ECG Interpretation: ECG Blog #330 - Pneumonia with 2 ECG Findings!

Today’s patient is an elderly man who was admitted to the hospital for symptoms of fever and coughing — with an admission diagnosis of community-acquired pneumonia. He was treated with antibiotics. A short while after hospital admission — the patient complained of chest pain, at which time the ECG in Figure-1 was obtained.

How would YOU interpret the ECG in Figure-1?
Clinically — What would you do?

Figure-1: This ECG was obtained for an episode of chest pain. The patient is an elderly man admitted to the hospital for pneumonia.

MY Thoughts on the ECG in Figure-1:

Unfortunately — there is no long lead rhythm strip for ECG #1. In addition — resolution is suboptimal, and the wide black lead change markers may be concealing beats. I suspect the rhythm is supraventricular with PACs (Premature Atrial Contractions) — but a longer rhythm strip lead would be needed to verify this.

PEARL #1: Something is wrong! You virtually never normally see an almost-all-negative QRS complex in lead I (especially when the T wave is also negative in this lead).
Further increasing my suspicion that something is wrong with this initial ECG in Figure-1 — is the finding of an all-positive QRS with positive T wave in lead aVR.
PEARL #2: Doesn't the QRS complex and ST-T wave in lead I — look like what we'd expect the QRS and ST-T wave to normally look like in lead aVR? (And doesn't the QRST in lead aVR — look like what we'd expect the QRST in lead I to look like?). This reversal from our normal expectations for the QRST in leads I and aVR strongly suggests there is LA-RA (ie, Left Arm-Right Arm) Lead Reversal.
PEARL #3: We can usually quickly distinguish between LA-RA lead reversal vs dextrocardia — by looking at R wave progression in the chest leads. Because the heart lies in the right hemithorax when there is dextrocardia — you will usually see "reverse" R wave progression in the chest leads (ie, R wave ampitude becoming progressively smaller as one moves across the chest from lead V1-to-V6).
LA-RA lead reversal is much more common than dextrocardia. In Figure-1 — R wave amplitude is increasing as one moves from lead V1-toV6, so I thought it unlikely that dextrocardia was present. That said — given how small R wave amplitude still is in the most lateral chest lead ( = lead V6) — I was not yet 100% certain that dextrocardia was ruled out.

BOTTOM LINE: The ECG in Figure-1 — should be promptly repeated! There are at least 2 reasons for this:

Reason #1: We want to see what this patient's ECG looks like with electrode leads correctly placed. (Along the way — we'll listen to the patient chest to verify that heart sounds are on the left and not the right side of the thorax).
Reason #2: There are a number of abnormal findings in the inferior leads in the ECG shown in Figure-1 — including Q waves, ST elevation and T wave inversion. Is this patient having an acute inferior MI?

The CASE Continues:

The lead reversal was not recognized — so the ECG in Figure-1 was never repeated.

Fortunately — there was another ECG available from this patient for comparison. As stated above — ECG #1 was obtained a short while after hospital admission, when this patient (who had been admitted for pneumonia) — developed chest pain.
For clarity — I have put the 2 ECGs that were obtained on today's patient together in Figure-2. I've labeled the hospital admission tracing as ECG #2 — which was done as part of the routine procedure for a patient admitted with pneumonia. To Emphasize: The patient was not having any chest pain at the time ECG #2 was recorded.

QUESTION:

Does your comparison of the 2 ECGs in Figure-2 confirm your interpretation of ECG #1?

Figure-2: The 2 ECGs that were obtained on today's patient.

How Figure-2 Helps:

Seeing what the hospital admission ECG looked like (as we do in Figure-2) — confirms that there was LA-RA Lead Reversal in ECG #1.

Note that leads I and aVR in the admission ECG ( = ECG #2) look as we expect them to — with an upright QRS complex and upright T wave in lead I — and — a predominantly negative QRS and no upright T wave in lead aVR.
There is no doubt that R wave progression is normal in ECG #2 (with transition where the R wave becomes taller than the S wave is deep, occurring as expected between leads V3-to-V4).

What Happens with LA-RA Lead Reversal?

