Think of Wenckebach (also) when you see SR with long PRI

Here is a radical view when you see SR with long PR interval.

Acceleration dependent LBBB

Image 1

This is sinus rhythm at about 88 bpm with a PR interval of 0.20 sec and a left bundle branch block (LBBB) configuration (QS in V1 and intrinsicoid delay in lead I).

Image 2

At another time while this patient is being monitored on telemetry, the QRS is narrow with PRI of 0.20 sec at a rate of about 58 bpm.

Image 3 (histogram)

The histogram markers identified the beginning (Image 4)and termination (Image 5) of the QRS changes.

Image 4 

Image 5 

This revealed that the widening of the QRS is noted at a higher heart rate. This is also known as acceleration dependent LBBB (aberrancy). Recognition of this phenomenon will only be possible if observed over time. Random 12L lead or rhythm strips will be interpreted as LBBB.

This is different in many aspects from aberration recorded in normal hearts in response to premature stimulation. The latter often manifest as right bundle branch block (RBBB) because the right bundle branch has a longer refractory period. Acceleration dependent aberrancy usually displays LBBB; appears at relatively slow rates, often below 75 a minute; is independent of any change in the duration of the preceding cycle; is independent of abrupt change in cycle length, often appearing with gradual acceleration and frequently with a small, 0.5 ms or shorter, change of the cycle length; after an acceleration of the rate it may appear only after a number of cycles, all the cycles equal in duration; rarely disappears with acceleration of the heart rate; and is nearly always a marker of cardiac abnormality.

Reference: 

Fisch C. 1983. Aberration: seventy five years after Sir Thomas Lewis. Br Heart J; 50: 297-302 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC481414/

# 603 

Orthodromic AV Reentry Tachycardia

What is the ECG rhythm interpretation?

Image 1

We will take the long lead II and analyze the highlighted section of the strip.

Image 2

First, this is a regular, narrow complex, short RP tachycardia. 

Image 3

This (first) beat is conducted with a normal PRI and QRS morphology.

Image 4

The second beat is conducted with a short PRI, wide QRS and a delta wave (red arrowhead). This is a pre-excited beat.  

Image 5

Accessory Pathway

The normal conduction of impulse is through the AV node.  In a very few, there is an extra pathway outside of the AV node (accessory pathway or AP)  that connects the atrium to the ventricle. This  accessory pathway can transmit impulse antegrade (atrium to ventricle) or retrograde (ventricle to atrium). During antegrade conduction (as seen in the diagram), the ventricle is activated by an impulse transmitted to the AV node (continuous arrow) and the AP (broken arrow). An impulse transmitted to the AP can activate a portion of the myocardium earlier than the impulse transmitted through the AV node. This preexcitation creates the delta wave. The rest of the myocardium is activated by the impulse transmitted through the AV node. The widened QRS complex is due to the fusion between the impulse transmitted through the AP and the AV junction. The PR interval is affected by the degree of preexcitation. In fully preexcited beats, the PRI is the full P wave duration.

 

Image 6

The third beat is a premature atrial beat or complex (PAC). The impulse is blocked at the AP because it is refractory but was transmitted in the AV node. Thus, creating a normal looking QRS.

 

Image 7

In the 4th beat, the impulse was able to travel retrograde (ventricle to atrium) because the AP has recovered. This created an inverted P wave and a short RP. It then travelled antegrade by way of the AV node creating the normal QRS.

 

Image 8

The 5th beat is the repetition of the circuit (ventricle - AP - AV node or orthodromic).

 

Here are the diagrams all together.

Image 9

#144

Sinus rhythm with long PRI mimicking junctional rhythm

Vignette: Elderly patient with history of chronic smoking, DM, HTN and dyslipidemia was brought in due to  weakness and fall. Patient is being worked-up for possible CVA.

What is the rhythm?

Image 1

This is a regular, wide QRS complex rhythm with left anterior fascicular block (LAFB) and right bundle branch block (RBBB). Our differential are: junctional rhythm or a SR with a long PR interval with P hidden from view as it merges with the T wave. 

Image 2

The rhythm strip revealed the P waves and the long PR interval.

Going back to the 12 lead, if you look closely in lead II you see distortions at the descending portion of the T waves.

For the case, it was found that it was indeed stroke. Managed as that and later sent for rehab and risk factors addressed.

#142 

Hyperkalemia in a patient with pacemaker

A 70 year old patient complaining of generalized swelling. 

This strip can can tell you 2 things: 

Image 1

-In V1 you can see the atrial spikes. This patient had an AICD. EF is in the 30's which could explain the low voltage ecg and poor R wave progression (cardiomyopathy).

-There is hyperkalemia as shown by a wide QRS and tall T waves in the precordial leads. (compare the 12L in the case and the 12L below when K was normal).

Image 2

The reason for the swelling was acute renal failure and the K was ~ 7.Calcium gluconate, glucose-insulin, sodium bicarb and kayexalate were given.

So, the 2 things that this strip can tell: cardiomyopathy - low voltage limb leads/poor R wave progression and hyperkalemia.

#115 

Hypokalemia

A pt who was admitted due to ascites and diarrhea.

Image 1

You can see ST depression and prolonged QT. "I would like to call it the invasion of the  ST on P's personal space". The K during this time is 2.2

What was done?

Institutions often trigger K protocol. So, K here was replaced.

Image 2

Image #2 (after something was done - K replacement). The strip looked normal and no more invasion of P-ersonal space. K came back to 4.

#130 

Wearable external defibrillator and dual chamber pacemaker (xray)

Implanted dual chamber pacemaker + a wearable external defibrillator (xray images)

#139 -

Atrial Flutter

This  is a middle aged patient who came in due to shortness of breath. No fever, no cough, no calf tenderness, no chest pain. VS 110's/60's 140 regular, afebrile sat 98% at 2L. Clear breath sounds, no murmur and no peripheral edema.

What is the rhythm?

Image 1

This is a regular wide complex tachycardia (~ 150 bpm) with a right bundle branch block (RBBB) morphology. For tachycardias that are in the 150 range, think of atrial flutter. The heart rate trend or the histogram often is "flat" (or no variation in rate).

Image 2

With intervention (AV nodal drugs), flutter waves will be visible. Sometimes in life the rhythms are so elusive and they will not show their classic features right away.

# 137 

Atrial fibrillation with entrance block and junctional tachycardia with Wenckebach exit block in Digoxin Toxicity

A patient was admitted due to confusion. What is the rhythm?

Image 1

For most, this would be interpreted as atrial fibrillation (AF) with probable ischemia because of the ST depression. This interpretation is partly correct and partly wrong.

If you notice, there is group-beating (QRS of 3's,2's, 2's,3's and 2's). You would expect AF to be an irregular rhythm and not like this with a pattern. You see patterns like this in atrial flutter (AFl). However, there are no flutter waves because this is really AF.

What is causing this group-beating? 

The strip above shows shortening of the RR interval then a pause. This shortening of the RR interval is one of the hallmarks of a Wenckebach. If you have read books authored by the late Dr. Marriott you will often encounter the words - group-beating is a "footprint" of a Wenckebach. 

What is driving the ventricle if AF cannot be regular like this? The answer is the junction. The ventricle is captured is by junctional beats but have some problem exiting creating progressive delay. So, there is shortening of the RR interval and eventually a dropped beat. There is an EXIT BLOCK.

What is the rate the of the junction?

This is computed by adding the beginning of the group to the R of the next group and then dividing it by 3 (in this case of 3:2 Wenckebach with the 3rd beat as the dropped beat). The answer here is called the interectopic interval. The rate of the junction is 110 bpm or there is junctional tachycardia.

Image 2

What about the AF?

The AF cannot penetrate the junction because there is an ENTRANCE BLOCK. Entrance block denotes failure of an impulse to reach, enter, suppress, reset, or discharge a dominant pacemaker. In our case, the dominant pacemaker is the junction.

Rhythm interpretation: AF with entrance block, junctional tachycardia with type I (Wenckebach) exit block or also called double tachycardia

This ladder diagram will help us understand what is happening (thanks to Jason Roedinger)

Image 3

Work-up for confusion was done.  Imaging was negative for stroke. Chemistry was normal . Digoxin level was 4.6 (upper range is 2.0). The drug was stopped. LOC improved and the patient was discharged. The patient has a long standing AF and CHF. Digoxin was one of the medications.

The rhythm (Wenckebach exit block) was due to digoxin toxicity. Digoxin toxicity can cause a lot of ECG abnormalities and this one is just one of them (including the ST scooping). Scooping of the ST segment does not mean digoxin toxicity. It can be seen in patient on digoxin at therapeutic levels. In this case, the confusion was due to digoxin toxicity.

* Here are other similar cases: 

http://europace.oxfordjournals.org/content/europace/10/9/1108.full.pdf

http://ecg.utah.edu/img/items/ecg_494.gif

Reference:

Fisch C and Knoebel SB. 2000. Electrocardiography of Clinical Arrhythmia. New York. Futura Publishing Co.

# 133 

ST elevation in the inferior leads due to wraparound LAD

An adult patient was admitted due to numbness and weakness of arm and left sided chest pain. VS were 149/90, HR = 66 , RR = 12 and afebrile. Baseline 12L was negative for STE's. CBC, Chemistry were normal and troponin came back negative, CXR showed no acute disease. 

While on telemetry, the patient had chest pain. 

