ECG Blog #82 — Serial STEMI Tracings

     

Interpret the ECG shown in Figure-1 — obtained from a patient with new-onset chest pain. There is an obvious acute STEMI (ST Elevation Myocardial Infarction). Follow-up ECGs on this patient are shown in Figure-2 (obtained a short while later) — and finally in Figure-3 (obtained post-cath/reperfusion).

• Is there evolution of the MI on these serial ECGs? What are the specific changes you see as you compare these sequential tracings?
• Which coronary artery is likely to be acutely occluded?
• Was acute reperfusion successful (Figure-3)?

Figure-1: This is ECG #1 (blue border) — from this patient with new-onset chest pain. There is sinus bradycardia with marked precordial ST elevation. Q waves have not yet formed in the anterior leads on this initial ECG #1. Note the hyperacute appearance of ST-T waves in leads V2,V3,V4. Surprisingly — reciprocal changes are minimal (no more than slight ST-T wave flattening/depression in the inferior leads). Despite this — there can be little doubt that this ECG #1 represents a large acute STEMI in evolution.

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What is the “Culprit” Artery?: We suspect acute proximal LAD occlusion as the “culprit” artery for the acute STEMI seen in Figure‑1. This is suggested by the ECG finding of diffuse precordial ST elevation that is especially marked in leads V2-to-V4.

• Acute occlusion of the LMain (Left Main) Coronary Artery is rarely seen in practice — because it usually leads to rapid demise of the patient. In addition to its uncommon occurrence — another clue that the ECG in Figure-1 does not represent LMain occlusion is that ST elevation is clearly more marked in lead V1 than in lead aVR. In contrast, with LMain disease or occlusion — ST elevation is generally more marked in aVR compared to V1.
• This patient is an ideal candidate for acute reperfusion — because there is marked ST elevation in Figure-1, but no anterior Q waves have yet formed. The cath lab should be immediately activated.

Two follow-up ECGs to Figure‑1 are shown below. For clarity — We use a different color border for each tracing:

• Figure-1 — ECG #1 (blue border) = the initial ECG obtained at presentation.
• Figure-2 — ECG #2 (red border) = obtained a short while after ECG #1.
• Figure-3 — ECG #3 (green border) = obtained after acute cath and angioplasty/stenting of the acutely occluded LAD.

As you evaluate these serial ECGs — Keep in mind the following Questions:

• Is there ECG evidence of evolution on these serial ECGs?
• Was acute reperfusion successful (Figure-3)?

Figure-2: This is ECG #2 (red border) — obtained a short while after ECG #1 from this patient with acute STEMI. Note that since ECG #1 — there has been interim development of RBBB (an rSr’ complex is now seen in V1 with wide terminal S waves in leads I,V6). The appearance of lead V2 is concerning — as the large new Q wave and now T wave inversion in this lead suggest ongoing evolution is in progress. 

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Figure-3: This is ECG #3 (green border) — obtained after acute catheterization and angioplasty/stenting of the acutely occluded LAD. The “good news” — is that this post-cath ECG #3 is encouraging! Note that the QRS complex has narrowed and RBBB is no longer present. The Q wave seen earlier in lead V2 of ECG #2 has resolved — and ST-T waves have essentially returned to baseline. R wave progression is essentially normal (with transition between V3-to-V4). It appears that acute reperfusion has salvaged significant myocardium!

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BOTTOM Line: Use of serial ECGs may be extremely valuable in following the course of acute MI. Lead-to-lead comparison of QRS morphology and ST‑T wave changes facilitates determining which changes are new — as well as providing insight to the likely benefit obtained from acute intervention.

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The LAD: Taking A Closer Look

The normal (expected) coronary anatomy of the LCA (Left-Coronary Artery) is depicted in schematic Figure-4:

• The LCA arises from the left aortic sinus. This vessel begins as the LMain (Left Main Coronary Artery), which is typically a short vessel (<10mm) that then bifurcates into the LAD (Left Anterior Descending Artery) and the LCx (Left Circumflex Coronary Artery).

Major Branches of the LAD: The LAD (Left-Anterior-Descending) Artery runs along the anterior epicardial surface of the heart in the interventricular groove on its path toward the cardiac apex. The LAD generally supplies the anterior wall of the heart, the cardiac apex and a major portion of the conduction system.

