ECG Blog #241 (56) — Fascinating Bigeminy

The 12-lead ECG and long lead II rhythm strip shown in Figure-1 was obtained from a man in his 60s who presented with a complicated course, including high fever and chest pain. The patient was unresponsive without a pulse on arrival in the ED (Emergency Department) — but promptly responded to resuscitation (albeit with hypotension) — at which time ECG #1 was obtained.

• Unfortunately — details of this patient's subsequent course were not available to me. That said — I thought the ECG in Figure-1 was fascinating and instructive enough to present the case without additional clinical follow-up.

 

QUESTIONS:

• What is the rhythm in Figure-1?
• What ELSE is going on in this tracing?
• Are there Osborn waves? IF so — What might this mean?

Figure-1: ECG and long lead II rhythm strip obtained following resuscitation of a patient with fever and chest pain (See text).

 

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NOTE: Some readers may prefer at this point to listen to the 5:35-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-56).

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Today's ECG Media PEARL #56 (5:35 minutes Audio) — What are Osborn Waves? (HINT: Osborn waves are not only seen with Hypothermia! ) 

 

 

MY Initial Approach to the ECG in Figure-1:

This is an especially challenging ECG — because QRS morphology is constantly changing in the 12-lead tracing. CONFESSION: I fully acknowledge that I was initially confused as to what was going on.

• PEARL #1: When in doubt about the etiology of a cardiac rhythm — Be systematic! Start with the long lead rhythm strip by addresing the 5 KEY parameters contained in the Ps, Qs & 3Rs Approach (See ECG Blog # 185).
• Because of the confusing, constantly-changing QRS morphology in the 12-lead ECG — I initially ignored the 12-lead — in the hope that understanding the rhythm would help me to sort out what was going on in the 12-lead.

My sequential thought process for assessing the rhythm in Figure-1 is outlined below. As part of my narrative — I include the questions I asked myself.

• There is group beating (ie, repetitive groups of 2 beats in a "long-short" pattern). So, although the ventricular rhythm is not Regular — some type of "organized" pattern to the rhythm is present.
• P waves are present! At least some of these P waves are conducting — as determined by the presence of P waves with a constant (and normal) PR interval preceding each of the QRS complexes that occur at the end of the longer R-R intervals (ie, RED arrows in front of beats #2,4,6,8,10 and 12 in Figure-2). This tells us there is an underlying sinus rhythm.
• The QRS complex is narrow for each of the sinus-conducted beats (ie, beats #2,4,6,8,10 and 12).

Figure-2: I've added RED arrows for those sinus P waves that we know are conducting. (See text).

 

QUESTION: In addition to the P waves highlighted by the RED arrows in Figure-2 — Are there more P waves on this tracing?

• HINT: What does the YELLOW arrow in Figure-2 suggest?

 

 

 

PEARL #2: I find the simple act of labeling P waves to be immensely helpful in facilitating rhythm recognition.

• I was not initially certain whether the hump in the ST segment of beat #3 (YELLOW arrow) represented another sinus P wave. But this hump looked to be about midway between the first 2 RED arrows in this figure — and the shape of this hump looked similar to the shape of other sinus-conducting P waves.
• Use of calipers provided me with the answer in a matter of seconds! (Figure-3).

 

Figure-3: Use of calipers allows us to walk out regular P waves throughout the rhythm strip (RED arrows). The atrial rate is ~80/minute. — NOTE: There is ever-so-slight variation in the P-P interval in Figure-3. This is common — and simply reflects slight sinus arrhythmia. But the presence of an underlying sinus rhythm (with almost regular sinus P waves) should be obvious.

 

QUESTION: Are all of the P waves in Figure-3 conducting? 

• HINT: Are the QRS complexes of beats #3,5,7,9,11 and 13 preceded by a P wave?

 

 

ANSWER: Beats #1,3,5,7,9,11 and 13 are not preceded by a P wave. Instead — an on-time sinus P wave occurs just after the QRS of these beats (PINK arrows in Figure-4).

• The fact that the on-time sinus P waves highlighted by PINK arrows are not followed by a QRS complex tells us that beats #1,3,5,7,9,11 and 13 can not possibly be conducted. Instead — these beats must originate from below the AV node! (ie, beats #1,3,5,7,9,11 and 13 can not possibly be PACs or PJCs — because if they were — they would reset the next sinus P wave!).

 

Figure-4: For clarity — I've colored in PINK the on-time sinus P waves that are not conducting. We know that these PINK P waves can not possibly conduct — because they occur in the refractory period of beats #1,3,5,7,9,11 and 13 — and they are not followed by a QRS complex.

 

PEARL #3: Use of simultaneously-recorded leads saves the day!

