Anterior OMI with RBBB has VF x 3: how to prevent further episodes of VF?

A middle-age woman with no previous cardiac history called 911 for chest pain.

This was her prehospital ECG:

What do you think?

There is sinus rhythm with RBBB and obvious LAD OMI (proximal LAD occlusion): hyperacute T-waves in I, aVL and minimal STE in V1, V2.

This is diagnostic of Acute LAD OMI

In case you are wondering what the Queen thought, here she is:

Notice that she also diagnoses Low Ejection Fraction.

The paramedics diagnosis was "Possible Anterolateral STEMI."  I don't know what the device algorithm interpretation stated.

I am not certain if there was a prehospital cath lab activation, but there should be.

On arrival in the ED, a bedside ultrasound showed poor LV function (as predicted by the Queen of Hearts) with diffuse B-lines.   

Initial BP was 120/96, HR 102, SpO2 98%. and this was recorded:

RBBB with proximal LAD Occlusion is very high risk.  

When this came off the machine, I turned to the resident in charge and whispered "This is very bad."

3 seconds later, she went into ventricular fibrillation.

We rapidly defibrillated her, and with return of normal sinus rhythm.

Several minutes later the patient developed V-fib again > 200J defibrillation with return to NSR.

Rapid sequence intubation was performed for airway protection in setting of recurrent V-fib and defibrillations. 

Chest X-ray also showed pulmonary edema.

The patient then had 2 subsequent episodes of V-fib requiring defibrillation, with return to NSR.

She was given 2 mg Magnesium.  Potassium was 4.5 mEq/L

While waiting for the cath team, and to prevent further episodes of VF,  lidocaine 100 mg administered followed by 50 mg q5 min x 3 afterwards (for a total of 250 mg over 15 minutes), followed by a lidocaine infusion of 3 mg/min

Lidocaine dosing: Lidocaine rapidly redistributes from the extracellular to the intracellular space.  A high extracellular (serum) level is toxic.  One must give it in serial boluses to give it time to redistribute.  Thus we gave 1.5 mg/kg, followed by 0.75, then 0.75, then 0,75 spaced 5 minutes apart.  Furthermore, it is rapidly metabolized and therefore an infusion is necessary to maintain adequate therapeutic levels.

The patient was transported to cath lab accompanied by the resident, with BP 50/30 en route improved with a push dose of 100 mcg epi.

She had no further episodes of VF.

Angiogram:

2. LAD: type III-IV vessel with a proximal thrombotic or embolic occlusion

(TIMI 0 flow).  The final angiographic result is very good.

Troponins

Initial troponin was 24 ng/L (barely above URL).  More proof that a huge STEMI may have normal or near normal initial troponin.   We showed this in this article in JAMA Cardiology.

Peak troponin was greater than 60,000 ng/L -- too high to measure.

Echo 9 months later:

Enlarged left ventricular cavity size (LVEDD 6.2 cms) with moderately reduced systolic function. Left ventricular cavity visually appears spherically remodeled.  The estimated left ventricular ejection fraction is 32%.  Akinesis of mid to distal anterior wall and anterior apical, lateral apical, inferior apical, and septal apical walls.

ECG many months later:

RBBB with well-formed Q-waves in V1-V6, also I, aVL.  Very large old anterolateral MI.

In spite of rapid reperfusion, there was a lot of myocardial damage.

Now, many months later, the Queen correctly diagnoses reperfused OMI and low EF (as well as RBBB and LAFB of course)

Why did I use lidocaine?

See reference below.  Lidocaine is effective at preventing even the first episode of VF during acute MI.  I do not give it in all, however.  I give it when there has already been one or more episodes of VF.  Why not amiodarone?  1) as far as I can tell, there is very little data on amiodarone for this indication  2) amiodarone has beta blockade effects which could be deleterious in a patient with large anterior MI with pulmonary edema and at risk for cardiogenic shock (and she did go into shock. 

Lidocaine does not have negative inotropic or chronotropic effects.

_________________

Lidocaine as prevention of further episodes of Ventricular Fibrillation.

