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).

ECG Blog #80 — CP & Coronary Anatomy

     Interpret the ECG shown in Figure-1 — obtained from a patient with new-onset chest pain.

• Localize the area(s) of acute infarction.
• Which coronary artery is likely to be acutely occluded?

Figure-1: ECG obtained from a patient with new-onset chest pain. Which coronary artery is likely to be acutely occluded? (See text).

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Interpretation of Figure 1:

     The rhythm is sinus. Intervals and axis are normal. No chamber enlargement. Regarding Q-R-S-T Changes:

• Small q waves are seen in leads II,III,aVF; and V5,V6.
• Transition is normal (occurs between lead V2-to-V3) — albeit the R wave is a bit taller-than-is-usually-expected in leads V2,V3.
• There is subtle-but-real ST elevation in each of the inferior leads (II,III,aVF) —  with suggestion of hyperacute T waves (especially in lead II). A similar pattern of slight J-point ST elevation is seen in leads V5,V6 — with suggestion of hyperacute T waves in these leads.
• There is marked ST depression in leads V1-thru-V4.

Impression: Sinus rhythm with acute infero-postero-lateral STEMI (ST Elevation Myocardial Infarction). The cath lab should be activated. We suspect acute LCx (Left Circumflex Artery) occlusion.

• Although q waves in the infero-lateral leads are small and narrow — these are the very same leads that manifest ST elevation with hyperacute T waves. While these might possibly be normal septal q waves — it is far more likely that they reflect ongoing acute infarction. In any case — We should know the answer shortly (if the q waves become larger as the infarct evolves – or – if they resolve after reperfusion).
• The ECG picture in leads V1,V2,V3 strongly suggests associated acute posterior infarction. We say this despite the reality that none of the standard 12 leads directly visualize the posterior wall of the LV (Left Ventricle). Therefore — to diagnose acute posterior MI, one either has to: i) Obtain additional leads that directly visualize the posterior wall (= leads V7,V8,V9); or ii) Perform a “Mirror” Test (turning the tracing over and holding it up to the light — which provides a mirror-image view of the anterior leads — Figure-2).

Figure-2: Diagnosis of acute posterior MI is made from Figure-1 by applying the “Mirror” Test (ie, turning the tracing over and holding it up to the light). Doing so transforms the anterior ST depression and tall R waves that were seen in leads V2,V3 of Figure-1 into Q waves and ST elevation once the tracing is flipped over (red rectangle encircles leads V1,V2,V3 that were flipped over).

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The Coronary Circulation: 

     The most common cause of acute MI is sudden total occlusion of a major coronary artery.  The area of the heart affected will depend on distribution to the area from the coronary circulation.

• Prompt recognition of acute coronary occlusion with rapid initiation of reperfusion therapy is essential for optimal outcome. For this — evaluation of the initial ECG is invaluable. Appreciation of normal coronary anatomy and common variants facilitates the process.

In Figure-3 — We present a schematic overview of normal coronary anatomy (Panel A). The two major vessels supplying the heart are the right and left coronary arteries. These most commonly arise from the right and left aortic sinuses, respectively.

• In most patients (80-90%) — the RCA (Right Coronary Artery) is a dominant vessel that supplies the RV (Right Ventricle) — and then continues as the PDA (Posterior Descending Artery) along the undersurface of the heart (unlabeled dotted vessel arising from the RCA in Panel A) to supply the inferior and posterior walls of the LV (Left Ventricle). Not shown — the AV nodal artery is most often supplied from the RCA.
• As suggested in Panel A — the LMain (Left Main Coronary Artery) is typically a short vessel (<10mm) that then bifurcates into the LAD (Left Anterior Descending Artery) and the LCx (Left Circumflex Coronary Artery).
• In ~15% of patients — there is a “left-dominant” circulation (shown in Panel B of Figure-3). In this case — the RCA is a smaller vessel than depicted in Panel A. To compensate — the LCx is typically larger and gives rise to the PDA (large unlabeled dotted vessel arising from the LCx in Panel B). In a left-dominant circulation — the inferior and/or posterior wall of the LV is supplied by the LCx.
• KEY Clinical Point: The existence of a left-dominant circulation in ~15% of patients explains why inferior and posterior MIs will not always be due to acute RCA occlusion. Similarly, since the AV nodal artery may be supplied by the LCx in a left-dominant circulation — AV block may also occasionally occur with LCx (rather than RCA) occlusion.

Figure-3: Overview of normal coronary anatomy. Panel A — the most common situation (80-90%), in which the RCA is a dominant vessel that supplies the RV as well as the posterior and inferior walls of the LV. Panel B — represents a left-dominant circulation, in which the LCx (rather than the RCA) supplies the posterior and inferior walls of the left ventricle.

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Localizing the “Culprit” Artery:

     While definitive identification of the “culprit” artery (acutely occluded vessel) will be forthcoming on cardiac catheterization — assessment of the initial ECG may provide important clues to the angiographer that facilitate knowing where to look.

• Given the presence of acute inferior infarction without anterior ST elevation in Figure-1 — the “culprit” artery is almost certainly either the RCA (Right Coronary Artery) or the LCx (Left Circumflex Coronary Artery).

ECG findings arising from acute RCA occlusion will vary depending on: i) Whether the patient has a dominant right or left circulation; ii) The relative site of occlusion within the RCA (ie, proximal or more distal occlusion); iii) Any prior infarctions that may have occurred; and, iv) The status of the collateral circulation. For simplicity — We describe expected ECG findings assuming no prior infarctions and no alteration in collateral circulation.

