no capture......

[bassnmedic]

53 yo male, guest of the State of Fla at the gray bar motel. Patient reports to the infirmary at 0800 hrs with complaints of substernal, crushing chest pain and just a general weak feeling. His initial v/s were B/P- 96/46, P- 62, R-16 and Ra SpO2@ 95%. patient has PmHx of HTN and Hep C. The prison nurse tells the Dr. the patients V/S and he orders a LR drip at 75cc/hr and bed rest.

At 0130 hrs(17 hours later) We get the call to come take a patient with "general illness" to ED for Eval. Upon arrival,we find the patient supine in bed, he is A+Ox 4, pale, cool and clammy, no radial pulses, nibp is 64/22 and has a weak carotid pulse of 32.....the IV is empty and my guess is has been for quite a while. chest pain is 8 with radiation to his shoulders, 3 lead EKG shows a Junctional rhythm at 32bpm w/o ectopy, this is confirmed with 12 lead minutes later. BGL is 101. We placed pt on O2 NRB@ 15lpm, reestablished IV of NS 300cc bolus with only slight improvement in B/P. Without hesitation we began pacing him starting at 70bpm and 10 mA and increasing the MA in increments of 10, eventually reaching 170 MA and 80bpm and never gained electrical or mechanical capture only the occasional contra lateral capture. Pacing was discontinued and Dopamine drip was started, ending up at 15mcg by the time we arrived at ED without significant increase in B/P. The patient ended up going to OR for pacemaker implant.

With all that said, I was wondering if Az, Rid or Dust or someone could shed some light as to why the pacer never captured?

[nsmedic393]

The most common problem would be placement of the pads. If that was correct i'm not sure...Perhaps thoracic impedance...was he a large lad?

As a side is it typical for your service try pacing before dopamine?

[hammerpcp]

With all that said, I was wondering if Az, Rid or Dust or someone could shed some light as to why the pacer never captured?

He wasn't talking to you Nsmedic393.

So like, why not Atropine?

[evjm]

Were the pads anterior-lateral or anterior-posterior? I haven't had to pace yet but I've heard from some the A-P requires less amperage for capture. Anyone have experiences with placement making the difference?

[vs-eh?]

Were the pads anterior-lateral or anterior-posterior? I haven't had to pace yet but I've heard from some the A-P requires less amperage for capture. Anyone have experiences with placement making the difference?

I am pretty sure (and correct me if I'm wrong) that the pads HAVE TO be placed A-P to pace using the "common" prehospital monitors (Zoll M and LP12). For cardioversion as well. Even if it is only an arrested patient, it is probably better to place the pads A-P incase of post-arrest pacing/cardioversion, and due to the fact that I believe it has been referenced that A-P placement delivers a more "efficient" shock.

I am going to assume this patient was having the ever popular inferior MI with right vent. involvement. Did the 12 lead indicate this?

Are you allowed to start pacing/dopamine for this on standing order without contacting a doctor?

I probably would have trialed atropine (quickly) continued the fluid (i.e. pressure infussion assuming clear chest/absent edema) and set up dopamine. I also would have called a doctor to bounce things of him/her.

I have only paced 1 person in the field. 1 degree ---> Mobitz 2 ----> 3rd degree @ 28-32bpm in about 2 mins. Massive inferior MI, no BP. But I have to patch first. Started the bolus, patched, atropine, pacing, dopamine (didn't get to it).

Pacing worked well...got electrical/mech capture at 56mV and upped to 62 for safety sake. He didn't like me much though...

[bassnmedic]

The pads were placed sternum and apex per our standing orders with good adhesiveness. I'm sorry , I forgot to mention that .5mg Atropine IVP was given post Dopamine. Yes VS, we are practicing under standing orders with out direct Med control contact.

The 12 lead never did confirm Inferior MI, only junctional Bradycardia. My train of thought was that maybe the patient had been in either 2nd or 3rd degree block during the day and the location and degree of block may have played a role in blocking the pacing from working.

As for the placement having to be A-P, that is not entirely correct. It does require less amps in the thinner patients. But, normal conduction through the heart runs sternum to apex, thus decreasing the threshold a little better in the avg. sized patient.

[Ridryder 911]

Wow!.. This type of situation is a pain in the gluteus and further south!..

I did not read if there appeared to be a high degree block sustained or a consideration of such in the rhythm ? I might had considered using the traditional Atropine trial dose of 0.5 mg to 1.0mg RIVP and see if it would had worked. As a possible treatment regime. If it is successful, then I would attempt to consult physician to seek some suggestions. I have had non capturing even maxed out on amps. In my experience I have several non-capturing in comparison to those capturing. I personally, do not feel there is any significant difference in A/P versus traditional anterior sternal/apex. As well, most EMS utilizes fast patch in lieu of the older version of pacer pads, which is recommended for anterior aspect.

Again, I agree Atropine can increase infarct size especially in high degree blocks (2nd degree/ type II to 3'rd degree) Although, I have seen it work quite effectively on nodal rhythms as you described especially those in higher nodal rhythms. Again.. if possible a consultation is not a bad idea... this situation is not good one This should also give the ER physician a heads up to prepare for a venous pacer to be placed ...

Sometimes even venous pacemaker will fail to capture, the ischemic or necrosed myocardial tissues will fail to respond to any electrical therapy. Traditional pacemaker placement is sometimes the only treatment that might be of success....

Your description of the scenario sounds like a a bad predicament, the type no one wants. It appears you handle the best you could given the situation.

[bassnmedic]

Due to the fact that Atropine can increase the size and severity of the infarct is why we save the atropine for last line tx. I did give the ED a heads up call for the cardiac alert. The patient was sent to to have a pacemaker later that morning. It was definitely a call I don't wish to see again anytime soon!

Todd

[buddha]

I can't quote the author of the study, but literature that came with our M-series indicated somewhere around 11% higher conversion rate with Anterior/Posterior pad placement vs. Sternal/Apex. This study may even be referred to in the AHA science guidelines. The label on the Zoll combi-pads even says they need to be A/P for pacing.

The 12 lead would have been the key for my treatment of this patient. Had it shown inferior AMI, fluid therapy definitely would have been my first goal and pacing would have been the second line. I would not give atropine to a confirmed MI - impossible to regulate the effect of the drug in a given patient. At least you can control the effect of a pacer, and bad effects go away with the flip of a switch. I believe the AHA guidelines recommend pacing before atropine in the presence of AMI.

Once inferior AMI was ruled out, I would have been quite comfortable giving atropine.

[hammerpcp]

Can we talk about this a bit? By what mechanism does atropine potentially worsen the myocardial infarction?

I found this so far.

EDIT: And this.

EDIT 2: And this.......

EDIT 3: This is a good article. It recommends anteroposterior placement for TCP and it suggests that if capture is not obtained pads should be moved (page 4). If that doesn't work they should be replaced. Did you try any of that?

Also, the second column on page two near the top addresses the atropine issue again. Did you have a twelve lead on this pt?