ACLS Drugs

Each of the ACLS Algorithms utilizes a number of drugs which we will classify as primary
drugs. The primary drugs are the medications that are used directly in an ACLS Algorithm.
Here are the Primary ACLS drugs broken down by ACLS Algorithm.
Each is a link to its respective page which covers, in detail, all aspects of the medication and it
use in each ACLS algorithm and in post resuscitation efforts.

ACLS Algorithms and Their Primary Drug

Vent. Fib./Tach.

Epinephrine
Vasopressin
Amiodarone
Lidocaine
Magnesium
Asystole/PEA

Epinephrine
Vasopressin
Atropine (removed from algorithm per 2010 ACLS Guidelines)
Bradycardia

Atropine
Epinephrine
Dopamine
Tachycardia

adenosine
Diltiazem
Beta-blockers
amiodarone
Digoxin
Verapamil
Magnesium

Acute Coronary Syndromes

Oxygen
Aspirin
Nitroglycerin
Morphine
Fibrinolytic therapy
Heparin
Beta-Blockers
Acute Stroke

tPA-tissue plasminogen activator

Glucose (D50)
Labetalol
Nitroprusside
Nicardipine
Aspirin

ACLS and Epinephrine

Epinephrine is the primary drug used in the pulseless arrest algorithm. It is
used for its potent vasoconstrictive effects and also for its ability to increase
cardiac output. Epinephrine is considered a vasopressor.
Indications for ACLS
1. 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.
2. Cardiac Output: epinephrine also binds to beta-1-adrenergic receptors of the
heart. This indirectly improves cardiac output by:
o

Increasing heart rate

Increasing heart muscle contractility

Increasing conductivity through the AV node

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

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

Intravenous Push/IO: 1mg epinephrine IV is given every 3-5 minutes.

IV infusion for bradycardia: 1mg epinephrine is mixed with 500ml of NS or

D5W. The infusion should run at 2-10 micrograms/min (titrated to effect).

Endotracheal Tube: 2-2.5mg epinephrine is diluted in 10cc NS and given

directly into the ET tube.

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.
Note: 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).

ACLS and Vasopressin

Vasopressin is a primary drug used in the pulseless arrest algorithm. In

high concentrations, it raises blood pressure by inducing moderate
vasoconstriction, and it has been shown to be more effective than
epinephrine in asystolic cardiac arrest (Wenzel V, Krismer AC, Arntz
HR, Sitter H, Stadlbauer KH, Lindner KH (January 2004). A
comparison of vasopressin and epinephrine for out-of-hospital

cardiopulmonary resuscitation. N. Engl. J. Med. 350 (2): 10513. doi:10.1056/NEJMoa025431.

PMID 14711909.)
One major indication for vasopressin over epinephrine is its lower risk for adverse side effects
when compared with epinephrine. With epinephrine, some studies have shown a risk of increased
myocardial oxygen consumption and post arrest arrhythmias because of an increase in heart rate
and contractility (beta 1 effects). Vasopressin also is thought too cause cerebral vessel dilation
and theoretically increase cerebral perfusion.
Trivia: Another name for vasopressin is antidiuretic hormone (ADH).
Routes

Vasopressin may be given IV/IO or by endotracheal tube.

Dosing

40 units of vasopressin IV/IO push may be given to replace the first or second dose of
epinephrine, and at this time, there is insufficient evidence for recommendation of a specific dose
per the endotracheal tube.
In the ACLS pulseless arrest algorithm, vasopressin may replace the first or second dose of
epinephrine

Amiodarone and ACLS

Amiodarone is considered a class III antiarrhythmic agent and is used for various types
tachyarrhythmias. Because of its associated toxicity and serious side-effects it should be used
cautiously and care should be taken to ensure that cumulative doses are not exceeded.

