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.

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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.