Fig. 36.2 ECG from Eisenmenger syndrome due to a ventricular septal defect (VSD). Sinus rhythm, dramatic evidence of right atrial enlargement (best seen in lead V1 as a tall early peak to the P wave). Normal PR interval. QRS axis deviated to the right (look for the iso-electric standard lead – where the R wave = the S wave. aVR is the closest, so the axis is at right angles to this, either –60° or +120°. Inspection of lead III and aVF shows it must go towards lead III and away from lead aVL, i.e. +120°). The QRS complex in lead V1 shows a rsR′ pattern, i.e. a late and very large R wave i.e. a ‘dominant’ R wave (i.e. R wave > S wave). The right axis deviation with dominant R wave in lead V1 are fairly pathognomonic of right ventricular hypertrophy (RVH). There are inverted T’s in V1–3, ‘repolarization changes’ or in old terminology ‘RV strain’.

Fig. 36.3 Congenital heart disease. (a) Atrial septal defect; oxygenated blood returning from the lungs to the left atrium crosses over into the right atrium, increasing the work of the right ventricle, and pulmonary blood flow. (b) Patent ductus arteriosus. Oxygenated blood is passed from the aorta into the pulmonary circulation, increasing blood flow through the lungs and left ventricle. (c) Tetralogy of Fallot. Pulmonary stenosis prevents blood easily entering the lungs, and a ventricular septal defect allows blood to shunt right-to-left, causing cyanosis. (d) Transposition of the great arteries. The systemic and pulmonary circuits are separate, unless there is persistence of the foramen ovale, ductus arteriosus, or a more complex shunting lesion.

Congenital heart disease (CHD) is an increasing common condition in adults. The common forms are:

Bicuspid aortic valve

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