REFERENCE

Prevention of primary ventricular fibrillation in acute myocardial infarction with prophylactic lidocaine

https://www.sciencedirect.com/science/article/abs/pii/S0002914904007799

Primary ventricular fibrillation (VF) during an acute myocardial infarction (AMI) occurs with a high incidence and mortality rate with or without thrombolysis. The incidence varies from 2% to 19% depending on the definition of “primary.” Primary VF in this study refers to fibrillation occurring in the absence of shock or pulmonary edema. Mortality rate, when primary VF occurs, is 2 to 4 times greater than when it does not. 

Lidocaine had been used for the prevention of VF since the 1960s after coronary care units became a standard setting for the treatment of AMI.⁷ 

Smith comment: Yes, believe it or not, when I started out in the mid 1980's, every patient with acute MI was started on a lidocaine drip!  I'll never forget when I ordered such an infusion in 1991 and then my patient started seizing and I looked up and the nurse had hung the lidocaine wide open!

However, the 1996 guidelines of the American Heart Association and the American College of Cardiology (AHA/ACC) for the treatment of AMI considered prophylactic lidocaine a class III indication.⁸ This recommendation was based on 4 meta-analyses that hypothesized that the increased mortality rate among patients who received lidocaine was due to asystole or atrial ventricular or sinoatrial block, although without supporting data.

Prevention of VF has been impeded by the publication of the 1996 recommendations of the American Heart Association and American College of Cardiology against the use of prophylactic lidocaine based on meta-analysis studies implying toxicity. This observational study of 4,254 patients with AMI reports the incidence and mortality rates of primary VF over 32 years. Of the 4,254 patients, 4,150 received prophylactic lidocaine, and 104 patients did not receive prophylactic lidocaine due to the 1996 guidelines, after which administration of prophylactic lidocaine was governed by physician choice. The incidence of primary VF was 0.5% among the 4,150 who received prophylactic lidocaine and 10% among the 104 who did not due to physician choice (p <0.0001). 

After 1996, 104 patients did not receive prophylactic lidocaine at the discretion of their physician after the publication of the 1996 AHA/ACC guidelines.⁸ During this 6-year period, 798 patients with AMI were treated, 13% of whom did not receive prophylactic lidocaine.

Among the 4,150 receiving prophylactic lidocaine, sinoatrial block occurred in 0.5% and complete infranodal atrial ventricular block occurred in 0.2%, all secondary to the site of infarction (concurrent serum lidocaine levels were <4g/ml). Asystole was an agonal rhythm in 4%; these patients had been off lidocaine for 48 hours. Mortality rates were 10.5% in patients without primary VF and 25% in patients with VF (p <0.001). Thus, prophylactic lidocaine markedly decreased the incidence of VF in 4,150 patients with AMI to 0.5% compared with trials before and after thrombolysis (2% to 19%) and with the 104 patients in this study who did not receive prophylactic lidocaine (10%). No

Lidocaine was given as a 75-mg bolus over a 90-second interval followed by a 2-mg/min continuous infusion. A second bolus of 50 mg followed in 5 minutes. The infusion was discontinued after 24 hours if ectopic ventricular beats were not observed. If breakthrough ventricular arrhythmias occurred, additional 50-mg boluses were given every 5 minutes, as needed to a maximum of 325 mg. 

Discussion

Five conclusions have been drawn from the results of this and other studies: (1) the incidence of primary VF before and during the thrombolytic era is unchanged and continues to be excessive; (2) primary VF is unpredictable; (3) when primary VF occurs, it portends poor outcomes in morbidity and mortality rates; (4) lidocaine is effective for preventing primary VF; and (5) lidocaine is not associated with an increased incidence of conduction defects when given properly.

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Another less relevant study

This was a recent study which excluded patients who received anti-dysrhythmics only after ROSC, so not nearly as relevant.  But it does show a strong association of better outcome with lidocaine vs. amiodarone.

