ECG Blog #65 (AFib - RVH - Wandering - MAT)

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? 

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.

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? 

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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. 

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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:

• For more on Wandering Pacemaker — Please see ECG Blog #155.
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• Click HERE for a link to our ECG Blog #93 (reproduced from our 1st Book on ECGs-2014) that reviews the basics of our Systematic Approach to 12-lead interpretation. 
• For more on Chamber Enlargement — GO TO — ECG Blog #92 (for LVH) — ECG Blog #75 (for RAA/LAA) — ECG Blog #77 (for RVH).
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• 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).