ECG Blog #174 (AV block – PACs – group beating)

The 2 lead II rhythm strips shown in Figure-1 were obtained from the same patient, just a few minutes apart. Unfortunately — no history is available.

• Note that there is group beating in both tracings. Is this Wenckebach? (ie, Is the rhythm in this figure 2nd-degree AV block, Mobitz Type I?).
• How certain are you of your answer?
• HINT: Find a pair of calipers — and USE them to figure out your answer!

Figure-1: Two lead II rhythm strips obtained minutes apart from the same patient. Is this 2nd-degree AV block of the Mobitz I type ( = AV Wenckebach)? 

COMMENT: The presence of group beating should be immediately noticed in Figure-1. That is, there are 2 groups of 3 beats (ie, in rhythm A — beats #3,4,5 and beats #6,7,8) — and multiple groups of 2 beats (ie, beats #11,12 in A — and in B, beats #2,3; 4,5; 6,7; 8,9, 10,11). Recognition of group beating can prove invaluable — because this finding instantly tells you: i) that some kind of repetitive pattern is present in the rhythm; and, ii) that you should strongly consider the possibility of some type of Wenckebach conduction.

• IF the rhythm in Figure-1 was AV Wenckebach — then at least several of the “FOOTPRINTS” of Wenckebach should be present. (This is a direct link to 32:20 in our ECG Video on the Basics of AV Block, and takes you to the part in which we discuss the “Footprints of Wenckebach”. If you click on SHOW MORE, below this video on the YouTube page — You’ll see a detailed linked Contents of all in this video!).
• Use of calipers instantly tells us that the rhythm in Figure-1 is not AV Wenckebach because: i) the P-P interval is definitely not regular (Usually the P-P interval is at least fairly regular when there is AV block); and, ii) the PR interval is not reliably increasing within groups of beats (We should see PR interval prolongation when there is AV Wenckebach) — SEE Figure-2!

Figure-2: We’ve labeled the P waves that were seen in Figure-1 (See text).

FIGURE-2: In Figure-2 — We’ve labeled sinus P waves with RED arrows. Additional P waves are highlighted by BLUE arrows. Note that the T waves under each of the BLUE arrows in Figure-2 are deformed (usually be a notch), compared to the T waves that are not hiding P waves within them (ie, NO P waves are hiding within the T waves of beats #3, 6, 9, 11 in A; and beats #2, 4, 6, 8 and 10 in B).

• Therefore — the BLUE arrows in tracings A and B in Figure-2 represent P waves. Compared to the P-P interval between 2 sinus P waves (ie, between 2 RED arrows) — each of the P waves highlighted by BLUE arrows occurs much earlier-than-expected, which means the P waves highlighted by BLUE arrows are PACs (Premature Atrial Contractions).
• Taking another look at the 2 rhythm strips shown in Figure-2 — we see that every 3rd P wave (ie, each of the BLUE arrows) — is a PAC. Therefore, the underlying rhythm in Figure-2 is Atrial Trigeminy (which is the term we use to describe an underlying sinus rhythm, in which every 3rd beat is a PAC).
• The PACs preceding beats #2, 5 and 8 are conducted. However, none of the other PACs in Figure-2 are conducted. Instead, the PACs following beats #10 and 12 in A — and following beats #1, 3, 5, 7 and 9 in B are all “blocked” (ie, non-conducted), and followed by a short pause.
• BOTTOM LINE: The underlying rhythm in Figure-1 is atrial trigeminy (ie, every 3rd P wave is a PAC). Some of these PACs are conducted. Others are “blocked”. All of the PACs in B are blocked — and this produces a form of group beating that simulates AV Wenckebach — BUT — there is no AV block in Figure-2, for the reasons we state above.
• P.S. — Use of calipers allows you to rule out AV block within seconds! It should take no more than a few seconds to determine that every 3rd P wave in Figure-2 occurs far too early to be a sinus rhythm (as would be expected when there is AV block).

BEYOND-the-CORE: As is often the case in “real life” — there is a final “twist” to the rhythm in Figure-2. Do you see it?

• HINT: Is P wave morphology for all of the P waves highlighted by RED arrows the same?
• NOTE: My answer below is complex. It is not meant to confuse — but rather to illustrate the challenges faced by the astute clinician when confronted with a truly complex “real life” tracing. Less experienced interpreters may want to ignore what I write below. My hope is that what I write below proves insightful, especially for more experienced interpreters.

ANSWER: Perhaps the greatest challenge the astute clinician faces when interpreting a complex arrhythmia that is less-than-perfect technically — is distinguishing between deflections that are due to artifact vs the slight variation in P wave, QRS and/or ST-T wave morphology that may normally occur in “real life”.

