ECG Blog #146 – (BBB – Primary ST-T Changes)

The ECG in Figure-1 was obtained from a patient with new-onset chest pain. It was interpreted as showing LBBB (Left Bundle Branch Block). As a result, the provider thought — “impossible to tell if anything acute is going on because there is LBBB”.

• Do you agree with that assessment?

Figure-1: 12-lead ECG from a patient with chest pain. How do you interpret this tracing?

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Clinical NOTE: In the past, it was thought that one could not diagnose an acute STEMI (ST Elevation Myocardial Infarction) in the presence of LBBB. This notion has been completely refuted. Although it will often be more difficult to diagnose acute ischemia/infarction in a patient with chest pain who presents in complete LBBB — in a surprising number of such patients, there will be at least strong suggestion on the initial ECG of acute STEMI despite the presence of underlying LBBB.

• When acute ECG changes in a patient with LBBB are subtle — diagnostic aids such as Smith-modified-Sgarbossa criteria may be helpful. At other times (such as for the ECG in Figure-1) — the diagnosis of acute STEMI is obvious without need to invoke modified Smith-Sgarbossa criteria. (NOTE: Search of Dr. Stephen Smith’s web site at the above link will provide numerous examples of how his criteria can be applied to clinical cases).

Interpretation of the ECG in Figure-1: The rhythm is sinus. The QRS complex is wide (≥0.12 second) — and QRS morphology is consistent with complete LBBB because there is a predominantly positive complex in lateral leads I and V6 — and, a predominantly negative QRS in lead V1. (For review of the Basics of BBB — Please see my ECG Blog #11). That said, there are a number of features that are distinctly atypical for simple LBBB. These include:

• i) The presence of septal Q waves in lateral leads I and aVL. Because the presence of LBBB alters the direction of initial septal activation (which can no longer proceed from left-to-right) — there should never normally be a septal q wave in a lateral lead when there is uncomplicated LBBB. The prominent Q waves in leads I and aVL of this tracing leave little doubt that infarction has occurred at some point in time.
• Beyond-the-Core: The presence of one or more lateral Q waves in association with LBBB do not indicate “lateral” infarction. Instead, they indicate septal and/or anteroseptal infarction — since the reason for their occurrence is that the LBBB has altered the direction of initial septal activation.
• ii) There is ST segment coving and primary ST elevation in lead aVL. This just shouldn’t be seen with typical LBBB. The most reliable way to recognize acute STEMI that occurs in association with LBBB is by the presence of frank ST elevation in a lead that should not show ST elevation. So, while it is admittedly challenging to determine if the anterior ST elevation that is seen in Figure-1 is a result of LBBB or acute anterior STEMI (because there is often some normal ST elevation in anterior leads with simple LBBB) — there should not be ST elevation in lateral or inferior leads.
• iii) There are reciprocal ST-T wave changes in each of the inferior leads. We know the inferior ST-T wave changes that are seen here are likely to be both real and acute — because these inferior ST-T wave changes are a “mirror-image” reflection of the ST-T wave in lead aVL. This reciprocal change picture shouldn’t be seen with uncomplicated LBBB.
• iv) The final abnormality occurs in the chest leads, and is indeed subtle — but it supports the above limb lead findings. That is, the ST segments in leads V5 and V6 are coved — and manifest a disproportionate amount of J-point ST depression (considering the modest amplitude of the R wave in these leads). This abnormal shape of the ST-T wave extends to lead V4. (We think there are also tiny-but-real q waves in lateral leads V5 and V6).

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Clinical Impression: In a patient with new-onset chest pain — the combination of the above findings should suggest an acute evolving STEMI until proven otherwise despite the presence of underlying LBBB.

• NOTE: Access to a prior ECG on this patient would clarify whether the LBBB in Figure-1 was new — and, would help to establish that the above noted changes are acute. But in the absence of a comparison tracing — the history (of new-onset chest pain) in this patient whose ECG shows LBBB with inappropriate lateral Q waves and primary ST-T wave changes despite the LBBB, should strongly suggest acute STEMI with need for immediate evaluation and reperfusion therapy until proven otherwise.

