ECG Interpretation Review #85 (Aberration – Left Anterior Hemiblock – Fascicular VT – Typical RBBB – WCT)

     The ECG and lead II rhythm strip shown in Figure-1 — was obtained from a 23-year old man who presented with “palpitations”. He was presumably healthy prior to the occurrence of this arrhythmia — and he was hemodynamically stable at the time this ECG was recorded.

• Is the rhythm more likely to be VT (Ventricular Tachycardia) or SVT (SupraVentricular Tachycardia) with aberrant conduction?
• What factors favor one or the other diagnosis?
• Adenosine was initially tried as treatment. When this was unsuccessful — Verapamil was tried. Comment on this selection of treatment.

Figure-1: ECG and lead II rhythm strip obtained from a 23-year old male with palpitations. He is hemodynamically stable. Is this more likely to be VT or SVT with aberration? NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.

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Interpretation of Figure-1: The rhythm appears to be a regular WCT (Wide-Complex Tachycardia). Unfortunately, angling of the ECG paper has introduced slight irregularity in measured intervals — but the “theme” of this smart phone photo is that of a regular WCT rhythm.

• The rate of this regular WCT is just over 200/minute.
• The QRS complex is wide. QRS morphology resembles the bifascicular block pattern of RBBB (Right Bundle Branch Block) with LAHB (Left Anterior HemiBlock).
• No P waves are seen.

Assessment: The differential diagnosis of a regular WCT rhythm without sinus P waves should always be, “VT until proven otherwise”. The patient should be treated accordingly. Statistically — at least 80-90% of such cases will be VT (especially if the patient is an older adult with a history of underlying heart disease). That said — there are a number of unique aspects to this case.

• This patient was not an “older adult with underlying heart disease”. Instead — he was a presumably healthy young adult who presented with palpitations, but who was hemodynamically stable. Certain types of VT rhythms are known to occur in a younger adult age group in the absence of underlying heart disease. Many of these rhythms are catecholamine-related and exercise-induced. A significant percentage of these VT rhythms (thought to account for up to 5-10% of all VT rhythms) are adenosine responsive — which is one reason in support of early trial of adenosine in the treatment approach to a regular WCT of uncertain etiology. In addition to young age of the patient and absence of underlying heart disease — certain ECG features sometimes clue the provider in to the likelihood that one of these special forms of VT may be operative (See discussion on RVOT VT in our ECG Blog #35).

Although VT should be presumed until proven otherwise for the regular WCT rhythm in Figure 1 — there is a possibility that QRS widening could instead be due to: i) Preexisting BBB (Bundle Branch Block); or ii) Aberrant conduction. That said — We feel neither is likely in this case.

• Our reason for stating this is the clear absence of “typical” RBBB morphology in lead V1 of Figure-1. Normally with RBBB — there should be an rSR’ complex in lead V1 with: i) S wave that descends to slightly below the baseline; and ii) A taller right “rabbit ear” (= R’ that is slender and taller than the initial positive component in lead V1). These same morphologic features of “typical” RBBB when seen in a patient with a WCT rhythm may also suggest aberrant conduction (Panel A and Panel B in Figure-2).
• In contrast — atypical QRS morphology in lead V1 is far less likely to be due to RBBB or aberrant conduction (Panels C, D, E and F in Figure-2). While atypical QRS morphology in lead V1 may clearly occur with RBBB in patients with ischemic heart disease, scarring from cardiomyopathy and/or RVH — one would expect an otherwise healthy young adult to manifest a fairly typical RBBB pattern (as in Panel A or B in Figure-2) — IF the reason for QRS widening was simple RBBB.

Figure-2: Use of QRS morphology in a right-sided lead (V1 or MCL-1) to distinguish between ventricular ectopy (including VT) vs aberrant conduction. Only a typical RBBB pattern (rsR’ with descent of S wave below the baseline and with terminal taller right rabbit ear) is predictive of aberration (A or B). Any other pattern (C, D, E, F ) predicts ventricular ectopy. (Figure reproduced from ACLS-2013-ePub).

