Knowing your acls drugs cold is the difference between running a code smoothly and watching a megacode fall apart in front of the instructor. The 2020 American Heart Association guidelines tightened the medication list, removed some old standbys, and put a hard focus on three things: right drug, right dose, right time. There are no open books at the testing station. You either know that epinephrine is 1 mg IV every 3 to 5 minutes during cardiac arrest, or you don't pass.

This reference covers every acls algorithm medication you need for certification and real-world resuscitation: cardiac arrest (VF, pulseless VT, asystole, PEA), bradycardia, tachycardia (stable and unstable), acute coronary syndromes, post-arrest stabilization, and acute stroke. Every dose comes from current AHA guidance. We also flag the medication errors that get providers in trouble — wrong concentrations of epinephrine, mis-mixed amiodarone, adenosine pushed through a distal IV — so you don't repeat them.

Think of the ACLS drug list as a small toolkit, not a pharmacopeia. You need maybe twelve drugs total to run any algorithm. That's manageable. What separates a smooth code from a chaotic one is the ability to call out the right drug, dose, and route within five seconds of recognizing the rhythm — and to know which drugs are wrong for which patient. A 65-year-old in inferior STEMI with right ventricular involvement does not get nitroglycerin. A patient in third-degree AV block does not get atropine. These pairings are tested every megacode and matter every shift.

The way most providers learn ACLS pharmacology is by repetition under simulated pressure, not by reading. Read the doses once. Then drill them — with a partner, with flashcards, with a acls practice test pdf printed out for the bus ride to work. Spaced retrieval beats highlighter every time. By the time you sit for your provider exam, the dose for any drug-rhythm pair should come without thinking. That's the test of mastery, and it's also the test of safe practice.

When the rhythm is shockable (ventricular fibrillation or pulseless ventricular tachycardia) or non-shockable (asystole or PEA), the drug priorities shift but the headline stays the same: epinephrine first, antiarrhythmic second. The acls vf vt algorithm calls for epinephrine after the second shock in shockable rhythms, and immediately after IV/IO access in non-shockable rhythms. Amiodarone or lidocaine are added only after defibrillation has failed to convert the rhythm.

Concentration is where new providers slip. Cardiac-arrest epinephrine comes pre-mixed as 1:10,000 (0.1 mg/mL) in a 10 mL prefilled syringe — 1 mg per syringe. The 1:1,000 vial (1 mg/mL) is for IM anaphylaxis at 0.3 to 0.5 mg, not for IV cardiac arrest. Grabbing the wrong concentration is one of the most common preventable errors during a code.

The pharmacology behind epinephrine in arrest is alpha-adrenergic vasoconstriction. Chest compressions generate the pressure gradient that drives blood through the coronaries and into the cerebral circulation, but compressions alone produce only a fraction of normal cardiac output. Alpha-1 vasoconstriction in the peripheral vascular bed shunts blood centrally and pushes coronary perfusion pressure up — typically from the low 20s into the 30s mm Hg, which is the threshold above which ROSC becomes likely. Beta effects exist but are not the point during arrest.

Amiodarone, by contrast, is a multi-channel antiarrhythmic. It blocks potassium channels (the Class III effect that prolongs repolarization), sodium channels (Class I), and has weak beta-blocking and calcium-channel-blocking effects. In refractory VF/pVT it stabilizes the membrane long enough for defibrillation to capture and convert the rhythm. Push the 300 mg bolus undiluted during arrest; mix only when starting the maintenance infusion. Lidocaine works through pure sodium-channel blockade — narrower mechanism, comparable outcome data, simpler dose calculation by weight.

The bradycardia algorithm pivots on one question: does the slow rhythm produce symptoms? Hypotension, altered mental status, chest pain, acute heart failure, or signs of shock turn an asymptomatic 45 bpm sinus brady into a drug-and-pacing situation. The acls bradycardia and tachycardia algorithms sequence is: atropine first, then transcutaneous pacing, then dopamine or epinephrine infusion. Run them in that order unless the block is high-grade — Mobitz II or third-degree — in which case skip atropine and pace.

Watch for the failure modes. Atropine doses below 0.5 mg paradoxically slow the heart by blocking pre-synaptic muscarinic receptors. So even when the patient is small, never give less than 0.5 mg. A patient with a transplanted heart will not respond to atropine at all — the donor heart has no vagal innervation — go straight to pacing or chronotropic infusion.