My favorite on-line “Quick GO-TO” reference for the most common types of lead misplacement comes from LITFL ( = Life-In-The-Fast-Lane). I have used the superb web page they post in their web site on this subject for years. It’s EASY to find — Simply put in, “LITFL Lead Reversal” in the Search bar — and the link comes up instantly.

This LITFL web page describes the 7 most common lead reversals. There are other possibilities (ie, in which there may be misplacement of multiple leads) — but these are less common and more difficult to predict.
By far (!) — the most common Lead Reversal is mix-up of the LA (Left Arm) and RA (Right Arm) electrodes. This is the mix-up that occurred in today’s case. For clarity — I’ve reproduced the illustration from LITFL on LA-RA reversal in Figure-3.

Figure-3: LA-RA Lead Reversal (adapted from LITFL).

What Should ECG #1 Look Like?

For clarity — I've taken the initial ECG in today's case ( = ECG #1) — and inverted lead I — switched leads II and III — and switched leads aVL and aVR ( = ECG #1A, which is the lower tracing in Figure-4).

Doesn't ECG #1A now look perfectly consistent with what we would expect ECG #1 to look like? Note that there is now: i) A positive R wave and positive T wave in leads I and aVL; and, ii) An essentially all negative deflection in lead aVR.

Figure-4: Applying the manipulations specified in Figure-3 for LA-RA Lead Reversal — reveals in ECG #1A what the initial ECG in today's case should have looked like IF the LA and RA electrodes had been properly placed.

QUESTION:

Considering that ECG #1A in Figure-4 shows us what ECG #1 (that was recorded in association with an episode of severe chest pain) should look like — HOW would you interpret ECG #1A?

ANSWER:

For clarity in Figure-5 — I've put the tracing done at the time of hospital admission ( = ECG #2) — together with the "corrected" initial ECG in today's case ( = ECG #1A), that was recorded after hospital admission, when the patient began to have chest pain.

Regarding ECG #2:

There appears to be a regular supraventricular rhythm at 80-85/minute. It's difficult to tell if this is a sinus or ectopic atrial rhythm because of the baseline artifact (and the lack of a clearly upright P wave in all 3 of the beats shown in lead II).
The QRS is narrow in ECG #2. LAHB is present (ie, the QRS is very negative in lead aVF — and still predominantly negative in lead II). There is no chamber enlargement.
A QS complex is seen in lead V1 — but otherwise there are no Q waves. R wave progression is normal — with transition occurring between leads V3-to-V4. S waves persist through to lead V6. ST-T waves show nonspecific flattening of the ST segment (with a hint of ST depression is several leads) — but these changes do not appear to be acute.
IMPRESSION: Since the patient in today's case was admitted for pneumonia, and was not having any chest pain at the time ECG #2 was recorded — it was appropriate to interpret this hospital admission ECG as not suggestive of an acute cardiac process.

Figure-5: Comparison of the "corrected" initial ECG in today's case ( = ECG #1A) — with the hospital admission ECG that was recorded before the onset of chest pain (See text).

Regarding ECG #1A:

There once again is a fairly regular supraventricular rhythm at ~75/minute, with 2 PACs. Lack of a clearly upright P wave for the 2 beats that we see in lead II suggest that this may not be a sinus rhythm.
There has been an axis shift since the admission ECG — since the QRS complex in lead II of ECG #1A is no longer predominantly negative.
Each of the inferior leads in ECG #1A show — a Q wave (which is quite large in leads III and aVF) — ST segment coving with a small-but-definite amount of ST elevation — and — T wave inversion.
There are reciprocal changes in high-lateral leads I and aVL — in the form of ST segment straightening, slight depression, and terminal T wave positivity
I suspect that electrode leads V1 and V2 may have been placed too high on the chest — because both leads show a terminal r'. R wave progression is poor (ie, Transition never occurs in the chest leads). That said — ST-T wave changes in the chest leads do not appear to be acute.

IMPRESSION — Putting It All Together:

The tracing labeled ECG #1A (which shows what ECG #1 would have looked like IF electrode leads had been properly placed) — was obtained in response to new-onset chest pain that only developed after this patient was admitted to the hospital.