• We have just established that beats #1,3,5,7,9,11 and 13 must be originating from below the AV node. This conclusion initially surprised me — because in the long lead II rhythm strip, these beats did not look wide, and they looked similar in morphology to the sinus-conducting beats that occur before them.
• For clarity — I have highlighted within blue-white rectangles in Figure-4 the appearance of beats #3, 9 and 13 in other simultaneously-recorded leads. 12 leads are better than one. It should now be obvious that QRS morphology of beats #1,3,5,7,9,11 and 13 is very different than the QRS morphology of sinus-conducted beats #2,4,6,8,10 and 12.

 

 

QUESTION: If beats #1,3,5,7,9,11 and 13 are not supraventricular — then WHERE are they coming from? 

• HINT: Looking within the blue-white rectangles in Figure-4 — How WIDE are these beats? — and WHAT conduction defect(s) is suggested by their morphology in other simultaneously-recorded leads?

 

 

 

ANSWER: Looking within the simultaneously-recorded leads in Figure-4 — beats #1,3,5,7,9,11 and 13 are slightly (but not greatly) wider than the sinus-conducted beats that precede them. This is best seen for beat #9 in lead V1 — in which the qR complex in this lead measures ~0.11 second in duration.

• QRS morphology for beats #1,3,5,7,9,11 and 13 is consistent with RBBB (widened, qR pattern in lead V1 + wide terminal S waves in lateral leads I and V6) and LPHB (very deep and rapidly descending S wave in lead I + predominant R waves in leads II and III).
• NOTE: For review of how to quickly determine the bundle branch blocks and hemiblocks — See ECG Blog #204 (for BBBs) and ECG Blog #203 (for hemiblocks).

 

 

PEARL #4: We have already established that non-conducting beats #1,3,5,7,9,11 and 13 must be originating from below the AV node. But the fact that these beats are not overly wide — and — that their QRS morphology is consistent with a known type of conduction defect (ie, RBBB/LPHB) — suggests that these bigeminal beats originate from somewhere within the conduction system.

• Simply stated — there are 3 branches to the conduction system. These are: i) the right bundle branch (RBB); ii) the left anterior hemidivision (LAH) of the left bundle branch; and, iii) the left posterior hemidivision (LPH) of the left bundle branch.
• The EASY way to determine the origin of an escape or ectopic beat that manifests a hemiblock pattern — is that the complex arises from the remaining fascicle. Thus, in Figure-4 — since beats #1,3,5,7,9,11 and 13 manifest RBBB/LPHB morphology — these must be fascicular beats arising from the left anterior hemifascicle!
• I schematically illustrate the mechanism of the rhythm in today's case in the laddergram shown in Figure-5.

 

 

Figure-5: Laddergram illustrating the mechanism for the rhythm in today's case. The rhythm is ventricular (or more precisely, fascicular) bigeminy — in which beats #1,3,5,7,9,11 and 13 originate from the left anterior hemifascicle (LAH) in the ventricles.

 

 

What About the REST of the ECG?

Take another look at 12-lead ECG in Figure-5. Keeping in mind that this patient presented to the ED unresponsive, with a history of an acute febrile illness + chest pain — and — knowing that the rhythm in the long lead II rhythm strip is fascicular bigeminy — WHAT are your concerns?

• QUESTION #1: Are there acute ST-T wave changes?
• QUESTION #2: Are there Osborn waves?

 

 

 

PEARL #5: It is often challenging to interpret a 12-lead ECG for acute ST-T wave changes when QRS morphology in each of the leads is constantly changing. To address this challenge — I suggest the following:

• FIRST — Identify sinus-conducted beats in each of the 12 leads! In Figure-5 — the sinus-conducted beats are beats #2,4,6,8,10 and 12.
• Look at leads in a given "lead area" together. For example — beat #2 in both leads II and III shows J-point notching and 1-1.5 mm of ST elevation. The 3rd inferior lead is lead aVF — and sinus-conducted beats #4 and 6 in lead aVF show similar J-point notching and ST elevation as was seen in the other inferior leads.
• The QRS complex is tiny for both of the sinus-conducted beats in high lateral leads I and aVL. It is difficult to draw conclusions regarding ST-T wave appearance in these leads.
• In the chest leads — there is normal R wave progression (with transition between leads V3-to-V4) for sinus-conducted beats #8 and 12. Unfortunately — sinus-conducted beat #10 is obscured by the lead change. Of concern — is ST elevation that begins in lead V2 (for beat #8) — and which then increases (up to 3mm!), and continues through to lead V6 (for beat #12). Small q waves and prominent J-point notching is seen in leads V5 and V6 for beat #12.

 

PEARL #6: It clearly is more difficult to assess ST-T waves for acute changes with premature ventricular beats. That said — there are times when acute ST elevation or abnormal ST depression may only be seen in PVCs. As a result — it is always worthwhile to look at PVCs on the ECG of a patient with new-onset symptoms, because sometimes you will see clear indication of acute ST-T wave changes that may not always be evident in normal sinus-conducted beats!

