Sudden CP and SOB with Inferior ST Elevation and in STE in V1. Is it inferior and RV OMI?

A 60-something had been having chest "soreness" on and off for one month when she presented with sudden chest discomfort and dyspnea starting about an hour prior to arrival.

Here is the triage ECG.

It was texted to me along with concern for inferior ST Elevation and STE in V1, possible inferior and right ventricular OMI:

There is a negative P-wave in lead II.  

You'll notice that the P-wave is abnormal everywhere.  

This is an ectopic atrial rhythm, and it is low in the atrium such that the atrium is depolarized AWAY from lead II and is inverted.  

In any ECG, there might be an atrial repolarization wave, or not.  When there is sinus rhythm, with conduction towards lead II, the atrial repolarization wave is negative, resulting in PR depression and depression of the first part of the ST segment (see schematics below).  This is why we measure the ST segment relative to the QRS onset (PQ junction): both intervals may be depressed by a normal atrial repolarization wave.  

In pericarditis, the atrial repolarization wave is exaggerated; hence, we get excessive PR depression.

In low atrial rhythms, on the other hand, when the atrial impulse is traveling from inferior to superior, the atrial repolarization wave is positive, and can result in a mimic of ST Elevation.  

This is what is happening in inferior leads, but ALSO in V1.

Ken Grauer says this is called the "Emery Phenomenon," but I can't find that in any search.

Here is a magnification of V1:

Here it is with the atrial repolarization wave outlined by a circle:

Case continued:

I responded that this was unlikely to be OMI, that it was probably an atrial repolarization wave, and to get serial EKGs and troponins.

The patient ruled out for MI, and probably had chest wall pain.

See below for more Learning about the Atrial Repolarization wave.

Here are some schematics:

Normal atrial repolarization wave

This schematic is from my book, The ECG in Acute MI

Here is another recent case:

A man in his sixties with chest pain

At this link, there is an extensive discussion by Ken Grauer

Here you can see how the atrial repolarization wave can mimic what appears to be significant ST Depression:

Look at this ST Depression (It's not real)

A 30-something with inferior ST Elevation. OMI? Pericarditis? Normal Variant ST Elevation?

This ECG was texted to me with the information that it was recorded on a 30-something male who presented to the ED with bilateral chest tightness.  

There is some inferior ST elevation.  There is a Q-wave in lead III.  

The ECG is certainly suggestive of inferior OMI.

Or is it Normal ST Elevation?  Or Pericarditis?

The physician had only moderate suspicion due to absence of ST depression in aVL

What do you think?

Meyers interpretation: (all I know is 30-something male with bilateral chest tightness): The lack of hyperacute T waves and lack of STD or TWI in aVL makes this inferior STE not definitive for OMI for me yet. I am not sure between normal variant and possible pericarditis, there are some features of each. I would need more clinical info, repeat ECGs, trops, echo, etc.

Smith: I agreed and thought that it was probably not inferior OMI due to (see references):

1) Absence of ST depression in aVL [99% sensitive for inferior OMI in our study (1, 2)]

2) Absence of T-wave inversion in aVL [also 99% sensitive in our study (1)]

3) Small T-wave in lead III

However, I was not entirely certain because of:

1) Straight ST Segments in all of II, III, and aVF (absence of upward concavity is unusual in normal variant STE and in pericarditis. [Convex ST segments were seen in only 7% of pericarditis in Amal Mattu's study; did not assess straight segments. (2)]

2) Terminal QRS distortion in aVF (I have previously studied terminal QRS distortion in lead V2 and V3 as never occurring when normal variant STE is in leads V2-V4, but have noticed more and more that it is at least a soft sign of OMI in other leads).  See this blog post.  This appears to be what Amal Mattu calls the "RT Checkmark Sign"(2, 3) (I will ask Amal and edit it later if I'm wrong.) 

There is Spodick's sign, which is a downsloping of the baseline T-P segment, in several leads.  This has long been associated with pericarditis but without much evidence until recently.  In the 2020 study by Amal Mattu, referenced below, it occurred in 5% of OMI and 29% of pericarditis).(2)  They did not study normal variant STE; it may be very difficult even in the setting of a study to differentiate normal variant from pericarditis as an outcome measure.

Clinical Course

I recommended a formal bubble contrast echocardiogram, serial troponins, and serial ECGs.

Serial ECGs were unchanged.

The echo was normal.

All Abbott high sensitivity troponin I were below the level of detection.

Epilogue

The pain resolved.  The patient had had some viral symptoms, and for this reason was diagnosed with pericarditis and treated with colchicine.

Comment: I have my doubts about pericarditis here: 

1) Pain was not pleuritic, positional, or sharp, and also was not persistent.  Pressure pain where MI is ruled out is more likely to be esophageal.

2) There is no PR depression

3) The ST elevation is far more in inferior than in lateral leads.

