ECG Blog #297 — Is this VT?

The ECG in Figure-1 was obtained from an older man with a chief complaint of chest pressure and shortness and breath for the past several days. He was hemodynamically stable at the time the tracing in Figure-1 was recorded.

• Is this VT (Ventricular Tachycardia)?
• How certain are you of your answer?

Figure-1: ECG obtained from an older man with chest pressure and shortness of breath.

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NOTE: For optimal clinical utility — I’ve divided my comments into 2 parts: i) My initial rapid assessment (that I completed within seconds of seeing this tracing); and, ii) My 2nd (more detailed) assessment of this tracing — with greater attention to specific ECG findings:

• The “good news” — is that the patient in today’s case was hemodynamically stable at the time the ECG in Figure-1 was recorded. Therefore, by definition — this gives us at least a “moment of time” to assess the rhythm without need for immediate cardioversion. 

My Initial Rapid Assessment (Completed within Seconds! ):

By the Ps, Qs, 3R Approach (ECG Blog #185):

• The rhythm is Rapid (clearly over 200/minute) — and Regular. The QRS complex looks wide (albeit not very wide) — and I do not see sinus P waves. Therefore — the rhythm in Figure-1 is a regular WCT ( = Wide-Complex Tachycardia), but without clear sign of atrial activity.
• KEY Point: Even before looking at morphologic features — statistical odds are at least 80% that an older patient in a regular WCT rhythm without clear sign of atrial activity will turn out to be in VT. (These odds probably exceed 90% if this patient has underlying heart disease).
• 
  
• NEXT Step: I favor the “3-Simple Rules” for rapid distinction between VT vs SVT rhythms (See ECG Blog #196 — including the Audio Pearl in this post, for more on this topic). The fact that there is “extreme” axis deviation in Figure-1 (ie, an all negative QRS complex in lead aVF) — and an almost all negative QRS in lateral chest lead V6 — further increase statistical likelihood that this WCT rhythm is VT. That said — There are 2 ECG findings against this rhythm being VT: i) That QRS widening is minimal; and, ii) The initial portion of the QRS complex in multiple leads manifests rapid depolarization (ie, extremely steep S wave descent in virtually every lead with a predominantly negative QRS complex).
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• BOTTOM Line: Statistical likelihood (for this patient who is an older man) — that the regular WCT rhythm in Figure-1 will turn out to be VT is at least 90%. While it should be emphasized that 90% is not the same as 100% — We need to assume VT (and treat the patient accordingly) — until proven otherwise.

More Detailed Assessment about Today's Case:

• The rate of the rhythm in Figure-1 is extremely fast. There are a number of ways to rapidly estimate very fast heart rates (See ECG Blog #210 — and ECG Blog #278 for detailed illustration of my Every-Other-Beat Method). The R-R interval for today's rhythm is just over 1 large box in duration — which corresponds to a heart rate ~240/minute.
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• We are told that today's patient was “hemodynamically stable” at the time the ECG in Figure-1 was recorded. However, this patient is “older” — the ventricular rate of this WCT rhythm is extremely fast (~240/minute) — and the patient was having symptoms (ie, “chest pressure" and "shortness of breath”) at the time this ECG was recorded. This raises the question: Was this patient truly hemodynamicaly stable?
• I have always felt that in such cases, “Ya Gotta Be There” in order to optimally assess hemodynamic stability (See ECG Blog #220 — for full discussion of this subject). While it may have been reasonable to initially opt for a trial of medical therapy — we need to recognize that at best, this patient’s “hemodynamic stability” is borderline. IF at any point during the treatment process the patient's condition worsens — prompt cardioversion will be needed.
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• It is sometimes difficult to accurately assess QRS duration at the bedside of a symptomatic patient in a very rapid arrhythmia. In Figure-1 — the QRS actually looks narrow in a number of leads (ie, in leads I, aVL, V1 — and in some of the leads with predominantly negative QRS complexes). Remember: QRS duration should be measured in that lead in which you can clearly see the beginning and end of the QRS complex — and in which the QRS looks widest! If we select lead aVR in Figure-1 — the QRS definitely looks wide!
• 
  
• It may also be difficult to assess atrial activity in rapid arrhythmias. We are looking for a number of different types of atrial activity: i) Are there sinus P waves? (ie, clearly upright P waves in lead II?); ii) Are there retrograde P waves? (ie, P waves that regularly occur after the QRS — and which are negative in the inferior leads, but positive in leads like aVR and V1?); iii) Are there "fib" waves? — "flutter" waves? — or other evidence of atrial activity?; and/or, iv) Do we see AV dissociation?
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• PEARL #1: Although the finding of AV Dissociation can provide strong support that a regular WCT rhythm is VT (See ECG Blog #217) — it is very difficult to identify AV dissociation when the rate of the WCT rhythm is fast. In my experience, many clinicians think they see "AV dissociation" — when in fact, no reliably regular underlying sinus rhythm can be found. This may lead to misdiagnosis. It's best not to call AV dissociation unless you can reliably demonstrate (ie, with calipers) a reproducibly regular underlying sinus rhythm amidst the wide complexes of the tachycardia.
• I do not see sinus P waves in Figure-1. I do not see clear evidence of retrograde atrial activity. The only possible indication of atrial activity that I see, is a small deflection following the QRS complex in lead V1. Given that I do not see this activity in other leads (and given that even if present, I cannot distinguish if this represents a positive or negative deflection) — I did not include this deflection in my assessment of the rhythm (because it does not provide diagnostic value).
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• BOTTOM Line: Even after more careful analysis — I was left with the same conclusion: Statistical likelihood that the regular WCT rhythm in Figure-1 will turn out to be VT is at least 90%. While 90% is not the same as 100% — We need to assume VT (and treat the patient accordingly) — until proven otherwise.
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• P.S. — If the rhythm in Figure-1 did turn out to be supraventricular (statistically unlikely — but possible) — I thought the most likely diagnosis would then be a reentry SVT rhythm (ie, AVNRT or orthodromic AVRT) — since AFlutter rarely presents with 1:1 AV conduction.

Follow-Up: The Case Continues:

The patient was treated with 1 dose of Adenosine without effect. Amiodarone was started — and several minutes later ECG #2 was obtained (bottom tracing in Figure-2).

• How would YOU interpret the repeat ECG?
• Does ECG #2 explain what the rhythm in ECG #1 was?
•    HINT: Look closely again for atrial activity in both tracings!

Figure-2: Comparison between the initial ECG — and the repeat ECG after a dose of Adenosine and beginning Amiodarone.

ANSWER:

The ventricular rate has significantly slowed in ECG #2 (from ~240/minute — to ~115/minute in ECG #2). The sawtooth pattern of AFlutter (Atrial Flutter) can now be seen in each of the inferior leads.

• The rhythm in ECG #2 is AFlutter with 2:1 AV conduction. Since the ventricular rate is 115/minute — the atrial rate is 2X 115 — or about 230/minute.
• 
  
• Note that QRS morphology in each of the 12 leads in ECG #2 looks almost identical to QRS morphology in the initial tracing (except for the QRS looking slightly narrower in ECG #2).

QUESTION:

• What about atrial activity in both tracings? (See Figure-3).

Figure-3: I've magnified leads V1,V2 in both tracings — with focus on the appearance of atrial activity (See text).

ANSWER:

The fact that QRS morphology is virtually identical in both ECG #1 and ECG #2 — confirms that the rhythm was supraventricular — and not VT.

