Atrial Flutter with Lead Reversal

 

Pt came is due to palpitations

ECG case digitized using PMCardioApp

What is the rhythm? 

1. ST - sinus tachycardia
2. AVRT - AV reentry tachycardia
3. AVNRT- AV nodal reentry tachycardia
4. AT/AFL-atrial tachycardia/flutter

VT or SVT (with aberrancy or fixed BB)?

A 73 yo patient with h/o diabetes, hypertension and heart failure who presented with palpitations. Is this VT or SVT with aberrancy or fixed bundle branch block?

Image 1 - ECG case 

This is a ("mostly") regular wide complex tachycardia (WCT) at a rate of about 214 bpm with a left bundle branch block (LBBB) morphology and left axis deviation (LAD). 

Rule-out VT

It is difficult to be certain if there is AV dissociation. There is no capture and fusion beat. If we use the Brugada algorithm, there is an RS complex best seen in V3-V6. The RS interval is less than 100 ms. There is no AV dissociation. This is a LBBB-like WQRST with R wave in leads V1 and V2 less than 30 ms, the RS interval is less than 60 ms and the V6 is rS and not QR,QS or monophasic R. Thus, this favors SVT with aberrant conduction than VT.

Rule-out AV nodal reentry tachycardia and orthodromic reentry tachycardia

At certain points, distinct positive/upright P waves in lead II and III can be seen very close to the QRS (arrows). A positive P wave in the inferior lead will rule out AVN reentry tachycardia (with aberrancy or fixed bundle branch block) and orthodromic AVR because if this was an AVN reentry tachycardia or AVRT, the P waves will be inverted because of retrograde atrial activation. 

Which SVT?

With 1:1 conduction at a rate of about 214 bpm, the SVT would be atrial tachycardia vs a slow atrial flutter. This is supported by the distinct P waves. 

A beta-blocker was given which reduced the rate and revealed 2:1 conduction. At times, you would be mistaken to interpret this as sinus tachycardia with a LBBB and left anterior fascicular block.

Image 2 - ECG case at a slower ventricular rate

At slower ventricular rate, the exta P waves can be seen.

Image 3 - ECG case at even a slower ventricular rate

Thus, the case is atrial tachycardia vs (slow) atrial flutter with 1:1 conduction with LBBB, LAD

#681

A Tricky Conversion (by Arnel C.)

A patient admitted with atrial fibrillation (AF) was later noted to have this. Do you see conversion to sinus rhythm?

Image 1 – ECG case

Image 2 - ECG case marked with arrows to highlight PR interval variation

This is a regular narrow QRS complex rhythm with a ventricular rate of about 80’s. Variation in the PR interval can be observed as marked with arrows. So, is this sinus rhythm with variable PR interval? This pattern cannot be explained by dual AV node conduction or concealed conduction. In dual AV node conduction, there are 2 pathways in the AV node which are designated as slow pathway (SP) and fast pathway (FP). In dual AV node conduction with dual AV node physiology, we should see 2 PRI’s (one short and one long) and the PRI change is usually sudden (Image 3).

Image 3- Sinus rhythm with dual AV node physiology. After QRS #5, there is sudden prolongation of PRI (~520 ms).

So can this be atrial flutter or atrial tachycardia (AT)?

Atrial flutter (AFL) and atrial fibrillation (AF) can occur in the same person. They can appear on the same electrocardiogram as atrial flutter-fibrillation or “impure atrial flutter”. According to Braunwald’s Heart Disease – A Textbook of Cardiovascular Medicine ( 10^th ed) -

“Atrial fibrillation (AF) is a supraventricular arrhythmia characterized electrocardiographically by low-amplitude baseline oscillations (fibrillatory or f waves) and an irregularly irregular ventricular rhythm. The f waves have a rate of 300 to 600 beats/min and are variable in amplitude, shape, and timing. In contrast, flutter waves have a rate of 250 to 350 beats/min and are constant in timing and morphology. In lead V1, f waves sometimes appear uniform and can mimic flutter waves (Image 4). The distinguishing feature from atrial flutter is the absence of uniform and regular atrial activity in other leads of the electrocardiogram.”

Image 4 – An example of atrial fibrillation with prominent f waves in V1 that mimicked atrial flutter. The typical f waves can be seen in lead II.

Treatment of atrial flutter with digitalis (digoxin) shortens the atrial refractory period and often converts atrial flutter to atrial fibrillation. Conversely treatment with sodium channel-blocking drugs (quinidine or procainamide) often converts atrial fibrillation to atrial flutter as transitional stage before restoration to sinus rhythm. During transition the flutter cycle tends to be irregular and the flutter morphology is variable.

Patients with markedly enlarged atria (and massive dilatation) tend to have slower rate or atrial flutter that could have rates of less than 200 beats per minute. Patients on antiarrhythmics can also decrease the atrial flutter rates. The resulting decrease in the atrial flutter rate will reveal the isoelectric interval we typically see in focal atrial tachycardia.

