Imagine you are overreading tracings that were done in an ED (Emergency Department). Unfortunately, you have NO clinical information on the patient whose ECG is shown in Figure-1.
- How would you interpret this ECG?
- Clinically — What do you suspect is going on with this patient?
Figure-1: 12-Lead ECG obtained from a patient who presented to the ED. Unfortunately — NO clinical information is available. How do you interpret this tracing? (See text). |
Descriptive Analysis of the ECG in Figure-1:
An upright P wave with a normal PR interval is seen in lead II. The ventricular rhythm is fairly regular — and the QRS complex is not widened (ie, not more than 0.10 second) — therefore, this is a sinus rhythm at ~60-65/minute.
An upright P wave with a normal PR interval is seen in lead II. The ventricular rhythm is fairly regular — and the QRS complex is not widened (ie, not more than 0.10 second) — therefore, this is a sinus rhythm at ~60-65/minute.
- All intervals are normal (ie, the PR interval is not more than 1 large box in duration — the QRS not more than 1/2 a large box — and the QT not more than 1/2 the R-R interval).
- There is a markedly leftward axis (ie, the QRS is predominantly positive in lead I — but all negative in lead aVF).
- There is no chamber enlargement.
- Q Waves — Small and narrow q waves are seen in leads I and aVL. Entirely negative QS complexes are seen in leads II, aVF; and V2, V3. Larger and/or wider-than-expected Q waves are seen in leads V4, V5 and V6.
- R Wave Progression — Transition is slightly delayed, since the R wave does not become taller than the S wave is deep until between leads V4-to-V5. NOTE: There is an initial positive deflection (r wave) in lead V1. This small initial r wave is then lost as the fragmented and entirely negative QS complex in lead V2 forms (ie, there is “Loss of R Wave” as we move from lead V1-to-V2).
- ST-T Wave Changes — There is nonspecific ST-T wave flattening in lead aVL. There is straightening of the ST segment takeoff in several anterior leads (slanted BLUE lines in Figure-2). Slight ST elevation is seen in lead V1 — and then 2-3 mm of J-point ST elevation is seen in leads V2, V3 and V4 (small PURPLE arrows above the dotted RED line baseline).
- Other Findings — There is fragmentation of the QRS that deforms the downslope of the S wave in a number of leads (small BLUE arrows).
Clinical Impression /Clinical Notes: As stated — We were not provided with any clinical information, other than that this patient presented to the ED.
- The rhythm is sinus at ~60-65/minute.
- Marked left axis deviation is present. It is difficult to determine if the reason for this is: i) LAHB (Left Anterior Hemi-Block); ii) Inferior MI of uncertain age; and/or, iii) Both LAHB + prior Inferior MI.
- Identification of fragmentation (ie, irregularities) in one or more QRS complexes (small BLUE arrows) suggests scarring — that may be the result of prior infarction, cardiomyopathy, or some other form of structural heart disease. Such fragmentation does not tell us whether heart disease is acute or has been present long-term — but it nonetheless is an invaluable clue for conveying that the patient in question almost certainly has some form of underlying structural heart disease.
- Returning to assessment of the inferior leads — the finding of fragmentation (irregularity) of S wave downslope in lead aVF — and especially the QRS shape in lead II (which suggests an initial Q wave, that is aborted by a small positive deflection that fails to reach to baseline, before continuing on as a deep S wave) — strongly suggests that there has been inferior MI at somepoint in time. Lack of any inferior lead ST elevation + the nonspecific ST-T wave flattening in lead aVL suggest this to be an old inferior MI.
- Finally — the small, thin initial r wave in lead III is against inferior MI, and strongly suggests LAHB.
- “My Take” — Inferior MI and LAHB are “competing” conditions — in that the presence of one may mask the other. Given the conflicting ECG findings described above — I strongly suspect that there is both LAHB + old inferior MI.
- Preservation of the initial r wave in lead V1 suggests (at least in theory) — that the septum remains intact (it is the initial left-to-right vector of septal depolarization that produces the initial r wave in lead V1; This is lost with septal infarction). We would therefore describe the location of the MI in Figure-2 as “anterior” or “antero-lateral” — but not “antero-septal” (because the initial r wave in lead V1 is preserved).
- Finding a prior ECG on this patient could be of invaluable assistance in answering this question — since this will tell you which of the above ECG findings were previously present. But without a prior ECG — it is virtually impossible to be certain ...
- The History is extremely important! We were told that the ECG in Figure-2 was recorded in the ED — but we were not told if the patient was asymptomatic or having new-onset chest pain at the time ... IF the history for this patient did not sound like an acute MI — this would support the likelihood that the changes were not new.
- Repeating the ECG in the ED a little while later may help. An acute evolving STEMI tends to show evolution of ECG changes, sometimes over a surprisingly short period of time.
- Doing an Echo in the ED may help! Seeing a large LV (left ventricular) aneurysm with reduced or absent contractility would support chronicity rather than acute MI.
- BOTTOM Line: Clinical correlation will be needed to arrive at a definitive answer (ie, history; finding a prior tracing; serum troponin values, Echo, serial ECGs in the ED, etc.). That said — the KEY Points from this blog post are: i) To recognize ECG findings suggestive of new or recent vs old infarction; ii) To realize that you may not be able to “date” the infarction on the basis of a single ECG without clinical correlation; and, iii) To appreciate that the ECG picture seen in Figure-2 would be perfectly consistent with development of LV Aneurysm following extensive Anterior MI.