Sunday, November 20, 2016

ECG Blog #131 (Acute STEMI – Acute Occlusion of LAD – LCx – RCA)

The 12-lead ECG shown in Figure-1 was obtained from a 51-year old man with new-onset chest pain. The patient has diabetes, and he continues to smoke.
  • How would you interpret this ECG?
  • What is the likely “culprit” artery?
Figure-1: 12-lead ECG obtained from a 51-year old man with new-onset chest pain. What is the likely “culprit” artery? NOTE — Enlarge by clicking on the Figure.
Although there is much artifact (especially in leads II and III) — this does not prevent appreciation of the obvious abnormalities on this tracing:
  • The rhythm is sinus tachycardia at a rate just over 100/minute. The PR and QRS intervals are normal — but the QT appears to be prolonged. The axis is normal. There is no chamber enlargement.
  • Q-R-S-T Changes: There are small and narrow q waves in most infero-lateral leads. R wave progression is normal, with transition occurring between leads V2-to-V3. There are dramatic ST-T wave changes. There is over 10mm of J-point ST segment depression in several anterior leads. All lateral leads show marked ST segment elevation, which nearly attains 10mm in lead V6!
IMPRESSION: There is an obvious acute STEMI (ST Elevation Myocardial Infarction). Localization of ST segment elevation to the lateral leads strongly suggests acute occlusion of the LCx ( = Left Circumflex Artery). This is supported by the finding of several millimeters of ST elevation in lead II, but virtually none in leads III and aVF. In contrast, with acute RCA ( = Right Coronary Artery) occlusion — ST elevation is localized to the inferior leads, with the relative amount of ST elevation typically more in lead III compared to lead II. The dramatic anterior ST depression strongly suggests acute posterior as well as lateral infarction. This distribution of marked and acute infero-lateral wall involvement is seen with acute occlusion of a dominant LCx artery.

Follow-Up: Fortunately, this large acute STEMI was immediately recognized. Cardiac catheterization with prompt reperfusion of a dominant LCx artery resulted in rapid resolution of virtually all ST-T wave abnormalities (Figure-2). The “good news” about this case is that treatment was so promptly initiated, that elevation of serum troponin was minimal. Together with resolution of ST-T wave abnormalities and lack of QRS amplitude loss or development of new Q waves — it is likely that almost all jeopardized myocardium was salvaged with minimal longterm damage from this event. That said, cardiac catheterization revealed severe multi-vessel underlying coronary disease — such that longterm prognosis remains guarded even if the patient completely stops smoking. If he doesn’t, his days are likely to be numbered ...
Figure-2: Follow-up ECG obtained after reperfusion of the acutely occluded LCx artery. Virtually all ST-T wave abnormalities that were seen in Figure-1 have resolved!
PEARLS: This case provides a wonderful clinical example of how prompt recognition and treatment of acute STEMI, with reperfusion of the “culprit” artery may result in life-saving myocardial salvage. Localization of the ST-T wave abnormalities in this case facilitated prediction of a dominant LCx artery as the source of the acute insult.
  • The dramatic and extensive amount of the ST-T wave changes seen in Figure-1 is most probably attributable to the acute insult of LCx occlusion on top of severe underlying multi-vessel disease.
Acknowledgment: — My thanks to Mustafa Alwan (from Amman, Jordan) for his permission allowing me to use this case and ECG.

Monday, July 4, 2016

ECG Blog #130 (AV Block – ABBB – RBBB – LBBB)

The 3 successive lead MCL-1 rhythm strips that are shown in Figure-1 were obtained from a 56-year old man with dyspnea, but no chest pain.
  • How would you interpret the rhythm?
Figure-1: Lead MCL-1 showing 3 successive rhythm strips from a patient with dyspnea. Can you explain what is happening? NOTE — Enlarge by clicking on the Figure.
Although there is slight distortion of some QRS complexes, and the ECG grid is not well seen — this is a fascinating tracing!

