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 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).
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.
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.
When can say that patient unstable bradycardia..??!
When he has one of those sign or symptom ( Hypotension, Alterd mental status, HF, Chest pain, sign of shock)
More than one
If patient presented with hypotension 80/40 and HR 46 and no other sign and symptoms.
Shall we administer atropine 1 mg or treat first hypotension with IVfluid , if not improve then administer atropine ..!!!
Unstable in this case would best be defined as bradycardia with signs of poor perfusion. This would be up to the doctors discretion to determine what signs of poor perfusion or present. I would say that it would require more than just seeing a blood pressure of 80/40, but this definitely would be a starting point to evaluate for other signs of poor perfusion. If other signs of hypovolemia are present, then it would be wise to administer IV fluid. Bolus is prior to the administration of atropine.
The physician would need to use their assessment, skills and judgment to make the determination which intervention would be appropriate.
Marongo morish says
For this reasons,you first treat the heigh blood pressure.and you continued checking up
What are the studies backing TCP as first line action for Mobitz II? Thanks!
You would need to qualify what you are asking. You would be referring to SYMPTOMATIC Mobitz II.
The following paper provides a thorough review of the science behind The treatment for any high-degree symptomatic block with transcutaneous pacing.
Compromising bradycardia: management in the emergency department
Dr Sarat says
What about use of epinephrine infusion for bradycardia caused of acute iwmi?
Is it contraindicated in such scenarios?
Epinephrine is not contraindicated in such situations. Epinephrine infusion may be used. Epinephrine and dopamine infusions may be used in certain situations like this to maintain adequate cardiac output, but they are not routinely administered to manage complete AV block in a non-perfused acute inferior wall myocardial infarction.
Is atropine typically successful for symptomatic mobitz type 1 (wenckebach) patients?!
Symptomatic Mobitz type one is very responsive to medications which include atropine.
Mia Adi-Clare says
What about isoprenaline as 2nd line as opposed to adrenaline/ dopamine? As this is what our unit uses. We never use adrenaline or dopamine for AVB awaiting PPM.
Isoprenaline (Isuprel) is not recommended within the AHA ACLS guidelines for treatment within the bradycardia algorithm. Kind regards, Jeff
PS L says
Any rationale behind not using in the current guidelines?
Bring the bradycardia algorithm food next door there would not be any common reason to deviate from the guidelines.
Kind regards, Jeff
Please could you share the rationale for dropping isoprenaline from the algorithm if you are aware of it? I note it is still in ESC and Australian guidelines? Thanks
What reasoning/evidence was used in the recommendation for increasing the atropine dose to 1mg instead of 0.5mg?
I’m sorry I can’t be more helpful with this answer. I wish I knew the answer to it, but the American heart Association has not made any information about this change readily available in their literature.
I am continuing to work on updates on the site and as soon as I get these complete, I will be doing a deep dive into this to see if I can determine what the scientific
Kind regards, Jeff
Dr saied says
Why maximum dose of atropin is 3 mg?
The total dose should be restricted to avoid Atropine-induced tachycardia, increased myocardial oxygen demand and the potential for worsening cardiac ischemia or increasing infarction size.
Kind regards, Jeff
James Matthew says
Hi. Please, what is broad complex bradycardia? In the treatment of this- is atropine effective and why?
Atropine works by poisoning the vagus nerve, thereby removing parasympathetic inputs to the heart. This works beautifully for vagally-mediated bradycardia (e.g. vagal reflexes, cholinergic drugs). However, it fails for bradycardias caused by other mechanisms (e.g. heart block beyond the AV node). Overall, atropine is completely effective in only 28% of patients with symptomatic bradycardia.
Why does atropine need to be administered every 3-5 minutes?
It’s not that it has to be administered every 3 to 5 minutes. It should repeated every 3 to 5 minutes if there is no response to the previous doses. If an increased and adequate heart rate is achieved then it does not need to be repeated.
The half-life of atropine is 20 to 30 minutes
The reason for waiting 3 to 5 minutes before repeating is to ensure that you have adequately circulated the previous dose and are seeing a complete response to that dose.
I’d like to know if it’s been known to have any effect on a junctional escape rhythm at 38bpm?
Atropine can have a positive effect for reducing junctional escape rhythms caused by bradycardia. Atropine is used sed to increase heart rate through vagolytic effects. This increase in heart rate reduces junctional escape rhythm’s because of the improved heart rate. Kind regards, Jeff
Christopher Ingram says
Is there a role for atropine in Afib with slow ventricular response?
There is no specific role. If a patient had symptomatic bradycardia with an underlying atrial fibrillation then atropine would be used for the treatment of the bradycardia. This would be the same whether or not the patient had underlying atrial fibrillation.
I hope that answers your question. If you have any further questions, please let me know.
Had a patient recently with bradycardic a-fib with a ventricular response rate of around 32 bpm. Said she had a sync opal episode after using bathroom. Atropine works wonderfully for this as this is what it was designed for. I gave 0.5 mg instead of 1.0 mg but it still was very effective for about thirty minutes.
I teach both ACLS & PALS and the Epi vs. Atropine debate has always bothered me. We used to use Epi for adults with Symptomatic Bradycardia and Epi is still included for pediatric Symptomatic Bradycardia. Why did they remove Epi from the adult algorithm? By the way, your site is extremely helpful.
Jeff with admin. says
For bradycardia in adults, one of the primary causes is myocardial injury/ischemia. IV push epinephrine may cause too profound of an increase in heart rate and further compromise myocardial function, and the patient could have complications. I believe that’s why epinephrine was removed from the bradycardia algorithm.
Since myocardial injury/ischemia is not typically a problem which causes bradycardia in children, I believe this is why they have continue to use epinephrine in the pediatric bradycardia.
Dennis Ray Kirby, Jr says
I’m a now retired paramedic, I always had great success with low dose dopamine for SYMPTOMATIC bradycardia non-responsive to atropine. I always preferred it due to not increasing so much the heart workload. Again, with great results. Too bad I didn’t have a PhD, maybe I could have written a paper that would have changed things…..like giving atropine, not giving it, now giving it again….bicarb, etc….lol.