ECG Blog #156 (LVH – RVH – LAA – RAA – Strain – Ischemia)

The ECG shown in Figure-1 was obtained from a 40-year old man. Without the benefit of any history — How would you interpret this tracing?

• Is there evidence of an acute coronary syndrome?
• Is there a common diagnosis that potentially explains all of the findings?

Figure-1: ECG obtained from a 40-year old man. How would you interpret this tracing? (See text). NOTE — Enlarge by clicking on the Figure.

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Interpretation: There is baseline artifact that is most marked in lead V1. That said — this tracing is definitely interpretable. Approaching the ECG in Figure-1 systematically — We note the following:

• Rhythm & Rhythm — The rhythm is sinus at a rate just under 100/minute.
• Intervals — The PR, QRS and QT intervals are all normal (ie, the PR interval is not more than 1 large box — QRS duration is not more than half a large box — and despite the fairly rapid rate, the QT interval is not more than half the R-R interval). NOTE: We review our rapid assessment approach for intervals in ECG Blog #89.

Axis — There is marked RAD (Right Axis Deviation) — as determined by predominant negativity in lead I, that occurs in association with a predominantly positive QRS complex in lead aVF.

• NOTE: Although the finding of a predominantly negative QRS complex in lead I (especially in association with a completely negative QRS in lead aVL) should prompt consideration of lead misplacement — this is not the explanation here. Instead, the fact that the P wave and T wave in lead I are both positive, in conjunction with the expected negative P wave in lead aVR — tells us there is no lead misplacement. Instead, there is simply marked RAD.

Chamber Enlargement — As assessment for chamber enlargement highlights the most important findings in this case — we dissect our approach:

• We review assessment for atrial abnormality in ECG Blog #75. Definite criteria for RAA (Right Atrial Abnormality) are met in Figure-1 — in that the P wave is very tall and peaked in each of the 3 inferior leads (the P wave is at least 3mm tall in lead II). In addition, P waves are even taller, as well as peaked and pointed in 5 out of the 6 chest leads (ie, leads V2-thru-V6). We emphasize that in the vast majority of cases, ECG diagnosis of RAA is made from assessment of the limb leads. The ECG in Figure-1 provides one of those rare instances in which P wave appearance in the chest leads assists to confirm our impression of RAA.
• PEARL: The presence of a very pointed P wave in either lead V1 and/or V2 is an insensitive, but highly specific ECG finding in favor of RAA that most often indicates marked RA enlargement and/or significant pulmonary hypertension. This is especially true when P wave amplitude of these pointed chest lead P waves is excessive, as it is here (It is rare indeed to see 5mm P waves in any ECG lead!).
• Although one might think that the deep negative component to the P wave in lead V1 indicates LAA (Left Atrial Abnormality) — we suspect instead, that this is simply further evidence in support of marked RAA. That’s because on occasion, the RA (right atrium) may enlarge so extensively, that it “flops over” and is viewed by right-sided lead V1 as producing a wave of depolarization moving away from V1. The fact that the negative component to the P wave in lead V1 is so narrow (nearly the mirror-image of the upright pointed and very skinny P wave in lead V2) — makes us suspect that this is what is happening here.
• We review assessment for RVH (Right Ventricular Hypertrophy) in ECG Blog #77. As emphasized in Blog #77 — we view the ECG diagnosis of RVH as a “Detective” Diagnosis — since rarely will any one single finding clinch the diagnosis. Instead — determination of RVH is usually made by deduction from identifying a combination of suggestive ECG findings. Among the findings we note in Figure-1 that suggest RVH include: i) Marked RAD; ii) Marked RAA (since it is rare for RVH not to be present when there is right atrial enlargement); iii) Predominant R wave in lead V1 (Normally the QRS should be predominantly negative in lead V1); iv) Persistenceof S waves through to lead V6 (Normally the QRS complex is all positive by the time one reaches lead V6); and, v) Diffuse T wave inversion suggestive of RV “Strain” (See below!).
• PEARL: There is actually a small q wave in lead V1, prior to the predominant R wave in this lead. In patients with RVH — this initial small q wave in lead V1 is often associated with pulmonary hypertension.

Q-R-S-T Changes — The last part of our systematic interpretation entails assessment of Q-R-S-T wave changes.

• Q Waves — We have already noted the QS complex in lead aVL, and the small q (qR complex) in lead V1. There is also a Q wave in lead aVR which is common, and not indicative of anything special.
• R Wave Progression — We have also already noted predominant positivity of the QRS complex in lead V1.

This leaves us with assessment of ST-T Wave Changes — which show ST-T wave depression in multiple leads!

• PEARL: There are 2 lead areas that typically manifest asymmetric ST-T wave depression with RV “Strain”. These are the inferior leads (ie, II,III,aVF) — and the anterior leads (usually V1,V2,V3). RV “strain” may be seen in one or both of these areas. Sometimes when there is marked RV “strain” — ST-T wave depression may extend further across precordial leads. This appears to be the situation in Figure-1.

CLINICAL IMPRESSION — While one might be tempted to ascribe the diffuse ST-T wave depression in Figure-1 to ischemia — it is far more likely to reflect marked RVH with Pulmonary Hypertension. That’s because this unifying diagnosis potentially explains all of the important ECG findings we have noted above = marked RAD — RAA — the qR pattern and predominant R wave in lead V1 — persistence of S waves through to lead V6 — and diffuse ST-T wave depression consistent with RV “strain”.

• Clinical Correlation — This 40-year old man has uncorrected Tetralogy of Fallot. This explains the findings of right atrial and right ventricular enlargement, with pulmonary shunting and pulmonary hypertension.
• For brief review of the principal clinical findings associated with Tetralogy of Fallot — CLICK HERE.

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Acknowledgment: My thanks to Haval Issa from Duhok, Iraq for his permission allowing me to use this tracing and clinical case.

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ECG Blog #155 (Arrhythmia – PACs – Wandering – MAT )

The ECG in Figure-1 was obtained from a woman in her 50s, who complained of intermittent chest discomfort in recent weeks. She was hemodynamically stable at the time this tracing was obtained.

• How would you interpret her ECG?
• HINT: The rhythm is not sinus ... 

Figure-1: ECG obtained from a woman in her 50s, with intermittent chest discomfort. How would you interpret this tracing? NOTE — Enlarge by clicking on the Figure.

Interpretation: The interesting part of this tracing is the rhythm. We have numbered the long lead II rhythm strip. What do you see?

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ANSWER: The rhythm is irregular. The QRS complex is narrow. P waves are present — albeit as you look from 1 beat to the next in the long lead II rhythm strip, it should be clear that P wave morphology changes ...

• We identify 3 different shapes of P waves on this tracing (Figure-2). That is, P waves are tall and pointed in front of beats #1,5,6,7 and 8 (RED arrows) — P waves are round in front of beats #2, 9 and 10 (BLUE arrows) — and, P waves are pointed, but not quite as tall in front of beats #3,4,11,12 (GREEN arrows).
• Each of the P waves in this long lead II is conducting. We know this because for each of these 3 different P wave shapes — all beats of that shape manifest the same PR interval.

Figure-2: Colored arrows highlight atrial activity in the long lead II rhythm strip. What is the rhythm? (See text).

The principal differential diagnosis for an irregular rhythm with different-shape P waves that are conducting is: i) Sinus rhythm with multiple PACs; ii) MAT (Multifocal Atrial Tachycardia); and, iii) Wandering pacemaker. Regarding this differential:

• This is not sinus rhythm with PACs — because there is no predominant underlying sinus rhythm. And, although R-R intervals are shorter in some places — there are no beats that are especially early (ie, there are no PACs).
• This is not MAT — because P wave morphology and the PR interval do not change from one-beat-to-the-next. Instead, there is gradual change in the site of the supraventricular pacemaker over the course of several beats. This strongly suggests the presence of a wandering atrial pacemaker.

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What is a Wandering Pacemaker?

Occasionally — the site of the atrial pacemaker may shift (wander) away from its usual site of origin in the SA (Sino-Atrial) Node. In most cases — wandering atrial pacemaker is a benign normal variant that occurs in patients without underlying heart disease. It may result from variationsin vagal tone (that slow SA nodal discharge and allow other atrial sites to temporarily emerge) — or there may be no obvious cause.

• ECG recognition of wandering pacer requires a long enough rhythm strip to appreciate gradual change over a period of beats from one P wave morphology to another. Technically, there should be at least 3 different atrial sites — in order to distinguish a wandering atrial pacemaker from a simple atrial escape rhythm. The clinical reality, is that most of the time — the period of monitoring available for our scrutiny will simply not be long enough to appreciate gradual shift in the site of the atrial pacemaker to at least 3 different sites. As a result, true wandering pacemaker is not a common diagnosis.
• KEY: All too often, even experienced interpreters fail to adequately assess the long lead rhythm strip. On seeing a few upright P waves — the “eye” tends to assume that the rest of the rhythm is also sinus. All it takes to avoid missing subtle deviations from strict sinus rhythm is a few careful seconds in which you ensure that you scrutinize the P wave preceding each QRS complex in the long lead rhythm strip. You’ll be amazed at how disciplined addition of these few extra seconds will easily pick up those cases in which the rhythm is not strictly sinus.
• P.S.: Other than the rhythm — there are minimal nonspecific ST-T wave abnormalities in several leads that do not appear to be acute. These include shallow T wave inversion in lead III, and relative ST-T wave flattening in leads II, aVF, V5, V6. Thus, the wandering pacemaker is likely to be unrelated to the cause of this patient's intermittent chest discomfort.

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COMMENT: The example of wandering atrial pacemaker in Figure-2 is unique in our experience for allowing definitive diagnosis of this rhythm in no more than a short long lead II rhythm strip. Most of the time, a much longer period of monitoring is needed.

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Acknowledgment: My thanks to Joshua Wyeth from Petoskey, MI, for his permission allowing me to use this tracing and clinical case.

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NOTE: For more on distinction between MAT, Wandering Pacer & Sinus Rhythm with PACs — Please see ECG Blog #65.

ECG Blog #154 (STEMI - Inferior - Posterior - LVH - Mobitz - AV Block)

The ECG in Figure-1 was obtained from a patient with new chest pain. He was hemodynamically stable at the time this tracing was obtained.

• How would you interpret the rhythm and, the rest of this ECG?
• NOTE: In addition to the artifact that is most pronounced in the lateral chest leads — there are 4 Major Findings. Two of these findings are admittedly subtle. How many of these 4 findings can you identify?

Figure-1: ECG obtained from a patient with new chest pain. Can you identify the 4 Major Findings on this tracing? NOTE— Enlarge by clicking on the Figure.

Interpretation: As always, once we ensure that the patient is hemodynamically stable — We begin our Systematic Approach with assessment of the Rate & Rhythm.

• Rate & Rhythm —The rhythm in this tracing is complex — so we will defer full interpretation for a few moments. As we will see shortly, it is clinically useful in this case to delay detailed rhythm analysis — because one of the biggest hints for interpreting this rhythm lies in what we find in the rest of the 12-lead ECG!
• What is obvious about the rhythm — is that the ventricular rhythm is fairly fast — that there is atrial activity — and, that as we step back a bit from the tracing, there is a repetitive pattern = group beating. That is, there are groups of 2 beats and occasionally just 1 beat. That this is not due to chance should be evident because the distance after the 2-beat groups until the next group begins is always the same! (ie, the R-R interval between beats #2-3; between #5-6; between #7-8; 9-10; and 12-13 is the same)! Similarly, the distance after the 1-beat groups until the next group begins is also the same! (ie, the R-R interval between beats #3-4; between #10-11; and between #13-14 is the same)!
• PEARL: The presence of group beating should always make you consider the possibility of some type of Wenckebach block.
• At this point in the interpretation process — We suggest deferring further assessment of the cardiac rhythm until after you have looked at the rest of the 12-lead ECG. After all, this patient presented with new-onset chest pain — and even before scrutinizing the “details”, it looks like something acute is going on! Continuing with our Systematic Approach — We note the following:
• Intervals —The PR interval appears to be changing — although it is useful to note that the PR interval is constant and normal at the onset of each of the small groups in this tracing (ie, the PR interval before beats #1, 3, 4, 6, 8, 10, 11, 13 and 14 is normal and equal)! The QRS complex is normal (ie, not more than half a large box in duration) — therefore, this is a supraventricular rhythm. The QT interval does not appear to be prolonged — although the irregular rate makes this challenging to assess.
• Axis —The frontal plane axis is normal (approximately +75 degrees).
• Chamber Enlargement — P waves are peaked in each of the inferior leads — but not quite tall enough to qualify for RAA (Right Atrial Abnormality), since P waves are less than half a large box tall. There is a fairly deep negative component to the P wave in lead V1 — which qualifies for LAA (Left Atrial Abnormality). Of note — LVH (Left Ventricular Hypertrophy) is probably present! Although neither of the 2 most common voltage criteria for LVH are satisfied in this tracing (ie, deepest S in V1,V2 + taller R in V5,V6 ≥35mm – or – R in aVL ≥12mm) — voltage criteria for LVH are satisfied in lead V6 (R in V6 ≥18-20mm). And although there clearly is much baseline wander + artifact in leads V4-thru-V6 — the ST-T waves in these leads suggests there may be LV “strain”. Recognition of probable LVH in this tracing is the 1st of the 4 major findings that are present. We suspect many observers may overlook this finding.
• Q-R-S-T Changes —There are small q waves in each of the inferior leads. In addition, leads II, III and aVF clearly show ST elevation (of at least 3-4mm) — which occurs in association with reciprocal ST depressionin lead aVL. In a patient with new chest pain — these limb lead findings are diagnostic of an acute inferior STEMI, which is the 2nd of the 4 major findings on this ECG. Otherwise — transition occurs normally in this tracing (ie, the R wave becomes taller than the S wave is deep between leads V3-to-V4). And although a QS complex is seen in leads V1 and V2 — a small-but-definite initial r wave is seen in lead V3. We therefore doubt this patient has had prior anterior infarction. Instead, we suspect the presence of LVH accounts for the lack of initial r wave in V1, V2.

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COMMENT: We suspect the “culprit artery” in this case is acute occlusion of the RCA (Right Coronary Artery) — because: i) In ~80-90% of patients — there is a dominant RCA circulation, which means that most acute inferior MIs are due to acute occlusion of the RCA instead of the LCx (Left Circumflex Artery); ii) The amount of ST elevation in lead III is > lead II (the opposite tends to be true with acute LCx occlusion); and iii) There is a significant amount of reciprocal ST depression in lead aVL (this is less likely to be seen with acute LCx occlusion).
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QUESTION: Most of the time with acute inferior STEMI — there will be ST depression in anterior leads due to associated acute posterior involvement.

• What might be the reason why there is virtually NO anterior ST depression in leads V1, V2 or V3 of Figure-1?

ANSWER:The KEY point to remember is that the ECG reflects the “balance” of competing forces occurring throughout the heart. As emphasized above — there is probable LVH + “strain”, based on the appearance of the QRS complex and ST-T wave in leads V5 and V6.

• In patients with marked LVH + “strain” — the anterior leads often show the opposite (mirror-image) picture of ST-T wave changes as are seen in lateral chest leads. We illustrate this in Figure-2 — taken from our ECG Blog #73 on ECG criteria for LVH.
• Return to the ECG in Figure-1. It is rare to see nearly flat ST-T waves in the anterior leads of a patient with as much inferior ST elevation as occurs in Figure-1. As the 3rd major finding in this case — we suspect there is associated acute posterior MI in this case. Given the presence of LV “strain” in V5, V6 — the baseline tracing of this patient most probably manifested prominent upright ST-T waves in the anterior leads (similar to those seen in leads V2 and V3 in Figure-2). As a result, with acute occlusion of the RCA — there was acute infero-postero STEMI that probably produced anterior ST depression, which we suspect was attenuated by the prominent upright ST-T waves that are so commonly seen in anterior leads of patients with LVH.

Figure-2: Illustrative precordial leads obtained from a patient with longstanding hypertension. QRS amplitude is markedly increased — easily satisfying voltage criteria for LVH. In addition, lateral chest leads (especially V5 and V6) demonstrate ST-T wave changes suggestive of LV “strain”. Note how the oppositepicture is seen in anterior leads V2 and V3, which instead of ST depression demonstrate prominent upright ST-T waves (See text).

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Returning to the RHYTHM in this Case: We have just diagnosed acute inferior STEMI (most probably with associated acute posterior involvement) — that is probably the result of acute RCA occlusion.

• PEARL: Whenever you see group beating in a patient with acute inferior STEMI — the chances are excellent that 2nd-Degree AV Block, Mobitz Type I (= AV Wenckebach) is the cause of the group beating! Awareness of this clinical reality greatly facilitates a more careful analysis of the rhythm.
• Beyond-the-Core: It is especially likely that the cause of group beating with acute inferior MI is AV Wenckebach when noneof the R-R intervals are longer than twice the shortest R-R interval on the tracing!
• For clarity — we outline groups of beats in the long lead II Rhythm Strip. Dotted BLACK rectangles highlight groups of 2 beats — and dotted RED rectangles highlight groups of 1 beat (Panel A in Figure-3). As noted earlier — we KNOW this represents true “group beating” — because all 2-beat groups are similar to each other, and all 1-beat groups similar.
• PEARL: The simple step of using calipers and labeling P waves is always amazingly helpful to me in facilitating my recognition of complex arrhythmias. To determine IF the underlying atrial rhythm is regular — I start with an R-R interval within which I can see 2 P waves. This tells me what the P-P interval will be (ie, the distance between the first 2 RED arrows in Panel B of Figure 3). Set your calipers precisely to this distance — and see if you can walk out regular atrial activity throughout the tracing. RED arrows in Figure-3 show that we can!
• We have already noted that the PR interval is constant and normal at the onset of each of the small groups in this tracing (ie, the PR interval before beats #1, 3, 4, 6, 8, 10, 11, 13 and 14 is normal and equal). This tells us that there IS conduction!
• IF we now focus our attention within the groups of 2 beats (ie, within the dotted BLACK rectangles) — it should be apparent that the PR interval increases until a beat is dropped. For example — the PR interval preceding beat #5 is longer than the PR interval preceding beat #4 — and then the next P wave (which occurs within, and which peaks the T wave of beat #5) is nonconducted. The cycle then begins again with shortening of the PR interval that precedes beat #6.
• The rhythm is therefore 2nd-Degree AV Block, Mobitz Type I (= AV Wenckebach), with alternating 3:2 and 2:1 AV conduction. We determine these conduction ratios on the basis that for groups within the BLACK rectangles — there are 3 P waves, but only 2 of them are conducting (ie, 3:2 AV conduction). And, within the RED rectangles — there are 2 P waves, but only 1 of them conducts (ie, 2:1 AV conduction). NOTE: The rhythm is the 4th major finding in this case!

