A middle-aged patient with no known significant past medical history had sudden onset of palpitations, diaphoresis, dyspnea. This lasted for roughly 30 seconds. EMS was called and he had palpitations again and had this monitor strip (labeled as leads I, II, and III):
He was awake with a normal blood pressure and no shock.
A rate of 302 is very fast for any tachycardia in an adult, but is particularly fast for ventricular tachycardia. The narrow spike at the beginning of each QRS suggests that the ventricle is activated through the fast conducting Purkinje system, and is probably a supraventricular rhythm. One typical SVT that occurs at a rate of 300 is atrial flutter. It is unusual, however, for the AV node to conduct at this rate.
No matter what the source, it is very fast.
Before this could be electrically cardioverted, the patient spontaneously converted to sinus rhythm (again, leads I, II, and III):
He arrived in the ED and had this 12-lead ECG:
That the patient tolerated his rhythm of 300 is very re-assuring and makes this rhythm much less life-threatening than if he had been syncopal, hypotensive, or in shock. It also suggests a structurally normal heart. A patient with cardiomyopathy would not tolerate this rate. He remained stable in the ED.
K was 3.6 mEq/L. Mg was 1.6 mEq/L.
Thinking the patient had suffered from VT, he was started on amiodarone.
Because of worry about primary ischemia as the underlying etiology, he went to the cath lab and coronaries were normal.
An echocardiogram showed normal anatomy and function.
While in the hospital, he again had symptoms and had another ECG recorded:
Considerations in the diagnosis:
The electrophysiologist noted A-V dissociation in lead-II (which is nearly diagnostic of ventricular tachycardia). I am unable to recognize it in this tracing.
An LBBB pattern by itself strongly suggests an SVT with LBBB-type aberrancy, as does the QRS duration of 120 ms. Most typical VT (but certainly not all) has a QRS duration of > 140. Few typical (i.e., not fascicular) VT have a QRS as short as 120 ms.
However, the fact that the patient has RBBB at baseline, and this ECG has LBBB, makes SVT (sinus, PSVT, flutter) with LBBB-aberrancy virtually impossible.
So now we know that it is wide, LBBB, not SVT with aberrancy, and not a typical VT. The ultrasound showing a structurally normal heart also makes typical VT unlikely.
If you can see A-V dissociaton as the electrophysiologist did, that clinches the diagnosis of VT.
This leaves us with the "idiopathic" ventricular tachycardias: probably fascicular VT or right ventricular outflow tract VT. These are "idiopathic" VT's which occur in an otherwise normal heart, and are, compared to typical VT, relatively narrow. See these cases for a more detailed explanation of fascicular VT.
Subsequent events;
For the second rhythm, the electrophysiologist suspected right bundle branch fascicular re-entry (I had not heard of it before) because of the presence of baseline RBBB when in sinus.
For the first rhythm, he suspected atrial flutter with 1:1 conduction.
At EP study, he was right on both counts, and underwent ablation of fascicular VT as well as cavo-tricuspid isthmus ablation to eliminate the atrial flutter loop.
The patient did very well.
Final Diagnosis:
1. Atrial Flutter at rate of 302 with 1:1 conduction and ventricular rate of 302 with RBBB.
2. Right Bundle Fascicular Re-entrant Tachycardia.
 |
| There is a wide complex tachycardia at a rate of 302. There is a narrow spike at the top of each wave, suggesting rapid conduction to the ventricle. Perhaps it is actually a narrow complex? |
He was awake with a normal blood pressure and no shock.
A rate of 302 is very fast for any tachycardia in an adult, but is particularly fast for ventricular tachycardia. The narrow spike at the beginning of each QRS suggests that the ventricle is activated through the fast conducting Purkinje system, and is probably a supraventricular rhythm. One typical SVT that occurs at a rate of 300 is atrial flutter. It is unusual, however, for the AV node to conduct at this rate.
No matter what the source, it is very fast.
