ECG Interpretation Review #67 (PAC – PVC – 12 Leads Better than One)

     The rhythm strip shown in Figure 1 was obtained from a patient with palpitations. The patient was hemodynamically stable.

• Does Figure 1 show atrial trigeminy (every 3rd beat a PAC )?

Figure-1: Lead II rhythm strip obtained from a patient with palpitations. Is this atrial trigeminy? (Figure reproduced from ACLS-2013-Arrhythmias: Expanded Version- pp 229-230). NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window (See text).

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Interpretation of Figure 1:

     The underlying rhythm in Figure 1 is sinus — as determined by the presence of upright P waves with fixed PR interval preceding beats #1,2; 4,5; 7,8; 10,11; and 13 in this lead II monitoring lead. The QRS complex of sinus beats is narrow.

• Every-third-beat occurs earlier-than-expected and looks slightly different. That is — the QRS complex of beats #3, 6, 9 and 12 each have a smaller r wave and less deep S wave than do sinus beats. The QRS complex for each of these early beats looks to be narrow and preceded by a premature P wave (red arrow in Figure 1). IF this were the case — the rhythm would be atrial trigeminy (every third beat a PAC [Premature Atrial Contraction] ).

QUESTION: Do you agree with the above assessment?

• HINT #1: Do we have enough information from Figure 1 to determine IF the QRS complex of each early beat is truly narrow?
• HINT #2: Look at Figure 2 — in which we have added a simultaneously recorded lead I rhythm strip. Does the QRS of each early beat still look narrow?

Figure-2: A simultaneously recorded lead I rhythm strip has been added to Figure-1. Note from the vertical time line that the notch which looked to be a premature P wave in Figure-1 is actually the initial part of the QRS complex in simultaneously recorded lead I. (Figure reproduced from ACLS-2013-Arrhythmias: Expanded Version- pg 230).

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12 Leads are Better than One

     We fully acknowledge that this is a trick tracing. We nevertheless have chosen it to emphasize a number of important points:

• POINT #1: 12 Leads are Better than One. It is easy to get fooled when you are not provided with complete information. Part of the QRS complex may sometimes lie on the baseline. When this happens — the QRS complex may look narrow in one lead — whereas in reality it is actually quite wide. At other times (as in Figure 1) — what looks like a preceding “P wave” may actually be the initial part of the QRS complex. Use of a simultaneously recorded multi-lead rhythm strip (or 12-lead ECG) may be invaluable in such cases for shedding light on the true nature the rhythm being assessed. With the extra information provided by lead I in Figure 2 — it is now apparent that every third beat (ie, beats #3,6,9,12) occurs early, is wide, and is not preceded by any premature P wave. Every third beat in Figure 2 is therefore a PVC. The rhythm is ventricular trigeminy.
• POINT #2: Assume that a Premature Beat is “Guilty” (ie, a PVC) until Proven Otherwise.  Statistically — most early occurring different-looking beats that are not clearly preceded by a premature P wave will be ventricular in etiology. The “onus of proof” therefore rests with the interpreter to establish that any abnormal-looking beats are aberrantly conducted (ie, supraventricular) — rather than the other way around. Assume a ventricular etiology until proven otherwise. And remember that you can not “prove” aberrant conduction with use of the incomplete information provided from a single monitoring lead.

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- For more information – GO TO:

• Link to ACLS-2013-Arrhythmias(Expanded) — and the epub version of this book.

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ECG Interpretation Review #66 (2nd Degree AV Block – PACs – Blocked PACs – Mobitz I – AV Wenckebach – Group Beating)

     Interpret the two sequential tracings in Figure 1. The patient is hemodynamically stable.

• Note group beating in Tracing A. Is this due to AV block? If so — What type of AV block?
• HINT: Interpretation of Tracing A becomes easier if you first interpret Tracing B obtained from the same patient a lit bit later. This is because the same phenomenon responsible for the abnormal findings is operative in both tracings.

Figure-1: Sequential tracings in a patient who initially manifests group beating (Tracing A) — and later manifests some irregularity with a brief pause following beat #6 (Tracing B). What is the cause of the abnormal findings seen in both tracings? (Figure reproduced from ACLS-2013-Arrhythmias: Expanded Version - pp 264-265). NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window (See text).

