Tuesday, February 14, 2023

ECG Blog #363 — How Many Directions?

The ECG in Figure-1 was obtained from an older woman — who presented with chest pain and palpitations over the previous hour. She had a history of hypertension, and was on medication for this — but she was otherwise healthy. BP = 140/90 mm Hg in association with the rhythm in Figure-1.
  • How would YOU interpret the rhythm in Figure-1?
  • Is this Ventricular Bigeminy?

Figure-1: ECG obtained from an older woman with palpitations. Is there Ventricular Bigeminy? (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:
This is a challenging tracing! As always — I favor starting by first assessing the cardiac rhythm.
  • Although there is a long lead II rhythm strip at the bottom of the tracing in Figure-1 — this is a bit confusing, because of marked overlap between this long lead II rhythm strip and the bottom portion of QRS complexes in simultaneously-recorded leads V2 and V3 above it. That said — it looks as if the bigeminal pattern of alternating QRS morphology every-other-beat continues throughout the tracing!

  • The QRS complex is wide for all beats on this tracing. This is best seen in lead I.
  • I do not see P waves anywhere on this tracing.
  • The Rate of the rhythm is fast. The problem assessing the heart rate — is uncertainty IF we should calculate the rate of similar-looking complexes — or — the total rate of all QRS complexes in this tracing. I favor the latter — which suggests an overall heart rate of ~180-190/minute.
  • A similar problem arises when trying to assess for Regularity of the rhythm in Figure-1. There clearly is a "bigeminal" pattern, albeit with changing QRS morphology every-other-beat. Assessment for "regularity" of the rhythm is made difficult — because the R-R interval between beats is virtually constant, even though QRS morphology is constantly changing. This differs from the "usual" bigeminal rhythm — in which we typically see a "regular regularity" in the form of alternating shorter-then-longer R-R intervals.
  • NOTE: I found it easiest to evaluate the overall regularity of today's rhythm by selecting a lead in which there are all positive complexes (such as lead I or lead V6) — and measuring the R-R interval from the onset of the R wave upstroke from one beat — to the onset of the R wave upstroke of the next beat (ie, In Figure-2 — Doesn't the R-R interval between the RED arrows in lead I look regular?).

  • PEARL #1: One of my favorite quotes in teaching ECG interpretation is, "12 leads are better than one". For example, in Figure-1 — Doesn't QRST morphology for all beats in lead I look similar? However, when we look at simultaneously-recorded leads II and III — it becomes obvious that QRS morphology is very different for alternate beats!

The Rhythm in Today's Case: Putting It All Together
As I stated at the onset of today's case — This is a challenging tracing! 
  • I initially thought that the rhythm in Figure-1 was ventricular bigeminy (ie, that every-other-beat was a PVC). That said — reasons why today's rhythm is not ventricular bigeminy are: i) There is no sign of sinus P waves anywhere on today's initial tracing (ie, For there to be ventricular bigeminy — there should be an underlying sinus rhythm, in which every sinus-conducted beat is then followed by a PVC); and, ii) At 180-190/minute — the overall heart rate in today's initial rhythm is much faster than is usually seen with a sinus tachycardia, making ventricular bigeminy highly unlikely. (Contrast today's rhythm with true ventricular bigeminy — that was seen in ECG Blog #343).

  • I next considered the possibility of some type of alternating bundle branch block. That said, on closer inspection — this seemed unlikely because: i) As was the reasoning against ventricular bigeminy — there is no underlying sinus rhythm; and, ii) Both QRS morphologies in Figure-2 manifest QRS widening — instead of alternate beats being narrow. Neither QRS morphology resembles RBBB conduction — so this would not be alternating RBBB with LBBB. (Contrast  today's rhythm with true alternating bundle branch block — that was seen in ECG Blog #306).

  • Therefore: Summarizing our findings up to this point — we have a bigeminal rhythm with alternating QRS morphology in which all QRS complexes are wide, but without any P waves. This leaves us with the diagnosis of BiDirectional VT (BDVT).

Figure2: I've labeled the initial tracing. The RED arrows in lead I reveal a surprisingly regular rhythm. To facilitate assessment of the 2 different QRS morphologies — I've placed one set of even-numbered beats in each of the 4 lead groups within a dotted RED-YELLOW rectangle. Although both even- and odd-numbered beats resemble lbbb morphology — the frontal plane axis for these 2 QRS morphologies is markedly different! (See text).

CASE Follow-Up:
Additional history revealed no digoxin use — and no herbal or new medications. Troponin was slightly positive (felt unlikely to represent acute MI). Electrolytes were normal.
  • The patient was treated with IV Amiodarone. The result is shown in ECG #2 — which I have put together with the initial ECG in Figure-3 to facilitate comparison.

Figure-3: Comparison of the initial tracing — with the ECG obtained after treatment with IV Amiodarone. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Figure-3:
Treatment with IV Amiodarone resulted in successful conversion to sinus rhythm ( = ECG #2). Of note — the QRS complex with after conversion to sinus rhythm is indeed wide.
  • Lead-to-lead comparison of QRS morphology in ECG #2 — with the lead-to-lead appearance of the 2 different QRS morphologies seen in even- and odd-numbered beats in ECG #1 — suggest that this patient's QRS morphology during sinus rhythm is different in enough leads to strongly suggest that ECG #1 did in fact represent BiDirectional VT!

    What is BiDirectional VT?
    There are 4 basic types of VT (Ventricular Tachycardia) morphology: i) Monomorphic VT; ii) Polymorphic VT (PMVT) — which includes Torsades de Pointes; iii) Pleomorphic VT; and, iv) BiDirectional VT (BDVT). I review these terms in the June 1, 2020 post of Dr. Smith's ECG Blog — and limit my comments here to BDVT:
    • BiDirectional VT — is by far the least common form of morphologic VT. This rhythm is characterized by beat-to-beat alternation of the QRS axis. It distinguishes itself from PMVT and pleomorphic VT — because a consistent pattern (alternating long-short cycles) is usually seen throughout the VT episode. As implied in its name, there are 2 QRS morphologies in BiDirectional VT — and they alternate every-other-beat.

    PEARL #2:
     It's helpful to appreciate that BiDirectional VT is difficult to recognize. This is because the rhythm is not common — the rate is usually rapid (so not easy to determine if P waves might be hiding within T waves or the wide QRS complexes) — and the rhythm can easily be mistaken for ventricular bigeminy or alternating bundle branch block. NOTE: When contemplating the diagnosis of BDVT — Consider one of the following conditions which are known to predispose to this arrhythmia:
    • Digitalis toxicity
    • Acute myocarditis
    • Acute MI
    • Hypokalemic periodic paralysis
    • CPVT (Catecholaminergic PolyMorphic VT )
    • Metastatic cardiac tumors
    • Some types of Long QT Syndrome
    • Herbal aconite poisoning

    NOTE: In view of reduced use of Digoxin in recent years — CPVT is probably the most common cause of BiDirectional VT. This familial cardiac arrhythmia is the result of gene mutation. 
    • The heart is structurally normal in patients with CPVT. As a result — the resting ECG tends to be normal.
    • These patients are at high risk for malignant arrhythmias. Typically — these arrhythmias are induced by exercise or intense emotional states (ie, associated with increased catecholamine discharge). As a result — ETT (Exercise Treadmill Testing) can be used to elicit BDVT, and therefore help to diagnosie CPVT.
    • The mechanism for malignant arrhythmias with CPVT is a result of gene mutation. This leads to an increase in intracellular Ca++ concentration — which facilitates after-depolarizations and triggered arrhythmic activity — often beginning with multiple PVCs that evolve to BiDirectional VT. When persistent — BDVT may deteriorate to VFib.
    • Treatment of CPVT is aimed at suppressing excess adrenergic activity — which is why ß-blockers are the drug of choice for both acute and longterm treatment. If this fails to control episodes — an ICD is indicated.  

    FINAL Note on Today's CASE:
    Unfortunately — I lack details on what happened in today's case. To the best of my knowledge — today's patient had none of the predisposing causes of BDVT — and it was not discovered why she had this arrhythmia. 


      Acknowledgment: My appreciation to Sadiq Ameen (from Sana's City, Yemen) for the case and this tracing.



      Related ECG Blog Posts to Today’s Case: