THE ECG IN LEFT ATRIAL HYPERTROPHY

Left atrial hypertrophy causes a double (bifid) P wave. Left atrial hypertrophy without left ventricular hypertrophy is classically due to mitral stenosis, so the bifid P wave is sometimes called ‘P mitrale’. This is misleading, because most patients whose ECGs have bifid P waves either have left ventricular hypertrophy that is not obvious on the ECG or and perhaps this is more common have a perfectly normal heart. The bifid P wave is thus not a useful measure of left atrial hypertrophy.

Figure 6.3 shows an ECG with a bifid P wave indicating left atrial hypertrophy. This was confirmed by echocardiography in the patient, who also had concentric left ventricular hypertrophy due to hypertension.

Significant mitral stenosis usually but not always leads to atrial fibrillation, in which no P waves, bifid or otherwise, can be seen. Occasional patients, such as the one whose ECG is shown in Figure 6.4, develop pulmonary hypertension and remain in sinus rhythm. There is then a combination of a bifid P wave with evidence of right ventricular hypertrophy. This combination does allow a confident diagnosis of severe mitral stenosis.

THE ECG IN LEFT VENTRICULAR HYPERTROPHY

Left ventricular hypertrophy may be caused by hypertension, aortic stenosis or incompetence, or mitral incompetence.

The ECG features of left ventricular hypertrophy are:

Left axis deviation is not uncommon, but is due more to fibrosis causing left anterior hemiblock than to the left ventricular hypertrophy itself.

The ECG is a poor guide to the severity of left ventricular hypertrophy. Numerous criteria have been proposed that claim to detect the presence of left ventricular hypertrophy from ECG measurements. Most depend on measuring R or S waves in different leads, and some take the width of QRS complexes into account. The most commonly used indicators are the Sokolow-Lyon voltage criteria. These define left ventricular hypertrophy as being present when the depth of the S wave in lead V₁ plus the height of the R wave in lead V₅ or V₆ (whichever is the greater) exceeds 35 mm, although the S wave is usually also deep in lead V₂.

Unfortunately, voltage criteria have a low sensitivity as detectors of left ventricular hypertrophy, and are essentially useless. They would frequently lead to a diagnosis of left ventricular hypertrophy in perfectly healthy young men, even in those who are not athletic ( Fig. 6.5).

The complete ECG picture of left ventricular hypertrophy is easy to recognize. The ECG in Figure 6.6 is from a patient with severe and untreated hypertension. It shows the ‘voltage criteria’ which, when combined with the T wave inversion in the lateral leads, probably are significant. In this case, the small Q waves in the lateral leads are septal and do not indicate a previous infarction. Note that the T wave inversion is most prominent in lead V₆, and becomes progressively less so in leads V₅ and V₄. This pattern of T wave inversion is sometimes referred to as ‘left ventricular strain’, but this is an old-fashioned and essentially meaningless term.

The most important cause of severe left ventricular hypertrophy is aortic valve disease: when aortic stenosis or incompetence causes left ventricular hypertrophy, aortic valve replacement must be considered. Aortic valve disease is frequently associated with left bundle branch block (LBBB) ( Fig. 6.7), which completely masks any evidence of left ventricular hypertrophy. The patient who is breathless, or who has chest pain or dizziness, and has signs of aortic valve disease and an ECG showing LBBB, needs urgent investigation.

Unfortunately, the severity of ECG changes is an unreliable guide to the importance of the underlying cardiac problem. The ECG in Figure 6.8 shows lateral T wave inversion, but does not meet the ‘voltage criteria’, in a patient with moderate aortic stenosis (aortic valve gradient 60 mmHg).

In contrast, the ECG in Figure 6.9 is from a patient with severe aortic stenosis and an aortic valve gradient of > 120 mmHg, yet it shows little to suggest severe left ventricular hypertrophy.

ECGS THAT CAN MIMIC LEFT VENTRICULAR HYPERTROPHY

The problems of differentiating between lateral T wave changes due to left ventricular hypertrophy and those due to ischaemia have been discussed in Chapter 5. The history and physical examination become extremely important, and the ECG must not be viewed in isolation. The ECG in Figure 6.10 is from a patient with chest pain that was compatible with, but not diagnostic of, angina and who had physical signs suggesting mild aortic stenosis. The T wave inversion is more prominent in leads V₄ and V₅ than in V₆, and is present in V₃. The T waves are upright in leads I and VL. These changes point to ischaemia rather than left ventricular hypertrophy, and ischaemia proved to be present in this patient.

The ECG in Figure 6.11 is from a patient with hypertension and breathlessness. He was shown to have left ventricular hypertrophy and coronary disease, but all the changes here could have been due to left ventricular hypertrophy alone.

When a breathless patient has an ECG with gross lateral T wave changes ( Fig. 6.12), hypertrophic cardiomyopathy is a possibility ( Box 6.4).

Lateral T wave changes associated with left anterior hemiblock often accompany left ventricular hypertrophy. However, there was no echocardiographic evidence of this in the patient whose ECG is shown in Figure 6.13. Here the changes must be due to conducting system disease.