Atrial tachycardia (AT) is defined as a regular atrial rhythm originating from the atrium at 100 bpm to 240 bpm. As mentioned above, atrial flutter can look like atrial tachycardia if patients are on antiarrhythmics or with atrial myopathy. Atrial tachycardia in a scarred atrium can be rapid and mimic atrial flutter. So, it is a matter of semantics to define AT or AFL based on surface ECG features.

How to prove that this is not sinus rhythm but either atrial flutter vs atrial tachycardia?

1.      Heart Rate Histogram or Heart Rate Trend

Image 5 – Heart Rate Histogram of the case

The Heart rate histogram is the graphical representation of the heart rate over time. It has a number of uses in cardiac telemetry. It can guide us that a rhythm could be atrial tachycardia or atrial flutter rather than sinus rhythm. Atrial tachycardia or atrial flutter will have a flat histogram (Image 5 and 6).

Image 6 – A “flat” histogram (from a GE system) from a patient with atrial flutter. The heart rate was 120’s for several hours. A histogram of sinus rhythm will show variations in heart rate.

2.      The Role of a premature ventricular complex (PVC) in arrhythmia diagnosis

A PVC can unmask a “hiding P wave”. In the case, the “hidden” P (arrows) wave was revealed by a properly time PVC. The atrial rate was about 187 bpm (Image 7).

Image 7 – After a wide QRS beat, 2 distinct P waves can be seen at a rate of about 187 bpm.

3.      The drop in rate

If you follow the heart rate histogram where the heart rate decreased, you can see the strip below. This further supports that case is not sinus rhythm but can either be atrial tachycardia vs. atrial flutter (Image 8). The atrial rate is about 187 bpm.

Image 8 – The arrow shows distinct P waves in leads II and V with a rate of about 187 bpm.

Back to the case

So, in the case presented is not sinus rhythm (no conversion) but could either be atrial flutter (slow) vs. atrial tachycardia with 2:1 AV conduction.

#678

The Lewis Lead: A lead placement to see oscillations

What is the rhythm?

Figure 1 - ECG case

If you suspect there are "extra" P waves that are not seen on the surface ECG, you can use the Lewis lead configuration (Figure 2).

Figure 2 - Lewis lead configuration 

This is done by placing the right arm electrode applied to the right side of the sternum at the RIGHT second intercostal space and the left arm electrode applied to the RIGHT fourth intercostal space.  This configuration was developed by Sir Thomas Lewis in the 1900's to magnify atrial oscillations during atrial fibrillation.

In the case presented, after changing the configuration to Lewis lead placement, flutter waves are best seen (especially in lead II).

Figure 3 - Flutter waves are better seen after Lewis lead configuration

Figure 4 - Usual lead placement vs. Lewis lead configuration

Here is the cropped version (Figure 4 - A - usual lead placement and B - Lewis lead configuration).

Interpretation: Atrial flutter

#148

The Wide QRS Complex Tachycardia Case

Thank you all for your response! This was one of the most interesting cases I have ever seen…

The story about this patient started 24 years ago, when he had his first episode of palpitations. At that time he was found to be hemodynamically unstable with irregular WCT rate of 270 bpm/min. I have no ECG tracing of that event but by his medical documentation he was urgently defibrillated and pre-excitation was recorded during sinus rhythm. The cardiologist pronounced that WCT as AF+WPW and hospitalized this patient. The EP study was performed and they noted two accessory pathways: left lateral and right postero-septal. However during that time, the patient refused ablation and signed against medical advice that he wants to be discharged. So, he left home with Amiodarone prescribed (which he didn’t use).

Over the next 20 years he was fine (!), but the problems started again few years ago. He started to have palpitations approximately once per a month and was forced to use Amiodarone every time. The last month it got even worse: he had symptoms almost on daily base, so he finally decided to get some help. He called EMS and the ECG #1 was recorded.

Image 1. WCT recorded pre-hospital

This is WCT, rate about 160/min. There is a RAD in limb leads, but it means nothing in context of difference between ventricular tachycrdia (VT) and supraventricular tachycardia (SVT) with aberration. VT can have any axis and it is dangerous to use only this criterion. There is monophasic R wave in leads V1 and leads V2 leaning toward VT, but the morphological findings in leads V5 and V6 suggest SVT. However, lead aVR and Vereckei criteria favoring VT. With the fact that 80% WCTs are VTs, it is absolutely reasonable to presume that this VT. He received Amiodarone and was converted to sinus.

Image 2. ECG after conversion shows pre-excitation

ECG after conversion in sinus rhythm shows delta wave (positive in inferior leads and V1, and negative in lead aVL). This is suggestive for left sided accessory pathway.

Image 3. Locations of accessory pathways (from Das and Zipes Electrocardiography of Arrhythmias)

If we now compare ECG in sinus rhythm with pre-hospital WCT, we could say it was antidromic AV reentry tachycardia (AVRT).

                          

Image 4. Example how PAC induce antidromic AVRT.   

       

They transferred him in hospital, where the ECG #2 was recorded.

