ACLS Medications

ACLS Medication Quick Practice Guide

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Epinephrine – ​Amiodarone – Atropine – Adenosine – Lidocaine

Each of the ACLS Medication Algorithms utilize several drugs which we will classify as the “primary ACLS drugs”.

The “primary drugs” are the medications that are used directly in an ACLS Algorithm. Here are the primary ACLS medications that are broken down and cover in detail all aspects of the medication and its use during cardiac arrest and post-resuscitation efforts.

This is not an all-inclusive ACLS medication list but covers many of the common drugs referred to in the ACLS class and algorithms. This is not to be used as medical advice and only is for understanding these medications from an educational point of view in reference to the ACLS course materials.

ACLS Medication


Epinephrine is the primary drug used in the cardiac arrest algorithm. It is used for its
potent vasoconstrictive effects and also for its ability to increase cardiac output. Epinephrine is
considered a vasopressor.

Epinephrine is used in the cardiac arrest algorithm as a direct IV push and also in the
bradycardia algorithm as an infusion. See the respective algorithm for more information about
their use in each.

Vasoconstriction effects:

Epinephrine binds directly to alpha-1 adrenergic receptors of the blood vessels (arteries and veins) causing direct vasoconstriction, thus, improving perfusion pressure to the brain and heart.

Cardiac Output:

Epinephrine also binds to beta-1-adrenergic receptors of the heart. This indirectly improves cardiac output by:
○ Increasing heart rate
○ Increasing heart muscle contractility
○ Increasing conductivity through the AV node


During ACLS, epinephrine can be given 3 ways: intravenous; intraosseous, and
endotracheal tube


Endotracheal Tube:

2-2.5mg epinephrine is diluted in 10cc NS and given directly into the ET tube.

IV infusions for bradycardia:

1mg epinephrine is mixed with 500ml of NS or D5W. The infusion should run at 2-10 micrograms/min (titrated to effect).

IV infusions for post-cardiac arrest hypotension:

The dosing is 2 to 10 micrograms/min.

Intravenous Push/IO:

1mg epinephrine IV is given every 3-5 minutes.

Epinephrine should be used with caution in patients suffering from myocardial infarction since epinephrine increases heart rate and raises blood pressure. This increase in HR and BP can increase myocardial oxygen demand and worsen ischemia.

There is no clinical evidence that the use of epinephrine, when used during cardiac arrest, increases rates of survival to discharge from the hospital. However, studies have shown that epinephrine and vasopressin improve rates of ROSC (return of spontaneous circulation).


Another ACLS Medication is Amiodarone, a class III antiarrhythmic agent and is used for the treatment of various types of tachyarrhythmias. Because of the toxicity and serious side effects of amiodarone, use it cautiously and do not exceed the cumulative total of 2.2 grams in 24 hours.

Indications for ACLS Within ACLS, amiodarone is used for its antiarrhythmic properties and is effective for the treatment of supraventricular arrhythmias and ventricular arrhythmias.

ACLS Medication

The mechanism of action for amiodarone’s antiarrhythmic properties remains unclear, but it continues to be the primary antiarrhythmic medication for the treatment of ventricular fibrillation and ventricular tachycardia within the cardiac arrest algorithm.

For cardiac arrest, amiodarone is used after the third shock for ventricular fibrillation and ventricular tachycardia which is unresponsive to shock delivery, CPR, and vasopressors. For tachycardia with a pulse, amiodarone may be considered, and expert consultation should be obtained prior to its use.


The ACLS Medication, Amiodarone can be administered by intravenous or intraosseous route. Dosing Within the VT/VF pulseless arrest algorithm, the dosing is as follows:
● 300mg IV/IO push → (if no conversion) 150 mg IV/IO push

For Tachycardia other than pulseless VT/VF, Amiodarone dosing is as follows:

● 150 mg over 10 minutes → repeat as needed if VT recurs → maintenance infusion of 1mg/min for 6 hours

*** The maximum cumulative dose in a 24-hour period should not exceed 2.2 grams. ***

*** When infusions exceed 2 hours, amiodarone can absorb into the plastic used for standard IV bags. This will change the medication concentration. Therefore, when an infusion exceeds 2 hours use a glass or polyolefin bottle for the administration container. ***


Atropine is the first-line ACLS 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 increased HR.