• Because rhythm strips A and B in Figure-2 were obtained just seconds apart — I would expect moment-to-moment fluctuations in P wave and/or QRS morphology to be minimal. Yet despite virtually no change in QRS morphology between tracings A and B — I thought the P waves under the RED arrows of beats #3,4; 6,7; 9,10; and 12 in A, were in general taller and more pointed than almost all of the other P waves. This made me wonder IF those smaller and rounder P waves in these 2 tracings might not reflect P waves arising from an alternate atrial site?
• That said — strongly against this possibility, is that fact that the R-R intervals between beats with successful RED-arrow P waves are virtually identical! I definitely would not expect this, if ectopic site atrial P waves were mixed in with sinus P wave activity.
• BOTTOM LINE: I suspect all P waves in tracings A and B of Figure-2, that are highlighted by RED arrows — are of sinus origin. I suspect there is just a lot of moment-to-moment variation in sinus P wave morphology. That said — I cannot prove this based only on these 2 tracings ...

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For MORE on PACs vs Wenckebach:

• Please see ECG Blog #66 and Blog #164 —

ECG Blog #173 (VT - AFib - Polymorphic - WPW)

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NOTE: My complete write-up of this case is found on the March 11, 2020 post on Dr. Smith's ECG Blog — CLICK HERE — 

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The Case: A young adult presented to the ED for with "heart awareness" and the ECG shown in Figure-1 — but with no more than slight shortness of breath. BP ~130/70.

Questions:

• What is the cardiac rhythm in Figure-1?
• How certain are you of your diagnosis?
• Is the clinical scenario consistent with what you might expect for this rhythm?

Figure-1: The initial ECG in this case.

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NOTE: My complete write-up of this case is found on the March 11, 2020 post on Dr. Smith's ECG Blog — CLICK HERE — 

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ECG Blog #172 (ST Elevation – J-Point – Osborn – OMI vs Repolarization)

The ECG shown in Figure-1 was obtained from a 52-year old man. There was concern about acute infero-lateral MI vs acute pericarditis.

• WHICH of these conditions do you think is present? How certain are you about the diagnosis?
• What are we missing?

Figure-1: ECG obtained from a 52-year old man. The differential diagnosis was acute infero-lateral MI vs acute pericarditis.

COMMENT: What we are missing — is a brief History about the circumstances surrounding this ECG. The patient was found outside during the winter months. His core temperature on arrival in the ED was 83 degrees Fahrenheit ( = 28 degrees Celsius).

Descriptive Analysis:

• Rate & Rhythm — The rhythm is sinus bradycardia at ~55/minute.
• Intervals — The PR interval is normal. The QRS complex is normal (ie, not more than half a large box in duration = ≤0.10 second). However, the QT interval is clearly prolonged; it is nearly 3 large boxes in duration (ie, ~560 msec).
• Axis — The mean QRS axis is normal (about +75 degrees).
• Chamber Enlargement — None.

Looking Next at Q-R-S-T Changes:

• Q Waves — There are very small and narrow q waves are seen in the infero-lateral leads (ie, leads II,III,aVF; and V5, V6).
• R Wave Progression — There is normal R wave progression, with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V2-to-V3.

Regarding ST-T Wave Changes:

• The most remarkable findings are: i) Prominent J-point notching (RED arrows in Figure-2) and/or J-point slurring (BLUE arrows) in multiple leads; and, ii) 1-1.5 mm of upward-sloping ST elevation in the inferior leads (II,III,aVF) — and in leads V2-thru-V6. Other leads show nonspecific ST-T wave flattening.

Figure-2: I’ve added to Figure-1 my measurement of the QT interval + ARROWS to highlight J-point notching/slurring (See text).

DISCUSSION: I intentionally omitted the history of cold exposure for several reasons. FIRST — Descriptive Analysis of this (or any other) ECG is the SAME regardless of the history.

• It is the Clinical Interpretation that will change, depending on clinical circumstances surrounding the case (See ECG Blog #93 — for “My Take” on use of a Systematic Approach to ECG Interpretation).

We have previously discussed the ECG findings of Hypothermia (See ECG Bog #149). Both that case and this one are similar in that: i) There is bradycardia; ii) There is QTc prolongation with associated ST elevation in multiple leads; iii) Other ECG findings of acute MI are lacking (ie, No Q waves, or no more than very small and narrow q waves; No reciprocal ST depression); and, iv) There are prominent Osborn waves ( = J-point notching) in multiple leads (RED arrows in Figure-2). The J-point slurring in this tracing (BLUE arrows) is also a temperature-related phenomenon.

