April 28, 2017

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 ( 10th 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

April 24, 2017

Practical Approach of Wide Complex Tachycardia in Cardiac Telemetry


Definition

A wide complex tachycardia (WCT) is defined as a cardiac rhythm with a rate of ≥ 100 bpm and QRS width/duration ≥120 ms or 0.12 sec. Other acronym used is WQRST.

If you read articles and journals, electrocardiographers will describe a WCT as right bundle branch block (RBBB) - like configuration or left bundle branch block (LBBB)-like configuration.

A RBBB is recognized by a QRS duration ≥ 120 ms with a predominantly positive portion in V1 (Figure 1A). LBBB has QRS duration of ≥120 ms with a predominantly negative terminal portion in V1 (Figure 1B).


Figure 1 – A. RBBB configuration in V1. B. LBBB configuration in V1.
A Wide Complex Tachycardia (WCT) can be:
  • Ventricular Tachycardia (VT)
  • Supraventricular tachycardia (SVT):
    • with aberrancy in the His-Purkinje system
    • with anterograde accessory pathway conduction
    • with bizarre baseline QRS
    • in presence of drug effect or electrolyte imbalance
  • Ventricular pacing
  • Electrocardiogram artifact
Providers in cardiac telemetry are faced with the daunting task of identifying whether a WCT is ventricular tachycardia (VT) or SVT with aberrancy. Ventricular tachycardia is a tachycardia requiring the participation of structures below the bundle of His. Supraventricular tachycardia (SVT) is a tachycardia requiring the participation of structures above the bundle of His.

Figure 2 – Diagram Diving Supraventricular Tachycardia and Ventricular Tachycardia



A narrow QRS complex is the considered normal and it requires highly synchronous activation of the ventricles which is made possible though the rapidly conducting His-Purkinje system (HPS).
The term aberrancy (aberration or aberrant intraventricular conduction) is used to describe transient bundle branch block (BBB) and does not include QRS abnormalities caused by preexisting BBB, preexcitation, or the effects of drugs/electrolyte. The mechanism of aberration can occur anywhere in the His-Purkinje system (red box in Figure 3). The transient BBB is due to impulse transmission of a supraventricular beat during period of physiologic refractoriness and/or depressed conductivity. The supraventricular electrical impulse is conducted abnormally through the ventricular conducting system. This results in a wide QRS complex that may be confused with a ventricular ectopic beat or PVC or VT.
Technicians often used other terms instead of aberrancy like bundle-switch, intermittent bundle, conduction change and intermittent ventricular conduction delay. However, the appropriate term should be aberrancy or aberrant intraventricular conduction.


Figure 3 - Cardiac Conduction System



Diagnosis by Statistics

The pretest probability that a WCT is VT is 80%. This means that 4 out 5 WCT is VT. If patients are known to have prior myocardial infarction and the symptom of tachycardia occurred after the probability increases to > 90%.

The Purpose for a Correct Diagnosis

The purpose of arriving at the correct diagnosis is to avoid harm to the patient. If SVT is treated as VT and given amiodarone or electrical cardioversion (which may not be harmful) it is not the optimal therapy. If it was atrial flutter, cardioversion will entail a risk of stroke.  If VT is treated as SVT (using diltiazem/verapamil), hemodynamic deterioration may occur. If SVT are managed as VT, they might be placed on long-term amiodarone which carries a number of long-term problems or an implantable defibrillator with repeated generator change. However, hunting the diagnosis is second only to stability of the patient. If the patient is unstable then immediate cardioversion and then once stable the various morphological characteristics and algorithms are used - – (Garner J and Miller J. 2013. Wide Complex Tachycardia – Ventricular Tachycardia or Not Ventricular Tachycardia,That Remains the Question. Arrhythmia & Electrophysiology Review 2013;2(1):2329)

Algorithms Focus on VT Characteristics

Most algorithms differentiating VT from SVT with aberrancy focus on characteristics unique to VT. If those characteristics are not present, then it is presumed SVT until proven. We should also recognize that algorithms find it hard to distinguish VT from pre-excited SVT.

