ACLS drugs for Bradycardia | ACLS-Algorithms.com

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    • Jeff with admin. says

      At intermediate rates (2-10 mcg/kg/min), dopamine acts to stimulate the beta1-adrenoceptors, resulting in improved myocardial contractility, increased SA rate and enhanced impulse conduction in the heart (i.e. increased heart rate and improved contraction). Kind regards, Jeff

      • Monthe Kofos says

        Brilliant response!
        I am watching a Blacklist episode right now where they are doing ACLS and trying to figure out why they were giving dopamine and I completely forgot about the three different responses. Thank you so much for reminding me! This is going to help me on my medical school boards now.

    • Monthe Kofos says

      Just to elaborate a little more, at low levels dopamine activates the D1 and D2 receptors, at middle doses dopamine activates the B1 and B2 receptors, and at high doses dopamine activates the alpha 1 and Alpha 2 receptors. It is one of those weird drugs where the actual dosing effects what receptor is being involved. I hope this helps!

  1. Carol L says

    Is there a place on your site where you talk about and explain about transcutaneous pacing (for someone who knows very little about it) or a website you would recommend to increase my understanding of what exactly it is and does?
    Thanks!

  2. malinarose says

    Ok just a checking…because Mobiz II and 3 rd degree HR block are located below the SA node Atropine probably won’t help in this problem? But in the brady alogrithm we start with atropine even in these conditions (Mobiz II and 3 rd Degree HR block) until we can get pacing ready.

    If you know it is a Mobiz II and a 3 rd degree should you not use atropine at all?
    If you see that the patient is having a septal MI on a 12 lead if you have one is it best to not use Atropine since it might decrease the preload?

    • Jeff with admin. says

      In the case where you are dealing with symptomatic bradycardia and an ongoing MI, atropine would be contraindicated and should not be given.

      In general, the use of atropine with Mobitz II and third-degree block should not be depended upon and would be a discretion call by the emergency team running the code.

      Kind regards,
      Jeff

      • Mei says

        hi Jeff,
        Just find it on the medscape

        “Mobitz type II AV blocks are associated with a poor prognosis, as the mortality rate associated with their progression to a complete heart block is approximately 80%. Therefore, this type of second-degree AV block should be immediately treated with transcutaneous pacing or atropine. Atropine helps in about 50% of cases, but it occasionally worsens the block with an increased heart rate. A temporary transvenous pacemaker, and possibly a permanent demand pacemaker, must ultimately be placed.”

        “Complete heart block in patients with an inferior MI usually responds to atropine. In most patients, it resolves within a few days without the need for a temporary or permanent pacemaker. ”

        here’s the link http://emedicine.medscape.com/article/164924-overview#a6

        what do you think? thank you

      • Jeff with admin. says

        The statements in these articles are correct. I concur with everything stated.

        The nuances and technicalities of the article are a little bit beyond the scope of basic ACLS, but they are correct.

        Kind regards,
        Jeff

  3. rob says

    So atropine is not to be used in a bradyarrhythmia when the etiology is presumed to be an AMI. How often is a bradycardic rhythms’ etiology not AMI. What are other causes of symptomatic bradycadia? Also could you direct me towards some literature that supports withholding atropine in the presence of bradycardia secondary to AMI. Thanks!

    • Jeff with admin. says

      It can be used but you should use it with caution. Here is the AHA quote and link to the reference:
      “Avoid relying on atropine in type II second-degree or third-degree AV block or in patients with third-degree AV block with a new wide-QRS complex where the location of block is likely to be in non-nodal tissue (such as in the bundle of His or more distal conduction system). These bradyarrhythmias are not likely to be responsive to reversal of cholinergic effects by atropine and are preferably treated with TCP or b-adrenergic support as temporizing measures while the patient is prepared for trans-venous pacing.” Reference: Pg. S749-750 Circulation Journal Nov. 2nd 2010

    • Mo says

      Pt coded and has a breathing rate of 8 per minute. Common causes of bradycardia? Hypoglycemia, overdose, vagal. So, you should give D50W, atropine, narcan.

  4. goar0701 says

    I am a little confused here, please some help!!!

    For the treatment of Hypotension (Just for ACLS purpose), can we use:

    Dopamine infusion of 10-20 mcg/kg/min. OR,
    Epinephrine infusion of 0.1-0.5 mcg/kg/min OR,
    Epinephrine infusion of 2 – 10 mcg/min.

    Thanks for your help!

    • Jeff with admin. says

      Treat hypotension as follows:
      Epinephrine 0.1-0.5 mcg/kg/min
      Dopamine 5-10 mcg/kg/min

      For chemical pacing with bradycardia:
      Epinephrine: Initiate at 2-10 mcg/min and titrate to response
      Dopamine: Initiate at 2-20 mcg/kg/min and titrate to response
      Kind regards,
      Jeff

  5. crackers says

    I think you mean “vagus nerve”…….but I get it.

    First let’s look at atropine and how it works. Atropine increases firing of the sinoatrial node (atria) and conduction through the atrioventricular node (AV) of the heart by blocking the action of the vegus nerve.

  6. kb says

    Hi,

    Do we need to dilute atropine in NS before giving IVP in Bradycardia Algorithm?or we can give undiluted?And how fast can we give?

    Thanks

    • Jeff with admin. says

      Atropine usually comes in prefilled syringes that are ready to push as is. These syringes can be given undiluted. If you must dilute the atropine, dilute to 0.1 mg/ml. You will push the atropine rapidly. The goal with all emergency medicines is to get them in as a bolus so that the entire medication is made available in the system at the same time. Always follow all medications with 20 ml of NS rapid IV push as well.