• NOTE: Neither patient (ie, not the patient from ECG Blog #149, nor the patient in today’s case) had acute MI or pericarditis — despite the presence of significant ST elevation in multiple leads.
• PEARL #1 — While impossible to completely rule out the possibility of acute MI or pericarditis from the ECG shown in Figure-1 — it is good to remember that ST elevation in multiple leads is one of the ECG Findings of hypothermia.
• PEARL #2 — Even if this hypothermic patient was having an acute STEMI (ST-Elevation MI) — cardiac catheterization would best be deferred until core temperature was raised. At that point, the ECG can be repeated — and, if ST elevation has greatly resolved (and the patient is not having chest pain) — then low core temperature (and not ongoing infarction) was the likely cause of the ST elevation.
• PEARL #3 — Prominent J-point notching can be a finding associated with acute ischemia and/or ongoing acute infarction. In this setting — ischemia-related Osborn waves may be predictive of increased risk of malignant ventricular arrhythmias — which is another reason why the history in today's course (which was "cold" exposure) was so important for determining clinical implications of the ECG in Figure-1. (NOTE: — More on the subject of ischemia-related Osborn waves will appear shortly in our ECG Blog #241).

ECG Blog #171 — "Magic" between Leads III & AVL

The only information provided on the patient whose ECG is shown in Figure-1 — was that the patient was a 54-year old man. NO history was available.

• IF this tracing was in your “pile-of-ECGs-to-be-read” — What would you do?

Figure-1: 12-lead ECG obtained on a 54-year old man. NO history available. What are your thoughts?

Descriptive Analysis: 

• Rate & Rhythm — The rhythm is sinus bradycardia at a rate between 55-60/minute.
• Intervals — The PR, QRS and QTc intervals are all normal. If anything, the QTc is relatively short (I measure ~380 msec).
• Axis — The mean QRS axis is normal (about +75 degrees).
• Chamber Enlargement — None.

Looking next at Q-R-S-T Changes:

• Q Waves — Small and narrow q waves are seen in the infero-lateral leads (ie, in leads II,III,aVF; and V4-thru-V6).
• R Wave Progression — Transition occurs normally (here, between leads V2-to-V3) — albeit the R wave in lead V2 has already become relatively tall (~7 mm).

Regarding ST-T Wave Changes:

• There is 1-1.5 mm of concave-up ST elevation in each of the inferior leads (ie, in leads II,III,aVF). The mirror-image opposite ST-T wave picture of what we see in lead III appears in lead aVL. In addition — there appears to be 1 mm of flat ST segment depression in lead I.
• In the chest leads — there is ~1.5 mm of J-point ST depression in lead V2. As has been previously mentioned — this occurs in association with an R wave in lead V2 that is already surprisingly tall (~7 mm).

Figure-2: Schematic representation of mirror-image relationships from Figure-1 (See text).

Putting It All Together: The KEYS to interpreting this tracing lie with appreciating several mirror-image relationships (Figure-2):

• When ST segment elevation in the inferior leads is acute — there is an almost “magic” mirror-image relationship between the way the ST-T wave looks in lead III, compared to lead aVL. These 2 leads are nearly 180 degrees opposed to one another — therefore they show reciprocal changes.
• Note in Figure-2 — how the mirror-image of the ST-T wave in lead aVL (within the light BLUE insert) — looks identical to the shape of the elevated ST-T wave in lead III (within the WHITE rectangle).
• Similarly, the mirror-image of the elevated ST-T wave in lead III (within the light BLUE insert) — looks identical to the shape of the inverted ST-T wave in lead aVL (within the WHITE rectangle).
• Confirmation that the above mirror-image relationships are real and represent an acute change consistent with acute inferior MI — is forthcoming from the clearly abnormal shelf-like ST depression we see in lead I.
• Further support of recent (if not ongoing acute) occlusion of the RCA (Right Coronary Artery) — is suggested by the positive Mirror Test we see for the QRST complex in lead V2 (For more on the Mirror Test — See ECG Blog #80). Anterior leads (ie, leads V1, V2 and/or V3) often manifest the mirror-image opposite picture of ongoing events in the left ventricular posterior wall — and the mirror-image of the QRST complex in lead V2 (within the light BLUE insert) shows a large Q wave + downward coved ST elevation, that leads to beginning T wave inversion.

BOTTOM Line: One has to interpret the ECG in Figure-1 as consistent with recent (if not ongoing acute) RCA occlusion until proven otherwise. Since this tracing was in your “pile-of-ECGs-to-be-read” — the responsibility falls on YOU to immediately look up the patient to find out WHAT is going on?

• In addition to acute infero-postero MI — there may also be acute RV involvement in Figure-1 — since rather than ST depression, the ST segment in lead V1 is not at all depressed as would be expected with acute posterior MI. That said — right-sided chest leads would be needed to know for certain if there is or is not associated acute RV involvement.

