ECG Blog #467 — The Cath Lab was Deactivated

I was sent the ECG in Figure-1 — obtained from a previously healthy man his 60s, who contacted EMS (Emergency Medical Services) for new-onset severe “burning” CP (Chest Pain) that radiated to the jaw and throat.

On seeing the ECG in Figure-1 — the EMS crew activated the cath lab.

• QUESTION: Do you agree with this decision by the EMS crew to activate the cath lab?

Figure-1: The initial ECG in today's case — done by EMS at the scene. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts on Today’s CASE:

Sometimes — “Ya gotta be there!” The words on paper in my initial paragraph (written above) — voice concern that this man in his 60s may be having an acute cardiac event. If similar concern is perceived by the EMS team in the field — then even before seeing the initial ECG, the patient is in a higher-risk category for having an acute cardiac event.

• As a result — any abnormalities on the initial ECG should prompt significant concern.

And — the initial ECG in Figure-1 is not normal ...

• The rhythm is sinus (small, but upright P wave in lead II ) — with some R-R interval variability (probable sinus arrhythmia).
• All intervals (PR, QRS, QTc) are normal — as is the frontal plane axis (about +50 degrees). No chamber enlargement.
• Regarding Q-R-S-T Wave Changes: There are no Q waves — and R wave progression is normal (with transition where the R wave becomes taller than the S wave is deep occurring normally between leads V3-to-V4). 

BUT — there are subtle-but-important findings regarding ST-T wave appearance. I've highlighted these in Figure-2. 

• Do you agree?

Figure-2: I've labeled the initial ECG in today's case.

Abnormal Findings in Figure-2:

• My "eye" was immediately drawn to lead V2 (within the RED rectangle). There should be slight gentle upsloping ST elevation in leads V2 and V3 in a normal tracing. This is not seen in lead V2 (the straight RED line that I've drawn in this lead highlighting this abnormal straightening of the ST segment). In a patient with new CP — recognition of this subtle-but-important finding is what prompts me within seconds to suspect an ongoing posterior OMI (Occlusion-based MI).
• In addition — the T wave in lead V2 looks taller-than-it-should-be given modest size of the QRS in this lead (RED arrow in lead V2). This suggests that there may already be some spontaneous reperfusion of an ongoing posterior OMI.
• In support of my suspicion of an ongoing posterior OMI — is the similar finding in neighboring lead V2 of another T wave that looks taller-than-it-should-be (within the BLUE rectangle).
• Any doubt that I may have had that these admittedly subtle lead V2 and V3 findings are real — was immediately dispelled by the shelf-like ST depression in lead V4. There is no way this shape and this amount of ST depression in this mid-chest lead is "normal" (especially since lack of increased R wave amplitude in this tracing rules out LV "strain" from LVH as a cause of ST depression).
• Additional findings of subtle but abnormal ST segment straightening are also seen in leads V5, I and aVL.
• And then there is the coved but non-elevated ST segment in lead III — that I felt was noteworthy, though of uncertain significance.

What do these Subtle Findings Mean?

When interpreting ECGs such as the initial tracing in today's case — We need to remember that we are not trying to "rule in" an acute STEMI.

• Instead — We need to remember that this man in his 60s presents with new cardiac-sounding CP that immediately places him in a higher-risk category for having an acute cardiac event. Therefore, in the absence of a prior baseline ECG for comparison — any abnormal findings on his initial tracing must be interpreted as acute until proven otherwise.
• Not to accept that the process of acute coronary occlusion is "fluid" and not "static" — is to ignore the pathophysiology of this process. It is also the best way to miss a lot of acute OMIs in need of prompt cath with PCI (ie, See recent publications by Ricci, Smith et al — Ann Emerg Med, 2025 — and — McClaren, Smith et al — JACC Adv. 2024,3:101314 — with detailed review of this pathophysiology in Podcast #2 in My ECG Podcast tab at the top of each page in this ECG Blog). 

