Wednesday, February 3, 2021

ECG Blog #190 — The "Culprit"? (LCx – RCA – LAD)

The ECG in Figure-1 was obtained from a middle-aged man with new-onset chest pain.

  • Where is the acute occlusion? What is the “culprit” artery?
  • Are additional leads needed to determine your answer?
  • WHY is it important to recognize the situation presented by this case?

  • Extra Credit: What might be the cause of the ST elevation in lead V3?


Figure-1: ECG obtained from a middle-aged man with new-onset chest pain (See text).

MY Thoughts on ECG #1:

The rhythm is sinus at a rate just under 60/minute. All intervals (PR, QRS, QTc) are normal. The frontal plane axis is normal at +60 degrees. There is no chamber enlargement.


Regarding Q-R-S-T Changes:

  • There is a suggestion of tiny, “just-now-beginning” Q waves in leads III and aVF ...
  • R Wave Progression: Transition (where the R wave becomes taller than the S wave is deep) occurs normally between leads V2-to-V3 — although change from the predominantly negative QRS complex in lead V2 — to the entirely positive R wave in lead V3 is more abrupt than usual.
  • There is dramatic ST elevation in each of the inferior leads ( = leads II, III and aVF). There is also ST elevation in lead V3. T waves in each of the leads with ST elevation are hyperacute (ie, much taller and “fatter”-at-their-peak than would normally be expected).
  • As opposed to the inferior lead ST elevation — there is marked mirror-image” (ie, reciprocal) ST-T wave depression in lead aVL. ST-T wave depression of a lesser extent is seen in lead I.
  • There is significant ST-T wave depression in lead V2.



NOTE: Some readers may prefer at this point to listen to the 6-minute ECG Media Pearl before reading my final interpretation. Feel free to review my Clinical Impression to ECG #1 (that appears just below ECG MP-7) at any time.



Today’s ECG Media PEARL #7 (4:50 minutes audio) — reviews the ECG findings of acute RV MI — as well as other pearls for determining the likely “culprit” artery.



MY Clinical Impression of ECG #1:

ECG #1 shows an obvious acute inferior STEMI — as evidenced by dramatic ST elevation in each of the 3 inferior leads. That said — the interesting part of this case relates to discussion of which other lead areas of the heart are affected — and — determining what is the “culprit” artery.

  • As discussed above in ECG Media PEARL #7 — among the reasons why the RCA (Right Coronary Artery) is almost certain to be the "culprit" artery are: i) LAD (Left Anterior Descending) occlusion of an LAD with "wraparound" is unlikely — because ST elevation in the chest leads is limited to lead V3ii) LCx (Left Circumflex) occlusion is also unlikely — because the relative amount of ST elevation in lead III is significantly more than in lead II (and LCx occlusion is more likely to result in a greater amount of ST elevation in lead II instead of lead III — as well as lateral ST elevation); iii) There is marked reciprocal ST depression in lead aVL (which further supports RCA occlusion — vs LCx occlusion, in which ST depression in lead aVL tends to be less marked)iv) Statistics — given that ~85% of people have a right-dominant circulation, which makes acute RCA occlusion much more likely statistically than LCx occlusion; andv) The findings in ECG #1 strongly suggest there is associated acute RV involvement — and the major blood supply to the right ventricle is provided by the RCA (and not by the LCx or the LAD).


PEARL: The ST depression in lead V2 of ECG #1 strongly suggests there is associated acute posterior MI. Posterior MI is very commonly seen with acute inferior MI (from either RCA or LCx occlusion) — because of the common blood supply that the inferior and posterior walls of the left ventricle typically share.

  • Acute posterior MI usually manifests ST depression in at least 2 of the first 4 chest leads. The fact that the ST-T wave in lead V1 is almost flat despite obvious ST depression in lead V2 — suggests that something else” must be producing ST elevation in lead V1 that is opposing to what otherwise would have been ST depression from the posterior MI. In the setting of acute RCA occlusion — it is this flattened (instead of depressed) ST-T wave in lead V1 that strongly suggests associated acute RV involvement.