Before this could be electrically cardioverted, the patient spontaneously converted to sinus rhythm (again, leads I, II, and III):
 |
| This shows sinus rhythm. There is a wide complex with a deep S-wave in lead I, strongly suggesting right bundle branch block. |
He arrived in the ED and had this 12-lead ECG:
 |
| Again, sinus rhythm, and with confirmation of RBBB. No ischemia. |
That the patient tolerated his rhythm of 300 is very re-assuring and makes this rhythm much less life-threatening than if he had been syncopal, hypotensive, or in shock. It also suggests a structurally normal heart. A patient with cardiomyopathy would not tolerate this rate. He remained stable in the ED.
K was 3.6 mEq/L. Mg was 1.6 mEq/L.
Thinking the patient had suffered from VT, he was started on amiodarone.
Because of worry about primary ischemia as the underlying etiology, he went to the cath lab and coronaries were normal.
An echocardiogram showed normal anatomy and function.
While in the hospital, he again had symptoms and had another ECG recorded:
 |
| This is very different from the first. It shows a regular wide complex tachycardia, with a left bundle branch block pattern and an inferior axis. The rate is 180. There are no P-waves. The QRS duration is only 120 ms, which is quite narrow for VT. |
The electrophysiologist noted A-V dissociation in lead-II (which is nearly diagnostic of ventricular tachycardia). I am unable to recognize it in this tracing.
An LBBB pattern by itself strongly suggests an SVT with LBBB-type aberrancy, as does the QRS duration of 120 ms. Most typical VT (but certainly not all) has a QRS duration of > 140. Few typical (i.e., not fascicular) VT have a QRS as short as 120 ms.
However, the fact that the patient has RBBB at baseline, and this ECG has LBBB, makes SVT (sinus, PSVT, flutter) with LBBB-aberrancy virtually impossible.
So now we know that it is wide, LBBB, not SVT with aberrancy, and not a typical VT. The ultrasound showing a structurally normal heart also makes typical VT unlikely.
If you can see A-V dissociaton as the electrophysiologist did, that clinches the diagnosis of VT.
This leaves us with the "idiopathic" ventricular tachycardias: probably fascicular VT or right ventricular outflow tract VT. These are "idiopathic" VT's which occur in an otherwise normal heart, and are, compared to typical VT, relatively narrow. See these cases for a more detailed explanation of fascicular VT.
Subsequent events;
For the second rhythm, the electrophysiologist suspected right bundle branch fascicular re-entry (I had not heard of it before) because of the presence of baseline RBBB when in sinus.
For the first rhythm, he suspected atrial flutter with 1:1 conduction.
At EP study, he was right on both counts, and underwent ablation of fascicular VT as well as cavo-tricuspid isthmus ablation to eliminate the atrial flutter loop.
The patient did very well.
Final Diagnosis:
1. Atrial Flutter at rate of 302 with 1:1 conduction and ventricular rate of 302 with RBBB.
2. Right Bundle Fascicular Re-entrant Tachycardia.
I'd first come across bundle branch reentrant tachycardia in a patient with muscular dystrophy and a WCT of unknown origin. The patient also had cardiomyopathy and an implanted pacemaker/ICD. The WCT happened to be of a low enough rate to not trip the ICD therapy. In my conversation with an EP doc on this patient's ECG, I learned that certain types of muscular dystrophy predispose a patient to bundle branch reentry (due to fibrosis in the myocardium and conduction system) amenable to ablation of the right bundle branch.
ReplyDeleteSome papers on that topic:
Finsler J, Stoellberger C, Keller H. Arrhythmia-related workup in hereditary myopathies. J Electrocardio. 2012;45:376-384.
Ramirez CJ, et al. Myotonic Dystrophy and Bundle-Branch Re-Entrant Tachycardia. Rev Esp Cardiol. 2002;55(10):1093-7.
Also, this paper from the Indian Pacing and Electrophysiology Journal has a great drawing showing the concept of BBR:
Mazur A, Kusniec J, Strasberg B. Bundle Branch Reentrant Ventricular Tachycardia. Indian Pacing Electrophysiol J. 2005;5(2):86-95. [PubMed Central: PMC1502081]
Thanks, Christopher!
DeleteDear doctor as you said this is atrial flutter with 1:1 conduction one should think of wpw as he 300 cannot get through av node.
ReplyDeleteDefinitely, but that would have a wide complex (delta wave). It is of course possible to hide a delta wave in those flutter waves.
ReplyDelete