Follow-up: Unfortunately, the cardiac catheterization lab was not immediately activated for this patient. The patient coded in the hospital, and could not be resuscitated.

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Acknowledgment: My thanks to Casey Caldwell for allowing me to use this tracing and clinical case.

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Additional Material: For Review on ECG Diagnosis of the Bundle Branch Blocks — See my 17-minute ECG Video on this subject at www.bbbecg.com —

• Please note that if you click on SHOW MORE on the You-Tube page under where this video appears — You’ll see a detailed linked Contents that will allow you to immediately find whatever key points you are looking for in this video.

ECG Blog #145 – (ST Depression – STEMI – BBB)

The ECG in Figure-1 was obtained from a 60-year old woman who presented to the ED (Emergency Department) with new-onset chest pain.

• The initial emergency care provider interpreted this tracing as showing complete RBBB ( = Right Bundle Branch Block). Do you agree? 
• Are you concerned about anything else?

Figure-1: 12-lead ECG from a patient with new-onset chest pain. How do you interpret this tracing?

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Interpretation: In a patient with new-onset chest pain — this tracing should be of obvious concern. The rhythm appears to be sinus tachycardia at a rate of ~120/minute. Complete RBBB is present. But there is much more going on than just RBBB ... 

• Beyond-the-Core NOTE: Although it clearly appears that there are upright P waves with a constant and normal PR interval in lead II — a number of leads also display some sort of ‘notching’ toward the tail end of the QRS complex (especially leads II, III, aVR, V4, V5). Caliper measurement suggests that the timing of these extra deflections is not quite at the precise midpoint between sinus P waves (as I would expect it to be if there was 2:1 AV conduction). Thus, although I am fairly confident that the rhythm here is indeed sinus tachycardia — I am not 100% certain, and would entertain the possibility that there could be 2:1 conduction … The point to emphasize is that sometimes it is simply not possible to be 100% certain of the rhythm at the time you need to initiate management. That said, in this case regardless of whether this rhythm is sinus tachycardia or atrial flutter (or atrial tachycardia) with 2:1 AV conduction — initial clinical priorities are similar.
• The QRS complex is wide. QRS morphology is consistent with complete RBBB (ie, predominantly upright QRS in lead V1 — with wide terminal S waves in leads I and V6). However, a deep Q wave is present in lead V1. This suggests that in addition to RBBB — septal infarction has probably occurred at some point in time.
• There is ST segment elevation in lead V1 (by ≥3mm! ). This should not be seen with simple RBBB (See my ECG Video Pearl #22 on the Basics of BBB in ECG Blog #204). Using the principle of “neighboring leads” — it should be apparent that there is also some coved ST segment elevation in neighboring lead V2! Normally with RBBB — one expects the ST-T wave to be at least slightly depressed in anterior leads in which a RBBB-pattern is seen.
• There is also marked ST elevation (of 3-4mm) in lead aVR. Virtually all other leads on this tracing manifest ST depression, which is marked (up to 5-6mm) in many leads! The finding of diffuse ST segment depression (ie, in at least 6-7 leads) in association with ST elevation in lead aVR strongly suggests diffuse subendocardial ischemia as the cause.

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Clinical Impression: At the least, the rhythm in this 60-year old woman with new chest pain is sinus tachycardia. Serial ECG monitoring should clarify whether extra P waves are or are not present. There is complete RBBB — evidence of prior septal infarction at some point in time — and, of most concern strong suggestion of diffuse subendocardial ischemia.

• Although on occasion, ST segment elevation may also be seen in lead V1 (in addition to aVR) when there is subendocardial ischemia — ST elevation is usually not seen in lead V2. Especially in view of the deep Q wave in lead V1 — one should consider the possibility of acute septal infarction.
• Otherwise, when the ECG picture of diffuse ST depression in association with ST elevation in leads aVR and V1 is seen — this is most often not due to acute coronary occlusion. Instead, severe coronary disease (ie, left-main, proximal LAD and/or multi-vessel disease) is most often found. Given the severity of this patient’s new-onset chest pain — the marked tachycardia — the RBBB conduction defect — and, the dramatic amount of ST segment deviation — prompt diagnostic cardiac catheterization is clearly indicated for this patient. This hopefully will suggest potential for life-saving PCI (percutaneous coronary intervention).

Follow-up: Cardiac catheterization confirmed the presence of very severe 3-vessel disease.

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Acknowledgment: My thanks to MG for allowing me to use this tracing and clinical case.
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Additional Material: For Review on ECG Diagnosis of the Bundle Branch Blocks — See my 13-minute ECG Video Pearl #22 on this subject (GO To ECG Blog #204).

ECG Blog #144 — An Alternating BBB?

The ECG and long-lead II rhythm strip shown in Figure-1 was obtained from a 58-year old man who was admitted to the hospital with a history of chest pain and “fatigue”.

• How would you interpret the tracing?
• Is there 3:1 and/or “high-grade” AV block?
• How many different types of conduction disturbances can you identify?
• Is there ECG evidence of a cause?
• What treatment is likely to be needed?

Figure-1: 12-lead ECG with long lead II rhythm strip obtained from a 58-year old man with chest pain and fatigue.

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Interpretation: This is a complex tracing. The easiest way I have found to derive the mechanism for complex arrhythmias such as this one — begins with the simple step of numbering the beats and labeling the P waves (Figure-2).

• NOTE: The value of using calipers as an aid for interpreting complex arrhythmias cannot be overemphasized. Using calipers allows you to rapidly determine if P wave and QRS rhythms are regular or not, and whether beats are (or are not) likely to be conducting. With minimal practice — you’ll find calipers dramatically increase your speed for interpretation, as well as improving your accuracy. The cardiologist who does not regularly use calipers to interpret complex arrhythmias will miss the diagnosis on more than one occasion …

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RED arrows in Figure-2 below indicate all P waves on the long lead II rhythm strip at the bottom of Figure-1. What conclusions can you now draw about this rhythm?

Figure-2: The beats from Figure-1 have been numbered. P waves have been labeled (RED arrows — See text).

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Interpretation of Figure-2: Red arrows show regular occurrence of P waves with similar morphology. Thus, there is an underlying sinus rhythm.

• The reason for slight variation in the P-P interval, is that there is sinus arrhythmia. (NOTE: A special type of sinus arrhythmia, known as “ventriculophasic sinus arrhythmia” — is commonly seen in association with 2nd- or 3rd-degree AV block, and this is probably what we are seeing here).
• Some beats in Figure-2 are conducting! Note that the PR interval preceding beats #1, 3, 5 and 7 is constant (albeit slightly prolonged beyond 0.20 second in duration). This means that beats #1, 3, 5 and 7 in Figure-2 are all being conducted (albeit with 1st-Degree AV Block).
• That said — other sinus P waves are not being conducted! We know that some of the other P waves are not being conducted — because there is no QRS complex near many of these other on-time but non-conducting P waves.
• Since the atrial rate (P-P interval) is regular (or at least, fairly regular) — and since some P waves conduct but others don’t — this means that some type of 2nd-Degree AV Block is present. This cannot be complete (3rd-degree) AV block — because there is some conduction!

QUESTION: Can you think ahead as to which type of 2nd-degree AV block is present in Figure-2? Does this represent Mobitz I? — or Mobitz II? — or high-grade AV block? — or, some indeterminate form of 2nd-degree AV block?

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Next STEP: Can you figure out which of the lettered P waves in Figure-3 have a chance to conduct, yet still fail to do so?

• To clarify which P waves are (or are not) conducting, we have made Figure-3 — in which we label each of the P waves in the long lead II rhythm strip.

Figure-3: We have labeled all P waves in Figure-2 with letters. Which of these P waves have a chance to conduct, yet fail to do so?

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Interpretation of Figure-3: As already noted — the P waves labeled a, d, g and j are all conducting (because the PR interval preceding beats #1, 3, 5 and 7 is constant).

• One should expect the P waves labeled b, e, and h to be able to conduct — because these P waves all occur near the middle of the R-R interval, at a time when no part of the conduction system should still be refractory. The fact that these on-time P waves do not conduct — is what tells us that there is 2nd-Degree AV Block.
• This leaves us with the P waves labeled c, f, and i. These P waves are not conducting — because no QRS complex follows them. However, these P waves labeled c, f and i never have a chance to conduct — because they occur immediately after beats #2, 4 and 6. That is, the P waves labeled c, f, and i all occur during the absolute refractory period that immediately follows the QRS complexes that precede them.
• NOTE: The term, “high-grade” AV Block means that more than 1 on-time P wave in a row that has a chance to conduct, fails to do so. We can not diagnose “high-grade” AV block in Figure-3 — because we never see 2 P waves in a row that have a chance to conduct yet fail to do so. It could be entirely possible that IF beats # 2, 4 and 6 were delayed a little bit more — that the P waves labeled c, f, and i would then have a chance to conduct.

QUESTION: What should we call beats #2, 4 and 6?

• HINT: In Figure-4, we have drawn in horizontal BLUE lines to show that the distance from the onset of beats #1, 3 and 5 — until the onset of beats #2, 4 and 6 is constant. This is just one of many relationships in this this tracing that can be instantly recognized by using calipers.

Figure-4: Horizontal BLUE lines show that the distance from the onset of beats #1, 3 and 5 — until the onset of beats #2, 4 and 6 is constant. How does awareness of this relationship facilitate determining the etiology of beats #2, 4 and 6?

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Interpretation of Figure-4: Beats #2, 4 and 6 are escape beats. When sinus P waves fail to conduct — one hopes for emergence of an “escape” pacemaker site that will prevent development of any prolonged pauses. Escape beats most often arise from the AV Node — though they can also arise from elsewhere in the atria, from the bundle of His, or from the ventricles.

• Escape beats are recognized because they are either not preceded by any P wave — or, because they are preceded by a P wave with a PR interval that is too short to conduct. Since most “escape” pacemakers are at least fairly regular — the R-R interval preceding escape beats tends to be fairly constant. This important clue is precisely what the equally long horizontal blue lines in Figure-4 show.
• PEARL: It is often difficult to tell which beats in complex AV block tracings are (or are not) being conducted. Knowing that most escape rhythms are at least fairly regular — the finding of one or more QRS complexes that clearly occur earlier-than-expected is a superb clue that such early beats are probably being conducted. The slower beats that are not preceded by P waves, but which are preceded by a constant R-R interval are usually the escape beats (For review of this concept — Click HERE to go to 25:30 in our AV Block Basics Video).

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The Concept of an Escape-Capture Rhythm: From a descriptive standpoint — there are several useful ways to classify the rhythm we see in Figure-4.

• There is group beating. That is, although the ventricular rhythm in Figure-4 is not completely regular — there IS a pattern. This pattern is, that shorter and longer R-R intervals alternate — with shorter intervals (as between beats #2-3; 4-5; and 6-7) being of similar duration — and longer intervals (as between beats #1-2; 3-4; and 5-6) also being of a different similar duration.
• The rhythm in Figure-4 is a bigeminal rhythm. This is just another way of stating that the pattern of this rhythm repeats every-other-beat.
• There is “Escape-Capture” Bigeminy. As we have discussed earlier — beat #2 is an “escape” beat — because it occurs after a short pause that is longer than the R-R interval that precedes sinus beats. Beat #3 is a “capture” beat — because the on-time sinus P wave that precedes it (ie, the P wave labeled “d”) occurs at a moment during the R-R interval when the conduction system has recovered, and is able to conduct this P wave to the ventricles. This is followed by another escape beat (beat #4) — and then another “capture” beat (the P wave labeled “g” is able to conduct). This sequence then repeats.

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SYNTHESIS: The rhythm in Figure-4 represents a form of 2nd-degree AV block. There is group beating, with repetitive short-long sequences. If we look at each sequence as beginning with a P wave that conducts (beats #1, 3, 5, 7) — the next P wave in each sequence fails to conduct (b, e, h). Before we can tell if the 3rd P wave in each sequence will be able to conduct — an escape beat arises (beats # 2, 4, 6). But this 3rd P wave in each sequence (ie, the P waves labeled c, f and i) never have a chance to conduct ...

• We cannot determine IF the rhythm in Figure-4 represents Mobitz I or Mobitz II — because we never see 2 consecutive P waves conducting. That is, we cannot tell if the PR interval would lengthen (as it should with Mobitz I AV block) — because we never see 2 consecutively conducted QRS complexes.
• We also cannot tell if the form of 2nd-degree AV block in Figure-4 represents “high-grade” AV block — because we never see 2 P waves in a row that should conduct, yet fail to do so.
• The P-P interval in Figure-4 is ~5 large boxes in duration. This corresponds to an atrial rate of ~60/minute.
• The R-R interval of the escape beats in Figure-4 (ie, the length of the horizontal blue lines) — is ~8 large boxes. This corresponds to an escape rate just under 40/minute. Thus, an important problem here is bradycardia … It is entirely possible that if either the atrial or escape rates were a little faster — that there would be 2:1 (instead of 3:1) AV conduction.
• If we now change how we look at the repetitive sequences in Figure-4, so that instead of beginning each sequence with a sinus-conducted beat, we begin with an escape beat (ie, with beats #2, 4, 6) — we then have repetitive long-short sequences — which is how the name “escape-capture” was derived.
• PEARL: It is well to appreciate that “Escape-Capture” Bigeminy (as is seen in Figure-4) is a common manifestation of 2nd-degree AV block.

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Remaining Issues: Several questions remain regarding this case. These include:

• Why is the QRS complex wide?
• Why are there 2 different morphologies for QRS complexes in the long lead II rhythm strip?
• What does the 12-lead ECG show? Is there a clue on the 12-lead tracing to the reason why this patient developed AV block?

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Addressing the Remaining Issues: To facilitate addressing these remaining issues — We repost a less cluttered 12-lead ECG (Figure-5).

Figure-5: Why does QRS morphology change in the long lead II rhythm strip? How would you interpret the 12-lead ECG? Technical Note: The 12-lead ECG is simultaneously recorded with the long lead II rhythm strip at the bottom. Unfortunately, due to the way in which lead changes are recorded — we do not see beat #2 in leads I, II and III of the 12-lead ECG (but we do see all of the other beats).

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Interpretation of Figure-5: Now that we have elucidated the behavior of atrial activity in this arrhythmia — we need to address QRST morphology.

• Note that there are 2 different QRS morphologies. The QRS complex appears to be widened for both of these morphologies. Looking first at QRS morphology for the sinus-conducted beats (ie, for beats #1, 3, 5 and 7) — the monophasic R wave in lead I for beat #1 — with predominantly negative QRS for beat #5 in lead V1 — with monophasic R wave for beat #7 in lead V6 — are consistent with LBBB as the reason why conducted beats #1, 3, 5 and 7 are wide.
• Although beats #2, 4 and 6 do not appear to be wide in the long lead II rhythm strip at the bottom of the tracing — a look at simultaneously obtained beat #4 in lead V1, and beat #6 in leads V4, V5 and V6 tells us that beats #2, 4 and 6 are in fact widened. The rSR’ for beat #4 in lead V1 — together with the wide terminal S wave for beat #6 in lead V6 — are consistent with RBBB as the reason why escape beats #2, 4 and 6 are wide.
• The escape beats could be arising either from the AV Node or the Bundle of His. In either case — escape beats manifest an alternating form of bundle branch block compared to sinus-conducted beats that consistently manifest LBBB conduction.
• NOTE: Although the term, “trifascicular block” has been discouraged in recent years because of potential ambiguity — this tracing clearly manifests signs of severe and multi-level conduction system disturbance, including: i) 1st-degree AV block (for conducting beats #1, 3, 5 and 7); ii) an indeterminate form of 2nd-degree AV block; and iii) alternating LBBB and RBBB conduction for the escape-capture bigeminal rhythm. Unless some potentially-reversible etiology is found — a pacemaker is likely to be needed.

