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Wide complex tachycardias: 2 cases. What is the diagnosis and management?

Posted May 09 2011 5:43pm
This is the most widely misunderstood problem in Emergency tachydysrhythmia care.  There are many textbooks and articles and preparatory tests that get this wrong.  So read carefully!

Case 1.

This is a 37-year-old male who states that he has paroxysms of chest palpitations which usually last about 15 minutes and get better with cough or changes in position. The previous evening at approximately 11 p.m., he began to have chest palpitations which lasted through the night until the morning of admission. Along with these palpitations, he had some headache with dizziness. He denied any chest pain or shortness of breath.  He did admit to crack cocaine use over the past several days.

There are no p-waves.  The rate is 180 and constant.  It is regular.  It is wide.
What is your differential diagnosis?
What are the treatment options in the ED?


Case 2.
This is a case that comes courtesy of Dr. Kyuhyun Wang (long time Hennepin EKG wizard and my mentor, now at the University of Minnesota).   It is from his marvelous Atlas of Electrocardiography, with permission.

This is an irregularly irregular rhythm.  The QRS is wide and bizarre, with multiple QRS morphologies and very short R-R intervals
What is your differential diagnosis?
What are the treatment options in the ED?
There is sinus rhythm with a very short PR interval and widespread delta waves.  This confirms that the first ECG was antidromic reciprocating tachycardia.  There are secondary repolarization abnormalities (ST depression) very typical of WPW.  This confirms that the first ECG was antidromic reciprocating tachycardia.

http://hqmeded-ecg.blogspot.com/search/label/wolff%20parkinson%20white%20WPW



Answer to Case 2:

This is irregularly irregular.  Only MAT and atrial fibrillation are irregularly irregular.  Since there are no p-waves, this is atrial fibrillation.  There is a wide complex.   Atrial fibrillation with a wide complex can be atrial fib with RBBB or LBBB or nonspecific intraventricular conduction delay, but these do not have extremely short R-R intervals and do not have multiple QRS morphologies. 

The shortest R-R interval is less than 200 ms, which is very short; this atrial fibrillation is able to be conducted to the ventricles at an extremely fast rate.  This and the multiform QRS can only be due to a bypass tract, as in WPW.  Any AV nodal blocker (adenosine, Ca channel blocker, beta blocker, digoxin) is contraindicated because is may increase the conduction rate through the bypass tract and result if ventricular fibrillation.  To treat this, one must convert the atrial fib to sinus, either chemically (e.g. procainamide) or (my preference) electrically.

The post cardioversion ECG of the second case is unavailable but might look similar to the one above, depending on the location of the bypass tract.Literature: This paper established adenosine as safe in ventricular tachycardia and led to new ACC/AHA guidelines which state that adenosine may be given in regular wide complex tachycardia:
Marill KA et al. Adenosine is safe and effective for differentiating wide-complex supraventricular tachycardia from ventricular tachycardia.  Crit Care Med 2009 Sep 37:2512. 
Summary of points

1) Any fast rhythm which worries you may be treated with electrical cardioversion.  If confused, use electricity.  If the patient is unstable, use electricity.
2) AV nodal blockers are only contraindicated when there is atrial fib with WPW
3) In regular tachycardias due to WPW (even wide ones!), AV nodal blockers are safe and effective.  They block the limb of the re-entrant rhythm which goes through the AV node, thus interrupting the circuit.
4) Atrial fib with WPW is very recognizable: there are bizarre QRS with multiple morphologies, and very fast rhythms with short R-R intervals.  If you can find any R-R interval shorter than 240 ms, then AV nodal blockers are definitely dangerous.
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