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ACLS Drugs for Bradycardia

 

ACLS Drugs for Bradycardia

When bradycardia is being treated in ACLS, if an underlying cause cannot be identified and corrected, medications are indicated.

There are three medications used in the bradycardia algorithm: atropine, epinephrine, and dopamine. Each drug and its use within the bradycardia algorithm is explained below.

Atropine

Atropine is the first drug used to treat bradycardia in the bradycardia algorithm. It is classified as an anticholinergic drug and increases firing of the SA Node by blocking the action of the vagas nerve on the heart resulting in an increased heart rate.

Atropine should be used cautiously in the presence of myocardial ischemia and hypoxia since it increases oxygen demand of heart and can worsen ischemia.

The dosing for Atropine is 0.5 mg IV every 3-5 minutes as needed, and the maximum total dosage that can be give is 3 mg.

Atropine should be avoided in hypothermic bradycardia and it will not be effective for Mobitz type II/Second Degree Block Type 2.

You may have read that Atropine is not effective for Mobitz II (2nd degree block type II) and Complete Heart Block (3rd degree block)
Click here to find out why

Epinephrine and Dopamine

Epinephrine and dopamine are second-line drugs for symptomatic bradycardia. They are both used as infusions in the bradycardia algorithm if atropine is ineffective.

New 2010 ACLS guidelines state that if bradycardia is unresponsive to atropine, an equally effective alternative to transcutaneous pacing is the use of an IV infusion of the beta-adrenergic agonists (dopamine or epinephrine).

Dosing:

Begin the epinephrine infusion at 2 to 10 mcg/min and titrate to patient’s response.

The goal of therapy is to improve the patient’s clinical status rather than target an exact heart rate.

Begin the dopamine infusion at 2 to 10 mcg/kg/min and titrate to the patient’s response.

Precautions

Prior to use of ACLS drugs in the treatment of symptomatic bradycardia, contributing factors of the bradycardia should be explored then ruled out or corrected.

Return to main ACLS Pharmacology page.


In your AHA Provider manual, you will see it stated under the bradycardia algorithm section that atropine is not effective for Mobitz II and Complete Heart Block. I have had a number of people ask why it is not effective. Here is an explanation:

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.

With 3rd degree block there is a complete block and disassociation of the electrical activity that is occurring in the atria and ventricles. Since atropine’s affect is primarily on the SA node in the atria, 3rd degree block would prevent its affect on the SA node from influencing the rate of ventricular contraction which is needed to improve perfusion.

With Mobitz-II, aka, Second-degree AV Block Type II, the situation is similar. There is a partial block in the electrical impulses from the atria (SA) to the ventricles, and thus the affects of atropine would not significantly change the status of the ventricles.
This block can also rapidly progress to 3rd degree block.

To summarize, Atropine may speed the firing rate of the SA node (atria), but the ventricles are not responding to anything the atria (SA node) puts out. Thus, the heart rates will not increase.

There may be some action at the AV-node with atropine, but the effect will be negligible and typically not therapeutic. Atropine in most cases will not hurt the patient with 3rd degree block unless they are unstable and you delay pacing to give atropine.

It is important to note that Mobitz II and Complete Heart Block may be associated with acute myocardial ischemia. In this case, if atropine is used and it increases the heart rate there is a high potential for worsening of the myocardial ischemia due to the increased oxygen consumption. The increased heart rate will also reduce diastolic filling time which may worsen coronary perfusion.

Since new onset mobitz II and Complete Heart Block are commonly associated with myocardial infarction, it would be ideal to keep the HR slow (50-60) to increase diastolic filling time. Anytime you increase HR, the diastolic filling time is what takes the biggest hit.

Transcutaneous Pacing should be the first line in symptomatic Mobitz II and Symptomatic Complete Heart Block. It is very safe & less painful than in previous times due to technology improvements. Research has shown that most individuals can tolerate > 15min of transcutaneous pacing without too much difficulty.

Now back to the bradycardia drugs

  68 Responses to “ACLS Drugs for Bradycardia”

  1. 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?

    • 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

  2. Why is the initial dose of Atropine 0.5 and no longer 1.0?

    • 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

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

    • Atropine has been shown through clinical use to have no effect on improving outcomes for the patient with asystole.

      Kind regards,
      Jeff

      • 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 ?

      • 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

  4. 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).

    • 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

  5. when the patients take the atropin alone why the response will be bradycardia then tachycardia??

    • 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

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

  6. Hi just looking at this topic from a different view point, with a bradycardia from a new 2nd degree type 2 AV block with narrow QRS (so likely AV node, not infranodal) what about giving a fluid bolus? increase the preload and stretch, starlings law wouldn’t this increase the intrinsic rate? and if this doesnt work pacing?

    Regards
    Mark

  7. Atropine is a parasympatholytic blocker. There are no parasysmpathetic fibers in the ventricles so Atropine would have no influence where it “can’t go”. This is most likely why it had been traditionally held in second degree Type II and 3rd degree heart blocks – the wider the complex the lower in the conduction system the rhythm originates. With the 2010 guideline changes, I believe the pendulum swung back to saying try the Atropine in case the block is not that low in the conduction system WHILE you are reaching out and setting up for TCP – it’s often quicket to get the drug on board than the TCP set up.

  8. I had tavb case in ER few days ago. Patient condition : BP110/70, HR 38, LOC and SOA, peripheral perfusion was good. cardiologist gave the patient atropine and NE. I didnt talk much with him. Jeff what do you think about NE in bradycardia case? Why didnt he give epi?

  9. Jeff you are just great. If you bradycardia and hypotension and the patient was in cardiac arrest previously, and the patient is in septic shock, epi and dopa are after norepinephrine. Even, dopa is not recommended because it increases mortality due to arrhythmias( dopa trigger arrhy).