4) The ST/T ratio in V6 is less than 25%

I think that normal variant ST elevation (early repolarization) is more likely.  

Final thoughts and New Study differentiating Pericarditis from OMI

Is it important to differentiate pericarditis from normal variant ST Elevation?  It can be!

Read this important post written by Pendell Meyers when he was a medical student:

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

3 References

2 Studies comparing acute OMI to pericarditis, one by Smith, one by Amal Mattu.  Unfortunately, since it is very difficult to make a definite diagnosis of pericarditis, neither study could even attempt to differentiate pericarditis from normal variant ST Elevation, and it is possible that a large percentage of patients in both studies had normal variant STE and non-cardiac chest pain.

1) Bischof JE, Worrall C, Thompson P, Marti D, Smith SW. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med 2016;34(2):149–54. Available from: http://dx.doi.org/10.1016/j.ajem.2015.09.035

This study showed that ANY ST depression in lead aVL is highly sensitive for inferior OMI, and that zero patients with pericarditis had this feature.

Of the 154 patients with catheterization laboratory diagnosis of inferior STEMI, 154 patients (sensitivity, 100%; CI, 98%-100%) had some degree of ST depression in lead aVL (at least 0.25mm).  In addition, all 154 patients demonstrated T-wave inversion in lead aVL (sensitivity, 100%; CI, 98%-100%).  Of the 49 pericarditis patients, zero (0%) had any ST-segment depression in lead aVL (CI, 0%-7%), and 7 (14%) of 49 (CI, 7%-27%) had T-wave inversion in aVL.  ------Of an additional 272 inferior OMI from a different cohort, 267 (98%) had STD in aVL.   

2) Witting MD, Hu KM, Westreich AA, Tewelde S, Farzad A, Mattu A. Evaluation of Spodick’s Sign and Other Electrocardiographic Findings as Indicators of STEMI and Pericarditis. J Emerg Med 58(4):562-569; April 2020;Available from: http://dx.doi.org/10.1016/j.jemermed.2020.01.017

Note that, in the Witting study, 3/42 pericarditis patients had ST depression.  It is not specified in what lead the ST depression was found.  Bischof et al. found zero STD in aVL.  

3) Lee DH, Walsh B, Smith SW. Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarization. Am J Emerg Med 34(11):2182-2185; November 2016; Available from: http://dx.doi.org/10.1016/j.ajem.2016.08.053

A man in his early 40s with chest pain: STD in V1-V4, but posterior lead are negative

Written by Pendell Meyers

A man in his early 40s with hyperlipidemia and family history of MI presented at 545 AM with acute onset substernal chest pain with nausea and diaphoresis. He reported that the pain began at 8pm last night, and was unclear whether it was constant or intermittent overnight, but his wife convinced him to present to the ED.

His triage ECG was performed at 0550 (no prior for comparison):

What do you think?

There is STD in precordial leads, maximal in V2-V4.  There is zero STE anywhere on the ECG.

It is yet another ECG diagnostic of posterior OMI, with STD present from V1-V5 and maximal in V2-V4. If you have been reading this blog for any length of time, you will have seen countless cases just like this one, and you will see the pattern over and over that these patients are very unlikely to be recognized as OMI and receive emergent reperfusion.

Smith comment on terminology of posterior MI: The posterior wall has been reclassified as part of the lateral wall, but we continue to refer to the portion of the lateral myocardium which which does not face any overlying leads of the standard 12-lead ECG as the posterior wall.(Bayes de Luna)

----Bayes de Luna A, Zareba W. New terminology of the cardiac walls and new classification of Q-wave M infarction based on cardiac magnetic resonance correlations. Ann Noninvasive Electrocardiol [Internet] 2007;12(1):1–4. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17286644

Case continued

This ECG was not recognized as OMI, but rather interpreted as "ST depression." Generalized chest pain workup was ordered.

At around 0730 the initial high sensitivity troponin I returned at >25,000 ng/L (the lab's upper limit of reporting, and consistent with a very large OMI).

The documentation is unclear as to whether the patient was having ongoing pain since triage. In response to the troponin another ECG was obtained at 0744, this time with posterior leads (unclear which leads are intended to be posterior, or where they were placed, but it appears that V4-V6 are likely V7-V9):

Posterior leads.
Ongoing active posterior OMI is evident by persistent STD in V1-V2. There is a hint of STE in V4-V6, but most cardiologists would say that it does not meet posterior leads criteria (0.5mm in just one lead).
Smith comment: Notice also that the ST Depression in V2 is still present. This is important in verifying the validity of the posterior leads.  Sometimes, posterior leads are recorded later after there has been spontaneous reperfusion (not simultaneously).  In order to assess posterior leads in relation to anterior STD, one much ascertain that the STD which prompted the recording of posterior leads is still present.