• Despite the final diagnosis — assuming the rhythm in ECG #1 was VT, and treating accordingly was the appropriate approach to initial management! We were not 100% certain about our diagnosis from Figure-1 — but we often have to begin management before knowing with certainty the etiology of the rhythm you are treating.
• Treatment with both Adenosine and Amiodarone was appropriate in this case. The fact that the QRS complex was only minimally widened in ECG #1 suggests that IF the rhythm was VT — that it might be a form of idiopathic VT (ie, VT in the absence of underlying heart disease) — and some idiopathic VTs do respond to Adenosine (See ECG Blog #197). And if instead, the rhythm was supraventricular — then it should be either converted or temporarily slowed by Adenosine.
• The advantage of IV Amiodarone as a treatment measure — is that it may effectively treat both ventricular and supraventricular tachyarrhythmias.
• 
  
• As to the question of atrial activity? — Slanted RED lines in the long lead II rhythm strip in ECG #2 highlight the 2:1 sawtooth pattern of AFlutter. Look at the RED arrows in lead V1 of this tracing.
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• Isn't the morphology of flutter waves (RED arrows) in lead V1 of ECG #2 the same as the morphology of the deflection highlighted by the BLUE arrows in lead V1 of the initial ECG?
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• PEARL #2: I did not initially realize that the deflection I was seeing in ECG #1 (BLUE arrows) represented 1:1 flutter activity! Sometimes the etiology of an arrhythmia will only become apparent after conversion to sinus rhythm, when you compare the "during" and "after" tracings. I found today's case fascinating — because it turns out that the initial rhythm in Figure-1 was AFlutter with 1:1 AV conduction! It is rare to see 1:1 AV conduction in a patient with AFlutter who is not on antiarrhythmic medication, and who does not have an accessory pathway.
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• PEARL #3: Despite a QRS morphology for the initial WCT rhythm in Figure-1 that strongly suggested the rhythm was VT (ie, extreme frontal plane axis — all positive QRS in lead aVR — almost all negative QRS in lead V6) — it turned out that the rhythm was supraventricular. Therefore — As helpful as QRS morphology may be for assessment of regular WCT rhythms — it is not perfect for distinguishing between VT vs SVT rhythms.
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• P.S.: Since we calculated the ventricular rate for the rhythm in ECG #1 to be ~240/minute — and since we determined this rhythm was AFlutter with 1:1 AV conduction — the initial rate of flutter waves was also 240/minute. Following IV Amiodarone — AV conduction decreased to 2:1 — and — the atrial rate of flutter waves was seen to decrease to ~230/minute (ie, 2:1 AV conduction, with a ventricular rate of ~115/minute).

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Acknowledgment: My appreciation to 陳俊宏 (Chun-Hung Chen from Taichung City, Taiwan) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm.
• ECG Blog #278 — Reviews one more example of how to quickly estimate a very rapid rate for this WCT rhythm.
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• ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm. 
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• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
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• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the video ECG Media Pearl #21 in this blog post.
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• ECG Blog #220 — Case Study that reviews my LIST #1: Distinction between VT vs SVT with preexisting BBB or aberrant conduction. (Audio Pearl = How to determine IF your Patient is Hemodynamically Stable).
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• ECG Blog #211 — WHY does Aberrant Conduction occur?
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• ECG Blog #217 — Reviews the concept of how AV Dissociation may help in the diagnosis of VT (including the Audio Pearl in this post).

ECG Blog #296 — Shark Fin Infarction — or Not?

An elderly man presented to the ED (Emergency Department) — with a 1-day history of abdominal pain and the ECG shown in Figure-1.

QUESTION:

• Despite the history of abdominal pain (and not chest pain) — Should the cath lab be activated?
• What is "Shark Fin" ST elevation?

Figure-1: Initial ECG in the ED — obtained from an older man with a 1-day history of abdominal pain. Should the cath lab be activated?

MY Initial Thoughts on ECG #1:

The entity of "Silent" MI (ie, infarction without a history of chest pain) — is more common than is generally appreciated, especially among older individuals (See ECG Blog #228 for more on "Silent" MI). My awareness of this entity led me to rapidly consider the need to activate the cath lab for the ECG shown in Figure-1 despite the lack of chest pain.

• I fully admit that my attention was instantly captured by the "eye-catching" abnormal complexes in the anterior leads V1, V2 and V3 of ECG #1! Could this represent "Shark Fin" ST elevation from a huge acute STEMI in a patient with need of prompt reperfusion?

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What is Shark Fin Morphology?