Comparison of ECG #1A with ECG #2 (in Figure-5) — confirms that the above-described ECG changes are new. In this context — these 2 serial tracings in Figure-5 should be interpreted as indicative of acute inferior OMI (Occlusion-based MI) — until you can prove otherwise.
Unfortunately — We do not have the details regarding when these 2 ECGs were obtained with respect to the precise timing of when the patient's chest pain began and ended. Without this precise timing — it's impossible to hone in on the sequence of events. For example — The fact that the inferior lead Q waves in ECG #1A are so large (in association with no more than modest ST elevation and T wave inversion) — suggests that some period of time (? hours) — may have passed since the onset of infarction.
T wave inversion in the inferior leads of ECG #1A — suggests that spontaneous reperfusion may have occurred. IF this patient's chest pain had resolved at the time this ECG was obtained — this would suggest that the "culprit" vessel ( = most likely the RCA = Right Coronary Artery) had spontaneously reperfused, and was now still open.
Finally — Given my suspicion of too-high placement of the V1,V2 electrodes — assessment for possible posterior involvement is problematic.

The "Lessons" To Be Learned:

Unfortunately — the LA-RA Lead Reversal in today's case was not recognized. Neither were the above-described ECG signs suggestive of infarction. Therefore, among the "Lessons to be Learned" from today's case include the following:

Lead I — usually manifests a predominantly positive QRS complex, because this left-sided lead normally sees the heart’s electrical activity as traveling toward lead I. It is of course possible to have right axis deviation — but you will virtually never see an all-negative (ie, QS) complex in lead I (as we almost did for the Qr complex in ECG #1) — unless there is: i) lead reversal; or ii) dextrocardia.
Lead aVR — usually manifests a predominantly negative QRS complex, because this right-sided lead normally views the heart’s electrical activity as traveling away from the remote (looking down from the right shoulder) viewpoint of lead aVR. Clearly, there are instances in which the QRS manifests positive activity in lead aVR — but the finding of an all negative QRS in lead I with an all positive QRS in lead aVR is virtually diagnostic of either lead reversal or dextrocardia!
The most time-efficient (and accurate) way to compare serial ECGs — is to interpret one of the ECGs completely — and to then look at both ECGs together — going lead-by-lead between the 2 tracings to see if there are significant differences. Had this been done in today's case — clinicians would have immediately realized that the switch from the predominantly negative Qr pattern in lead I and all positive R wave in lead aVR of ECG #1 — to the almost completely opposite QRS orientation in ECG #2 for these same leads — simply did not make physiologic sense.
Finally — Correlation between the timing of serial ECGs with respect to the presence and relative severity of chest pain at the time each ECG is done — is essential for optimal understanding of the sequence of physiologic events. This is the way to tell IF the "culprit" artery for an acute event is likely to still be occluded — or whether it is more likely to have spontaneously reopened. Awareness of this information is essential for optimal clinical decision-making regarding treatment modalities.

==============================

Acknowledgment: My appreciation to Anis Ahmad and Kianseng Ng (from Malaysia) for the case and this tracing.

==================================

Related ECG Blog Posts to Today’s Case:

ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post revieews the basics for predicting the "culprit artery". NOTE: The Audio Pearl reviews the concept of why the term "OMI" ( = Occlusion-based MI) should replace the more familiar term STEMI.
ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post).
ECG Blog #222 — Reviews the concept of Dynamic ST-T wave Changes (and how this ECG finding can assist in determining if acute cardiac cath is indicated).
ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?").
ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).
ECG Blog #175 — shows a case of true Dextrocardia! (and reviews the basics about the many different forms of Dextrocardia!).
ECG Blog #264 — shows a case of LA-RA lead reversal.
The November 19, 2020 post in Dr. Smith's ECG Blog — in which I present an easy-to-overlook but important case in which LA-LL lead reversal was missed (with the "tip-off" being recognition of a taller P wave in lead I > lead II).
The August 28, 2020 post in Dr. Smith's ECG Blog — My Comment (in my Addendum, at the very bottom of the page) reviews expected findings when there is LA-LL lead reversal (Tipoff = the P in lead I is larger than the P in lead II).
The July 29, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews this case in which there were 2 technical errors that multiple physicians failed to recognize ( = LA-RA lead reversal and too high placement of leads V1, V2 on the chest).
The February 11, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews this case in which there was LA-RA lead reversal.