Dopamine is dose-dependent in how it acts. From 5 to 10 mcg/kg/min, beta-1 stimulation drives heart rate and contractility. Above 10 mcg/kg/min, alpha-1 vasoconstriction dominates and the drug behaves more like norepinephrine. Titrate to a heart rate above 60 and a mean arterial pressure above 65. Epinephrine infusion at 2 to 10 mcg/min is an equivalent option — sometimes preferred when the patient also has hypotension that needs more aggressive support, since epinephrine has a broader receptor profile at any given infusion rate.

For Mobitz II and complete heart block, transcutaneous pacing is the bridge to a transvenous wire and ultimately a permanent pacemaker. Set the pacer to 60 to 80 bpm output and start at 20 mA, increasing until you see consistent electrical and mechanical capture. Mechanical capture means a pulse — confirm by palpating the femoral artery, not the radial, because the pacer's electrical artifact corrupts upper-extremity pulse palpation. Sedate with a low-dose benzodiazepine or short-acting opioid; pacing is painful.

Stable tachycardia gives you time for drugs. Unstable tachycardia — hypotension, altered mental status, ischemic chest pain, acute heart failure — gets synchronized cardioversion, not pharmacology. The rate cut-off most providers use is 150 bpm, but the actual trigger is hemodynamic instability, not the number on the monitor.

For stable, narrow-complex, regular tachycardia, adenosine is both diagnostic and therapeutic. If the rhythm breaks, it was AV-nodal reentry. If the rhythm slows just long enough for you to see flutter waves or atrial fibrillation, you've made a diagnosis without converting anything. Either way you learn something. The single most common adenosine failure is putting it through a hand or forearm IV — the half-life is under 10 seconds and the drug is gone before it reaches the AV node. Antecubital or central access only, with an instant 20 mL flush.

For wide-complex tachycardia with a pulse, the differential matters before the drug. Monomorphic stable VT can be treated with amiodarone 150 mg IV over 10 minutes or procainamide 20 to 50 mg/min until the arrhythmia breaks, QRS widens by 50%, or you hit 17 mg/kg. Polymorphic VT with a long QT (torsades) gets magnesium 1 to 2 g IV — never amiodarone or other QT-prolonging drugs, which make the situation worse. SVT with aberrancy can mimic VT; when in doubt, treat as VT.

Diltiazem at 0.25 mg/kg IV is the rate-control drug for atrial fibrillation with rapid ventricular response in patients without WPW. Onset within 2 to 7 minutes; repeat at 0.35 mg/kg if needed. Beta-blockers (metoprolol 5 mg IV) are an alternative. Both are contraindicated in pre-excited AFib (WPW with wide-complex AFib) — these patients need procainamide or cardioversion because AV-nodal blockers will preferentially route conduction down the accessory pathway and can trigger VF.

Acute coronary syndrome treatment in ACLS follows the legacy MONA-B framework — Morphine, Oxygen, Nitroglycerin, Aspirin, Beta-blocker — but the order and the indications have shifted. Aspirin and nitroglycerin still go up front. Oxygen is now reserved for patients with SpO2 under 90% or signs of respiratory distress; routine oxygen in normoxic ACS does not help and may harm. Morphine has dropped to last-line. aha acls guidance still tests MONA-B because it is a stable framework — just know the modern caveats.

Time-to-PCI is the metric that drives STEMI outcomes. Door-to-balloon under 90 minutes is the goal; if your facility cannot meet that, thrombolytic alteplase (tPA) is the bridge. Pre-hospital ECG transmission shaves crucial minutes — most cath labs activate while the patient is still in the ambulance.

Dual antiplatelet therapy starts in the ED. Aspirin 162 to 325 mg chewed is dose one. A P2Y12 inhibitor — clopidogrel 600 mg loading dose, ticagrelor 180 mg, or prasugrel 60 mg in select patients — follows. Anticoagulation with unfractionated heparin (60 units/kg bolus, then 12 units/kg/hr infusion targeting an aPTT of 1.5 to 2.5 times control) or a low-molecular-weight heparin like enoxaparin 1 mg/kg subcutaneous every 12 hours rounds out the pharmacy. High-intensity statin therapy (atorvastatin 80 mg or rosuvastatin 40 mg) starts before discharge regardless of baseline lipid levels.

