Friday, February 12, 2021

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


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.


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:

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:

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:

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.


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:


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 rhythmAm J Cardiol [Internet] 2013;112(9):1379–83. Nov 2013. Available from:

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:

"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.


  1. So, and please forgive the uneducated/inexperienced/hobbyist question here, why does delaying repolarization (whether by blocking IKr or by enhancing plateau INa or both) make electrical cardioversion work more reliably and at lower energy levels? Thanks for the great blog post and for all the work that you guys put into helping folks learn this.

    1. I am not an electrophysiologist, and even if I were, sometimes the macro effects of a drug are not easily explained by the underlying ion shifts. Here is one pure guess: cardioversion works either way, but atrial fib re-establishes itself so instantaneously that you can't notice that there ever was successful conversion. With ibutilide, the prolonged repolarization prevents atrial fib from taking over again.

    2. Thanks for the reply. That's an interesting thought, and it does make sense.

    3. Thanks for the reply. That answer, combining cardioversion's ability to disrupt the AF in the first place with the longer repolarization time and refractory period's ability to "hold off" persistent AF by not presenting any good re-entry circuits to fire up in, makes sense. I hadn't really thought about AF being so persistent that it would just get started again right after a shock. Thanks for the learning experience.


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