Below is a common and important ECG that somehow hasn’t made it onto this blog yet!
A middle aged man presented with acute shortness of breath. He was hemodynamically stable but in mild respiratory distress, with diffuse B-lines and requiring BIPAP.
Here is his initial ECG:
|What is your interpretation? What is the rhythm? Are there signs of acute coronary occlusion?|
This shows an irregularly irregular wide complex tachycardia at a rate of about 120. Of course, whenever confronted with a wide complex tachycardia, one must consider ventricular tachycardia. However, unless it is polymorphic VT (which has multiform QRS complexes), VT is never this irregular. An irregularly irregular rhythm must put atrial fibrillation (AF) at the top of the differential.
The QRS complex is classic for LBBB except that V1 and V2 do not show a large, predominant S-wave. It is possible that lead misplacement may account for these two leads, but the rest of the precordial leads and high lateral leads have morphology diagnostic of LBBB. Thus, this is most likely AF with LBBB. Is there coronary occlusion? If there is, it is not evident on this ECG: it does not meet either the original or modified Sgarbossa criteria.
The differential diagnosis of irregularly irregular wide complex tachycardia is an important one, as it includes dangerous etiologies such as Pre-excited AF (AF with WPW), polymorphic VT, and hyperkalemia-induced arrhythmias, in addition to the more common etiology of Atrial Fib with aberrancy (including LBBB and RBBB).
Unfortunately, the common management for AF with aberrancy (AV nodal blockers to slow the ventricular response) is contraindicated in AF with WPW, as it can precipitate ventricular fibrillation.
How do we know it is NOT AF with WPW?
1) In AF with WPW, the QRS has multiple waveforms. In this ECG, there are slight variations, but they are all basically the same.
2) Most important, in AF with WPW, there can be very short RR intervals because the accessory pathway can have a very short refractory period, allowing it to conduct to the ventricles with RR intervals less than 250 ms. In this case, the shortest RR interval is about 360 ms.
As in all ECG interpretation, finding an old ECG is often very helpful. Identical QRS morphology from a prior known supraventricular rhythm would confirm that the tachycardic rhythm is indeed supraventricular, and would allow a degree of safety in giving AV nodal blocking agents.
Here is the patient’s prior EKG:
|Sinus rhythm with LBBB. All leads have nearly identical morphology as the presentation ECG above, except that V1 and V2 in this prior ECG (in contrast to the presenting ECG) are typical for LBBB. The fact that all other leads match supports the possibility that lead placement is to blame for the first ECG. But it is uncertain.|
This ECG was taken as evidence that the first ECG was, as suspected, AF with LBBB. The patient was given 20mg, then 25mg of diltiazem IV, which lowered the rate satisfactorily.
The patient then spontaneously converted to sinus rhtythm without further therapy (This is not necessarily a result of the diltiazem, which does not generally “convert” AF; it only slow the ventricular response. Thus, the conversion to sinus is likely coincidental):
Sinus rhythm with LBBB. V1 is slightly more similar to baseline, but the abnormality (from classic LBBB) in V2 remains. There is likely still lead misplacement.
1) With the exception of polymorphic VT (multiple QRS complexes), VT is fairly regular.
2) Irregularly irregular wide complex tachycarrhythmias include dangerous etiologies such as Preexcited AFib which must be suspected in order to avoid harms of AV nodal blocking agents.
3) However, AFib with preexisting bundle branch block is the most common overall etiology.
4) A prior ECG with identical morphology is helpful in determining whether a wide complex rhythm is supraventricular.
5) You must memorize the morphology of LBBB and be able to recognize it instantly.