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Characteristics of Mobitz I 2nd-Degree AV Block (AV Wenckebach)

    Recognition of the phenomenon of “group beating” should always suggest the possibility of a Wenckebach conduction disorder. That said — this case presents a wonderful example of why group beating does not always mean that a Wenckebach block is present.

• Second-degree AV block of the Mobitz I type (also known as AV Wenckebach) — is by far the most common form of 2nd-degree AV block. Mobitz I is characterized by: i) Progressive lengthening of the PR interval until a beat is dropped; ii) Group beating; iii) A regular (or at least fairly regular) atrial rate; and iv) The pause that contains the dropped beat is less than twice the shortest R-R interval. These features collectively (among a few others) are known as “the Footprints of Wenckebach”. They are all present in Figure 2.

Figure-2: Mobitz I 2nd degree AV block with all of “the footprints” mentioned above. There are two “groups” of beats (beats #1,2,3; and #4,5). The P-P interval is regular (in this case at a rate of 100/minute). Within groups — the PR interval progressively lengthens until a beat is dropped (the P wave following beats #3 and #5 is nonconducted). The pause containing the dropped beat is less than twice the shortest R‑R interval (that is — the pause between beats #3-4 is less than twice the R-R interval between beats #2-3). (Figure reproduced from ACLS-2013-Arrhythmias: Expanded Version- pg 237).

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Beyond-the-Core: The reason we specify “AV Wenckebach” rather than just, “Wenckebach” for the conduction disorder shown in Figure 2 — is that there are many types of Wenckebach conduction disorders. Second-degree AV block of the Mobitz I type is just one of these (albeit the most common form seen).

• One may also see Wenckebach-conduction in the form of retrograde block out of the AV node; Ventricular tachycardia with retrograde Wenckebach; SA node Wenckebach; and atrial fibrillation or flutter with Wenckebach conduction, to name just a few.
• Among the above footprints most helpful in identifying some of these other forms of Wenckebach conduction are “group beating” and pause containing the dropped beat being less than twice the shortest R-R interval.

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Why Despite Group Beating – Figure 1 is Not AV Wenckebach

     Before addressing specific interpretation of the rhythm in Figure 1 — We list reasons why sequential Tracings A and B are not the result of Mobitz I 2nd degree AV block. This is easiest to do by adding red and blue arrows to highlight P waves in these tracings (Figure 3). Note the following:

• The PR interval does not progressively increase within the groups of beats (from beat #1-to-2; from beats #3-to-4-to-5; from beats #6-to-7-to-8).
• The atrial rhythm in Tracing A is clearly not regular.

Figure-3: Addition of arrows to Figure 1 to highlight atrial activity (See text). (Figure reproduced from ACLS-2013-Arrhythmias: Expanded Version - pp 264-265).

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Interpretation of the Sequential Tracings in Figure 3

     The underlying rhythm for both tracings in Figure 3 is sinus arrhythmia. In Tracing A — a short pause follows each group of sinus-conducted beats. There is subtle-but-real peaking of the T wave of beats #2, 5 and #8 in Tracing A (blue arrows). That this peaking is real and not due to artifact — is determined by the fact that the T wave of all other beats in Tracing A is smoother and of smaller amplitude. This peaking of T waves must therefore reflect blocked PACs.

• A similar phenomenon is operative in Tracing B — and much easier to see. Note that beat #4 in Tracing B occurs early. The T wave just preceding beat #4 in Tracing B is again peaked (blue arrow) — strongly suggesting that a PAC is hidden within this T wave. The reason the QRS complex of beat #4 looks slightly different — is that beat #4 is a PAC conducted with aberration.
• A short pause follows beat #6 in Tracing B. The commonest cause of a pause is a blocked PAC. Once again — “telltale” notching of the T wave of beat #6 in Tracing B (blue arrow) indicates this is due to another blocked PAC.

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Summary Take-Home Points:

     Awareness and recognition of the phenomenon of “group beating” is an important concept that will often help streamline your interpretation. Some type of Wenckebach conduction will often be the cause. However — there are other reasons for group beating that need to be kept in mind. Remember:

• The commonest cause of a pause is a blocked PAC (not AV block). Although often quite subtle (as they are in Tracing A) — blocked PACs will be found IF you look for them.
• Routine use of a systematic approach to rhythm interpretation is essential for accurate interpretation. We use this memory aid: “Watch your Ps & Qs — and the 3Rs”. (Click HERE for brief Review.) Using this systematic approach should make it immediately obvious that AV Wenckebach is not the cause of group beating in this example — because the atrial rhythm in Tracing A is definitely not regular!

     In Summary — the 2 tracings in Figure 3 reflect the same phenomenon. There is underlying sinus arrhythmia that is punctuated by multiple PACs. Most of these PACs are blocked.

• The PAC that notches the T wave of beat #3 in Tracing B is conducted with aberration.
• The T wave of beat #6 in Tracing B is unmistakably peaked.
• Recognition that the “theme” for Tracing B is the occurrence of PACs alerts us to carefully focus on T wave morphology at the beginning of each pause in Tracing A. Doing so facilitates identifying the subtle-but-real deformity brought about by hidden PACs within the T waves of beats #2, 5 and 8 in Tracing A.

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- For more information – GO TO:

• Brief review of the Ps,Qs & 3R Approach to Rhythm Interpretation.
• The Basics of AVBlock (including links to examples of AV block mimics).
• Link to ACLS-2013-Arrhythmias(Expanded) — and the E-Pub version of this book.

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ECG Interpretation Review #65 (SVT - RVH - COPD - RAA - MAT - Multifocal Atrial Tachycardia - Wandering Pacer - PACs - Schamroth Sign)

The ECG in Figure 1 was obtained from a patient who presented with shortness of breath.

• How would you interpret this 12-lead tracing? What is the rhythm?
• Is a pulmonary or cardiac etiology a more likely cause of this rhythm?

Figure-1: 12-lead ECG obtained from a patient with shortness of breath. Is a cardiac or pulmonary etiology more likely? (Figure reproduced from ACLS-2013-Arrhythmias: Expanded Version - pp 133-135). NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window (See text).

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Interpretation of the RHYTHM:

     Although there is no long lead II rhythm strip — We can nevertheless interpret the rhythm from surveillance of all 12 leads on this tracing.

• The QRS complex is narrow. The rhythm is irregular.
• Despite the overall irregularity of this rhythm — this is not AFib (Atrial Fibrillation). Instead, definite atrial activity is seen in each of the inferior leads (II,III,aVF). This is especially true in lead II — where several different P wave morphologies are seen. The rhythm is therefore MAT (Multifocal Atrial Tachycardia).
• It is easy to understand how the irregularly irregular rhythm in Figure 1 might be mistaken for AFib — IF monitoring was performed from a single lead in which P waves are not readily seen. Thus, there is no indication that the rhythm is MAT from inspection of leads I; V1,V2,V3 — and the inferior leads are really the only place where beat-to-beat change in P wave morphology is readily apparent.

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Interpretation of the REST of the 12-LEAD ECG in Figure -1:

     Having interpreted Rate and Rhythm — We continue our Systematic Approach by next assessing for Intervals (PR-QRS-QT) – Axis – Hypertrophy (= Chamber Enlargement) — and Ischemia/Infarction (= Q‑R‑S‑T Changes):

• Intervals: As stated — the QRS is narrow. Determination of the PR interval is not relevant in this tracing due to constantly changing P wave morphology. The QT looks to be within the normal range (not more than half the R-R interval) — although assessment of QT interval duration becomes challenging (and far less accurate) when the rate is rapid and irregular as it is here.
• Axis: The axis is vertically oriented — although still within the normal (0-to-90 degree) range. We estimate the mean QRS axis to be about +80 degrees (since the QRS is no more than barely positive in lead I ).
• Hypertrophy: RAA. Possible RVH. No LVH. (See Putting It All Together below.)
• QRST Changes: Other than a possible q in lead aVL — there are no Q waves. Transition is delayed in the precordial leads (the R wave does not become taller than the S wave is deep until between V5-to-V6). There are nonspecific ST-T wave abnormalities — but there are no acute changes.

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Putting It All Together: Figure-1 = MAT

     The unifying theme in this case stems from awareness that the cardiac rhythm is MAT. As suggested by its name — with MAT there are multiple forms of atrial activity at a rapid (tachycardia) rate. MAT almost always occurs in one of 2 common clinical settings:

• Clinical Setting #1: Pulmonary disease (COPD; long-term asthma; pulmonary hypertension).
• Clinical Setting #2: Acutely ill patients with multisystem disease (ie, with sepsis; shock; electrolyte and/or acid-base disorders).