The algorithms developed utilize the 12 lead ECG. However, in this age of ECG telemetry, most wide QRS tachycardia are captured and saved in central telemetry which can view all the limb leads and a V1 +/- V6.

Figure 4 – Typical Central Telemetry Set-up

ECG Criteria/Features in Cardiac Telemetry Supporting VT

·       Fusion Beat
·       Capture Beat
·       V1 and V6 Morphology
·       aVR algorithm (Vereckie algorithm)
·       “K. Wang Logic”

AV dissociation

During VT, there is independent beating of the atria and ventricles. In patients with underlying sinus rhythm, the atria are depolarized by an impulse coming from the sinoatrial (SA) node while the ventricles are controlled by an ectopic ventricular beat. The atrial rate is slower compared to the ventricular rate. AV dissociation is difficult to spot but not impossible. AV dissociation is easier to see in slower VT but difficult to appreciate during fast rates. Multiple simultaneous leads are needed to compare distortions and determine if those distortions are indeed P waves.



Look for AV dissociation in the case below. Map the P waves and the QRS.


Figure 5 – WCT case for AV dissociation

Distinct P waves are marked in red arrows and not so obvious P waves are marked with blue arrows. To check if those are indeed real P waves, you can do simultaneous lead comparison. Take for example the identified P wave before R5. The P wave is upright in II and aVF and inverted in aVR. Other P waves in this case are hidden from view or are buried in the QRS. From 2 sequential P waves, we can then use a caliper to march the P waves.



Figure 6 – P waves marked with arrows



The P to P interval is 18 small boxes (cycle length 720 ms) or an atrial rate of about 83 bpm.  The R to R interval is 14 small boxes (cycle length 540 ms) or a ventricular are of about 107 bpm. At that rate difference, we can see dissociation. Another way of visual recognition is using a ladder diagram. However, this might be time consuming in the acute setting. For educational purposes the ladder diagram is presented below. The diagram will show independent beating of the atria and ventricles or AV dissociation.



Figure 7 – Ladder diagram showing AV dissociation



 Fusion Beat

The ventricles may be also be depolarized both by the ectopic ventricular impulse and a supraventricular impulse resulting in a QRS complex that is intermediate in morphology between the sinus beat and the ectopic ventricular beat. This complex is a fusion beat.
The previous ECG case featuring AV dissociation will be used. In the strip below, the morphology of R4, R10 and R16 is different compared to the rest of the R waves. The duration of these 3 R waves is about 0.12 seconds (vs. 0.16 sec).




Figure 8 – Fusion beats highlighted with arrows



The reason for the difference in QRS morphology is because R4, R10 and R16 are fusion beats. This is best illustrated in the ladder diagram.




Figure 9– Ladder diagram showing fusion beats



Below is another example of a fusion beat (red arrows) which supports that the WCT is VT and not SVT with aberrancy. The first 4 complexes are sinus beats. After the 5th complex is the full duration of the WCT. If you only use leads II and V1, it will be difficult for you to appreciate the difference in the shape of complex #5 which is a fusion beat. However, if you use full disclosure to see all limb leads, you will appreciate that complex #5 is different in shape from the first 4 complexes and the WCT.




Figure 10 – Fusion beat highlighted by arrows



Capture beat

During slower VT, occasional supraventricular impulse may be transmitted through the AV node and depolarize the ventricles resulting in a normal looking QRS (capture beat) in the middle of wide QRS beats.

The interval of a capture beat is shorter than during the tachycardia or its rate is faster compared to the WCT.

The complexes below (red box) are captured beat. It has the same morphology or shape with that of a sinus beat (latter part of the strip). The presence of the capture beats means that the WCT is VT.








Some of the telemetry systems have 6 wires. The 4 wires are for the limbs and the other 2 wires are chest leads. These 2 wires can be positioned in the V1 and V6 position. Thus, the interpretation of an electrocardiographer in WCT diagnosis is dependent on correct lead positioning.
The following morphology in V1 and V6 supports VT:
       RBBB-VT
v  V1 -  Monophasic R, QR, or RsR’ (rabbit ear with right greater than left)
v  V6 – R/S ratio < 1, QR or QS, monophasic R
       LBBB-VT
v  V1- Initial r > 30 ms, nadir of S > 60 ms, notched downstroke
v  V6 – any q, QS or QR



These features are difficult to remember. So, a cheat sheet is handy in telemetry stations.