This is exactly the problem with posterior leads. Those who can see posterior OMI on the standard 12 lead ECG don't need the posterior leads, and those who can't see posterior OMI on the standard 12-leads may be misled by posterior leads because of their very low voltage. In the end, neither provider has their decision making improved by posterior leads. 

We have no cases on this blog in which posterior leads truly helped when the standard 12 leads did not have STD maximal in V1-V4. Even when they do show very small STE in posterior leads that agrees with STD maximal in V1-V4, the smaller voltage on the posterior leads causes the amount of STE to be very very small, so small that humans report that there is no STE at all.

Smith comment: Posterior leads may be beneficial if the standard 12-lead is non-diagnostic.  There is literature to support this (see below literature on posterior leads).  However, that literature always requires at least 1 mm of ST Depression in 2 consecutive precordial leads for the diagnosis of Posterior MI. If that amount does not exist, the ECG is considered nondiagnostic. But in fact many ECGs with minimal ST Depression in V2 and V3 are diagnostic.  This is because V2 and V3 normally have baseline ST Elevation. ANY AMOUNT of ST depression is abnormal in these 2 leads.  Thus many "non-diagnostic" 12-lead ECGs really are diagnostic.  (I often say that "It is not the ECG that is not diagnostic; it is the interpreter.) See example ECG of tiny STD, at the bottom.

Case continued

ED bedside US: "inferolateral wall motion abnormality."

The patient was taken for cath at around 0900 (more than 3 hours after ED arrival). A proximal LCX occlusion (100%, TIMI 0) was found and stented.

The second troponin also resulted at >25,000 ng/L, and no further troponins were ordered.

Here is the ECG after cath:

Resolving STD,  posterior reperfusion T waves, and developing R waves (like posterior Q waves). 

2 days later:

Similar to prior, increasing R waves, and persistent STD (this is consistent with developing posterior aneurysm, or at least "persistent ST deviation after old MI").


See this ECG of a patient with proven inferior-posterior aneurysm, from Smith's book:

Learning Points:

The most important and reproducible finding for posterior OMI on the standard 12-lead ECG is ST depression maximal in V1-V4. We are studying this now, have published this in abstract form, and are currently writing a full manuscript.  We did not record posterior leads for the study, but we did find that ST depression maximal in V1-V4 had 88% sensitivity for OMI.

See these other cases of posterior OMI, many of which were missed, and some of which died:

Cardiologist declines taking patient to the cath lab. Patient dies.

Interventionalist at the Receiving Hospital: "No STEMI, no cath. I do not accept the transfer."

"It isn't a STEMI," so cath lab refusal (again). Were they right?

A middle aged man with ST depression and a narrow window of opportunity

A man in his 50s with 2 hours of chest pressure

A woman in her 70s with bradycardia and hypotension

You have two hours to save this patient's life

A man in his early sixties with palpitations

A female in her 60s with sudden chest pressure

How much time are you willing to wait for OMI to become STEMI (if it ever does)?

Chest pain and Concordant ST Depression in a patient with aortic valve and previously normal angiogram

Right Bundle Branch Block and ST Depression in V1-V3. Is that normal? And a complication.

See this case of posterior MI with tiny ST depression:

This was texted to Dr. Smith with "46 year old with chest pain".  

He texted back: "Posterolateral OMI, activate the cath lab".  

This is diagnostic because V2 and V3 have a tiny amount of ST depression which should not be there, AND also a tiny amount of STD in III and aVF, which is reciprocal to a tiny amount of STE in aVL.  And it all fits together as a posterolateral OMI. Cath showed 100% obtuse marginal occlusion and peak troponin I was 85 ng/mL, a very large OMI.

More Discussion by Smith on Posterior Leads

This is a letter to the editor that is a great review: Wong C-K. Usefulness of leads V7, V8, and V9 ST elevation to diagnose isolated posterior myocardial infarction. Int J Cardiol [Internet] 2011;146(3):467–9. Available from: http://dx.doi.org/10.1016/j.ijcard.2010.10.137

The below 2 studies by Matetzky are the best prior evidence on posterior leads vs. ST Depression in V1-V4.  Studies comparing the 2 lead locations compare 1 mm ST depression in V1-V4 with 0.5 mm STE in posterior leads (actually, only one of the 2 studies specified the amount of ST depression and number of leads).  This ignores the fact that most people have at least 1 mm of STE at baseline in leads V2 and V3.  Thus, ANY ST depression in V2 or V3 is abnormal: to require 1 mm STD in these leads will result in poor sensitivity.

