Challenging Rhythms in an 80-something Man

 

Written by Magnus Nossen and Ken Grauer

You are shown the ECG that appears in Figure-1 — obtained from an 80-something year old man. Other than sinus rhythm — What else do you see in this tracing?

• Note: The ECG in Figure-1 was initially recorded using the Cabrera Format (See Comment by Dr. Grauer at the bottom of the page in the October 26, 2020 post for review of the Cabrera Format). The image was recorded with a paper speed of 50mm/sec; below it was been "compressed" to 25mm/sec.

Figure-1: The initial ECG in today's case.

Figure-1: While at first glance the rhythm in Figure-1 might be mistaken for sinus tachycardia in fact, this is not the rhythm. Instead there is 2:1 atrial activity that is best seen in lead V1 (See Figure-2).

 

There are several clues that suggest today's initial rhythm is not sinus in origin.

• The rate of ~100/minute would be fast for an 80-something year old adult — unless something acute is going on (infection, shock etc.). 
• If the upright deflection in lead V1 was a single sinus P wave — then the PR interval would be longer-than-expected for this to be sinus tachycardia.
• Whenever the PR interval looks longer-than-it-should-be for a supraventricular rhythm — there may be another P wave hidden within the QRS complex! (This is the "Bix Rule" — See Pearl #1 in Dr. Grauer Comment in the July 16, 2024 post).
• There is no distinct, upright P wave in lead II — as there should be if the rhythm was sinus. Also, sinus P waves are usually not all positive in lead V1 like in today's ECG (unless there is RAA).
• The presence of a pseudo-r' deflection in lead V1 is common as a "hiding place" for either extra or retrograde P waves.

Grauer: My “Go To” Leads when looking for less obvious atrial activity in a supraventricular rhythm — are leads II and V1 (as the best leads to look at first) — but also leads III, aVF and aVR, each of which may be surprisingly helpful for finding retrograde P waves or flutter waves.

Interpretation: The rhythm in the initial ECG in today's case is supraventricular with 2:1 AV conduction. The ventricular rate is ~100/minute. Since there are 2 P waves within each R-R interval, the atrial rate must be twice the ventricular rate, or ~200/minute. The differential diagnosis is between ATach (Atrial Tachycardia) vs AFlutter (Atrial Flutter). Although a subtle "sawtooth" pattern may be present in the inferior leads — an atrial rate of ~200/minute would be slow for untreated AFlutter.

Figure-2: Colored arrows highlight flutter waves, with 2:1 AV conduction.

Patient history: It turns out that today’s patient is an 80-something year old man with longstanding hypertension and paroxysmal atrial fibrillation. The AFib had been well controlled on Flecainide for many years. He presents now with an episode of syncope at rest. 

On questioning the patient reported intermittent palpitations in recent months. The initial ECG was wrongly interpreted as showing sinus rhythm. He was admitted to the hospital with a suspected diagnosis of Sick Sinus Syndrome (Paroxysmal AFib accounting for palpitations — and bradycardic spells accounting for the syncope). 

Nossen: I initially saw the ECG in Figure-1 — knowing only that the patient was an elderly man on Flecainide, who presented to the ED for syncope. I was told that an episode of a WCT (Wide Complex Tachycardia) was captured on telemetry. However, having noticed the 2:1 atrial activity in lead V1 — I was not at all convinced that the episode was VT.

In Figure-3 — is the wide tachycardia rhythm that was captured on telemetry:  

Figure-3: Rhythm captured on telemetry. (Recording speed = 25 mm/second.)

Figure-3: The ECG in Figure-3 shows a regular WCT with a heart rate of 180/minute. There is overlap of the 5 chest leads that we see, and we have lost most of the lead V6 recording. Within approximately 3 minutes telemetry recorded spontaneous conversion of the rhythm, as shown in Figure-4 below.

Figure-4: Spontaneous conversion of the WCT in Figure-3. (Recording speed = 25 mm/second.)

What do you make of the clinical scenario in today's case up to now?

• Do you agree that the WCT rhythm is VT?
•     What other possible explanations might there be?
•         Will you recommend ICD placement for this patient?

Nossen: I was suspicious that the underlying rhythm was AFlutter throughout the above clinical scenario. Use of Flecainide could account for the slower-than-expected flutter rate of ~200/minute that we saw in Figure-2. And, perhaps once the flutter rate dropped below 200/minute — 1:1 AV conduction of AFlutter became possible (with the marked increase in QRS widening that we see in Figure-4 being attributed to Flecainide toxicity). Therefore — No VT, but instead 1:1 AFlutter with Flecainide-induced QRS widening!

