Pages

February 13, 2017

Atrial Tachycardia and AV Block



A 70 yo patient with history of diabetes and hypertension is admitted due to tachycardia. What is your ECG interpretation?



Figure 1 - ECG case





Figure 2 - ECG case marked

This is an irregular narrow complex rhythm with a ventricular rate of about 40 bpm (4 QRS x 10) with an initial atrial rate of about 120 bpm then a sudden decrease in atrial rate of about 80 bpm.

What is the rhythm?

The clue to the diagnosis of the rhythm is the sudden decrease in the atrial rate which is from about 120 bpm to about 80 bpm. If this was sinus tachycardia to sinus rhythm, the change in rate will be gradual. However, in this case, the change in rate was abrupt or sudden. An atrial rhythm with this rate (~120 bpm) with isoelectric baseline between P waves is indicative that the initial rhythm in the ECG strip is atrial tachycardia or AT (red arrows). After the atrial tachycardia there is spontaneous conversion to sinus rhythm (blue arrows). The light green arrow points to a possible premature atrial complex.

Is this Complete Heart Block?

In complete heart block, whether the escape pacemaker is from the AV junction or lower, the R to R interval is regular. If the R to R interval is irregular then some of the impulses were conducted. The R to R in this strip is not regular (1440 to 1280 ms). Thus, this is not complete heart block.

Some Form of AV Block

In the case presented during atrial tachycardia (~125 bpm), the R to R is regular (1440 ms) with 3 organized P waves between 2 QRS complexes. It would indicate 3:1 AV conduction. In fast atrial rhythms like atrial tachycardia and atrial flutter, some of the atrial impulses are not conducted to the ventricles because of the modulating role of the AV node. Failure of the AV node to conduct during fast atrial rhythms should not be considered pathological AV block. One of the functions of the AV node is synchrony of atrial and ventricular contraction. Failure of the AV node to conduct every atrial impulse occurring at fast rates should be considered a normal physiologic finding caused by normal refractoriness. So, terminologies like 3:2 AV conduction is appropriate than 3:2 AV block. This electrophysiologic phenomenon is often called decremental conduction. This means as the cycle length is progressively shortened (rate is increased), conduction delay is increased.  

However, as we note on the strip, 2:1 AV conduction is noted at slower atrial rate (~80 bpm). Under normal conditions, the AV node must have recovered from the previous supraventricular impulse. Thus, there must be some form of AV block.
During the course of monitoring, the ventricular rate was mostly in the 40’s (2:1 AV conduction) and recurrent episodes of AT with block.

The Electrophysiologic Study (EP)

The EP study showed focal atrial tachycardia (AT) in the superior lateral right atrium (ablation done) and intranodal AV block. A permanent pacemaker was placed.

What happened next?

There was no recurrence of the AT. The patient was noted to be V-pacing most of the time and was discharged after a few days.

Take Home Message
  •        If you see some form of AV block but the R to R interval is not regular then it is not complete heart block.
  •       Sometimes, the AV blocks we see on the surface ECG cannot be classified according to textbook definitions.
  •       Sudden or abrupt change in atrial rate would rule-out sinus tachycardia and we should consider atrial tachycardia.
  •       During fast atrial rhythms (atrial tachycardia/atrial flutter), 3:2 or 2:1 AV conduction is an appropriate term to use than AV block.


Interpretation: Atrial tachycardia with 3:1 AV conduction and sinus rhythm with 2:1 AV conduction.


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
Das and Zipes. 2012. Electrocardiography of arrhythmias : a comprehensive review. Elsevier PA
Fisch C and Knoebel SB. 2000. Electrocardiography of Clinical Arrhythmia. New York. Futura Publishing Co.
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
Josephson M. 2008. Clinical Cardiac Electrophysiology: Techniques and Interpretations, 4th Edition. Lippincott Williams & Wilkins PA
Kumar UN et al. 2006. The 12L Electrocardiogram in Supraventricular Tachycardia. Cardiology Clinics ;24: 427-437
Saoudi N et al.2001. Classification of Atrial Flutter and Regular Atrial Tachycardia According to Electrophysiologic Mechanism and Anatomic Basis: A Statement from Joint Expert Group from the Working Group of Arrhythmias of the European Society of Cardiology and North American Society of Pacing and Electrophysiology. Journal of Cardiovascular Electrophysiology 12: 852-866
Stahmer SA and Cowan R. 2006. Tachydysrhythmias. Emergency Medicine Clinics of North America 24:11-40
Surawicz B and Knilans TK. 2008. Chou’s Electrocardiography in Clinical Practice. 6th ed. PA. Saunders-Elseiver
Zimetbaum P and Josephson. 2009. Practical Clinical Electrophysiology. Lippincott Williams & Wilkins PA
Zipes D and Jalipe J. 2014. Cardiac Electrophysiology: From Cell to Bedside 6th ed. Elsevier PA

#672


No comments:

Post a Comment

Note: Only a member of this blog may post a comment.