Thus, my practice is the following: if there is STD of any amount that is maximal in V1-V4, especially V2 and V3, I will not let absence of STE in posterior leads dissuade me from the diagnosis of posterior OMI.  One might use posterior leads to detect ST depression in those leads, which will support the unlikely possibility that the ST depression in V1-V4 is due to subendocardial ischemia.(Wong)

Baseline ECG has STE in V2, V3 (Surawicz, Macfarlane):

Surawicz B, Parikh SR. Prevalence of male and female patterns of early ventricular repolarization in the normal ECG of males and females from childhood to old age. J Am Coll Cardiol [Internet] 2002;40(10):1870–6. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12446073.

Macfarlane PW, Browne D, Devine B, et al. Modification of ACC/ESC criteria for acute myocardial infarction. J Electrocardiol [Internet] 2004;37 Suppl:98–103. Available from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15534817

This study by Shah et al. shows that the STD of subendocardial ischemia (in contrast to posterior OMI) is maximal in V5 and V6.

Shah A, Wagner GS, Green CL, et al. Electrocardiographic differentiation of the ST-segment depression of acute myocardial injury due to the left circumflex artery occlusion from that of myocardial ischemia of nonocclusive etiologies. Am J Cardiol [Internet] 1997;80(4):512–3. Available from: https://europepmc.org/article/med/9285669

However, STD in V1-V4 can occasionally be due to subendocardial ischemia.  

Poh K-K, Chia B-L, Tan H-C, Yeo T-C, Lim Y-T. Absence of ST elevation in ECG leads V7, V8, V9 in ischaemia of non-occlusive aetiologies. Int J Cardiol [Internet] 2004;97(3):389–92. Available from: http://dx.doi.org/10.1016/j.ijcard.2003.10.022.  These authors studied 35 patients with ST depression on exercise test. None had posterior ST Elevation and many had posterior ST depression.

Thus, if posterior leads also show ST depression, then subendocardial ischemia is probable!!  This review supports that, if it is subendocardial ischemia, it should manifest as STD in posterior leads in addition to anterior leads.  The subendocardial ischemia is diffuse, with ST depression pointing outward from all walls except for the "base" of the heart, which has no wall, and therefore the combined ST depression vector is towards the apex (V5, V6)

Matetzky-1:

Matetzky S, Friemark D, Feinberg MS. Acute myocardial infarction with isolated ST-segment elevation in posterior chest leads V7-V9: “hidden” ST-segment elevations revealing acute posterior infarction. J Am Coll Cardiol 1999;34(3):748–53.

33 patients with proven posterior OMI.  Admission ECG. ST-segment elevation was present in leads V7 and V9 in 30 patients (91%) and in all 33 patients in lead V8. ST-segment depression (ST2) was noted in leads V1 through V3 in 20 patients (61%), and in 22 patients (67%) in at least two consecutive leads of the anterior chest leads V1 through V6 (Figs. 1A and 2). Prominent R-waves appeared in lead V1 in 3 patients (9%) and in lead V2 in 14 (44%). The method of measurement of STD was not specified.

Matetzky-2:

Matetzky S, Freimark D, Chouraqui P. Significance of ST segment elevations in posterior chest leads (V7-V9) in patients with acute inferior myocardial infarction: application for thrombolytic therapy. J Am Coll Cardiol 1998;31(3):506–11.

46 of 87 inferior MIs with posterior leads had posterior ST elevation of at least 0.5 mm in 2 consecutive leads of V7-V9.  

Results:

Comparison of ST segment elevation in leads V7 to V9 and ST segment depression in leads V1 to V3. Significant ST segment depression in leads V1 to V3 was noted in 52 patients (60%). The occurrence of ST segment depression in the precordial leads agreed only partially with the occurrence of ST segment elevation in the posterior chest leads. In 10 Group A patients (22%), ST segment depression was not present on the admission ECG, and 16 patients (31%) with ST segment depression in leads V1 to V3 had no ST segment elevation in leads V7 to V9 (Fig. 1).

When ST segment elevation in leads V7 to V9 and ST segment depression in leads V1 to V3 at hospital admission were compared with respect to diagnostic accuracy of posterior involvement (at least severe hypokinesia), ST segment elevation in leads V7 to V9 had a similar sensitivity (80% vs. 72%, p 5 0.34) but a higher specificity (84% vs. 57%, p 5 0.02) and test accuracy (82% vs. 66%, p 5 0.01).

In this study, they required at least 1 mm STD in 2 consecutive leads.

Matetzky-2 makes the following claim (with the references below):

During the acute phase of inferior infarction, ECG detection of posterior infarction rested on the appearance of concomitant ST segment depression in leads V1 to V3  (2–7). However, these changes are relatively insensitive and not specific (3,7,9,10) and may represent inferoseptal infarction (11) or, as suggested earlier by a number of other investigators (12–16), anterior ischemia or non–Q wave MI.

Here are the references:

3. Croft CH, Woodward W, Nicod BP, et al. Clinical implications of anterior S-T segment depression in patients with acute inferior myocardial infarction. Am J Cardiol 1982;50:428 –30.

