ECG Blog #37 — AFib and Lead Reversal?

I discovered the 12-lead ECG shown in Figure 1 in “the files”. It was obtained from a patient who was hemodynamically stable despite the rapid rate. Unfortunately – I have no follow-up. Three diagnoses should come to mind on review of this tracing. The first two diagnoses should be thought of within seconds; the 3rd on some reflection. 

• What 2 diagnoses should immediately come to mind? 
• What is the 3rd diagnosis that should become apparent on reflection of QRS morphology in the various leads? 
• Imagine a scenario of a young adult presenting with this 12-lead ECG and having palpitations, but being otherwise stable. How might you proceed clinically? 

Figure 1 – 12-lead ECG from a young adult who is stable despite the rapid rate. What 3 diagnoses should be considered? 

INTERPRETATION: The rhythm is exceeding rapid and irregular. No P waves are seen. The QRS is wide. The rhythm therefore qualifies as an irregular WCT (Wide-Complex Tachycardia). As discussed in detail in ECG Blog #36 – the underlying rhythm of this irregular WCT without P waves is AFib (Atrial Fibrillation) – which is the 1st diagnosis to be made that we allude to. Additional points we highlight about this rhythm include the following: 

• Although VT (Ventricular Tachycardia) may at times be slightly irregular – We exclude VT from our differential diagnosis of Figure 1 because of the marked persistent irregularity seen on this tracing (with some R-R intervals being almost twice the duration of others). 
• The rate of the AFib seen in Figure 1 is much faster than usual – attaining 250-to-300/minute in various parts of the tracing (in which the R-R interval appears to be no more than 1 large box in duration). This is clearly too fast for conduction to be proceeding down the normal AV nodal pathway. Therefore – there must be an AP (Accessory Pathway) that allows AFib impulses to bypass the AV node. The finding of AFib with QRS widening and an exceedingly rapid rate (>220/minute in parts of the tracing) is virtually diagnostic of WPW (Wolff-Parksinson-White) syndrome, which is the 2nd diagnosis to be made from Figure 1. 
• The importance of distinguishing the common form of rapid AFib (with rates in the 120-180/minute range) from excessively rapid AFib with WPW – lies with recommendations for treatment. The usual AV nodal blocking drugs recommended for controlling the ventricular response of rapid AFib are contraindicated when AFib occurs in association with WPW. Thus – verapamil, diltiazem, digoxin (and possibly β-blockers) may all potentially accelerate forward (antidromic) conduction down the AP, thereby further increasing the already excessively rapid rate, thereby predisposing to deterioration to ventricular fibrillation. 
• Recommended treatment of very rapid AFib with WPW includes procainamide, amiodarone, and ibutilide (See references below for additional discussion of treatment options). Immediate cardioversion is indicated if hemodynamic decompensation occurs at any time during the treatment process. 

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About the 3rd Diagnosis in Figure 1: Careful review of QRS morphology in Figure 1 should suggest a 3rd diagnosis = lead misplacement! Overall QRS appearance simply does not make sense … 

• Five of the 6 limb leads are decidedly negative – yet the QRS deflection in lead aVF is positive. This can’t be … 
• R wave progression in the 6 precordial leads is totally erratic – going from entirely positive (in V1) – to entirely negative (by V2) back to positive and then again negative by the time one reaches lead V6. Again – this can’t be … 
• Steurer, Brugada et al have provided us with 3 clues to help rule out AP conduction with WPW (See References below). These clues are: i) A negative QRS in V4-to-V6 (implies an apical origin of the tachycardia – and since all accessory pathways enter the base of the ventricles, AP conduction is excluded); ii) A QR complex in any of the 5 leads, V2-to-V6; and iii) the presence of more QRS complexes than P waves (since in any form of preexcited tachycardia the atria are involved in every beat). In Figure 1 – a QR is seen in lead V3; and a QS is seen in lead V6 – yet we know that Figure 1 has to represent AP conduction during AFib in a patient with WPW (since there is no other logical explanation for the excessively rapid rate). The reason for inconsistency with the Steurer/Brugada criteria has to be erroneous lead placement. 

IMPRESSION: Despite my lack of follow-up on this case – this 12-lead ECG is highly instructive on a number of important issues including: i) Presumed diagnosis of WPW from the finding of excessively rapid AFib with QRS widening (with associated clinical implications for treatment); ii) Awareness of Steurer/Brugada criteria for ruling out AP conduction in WCT rhythms; and iii) Need for vigilance in assessing QRS morphology for picking up less commonly recognized forms of lead misplacement (the ECG technician in this case was doubtlessly more scared than the patient by the excessively rapid rate – ergo, my explanation for this bizarre manifestation of leads that simply do not make anatomic sense). 

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BONUS: For Those Who Do Not Believe All They Read – There is a reason why QRS morphology shown in Figure 1 made NO sense – namely, that the tracing was inexplicably rotated by 180 degrees. Figure 2 now shows correct lead placement after rotation of the tracing by 180 degrees. Note a much more plausible QRS morphology with now easy-to-decipher delta waves.

Figure 2 – Correct orientation for the 12-lead ECG in this case (after rotating Figure 1 by 180 degrees). The characteristic picture of very rapid AFib with WPW (and obvious delta waves) is now apparent.

BOTTOM LINE: The original tracing in Figure 1 represents one more way in which leads may be mislabeled. While recognition of very rapid AFib with WPW was possible when leads were mislabeled (as discussed above) – the ECG picture makes much more sense with correct orientation of all 12 leads as shown in Figure 2. 

• MORAL of the Story – Not all tracings "in the files" are correctly labeled.
• Special Credit – to Jason Roediger, CCT, CRAT (from Richmond, VA) for not being fooled for a second by the ECG in Figure 1.

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REFERENCES: 

• Steurer G, Gursoy S, Brugada P, et al: The Differential Diagnosis on the ECG between VT and Preexcited Tachycardia. Clin Cardiol 17:306-308, 1994. 
• Marriott HJ: Emergency Electrocardiography (Trinity Press, Naples, FL, 1997 – pg 71). 

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• See ECG Blog #18 and Blog #36 – and Section 12.0 (from ACLS-2013-ePub) on Management of Very Rapid AFib with WPW. 
• See ECG Blog #76 – for Review of How to Localize the AP (Accessory Pathway) from the surface ECG.