Figure 12 – V1 and V6 morphology criteria for VT (top) and SVT with RBBB morphology (bottom)
 (From Garner J and Miller J. 2013. Wide Complex Tachycardia – Ventricular Tachycardia or Not Ventricular Tachycardia, That Remains the Question. Arrhythmia & Electrophysiology Review 2013;2(1):2329)








Figure 13 – V1 and V6 morphology for VT (top) and SVT with LBBB morphology (bottom)
(From Garner J and Miller J. 2013. Wide Complex Tachycardia – Ventricular Tachycardia or Not Ventricular Tachycardia, That Remains the Question. Arrhythmia & Electrophysiology Review 2013;2(1):2329)


aVR Algorithm (Vereckie Algorithm)
Several criteria and/or algorithm had been developed through the years.
       Sandler and Marriot Criteria (1965)
       Wellen’s Criteria of RBBB (1978)
       Kindwall criteria of LBBB (1988)
       Brugada algorithm (1991)
       Griffith algorithm (1994)
       Bayesian Analysis (2000)
       Vereckie Algorithm I (2007)
       Vereckie  Algorithm II  (2008)
       Pava Criteria of lead II (2010)

A lot of these used several leads and the famous Brugada criteria utilize a 12-lead ECG. In 2008, the group of Dr. Vereckie used a four-step decision tree (algorithm) using only aVR. They hypothesized that aVR might be more sensitive than the other leads in differentiating WCT because, in normal sinus rhythm and SVT, ventricular activation wavefront proceeds in a direction away from aVR, typically yielding a QS complex in aVR. Their study showed that the new aVR algorithm devised for differential diagnosis of wide QRS complex tachycardias have superior overall test accuracy and greater sensitivity and negative predictive value in VT diagnosis compared with the Brugada algorithm.




The new Vereckie algorithm is shown below. The algorithm in a stepwise fashion looks at aVR for (1) an initial R wave, (2) initial r or q wave > 40 ms, (3) a notch in the descending limb of a predominantly negative QRS and (4) vi/vt ≤ 1. Vi stands for voltage change in the initial or first 40 ms and vt stands for voltage change in the terminal or last 40 ms. Anything answered yes in the algorithm is VT.


Figure 14 – The New Vereckie Algorithm


Again, a cheat sheet will come very handy in telemetry stations. Shown below is the graphic morphology of the algorithm.


Figure 15 – Morphologic features supporting VT in the New Vereckie Algorithm (From Garner J and Miller J. 2013. Wide Complex Tachycardia – Ventricular Tachycardia or Not Ventricular Tachycardia, That Remains the Question. Arrhythmia & Electrophysiology Review 2013;2(1):2329)




“K. Wang Logic”

Dr. Kyuhyun Wang (Dept. of Medicine - University of Minnesota) is one of the best electrocardiographer I found in cyberspace and happened to be an internet acquaintance. He is like following the lines of Dr. Henry Marriott. In 2013, he published Atlas of Electrocardiography. In there, I found 3 simple logical reasoning to differentiate VT from SVT with aberrancy in patients in sinus rhythm which is highly applicable in cardiac telemetry because we can see the beginning of the WCT. Thus, I am calling it the “K. Wang Logic”.



If  the patient in sinus rhythm (SR), it is easy to identify VT and SVT with aberrancy:
1.       When the run of WCT is preceded by a premature P wave (often the P wave has a different morphology), then it is SVT with aberrant conduction.
The ECG case below is from a 75 yr old patient with pontine infarct with several episodes of wide and narrow complex tachycardia. The tachycardia starts with a premature atrial complex (red arrow) with a long PRI. The P wave has a different morphology or shape during that of sinus rhythm. Following the “K. Wang logic”, this WCT is SVT with aberrancy.
Further examination of the strip, will reveal inverted P waves (II, III and aVF) right after the R waves (blue arrows). This indicates retrograde atrial activation. This supports that this SVT most likely typical AV nodal reentry tachycardia (AVNRT).