Indications for ACLS

Amiodarone is an antiarrhythmic that is used to treat both

supraventricular arrhythmias and ventricular arrhythmias.
The mechanism of action of amiodarone remains unknown, but
within the framework of ACLS, amiodarone is used primarily to
treat ventricular fibrillation and ventricular tachycardia that
occurs during cardiac arrest and is unresponsive to shock
delivery, CPR, and vasopressors.
Amiodarone should not be used in individuals with polymorphic
VT as it associated with a prolonged QT interval which is made worse with antiarrhythmic
drugs.
Amiodarone should only be used after defibrillation/cardioversion and first line drugs such as
epinephrine and vasopressin have failed to convert VT/VF.
Route

Amiodarone can be administered by intravenous or intraosseous route.

Dosing

The maximum cumulative dose in a 24 hour period should not exceed 2.2 grams.
Within the VT/VF pulseless arrest algorithm, the dosing is as follows:
300mg IV/IO push (if no conversion) 150 mg IV/IO push (after conversion) Infusion #1
360 mg IV over 6 hours (1mg/min) Infusion #2 540 mg IV over 18 hours (0.5mg/min)
For tachyarrhythmias other than life threatening, expert consultation should be considered before
use.
For Tachycardia other than pulseless VT/VF, Amiodarone dosing is as follows: (see above note)
150 mg over 10 minutes repeat as needed if VT recurs maintenance infusion of 1mg/min
for 6 hours

Amiodarone should only be diluted with D5W and given with an in-line filter.
Infusions exceeding 2 hours must be administered in glass or polyolefin bottles containing D5W.

ACLS and Lidocaine

Although lidocaine was removed from the 2010 Simplified

Pulseless Arrest Diagram, it is still considered a suitable alternative
if amiodarone is ineffective in cardiac arrest from VT/VF.
Lidocaine was removed in the AHA Simplified Pulseless Arrest
Diagram to help reduce emphasis on the use of medications and
place more emphasis on high quality CPR and early
defibrillation.
Indications for ACLS

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.

The overall benefits of lidocaine for the treatment arrhythmias in cardiac arrest has come under
scrutiny. It has been shown to have no short term or long term efficacy in cardiac arrest.
Routine prophylactic use is contraindicated for acute myocardial infarction.
Side Effects

Lidocaine should be used with caution due to negative cardiovascular effects which include
hypotension, bradycardia, arrhythmias, and/or cardiac arrest. Some of these side effects may be
due to hypoxemia secondary to respiratory depression.

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, and seizures, then coma, respiratory arrest, and cardiovascular
depression.
There are several conditions that increase the potential for lidocaine toxicity:
1. Liver dysfunction increases the risk of toxicity due to lidocaine being
metabolized by the liver.
2. Low protein increases the risk of toxicity because lidocaine is protein bound.
3. Acidosis can also increase the risk of toxicity since acidosis increase the
potential of lidocaine to dissociate from plasma proteins.
Dosing

Cardiac Arrest from VT/VF:

Initial dose: 1 to 1.5 mg/kg IV/IO

For refractory VF may give additional 0.5 to 0.75 mg/kg IV push, repeat in 5
to 10 minutes; maximum 3 doses or 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 maximum total dose of 3
mg/kg

Maintenance infusion:

1 to 4 mg/min (30-50 mcg/kg/min)

Discontinue a lidocaine infusion immediately if signs of toxicity develop.

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 patients response.

The goal of therapy is to improve the patients clinical status rather than target an exact heart
rate.
Begin the dopamine infusion at 2 to 10 mcg/kg/min and titrate to the patients 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.

ACLS and Adenosine:

Adenosine should be used within the tachycardia algorithm when vagal maneuvers fail to
terminate stable narrow-complex SVT.
Adenosine is the primary drug used in the treatment of stable narrow-complex SVT
(supraventricular Tachycardia). It can now also be used for regular monomorphic wide-complex
tachycardia.

When given as a rapid IV bolus, adenosine slows cardiac conduction

particularly effecting 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.
A change from the 2010 guidelines now has adenosine given up to two times rather than three.
Dosing

The first dose of adenosine should be 6 mg administered rapidly over 1-3 seconds followed by a
20 ml NS bolus. If the patients rhythm does not convert out of SVT within 1 to 2 minutes, a

second 12 mg dose may be given in similar fashion. All efforts should be made to administer
adenosine as quickly as possible.
Precautions

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