Does Atropine work on a 3rd degree HB?

BigBad

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My teacher says its only affects the heart at the AV node and above so no point in giving it in a 3rd degree hb.


Anyone ever see it work in the field?
 
I have never seen it work because the generally very ill 3rd degree HB patients get paced straight away.
 
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At best, I've seen/heard of Atropine working transiently. There is a reason why pacing is the preferred intervention in those patients... Atropine doesn't work all that well, if at all.
 
The vagus (parasympathetic) nerves that innervate the heart release acetylcholine as their primary neurotransmitter. ACh binds to muscarinic receptors that are found principally on cells comprising the sinoatrial (SA) and atrioventricular (AV) nodes.

Increases in vagal activity to the SA node decreases the firing rate of the pacemaker cells by decreasing the slope of the pacemaker potential (phase 4 of the action potential); this decreases heart rate. Similar electrophysiological effects also occur at the AV node; however, in this tissue, these changes are manifested as a reduction in impulse conduction velocity through the AV node.

Atropine is a muscarinic receptor antagonist that is used to inhibit the effects of excessive vagal activation on the heart, which is manifested as sinus bradycardia and AV nodal block. Therefore, atropine can temporarily revert sinus bradycardia to normal sinus rhythm and reverse AV nodal blocks by removing vagal influences.

Unfortunately, in a complete 3rd degree block atropine may accelerate the SA node, noted as an increase in P wave activity, but since the ventricular rate is initiated by the purkinje fibres, an increase in SA nodal activity will have no effect. This is why pacing is the treatment of choice.
 
Just to add to what Artickat said:

* newer research suggests there may be more vagal innervation of the ventricular myocardium than previously thought. However, where this is of pharmacological significance is debatable.

* in some patients where blockade of the AV node occurs higher up in the junction, an escape pacemaker may originate in the His bundle. This may be atropine-responsive, and if there's no additional BBB, the associated escape complexes may appear narrow.
 
If the AV Node is functioning as the ventricular pacemaker, atropine will allow it to speed up some by removing vagus stimulus, as noted above. Of course, you wouldn't be seeing a typical 3* block like you're used to... You'd see an atrial rate and a separate ventricular rate with a narrow QRS. I doubt that happens all that often. In any event, once the atropine wears off, the ventricular rate will slow right back down... So if you see a third-degree heart block in a wide or narrow QRS, know that while atropine may work, it's effects will likely be short-lived and you'd better be considering (and preparing to use) other options, such as TCP.
 
What it can also do is exacerbate the block making it go from 3°AVB to a High grade block (I've seen this happen before). A high grade block is a wide complex rhythm around 15 with A-Flutter. Very bad joo joo.
 
What it can also do is exacerbate the block making it go from 3°AVB to a High grade block (I've seen this happen before). A high grade block is a wide complex rhythm around 15 with A-Flutter. Very bad joo joo.
Something I generally prefer to avoid...
 
Hence why many of us refuse to describe A-V Dissociations as blocks (as they are not really blocks..*School of Marriot Cardiology). In patients with such terminal problems, one is really only urinating in the wind by giving Atropine, either little to no response and if it does respond a short response time. Alike was said, increasing work demand = increasing oxygen consumption= increasing infarct size.

I do wonder why though, AHA is emphasizing the usage of vasopressor therapy in lieu of TCP. Yes, I recognize the effects can be achieved but with the simplicity and response of TCP, why the switch or emphasis now on such as Dopamine to achieve these results?

R/r 911
 
I do wonder why though, AHA is emphasizing the usage of vasopressor therapy in lieu of TCP. Yes, I recognize the effects can be achieved but with the simplicity and response of TCP, why the switch or emphasis now on such as Dopamine to achieve these results?

The way I read it, they're just saying that either therapy can be used.

"TCP may be useful for the treatment of symptomatic bradycardias. There are limited studies comparing TCP with drug therapy for the treatment of symptomatic bradycardia. A randomized controlled trial in which atropine and glycopyrrolate were compared with TCP showed few differences in outcome and survival, although the TCP group obtained a more consistent heart rate.363 In a study evaluating the feasibility of treatment with dopamine as compared with TCP, no differences were observed between treatment groups in survival to hospital discharge.370 TCP is, at best, a temporizing measure. TCP is painful in conscious patients, and, whether effective or not (achieving inconsistent capture), the patient should be prepared for transvenous pacing and expert consultation should be obtained." (ACLS 2011; Neumar et al.)


Seems like they're basing the recommendation on this trial:

"OBJECTIVE:

To evaluate the feasibility of a prehospital randomized controlled trial comparing transcutaneous pacing (TCP) with dopamine for unstable bradycardia.
METHODS:

Unstable bradycardic patients who failed to respond to a fluid bolus and up to 3mg atropine were enrolled. The intervention was dopamine or TCP with crossover to dopamine if TCP failed. The primary outcome was survival to discharge or 30 days. Randomization compliance, safety, follow-up rates, primary outcome, and sample size requirements were assessed.
RESULTS:

Of 383 patients with unstable bradycardia, 151 (39%) failed to respond to atropine or fluid and were eligible for enrollment and 82 (55%) were correctly enrolled. Fifty-five (36%) of eligible patients could not be enrolled for practical reasons; 3 had advance directives, 32 met inclusion criteria on arrival at hospital and in 20 cases, paramedics chose not to enroll based on the circumstances of the case. The remaining 13 were missed cases; 8 were missing randomization envelopes and in 5, the paramedic forgot. Randomization compliance was 95% (78/82). Forty-two (51%) patients were randomized to TCP and seven of these crossed over to dopamine. Two cases were randomized but did not receive the intervention; either due to lack of time or loss of IV access. Three adverse events occurred in each group. Survival to discharge or 30 days in hospital was 70% (28/40) and 69% (29/42) in the dopamine and TCP groups, respectively with 100% follow up. To detect a 10% relative difference in 30 days survival between treatment arms, a sample size of 690 per group would be required.
CONCLUSIONS:

It is feasible to conduct a prehospital randomized controlled trial of TCP for unstable bradycardia and a definitive trial would require a multi-centre study."



Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, Passman RS, White RD, Hess EP, Tang W, Davis D, Sinz E, Morrison LJ. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010 Nov 2;122(18 Suppl 3):S729-67.

Morrison LJ, Long J, Vermeulen M, Schwartz B, Sawadsky B, Frank J, Cameron B, Burgess R, Shield J, Bagley P, Mausz V, Brewer JE, Dorian P.A randomized controlled feasibility trial comparing safety and effectiveness of prehospital pacing versus conventional treatment: 'PrePACE'.
Resuscitation. 2008 Mar;76(3):341-9. Epub 2007 Oct 22.
 
I love learning on a Friday morning thank you all! I have heard you can try it if you want while the pacer is getting set up but it probably wont work. My instructor said that when he was in school they said if you give a guy with a 3rd deg HB Atropine you will kill him. Now the AHA says well you can try it if you want.... Interesting things are always changing
 
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