There are three medications used in the bradycardia algorithm: atropine, epinephrine, and dopamine. Read about each drug and its use within the bradycardia algorithm below.
When symptomatic bradycardia occurs, the primary objective is to identify and treat the cause of the problem. Medications are indicated if symptomatic bradycardia cannot be corrected by treating an underlying cause or if the cause cannot be determined.
2020 AHA UpdateThe single-dose administration of atropine was increased from 0.5 mg to 1 mg. Now give 1 mg for the first dose and then repeat every 3-5 minutes at the 1 mg dose. Also, the dopamine infusion rate for chemical pacing was changed to 5-20 mcg/kg/min. The previous rate from the 2015 guidelines was 2-20 mcg/kg/min.
Atropine
Atropine is the first line medication for the treatment of bradycardia. The administration of atropine typically causes an increase in heart rate. This increase in the heart rate occurs when atropine blocks the effects of the vagus nerve on the heart. When the vagus nerve is blocked, the SA node increases its rate of electrical discharge and this, in turn, results in the increased HR.
Use atropine cautiously in the presence of myocardial ischemia and hypoxia because it increases oxygen demand on the heart and can worsen ischemia.
The dosing for Atropine is 1 mg IV every 3-5 minutes as needed, and the maximum total dosage for administration is 3 mg.
Atropine should be avoided with bradycardia caused by hypothermia and, in most cases, it will not be effective for Mobitz type II/Second-degree block type 2 or complete heart block.
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
Atropine for Mobitz II and Complete Heart Block
In your AHA provider manual, you will see it stated in the bradycardia 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. Read below for the explanation.
First, let’s look at atropine and how it works. Atropine increases the firing of the sinoatrial node (atria) and conduction through the atrioventricular node (AV) of the heart by blocking the action of the vagus 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 effect is primarily on the SA node in the atria, a 3rd-degree block would prevent its effect 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 effects 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. In most cases, atropine will not hurt the patient with 3rd-degree block unless they are unstable and cardiac pacing is delayed in order to administer atropine.
Caution with Atropine
It is important to note that Mobitz II and complete heart block may be associated with acute myocardial ischemia. If atropine is used when there is ongoing myocardial ischemia this may worsen myocardial ischemia because of an increase in oxygen consumption. The increased heart rate will also reduce the diastolic filling time which may worsen coronary perfusion.
Since new-onset Mobitz II and complete heart block are commonly associated with myocardial infarction, it is recommended to maintain a slow HR (50-60) in order to increase the diastolic filling time. Any time you increase HR, the diastolic filling time is reduced and this reduces the coronary perfusion.
Transcutaneous pacing should be the first line action for symptomatic Mobitz II and symptomatic complete heart block. It is very safe & less painful than in previous times due to technological improvements. Research has shown that most individuals can tolerate > 15min of transcutaneous pacing without significant pain or discomfort.
Now back to the bradycardia drugs
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.
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:
IV infusion for bradycardia:
- 1mg epinephrine is mixed with 500ml of NS or D5W. The infusion should run at 2-10 mcg/min and titrate to the patient’s response.
- Dopamine 400 mg is mixed with 250 ml NS. Begin the dopamine infusion at 5 to 20 mcg/kg/min and titrate to the patient’s response.
The goal of therapy is to improve the patient’s clinical status rather than target an exact heart rate.
Precautions
Prior to the use of ACLS drugs in the treatment of symptomatic bradycardia, contributing factors of the bradycardia should be explored then ruled out or corrected.
Brenna says
why give dopamine for bradycardia???????
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!
Ren says
Because dopamine has some alpha effects
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!
Jeff with admin. says
The following link is just as good an explanation as any on the web: Transcutaneous pacing. Kind regards, Jeff
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
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.
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
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.
Jeff with admin. says
Yes vagus nerve. Thanks for sharing your comments. Kind regards, Jeff
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
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
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
Jon heacock says
Got it. Thanks for the clarification.
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
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.
arkawal4 says
Why is the initial dose of Atropine 0.5 and no longer 1.0?
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
KM says
Hi,
can I know what’s the reason for the relatively recent exclusion of atropine in patients with asystole ?
Thanks !
Jeff with admin. says
Atropine has been shown through clinical use to have no effect on improving outcomes for the patient with asystole.
Kind regards,
Jeff
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
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
lara says
when the patients take the atropin alone why the response will be bradycardia then tachycardia??
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