ECG Blog #335 — Is there Proof?

You are given the ECG shown in Figure-1 — and told only that the patient is a 40-year old man, who was hemodynamically stable.

QUESTION:

• How would YOU interpret this tracing?

==============================

NOTE: Unfortunately — no long lead rhythm strip was recorded. That said — it turns out that a long lead rhythm strip was not needed for definitive diagnosis.

==============================

Figure-1: 12-lead ECG obtained from a 40-year old man. He was hemodynamically stable at the time this ECG was recorded.

MY Approach to the ECG in Figure-1:

As always – I favor beginning interpretation with assessment of the long lead rhythm strip — using the Ps, Qs & 3R Approach to recall the 5 KEY Parameters (See ECG Blog 185). I find it easiest (and most productive) to delay assessing the 12-lead ECG until after I’ve had a chance to look at the rhythm.

• The rhythm is fast and regular (although not quite as fast as one might think from initial inspection = about 115/minute). The QRS is wide. Regular sinus P waves that conduct are not seen (ie, there is no upright P wave with constant and normal PR interval before each QRS complex in lead II).

What Have We Described for the Rhythm in Figure-1?

We have described a regular WCT ( = Wide-Complex Tachycardia) rhythm at ~115/minute — but without clear sign of normally conducting sinus P waves.

• PEARL #1: As emphasized often on these ECG Bogs — the most common cause (by far!) of a regular WCT rhythm without sinus-conducting P waves is VT (Ventricular Tachycardia). Depending on clinical circumstances of the case at hand — between 80-to-90+% of such rhythms will turn out to be VT. For that reason — ALWAYS assume VT until proven otherwise!
• 
  
• PEARL #2: Prominent among ECG features that may assist in the diagnosis of a regular WCT — is QRS morphology. VT is favored IF — QRS morphology does not resemble any known form of conduction defect (ie, LBBB or RBBB, with or without a hemiblock). This is the case with the ECG in Figure-1. Although the predominantly upright qR pattern in lead V1, with wide terminal S wave in lead V6 resembles RBBB (Right Bundle Branch Block) conduction in the chest leads — the indeterminate frontal plane axis (ie, leads I,II,III all predominantly negative) is not typical for RBBB conduction in the limb leads. That said — I thought QRS morphology in ECG #1 was clearly not definitive for a ventricular etiology.
• 
  
• NOTE: For review of "My Take" on the ECG approach for assessing the regular WCT rhythm — Check out ECG Blog #196 — Blog #220 — Blog #263 — and Blog #283 —

CHALLENGE: 

Returning to today's case — there is 1 ECG feature that is all but definitive for VT in Figure-1. What might this be?

• HINT: Take Another LOOK at the ECG in Figure-1. WHY might QRS morphology in lead II be changing?

ANSWER:

• See Figure-2 ...

Figure-2: RED arrows highlight why QRS morphology in lead II is subtly changing (See text).

Why QRS Morphology in Lead II is Changing:

There are 5 RED arrows in Figure-2. These arrows represent atrial activity — that is best seen under the 1st RED arrow — partially seen under the next 3 RED arrows (as these P waves distort the initial part of the QRS complex) — and almost completely hidden within the QRS under the last RED arrow.

• PEARL #3: The fact that the position of the 5 P waves highlighted by these RED arrows is constantly moving with respect to its neighboring QRS complex — tells us that these P waves are unrelated to QRS complexes (ie, there is complete AV dissociation for these 5 beats). This finding of complete AV dissociation of a regular atrial rhythm from the wide tachycardia (at least for a significant portion of the WCT rhythm) — is virtually diagnostic of VT (See ECG Blog #133 — Blog #134 — and Blog #151 for additional examples illustrating how AV dissociation allows you to confirm the diagnosis of VT!).
• 
  
• PEARL #4: Although the ECG finding of AV dissociation provides invaluable assistance for confirming the diagnosis of VT — it will usually not be seen with the most problematic forms of VT (which are those VTs that occur at faster heart rates). This is because the faster the ventricular rate of VT — the more likely it is that underlying sinus P waves will be hidden (ie, within QRS complexes or within ST-T waves). It is because the ventricular rate of the WCT rhythm in today's case was relatively slow (ie, only ~115/minute) — that we are able to identify AV dissociation for the 5 P waves highlighted by RED arrows in Figure-2 (Note that we do not see evidence of AV dissociation in the rest of today's tracing).
• 
  
• PEARL #5: In my experience — AV dissociation is greatly overdiagnosed! There is a tendency to label as "AV dissociation" any (and sometimes all) unexpected deflections seen in a WCT tracing. Most of the time (in my experience) — these "extra" deflections are not underlying P waves — but rather reflect artifact that is so common in symptomatic patients with marked tachycardia. Because of the clinical implications of identifying true AV dissociation in a regular WCT rhythm (ie, it virtually proves the rhythm is VT!) — I favor only diagnosing AV dissociation when you can be certain it is present (ie, when you can reliably identify at least a series of regular underlying P waves at a constant rate — as is possible for the 5 consecutive RED arrows seen in Figure-2).
• 
  
• PEARL #6: As I've emphasized — the rate of the regular WCT rhythm in today's tracing is not fast. It is ~115/minute — which lies at the limit between a "slower" form of VT = AIVR (Accelerated IdioVentricular Rhythm — which is often benign and associated with reperfusion) — and a "faster" VT rhythm (with much higher risk of deterioration to VFib and cardiac arrest). As a result — the clinical significance of today's rhythm will depend on the patient's hemodynamic stability — and — on clinical factors such as whether this rhythm represents a positive (and transient) sign that reperfusion of the "culprit" artery has just occurred. KEY POINT: Depending on these factors — the risk of today's rhythm deteriorating to VFib and cardiac arrest might be limited — and cardioversion or antiarrhythmic treatment might not necessarily be needed (See ECG Blog #108 and Blog #125 for more on AIVR).

CASE Follow-Up:

My follow-up to today's case is limited. I know that this patient had a recent MI — which suggests that the rhythm in Figure-2 may represent AIVR that developed in response to coronary reperfusion. Unfortunately — I lack confirmation of this.

• In the absence of more clinical information — I'd consider optimal interpretation of today's rhythm = "Ventricular Tachycardia at a rate of 115/minute". 
• I'd emphasize the need for clinical correlation to determine IF antiarrhythmic treatment, cardioversion — or — a "tincture of time" (ie, with no active treatment) is likely to represent the BEST approach to initial management.

==================================

Acknowledgment: My appreciation to Ahmed Shaaban (from Cairo, Egypt) for the case and this tracing.

==================================

 

Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
• ECG Blog #185 — Reviews my Systematic Approach to Rhythm Interpretation.