    Nelhom

  10. One of my practice tests keeps giving the atropine dose as 0.5-1 mg. I can’t find anywhere that says it’s ok to give 1mg of atropine as an initial dose for bradycardia. Is this an ok practice or a trick question?

  11. I always thought Atropine was not used in Mobitz II and CHB because of where it works-the SA node. In high degree blocks the electrical signal does not pass through the Bundle of His and so increasing the number of signals generated by the SA node will not increase the ventricular rate. It is the ventricular rate that determines cardiac output so you need to go to a more direct approach with a pacemaker or epinephrine

    • Yes, this is true. Atropine may have not have an effect because it primarily acts by increasing the firing of the sinoatrial node (atria) and conduction through the atrioventricular node (AV) of the heart. Basically, with 3rd degree block there is a complete block and disassociation of the electrical activity that is occurring in the atria and the ventricles.
      Atropine may speed the firing rate of the SA node (atria), but the ventricles are not responding to anything the atria (SA node) puts out. Thus, the heart rates will not increase.
      There may be some action at the AV-node with atropine, but the effect will be negligible and typically not therapeutic. Atropine in most cases will not hurt the patient in with 3rd degree block unless they are unstable and you delay pacing to give atropine.
      However, the major reason why you would not want to give it is because of the risk of worsening already existing myocardial ischemia as is common with a new onset of 2nd degree block Type 2 or complete heart block.
      The explanation on the site was vague regarding where atropine has it affects. I have modified this section and hopefully it will be a little more clear.
      Kind regards,
      Jeff

  12. Hello,
    How would you set up the Dopamine and Epi infusions?

    • The standard concentration for a dopamine drip is 800mg in 500 ml D5W or 1600 mcg/ ml. Dopamine infusion is a weight based infusion so you would need to calculate the infusion rate. For bradycardia you will infuse at 2 to 10 mcg/kg/min and titrate based upon the patients response.

      Here is the formula for calculating the infusion rate:

      Ordered dose x patient weight in kilograms x 60 minutes divided by the solution concentration.

      So here is an example:
      The patient weighs 50 kg and you want to infuse the drip at at 6 mcg/kg/min then you would calculate it as follows:
      6 mcg x 50 kg x 60 minutes divided by 1600 mcg/ml = 11.25 ml/hr



      The standard concentration for an epinephrine drip is 3mg in 250 ml D5W or 3000 mcg/250 ml = 12 mcg/ml. So if you want your epinephrine infusion to run at 6 mcg/min then you would calculate it as follows. First, to simplify the drip calculation for any drug ordered as mcg/minute calculate the infusion rate for 1 mcg/minute of 3000 mcg/250 ml solution (12 mcg/ml) as shown here:
      1 mcg x 60 min
      ———————— = 5 ml/hour (infusion rate)
      12 mcg/ml (drug concentration)
      Once you’ve calculated the infusion rate for 1 mcg/min which is 5 ml/hour, you can
      easily determine the titration rates, as shown below:
      2 mcg x 5 = 10 ml/hour (2 mcg/minute)
      3 mcg x 5 = 15 ml/hour (3 mcg/minute)
      4 mcg x 5 = 20 ml/hour (4 mcg/minute)
      5 mcg x 5 = 25 ml/hour (5 mcg/minute)

      Kind regards,
      Jeff

  13. Why is noenates contra indicated for atrophine

    • I have done some searching to find out the answer and the only thing that I could clearly deduce was that research has shown no proven benefit of routine use of atropine in neonatal resuscitation.
      If I do discover anything else about this, I will post it on the site.

      Kind regards,
      Jeff

      • I just wanted to add that in PALS, we teach not to use atropine routinely for infants and children because they have a much higher vagal tone than adults If their bradycardia is not due to vagal stimulation, and you give atropine, their heart rate will shoot way up, and you will still have cardiovascular compromise, just with the opposite problem (tachycardia). PALS teaches that you only use atropine if you vagaled them or watched them vagal (suction, etc.). I do not teach NRP, but I assume it is similar reasoning. Or, it could be that they cannot handle the increase in myocardial O2 demand/consumption.

  14. Why is there a difference in an Epi infusion for post cardiac arrest care compared to during an arrest. In the post care it is weight based, whereas most of the time it is a standard 2-10 mcgs per min.
    Thanks,
    Angela

    • I believe that the weight based is because that is how the folks doing the research on post-cardiac arrest care ran their trials. I think weight based was what they had the best outcomes with as compared to the non-weight based.
      Kind regards,
      Jeff

      • I think that you both are referring to Dopamine. Epi is always infused as a standard 2-10 mcgs/min. Am I wrong?

      • Hi Dualdoc,
        Thanks for your input. Just passing this along. For post-cardiac arrest the Epinephrine is weight based. Reference is page 76 of the AHA Provider manual.
        States: Treatment of Hypotension–Epinephrine 0.1-0.5 mcg/kg/min titrate to achieve a minimum SBP > 90 mmHg or mean arterial pressure of > 65 mmHg.
        (70kg adult this would work out to 7-35 mcg/min)
        Kind regards,
        Jeff

  15. Hello

    I have also read that epi shoud be used cautiously when MI is suspected. In type 2/2 and type 3 would you use dopamine infusion instead….OR…is the epi ok bc it’s an infusion and not rapid IVP?

    Thanks!
    Andi

    • Either epinephrine or dopamine is ok. Due to the fact that the infusion dose is very small and you will not have the profound affect as when you give IVP. The epi drip should not increase the myocardial oxygen demand any more than the dopamine. If MI suspected PCI should be the priority.
      Kind regards,
      Jeff

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