Monday, March 2, 2015

A 50-something male with Dyspnea

A middle-aged male presented with dyspnea.  An ECG was recorded.
What is going on?  See below.























There is sinus rhythm.  There is notable ST depression in V1-V4, maximal in V2 and V3.  At first glance, it appears to be a posterior STEMI.

But one must always read ST and T-wave abnormalities in the context of the QRS.  There is a large R-wave in V1-V3.  One can see a large R-wave in posterior MI, and so one feels as if one's first impression is confirmed.

However, Right ventricular hypertrophy (RVH) also results in large right precordial R-waves and secondary ST and T-wave abnormalities that mimic ischemia.

One should always look for an S-wave in lead I.  And there it is.   There is right axis deviation.  All this is strongly suggestive of RV hypertrophy.

So a cardiac ultrasound was done:

--Pulmonary hypertension: The estimated pulmonary artery systolic pressure is 72 mmHg + RA pressure.
--Right ventricular enlargement .
--Decreased right ventricular systolic performance .
--Right atrial enlargement but the inferior vena cava is small in size.
--Left ventricular hypertrophy concentric .
--The estimated left ventricular ejection fraction is 75 %

--There is no left ventricular wall motion abnormality identified.


The patient ruled out for MI.

Also, the the workup for PE was done and was negative.  Etiology was airway disease.  McGinn (S1Q3T3) is present here but is a very soft sign of PE.  In a large group of dyspneic patients worked up for PE, those without PE had a 3% incidence of S1Q3T3 and those with PE had an incidence of 8%, for very low positive and negative predictive values.  Also, PE does not give large R-waves in right precordial leads. 


Learning Point:

1.  Abnormal ST elevation and/or depression, and/or T-wave inversion (abnormal repolarization), may be primary (due to ischemia, for instance), or these may be secondary to abnormal depolarization (an abnormal QRS, such as LVH, RVH, LBBB, RBBB, and others).

Thus, one must always closely examine the QRS to be certain that it does not harbor abnormalities that explain the repolarization abnormalities.

2.  Right ventricular hypertrophy often results in right precordial ST depression and T-wave inversion that mimics ischemia.  In particular, it mimics posterior STEMI.

17 comments:

  1. Nice post Steve, just curious about the D-dimmer lab results? McGinn-White sign also seen on this ECG. Thanks

    This ECG certainly mimics posterior wall infarction at the first glance.

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    1. Jason, the workup for PE was done and was negative. Etiology was airway disease. McGinn (S1Q3T3) is a very soft sign of PE. In a large group of dyspneic patients worked up for PE, those without PE had a 3% incidence of S1Q3T3 and those with PE had an incidence of 8%, for very low positive and negative predictive values. Also, PE does not give large R-waves in right precordial leads.

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  2. There is also a S1Q3T3 as a hint to PHT in this ECG.

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  3. nice ecg. thanks..

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  4. Is this vertical axis or RAD?

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    1. there is slightly more area under the curve of the S-wave than the R-wave (in lead I). Just barely > 90 degrees, therefore RAD.

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  5. Nice ECG thank you!But the P-waves look normal,if the pulmonary pressure is so high 72mmHg, P-wave should be pathologic.Isn't it?

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    Replies
    1. That is just not a reliable finding.

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  6. If it is airway desease,why the P-waves are normal?

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    Replies
    1. That is just not a reliable enough finding.

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  7. Dr Smith if we had run V7 V8 V9 would we still see ST elevation leading to a false positive for posterior MI?

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    1. Whether precordial ST depression shows on posterior leads depends on how well the voltage conducts from the heart to the posterior chest, which is a long distance and through the air of the lungs. This depends on 1) whether the ST depression "force" is coming from the subendocardium of the anterior wall, which is close to the overlying leads or from the epicardium of the posterior wall (Since it is due to RVH, it is coming from the subendocardium of the very anterior and hypertrophied RV), in which case it is close to the recording leads and likely to show high voltage ST shift, or if the force is coming from the subepicardium of the posterior wall, as in a posterior STEMI, in which case any anterior ST depression is more likely to show on posterior leads. Any ST depression in the anterior leads will have reciprocal ST elevation in posterior leads; the question is a matter of voltage -- how far does it have to go and how much air is between them. This is why ST elevation on posterior leads had a "criterion" of only 0.5 mm - the voltage doesn't show well. It is also why many posterior STEMI show well on the anterior leads but NOT on posterior leads. Overall, though, posterior leads are more sensitive at 0.5 mm. Complicated, no?

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  8. Thanks doc I think I understand the how the distance will affect the voltage and why a lower criteria is used for posterior elevation.

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  9. STD in Rt Precordial leads are asymmetrical- unlikely MI

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    1. Jyoti,
      Plenty of posterior MIs have this kind of ST depression.
      Steve

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