P.S. — Unfortunately — follow-up in this case is lacking. The patient was seen years ago — and I have no further information on the case. Nevertheless, I thought it worthwhile to discuss how even when no clinical information is available — how the mirror-image opposite relationships we see in this tracing tell us we have to assume these ECG changes are acute until we prove otherwise.

ECG Blog #170 (Atypical Chest Pain - Mirror Image - Troponin - Lcx - Lad)

The ECG in Figure-1 was obtained from a 30-year old man with an unusual story. He was admitted to the hospital to “Rule Out MI” — with what was described as “atypical” chest pain, that was not thought to be cardiac in etiology. Serial troponins were negative. His initial ECG (not shown) was interpreted by a capable emergency physician as “normal”. The patient had a normal Stress Echo, in which he attained his target heart rate and showed no wall motion abnormality. He was about to be discharged from the hospital with a diagnosis of atypical non-cardiac chest pain. His pre-discharge ECG ( = ECG #2) is shown in Figure-1. There were no new symptoms at the time ECG #2 was done. How would you interpret this pre-discharge ECG ( = ECG #2)?

• What would you do, given that all testing to this point had been normal?

Figure-1: This is the follow-up ECG, obtained on this 30-year old man who was about to be discharged from the hospital. His initial ECG (not shown) was interpreted as “normal”. Serial troponins, and Stress Echo were completely normal (See text).

COMMENT: We can’t comment on the initial ECG — since it is not shown. What we can say — is that ECG #2 is not a normal tracing! Presumably, had the initial ECG been as abnormal as this 2nd ECG — the capable clinician who interpreted that initial tracing would presumably have at least seen some of the abnormalities — BUT — We can’t comment on what we are not shown ...

Descriptive Analysis of ECG #2:

• Rate & Rhythm — It’s hard to be certain what the cardiac rhythm is! This is clearly a supraventricular rhythm — because the QRS complex is decidedly narrow. But there is no long lead rhythm strip. The R-R interval is not completely regular. It looks like there is atrial activity in front of some QRS complexes — but a clearly upright P wave is lacking in lead II. I’d guess this is an ectopic atrial rhythm, perhaps with some junctional escape beats — but I can’t rule out the possibility of a nearly regular AFib. A longer period of monitoring is clearly needed to determine for certain ... Bottom Line: The above said — Since the rhythm is supraventricular, we can assess ST-T waves in ECG #2 for potential ischemic changes!
• Intervals — The PR interval is irrelevant in this tracing — since we don’t see consistent atrial activity. As noted — the QRS complex is narrow. The QTc interval appears to be normal.
• Axis — The mean QRS axis is normal (about +25 degrees).
• Chamber Enlargement — None.

Looking next at Q-R-S-T Changes:

• Q Waves — Small and narrow q waves are seen in high lateral leads I and aVL.
• R Wave Progression — Transition occurs normally (here, between leads V2-to-V3) — albeit abruptly (ie, the QRS was almost all negative in lead V2 — and abruptly becomes almost all positive by lead V3).
• Regarding ST-T Wave Changes:
• There is 1-2mm of concave-up ST elevation in leads I and aVL. The mirror-image opposite ST-T wave picture of what we see in lead aVL appears in lead III. Of note — there is ~2mm of J-point ST depression in lead III — and 1-1.5mm of J-point ST depression in leads II and aVF.
• The ST-T wave in lead V2 is somewhat distorted by artifact (ie, the contour of the ST segment in V2 is not at all smooth). That said — the T wave looks disproportionately peaked in V2, with a disproportionately wide base — however, other than nonspecific ST-T wave flattening in leads V4-thru-V6, there do not appear to be acute changes in the remaining chest leads.

Putting It All Together: The limb leads in ECG #2 are clearly abnormal. ST elevation in high-lateral leads — with a mirror-image opposite appearance of the ST-T in lead aVL compared to lead III should suggest an acute cardiac event until you prove otherwise (For more on this point — Please see My Comment at the bottom of the page in the 10/6/2018 SSmith ECG Blog post).

Follow-Up on This Case: Based on the abnormal pre-discharge ECG in Figure-1 — the cardiologist took this patient to the cath lab. He was found to have a very tight stenosis of a dominant LCx (Left Circumflex) coronary artery — which was successfully stented.

• It is fortunate that this pre-discharge ECG was obtained and interpreted before sending this patient home.
• Learning Point: The initial ECG in a patient with significant coronary disease may not always be abnormal. Serial troponins and stress testing may also be normal. None of this rules out the possibility of severe underlying coronary disease.