ECG Interpretation Review #29 (Infarction- Hemiblock- Normal Q Waves)

Interpret the ECG shown below in Figure 1, obtained from a 50-year-old man with a history of longstanding hypertension.  Is there is evidence of prior infarction?

Figure 1 – 12-lead ECG from a patient with longstanding hypertension.
Is there evidence of prior infarction?

INTERPRETATION: There is normal sinus rhythm at 60/minute.  Intervals are normal.  There is significant LAD (left axis deviation) sufficient to qualify as LAHB (left anterior hemiblock) — since the QRS complex in lead II is predominantly negative (which places the QRS axis at more negative than minus 30 degrees).  There is no evidence of chamber enlargement.  The remarkable findings on this tracing lie with assessment of Q-R-S-T morphology.  They include:

• a deep Q wave (QS complex) in lead III.
• a subtle r’ in lead V1 with some concave upward J-point ST segment elevation in V1,V2.
• early transition between V1-to-V2 (with a surprisingly tall R wave already by lead V2).
• persistence of S waves throughout the precordial leads.

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IMPRESSION:  The significance of the above findings that we note in our descriptive analysis is uncertain.  Isolated Q waves (even when deep) are often found in leads III and/or aVF without necessarily implying that there has been prior inferior infarction (See below).  

• Unless there are Q waves in each of the 3 inferior leads (II, III, and aVF) — we tend to interpret this finding as a “Q wave in lead III of uncertain significance”.  A terminal r’ in lead V1, and persistence of S waves across the precordial leads are findings that are often associated with pulmonary disease — but the rest of this tracing is not suggestive of this.  
• Slight J-point ST elevation with upward concavity in a few isolated anterior leads, but in the absence of other evidence of acute infarction — is usually a benign finding.  
• The most eye-catching finding on this tracing is the abrupt early transition caused by the unexpectedly tall R wave in lead V2. Possible reasons for this finding include posterior infarction, cardiomyopathy, abnormal body habitus, anatomic chest wall abnormality and/or lead misplacement.  
• Clinical correlation (and comparison with a prior tracing) is essential to determine which of these possibilities may be operative.

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Leads with Normal Q Waves/T Wave Inversion:  Five leads (III,aVR,aVL,aVF,V1) may normally display moderate-to-large Q waves and/or T wave inversion in otherwise healthy adults. Thinking of a “reverse Z” (à la Zorro) may help recall which leads these are (Figure 2).

Figure 2 – Leads that may normally display large Q waves or T inversion. 

We emphasize the following additional points regarding variants in Q and T wave morphology:

• Small and narrow normal septal q waves will often be seen in one or more lateral leads (I,aVL,V4,V5,V6) in asymptomatic individuals without heart disease.
• In general we can ignore lead aVR (a Q and/or T inversion in aVR is not indicative of MI/ischemia).
• Isolated T wave inversion (or an isolated Q wave) in lead III, aVF or aVL (as in Figure 2) — is most likely not to reflect ischemia IF the QRS is also negative in these leads.     But IF ischemia or infarction is present — then lead II (in addition to III and aVF) should also show a Q wave and/or T wave inversion.
• In adults — Lead V1 typically shows a QS or rS complex and T wave inversion. The QS may normally persist until V2 (but there should normally be at least some r wave by V3).  
• In children — all bets are off! (children often manifest a Juvenile T wave variant in which there may normally be T wave inversion in leads V1-thru-V3,V4).

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ADDENDUM (December 22, 2017):

• BOTTOM Line: It is difficult to know from this single tracing whether the isolated QS complex in lead III is a marker of a prior, silent inferior infarction — or, whether it is an incidental finding of no consequence. 
• If it does reflect prior inferior infarction — then the abrupt transition by lead V2 (with a markedly positive QRS complex in this lead) might reflect prior associated posterior involvement. At times, the presence of LAHB may mask prior inferior infarction (and vice versa) — since there is some opposition of forces in these 2 clinical conditions. Therefore, the ECG picture seen here could also reflect both LAHB and prior infero-postero infarction. 
• What can be said — is that there do not appear to be any acute changes on this ECG. At the least — a more detailed history on this patient is indicated, asking about any potential symptoms that might signal a prior event. Whether further evaluation beyond that is indicated would depend on clinical correlation ...