ECG Blog #313 — Acute Post-Partum MI?

The ECG in Figure-1 — was obtained from a 40-year old woman 10 days after a normal vaginal delivery. She presented to the ED (Emergency Department) with a history of progressive dyspnea over the previous 3 days.

QUESTIONS:

• In view of this history — How would YOU interpret the ECG in Figure-1?
• Many staff physicians were concerned about an acute MI. Do YOU agree?

Figure-1: Initial ECG from a woman 10 days post-partum — who presented to the ED with progressive dyspnea. (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 ~110/minute. 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. 

Additional relevant ECG findings include:

• Overall low voltage (especially in the chest leads).
• Incomplete RBBB (ie, rSR' pattern in lead V1 — with normal QRS duration and narrow terminal s waves in leads I and V6).
• An indeterminate frontal plane Axis (ie, nearly isoelectric complexes in most limb leads).
• An S1Q3T3 pattern is present!

 

Regarding Q-R-S-T Changes:

• There is a Q wave in lead III — as well as small q waves in leads I, II, aVF.
• Regarding R Wave Progression — a tiny initial r wave (positive deflection) is seen in lead V1 — consistent with the incomplete RBBB pattern noted above. An rSr' pattern persists in lead V2 — but the fact that the P wave is positive in both leads V1 and V2 indicates that these rSr' patterns in leads V1,V2 are "real" (ie, they are not due to chest lead misplacement). 
• QRS complexes remain extremely small across the chest leads — with nearly isoelectric QRS complexes in leads V3-thru-V6. There is persistence of S waves across all chest leads (with a significant S wave still present in lateral lead V6).
• ST segments are coved — with a hint of ST elevation in a number of leads (ie, leads III, aVR, V1, V2). Perhaps the most remarkable finding is the deep (considering the small R wave amplitude) and symmetric T wave inversion that is seen in the inferior leads — and — in leads V1-thru-V6.

 

IMPRESSION: 

The History is KEY in today’s case: Rather than an acute cardiac event — the history of progressive dyspnea 10 days post-partum in a younger woman should immediately suggest the following entities: i) Post-Partum Cardiomyopathy; ii) Takotsubo Cardiomyopathy; and, iii) Acute PE (Pulmonary Embolism). 

• Even before results from bedside Echo were seen — the ECG in Figure-1 should strongly suggest acute PE as the presumed diagnosis until proven otherwise.

 

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The ECG Diagnosis of Acute PE:

As I've discussed on prior ECG Blog posts (See ECG Blog #233) — the ECG is far from optimal as an investigative tool for the diagnosis of acute PE. That said — there are times when the ECG, in conjunction with the clinical history — can be extremely helpful in suggesting the diagnosis even before additional testing can be accomplished. The ECG in Figure-1 provides an excellent example of this situation.

• PEARL #1: The ECG is unlikely to identify patients with smaller PEs. Do not expect to see anything on the ECG of these patients (This may be a "blessing in disguise" — as the longterm benefit of anticoagulating such patients is debatable). Sensitivity of the ECG for suggesting the possibility of acute PE is clearly better with large (especially submassive) PEs.

 

PEARL #2: One of the problems with using the ECG as a diagnostic tool for detecting acute PE — is that there is no single ECG finding definitive for this diagnosis. Instead, acute PE may be suggested by a combination of several supportive ECG findings that occur in association with the “right” clinical scenario (ie, recent onset of unexplained dyspnea, syncope and/or shock — especially in a patient predisposed or with a prior history of venous thromboembolism).

• The clinical setting of today's case serves as a "perfect set-up" for development of acute PE (ie, an otherwise healthy, adult woman who presents with progressive dyspnea during the first 2 weeks post-partum).
• 
  
• For clarity — I summarize the KEY ECG findings to look for when considering the diagnosis of acute PE in Figure-2. These ECG findings are expanded on in the ADDENDUM below (See Figure-3 and Figure-4 — and the attached Audio Pearl).

 

Figure-2: ECG findings associated with acute PE. There is no single ECG finding that is diagnostic of acute PE. Instead, the diagnosis may be suggested by the presence of at least several of these ECG findings when they occur in the “right” clinical setting (See text).

 

WHAT are the ECG Findings in Today's Case?

