Saturday, April 27, 2013

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 (= QRST 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.

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).
     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.

MAT is neither AFib – Wandering Pacer – orSinus 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.

     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? 

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.

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. 

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).

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.

- For more information – GO TO:

  • For more on Wandering PacemakerPlease see ECG Blog #155.

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

  • 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).

Tuesday, April 2, 2013

ECG Blog #64 — AV Block and/or Escape beats?

Interpret the 2 rhythm strips below using the Ps,Qs,3R Approach. The patient is hemodynamically stable in each case.
  • Is there AV block or not? If so – Describe the type of AV block present.
  • HINT: A similar mechanism is operative in each tracing.

Figure 1: Tracings A and B were each obtained from an asymptomatic young adult. Is there AV block? HINT: A similar mechanism is operative in each tracing.

ANSWER to Tracing A in Figure 1:
The first 4 beats in Tracing A are sinus conducted. The QRS complex is narrow throughout – although there is slight change in QRS morphology beginning with beat #5.
  • Note that there is gradual slowing in the rate of the sinus bradycardia seen for the initial 4 beats. That is, the R-R interval between sinus beats (red arrows in Figure-2) increases from 6.2 large boxes (between beats #1-2) – up to an R-R of 7.0 large boxes (between beats #3-4).
  • No P wave precedes beat #5. This QRS complex is narrow (albeit slightly different in morphology compared to the QRS for sinus conducted beats). Beat #5 is a junctional escape beat.
  • Note that the R-R interval preceding beat #5 is a bit over 7 large boxes in duration. Thus, it is appropriate (and downright fortunate) that this AV nodal escape beat occurred – since the underlying sinus bradycardia rhythm has continued to slow down. Note also that the R-R interval for each of the junctional escape beats in Tracing A manifests the same R-R interval (7.4 large boxes) – which corresponds to an appropriate AV nodal escape rate at ~40/minute.
  • Finally – note that each junctional escape beat (beats #5,6,7) is followed by a negative P wave in this lead II (blue arrows). This reflects retrograde atrial conduction from junctional beats that continually resets the sinus node and serves in this way to perpetuate the junctional escape rhythm.

Figure 2: Addition to Tracing A of red arrows (denoting sinus beats) – blue arrows (denoting retrograde atrial conduction from junctional escape beats) – and measurement of R-R intervals (See text).

BOTTOM Line Regarding Tracing A in Figure 1:
There is no evidence of any AV block at all in Tracing A. On the contrary, in view of the fact that this tracing was obtained from a presumably healthy and otherwise asymptomatic young adult – there is not necessarily any abnormality at all. We simply see progressive sinus bradycardia with an appropriate AV node escape rhythm arising once the sinus rate drops below 40/minute.
  • Marked sinus bradycardia as seen here could be normal for this patient IF this young asymptomatic individual was an endurance athlete. In this case – no intervention would be needed. On the contrary – sinus bradycardia to this degree with need for an AV nodal escape rhythm to arise would be cause for concern IF the patient was an older adult with a history of weakness or syncope. Clinical correlation is everything.
  • There is no evidence of any AV dissociation in Tracing A. This is because all P waves seen on this tracing are related to neighboring QRS complexes (either appearing before the QRS and conducting – or appearing after the QRS reflecting retrograde AV conduction from junctional escape beats).

Review of Tracing B in Figure-1:
Figure 3: Addition to Tracing B of vertical red arrows (denoting sinus beats) – a blue arrow (denoting retrograde atrial conduction following beat #3) – and slanted red arrows denoting nonconducting P waves that precede the QRS complex of beats #6-thru-9 (See text).

ANSWER to Tracing B:
The underlying rhythm in Tracing B is sinus – as determined by the presence of an upright P wave with fixed PR interval preceding beats #1 and #2.
  • Beat #3 is premature. It is slightly wider and quite different in morphology compared to other beats on this tracing. Beat #3 is not preceded by a premature P wave. We suspect that beat #3 is a PVC (although acknowledge that it could be a fascicular escape beat given that it is not overly wide).
  • Regardless of the origin of beat #3 – this premature beat is followed by a retrograde P wave (blue arrow). Just like the situation in Tracing A – retrograde atrial conduction resets the sinus node. As a result – there is no P wave preceding beat #4. Given how similar QRS morphology of beat #4 is to the first two sinus beats – this defines beat #4 as a junctional escape beat.
  • The remaining beats in Tracing B (beats #5,6,7,8,9) represent a fairly regular albeit slightly accelerated junctional escape rhythm at ~65/minute.
  • Sinus node activity gradually returns toward the end of the tracing (slanted red arrows preceding beats #6,7,8 with a PR interval too short to conduct).

NOTE: We are uncertain if the P wave preceding beat #9 is or is not conducting. We suspect that it is not, because the PR interval preceding it appears to be slightly shorter than the PR preceding sinus beats #1 and #2. Clinically – it does not matter if the P wave preceding beat #9 is conducting or not – since the “theme” of this rhythm remains unchanged. In either case – Our Interpretation for Tracing B is the following:
  • Underlying sinus rhythm (beats #1 and #2). One PVC is seen (beat #3).
  • Resultant AV dissociation by default beginning with beat #4 – with a fairly regular albeit slightly accelerated junctional escape rhythm. That said – there is no evidence of any AV block in Tracing B, since P waves never fail to conduct when given a chance to do so. The PR interval preceding beats #6-thru-9 is simply too short to conduct.
  • Given that Tracing B was obtained from a presumably healthy and asymptomatic young adult – no intervention is needed.
Presumably sinus rhythm is restored in Tracing B. If this has not yet occurred by beat #9 – it looks like it will occur soon thereafter.

For more information – GO TO: