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Session V: Clinical Scenarios/Device Management-61 ...
Workshop #8 Device Cases - Asirvatham
Workshop #8 Device Cases - Asirvatham
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Video Transcription
This is Sam Asirvadam. This workshop will just focus on some issues with device cases, radiology, electrocardiographic correlation and some troubleshooting. So I'm going to show you ECG tracing from a patient with a CRT device that's been in about a year. Patient has not had any clinical improvement. What would be an explanation for why the patient is a non-responder? So I'll show the ECG, paced rhythm, and the options. Is it the PVCs? Is there lack of atrioventricular synchrony, failure to capture on the left ventricular lead, possible need for a left ventricular lead offset, or potentially all of the above? So it really can be any or all of these reasons. So if we look through a few things here, first we look at the overall vector. So left bundle pattern and R-wave, initial R-wave in one. This suggests that predominant activation is the right ventricle. So it could be there's an issue with the left ventricular lead or just needs an offset. Just in this 12 lead, we have PVCs. So frequent PVCs, they could be minimizing pacing from the CRT system, or enough PVCs could themselves be affecting ventricular function. We also know sometimes we can see a P-wave. So this is a patient who may have had a CRT system placed without an atrial lead because the patient was at atrial fibrillation at that time and now is in sinus rhythm. So this loss of AV synchrony can greatly diminish and completely offset any advantages that you could have from ventricular synchronization. Just an example of some potential things that we can look at with the 12 lead ECG when troubleshooting failure to respond to CRT. We think about frequent PVCs, we think about AV synchrony, and we look at the ECG to see what we can tell about the ventricular pacing. So this is a question that I'm going to show you an EKG and chest X-ray and need to see what you suspect about the system. So this is the electrocardiogram and an AP chest X-ray. So is what you're seeing consistent with a normal endocardial system, a normal epicardial system, a coronary sinus implant, or an arterial implant? ECG X-ray. So this is consistent with an arterial implant. So why is that? So let's start with the ECG. We notice a right vundral branch block pattern, negative and lead one. So that's consistent with left ventricular pacing. A left ventricular pacing could be an epicardial system. It could be an endocardial system, purposely placed endocardial system through a transeptal puncture or potentially placed inadvertently either through an artery or a PFO, or it could be coronary sinus-based left ventricular pacing. Now it's hard to know which of those three it is looking at the ECG alone, but epicardial implants like epicardial foci or PVCs or VT tend to be very slurred up strokes on the QRS, whereas this is pretty sharp. So suggesting an endocardial implant from the left ventricle, probably inadvertently. One thing that we can also look at when we correlate is with the chest X-ray. And the chest X-ray, the telltale signs of an arterial implant is it crosses the clavicle and goes in the center of the cardiac stem, the cardiac silhouette. SVC would be here, pulmonary artery would be here, aortas in the middle. So arterial implant going into the left ventricle. That central location along with the right bundle branch block should make you think about this and hope that it's recognized when inadvertent and taken out. In this patient, unfortunately it wasn't, thrombi had formed on the lead and the patient had presented with unexplained stroke. So here a pacing lead is placed at a site that I'm going to show and point to you. And we want to try to correlate that lead location with what you anticipate will be an issue. So this is the yellow arrow and this is the location anatomically. If we were to target this location, this is looking from the left side of the heart. Aortic, leaflets, non-coronary and right coronary, coronal section, crest of the interventricular septum, atrial septum, mitral valve, tricuspid valve. What do you think is likely to be associated with this? Is it high thresholds? I'm sorry, least likely associated. So all of these are possible, but what's least likely associated with this site? Is it high thresholds, his bundle capture, injury to the compact aveno, interventricular perforation or far field sensing of atrial signals? So question is, if you put a lead where this arrow is shown, which of these do you not expect, least likely to occur? So compact AV node injury would be not expected in this region. Many of you would have recognized this region is the membranous septum, fusion of the right and non-coronary sinuses at the level of the tricuspid valve. Membranous septum is home to the bundle of his. So bundle of his is the only structure in the membranous septum. If we targeted that site, we might capture the his bundle directly. Thresholds tend to be high because of the insulation around the his bundle. And if you're not having simultaneous ventricular capture, thresholds tend to be higher. You could perforate with a screw, a large helix through the membranous septum. Because this is all atrial tissue of the interatrial septum in the region of the non-coronary sinus, you could get far field atrial sensing. What you won't get is AV node, compact AV nodal damage. Unlike the membranous septum where the his bundle is located, the compact AV node is atrial and a mid-septal structure. So damage to the AV node, the compact AV node is unlikely. It's possible to damage the his or maybe even the proximal right bundle when targeting casing and locations for the conduction system at the level of the his or perihisin region. So coronary sinus angiography is what I'm going to show here. I'm going to show you the RAO and lateral projections. And to see what abnormality do you think is being seen here. So this is the right anterior oblique projection. And then the left anterior oblique projection. So retrograde coronary venography is being done perhaps in anticipation of placing a left ventricular lead. So which are you seeing here? Is it a fistula, perforation, prominent business valve, prominent ventricular valve, prominent thebesian valve, or a coronary sinus diverticule? Here's the image again. And this is a prominent business valve. So a few things