Drug Overdose with a Fascinating Arrhythmia

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

MY Comment by KEN GRAUER, MD (6/13/2020):

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

Today’s case features another look at a fascinating arrhythmia that Dr. Smith first posted on June 10, 2011. The patient presented to the ED following a drug overdose with oxcarbazepine. Although details of the case beyond this were not available — we’ll assume this patient was hemodynamically stable at the time the ECG in Figure-1 was recorded.

• What is the cardiac rhythm in Figure-1?
• Is there AV block?
• HOW would you proceed in assessing this arrhythmia?
• Considering the clinical context (ie, a drug overdose) — HOW would you manage this patient?

Figure-1: The initial ECG in the ED for this case (See text).

My THOUGHTS on ECG #1: This is an extremely challenging ECG. In the interest of illustrating an approach to complex arrhythmia interpretation — I thought I’d walk through the Step-by-Step Process I used to evaluate this tracing.

There are 5 KEY Parameters to assess in evaluation of any arrhythmia. I like to recall these by the saying, “Watch your P’s and Q’s, and the 3 R’s”:

• Are there P waves? — or, if no clear P waves, then are there signs of atrial activity (such as “fib waves” or atrial flutter)?
• Is the QRS wide? — for which we accept anything more than half a large box in duration (ie, >0.10 second) as qualifying as a “wide” QRS.

And the 3 Rs:

• Rate? — What is the ventricular (and the atrial) rate?
• Regularity? — Is the ventricular (and atrial) rhythm regular?
• Related? — Is there a specific relationship between QRS complexes and neighboring atrial activity?

It does not matter in what sequence the Ps, Qs and 3Rs are assessed, and I often vary the sequence depending on whether atrial activity, QRS width, and/or rhythm regularity is easiest to evaluate for the rhythm at hand.

• PEARL #1 — In applying the 5 Parameter approach — I like to begin by labeling P waves. Especially in a more complex arrhythmia — the simple act of labeling P waves can be tremendously helpful in focusing your attention when assessing the relationship (if any) between P waves and neighboring QRS complexes (RED arrows in Figure-2).
• PEARL #2 — Evaluate for the presence and nature of atrial activity. This essential step is greatly facilitated by: i) Use of calipers; and, ii) Looking at simultaneously-recorded leads. Some of the P waves in Figure-2 are obvious — but others are not. That said — Common things are common! It is much more likely for there to be an underlying regular (or almost regular) sinus rhythm (as can be marched out by calipers) — than for there to be regular P waves most of the time, but with intermittent “skips” of P waves due to sinus node exit block. BLUE arrows in several simultaneous leads in Figure-2 highlight deflections confirming that the RED arrows are all placed over sinus P waves, many of which are partially hidden because they coincide with (distort) the beginning or end of the QRS complex. And, the RED arrow we placed over the terminal portion of the T wave of beat #11 in the long lead II does point to a subtle notch in the T wave, that corresponds to a definite notch in the T wave of beat #11 in lead V1 (the longest vertical BLUE arrow). We have therefore confirmed that a regular sinus rhythm continues throughout the long lead II rhythm strip in Figure-2.
• Now that we’ve identified P waves — we need to continue with assessment of the other 4 Parameters: i) With 1 exception ( = beat #11) — the QRS complex is narrow; ii) Parts of the rhythm in Figure-2 look Regular— but other parts are not; iii) The ventricular Rate for those parts that look fairly regular is ~80-85/minute; and, iv) The Relationship between P waves and neighboring QRS complexes is complicated — and requires closer evaluation (See below).

Figure-2: We’ve added RED arrows to highlight sinus P waves. Using calipers and the principle of simultaneously-recorded leads allows us to verify that regular sinus P waves do continue throughout this rhythm strip (See text).

PEARL #3 — Start with what you know! Even complex arrhythmias usually contain both easier and more difficult parts to interpret. Begin with the easier parts!

• Beat #11 occurs earlier than expected. This beat is wide — it looks very different than virtually all other QRS complexes — and it is not preceded by a P wave. Therefore, beat #11 is a PVC.
• The other “easier part” of this tracing to interpret — is realization that the PR interval is too short to conduct many of the beats on this tracing. For example — There is NO way that the PR interval preceding beats #1, 2, 10, 14, 15 and 16 could be conducting!
• There is also NO way that beats #3, 4, 5 and 6 are conducting — because sinus P waves (RED arrows) occur either during or after the QRS complex for each of these beats.

PEARL #4 — Look to see if there are any sinus-conducted beats? Usually this is easy to determine — but it is anything but easy in Figure-2! As Dr. K. Wang emphasized in his 2011 commentary on this tracing — beat #8 holds the KEY to interpreting this arrhythmia.

• The reason we strongly suspect that beat #8 is being conducted — is that the longest PR interval in this tracing precedes this beat.
• We suspect that beat #13 is also conducted — because the PR interval preceding it is equal to the PR interval preceding beat #8.
• In contrast — the PR interval preceding beat #9 is slightly shorter — so beat #9 is probably not conducted.
• This leaves us with all beats in Figure-2 accounted for — except for beats #7 and 12 — which we save for later because assessment of these 2 beats is among the “harder parts” of this tracing.

Putting It ALL Together:

• What we have established thus far — is that with the exception of 1 PVC (ie, beat #11) — the rhythm in Figure-2 is supraventricular (narrow QRS) and fairly regular — but that most of the regular sinus P waves that are present are not conducting.
• Since those beats that are not conducting manifest a narrow QRS complex that looks identical to sinus-conducted beats #8 and 13 — this means that the non-conducted beats must be arising from the AV node. And since the rate of these non-conducted beats is ~80-85/minute — this means that part of the time, there is an accelerated junctional rhythm in Figure-2 (a rate of ~80-85/minute being well above the usual 40-60/minute rate range for a junctional “escape” rhythm).
• Finally — the fact that there is an underlying regular sinus P wave rhythm, with many of these sinus P waves being unrelated to neighboring QRS complexes — defines the presence of AV Dissociation.

PEARL #5 — As emphasized in our May 24, 2020 post — AV dissociation is never a “diagnosis” per se. Instead — it is a condition caused by “something else”. The 3 Causes of AV Dissociation are: i) AV Block (of 2nd- or 3rd-degree); ii) AV dissociation by “usurpation” — in which P waves transiently do not conduct because an accelerated junctional rhythm takes over (ie, “usurps” control of the rhythm); and, iii) AV dissociation by “default” — in which a junctional escape rhythm takes over by “default” (ie, because of SA node slowing) — as may occur if a medication such as a ß-blocker is being used. In Figure-2:

• None of the P waves that failed to conduct had a chance to conduct — because the PR interval was either too short to conduct — or the P wave occurred during or immediately after the QRS complex. Therefore — despite the fact that a majority of P waves in Figure-2 are not conducting — there is no evidence of any degree of AV block.
• The rate of sinus P waves (RED arrows) in Figure-2 is ~80/minute. Since this is a normal sinus rate — this can not be AV dissociation by “default”.
• Instead — the cause of AV dissociation in Figure-2 must be AV dissociation by "usurpation" — which occurs here because an accelerated junctional rhythm intermittently exceeds the rate of the sinus pacemaker.
• KEY Point re Clinical Implications of this Rhythm: Recognition that there is no AV block in Figure-2 — and, that the cause of the AV dissociation is an accelerated junctional rhythm, has important clinical implications. While we don't know details of this case — it would seem that an accelerated junctional rhythm would not be unexpected in association with a drug overdose. Chances are excellent that the accelerated junctional rhythm (and resultant AV dissociation) will resolve spontaneously as the patient’s clinical condition improves. Unlike AV dissociation due to 2nd- or 3rd-degree AV block — NO specific treatment for the rhythm in Figure-2 is likely to be needed.

PEARL #6 (Beyond-the-Core): As discussed in the May 24, 2020 post — there is a special type of AV dissociation known as “isorhythmic” AV dissociation — in which the sinus P wave rate is almost identical to the rate of the accelerated junctional focus. A characteristic of this unique arrhythmia — is that there is often a “back-and-forth” change in the rate of the 2 competing pacemakers. We see this phenomenon in Figure-2.

PEARL #7 — Don’t forget to interpret the rest of the 12-lead ECG! A common mistake after working through a complex arrhythmia is to forget to inspect the rest of the 12-lead tracing (Figure-2).

• As noted above — there is 1 PVC in this tracing (beat #11) — there are a few sinus-conducted beats — and there is AV dissociation due to an accelerated junctional rhythm for most of the tracing. We can still assess QRST morphology when the rhythm is junctional.
• The QTc interval is normal. The frontal plane axis is normal at +20 degrees. There is no chamber enlargement. There are no Q waves. R wave progression is normal (with transition occurring between leads V3-to-V4). There are nonspecific ST-T wave abnormalities (ie, T wave inversion in leads V1,V2 + ST segment flattening with some ST depression, particularly in lateral leads). These ST-T wave changes do not look acute — and I suspect they’ll resolve as the junctional rate slows and the patient’s clinical condition improves.

BEYOND-the-CORE on this Cardiac Rhythm: The above discussion followed my step-by-step thought process in assessing the cardiac rhythm in Figure-2. That said — a number of findings remain unexplained ...

• NOTE: Although the above description of my “thought process” seems long — It literally took less than 1 minute in “real time” to derive the above conclusions.
• SUGGESTION for Viewing the Laddergrams that Follow: The BEST way to explain the remaining fine points of this arrhythmia is by sequential construction of a laddergram. For the following 10 Figures — you’ll note that these laddergrams superimpose one on another. Optimal viewing will be on a computer. CLICK on Figure-3 to enlarge it — and then click the Forward Arrow on your keyboard for sequential development of the laddergram. The newest addition to each step is in BLUE. Legends explain my thought process. Regardless of your prior experience using laddergrams — I bet you’ll have a much better understanding of what is going on after sequential viewing of these next 10 Figures!

Beginning with Figure-3:

Figure-3: It’s easiest to begin construction of a laddergram by filling out atrial activity. RED vertical lines in the Atrial Tier correspond to P waves (RED arrows) in the long lead II rhythm strip.

Figure-4: Next — I’ve filled in the Ventricular Tier with BLUE arrows that correspond to each of the supraventricular QRS complexes in the long lead II.

Figure-5: I’ve added the arrow representing the PVC (BLUE arrow). Note that the PVC begins in the ventricles — and conducts backward (retrograde) through at least a portion of the AV Nodal Tier.

Figure-6: For clarity — I’ve added the numbers of each beat to the laddergram.

Figure-7: It’s time to start filling in the AV Nodal Tier. It’s easiest to begin with those beats that you know are sinus-conducted (ie, beats #8 and 13).

Figure-8: Looking closer at beat #11 — this is an interpolated PVC, because it occurs in between 2 supraventricular beats without the usual compensatory pause. As suggested in the laddergram — retrograde conduction from the PVC (dotted BLUE line) is enough to delay forward transmission of the next sinus P wave (ie, the P wave that notches the terminal part of the T wave of beat #11 then conducts with a prolonged PR interval — shown by the slanted BLUE line). (NOTE: For full discussion of interpolated PVCs — See the April 9, 2020 post).

Figure-9: BLUE circles within the AV Nodal Tier represent the accelerated junctional rhythm.

Figure-10: Retrograde conduction from the junctional rhythm prevents all sinus P waves but one from reaching the ventricles. This leaves us to explain what happens with beat #7 ...

Figure-11: The P wave just after beat #6 occurs later after the QRS than any other P wave. I suspect this P wave is conducting, albeit with a prolonged PR interval because of retrograde conduction from the preceding junctional beat. Beat #7 occurs much earlier-than-expected — so the reason QRS morphology looks different is aberrant conduction.

Figure-12: The finished laddergram. Note alternation between the accelerated junctional rhythm and occasional sinus-conducted P waves. Beyond-the-Core: Because the sinus P wave that occurs right after beat #6 “captures” the ventricles (with beat #7) — this delays the next junctional beat, which allows the sinus P wave in front of beat #8 enough time to conduct. But right after this — the accelerated junctional rhythm resumes for beats #9 and 10, until the interpolated PVC (beat #11) occurs. But because conduction of the next P wave (that falls at the end of the T wave of beat #11) is delayed, the sinus P wave in front of beat #13 is given enough time to conduct. But right after this — the accelerated junctional rhythm resumes for beats #14, 15 and 16.