PEARL: As we have done with several of our recent ECG Blog posts — We begin by noting 3 Helpful Steps for facilitating interpretation of complex arrhythmias: i) Look first for an underlying rhythm; then, ii) Use calipers (as by far the fastest, easiest, and most accurate way to seek out atrial activity and determine relationships between P waves and neighboring QRS complexes); and, iii) On a copy of the rhythm strip (so that you do not write on the original tracing)Mark the presence of sinus P waves that you can clearly see. We have done this in Figure-2:
Figure-2: We have numbered the beats in the middle (Panel B) and lower (Panel C) tracings, and marked (with RED arrows) the presence of sinus P waves that we clearly saw in Figure-1 (See text).
Interpretation: Use of calipers makes it readily apparent that regularly occurring sinus P waves are present throughout this tracing (RED arrows). There is some conduction. That said, there are 2 different QRS complexes, and the PR interval is not the same in front of all conducting beats ...
  • Start with What You Know — Focusing on the middle and lower tracings in Figure-2 (Panels B and C) — beats #1, 2, 12, 13 and 14 are all preceded by a similar-looking P wave with a constant PR interval. This tells us that these beats are clearly being conducted.
  • Unfortunately, the ECG grid is not clear. There is also no 12-lead ECG on this patient — which means that our assessment of QRS morphology is limited to this single right-sided MCL-1 monitoring lead. That said, the QRS complex for all beats on this tracing looks to be widened. The predominantly negative rS configuration of beats #1,2,12,13 and 14 is consistent with LBBB (Left Bundle Branch Block).
  • Beats #3,4,5,6,7,8,9,10 and 11 also appear to be conducted — as the PR interval preceding these beats looks to be constant. However, QRS morphology of these beats in this right-sided MCL-1 lead suggests a change to RBBB (Right Bundle Branch Block) conduction. If confirmed on a 12-lead — this would mean there is ABBB (Alternating Bundle Branch Block).
  • There is also 2:1 AV Block in some parts of Figure-2. Interestingly — 2nd-Degree AV Block with 2:1 AV conduction occurs in association with the QRS complexes manifesting LBBB (ie, beats #1,2,12,13 and 14). In contrast — 1:1 AV conduction occurs in association with the QRS complexes manifesting RBBB (ie, beats #3,4,5,6,7,8,9,10 and 11). The question is why?
The Parts of this Tracing We are Not Certain About …
There are some additional confounding findings on this tracing. These relate to a highly unusual pattern of variation in the PR interval that was not apparent to us on initial assessment of this tracing (Figure-3).
Figure-3: Caliper measurement reveals a highly unusual pattern of PR interval variation, which we have color coded for clarity (See text).
Explanation of Figure-3: It turns out that the PR interval preceding all beats with LBBB morphology is the same (short RED horizontal lines). The PR interval preceding all beats with RBBB morphology is also constant (short YELLOW horizontal lines) — however, this PR interval (the yellow lines) is slightly longer than the PR interval preceding LBBB beats (red lines). To add to the complexity — the PR interval preceding the 1st RBBB beat in a run inexplicably has an even longer PR interval (BLUE horizontal lines in Figure-3).
  • The fact that other than this 1st RBBB beat in Panels A and B — the PR interval preceding each RBBB beat is the same (yellow lines) clearly indicates that these RBBB-pattern beats are being conducted. However, we cannot explain the changing PR interval relationship over the course of Figure-3 that we just described, as it is not what would be expected with simple Wenckebach conduction, dual AV nodal pathways, or vagotonic AV block.
BOTTOM Line: This is a fascinating tracing that we admittedly cannot completely explain. That said, we can state the following:
  • There is 2nd-Degree AV Block, with intermittent 2:1 AV conduction. This is associated with an unusual pattern of variation in the PR interval, as shown by the color-coded PR intervals in Figure-3.
  • There is significant bradycardia during 2:1 AV conduction (the ventricular rate drops down to the 40s).
  • There appears to be ABBB (Alternating Bundle Branch Block). It is rare to see true alternating bundle branch block. When this phenomenon does occur, it almost always indicates severe His-Purkinje disease. Given the associated AV block with significant bradycardia — it is highly likely that a pacemaker will be needed.
Concluding NOTE:
This case illustrate how even when we are unsure of certain aspects in our interpretation — we can still arrive at the appropriate next step in management.
  • Additional comments are welcome!
  • P.S. — I think between the comment below by Jan S and my reply (7/5/2016) — that we may have arrived at reasonable explanation for the unusual variation in PR intervals ...
Acknowledgment: — My thanks to Bady Hanna Adly (from Asyut, Egypt) for his permission allowing me to use this case and ECG.

Friday, July 1, 2016

ECG Blog #129 (PVC – Late-Cycle – End-Diastolic – AIVR – Fusion – WPW – Laddergram)

How would you interpret the lead V1 rhythm strip shown in Figure-1?
  • How certain are you of your diagnosis?
  • How would you describe this rhythm in words?
  • Why does beat #8 look so different from all other beats in this tracing?
  • What clinical situation is commonly associated with arrhythmias such as the one shown here?
Figure-1: Long lead V1 rhythm strip showing a changing rhythm. Can you explain what is happening? NOTE — Enlarge by clicking on the Figure.
PEARL: 3 of the most Helpful Steps for facilitating interpretation of the mechanism of complex arrhythmias are: i) To look first for an underlying rhythm; then, ii) To mark the presence of sinus P waves that you can clearly see; and, iii) To use calipers (as by far the fastest, easiest, and most accurate way to seek out atrial activity). We have done this in Figure-2:
Figure-2: We have marked (with RED arrows) the presence of sinus P waves that we clearly saw in Figure-1 (See text).
Interpretation: It should now be apparent that the underlying mechanism of the rhythm in Figure-2 is sinus. This is true even though the number of sinus-conducted beats in this tracing is limited. Nevertheless, similar-shaped sinus P waves with a constant and normal PR interval precede beats #1, 3, 6, 7, 9, 11 and 13.
  • To determine the rate of the underlying sinus rhythm — We look for 2 consecutive sinus-conducted beats. This occurs for beats #6 and 7 — which tells us that the underlying sinus rate is just under 100/minute (because the R-R interval between beats #6-7 is just over 3 large boxes in duration).
  • Beats #2, 4, 5, 10 and 12 are wide. These beats are either not preceded by any P wave — or preceded by an on-time P wave that notches the very beginning of the QRS complex with a PR interval that is too short to conduct. Therefore these beats must be ventricular in etiology. We call these beats “PVCs”  ( = Premature Ventricular Contractions) — even though they occur relatively late in the cycle (usually just before the next on-time sinus P wave is able to conduct). So these ventricular beats do occur “early” (ie, all of them except perhaps beat #5 occur before the next on-time sinus-conducted QRS complex would be seen) — but barely so. As a result, these late-cycle PVCs are also known as end-diastolic PVCs.
  • Clinically — this late-cycle feature of the PVCs seen in Figure-2 is similar to the phenomenon of AIVR (Accelerated IdioVentricular Rhythm), in which a ventricular rhythm at a slightly accelerated rate (usually between 60-110/minute) is seen in patients with recent acute infarction who have just reperfused the infarct-related artery. Note that this is the picture we see for ventricular beats #4 and 5, which if they were followed by additional ventricular beats at similar R-R interval spacing, would constitute AIVR at a rate of ~75/minute. NOTE: Although we are given no clinical information about this patient — the finding of a bigeminal pattern of end-diastolic PVCs with 2 consecutive ventricular beats at a rate consistent with AIVR is characteristic enough to prompt consideration of the possibility that the rhythm in Figure-2 might represent a reperfusion rhythm!
What about Beat #8?
We save assessment of beat #8 for last — since the explanation for why this beat looks different from all others in Figure-2 might not initially be apparent.
  • This illustrates the 4th Helpful Step we favor for interpretation of virtually any complex arrhythmia = iv) Save assessment of the more challenging part(s) of any given tracing for last, waiting until after you are able to explain the more easily interpretable parts of the tracing.
  • We KNOW beats #1,3,6,7,9,11 and 13 in Figure-2 are normally-conducted sinus beats.
  • We KNOW beats #2,4,5,10 and 12 are ventricular beats.
  • What if a ventricular beat and a sinus-conducted QRS complex got together to “have children”. What would the QRS complex and the T wave of the children look like? Wouldn’t such a beat look like beat #8?
  • Beat #8 is a Fusion Beat. Conditions for fusion are present — in that beat #8 is preceded by an on-time P wave of similar shape as other sinus P waves, but with a shorter preceding PR interval.
Illustration of what is happening with beat #8 is facilitated by use of a Laddergram (Figure-3):
Figure-3: Laddergram illustrating the reason for the short PR interval preceding beat #8 (See text).
Explanation of Figure-3: We discussed and illustrated the phenomenon of Fusion in our ECG Blog #128. The key to distinguishing a fusion beat from an aberrantly conducted PAC (Premature Atrial Contraction) — is that the P wave preceding a fusion beat is on-time and not premature.
  • As can be seen in the laddergram shown in Figure-3 — the PR interval of the preceding P wave (RED arrow just before beat #8) is shorter than the PR interval preceding pure sinus-conducted beats. This is because this P wave is only able to partially penetrate through the ventricles before meeting up with an oppositely directed wavefront originating from a near-simultaneously occurring ventricular beat.
  • The result is a fusion beat, with a QRS complex and T wave that looks intermediate between sinus-conducted beats and pure ventricular beats. Verify this yourself. Fusion beat #8 manifests a similar upright shape as do other ventricular beats — but the QRS is not as wide, and the negative ST-T wave not as deep because fusion with a narrow, predominantly negative sinus beat (similar to that seen for beat #7) counteracts the QRS/T wave appearance of ventricular beats.
  • Bottom Line — Although we have already conclusively proven that beats #2,4,5,10 and 12 in Figure-3 are ventricular in etiology — recognition that beat #8 is a fusion beat provides yet one more sign of a definitive ventricular etiology.
A Few Final Points (Beyond-the-Core): It is interesting how QRS morphology of the ventricular beats seen in Figure-3 changes with regard to the single or double peaking of each R wave. We are not sure of the reason for this, other than our awareness that ventricular beats from the same focus may sometimes vary in morphology. This could be because the pathway through the ventricles is not always exactly the same — or perhaps in this case, by the fact that several ventricular beats in Figure-3 are seemingly altered by an on-time P wave that deforms the initial upslope of the R wave. Some degree of fusion might be occurring in a few of these beats, accounting for slight variation in QRS morphology. Practically speaking — none of this matters, since the “theme” of this arrhythmia remains clear — namely, an underlying sinus rhythm with an intermittent bigeminal pattern of late-cycle PVCs, as well as one ventricular couplet with a relatively long R-R interval.
  • Although the P-P interval of sinus P waves is quite regular during the latter portion of this tracing (RED arrows in Figure-3) — we have to acknowledge that we lose track of P waves earlier in the rhythm strip — and, we do not see any P wave occurring during the relatively long R-R interval between beats #4-5. I do not know why. That said, this also is unimportant clinically — as the “theme” of this arrhythmia (just stated above) remains clear. One cannot always explain all findings that appear on every ECG — and, one does not always have to try ...
  • Finally — despite what superficially looks like a short PR interval with initial delta wave slurring preceding some of the wide beats — this is not WPW! That’s because the QRS complex remains wide for beats such as #4 and 5, which are not preceded by either P waves or by any initial slurring. In addition, the coupling interval preceding beats #8 and 10 is different, whereas it should be the same in WPW with variable preexcitation (Concertina effect).
Concluding NOTE:
This case provides a superb example of how to apply the 4 Helpful Steps I find most useful for facilitating interpretation of complex arrhythmias. Recognition that the underlying rhythm is sinus, with a late-cycle pattern of ventricular bigeminy plus one definite fusion beat — are the key points to appreciate.
Additional Reading: — The links below may be of interest regarding selected concepts discussed in this case:
  • For more on Fusion Beats — Please see my ECG Blog #128 —
  • For more on Laddergrams — Please see my ECG Blog #69 —
  • For more on the Concertina Effect with WPW — Please CLICK HERE for the link to the brief commentary by Singla et al. —

