Here is the EKG:
- Rate: tachycardia at 200.
- Axis: leftward axis
- Rhythm: regularly irregular
- Associated features: diffuse ST-T changes (not ischemic related) and QRS alternans (not related to pericardial effusion), which are both just related to rate and disappear as the rate slows.
The first interpretation would be to figure out the differential diagnosis for a regularly irregular rhythm in coupled beats. Without looking into more rare causes of coupled beats, the common causes includes atrial bigeminy, ventricular bigeminy, second degree AV block, and atrial flutter with variable conduction. Looking more closely at lead II below, we can see flutter waves appear, in a conduction pattern of a 3:2 block.
Our EKG:
The electrophysiology of atrial flutter is one of a macro-re-entrant circuit that occurs in the right atrium, involving the inferior vena cava at the tricuspid isthmus (site of ablation to abate rhythm). This macro re-entrant circuit causes an atrial rhythm (flutter waves) that is strikingly regular at about 300bpm. To protect from ventricular rhythms reaching 300bpm and possibly degenerating into V Fib, the AV node attempts to blunt this circuit via a conduction blockade. This blockade can occur at a fixed block (2:1, 3:1, 4:1, etc.) creating a regular rhythm, or a variable block, creating an irregular rhythm.
On EKG, you should look for the classic “sawtooth” flutter waves at rate of 300bpm (typical flutter is anticlockwise, with positive flutter waves in V1, and negative flutter waves in II, III, aVF), with ventricular rates of around 150 for 2:1 blocks (Or 100 for 3:1, or 75 for 4:1…). Also look for absence of an isoelectric baseline. This specific EKG shows an odd 3:2 conduction pattern, which can be explained by the Wenckebach phenomenon. This is a progressive prolongation of the PR interval culminating in a non-conducted P wave. In addition to this occurring with bradycardia during Mobitz type 1 2nd degree AV block, this can similarly occur in atrial flutter. As a result, in atrial flutter, as the atria is firing p waves (flutter waves), at 300bpm, the AV node is slowly slipping in it’s ability to conduct these beats, leading to a dropped (or blocked) beat.
Looking at our EKG:
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Back to our case:The patient first failed vagal maneuvers and then received Adenosine (6mg -> 12mg -> 12mg). After all three, the rhythm remained unchanged. (At some point the rate went to 300 bpm, which might have been a brief moment of 1:1 conduction.) We then tried rate control with a longer acting AV node blocker, IV Diltiazem, and the EKG slowed down to this:
The patient was then admitted to the floor and eventually got an EP study, which showed: “Atrial flutter cycle length 283ms; Typical counterclockwise rotation on surface ECF; AF was terminated during linear ablation at the Cav-tricuspid isthmus followed by normal sinus rhythm.” After receiving this ablation, the patient was discharged with the following EKG:
To learn more about atrial flutter with Wenckebach phenomenon, and to see a more comprehensive view of the differential for coupled beats, please check out this amazing podcast: https://vimeo.com/90269984
References:- Brown K. (2003). Emergency Dysrhythmias & ECG Injury Patterns. Thomson Delmar Learning. Copywrite 2003
- Carnell J., Singh A. (2008). An Evidence-Based Approach To Supraventricular Tachydysrhythmias. Emergency Medicine Practice.NET. April 2008, Vol 10, # 4
- Hampton J., Wagner G. AV Block: 2nd degree, Mobitz I (Wencheback Phenomenon). LifeInTheFastLane.com
- Larkin J., Burns E.,Cadogan M. Atrial Flutter and AVNRT. LifeInTheFastLane.com
- Mattu, Amal. Searching for P waves: atrial flutter, How to avoid misdiagnosing atrial flutter and a few others. EKGUMEM.com
- Phang R., Prutkin J., Ganz L. Overview of Atrial Flutter. UpToDate.com. May 2013
- Wang K. The Beautiful World of Electrocardiography – Part One. umn.edu/cardiology/faculty/wang/home.html. Vimeo.com
GuyCarmelli
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