• The major branches of the LAD are i) the Septal perforator vessels; and ii) Diagonal branches.
• Septal branch anatomy is highly variable. We show 2 septal branches in Figure-4 (S-1; S-2) — but instead there may be only one septal branch or many septal branches, depending on individual anatomy. The 1st septal branch is typically the largest; its takeoff is generally just after the takeoff of the 1st diagonal branch.
• The interventricular septum is the most densely vascularized area of the heart. This is as it should be given the integral role of the septum in providing blood supply to the heart’s conduction system. Septal perforators normally run a vertical path downward following their takeoff from the proximal LAD.
• Downward penetrating septal branches from the LAD typically connect with upward penetrating septal branches from the PDA branch of the RCA. In this way — there is usually a network of collaterals from both LCA and RCA systems in the event of disease in one system. How adequately collaterals from one system compensate for disease in the other is subject to individual variation (as well as to how rapidly occlusive disease develops).
• Clinical Note: Very proximal LAD lesions have been known as “widow-makers”. Especially if proximal to the 1st septal perforator (and the 1st diagonal branch) — these lesions are virtual “left-main-equivalents” because of the extent of injury and conduction system damage they cause.
• Diagonal branch anatomy is also highly variable. We show 2 diagonal branches in Figure-4 (D-1; D-2) — but there may be 1, 2, or 3 diagonal branches supplying the anterolateral wall of the heart. Occasionally — there is no diagonal branch per se, but rather a discrete ramus intermedius arising from between the LAD and LCx to supply the anterolateral surface (not shown on Figure-4). Typically — it is the 1st diagonal branch that is the largest.
• Clinical Note: Considerable variation in number and course of diagonal branch anatomy (and the angulated path that these vessels follow) may require multiple views on cath to determine if occlusion is present.
• NOTE-2: Additional variations in anatomy are not uncommon. One to be aware of is a “wraparound” LAD — in which the LAD is a larger and longer vessel, to the point of extending beyond the cardiac apex and “wrapping around” to supply the undersurface (= inferior wall) of the heart. Awareness of this anatomic variant provides one explanation for the ECG pattern of simultaneous ST elevation in inferior and anterior lead areas that may sometimes be seen due to acute occlusion of a single vessel.

Figure-4: Normal coronary anatomy of the left coronary artery and its major branches. The LCA (Left Coronary Artery) begins as a short LMain (Left Main Coronary Artery) branch — which then bifurcates into the LAD (Left Anterior Descending Artery) and the LCx (Left Circumflex Artery). Panel A — anterior view. Panel B — RAO (Right-Anterior Oblique) view. Abbreviations: S‑1,S‑2 (Septal Perforator branches); D‑1,D‑2 (Diagonal branches); M‑1,M‑2 (Obtuse Marginal branches from the LCx).

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Acute LAD Occlusion:

ECG findings arising from acute LAD occlusion may vary depending on: i) The relative site of occlusion within the LAD (ie, proximal to septal perforators and the 1st diagonal or more distal occlusion); ii) Any prior infarctions that may have occurred; iii) Presence of any anatomic variants (such as a “wrap-around” LAD circulation); and iv) The status of the collateral circulation. For simplicity — our comments below relate to expected ECG findings assuming no prior infarctions; no alteration in collateral circulation; and no anatomic variants.

• Acute LAD occlusion leads to acute anterior MI. This may be extensive and also involve the lateral wall.
• The most typical ECG manifestation of acute LAD occlusion is ST elevation in anterior leads (usually in ≥2 leads between V1-to-V4).

PEARL: ST elevation in lead aVL — may provide an invaluable clue to the location of the acutely occluded coronary artery. According to a study by Birnbaum et al (Am Heart J 131:38, 1996):

• Suspect acute LAD occlusion proximal to the 1st Diagonal IF in addition to ST elevation in aVL — there is also ST elevation in leads V2-through-V5. This is the most common situation when there is ST elevation in lead aVL.
• Suspect 1st Diagonal branch occlusion IF in addition to ST elevation in aVL — there is ST elevation in lead V2 (but not in V3,V4,V5).
• Suspect LCx occlusion (especially of the 1st obtuse marginal branch) — IF there is ST elevation in aVL but not in lead V2 (and not in other anterior leads).

NOTE: Anterior ST elevation without ST elevation in lead aVL — usually suggests more distal LAD occlusion after takeoff of the 1st Diagonal.

• PEARL: In addition to recognizing ST elevation in lead aVL with marked anterior ST elevation — there are 2 additional ways to identify patients at high risk of impending proximal LAD occlusion. These are: i) Recognition of Wellens’ Syndrome (Click here for more on Wellens' Syndrome); and ii) Recognition of DeWinter T Waves (See ECG Blog #53).