7. Lew AS, Weiss AT, Shah PK, et al. Precordial ST segment depression during acute inferior myocardial infarction: early thallium-201 scintigraphy evidence of adjacent posterolateral or inferoseptal involvement. J Am Coll Cardiol 1985;5:203–9.

9. Mukharji J, Murray S, Lewis SE, et al. Is anterior ST depression with acute transmural inferior infarction due to posterior infarction? A vectorcardiographic and scintigraphic study. J Am Coll Cardiol 1984;4:28 –34.

10. Cohen M, Blanke H, Karsh KR, Holt J, Rentrop P. Implications of precordial ST segment depression during acute inferior myocardial infarction: arteriographic and ventriculographic correlations during the acute phase. Br Heart J 1984;52:497–501.

What to do when Atrial Fib with RVR will not Electrically Cardiovert. And how do you measure the QT in Atrial Fib?

This middle-aged male patient has a history of paroxysmal atrial fibrillation, and on this day of admission had sudden onset of palpitations and he knew it was atrial fib again.  He presented only a few hours after onset.  He complained of severe chest pressure.  Here is his ED ECG:

Atrial Fibrillation with very rapid ventricular rate which varied from 130-170.  

There is some moderate ST depression in V4-V6 which is likely due to ischemia.

What is the QT interval?  Is the computer's measurement correct?  

How do you correct the QT in atrial fib?  

And does it matter?

Because he was complaining of severe chest pressure, immediate cardioversion was indicated.  He was given etomidate 10 mg and, after sedation, cardioverted with 200 Joules biphasic.  There was no response.  So he was given 2 g of Magnesium.  Then he was cardioverted again.  Again there was no response.

What would you do?  Below is my management approach, and what was done in this case:

I give 1 mg of ibutilide IV over 10 minutes, then cardiovert again.  Ibutilide blocks the potassium rectifier channel, prolonging repolarization, and therefore prolonging the QT interval and helping to convert atrial fib.  In the 2 studies cited below, if electrical cardioversion did not work, then repeating the electrical cardioversion after giving 1 mg of ibutilide resulted in sinus rhythm in 100% of cases.  

Contraindications are : QTc (Bazett) > 480 ms, Ejection fraction < 30%.  These are only absolute contraindications if the patient is not requiring emergent cardioversion due to severe ischemia, pulmonary edema, or shock.

Other relative contraindications are K+ level ﹤ 3.5, mEq/L, QT﹥440 ms, and presence of other QT prolonging medications.

Before using ibutilide, it is important to read the New England Journal abstract at the bottom of the page, and my associated notes on the study.  

But how do you calculate the corrected QT in atrial fibrillation?  

The formulas are given below

[the last (Hodges) is expressed in two equivalent formulas, one with the heart rate, as is typically seen, and one with the RR interval as the others are presented].

RR is always the PRECEDING RR interval, meaning that the QT interval of one complex is modified by the RR interval of the preceding complex.

RR interval is in seconds, not milliseconds!

·       Bazett’s formula: QTc = QT / √RR  (QT divided by square root of RR interval)

·       Frederica’s formula: QTc = QT / √3(RR)  (QT divided by cube root of RR interval)

·       Framingham formula: QTc=QT+0.154*(1–RR)

·       Hodges formula: QTc = QT + 1.75*(HR−60)    
                                         = QT + 105/RR − 105

What is the QT in this ECG?

After reading the below 3 articles at the far bottom, my takeaway is this for rapid estimation in the ED:

1. look at lead II across the bottom

2. Find the complex with the longest preceding RR interval

3. Rule of thumb: In this complex, if the QT ﹤ half of the preceding RR interval, it is safe

4. If it is ﹥ half the RR, then measure all it, using the preceding RR interval and the Fridericia formula.

On this ECG: 

1) the first RR interval in lead II is the longest 

2) the QT following this is 310 ms. (compare with computer at 286 - not so different)

3) that preceding RR interval is 500 ms, equivalent to a heart rate of 120.

4) Calculate Fridericia QTc using this calculator

= 391 ms 

Case continued:

We found that the patient's QTc was not too long.  We did a bedside ultrasound that showed excellent function.  The K level was normal.

So we gave 1 mg IV ibutilide and cardioverted again, successfully.  See repeat ECG below.

The patient was discharged on a beta blocker after his QTc normalized.  His CHAD2VASC score was 2 and HAS BLED score was 1, so he was started on Rivaroxaban. 

See also a slide at the bottom that shows comparative data for various antidysrhythics for conversion of atrial fib.

