5.4 Core ACLS Drugs and Doses
Key Takeaways
- Epinephrine 1 mg IV/IO every 3-5 minutes is the universal cardiac-arrest vasopressor; its benefit is alpha-1 vasoconstriction that raises coronary perfusion pressure during CPR.
- For shock-refractory VF/pVT: amiodarone 300 mg IV/IO bolus then 150 mg, OR lidocaine 1-1.5 mg/kg then 0.5-0.75 mg/kg.
- Atropine 1 mg (max 3 mg) is for symptomatic bradycardia; adenosine 6 mg then 12 mg is for stable regular narrow-complex SVT — keep these peri-arrest drugs separate.
- Stable VT antiarrhythmics: procainamide 20-50 mg/min (max 17 mg/kg), amiodarone 150 mg over 10 min, or sotalol 100 mg over 5 min — give only one.
- Magnesium sulfate is for torsades de pointes (polymorphic VT with long QT), not for routine VF/pVT.
The Arrest Drugs: Epinephrine and Antiarrhythmics
Mastering ACLS pharmacology means connecting each drug to its rhythm, indication, dose, route, and timing — the exam buries wrong doses and wrong-pathway drugs as distractors. The 2020 ACLS algorithms anchor these numbers.
Epinephrine is the one drug given in every cardiac arrest. The dose is 1 mg IV/IO every 3-5 minutes. Its arrest benefit is alpha-1 adrenergic vasoconstriction, which raises aortic diastolic pressure and therefore coronary perfusion pressure during compressions — higher coronary perfusion pressure correlates with ROSC. For non-shockable rhythms (PEA/asystole), give epinephrine as soon as possible; for shockable rhythms (VF/pVT), give it after the second shock, so that defibrillation and CPR are not delayed.
Antiarrhythmics for refractory VF/pVT are given after shocks plus epinephrine have failed:
- Amiodarone 300 mg IV/IO bolus, then a second dose of 150 mg for recurrent/refractory VF/pVT.
- Lidocaine is the alternative: 1-1.5 mg/kg first dose, then 0.5-0.75 mg/kg for repeat doses (max ~3 mg/kg).
Cardiac-arrest drug table
| Drug | Arrest dose | Indication |
|---|---|---|
| Epinephrine | 1 mg IV/IO q3-5 min | All arrests (VF/pVT/PEA/asystole) |
| Amiodarone | 300 mg, then 150 mg | Shock-refractory VF/pVT |
| Lidocaine | 1-1.5 mg/kg, then 0.5-0.75 mg/kg | Alternative to amiodarone |
| Magnesium | 1-2 g IV/IO | Torsades de pointes only |
Shockable vs. non-shockable drug timing
The timing of epinephrine differs by rhythm, and the exam tests this. In non-shockable arrest (PEA/asystole), epinephrine is given as early as possible — earlier epinephrine is associated with better outcomes when no shock is indicated. In shockable arrest (VF/pVT), the first priorities are shock and CPR, so epinephrine is given after the second shock, and the antiarrhythmic (amiodarone or lidocaine) comes still later, typically after the third shock for persistent VF/pVT.
The mental model: in a shockable rhythm, electricity is the cure and drugs are adjuncts; in a non-shockable rhythm, there is no shock to give, so epinephrine and cause-correction move to the front.
The Peri-Arrest Drugs: Atropine, Adenosine, Dopamine
These drugs treat patients with a pulse and must never be confused with the arrest agents.
Atropine (vagolytic, acts at the AV node): 1 mg IV every 3-5 minutes, maximum 3 mg for symptomatic bradycardia. It does NOT work in PEA/asystole or in infranodal high-grade blocks.
Adenosine (transient AV-nodal block): 6 mg IV rapid push with a saline flush, then 12 mg if needed, for stable, regular, narrow-complex SVT. It can also be a diagnostic/therapeutic trial in regular monomorphic wide-complex tachycardia. It is useless and potentially harmful in irregular or polymorphic rhythms. Adenosine's half-life is under 10 seconds, so administration technique (fast push, immediate flush, proximal vein) is itself tested.
Dopamine and epinephrine infusions support refractory symptomatic bradycardia: dopamine 5-20 mcg/kg/min or epinephrine 2-10 mcg/min, co-equal to transcutaneous pacing.
Stable-VT antiarrhythmics (tachycardia algorithm)
| Drug | Stable-VT dose | Note |
|---|---|---|
| Procainamide | 20-50 mg/min until suppressed or max 17 mg/kg; maint 1-4 mg/min | Avoid long QT/CHF |
| Amiodarone | 150 mg over 10 min; maint 1 mg/min x 6 h, then 0.5 mg/min x 18 h | Most familiar |
| Sotalol | 100 mg (1.5 mg/kg) over 5 min | Avoid long QT |
Note the two different amiodarone doses: a 300 mg bolus in cardiac arrest versus 150 mg over 10 minutes for the stable, perfusing VT patient. Mixing these up is a classic exam trap.
Indication Matching and Common Drug Traps
The fastest way to lose ACLS points is to give the right drug to the wrong rhythm. Build the habit of asking: does this patient have a pulse, and what is the rhythm pathway?
Drug-to-pathway map
- Pulseless VF/pVT: shock first, then epinephrine 1 mg q3-5 min, then amiodarone 300/150 mg (or lidocaine).
- Pulseless PEA/asystole: epinephrine 1 mg ASAP, CPR, treat H's and T's; no shock, no atropine, no antiarrhythmic.
- Symptomatic bradycardia: atropine 1 mg (max 3), then pacing or dopamine/epi infusion.
- Stable narrow regular SVT: vagal, then adenosine 6 then 12 mg.
- Stable wide regular VT: procainamide, amiodarone, or sotalol — one only.
- Torsades: magnesium 1-2 g.
Routes, intervals, and ceilings to memorize
Every arrest drug goes IV or IO, never relying on the endotracheal route. Epinephrine repeats on a strict 3-5 minute clock. Atropine stops at a cumulative 3 mg. Lidocaine's total ceiling is roughly 3 mg/kg. Amiodarone carries two distinct doses depending on context — a 300 mg bolus in arrest versus 150 mg over 10 minutes in the perfusing tachycardia patient. Adenosine demands a rapid push plus immediate saline flush because of its ultra-short half-life. Locking these intervals and ceilings into memory is what separates a passing megacode from a failing one.
Common traps
- Giving atropine for PEA/asystole because the monitor looks slow — atropine has no role there.
- Using adenosine in irregular or polymorphic wide-complex tachycardia.
- Confusing amiodarone 300 mg bolus (arrest) with 150 mg over 10 min (stable VT).
- Letting drug preparation interrupt CPR or defibrillation — electricity and compressions outrank drugs in arrest.
- Stacking two antiarrhythmics without expert consultation (additive proarrhythmia and hypotension).
Scenario anchor: A stable patient with regular narrow-complex tachycardia fails vagal maneuvers, so adenosine 6 mg then 12 mg is reasonable. Contrast that with VF arrest, where shock, CPR, epinephrine 1 mg, and amiodarone 300 mg drive the loop — same chapter, completely different drugs.
What is the initial amiodarone dose for VF/pulseless VT that persists after shocks and epinephrine?
What is the primary mechanism by which epinephrine benefits a patient in cardiac arrest?
A patient in pulseless electrical activity (PEA) shows a slow, organized rhythm on the monitor. Which drug is NOT indicated?
A patient has stable monomorphic VT and you choose an antiarrhythmic. Which dosing is correct?