Atypical Wenckebach interrupted by bigeminal PAC's

Is this Mobitz II?

Image 1 - Long lead II

The rhythm is sinus at a rate about 94 bpm with a long PRI or first degree AV block. The middle of the strip seemingly shows sudden onset of bradycardia. Remember that the most common cause of sudden onset of bradycardia in premature atrial complex (PAC). However, it cannot be seen in lead II.

Image 2 - Full disclosure

The full disclosure image revealed the PAC in V2 and not on the rest of the leads. There is no preferred lead to look these nibs. You have to train your eyes to spot those distortions.

The second point what this strip would teach us is the existence of atypical Wenckebach. The PRI was measure using an electronic caliper. The PRI remained prolonged (310 ms) then it increased to 320 ms then it was interrupted by a PAC's. The latter PRI are shorter then there is gradual increase in the PRI. Also remember that when the Wenckebach cycle is longer than 5:6, the PRI prolongation becomes unpredictable and does not behave your typical Wenckebach cycle where most student memorize the longer-longer drop. Atypical Wenckebach does not behave that way.

#131

Differential diagnosis of long RP tachycardia with inverted P waves in the inferior leads

A 60 yo with h/o HTN c/o SOB. What is the rhythm?

Image 1

This is a regular narrow complex tachycardia (NCT) at  rate of about  167 bpm. P waves are inverted in II, III and aVF and upright in AVR. The PR interval is shorter compared to the RP interval. So, this is a regular narrow complex long RP tachycardia.

The differential diagnosis for long RP tachycardia with inverted P waves in the inferior leads are:

• atrial tachycardia
• atypical AV nodal reentry tachycardia (AVNRT)
• persistent form of junctional reciprocating junctional tachycardia (PJRT)
• junctional tachycardia

Reference:

Das and Zipes. 2012. Electrocardiography of arrhythmias : a comprehensive review. Elsevier PA

# 136

A patient with chest discomfort and wide QRS tachycardia: VT or not VT? by Dr. Bojana Uzelac

This ECG case was posted in FB ECG Rhythms page on - 10.29.15 - https://www.facebook.com/ecgrhythms/posts/629361277166523

Image case:

Vignette:

(Courtesy of Dr Milena Popovic) This is ECG is from 80 yo woman complaining of chest discomfort and palpitations for one hour. She is hemodynamically stable at the moment of examination. No previous ECGs are available to compare. What do you think about rhythm here: VT or SVT?

***

Thank you all for such interesting discussion!

This was a case of wide complex tachycardia (WCT) rate about 140/min; actually, this was atrial flutter 2:1 conduction with left bundle branch block (LBBB).

As I mentioned in my comments on ECG Rhythms page and in the FB Group EKG club, this woman was admitted to a hospital because of acute coronary syndrome (ACS). Initially in ED, she had chest discomfort and palpitations. While waiting for her lab results, physicians tried to decrease her heart rate with labetalol IV (Presolol). Although she stayed hemodynamically stable, Presolol didn’t work and her symptoms didn’t improve. Her Troponin level came back highly elevated 10,3ng/dl, and she was hospitalized as an ACS. In the hospital, they were worried that this WCT could actually be VT. So, they gave her Amiodarone in attempt to convert her. That worked and she was successfully converted into sinus rhythm (Picture 1).

Picture 1. 12 Lead ECG post-conversion

As you can see this is sinus rhythm with LBBB morphology, rate about 96/min. PR interval is borderline for AV block 1^st degree: 0.20 sec but the most important fact: the QRS morphology during sinus rhythm match with the QRS morphology during WCT, meaning that origin of WCT is supraventricular.

Our patient is still in the hospital and she is doing well.  

So, what would be correct approach to patients like this? 

The initial rhythm is very similar to VT. As Ken Grauer mentioned in his comment in EKG club, reasons why should we suspect VT are:  i) The QRS is all negative in lead III; ii) the initial slope of the downslope of the S in V1 is slow (and not steep as would suggest lbbb aberration); and iii) there is a fat initial R wave in V2 (makes SVT less likely); and iv) VT is MUCH more likely than SVT with aberration in an 80 yo.

The smartest thing for a PROVIDER to do and the safest for PATIENT is to treat this rhythm as VT until proven otherwise! Remember, 80% of WCTs are VTs!

But, some findings on our first ECG are revealing that this tachycardia is supraventricular in origin. In leads V1-V3, there are clearly visible blips preceding every QRS. These blips are small and so close to QRS that make pseudo R waves in lead V1. Another blip is hidden and (as Chandran Pv said in his comment in EKG club) there is also notching at the beginning of ST segment, indicating atrial activity in addition to the visible blips. Atrial rate in this case is about 280/min. That makes AV conduction ratio of 2:1.

Picture 2. Atrial activity is shown with red lines. Green circles are for visible waves and blue arrows indicate a place of hidden blips.

If you are suspicious about my theory of hidden flutter waves, you could name this rhythm as sinus tachycardia. In other words, only visible P waves in green circles are recognized as atrial activity.

Let us compare leads V1-V3 during WCT and during sinus rhythm.

Picture 3. Leads V1-V3 during tachycardia and in sinus rhythm showing significant differences. 

There are distortions in the ST segments in leads V1-V3 (notching at the beginning as shown by blue arrows) during WCT, while after conversion these blips are gone. ST segment in sinus rhythm is smooth (blue lines).

Pseudo R waves in lead V1 as I’ve mentioned before are labeled with green circle in picture 3. These blips disappeared during sinus rhythm; instead there is QS with smooth initial part (green lines).

Shape and amplitude of atrial activity waves are not same in these two rhythms: P' s are more prominent (rounded and bigger as shown in purple arrows) during sinus rhythm.

PR intervals are significantly different: the longer ones are during sinus rhythm (labeled with red lines).  

Facts above should prove that rhythm from left side of picture 3. is not sinus tachycardia.

Picture 4. Inferior leads during WCT are showing saw-tooth shape suggesting atrial flutter. On contrary, P waves are clearly visible in sinus rhythm (red circles).

Inferior leads (especially lead II) are showing saw-tooth shape during tachycardia. After conversion there are distinct P waves preceding every QRS.

Take home point once again: WCT associated with ACS is VT until proven otherwise. And in practice, it usually turns out to be VT.

This case was a rare example of supraventricular origin of WCT in patient with ACS. But remember, this is an exception! 

Complete heart block with junctional escape rhythm

Image 1

Complete heart block will always have REGULAR VENTRICULAR BEATS(escape beats either ventricular or junction in origin). If the RR interval is irregular then some of the supraventricular impulses are conducted. Hence, not CHB. 

Image 2 - ladder diagram

For this strip:

Sinus rhythm with complete heart block with junctional escape rhythm

#183

Escape and the Capture by Dr TÍNH NGUYỄN CHÍ

In long lead II, the first complex is the normally conducted PQRST one, the next is the blocked P and the next is a ventricular escape beat ( we can see clearly the wide complex in D3 and D1 at the same time ) and then the cycle repeats. In this case, we see a particular pattern -  escape ventricular beat, next is the captured beat  and the next is the blocked P wave and the cycle repeats ( escape beat- capture beat- blocked P wave ). So this 2^nd degree AV Block and with the specific pattern ( Escape beat-capture beat- block P wave ). So it is called : Escape-capture Bigeminy.

Can atrial fibrillation (AF) be regular?

Adult with h/o HTN, DM, dyslipidemia, s/p cabg, s/p mvr, tvr c/o fever What is the rhythm?

Image 1

This is a regular  wide QRS rhythm at a rate of about 60 bpm  with no discernible P waves. There is right bundle branch block or RBBB (rsR in V1 and wide S in lead I) and left anterior fascicular block. 

A rhythm that can generate regular wide QRS rhythm with no P waves is AF with ventricular pacing. There are no pacer spikes seen (also this pt really has no pacemaker). 

Atrial flutter can also generate a regular rhythm with wide QRS complexes in the presence of a fixed bundle branch block or or aberrancy. In this case, it is difficult to appreciate the typical flutter wave morphology even with a 12 lead.