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Follow-Up:

     The clinical presentation and ECG features shown in Figure-1 for this case are most suggestive of Fascicular VT as the reason for QRS widening This is because:

1. The patient is a 23-year old man who was previously healthy — and who presented with palpitations in a hemodynamically stable condition (ie, an unlikely scenario for an ischemic form of VT).
2. Despite superficial resemblance to a bifascicular block pattern of RBBB/LAHB — QRS morphology in lead V1 is clearly atypical for RBBB since: a) the S wave does not descend to below the baseline; and b) the R’ is far wider than is usually seen for typical RBBB.

     This patient was initially treated with Adenosine. There was no response. Verapamil was then given. Spontaneous conversion to sinus rhythm occurred a short while later.

• We emphasize that the calcium blockers Verapamil and Diltiazem are contraindicated for treatment of ischemic VT. In a patient with ischemic VT who is only tolerating the arrhythmia because of compensatory vasoconstriction — the vasodilatory and negative inotropic properties of Verapamil/Diltiazem are likely to precipitate acute deterioration. Surprisingly — fascicular VT often responds to calcium blockers. While not advocating empiric use of calcium antagonists for WCT rhythms until definitive diagnosis of fascicular VT is made — this treatment was effective in this case.
• When in doubt — Cardioversion is the safest treatment for WCT rhythms not responding to trial of medication. Referral to EP (ElectroPhysiology) is indicated for further assessment and consideration of ablative therapy in this case.
• For more details on Fascicular VT – Please see our ECG Blog #38 -

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Acknowledgment: My appreciation to Ong Jiann Ruey – who contributed the case and the tracing shown in Figure 1.
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Figure 2 excerpted from ACLS-2013-ePub.

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- Please see our ECG Blog #38 — for a similar case/full discussion of Fascicular VT -

- Our ACLS Comments #11 reviews the approach to the regular WCT rhythm. Here is the part that assesses using QRS morphology in WCT assessment — 

ECG Interpretation Review #84 (ST Depression – ST Flattening – Nonspecific ST-T Wave Changes)

     Interpret the ECG shown in Figure-1 — obtained from an adult with a recent history of atypical chest discomfort.

• Would you classify the ECG shown in Figure-1 as a “normal” tracing?
• If not — Why not?

Figure-1: ECG obtained from an adult with atypical chest discomfort. Would you interpret this ECG as a “normal” tracing? (Figure reproduced from ECG-2014-ePub). NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.

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Interpretation of Figure-1: The rhythm is sinus bradycardia and arrhythmia (heart rate ~60/minute, or a bit below this). The PR, QRS and QT intervals are all normal — as is the axis (which is about +30 degrees). There is no chamber enlargement.

• Q-R-S-T Changes: A small and narrow q wave is seen in lead aVL. Transition is slightly delayed (the R wave becomes taller than the S wave is deep between V4-to-V5). The most remarkable finding on this ECG is ST segment flattening with slight ST depression in multiple leads.
• The amount of actual ST segment depression on this tracing is minimal (no more than 1mm in the inferior leads) — yet there is no denying that ST depression is present (See blow-up inserts in the inferior leads in Figure-2).
• There is no ST depression at all in leads I and V2-thru-V6 (Figure‑2). That said — ST-T waves are not normal in these leads. Instead — there is subtle-but-real ST segment straightening that resembles the picture in Panel B of Figure‑3.

BOTTOM Line: The ECG in Figure-2 is not normal. Instead — there is diffuse nonspecific ST flattening and slight ST depression. These changes are subtle but real. Clinical correlation is essential for knowing how to interpret this ECG finding. This patient may have coronary disease — possibly even severe coronary disease. On the other hand — these changes are not acute and they could be due in part or in combination to any of the other potential causes of ST depression (drug effect, electrolyte disorder, hyperventilation, acutely ill patient, etc.). We simply cannot tell on the basis of this single ECG.

Figure-2: Reproduction of the ECG in Figure-1, with blow-up inserts illustrating subtle ST-T wave abnormalities. Note that there is ST depression (of ~1mm) in the inferior leads. There is also ST segment flattening (straightening) but no depression in leads I and V2-thru-V6 (red arrows in blow-up inserts in V5,V6). Although T wave amplitude in lead aVL is reduced — note that gradual transition from ST segment-to-T-wave is preserved in this lead (blue arrow) — compared to clear straightening of the ST segment in leads V5,V6 (red arrows). This is not a “normal” ECG. (Figure reproduced from ECG-2014-ePub).

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Recognizing Subtle ST Changes: ST Segment Straightening

Consensus among expert electrocardiographers is lacking regarding the definition of a “normal” ECG. Much of this relates to semantics — since minor ST‑T wave abnormalities generally provide no more than a nonspecific suggestion to potential etiologies. That said — We feel it is important to hone in on recognizing even minimal abnormalities, if for no other reason than to let those reading our interpretation be aware that we saw the abnormality in question but did not think it clinically important for the case at hand.

• The above said — there are times when even minimal ST-T wave changes may have clinical relevance. In addition — routine attention to recognizing subtle ST-T wave changes will go a long way toward improving one’s ECG interpretation ability.
• For example — What is the difference between the ST segment shown in Panel A vs Panel B in Figure-3? Is the admittedly subtle difference in ST‑T wave appearance between these two complexes likely to be of clinical significance? If so — How?

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Figure-3: Compare the ST segment in Panel A with Panel B. What is the difference? Is this likely to be clinically significant? (Figure reproduced from ECG-2014-ePub).

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Answer to Figure-3: The ST-T wave in Panel A is normal. Note the smooth contour at the point of transition between the end of the S wave and the beginning of the ST segment. Note an equally smooth contour at the end of the ST segment and the point where the ascending limb of the T wave begins.

• In contrast — Note the sharp angle in Panel B at the point where the straight (flat) ST segment ends and the ascending limb of the T wave begins (red arrow). While admittedly “splitting hairs” — the ST-T wave in Panel B is not normal. Instead — there is nonspecific ST segment straightening (ie, loss of that smooth transition between end of the ST segment and the beginning of the T wave ascending limb).
• We emphasize that “nonspecific ST segment straightening” — is a descriptive finding. It is nonspecific. It may mean nothing — especially if only seen in a single lead. In any case — it is not an acute change. On the other hand — ST segment straightening as occurs in Panel B may at times be a nonspecific indicator of underlying coronary disease — especially when this finding is seen in more than one lead. Clinical correlation is everything.

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Figures 1,2,3 excerpted from ECG-2014-ePub.

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ECG Interpretation Review #83 (PSVT – AVNRT – AVRT – Alternans – Electrical – Reentry – Pericardial Tamponade)

     Interpret the 3-lead rhythm strip shown in Figure-1 — obtained from a patient in a fairly (but not completely) regular SVT rhythm.

• What is the reason for the slight change in QRS morphology from beat-to-beat?

Figure-1: 3-lead rhythm strip — obtained from a patient in a regular SVT rhythm. What is the reason for the slight change in QRS morphology from beat-to-beat? (Figure reproduced from ECG-2014-ePub). NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.

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Answer to Figure-1: Although one might at first be tempted to interpret the rhythm as a form of bigeminy — a more accurate interpretation would be electrical alternans. While we would accept general description of this rhythm as representing a “regular” SVT (SupraVentricular Tachycardia) — there is in fact slight-but-real phasic variation in the R‑R interval occurring every-other-beat. This is not due to a form of bigeminy — but rather to R‑R alternans. In addition — there is both QRS alternans (red and blue double arrows in Figure-2) — and T wave alternans (red and blue circles in Figure-2). That is — QRS morphology changes every-other-beat. This is subtle in lead V1 — but more noticeable in lead V2 where the initial R wave manifests an obvious difference in height from one beat to the next. Similarly — T wave morphology changes every-other beat, with this clearly more noticeable in lead V2 which manifests extra peaking of every-other-T wave (red and blue circles in lead V2).