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     Putting together the ECG findings seen in Figure 1 strongly suggests that this patient with shortness of breath has significant pulmonary disease:

• The mean QRS axis is vertically oriented. This is common in patients with longstanding COPD (Chronic Obstructive Pulmonary Disease) — in whom hyperinflation and low set diaphragms often results in a relatively vertical mean QRS axis.
• Mean QRS voltage is reduced. Although not quite satisfying ECG criteria for “low voltage” (ie, QRS amplitude not more than 5mm in any limb lead) — QRS voltage in both limb and precordial leads is clearly less than is normally seen. The insulating effect of air prevalent in the emphysematous chest of patients with COPD accounts for the reduction in voltage.
• There is probable RAA (Right Atrial Abnormality) — suggested by the finding that several of the different-shaped P waves in lead II appear to be tall and peaked. RAA is an indirect ECG sign of RVH (the only condition that results in right atrial but not right ventricular enlargement is tricuspid stenosis).
• We suspect probable RVH. Admittedly — ECG diagnosis of RVH in an adult is extremely difficult. This is because anatomic mass of the adult LV (left ventricle) is normally many times greater than mass of the adult RV (right ventricle). As a result, even when RV mass is significantly increased — it will often not be by enough to produce a predominance of right-sided forces. Therefore — hallmark ECG findings of RVH such as tall R wave in lead V1 and right-sided “strain” (ST-T depression in inferior and/or anterior leads) are often not seen until very late in the course of adult pulmonary disease (by which point there is often pulmonary hypertension). That said — the constellation of other ECG findings listed above in this patient with acute dyspnea suggest at least possible (if not probable) RVH, even in the absence of definitive ECG signs.
• There is persistence of precordial S waves. Normally — electrical activity in lateral precordial leads V5,V6 is all positive, reflecting the predominant direction of depolarization toward the much larger left ventricle. In patients with pulmonary disease — small-to-moderate-sized S waves often persist in left-sided precordial leads. Note in Figure 1 — that: i) Transition is delayed (the R wave does not become greater than the S wave until between leads V5‑to‑V6); and ii) A substantial S wave (of 5 mm) is still seen in lateral lead V6.
• Lead I is almost a null vector. That is — the P wave, QRS complex and ST-T wave in lead I are all of tiny amplitude. This finding (known as “Schamroth’s sign”) — is highly suggestive of significant pulmonary disease (and probable RVH) provided that there is: i) No lead misplacement; and ii) Other ECG signs of pulmonary disease. The tiny 2-3 mm R wave and flat ST-T wave seen in Figure 1 qualifies as a “Schamroth sign” in this tracing.
• The patient has shortness of breath as their chief complaint.
• The cardiac rhythm is MAT. Even as an isolated finding — MAT should make you strongly consider significant pulmonary disease. In the context of this case, it makes RVH likely.

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MAT is neither AFib – Wandering Pacer – or – Sinus Tach with PACs:

     MAT is not AFib. Although both are irregularly irregular rhythms — no P waves at all are present in AFib, whereas multiple different-shaped P waves are seen with MAT. The importance of distinguishing between AFib vs MAT — is that treatment considerations are very different for these two arrhythmias. Rate control by use of drugs is rarely needed with MAT (that generally responds best to treatment of the patient’s underlying pulmonary condition or multisystem disease).

• In our experience — MAT is the 2nd most commonly overlooked cardiac arrhythmia (next to AFlutter). MAT is easy to overlook — because the overwhelming majority of sustained irregular SVT rhythms will turn out to be AFib.
• The best way to avoid overlooking MAT is to: i) Think of this diagnosis when you see an irregular rhythm in an acutely ill patient, especially if they have severe pulmonary disease; and ii) Always get a 12-lead when assessing irregular rhythms.

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     MAT is also not sinus tachycardia with PACs. Consider the two lead II rhythm strips shown in Figure-2:

• Is MAT present in one or both of these tracings?

Figure-2: Is MAT present in one or both of these tracings? (Figure reproduced from ACLS-2013-Arrhythmias: Expanded Version - pp 133-135).