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RETURN to Figure-1: Is this Proximal LAD Occlusion?

Application of the above concepts to the ECG shown in Figure-1 (reproduced below in Figure-5) — supports our presumption of a proximal LAD occlusion. Although this patient “failed to read the textbook”, in that there is no ST elevation in lead aVL — proximal LAD occlusion is still strongly suggested because: i) There is marked ST elevation in all anterior leads, including significant ST elevation in lead V1; ii) ST elevation in lead V1 is clearly more than in lead aVR (virtually no ST elevation in aVR); and, iii) The patient developed septal Q waves (in lead V2) as well as RBBB on the follow-up tracing (Figure-2). RBBB and the septal Q wave fortunately resolved following the good result obtained from acute reperfusion.

Figure-5: This is ECG #1 (reproduced from Figure-1) — obtained from this patient with new-onset chest pain. Despite lack of ST elevation in lead aVL — we strongly suspect proximal LAD occlusion (See text).

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Link to Section 10.0 for pdf download on the ECG Diagnosis of Acute MI (from our ECG-2014-ePub).

• ECG Changes of Acute MI — begins in Section 10.1 - 
• Discussion of the Coronary Circulation (and determining the "culprit" artery) — begins in Section 10.16 - 
• See ECG BLOG #80 for a case involving differentiation between acute RCA vs LCx occlusion.

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ECG Blog #81 — Tall R Wave in V1 ...

There is a tall R wave in lead V1 of the ECG that is shown below (Figure-1). No history is available.

• What is the likely cause of this Tall R Wave in Lead V1?

Figure-1: 12-lead ECG showing a tall R wave in lead V1. What is the likely cause of this tall R wave? 

Normal Appearance of the QRS in Lead V1

When the rhythm is supraventricular — the QRS complex in lead V1 should be predominantly negative under normal circumstances. This is because this right-sided lead (V1) normally sees electrical activity as moving away from V1 (or toward the large left ventricle). This concept is illustrated in schematic Figure-2.

• The finding of predominant positive activity in lead V1 (an R wave that equals or exceeds the S wave in this right-sided lead) — is not “normal”. This is the premise on which one of our 6 “Essential Lists” in ECG Interpretation is based (Figure-3 below).

Figure-2: Transverse (cross-sectional) view of the heart — illustrating precordial lead appearance in leads V1-through-V6. Transition occurs in the above Figure between lead V2-to-V4. Note that the QRS complex in lead V1 is predominantly negative under normal circumstances (red box). Septal depolarization normally moves left-to-right (small black arrow). The major component of ventricular activation moves to the left and posteriorly (large red arrow) — which reflects the relative size and anatomic position of the left ventricle. This explains why lead V1 normally sees predominant electrical activity as moving away from this right-sided lead. 

LIST #6: Causes of a Tall R Wave in Lead V1

It is easy to overlook the finding of a tall (or relatively tall) R wave in lead V1. It is equally easy to overlook the finding of early transition — in which the R wave in precordial leads V2 or V3 becomes disproportionately tall much sooner than expected.

• The KEY to not overlooking the ECG findings of a tall R wave in lead V1 or early transition — is to routinely apply a Systematic Approach to your ECG interpretation. This is our purpose for including the “R” component (looking for R Wave progression) when assessing for “Q-R-S-T” Changes.
• The purpose of our LIST #6 which we present in Figure-3 — is to facilitate recall of the principal causes of a disproportionately tall R wave in lead V1. The best way not to overlook any of the causes — is to work through each of the entities on this list whenever you recognize that the R wave in lead V1 is taller than you expect.
• NOTE: Awareness of these causes is especially important — because computerized ECG interpretations typically fail to pick up a taller-than-expected R wave in leads V1,V2,V3.

Figure-3: The Common Causes of a Tall R Wave in Lead V1 = LIST #6. Normal variant is a diagnosis of exclusion. 

Taking a Closer Look at LIST #6:

The way to narrow down which of the entities on List #6 is likely to be the cause of a tall R wave in lead V1 — is to look for associated findings in the remaining leads.

