Case submitted by anonymous. Written by Smith. Ken's piece at the bottom is excellent.
A 50-something presented with sudden onset palpitations 8 hrs prior while sitting at desk at work. He had concurrent sharp substernal chest pain that resolved, but palpitations continued. Over past 3 months, he has had similar intermittent episodes of sharp chest pain while running, but none at rest. Past medical history includes coronary stenting 17 years prior. A brief chart review revealed his most recent echo in 2018, with LV EF 67%, “very small” inferior wall motion abnormality.
Initial ED ECG:What do you think?
This was shown to me with no clinical information and I said "It is VT until proven otherwise." Why did I say that?
1. It does not look like RBBB or LBBB; therefore, if there is aberrancy, it is atypical aberrancy
2. The rapidity of onset of the QRS is slow (in SVT with aberrancy, the first part of the QRS is through fast conducting Purkinje fibers and is therefore narrow). Look at the R-wave in V4: it takes 60 ms to reach its peak. It should be less than 30 ms.
3. It has a "Northwest Axis" (towards aVR). Correspondingly, as Ken notes below, the inferior leads are 100% negative, which virtually never happens in SVT.
4. There is a 40 ms q wave in aVR.
5. The 2 R-waves in V1 fulfill Brugada criterion of having the first R larger than the 2nd R (in true RBBB, the first r-wave is small and the 2nd R'-wave is large)
6. There is a deep S-wave in V5 and V6.
7. The 15th beat (2nd beat of V1-V3) appears to be a fusion beat, which is all but diagnostic of VT.
8. Ken notes AV dissociation. I find AV dissociation in VT to be very difficult to differentiate from artifact, as there are always random blips on tachycardia tracings.
So there are MANY features of VT and virtually zero features of SVT with aberrancy.
Then we must consider clinical data other than the ECG, for a pretest probability:
Of all wide complex tachydysrhythmias, the majority are VT.
If you take old people with a history of MI (he had a stent), that percentage goes far higher since there is scar tissue that acts as a nidus for the PVCs that initiate VT. The history of inferior wall motion abnormality confirms this.
A bedside echo showed good contractility.
The interpretation was SVT with aberrancy (erroneous).
The choice was to use electrical cardioversion with sedation.
No adenosine was given (if you believe it is SVT, this is worth a try). However, this is not SVT. If it is VT, adenosine is safe but not effective.
Shocked x 2 without effect. Pads were placed with ultrasound guidance, so they were in the correct position.
What to do now?
If you believe it is SVT, then try adenosine.
If you don't know what the dysrhythmia is, then try procainamide. Procainamide is proven better and safer than amiodarone for VT (Procamio randomized trial) AND it also works for SVT. So I would give procainamide.
Warning: if this is VT, a calcium channel blocker can result in shock and death.
K returned 3.6 mEq/L
2 g IV Mg was given. 10 mEq IV K (with plan for 40 mEq PO KCl) was given.
Heparin bolus (4000u), infusion
Plan for rate control
25 mg IV diltiazem given
HR = 143
25 mg IV repeat dose diltiazem given
HR = 143
Diltiazem drip 10 mg/ hr for ~20 min
HR remained 140 - 155
Then the patient developed Cardiogenic shock and echo had poor contractility
Amiodarone load given. Patient intubated.
Repeat cardioversion was then successful.
Cardiology was consulted and the patient underwent coronary angiogram which showed diffuse severe three-vessel disease.
Episodes of angina over past couple of months had been progressive.
--High sensitivity troponin I rose to peak at 2900 ng/L.
--Formal bubble contrast echo showed EF 35% with anterior, anterolateral and inferolateral akinesis.
--Coronary angiogram shows diffuse severe three-vessel disease.
--Patient will need CABG
1. Calcium channel blockers must be avoided in VT (unless it is fascicular VT, which has a different morphology. Read this post:
2. Pretest probability: Even before the ECG, a patient with a history of coronary stent has a 90% chance that his wide complex tachycardia is VT.
3. VT can be perfectly hemodynamically stable if the patient has good cardiac contractility. The reason that VT is associated with instability is that so many cases of VT are in patients with very poor LV function.
