Saturday, March 19, 2016

ECG Blog #121 (Arrhythmia — multiple Q waves — WPW — delta waves — Concertina Effect — Wandering Pacemaker — pseudo-infarction)

The ECG in the Figure-1 was obtained from a previously healthy 19-year old man, presumably as part of a vigorous pre-exercise evaluation. No symptoms.
  • How would you interpret this­­ tracing?
  • In view of this presentation — What clinical entities should be considered in your differential diagnosis? How might you proceed in your evaluation?
Figure-1: 12-lead ECG and long lead II rhythm strip obtained from an asymptomatic, young adult man as part of a pre-exercise evaluation. Can you explain the unusual findings in this otherwise healthy 19-year old? NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
Interpretation: This ECG is markedly abnormal for a 19-year old man. The long lead II rhythm strip at the bottom shows a phasic arrhythmia, with upright P waves with a fixed PR interval preceding each QRS complex. This is most likely marked sinus arrhythmia — though it is hard to rule out the possibility that the slight reduction in P wave amplitude that seems to occur with slower rates might be due to a wandering atrial pacemaker. In either case — the rhythm is benign in a 19-year old man.
  • It is the remainder of the ECG that is of most interest. All intervals (PR, QRS and QT) appear to be normal. The mean QRS axis is indeterminate (predominantly negative in both leads I and aVF). There is no chamber enlargement. What IS distinctly unusual — is inferior negativity of the QRS, and an almost reverse R wave progression in the chest leads with small q waves in leads V4,V5,V6. There is T wave inversion in lead aVL, with T waves otherwise upright (albeit a bit peaked). BOTTOM LINE: This is not a “normal” ECG for an otherwise healthy 19-year old!
What Next?
The finding of a clearly abnormal 12-lead ECG for this young adult should raise a number of considerations (ie, previously undetected congenital heart disease; some type of cardiomyopathy; a prior episode of myocarditis that spontaneously resolved; etc.). An Echocardiogram was obtained, looking for underlying structural heart disease — but, the Echo was essentially unremarkable.
  • HINT: Look carefully at the terminal part of the PR interval in leads II and III. Is the terminal portion of the PR segment flat?
COMMENT: The terminal portion of the PR segment in leads II and III slopes downward. Consultation with EP Cardiology confirmed suspicion that this ECG represents a Pseudo-Infarction Pattern in a patient with WPW.
  • There are pros and cons to pre-participation ECG evaluation of otherwise healthy young adult athletes. The obvious goal of such evaluation is to detect occult cardiac conditions that might prove hazardous if unrestricted physical exertion is allowed. Among the problems with routinely obtaining pre-participation ECGs are: i) cost; ii) poor sensitivity of such screening (ie, a “normal ECG” may reduce risk, but in no way rules out all risk); and iii) potential for false positive results (ie, many unusual ECG patterns of no consequence may be seen in athletic individuals). That said — the degree of abnormality for the ECG shown in Figure 1 is so atypical for an otherwise healthy 19-year old, that search for the cause is clearly indicated.
  • NOTE: I fully acknowledge not considering WPW when I first saw this tracing. Delta waves as we typically think of them — are just not seen. However, the list of potential causes of this unusual ECG picture dramatically decreased once a high quality Echocardiogram failed to suggest any form of underlying structural heart disease. The Lesson-to-be-Learned — is that depending on the relative amount of preexcitation and the location of the accessory pathway — the appearance of WPW on ECG may be varied and subtle. The inferior pseudo-infarction pattern seen here is due to negative delta waves in leads II and III. Delta waves are otherwise not readily recognizable on this tracing.
P.S. — Please LOOK AGAIN at the long Lead II Rhythm Strip!
Excellent comments and questions by Nguyen Chi Tinh and Pham Le Tra (both from Vietnam) on the internet EKG Club inspired me to take another closer look at the long lead II rhythm strip that appeared at the bottom of Figure-1 (See Figure-2 below).
  • Question: How do you make a diagnosis of Wandering Atrial Pacemaker? Is that what we see in the long lead II rhythm strip shown here?
  • In addition to subtle change in P wave morphology — Is anything else changing as one moves across this long lead II rhythm strip? (HINT: Look at the RED arrows in Figure-2 — and compare what you see with the P-QRST complex for beats #5 and 6).