Impression: In this patient with new CP — the ECG in Figure-1 should suggest the possibility of an evolving posterior OMI. 

• While fully acknowleding that STEMI criteria are not satisfied in this initial ECG (and that many interventionists would not take this patient to the cath lab on the basis of this single ECG unless the patient was having refractory CP) — the physiologic reason for the lack of more obvious abnormalities may be the result of some spontaneous reperfusion (suggested by disproportionately taller-than-expected T waves in anterior leads V2,V3).
• This could account for the lack of ST elevation on this tracing (ie, "pseudonormalization" phase — that occurs between the stage of ST elevation and reperfusion ST-T wave changes). 
• Whether ST coving in lead III is the result of associated inferior OMI is uncertain from this single ECG. 
• Finally, given this patient's age and the diffuseness of the above-noted ST-T wave abnormalities — there may be underlying multivessel disease. 
• Bottom Line: Additional evaluation (serial ECGs, Troponins) with prompt transport to a cath-capable facility is needed.

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The CASE Continues:

The patient was promptly transported to the nearest ED facility. The ECG was repeated on arrival in the ED — as shown in Figure-3.

• The ED physician interpreted the patient's "burning" CP that was with associated nausea as GERD (esophageal reflux). As a result — initial treatment consisted of a GI cocktail.
• The patient's CP had decreased at the time the repeat ECG (shown at the bottom of Figure-3) was recorded. As a result — the cath lab was deactivated.

QUESTIONS:

• Do you agree with this management in the ED?
•     — Is ECG #2 an unremarkable tracing?

Figure-3: Comparison between the initial ECG vs the repeat ECG in the ED.

My Thoughts on Figure-3:

There are subtle-but-important differences between the 2 ECGs that are seen in Figure-3.

• KEY Point: It would be easy to overlook these differences if these tracings were not placed side-by-side to facilitate lead-by-lead comparison.
• There has been a slight change in the frontal plane axis (ie, The isoelectric QRS that is now seen in lead aVF of ECG #2 indicates a more horizontal axis). This slight axis shift probably accounts for the intermittent QS that we now see in lead III. That said — I do not think there has been any significant ST-T wave change in the limb leads.

In the chest leads:

• The T waves in leads V2 and V3 appear less prominent in ECG #2.
• There is less baseline wander and less baseline artifact in leads V4,V5,V6 of ECG #2. As a result — assessment of ST-T wave appearance is much more reliable in this repeat ECG. Whereas I put a BLUE question mark over the variable ST-T wave appearance in lead V6 of ECG #1 — there is now no doubt that there is abnormal ST segment flattening with slight ST depression in leads V4,V5,V6.

Bottom Line: Overall – I think ST-T wave changes in ECG #2 may be slightly less. This may be explained by the decrease in the patient's CP at the time of the repeat ECG. But the definite ST segment flattening and depression in leads V4,V5,V6 is real — and given the history of new severe CP — this has to be assumed as acute ischemia until proven otherwise.

• The call for cath lab activation should not have been deactivated on the basis of this 2nd ECG.

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The CASE Continues:

• The initial Troponin was negative.
• Although the patient's CP had decreased on arrival in the ED — it never went away.
• A bit later, while still in the ED — the patient's CP worsened, at which time ECG #3 was recorded (which I've placed next to ECG #2 in Figure-4).

QUESTIONS:

• How to interpret the 2 ECGs in Figure-4 given the clinical context of this case?
•     — What to do?

Figure-4: The ECG was repeated while the patient was still in the ED because of worsening of his CP.

ANSWER:

Looking at ECG #3 — the answer is now obvious.

• In ECG #3 — We now see definite hyperacute ST-T waves in leads III and aVF — with marked reciprocal changes in high-lateral leads I and aVL.
• The previously taller T waves in leads V2 and V3 — have been replaced by marked ST depression that begins in lead V2 and extends through until lead V6.
• There is now more ST elevation in lead aVR.
• IMPRESSION: There is an obvious acute infero-postero OMI in progress. Correlating the timing of the severity of this patient's CP with serial ECG changes suggests that the taller-than-expected T waves that were initially seen in leads V2,V3 did reflect spontaneous reperfusion — BUT — recurrence of CP severity in association with ECG #3 and worsening of ECG changes in virtually all 12 leads suggests there has been spontaneous reocclusion. The diffuseness of these ST-T wave changes in ECG #3 suggest there may be underlying multi-vessel disease.

Cardiac Cath was performed:

• The patient had multi-vessel disease — including a 90% LAD lesion — 70% LCx lesion — and "chronic near-occlusion" of the RCA.
• The patient was scheduled for CABG.

Lessons To Be Learned:

• In a higher-risk patient (such as the patient in today's case) — detection of subtle ECG abnormalities on the initial ECG may be extremely important. Frank ST elevation will not be seen in 1/3 or more cases of acute coronary occlusion. Especially if the history of symptoms is fluctuating — ECG changes may be subtle if the tracing is recorded during the period "pseudo-normalization".
• The initial Troponin may be negative despite ongoing acute infarction (even when high-sensitivity Troponins are used). Physiologically — this may occur as a result of very brief coronary occlusion, followed so soon after by spontaneous reperfusion. This is why clinical correlation of each ECG recorded with notation of the presence and severity of CP is so important.
• What spontaneously opens — may just as easily spontaneously reclose. For this reason — even though CP may decrease and the ECG may "improve" — if an ongoing OMI is in process, the patient still needs prompt cath with PCI to prevent reocclusion.
• In a patient with an ongoing OMI — reduced CP is not the same as completely resolved CP. As long as any CP continues — the acute event is still ongoing (such that prompt cath with reperfusion is still needed).
• The paradigm of waiting until STEMI criteria are satisfied is outdated and dangerous. Even when cardiac cath is ultimately performed — precious time is wasted, with potential loss of precious myocardium as a result of this delay (as occurred in today's case).

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Acknowledgment: My appreciation to Cortland Ashbrook (from Spokane, WA, USA) for the case and this tracing.

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ECG Blog #466 — Do You See What I See?

I was sent the ECG in Figure-1 — without clinical information.

• I interpreted the rhythm as AFib (Atrial Fibrillation).

QUESTION:

• Do you see anything else?

Figure-1: The initial ECG in today's case.

Take another LOOK.

• To facilitate description — I've numbered the beats in Figure-2.

Figure-2: I've numbered the beats from Figure-1.

Confession: I initially looked at this tracing too quickly ...

• The QRS complex is narrow. As a result — the rhythm is supraventricular.
• I initially thought the rhythm was irregularly irregular, albeit with a number of baseline undulations — but no distinct P waves. I therefore interpreted the rhythm as AFib with a controlled ventricular response (with those baseline undulations representing "fib" waves).
• I thought the tracing was otherwise unremarkable — other than minimal nonspecific ST-T wave changes, but nothing that looked acute.

QUESTION:

• Do you agree with my initial interpretation?

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Looking Closer ...

• Beginning with beat #12 — the rhythm becomes quite regular. As shown in Figure-3 — RED arrows highlight what now appears to be atrial activity that had been present all along.

Figure-3: I've labeled atrial activity in today's rhythm (See text).

QUESTION:

• How can we be certain that the RED arrows in Figure-3 are truly highlighting atrial activity?

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ANSWER:

• The KEY is to appreciate (and make use of) simultaneous leads. As shown in Figure-4 — the shallow negative deflection that precedes beats #11-thru-16 with a constant PR interval is a P wave. We know this — because we now clearly see distinct P waves with the same constant PR interval in simultaneously recorded leads V4,V5,V6.
• And, if we look a few seconds earlier in the long lead V1 rhythm strip — no such P waves were present in lead II for the first 5 beats in this tracing (within the BLUE rectangle).
• Therefore: Today's patient was in AFib at the beginning of this ECG — until there was spontaneous conversion to sinus rhythm (that began with beat #11).