The QTc is normal even after receiving ibutilide, which often would prolong it significantly

References

Use of Ibutilide to Facilitate Electrical Cardioversion of Atrial Fibrillation

Ibutilide, like other class III antiarrhythmic drugs, blocks delayed rectifier potassium current.  Vaughan Williams classification

Facilitating Transthoracic Cardioversion of Atrial Fibrillation with Ibutilide Pretreatment. Hakan Oral, New Engl J Med June 17, 1999; 340(24):1849-54. 

https://www.nejm.org/doi/full/10.1056/NEJM199906173402401

Abstract 

Background. Atrial fibrillation cannot always be converted to sinus rhythm by transthoracic electrical cardioversion. We examined the effect of ibutilide, a class III antiarrhythmic agent, on the energy requirement for atrial defibrillation and assessed the value of this agent in facilitating cardioversion in patients with atrial fibrillation that is resistant to conventional transthoracic cardioversion. 

Methods. One hundred patients who had had atrial fibrillation for a mean (±SD) of 117±201 days were randomly assigned to undergo transthoracic cardioversion with or without pretreatment with 1 mg of ibutilide. We designed a step-up protocol in which shocks at 50, 100, 200, 300, and 360 J were used for transthoracic cardioversion. If transthoracic cardioversion was unsuccessful in a patient who had nreceived ibutilide pretreatment, ibutilide was administered and transthoracic cardioversion attempted again. 

Results. Conversion to sinus rhythm occurred in 36 of 50 patients who had not received ibutilide (72 percent) and in all 50 patients who had received ibutilide (100 percent, P<0.001). In all 14 patients in whom transthoracic cardioversion alone failed, sinus rhythm was restored when cardioversion was attempted again after the administration of ibutilide. Pretreatment with ibutilide was associated with a reduction in the mean energy required for defibrillation (166±80 J, as compared with 228±93 J without pretreatment; P<0.001). Sustained polymorphic ventricular tachycardia occurred in 2 of the 64 patients who received ibutilide (3 percent), both of whom had an ejection fraction of 0.20 or less. The rates of freedom from atrial fibrillation after six months of follow-up were similar in the two randomized groups.

Conclusions. The efficacy of transthoracic cardioversion for converting atrial fibrillation to sinus rhythm was enhanced by pretreatment with ibutilide. However, use of this drug should be avoided in patients with very low ejection fractions. (N Engl J Med 1999;340:1849-54.) 

Important aspects to this study:

They included patients who had had a fib for less than 48 hours.

They excluded patients with a fib for longer than 48 hours unless they proved, by TE echo, to not have an atrial clot OR unless they anticoagulated them for 3 weeks first.

Therefore, our patients who have been in afib < 48 hours, or who have been on anticoagulants, apply.

They excluded anyone with a QTc > 480ms because ibutilide can lead to torsade.  As far as I can tell, they did not state their correction formula or how they measured the raw QT and in what lead.

The dose was 1mg over 10 minutes.

2 of 64 patients who received ibutilide went into torsades de pointes. Both had low ejection fractions, <20% and both were easily controlled. 

The authors recommend not using ibutilide for this indication in stable patients if the EF is < 30%. However, it is still an option in unstable patients. 

Ibutilide increased the QTc significantly (432+/-37 before vs. 482+/-49 afterward).

Although the point is not discussed in the paper, I would not send such a patient home unless the QT is corrected, by time or magnesium.

_____________________

This emergency department study also had a 100% conversion rate with the combination of ibutilide and electrical cardioversion.

Domanovits H, Schillinger M, Thoennissen J, et al. Termination of recent-onset atrial fibrillation/flutter in the emergency department: a sequential approach with intravenous ibutilide and external electrical cardioversion. Resuscitation [Internet] 2000;45(3):181–7. Available from: http://dx.doi.org/10.1016/s0300-9572(00)00180-5
__________________________

The 2 studies below used ibutilide alone, without electricity, and had substantially lower conversion rates.

Vinson DR, Lugovskaya N, Warton EM, et al. Ibutilide Effectiveness and Safety in the Cardioversion of Atrial Fibrillation and Flutter in the Community Emergency Department. Ann Emerg Med [Internet] 2018;71(1):96–108.e2. Available from: http://dx.doi.org/10.1016/j.annemergmed.2017.07.481

In this ED study from Annals of Emergency Medicine, they used ibutilide alone, not in combination with electrical cardioversion, and success was much lower.

____________________________

Efficacy and Safety of Repeated Intravenous Doses of Ibutilide for Rapid Conversion of Atrial Flutter or Fibrillation.  Stambler BS et al. Circulation 1996;94(7):1613–21. Available from: https://doi.org/10.1161/01.CIR.94.7.1613

Using Ibutilide Alone, without electricity, is effective, but not nearly as effective as ibutilide + electricity.  This study, using a 2nd 1 mg infusion if necessary, had a 30% conversion for fib and 60% for flutter, with efficacy better for those with a shorter duration of atrial fib.  Conversion rate for placebo was 2%.  Thus, a second infusion of 1 mg may be safely given.  They excluded patients with a QTc over 440 ms.  The infusion was stopped if the QTc went over 600 ms.  As with the previous study, the method of QT measurement and the correction formula were not specified.