Smida T et al.  A retrospective 'target trial emulation' comparing amiodarone and lidocaine for adult out-of-hospital cardiac arrest resuscitation.  DOI: 10.1016/j.resuscitation.2025.110515

https://pubmed.ncbi.nlm.nih.gov/39863130/

Abstract

Objective: The administration of amiodarone or lidocaine is recommended during the resuscitation of out-of-hospital cardiac arrest (OHCA) patients presenting with defibrillation-refractory or recurrent ventricular fibrillation or ventricular tachycardia. Our objective was to use 'target trial emulation' methodology to compare the outcomes of patients who received amiodarone or lidocaine during resuscitation.

Methods: Adult, non-traumatic OHCA patients in the ESO Data Collaborative 2018-2023 datasets who experienced OHCA prior to EMS arrival, presented with a shockable rhythm, and received amiodarone or lidocaine during resuscitation were evaluated for inclusion. We used propensity score matching (PSM) to investigate the association between antiarrhythmic and outcomes. Return of spontaneous circulation (ROSC) was the primary outcome. Secondary outcomes included the number of post-drug defibrillations and survival to hospital discharge.

Results: After application of exclusion criteria, 23,263 patients from 1,707 EMS agencies were eligible for analysis. Prior to PSM, 6,010/20,284 (29.6%) of the patients who received amiodarone and 1,071/2,979 (35.9%) of the patients who received lidocaine achieved prehospital ROSC. Following PSM, lidocaine administration was associated with greater odds of prehospital ROSC (36.0 vs. 30.4%; aOR: 1.29 [1.16, 1.44], n = 2,976 matched pairs). Lidocaine administration was also associated with fewer post-drug defibrillations (median: 2 [0-4] vs. 2 [0-6], mean: 3.3 vs. 3.9, p < 0.01, n = 2,976 pairs), and greater odds of survival to discharge (35.1 vs. 25.7%; OR: 1.54 [1.19, 2.00], n = 538 pairs).

Conclusion: Our 'target trial emulation' suggested that lidocaine was associated with greater odds of prehospital ROSC in comparison to amiodarone when administered during resuscitation from shock refractory or recurrent VF/VT.

  

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MY Comment, by KEN GRAUER, MD (4/9/2025):

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Dr. Smith insightfully noted on seeing the initial ED ECG in today's case, "This is very bad ...".  I focus my comment on expanding as to why this is so.

• For clarity in Figure-1 — I've reproduced and labeled this initial ED ECG.

Findings on the Initial ED ECG:

The main difference between the prehospital ECG (shown above in Dr. Smith's discussion) — and this initial ED ECG in Figure-1 — is the presence of 2 PVCs in the long lead rhythm strip.

• Confession: I remain confused by the literature I have read as to whether (and if so, by how much) risk is increased by the R-on-T phenomenon (ie, in which the R wave of a PVC falls on the so-called "vulnerable period" — that corresponds to the ascending part of the preceding T wave). First observed almost 100 years ago — we now appreciate that while R-on-T PVCs is not a common phenomenon — its occurrence has been shown to precede VT/VFib in a variety of situations, including acute coronary occlusion.
• For clarity — I've labeled the peak of the T wave with GREEN arrows for a number of sinus-conducted beats in the long lead II rhythm strip of Figure-1. Note that the 1st PVC in this rhythm strip clearly occurs on the peak of the preceding T wave ( = the R-on-T phenomenon), thereby increasing potential risk of precipitating VT/VFib in today's patient (In contrast — the 2nd PVC = beat #11, occurs later in the cycle, and is not an R-on-T).

There is Low Voltage:

As per My Comment in the December 13, 2023 post — the recognition of low voltage (either isolated to the limb leads — or in both limb and chest leads) — should prompt consideration of a differential diagnosis.

• Despite RBBB — Today's initial ED ECG clearly shows diminished QRS amplitudes in each of the limb leads (ie, <5 mm in all 6 limb leads) — as well as low voltage in all chest leads except for lead V3.
• Among the causes of Low Voltage that I list in this Dec. 13, 2023 post is myocardial stunning = a transient marked reduction in cardiac contractility, that occurs in response to a major acute insult such as cardiac arrest, after a sustained tachyarrhythmia — or a large acute MI.