Figure-4: The vertical RED line shows the presence of distinct P waves in 4 simultaneously recorded leads (leads V4,V5,V6 — and in the long lead V1 rhythm strip).

QUESTION:

• Was the rhythm still AFib right before spontaneous conversion to sinus rhythm with beat #11?
• 
  
•    HINT: Look at spontaneously recorded lead V3 ...

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ANSWER:

• I thought we were seeing 4 consecutive atrial waves with a fixed P-P interval in lead V3 (BLUE arrows in Figure-5). The rate of these 4 atrial deflections is ~250/minute, which suggests that this patient began with AFib with a controlled ventricular response — then transiently developed AFlutter (or ATach) before manifesting a short pause, after which there was spontaneous conversion to sinus rhythm.

Figure-5: BLUE arrows in lead V4 highlight a 4-beat run of regular atrial activity shortly before spontaneous conversion of today's rhythm to sinus (See text).

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LESSONS to be Learned:

• It's good to stay humble — as you never know when you might overlook an important finding that you should have picked up. I initially looked at today's tracing too quickly — and, as a result — I missed the spontaneous conversion of this patient's AFib to a sinus rhythm that occurred with beat #11. Today's case highlights how it's important to survey the entire rhythm strip when assessing for regularity of the rhythm.
• KEY Point: One of the best clues for uncovering the mechanism of a complex rhythm (and for detecting hidden P waves) — is to Look for the "break" in the rhythm! By this I mean to look for any short pause, paying extra attention to events just before, during and just after the pause (ie, the "break" in today's rhythm is seen between beats #10 and 11, as the R-R interval is longest between these 2 beats).
• NOTE: It is not common to see a patient going in-and-out of AFib during a single 12-lead recording. That said — Be aware that this can happen. AFib may spontaneously convert to AFlutter — and vice versa — sometimes passing from 1 rhythm-to-the-other multiple times. 
• Clinically — Although initial treatment of AFib and AFlutter is similar, there are some important different management considerations to be aware of: i) AFib is a much more common rhythm; ii) While medications to treat both rhythms are generally similar — it may be easier to control the ventricular response of AFib with medication; iii) AFlutter is typically more responsive to electrical cardioversion (and often requires much lower energies for cardioversion than does AFib);  — and, iv) For persistent AFib or persistent AFlutter — the response to ablative therapy is somewhat different (typical AFlutter tends to be easier to "cure" by ablation — although in experienced centers, ablation of many cases of AFib will be successful).
• Patients who go in-and-out of AFib are said to have PAF (Paroxysmal AFib). It is estimated that about half of all patients with AFib have PAF. Clinically, the risk of stroke for patients with PAF is probably about the same as the risk of stroke with persistent AFib ( = a long discussion beyond the scope of this ECG Blog).
• Finally — It's good to appreciate when seeing a patient with presumably new AFib — that the overall results of literature studies suggest that if you do nothing to actively treat your patient's AFib — that ~1/2 of these patients with AFib will spontaneously convert to sinus rhythm over the next 24 hours.

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Acknowledgment: My appreciation to Sam Ghali  (from Jacksonville, Florida — @EM_RESUS) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.

 

ADDENDUM (1/25/2025):

—  — 

ECG Media PEARL #51a (7:40 minutes Audio) — Reviews of "Some Simple Steps to Help Interpret Complex Rhythms" ).

 

ECG Blog #465 — A Tale of Syncope & 2 Rhythms

The ECG in Figure-1 was obtained from an older woman who presented to the ED (Emergency Department) because of a syncopal episode. She was asymptomatic at the time this ECG was recorded.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
•   Is there AV block?  If so — What kind?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Figure-1:

As always — I favor the Ps, Qs, 3R Approach as an optimally time-efficient way to assess any arrhythmia, including the AV blocks (See ECG Blog #185).

