The ECG was recorded from a 35 year old man who had presented with a six month history of chest pain and lightheadedness on exertion
ECG. Rhythm: Sinus rhythm is present, all beats are conducted with a normal PR interval. The ninth complex in the rhythm strip occurs earlier than expected. The QRS complex is of the usual configuration for this patient but the P wave that precedes it is different to the others in this lead. An ectopic focus within the atria is responsible for initiating atrial contraction and gives rise to an atrial premature beat.
Morphology: The QRS duration is prolonged beyond the upper limit of normal (.10 seconds). The normal Q wave in lead V5 or V6 that represents septal depolarization is absent. There is no secondary R’ wave in VI as occurs in RBBE. These are the diagnostic features of left bundle branch block. Several other ECG changes that may occur in LBBB are seen in this ECG although they are not essential to make the diagnosis. The QRS complexes in leads facing the left ventricle (I, aVL and V6) show an M shaped pattern and there are secondary changes in the ST segments which are depressed and accompanied by T wave inversion. The initial R waves that are normally seen in the right sided precordial leads are absent in this record and the complexes in these leads are changes in these leads – the ST segments are elevated and the T waves are tall. As explained elsewhere these changes should not be interpreted to indicate ischaemia in the presence of LBBB.
Comment. In left bundle branch block activation of the left ventricle occurs from the right bundle branch. The interventricular septum is the first part of the ventricular myocardium to be activated and this occurs in the opposite direction to normal ie from right to left. Depolarization of the right ventricle now occurs- directed from left to right, and finally delayed activation of the left ventricle occurs – directed from right to left. This sequence gives rise to the notched appearance in leads facing the left ventricle – the first positive (r) deflection coming from septal activation. The negative component arises from right ventricular activation which occurs in the opposite direction and the final positive component (the R’ wave) from activation of the left ventricular free wall. The sequence might also give rise to a wide notched QS complex in leads facing the right ventricle; in practice the notch is usually small or absent.
One important practical consequence of LBBB arises from the fact that depolarization of the AV septum at the start of ventricular activation occurs in the opposite direction to normal: none of the morphological changes recorded have the same significance as when septal depolarization occurs normally. It is impossible therefore to make deductions about the presence (or absence) of ischaemia, infarction or chamber hypertrophy if the record shows LBBB.
Left bundle branch block is nearly always associated with organic heart disease. It is seen in ischaemic disease, hypertensive heart disease as well as in idiopathic conducting system disease. It is often found in restrictive, dilated and hypertrophic cardiomyopathy. The patient was shown to have the typical features of hypertrophic cardiomyopathy on echocardiography.
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