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 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 vagus 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 given 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
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 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 affect is primarily on the SA node in the atria, a 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 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 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
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).
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 20 mcg/kg/min and titrate to the patient’s response.
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.