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Case #35

You're about to start rounds with your teaching attending. He is a cardiologist and likes to bring an EKG with him every day for you to interpret. He hands you the EKG below and says, this patient was admitted "palpitations and syncope" and this is one of the EKG's they got. He has already ruled out for myocardial infarction (enzymes negative) and never had any chest pain, diaphoresis, or shortness of breath. His only complaint was palpitations and blacking out and a large laceration on his forehead from the fall. What is your interpretation of the EKG.

Click here for Larger Image of EKG

 

So this EKG is full of findings, however we have to figure out if these are real or not. Approaching it systematically we begin with the underlying rhythm. The p wave is Up in II, III, AVF and down in AVR, the rhythm is regular and at a rate of 120's so we have Sinus Tachycardia @ 120's.

The P wave morphology is all negative in v1 and > 1mm (1 small box) so Left atrial abnormality/enlargement can be called.

The P-R interval is .08 !! At this point the first thing to think of is Ventricular Pre-excitation (WPW) but at the same time we have to be sure that the p wave we are seeing is really the one that is driving the rhythm, not a retrograde p wave or ectopic p wave causing a shorter P-R but not truly being Pre-excitation. As we said in the beginning with the rhythm, the p wave is a normal axis for sinus. So we can confidently conclude that the P-R is truly shortened to Pre-excitation So now we have in the back of our minds before we go to the QRS complex that we are thinking WPW and to look for that specific pattern.

The QRS - First there are no significant q waves. The Axis is >90 and consistent with Right axis deviation. The R wave voltage in v1 is greater than 15 mm, and there is an R'. The differential here could be RVH, Posterior infarct, RBBB, but we will get to this shortly as it is all related to the main diagnosis.

The duration of the QRS is increased @ .12 seconds and this would be consistent with WPW and RBBB. How ever because we already know there is a short p-r it would most probably be WPW. Sure enough we find the delta wave which takes us away from RBBB and towards WPW. In this case, the best place to find the "delta" waves which are present would be in v2-v5. Looking even closer you can tell that the second half of the QRS is fairly narrow and strait and it is the initial QRS forces that look slurred from the delta wave. If you look below at figure 1, the arrows are pointing to the delta waves in

Figure 1

v5. This is due to the an extra "path" to the ventricles causing the ventricle in the vicinity of the extra path to start depolarizing before it is supposed to. This depolarization starts before the impulse from the AV node reaches the ventricles, and causes the P-R interval to be shorter. Think of the QRS as really being two waves in one.

Wave 1- Sinus node -> AV node -> Bundle of His -> Perkinje fibers -> Ventricles

Wave 2- Sinus node -> accessory pathway to Left or Right Ventricle -> Ventricles (causing delta wave)

The next thing to due is to classify this as WPW type A or Type B. Type A is when the QRS vectors are all positive in the precordial leads and Type B is when it starts out positive in v1 but ends up being negative. So with this EKG we can say this is type A. Type B are mostly associated with Right sided accessory paths, and type B are usually associated with Left Sided paths. With this case representing type A, it is this Right sided path that lead's to the Right Axis and RsR' pattern. Think of it like this. In RBBB, the left is still working so the vector goes from left to right. So the same can be inferred here. With the accessory path being on the left, it starts on the left as well and moves to the right creating the R' and Right Axis. Also in the face of WPW it is very difficult to diagnose RBBB/LBBB, and RVH/LVH as the early slurring causes bizarre QRS morphologies which may lead to false negatives or false positives of all.

Next the ST- and Twave changes. There is T wave inversions in almost all the precordial leads and II, III and AvF and also ST depression in the same leads. This is concerning, but at the same time, this is VERY TYPICAL for WPW pattern. Simi lair to changed with LVH with strain, WPW can lead to the repolarization abnormalities leading to T wave and ST depression opposite to the QRS vector. Also since this patient has ruled out for infarction we can also confidently say that these changes are also secondary to WPW.