04 Sep 1997: CJ @bora.dacom.co.kr-Kosin University Gospel Hospital- Korea

Pacemaker induced cardiac perforation and pericarditis.

ECG AFTER PM INSERTION REVEALS INTERMITTENT CAPTURE. CXR DEMONSTRATES ELECTRODE CATHETER IN THE PERICARDIAL SAC. LAST ECG WITH CHEST PAIN SHOWS NORMAL SINUS RHYTHM AND EPICARDIAL INJURY CURRENT FROM PERICARDITIS DUE TO BLEEDING INTO THE PERICARDIUM.

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The ST elevation and the story are very suggestive of pericarditis, due to perforation of the catheter into the pericardial sac. The patient's echo did not show any sign of pericardial fluid and I believe it unlikely that there was bleeding. This is an important point as the RV at times seems to tolerate perforation well and not to bleed and progresses to cardiac tamponad.

The first EKG looks as if it is Junctional @around 50. The #2 EKG I can see the pacers spikes. The #3 looks like she has a elevated ST. Is she having a MI? I just looked at the #2 EKG she looks like she has some pacers not capturing?

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The question, is this a myocardial infarction, is critical. The patient was know for angina (with normal coronary arteries) and had just had her diltiazem and metoprolol stopped abruptly. It is conceivable that she was having an acute event. The fact that the ST elevation is so wide spread and that there is no ST depression (reciprocal changes) argues against this being an MI.

If we had decided that it was an acute MI and given thrombolytics one would suppose that there could have been bleeding into the pericardial space and tamponad. Further the wisdom of thrombolysis after a central line insertion is troublesome. In the end angiography probably would have been the safest approach to ensure that there was not an acute occlusion.

Patient has junctional escape rhythm at rate of 50, so should not have syncope unless the BP is low from the meds, or the rate is sometimes much lower. paced rhythm shows RBBB in lead V1, suggesting the LV is being paced. The X-ray shows the pacing catheter in the LV or the pericardium over the lateral LV. The previous ECG showed one non-paced beat. The last ECG shows pericarditis, compatible with details of the described pain. Nice case.

The catheter has perforated the ventricle. The patient resumed sinus rhythm probably the junctional rhythm was due to drugs.

There are two of us here, a computer scientist and echocardiography technician. This is an interesting set of ECGs. Tracing 1: Narrow complex bradycardia rate about 53. P-waves absent. Possibly 3rd AV block. Tracing 2: Appears that pacemaker has taken over at rate of about 75. Tracing 3: P-wave has returned. Pacemaker spike absent. In lead 3, QRS has reversed. V leads show reduce of QRS amplitude and increase of T-wave. Possibility of eschemia and fear of infarct extension.

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The fist tracing does not show P waves and suggests that this is a nodal rhythm where the P waves are not seen as they are hidden in the QRS complex or just not present. This is probably due to sinus node exit block or arrest, but it is also possible that this is atrial fibrillation (fine) with complete heart block with a nodal escape. This last rhythm can be seen in digitalis excess in patients with atrial fibrillation where the digitalis dose is high and the patient's rhythm becomes regular. In this case though the nodal rhythm is usually faster. In this case complete heart block is unlikely but not impossible.

A point to remember is that this patient was not having an MI and so ischemia and extension of an MI are unlikely.

The first tracing shows a slow idiojunctional rhythm. The second tracing shows a idioventricular rhythm induced by an artificial pacemaker with intermittent failure of capture. The symptoms of chest pain that get better with sitting up, the unusual location of the electrode at the chest X-ray and the findings at the ECG ( positive R wave in the aVR resemble the R wave usually seen in aVL during the apical RV pacing, and the negative QRS complexes from V1 to V6 ), suggest RV perforation. Unfortunately we couldn't see the ventricular capture in the lead I that shows in the case of perforation a small and negative QRS complexes that associated with important R wave in the lead aVR and negativity in the leads II,III, aVF and from V1 to V6 makes the diagnosis of RV perforation. Failure of capture and sensing problems are usually seen in this situation ( Carvalho e cols. ARQ.BRAS.CARDIOL vol 35:413-417,1980 ). The last ECG shows sinus rhythm with ST segment elevation that could be to pericarditis.

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Temporary pacing catheters probably perforate more than we realize. One sign is failure to pace the ventricle or a high pacing threshold. In this case the lead was displaced out from the apex and give an abnormal ECG but this is not always the case as not all perforated catheters assume a position over the LV.

The tip of a pacing catheter causes a ventricular depolarization that is positive if it moves in the direction of an EKG lead. Hence one expects a positive R in AVL with right ventricular pacing and a positive R in AVR with left ventricular pacing.

Perforation of the RV with tracking of the lead in the pericardial space, ST elevation from epicardial irritation from the temp wire?

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There certainly was a perforation, but I am not sure where it occurred. The RV apex is extremely thin and in some cases is only one or two cells thick. It is therefore surprising that more catheters don't perforate!

In this case though I suspect the perforation was higher up and that the catheter tracked down into the pericardial space.

The 1st EKG shows Bradycardia with Junctional rhythm at rate of about 50 BPM. 2nd EKG shows improperly paced rhythm. 3rd EKG is consistent with pericarditis.

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One word of caution about the failure to capture of this pacer. Remember that this was a temporary pacer and failure to capture or sense could represent some one adjusting the output or sensitivity dials.

Sat, 18 Oct 97 : club-internet.fr

I think you went through the pericardium of this poor woman who got a iatrogen sinus failure.

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The first EKG is a nodal rhythm and at first it was felt that the this was due to the combination of the metoprolol and the diltiazem. After several days off of her medications her heart rate was still relatively slow, and because of the patient's chest pain she was eventually restarted on her diltiazem and a pacemaker implanted.

The patient had an uneventful atrial pacemaker implant. An atrial pacer was selected partly as we were unsure how the extremely flexible temporary pacing wire had perforated and we did not want to repeat the event with a larger and stiffer permanent lead. Of interest, in spite of a slow sinus rate, her A/V nodal conduction was normal with 1:1 conduction maintained beyond 120/min. This suggests that the sinus node itself or conduction out of the sinus node was a major factor with this patient.

I agree that the temporary wire is in the pericardium. It is interesting in that it was still pacing and that this wire was a thin semi-floater pacing wire which is extremely flexible. The EKG suggests pericarditis with ST elevation and the patient had pleuritic chest pain which slowly improved over several days with indomethacin after the wire was removed. The pain did recurred several weeks later and again responded to indomethacin. She is doing well with her atrial pacemaker.