Acute LAD Occlusion:

As per Dr. Smith — the patient's initial tracings are diagnostic of acute LAD OMI.

• In addition to sinus rhythm with the 2 PVCs that we see in ECG #2 — there is RBBB (in the form of an rSR' or QR in lead V1 — with predominant positivity of the QRS continuing in leads V2,V3).
• Although difficult to determine if there is an initial Q wave or r wave in lead V1 — a definite small q wave is seen in lead V2, with infarction Q waves continuing in the remaining chest leads. Small q waves are also probably present in leads I,II,aVL.
• Considering the small size of QRS complexes — there is marked ST elevation in leads I,aVL; and in leads V1,V2 — with ST coving in lead V3 — and ST elevation and/or hyperacute T waves in V4,V5,V6. (Remember that the ST-T wave in right-sided leads V1,V2 should be negative with RBBB — and instead the ST-T wave is markedly elevated in these leads).
• There is marked reciprocal ST depression in each of the inferior leads.

2 More Interesting ECG Findings:

• T-QRS-D (Terminal QRS Distortion) is seen in lead V2 (for illustration of T-QRS-D — See My Comment in the November 14, 2019 post).
• Finally — ECG #2 provides a nice example of how PVCs may sometimes show diagnostic ST elevation (seen in lead aVL for beat #5). This is a helpful PEARL to be aware of — since on occasion, acute ST-T wave changes of acute MI may only be seen in PVCs, and not in the rest of the tracing (See My Comment in the October 8, 2018 post).

Impression: Putting the above observations together — the ECG findings that suggest higher risk for this initial ED tracing include:

• The R-on-T phenomenon (for beat #4).
• Diffuse low voltage, which given the clinical setting suggests myocardial stunning.
• An initial ECG with RBBB and ST-T wave abnormalities in virtually all 12 leads, in which there is marked ST elevation and reciprocal ST depression — and in which infarction Q waves are already seen in at least 8 leads. Taken together, these findings suggest an ongoing extensive antero-lateral STEMI. 

Figure-1: The initial ECG obtained in the ED (which is the 2nd tracing in today's case — obtained after the prehospital ECG that Dr. Smith shows above). 

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Reflections on Lidocaine:

Among the first of my academic publications was a manuscript in which I asked the clinical question, "Should Prophylactic Lidocaine be Routinely Used in Patients Suspected of Acute MI?" (J Fla Med Assoc 69:377-379, 1982).

• This was before thrombolytics gained full use in our admitting hospital. As a result — I got to witness first-hand how the incidence of primary VFib appeared to dramatically decrease in our ICU as a result of the new practice at that time of using prophylactic Lidocaine on acute MI patients.
• I later got to trace the evolution of Lidocaine use in the series of ACLS books that I wrote — to which I dedicated a full chapter on Lidocaine pharmacokinetics in my 1st edition (1984) — with emphasis on this drug continued in my next several editions, until the progressive changeover in favor of IV Amiodarone — such that by the time of the last edition I wrote (in 2013), Lidocaine was essentially relegated to a 3rd-line agent for VT/VFib.
• To Emphasize: Even with widespread use of ACLS Guidelines in years past — clinical practice on the emergency use of antiarrhythmic medication is subject to variation, depending on clinician experience and practice, as well as regional use patterns. Add to this the sobering clinical reality of how difficult it is to get objective, controlled, prospective data in the emergency situation of cardiac arrest and life-threatening arrhythmias.

The above said — today's case as described by Dr. Smith illustrates the highly effective use of IV Lidocaine boluses, followed by IV Lidocaine infusion that successfully abolished what otherwise would probably have developed into refractory VFib.

 

Newest Lecture: Replace STEMI/NSTEMI with OMI/NOMI, and AI in the ECG Diagnosis of OMI

 

I gave this Grand Rounds to UC Riverside a couple weeks ago.  

It is my most up to date lecture on OMI NOMI and Use of AI, especially the Queen of Hearts, in the Diagnosis of Occlusion MI.

