One very sophisticated reader, Ken Grauer, came up with another interpretation of the last rhythm strip.
Here is the strip:
Here is K. Wang's ladder diagram and interpretation:
Answer: b) NSR and AV junctional acceleration with AV dissociation and occasional capture beats.
What bothered me about this being an accelerated junctional rhythm (interrupted each 3rd beat by sinus capture) - was that the R-R interval for the 1st junctional beat in each sequence (= the R-R between beats #3-4; 6-7; 9-10; and 12-13) is slightly different (shorter) than the R-R interval of the subsequent beat (= the R-R between beats #4-5; 7-8; 10-11; and 13-14) - whereas if this was AV dissociation by usurpation with junctional acceleration I would have expected them to be the same ....
Why couldn't the mechanism be the one I drew - whereby there are PJCs (beats #4,7, 10, 13) that conduct retrograde enough to slow down forward conduction of the next sinus impulse. Admittedly - that next sinus impulse is slowed down to a greater extent than usually occurs with such concealed conduction (perhaps due to switching to some alternate slow conduction pathway ... ).
Just wondering if Dr. Wang might consider my alternate mechanism plausible. In any case - GREAT TRACING - and what IS agreed is that there is AV dissociation from some junctional intervention and no evidence of any AV block.
Here is K. Wang's Respsonse:
Here is the strip:
Here is K. Wang's ladder diagram and interpretation:
Answer: b) NSR and AV junctional acceleration with AV dissociation and occasional capture beats.
Discussion. As
diagrammed, P waves from the sinus impulse occur regularly at a rate
of 65/m (P1,2,3...etc). The blips pointed by the arrows are not r' of rSr',
but sinus P waves, judging from the timing. If it were an r', then all QRSs would have it. The primary problem in
this patient is AV junctional acceleration. P1 is conducted to R1. P2 was going
to be conducted but accelerated junctional beat (R2) occurred sooner than that.
P2 and R2 are dissociated because they occur close together during the physiologic
refractory periods of each other. R3 is the accelerated junctional beat which
failed to conduct to the atria and next sinus P wave is uninterrupted and
occurs on time and conducts to the ventricle (R4). And the cycle repeats.
Thus, there is AV dissociation without any AV block.
The primary problem is junctional acceleration. What is the clinical significance of junctional acceleration? One has to consider digitalis intoxication, myocardial ischemia or infarction, or excess amount of catecholamines circulating which means any stressful condition. Again, a given ECG tracing can be dissected into primary disorder and secondary manifestations and ask what is causing the primary disorder, so that the patient can be treated appropriately, promoting quality patient care.
Here is Ken Grauer's ladder diagram and interpretation:
Thus, there is AV dissociation without any AV block.
The primary problem is junctional acceleration. What is the clinical significance of junctional acceleration? One has to consider digitalis intoxication, myocardial ischemia or infarction, or excess amount of catecholamines circulating which means any stressful condition. Again, a given ECG tracing can be dissected into primary disorder and secondary manifestations and ask what is causing the primary disorder, so that the patient can be treated appropriately, promoting quality patient care.
Here is Ken Grauer's ladder diagram and interpretation:
What bothered me about this being an accelerated junctional rhythm (interrupted each 3rd beat by sinus capture) - was that the R-R interval for the 1st junctional beat in each sequence (= the R-R between beats #3-4; 6-7; 9-10; and 12-13) is slightly different (shorter) than the R-R interval of the subsequent beat (= the R-R between beats #4-5; 7-8; 10-11; and 13-14) - whereas if this was AV dissociation by usurpation with junctional acceleration I would have expected them to be the same ....
Why couldn't the mechanism be the one I drew - whereby there are PJCs (beats #4,7, 10, 13) that conduct retrograde enough to slow down forward conduction of the next sinus impulse. Admittedly - that next sinus impulse is slowed down to a greater extent than usually occurs with such concealed conduction (perhaps due to switching to some alternate slow conduction pathway ... ).
Just wondering if Dr. Wang might consider my alternate mechanism plausible. In any case - GREAT TRACING - and what IS agreed is that there is AV dissociation from some junctional intervention and no evidence of any AV block.
Here is K. Wang's Respsonse:
An interesting comment and a legitimate argument by observing
slight difference in the R-R intervals of what I claim to be junctional beats,
an astute observation. Yes, junctional rhythm is very regular rhythm, and I
would have been happier if they occurred with exactly the same interval. The
slight difference in this case may be due to some degree of penetration of the
impulse from P2,4 and 6 into the junction (some degree of concealed
conduction). In my view, the argument against your diagram is that that long
P2-R3 interval will become too short (P3-R4) too quickly. Also, a premature
junctional beat would have occurred more prematurely. His bundle recording
would have settled the issue, which this patient did not have. It is an
important issue because an accelerated junctional rhythm and junctional
trigeminy (which is what you are advocating) have different clinical
implications (see the discussion of the case). It is also interesting that we
two are applying concealed conduction at different places of the same tracing.
Thank you for showing interest in our program and generating
interesting discussion.
K. Wang.
My impression is that Ken's interpretation is very viable, but that the differences in R-R interval are tiny and that K.'s interpretation is more likely.
As Ken says, the important thing is not which of these is correct, but that in both interpretations, there is no AV block, only AV Dissociation.
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