ECG Effects of Ibutilide

The QT and QTc intervals were significantly (P<.0001) prolonged from baseline in the ibutilide-treated patients. From baseline QT and QTc intervals of 347±45 and 414±31 ms, respectively, the 1.0 mg/0.5 mg ibutilide dose prolonged these intervals by 73±75 and 62±66 ms to 420±78 and 477±62 ms, respectively, at minute 30 after the start of the infusion. From baseline QT and QTc intervals of 343±51 and 416±31 ms, the 1.0 mg/1.0 mg ibutilide dose prolonged these intervals by 71±82 and 63±68 ms to 414±92 and 478±70 ms at minute 30. These changes in QT and QTc were significantly greater (P<.0001) than the changes in the placebo group (5±29 and 9±34 ms). The QRS duration was not altered significantly across dose groups from baseline to minute 30.

Proarrhythmia

Polymorphic ventricular tachycardia developed in 15 of 180 ibutilide-treated patients (8.3%) and in no placebo-treated patients. Among the ibutilide-treated patients, 7 patients also developed episodes of nonsustained monomorphic VT. In 3 patients (1.7%), polymorphic VT was sustained and required DC cardioversion, and in 12 patients (6.7%), polymorphic VT was nonsustained and resolved spontaneously or with discontinuation of ibutilide (Table 3). Six patients with polymorphic VT were given magnesium sulfate (2 to 4 g IV) to prevent recurrences. In all patients, the first episode of polymorphic VT occurred either during or shortly after the end of the last ibutilide infusion. Eleven of 15 episodes (73%) occurred during or within 10 minutes of the first 1.0 mg ibutilide dose, and 4 episodes occurred in 144 patients (2.8%) who received the second 0.5 or 1.0 mg ibutilide dose.

Measurement of corrected QT in Atrial Fibrillation 

Dash A, Torado C, Paw N, Fan D, Pezeshkian N, Srivatsa U. QT correction in atrial fibrillation - Measurement revisited. J Electrocardiol [Internet] 2019;56:70–6. Available from: https://www.sciencedirect.com/science/article/pii/S0022073619302237

Abstract

Background: QT interval measured in the electrocardiogram (ECG) varies with RR interval challenging the calculation of corrected QT (QTc) in Atrial fibrillation (AF).

Objectives: To identify the ideal Lead, number of complexes and the formula to measure QTc that correlates best between AF and sinus rhythm (SR).

Procedure: We identified ECGs from patients with AF before and after conversion to SR. After excluding patients on drugs and clinical conditions that prolong QT interval, QTc was calculated from all the leads using the formulae: Bazett (BF), Fridericia (FF), Framingham(FrF), Hodges (HF), Saige (SF) and Rautaharju (RF) during AF and SR. After identifying the lead with best linear correlation, we calculated QTc following the longest RR, multiple QRS complexes and average automated RR interval during AF and compared to SR.

Findings: In 52 patients (male 69%, age 63 ± 9 yrs), QTc measured from Lead II correlated best with SR in majority of the formulae. QTc was consistently shorter with linear formulae. While BF overestimated QTc, FF was optimal comparing AF vs SR (416 ± 33 vs 411 ± 38 ms, ns) calculated from single, multiple or average automated RR interval. Bland Altman analysis of the average automated QTc versus the delta of individual automated QTcs shows the least variation in the QTc calculated by FF.

Conclusions: BF in commercial software is not ideal for measurement of QTc in AF, Fridericia Formula in lead II from the average RR from automated ECG measurement maybe utilized for the calculation of QTc.

___________________

Musat DL, Adhaduk M, Preminger MW, et al. Correlation of QT interval correction methods during atrial fibrillation and sinus rhythm. Am J Cardiol [Internet] 2013;112(9):1379–83. Nov 2013. Available from: http://dx.doi.org/10.1016/j.amjcard.2013.06.027.

These authors compared Bazett, Fridericia, and Framingham QT measurements on 54 patients with atrial fibrillation.  They measured QTc while patients were in Afib and then again after conversion, when they were in sinus rhythm.  They measured the lead with the longest QT, and measured all complexes during a 10 second time period (one 12-lead ECG), then averaged them. The RR interval was also a 10 second average.   They found that Bazett’s formula overestimated QTc in Afib while Fridericia’s formula was the most accurate.  They do not answer the vexing question of how to  quickly measure and correct for QT; the traditional answer is to correct the QT interval by using the preceding RR interval.   