• As shown in the long lead II rhythm strip at the bottom of Figure-1 — the Rhythm is regularly irregular (ie, there is group beating, with repetitive short-long cycles). As a result — the Rate of the rhythm is not constant, although the overall ventricular rate is not overly rapid.
• P waves are present.
• The QRS is wide (ie, more than half a large box in duration). Looking at the 12-lead ECG that appears above the long lead II rhythm strip — QRS morphology appears to be consistent with LBBB (Left Bundle Branch Block) conduction, in that the QRS is all upright in left-sided leads I,V6 — and predominantly negative in right-sided lead V1, as well as in other anterior chest leads.

This leaves us with needing to assess the 5th Parameter — which is determining whether those P waves that are present, are Related to neighboring QRS complexes?

• To answer this question — I’ve labeled the P waves that we see in the long lead II rhythm strip with RED arrows (Figure-2).
• 
  
• PEARL #1: To facilitate determining if any of the P waves that you see are conducting — Label the P waves you identify! Doesn't this simple step of labeling P waves make it easier to determine which P waves are (or are not) Related to neighboring QRS complexes?

Figure-2: I've labeled P waves in today's initial ECG with RED arrows.

Are P Waves Related to Neighboring QRS Complexes?

Focus on QRS complexes that end each of the pauses in Figure-2 (ie, on beats #3,5,7,9 and 11).

• Isn't the PR interval that precedes beats #3,5,7,9,11 constant? This tells us that each of these beats is being conducted to the ventricles. (NOTE: Although we do not see far enough in front of beat #1 to assess the PR interval — by its similarity to the overall pattern in this tracing, we can presume that beat #1 is also being conducted to the ventricles).
• Next — Focus on the 2nd beat in each group (ie, on beats #2,4,6,8,10,12). Although somewhat difficult to tell because the P wave in front of each of these beats is partially hidden within the preceding T wave — Doesn't it appear that the PR interval before beats #2,4,6,8,10,12 is also constant, as well as being equal to the PR interval before beats #1,3,5,7,9,11?

For clarity in Figure-3 — I've drawn a laddergram of the long lead II rhythm strip from today's initial ECG. Note the following:

• Group beating (repetitive 2 beat groups throughout the tracing).
• A fairly (albeit not completely) regular atrial rhythm.  
• QRS widening (that we determined is consistent with LBBB conduction).
• All 12 QRS complexes in Figure-3 are preceded by P waves that manifest the same constant PR interval (ie, the slope of the RED lines within the AV Nodal Tier remains constant). 
• The PR interval of conducted beats is not prolonged.
• Every 3rd P wave is not conducted (ie, every 3rd P wave fails to make it out of the AV Nodal Tier).

Conclusion: The finding of a fairly regular atrial rhythm with failure of one or more on-time P waves to conduct to the ventricles defines today's initial rhythm as a form of 2nd-degree AV block.

• QUESTION: Which type of 2nd-degree AV block? 

Figure-3: Laddergram of the long lead II rhythm strip from Figure-2.

PEARL #2: As reviewed in detail in the ADDENDUM below — there are 3 Types of 2nd-degree AV block. These are:

• Mobitz I, 2nd-degree AV block ( = AV Wenckebach) — in which the PR interval increases until a beat is dropped.
• Mobitz II — in which the PR interval remains constant for consecutively conducted beats until one or more QRS complexes are non-conducted.
• 2nd-degree with 2:1 AV block — in which because of the fact that we never see 2 consecutively conducted beats — We are not able to tell if the PR interval would lengthen before dropping a beat IF given the chance to do so.
• 
  
• BOTTOM Line: By the above definitions — the rhythm in Figure-3 appears to be the Mobitz II form of 2nd-degree AV block because: i) The QRS is wide; ii) On-time sinus P waves are not conducted to the ventricles (which happens with every 3rd P wave in Figure-3); — and, iii) The PR interval remains constant for consecutively conducted beats.
• KEY Point: Distinction between the Mobitz I and Mobitz II forms of 2nd-degree AV block is important — because the clinical course of Mobitz I is often fairly benign — whereas patients with Mobitz II are much more likely to need a permanent pacemaker.