Another example of a conducting tissue abnormality that could be mistaken for left ventricular hypertrophy is the Wolff-Parkinson-White (WPW) syndrome. The ECG in Figure 6.14 is from a young man with the WPW syndrome type B. There is left ventricular hypertrophy according to voltage criteria, and there is also lateral T wave inversion, but the diagnosis is made from the short PR intervals and the delta waves. The height of the QRS complexes and the T wave inversion in this situation do not indicate left ventricular hypertrophy.

THE ECG IN RIGHT ATRIAL HYPERTROPHY

Right atrial hypertrophy causes tall and peaked P waves, which are sometimes described as ‘P pulmonale’. There is, in fact, such variation within the normal range of P waves that the diagnosis of right atrial hypertrophy is difficult to make. Its presence can be inferred when peaked P waves are associated with the ECG changes of right ventricular hypertrophy. Evidence of right atrial hypertrophy without right ventricular hypertrophy will usually only be seen in patients with tricuspid stenosis ( Fig. 6.15).

The ECG in Figure 6.16 is from a patient with right atrial and right ventricular hypertrophy due to severe chronic obstructive pulmonary disease.

THE ECG IN RIGHT VENTRICULAR HYPERTROPHY

The ECG changes associated with right ventricular hypertrophy are:

In extreme cases it is easy to diagnose right ventricular hypertrophy from the ECG. The ECG in Figure 6.17 came from a patient incapacitated by breathlessness due to primary pulmonary hypertension.

As with the ECG in left ventricular hypertrophy, none of the ECG changes of right ventricular hypertrophy individually provide unequivocal evidence of right ventricular hypertrophy ( Table 6.1). Conversely, it is possible to have marked right ventricular hypertrophy without all the typical ECG features being present. Minor degrees of right axis deviation are seen in normal people, and a dominant R wave in lead V₁ is occasionally seen in normal people, although it is never more than 3 or 4 mm tall. A dominant R wave in lead V₁ may also indicate a ‘true posterior’ myocardial infarction (see Ch. 5). There may be variation in the T wave inversion in leads V₁ and V₂ in normal subjects (see Ch. 1) and, particularly in black people, the T wave can be inverted in leads V₂ and V₃.

The ECG in Figure 6.18 shows a dominant R wave in lead V₁ but no other evidence of right ventricular hypertrophy. This could indicate a posterior myocardial infarction (see Ch. 5), but this trace was from a young man who was asymptomatic, who had no abnormalities on examination, and whose echocardiogram was normal. This is a normal variant.

The ECG in Figure 6.19 is from a young woman who had become progressively more breathless since the birth of her baby 4 months previously. She had had no chest pain. No previous ECGs were available. The anterior T wave changes could be a normal variant in a black woman. T wave inversion in leads V₃-V₄ could indicate anterior ischaemia, but the important point here is that the T wave inversion is most prominent in leads Vi-V₂, and becomes progressively less in V₃-V₄. This is characteristic of T wave inversion due to right ventricular hypertrophy. In this case the T wave inversion, combined with right axis deviation and a persistent S wave in lead V₆, suggests right ventricular hypertrophy. The patient was shown to have had recurrent small pulmonary emboli.

A prominent S wave in lead V₆ is sometimes called ‘persistent’ because this lead should show a pure left ventricular type of complex with a dominant R wave and no S wave. The ‘transition point’, when the R and S waves are equal, indicates the position of the interventricular septum and this is normally under the position of lead V₃ or V₄. In the ECG in Figure 6.20 a transition point is not present at all, and lead V₆ shows a small R wave and a dominant S wave. This is due to the right ventricle underlying more of the precordium than usual. This change is characteristic of chronic lung disease.

When breathlessness is accompanied by a sudden change in rotation, a pulmonary embolus is likely. The ECG in Figure 6.21 is from a patient who had had a normal preoperative ECG but who developed breathlessness with atrial fibrillation a week after cholecystectomy. The deep S wave in lead V₆ is the pointer towards a pulmonary embolus being the cause of the atrial fibrillation.

As with the ECG in left ventricular hypertrophy, it is the appearance of changes in serial recordings that provides the best evidence of minor or moderate degrees of right ventricular hypertrophy. In the majority of cases in which the ECG suggests right ventricular hypertrophy, it is not possible to diagnose the underlying disease process with certainty.

CARDIAC RESYNCHRONIZATION THERAPY (CRT)

Patients with severe heart failure, especially those whose ECG shows left bundle branch block with a broad QRS complex, may have dyssynchronous cardiac contraction. Instead of both sides of the left ventricle contracting simultaneously in systole, there is a substantial delay between contraction of the left ventricular septum and the free wall. This reduces the stroke volume and exacerbates the heart failure. Contraction can be resynchronized by pacing the left ventricular free wall and the septum simultaneously. This is achieved by two pacing leads one placed in a branch of the coronary sinus (the venous side of the coronary circulation, which drains into the right atrium), with a second, right ventricular, lead to pace the septum. This technique, ‘cardiac resynchronization therapy’ (CRT), is also known as biventricular pacing, or simply ‘bivent’. Resynchronization improves both cardiac output and symptomatic heart failure. In addition to right ventricular and coronary sinus leads, there will usually be an atrial lead if sinus rhythm is present, because atrial systole may make an important contribution to cardiac output ( Fig. 6.22).