no capture......

[bassnmedic]

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?

Yes, we did go through all all our troubleshooting steps, pads moved and replaced. The 12 Lead was done quickly after the 3 lead and confirmed only Junctional Bradycardia.

Take care,

Todd

[bassnmedic]

We have gotten a little off track on this thread which is ok with me, but I was really trying to figure out if there is any pathophysiological reason the pacing may have not worked. Could there have been a high degree earlier in the day that changed to the junctional rhythm that was preventing the pacer from working as it was supposed to?

[AZCEP]

The conduction system defect is unlikely to cause the TCP to be unable to capture. The pacer isn't relying on the intrinsic conduction system too much anyway. It would be likely that the events played out as you suspected, but instead of the damage to the conduction system, perhaps the ischemic/injured myocardium was unable to accept the stimulus.

When a degree of acidosis presents, the tissue just doesn't want to respond like we expect it too.

Patient factors aside, it may be time to take the pacer to your bio-med person to give it a good going over.

[buddha]

Increased myocardial workload causes increased myocardial oxygen demand. If myocardium is already starved for oxygenat a rate of 40, do you really want to give atropine and increase the rate to 100 or would you like to pace at a rate just high enough to balance the patient's need for perfusion against killing off myocardium??

[bassnmedic]

Thanks for everyone's input, it has been helpful and informative.

[hammerpcp]

Increased myocardial workload causes increased myocardial oxygen demand. If myocardium is already starved for oxygenat a rate of 40, do you really want to give atropine and increase the rate to 100 or would you like to pace at a rate just high enough to balance the patient's need for perfusion against killing off myocardium??

Did you read those articles?

[zzyzx]

Here's what the AHA says about atropine (taken from the just-published ACLS book):

"In the absense of immediately reversible causes, atropine remains the first-line drug for acute symptomatic bradycardia. Failure to respond to atropine is an indication for TCP, although use of second-line drugs such as dopamine and epinephrine may be successful. For bradycardia, give atropine at .5 mg IV every 3 to 5 minutes to a total dose of 0.04 mg/kg (max total dose of 3 mg). Atropine doses of less than .5 mg may paradoxically result in further slowing of the heart rate. Use atropine cautiously in the presence of acute coronary ischemia or MI. An atropine-mediated increase in heart rate may worsen ischemia or increase infarct size. Do not rely on atropine in Mobitz type II second-degree or third-degree AV block or in patients with third-degree AV block with a new wide QRS complex. Hemodynamically unstable and clinically deteriorating patients require immediate pacing. All other away patients should have sedation before pacing."

I'm taking this out of context, and I should explain that they say you shouldn't delay pacing if the patient is unstable and has a high-degree block.

[northernmedic]

AP or AL placement of pads will work for pacing (at least with the LP 12). I recently encountered a similar situation where there was no response with atropine and there was electrical capture with pacing but no mechanical capture. I generally have 1 or 2 patients a month that I end up pacing and on the 3 occasions I have no received capture, it was in a situation where the pt had a massive MI and ended up in a 2nd or 3rd degree block. I think AZCEP mentioned above that acidosis makes it harder to get capture. My ultimate reasoning: S**t happens and patients die. Also that's why we have orders for catecholamine infusions if we need them. It sucks to have to patch for orders for pacing when a patient is heading south, glad we don't have to do that here.

[buddha]

To reiterate from the above post:

Use atropine cautiously in the presence of acute coronary ischemia or MI. An atropine-mediated increase in heart rate may worsen ischemia or increase infarct size.

[Aussieaid]

Hi all,

I usually just read these forums but figured it wouldn't kill me to post for once :lurk: [/font:11babba7ee] (I figure someone here might be kind enough to help me when I get beaten into the ground - if I put my foot in my mouth!!!)

Sounds like Bass did all the troubleshooting..

I would be in agreement with AZCEP. This guy is probably extremely acidotic by this stage and that really increases your pacemaker capture threshold. The guy has a history or hypertension and presents in the first place with a SBP in the 90's hours prior to you being called. Compound that with the fact that it only takes 40 minutes of renal hypoperfusion to go into renal failure and it adds to the acidosis and the risk of hyperkalemia which can also increase the capture threshold......whew, take a deep breath.

Other causes of increased capture threshold include hypoxia, hyperglycemia, certain antiarrhymic drugs, verapamil, beta-blockers and alkalosis.

So take your pick.

By the way could they do any kinds of gases or labs at the infirmary, like maybe an I-stat. That would have been a big help for you.

Also agree that the heart was probably just a little "pooped" by this stage and just didn't have enough "ZAP" left to respond. :mrgreen:

Thanks for letting me play in the sandbox.. :smilebox: