The ECG in Figure-1 — was obtained from a middle-aged woman with positional tachycardia and diaphoresis with change of position from suprine to sitting. Although CP (Chest Pain) was not a prominent symptom — ACS (Acute Coronary Syndrome) was suspected from the chest lead T wave inversion seen on this ECG.
QUESTIONS:
- How would YOU interpret the ECG in Figure-1?
- Do you agree with the diagnosis of ACS?
- WHY — or Why Not?
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| Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
My THOUGHTS on the ECG in Figure-1:
The rhythm is sinus tachycardia at ~105/minute (ie, The R-R interval is regular — and just under 3 large boxes in duration). The PR interval is normal. The QRS complex is narrow — but the QTc appears to be prolonged (although this is more difficult to assess given the tachycardia). No chamber enlargement. A small, narrow (and normal) septal q wave is seen in leads I and aVL.
Additional relevant ECG findings include:
- There is an rSr' pattern in leads III and aVF — but not in right-sided lead V1. Although an rSr' pattern in either lead III or aVF is more of a descriptive finding — the potential relevance of this pattern in today's case is that this terminal right-sided activity (that writes the r' in these vertical/right-sided leads) sometimes serves as a proxy for an IRBBB (Incomplete Right Bundle Branch Block) pattern.
- There is poor R wave progression — with transition (where the R wave becomes taller than the S wave is deep) being delayed until between leads V5-to-V6.
- S waves persist in the chest leads through to lead V6.
Regarding ST-T wave findings:
- The most remarkable ECG finding in Figure-1 — is the fairly deep and symmetric T wave inversion, that begins in lead V1 — and continues through until lead V5.
- Nonspecific ST-T wave flattening is seen in most of the remaining leads.
IMPRESSION:
While the History in today’s case was not especially suggestive of ACS (ie, There was no mention of CP) — this history was also not suggestive of any other specific diagnosis. That said — the ECG in Figure-1 should prompt the following considerations:
- The symmetric chest lead T wave inversion in ECG #1 could be a sign of coronary disease, potentially with acute ischemia. And as per ECG Blog #350 — this could represent Wellens' Syndrome IF this chest lead T wave inversion was new and occurred in a patient who initially had a normal ECG, and then had an episode of transient CP that had resolved at the time this ECG with chest lead T wave inversion was recorded.
- PEARL #1: Before attributing the chest lead T wave inversion seen in ECG #1 to Wellens' Syndrome — it is essential to inquire IF the patient had a prior episode of CP that has now resolved at the time the T wave inversion is seen.
- Alternatively — the symmetric chest lead T wave inversion in ECG #1 could be a sign of Takotsubo Cardiomyopathy — especially given hemodynamic instability reported in the history — and, what appears to be QTc prolongation (See ECG Blog #277).
- As another alternative consideration — Diffuse ST-T wave abnormalities (including T wave inversion) as are seen in ECG #1 could be the result of a non-cardiac condition — including marked metabolic and/or electrolyte disturbance, CNS catastrophe (ie, stroke, intracerebral or subarachnoid bleed, trauma, tumor), severe anemia, "sick" patient, etc.
- PEARL #2: Acute PE remains one of the most commonly overlooked diagnoses. As per links that I provide below — IF the diagnosis of acute PE is not thought of, this entity will be missed! (See ECG Blog #313 — as well as My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog).
- As emphasized in previous ECG Blog posts — Figure-2 lists the series of ECG findings most commonly associated with acute PE. Of these — acute RV "strain" is the most suggestive ECG sign. Statistically, in an adult population with new symptoms — the finding of symmetric, anterior lead T wave inversion (as seen in Figure-1) is much more likely to reflect RV "strain" than acute coronary disease.
- Additional, potentially supportive ECG signs of acute PE in Figure-1 include: i) Sinus tachycardia; ii) Poor R wave progression, with persistence of S waves through to lead V6; and, iii) The rSr' morphology (ie, IRBBB proxy) seen in leads III and aVF.
- To EMPHASIZE: While the ECG picture in today's tracing is clearly not definitive for the diagnosis of acute PE — seeing anterior T wave inversion in association with sinus tachycardia in this patient with signs of hemodynamic instability (ie, positional tachycardia with diaphoresis on change of position from supine to sitting) — should at least prompt consideration of this diagnosis.
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| Figure-2: ECG Findings associated with acute PE. |
CASE Conclusion:
As noted in my presentation above — the ECG in Figure-1 was initially interpreted as suggestive of ACS. Cardiac cath was planned — until the patient had an episode of syncope with severe hypotension.
- Stat Pulmonary CT angiography was ordered — and confirmed acute PE.
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P.S. = PEARL #3: An Often Forgotten Clinical NOTE ...
Initial assessment of the patient for possible acute PE begins by counting the respiratory rate. During my decades of working with residents when hospital Attending — by far, the most commonly overlooked vital sign was respiratory rate.
- KEY Point: The respiratory rate that is written on the chart does not count! I cannot tell you how many times such "written" documentation was off, due to the tendency to inscribe a normal number instead of counting for 30 seconds because "the patient looked like they were breathing normally".
- Patients may "look" like they are breathing normally — when in fact they are tachypneic if you simply take the time to watch them and count the number of rapid, shallow respirations. All it takes is a few seconds of concentration for you to determine how fast the patient is breathing. And, IF the patient's respiratory rate is increased — and their initial ECG looks like the initial ECG in today's case — You have made the diagnosis of acute PE until proven otherwise!
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Acknowledgment: My appreciation to Mahtab Parvizpour (from Khorramabad, Iran) for the case and these tracings.
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Related ECG Blog Posts to Today’s Case:
- ECG Blog #313 — Reviews in detail a case that illustrates the ECG diagnosis of acute PE.
- ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
- ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
- My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).
- ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
- ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”.
- ECG Blog #209 — Reviews the ECG diagnosis of Wellens’ Syndrome (What it is — and what it is not! ).
- ECG Blog #277 — Reviews findings in Takotsubo Cardiomyopathy.
ADDENDUM (6/21/2024): 
I've excerpted below in Figure-3 and Figure-4 — several pages from my ECG-2014-ePub — that summarize the ECG findings of acute PE (Pulmonary Embolus) — as well as an Audio Pearl relevant to today's topic.
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Figure-3: Summary of KEY findings in the ECG diagnosis of acute PE. 
Figure-4: Summary (Continued) of KEY findings in the ECG diagnosis of acute PE. ECG Media PEARL #49 (7:40 minutes Audio) — Reviews the ECG finding of Anterior T Wave Inversion (with emphasis on not overlooking acute PE as the cause!).
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Good Morning Prof! Another great case!
ReplyDeleteTHANK YOU as always for your kind comments! — :)
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