 Figure 16 – A WCT preceded by a PAC



2.       If the WCT is preceded by a regularly (not prematurely) occurring sinus P wave (the PR interval is shorter than that of normally conducted sinus beats), it is ventricular tachycardia





Figure 17 – A WCT preceded by  a regular sinus P wave with short PRI



  
3.       If the WCT is not preceded by a P wave, it is ventricular tachycardia



Figure 18 – A WCT not preceded by a P wave



Conclusion

The diagnosis of VT has undergone evolution.  There is still “no one criterion to end all criteria”. People in front of telemetry monitors are by default forced to be familiar with all available criteria. However, there will be some ECG’s that will not “read” books and journals. Thus, if uncertain about the diagnosis of a WCT, it is wise to treat it as VT. You will be correct 80% of the time. However, we should still try to create a logical explanation why a WCT is VT and not just depend on statistics.



References:

Blomström-Lundqvist C, Scheinman M, Aliot E, et al. 2003. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias) Developed in Collaboration with NASPE-Heart Rhythm Society. J Am Coll Cardiol. ;42(8):1493-1531. 
Bonnow et al. 2014. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 10th Edition. PA.Saunders
Brugada P et al. 1991. A New Approach to the Differential Diagnosis of a Regular Tachycardia With a Wide QRS Complex Circulation 83:1649-1659 (http://circ.ahajournals.org/content/83/5/1649)
Das and Zipes. 2012. Electrocardiography of arrhythmias: a comprehensive review. Elsevier PA
Fisch C and Knoebel S. 1992 .Vagaries of Aberrancy. Br Heart J 67:16-24
Fisch C and Knoebel SB. 2000. Electrocardiography of Clinical Arrhythmia. New York. Futura Publishing Co.
Fisch C. 1983. Aberration: seventy five years after Sir Thomas Lewis. Br Heart J; 50: 297 -302
Fisch C., Zipes DP and McHenry PL. 1973. Rate Dependent Aberrancy. Circ 48:714-724
Garner J and Miller J. 2013. Wide Complex Tachycardia – Ventricular Tachycardia or Not Ventricular Tachycardia,That Remains the Question. Arrhythmia & Electrophysiology Review 2013;2(1):2329
Goldberger A. 2013. Goldberger’s Clinical Electrocardiography : A Simplified Approach 8Ed. Ph Elsevier
Issa Z, Miller J and Zipes D. 2012. Clinical Arrhythmology and Electrophysiology: A Comprehensive Review - A Companion to Braunwald’s Heart Disease 2nd Ed. PA Saunders
Miller et al. 2006. The Value of 12-Lead ECG in Wide QRS Tachycardia Cardiology Clinics 24:439-451
Surawicz B and Knilans TK. 2008. Chou’s Electrocardiography in Clinical Practice. 6th ed. PA. Saunders-Elseiver
Vereckie A et al. 2008.New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm ;5:89 –98  (http://lab230.com/files/Miller_Criteria_for_wide_complex_tachycardias-_EHJ.pdf)

Wang K. 2013. Atlas of Electrocardiography. India. JP Brothers Medical Publishers

April 23, 2017

ECG characteristics of Torsades de Pointes (TdP)


Torsades de Pointes (TdP) was coined by Dessertnne in 1966 as a polymorphic ventricular tachycardia characterized by twisting of points.



Image 1 

ECG features:

1. Change in amplitude (QRS) and twisting of the QRS complexes around the isoelectric line

2. Short-long-short pattern of R-R cycles (short-coupled PVC followed by a compensatory pause and then another PVC that falls close to the peak of the T wave).

3.Usually shows a warm-up phenomenon

4. Frequently terminates spontaneously (in contrast to VF that does not terminate without defibrillation).

TdP - (suggested) to be confined to polymorphic VT with marked QT prolongation (> 500 ms) and QT-U deformity because of distinct mechanistic and therapeutic entity.

- http://circ.ahajournals.org/cgi/content/full/121/8/1047

#180