It's important to be aware of the pattern of "Shark Fin" ST segment elevation — in which the QRS complex looks wide, because it blends in with ST segments that show extreme ST elevation in multiple leads. As a result — the boundary between the end of the QRS complex and the ST segment becomes indistinguishable in those leads showing marked ST elevation or depression.

• As discussed in the illustrative case in ECG Blog #265 — "Shark Fin" ST segment elevation is most often a sign of severe transmural ischemia that results from acute coronary occlusion. Consideration of prompt cardiac cath is essential for clarifying the anatomy — since in many (most) cases, prognosis is likely to be poor unless there is prompt reperfusion.
• The KEY for confirming that "Shark Fin" morphology is the cause of the striking ECG picture this produces — is to find 1 or 2 leads in which you can clearly define the limits (end point) of the QRS complex (See Figure-2 below):

Figure-2: I've labeled today's ECG from Figure-1 — to facilitate recognition of "Shark Fin" ST elevation in the anterior leads (See text).

Taking a Closer Look at ECG #1:

Assessing today's tracing systematically:

• The rhythm is sinus tachycardia at ~115/minute (RED arrow in lead II of Figure-2 highlighting the upright sinus P wave in this lead). Regarding "Intervals" — the PR interval is not prolonged. Assessing the QTc is difficult with this degree of tachycardia — though I thought the QTc at most to be no more than slightly prolonged. It was assessment of QRS duration that posed the greatest difficulty!

The QRS complex clearly looks wide in leads V1 and V2 — but not so much in other leads. This was initially confusing to me.

• Leads V1, V2 and V3 were recorded simultaneously with the corresponding portion of the long lead II rhythm strip below the 12-lead. I thought lead V3 was KEY to assessment of QRS duration — as we can clearly see the end point of the QRS complex in this lead. I therefore drew a dotted BLUE line parallel to the heavy ECG grid line in Figure-2, corresponding to the end of the QRS complex. This suggests that the QRS complex is actually no more than minimally prolonged (ie, ~0.10-0.11 second).
• Taking the vertical dotted BLUE line as the end point of the QRS complex  in Figure-2 suggests: i) That the QRS complex is slightly widened and upright in leads V1,V2; and, ii) That there is extreme ST segment elevation in leads V1,V2,V3 (with the point marking the amount of ST elevation beginning just to the right of this dotted BLUE line in these 3 leads). This dramatic amount of ST elevation then descends into deeply inverted T waves in each of these 3 anterior leads.

My "Bottom Line" Impression of ECG #1:

I was left with uncertainty as to the cause of the highly unusual appearance of the QRST complexes in anterior leads V1, V2 and V3.

• QRS morphology is clearly abnormal — in that the QRS is slightly (but not markedly) widened — and the QRS is all positive in leads V1 and V2 (and still predominantly positive in lead V3). In association with wide terminal S waves in lateral leads I and V6 — this picture is consistent with IRBBB (Incomplete Right Bundle Branch Block).
• My initial impression regarding the dramatic amount of "Shark Fin" ST elevation in the 3 anterior leads — was acute LAD (Left Anterior Descending) coronary artery occlusion, causing acute antero-septal STEMI with the bifascicular block (RBBB/LAHB) that is so commonly seen in association with acute proximal LAD occlusion. That said, if this was the cause of the unusual anterior lead appearance — I would not have expected to already see such deep anterior T wave inversion.
• Then I thought that perhaps we are seeing a Brugada-1 ECG pattern (See ECG Blog #238 on Brugada Phenocopy) — that is superimposed on IRBBB/LAHB in a patient with acute LAD occlusion, with deWinter-like T waves in lateral chest leads V4-thru-V6 (ie, Note J-point ST depression that ascends to form prominently peaked T waves — as reviewed in ECG Blog #183). 
• Finally — There are deep, wide Q waves in each of the inferior leads, indicative of inferior MI of uncertain age (with or without associated LAHB).

The CASE Continues:

Clinical follow-up in today's case was very surprising! (See Figure-3).