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Are there Acute Changes on the 12-Lead ECG? The final part of this tracing to assess is the ST-T wave changes on the 12-lead ECG. This assessment is especially challenging because of the multiple conduction defects that are present. We proceed as follows:

• Regarding the sinus beats that conduct with LBBB morphology — the  ST-T wave for beat #1 in lead I manifests a T wave that is inappropriately concordant (upright) with the QRS complex in this lead. Normally, the ST-T wave should be oppositely directed to the last QRS deflection in lead I with LBBB. This finding of inappropriate T wave concordance suggests possible ischemia.
• Much more remarkable is the persistent ST segment coving and increasingly deeper symmetric T wave inversion for escape beat #4 that is seen as one moves from lead V1-to V2-to V3. The amount of T wave inversion expected in anterior leads with RBBB should be maximal in lead V1. Especially in view of the relatively small QRS amplitude for beat #4 in leads V2 and V3 — this very deep and symmetric T wave inversion is clearly is a manifestation of ischemia, and may represent recent infarction as the precipitating cause of AV block.
• Finally — the downward “s” wave in lead V2 for the RBBB pattern of beat #5 is fragmented. This suggests scar, and may be consistent with recent infarction.

Conclusion: Admittedly, QRST assessment is challenging on this 12-lead ECG given technical issues and extensive underlying conduction defects. Nevertheless — the findings we highlight above should raise suspicion of recent extensive infarction as the potential cause of AV block.

FINAL Interpretation of this Tracing: Underlying sinus arrhythmia with 1st-degree AV block. Escape-capture bigeminal rhythm, with 2nd-degree AV block of indeterminate severity, but with at least a 2:1 AV block conduction disturbance. Underlying LBBB for sinus-conducted beats — which alternates with RBBB for escape beats. This suggests severe conduction system disease. ST-T wave changes suggest ischemia and/or recent infarction.
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P.S.: An “unknown” commenter (below) asked whether the P waves labeled b, e and h might actually be conducting with a very long PR interval? — because the distance from onset of each of these P waves, until the next QRS complex (ie, the distance from b-to-beat #2; e-to-beat #4; h-to-beat #6) appears to be the same! If this was true — then the PR interval “increment” would be extremely long. That is, the relative increase in PR interval for the P waves before beats #1 and 2 would be much more than is usually seen with a typical Mobitz I form of 2nd-degree AV block (ie, the PR interval for beat #2 if “b” was conducting would be over 0.80 second! ). That said, nothing else about this tracing is “typical” — and without additional ECG monitoring strips, we cannot rule out the possibility of dual AV node conduction pathways with change to the slow conduction pathway accounting for the extremely large PR interval increment from one conducting P wave to the next. In this case, the rhythm would be 2nd-degree AV block, Mobitz Type I — with the non-conducting P waves for each Wenckebach cycle being c, f and i. There would still be underlying alternating bundle branch block (from LBBB to RBBB conduction) in this patient with severe conduction system disease. A pacemaker will be needed. Moral: Some complex arrhythmias may have more than a single potentially plausible explanation!    
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Acknowledgment: My thanks to Chu Thanh & Nguyen Chi Tinh (from Vietnam) for allowing me to use this tracing and clinical case.
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• For more on AV Blocks — Check out our Video @ www.avblockecg.com —
• For more on assessment of ST-T wave changes with BBB — Check out our Video @ www.bbbecg.com —

NOTE: For any of our ECG Videos — If you click on SHOW MORE that appears under the video on the YouTube page — You will find a timed Linked Contents of all that appears in the video!