Thursday, June 30, 2016

ECG Blog #128 (VT – Fusion – WCT – Sinus Tachycardia)

How would you interpret the lead II rhythm strip shown in Figure-1?
  • How certain are you of your diagnosis?
  • Are the P waves preceding beats #6 and #7 conducting?
  • Challenge Question: How many different-shaped beats are there on this tracing?
Figure-1: Long lead II rhythm strip showing a changing rhythm. Can you explain what is happening? NOTE — Enlarge by clicking on the Figure.
Interpretation: This is a challenging case. The easiest way to approach the interpretation of more difficult arrhythmias such as this one, is to begin with that part of the tracing that is easiest to interpret. 
  • To do this — Mentally block out the first 7 beats on this tracing. If ALL you had to worry about was the last 6 beats in Figure-1 (ie, beats #8-thru-13) — How would you interpret the rhythm in Figure-2?
Figure-2: The first 7 beats from Figure-1 have been blocked out. How would you interpret the arrhythmia represented by beats #8-thru-13?
Answer to Figure-2:
Beats #8-thru-13 are regular at a rate of 110 beats/minute. The QRS complex is narrow, and each QRS is preceded by normal appearing (upright) P waves with a normal PR interval. Beats #8-thru-13 represent Sinus Tachycardia.
  • Now mentally block out the last 8 beats on this tracing. If all you had to worry about were the initial 5 beats — How would you interpret the arrhythmia in Figure-3?
Figure-3: The last 8 beats (#6-thru-13) from Figure-1 have been blocked out. How would you interpret the arrhythmia represented by beats #1-thru-5?
Answer to Figure-3:
Beats #1-thru-5 are regular at a rate of just over 100 beats/minute (the R-R interval is just under 3 large boxes in duration). The QRS complex of these beats is wide, bizarre, and not preceded by atrial activity. This suggests a ventricular etiology. Since the usual rate of an idioventricular escape rhythm is much slower (in the range of 30-40 beats/minute) — We describe the arrhythmia represented by beats #1-thru-5 in Figure-3 as an Accelerated IdioVentricular Rhythm ( = AIVR).
  • Return to Figure-1. Now focus on the more difficult part of the tracing = beats #5-thru-8. Can you figure out what is going on in Figure-4?
Figure-4: Beats #1-thru-4 and #9-thru-13 from Figure-1 have been blocked out. Can you figure out what is happening with the remaining beats #5-to-8?
HINT to Figure-4: Sequential consideration of the following 4 questions may lead you to the diagnosis:
  • What kind of beat is beat #8? (See Answer to Figure-2).
  • What kind of beat is beat #5? (See Answer to Figure-3).
  • Would you expect the P wave preceding beat #6 to be able to conduct normally? If not — Why not?
  • Think of beats #5 and #8 as “parent beats”. If these parent beats (#5 and #8) were to mate (ie, combine) and “have children” — What would you expect the children to look like?
Answer to Figure-4:
Since the rhythm in Figure-2 is sinus tachycardia, beat #8 must be a sinus-conducted beat. Similarly, since the rhythm represented by Figure-3 is AIVR — beat #5 must be a ventricular beat.
  • Note that the PR interval preceding beat #6 is shorter than the PR interval preceding other sinus-conducted beats (beats #8-thru-13 in Figure-1). It is too short to conduct normally.
  • Note also that although the QRS complex of beat #6 is entirely upright — it is not nearly as wide as the other upright (ventricular) beats (beats #1-thru-5 in Figure-1). Beat #6 is a Fusion Beat.
Fusion beats occur as a result of simultaneous occurrence of supraventricular and ventricular impulses. This concept is illustrated in Figure-5.
  • Panel A in Figure-5schematically shows the pathway of normal conduction (SA Node–to–AV Node – to bundle branches). This results in a sinus-conducted beat (S) with a normal PR interval and a narrow QRS complex.
  • In contrast, Panel B — begins in the ventricles (V). This results in a wide QRS complex without preceding atrial activity.
  • The phenomenon of Fusion is represented in Panel C — in which there is simultaneous (or near simultaneous) occurrence of a supraventricular and ventricular complex. Depolarization wavefronts meet before they are able to complete their path, and the ECG appearance of the resultant fusion beat takes on characteristics of both the supraventricular and ventricular complex (F).