2. Learn to differentiate VT from SVT with aberrancy. Here are many discussions of, and cases of, SVT with aberrancy.
3. Electrical Cardioversion works for both, but when it does not, try procainamide (in addition to optimizing K and Mg). Procamio randomized trial.
MY Comment, by KEN GRAUER, MD (9/20/2023):
- Today's case is insightful in many ways — especially since despite prompt electrical cardioversion, we are told that this patient "was shocked X 2 without effect".
- There is no need to "prove otherwise" in today's rhythm — because ECG #1 (that I've reproduced in Figure-1) — already provides proof that this rhythm is VT.
- Definitive diagnosis that ECG #1 is in fact VT is more than academic. This is because the treating clinicians failed to make an accurate rhythm diagnosis — and, as a result — the wrong treatment was continued, with nearly lethal consequence (ie, IV loading with Diltiazem — followed by IV Diltiazem infusion for ~20 minutes resulted in severe hypotension).
- Why do I say there is proof in ECG #1 that the rhythm is VT?
- IV Diltiazem (and/or IV Verapmil) can be a treatment of choice in selected hemodynamically stable patients with Fascicular VT. That said — How do we know that IV Diltiazem was contraindicated in today's case?
- The fact that the 50yo man in today's case has known coronary disease (including exercise-induced angina over the previous 3 months) — means that even before looking at his initial ECG — statistical odds that his regular WCT rhythm will be VT are at least 90%.
- These statistical odds can be increased to over 95% likelihood of VT within a focused 5-to-10 second assessment that notes: i) There is extreme frontal plane axis deviation (ie, an all negative QRS in each of the inferior leads — which is virtually never seen in SVT rhythms); ii) QRS morphology in lead V1 is atypical for RBBB conduction because of the lack of an S wave, and the taller "left rabbit ear" (While this does not completely rule out the possibility of rbbb conduction — it does make SVT much less likely); and, iii) The almost-all-negative QRS complex in lead V6 (which will almost always have more positive activity in supraventricular rhythms).
- This is clinically relevant — because obtaining hard copy of what happened immediately after synchronized shock was delivered (even if the WCT rhythm resumes quickly thereafter) will often provide ECG clues to a definitive rhythm diagnosis. And IF it these clues would have been recognized — the inappropriate use of IV Diltiazem might have been avoided.
- Perhaps the reason clinicians in today's case thought the regular WCT rhythm that this patient presented in was SVT with aberrancy — was that the patient reported "hours" of palpitations?
- As I discussed and documented in Lesson 1 of My Comment at the bottom of the page in the April 2, 2022 post of Dr. Smith's ECG Blog — certain patients may remain in sustained VT not only for hours — but even for days!
- The 2nd most common form of idiopathic VT is Fascicular VT — which interestingly does often respond to IV Verapamil or Diltiazem (See Figure-3 below in the APPENDIX for my Summary of Idiopathic VT).
- That said — Today's patient does not have the simple form of Fascicular VT that responds to IV Verapamil or Diltiazem — because today's patient has underlying heart disease (as well as a history of exercise-induced angina in the 3 months prior to presentation). In addition — ECG features of the initial rhythm are atypical for the simple form of Fascicular VT likely to respond to calcium blockers (ie, marked QRS widening — extreme frontal plane axis deviation — almost-all negative QRS in lead V6).
- Since today's patient does not have this simple form of Fascicular VT — he almost certainly has an ischemic (scar-based) form of VT. The reason IV Diltiazem and Verapamil are contraindicated in ischemic VT — is that these calcium channel blockers are negative inotropes and vasodilators (the consequences of which were seen in today's case when the patient developed hypotension and cardiogenic shock following IV Diltiazem).
- It is not often that we see Fusion Beats in rapid regular WCT rhythms — because most of the time, the fast ventricular rate completely usurps any underlying supraventricular rhythm. However, when we do — this virtually proves that the WCT is VT — because unexpectedly narrow QRS complexes are unlikely to occur unless there is "capture" of a supraventricular impulse that somehow "gets through" and "fuses" with a ventricular beat.
