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 and Complete Heart 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.
First, it is important to note that Mobitz II and Complete Heart Block are commonly associated with acute myocardial ischemia.
It is not so much that the Atropine won’t increase the heart rate when given for Mobitz II and Complete Heart Block. In fact it will probably increase the HR, but this has a high potential of inducing more myocardial ischemia as the HR will double or triple. This will also reduce diastolic filling time which will worsen coronary perfusion.
Since Mobitz II and Complete Heart Block are almost always 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. Mobitz I is not usually associated with MI.
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
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.
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
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