Replace STEMI/NSTEMI with OMI/NOMI and AI in the ECG Diagnosis of OMI

If you want to find it in the future, you can always find it at the banner above:

Unresponsive and Acidotic: OMI? Acute, subacute, or reperfused? What is the rhythm? Why RV dysfunction? Can CT scan help?

This was written by one of our really fine 3rd year residents, Katie Buerk.

This case was a 69 year old male, brought in by ambulance, after being found unresponsive in bed by family earlier that day. He had last been seen 3-7 days ago. For the medics, he was bradycardic in the 20-30s. They were unable to obtain a blood pressure.

 

On arrival to the ED, he was breathing spontaneously, had faint pulses, and was cool to the touch. His heart rate was in the low 20s and we were also unable to obtain a blood pressure. His temperature was 32.8 C. A quick POCUS which showed significantly reduced ejection fraction and trace B lines. He was given 50 mcg epinephrine with good response in both heart rate and blood pressure.

 

His rhythm on telemetry seemed to be sinus bradycardia vs junctional rhythm. Telemetry also showed possible ST elevation and peaked T waves, so he was given 2 g calcium gluconate empirically.

 

What do you think?

 

There is a regular wide complex rhythm without P waves at a rate of less than 100.  Thus, this could be junctional, but is far more likely to be accelerated idioventricular rhythm (AIVR).  AIVR is often a reperfusion rhythm.  The AIVR has an RBBB configuration; thus, it is originating from the LV.  There is also left axis deviation; thus it is originating in the inferior LV.  The ST segments in AIVR can be analyzed similarly to LBBB (excessively discordant ST Elevation or Depression/concordant STE or STD).  

In this case, there is excessively discordant STD in V2 and concordant STD in V3.  Thus, it is diagnostic of Posterior OMI.  

The AIVR suggests that it is a reperfused posterior OMI, and that is certainly possible, but I think one must assume it is active until proven otherwise.

The PMCardio Queen of Hearts AI Model thinks it is a reperfused OMI:

Case continued:

Initial EKG demonstrated ST depression in V1-V4, concerning for posterior OMI. Cardiology was consulted.

His heart rate had improved to the 80s after epinephrine administration. Subsequently, he became increasingly bradycardic and was noted to have myoclonic movements. At that time, he had no pulses and was in asystole on the monitor. CPR was initiated and he underwent 1 round of ACLS (CPR + 1 mg epi). During CPR, he started moving all four extremities spontaneously. During first pulse check, ROSC was achieved. We proceeded with intubation using ketamine and rocuronium. He was given 2 amps of bicarb empirically prior to intubation due to concern for profound acidosis. Norepinephrine started after intubation due to persistent hypotension.

 

Post intubation we obtained: 

This still shows AIVR with excessively discordant ST depressions in V1-V4.

 

 

His initial labs returned notable for pH 7.01, bicarb 10, and pCO2 41. His lactate was 22. His blood gas demonstrates profound metabolic acidosis, driven by the lactate, with insufficient respiratory compensation. He was noted to have a glucose of 591 and an anion gap of 30. Potassium was 3.7.

 

His potassium was replaced, he was given 300 mg rectal ASA, and an insulin drip ordered. He was hyperventilated at a rate of 28 to provide some compensation for the metabolic acidosis.

 

He was persistently bradycardic, requiring 2 x 50 mcg epinephrine to maintain HR >60. Epinephrine drip was started and norepinephrine was discontinued. He was given vancomycin and cefepime empirically, though we overall had low concern for sepsis as the etiology of his presentation.

 

At this time, there had been multiple discussions with cardiology team, who were debating taking this patient to the cath lab. They felt that the asystolic arrest suggested a different etiology of cardiac arrest. With the severe acidosis and absence of ST elevation, they felt there was more likely to be a non-cardiac etiology of his presentation. Cath lab had not yet been activated, so he was taken to CT for a head and chest/abdomen/pelvis angiogram to rule out other causes of cardiac arrest.

