What Lies Beneath
Firefighter / Paramedic
Acute Care Nurse Practitioner
Expert commentary and peer review by
Dr. Jesse McLaren
This case was kindly submitted by Dr. Paco Dardon (@PacoDardon), and it’s a privilege to present it as a formal review due to the many pathophysiological, and electrophysiological, phenomenon at play.
A 65 y/o Female was admitted to the ICU for septic shock. She was critically ill despite aggressive vasopressor therapy. A 12 Lead ECG was recorded secondary to bizarre telemetry findings at bedside.
From afar, there is gross tachycardia, cadence irregularities, and narrow QRS complexes that may, or may not, be Sinus in origin; and finally – a cacophony of wide complexes that might very well be ventricular in origin. Said differently, it’s a mess.
This particular onslaught of ECG madness is prime setting for frustration as you attempt to navigate complex diagnostics while simultaneously holding on to the big picture of patient care trajectory.
McLaren: ACLS attempts to simplify this process, suggesting cardioversion for unstable tachycardias, and anti-arrhythmics for stable wide complex tachycardias.
Given that a significant part of said trajectory is predicated on the ECG – for example, immediate cardioversion – it’s important to pause, take a deep breath, and consider the nuance.
Question 1: What is the rhythm?
The simple process of identifying atrial and ventricular activity – and how they relate to each other – can answer our first question and guide immediate management.
Are there Sinus P waves? If so, do they march out in a mostly predictable pattern? Yes! Below I have them isolated in both Leads I and V1 in red arrows. These leads were specifically chosen because, serendipitously, they afford maximal insight regarding Atrial activity.
McLaren: Not only is there regular atrial activity, but it looks like normal Sinus activity with upright P waves in Lead I (and II), and biphasic P waves in V1.
As previously mentioned, some of the QRS complexes are narrow, others wide. Given that the wide complexes are so gripping, from a visual perspective, we must deploy concerted attention to the juxtaposition of those that are regular versus those that arrive early. As demonstrated below, regular QRS complexes are marked in blue while those premature are green.
By process of elimination, we can now see that the only remaining QRS complexes are narrow – and since they are subsequent to a previously defined Sinus P wave (with a respective PR interval that is appropriate for the current heart rate), we can reliably designate these particular beats to be the true underlying, native rhythm.
The blue arrows show RBBB morphology, and it’s tempting to deploy a compulsory diagnosis of PVC’s, but remember: these wide QRS complexes arrive subsequent to a regularly timed P wave. They are not premature, by definition.
The green arrows, however, do show premature complexes. Paradoxically, though, the third green arrow identifies a QRS that is more narrow than the RBBB complexes surrounding it.
McLaren: We’ve answered the first question – Sinus Tachycardia with episodic runs of wide QRS (RBBB morphology) and PVC’s. We can, therefore, put down the defibrillation pads, set aside the amiodarone, and look further at the ECG.
Question 2: What explains the conduction abnormalities?
Ladder diagrams are essential as they provide visual insight of the conduction abnormalities at hand.
Beat 1: Sinus, narrow QRS complex.
(For didactic purposes, I’m going to skip ahead to Beats 6 and 7 as this will help explain what is happening in Beats 2 and 3.)
Beat 6: Sinus with normal antegrade passage through the AVN and His, however the impulse encounters a refractory right bundle branch. The reason for this is Phase III block.
When an impulse encroaches on the natural refractory period of the previous beat, it will encounter block. This can be cycle length-, or time-dependent. The block itself is functional and does not necessarily imply gross conduction disease.
Below is an example of functional, time-dependent Phase III block.
Courtesy of @AThomazAndrade
Back to the case:
Beat 4 arrives early, which necessarily prolongs the refractory period of Beat 5, and although Beat 6 arrives on time, it no less encounters a refractory right bundle.
RBBB is perpetuated in Beat 7 by a process called concealed transeptal conduction. The assumption is that a premature complex discharged prior to Beat 1, which prolonged its respective refractory period in the same manner as Beat 5.
Concealed transeptal conduction is unexpected persistence of aberrancy. In today’s case, there is persistence of RBBB. Typically, the bundles recover after gradual changes of time-, or cycle length dependency (i.e. slowing of the heart rate).
Alternatively, cessation of aberrancy may be the result of a phenomenon commonly referred to as “Peel Back.” At times, a premature impulse can invade the bundle branches and “strip” them of induced refractoriness, thereby restoring baseline Absolute, and Relative, Refractory Period properties.
In the below example, a premature extrasystole invades the bundle branches, and the subsequent aberrancy is perpetuated via concealed transeptal conduction. A secondary extrasystole “strips” the bundles of refractoriness via Peel Back with restorative narrow QRS conduction downstream.
Courtesy of @AThomazAndrade
Back to the case:
Beat 2 and Beat 3 manifest RBBB due to Phase III block, and perpetuation of such is via transeptal concealed conduction.
Beat 4: This is a premature ectopic complex of ventricular origin (i.e. PVC). The proximal P wave does not conduct because it encounters a refractory AVN, most likely from the influence of the PVC itself (a different form of concealed conduction, except this time at the level of the AVN).
We have established that Beats 2 and 3 manifested RBBB because of Phase III block with subsequent perpetuation via transeptal conduction. Beat 4 abruptly halts this repetitious cycle via Peel Back.
Beats 9-12: Continuation of the previously described events, all inducible by the pause (and thus, prolongation of refractoriness) created by the PVC of Beat 8.
Beat 13: This premature complex manifests a shorter coupling interval (red horizontal line) with its paired QRS than that which is seen in Beats 4 and 8 (blue horizontal lines). Moreover, this complex is even more narrow than the RBBB morphology surrounding it. The hypothesis here is that an additional His extrasystole of the contralateral chamber fuses with the same quadrigeminal PVC. Although the ladder diagram shows a proximal focus in the conduction system, it could just as easily be more distal.
Beats 14-16: Sinus with narrow QRS, then RBBB due to Phase III block with perpetuation via transeptal concealed conduction.
Summarily, we have answered the second question, providing further reassurance about the initially troubling wide complex rhythm.
Question 3: What else is going on?
During narrow QRS conduction there is a peculiar T wave finding, as demonstrated below in Leads V1-V3.
QT prolongation is usually attributable to reversible causes, including 1) medication use, 2) electrolyte depletion [e.g. hypokalemia, hypomagnesemia], and/or 3) CNS dysfunction.
McLaren: This adds another reason against the use of Amiodarone. Not only is it unnecessary with knowledge that the wide complex rhythm is inherently Sinus, but in the setting of long QT it could provoke Torsades. The combination of prolonged QT and deep T wave inversion throughout the precordium is typical of Takotsubo syndrome, or Stress Cardiomyopathy – which can occur in the context of a physiologically distressed ICU patient, further compromising their hemodynamics.
Surawicz and Knilans report that intense catecholamine surge, or severe maladjustment of the autonomic nervous system, can manifest “cerebral T waves” in the absence of an acute intracranial process.
Indeed, bedside Echocardiogram revealed severe left ventricular impairment of Takotsubo cardiomyopathy. The coronary angiogram revealed no critical stenosis, or acute plaque ulceration. Furthermore, pertinent electrolyte values (e.g. potassium) were within normal parameter.
Takotsubo should be a diagnosis of exclusion after angiography reveals no obstructive coronary disease, and repeat Echo displays left ventricular recovery.
Detailed analysis via ladder diagram revealed that no Adenosine, Amiodarone, or cardioversion is warranted. In fact, as previously mentioned, Amiodarone could be harmful. All effort should be focused on the underlying cause for this patient in septic shock.
The additional complication of Stress Cardiomyopathy (assuming obstructive coronary disease has been excluded) requires hemodynamic support, prevention of thrombogenesis, and avoiding QT-prolonging medications.
McLaren: We started with a mainly wide complex tachycardia. Rhythm analysis identified Sinus Tachycardia, and conduction analysis explained the variable complexes, shifting our concern from the tachycardia itself to the underlying cause. Then, the remaining ECG interpretation identified long QT, and T wave inversions, from cardiomyopathy.
Chiale, P. A., et al. (1994). Overdrive prolongation of refractoriness and fatigue in the early stages of human bundle branch disease. JACC, Vol 23, No 3; 724-32.
Friedman, M., et al. (2006). Transient unexpected improvement of AV conduction: What is the mechanism? Indian Pacing and Electrophysiology Journal, 6(3), 182-83.
Saini, A., et al. (2018). Alternating bundle branch block: What is the mechanism? Circulation, Vol 137, No 11, 1192-94.
Raymond-Paquin, A., et al. (2022). Multifaceted left bundle branch block: What are the mechanisms? JACC, Vol 4, No 5, 306-09.
Josephson, M. E., et al. (2017). Paroxysmal atrioventricular block: Electrophysiological mechanism of Phase 4 conduction block in the His-Purkinje system: A comparison with Phase 3 block. Pacing Clin Electrophysiol., 40, 1234-41.
Larsen, T. R., et al. (2019). Resolution of bundle branch block: Unusual finding. Circulation, Vol 139, No 16, 1974-76.
Surawicz, B. & Knilans, T. K. (2008). Chou’s Electrocardiography in Clinical Practice (6th ed). Chapter 22: Electrolytes, Temperature, Central Nervous System Diseases, and Miscellaneous Effects. Saunders-Elsevier: Philadelphia, PA.