Beta-blockers reduce myocardial oxygen demand and limit infarct size. Metoprolol 5 mg IV every 5 minutes for three doses, then transition to oral, is a common regimen. Hold for hypotension, bradycardia, signs of decompensated heart failure, or known cocaine use within the past 24 hours — in cocaine-induced ACS, beta-blockers leave alpha receptors unopposed and worsen coronary vasoconstriction. ACE inhibitors started in the first 24 hours improve long-term outcomes, particularly in patients with reduced ejection fraction or anterior MI.

Return of spontaneous circulation does not end the code. The first 60 minutes post-arrest are when patients re-arrest, when hypotension cooks the brain, and when targeted temperature management starts. Norepinephrine 0.1 to 0.5 mcg/kg/min is the first-line vasopressor for post-arrest hypotension — start it before the patient circles back down. Dobutamine 5 to 20 mcg/kg/min adds inotropy for cardiogenic shock with poor cardiac output.

Two drugs you started during the arrest continue: an amiodarone maintenance drip at 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours, and consider lidocaine maintenance if that was your bolus antiarrhythmic. Keep MAP above 65, SpO2 92–98%, glucose 144–180 mg/dL, and start targeted temperature management between 32–36°C. acls algorithm post-arrest checklists exist for a reason — running through them by memory is how cases get missed.

Avoid hyperoxia. Targeting an SpO2 of 100% with high FiO2 worsens neurologic outcomes — titrate FiO2 down to maintain SpO2 between 92 and 98%. Avoid hyperventilation. A respiratory rate of 10 breaths per minute with normal tidal volume is the post-arrest target; over-breathing the patient drops PaCO2, causes cerebral vasoconstriction, and reduces cerebral perfusion at exactly the wrong moment. Obtain a 12-lead ECG immediately and activate the cath lab if STEMI criteria are met — coronary intervention after arrest is associated with better neurologic recovery.

Acute ischemic stroke has its own pharmacology pathway running parallel to the cardiac arrest algorithms. Alteplase (tPA) is the only proven thrombolytic for stroke at a dose of 0.9 mg/kg with a maximum of 90 mg total. Give 10% of the calculated dose as a bolus over one minute, then infuse the remaining 90% over 60 minutes. The treatment window is 3 hours from last known well, extended to 4.5 hours in eligible patients without contraindications.

The contraindication list is long — recent surgery, history of intracranial hemorrhage, INR over 1.7, platelet count under 100,000, blood pressure over 185/110, and several others. Memorize the absolutes. Blood pressure must be aggressively managed below 185/110 before tPA — most centers use labetalol 10–20 mg IV. Tenecteplase (TNK) at 0.25 mg/kg is now an increasingly common alternative, given as a single bolus over 5 seconds.

Door-to-needle time under 60 minutes is the quality benchmark for stroke thrombolysis. The time chain runs door to CT in 25 minutes, CT read in 45, and needle in by 60. NIH Stroke Scale (NIHSS) is documented before and after tPA, then every 15 minutes for the first two hours. Worsening neurologic exam during infusion raises the question of intracerebral hemorrhage — stop the drug, reverse with cryoprecipitate and tranexamic acid, and image immediately. Mechanical thrombectomy is now standard for large-vessel occlusions within 24 hours of last known well, often combined with IV tPA.

Medication errors during codes cluster around a handful of patterns. Epinephrine concentration mix-ups top the list — every emergency department has stories about 1:1,000 vials pulled by mistake from the cardiac drawer. The fix is segregation: 1:1,000 lives in the anaphylaxis or IM drawer, never next to the cardiac-arrest prefilled syringes. acls medical training programs hammer this because the error is high-frequency and high-severity.

Adenosine failures usually trace back to IV location and flush technique. Anything distal to the antecubital fossa metabolizes the drug before it reaches the heart. The flush has to chase the bolus instantaneously — most providers use a three-way stopcock pre-loaded with 20 mL saline so a second nurse can push immediately after the adenosine. The third common error is amiodarone reconstitution: the manufacturer-approved diluent is D5W, not normal saline or sterile water, and substituting either causes the drug to precipitate. Refractory VF/pVT with an amiodarone bolus pushed in saline can mean you gave a half-dose of crystallized drug.

