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.
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 0.5 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 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 2 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 use of ACLS drugs in the treatment of symptomatic bradycardia, contributing factors of the bradycardia should be explored then ruled out or corrected.
James Matthew says
Hi. Please, what is broad complex bradycardia? In the treatment of this- is atropine effective and why?
ACLS says
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.
Kind regards,
Jeff
Anna says
Why does atropine need to be administered every 3-5 minutes?
ACLS says
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.
Kind regards,
Jeff
Luke says
I’d like to know if it’s been known to have any effect on a junctional escape rhythm at 38bpm?
Luke says
Atropine*
ACLS says
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?
ACLS says
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.
Kind regards,
Jeff
Kathryn says
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.
Kind regards,
Jeff
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.