It did not show pulmonary embolism or intra-abdominal pathology, but it did show this:

See the dark area at the bottom of the image?  This is the posterior wall and there is no contract perfusing that posterior wall.  

There is Transmural ischemia of Occlusion MI.

Spectral CT

This spectral CT image really highlights the dense transmural ischemia of the posterior wall.

Here you can also see that there is dense ischemia of the RV.

 

CT showed hypoperfusion of the right ventricular wall and the posterior wall, as well as significant calcifications of the LAD. There were no other radiographic findings to explain his presentation.

 

Third EKG obtained 100 minutes after the first:

Same interpretation: AIVR with excessively discordant ST depression.

 

Initial troponin returned and was 42,747 ng/L.

This very high initial troponin tells us that the infarct is subacute and much, or most, of the damage is already done.

The patient went to the cath lab relatively quickly, at 160 minutes after arrival.  He received an additional 300 mg rectal aspirin and 5000 unit heparin bolus in the ED. 

Coronary Angiography 

 

--First Diagonal occluded

--RCA: 95% distal disease with total occlusion of RPAV with the vessel small and no PCI option to RCA or RPAV RPDA severe diffuse disease, small vessel

 --Ramus: Small vessel with severe diffuse disease

There was no possibility of PCI/stent

 

Echo:

Decreased left ventricular systolic performance mild to moderate.

The estimated left ventricular ejection fraction is 40-45%.

Probable anterior and anterolateral wall hypokinesis.

 

Right ventricular enlargement.

Decreased right ventricular systolic performance.

Assessment:

Cardiology thought this was cardiogenic shock from RV dysfunction.

Smith Comment: the RV was very ischemic on the CT scan and dysfunctional on echo, and this does explain the shock.  But I'm not sure how to explain the RV ischemia based on either ECG or angiogram.  There was no pulmonary embolism.

Case Continued

The post cath course was very complicated with cardiogenic shock and severe dysrhythmias that were eventually controlled, but he did not recover neurologically.

 

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MY Comment, by KEN GRAUER, MD (4/6/2025):

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As per discussion above by Dr. Smith — the patient in today's case did not survive. His case was complicated by failure to respond to intense treatment efforts (as described above by Dr. Smith). 

• I focus my comments on the series of the 3 ECGs that were done in this case, each of which are extremely challenging — yet richly illustrative with important principles for the interpretation of difficult tracings in a critically ill patient.

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In Summary: Today's case regards a 69-year old man, who was found unresponsive in bed by his family. Given that the patient was last seen "3-to-7 days earlier" — it is likely that he was in the critical state noted on arrival in the ED for a prolonged period of time.

• On arrival in the ED — he was breathing spontaneously, but hypothermic, markedly bradycardic and without an obtainable blood pressure. In short — with a very guarded likelihood for a positive outcome.
• Telemetry initially was interpreted as showing sinus bradycardia vs a junctional rhythm. Because of peaked T waves — the patient was appropriately treated empirically with IV Calcium (No rhythm strips of this available).
• Subsequent serum K+ came back = 3.7 mEq/L (which given this patient's profound acidosis — suggests a true serum K+ significantly lower than 3.7).
• The patient was warmed and treated with vasopressor agents — which succeeded in improving his heart rate and blood pressure.

Around this time — an initial ECG was obtained (which I have reproduced in Figure-1).

• Clinician notation regarding interpretation of this tracing was, "Initial EKG demonstrated ST depression in V1-V4, concerning for posterior OMI. Cardiology activated via Pathway B".

QUESTION: 

• How did YOU interpret the initial ECG in today's case? 
•    — Please take another LOOK at this tracing. Do you agree with the clinician notation of their interpretation?

Figure-1: The initial 12-lead ECG obtained in the ED.

MY Thoughts on ECG #1:

To emphasize — clinicians appropriately suspected hyperkalemia, and treated the patient with IV Calcium. But serum K+ was not elevated (ie, The returning lab value = 3.7 mE/L was probably falsely elevated by the severe underlying acidosis). 

• I completely agree that my initial concern on hearing this case and seeing this initial ECG — was that QRS widening and the large, peaked T waves represented hyperkalemia. But this patient was not hyperkalemic!
• I also completely agree that it looks like in addition to RBBB — there is excessive ST depression in anterior leads V2,V3 of Figure-1 — which given the clinical scenario would suggest the possibility of a large, ongoing posterior OMI.
• 
  
•  QUESTION: How did YOU interpret the rhythm?

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MY Thoughts regading the Rhythm in ECG #1:

Although one might easily consider a bifascicular block ( = RBBB/LAHB) — We do not see P waves.

• There is marked baseline artifact in this initial ECG — perhaps the result of tremor or shivering in this hypothermic patient. 
• That said, the overall rhythm in Figure-1 is fairly regular — with obvious QRS widening. And even though marked artifact complicates assessment of atrial activity — I don't see P waves.
• And although the all upright R wave in lead V1 could be consistent with RBBB conduction — and the marked left axis could be consistent with LAHB — the complete lack of a triphasic complex in V1 — and the entirely negative QS complexes in each of the inferior leads are both against this rhythm being supraventricular!
• In addition — the all negative (QS complexes) in leads V4,V5,V6 are virtually never seen in a supraventricular rhythm. And while hyperkalemia may widen the QRS and negate the presence of P waves (with a sinoventricular rhythm) — the serum K+ was not elevated.
• BOTTOM Line: The rhythm in Figure-1 is not supraventricular. Instead — this rhythm is AIVR (Accelerated IdioVentricular Rhythm).

QUESTION:

• Did YOU notice beat "X" ( = beat #6) in Figure-2?

ANSWER:

• Support that the rhythm in today's initial ECG is AIVR is forthcoming from the presence of beat "X" — because: i) This beat occurs earlier-than-expected; — and, ii) Beat #6 is clearly narrower than all other beats in Figure-2, with a much straighter (steeper) S wave descent — which strongly suggests that this beat is supraventricular (in distinction to the other wider 13 beats in this tracing — that therefore must be ventricular).

Learning Points: I have seen the best of cardiologists and emergency clinicians skip assessment of the rhythm (therefore not realizing the rhythm they are looking at is not the usual sinus rhythm). 

• BEST way to avoid overlooking important landmarks of the cardiac rhythm — is to begin your interpretation of every ECG you encounter, by spending 3-4 seconds letting your "educated eye" focus on the long lead II rhythm strip — to ensure that upright P waves precede each QRS with fixed PR interval. If you do not see this — then the rhythm is not sinus.
• The BEST clue to the etiology of a challenging rhythm that for the most part is regular — is to look for the "break" in the rhythm! Beat #6 clearly occurs earlier than any other beat in Figure-2 — which should "catch" your eye, and entice you to look closer.
• P.S.: Even though ECG #1 represents AIVR — I completely agree with the clinician concern that the disproportionate amount of ST depression in leads V2,V3 may represent acute ongoing posterior OMI — so this tracing once again illustrates that on occasion, acute infarction may be suggested by ventricular beats.

Figure-2: I've added an "X" to today's initial ECG. What does this "X" indicate?

The CASE Continues:

Some time later in the management of today's case (ie, after an asystolic episode — from which the patient was successfully resuscitated) — a 2nd ECG was obtained, which I have reproduced in Figure-3.

• Clinician notation regarding interpretation of ECG #2 was, "This ECG continued to demonstrate ST depression in leads V1-thru-V4".

QUESTION: 

• How did YOU interpret this repeat ECG in Figure-3?
•    — Please take another LOOK at this tracing — and compare this ECG #2 with ECG #1 (that was shown in Figure-2). Do you agree with the clinician notation of their interpretation of ECG #2?

Figure-3: Repeat ECG obtained after ROSC from an asystolic episode.

MY Thoughts on ECG #2:

One of the most common oversights that I see repeated by even experienced cardiologists and emergency providers — is the failure to compare lead-by-lead serial tracings.