So, a likely interpretation is atrial fibrillation with complete heart block with a junctional escape rhythm with a right bundle branch block. The typical RBBB morphology is suggestive of supraventricular activation of the ventricles.



# 154

A reentry phenomenon

Image 1

Came in due to CP. trop neg x3, pro-BNP-~ 10000, echo EF ~55, no WMA. Asymptomatic during at the time these ecg changes were noted. What do you think is happening here? 

Image 2 -ladder diagram

The tracing started as a sinus rhythm at about 70's bpm. After a PVC, retrograde P waves can be seen which can be seen distorting the ST segment. This created a short RP/long PR complex. The ladder diagram shown illustrates that as the impulse from the PVC was retrogradely conducted, it found the slow pathway in the AV node able to conduct (long PRI).  That same impulse later found the fast pathway able to conduct retrogradely. So, it created it the short RP. It then continued a few cycles. This arrhythmia was terminated by PVC's.

Image 3 - dual AV node physiology

This case illustrates dual AV node physiology (Image 3). In some persons, the AV node has 2 conducting pathways. One pathway is able to conduct fast and the other one is able to conduct slow. The fast pathway recovers slow (long refractory period) and the slow pathway recovers fast or short refractory period. These pathway can also conduct impulse retrogradely or in reverse direction. 

#176

Complete Heart Block or Not?

No clinical history. What is the interpretation?

Image 1 - Long lead II

The rhythm is sinus at a  rate of about 68 bpm. Some of the P's are hidden from view or are merged with the QRS. The QRs interval is irregular. If you see an irregular RR interval then you should right away think that some of the sinus beats were conducted. Thus, this is not complete heart block (CHB).

In CHB, because the sinus beats cannot traverse the AV node then the ventricles are under the control of another pacemaker like the AV junction or the from the ventricles. These subsidiary or back-up pacemakers generate a regular pattern.

If you rely on lead II alone then a complex-looking arrhythmia becomes impossible to decipher. Then we need simultaneous leads in full disclosure view.

Image 2 - Full disclosure view with ladder diagram

What are clues of a captured QRS?

Sudden shortening of the RR interval would mean that the R with a shorter RR interval is conducted. In this strip, it is difficult to do that. Another clue is to use the morphology of the QRS. In using QRS morphology, you can use any lead where you can spot an obvious difference. In this case, we can use V1. 

R1, 4,5 and 7 shared the same QRS morphology and R2,3, 6 and 8 have the same morphology. 

Using deductive reasoning, R1 is near a P wave within a conductible distance and R2 is merging with the 3rd P wave. So, R1 is a captured beat and R2 is a junctional beat. If we follow the reasoning, then R1,4,5 and 7 are captured beats and R2,3,6 and 8 are junctional beats.

To make it easier to understand, a ladder diagram is constructed. By looking at the ladder diagram in R4 and R5 then there is some form of second degree AV block type I and an episode of advanced heart block considering (4 consecutive P waves are not conducted).

For this case, the 12L captured says SR, LAFB, first degree heart block. The initial  PRI I saw was ~ 300 ms. After years of watching strips, I know this P will drop and will manifest itself. Indeed it had several cycles of Wenckebach. The heart rate dropped some more and also captured this interesting portion. I know this 10 sec strip will stir imaginations and the challenge. 

#189

Bilateral Bundle Branch Block

A patient c/o of dizziness.

Image  1

The rhythm is sinus at a rate of about 100 bpm. The first 8 QRS complexes has a left bundle branch block configuration with PRI of 0.20 sec. The next QRS complexes has a right bundle branch (RBBB) configuration with QR configuration in V1 and wide S in I with PRI of 0.32 sec.

Is this dual AV node physiology + rate-related aberrancy?

It is possible to have normal PRI and a long PRI in one strip because some individuals have 2 pathways in the AV node where a supraventricular impulse can pass. The fast pathway will create a short PRI and a slow pathway will create a long PRI on the surface ECG.

It is also possible that RBBB and LBBB would appear depending on the heart rate.

In most "funky" arrhythmia, there is a unifying phenomenon

In this case, there is alternating QRS morphology (LBBB and RBBB) and changing PRI interval. So, is there is unifying phenomenon to explain this?

"AV conduction delay or block can be assumed to be caused by bilateral bundle branch block (BBB) only in the presence of alternating or intermittent RBBB and LBBB with a changing PR interval. - Fisch and Knoebel 2000."

In the first 8 QRS complexes, the sinus impulse is blocked in the left bundle and transmitted in the right bundle. After that the sinus impulse was blocked in the right bundle but delayed in the left bundle.

The unifying explanation for this strip is Bilateral bundle branch block. The bradycardia noted during admission could have been the AV block (block on both branches) expected among these groups of patients.

In this case, the patient came in due to dizziness and heart rate dropped to the 30's. This patient eventually had a pacemaker.

A 2:1 AV block is not right away a Mobitz II

Most 12 lead ECG's are random captures of cardiac activity. For STEMI cases, the 12 lead will do but for arrhythmia recognition longer strips are needed.

Image 1 - covered 2:1 

It is time to use full disclosure in telemetry

No clinical info. What is the rhythm?

Image 1 long lead II

This is an irregular narrow complex tachycardia. Can this be atrial fibrillation (AF)?  AF cannot create equal RR intervals. If you use a caliper, you will see that some RR intervals are the same. AF is generally irregular unless there is complete heart block or entrance block and the depolarization of the ventricles is by an AV junctional pacemaker. So, what is this?

Image 2 - Full disclosure strips

Some telemetry systems probably the older generations cannot generate the 7 leads in screen or page. If you are in that situation, it means it is time to upgrade your system.

Here in full disclosure you can see distinct + P waves in V1 and you can simultaneously compare it in II, III and aVF (+ P). The computed atrial rate is about 230 bpm (1500/6.5 small squares). There is also group-beating. Indicative of a Wenckebach phenomenon. 

During my early blogging days,  I interpreted this as atrial tachycardia (AT) for the sole reason that the atrial rate is about 230 bpm. Several textbooks that you will read will say that AT will have an atrial rate of about 150-250 bpm and atrial flutter (AFl) will have flutter rates of about 250-350 bpm. 

The chapter on atrial tachycardia (AT) from the book by Das and ZIpes (Electrocardiography of Arrhythmias, 2012) will make you consider AT vs AFl. AT it defined as a regular atrial rhythm originating from the atrium at 100-240 bpm and previous classification was based in ECG that it has a constant rate and isoelectric line between two consecutive P waves . AT can have a reentrant mechanism around a scar in the atrium. This can mimic the pattern of atypical atrial flutter (noncavotricuspic dependent). 

AFl is also typically a reentrant arrhythmia that is regular (tachycardia) with rates above 240-340 bpm and without an isoelectric baseline. However, AFL can also show isoelectric intervals between flutter waves in diseased atrial, or in the presence of antiarrhythmic drug therapy. AFl rate can slow with progression of atrial myopathy or with use of antiarrhythmic drugs such as amiodarone.

With this reasoning it is sensible to label this strip as AT vs AFl until proven by electrophysiology study.

Interpretation: AT with a block vs AFl with variable block

Reference:

Das and Zipes. 2012. Electrocardiography of arrhythmias : a comprehensive review. Elsevier PA

#191

A common source of confusion

This patient came in due to altered level of consciousness. 

Is there pacemaker malfunction?

Figure 1 - ECG case

There is no malfunction here. R8 to R11 are pseudofusion complexes. Pacer artifacts are seen ON the  QRS complexes (native looking or intrinsic or normal-looking complexes) but the pacer impulse did not change the shape or morphology of the QRS complex.

Pseudofusion beats (together with fusion) on the ECG is a common source of confusion. It indicates that the pacemaker stimulus did not alter the intrinsic QRS morphology on the surface ECG. This is because the pacemaker stimulus occurred after the normal depolarization of the ventricles has started. Thus, it cannot be affected by the pacemaker stimulus. 

