Welcome back to another Clinical Image of the Week from the case files of the Brown EM Residency!
HPI: A 60 year old female presents with palpitations after walking on the beach with friends. She states she was sitting at her favorite clam shack, and felt the onset of a “rapid heart rate”. Thinking she was dehydrated, she drank some water, and her palpitations resolved after five minutes. After returning home, the palpitations recurred, and after 40 minutes she felt “really tired, really washed out”, but at no point had any chest pain, dyspnea, or lightheadedness. She looked “gray” to her husband, so he called 911.
Vitals: BP 160/110, HR 210, T 98.7 °F, RR 22, SpO2 99% on RA
Notable PE: Pale and anxious appearing. On auscultation, tachycardic without murmur, rub, or gallop. Regular rhythm. Intact and equal pulses throughout. Mild increased work of breathing. Lungs are clear bilaterally. No lower extremity edema.
The following EKG was obtained:
Stable Monomorphic Ventricular Tachycardia
The age old question: Is it VT or SVT with aberrancy? Do I manage these differently?
(Note that the EKG reading says ‘Acute MI’. Don’t depend on the machine reading!)
As a general rule of thumb, ventricular tachycardia will have QRS complexes >140 ms, and there should be no p waves proceeding each QRS complex (implying sinus rhythm).
There’s been quite a bit of literature looking at the delineation between ventricular tachycardia and SVT with aberrancy. Lets take a look at some:
Brugada, et al prospectively analyzed 384 patients with VT and 170 patients with SVT (with aberrancy), and came up with the following clinical decision rules:
1: Is there an absence of RS waves in all precordial leads (i.e. is the QRS concordance across all precordial leads the same)? If yes, think VT.
2: Is the R to S interval >100 msec (implying conduction originating in the ventricular myocardium versus conduction pathways)? If yes, think VT.
Unfortunately, the Brugada criteria did not fare quite as well in validation studies. Along came the Verecki criteria, which restricted the analysis to lead aVR only. They looked for the presence of an initial R wave (implying conduction moving from the apex of the heart towards the base), the width of an initial R or Q wave >40 msec (implying myocardial conduction versus conduction fibers), and notching on the initial downstroke of a predominantly negative QRS complex. Any 1 of these 3 criteria being positive, was a diagnosis of VT.
Well, by now, most people’s heads were spinning. In an effort to simplify this whole process, the Sasaki rule was devised. They applied both of the above rules to 107 patients with wide complex tachycardias and examined the diagnostic accuracies of each. Their rule was simpler and more accurate than both of the above rules:
1: Initial R in aVR (from the Verecki)? If no, then step 2.
2: Longest RS >100 msec (from the Brugada, see above)? If no, then step 3.
3: Initial R or Q >40 msec (from the Verecki). No, then think SVT.
A few more thoughts:
- There is no single criterion or combination of criteria that provides complete diagnostic accuracy. For instance, there have been no validation studies of the Sasaki rule.
- Of wide complex tachycardias, ventricular tachycardia is the most common.
- If your patient has a history of structural heart disease, ischemic heart disease, or heart failure (especially if elderly), presume ventricular tachycardia (up to 90% of cases).
- If you’re unsure of the diagnosis, treat as though it is VT. Speaking of which…
Treatment of wide complex tachycardia:
- ABCs. ABCs. ABCs.
- Pulseless? Begin ACLS.
- Unstable (chest pain, hypotensive, altered mental status, heart failure)? Synchronized cardioversion.
- Stable? Electric or chemical conversion. You can also safely use adenosine in these patients assuming the rhythm is regular, which will convert a patient in SVT and not harm a patient in VT.
- An irregular rhythm with a wide QRS could be WPW. Do not use adenosine in this scenario. Wait, didn’t I already do a post on this? I sure did.
The patient received an amiodarone bolus with resolution to sinus rhythm. Cardiology was consulted afterwards and agreed with a VT diagnosis after viewing EKG. The patient was placed on an amiodarone drip and transferred to the CCU where she underwent electrophysiology studies.
The contents of this case were deliberately altered to protect the identity of the patient. All content in this report are for educational purposes only. The patient consented to the use of these images.
Faculty Reviwer: Dr. Gita Pensa
Guest Reviewer: Dr. Arslan Johnghar of Cardiology
See you next week!
1: Brugada, et. al. A New Approach to the Differential Diagnosis of a Regular Tachycardia with a Wide Complex QRS Complex. Circulation. 1991; 83(5):1649-59.
2: Sasaki, K. A New Simple Algorithm for Diagnosing Wide QRS Complex Tachycardia: Comparison with Brugada, Verecki and aVR Algorithms. Circulation. 2009; 120:S671.
3: Verecki, et. al. New Algorithm Using Only Lead aVR for Differential Diagnosis of Wide QRS Complex Tachycardia. Heart Rhythm. 2008; 5(1):89-98.
4: Karuturi. Fusion Beat – Ventricular Tachycardia. <http://www.imnotebook.com/content/fusion-beat-ventricular-tachycardia>. 2011.
5: Smith. Wide Complex Tachycardia: Ventricular Tachycardia or Supraventricular Tachycardia with Aberrancy. <http://hqmeded-ecg.blogspot.com/2011/10/wide-complex-tachycardia-ventricular.html>. 2011.
6: Supraventricular Tachycardia with Aberrancy Versus Ventricular Tachycardia. <http://www.foamem.com/2013/07/23/supraventricular-tachycardia-svt-with-aberrancy-versus-ventricular-tachycardia-vt/>. 2013.