Figure-2: Taking another look at the long lead II rhythm strip that appeared at the bottom of Figure-1. Why is P wave morphology changing as one moves across this long lead II rhythm strip? Is anything else changing?
Answers: 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 variations in vagal tone (that slow SA nodal discharge and allow other atrial sites to temporarily emerge) — or there may be no obvious cause. To make the diagnosis — there should be at least 3 different P wave morphologies (representing shift to at least 3 different sites in the atria) — with gradual change over several beats (not abruptly! ) from one P wave morphology to the next. As you might imagine — this requires a fairly long period of monitoring! — which is perhaps the main reason we so often fail to recognize wandering pacemaker when it is present (most rhythm strips are no more than a limited number of seconds long …). Given the usual benign consequence of wandering atrial pacemaker — it is generally of no clinical significance that we fail to recognize it in asymptomatic and otherwise healthy individuals. Therefore, even IF the change in P wave morphology that we see in the long lead II rhythm in Figure-2 was due to shift from one atrial pacemaker to another — we technically could not diagnose a “wandering pacemaker” — because we do not see 3 different P wave morphologies.
  • That is not what is happening in the long lead II rhythm strip! Instead — the 2 RED arrows in Figure-2 represent subtle-but-real downsloping of the negative delta wave that is intermittently present to varying degrees in lead II!
  • Beats #4,5 and 6 in lead II appear to be conducting normally. Beginning with beats #7 and 8, a small and narrow q wave develops. Over the course of the next several beats, this q wave deepens and widens — eventually developing subtle downsloping toward the end of the P wave for the last few beats in the tracing. The effect looks similar to the appearance of the P-QRS juncture highlighted by the RED arrows at the beginning of the tracing. While easy to overlook these subtle changes (I missed them initially! ) — they are unmistakable in this 19-year old diagnosed by EP to have WPW when you compare normal conduction (beats #4,5,6) with P-QRS appearance at the beginning and at the end of this tracing.
  • Thus, after the first 3 beats, that are conducted over the AP (Accessory Pathway) — we are seeing several normally conducted beats (beats #4,5,6) — and then progressive shortening of the PR interval with corresponding widening of the QRS complex as a delta wave again develops after the middle of this long lead II rhythm strip. This cyclic pattern, with gradual change in the relative amount of preexcitation that we see here in this patient with newly diagnosed WPW is known as the Concertina Effect.
  • The “good news” — is that on those occasions when you do see a definite Concertina Effect (the Concertina Effect is not a very common phenomenon in patients with WPW) — it is a surprisingly good indicator of a relatively long AP refractory period. As a result, excessively fast rates with AP-associated SVT rhythms are much less likely in such patients (since a longer refractory period limits the number of impulses that can be transmitted over the AP). This portends a relatively lower risk of sudden death during a WPW-related tachyarrhythmia. Thus, recognition of the Concertina Effect in this 19-year old with newly diagnosed WPW at least provides positive prognostic information (ie, if ablation of the AP is not initially done — at least the relative risk of a potentially lethal WPW-associated tachyarrhythmia is lower).
  • NOTE: Other non-invasive markers of lower risk of sudden death in patients with WPW include: i) Intermittent preexcitation during sinus rhythm; and ii) Abrupt loss of AP conduction (ie, loss of the delta wave) during exercise (which explains one of the benefits of exercise testing of younger patients with WPW).
Acknowledgment: My thanks to Massimo Bolognesi, MD (of Cesena, Italy) for allowing me to use this tracing and clinical case.
Additional Reading:
  • For more on Wandering Pacemaker — Please check out my ECG Blog #65 (Scroll down the page to just above Fig. 2 for discussion regarding distinction between MAT vs AFib vs Wander Pacer vs multiple PACs).
  • For more on the Concertina Effect — Please check out the brief manuscript by Singla V et al: BMJ Case Rep 2013 (doi:10.1136/bcr-2013-009328).

