QRS complexes are abnormally wide in the presence of bundle branch block (see Ch. 2), or when depolarization is initiated by a focus in the ventricular muscle causing ventricular escape beats, extrasystoles or tachycardia (see Ch. 3). In each case, the increased width indicates that depolarization has spread through the ventricles by an abnormal and therefore slow pathway. The QRS complex is also wide in the Wolff-Parkinson-White syndrome (see p. 79, Ch. 3).

INCREASED HEIGHT OF THE QRS COMPLEX

An increase of muscle mass in either ventricle will lead to increased electrical activity, and to an increase in the height of the QRS complex.

Right ventricular hypertrophy

Right ventricular hypertrophy is best seen in the right ventricular leads (especially V₁. Since the left ventricle does not have its usual dominant effect on the QRS shape, the complex in lead becomes upright (i.e. the height of the R wave exceeds the depth of the S wave) – this is nearly always abnormal ( Fig. 4.3). There will also be a deep S wave in lead V₆.

Fig. 4.3 The QRS complex in right ventricular hypertrophy

Right ventricular hypertrophy is usually accompanied by right axis deviation (see Ch. 1), by a peaked P wave (right atrial hypertrophy), and in severe cases by inversion of the T waves in leads V₁ and V₂, and sometimes in lead V₃ or even V₄ ( Fig. 4.4).

Fig. 4.4 Severe right ventricular hypertrophy
Note

• Sinus rhythm, rate 63/min

• Right axis deviation (deep S waves in lead I)

• Dominant R waves in lead V₁

• Deep S waves in lead V (clockwise rotation)

• Inverted T waves in leads II, III, VF and V₁–V₃

• Flat T waves in leads V₄–V₅

Pulmonary embolism

In pulmonary embolism the ECG may show features of right ventricular hypertrophy ( Fig. 4.5), although in many cases there is nothing abnormal other than sinus tachycardia. When a pulmonary embolus is suspected, look for any of the following:

Fig. 4.5 Pulmonary embolism
Note

• Sinus rhythm, rate 75/min

• Right axis deviation

• Peaked P waves, especially in lead II

• Persistent S wave in lead V₆

• T wave inversion in leads V₁–V₄

1. Peaked P waves.

2. Right axis deviation (S waves in lead I).

3. Tall R waves in lead V₁.

4. Right bundle branch block.

5. Inverted T waves in lead V₁ (normal), spreading across to lead V₂ or V₃.

6. A shift of transition point to the left, so that the R wave equals the S wave in lead V₅ or V₆ rather than in lead V₃ or V₄ (clockwise rotation). A deep S wave will persist in lead V₆.

7. Curiously, a ‘Q’ wave in lead III resembling an inferior infarction (see below).

However, do not hesitate to treat the patient if the clinical picture suggests pulmonary embolism but the ECG does not show the classical pattern of right ventricular hypertrophy. If in doubt, treat the patient with an anticoagulant.

Left ventricular hypertrophy

Left ventricular hypertrophy causes a tall R wave (greater than 25 mm) in lead V₅ or V₆ and a deep S wave in lead V₁ or V₂ ( Fig. 4.6) – but in practice such ‘voltage’ changes alone are unhelpful in diagnosing left ventricular enlargement. With significant hypertrophy, there are also inverted T waves in leads I, VL, V₅ and V₆, and sometimes V₄, and there may be left axis deviation. It is difficult to diagnose minor degrees of left ventricular hypertrophy from the ECG.

Fig. 4.6 Left ventricular hypertrophy
Note

• Sinus rhythm, rate 83/min

• Normal axis

• Tall R waves in leads V₅–V₆ (R wave in lead V₅, 40 mm) and deep S waves in leads V₁–V₂

• Inverted T waves in leads I, VL and V₅–V₆

THE ORIGIN OF Q WAVES

Small (septal) ‘Q’ waves in the left ventricular leads result from depolarization of the septum from left to right (see Ch. 1). However, Q waves greater than one small square in width (representing 40 ms) and greater than 2 mm in depth have a quite different significance.

The ventricles are depolarized from inside outwards ( Fig. 4.7). Therefore, an electrode placed in the cavity of a ventricle would record only a Q wave, because all the depolarization waves would be moving away from it. If a myocardial infarction causes complete death of muscle from the inside surface to the outside surface of the heart, an electrical ‘window’ is created, and an electrode looking at the heart over that window will record a cavity potential – that is, a Q wave.

Fig. 4.7 The origin of Q waves

Q waves greater than one small square in width and at least 2 mm deep therefore indicate a myocardial infarction, and the leads in which the Q wave appears give some indication of the part of the heart that has been damaged. Thus, infarction of the anterior wall of the left ventricle causes a Q wave in the leads looking at the heart from the front – V₂-V₄ or V <; ( Fig. 4.8) (see Ch. 1).

Fig. 4.8 Acute anterior myocardial infarction, and probable old inferior infarction
Note

• Sinus rhythm, rate 80/min

• Normal axis

• Small Q waves in leads II, III and VF – associated with flat ST segments and inverted T waves – indicate old inferior infarction

• Small Q waves in leads V₃–V₄ – associated with raised ST segments – indicate acute anterior infarction

If the infarction involves both the anterior and lateral surfaces of the heart, a Q wave will be present in leads V₃ and V₄ and in the leads that look at the lateral surface – I, VL and V₅-V₆ ( Fig. 4.9).

