First call for a paramedic student

captaindepth said:
By the time we arrived the receiving ED we had administered 800ml of fluid and still were unable to auscultate a BP. The pt remained alert throughout transport with no changes in mentation, so we did NOT pace and only administered ASA and O2. Cath Lab was activated prior to us leaving the scene and the pt went up 15 minutes after arrival in the ED. I did not get follow up and know nothing after that.

I called the rhythm a sinus brady with a significant 1* AV block, ST segment elevation in the inferior leads and reciprocal changes in the high lateral leads. I believe the RCA is the involved coronary artery.
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Sounds good to me.
 
Do you think pacing would put unwarranted stress on the myocardium? He is perfusing the brain enough to remain alert and had no changes in presentation throughout pt contact. I'm not sold that pacing would be beneficial.
 
Rather rich for the Lifepak to gripe about the data quality...

Nice call.
 
With pacing you can control how high the heart rate increases, there is no telling how high the rate will increase with giving atropine. You want to get a stable heart rate without causing increase cardiac demand. Remember a nice slow heart rate improves diastole time which is needed to perfuse the coronary arteries .
 
tpchristifulli said:
With pacing you can control how high the heart rate increases, there is no telling how high the rate will increase with giving atropine. You want to get a stable heart rate without causing increase cardiac demand. Remember a nice slow heart rate improves diastole time which is needed to perfuse the coronary arteries .
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Agreed, provided there's enough diastolic pressure to do so.

Definitely agree about TCP > Atropine in the presence of an AMI.
 
Just a brady patient that's cool probably no need to pace at all.

A brady patient who is lethargic, cool/pale/profuse, and an unobtainable BP is getting either paced or atropine as my treatment plan. Mix in a MI and I'm going for pacing.
 
I guess im having trouble finding the threshold for more advanced interventions. I get wanting to pace the pt but what is the end goal of treatment? normal mentation? SBP > 90mmHg?

The pt continued to be AAOx 4 with a GCS of 15 throughout transport, why pace? Unable to auscultate BP in the ambulance but there must be adequate profusion if he continues to mentate appropriately.
 
captaindepth said:
I guess im having trouble finding the threshold for more advanced interventions. I get wanting to pace the pt but what is the end goal of treatment? normal mentation? SBP > 90mmHg?

The pt continued to be AAOx 4 with a GCS of 15 throughout transport, why pace? Unable to auscultate BP in the ambulance but there must be adequate profusion if he continues to mentate appropriately.
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I didn't see "pale/cool/ and extremely diaphoretic" thanks to the advertisement banner right in the middle of the paragraph. If he's showing such severe signs of hypoperfusion, then he needs to be paced for sure. Mental status isn't a sole indicator for how well someone is getting perfused.

He is obviously trending downwards, especially after no response to an 800ml fluid bolus. You want to intervene before he kicks the bucket. Pacing would be the best option, with a last resort for pressors.

Or just give him 1mg epi IVP since he's headed for cardiac arrest. That'll wake him up.
 
captaindepth said:
I guess im having trouble finding the threshold for more advanced interventions. I get wanting to pace the pt but what is the end goal of treatment? normal mentation? SBP > 90mmHg?

The pt continued to be AAOx 4 with a GCS of 15 throughout transport, why pace? Unable to auscultate BP in the ambulance but there must be adequate profusion if he continues to mentate appropriately.
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The pt may be AAOx4 but is lethargic which is a sign of inadequate profusion (add in the other vitals signs)
 
captaindepth said:
You are dispatched for a 60-70y/o male pt with chest pain @ 0630

U/A Pt was pale/cool/ and extremely diaphoretic. Pt appeared lethargic but alert and able to answer questions appropriately. BP unobtainable (manual attempt x 2), no distal pulses, and a RR of 20. The wife sates he had been awake for approx 30minutes before he had sudden weakness and shortness of breath.

You are in an urban system with about a 15 minute transport to a Level I trauma center with all services available.

Here is the initial 4 lead EKG obtained in the house:
View attachment 1539

What are your treatment priorities? Any pharmacological interventions you would consider? How long should the on scene time be? and how would you transport the pt, emergent vs. nonemergent?
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Junctional bradycardia with short-coupled extrasystoles (likely early after-depolarizations)...nasty nasty nasty. I'm very concerned for ventricular arrhythmias given the slow rate and EADs.

Fluids, atropine, set up for pacing/begin pacing. (of course Code STEMI)
 
Just out of curiousity is anyone going to Dopamine or an Epi drip before pacing this guy? or at least thinking about it?
 
Rialaigh said:
Just out of curiousity is anyone going to Dopamine or an Epi drip before pacing this guy? or at least thinking about it?
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No. I don't see any evidence that the addition of a pressor would improve the state. We've got what appears to be an electrical problem, perhaps due to extreme vagal tone (Bezold-Jarisch). If this weren't a narrow complex rhythm I'd move more towards those treatments though.
 
Christopher said:
Junctional bradycardia with short-coupled extrasystoles (likely early after-depolarizations)
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Are you not buying these P waves, Chris?
 
Brandon O said:
Are you not buying these P waves, Chris?
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I saw no evidence of consistent P-waves in the 3- or 12-Leads.

EDIT: just saw the V4R 12-Leads...did not realize those were new attachments.

Consistent PRi of ~440? Obviously sinus brady, 1AVB. Even more likely to push atropine with those findings.
 
Christopher said:
No. I don't see any evidence that the addition of a pressor would improve the state. We've got what appears to be an electrical problem, perhaps due to extreme vagal tone (Bezold-Jarisch). If this weren't a narrow complex rhythm I'd move more towards those treatments though.
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What about decreased blood flow to the SA and AV nodes causing the slow rate and conduction delay? With such a slow atrial rate would atropine just decrease the 1* AV block and speed up the AV nodal conduction? Or would it actually increase the SA rate therefore increasing the HR?
 
captaindepth said:
What about decreased blood flow to the SA and AV nodes causing the slow rate and conduction delay?
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That dramatic of an effect would be unusual from systemic hypotension. Local perfusion problems (e.g. occlusion) are more often the cause of myocardial ischemia. (Systemic hypoxia can annoy the heart though.) Probably the MI in this case.

With such a slow atrial rate would atropine just decrease the 1* AV block and speed up the AV nodal conduction? Or would it actually increase the SA rate therefore increasing the HR?
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The most important effect would be on the SA node. Possibly you could get rid of the block, but it's neither here nor there since a 1st degree block never killed nobody.
 
captaindepth said:
What about decreased blood flow to the SA and AV nodes causing the slow rate and conduction delay? With such a slow atrial rate would atropine just decrease the 1* AV block and speed up the AV nodal conduction? Or would it actually increase the SA rate therefore increasing the HR?
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That's a reasonable assumption given the distribution of ST-elevation and likely infarct related artery. I'm not concerned about shortening the delay in the 1AVB, but instead increasing the rate.
 
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