Monday, September 19, 2022

ECG Blog #333 — An Elderly Man with a Stroke


The ECG in Figure-1 — was recorded pre-hospital by the EMS (Emergency Medical Services) team, obtained from an elderly man with an acute stroke. There was no chest pain. The patient was hemodynamically stable.
  • How would YOU interpret this ECG?
  • Clinically — What do you suspect as the cause of these ECG findings? Does this explain the cardiac rhythm?

Figure-1: The 12-lead ECG recorded by the EMS team in today's case.

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NOTE: Interpretation of today's tracing is especially challenging because (as is common with pre-hospital ECG machines): i) There is no simultaneously-recorded long lead rhythm strip; and, ii) QRS amplitude is often "cut off" — such that in Figure-1, full amplitude of some QRS complexes in leads II, III, aVL, aVF and V3 is simply not seen.
  • Also complicating interpretation of the ECG in Figure-1 — is the constantly changing QRS morphology.
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MY Thoughts on the Rhythm in Figure-1:
As noted — constantly changing QRS morphology and lack of a long lead rhythm strip complicate interpretation. For clarity in Figure-2 — I've numbered the 15 beats in today's tracing.
  • Beats #1, and 8 (which is partially hidden by the vertical black lead change marker) — and beats #12-thru-15 all manifest a narrow QRS. Although this makes for a total of only 7 narrow-complex beats — this appears to be the underlying rhythm. This underlying rhythm looks to be irregular (ie, with variable R-R intervals— and, I do not see any P wave in lead II (and IF there were sinus P waves — I would expect to see one in lead II between beats #1-2). Therefore — the underlying rhythm in Figure-2 appears to AFib (Atrial Fibrillation), here with a controlled ventricular response.
  • In support that the underlying rhythm in Figure-2 is AFib — are the irregularly irregular undulations between QRS complexes that appear in the baseline, and which are best seen in lead V1. These are "fib waves".

  • This leaves us with beats #2-thru-6 and beats #9,10,11 — which all manifest a wide QRS complex. These wide beats are surprisingly regular (with no more than minimal variation in the R-R interval) — with a ventricular rate of ~85/minute

  • PEARL #1: The fact that in the setting of underlying AFib — these 8 wide beats manifest an almost regular rhythm strongly suggests that these beats represent a ventricular rhythm (which at a rate of ~85/minutequalifies this rhythm as AIVR = an Accelerated IdioVentricular Rhythm — See ECG Blog #108).

  • PEARL #2: The wide beats in Figure-2 are not the result of aberrant conduction. There simply is no reason for beats #2-thru-6 and #9,10,11 to conduct with a wide QRS complex — because these beats occur late in the cycle (whereas aberrant conduction almost always occurs with a much shorter coupling interval that falls within the relative refractory period). Instead — the R-R interval preceding the 1st ventricular beat in each run (ie, the R-R interval before beat #2 and before beat #9) — is virtually the same as the R-R interval between consecutive ventricular beats (which is exactly what we'd expect for an escape rhythm!).
  • PEARL #3: QRS morphology of the wide beats in Figure-2 is not consistent in all leads with LBBB (Left Bundle Branch Block) conduction. Although the monophasic R wave in high-lateral leads I and aVL does resemble LBBB conduction — the equiphasic (R=S) complex in lead V2 for beats #9,10,11 is not consistent with this, or any other form of conduction defect.
  • PEARL #4: In final support that the wide beats in Figure-2 represent an accelerated ventricular rhythm — is the finding that beat #2 is a fusion beat! (See ECG Blog #128). This is best seen by comparing the shape and width of the QRS complex and T wave of beat #2 in leads I and II — with the shape and width of the supraventricular beat before it ( = beat #1) — and the ventricular beat after it ( = beat #3). The only way to produce the intermediate appearance of beat #2 — is if beat #2 represents near-simultaneous occurrence of both a supraventricular and ventricular beat!

Figure-2: I've numbered the beats in Figure-1.

Interpreting the Rest of the 12-Lead ECG:
Now that we've established that the underlying rhythm in Figure-2 is AFib (that is twice interrupted by runs of AIVR) — we can focus attention on interpreting the remainder of today's tracing.
  • PEARL #5: The KEY to assessing acute ST-T wave changes in association with an intermittent ventricular rhythm — is to focus attention in each of the 12 leads on all supraventricular beats (which in Figure-2 entails assessing ST-T wave morphology for each of the narrow beats).
  • In leads I,II,III — beat #1 is supraventricular. In leads aVR,aVL,aVF — beat #7 and beat #8 are supraventricular (but we unfortunately do not see the ST-T wave for beat #8). Both beats #1 and 7 reveal T wave inversion in the inferior leads for these 2 supraventricular beats.
  • There are no supraventricular beats in leads V1,V2,V3 (so we can not reliably assess for ST-T wave changes in these leads).
  • There are 4 supraventricular beats in leads V4,V5,V6 — all of which show modest T wave inversion, with what appears to be modest J-point ST depression.

  • BOTTOM LINE: There is a small-to-modest amount of symmetric T wave inversion in 6/9 leads that we were able to assess for this in. A number of these leads also show slight J-point ST depression. These ST-T wave changes may represent: i) Ischemia (which could be recent or acute); — and/orii) These ST-T wave changes may represent reperfusion T waves following recent infarction.


Putting It All Together:
Although today's patient did not complain of chest pain — this elderly man was having an acute cardiovascular event in the form of an acute stroke. Clearly age and the underlying AFib rhythm predisposed this patient to developing stroke.
  • In a small-but-significant percentage of patients with acute thromboembolic stroke — an acute MI is the precipitating cause. Perhaps the most common clinical setting for seeing AIVR — is as a reperfusion arrhythmia following acute OMI ( = Occlusion-based Myocardial Infarction).

  • PEARL #6: On occasion (ie, when the clinical setting is "right") — the 1st ECG clue that a patient is having an acute MI may be the unexpected development of AIVR. Given the age of today's patient — his ongoing acute stroke — diffuse T wave inversion (with some ST depression) — and runs of AIVR — spontaneous reperfusion from acute MI should be suspected!

  • PEARL #7: As emphasized in ECG Blog #228Not all patients with acute MI have chest pain. Instead, the estimated incidence of "Silent" MI may be as high as between 20-40% of all MIs (depending on the definition used). As a result — lack of chest pain in today's case does not rule out the possibility of acute MI given predisposing factors of advanced age and acute stroke, in association with diffuse T wave inversion and runs of AIVR. 

CASE Conclusion:
Unfortunately — I do not have follow-up on this case. That said — the "Lesson-to-be-Learned" — is that despite the absence of chest pain in today's case — serial troponins and repeat ECGs were indicated as soon as the patient arrived at the hospital.  


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Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).  

  • ECG Blog #108 — Reviews the concept of AIVR.
  • ECG Blog #321 — Reviews another case of an AIVR rhythm.

  • ECG Blog #128 — Reviews the concept of how Fusion Beats can help to prove a wide-complex rhythm is ventricular (and not the result of aberrant conduction).

  • ECG Blog #228 — Reviews the concept of "Silent" MI (How common this is — and How these patients present).

  • ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused (with Audio Pearl MP-11 in Blog #294).





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