• Since the PVCs in Figure-5 are of fascicular etiology (ie, originating from within the conduction system) — it is even more likely that we may be able to see acute ST-T wave changes in at least some of these fascicular beats. Note the worrisome shape and marked amount of ST elevation in lateral chest leads V4, V5 and V6 for fascicular beats #11 and 13!

 

 

What about the Osborn Waves?

Note the profound J-point notching in the inferior and lateral chest leads (YELLOW arrows in Figure-6)! This patient was not hypothermic (On the contrary — this patient presented with an acute febrile illness).

• I interpreted the profound J-point notching in Figure-6 as most probably representing Osborn waves. Review of J Wave Syndromes (of which Osborn waves are one of the key entities) — is the subject of today's Audio Pearl (ECG-MP-56).
• An Osborn wave is a deflection with a dome or hump that occurs at the J-point, which is the point where the end of the QRS complex joins with the beginning of the ST segment. While Osborn waves are most commonly associated with hypothermia — it's important to appreciate that this ECG finding has been associated with a number of other conditions, including cardiac arrest and acute myocardial infarction.

 

PEARL #7: More on Osborn waves can be found in my Audio Pearl above (ECG-MP-56). That said — several points merit repetition:

• J Wave Syndromes represent a spectrum of disorders, with certain repolarization variants at one end of the spectrum — and Brugada Syndrome at the other end. Hypothermia-induced Osborn waves represent another part of this spectrum.
• Until recently — awareness was lacking that acute development of exaggerated J waves (ie, Osborn waves) could be a manifestation of acute ischemia (Antzelevitch and Yan and Rituparna et al). This appears to be a transient finding — in which persistence of acute ischemia leads to integration of J-point prominence into the increasingly elevated ST segments. While not commonly reported at the present time — I suspect increased awareness of ischemia-induced Osborn waves will result in more frequent detection of this phenomenon.
• Admittedly — proof is lacking in today's case that J-point prominence in Figure-6 represents ischemia-induced Osborn waves. Support of this assumption could be forthcoming: i) IF a prior baseline ECG on this patient could be found, in which prominent J waves were absent (thus proving that both ST elevation and the J waves were new); and/or, ii) IF serial tracings on this patient showed evolution in the amount of J-point prominence, with resolution after acute reperfusion. That said — given the high (not low) body temperature + the history of chest pain + the ominous shape and amount of diffuse ST elevation in Figure-6 — I felt it likely that J-point prominence highlighted by the YELLOW arrows was ischemia related.
• Clinically — the importance of recognizing ischemia-induced Osborn waves, is that this finding appears to identify patients at high risk for development of malignant ventricular arrhythmias (Rituparna et al). Prompt cath with acute reperfusion seems especially indicated in such patients to reduce risk of VFib. 

Figure-6: I've added YELLOW arrows to the 12-lead ECG from Figure-5 to highlight Osborn waves (See text).

 

In SUMMARY: The rhythm in today's case is fascicular bigeminy. There is diffuse, worrisome ST elevation in multiple lead areas suggestive of an acute evolving STEMI. J-point promience in multiple leads suggests ischemia-related Osborn waves — and adds to concern regarding increased risk for malignant ventricular arrhythmias.

• Unfortunately, additional follow-up in this case is lacking.

 

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Acknowledgment: My appreciation to Ong Hooi Yee (from Malaysia) for allowing me to use this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Systematic Approach to Rhythm Interpretation. 
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
• ECG Blog #188 — Reviews HOW to Read and Draw Laddergrams.
•  
• ECG Blog #204 — Reviews rapid assessment of the Bundle Branch Blocks. 
• ECG Blog #203 — Reviews rapid assessment of the Hemiblocks.
•  
• Antzelevitch C, Yan G-X: J Wave Syndromes. Heart Rhythm 7(4): 549-558, 2010 — is a detailed review by these experts that contains all one could hope to know regarding the etiology and pathophysiology of J Wave Syndromes (including Osborn waves — Brugada Syndrome — and arrhythmogenic Early Repolarization patterns).
• Rituparna S et al: Occurrence of "J Waves" as a Marker of Acute Ischemia (and their Cellular Basis). Pacing Clin Electrophysiol 30(6): 817-819, 2007. 
• ECG Blog #149 — Reviews a case of Osborn Waves from Hypothermia. 
• ECG Blog #172 — Reviews another case of Osborn Waves from Hypothermia. 
• The November 22, 2019 post in Dr. Smith's ECG Blog — Please scroll down to the BOTTOM of the page for My Comment on this case with "Shark Fin" ST elevation and Osborn Waves from acute STEMI. 
• The September 23, 2020 post in Dr. Smith's ECG Blog — Please scroll down to the BOTTOM of the page for My Comment on this additional case of Osborn Waves from acute STEMI.