The dosing for Atropine is 1 mg IV every 3-5 minutes as needed, and the maximum total dosage for administration is 3 mg.

*** Use atropine cautiously in the presence of myocardial ischemia and hypoxia because it increases oxygen demand on the heart and can worsen ischemia. ***

Additional Information

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). 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 a 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 a 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 a 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 of 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.


When vagal maneuvers fail to terminate stable narrow-complex SVT, the primary ACLS medication of choice is adenosine. For an unstable patient with a regular and narrow QRS complex, adenosine may also be considered prior to synchronized cardioversion. Adenosine is the primary drug used in the treatment of stable narrow-complex SVT (Supraventricular Tachycardia). Now, adenosine can also be used for regular monomorphic wide-complex tachycardia. 

ACLS Medications

When given as a rapid IV bolus, adenosine slows cardiac conduction, particularly affecting conduction through the AV node. The rapid bolus of adenosine also interrupts reentry (SVT-causing) pathways through the AV node and restores sinus rhythm in patients with SVT. When injected into the body, adenosine is rapidly absorbed by red blood cells and blood vessel endothelial cells and metabolized for natural uses throughout the body. In light of this adenosine should be administered by RAPID intravenous bolus so that a significant bolus of adenosine reaches the heart before it is metabolized.


The first dose of adenosine should be 6 mg administered rapidly over 1-3 seconds followed by a 20 ml NS bolus. If the patient’s rhythm does not convert out of SVT within 1 to 2 minutes, a second 12 mg dose may be given in a similar fashion. All efforts should be made to administer adenosine as quickly as possible.


Some side effects of adenosine administration include flushing, chest pain/tightness, brief asystole, or bradycardia. Make sure that adenosine is not used for irregular, polymorphic wide-complex tachycardia and unstable VT. Use in these cases may cause clinical deterioration.


Lidocaine may be considered a suitable antiarrhythmic that can be used to treat cardiac arrest from VT/VF. Lidocaine is now included in the AHA Cardiac Arrest diagram along with amiodarone. Emphasis should not be on the use of ACLS medications and it is the AHA recommendation to place more emphasis on high-quality CPR and early defibrillation.

In ACLS, Lidocaine is used intravenously for the treatment of ventricular arrhythmias. (VT/VF). It is also useful for the treatment of stable monomorphic VT with preserved ventricular function and for stable polymorphic VT with preserved left ventricular function, normal QT interval, and correction of any electrolyte imbalances.


Lidocaine Toxicity

Symptoms of lidocaine toxicity progress in the following predictable pattern. It begins with numbness of the tongue, lightheadedness, and visual disturbances and progresses to muscle twitching, unconsciousness, seizures, then coma, respiratory arrest, and cardiovascular depression.

There are several conditions that increase the potential for lidocaine toxicity:

● Liver dysfunction increases the risk of toxicity due to lidocaine being metabolized by the liver.

● Low protein increases the risk of toxicity because lidocaine is protein bound.

● Acidosis can also increase the risk of toxicity since acidosis increases the potential of lidocaine to dissociate from plasma proteins.


Cardiac Arrest from VT/VF:
● Initial dose: 1 to 1.5 mg/kg IV/IO
● For refractory VF may give an additional 0.5 to 0.75 mg/kg IV push, repeat in 5 to 10 minutes; maximum 3 doses or a total of 3mg/kg

Perfusing Arrhythmia:
For stable VT, wide-complex tachycardia of uncertain type and significant ectopy:
● Doses Range from 0.5 to 0.75 mg/kg and up to 1 to 1.5mg/kg
● Repeat 0.5 to 0.75 mg/kg every 5-10 minutes with a maximum total dose of 3 mg/kg
*** Discontinue a lidocaine infusion immediately if signs of toxicity develop. ***

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