I list below those positive and negative ECG findings from Figure-2 — as they are relevant to today's case:

• Sinus Tachycardia — While not absolutely essential for the diagnosis, a rapid heart rate (usually to at least 90/minute) is a common and expected finding in patients with hemodynamically significant acute PE. The heart rate in Figure-1 is over 100/minute.
• 
  
• Acute RV “Strain” — Awareness of ECG evidence of RV (Right Ventricular) Strain is one of the most important ECG indicators of acute hemodynamically significant PE. Unfortunately, this sign remains all-to-often unappreciated and misinterpreted as coronary ischemia (as it was in today's case). RV “strain” manifests as ST depression and/or T wave inversion that typically occurs in anterior leads (V1,2,3) — and/or — in inferior leads (II,III,aVF). Abnormal ST-T wave changes consistent with acute PE are seen in both of these lead areas in Figure-1 (and these changes extend out to the lateral chest leads = until lead V5!).
• 
  
• S1-Q3-T3 — Whereas the diagnostic value of this pattern is minimal at best when seen as an isolated finding — a definite S1Q3T3 pattern can be extremely helpful IF seen in association with other ECG evidence of acute PE. Such is the case in Figure-1.
• 
  
• There is no RAA.
• There is an indeterminate frontal plane axis (ie, nearly isoelectric QRS complexes in most limb leads).
• An incomplete RBBB pattern is present (ie, Narrow QRS with rSr' in leads V1,V2 — with a terminal narrow s wave in lateral leads I and V6).
• There is no tall R wave in lead V1.
• Persistent Precordial S Waves — Poor R wave progression with persistence of S waves across the chest leads (through to lead V6) — is another ECG sign seen here that is consistent with new or chronic pulmonary disease.
• ST Elevation in Lead aVR and/or Lead III — Among the unappreciated benefits of lead aVR in ECG interpretation, is awareness that acute right heart “strain” (as seen with large acute PE) may often produce ST elevation in right-sided lead aVR. Although subtle — there is at least a hint of ST elevation in the 3 "right-sided" leads in Figure-1 (ie, in leads III, aVR, V1).
• Atrial fibrillation is not present.

 

PEARL #3: Boey et al (Singapore Med J 56:533-537, 2015) — make the point that in addition to the ECG findings noted in Figure-2 — more extensive and severe PE has been associated with: i) Low QRS voltage; ii) Pseudo-infarction patterns (ie, Q waves in leads III, aVF); and/or, iii) ST segment changes that extend to leftsided chest leads (ie, leads V4,V5,V6).

• NOTE: All 3 of these ECG findings that have been associated with more severe PE are present in today's case!

Putting It All Together: The one unifying diagosis that explains all of the ECG findings noted above in Figure-1, in this 40-year old post-partum woman who presented to the ED with progressive dyspnea (but no mention of chest discomfort) — is acute PE.

• The "beauty" of the initial ECG in today's case — is that it expedited an accurate presumptive diagnosis of extensive acute PE within minutes!

CASE FOLLOW-UP: 

The patient was hypotensive on arrival in the ED. Stat Echo in the ED revealed a compressed left ventricle — septal flattening with paradoxical movement — and a grossly dilated right ventricle. These Echo findings ruled out Takotsubo and Post-Partum Cardiomyopathy — and confirmed the diagnosis of massive acute PE.

• The patient was immediately treated with Streptokinase — which fortunately resulted in significant improvement.
• Subsequent CT Angiography of the Chest confirmed extensive bilateral PE.
• The patient continued to improve — and she was soon discharged from the hospital in stable condition on oral anticoagulation.

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Acknowledgment: My appreciation to Dr. Rasheed (from Sana'a, Yemen) for making me aware of this case and allowing me to use this tracing.

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Related ECG Blog Posts to Today’s Case: 

• 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).
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• 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”. 
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• ECG Blog #209 — Reviews the ECG diagnosis of Wellens’ Syndrome (What it is — and what it is not! ).
• ECG Blog #59 — Reviews the causes of Giant T Wave Inversion.

 

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ADDENDUM (6/16/2022): 

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.

  

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.

—  — 

Today’s 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!).

• NOTE #2: Among the topics discussed in this Audio Pearl are the ECG findings with acute PE (See Figure-3 and Figure-4 in the ADDENDUM below) — Wellens' Syndrome (reviewed in ECG Blog #209) — and — Giant T Wave Syndrome (reviewed in ECG Blog #59).