we notice from this retrograde venography. CS ostium, typical position of the business valve or valve of the lateral vein. Is where the body of the CS diverges as an atrial vein, vein of Marshall, and the great cardiac vein. Usually the same site you get a lateral or posterolateral vein. Now you could also get valves and mouths of other veins and the thebesian valve right at the CS ostium. These generally are not prominent and allow you to cross. The business valve can be prominent and difficult. Wires will sometimes coil up here. But it is a valve that opens and closes with retrograde blood flow. So just gentle probing will usually allow you to get across that valve and you can complete the procedure. Occasionally it's nearly occlusive. And when that's the case, if you stay on venography or do arteriography, venous phase imaging, you'll see posterior veins draining the blood from the left ventricle. And you could use one of those veins to try to get to the left heart border. So prominent valves, occasional difficulty with placing CS based left ventricular leads. I'm going to show you an ECG and we're going to try to determine the location of the pacing lead. So this is the ECG pattern. Take a look at this. And is this most consistent with the right ventricle, middle cardiac vein lead, anterior interventricular vein lead, posterolateral vein lead, or something else? So based on some of our prior discussions, I think without the X-ray, you should recognize this is posterolateral vein facing. How do we know that? There is a right bundle-like pattern suggesting there is at least a lead capturing left ventricle. It's completely negative in one, completely negative in one. Free wall of the left ventricle. Free wall, but it's posterior free wall. It's 2,3-AVF are predominantly negative. Posterolateral LV is where you anticipate seeing on the LAO projection. So free wall of LV, negative in one, positive in lead V1, and closer to the feet, so negative in leads 2,3-AVF. So in this case, we're going to look at not so much where the lead is, but knowing that the lead is in the same location and facing at different outputs from the same location, the vector for facing is the tip of the LV lead to the ICD lead. In this case, the coil, but more commonly with present systems would be the ring electrode of, could be the ring electrode of the RB lead. Why does this change occur? So we see here 2,3-AVF negative. Increased output, the axis flips positive in 2,3-AVF. So is this migration of the lead? Is it a VT we are inducing and maybe a training with facing that gives this morphology? Anodal stimulation, or it really could be any or all of the above. Low output, high output. So this is most likely an example of anodal stimulation. We haven't moved the lead. It's only output that we're changing. It's uncommon when it's the RB-ICD coil, but depending on contact, how much of the coil has contact with cardiac tissues like with fibrosis, it's possible to get anodal stimulation. Stimulation from the anode, the coil or ring electrode, depending on the configuration rather than the tip or the cathode. And because of that change, the coil is at a higher site, 2,3-AVF are positive when we get that anodal stimulation. So general putting it together in terms of ECG by V pacing, two leads, lead one and V1. RV pacing, RV capture, predominant RV in a by V system. It'll be positive in lead one, towards lead one, negative in V1, away from V1. LV, free wall, sites that you like for by V pacing. Lead one is negative. V1 will be positive towards V1. When we stimulate from both, we like to see some fusion. We like to see something that looks in between these two. Maybe less negative in one, but still negative. Maybe not quite as tall in V1. But if we saw simultaneous pacing, looks just like RV, then either we have loss of LV capture, or there's so much scar around where the LV lead is that we need a headstart, an offset for the LV lead, or there could be anodal stimulation. And in this cartoon example, if we give LV a little offset, you may get something that's like a fused vector, a hybrid vector between RV and LV stimulation. So it's a patient with chronic atrial fibrillation and a single-chamber pacemaker set BVI at 70. Pacemaker malfunction was diagnosed based on this tracing, but what is it that we see? Oversensing, failure to capture, undersensing, combinations, B and C are off. So this is the tracing. So kind of basic troubleshooting, I think many of you would be familiar, but a revision. So there's evidence of all of these. So failure to capture, probably easiest to recognize, we see output here, but no captured QRS. There's oversensing because your timing cycle is reset. So you can walk back and you anticipate there's an oversensed event somewhere here. There's undersensing because this pacing is too quick. So over pacing, so did not sense, paced and put the patient into a polymorphic PT. So sometimes when troubleshooting cases and we see one abnormality, important to look and see what else there may be, may give clues to the type of lead malfunction, primary etiology, and see whether any troubleshooting options are possible. Thank you very much for your attention.
Video Summary
The workshop focuses on issues with device cases, radiology, electrocardiographic correlation, and troubleshooting. The first ECG tracing shows a patient with a CRT device who has not had any clinical improvement. The possible reasons for the patient being a non-responder are explored, including PVCs, lack of atrioventricular synchrony, failure to capture on the left ventricular lead, and the need for a left ventricular lead offset. The second ECG and chest X-ray demonstrate an arterial implant due to the right bundle branch block pattern and the central location of the lead in the chest X-ray. The third case involves a lead placed in the membranous septum, which is unlikely to cause compact AV node injury but can lead to high thresholds. The fourth case shows prominent valve in the coronary sinus, creating difficulty in placing a left ventricular lead. The last case involves an ECG pattern that indicates posterolateral vein pacing. Changing the output leads to anodal stimulation instead of the desired simultaneous pacing. The final case shows evidence of failure to capture, oversensing, and undersensing in a patient with a single-chamber pacemaker.
Keywords
device cases
radiology
electrocardiographic correlation
troubleshooting
CRT device
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