      Kind regards,
      Jeff

  7. Benjamin Leong says

    Why is it a concern to give atropine for bradycardia in the setting of ACS, when ANY therapy to restore the heart rate (pacing, dopamine etc) WILL also increase the myocardial oxygen demand?

    If the patient was unstable due to the bradycardia, and you have to bring the heart rate back up, why is atropine singled out to be ‘bad’?

    • Jeff with admin. says

      The main reason that atropine needs to be used with more caution in the ACS setting is it is harder to control and predict its effect on the patient. Pacing can be titrated and well controlled during its use. A dopamine or epinephrine drip can be controlled in the same way but with control of the amount of medication being infused. Atropine is a bolus injection and there is no way to control the effect on the heart rate when giving this type of injection.
      Kind regards,
      Jeff

    • Dr yatin khairnar says

      As dopamine and epinephrine are given in infusion for, the rate can be controlled and so the heart rate can be controlled without increasing myocardial oxygen demand. But on the contrary atropine being given bolus, so one can not control the heart rate

  8. Jon says

    Jeff,

    First of all. Thanks for your feedback.

    According to ACLS guidelines, can a Pt be treated with more than one algorythm at a time? For example a Pt is Sinus Brady and hypotensive with a right sided AMI?

    Are there any other examples that you can think of in which a Pt could be treated with more than algorithm?

    • Jeff with admin. says

      It is ok to use any one of the algorithms in coordination with the ACS or Stroke algorithm. You may have a variety of scenarios occur simultaneously. Here are some examples: ACS+Unstable Tachycardia, ACS+Stable Tachycardia, ACS+Bradycardia. Watch symptoms and treat using ACLS protocols accordingly.
      Kind regards,
      Jeff

  9. Jerry says

    I have sort of high BP, bradycardia (41 low end of range) and Frequent PACs with some atrial runs. Is there is a medication that could ideally help with all of these – or at least some – without causing more problems in one of more problem areas

    • Jeff with admin. says

      Unfortunately, I cannot offer any medical advice on this site since it is for education purposes only. I can say that I really don’t know of any one medication that could help with all of the problems you listed. You should get a consultation with a good cardiologist to help with this situation.

      Kind regards,
      Jeff

  10. Arun G Arali says

    Why not use Dobutamine instead of Dopamine for bradycardia?
    Dobutamine is the closest in profile to Isoprenaline, which is an excellent drug in the management of bradycardia, when pacing is not available.
    Why do the AHA guidelines put Dopamine ahead of Dobutamine in the management of bradycardia? Is Dobutamine a bad choice in a patient with bradycardia compared to Dopamine?
    Adrenaline being the primary catecholamine, I agree has a place. But, why Dopamine? Why not Dobutamine? In a patient needing a chronotropic agent (heart rate of 45 to 50bpm), a patient who has normal or slightly higher blood pressure and is not in shock, is Dopamine a better choice than Dobutamine?

    • Jeff with admin. says

      To my knowledge dobutamine is not commonly used for bradycardia, has insignificant effects on heart rate and mostly improves myocardial contractility. It is not recommended in any of the AHA literature that I can find. I would say that Dobutamine would be a bad choice. Dopamine has a much more profound effect on the heart rate.

      Kind regards,
      Jeff

      • CICUnurse says

        In my experience, dobutamine causes significant vasodilation (reduces SVR) to offset the positive benefits if increased heart rate and contractility. For this reason is is not considered a pressor and also would not help a hemodynamically unstable bradycardic patient.

    • Jeff with admin. says

      The dose of 0.5mg has been found to be effective for the treatment of bradycardia. This has been the standard initial dose since at least 2000. Also, you may be thinking about the previous 1.0mg dosing of atropine for PEA and asystole. This was changed in 2010 and atropine is no longer recommended for the treatment of PEA and asystole.

      Kind regards,
      Jeff

  11. KM says

    Hi,
    can I know what’s the reason for the relatively recent exclusion of atropine in patients with asystole ?
    Thanks !

      • KM says

        Thanks for the prompt reply! Was just wondering: so was the previous (outdated) ACLS recommendation of 2.4mg atropine in asystole not based on demonstrable benefit in clinical studies ? Or is it that new evidence from better studies overrided that ?

      • Jeff with admin. says

        More recent studies and clinical evidence has shown that atropine is not and never was effective for the treatment of asystole. Prior to 2010, the use of atropine was included because there was a hypothetical justification for atropine based on physiology and pathophysiology.
        Quote from AHA: “Available evidence suggests that routine use of atropine during PEA or asystole is unlikely to have a therapeutic benefit.”

        Kind regards,
        Jeff

  12. zane reid says

    Why are cholinergics avoided in hypothermia bradycardia and how would these factors affect a thermoregulation crisis of the body? Both cold emergencies(hypothermia) and hot emergencies(heat cramps, heat exhaustion, heat syncope, and heatstroke).

    • Jeff with admin. says

      I don’t think it is so much that they are avoided, it is that when the body’s temperature is deranged significantly, the enzymatic reaction and cellular activity is altered drastically and drugs such as atropine won’t be effective. I think that most physicians would still use it.

      Kind regards,
      Chris

    • Jeff with admin. says

      I don’t really understand your question, but here is how atropine works.
      Atropine blocks the action of the vagus nerve. The main action of the vagus nerve is to decrease heart rate. Atropine will increase the heart rate.

      If you need any further help, please clarify your question a little more.

      Kind regards,
      Jeff

    • anuj says

      This is initially due to blockage of muscarinic M1 autoreceptors on vagal nerve ending augmenting Ach release

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