A weekly ECG / EKG review blog looking at some interesting ECG's from the world of Emergency Medicine.
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Friday, 15 February 2013
ECG of the Week - 18th February 2013
Final part of the ECG trilogy.
Check out part 1 here and part 2 here. The nursing staff come and get you to say the patient's rhythm has changed on the monitor and they've ran off a new ECG.
Rate: v-rate 100 bpm, a-rate ~140 bpm Regularity: V-regular, A-regular P-waves: Present, not paced, rate of ~140 best appreciated in V1-V3 superimposed on the T-waves and initial deflection of the QRS in V3. PRi: not associated or intermittent capture? Some consistency seen, other times none. There is an alternans seen in V3 that appears related to a seemingly 2:1 association of atrial activity to V-pace. Given the prior ECG showed a A-V conduction time of ~300ms and these PRi's are ~200ms, this might be coincidental. QRSd: wide-wide at 180ms, RBBB-morphology V-pacing
Axis: pathological left, almost -90 QTi/QTc: a bit prolonged ST/T-waves: excessive discordance in II/III/aVF
DDx: Yikes. Looks like atrial tachycardia/sinus tachycardia with upper rate behavior on the pacemaker. RBBB morphology is not a great sign in RV-pacing (not known if that, but likely) esp when underlying rhythm exhibited LBBB morphology during normal A-V conduction. The excessive discordance in the inferior leads signals perhaps an ongoing ischemic event.
I'm not a pacemaker ninja, so consider this a guess on a pretty neat ECG :)
Nice thoughts Christopher. I don't have much of substance to add, but did notice two curiosities...
1) Well you actually noticed this one, I missed it, but there is a subtle alternans to the QRS compelxes in several leads (II, III, AVF, V2-V6). Now that you mention it though, according to Wellens (I just read this two days ago) this is possibly a sign of "severe and extensive cardiac ischemia" in the setting of a paced rhythm. I'm not sure how validated that sign is since he doesn't provide any references and I've never really looked for it before, but there it is.
2)The QRS complexes in I and aVR are almost identical (throw in V1 for that matter). Not an interesting thing in and of itself, but maybe a bit more intriguing since their j-points are markedly different. Again, I don't know if that really means anything, but it's an interesting development in light of all these possible-ischemic findings that are piling up. Then you gotta wonder, what causes an elevated J-point in aVR and V1 and ST-depression in I. I hate people who overcall LMCA/triple-vessel disease, but maybe...
Whoops, a third thing to add. 3) The very last complex is partially cutoff, but it looks like it's very likely a fusion beat. So no complete AV block, just dissociation caused by the tachyarrhyhtmia overloading the already sluggish AV node and allowing the ventricular pacer to usurp by default?
Christopher commented last night that this might have been the most interesting of the bunch, and I'm inclined to agree.
I already regret even mentioning aVR, but I have to clarify that I only mean to point out the possibility of underlying and maybe exacerbated triple-vessel CAD (not a crazy idea with a Hx of cardiomyopathy, possibly ischemic?), not that I think this is the presentation of an acute LMCA lesion. After pericarditis, "LMCA occlusion" is one of the most over-called signs in all of "internet cardiology," so I don't want someone running away with this possibly insignificant finding...
RBBB-morphology v-pacing...ruh roh.
ReplyDeleteRate: v-rate 100 bpm, a-rate ~140 bpm
Regularity: V-regular, A-regular
P-waves: Present, not paced, rate of ~140 best appreciated in V1-V3 superimposed on the T-waves and initial deflection of the QRS in V3.
PRi: not associated or intermittent capture? Some consistency seen, other times none. There is an alternans seen in V3 that appears related to a seemingly 2:1 association of atrial activity to V-pace. Given the prior ECG showed a A-V conduction time of ~300ms and these PRi's are ~200ms, this might be coincidental.
QRSd: wide-wide at 180ms, RBBB-morphology V-pacing
Axis: pathological left, almost -90
QTi/QTc: a bit prolonged
ST/T-waves: excessive discordance in II/III/aVF
DDx: Yikes. Looks like atrial tachycardia/sinus tachycardia with upper rate behavior on the pacemaker. RBBB morphology is not a great sign in RV-pacing (not known if that, but likely) esp when underlying rhythm exhibited LBBB morphology during normal A-V conduction. The excessive discordance in the inferior leads signals perhaps an ongoing ischemic event.
I'm not a pacemaker ninja, so consider this a guess on a pretty neat ECG :)
By 2:1 I meant 3:2 association.
ReplyDeleteNice thoughts Christopher. I don't have much of substance to add, but did notice two curiosities...
ReplyDelete1) Well you actually noticed this one, I missed it, but there is a subtle alternans to the QRS compelxes in several leads (II, III, AVF, V2-V6). Now that you mention it though, according to Wellens (I just read this two days ago) this is possibly a sign of "severe and extensive cardiac ischemia" in the setting of a paced rhythm. I'm not sure how validated that sign is since he doesn't provide any references and I've never really looked for it before, but there it is.
2)The QRS complexes in I and aVR are almost identical (throw in V1 for that matter). Not an interesting thing in and of itself, but maybe a bit more intriguing since their j-points are markedly different. Again, I don't know if that really means anything, but it's an interesting development in light of all these possible-ischemic findings that are piling up. Then you gotta wonder, what causes an elevated J-point in aVR and V1 and ST-depression in I. I hate people who overcall LMCA/triple-vessel disease, but maybe...
Whoops, a third thing to add.
3) The very last complex is partially cutoff, but it looks like it's very likely a fusion beat. So no complete AV block, just dissociation caused by the tachyarrhyhtmia overloading the already sluggish AV node and allowing the ventricular pacer to usurp by default?
Christopher commented last night that this might have been the most interesting of the bunch, and I'm inclined to agree.
I already regret even mentioning aVR, but I have to clarify that I only mean to point out the possibility of underlying and maybe exacerbated triple-vessel CAD (not a crazy idea with a Hx of cardiomyopathy, possibly ischemic?), not that I think this is the presentation of an acute LMCA lesion. After pericarditis, "LMCA occlusion" is one of the most over-called signs in all of "internet cardiology," so I don't want someone running away with this possibly insignificant finding...
ReplyDelete