxiety.

An extra hump on the end of the T wave, a ‘U’ wave, is characteristic of hypokalemia. However, U waves are commonly seen in the anterior chest leads of normal ECGs ( Fig. 1.43), where they can be remarkably prominent ( Fig. 1.44). It is thought that they represent repolarization of the papillary muscles. A U wave is probably only important if it follows a flat T wave.

THE QT INTERVAL

The QT interval (from the Q wave to the end of the T wave) varies with the heart rate, gender and time of day. There are several different ways of correcting the QT interval for heart rate, but the simplest is Bazett’s formula. In this, the corrected QT interval (QT_C) is calculated by:

An alternative is Fridericia’s correction, in which QT_C is the QT interval divided by the cube root of the R-R interval. It is uncertain which of the corrections is clinically more important.

The upper limit of the normal QT_C interval is longer in women than in men, and increases with age. Its precise limit is uncertain, but is usually taken (following Bazett’s correction) as 450 ms for adult men and 470 ms for adult women.

THE ECG IN ATHLETES

Any of the normal variations discussed above can be found in athletes. There can be changes in rhythm and/or ECG pattern, and the ECGs of athletes mayalso show some features that might be considered abnormal in non-athletic subjects, but are normal in athletes (see Box 1.5). Figure 1.45 shows the short and varying PR interval of an ‘accelerated idionodal rhythm’ (also known as a ‘wandering atrial pacemaker’). Here the sinus node rate has slowed, and the heart rate is controlled by the AV node, which is discharging faster than the SA node.

The ECGs in Figures 1.45, 1.46 and 1.47 were all recorded during the screening examinations of healthy young footballers.

THE ECG IN PREGNANCY

Minor changes in the ECG are commonly seen in pregnancy (see Box 1.6). Ventricular extrasystoles are almost universal.

THE ECG IN CHILDREN

The normal heart rate in the first year of life is 140-160/min, falling slowly to about 80/min by puberty. Sinus arrhythmia is usually quite marked in children.

At birth, the muscle of the right ventricle is as thick as that of the left ventricle. The ECG of a normal child in the first year of life has a pattern that would indicate right ventricular hypertrophy in an adult. The ECG in Figure 1.48 was recorded from a normal 1-month-old child.

The changes suggestive of right ventricular hypertrophy disappear during the first few years of life. All the features other than the inverted T waves in leads V₁ and V₂ should have disappeared by the age of 2 years, and the adult ECG pattern should have developed by the age of 10 years. In general, if the infant ECG pattern persists beyond the age of 2 years, then right ventricular hypertrophy is indeed present. If the normal adult pattern is present in the first year of life, then left ventricular hypertrophy is present.

The ECG changes associated with childhood are summarized in Box 1.7.

FREQUENCY OF ECG ABNORMALITIES IN HEALTHY PEOPLE

The ECG findings we have discussed so far can all be considered to be within the normal range. Certain findings are undoubtedly abnormal as far as the ECG is concerned, yet do occur in apparently healthy people.

The frequency with which abnormalities are detected depends on the population studied: most abnormalities are found least often in healthy young people recruited to the armed services, and become progressively more common in populations of increasing age. An exception to this rule is that frequent ventricular extrasystoles are very common in pregnancy. The frequency of right and left bundle branch block has been found to be 0.3% and 0.1% respectively in populations of young recruits to the services, but in older working populations these abnormalities have been detected in 2% and 0.7% respectively of apparently healthy people.

1. Does the ECG really come from that individual? If so, is he or she really asymptomatic and are the findings of the physical examination really normal?

2. Is the ECG really abnormal or is it within the normal range?

3. If the ECG is indeed abnormal, what are the implications for the patient?

4. What further investigations are needed?

THE RANGE OF NORMALITY

Normal variations in the P waves, QRS complexes and T waves have been described in detail. T wave changes usually give the most trouble in terms of ECG interpretation, because changes in repolarization occur in many different circumstances, and in any individual, and variations in T wave morphology can occur from day to day.

Box 1.8 lists some of the ECG patterns that can be accepted as normal in healthy patients, and some that must be regarded with suspicion.

THE PROGNOSIS OF PATIENTS WITH AN ABNORMAL ECG

In general, the prognosis is related to the patient’s clinical history and to the findings on physical examination, rather than to the ECG. An abnormal ECG is much more significant in a patient with symptoms and signs of heart disease than it is in a truly healthy subject. In the absence of any other evidence of heart disease, the prognosis of an individual with one of the more common ECG abnormalities is as follows.

FURTHER INVESTIGATIONS

Complex and expensive investigations are seldom justified in asymptomatic patients whose hearts are clinically normal, but who have been found to have an abnormal ECG.

An echocardiogram should be recorded in all patients with bundle branch block, to assess the size and function of the individual heart chambers. Patients with LBBB may have a dilated cardiomyopathy, and the echocardiogram will then show a dilated left ventricle which contracts poorly. Alternatively they may have ischaemia, and the echocardiogram will show some segments of the left ventricle failing to contract or contracting poorly. Patients with LBBB may also have unsuspected aortic stenosis. Patients with RBBB may have an atrial septal defect or pulmonary hypertension, but quite frequently the echocardiogram shows no abnormality.

Echocardiography may be helpful in establishing the cause of T wave inversion, which might be due to ischaemia, ventricular hypertrophy or cardiomyopathy.

Patients with frequent ventricular extrasystoles seldom need detailed investigation, but if there is any question of underlying heart disease an echocardiogram may help to exclude the possibility of a cardiomyopathy. It is also worth checking their blood haemoglobin level.

In patients with atrial fibrillation, an echocardiogram is useful for defining or excluding structural abnormalities, and for studying left ventricular function. An echocardiogram is indicated if there is anything that might suggest rheumatic heart disease. Since atrial fibrillation can be the only manifestation of thyrotoxicosis, thyroid function must be checked. Atrial fibrillation may also be the result of alcoholism, and this may be denied by the patient, so it may be fair to check liver function.

Table 1.1 shows investigations that should be considered in the case of various cardiac rhythms and indicates which underlying diseases may be present.

TREATMENT OF ASYMPTOMATIC ECG ABNORMALITIES

It is always the patient who should be treated, not the ECG. The prognosis of patients with complete heart block is improved by permanent pacing, but that of patients with other degrees of block is not. Ventricular extrasystoles should not be treated because of the risk of the pro-arrhythmic effects of antiarrhythmic drugs. Atrial fibrillation need not be treated if the ventricular rate is reasonable, but anticoagulation must be considered in all cases. In the case of patients with valve disease and atrial fibrillation, however, anticoagulant treatment is essential.