• In the 80-90% of patients with a right-dominant circulation (Panel A in Figure-3) — the most typical manifestation of acute RCA occlusion is ST elevation in all 3 inferior leads (II,III,aVF) = acute inferior MI.
• Acute RV (Right Ventricular) MI — is likely to be seen when there is proximal RCA occlusion. More distal RCA occlusion may spare much of the right ventricle.
• PEARL: Proximal RCA occlusion is suggested when ST elevation in lead III is more than in lead II (especially if there is marked ST depression in lead aVL). This picture is seen in Figure-4. In contrast — a left-dominant LCx occlusion is suspected when there is inferior MI with less ST elevation in lead III and less ST depression in lead aVL (especially if there is significant ST elevation in leads V5,V6).
• Posterior MI — is commonly seen with RCA occlusion (because the RCA most often supplies both inferior and posterior walls of the LV). Posterior MI may also be seen with LCx occlusion IF there is a left-dominant circulation. In either case — there will usually be ECG evidence of inferior MI when there is posterior MI.

Figure-4: Acute infero-postero MI from acute proximal RCA occlusion. Note ST elevation in lead III > II with marked reciprocal ST depression in lead aVL. Posterior involvement is suggested by the ST depression in lead V2 (positive “mirror” test). There may also be acute RV involvement.

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Additional Points regarding Acute RCA Occlusion: 
     Keeping in mind the areas of the heart most commonly supplied by the RCA facilitates recognizing acute occlusion of this vessel (Figure-4):

• Lead III is more rightward (at +120 degrees) than lead II (at +60 degrees). As a result — acute occlusion of the RCA generally produces more ST elevation in lead III than in lead II (Figure-4).
• The electrical perspective of lead aVL is virtually opposite that of lead III. As a result — the shape of the reciprocal ST depression in Lead aVL often looks like the mirror-image opposite of the ST elevation in lead III. ST-T wave changes in aVL are typically marked when there is proximal RCA occlusion — and are generally more prominent than in lead I.
• Posterior MI is suggested in Figure-4 — because of the positive “Mirror Test” for lead V2 (ie, flipping lead V2 over would result in a Q wave with slight-but-real hyperacute ST elevation in this lead).
• NOTE: Associated posterior MI may be seen when acute inferior MI results from either RCA occlusion or a left-dominant LCx occlusion. However, associated acute RV (Right Ventricular) MI localizes the “culprit artery” to the RCA — because the right ventricle is not supplied by the LCx (Left Circumflex Artery). While use of right-sided leads is needed for definitive diagnosis of acute RV MI — a hint that RV MI may be present is sometimes provided by right-sided lead V1 — IF there is ST coving or slight elevation in lead V1 but ST depression by lead V2.
• Beyond-the-Core: We suspect that there may also be associated acute RV MI in Figure-4 — because the ST-T wave in lead V1 is relatively flat. Normally, with acute posterior MI — there is similar-appearing ST-T wave depression in each of the anterior leads (V1,V2,V3). In contrast, when there is also acute RV MI — right-sided ST elevation in lead V1 cancels out some of the ST depression that would have been seen from the posterior infarction. Bottom Line: Suspect associated acute RV MI with acute infero-postero MI from proximal RCA occlusion — IF you see ST segment coving with slight ST elevation in lead V1. The finding of a flat (instead of depressed) ST segment in lead V1 (as is seen in Figure-4) — suggests that there may be some canceling out of V1 ST depression by acute RV ST elevation. IF important to know — right-sided leads would answer this question.
• Clinical Note: It is well to remember that 2nd-degree AV Block, Mobitz Type I — is most often seen in association with acute RCA occlusion (since the RCA usually supplies the AV nodal artery). That said — Mobitz I may occasionally be seen with acute LCx occlusion of a left-dominant circulation (in which case the AV nodal artery will usually be supplied by the Lcx).

Returning to FIGURE-1: Acute Circumflex Occlusion

     With the above as background — Let us now return to the initial ECG in Figure-1 that we presented at the onset of this case (which we reproduce below in Figure-5):

• There is acute infero-postero-lateral MI.
• The “culprit” artery is likely to be a dominant-left Circumflex (LCx) because: i) ST elevation in lead III is less than in lead II; ii) There is no ST elevation in lead aVL; iii) There is no hint of acute RV involvement (ST depression is prominent in V1 — whereas we’d expect either a flat or coved ST segment with slight elevation in V1 if there was associated RV involvement); and, iv) There is ST elevation in V5,V6 — and this ST elevation in lead V6 is clearly more than it is in lead III.

Figure-5: ECG obtained from a patient with new-onset chest pain (this ECG was initially shown in Figure-1) There is acute infero-postero-lateral MI. The “culprit” artery is most likely to be the LCx in a dominant-left circulation (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 - 
• Mirror Test (Posterior MI) — begins in Section 10.33 -
• See ECG BLOG #82 — for a case involving LAD vs LMain occlusion -

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A POEM regarding Rhythm Interpretation (by Ken Grauer, MD)

On a lighter note — I thought I would share the short poem I just wrote regarding rhythm interpretation. I was inspired by those who negate the use of lead II as "giving no clue".

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TITLE: 12 Leads are Better than One (Ken Grauer, MD):

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1 lead alone is lacking,

If you only use one you are slacking.

A 12-lead is better than one,

It helps with the answer, while before you had none.

This of course all assumes that your patient is stable,

Because if not — then a shock you must enable.

But using lead II not alone,

Will allow you your rhythm skills to best hone!