Tuesday, December 22, 2015

ECG Blog #120 (ECG Video-16) - Chest Pain with Giant T Waves

This is the 16th installment of my ECG Video Blog (12 minutes). Today's ECG was obtained from a 50-year old man with chest pain. How would you systematically interpret his ECG? What diagnostic entities should you consider? Click on the link below for a detailed linked CONTENTS (so that you can easily navigate through the video).

NOTE: There are advantages to using a video format format. These include:
  • Ability to illustrate concepts not done full justice by the written word.
  • Greater dispersion of my content through Google & YouTube. This material is free for anyone to use.
LINKS to my ECG Video-Blog installments:
  • ECG Video-Blog #1-Revised (= Blog #95) — Is there AV Block?
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  • ECG Video-Blog #2 (= Blog #96) — Bundle Branch Blocks
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  • ECG Video-Blog #3 (= Blog #97) — SVT with marked ST Depression
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  • ECG Video-Blog #4 (= Blog #98) — Clinical Arrhythmia Mgmt (Part I )
  • ECG Video-Blog #5 (Blog #99) — Clinical Arrhythmia Mgmt (Part 2 )
  • ECG Video-Blog #6 (= Blog #100) — Clinical Arrhythmia Mgmt (Part 3 )
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  • ECG Video-Blog #7 (= Blog #101) — Wide Tachycardia + Chest Pain
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  • ECG Video-Blog #8 ( = Blog #105) — Basics of AV Block
  • ECG Video-Blog #9 ( = Blog #110) — Complete AV Block? / Laddergrams
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  • ECG Video-Blogs #10,11,12 ( Blog #113) — Rhythm Diagnosis Basics
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  • ECG Video-Blog #13 ( = Blog #116) — Essentials of Axis / Hemiblocks
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  • ECG Video-Blog #14 ( = Blog #117) — Brugada Syndrome
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  • ECG Video-Blog #15 ( = Blog #118) — QRST Changes
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  • ECG Video-Blog #16 ( = Blog #120) — Giant Waves
  •    Click Here for Timed Contents to the Giant T Waves Video!
         This is the 16th installment of my ECG Video Blog. This video is 12 minutes long. The case is about a 50-year old man with chest pain, whose ECG is shown in Figure 1. 
    • How would you interpret his 12-lead ECG (Figure 1).
    • What diagnostic entities should you consider in your differential diagnosis?
    • NOTE: I aimed my content at an Intermediate level interpreter (with emphasis on BASIC concepts plus LOTS of PEARLS for more advanced interpreters along the way). 
    Hope you enjoy this! I welcome your feedback! (Ken Grauer, MD –
    Figure-1: 12-lead ECG obtained from a 50-year old man with chest pain. How would you interpret this tracing? What clinical entities should you consider? NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
    Table: The 2-Step Systematic Approach to ECG Interpretation.
      Figure-2: Entities associated with Giant T Wave Inversion.
      GT — on YouTube to view this ECG Video (12 minutes). —
      • Click Here  — for a Timed CONTENTS of Video-Blog #16 on Giant T Waves.
      • Please also see our ECG Blog #59 (on Giant T Wave Inversion).
      • Addition details on this case are explained in my Comment on ECG Guru (for 12/15/2015).
      • Please also check out my ECG Video Blog page on Google. The link is easy to remember = -
      NOTE: For a Power Point Show (.ppsx) version of my Video Blogs - CLICK HERE. This folder will contain links to download a .ppsx version that allows faster viewing:
        • Download the .ppsx to your computer desktop.
        • The PPT show is without automatic sound. YOU activate only the Audio clips you want.
        • Hover your mouse over the highlighted Audio. You may play and/or pause if/as you like.
        • Feel free to use this .ppsx for teaching with my blessings!
        Acknowledgment — to Dawn Altman of the ECG Guru — for allowing the use of this case & tracing.

        Thursday, December 17, 2015

        ECG Blog #119 (Anterior T Wave Inversion – Ischemia – Long QT – Acute PE)