PEARL #3: There are a number of ECG and clinical Clues that may help to determine IF the type of 2nd-degree AV block you are looking at is more likely to be a Mobitz I or Mobitz II block. These clues include the following:

• Mobitz II is rare. In my experience — well over 90-95% of all 2nd-degree AV blocks will turn out to be Mobitz I.
• The QRS complex will most often be wide with Mobitz II. As a result — Mobitz II is very unlikely if the QRS is not wide. In contrast — the QRS is most often narrow with Mobitz I (although exceptions exist IF in a patient with Mobitz I — there is preexisting bundle branch block).
• Mobitz I is most often associated with recent or acute inferior infarction. In contrast — Mobitz II is most often associated with anterior infarction.
• The PR interval for beats that conduct with Mobitz I is often prolonged (sometimes markedly so). In contrast — the PR interval of conducting beats with Mobitz II is more often normal, or no more than minimally prolonged.
• It is unlikely to switch back-and-forth from Mobitz I to Mobitz II (or vice versa). Therefore, IF on review of additional monitoring on your patient you see clear evidence of Mobitz I (ie, progressive PR interval lengthening until a beat is dropped) — then it is likely that all tracings on that patient (including those with 2:1 AV block) — are also Mobitz I.

Regarding Today's CASE ...

• Because of the implication that pacing will be needed if today's rhythm is Mobitz II — We want to be as certain as possible that the PR interval is not increasing with consecutively conducted beats. As noted earlier — it is difficult to be certain of this in Figure-2, because the onset of the 2nd P wave in each 2-beat group is partially hidden within the preceding T wave.
• The 12-lead ECG that is seen in Figure-2 does show LBBB — but there is no clear sign of acute, recent or previous infarction.
• Conclusion: I strongly suspect the rhythm is Mobitz II — but I cannot be 100% certain this from this single ECG.

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The CASE Continues:

Today's patient had another syncopal episode. Her ECG at that time is shown in Figure-4.

QUESTIONS:

• How would YOU interpret the ECG in Figure-4?
•   Is there AV block?  If so — What kind?

Figure-4: Repeat ECG obtained following another syncopal episode.

MY Thoughts on Figure-4:

The rhythm in Figure-4 is now slower, but regular. The R-R interval is ~8 large boxes in duration — corresponding to a rate a bit less than 40/minute. P waves are seen. The QRS is obviously wide.

• As per PEARL #1 — Assessment of whether P waves are (or are not) related to neighboring QRS complexes is most easily accomplished by labeling P waves — which I have done in Figure-5.

Figure-5: I've labeled the P waves in Figure-4.

Are P Waves in Figure-5 Related to the QRS?

In Figure-5 — I've labeled those P waves that we can readily identify with RED arrows. Although there is slight variation in the P-P interval — this type of ventriculophasic sinus arrhythmia is common with 2nd- and 3rd-degree AV blocks.

• Given that it makes more sense for the underlying atrial rhythm to remain regular (rather than to all-of-a-sudden drop several beats) — I added PINK arrows in Figure-5 where I expected to find 2 additional P waves. (Slight distortion at the beginning of the QRS of beat #3 — and at the end of the T wave of beat #3 — strongly suggests that P waves do lie below these 2 PINK arrows).

Putting Together what we've determined in Figure-5:

• The QRS is wide.
• The ventricular rhythm is essentially regular (with minor variation in the R-R interval due to ventriculophasic sinus arrhythmia). The ventricular rate is just under 40/minute.
• An almost regular atrial rhythm is present (colored arrows in Figure-5). Focusing on the P waves before each of the 6 beats in the long lead II rhythm strip — the PR interval continually changes. Thus, P waves “are marching through” the QRS — such that there appears to be complete AV dissociation (ie, None of the P waves in Figure-5 are being conducted to the ventricles).