__________

Tooley J, Ouyang D, Hadley D, et al. Comparison of QT Interval Measurement Methods and Correction Formulas in Atrial Fibrillation. Am J Cardiol [Internet] 2019;123(11):1822–7. Available from: http://dx.doi.org/10.1016/j.amjcard.2019.02.057

"Determining QT from a 5-beat average resulted in a QTc that was 19.0 ms higher (interquartile range 0.30 to 43.7) in AF than SR. After correcting for residual effect of HR on QTc, there was not a significant difference between QTc in AF to SR. In conclusion, measuring QT over multiple beats produces a more accurate measurement of QT in AF. Differences between QTc in AF and SR exist because of imperfect HR correction formula and not due to an independent effect of AF."

This is a slide you can see at minute 43:50 of my 2014 lecture on SVTs, including atrial fibrillation.

http://hqmeded-ecg.blogspot.com/2014/09/one-hour-lecture-supraventricular.html

A 50-something with cocaine chest pain and ST Elevation in V1 - V3

This case was expertly managed by Aaron Robinson (https://twitter.com/ARobinsonMD), one of our Hennepin EMS fellows, and by Danika Evans, a superb Hennepin G3 resident. 

This ECG was texted to me with the words "Cocaine" and "Chest pain."

There were no previous ECGs available for review.

There are QS-waves in V1 and V2.  There is ST Elevation in V1-V3, with large T-waves.  This looks scary and looks a lot like an LAD OMI.  However, there is also T-wave inversion in V5 and V6.  

There is also high voltage.  

I don't think this meets any of the many different voltage criteria for LVH, all of which are relatively insensitive and nonspecific, but it does look like LVH because of:

 1) the relatively high voltage, especially in V5 and V6 

2) slight ST depression with T-wave inversion in V5 and V6. 

3) STE in V1 and V2 primarily

4) QS-waves in V1 and V2 (QR-waves would be unusual in LVH)

Such morphology is usually LVH and not OMI.

STE in V1 and V2 may be septal STEMI, but usually not with T-wave inversion in V5 and V6 (see many examples below)

He also sent this one, recorded 41 minutes later: 

There is a slight change in leads V3 and V4, but probably due to lead placement, with these 2 leads slightly farther around the chest on ECG 2 than ECG 1.

I wrote: "Wow. That is a really tough one. V2 and V3 look exactly like anterior LAD OMI. But then V5 and V6 make it look like it is LVH."

"What does the echo look like? An anterior wall motion abnormality should be pretty obvious. So if you do not see one, then this is probably an LVH mimic. It would not be a bad idea to do a pathway B"

But he beat me to it and was already in the process of obtaining a bedside echo. 

Here is one representative parasternal short axis view of the LV:  

The anterior wall is at the top, closest to the probe

This clearly shows excellent anterior wall motion and very thick LV wall.

Therefore, it is very unlikely that V1 and V2 represent anterior OMI.

This ECG was recorded at 82 minutes:

No Evolution; this supports absence of OMI

Troponin I (hs) were: 0 hour: 7 ng/L, 2 hour: 9 ng/L, 4 hour: 8 ng/L (Rules out Acute MI)

Thus, the chest pain was non-ischemic.

Formal echo the next day showed:

CONCLUSIONS -- SUMMARY

 

Moderately increased left ventricular wall thickness.

Normal left ventricular size and systolic function with an estimated EF of 68%.

No regional wall motion abnormality.

Dynamic intracavitary gradient, peak 34 mmHg at rest and mmHg with Valsalva.

Indeterminate left-sided diastolic parameters.

  

The hypertrophy is somewhat more prominent at the apex. This, in conjunction with the dynamic intracavitary gradient, raises concern for hypertrophic cardiomyopathy. 

Learning Points

Right precordial ST Elevation: Septal STEMI vs. LVH:

Here is a typical case of massive LVH, with secondary ST Elevation in V1 and V2.  Note that there is a QS-wave in V1, STE is in V1 and V2, there is ST depression in V5 and V6, with negative T-waves in V5 and V6.

Notice the T-waves are negative in V5 and V6

Examples of Septal STEMI. Note that, even though there is ST depression in V5 and V6 (reciprocal to the STE in right precordial leads), there is no T-wave inversion in V5-V6!)

A man in his 50s with "gas pain"

Developed into this:

A woman in her 70s with chest pain

Chest Pain and RBBB. What do you think?

Chest pain in a patient with previous inferior STEMI. Scrutinize both the ECG and the history!

Septal STEMI with lateral ST depression, then has collateral reperfusion resulting in Wellens' waves

Septal STEMI with ST elevation in V1 and V4R, and reciprocal ST depression in V5, V6

This is a Septal OMI.  

Full LAD Occlusion with STE in V1-V3, STD in V5 and V6, but does not have the elements of LVH described above.

This was missed, ruled in by serial troponins, found to have LAD OMI next day.  Peak troponin I of 80 ng/mL (very large MI)