ECG Blog #167 (Reciprocal-OMI-Normal)

You are “On” for interpreting a series of tracings from your local hospital. The ECG in Figure-1 was in your “pile” of tracings to interpret. No clinical information is provided.

• How would you interpret this ECG?
• Clinically — What should you do?

Figure-1: 12-Lead ECG in your “pile” of tracings to interpret. No clinical information is provided (See text).

COMMENT: Having worked in a clinical outpatient setting for 30 years, during which time I was charged with overreading all ECGs that were ordered by 35 medical providers — I am well familiar with the assignment of having a “pile” of tracings to review on patients I did not know, and about whom little or no clinical information was provided on the tracing.

• As is “usual” in such cases — the clinician who ordered the ECG will have already examined the patient and interpreted the ECG. But written documentation of HOW they interpreted the ECG usually would not appear on the tracing given to me for review.
• The TASK of the OVER-READER: To determine if there is anything important on the ECG that may have been overlooked — and to follow-up on this as appropriate. With time always at a premium — one obviously must be selective in deciding which tracings mandate follow-up ...

Descriptive Analysis of the ECG in Figure-1: There is a fairly regular sinus rhythm at ~85/minute. Overall voltage is reduced in both the limb and chest leads (although criteria for “low voltage” are not technically reached — since QRS amplitude in at least one of the limb leads [lead I] is >5 mm).

• Intervals — The PR interval is normal (ie, not more than a large box in duration). The QRS is narrow. The QTc is probably at the upper limits of normal.
• Axis — The mean QRS axis is normal (about +15 degrees).
• Chamber Enlargement — None.

Looking next at Q-R-S-T Changes:

• Q Waves — A definite Q wave is seen in lead III. Given tiny amplitude of the R wave in this lead — this is a large Q wave in lead III. I believe a tiny q wave is also seen in lead aVF (though this is admittedly difficult to discern given how tiny the QRS complex is in this lead).
• R Wave Progression — Transition is slightly delayed in the chest leads (ie, the R wave does not become taller than the S wave is deep until between V4-to-V5).

Regarding ST-T Wave Changes: 
Because of the small amplitude of the QRS complex in all limb leads (especially in lead aVF) — ST-T wave deviations are correspondingly small. As a result — assessment of ST-T wave deviation must be considered in proportion to QRS amplitude in the lead being assessed!

• There is ST elevation in each of the inferior leads! Relative to the R wave — the amount of ST elevation in lead III is more than 50% of R wave height, and 100% of R wave height in lead aVF! In addition — there is beginning T wave inversion in both of these leads, and probably also in lead II. As noted previously — there is a large Q in III, and a small-but-present q in aVF.
• There is mirror-image (reciprocal) ST depression in lead aVL when one compares this to the SHAPE of the ST elevation in lead III. This mirror-image relationship is best appreciated in Figure-2, in which I have superimposed the mirror-image of lead III (in GREEN) to the right of upright lead aVL (in RED). I’ve superimposed the mirror-image of lead aVL below upright lead III. 
• PEARL: There is an almost "magic" mirror-image relationship between leads III and aVL in many (if not, almost all) cases of acute inferior MI.
• Otherwise — there are some non-specific ST-T wave changes in the chest leads (ie, relative flattening of the T wave in most chest leads), and perhaps slight ST coving (but not elevation) of the ST segment in leads V4, V5 and V6. That said, there is really no anterior ST depression.

Figure-2: Blow-up of the 6 limb leads from Figure-1. Mirror-image blow-ups of leads III and aVL have been added (See text).

Clinical Impression / Clinical Notes on the ECG in Figure-1:

The ECG in Figure-1 is virtually diagnostic of recent, if not acute inferior MI. The presence of ST elevation in each of the inferior leads — in association with mirror-image ST depression in lead aVL — tells us to assume acute MI is ongoing until proven otherwise.

• As suggested above — given tiny QRS amplitude in the limb leads, the relative amount of ST elevation in the inferior leads is considerable!
• The Q wave in lead III is large! That said, it has been shown that even “large” Q waves may form within the first 1-2 hours of acute MI — so definitive information regarding the “age” of this MI is not forthcoming based on the size of the inferior Q waves seen here.
• There is beginning T wave inversion in the inferior leads. This suggests that this acute MI may not have just happened (ie, within the past 1-to-a-few hours) — though, on the other hand, this MI could be quite recent, because depth of these inferior T waves is minimal.
• Persistence of reciprocal ( = mirror-image) ST depression in lead aVL that is as deep as the ST elevation in lead III is tall (as we see in Figure-2) — is usually an acute finding.
• Most cases of acute inferior MI are associated with acute posterior involvement. However, none of the anterior ST depression usually associated with acute posterior involvement is seen here.

BOTTOM LINE: Clinical correlation is impossible without some history. That said, the ECG in Figure-1 is diagnostic of inferior MI, that could be quite recent in what may be an ongoing process.

• NOTE: The most likely “culprit artery” is the RCA (Right Coronary Artery) because: i) 80-90% of patients have a dominant right circulation, in which the RCA provides the primary blood supply to the inferior wall of the left ventricle; ii) The presence of more ST elevation in lead III than lead II (as is seen here) suggests the RCA rather than the LCx (Left Circumflex) as the “culprit” artery; and, iii) The presence of marked reciprocal ST depression in lead aVL also suggests the RCA (rather than the LCx) as the culprit artery. (For more on determining the likely “culprit" artery — See ECG Blog #80).

WHAT To Do in this Case? Unfortunately — NO historical information has been provided. By far, the BEST way to judge probable “age” of an acute MI is by correlating the history to ECG findings.

• As the clinician assigned to overread this ECG — the 1st thing I would do is immediately find the chart on this patient to see what was going on clinically. If the chart could not be quickly found, or if information on the chart was incomplete — I would call the medical care provider. We simply need to find out some History on this patient.
• IF the medical provider was not available — I’d call the patient.
• BOTTOM Line: IF the history in this case was at all suggestive of recent onset of symptoms — then acute intervention (ideally by cardiac catheterization with angioplasty as appropriate) would be indicated.

Follow-up of this Case:

• It turned out that this patient was seen for symptoms. Unfortunately, the possibility of an MI that was ongoing was not recognized. The patient died before referral was made ...

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Acknowledgment: This case was sent to me from Malaysia.

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ECG Blog #166 (ST-T – AFib – LVH – SVT)

The ECG that appears in Figure-1 was obtained from a 65-year old woman who presented in acute heart failure (HF). She was on multiple medications. She was short of breath — and had been having intermittent chest discomfort.

• How would you interpret this ECG?
• Is it surprising that this patient presented in HF?
• What might account for the ST-T wave changes that are seen in many leads on this tracing?

Figure-1: 12-Lead ECG obtained from a 65-year old woman who presented in acute HF (See text).

Descriptive Analysis of the ECG in Figure-1: 
The rhythm is rapid and irregularly irregular. No P waves are seen in any of the leads. This defines the rhythm as AFib (Atrial Fibrillation) — seen here with a rapid ventricular response. Since most R-R intervals look to be a little less than 2 large boxes in duration — the average ventricular rate is over 150/minute (probably ~160-180/minute range).

• Intervals — The QRS complex is of normal duration. (The PR interval is not relevant when the rhythm is AFib — and the QTc interval is meaningless at as fast of a rate as seen here.).
• Axis — The mean QRS axis is normal (between +60-70 degrees).
• Chamber Enlargement — There is LVH (Left Ventricular Hypertrophy). The sum of the deepest S in V1,V2 + tallest R in V5,V6 ≥35 mm (Criteria for LVH used in this case are discussed in more detail below! ).

Looking next at Q-R-S-T Changes:

• Q Waves — No Q waves are seen.
• R Wave Progression — Transition is normal (occurs between lead V2-to-V3, albeit the R wave is already fairly tall by lead V2).
• ST-T Wave Changes — As an overall assessment, there is ST segment “scooping” and/or slight depression in multiple leads. We would describe this as diffuse NS (Non-Specific) ST-T wave abnormalities.

Figure-2: Common causes of ST-T wave depression (See text).

Clinical Impression / Clinical Notes: The rhythm is rapid AFib. In patients with new-onset AFib — loss of the atrial "kick" and the rapid ventricular response that so often accompanies new AFib (which significantly reduces the period of diastolic filling) — are reasons why new-onset HF and AFib are so commonly associated!

• Of interest in Figure-1 — Note the marked change in appearance of the QRS complex from beat-to-beat in lead aVL. This most likely reflects respiratory variation in this acutely ill patient with heart failure.
• As noted earlier — there is LVH.
• There are diffuse, nonspecific ST-T wave abnormalities that may be due to i) LV "Strain"; ii) Ischemia; iii) Drug effect; iv) Electrolyte Disturbance; v) Tachycardia; and/or, vi) Any combination of the above (Figure-2).

BOTTOM Line: There is rapid AFib — which is presumably new. That said — at least the ST-T wave changes that we see in Figure-1 do not appear to be acute in this patient with intermittent chest discomfort (ie, other than lead aVL — there is no ST elevation). Clinical correlation will be needed to determine which of the causes of ST-T wave depression that are listed in Figure-2 are likely to be operative in this case.

Looking closer at the ECG diagnosis of LVH in Figure-1:

• There are numerous criteria in the literature for ECG diagnosis of LVH. For simplicity — we summarize the criteria we favor in Figure-3. We discuss this topic fully in ECG Blog #73.
• In my opinion — there is an “art” to the ECG diagnosis of LVH. Clinical factors — including patient age, race and the presence of certain underlying heart diseases (such as longstanding hypertension or heart failure) predispose a patient to LVH. As a result — even when numerical criteria for LVH voltage fall slightly shy of the lower LVH voltage threshold — “probable” LVH can still be strongly suspected in an older adult with underlying heart disease, especially if ST-T wave changes of LV “strain” (or a “strain” equivalent) are present.
• To facilitate application of Figure 3 — We’ve counted R wave and S wave amplitude in several key leads for the ECG in this case, which we show in Figure-4. Voltage criteria for LVH are satisfied in this case by: i) Sum of the S in V1 (16 mm) + R in V5 (21 mm) ≥35 mm; and, ii) Sum of the R wave in lead II ≥20 mm.