• Comparison of ECG #1 with ECG #2 should reveal: i) That QRS voltage has dramatically decreased in ECG #2 (especially in the limb leads); ii) That the QRS is clearly more narrow than it was in ECG #1; — and, iii) That there is now predominant positivity of the QRS in leads V4,V5 — whereas the QRS in these leads was entirely negative in ECG #1.

Learning Points: 

• If you did not initially recognize that ECG #1 was not a supraventricular rhythm — the dramatic change in QRS width and appearance that we now see in ECG #2 should have clued you into this.
• The tiny voltage that we now see in this supraventricular rhythm in ECG #2 is a poor prognostic sign — that in today's case probably represents cardiac "stunning" with significantly reduced cardiac output.
• P.S.: I fully acknowledge that I do not know what the rhythm in Figure-3 is. I believe the above points indicate this is a supraventricular rhythm — that manifests QRS widening consistent with RBBB conduction, but without P waves that I can see (with amplitude so greatly reduced that I have no idea if P waves are or are not somehow present).

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The CASE Continues:

Some time later in the management of today's complicated case (ie, after multiple therapeutic interventions) — a Troponin value of ~40,000 apparently prompted the recording of a 3rd ECG (which I have reproduced and labeled in Figure-4).

• I do not see any clinician notation regarding interpretation of ECG #3.

QUESTION: 

• How did YOU interpret this 3rd ECG that I have labeled in Figure-4?
•    — What is the rhythm?
•        — HINT: What are the arrows pointing to? What about beats #13,14,15?

Figure-4: The 3rd ECG — obtained after return of a Troponin ~40,000.

MY Thoughts on ECG #3:

I found it helpful to interpret ECG #3 in the context of knowing this patient was previously in both AIVR (in Figure-2), as well as in a supraventricular rhythm of uncertain etiology (in Figure-3).

• My "eye" was immediately drawn to beats #13,14,15 in the long lead II rhythm strip — as QRS morphology of these beats is clearly different from the previous 12 beats in this tracing.
• Beat #13 clearly occurs earlier-than-expected — so this should clue us in that something else is occurring.
• I believe we are for the first time seeing some P waves (RED arrows in the long lead II). To emphasize that the amplitude of this atrial activity is tiny — but we do see similar signs of atrial activity in simultaneously-recorded leads II,III; and V4,V5,V6 (PINK arrows) — so I believe these are indeed P waves. 
• In further support that these colored arrows are highlighting atrial activity — is that QRS morphology of beat #15 is intermediate between QRS morphology of the first 12 beats — and of beats #13,14.
• Now although the QRS in the long lead II does not look overly wide for the first 12 beats — simultaneously-recorded lead V1 tells us that the QRS for these first 12 beats is actually very wide!
• And — the fact that the first sinus P wave (1st RED arrow in the long lead II rhythm strip) manifests a PR interval that is too short to conduct before beat #2 — tells us that the rhythm for the first 12 beats must be ventricular (ie, AIVR).
• Support that this assumption is correct is forthcoming from the slightly longer PR interval before beat #15, which is a fusion beat between supraventricular beats #13,14 — and the AIVR that we see for the first 12 beats. It is because the PR interval before beat #15 is longer than the PR interval before beat #2 — that there is enough time for this P wave to partially traverse a portion of the ventricles (and thereby produce a fusion beat).
• Note that in contrast to the AIVR that we saw in Figure-2, in which there were completely negative QS complexes for leads V4,V5,V6 — there is a small, but-definitely-present initial R wave before beats #13,14 in leads V4,V5,V6 — whereas there is no initial R wave before beat #15 in leads V5,V6.

Learning Points: 

• As noted — it is all-too-easy to overlook subtleties in a complex rhythm if you do not religiously spend those 3-4 "magic" seconds taking an "educated look" at each beat in the long lead rhythm strip (assessing for atrial activity — and looking for any "break" in regularity of the rhythm).
• Today's patient was in persistent shock. While I do not believe that any additional intervention could have saved this unfortunate patient — persistence of AIVR (especially if unrecognized) may exacerbate persistent hypotension.