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ACLS 9 min read

ACLS Medications Explained: Every Drug in the Algorithms

By the CardioLens Team

In a code, the algorithm gives you the sequence — but the drugs are where hesitation shows. Knowing what each ACLS medication does, why it's there, and the exact dose lets you speak up with confidence when the team is looking for the next step.

This is a working guide to every medication in the core ACLS algorithms, organised by where it appears.

Educational reference only. Doses reflect widely taught AHA ACLS recommendations, but guidelines are revised and institutions vary. Always follow current AHA guidance and your local protocols.

Cardiac Arrest: Shockable and Non-Shockable

Epinephrine — the one constant

Epinephrine is given in every cardiac arrest, shockable or not. As a potent alpha-agonist it raises systemic vascular resistance, which increases coronary and cerebral perfusion pressure during compressions.

  • Dose: 1 mg IV/IO every 3–5 minutes.
  • Timing: In non-shockable rhythms (asystole/PEA), give it as soon as possible. In shockable rhythms (VF/pVT), give it after the second shock, once defibrillation has had its chance.

Amiodarone — the first-line antiarrhythmic

For VF or pulseless VT that persists after defibrillation and epinephrine, amiodarone is the preferred antiarrhythmic. It prolongs the action potential and refractory period across multiple ion channels.

  • Dose: 300 mg IV/IO first dose, then 150 mg for a second dose if needed.

Lidocaine — the alternative

Lidocaine is an acceptable alternative to amiodarone for refractory VF/pVT, particularly where amiodarone is unavailable.

  • Dose: 1–1.5 mg/kg IV/IO first dose, then 0.5–0.75 mg/kg every 5–10 minutes (maximum 3 mg/kg).

Special Reversible Causes

These drugs aren't part of the routine arrest sequence — they target specific reversible causes (the H's and T's). Giving them requires that you've identified the underlying problem.

Magnesium sulfate

Reserved for torsades de pointes (polymorphic VT with a long QT). It is not recommended for routine use in cardiac arrest.

  • Dose: 1–2 g IV/IO, diluted, for torsades.

Calcium chloride and sodium bicarbonate

Not routine. Consider for specific situations — for example, calcium for known or suspected hyperkalaemia or calcium-channel-blocker toxicity, and sodium bicarbonate for hyperkalaemia or tricyclic antidepressant overdose. Both are guided by the clinical scenario, not the arrest itself.

Symptomatic Bradycardia

Atropine — first line

Atropine blocks vagal (parasympathetic) tone at the SA and AV nodes, increasing the heart rate. It's the first drug for symptomatic bradycardia.

  • Dose: 1 mg IV every 3–5 minutes, to a maximum total of 3 mg.
  • Caveat: It is often ineffective in high-grade (Mobitz II or third-degree) block, where the problem is below the AV node — don't let it delay pacing.

When atropine fails: pacing and infusions

If atropine doesn't work, move to transcutaneous pacing and/or a chronotropic infusion:

  • Epinephrine infusion: 2–10 mcg/min, titrated to response.
  • Dopamine infusion: 5–20 mcg/kg/min, titrated to response.

Tachycardia With a Pulse

Adenosine — for regular narrow-complex SVT

Adenosine briefly blocks conduction through the AV node, which can terminate re-entrant SVT and, when it doesn't, unmask the underlying atrial rhythm. It has a half-life of only a few seconds, so it must be pushed fast and flushed immediately.

  • Dose: 6 mg rapid IV push, followed by a 12 mg dose if needed.
  • Use: Stable, regular, narrow-complex SVT. It can also be considered for stable, regular, monomorphic wide-complex tachycardia (both diagnostic and therapeutic) — but not for irregular or polymorphic rhythms.

Do not give AV-nodal blockers (adenosine, calcium-channel blockers, beta blockers) in pre-excited atrial fibrillation (WPW). Blocking the AV node can accelerate conduction down the accessory pathway and precipitate VF.

Antiarrhythmics for stable wide-complex tachycardia

For stable wide-complex tachycardia where you elect medical management, options include procainamide, amiodarone, or sotalol. If the patient is unstable at any point, the answer is synchronised cardioversion — not another drug.

Quick-Reference Doses

DrugSettingDose
EpinephrineCardiac arrest1 mg IV/IO q3–5 min
AmiodaroneRefractory VF/pVT300 mg, then 150 mg IV/IO
LidocaineRefractory VF/pVT (alt.)1–1.5 mg/kg, then 0.5–0.75 mg/kg
MagnesiumTorsades de pointes1–2 g IV/IO
AtropineSymptomatic bradycardia1 mg IV q3–5 min (max 3 mg)
Epinephrine infusionBradycardia2–10 mcg/min
Dopamine infusionBradycardia5–20 mcg/kg/min
AdenosineRegular SVT6 mg, then 12 mg rapid push

Key takeaway: ACLS pharmacology comes down to a few patterns — epinephrine in every arrest, amiodarone (or lidocaine) for shock-refractory VF/pVT, atropine then pacing for bradycardia, and adenosine for regular SVT. Reserve magnesium, calcium, and bicarbonate for the reversible causes they actually treat. Memorise the doses so the drug is never the thing you hesitate on.

Practicing in CardioLens

The ACLS Algorithms in CardioLens map every one of these medications to the rhythm and decision point where it belongs, with shockable versus non-shockable pathways laid out side by side. The MEGA CODE simulations then put the drugs in context — you'll choose epinephrine vs. amiodarone, recognise when atropine won't work, and avoid nodal blockers in pre-excited AF, all with realistic consequences for each choice.

Sources

  • American Heart Association Guidelines for CPR and Emergency Cardiovascular Care
  • AHA Advanced Cardiovascular Life Support (ACLS) Provider Manual
  • Braunwald's Heart Disease, 12th Edition

For educational purposes only — not a diagnostic tool.

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