Reference:

Bonnow et al. 2011. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 9th Edition. PA.Saunders 

#192

Telemetry captured the cause of syncope

Image 

A patent was admitted due to syncope. Telemetry captured transition from atrial flutter to asystole of more than 5 seconds which was interrupted by a junctional escape beat. Eventually a permanent pacemaker was implanted.

Interpretation: tachy-brady syndrome/sinus node dysfunction

#194

From the ECG vault

What is your interpretation?

Image 1

This is an irregular rhythm with no P to QRS relationship. The QRS duration is about 0.10 sec as measured using aVR. 

Lead I is predominantly positive and aVF is predominantly negative  or there is left axis deviation. There is qR pattern  in aVL and there is rS pattern in II, III and aVF. This QRS morphology suggest left anterior fascicular block (LAFB).

Image 2

As to the P waves, there is a bigeminal pattern. Bigeminal pattern P waves can be seen in PAC in bigeminy or sinoatrial block. 

Without R3 and R7, the pattern is of complete heart block (CHB) with a junctional escape with LAFB. R3 and R7 could  be premature junctional beats conducted with LAFB. R3 and R7 cannot be PAC's because supraventiruclar impulse cannot be conducted in CHB.

So, this is sinus rhythm with bigeminal pattern probably sinoatrial block, complete heart block with junctional escape conducted  with LAFB and premature junctional complexes.

* If you have another probable explanation, feel free to post. As seasoned ECG reader would say, an ECG can have multiple possible explanations. 

Several tricks of a PJC in one strip

A pt s/p post surgery. Asymptomatic at this time.

Image 1 (rhythm strip lead 2)

It shows sinus rhythm with inverted waves before  R2 and after R10, a longer PRI in R5 and R8 and  AV dissociation in R12 and R14.

Image 2 Ladder diagram

All those findings is due to one phenomenon: premature junctional complex (PJC) affecting the behavior of the surface ECG. R2 with an inverted P wave and a PRI of about 0.16 sec due to a conducted PJC with a delayed anterograde conduction. That is why the PRI normal. 

R5 and R8 had a longer PRI compared to the rest because of concealed conduction of PJC's in the AV node. Concealed means not seen on the surface ECG but manifest as unexpected ECG behavior. In this case the sudden PRI prolongation. The "unseen" PJC made the partially refractory so that the next beat that is conducted in the AV node is delayed. This delay created the long PRI on the surface ECG.

The inverted P wave after R10 is due atrial depolarization of a PJC that is blocked going to the ventricles.

R12 and R14 are conducted PJC's but the atrium is depolarized by an impulse from the sinoatrial node. So, we see an upright P wave that is very close to a QRS which resulted to AV dissociation.

#498

Very wide QRS rhythm

An adult pt came in with h/o of HTN, DM 2 and end-stage renal disease is c/o dyspnea and change in sensorium.

Image 1

This is a VERY WIDE QRS rhythm. Consider toxic and metabolic causes.

The K  was 8.5. Because of the dyspnea, pt was intubated. Calcium gluconate, NaHCO3, insulin and kayexalte was given. Dialysis was also done. After a few days pt was discharged.

#420

A rare cause of bradycardia: non-conducted PJC's in bigeminy

Image 1 - Long lead II

This is best appreciated in a ladder diagram.

Image 2 Full disclosure and ladder diagram

The rhythm is sinus at a rate of about 50 bpm. Every other sinus beat is followed by an inverted (negative) P wave. This negative P wave is atrial activation from a premature junctional beat (in bigeminy). However, the PJC's are not conducted to the ventricles.

Machine interpretation: atrial fibrillation. Do you agree?

Image 1 Long lead II

This is an irregular wide QRS rhythm with LBBB-like morphology. The machine interpreted it as atrial fibrillation. Do you believe the machine?

Image 2 Full disclosure image

If you look at lead II, then you will be deceived but the presence of a P wave in V1 proves that this is sinus. The P to P interval is 0.72 sec or an atrial rate of about 83 bpm. If you use a caliper and march the P, you will notice that some of the P wave are hidden from view.

