ECG Blog #339 — Is it SA Block?

 

The ECG in Figure-1 — was obtained from an older old man who presented to the ED (Emergency Department) with chest pain.

• Providers were concerned about SA block. Do you agree?
• What else do you see?

Figure-1: Initial ECG of a patient with chest pain. Is there SA block?

MY Approach to the ECG in Figure-1:

As always – I favor beginning interpretation with assessment of the long lead rhythm strip — using the Ps, Qs & 3R Approach to recall the 5 KEY Parameters (See ECG Blog 185). I find it easiest (and most productive) to delay assessing the 12-lead ECG until after I’ve had a chance to look at the rhythm.

• The rhythm in Figure-1 is not regular — but it does show a "bigeminal" pattern of group beating (ie, repetitive groups of 2 beats — seen here as a repetitive pattern of alternating "longer-than-shorter" R-R intervals).
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• The QRS is narrow (ie, not more than half a large box in duration in any lead = not more than 0.10 second). Therefore — the rhythm is supraventricular.
• P waves are present. It's easiest to focus on the 2 long lead rhythm strips — in which details of QRS complexes and P waves are perhaps easiest to see in the long lead V1.

The Importance of P Waves:

IF one focuses on the long lead V1 rhythm strip in Figure-1 — it appears that a P wave precedes each QRS complex on this tracing.

• The PR interval is normal (ie, between 0.12-0.21 second in lead II) — and appears to be of equal duration for all 10 beats on this tracing.
• The 1st beat in each pair (ie, beats #1,3,5,7 and 9) — appears to be sinus-conducted (ie, upright P wave with a constant and normal PR interval).

PEARL #1: As discussed in ECG Blog #232 and Blog #312 — recognition of a bigeminal supraventricular pattern when the 1st beat in each pair is conducted, should suggest the following differential diagnosis:

• Sinus rhythm with atrial or junctional bigeminy (ie, every-other-beat is a PAC or a PJC).
• Sinus rhythm with atrial trigeminy — in which every-third P wave is a PAC that is "blocked" (non-conducted).
• Some form of SA ( = Sino-Atrial) Block.
• Mobitz I, 2nd-Degree AV Block ( = AV Wenckebach) with 3:2 AV conduction.
• Mobitz II, 2nd-Degree AV Block (with non-conduction of every 3rd P wave).

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Beyond-the-Core: Technically, there are a few additional causes of a bigeminal rhythm that need not be considered in today's case, because the rhythm is either not strictly supraventricular — or — because the 1st beat in each group is not sinus-conducted. These additional causes include:

• Ventricular bigeminy (ie, every-other-beat is a PVC).
• Atrial fibrillation, atrial tachycardia or atrial flutter with Wenckebach conduction.
• "Escape-Capture" (the 1st beat in each group is a junctional or ventricular escape beat — followed by a conducted beat).

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PEARL #2: Since atrial activity provides the essential clue to the etiology of a bigeminal rhythm — the KEY Question — is whether the morphology of all P waves in today's tracing is the same?

• IF P wave morphology (and the PR interval) are both the same for each of the 10 beats on today's tracing — then all P waves are sinus-conducted.
• IF on the other hand — P wave morphology for each of the early beats (ie, beats #2,4,6,8 and 10) is different — then these early beats must be PACs (Premature Atrial Contractions), and the rhythm is atrial bigeminy.
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• KEY Point: An ectopic P wave arising from a site in the atria that lies close to the SA node — may look very similar to a sinus P wave in one or more leads. But non-sinus P waves will not look the same as sinus P waves in all 12 leads. For this reason — it is important to closely examine P wave morphology in as many of the 12-leads as possible.

Take Another LOOK at today's tracing (See Figure-2):

• HINT: Compare P wave morphology in Figure-2 for the 3 leads with colored arrows. Is morphology for the RED and YELLOW-arrow P waves exactly the same for each of the 3 simultaneously-recorded leads that I have labeled?

Figure-2: I've labeled selected atrial activity from Figure-1 (See text).

ANSWER:

There are subtle-but-real differences in P wave morphology between the RED and YELLOW-arrow P waves in Figure-2:

• In lead II — the RED-arrow P wave is clearly larger than the YELLOW-arrow P wave. In support that this finding is real (and not the result of artifact or the normal variation that may be seen from one P wave to the next) — is the fact that the first P wave in each of the 5 groupings in the long lead II rhythm strip is larger.
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• In lead III — the YELLOW-arrow P wave is barely seen, whereas a definite P wave can be seen under the RED arrow.
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• In lead V1 — the negative component of the RED-arrow P wave is larger. Once again, we see that the negative component of the 1st P wave in each of the 5 groupings in the long lead V1 is larger.
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• PEARL #3: In my experience — SA block is rare! In contrast — atrial bigeminy is a common rhythm disturbance. As a result, I start from the premise that before I will diagnose SA block as the cause of a bigeminal rhythm — I know that I'll probably be able to see subtle-but-real differences in P wave morphology between the 2 beats in each group IF I look in enough different leads. Only when there truly is no difference in P wave morphology in multiple leads do I contemplate SA block.

IMPRESSION: There are subtle-but-real differences in P wave morphology between the 2 P waves in each grouping in Figure-2. Therefore — we can rule out AV block (both Mobitz I and Mobitz II) — because P waves should be both regular and have the same morphology with either form of AV block.

• We ruled out SA block — because morphology of all P waves should be the same with this rare arrhythmia.
• We can rule out blocked PACs — because the T waves of the 2nd beat in each grouping (ie, the T waves of beats #2,4,6,8,10) look identical to the T waves of the 1st beat in each grouping (ie, there is no sign of a "hidden" blocked PAC).
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• Therefore — the rhythm in Figure-2 is atrial bigeminy!