Figure-5: Illustration of the concept of fusion beats. Panel A — Sinus-conducted beat (S). Panel B — Ventricular beat (V). Panel C — Fusion beats (F1 and F2).
NOTE: Depending on whether the wavefronts in Panel C of Figure-5 meet high or low in the ventricles — the fusion beat will take on more characteristics of either the supraventricular complex (F2 in Panel C) — or, of the ventricular complex (F1 in Panel C).
  • Clinically — the reason recognition of fusion beats is important, is that it proves anomalous complexes in a tracing must be of ventricular etiology!
SUMMARY: Now look at Figure-6 — in which we have labeled Figure-1 with RED arrows to indicate the series of regularly-occurring sinus P waves which are clearly seen to begin just before beat #6.
  • Close inspection just before widened beat #5 reveals a subtle-but-definite small hump at the onset of the R wave of this beat. This small hump is almost certainly one more P wave (BLUE arrow) — that occurs right on time (ie, at the appropriate P-P interval distance just before the last RED arrow). No sinus P waves are seen before this blue arrow ...
Figure-6: Long lead II rhythm strip taken from Figure-1. We have labeled the regularly-occurring sinus P waves that are clearly seen with RED arrows. The BLUE arrow indicates yet one more on-time P wave that deforms the initial part of beat #5.
From Figure-6 — It should now be apparent that the arrhythmia begins with a 5-beat run of AIVR (at ~100-105/minute). Sinus tachycardia at a slightly faster rate (~110/minute) then takes over (beats #8-thru-13). Beats #6 and #7 manifest a QRS morphology intermediate between that of the ventricular and supraventricular beats, with the former beat (#6) more closely resembling the morphology of ventricular beats (as was the case for F1 in Panel C of Figure-5) — and the latter ( = beat #7) most closely resembling the morphology of the QRS complex during sinus tachycardia (as was the case for F2 in Figure-5).
  • The appearance of beats #6 and #7 in Figure-6 is as might be anticipated considering the PR interval that precedes each of these fusion beats. That is, the very short PR interval preceding beat #6 would not be expected to allow sufficient time for deep penetration of the supraventricular impulse (P wave) into the ventricles. Thus, beat #6 much more closely resembles the beats of ventricular etiology.
  • In contrast — the PR interval preceding beat #7 is almost normal. As a result, this supraventricular impulse (P wave) should have had time to travel relatively far down the conduction system before fusion occurred (explaining why the beat more closely resembles the morphology of supraventricular beats).
  • KEY POINT — Clinically, recognition that beats #6 and #7 in this tracing are fusion beats confirms the ventricular etiology of beats #1-thru-5.
CHALLENGE Question — Return a final time to Figure-6. In addition to beats #6 and #7 — there are 3 more fusion beats in this tracing. Can you spot them?
  • PEARL — One looks for fusion beats not only by examining the QRS complex — but also by close inspection of each T wave!
ANSWER to Challenge Question:  Beats #5, #8 and #9 are all fusion beats! The KEY to recognizing fusion beats is to look for the ever-so-slight subtle differences that may be present in either the QRS complex and/or the T wave between the beat(s) in the question and the complexes of known etiology.
  • Careful inspection of beat #5 reveals that its R wave is not quite as tall and its T wave not quite as deep as the other ventricular beats. Note also that the very initial portion of the upstroke of this R wave is deformed. A P wave is hiding here — and accounts for the slight degree of fusion that this beat manifests (BLUE arrow in Figure-6).
  • Beats #8 and #9 are also fusion beats. Careful comparison of these beats with beats #10-thru-13 reveals that they have a slightly narrower QRS complex and, a T wave that is smaller and less peaked.
NOTE: For more on Fusion Beats — See our ECG Blog #129