Tuesday, February 12, 2019

ST Depression and T-wave inversion in V2 and V3.

A middle aged male dialysis patient was found disorganized and paranoid.  He had no chest pain or dyspnea.

An ECG was recorded.  The clinician was worried about his ECG and showed it to me:
What do you think?

When I saw this ECG, I immediately recognized right ventricular hypertrophy as the cause of the ST depression and T-wave inversion in leads V2 and V3.   In other words, I was certain that this was a chronic finding on the ECG.  The worried clinician stated there are no old ECGs to compare with, and no records.  I remained certain that this was RVH as the findings are classic: Large R-wave in V1, large S-wave in lead I, and typical right precordial ST-T that mimic posterior STEMI.

If the QRS were normal, and the patient had chest pain, I would have said this was posterior MI, or possibly hypokalemia (see this post: Are These Wellens' Waves??).

Later, however, we found written records from an outside hospital:

EKG read:
Normal sinus rhythm
Right ventricular hypertrophy with repolarization abnormality
Nonspecific T wave abnormality
Prolonged QT
Abnormal ECG
No significant change since 05-17-18

Previous echo
Final Impressions:
1. Normal LV size, moderately increased wall thickness, normal global systolic function with an estimated EF of 60 - 65%.
2. Right ventricular cavity size is severely enlarged, global systolic RV function is severely reduced.
3. Severely enlarged right atrium.
4. Mildly enlarged left atrium.
5. Severe tricuspid regurgitation.
6. Severely increased estimated pulmonary pressures by tricuspid regurgitation velocity and right atrial pressure (96 mmHg plus RAP).
7. The inferior vena cava is dilated, respiratory size variation less than 50%, consistent with elevated right atrial pressure.

Learning Point:

Whenever there is abnormal repolarization (abnormal ST-T), look for abnormal depolarization (abnormal QRS).  This might include RVH, LVH, LBBB, RBBB, IVCD, WPW, paced rhythm and more.  If present, assess whether the ST-T abnormalities fit with the abnormal QRS.

2. Learn this pattern, as it is classic for RVH.  Here are some more cases of RVH, and/or large R-wave in V1, with ST-T abnormalities:

Young Woman with history of repaired Tetralogy of Fallot presents with chest pain

ST Depression and T-wave Inversions after ROSC from Resp and Cardiac Arrest after Head Trauma

A 50-something male with Dyspnea

Comment by KEN GRAUER, MD (2/12/2019):
Excellent case presented by Dr. Smith from the perspective of ECG teaching. For clarity — I’ve labeled the ECG in Figure-1.
Figure-1: ECG in this case — obtained from a middle-aged dialysis patient. No chest pain or dyspnea. (See text regarding labeling).
The interesting teaching points that impressed me about this case include the following:
  • How the History is of such critical importance! As per Dr. Smith — the fact that this middle-aged man had neither chest pain nor dyspnea dramatically reduced the likelihood of an acute cardiac or pulmonary event even before looking at the ECG. I would have interpreted this tracing very differently had the patient presented to an ED with severe new-onset chest pain or new dyspnea.
  • It is helpful that records from an outside hospital contained written interpretation of a prior ECG on this patient. This suggested that at least some of the findings present in ECG #1 (in Figure-1) were present previously. CAUTION: While clearly much better than nothing — in my experience, written report of ECG findings (even from a cardiologist) is NO substitute for finding an actual prior ECG in the old chart. Too-numerous-times-to-count I have found important ECG findings either undercalled or overcalled in a prior written report. The tracing in this case (in Figure-1) is complex. In my opinion, the only way to know if all findings are old is by lead-to-lead comparison with a prior ECG.
  • Availability of a previous Echo report can be an invaluable teaching tool — as well as proving to be tremendously helpful clinically in this case. Access to the previous Echo report in this case makes up for not having an actual copy of the prior ECG — because the previous Echo confirms high likelihood that ECG findings in this case are probably not new.
  • Regarding use as a teaching tool — the previous Echo showed severe RAE, severe RVH and markedly increased right-sided pressures — as well as mild LAE and moderate LV wall thickening. How well does the ECG in Figure-1 predict each of these findings? (See below).
The ECG in Figure-1 shows sinus rhythm at ~85/minute. Additional ECG findings (as well as non-findings) that I see include the following:
  • No sign of either LAE or RAE. Although the sinus P wave in lead II is a good size (RED arrow) — it is neither notched (as is common with LAE), nor tall enough or pointed enough in any of the inferior leads to qualify for RAE. The negative component to the P wave in lead V1 is neither deep enough nor wide enough to qualify for LAE. The positive component to the P wave in leads V1 and V2 is neither tall nor peaked, as may be seen with RAE.
  • No sign of LVH. The Echo showed moderately increased LV wall thickness. While sensitivity of the ECG is limited for picking up this type of LVH — I always find it insightful to correlate ECG findings with the far more accurate anatomic assessment possible in Echo evaluation.
  • Incomplete RBBB is presentI measure QRS width at between 0.09-0.10 second — which is within the normal range. A multiphasic (rsR’s’) complex is present in lead V1 (within the BLUE oval in V1) — in association with narrow terminal S waves in both leads I and V6 (within BLUE ovals in these leads). This qualifies as incomplete RBBB. It is common with either complete or incomplete RBBB to also see an rsR’ complex in right-sided lead III (as we do here). It is not common to see a 4-phase QRS complex (rsR’s’) in lead V1 due to simple complete or incomplete RBBB. That said, I still feel description of QRS morphology here best qualifies as incomplete RBBB. NOTE: Some anterior ST-T wave depression may be seen with incomplete RBBB. However, the amount of anterior ST-T wave depression seen here is clearly more than one should expect from simple incomplete RBBB.
  • ECG findings in favor of RVH in Figure-1 include — the relatively tall R’ wave in lead V1 — presence of numerous S waves on this tracing (ie, in leads I, II, aVL; and V2-through-V6) — the presence of incomplete RBBB — and, ST-T wave depression in leads V1-V3 consistent with RV “strain”. Clearly, the QRS complex is not wide enough to qualify as complete RBBB. Most of the time with incomplete RBBB — the R’ deflection in lead V1 is not nearly as tall as it is in Figure-1, unless there is also “something else” (ie, RVH).
  • ECG findings atypical for the dramatic degree of RAARVH and increased right-sided pressures indicated by Echo include: iLack of ECG findings suggestive of RAA; andiiLack of any hint of RV “strain” in the inferior leads. The 2 lead areas to look at when assessing for RV “strain”, are the inferior leads (II,III,aVF— and the anterior leads (V1,V2,V3). While true that RV “strain” will not always be seen in both of these lead areas — the fact that there is no sign at all of inferior ST-T wave depression (within the PURPLE rectanglesand, the somewhat less usual pattern of ST-T wave depression in the anterior leads (within RED rectangles, showing maximal ST-T wave depression in lead V2, despite only modest R wave amplitude in this lead) — to me suggested that the anterior ST-T wave depression might reflect acute cardiac or pulmonary disease. I’ll emphasize that the negative history for chest pain and dyspnea + dramatic abnormalities on the previous Echo strongly support supposition that the ECG findings in Figure-1 are not acute. My point is simply that I would not be at all certain of the chronicity of these findings had I just seen this ECG without benefit of the history and prior Echo report.
Our THANKS to Dr. Smith for presenting this highly insightful case.