Figure-3: Criteria we favor for the ECG diagnosis of LVH — excerpted from ECG Blog #73. NOTE — Only 1 voltage criterion need be met for LVH by voltage to be satisfied (See text).

Figure-4: We’ve counted R wave and S wave amplitude from Figure-1 in several key leads. Applying criteria suggested in Figure-3 — voltage for LVH is satisfied (See text).

Looking closer at the 6 Common Causes of ST-T Wave Depression from Figure-2:

• There are actually over 50 causes of ST-T wave changes on ECG. Although many of these causes are cardiac-related — there are also many that are not cardiac-related. Among the many non-cardiac causes of ST-T wave changes are hyperventilation; temperature extremes (excessive heat or cold exposure); anxiety or emotional stress; anemia; tachycardia; sleep deprivation; pulmonary disease; electrolyte abnormalities; central nervous system disorders; certain medications; and severe medical illness (among others). BOTTOM Line: Rather than attempting to commit to memory an exhaustive list of conditions that may predispose to ST-T wave changes — it suffices to appreciate the variety of entities that may produce changes on ECG. Remember: Many of these conditions are non-cardiac.
• NOTE: In general — causes of T wave abnormalities (including T wave flattening or frank T wave inversion) are similar to potential causes of ST segment depression.
• PEARL #1: The purpose of formulating the short list that we show in Figure-2 — is that it simplifies your task as the interpreter. As soon as you recognize generalized ST-T wave changes on an ECG — Consider this short LIST. Often — more than a single cause will be operative. For example — the patient in this case was an older woman on multiple medications, who presented in heart failure. As a result — she might be taking Digoxin and/or a Diuretic (which might contribute to electrolyte disturbance). She has heart failure and voltage for LVH — so the ST-T wave changes may reflect LV “strain” (or a strain equivalent). In addition, the ST-T wave changes we see in Figure-1 could reflect ischemia in this patient with intermittent chest discomfort. Finally, the very rapid ventricular rate may be contributing to ST-T wave flattening and depression that will resolve once the rate slows. BOTTOM Line — All of the potential causes of ST-T wave depression listed in Figure-2 may be contributing in varying degree to the ECG picture we see in Figure-1.

PEARL #2: The Shape of the ST-T wave may suggest which one (or more) of the 6 entities in our LIST is (are) most likely to be operative in a given patient (See bottom half of Figure-2):

• Ischemia — is suggested by symmetric T inversion (RED arrow in Panel B) — especially when seen in two or more leads of a given lead group (ie, in leads II, III and aVF — or in both leads I and aVL).
• Strain — from LVH, is suggested by asymmetric ST depression occurring in one (or more) of the lateral leads (less often in the inferior leads). Note the initial slow sagging of the ST segment with LV “strain” (BLACK arrow in Panel A) — with more rapid return to the baseline. “Strain” is more likely to be the cause of ST depression when voltage for LVH is present — although occasionally, there may be ST-T wave changes suggestive of “strain” without accompanying voltage.
• "RV strain" — is suggested IF the picture in Panel A of Figure-2 is seen in right-sided leads (leads II,III,aVF; or V1,V2,V3) in a patient with RVH.
• Use of Digoxin may affect ST-T waves in one of 3 ways: i) There may be “scooped” ST depression in multiple leads (that simulates an inverted ice cream cone, as in Panel D of Figure-2); or, ii) Digoxin “effect” may produce a "strain"-like pattern (identical to Panel A); or, iii) Despite use of an appropriate amount of  Digoxin — there may be little-to-no effect on the ST-T wave. In my experience (from correlating ECG ST-T wave appearance to serum Digoxin levels over many years) — the serum Digoxin level correlates poorly with the amount of ST-T wave scooping or depression. Thus, despite even high serum Digoxin levels — some patients fail to manifest ST-T wave abnormalities — whereas other patients show marked ST-T wave changes despite surprisingly low serum Digoxin levels.
• Finally — Panel C in Figure-2 shows a non-specific ST-T wave pattern, in which the T wave and ST segment are flattened (if not slightly depressed). This pattern is called “nonspecific” — because any of the many potential causes of ST-T wave abnormalities may be operative.
• BOTTOM Line (regarding ST-T wave changes in Figure-1) — The depressed ST segments manifest a scooped appearance in many leads. We therefore need to find out IF this patient who is on multiple medications (and who is in heart failure) is taking Digoxin? That said — any (or all) of the causes listed in Figure-2 may be contributing to the ST-T wave changes that we see in Figure-1.