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What About the Rest of the 12-Lead ECG?

Returning to the 12-lead ECG in Figure-2 — this is a very abnormal tracing from this older man who presented to the ED with chest pain!

• Take Another LOOK at the 12-lead tracing (Figure-3):

Figure-3: For ease of interpretation — I show only the 12-lead ECG from today's case. We've already established that the rhythm is atrial bigeminy (ie, sinus rhythm + every-other beat is a PAC). 
— QUESTION: What else do you see? —

MY Thoughts on the 12-Lead ECG:

As previously noted — the underlying rhythm in Figure-3 is atrial bigeminy. Additional findings include the following:

• There is low voltage in the limb leads (ie, No limb lead >5 mm). There is also surprisingly low voltage in lateral chest leads V5,V6 (which usually manifest significant R wave amplitude).
• Intervals (PR, QRS, QTc) are normal. That said, although the QRS complex does not measure out to be “wide” (ie, It is not more than 0.10 second in duration) — the QRS in the limb leads “looks wide”, because there is fragmentation (notching) of QRS complexes in all 6 limb leads.
• There is marked LAD (Left Axis Deviation) — as a result of the all-negative fragmented QS complexes in each of the inferior leads. Whether this is the result of LAHB (Left Anterior HemiBlock) — inferior infarction of uncertain age — and/or some combination of both is uncertain.
• There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves: As noted — There are fragmented inferior lead QS complexes. A Q wave is also seen in lead V6. Although small in size — given how tiny the R wave amplitude in lead V6 is — this is a significant (ie, infarction-related) Q wave.
• R Wave Progression: Transition (where the R wave becomes taller than the S wave is deep) — occurs appropriately (here between leads V2-to-V4). That said — the tiny R wave amplitude in lateral chest leads V5,V6 is clearly abnormal.
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• ST-T Wave Changes: There is ST segment coving and elevation, with terminal T wave inversion in each of the inferior leads. Subtle reciprocal ST segment depression is seen in lead aVL. The nonspecific ST-T wave flattening in the other high-lateral lead ( = lead I) — is probably also a reflection of reciprocal changes.
• In the Chest Leads — there is "shelf-like" ST depression in leads V1-thru-V4 (maximal in leads V2,V3). There is subtle-but-real ST elevation in lead V6.

Putting It All Together:

Given the History of this patient (ie, an older man who presented to the ED for chest pain) — the ECG in Figure-3 is diagnostic of recent or acute infero-postero-lateral OMI (Occlusion-based Myocardial Infarction).

• The marked fragmentation (notching) seen in virtually all limb leads (and also to a lesser extent in lateral chest leads V5,V6) — suggests "scar" from either infarction and/or cardiomyopathy. This finding, in addition to the QS complexes in each of the inferior leads — suggests that there has been inferior infarction at some point in time. That said, without a prior ECG for comparison — we can not rule out the possibility that these findings may be recent (or even acute). To Emphasize: Significant Q waves have been known to develop in as little as 1-2 hours after the onset of symptoms.
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• The amount of ST elevation seen in the inferior leads is modest, albeit this is difficult to assess given how small QRS complexes are in these leads. Similarly, the amount of reciprocal ST depression in high-lateral lead aVL is also modest. Therefore, without the benefit of a prior ECG for comparison — we simply can not say from this single ECG alone whether inferior lead changes are new — old — or — reflect an additional "new" event superimposed on prior infarction.
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• On the other hand — the marked shelf-like ST depression in anterior chest leads constitutes a positive "Mirror" Test for acute posterior OMI (See LINKS to related Blogs below) — and, in this patient with new chest pain — has to be assumed acute until proven otherwise!
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• The loss of R wave amplitude in lateral chest leads — in association with a small-but-definite Q wave with coved ST elevation in lead V6 must also be assumed to reflect acute lateral infarction until proven otherwise.
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• As to identification of the probable "culprit artery" — the finding of potentially acute ST-T wave changes in infero-postero-lateral lead areas — with a comparable amount of ST elevation in lead II and lead III — suggests either acute occlusion of the LCx (Left Circumflex) coronary artery and/or multi-vessel disease.
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• Finally — the finding of greatly reduced QRS amplitude ( = low voltage) in multiple leads, in a patient with acute infarction — may indicate myocardial "stunning" with markedly reduced LV function (See ECG Blog #272 for more on the causes and clinical significance of low voltage on ECG).
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• P.S.: Of Note — Our assessment of the cardiac rhythm in today's case determined that the bigeminal rhythm was not the result of AV block. Chances are that if (as) this patient recovers and regains normal LV function — that his atrial bigeminy will also resolve.

CASE Follow-Up:

Unfortunately — I did not receive clinical follow-up on today's case. I also did not receive any additional ECGs on this patient. Serial ECG could have been enlightening as to refining the anatomic area(s) of acute infarction — as well as shedding light on when the recent infarction most probably occurred. 

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Acknowledgment: My appreciation to Kire Todorov (from Macedonia) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Use of a Systematic Approach to Rhythm Interpretation. 
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #312 — Reviews the ECG diagnosis of SA Block (as well as the Differential Diagnosis of a Bigeminal Rhythm).
• ECG Blog #232 — More on the ECG diagnosis of a bigeminal supraventricular rhythm.
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• ECG Blog #272 — Reviews the causes and clinical significance of Low Voltage (especially in association with recent/acute infarction).
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• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery (and discusses the concept of why "OMI" is a much better term than "STEMI", which has become outdated).
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• ECG Blog #317 — More on use of the Mirror Test (compared to use of posterior leads) for detection of acute Posterior MI.
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• ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).
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• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post). 
• ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.
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• The September 21, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI.
• The February 16, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) emphasizes utility of the Mirror Test for diagnosis of acute Posterior MI. 
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• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.