Before going further, why did we say that this is LBBB-like morphology or properly called intraventricular conduction defect/delay (IVCD). It is because even though there is a QS pattern in V1, there is no broad, notched, monophasic R in I.

However, the 12L confirmed that it has an LBBB morphology.

Image 3 12L

Rule-out CHB

We can right away rule-out complete heart (CHB) block because the RR interval is NOT regular. In CHB, because there is complete AV dissociation, the ventricle is always in under the control of either a junctional or ventricular pacemaker. In this case, the sinus beats are conducted.

Differentiating beats by examining QRS morphology

Image 4 Measurement and ladder diagram

I have learned from Dr. Marriott's writings that QRS morphology can give a clue to the source of the impulse. There is no rule which lead will consistently show difference in morphology. In our case, we can use lead I. There are 2 QRS morphology (red circle and blue circle). So, R1,R2,R5,R6 and R7 (red circle) with the same morphology and the same PR interval (0.54 sec) are all sinus beats with long PRI and an LBBB-like morphology.

R3, R4 and R8 (blue circles) are a challenge here. The fastest way to make sense of these beats is the progressive shortening of the RR interval from R2to R4 (0.86 sec to 0.74). The RR interval of R4R5 is 1.31 sec which is less than 2x than R3R4. This fits the logical thought of a Wenckebach. The daunting challenge is here is that the P waves are hidden in the QRS in these beats but in other strips, the P waves near the QRS. That is why I know there is a P wave in there.

So, this is sinus rhythm with a long PRI (first degree AV block), second degree AV block type I, LBBB.

Is this a STEMI or an optical illusion? - by Dr. Bojana U.

Case posted in FB ECG Rhythms page on 09.18.2015- https://www.facebook.com/ecgrhythms/photos/a.219235038179151.30858.219229508179704/625971030838881/?type=3&theater

Thank you all for such interesting discussion!

Many things on this ECG are not what they appear to be. In that context, you can consider this tracing as an optical illusion!

First finding that stands out is inverted P waves in inferior leads and V3-V6. Second, PR interval seems to be very, very short. If you look at lead I only, you could say that PR interval is barely 60msec. So, this must be a junctional rhythm, right?

Next, if measured from TP line, there are no doubts about diffuse ST elevations in leads: II, III, aVF and V3-V6. STEs in inferior leads are 1mm high and almost horizontal shape in lead III; making very worrisome signs for chest discomfort patient. Actually, this patient was admitted to hospital as inferior wall STEMI!

What if I tell you that all of that is an illusion? PR interval on this ECG is normal, and there are actually NO ST segment elevations!!! Would you believe me??

In normal ECG, P waves are positive in leads I, II, III and aVF and negative in aVR.  They can be biphasic in V1, but are usually positive in the rest of the precordial leads. But, in this ECG P waves are NEGATIVE in inferior leads and in V3-V6.  This indicates retrograde conduction to the atria. The cardiac pacemaker must be anatomically lower than sinus node and the impulse from there continues in a backward direction through the atria. That means that the rhythm could be originate in the AV node (junctional rhythm) or in low atria (ectopic or low atrial rhythm).

Actually, the literature has shown many variety and has been confusing over the past years about precise anatomically location of junctional pacemakers. According to Bill Nelson it is generally believed that most pacemaker cells in the AV junction are in the perinodal cells or in the Hiss bundle, not in the AV node itself.

In junctional rhythm P and QRS relation could be: P wave preceding; superimposed on; or after QRS. If P wave precedes QRS complex these Ps are retrograde with a short PR interval (<120msec).

Picture 1. P and QRS relations in junctional rhythm

Heart rate in junctional rhythm is usually ≤60/min, but it can be 60-100/min (called accelerated junctional rhythm) or >100/min (called junctional tachycardia).

In our case, we should carefully observe PR interval in all leads.

Picture 2. PR interval measured in limb leads

Looking in lead I only, PR interval seems to be very short. But it is an optical illusion! We are used to see uniform and completely positive P wave in lead I. In this case the P wave is biphasic, meaning P1 component is isoelectric (slightly negative?) and P2 is positive deflection.

