why we can't give IV Atropine for 2nd degree heart block type 2?

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    Anyone can help to explain to me why Atropine can be given for complete heart block but not for 2nd degree heart block type 2?? I tried to find the answer through the website but I couldn't find it. Can someone explain to me how this medication react on these condition??
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  4. 1
    because it's action is nodal, and if you're dealing with 2nd degree type II the effect would be minimal. with 3rd degree there would be no effect.
    stressgal likes this.
  5. 0
    Thanks for the response... Actually, my tutor told me that I can't give Atropine to 2nd degree type II but to give it for 3rd degree. If there is a minimal effect for 2nd degree, supposingly we should give the Atropine, right? I'm confused. Please elaborate. Thanks..
  6. 0
    Quote from erintiong
    Thanks for the response... Actually, my tutor told me that I can't give Atropine to 2nd degree type II but to give it for 3rd degree. If there is a minimal effect for 2nd degree, supposingly we should give the Atropine, right? I'm confused. Please elaborate. Thanks..
    Why would you give a drug that has minimal effect? Why not pace if the patient is not pumping effectively?

    And you should ask your tutor for an explanation as to why she or he would give atropine for 3rd degree. Other than narrow complex QRS it is not even indicated by ACLS protocols. And ACLS is very very very conservative. Why not epi or even dopamine before atropine? Why run to a drug that will likely have no effect? Why waste your time when you could be giving epi and setting up for pacing, because ultimately pacing is what you will need until if/when it can be reversed or a permanent pacer is put in.
  7. 0
    Second degree type II (Mobitz II) block generally occurs in the fascicles below the His bundle. Recall the sequence of conduction fibers

    Sinus Node - Atrial Fibers - AV Node - His Bundle - Bundle Branches/Fascicles

    Atropine works at the AV node. Because the conduction abnormality is distal to the site of action for atropine, the drug would have little/no effect.

    Cases of third degree which are medication induced can show response to atropine by enhancing AV conduction. Some cases, though- heart transplant, surgically induced conduction injury (valvular/septal surgery) would not be responsive to medical therapy and may need a temporary/permanent pacing.
  8. 4
    Quote from TakeBack
    Atropine works at the AV node. .
    Actually it's primary effect occurs at the SA node (by increasing SA-node firing, thus increasing heart rate) ...and can speed conduction through the AV-node. (which is why atropine 'speeds-up' sinus rhythms...if it's effect were only at the AV-node you wouldnt see a corresponding increase in sinus rates)

    anyway, that's kinda slicing hairs.... BUT...once you understand that atropine works by jump-starting the SA-node you can better understand why (and why not) it might work in certain blocks.

    In MOBITZ II, at least one of the p-waves is conducting (properly) through the AV-node and causing a ventricular contraction (which is your heart rate). So...lets say your patient is in a MOBITZ II block with a heart rate of 30 ( but a sinus/p-wave rate of 60). Atropine could POTENTIALLY help speed the rate up by increasing the p-wave/sinus rate...So to follow this example your patients p-wave rate jumps to 120...but the heart rate is now 60 (as a ventricular beat is following every-other p-wave).

    BUT...like others will mention, ACLS protocols do not readily advise atropine in these cases because it can make the block worse...it could degenrate into a third degree heart block...

    NOW...if atropine primarily functions by increasing SA-node firing, you can understand why it wont help in 3rd degree... because even if you could speed the SA/sinus rate up, the ventricles arent responding to anything the atria are doing and thus the heart rates wont increase. (there may be some action at the AV-node with atropine...but the effect is negligable(sp?) and typically not therapeutic). BUT...atropine wont/cant make a 3rd degree block any worse.

    SO...your teacher was kinda right and kinda wrong. The answer is: atropine CAN help sometimes in type2 but CAN be dangerous.... AND...even though atropine may have a miniscule effect on 3rd degre...you cant make it worse...
    I_See_You_RN, AmyCardsNP, dianah, and 1 other like this.
  9. 0
    Quote from Dinith88
    Actually it's primary effect occurs at the SA node (by increasing SA-node firing, thus increasing heart rate) ...and can speed conduction through the AV-node. (which is why atropine 'speeds-up' sinus rhythms...if it's effect were only at the AV-node you wouldnt see a corresponding increase in sinus rates)

    anyway, that's kinda slicing hairs.... BUT...once you understand that atropine works by jump-starting the SA-node you can better understand why (and why not) it might work in certain blocks.

    In MOBITZ II, at least one of the p-waves is conducting (properly) through the AV-node and causing a ventricular contraction (which is your heart rate). So...lets say your patient is in a MOBITZ II block with a heart rate of 30 ( but a sinus/p-wave rate of 60). Atropine could POTENTIALLY help speed the rate up by increasing the p-wave/sinus rate...So to follow this example your patients p-wave rate jumps to 120...but the heart rate is now 60 (as a ventricular beat is following every-other p-wave).

    BUT...like others will mention, ACLS protocols do not readily advise atropine in these cases because it can make the block worse...it could degenrate into a third degree heart block...

    NOW...if atropine primarily functions by increasing SA-node firing, you can understand why it wont help in 3rd degree... because even if you could speed the SA/sinus rate up, the ventricles arent responding to anything the atria are doing and thus the heart rates wont increase. (there may be some action at the AV-node with atropine...but the effect is negligable(sp?) and typically not therapeutic). BUT...atropine wont/cant make a 3rd degree block any worse.

    SO...your teacher was kinda right and kinda wrong. The answer is: atropine CAN help sometimes in type2 but CAN be dangerous.... AND...even though atropine may have a miniscule effect on 3rd degre...you cant make it worse...
    Actually, I never said it only works at the AV node. (???)

