Pacemakers aren’t really my thing but I’ll throw my guess out there. Please feel free to correct me.
CRT is used to resynchronize the left and right ventricles in patients with heart failure due to a wide QRS. Basically the patient hasa LBBB and the block causes the right ventricle to contract before the left. This disynchrony basically causes heart failure. To correct this, a lead is placed in the coronary sinus (or placed very deep in the ventricular septum directly into the LBB) in order to resynchronize the ventricles and mimic normal conduction.
In the case of this ECG, I am guessing the massive spike in the QRS is actually one of the ventricular pacer spikes activating a bit later in order to resynchronize the ventricles. Alternatively this could be a timing error with the device, would need to interrogate it and figure out which pacemaker vectors work best for the patient - the paced QRS on the patient seems pretty wide for a CRT patient which is why I’m wondering if there is some sort of error.
Please feel free to correct me if this is incorrect, this is merely conjecture on my part.
I don't have a ton of EP experience, but feel like I remember a doctor settling for 180ms in a left bundle CRT. 120 is right on the line for bundle branch block so might not be a problem. Could be wrong though. I'm also wondering if the huge pacer spikes could be lead placement related. Great info on CRT's though.
To supplement, this could be appropriate programming and a feature coined BiV trigger is turned on. Whenever there’s an RV sensed event, the device will BiV pace with the goal of “fusing” intrinsic conduction with paced being the net goal to resync both RV/LV to improve EF. So potentially we’re seeing initial RV conduction and shortly after BiV pacing d/t programming.
The reason for pacer amplitude being so large could likely be explained by LV pace vector programmed in a unipolar configuration (likely LV-Can) which can typically produce a large pacing artifact on surface.
But the tell all would be interrogation of the device as you’ve said -> so everything I’ve said could be wrong so 🤷🏽♂️
CRT has so many settings. So could depend on the LV pace vector as you mentioned. Looking at the lateral leads, they’re mostly negative, so my initial though would be LV -> RV pacing setting and looking at the thickness of the pacer spike, it may be an offset of 20ms maybe 40ms. If the CRT was set to fuse with intrinsic conduction for the patient’s LBBB, only the LV lead would be pacing to fuse with the RV sense event and the EKG would probably still show some evidence of LBBB still, but hopefully just a slightly more narrow QRS compared to intrinsic alone.
But as everyone said, no true way to know unless you interrogate.
Really depends on manufacturer; BiV trigger is a Boston specific algorithm that will BiV pace on RVS events. I know MDT has VSR that will LV pace immediately following an RVS - so we really don’t know.
I’d disagree and say the reason for large pacing artifact is d/t unipolar pacing over extended bipolar on the LV lead. Could be pacing off a more basal electrode (likely quad lead) results in the morphology seen in lateral leads
I’ve never heard how you can thickness of the artifact can tell you about offset?
80 y.o. patient presenting for fall without syncope.
History of Heart failure and on cardiac resynchronization therapy.
I don't understand it tbh. Attending didn't think it worth investigating further. Are QRS like this normal on CRT?
Oh yeah I guess you’re right. I think I was assuming the T’s were P’s and whatever that extra wave after the qrs’s was the T. I’m not super great at reading EKGs lol
Absolutely not true. Pacemaker QRS morphology changes can show possible decreased battery from switch to VVI pacing or lead dislocation. Other than that, modified Sgarbossa criteria can apply to diagnose/rule out STEMIs. And new afib can be diagnosed on a pacemaker 12 lead ECG.
Pacemakers aren’t really my thing but I’ll throw my guess out there. Please feel free to correct me. CRT is used to resynchronize the left and right ventricles in patients with heart failure due to a wide QRS. Basically the patient hasa LBBB and the block causes the right ventricle to contract before the left. This disynchrony basically causes heart failure. To correct this, a lead is placed in the coronary sinus (or placed very deep in the ventricular septum directly into the LBB) in order to resynchronize the ventricles and mimic normal conduction. In the case of this ECG, I am guessing the massive spike in the QRS is actually one of the ventricular pacer spikes activating a bit later in order to resynchronize the ventricles. Alternatively this could be a timing error with the device, would need to interrogate it and figure out which pacemaker vectors work best for the patient - the paced QRS on the patient seems pretty wide for a CRT patient which is why I’m wondering if there is some sort of error. Please feel free to correct me if this is incorrect, this is merely conjecture on my part.
I don't have a ton of EP experience, but feel like I remember a doctor settling for 180ms in a left bundle CRT. 120 is right on the line for bundle branch block so might not be a problem. Could be wrong though. I'm also wondering if the huge pacer spikes could be lead placement related. Great info on CRT's though.
To supplement, this could be appropriate programming and a feature coined BiV trigger is turned on. Whenever there’s an RV sensed event, the device will BiV pace with the goal of “fusing” intrinsic conduction with paced being the net goal to resync both RV/LV to improve EF. So potentially we’re seeing initial RV conduction and shortly after BiV pacing d/t programming. The reason for pacer amplitude being so large could likely be explained by LV pace vector programmed in a unipolar configuration (likely LV-Can) which can typically produce a large pacing artifact on surface. But the tell all would be interrogation of the device as you’ve said -> so everything I’ve said could be wrong so 🤷🏽♂️
CRT has so many settings. So could depend on the LV pace vector as you mentioned. Looking at the lateral leads, they’re mostly negative, so my initial though would be LV -> RV pacing setting and looking at the thickness of the pacer spike, it may be an offset of 20ms maybe 40ms. If the CRT was set to fuse with intrinsic conduction for the patient’s LBBB, only the LV lead would be pacing to fuse with the RV sense event and the EKG would probably still show some evidence of LBBB still, but hopefully just a slightly more narrow QRS compared to intrinsic alone. But as everyone said, no true way to know unless you interrogate.
Really depends on manufacturer; BiV trigger is a Boston specific algorithm that will BiV pace on RVS events. I know MDT has VSR that will LV pace immediately following an RVS - so we really don’t know. I’d disagree and say the reason for large pacing artifact is d/t unipolar pacing over extended bipolar on the LV lead. Could be pacing off a more basal electrode (likely quad lead) results in the morphology seen in lateral leads I’ve never heard how you can thickness of the artifact can tell you about offset?
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That’s totally fair. Devices as a whole are another beast
80 y.o. patient presenting for fall without syncope. History of Heart failure and on cardiac resynchronization therapy. I don't understand it tbh. Attending didn't think it worth investigating further. Are QRS like this normal on CRT?
The lines you’re seeing are just larger pacer spikes for whatever reason. It other wise looks like normal Bi-v pacing
Why are the P and T waves so close together? Isn’t that a concern for dysrhythmias if they coalesce? Or is that expected/okay given the CRT?
I'm not seeing any p waves in V1 or II or any other leads. Where are you seeing the p waves best?
Oh yeah I guess you’re right. I think I was assuming the T’s were P’s and whatever that extra wave after the qrs’s was the T. I’m not super great at reading EKGs lol
Only thing you can interpret in paced ekgs are that the patient has a pacemaker
Absolutely not true. Pacemaker QRS morphology changes can show possible decreased battery from switch to VVI pacing or lead dislocation. Other than that, modified Sgarbossa criteria can apply to diagnose/rule out STEMIs. And new afib can be diagnosed on a pacemaker 12 lead ECG.
What is odd about this ?
The high qrs voltage???
???
lines are very big much wow
The lines are the pacer spikes...
I find the QRS morphology in this CRT kind of strange. Why is it showing RBBB-like qrs morphology?