• Clinical implications of these forms of electrical alternans in a patient with SVT — are that reentry is almost certain to be involved in the mechanism. There may or may not be a concealed accessory pathway.

Figure-2: We have labeled the 3-lead rhythm strip recorded in Figure-1. There is slight shortening of the R-R interval every-other beat = R‑R alternans. In addition — there is both QRS alternans (red and blue double arrows) — and T wave alternans (red and blue circles in Figure-2). That is — QRS and T wave morphology changes every-other-beat.  (Figure reproduced from ECG-2014-ePub).

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What is Electrical Alternans?

     The fascinating phenomenon of electrical alternans — is a relatively uncommon clinical entity that is frequently misunderstood. It is often overlooked when it does occur. A look at Figure-1 explains why: This ECG sign can be subtle indeed.

• Electrical alternans is a general term that encompasses a number of different pathophysiologic mechanisms. Its occurrence is not limited to pericardial tamponade — but instead has been associated with an expanding array of clinical conditions.
• Distinction should be made between electrical and mechanical alternans. The term “alternans” itself — merely indicates that there is phasic fluctuation in some cardiac signal from one beat to the next within the cardiac cycle. This may be in the strength of the pulse (or the blood pressure recorded) — or it may be in one or more waveforms in the ECG recording.

NOTE: It may be helpful to first define other alternans phenomena that may sometimes be confused with the various ECG manifestations (especially since these other forms of alternans phenomena may also be seen with cardiac tamponade).

• Pulsus alternans — is a mechanical form of alternans. The rhythm is regular — but cardiac output varies from beat-to-beat. It is seen with severe systolic dysfunction. Pulsus alternans should be distinguished from a bigeminal pulse — in which a weaker beat follows the stronger beat by a shorter time interval (as occurs when the alternating beat is a PVC, which understandably generates less cardiac output).
• Pulsus alternans should also be distinguished from pulsus paradoxus — in which there is a palpable decrease in pulse amplitude (or a measured drop of >10mm in blood pressure) during quiet inspiration. While pulsus alternans and paradoxus may both be seen with pericardial tamponade — they are different phenomena than the various types of electrical alternans.

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Electrical Alternans: Definition/Features/Mechanisms

     Electrical alternans — is a beat-to-beat variation in any one or more parts of the ECG recording. It may occur with every-other-beat — or with some other recurring ratio (3:1; 4:1; etc.). Amplitude or direction of the P wave, QRS complex, ST segment and/or T wave may all be affected (although P wave alternans is rare). Alternating interval duration (of PR, QRS or QT intervals) may also be seen.

• Electrical alternans — was first observed in the laboratory by Herring in 1909. It was reported clinically by Sir Thomas Lewis a year later, who characterized the phenomena as occurring, “either when the heart muscle is normal but the heart rate is very fast or when there is serious heart disease and the rate is normal”. This 1910 description by Lewis serves well to this day to remind us of the 2 principal clinical situations in which electrical alternans is most often encountered: i) Supraventricular reentry tachycardias; and ii) Pericardial tamponade.

Mechanisms: There are 3 basic types of electrical alternans phenomena — each relating to a different pathophysiologic mechanism: i) Repolarization alternans; ii) Conduction and Refractoriness alternans; and iii) Alternans due to abnormal cardiac motion. A common cellular mechanism may underlie each of these processes relating to abnormal calcium release or reuptake within the sarcoplasmic reticulum.

