• Atrial contraction is associated with the P wave of the ECG.

• Ventricular contraction is associated with the QRS complex.

• Atrial contraction normally precedes ventricular contraction, and there is normally one atrial contraction per ventricular contraction (i.e. there should be as many P waves as there are QRS complexes).

• The P waves – can you find them? Look for the lead in which they are most obvious.

• The relationship between the P waves and the QRS complexes – there should be one P wave per QRS complex.

• The width of the QRS complexes (should be 120 ms or less).

• Because an arrhythmia should be identified from the lead in which the P waves can be seen most easily, full 12-lead ECGs are better than rhythm strips.

THE INTRINSIC RHYTHMICITY OF THE HEART

Most parts of the heart can depolarize spontaneously and rhythmically, and the rate of contraction of the ventricles will be controlled by the part of the heart that is depolarizing most frequently.

The stars in the figures in this chapter indicate the part of the heart where the activation sequence began. The SA node normally has the highest frequency of discharge. Therefore the rate of contraction of the ventricles will equal the rate of discharge of the SA node. The rate of discharge of the SA node is influenced by the vagus nerves, and also by reflexes originating in the lungs. Changes in heart rate associated with respiration are normally seen in young people, and this is called ‘sinus arrhythmia’ ( Fig. 3.1).

A slow sinus rhythm (‘sinus bradycardia’) can be associated with athletic training, fainting attacks, hypothermia or myxoedema, and is also often seen immediately after a heart attack. A fast sinus rhythm (‘sinus tachycardia’) can be associated with exercise, fear, pain, haemorrhage or thyrotoxicosis. There is no particular rate that is called ‘bradycardia’ or ‘tachycardia’ – these are merely descriptive terms.

ABNORMAL RHYTHMS

Abnormal cardiac rhythms can begin in one of three places ( Fig. 3.2): the atrial muscle; the region around the atrioventricular (AV) node (this is called ‘nodal’ or, more properly, junctional′); or the ventricular muscle. Although Figure 3.2 suggests that electrical activation might begin at specific points within the atrial and ventricular muscles, abnormal rhythms can begin anywhere within the atria or ventricles.

Sinus rhythm, atrial rhythm and junctional rhythm together constitute the ‘supraventricular’ rhythms ( Fig. 3.3). In the supraventricular rhythms, the depolarization wave spreads to the ventricles in the normal way via the His bundle and its branches ( Fig. 3.4). The QRS complex is therefore normal, and is the same whether depolarization was initiated by the SA node, the atrial muscle, or the junctional region.

In ventricular rhythms, on the other hand, the depolarization wave spreads through the ventricles by an abnormal and slower pathway, via the Purkinje fibres ( Fig. 3.5). The QRS complex is therefore wide and is abnormally shaped. Repolarization is also abnormal, so the T wave is also of abnormal shape. Remember:

Abnormal rhythms arising in the atrial muscle, the junctional region or the ventricular muscle can be categorized as:

THE BRADYCARDIAS – THE SLOW RHYTHMS

It is clearly advantageous if different parts of the heart are able to initiate the depolarization sequence, because this gives the heart a series of failsafe mechanisms that will keep it going if the SA node fails to depolarize, or if conduction of the depolarization wave is blocked. However, the protective mechanisms must normally be inactive if competition between normal and abnormal sites of spontaneous depolarization is to be avoided. This is achieved by the secondary sites having a lower intrinsic frequency of depolarization than the SA node.

The heart is controlled by whichever site is spontaneously depolarizing most frequently: normally this is the SA node, and it gives a normal heart rate of about 70/min. If the SA node fails to depolarize, control will be assumed by a focus either in the atrial muscle or in the region around the AV node (the junctional region), both of which have spontaneous depolarization frequencies of about 50/min. If these fail, or if conduction through the His bundle is blocked, a ventricular focus will take over and give a ventricular rate of about 30/min.

These slow and protective rhythms are called ‘escape rhythms’, because they occur when secondary sites for initiating depolarization escape from their normal inhibition by the more active SA node.

Escape rhythms are not primary disorders, but are the response to problems higher in the conducting pathway. They are commonly seen in the acute phase of a heart attack, when they may be associated with sinus bradycardia. It is important not to try to suppress an escape rhythm, because without it the heart might stop altogether.

EXTRASYSTOLES

Any part of the heart can depolarize earlier than it should, and the accompanying heartbeat is called an extrasystole. The term ‘ectopic’ is sometimes used to indicate that depolarization originated in an abnormal location, and the term ‘premature contraction’ means the same thing.

The ECG appearance of an extrasystole arising in the atrial muscle, the junctional or nodal region, or the ventricular muscle, is the same as that of the corresponding escape beat – the difference is that an extrasystole comes early and an escape beat comes late.

Atrial extrasystoles have abnormal P waves ( Fig. 3.11). In a junctional extrasystole there is no P wave at all, or the P wave appears immediately before or immediately after the QRS complex ( Fig. 3.11). The QRS complexes of atrial and junctional extrasystoles are, of course, the same as those of sinus rhythm.

Stay updated, free articles. Join our Telegram channel

Join