  • For “My Take” on the ECG diagnosis of RVH  CLICK HERE.
  • For “My Take” on the ECG diagnosis of LAE & RAE  CLICK HERE.


  1. How to differentiate between incomplete RBBB and RVH with strain ?

    1. Any RBBB, whether complete or incomplete, should have a significant S-wave in V1. Here it barely goes below the isoelectric line.

    2. One cannot always distinguish between incomplete RBBB and RVH — and sometimes both conditions may coexist. RVH is often a very difficult diagnosis to make on ECG in an adult (Please see LINK I provide above under “For More Detail” at the end of My Comment). Controversy exists among experts regarding how tall the R’ wave needs to be in a patient with RBBB for one to be able to say there is “also RVH”. And while in theory complete or incomplete RBBB should manifest a neat triphasic rsR’ complex (with taller right rabbit ear) in lead V1 — complication by presence of “something else” in addition to RBBB (ie, prior infarction; scar from cardiomyopathy; another conduction defect; severe underlying pulmonary disease; etc) — may all contribute to alter appearance of the QRS in lead V1.

  2. The ST depression from RVH "strain" starts from near the baseline (the level of the end of the PR segment) and down sloping just like in this case, while the ST depression in V1-3 of posterior STEMI begins lower than the baseline and more or less horizontal, which is the up-side-down of the ST elevation of the posterior wall.
    So, the ST depression of RVH and posterior MI look different. This is a good case of RVH as described by Dr. Smith.
    K. Wang.

    1. @ Unknown — As always, a picture is worth 1,000 words — and “one size does not fit all”. There often is a “different look” between RV strain vs acute posterior MI (vs posterior MI that is less acute … ) — but MANY factors in the remaining leads may influence whether a “shape” in one or more anterior leads is more likely to be one or the other condition. In this case, in my opinion (as I wrote above) — rather than posterior MI, I would have been concerned about possible acute cardiac (ischemia) or pulmonary (acute PE) disease had I not known the history and not known results of the prior Echo. I completely accept that others may view this tracing differently.

    2. By the way, a posterior MI is often a part of infero-posterior or postero-latera MI. So helpful clues are available in the inferior or lateral leads. Rarely, it is isolated, in which case the above mentioned difference between the ST depression of RVH and posterior MI is useful.
      K. Wang.

    3. One more thing; of course if the ST depression is from RVH, there will be findings of RVH in other leads, as mentioned above by Drs Smith and Grauer, such as right axis deviation, deep S waves in leads I, aVL and lateral precordial leads. I used to say one can not think of RVH without right axis deviation (RAD). This case barely makes it. One more "by the way": In my observation, there are two kinds of RVH; one not due to COPD (such as from primary pulmonary hypertension) and one due to COPD. Both will have all the findings of RVH except the R wave behavior; the R waves are tall in V1-3 in RVH not due to COPD, while they are small or practically absent in these leads in RVH due to COPD.
      K. Wang.

    4. THANKS so much K for your excellent comments! I'll add that in my experience, I have seen cases of COPD that do manifest a predominant R wave in lead V1 — with the point being that by the time you finally see such an ECG picture, it is LATE in the course of their severe pulmonary disease, and often associated with pulmonary hypertension.


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