Once again, I don’t have any clinical information but how would you describe and interpret this ECG? It’s probably unreasonable for you to be expected to make a definite diagnosis but based on what you can see, what are the most likely possibilities?

The Answer

This time, for a change, we’ll start with the conclusion. This is an example of mirror-image dextrocardia, as several of you suspected, but’s it’s not an obvious, straightforward case to diagnose because in addition there is atrial fibrillation and right bundle branch block.

Dextrocardia is usually recognised electrocardiographically by all the deflections in lead I being negative and all the chest lead QRS complexes being negative with diminishing amplitude towards V6. In this case, because the rhythm is atrial fibrillation, there are no negative P waves in lead I to support a suspicion of dextrocardia. Yes, the QRS is negative in lead I but this can have a number of causes including right ventricular hypertrophy, left posterior fascicular block, swapped left arm and right arm connections and lateral myocardial infarction. When we turn to the chest leads to help us, we find that although the QRS complexes show diminishing amplitude from V2 to V6, there is not a persisting negativity; in fact, all the chest leads show predominantly positive complexes.

The complicating factor here, of course, is the right bundle branch block (RBBB). The characteristic ECG appearances in RBBB are due primarily to delayed and prolonged depolarisation of the right ventricle (RV): initially, ventricular depolarisation is normal, with left-to-right activation of the septum and rapid activation of the left ventricle, but then the ECG shows a broad terminal deflection due to RV depolarisation. In mirror-image dextrocardia, the morphological RV (the one that has a moderator band and receives deoxygenated blood which it pumps up to the lungs) is of course on the left. This means that initial septal activation takes place from right to left, producing an initial small R wave in all the chest leads, which are all to the left of the ventricles. There is then depolarisation of the rest of the LV, which of course is on the right in dextrocardia, and this produces an S wave in all the chest leads. Note that this S wave gets smaller from V1 to V6, as the chest electrodes get further and further from the morphological LV. There is then the delayed and prolonged depolarisation of the morphological RV, which proceeds towards the left, producing a broad terminal R wave from V1 to V6 that diminishes in amplitude as the chest electrodes become progressively remote from the RV.

This ECG is therefore completely consistent with mirror-image dextrocardia, and just to prove it here are two repeat recordings, one with right sided chest leads and one with swapped right arm and left oarm connections in addition to right sided chest leads.

I am very grateful to Kate Hardy, PTP student at the University of Sunderland, for sharing these ECGs with me.