Figure-3: Labeling of Figure-1 to illustrate the presence of 1-beat and 2-beat groups (Panel A). In Panel B — RED arrows illustrate the presence of a regular underlying sinus rhythm (See text).

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LADDERGRAM Illustration of the Rhythm: We conclude this blog post with a laddergram of the rhythm (Figure-4). While construction of laddergrams can be quite complex when the rhythm is challenging — we emphasize that readinga laddergram that has already been constructed for you is EASY.

• Vertical RED lines in Figure-4 show the underlying regular atrial rate. Note that each vertical line in the Atrial Tier lies directly under its corresponding P wave in the long lead II rhythm strip.
• Focus your attention next on the Ventricular Tier. Each line with an arrow corresponds to conduction of a QRS complex through the ventricles.
• Finally — See how the middle = AV Nodal Tier illustrates the Wenckebach mechanism. Within each of the 2-beat groups (ie, beats #1-2; 4-5; 6-7; 8-9; and 11-12)  — the degree of slanting increases. This corresponds to progressive lengthening of the PR interval within a group until a beat is dropped — and then, the PR interval shortens (the amount of slanting decreases) as the next cycle begins.

Figure-4: Laddergram illustration of Figure-3 (See text).

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SUMMARY of this Case: This is indeed a challenging ECG to interpret — with 4 major findings: i) acute inferior STEMI; ii) probable LVH with “strain”; iii) probable associated acute posterior infarction; and iv) 2nd-Degree AV Block, Mobitz Type I ( = AV Wenckebach), with alternating 3:2 and 2:1 AV conduction.

• The 2 most important findings to appreciate are interpretation of the cardiac rhythm, and recognition of the acute STEMI. Extra Credit to you if you picked up on LVH and the associated posterior infarction.
• Among the most important “Take-Home” Points of this case are learning how to recognize the phenomenon of group beating — and, realizing that once you see true group beating in the setting of acute inferior STEMI — the most likely etiology of the rhythm will be Mobitz I. With practice — this should literally take no more than a handful of seconds to recognize! You can then verify that Mobitz I is truly the etiology of the rhythm by: i) Using your calipers to verify that regular P waves are present; and, then ii) Focusing your attention within each group of beats to see if the PR interval progressively lengthens until a beat is dropped — before then restarting the next cycle with a shortened PR interval.
• CHALLENGE: Test your newly acquired skill by interpreting the 12-lead ECG and rhythm strip shown in Figure-5. Detailed assessment of this tracing is explained (and illustrated with laddergram) in our ECG Blog #55.

Figure-5: 12-lead ECG and long lead II rhythm strip obtained from a 50-year-old woman with chest pain. What is going on? What is the rhythm? Detailed answers appear in our ECG Blog #55.

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Acknowledgment: My thanks to Gëzim Berisha from Kosovo-Prishtina, for his permission allowing me to use this tracing and clinical case.
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NOTE: The following blogs and reference materials provide more information on topics mentioned in this case:

• Our 1-hour ECG Video on the Basics of AV Block = EASY LINK = www.avblockecg.com — NOTE: If you click on SHOW MORE (on the YouTube page, under the video) — you’ll see a detailed linked Contents that will facilitate quickly finding whichever part of this video you will to review!
• Our suggested Systematic Approach to 12-Lead ECG Interpretation — See ECG Blog #93.
• Step-by-Step illustration of How to Draw Laddergrams — See ECG Blog #69.
• Here are a few cases of Acute MI + AV Block — See ECG Blog #48 and Blog #55.
• Click HERE — For free Download of our Section 20 (from ACLS-2013-ePub) on AV Block/AV Dissociation.
• Review of ECG Criteria for Atrial Abnormality (in ECG Blog #75) — and for LVH (in Blog #73).