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ANSWER to Figure 2:

     The rhythm in Tracing A of Figure-2 is MAT. Note that P wave morphology erratically and continually changes from beat-to-beat. In contrast — Tracing B represents sinus tachycardia with PACs. As opposed to MAT — there is an underlying sinus rhythm with intermittent periods of the same sinus P wave appearing consecutively for at least a few beats in a row.

• Note similar P wave morphology (and similar PR interval) for beats #1,2,4,5, and 8 in Tracing B of Figure-2. These are the P waves of the underlying sinus rhythm.
• The irregularity in Tracing B is produced by the multiple PACs that are present (beats #3,6,7). Note variation in P wave morphology for these PACs. That said — clear indication of underlying sinus rhythm suggests that the rhythm is not MAT.
• Realize that Figure-2 represents no more than a “snapshot” of what is occurring clinically. Tracings A and B merely constitute a 4-second rhythm strip. True appreciation for the real degree of variation in rate and P wave morphology can only be determined by a longer period of monitoring.

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Clinical NOTE: Variations on the “MAT Theme"

     Many possibilities exist for “middle ground” irregular SVT rhythms that manifest P waves. For example — rhythms otherwise suggestive of being “MAT” are not always “tachycardic”. Moreover — the point of transition between sinus rhythm with multiple different-shaped PACs into “MAT” is often elusive.

• Most of the time — it will be obvious when the rhythm is sinus tachycardia with PACs. That said — it may at times be difficult (impossible) to distinguish between MAT vs Sinus Tach with PACs.
• The “good news” — is that clinically it does not matter which of the two are present. This is because clinical implications of MAT vs Sinus Tach with multiple PACs are the same when either rhythm is seen in a patient with one of the clinical settings predisposing to MAT. In either case — priority rests with identifying and treating the underlying disorder.
• Final Caveat: — MAT is not a wandering pacemaker. Rather than beat‑to‑beat change in P wave morphology (as is seen with MAT) — there is gradual shift in P wave morphology with wandering pacemaker (Figure 3). Wandering pacemaker is often a normal variant. MAT is anything but a “normal” variant.

Figure-3: Wandering pacemaker. There is gradual change in P wave morphology as the site of the atrial pacemaker changes. Initially the P wave in lead II is an upright sinus complex (red arrow preceding beat #4) — with gradual change to an isoelectric P wave (blue arrow that precedes beat #5) — followed by eventual resumption of sinus rhythm with beat #17 toward the end of the bottom tracing. Note that there is minimal change in heart rate throughout the rhythm strip. (Figure reproduced from ACLS-2013-Arrhythmias: Expanded Version - pp 133-135).

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Beyond-the-Core: MAT vs Wandering Pacer

     It should be apparent from Figure-3 that a more extensive period of monitoring would really be needed to definitively diagnose “wandering pacemaker”. Technically — Figure-3 does not qualify, because only two different atrial sites are seen. Nevertheless, we use this illustration because it highlights gradual change from one P wave morphology (upright for beats #1,2,3,4 and #17,18,19,20,21) to another (isoelectric P wave for beats #5-thru-16).

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Bottom Line: MAT vs Wandering Pacer 

     MAT and wandering pacer represent two ends of a spectrum. In a sense — MAT is simply a “wandering pacemaker” with a rapid rate and beat-to-beat change in P wave morphology. Clinical judgement (with awareness of the patient’s medical history) will therefore be needed for assessment of middle-ground cases in which the rate is slower and P wave variation is intermediate between strict definition of MAT vs wandering pacemaker.

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- For more information – GO TO:

• Click HERE for a link from our ECG-2011-E-Pub that reviews the basics of our Systematic Approach to 12-lead interpretation. -
• Click HERE for my web page on Chamber Enlargement. -
• Link to My COMMENT on the ECG Guru web site regarding Use of Schamroth's Sign in the diagnosis of RVH (this post and tracing presented in excellent fashion by Jason Roediger).

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Please CHECK OUT our 2 newest publications:

• ACLS-2013-Arrhythmias (Expanded Version) - 292 pages; 8.5 X 5.5" pages; spiral bound.
• ACLS-2013-ePub (which contains the same content as ACLS-2013-Arrhythmias in electronic format).

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