Fig. 4.9 Acute anterolateral myocardial infarction and left anterior hemiblock
Note

• Sinus rhythm, rate 110/min

• Left axis deviation (dominant S waves in leads II and III)

• Q waves in leads VL and V₂–V₃

• Raised ST segments in leads I, VL and V₂–V₅

Infarctions of the inferior surface of the heart cause Q waves in the leads looking at the heart from below – III and VF ( Figs 4.8 and 4.10).

Fig. 4.10 Acute inferior infarction; lateral ischaemia
Note

• Sinus rhythm, rate 70/min

• Normal axis

• Q waves in leads III and VF

• Normal QRS complexes

• Raised ST segments in leads II, III and VF

• Inverted T waves in lead VL (abnormal) and in lead V₁ (normal)

When the posterior wall of the left ventricle is infarcted, a different pattern is seen ( Fig. 4.11). The right ventricle occupies the front of the heart anatomically, and normally depolarization of the right ventricle (moving towards the recording electrode V^ is overshadowed by depolarization of the left ventricle (moving away from Vi). The result is a dominant S wave in lead V_l. With infarction of the posterior wall of the left ventricle, depolarization of the right ventricle is less opposed by left ventricular forces, and so becomes more obvious, and a dominant R wave develops in lead V₁. The appearance of the ECG is similar to that of right ventricular hypertrophy, though the other changes of right ventricular hypertrophy (see above) do not appear.

Fig. 4.11 Posterior myocardial infarction
Note

• Sinus rhythm, rate 70/min

• Normal axis

• Dominant R waves in lead V₁

• Flattened T waves in leads I and VL

For more on myocardial infarction, see pp. 214-241

The presence of a Q wave does not give any indication of the age of an infarction, because once a Q wave has developed it is usually permanent.

ABNORMALITIES OF THE ST SEGMENT

The ST segment lies between the QRS complex and the T wave ( Fig. 4.12). It should be ‘isoelectric’ – that is, at the same level as the part between the T wave and the next P wave – but it may be elevated ( Fig. 4.13a) or depressed ( Fig. 4.13b).

Fig. 4.12 The ST segment

Fig. 4.13 (a) Elevated ST segment. (b) Depressed ST segment

Elevation of the ST segment is an indication of acute myocardial injury, usually due either to a recent infarction or to pericarditis. The leads in which the elevation occurs indicate the part of the heart that is damaged – anterior damage shows in the V leads, and inferior damage in leads III and VF (see Figs 4.8 and 4.10). Pericarditis is not usually a localized affair, and so it causes ST elevation in most leads.

Horizontal depression of the ST segment, associated with an upright T wave, is usually a sign of ischaemia as opposed to infarction. When the ECG at rest is normal, ST segment depression may appear during exercise, particularly when effort induces angina ( Fig. 4.14).

Fig. 4.14 Exercise-induced ischaemic changes
Note

• In the upper (normal) trace, the heart rate is 55/min and the ST segments are isoelectric

• In the lower trace, the heart rate is 125/min and the ST segments are horizontally depressed

Downward-sloping – as opposed to horizontally depressed – ST segments are usually due to treatment with digoxin (see p. 101).

ABNORMALITIES OF THE T WAVE

INVERSION OF THE T WAVE

The T wave is normally inverted in leads VR and V₁, sometimes in leads III and V₂, and also in lead V₃ in some black people.

T wave inversion is seen in the following circumstances:

1. Normality

2. Ischaemia

3. Ventricular hypertrophy

4. Bundle branch block

5. Digoxin treatment.

Leads adjacent to those showing inverted T waves sometimes show ‘biphasic’ T waves – initially upright and then inverted.

MYOCARDIAL INFARCTION

After a myocardial infarction, the first abnormality seen on the ECG is elevation of the ST segment ( Fig. 4.15). Subsequently, Q waves appear, and the T waves become inverted. The ST segment returns to the baseline, the whole process taking a variable time but usually within the range 24–48 h. T wave inversion is often permanent. Infarctions causing this pattern of ECG changes are called ‘ST segment elevation myocardial infarctions’ (STEMIs) (see p. 130).

Fig. 4.15 Development of inferior infarction
Note

• Three ECGs have been recorded over 24 h, and have been arranged horizontally

• Sinus rhythm with a normal cardiac axis in all three ECGs

• The first record is essentially normal 6 h after the onset of pain, the ST segments have risen in leads II, III a VF, and the ST segment is depressed in leads I, VR and VL. A Q wave has developed in lead III

• 24 h after the onset of pain, a small Q wave has appeared in lead II, and more obvious Q waves can be seen in leads III and VF. The ST segments have returned to the baseline, and the T waves are now inverted in leads III and VF

If an infarction is not full thickness and so does not cause an electrical window, there will be T wave inversion but no Q waves ( Fig. 4.16). Infarctions with this pattern of ECG change are called ‘non-ST segment elevation myocardial infarctions’ (NSTEMIs). The older term for the same pattern was ‘non-Q wave infarction’ or ‘subendocardial infarction’.

Fig. 4.16 Anterior non-ST segment elevation myocardial infarction
Note

• Sinus rhythm, rate 62/min

• Normal axis

• Normal QRS complexes

• Inverted T waves in leads V₃–V₄

• Biphasic T waves in leads V₂ and V₅

VENTRICULAR HYPERTROPHY

Left ventricular hypertrophy causes inverted T waves in leads looking at the left ventricle (I, II, VL, V₅-V₆) (see Fig. 4.6). Right ventricular hypertrophy causes T wave inversion in the leads looking at the right ventricle (T wave inversion is normal in lead V_l, and may be normal in lead V₂, but in white adults is abnormal in lead V₃) (see Fig. 4.4).