A 48-year-old male with a past medical history of SVT, atrial flutter/fibrillation, hypertension, and hyperlipidemia presents to the ED with chest pain, shortness of breath, and palpitations that started 3 hours prior to arrival. His symptoms started suddenly. He has been compliant with all of his home medications. An index ECG above was obtained in triage (Figure 1).
Interpretation:
Rate: 262 bpm; Rhythm: regular wide complex tachycardia; Axis: right axis deviation (I: neg, II: pos., aVF: pos) Intervals: PR: n/a, no p-waves; QRS: 223, wide; QT: 326, normal; P-Waves: no p-wave preceding QRS; QRS Complex: wide; ST Segment/T-waves: no T-wave inversions
Initial rhythm: SVT with aberrancy
This patient was brought back to the resuscitation bay and placed on pads. The treating team initially attempted vasovagal maneuvers twice without any success. They then gave adenosine 6 mg IV and obtained the following ECG (Figure 2):
Figure 2. Repeat ECG s/p adenosine 6 mg IV.
Interpretation:
Rate: 131 bpm; Rhythm: regular narrow complex tachycardia, P waves are marched out with red dots; Axis: normal axis (I: pos, II: pos., aVF: pos) Intervals: PR: QRS: 89, narrow; QT: 367, normal; P-Waves: 2 P waves to 1 QRS complex; QRS Complex: good R wave progression; ST Segment/T-waves: no T-wave inversions
New rhythm: Atrial flutter 2:1
After adenosine converted the rhythm to atrial flutter 2:1, the patient received metoprolol 5 mg IV 3 times, and the rate persistently stayed exactly at 130. Cardiology was consulted, and the patient was admitted to the Cardiac ICU, where he ultimately underwent an electrophysiology (EP) study and ablation diagnosing him with atypical left atrial flutter with plans to consider an atrial fibrillation ablation in the future. It is believed the wide QRS complex in the initial ECG was a rate-related bundle branch block.
Discussion:
Wide complex tachycardias (WCTs) can be very tricky to determine the underlying etiology, even after thorough analysis and repeat ECGs. In some case, the true arrhythmia is only confirmed in the EP lab. The differential for WCTs is broad and includes ventricular tachycardia (VT), SVT with aberrant conduction, or antidromic atrioventricular reentrant tachycardia (AVRT, which is a subset of Wolff-Parkinson-White). When you are handed an ECG that shows a WCT, consider the following algorithm to help you differentiate between VT and SVT to aid in determining your management (Figure 3) (1,2):
Figure 3. Brugada algorithm to interpret WCTs.
Step #1:
Are there any RS complexes in leads V1-6? If you are seeing only R’s or only S’s without both aspects of the QRS complex, this is likely VT.
Step #2:
If there are RS complexes, how wide is the interval? If >100 msec, likely VT (Figure 4). If <100 msec, continue going through the pathway to consider SVT.
Figure 4. RS complex >100 msec.
Step #3:
Is there AV dissociation? If there are P waves present, do they look like they’re at a different rate than the QRS complexes? If yes, this is possibly VT. However, if there is no dissociation or no P waves seen at all, continue the pathway.
Step #4:
Do we meet morphologic criteria for VT in leads V1, V2, and V6? What does this look like? In leads V1 and V2, look for a right bundle branch block or a left bundle branch block. In V6, look for a LBBB-like pattern with QS waves (Figure 5) or with qR waves (Figure 6).
Figure 5. LBBB pattern with QS waves.
Figure 6. LBBB pattern with qR waves.
At the end of this algorithm, if your patient does not meet any of these criteria, you should consider SVT as the more likely arrhythmia and try adenosine to unmask the rhythm. The benefit of using adenosine is that the effects are typically transitory and have a lower risk of pushing a patient into VT/VF, but you should always have the pads on the patient in case they become unstable. If you have any doubt about the rhythm, it is always safest to treat it as VT.
It has been reported that the Brugada algorithm has a sensitivity of 0.987 and specificity of 0.965 for identifying VT compared to a sensitivity of 0.965 and a specificity of 0.987 for SVT, but other studies have suggested that there is user variability potentially skewing these results and limiting its clinical value in the ED (3,4).
Regarding atrial flutter, which was ultimately diagnosed in the EP lab, this is a common cause of SVT. The QRS is typically narrow but can widen if there is a pre-existing or rate-related bundle branch block, or if the patient has an accessory pathway between the atria and ventricles. The typical atrial activity rate is around 300 bpm, but the ventricular rate is a fraction of this, usually either 2:1, 3:1, or 4:1. For example, this patient’s repeat ECG after adenosine demonstrated a narrow-complex tachycardia with a 2:1 block at a heart rate of 131 bpm.
Figure 7. Atrial flutter with 2:1 block.
Patients who are in atrial flutter will have very persistent rates with minimal variation. While beta blockers or calcium channel blockers help control the ventricular rate, patients typically require an ablation for definitive management.
Take Away Points:
If you have a stable patient with a WCT, place pads on the patient and consider using the Brugada algorithm to try to differentiate the rhythm.
When in doubt it is always safest to treat the rhythm as VT.
If you have a low suspicion for WPW, adenosine can be considered to try to reevaluate the underlying etiology.
If the underlying rhythm is VT, adenosine will not likely change the rate/rhythm but will not harm the patient.
If the patient is unstable, perform synchronized cardioversion on the patient rather than going through the Brugada pathway.
Authored by Megan Buranosky, MD and Ari Edelheit, MD.
References:
Buttner, R. (2024, Oct 8). VT versus SVT. Life in the Fast Lane. https://litfl.com/vt-versus-svt-ecg-library/
Buttner, R and Burns, E. (2024, Oct 8). Atrial Flutter. Life in the Fast Lane. https://litfl.com/atrial-flutter-ecg-library/
Brugada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991; 83:1649.
Isenhour, J.L., Craig, S., Gibbs, M., Littmann, L., Rose, G. and Risch, R. (2000), Wide-complex tachycardia: Continued Evaluation of Diagnostic Criteria. Academic Emergency Medicine, 7:769-773. https://doi.org/10.1111/j.1553-2712.2000.tb02267.x