- I am always surveying regular WCT rhythms for a "break" in the rhythm — and/or for some unexpected change (ie, narrowing) in the QRS. My eye was therefore immediately drawn to the distinctly different-looking (and narrower) beat #7 (that I have labeled F/C in Figure-2). And although beat #17 does not look much different from the other 23 beats in the long lead II rhythm strip — there is no doubt that this beat is different and narrower than all other simultaneously-recorded beats in leads V1,V2,V3. The only way for the ventricular beats in ECG #1 to become narrower (apart from rare "supernormal" conduction) — is if there is fusion with underlying supraventricular impulses (CLICK HERE — for more on Fusion Beats).
- The diagnosis of VT is not nearly as difficult when the rate of the WCT rhythm is not overly fast. This is because diagnostic fusion beats and AV dissociation are much more likely to be seen in these relatively slower ventricular rhythm.
- Today's regular WCT is ~140/minute — which is usually fast enough that identification of AV dissociation is typically challenging, if not impossible (ie, underlying sinus P waves will usually be hidden within QRS complexes and ST-T waves at this rapid a rate). That said — We can definitively diagnose AV dissociation in today's tracing!
- Although it is often difficult to distinguish movement artifact from definite underlying P waves — the RED arrow P wave in the long lead II rhythm strip immediately caught my eye!
- Once I knew that at least 1 definite underlying P wave was present — I diligently looked for more. This told me that the ORANGE arrow deflections were all clearly highlighting other underlying P waves. (There is no R wave in the QRS complex of ventricular beats in the long lead II rhythm strip — so the initial positive deflection seen at the beginning of the QRS of beats #2, 5, 8, 18, 21 and 24 is the superposition of regularly-occurring underlying sinus P waves on the QS complexes of the VT rhythm.)
- Note that 2 consecutive ORANGE arrow P waves (in the T waves of beats #12 and 13) follow the RED arrow P wave — which told me the underlying sinus P-P interval. Even without calipers — the above process (which took me no more than seconds to recognize) indicated enough on-time regular P waves to confirm AV dissociation — which told me 100% that ECG #1 is VT.
- In the "peace and quiet" of my office — Knowing the underlying P-P interval allowed me to map out (with PINK arrows) regular-occurring underlying sinus P waves throughout the rest of the rhythm strip (with many of these PINK arrow P waves producing extra "peaking" of T waves, as for the T waves of beats #3,6,9,16,19,22).
- To EMPHASIZE: I knew there was AV dissociation from recognition of the RED and ORANGE arrow P waves — that with practice, can be recognized at the bedside without calipers in no more than a few seconds.
- Final POINT: For there to be "capture" and "fusion" — an on-time sinus P wave should be seen to occur at a point in the cardiac cycle in which conduction of a supraventricular impulse would be likely. Note that the long vertical BLUE arrow extending upward from the PINK arrow P wave in the T wave of beat #16 does occur at a point in which conduction of the F/C complex would be likely.
- CLICK HERE — for more on use of AV Dissociation in the diagnosis of VT.
- Although detection of fusion, capture and/or AV dissociation will not often be found in those more-difficult-to-diagnose faster VT rhythms — these ECG findings were all present in todays case — allowing a definitive diagnosis if recognized.
- But even if fusion, capture and AV dissociation were not identified — the diagnosis of presumed VT and treat accordingly until proven otherwise needs to quickly be made at the bedside.
- It should be clear that today's patient did not have idiopathic VT — because the patient has known coronary disease. As a result — IV Diltiazem was contraindicated.
- Hard Copy tracings need to be recorded during cardioversion — since even if the patient's regular WCT resumes soon after electricity is delivered — the etiology of the WCT will often be revealed. This may have provided key information confirming ischemic VT, that would have immediately favored either IV Amiodarone or IV Procainamide (instead of the diversion of using IV Diltiazem bolus and drip that led to shock).
|Figure-3: Review of KEY features regarding Idiopathic VT (CLICK HERE — for the source of this Summary).|