• Serum K+ = 5.3 mmol/L (ie, no more than minimally elevated).
• Serial Troponins were normal!
• Serial ECGs over the course of the next day failed to show any significant evolution.
• Echo revealed normal systolic and diastolic function without regional wall motion abnormality.
• It turned out that the cause of the patient's acute illness was a right inguinal hernia which led to bowel obstruction with perforation. On operation — intestinal perforation was found with multiple necrotic patches spread throughout the ileum (Figure-3).
• Throughout the patient's course — he never developed chest pain.
• Given no positive findings for an acute cardiac event — cardiac catheterization was not deemed necessary.

Figure-3: Clinical follow-up findings in today's case. Chest X-ray (upper Left) — showed greatly distended intestine, suggestive of bowel obstruction. CT scan and intra-operative photograph revealed right inguinal hernia with bowel obstruction and perforation (with multiple necrotic patches throughout the ileum).

Acute Abdomen as a Cause of Pseudo-Infarction on ECG:

There is a literature documenting a number of cases in which an acute abdomen resulted in an ECG picture suggestive of an acute cardiac event — but for which clinical follow-up revealed no infarction (ie, Pseudo-Infarction ECG patterns).

• Cattermole and McKay (Emerg Med J 23:e48, 2006) — reviewed the literature and reported on an older woman with a rectus sheath hematoma — whose ECG was mistaken for acute inferior MI.
• Herath et al (BMC Cardiovascular Disorders 16:245, 2016) — reported a case of intestinal obstruction with gastric distension, that resulted in dynamic ECG changes mimicking an evolving anterior MI. Of interest — ECG changes resolved promptly following gastric decompression.
• Mixon and Houck (Tex Heart Inst  30:155-157, 2003) — reported a case of intestinal obstruction which altered the anatomy, resulting in actual compression of the right ventricle (and the ECG finding of marked anterior lead ST elevation).
• Other acute abdominal conditions (including cholecystitis and pancreatitis) — have also been shown to produce pseudo-infarction ECG patterns.

NOTE: The mechanism responsible for producing pseudo-infarction patterns in association with acute abdominal conditions is uncertain. Among the mechanisms postulated include:

• Catecholamine surge — secondary to pain and/or the acute abdominal condition itself (perhaps via a similar mechanism to the catecholamine surge associated with Takotsubo Cardiomyopathy).
• Change in the anatomic position of the heart (and/or direct compression of a portion of the heart) — that might be caused by physical contact from gastric and/or intestinal obstruction.
• Increased vagal tone from pain — causing coronary artery spasm or other reflex mechanism that results in ECG changes.
• Variant (Pinzmetal) angina with coronary vasospasm — perhaps precipitated by increased sympathetic tone associated with an acute abdomen.

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Acknowledgment: My appreciation to 陳俊宏 (Chun-Hung Chen from Taichung City, Taiwan) 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 (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23-LINK in Blog #205).

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• ECG Blog #228 — reviews the entity of "Silent" MI with an illustrative case (the Audio Pearl in this post reviews How Often Silent MIs occur).
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• ECG Blog #265 — which reviews in detail a case of "Shark Fin" ST elevation due to ischemia/infarction from CO poisoning.
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• ECG Blog #238 — which reviews in detail the entity of Brugada Phenocopy (including an ECG Video Pearl on the essentials of Brugada Syndrome).
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• ECG Blog #183 — reviews the ECG pattern of deWinter-like T-waves (with variations of this pattern discussed in the accompanying Audio Pearl).
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• The November 22, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was cardiac arrest, ischemic Osborn waves, with massive Shark Fin ST deviation from acute STEMI.

• The June 11, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was an underlying Bifascicular Block (RBBB/LPHB), in addition to Shark Fin ST elevation & depression. 

• The January 24, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) adds to this case, in which there was an underlying Bifascicular Block (RBBB/LAHB), in addition to Shark Fin ST elevation & depression — followed by progressive Low Voltage due to Myocardial Stunning from the huge infarct.

ECG Blog #295 — Why is the 1st Beat Different?

The ECG in Figure-1 was obtained from an older patient with new chest pain.

• What is the cause of the rhythm?
• WHY is the 1st beat always different?

Figure-1: ECG obtained from an older patient with new chest pain.

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NOTE #1: This tracing is a smart phone photo that was sent to me for my comment. This is the reason for the slanting and slight distortion. That said — I believe the image still is good enough for accurate interpretation.

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NOTE #2: Some readers may prefer at this point to listen to the 3:45 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-41a).

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Today's ECG Media PEARL #41a (3:45 minutes Audio) — Reviews HOW to recognize within seconds (!!!) a Mobitz I (AV Wenckebach) 2nd-degree AV Block, in which there is ongoing Inferior STEMI.

MY Thoughts on the ECG in Figure-1:

There are 2 parts to this tracing: i) The cardiac rhythm (as shown in the long lead II rhythm strip); and, ii) The 12-lead ECG above it. I generally like to start my initial assessment by taking at least a brief look at the long lead rhythm strip — though sometimes (as in today’s case) — I need to switch my attention to the simultaneously-recorded 12-lead ECG in order to complete assessment of the cardiac rhythm.

• My initial impression on looking at the long lead II rhythm strip in Figure-1 — was that there is group beating! That is — we see 3 groups, each with 4 beats — and each with similar timing.
• Of Note — the 1st beat in each group (ie, beats #1, 5, 9 13) looks different than other beats in the group! 
• Also of Note — is that the duration of each of the short pauses in this rhythm (ie, the R-R intervals between beats #4-5; 8-9; and 12-13) are the same. It should be clear that this pattern of rhythmicity is not by chance!

Continuing my approach to assessment of the rhythm — I next considered the 5 KEY parameters (See ECG Blog #185 for review of the Ps, Qs, 3R Approach that I favor for Rhythm Interpretation):

• There are P waves! Of note — at least some of these P waves are related to neighboring QRS complexes (ie, the PR intervals preceding beats #1, 5, 9 and 13 are equal — therefore these beats are “Related” — in that these P waves are conducted to the ventricles).
• The QRS complex is narrow everywhere! To verify this — I looked at all beats in each of the 12 leads in the ECG above the long-lead rhythm strip.
• The remaining 2 parameters are Rate and Regularity. We have already addressed “regularity” — in that there is a “regular irregularity” to the rhythm (ie, a “pattern” — in the form of group beating). 
• As to the parameter of "Rate" — the ventricular Rate varies. In order to determine IF the atrial Rate is regular — we need to first complete our search for P waves.

PEARL #1: I’ll emphasize that one of the most helpful things to do for assessment of complex arrhythmias — is to label P waves. This is usually EASY to do with use of calipers. Simply set your calipers to the P-P interval between any 2 P waves in a row that you are sure about — and then see IF you are able to “walk out” P waves throughout the rest rest of the tracing.

• In Figure-2 — we can definitely distinguish the first 2 P waves in the long lead rhythm strip (ie, the first 2 RED arrows in Figure-2). Note how each of the subsequent RED arrows falls on a deflection resembling a P wave (even when this occurs during the ST-T wave) — throughout the entire rhythm strip. Thus, the atrial rhythm is regular at a Rate of ~100/minute! 
• 
  
• Now that we have labeled all P waves in today's rhythm with RED arrows — Isn’t it much easier to assess the potential relation that each of these P waves might have with its neighboring QRS?

Figure-2: I've labeled the P waves with RED arrows. The atrial rhythm is regular at ~100/minute. QUESTION: Is there evidence on the 12-lead ECG of acute inferior MI? (See discussion below!).

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PEARL #2: The finding of group beating in a rhythm in which the atrial rhythm is regular should immediately suggest the possibility of some form of Wenckebach conduction.

• The likelihood of AV Wenckebach ( = 2nd-degree AV Block of the Mobitz I type) — becomes much greater when group beating in a rhythm with a regular atrial rhythm occurs in the setting of acute inferior MI.
• For clinical examples of acute inferior MI with Mobitz I 2nd-degree AV Block ( = AV Wenckebach) — See ECG Blog #55 — ECG Blog #154 — ECG Blog #224 — and ECG Blog #232.

NOTE: At this point in my interpretation — I shifted my attention from the long lead II rhythm strip, in order to focus on the 12-lead ECG. 

• I did this because IF today's patient (who presented with new chest pain) was in the process of evolving an acute inferior MI — then even before completing assessment of the complex rhythm in Figure-2 — statistical likelihood that this rhythm will end up representing some form of AV Wenckebach will be greatly increased (and knowing will make it much easier for me to find confirmation of this when I return for final interpretation of this complex rhythm)!

QUESTION:

• Do YOU see evidence on the 12-lead ECG in Figure-2 of evolving acute inferior MI?

ANSWER:

We have already noted the following regarding today's ECG: i) There are 2 different QRS morphologies in this tracing that are seen in this tracing; ii) All beats on the 12-lead ECG are narrow — which means that all beats are supraventricular; and, iii) The fact that the PR interval preceding each of the beats that end one of the short pauses is the same (ie, the PR interval before beats #1, 5, 9 and 13 is the same!) — means that these 4 beats are definitely conducted!

• Focus your attention on the ST-T waves for beat #1 in simultaneously-recorded leads II and III — and on beat #5 in simultaneously-recorded leads aVF and aVL. Each of the ST segments in the 3 inferior leads for these beats is elevated — with the picture of mirror-image reciprocal ST depression in lead aVL. This is diagnostic of acute inferior MI.
• I found it interesting that this ECG evidence of acute inferior MI is much more easily appreciated for beats #1 and 5 — than for beats #2,3,4 and 6.
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• In the chest leads — beat #9 in simultaneously-recorded leads V1,V2,V3 suggests ongoing acute posterior MI (ie, early transition with a tiny isoelectric QRS in lead V1, and predominant R waves already by lead V2 — with associated ST depression in lead V2, but not in lead V1).
• Because the 12-lead ECG is abruptly cut off after the QRS complex of beat #13 — we do not see the ST-T wave of this last beat well in the lateral chest leads. But it's clear that there is abnormal ST depression in leads V4, V5, V6 for beats #11 and 12.
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• Putting It All Together: I interpreted the 12-lead ECG in Figure-2 as diagnostic of acute infero-postero MI. Lack of any ST depression in lead V1 suggested associated acute RV involvement — which strongly suggests that the "culprit" artery is the proximal RCA (Right Coronary Artery — See ECG Blog #190, including the Audio Pearl in this post for more on the ECG recognition of acute RV MI).

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NOTE: The results of Cardiac Catheterization of today's patient confirmed my clinical suspicion. There was diffuse disease of the RCA (including proximal, mid- and more distal segments) — with total occlusion, confirming this as the "culprit" vessel. In addition — there was multi-vessel disease in the form of an 80% mid-LAD lesion and 70-80% LCx lesion.

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NOTE: At this point in my interpretation — I shifted my attention back to the long lead II rhythm strip — in order to complete my assessment of the cardiac rhythm.

• PEARL #3: "Armed" with the knowledge that the 12-lead ECG showed acute inferior infarction — I virtually knew that the group beating with regular atrial rhythm that we see in the long lead II rhythm strip was going to represent some form of AV Wenckebach.
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• The next 4 Figures that I show illustrate by means of colored arrows my deductive process. I'll emphasize that total time it took me to work through what I show in the next 4 Figures was less than 15 seconds!
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• PEARL #4: The only way I could arrive at my final rhythm diagnosis so fast — was to use calipers. In my opinion — it is impossible to time-efficiently interpret complex rhythms such as this one without using calipers.
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• For clarity — I illustrate the mechanism of today's rhythm in the Laddergram shown in Figure-7. For those interested — I provide links to posts which review step-by-step description of how to read (and/or draw) laddergrams — with numerous detailed laddergrams that I have shown in prior posts on my ECG Blog #188.

Figure-3: RED arrows highlight our observation that the PR interval preceding each of the beats that end one of the short pauses is the same (ie, the PR interval before beats #1, 5, 9 and 13 is the same!). This tells us that these 4 beats are conducted.