What About the ST Elevation in Lead V3?

This leaves us trying to explain WHY there is isolated ST elevation in lead V3 among the 6 chest leads? The answer is not immediately apparent. Consider the principal differential diagnosis when ST elevation is seen in both inferior and anterior leads:

  • There could be acute RCA occlusion causing inferior MI with acute RV involvement. ST elevation is generally best seen with acute RV MI in right-sided leads. This ST elevation tends to be maximal in leads V3R and/or V4R — but you can sometimes also see some ST elevation in lead V1 (which after all, is a right-sided lead). On occasion, when RV MI is severe (with marked RV dilatation) — you can even see ST elevation extending on a standard ECG from lead V1 until lead V2 or V3. Perhaps the ST elevation that we see in lead V3 of ECG #1 is simply a reflection of severe RV MI for which ST elevation in lead V2 was countered by simultaneous ST depression from posterior MI?
  • Lead misplacement of one or more chest leads may be contributing to the problem. Abrupt transition from a predominantly negative QRS complex in lead V2 — to an all-positive QRS complex in lead V3 suggests that positioning of one or more chest leads may be off — and that could contribute to the unlikely picture we see here of a flat ST segment in lead V1 — that quickly evolves to definite ST-T depression in lead V2 — followed just 1 more lead over by marked ST elevation in lead V3. I wouldn’t physiologically expect such abrupt changes in ST-T wave morphology unless there was faulty lead placement of one or more chest lead electrodes.
  • There could be acute occlusion of a large LAD vessel with “wraparound” the inferior surface of the left ventricle. However if acute occlusion of a “wraparound” LAD was the reason for ST elevation in lead V3 — I would have expected more ST elevation in other anterior chest leads and no ST depression in lead V2. Finally, the relative amount of ST elevation in anterior leads is generally significantly more than in inferior leads when there is acute occlusion of a “wraparound” LAD — and that is the opposite of what we see here.
  • There could be multivessel disease. It’s difficult to predict the ultimate effect on the ECG when there is severe multi-vessel disease and altered compensatory patterns of collateral flow.
  • OR — there could be an anatomic variant in the RCA, in which a branch from this vessel flows more anteriorly than usual to supply a portion of the LV anterior wall. Proximal occlusion of the RCA in this instance might result in necrosis of a localized portion of the anterior wall, which might be detected by the isolated ST elevation we see in lead V3 of ECG #1.


Are Right-Sided Leads Needed Here to Diagnose Acute RV MI?

As emphasized above — the most definitive way to diagnose acute RV MI is by seeing ST elevation in right-sided leads. 

  • That said — I described a bit earlier in the PEARL above how in the setting of acute RCA occlusion, the finding of ST depression in lead V2 with a flat ST segment in lead V1 was suggestive evidence of acute RV involvement.
  • Confirmation of acute RV MI was forthcoming by obtaining right-sided leads (See Figure-2in which leads V4RV5R and V6R are now shown). The huge amount of ST elevation in these right-sided leads is as much as you’ll probably see (ie, most cases of acute RV MI show a much more modest amount of right-sided ST elevation).

Figure-2: Right-sided leads V4R, V5R and V6R have been added to Figure-1 (See text).

FOLLOW-UP to this Case:

Immediate cardiac catheterization was not available at the facility where this patient was seen. The patient was instead promptly treated with thrombolytic therapy with excellent result. Within 1 hour of initiating treatment — virtually all of the ST elevation had resolved, in association with marked clinical improvement of the patient.

  • I conclude today’s case with a several page excerpt from my ECG-2014-ePub — in which I summarize KEY aspects for recognition of acute RV MI (See Figure-3 and Figure-4).


FOR Other Examples of Acute RV MI:

Figure-3 (together with Figure-4): Reviews the ECG Essentials of RV MI (Excerpted from my ECG-2014-ePub).



Figure-4 (continued from Figure-3): Reviews the ECG Essentials of RV MI (Excerpted from my ECG-2014-ePub).



Acknowledgment: My appreciation to Hosain Saleh (from Damascus, Syria) for the case and this tracing.