Image 1 - ECG case

There are ST elevations in I, II, III and aVF and ST depression in aVR and aVL. STE in I with STE in II, III and aVF was an odd combination. 

Here is the serial telemetry changes.

Image 2 - Serial telemetry changes

Cardiology was on board and heart cath was done. There were no significant stenosis in right coronary artery (RCA) , left anterior descending (LAD) artery was wrapping around the apex with subtotal occlusion after the second diagonal. Intervention was done. The patient was eventually discharged.

The STE in the inferior leads was not due to RCA pathology but was due to wrap around LAD.

Image 3 -  Wraparound LAD 

*Image adapted from Akdemir et al. 2004. Simultaneous Ant and Inf MI due to occlusion of LAD. Turk J Med Sc (34):121-126

#129 

Watershed Infarct in a patient who had Torsades de Pointes

A patient was found to have watershed infarct after cardiac arrest.

MRI

The MRI (DWI - diffusion weighted image) image shows watershed infarct involving an internal border zone (LCA abd MCA) and cortical border zone (MCA and PCA). They are between adjacent arterial perfusion beds.

ECG

The reduction in perfusion can be due to pump failure caused by cardiac arrest or arrhythmia, or reduced cardiac output due to a variety of causes. In this case, the ecg showed prolonged QT, and a tachyarrhythmia with QRS complexes of changing amplitute (Torsades de pointes). This tachyarrhythmia caused the hypoperfusion and the watershed infarct.

References:

Caplan LR. Etiology and Classification of Stroke. In UpToDate, Kasner ES (Ed). Waltham, MA, 2012

Daroff et al. (2008).Bradley's Neurology in Clinical Practice 6th Ed. PA:Elsevier

#118 

Pericarditis

A 40 year old patient with no cardiac risk factor was admitted complaining of pleuritic chest pain with positive troponins.

The 12L showed ST elevations in inferior wall and precordial leads, PR elevation in aVR and PR depressions consistent with pericarditis.

Echocardiography revealed normal EF and no wall motion abnormalities. Patient was managed as pericarditis and later discharged.

#116

Dextropostion from Volvulus

An elderly was admitted due to abdominal pain and abdominal distention. Chest xray showed elevation of the left hemidiaphragm and plain abdominal films revealed dilated proximal bowel loops and the "coffee bean" sign. This was due volvulus and surgery was done.

Image 1 (xrays)

Something interesting was seen on the 12L.

The ECG showed reversal of R-wave progression pattern (decreasing amplitude from V1 to V6). The limb leads complexes looked normal (no signs of lead reversal leading us to think that this is dextrocardia and there is no dextrocardia in the chest xray). The direction of the apex in this case is a bit to the right due to the elevation of the left diaphragm and intestinal contents. Thus, this is dextroposition.

Ventricular orientation is best estimated from the precordial leads. Normal levocardia has a pattern of low voltage right chest leads with positive forces of higher amplitude in the mid and left chest lead. This pattern is reversed in dextrocardia. 

References:

- Bharate S and Lev M. Positional Variations of the Heart and Its Component Chambers. Circulation 1979:59:886-887

(http://circ.ahajournals.org/content/59/5/886.citation)

Khaity P and Marelli A. Clinical Use of Electrocardiophy in Adults with Congenital Heart Disease. Circulation 2007;116:2734-2746 

(http://circ.ahajournals.org/content/116/23/2734)

Walsh el al. Electrocaridography and Introduction to Electrophysiologic Techniques. Nada's Pediatric Cardiology 2006. Philadelphia PA

Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice (6th edition), Saunders 2008.

#110

For a very fast irregular wide QRS rhythm : consider WPW

A patient complaining of chest discomfort. What is the rhythm?

Image 1

This is an irregular wide ("bizarre") complex tachycardia at at a rate of about 250 bpm.

"The presence of WPW syndrome is suspected from a rhythm strip the  ventricular rate during atrial fibrillation is during AF exceeds 200 bpm. Such a  rapid ventricular response is unusual if the impulses were conducted via the  normal AV conduction system".

Reference: Surawicz B and Knilans TK. 2008. Chou’s Electrocardiography in Clinical Practice. 6th ed. PA. Saunders-Elseiver

Image 2

This is the 12L during sinus rhythm showing the hallmarks of WPW: short PRI, delta wave and widening of the QRS

Here is also a comment courtesy of Jason Roediger:

"Atrial fibrillation predominantly conducted with preexcitation. Wolff-Parkinson- White (W-P-W) syndrome. Based on the negative polarity of the QRS complex in lead  V1, the accessory pathway is probably situated on the right-side of the heart. Only the 8th, 9th, and 10th beats are conducted normally whereas the remainder of  them have Delta waves. It is highly unlikely that you would see this level of irregularity in ventricular tachycardia. Note that the longest RR interval, between the 13th and 14th beats, is greater than twice the shortest RR interval  between the 4th and 5th beats. That's more than 100% difference between the two RR intervals. Superficially, this is mimicking LBBB, however what looks like fat little r-waves in the anteroseptal leads are actually Delta waves. When LBBB is  seen with little r-waves in these leads, they are usually very narrow."

#107

What kind of block

Basic ECG Review

AV block is more common in IWMI

Vignette: 65 yo with h/o  HTN, DM, dyslipidemia 

c/o of chest pain

Image 1

The rhythm is sinus tachycardia at about 107 bpm with complete heart block (CHB) with a junctional escape rhythm (50 bpm). There are ST elevations in II, III and aVF with ST depression more pronounced in aVL than I. ST-T wave changes can be seen in precordial leads extending to V4. This is inferior wall STEMI (IWMI)with  complete heart block. AV block is more common in IWMI because the AV node is  supplied by the right coronary artery (RCA).

Image 2

P waves are marked. Some of the P waves are (partly) hidden from view (blue arrowheads)

Echo showed EF between 45 - 50 %,with severe inferior and inferolateral  hypokinesis. Angiogram revealed lesion in the RCA and intervention was done.Patient was discharged a few days later in sinus rhythm (with no CHB). 

#585  

Going away rhythm

I have seen 2 rhythm types on the natural course  of dying (peacefully). In the first, the heart rate holds for a few hours (AF or sinus) then gradually declines and the latent pacemaker kick-in one-by-one (junctional to ventricle). The other one is the one I'll post here. So this is not the sudden cardiac death (SCD) where people get excited.

These are 5 strips (~ 4 minutes duration) captured in a DNR pt. Pt was in no distress during the whole process.

Pls note timestamp on the upper left part of the strip.

Image 1 

The rhythm is regular and narrow with ST changes.The latter part of the strip shows wide QRS rhythm most likely AIVR.

Image 2 

Few seconds later, it turned into a fast wide QRS rhythm (likely VT)

Image 3

About 7 second later, change in morphology is seen (best seen in II, aVF and aVL)

Image 4

About 2 minute later, looked like the QRS voltages becomes smaller and the rate  becomes slower (agonal rhythm).

Image 5 

About 4  minutes after, asystole can be observed.

#514 

A common mistake is to call this pattern Mobitz II block

An elderly c/o of dizziness. What is the rhythm?

Image 1

As you can see, the P to P rate is about 100. Some of the P's are hiding in the T waves and distorting it. So this is 3:1 AV block. This is high-degree AV (or advanced) AV block.

According to Dr. Goldberger, a subset of second degree heart block occurs when there are multiple consecutive non-conducted P waves present (P-QRS ratios of 3:1 or 4:1). This is referred to as high-degree (or advanced) AV block. It can occur at any level of the conduction system.A common misnomer is to call this pattern Mobitz II block. 

This case went to complete heart block and a pacemaker was eventually inserted.

Reference: 

Goldberger A. 2013. Goldberger’s Clinical Electrocardiography : A Simplified Approach. 8Ed Ph Elsevier

#392 

Basic ECG Interpretation

What is your interpretation?

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Interpretations:

1. Sinus tachycardia with 3:1 AV conduction, right bundle branch block (Advanced or high-grade AV block)

2. Agonal Rhythm

3. 2 to 1 AV block

4. Sinus tachycardia with first degree AV block

5. Atrial Flutter with 4:1 AV conduction

6. Atrial fibrillation with slow ventricular response

7. Sinus rhythm with junctional rhythm (isorhythmic AV dissociation)

8. Sinus tachycardia, complete heart block, junctional escape rhythm with RBBB, inferior wall MI

9. Sinus rhythm with non-conducted premature atrial beat

10. Sinus rhythm, second degree AV block type I (typical Wenckebach/Mobitz I) with 5:4 AV conduction

11. Sinus rhythm, complete heart block with junctional escape

12. Atrial fibrillation

13. Sinus rhythm, second degree AV block type I (atypical Wenckebach or Mobitz I)

14. Sinus bradycardia

15. Normal sinus rhythm

16. Sinoatrial block type I

17. Sinus rhythm, second degree AV block type II (Mobitz II), RBBB

18. Sinus arrhythmia

19. Atrial tachycardia

20. Sinus rhythm converting to polymorphic ventricular tachycardia

21.Orthodromic AV reentry tachycardia

22. Multifocal atrial tachycardia, hyperkalemia

23. Supraventricular tachycardia or SVT probably AV nodal reentry tachycardia (AVNRT)

24. Ventricular tachycardia (5th QRS is a fusion beat)

25. Torsades de Pointes