Image 5. The first WCT recorded in hospital

This is WCT with a rate of about 160 bpm/min and very similar morphology to the pre-hospital WCT (Image 1). The only difference is slightly irregular rhythm. The cardiologist read this as AF+WPW, but I have doubts about that. If the atrial rhythm was really AF, it would produce much faster ventricular response, not only 160/min. In theory, this may be atrial flutter with variable conduction associated with WPW, but I’m still leaning toward antidromic AVRT. The reason for irregularity could be cycle length changes. In AVRT this could happen because of  one of these:

a)      The tachycardia CL usually changes as a result of changes in AV nodal conduction properties mostly owing to changes in autonomic tone.

b)      Tachycardia CL can also change if the patient has dual AV nodal pathways and the conduction via the AV node alternates between slow and fast AV nodal pathways. Alternatively, AVRT can change to AVNRT.

c)      Tachycardia CL changes can occur if the patient has more than one AP. (Das and Zipes)

He was hospitalized in Coronary unit, received Amiodarone and converted again.

The same episode of palpitations happened next day.

Image 6. WCT recorded second day in hospital

This is WCT with the same QRS complexes morphology in the limb leads as the first two, but with different findings in precordial leads. There is a positive concordance, strongly suggestsive of  VT, according to classic Brugada criteria.

However, there is another Brugada’s paper, not so famous - Steurer G, et al. The Differential Diagnosis on the Electrocardiogram BetweenVentricular Tachycardia and Preexcited Tachycardia. Clin. Cardiol. 1994;17:306-308.

Algorithm for the differential diagnosis between VT and preexcited tachycardia on the 12-lead surface ECG (SE 75%, SP 100%):

1)      Predominantly negative QRS complexes in the precordial leads V4 to V6?    YES=VT

NO

2)      Presence of a QR complex in one or more of the precordial leads V2 to V6?   YES=VT

NO

3)      AV relation different from 1:1? (More QRS complexes than P waves?)           YES=VT

NO= Pre-excitated tachycardia

According to this paper, this is pre-excited tachycardia.

One to remember: our hearts don’t read algorithms. This is example that WCT can have positive concordance and still not be VT.

During all these later episodes he was hemodynamically stable with normal vitals. They decided to transfer him into EP unit and he agreed with ablation this time.

Waiting for ablation, during two days, he had several WCT episodes with same ECG…

Image 7. WCT with different morphology than previous

What happened here? This WCT is completely different than all recorded previously. This is AFL with 2:1 conduction and rate-related LBBB. Accessory pathway is not included in this tachycardia. Again Amiodarone was given and he was converted.

Image 8. Sinus rhythm recorded just after conversion

Beside the same pre-excitation pattern as previous sinus ECG, there are diffuse STDs (probably caused by tachycardia) and one PAC at the end of strip. 

Third day narrow complex tachycardia was recorded two times (with identical morphology).

Image 9. Narrow complexes tachycardia in same patient

“Wow! Is there the end here?”-you are probably asking.

This is SVT with P wave after QRS complex (best seen in lead I, II and V1). So, here are two options:

1)      AFL with 2:1 conduction (the Bix rule: “If “P” wave is between QRS complexes, the most likely there is another “P” hidden into QRS complexes, favoring AT or AFL). But I’m not sure this is AFL: the rate is nearly the same when rate-related LBBB appeared (in several ECGs).

2)      The other option is orthodromic AVRT, as short RP SVT.  

He finally got in the Cath lab and they performed left lateral accessory pathway ablation. In short, this is the Cath lab report: …”Intracardiac recording revealed the earliest local activity in the ablation catheter placed in lateral mitral annulus (V-delta 35ms; A:V 2:1). Using conventional RF energy (50W, 60 C, 120sec) after 7 second the loss of pre-excitation was registered…After that,  the absence of accessory pathway was proven with differential pacing from RV and LV. During whole procedure the only recorded arrhythmia was antidromic AVRT, which was successfully converted in sinus with over-drive pacing. No VT was induced.  (They didn’t mention the other accessory pathway from 1992. at all!) After ablation there were no signs of pre-excitation in ECG.

Image 10. Post-ablation ECG

I’m not sure why there was difference between two EP studies and why another pathway wasn’t seen now.

After few days this patient was discharged in good condition.

Bojana

Atrial Flutter

No clinical hx. This ECG case is an exercise to find organized atrial activity. What is the rhythm?

Figure 1 - Lead II of the ECG Case

This is regular wide QRS tachycardia at a rate of about 136 bpm. 

Utility of a PVC in Arrhythmia Diagnosis

Most will thought of a premature ventricular complex (PVC) as a nuisance. However, a PVC can unmask or help in arrhythmia diagnosis.

A PVC can unmask hiding P waves

Figure 1 - A PVC in the middle of a regular wide-QRS complex rhythm.

 

It might look like sinus tachycardia with right bundle branch block (RBBB)

Atrial Flutter : The Great Mimic

A 70 yo patient with h/o CAD, stroke, hyperlipidemia admitted due to confusion due to sepsis.

Figure 1 - ECG case

This ECG shows:

a. Sinus tachycardia with short PR interval

b. Atrial flutter

c. Wolff-Parkinson-White Pattern

d. Junctional tachycardia