• Nossen Note: I went back as best I could, trying to correlate Flecainide dosing with the atrial rate of flutter during the patient's hospital stay. Prior to admission — the patient was on 150 mg bid of Flecainide (300 mg/day), which is a high dose of drug. On this dose — the atrial rate varied between ~180-200/minute during the 24 hours after admission. Ultimately, Flecainide was withdrawn — with resultant increase in the flutter rate to ~250-300/minute.

To further explore the possibility of underlying AFlutter persisting throughout this patient's hospital admission — I reviewed all telemetry recordings, 2 of which are shown below in Figure-5 and Figure-6. 

Figure-5: Additional telemetry tracing (atrial activity labeled).

Figure-6: Additional telemetry tracing. RED arrows highlight 2:1 AFlutter (with peaking of each T wave in lead V1 resulting from hidden flutter waves).

Nossen: Figures-5 and -6 clearly show an underlying atrial tachyarrhythmia at ~180/minute. I went through all the telemetry recordings and found that the patient had a number of short WCT episodes. Before each of these WCT episodes — the atrial rate decreased. Whenever the atrial rate remained over 190/minute — there was always 2:1 or 3:2 conduction of atrial flutter. 

Why is the R-R interval sometimes irregular in parts of Figure-5?

Grauer: It is common for AFlutter to manifest periods of group beating due to dual-level Wenckebach conduction out of the AV node. Despite consecutively non-conducted flutter waves — this is not a conduction "block" — but rather an expected reduced conduction by an AV node presented with too many rapid flutter impulses to be able to conduct them all.

The intricate relationships prevalent with dual-level AV conduction are easiest to appreciate by means of a laddergram — which I show in Figure-7. Many combinations of Wenckebach conduction out of 2 or more levels within the AV node are possible (ie, the relationships illustrated in my Figure-7 laddergram do not represent the only possibility).

The "good news" — is that Wenckebach conduction out of the AV node is usually not a fixed (ie, pathologic) conduction defect. Instead — the chances are excellent that normal AV conduction will resume once sinus rhythm is restored!

Figure-7: Proposed laddergram for the lead V1 rhythm strip in Figure-5.

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Regarding Flecainide: Flecainide toxicity is a relatively uncommon, but extremely important condition to recognize. Among the potential manifestations of Flecainide Toxicity are the following:

• QRS widening, which may be marked, often with bizarre QRS morphology that does not resemble any known form of conduction block.  
• Slowing of conduction in atrial and ventricular tissue, as well as in the His-Purkinje system.
• VT as a proarrhythmic effect. 
• Facilitating conversion of AFib to AFlutter as another proarrhythmic effect. 
• Because of Flecainide’s adverse effect on conduction through atrial, ventricular and His-Purkinje tissue — the usual diagnostic and therapeutic effects of antiarrhythmic agents may be much less effective (if they are effective at all). This probably accounts for the refractoriness of Flecainide-induced proarrhythmia to antiarrhythmic treatment.

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Conclusion: The WCT rhythm in today's case was the result of intermittent 1:1 AV conduction of AFlutter (and not the result of VT). This patient had been on longterm Flecainide, but was not receiving a ß-blocker! This facilitated episodes of AFlutter with 1:1 AV conduction.

• Marked QRS widening with an unusual QRS morphology (that resembles VT) was the result of Flecainide toxicity.
• Flecainide was discontinued. A ß-blocker was started. After withdrawing Flecainide, the rate of AFlutter increased, approaching a rate of 300/minute.
• Despite ß-blocker treatment — 2:1 AV conduction persisted, with a ventricular response of ~150/minute. The decision was then made to electrically cardiovert the patient — and to then refer him for ablation of his AFlutter.

Learning Points:

• Diagnosis of AFlutter may be challenging — especially when flutter waves are not readily visible in the usual leads. 
• Flutter waves may simulate the sinus P waves of sinus tachycardia. Always consider 2:1 AFlutter when sinus tachycardia does not fit the clinical picture.
• Be aware of the signs of Flecainide toxicity — especially of the tendency to slow the atrial rate of AFlutter (and in patients who are not on an AV nodal blocker — to precipitate 1:1 AV conduction).
• Regardless of how bizarre QRS morphology during a WCT rhythm may be — Consider 1:1 AV conduction of AFlutter (and not VT) if the patient is taking Flecainide.