        The ECG in the Figure-1 was obtained from a previously healthy 43-year old woman who presented to the ED (emergency department) with chest pressure and shortness of breath over the past day. She was alert but hypotensive at the time this ECG was recorded.
        • How would you interpret this­­ tracing?
        • In view of this presentation — What clinical entities should be considered in your differential diagnosis?
        Figure-1: 12-lead ECG obtained from a previously healthy 43-year old woman with chest pressure and dyspnea. NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
        Interpretation: This ECG is markedly abnormal. The rhythm is sinus tachycardia at a rate just over 100/minute. The PR and QRS intervals are normal — but the QT interval appears to be markedly prolonged. The axis is normal. There is no chamber enlargement.
        • Regarding QRST Changes Q waves are present in leads III and aVF. There is poor R wave progression in the chest leads, with late transition to a predominant R wave not occurring until between lead V5-to-V6. But the most remarkable finding, is deep symmetric T wave inversion that is most pronounced in leads V1, V2 and V3. Several additional leads show ST segment coving with a lesser degree of T wave inversion.
        Impression: Clinical correlation is essential for optimal interpretation of this tracing. Deep, symmetric T wave inversion may clearly be a manifestation of ischemia and/or an acute coronary event. Hypertrophic cardiomyopathy (especially when there is apical hypertrophy) is also known to produce deep symmetric T wave inversion in multiple leads. The markedly prolonged QT interval in association with the pronounced ST-T wave changes seen here could be consistent with a CNS (central nervous system) event such as stroke, intracerebral or subarachnoid bleed, coma, seizure or trauma. That said, the clinical scenario of hypotension plus new-onset dyspnea in a previously healthy young adult with this ECG is most suggestive of acute PE (Pulmonary Embolism) as the diagnosis. Massive PE was confirmed on further evaluation.
        ECG Diagnosis of Acute PE:
        ECG diagnosis of acute PE is difficult — because there is no single ECG finding definitive for this diagnosis. Instead, acute PE may be suggested by a combination of supportive ECG findings (Table-1) that occur in a patient with the “right” clinical scenario (ie, recent onset of unexplained dyspnea, syncope and/or shock, especially in a patient predisposed or with a prior history of venous thromboembolism). This case is an excellent example in which it is the sum of ECG findings (many of which are admittedly subtle) — in the context of the clinical presentation that suggests acute PE as the diagnosis.
        Table-1: ECG findings suggestive of acute PE. There is no single ECG finding that is diagnostic of acute PE. Instead, the diagnosis is suggested by the presence of at least several of these ECG findings when they occur in the “right” clinical setting.
        NOTE: The ECG is far less likely to help in the diagnosis of relatively small (ie, subsegmental) PEs that are not hemodynamically significant, and which are often only discovered on Chest CT performed on patients with less convincing symptoms. This is probably a “good thing” — since evidence is lacking that treatment of incidentally discovered, non-hemodynamically significant subsegmental PEs is beneficial (and it certainly is not without potential for harm). In our opinion — it is therefore a “benefit-in-disguise” that the ECG is unlikely assist in detection of relatively smaller pulmonary emboli.
        We list below the ECG Findings we note in Figure-1 that are consistent with the diagnosis of acute PE:
        • Sinus Tachycardia — While not absolutely essential for the diagnosis, a rapid heart rate (usually to at least 90/minute) is common and expected in patients with hemodynamically significant acute PE. The heart rate in Figure-1 is over 100/minute.
        • Acute RV “Strain” — Awareness of ECG evidence of RV (Right Ventricular) Strain is one of the most important ECG indicators of acute hemodynamically significant PE. Unfortunately, this sign remains all-to-often unappreciated and misinterpreted as coronary ischemia. RV “strain” manifests as ST depression and/or T wave inversion that typically occurs in anterior leads (V1,2,3) and/or in inferior leads (II,III,aVF). By itself — there is no way to be certain of the cause of the anterior T wave inversion seen here in Figure-1. But the clinical scenario (ie, new-onset dyspnea plus hypotension) and, the combination of other ECG signs listed here should strongly suggest acute PE as the diagnosis until proven otherwise. Note in this case how diffuse ST-T wave changes are (involving virtually all leads on this tracing). In addition — the QT interval is markedly prolonged in this previously healthy 43 year old adult who is alert but hypotensive. Coronary ischemia typically produces a more localized ST-T wave pattern of abnormality without such marked QT lengthening. Alert status, young adult age, and lack of LVH voltage are against either stress or hypertrophic cardiomyopathy, or CNS catastrophe as the cause. This leaves acute PE as our working diagnosis until proven otherwise. Although a long QT is not typically thought of as an ECG sign of acute PE — RV “strain” and this patient’s compromised hemodynamic status may explain this finding.
        • S1Q3T3 — The diagnostic value of finding the combination of an S wave in lead I + a Q wave and T wave inversion in lead III is generally overrated. In our experience, it is rare (if ever) that the isolated finding of an S1Q3T3 will make the diagnosis of a new significant PE. That said, this ECG sign may indeed be helpful IF seen in association with other ECG evidence of acute PE. Such is the case here.
        • RAARight Atrial Abnormality is another ECG indicator of acute right heart strain. RAA is most often diagnosed by the finding of a tall, peaked and pointed P wave (≥2.5 mm) seen in one or more of the inferior leads. Less commonly — RAA may be suggested by the finding of a pointed upright P wave in lead V1 and/or V2. Even though the amplitude of the pointed P wave seen in these leads in Figure-1 is small — this finding in context with the other signs noted is consistent with the diagnosis of acute PE.
        • Persistent Precordial S Waves — Poor R wave progression with persistence of S waves across the chest leads (through to lead V6) — is another ECG sign seen here that is consistent with new or chronic pulmonary disease.
        • ST Elevation in aVR — Among the unappreciated benefits of lead aVR in ECG interpretation, is awareness that acute right heart “strain” (as seen with large acute PE) may often produce ST elevation in right-sided lead aVR. Note how right-sided lead III also produces a similar picture in Figure-1.
        • Other ECG Signs NOT Seen in Figure-1 — These include new-onset atrial fibrillation — right axis deviation (or an indeterminate axis) — and/or complete or incomplete RBBB (Right Bundle Branch Block).
        BOTTOM LINE: This case provides a wonderful example of how clinical correlation plus the complete ECG picture can combine to strongly suggest the diagnosis of a large acute PE long before results from the CT scan come back. Prompt recognition of this life-threatening entity is essential to optimize the chance for favorable outcome.
        PEARL: The ECG finding of deep, symmetric T wave inversion in anterior leads can be an indication of coronary ischemia — but, recognition of this finding should always prompt consideration of the possibility that the patient has a large acute PE!
        Acknowledgment: My thanks to Hasan Jalal (of Jordan) for allowing me to use this tracing and clinical case.