Figure-4: Note that the 2nd PR interval in each group of 4 beats is slightly longer (YELLOW arrow) — than the PR interval that precedes the 1st beat in each group (RED arrow).

Figure-5: BLUE arrows highlighting the 3rd P wave in each group continue to show progressive lengthening of the PR interval within groups of beats.

Figure-6: Further PR interval lengthening (GREEN arrows) — followed by a non-conducted P wave (BLACK arrows) — confirms the diagnosis of 2nd-Degree AV Block of the Mobitz I Type ( = AV Wenckebach) — with 5:4 AV conduction (ie, 4 of the 5 P waves in each group are conducted — with the 5th P wave blocked).

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Final QUESTION:

• The final issue to resolve in today's complex tracing is the question of WHY the 1st beat in each of the 4-beat groups looks different?

ANSWER = PEARL #5: What makes today's ECG especially challenging is having to account for WHY the QRS complex of beats #1, 5, 9 and 13 looks different from other QRS complexes on this tracing. 

• Return for a moment to the 12-lead ECG shown in Figure-2. The reason beats #1, 5, 9 and 13 all look different — is that these beats all conduct with LAHB (Left Anterior HemiBlock) aberration, as they manifest predominant negativity in each of the inferior leads. But unlike the overwhelming majority of aberrantly-conducted beats — it is relative bradycardia (ie, slight slowing of the heart rate) rather than tachycardia that precipitates aberrant conduction. This is contrary to what one would anticipate — since improved conduction (not LAHB) is normally expected following a longer preceding R-R interval. 
• The mechanism of this paradoxical form of bradycardia-dependent block (sometimes called “Phase 4” block) has been described by Marriott. The mechanism is complex (Marriott HJL, Boudreau Conover MH: Advanced Concepts in Arrhythmias, Mosby, St. Louis, 1983, pp 164-166). Suffice it to say that this form of bradycardia-dependent aberrant conduction is not common — and that when it does occur, it is usually associated with significant underlying heart disease. This was borne out in today's case — in which cardiac catheterization showed acute RCA occlusion with a background of severe multi-vessel coronary disease.

I schematically illustrate the mechanism of today's arrhythmia in the Laddergram shown in Figure-7.

• For those interested — I presented a step-by-step laddergram illustration of another case with a similar form of bradycardia-dependent AV Wenckebach in the August 17, 2020 post of Dr. Smith's ECG Blog.

Figure-7: Laddergram illustration of today's arrhythmia. The dotted BLUE lines in the Ventricular Tier for beats #1, 5, 9 and 13 schematically illustrate that the reason the QRS complex of these beats looks different — is that these beats conduct with LAHB aberration.

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Acknowledgment: My appreciation to Arshad Ali (from Karachi, Pakistan) for the case and this tracing.

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Relevant LINKS to Today's Case:

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Additional Relevant Material to Today's Case:

• See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to rhythm interpretation.
• 
  
• Inferior STEMI + AV Wenckebach — See ECG Blog #154 —
• Mobitz I + Acute MI — See ECG Blog #55 —
• Inferior MI with Mobitz I — See ECG Blog #224 —
• Recent Inferior MI with Mobitz I — See ECG Blog #232 —
• ECG Diagnosis of acute RV MI — See ECG Blog #190 —

How to Draw a Laddergram (Step-by-Step Demonstration) 

• See ECG Blog #69 — for a Step-by-Step description on drawing a Laddergram.
• See ECG Blog #188 — for a brief ECG Video review on the basics of what a Laddergram is — with LINKS at the bottom of the page to more than 50 ECG blog posts in which I review illustrative laddergrams.
• See ECG Blog #164 — for a user-friendly rhythm-solving approach to AV Wenckebach, followed by Step-by-Step construction of the Laddergram.
• ECG Blog #236 — Reviews in our 15-minute Video Pearl #52 how to recognize the 2nd-Degree AV Blocks (including "high-grade" AV block). 
• ECG Blog #186 — Reviews when to suspect 2nd-Degree, Mobitz Type I.
• 
  
• CLICK HERE — to DOWNLOAD my Free PowerPoint Laddergram STENCIL for your use as desired.

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