PEARL #4: Clearly, there is at least 2nd-degree AV block in Figure-5 — because many of the on-time P waves are not being conducted to the ventricles (ie, There are many more P waves than QRS complexes in this tracing). 

• As discussed in ECG Blog #405 — the KEYs for determining if complete (3rd-degree) AV block is present are: i) Whether there is an underlying regular (or almost regular) atrial rhythm; and, ii) Whether all P waves fail to conduct despite having an adequate opportunity to conduct. To satisfy these conditions — the rhythm strip must be long enough for P waves to occur during all parts of the R-R interval, and still fail to conduct.
• PEARL #5: Escape rhythms from the AV Node, the His or the ventricles — tend to be regular. As a result — the BEST clue for suggesting that AV block is not complete — is if the ventricular rhythm is not regular. The occurrence of one or more QRS complexes earlier-than-expected usually means that those earlier beats are being conducted.
• 
  
• Conclusion: As a result, I strongly suspect that the rhythm in Figure-5 is complete AV block because: i) The QRS is wide; ii) The ventricular rate is slow and regular; iii) The atrial rate is regular; — and, iv) None of the P waves appear to be conducting to the ventricles despite many of these on-time P waves occuring in parts of the cycle during which we would expect P waves to be able to conduct.
• Beyond-the-Core: Technically, we can not rule out the possibility that some P waves might be able to conduct if "given the chance" — since we do not truly see P waves occurring over all parts of the R-R interval. To see this — we would probably need another 20-to-30 seconds of monitoring. That said — the failure to conduct consecutive P waves at many points in this 10-second rhythm strip suggest at the very least, that there is high-grade (if not complete) AV block. 

QUESTIONS:

Take another LOOK at the 2 ECGs in today's case. To facilitate comparison — I have placed these tracings together in Figure-6. 

• Did YOU notice how different the QRS complex looks in each tracing? — WHY is this so?
• What about the appearance of ST-T waves in ECG #2?

Figure-6: Side-by-side comparison of the 2 ECGs in today's case. 

 

ANSWER: QRS morphology in ECG #1 (TOP tracing) is consistent with LBBB conduction (ie, all positive in left-sided leads I and V6 — but predominantly negative in the anterior chest leads). The constant PR interval preceding each beat in ECG #1 tells us that each of the 12 QRS complexes in this tracing is being conducted — although every third P wave is not. Thus, the rhythm in ECG #1 is 2nd-degree (not 3rd-degree) AV block.

• In contrast — the QRS complex is wider in ECG #2, with a very different QRS morphology (ie, resembling RBBB conduction in lead V1 — albeit with marked right axis in the limb leads). In association with the much slower ventricular rate and the constantly changing PR interval throughout this tracing — this suggests there is now a ventricular "escape" focus (which supports our assumption that the rhythm is now complete AV block).
• If any of the P waves in ECG #2 were to be conducting — we would expect to see a return to the LBBB conduction morphology that we saw in ECG #1.
• The laddergram in Figure-7 schematically illustrates failure of all atrial impulses to conduct in ECG #2 — because there is now complete AV block (dotted line in the AV Nodal Tier) — with resultant slow ventricular "escape".

Figure-7: Laddergram showing complete AV block in ECG #2.

To conclude the case — Take another LOOK at ST-T wave morphology in ECG #2 (BOTTOM tracing in Figure-6). Although none of the QRS complexes in this tracing are being conducted — Doesn't ST-T wave morphology look abnormal? (ie, There is ST segment coving with deeper-than-expected T wave inversion in leads V1-thru-V4).

• It's possible that the reason for the slower heart rate and progression to complete AV block is the result of a recent event. Serial troponins and ECGs are indicated to rule out an acute or recent MI.

