Abstract
The electrocardiogram (ECG) represents a summation of electrical activity in the heart, derived from extracellular electrode recordings obtained from the body surface. Although a detailed description of ECG analysis for detecting cardiac pathology is beyond the scope of this book, this chapter provides a simplified outline of the electrical basis of the normal ECG.
The electrocardiogram (ECG) represents a summation of electrical activity in the heart, derived from extracellular electrode recordings obtained from the body surface. Although a detailed description of ECG analysis for detecting cardiac pathology is beyond the scope of this book, this chapter provides a simplified outline of the electrical basis of the normal ECG.
Describe the normal ECG
The normal ECG, as recorded using lead II, is shown in Figure 58.1. Heart rate (HR) may be calculated from the ECG most simply by dividing 300 by the number of large squares between adjacent QRS complexes. For example, if there are five large squares between adjacent QRS complexes, the HR is 60 bpm (note: this shortcut is only valid for regular heart rhythms and standard UK paper speeds).
The P wave represents atrial depolarisation. The smaller muscle mass of the atria compared with the ventricles results in the P wave having a smaller amplitude than the QRS complex. The duration of the P wave is normally <100 ms, or <2.5 ‘small squares’.1 P waves are absent in atrial fibrillation, where there is uncoordinated atrial depolarisation. In mitral stenosis, left atrial hypertrophy results in a larger, and sometimes bifid, P wave.
The PR interval is the time between the onset of atrial and ventricular depolarisation, which represents atrioventricular (AV) nodal delay. It is conventionally measured as time from the beginning of the P wave to the beginning of the Q wave rather than the R wave. The normal PR interval is 0.12–0.2 s; that is, three to five small squares. First-degree AV nodal block is characterised by a prolonged PR interval, whilst the δ-wave of Wolff–Parkinson–White syndrome characteristically shortens the PR interval.
The QRS complex represents ventricular depolarisation and its propagation. The normal QRS complex is <0.12 s; that is, three small squares. A widened QRS complex may occur in a bundle branch block – a conduction defect in either the right or left bundle branches. Pathological Q waves may result from a pulmonary embolus, which classically gives an S1Q3T3 pattern, or a previous myocardial infarction. Pathological Q waves have a duration >40 ms (one small square) or an amplitude ≥25% of the subsequent R wave.
The ST segment is the isoelectric segment that follows the QRS complex. The ST segment corresponds to the plateau phase of the cardiac action potential. Myocardial ischaemia or infarction may cause the ST segment to become depressed or elevated respectively.
The T wave represents the wave of ventricular repolarisation. Repolarisation of cardiac myocytes is not nearly as rapid as depolarisation; the T wave is therefore wider than the QRS complex. Inverted T waves may be caused by ventricular ischaemia.
The QT interval is the time from the onset of ventricular depolarisation to the completion of ventricular repolarisation. The QT interval therefore represents the duration of the cardiac action potential. As discussed in Chapter 57, the duration of the cardiac action potential shortens with increasing HR. The QT interval is therefore routinely ‘corrected’ (QTc) for HR using an algorithm, the most popular of which is Bazett’s formula (QT interval divided by the square root of the R–R interval, the time between consecutive R waves). Normal QTc is <0.44 s; that is, 11 small squares. A prolonged QTc interval is associated with a propensity to ventricular tachyarrhythmias.
Figure 58.1 The normal ECG.
How does cardiac electrophysiological activity generate ECG signals?
The ECG signals are generated from the changing electrical fields around the heart as the cardiac myocytes undergo a coordinated depolarisation, followed by a coordinated repolarisation:
The exterior of the normal resting membrane is positive relative to the interior (see Chapter 51).
When an action potential is triggered, the exterior of the membrane becomes negative relative to the interior (see Chapter 52).
Following the action potential, the cell membrane returns to its resting state, where its exterior is positive relative to its interior.
Each time the cell membrane changes polarity, local currents are generated.
An ‘observer’ watching this process take place from a vantage point outside the cell would see a ‘waveform of depolarisation’ sweep over the cell membrane, switching the polarity of charge from positive to negative, followed by a ‘waveform of repolarisation’, switching the polarity of the membrane back to positive (Figure 58.2).
