Severe Right Ventricular Hypertrophy

This 23 year old presented to the Emergency Department with pharyngitis, but also complained of dyspnea on exertion. This ECG was recorded:

The wide complex (QRS 155 ms) may distract your attention from the rhythm, which is simply sinus. There are massive S-waves in lateral leads, with an extreme right axis deviation (180 or -180, same thing). There are massive R' waves of RBBB in the right precordial leads. The combination of wide S-wave in V5 and V6, and large R' wave in lead V1 is diagnostic of RBBB. The precordial voltage is extreme, approximately 60 mm (6.0 mV) in V1.

So this is diagnostic of massive Right ventricular hypertrophy. One might be concerned for ischemia because of the large amount of ST depression and T wave inversion in V1-V3. Some discordant (in the opposite direction of a high voltage or bundle branch block QRS) ST depression and T inversion is usually found at baseline in RBBB, but this is more than usual. However, the voltage is also more than usual. The ratio of the ST depression to QRS voltage is about 4mm to 60 mm, or 0.067, which is normal. The troponin was mildly elevated due to demand ischemia of the RV.

Further history revealed congenital pulmonic stenosis which was dilated at age 7 days. The patient did not have further followup. Echocardiogram revealed an estimated peak systolic pulmonary pressure of 127 mmHg with RV enlargement and severe hypertrophy.

Comment on Posterior STEMI

I had a very good question regarding the post on posterior STEMI, and I wanted to be sure that the answer gets attention:

smallville said...

While your blog does an excellent job of highlighting posterior STEMIs that were mistaken, are there any solid criteria to help provide a DDx between anterior or subendocardial ischemia and posterior STEMI? Will posterior ST alteration always be limited to v2-v4?


This is a very good question, and not easily answered because there is very little solid research on this.

First, you should know that when there is precordial ST depression due to subendocardial ischemia, it is not necessarily due to anterior wall ischemia. Data from stress testing shows that subendocardial ischemia DOES NOT LOCALIZE on the ECG, and usually is in leads II, III, aVF and V4-V6. But, again, this does not tell you which artery is involved.

Second, ST depression in V1-V3, vs. V4-V6, is much more likely to be posterior than subendocardial ischemia.

Third, patients at higher risk of NSTEMI (older, more risk factors, h/o angiogram with multivessel disease) are much more likely to have subendocardial disease (vs., for instance, a younger smoker).

Fourth, patients with reasons to have demand ischemia (tachycardia, sepsis, GI Bleed, etc.) are much more likely to have subendocardial ischemia (like in a stress test); those with posterior MI are much more likely to present with onset of chest pain and with normal vital signs.

Fifth, look for tall R-waves in V1-V3 (the analog of Q-waves in other locations).

Sixth, an upright T-wave is much more likely to represent posterior MI, but probably signifies reperfusion of the artery rather than persistent occlusion. An inverted T-wave can be either subendocardial or posterior.

Seventh, placement of posterior leads is very helpful. Take leads V4-V6 and place them at the level of the tip of the scapula, with V4 placed at the posterior axillary line ("V7"), V6 at paraspinal area ("V9"), and V5 ("V8") between them. At lease 0.5 mm of ST elevation in 2 consecutive leads is very accurate for posterior MI.

References on posterior leads:

1) Matetzky S et al. Acute myocardial infarction with isolated ST-segment elevation in posterio chest leads V7-V9: "hidden" ST -segment elevation revealing acute posterior infarction. JACC 1999;34:748-53
2) Matetzky S et al. Significance of ST segment elevations in posterior chest leads (V7-V9) in patients with acute inferior myocardial infarction: application for thrombolytic therapy. JACC 1998;31 506-11.
3) Wung SF et al. New electrocardiographic criteria for posterior wall acute myocardial ischemia validated by a percutaneous transluminal coronary angioplasty model of acute myocardial infarction. Am J Cardiol 2001;87:970-4; A4.

Altered Mental Status, Tachycardia, Hypotension, Hyperglycemia, Ill appearing

This diabetic patient with the ECG below was brought in by medics confused, tachycardic, and hyperglycemic, Kussmauling. The computerized ECG algorithm diagnosed Acute MI (I'm not sure why).

The ECG is diagnostic of hyperkalemia, with QRS of 180 ms. The QRS improved immediately after giving 2 doses of Calcium gluconate. K returned at 7.3, with a pH of 6.91, HCO3 of less than 3. After a total of 5 doses of Ca gluconate, 6 doses of bicarb, 4 liters of fluid, and insulin, this patient with extremely severe diabetic ketoacidosis stabilized. He had some demand ischemia, with maximum troponin of 1.5, but there was no acute coronary syndrome.

His ECG from the next AM is shown below; the QRS is now less than 120 ms.

Left Ventricular Hypertrophy May Result in Profound ST Elevation

This 75 year old man presented with weakness. His blood pressure was 220/80. He was found to have renal failure. He ruled out for MI.

There are 4 mm of ST elevation in leads V2 and V3, but it not out of proportion to the very large (greater than 50 mm) preceding S-wave. This is typical of severe LVH with repolarization abnormalities.

It would be an unusual EKG for anterior STEMI.

In fact, it is very difficult to find a case of anterior MI with extreme voltage like this; this is probably because profound ischemia of LAD occlusion (STEMI) alters the QRS voltage and attenuates the severity of the electrocardiographic LVH voltage.

If anyone out there has such a case (proven LAD occlusion with very large voltage suggestive of LVH), please send it to me!