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Summary of Today's CASE:

The patient in today's case is an older woman who presented to the ED for a syncopal episode. Although she was asymptomatic at the time her initial ECG was recorded — this initial tracing (shown in Figure-1) showed frequent non-conducted P waves as a result of 2nd-degree AV block of the Mobitz II type.

• As emphasized — clinical implications of Mobitz II are clearly more worrisome than for the much more common Mobitz I type of 2nd-degree AV block. For this reason — permanent pacing will often be needed when the rhythm is Mobitz II.

Today's patient then had a 2nd syncopal episode. Her repeat ECG at this time (shown in Figure-4) — now showed complete AV block, with a slow ventricular "escape" rhythm.

• Final Follow-Up: A recent event was ruled out. Thus, this case showed progression of Mobitz II to complete AV block. The patient received a permanent pacemaker.

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Acknowledgment: My appreciation to Rajeesh R Pillai (from Kollam, Kerala, India) for the case and this tracing.

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ADDENDUM (1/18/2025): 

• I've included below an Audio Pearl — a Video Pearl — and links for download of PDFs reviewing the ECG diagnosis of AV Blocks.

—  —

ECG Media PEARL #4 (4:30 minutes Audio): — takes a brief look at the AV Blocks — and focuses on WHEN to suspect Mobitz I.

My GOAL in the 15-minute ECG Video below — is to clarify ECG diagnosis of the 2nd-Degree AV Blocks, of which there are 3 Types:

• Mobitz I ( = AV Wenckebach).
• Mobitz II.
• 2nd-Degree AV Block with 2:1 AV conduction.

This 15-minute ECG Video (Media PEARL #52) — Reviews the 3 Types of 2nd-Degree AV Block — plus — the hard-to-define term of "high-grade" AV block. I supplement this material with the following 2 PDF handouts.

• Section 2F (6 pages = the "short" Answer) from my ECG-2014 Pocket Brain book provides quick written review of the AV Blocks (This is a free download).
• Section 20 (54 pages = the "long" Answer) from my ACLS-2013-Arrhythmias Expanded Version provides detailed discussion of WHAT the AV Blocks are — and what they are not! (This is a free download).

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs and 3R Approach to Systematic Rhythm Interpretation.
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 
  
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).
• 
  
• ECG Blog #256 — and Blog #342 — Review  of SSS (Sick Sinus Syndrome).
• 
  
• ECG Blog #295 — Reviews the concept of bradycardic-induced BBB ( = Phase 4 block). This is discussed near the bottom of the page (ie, in Pearl #5 — that appears just under Figure-6).
• 
  
• The July 5, 2018 post in Dr. Smith's ECG Blog — (Please see My Comment at the bottom of the page for Review on the ECG diagnosis of Sick Sinus Syndrome).
• 
  
• ECG Blog #192 — The 3 Causes of AV Dissociation.
• ECG Blog #191 — Reviews the difference between AV Dissociation vs Complete AV Block.
• ECG Blog #389 — ECG Blog #373 — and ECG Blog #344 — for review of some cases that illustrate "AV block problem-solving".
• ECG Blog #251 — Reviews the concepts of Wenckebach periodicity and the "Footprints" of Wenckebach.
• ECG Blog #164 — Reviews a case of typical Mobitz I 2nd-Degree AV Block (with detailed discussion of the "Footprints" of Wenckebach). 
• 
  
• ECG Blog #236 — for an ECG Video Pearl on the 3 Types of 2nd-degree AV block.
• ECG Blog #344 — thoroughly reviews the Types of 2nd-degree AV block (Mobitz I vs Mobitz II vs 2:1 AV Block).
• 
  
• ECG Blog #63 — Mobitz I, 2nd-degree AV block with junctional escape.
• 
  
• ECG Blog #405 — ECG Video presentation that reviews the distinction between AV Dissociation vs Complete (3rd-degree) AV Block (For a LINKED Contents to this ECG Video — Click on MORE in the Description under the video on YouTube).