The measured PR interval is a little above 120 ms. This is shown in Picture 2 by drawing a vertical line in simultaneous leads from the onset of the P wave to the QRS complex.

So, we have an abnormal (retrograde) P wave and a NORMAL PR interval here. Per Chou, the old name for this rhythm is coronary sinus rhythm, but it has been replaced by the terms ectopic atrial rhythm (sometimes designated low or left atrial) or AV junctional rhythm. This is because inverted P waves in II, III and aVF with normal PR intervals can be elicited by stimulating sites other than the coronary sinus and because PR duration may be normal when  the junctional impulse conducted anterogradely is delayed .

All terms meaning the same: that the ectopic pacemaker is located in the low atrium, producing retrograde conduction through the atria and normal delay through the AV node. Actually, the pacemaker focus is within the atrial myocardium.

Picture 3. Frequency of atrial ectopic sites

Seventy-five percent of atrial ectopic foci are located in right atrium, while 25% is located in left one.

The exact place of ectopic focus in atria would determinate P wave morphology. In general it is impossible to locate ectopic focus without electrophysiology studies, but some findings could be helpful. Especially we can use P wave morphology to differentiating right atrial from left atrial foci (see the algorithm). Also, in general: the more deeply P waves are in inferior leads, the more inferiorly is located atrial ectopic focus. Low amplitude, biphasic or even positive P is for more superiorly located ectopic focus.

Picture 4. One of algorithms to identified site of ectopic atrial rhythm

The causes of this ectopic rhythm are many; and vary from completely benign to serious. Low atrial rhythm has been reported in acute amlodipine intoxication. A rare autosomal dominant disorder in four generations of a family with congenital heart diseases and low atrial rhythm has also been documented recently. It is often seen in pediatric population, especially with congenital heart diseases. Also, it has been reported in adult population with atrial septal defect. This rhythm is sometimes seen in inferior wall MI.

The next ‘illusion’ on this ECG is presence of STEs.

 

Picture 5. “STEs” in inferior leads and in V6 suggesting for STEMI

Bill Nelson was writing about an eponym- “Emery phenomenon”. It is named by Dr. James Emery who described this interesting phenomenon in his article from 1978. He reminds that for every atrial P wave there must be an atrial T wave. Normally, the sinus node P waves are positive in the limb leads, and the “T of the P” is a negative deflection; but unseen, because it occurs during the QRS complex. When atrial depolarization is ectopic and recorded as a negative event, the “T of the P” becomes positive, and can distort the end of QRS complex, simulating ST elevation. (From Nelson’s ECG site) - http://www.nelsonsekgsite.com/

Picture 6. Illustration of Emery phenomenon

This patient was admitted to hospital and MI was rule out by negative serial troponin’s level and by cardiac ECHO without LV wall motion abnormality.

After few hours, actually, this rhythm disappeared spontaneously. It was replaced with normal sinus rhythm. His symptoms resolved with BP control.

  

Picture 7. Moment of spontaneously termination of low atrial rhythm

Picture 8. Sinus beats clearly show no STEs (red lines). Slightly differences in QRS morphology during low atrial rhythm comparing to sinus rhythm are shown with green circles.

So, there is not truly STEs on this ECG; it is more like QRS distortion, QRS complex is simply shifted due to Emery phenomenon.

The cause of appearance of this rhythm to our patient remains unknown. The Amlodipine’s serum level in this case wasn’t measured.

Very important note! Ectopic atrial rhythm can be seen in truly STEMI. So, STEs in this rhythm could be caused from real deal ischemia! Keep that in your mind, please.

This ECG (picture 9.) is from another patient with proven inferior STEMI. But, in this other case you have some helpful findings strongly favoring STEMI. They are: size of T waves and notching QRS complexes in inferior leads; but more important is presence of reciprocal changes in lead aVL.

Picture 9. Ectopic atrial rhythm associated with true inferior wall STEMI in another patient.