Closed-loop communication is the human-factors fix for most dosing errors. The leader says "epinephrine 1 mg IV." The nurse repeats "epinephrine 1 mg IV" while drawing it. The leader confirms "correct, push it." The nurse says "epinephrine 1 mg IV pushed." Four short statements, but they catch 60% of the dosing errors that simulation studies measure when the loop is open. Add the time stamp on the recorder's sheet and you have a defensible record of administration.

The other underappreciated error is route. IO access is equivalent to IV for every ACLS drug — same dose, same flush, same outcome. Endotracheal administration is the historical fallback for some drugs (NAVEL: Naloxone, Atropine, Vasopressin, Epinephrine, Lidocaine), but doses must be 2 to 2.5 times the IV dose and diluted in 5 to 10 mL of sterile water or saline. ET is a last resort — get IO if IV access fails, and reserve ET routes for the rare case when neither IV nor IO is possible.

Memory aids fail under stress, but the well-known ones still earn their place because they survive cognitive overload. EAL — Epinephrine, Amiodarone, Lidocaine — is the VF/pVT drug sequence. MONA-B — Morphine, Oxygen, Nitroglycerin, Aspirin, Beta-blocker — frames ACS drug therapy with the modern caveats already noted. ABCD-A — Aspirin, Beta-blocker, Clopidogrel, Diuretic/Digoxin, ACE inhibitor — covers the post-discharge ACS pharmacy.

For pharmacology basics, remember the receptor map: alpha-1 (vasoconstriction — epinephrine, norepinephrine, phenylephrine), beta-1 (chronotropy, inotropy — dopamine, dobutamine, epinephrine), beta-2 (bronchodilation — albuterol, also epinephrine), and muscarinic (parasympathetic — atropine blocks it). The acls precourse self-assessment answers resource is built around these same patterns — once you know which receptor each drug hits, you can predict the side effect profile without memorizing it separately.

For doses, anchoring numbers help. Epinephrine cardiac arrest = 1 mg. Atropine bradycardia = 1 mg. Adenosine first push = 6 mg, second = 12 mg. Amiodarone first = 300 mg, second = 150 mg. Magnesium torsades = 2 g. Notice the pattern: most ACLS doses are round numbers (1, 6, 12, 150, 300, 2 g) — not 7.5 mg or 235 mg.

That is intentional. The AHA picks doses that are easy to remember and easy to draw up under stress. When you see a non-round dose (lidocaine 1–1.5 mg/kg), it is weight-based for a pharmacologic reason — the therapeutic window is narrower and a flat dose would over-treat small patients or under-treat large ones.

The other practical mnemonic for codes is the H's and T's for reversible causes during ongoing arrest: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo/Hyperkalemia, Hypothermia; Toxins, Tamponade (cardiac), Tension pneumothorax, Thrombosis (pulmonary or coronary). Each has a specific drug or intervention — calcium and bicarbonate for hyperkalemia, dextrose for hypoglycemia, naloxone for opioid toxin, needle decompression for tension pneumo, thrombolytics for massive PE. Knowing the H's and T's by reflex is what separates good code leaders from people who keep pushing epi and amiodarone while the patient stays in PEA.

Pharmacology accounts for roughly a quarter of the ACLS provider exam and a much larger share of practical megacode failures. The dose-and-indication pairs in this reference are the same ones the AHA tests, the same ones a code-blue team uses at 03:00, and the same ones a megacode instructor expects you to call out without prompting. There is no partial credit for almost-right. Six milligrams of adenosine is not seven, and 300 mg of amiodarone is not 200.

The most efficient way to lock these in is repetition under time pressure. Run mock megacodes with a teammate calling the rhythm and you calling the drug, dose, and route in under five seconds. Then switch. Pair that with a paper-based acls practice test pdf for spaced retrieval and a structured acls certification course for the rest of the curriculum. By exam day, naming the dose for any given rhythm should feel automatic — that's the bar for safe ACLS practice.

If you're due for renewal, the medication list barely changes between provider cycles, but the receptor pharmacology and the situational drugs (calcium, bicarb, naloxone) shift with new evidence. Review the current AHA focused updates each renewal cycle so you don't drift on doses. The acls renewal process is the right time to refresh, not the week before your card expires.