• Repolarization alternans — entails beat-to-beat variation in the ST segment and/or T wave. Alternation in ST segment appearance (or in the amount of ST elevation or depression) — is often linked to ischemia. In contrast — T wave alternation is more often associated with changes in heart rate or in QT duration (especially when the QT is prolonged). In patients with a long QT — T wave alternans may forebode impending Torsades de Pointes. Both ST segment and T wave alternans have been known to precede malignant ventricular arrhythmias. Thus, this type of electrical alternans may convey important adverse prognostic implications when seen in certain situations. That said — a variety of clinical conditions have been associated with repolarization alternans, such that adverse prognostic implications do not always follow. Among these clinical conditions are congenital long QT syndrome — severe electrolyte disturbance (hypocalcemia; hypokalemia; hypomagnesemia) — alcoholic or hypertrophic cardiomyopathy — acute pulmonary embolus — subarachnoid hemorrhage — cardiac arrest and the post-resuscitation period — and various forms of ischemia (spontaneous or induced by treadmill testing or other stimulus).
• Conduction and Refractoriness alternans — entails variance of impulse propagation along some part of the conduction system. This may result from fluctuations in heart rate or in nervous system activity or from pharmacologic treatment. ECG manifestations from this form of alternans may include alternating appearance of the P wave, QRS complex or alternating difference in P-R or R-R interval duration. In particular — QRS alternans during narrow SVT rhythms has been associated with reentry tachycardias. While identification of QRS alternans during a regular SVT often indicates retrograde conduction over an AP (Accessory Pathway) — this phenomenon has also been seen in patients with simple PSVT/AVNRT that exclusively limits its reentry pathway to the AV Node. Therefore — identification of QRS alternans during a regular SVT does not prove the existence of an accessory pathway. Conduction and refractoriness alternans may be seen with WPW-related as well as AV Nodal-dependent reentry tachycardias — atrial fibrillation — acute pulmonary embolus — myocardial contusion — and severe LV dysfunction.
• Cardiac Motion alternans — is the result of cardiac movement rather than electrical alternation. The most important clinical entity associated with motion alternans is large pericardial effusion — though motion alternans has also been observed in some cases of hypertrophic cardiomyopathy. It is important to appreciate that not all pericardial effusions produce electrical alternans. Development of total electrical alternans (of P wave, QRS complex and T wave) — is likely to be a harbinger of impending tamponade. Unfortunately — the sensitivity of total electrical alternans is poor for predicting tamponade (ie, most patients who develop tamponade do not manifest preceding electrical alternans). Therefore — it may be helpful if you see total electrical alternans in a patient with a large pericardial effusion — but failure to see this ECG sign in no way rules out the possibility that tamponade is occurring. Echo studies in patients with documented cardiac tamponade confirm that electrical alternans is synchronous with and a direct result of the pendulous movement of the heart within the enlarged, fluid-filled pericardial sac of a patient with large pericardial effusion.

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Electrical Alternans: KEY Clinical Points

     In summary, electrical alternans is not common — but it does occur. You will see it. You have probably already seen it a number of times without even realizing it. Electrical alternans is a fascinating but advanced concept.

• In our experience — electrical alternans is most often seen in association with regular SVT rhythms (as seen in Figure-1). Seeing it in this context suggests (but does not prove) the existence of an AP (Accessory Pathway). Regardless of whether the mechanism of the regular SVT is AVNRT or AVRT — it is likely that reentry is involved. This conclusion may prove useful in contemplating potential investigative and therapeutic interventions.
• In a patient with pericarditis — a large heart on chest X-ray — or simply unexplained dyspnea — recognition of electrical alternans should suggest the possibility of a significant pericardial effusion that may be associated with tamponade. That said — electrical alternans is a nonspecific ECG sign that may also indicate myocardial ischemia, LV dysfunction and/or possibility of any of a number of other precipitating factors. BOTTOM Line: If you see electrical alternans — Look for an underlying clinical condition that may be responsible for this ECG sign.
• Development of electrical alternans per se — conveys no adverse prognostic implications beyond those associated with severity of the underlying disorder. Two exceptions to this general rule are: i) In a patient with QT prolongation or severe ischemia — recognition of electrical alternans may portend deterioration to Torsades or VT/VFib; and ii) In a patient with a large pericardial effusion — development of total electrical alternans (of P wave, QRS complex and T wave) suggests there may now be tamponade.

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ACKNOWLEDGMENT: My appreciation to Jenda Enis Stros for allowing me to use the ECG in Figure‑1.

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- For more information – GO TO:

• Figures 1,2 excerpted from ECG-2014-ePub (recently published!). More on electrical alternans in Section 14 of ECG-2014-ePub.

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