• WPW — Look for the QRS to be wide with delta waves and a short PR interval.
• RBBB — Look for the QRS complex to be wide with an rSR’ (or equivalent) in lead V1 and wide terminal S waves in leads I,V6.
• RVH — Look for ECG criteria of RVH including right or indeterminate axis; RAA (Right Atrial Abnormality); tall R wave in V1; RV “strain”; persistent precordial S waves  (See ECG Blog #77).
• Posterior MI — Look for ECG evidence of associated inferior infarction and for a positive “mirror test” (See ECG Blog #56).
• Hypertrophic Cardiomyopathy — See below.
• Normal Variant — to be considered only after the above 5 causes have been ruled out. Thus, the diagnosis of “normal variant” as the reason for a disproportionately tall R wave in lead V1 — is a diagnosis of exclusion!
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• P.S. — My List in Figure-3 is not all-inclusive. For example — uncommon conditions such as dextrocardia or a mix-up in the chest leads could also result in an unexpectedly tall R wave in lead V1. Other entities (ie, a drug toxicity, hyperkalemia, Brugada syndrome) — may also alter the appearance of the QRS complex in lead V1, but these entities will usually be suggested by the clinical history.

HOW to Recognize Hypertrophic Cardiomyopathy on ECG? 

Be aware of the 5th cause in List #6 of a Tall R in Lead V1 — which is HCM (Hypertrophic CardioMyopathy). Although not overly common — HCM is an important potential cause of sudden death (especially in young athletes). Echo is diagnostic! On the other hand — ECG findings are highly variable. These may include a moderately tall R wave in lead V1 which suggests prominent septal forces. It might also include deep septal Q waves; LVH by voltage; IVCD/LBBB — or no ECG changes at all. The reason for emphasizing awareness of HCM is the risk of sudden death that HCM poses among previously healthy young adults. While cost concerns prohibit mass screening by Echo of all young adults — Echo is indicated when there is a history of syncope during exercise; with a positive family history for early sudden death; when a non-innocent murmur is heard — or when a pre-participation ECG reveals abnormal findings that may be consistent with the diagnosis.

Returning to FIGURE-1: What is the Cause of the Tall R in V1?

Let’s apply List #6 to the ECG in Figure-1 (reproduced below in Figure-4). The QRS complex looks to be slightly wide. The rhythm appears to be sinus — as suggested by the presence of an upright P wave in lead II. The PR interval in lead II looks normal. The QT is not prolonged. The most remarkable finding on this tracing — is the very tall R wave in lead V1. This is clearly not expected — and should prompt consideration of the 6 entities in LIST #6 as a possible explanation.

• We suspect that the answer will probably also explain: i) the marked left axis (and/or QS complex in inferior leads); and ii) ST flattening and shallow T inversion seen in multiple leads.

Figure-4: We reproduce Figure-1 of this ECG showing a tall R wave in lead V1. What is the likely cause?

ANSWER to Figure-4:

No history is available. The rhythm in Figure-4 appears to be sinus. The QRS looks slightly wide. As we work through List #6 (Figure-3) — We note the following:

• This is clearly not a “normal variant” tracing. Other than the tall R wave in lead V1 — there is really nothing to suggest RVH (no right axis; no RAA; no RV “strain” in lead V1). And although it almost looks as if there are inferior Q waves — this is not the usual picture of inferior infarction, and the “mirror test” is not suggestive of posterior infarction.
• Finally — the patient does not have RBBB. There is no rSR’ in lead V1 — and no S wave is seen in lead I. The QRS complex is also not as wide as is generally seen with bundle branch block.
• The patient has WPW! It is important to appreciate that the QRS complex is not always overly wide with WPW. This is because there may occasionally be simultaneous conduction down both normal and accessory pathway — which will result in only partial pre-excitation. It is because of awareness of LIST #6 — that one looks extra hard for delta waves whenever the finding of a tall R wave in V1 is seen. Close inspection reveals such delta waves are seen (red and blue arrows in Figure-5).

Figure-5: Arrows highlight delta waves that were subtly present in the ECG shown in Figure-4. The QRS complex with WPW will not always be overly wide — as there may only be partial pre-excitation (if impulses are simultaneously conducted down normal and accessory pathway). Although the PR interval looks to be normal in lead II of this tracing — it appears to be short in leads V4,V5,V6 (red arrows in these leads). Delta waves are present. They are negative in the inferior leads (blue arrows) — and positive in other leads in which they are seen (red arrows). No delta wave is evident in leads aVR, aVL or V2. 

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For more information — GO TO:

• See ECG Blog #93 ( = Basic Concepts #6)  — for Review of the Systematic Approach to ECG interpretation.
• CLICK HERE — to download a pdf of Section 10.41 on Causes of a Tall R Wave in Lead V1 (from our ECG-2014-ePub).