    Quote from Dinith88
    ..if it's effect were only at the AV-node you wouldnt see a corresponding increase in sinus rates
    The relevant point to the OP (AV block, not sinus dz) is that it speeds AVN conduction. It's action at the SAN is irrelevant b/c the conduction abnormality in type II is supra- or infra-hisian, and in CHB there is no effective nodal conduction. You could also mention that it causes mydriasis, but that has no bearing on its effects in AV block.

    Second, there are muscarinic receptors in the SAN and AVN. Antagonizing these receptors has effects at both sites. To say that the effect of atropine on the AVN is negligible is incorrect.

    Re: Mobitz II, the disease is infranodal. The anticholinergic effects of atropine will not have a clinical effect if the rhythm is truly type II. The fact that there is no PR prolongation in type II reveals that there is no nodal influence as there is in type I (Wenke).

    Per AJCC:

    "Identifying the location of block is important clinically, because treatment modalities for the 2 types of block are different. If the patient with 2:1 Wenckebach becomes symptomatic, it will usually respond to atropine, and pacing may be required for a time. Wenckebach is usually temporary. Mobitz II does not respond to atropine, and transcutaneous or transvenous pacing is the appropriate treatment. It does not reverse as readily, and the patient may require a permanent pacemaker. It is not unusual for Mobitz II to progress to trifascicular heart block (complete heart block with a wide QRS escape rhythm)."
  10. 0
    Quote from TakeBack
    Actually, I never said it only works at the AV node. (???)



    The relevant point to the OP (AV block, not sinus dz) is that it speeds AVN conduction. It's action at the SAN is irrelevant b/c the conduction abnormality in type II is supra- or infra-hisian, and in CHB there is no effective nodal conduction. You could also mention that it causes mydriasis, but that has no bearing on its effects in AV block.

    Second, there are muscarinic receptors in the SAN and AVN. Antagonizing these receptors has effects at both sites. To say that the effect of atropine on the AVN is negligible is incorrect.

    Re: Mobitz II, the disease is infranodal. The anticholinergic effects of atropine will not have a clinical effect if the rhythm is truly type II. The fact that there is no PR prolongation in type II reveals that there is no nodal influence as there is in type I (Wenke).

    Per AJCC:

    "Identifying the location of block is important clinically, because treatment modalities for the 2 types of block are different. If the patient with 2:1 Wenckebach becomes symptomatic, it will usually respond to atropine, and pacing may be required for a time. Wenckebach is usually temporary. Mobitz II does not respond to atropine, and transcutaneous or transvenous pacing is the appropriate treatment. It does not reverse as readily, and the patient may require a permanent pacemaker. It is not unusual for Mobitz II to progress to trifascicular heart block (complete heart block with a wide QRS escape rhythm)."
    "...supra-infra-hisian...and muscarinic receptors..."... Hmm. You are indeed wise. But...do you still deny atropine has any effect on the SA node?

    And regardless of the various phlegm's, vapors, and humors of how atropine works, it isnt a wise drug to give in any high-degree AV-blocks if there are other options. And despite your big black quotes... when you give atropine it's a fact that the atrial rate (p-waves) will increase...in a (for example) 2:1 mobitz II, this will in turn increase the ventricular rate (or make it worse/3rd degree). Simple. Regardless of the bold quotes.
  11. 0
    Quote from Dinith88
    "...supra-infra-hisian...and muscarinic receptors..."... Hmm. You are indeed wise. But...do you still deny atropine has any effect on the SA node?

    And regardless of the various phlegm's, vapors, and humors of how atropine works, it isnt a wise drug to give in any high-degree AV-blocks if there are other options. And despite your big black quotes... when you give atropine it's a fact that the atrial rate (p-waves) will increase...in a (for example) 2:1 mobitz II, this will in turn increase the ventricular rate (or make it worse/3rd degree). Simple. Regardless of the bold quotes.
    But... i should digress at this point as i dont want to seem confrontational. You are correct that in mobitz-2 the majority of literature states atropine usually wont help and can make things worse.
  12. 0
    Hey all,

    Atropine works by blocking areas of the heart that are innervated by the vagus nerve. We know the vagus nerve only connects to the SA and AV node directly.

    The reason atropine is contraindicated in High level blocks (2nd type II and 3rd/CHB) is these blocks are below the level of the AV node. 2nd degree type 1 is usually at the level of the AV node and might benefit from atropine/vagal blockade. 2nd degree type II and 3rd degree/CHB originate below the AV node.

    Imagine we give atropine and it blocks the parasympathetic system/Vagus nerve (which is the brake pedal for the heart). It should increase SA to AV rate.

    Since 2nd degree type II and 3rd degree originate below the AV node, we run the risk of increasing the disassociation between the atria and ventricles.

    In 2nd degree type II and CHB/3rd degree all or most of the impulses from from the atria are not getting to the ventricles. That’s why we we have P waves that are not causing contractions in 2nd degree II and 3rd degree.

    If we just increase atrial rate that will not help our patient. We need to increase the ventricular rate to increase blood pressure.


    The atrial impulses can’t get to the ventricles so we run the risk of increasing the atrial rate with out concurrently increasing the ventricular rate. You can make 2nd degree type II in to 3rd degree or 3rd degree into ventricular aystole.

    So you might be able to increase SA-AV rate, but since 2nd degree II and 3rd degree is beneath the AV you would not concurrently increase the ventricular rate therefore increasing the dissociation.

    Pacing is the treatment of choice for the high level blocks.

    Unfortunately your instructor was wrong. We are not supposed to give atropine to 3rd degree as a primary intervention.

    The guidelines state “prepare for immediately pacing for higher level blocks”.

    I hope this helps

    Jeff Laabs RCP


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