This is a 89 yo female admitted to the hospital for change in mental status. She is currently confused and not able to give a history. She came from a nursing home and has very low functional status and the family made it very clear they wanted nothing invasive done to her. The nurse you spoke to over the phone says she has been deteriorating for a few days with decrease PO intake and lethargy. She did mention that she wa having some chest discomfort yesterday but since than is more confused than anything else. She has long standing, DM, HTN, COPD, CRI, Hypothyroidism, Diverticulosis, PUD. Physical exam is essentially normal except for dry mucous membranes and some temporal wasting. Vitals are stable. Her Chest x-ray is clear and this is her EKG. What is your interpretation.

Click here for better quality Image of EKG

Starting from the beginning we can see that the rhythm strip at the bottom shows a regularly irregular pattern. Looking at all the P waves, the main driving rhythm is Sinus, with a short run of Atrial Bigeminy, ie a Premature atrial contraction after every sinus beat (beats 3, 5, 7, 9) and than returns back to Sinus rhythm. Notice the morphology of the p waves, and timing of the p waves are earlier than the fixed R-R intervals.

The next significant finding is the QRS complex. The most obvious abnormality is the wide qrs and the large R' in v1. Given that the qrs is wide, and there is a large R', and there is also a large slurred s wave in lead 1, there must be Right Bundle Branch block present. Also what goes along with that is the t wave finding in v1, being opposite that major qrs vector. However what is important to think about in this setting is the other differential of a large R in v1, that being RVH and Posterior infarction. The other differential is Lead misplacement, which is not the case here. Given the chest pain and the ST changes, posterior infarction must be considered, however what goes against this is first off, the T wave. The t wave in v1 in typical posterior infarction would be upright. Also, looking at II, III and AvF, we would expect some t wave or ST changes to suggest posterior infarction. Another strike against posterior infarction is an R', and it is highly unlikely that the posterior infarction would manifest as an R' rather than a pure R wave. So posterior infarction is out.

The other interesting finding is the size of the R', is greater than 15 mm. It is well known that in the setting of a RBBB, which is clearly present here, that diagnosing RVH is very difficult. In this case we do have a borderline Right axis and a R" greater than 15mm. A paper by Barker et al (Barker, Am Heart J 38:376,1949) stated that in the presence of Right Bundle Branch Block, if the R' is greater than 15 mm RVH is present. Going by that alone, we can say it is present. Later it was found that this was a very unreliable marker for RVH in the presence of RBBB. The other more reliable predictor of diagnosing RVH in RBBB is the initial QRS vector, i.e. the first half of it. Chou et al, (Chou, Vectorcardiography, Amsterdam, 1976 pge 21) in his paper found that the likely hood increases of RVH in the presence of RBBB if the initial vector is a right axis deviation. In our case, the initial vector is actually a normal axis. So diagnosing RVH here is really unreliable. So we can call it here, but keeping in mind that chances of a false positive is high.

The other findings that are important are the deep q waves and ST changes in v1-v3 which are consistent with a recent antero-septal myocardial infarction and in fact her troponins came back positive, however conservative management was taken and she was put on a heparin drip so the exact lesion was never found.