Monday, February 29, 2016

Nausea and Vomiting, Again. This ECG is loaded with information.

A middle-aged diabetic dialysis patient presented with 24 hours of nausea and vomiting associated with ~6 pound weight loss.  Patient stated his dry weight is around 85 kg.  The emesis is nonbloody and nonbilious.  He did have one episode of diarrhea.  He denied fevers and chills, abdominal pain, chest pain, or SOB.  Has been able to intermittently tolerate PO intake.  He is worried that he may be dehydrated.  He did not finish his dialysis run today.
Someone thought this was slow VT with a "northwest" axis (towards aVR, or -135 degrees), but there are definite P-waves (with a long PR interval).  
P-waves are best seen (as always) in II and V1, biphasic in V1 (as always).

The QRS duration is 150 ms, with a large R-wave in V1 and a wide negative QRS in lateral leads.  
Thus there is RBBB

There appears to also be right ventricular hypertrophy, as the R' wave in V1 is greater than 15 mm.

Besides the above, what is your diagnosis?

This ECG was texted to me with no clinical information, and I texted back:

"RBBB with RVH and inferior-posterior-lateral subacute MI.  Duration of symptoms is greater than 12 hours.  First troponin I will be high, maybe 60 ng/mL (60,000 ng/L)" (See short discussion below of the relation of troponin to infarct size)

Why did I think there was any acute MI, and why subacute?   (Why did I think the symptoms were prolonged)?

Answer: There are well-formed Q-waves in inferior and lateral leads.  In RBBB, V5 and V6 usually have a narrow R-wave followed by a wide S-wave (see the old ECG below, Figure 2).  But in the above ECG, V5 and V6 only have a Q-wave.  Inferior leads have only a minimal residual r-wave, preceded by large Q-waves.

The R-waves in V1-V3 are very large, suggesting posterior completed infarction vs. RV hypertrophy.  Posterior MI leads to loss of posterior depolarization amplitude and thus to increase in anterior depolarization amplitude.  These would be Q-waves if recorded from posterior leads, but since they are recorded anterior, they appear as enlarged R-waves.  In figure 3, I have inverted the image vertically to simulate recording leads from the opposite polarity (see Figure 3).

Here is the patient's previous ECG (Figure 2):
Previous ECG.  Normal RBBB, no evidence of ischemia.  R-waves of of normal height.  There are no significant inferior or lateral Q-waves.  There is no ST elevation in any lead.

Figure 3 (Figure 1 flipped vertically)
This is the presentation ECG flipped vertically.  Doing so is analogous to recording all leads from the opposite polarity: for instance, it is similar to recording V1-V3 from posterior leads.  One difference is that actual posterior leads must be recorded with much intervening lung, which dampens the voltage (amplitude).  By inverting the image, the amplitudes recorded from the precordial leads are maintained.
One can now see that these large R-waves are Q-waves and the ST depression, as seen from the posterior wall, is really ST elevation!

Patient course

The first troponin returned at 200 ng/mL!!

The cath lab was activated.  The culprit was a 100% occluded circumflex.  It was opened and stented.  the Troponin peaked at 500 ng/mL!  One would think that such a high troponin would be correlated with very poor ejection fraction, but as I explain below, peak troponin is not a reliable indicator of infarct size.

There was also a calcified 95% RCA and calcified 60% LAD.

The echocardiographic ejection fraction (EF) was 50%, with a posterior-lateral- and inferior wall motion abnormality.

Several days later this ECG was recorded:
There is persistent ST deviation, but much decreased from before.  4mm of ST depression in V1 and V2 has diminished to 1-2 mm, consistent with reperfusion.
The persistent ST deviation, however, suggests possible development of a future ventricular aneursym.  However, it is too early to make any conclusions.  Much ST deviation may persist for weeks before entirely resolving.

This ECG was recorded 6 days after first

There is some persistent ST deviation.  This may be permanent and may be associated with echocardiographic dyskinesis (aneurysm).

LV aneurysm is common in completed, full thickness (transmural) MI, which is what we have here.  It is uncommon in the age of reperfusion therapy,  as most STEMI get treated reasonably early, before transmural infarct.

Patients with completed, transmural infarct are also at risk for post-infarction regional pericarditis and myocardial rupture.  LV aneurysm puts them at risk for a mural thrombus, which puts them at risk for embolism, especially embolic stroke.

Peak Troponin and Infarct Size:

60 ng/mL would be a very high first troponin.  Most STEMI peak at over 10 ng/mL; most NonSTEMI at less than 10 ng/mL.  A very large anterior MI may have peak troponins in the 80-300 range, and I have seen it up to 500 in a 24 hour old, non-reperfused left main occlusion (it would have been much higher still if measured after reperfusion).  However, peak troponin levels are very variable and not a reliable measure of infarct size because they are dependent on too many variables:
1) the amount of myocardium at risk
2) the duration of ischemia
3) the density of ischemia (are there collaterals?)
4) the persistence of occlusion (opening and closing spontaneously?), and
5) reperfusion (which releases large amount of troponin).

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