Mastering acls drug doses is the single most important pharmacology task standing between you and a passing score on your Advanced Cardiovascular Life Support exam. Every algorithm — cardiac arrest, bradycardia, tachycardia, and post-cardiac arrest — pivots on the right medication, the right dose, the right route, and the right timing. The American Heart Association expects providers to recall these numbers under pressure without hesitation, because in a real code, fumbling for a reference card costs perfusion seconds the brain cannot afford.
This study guide consolidates the entire 2026 ACLS pharmacology curriculum into one resource. You will learn the core arrest medications (epinephrine, amiodarone, lidocaine), bradycardia medications (atropine, dopamine, epinephrine infusion), tachycardia medications (adenosine, diltiazem, beta-blockers, procainamide, sotalol), and post-arrest infusions. We cover indications, contraindications, mechanisms of action, common errors, and the exact moments in each algorithm when the drug must be pushed.
The AHA 2020 Guidelines, reaffirmed by the 2025 Focused Update, emphasize high-quality CPR first and pharmacology second — but pharmacology still determines return of spontaneous circulation (ROSC) in many shockable and non-shockable rhythms. Epinephrine 1 mg IV/IO every three to five minutes remains the workhorse vasopressor. Amiodarone 300 mg first dose, then 150 mg, remains the antiarrhythmic of choice for refractory ventricular fibrillation and pulseless ventricular tachycardia.
Beyond the arrest cart, the modern ACLS provider must also know reversal agents (naloxone, flumazenil cautions, calcium for hyperkalemia, sodium bicarbonate for tricyclic overdose), thrombolytics for acute coronary syndromes and stroke, and the increasingly tested role of magnesium sulfate in torsades de pointes. The exam routinely mixes algorithm questions with pharmacology stems, so isolated drug memorization is not enough — you need integrated recall.
Throughout this guide we use mnemonics, dosing tables, and clinical pearls that align with the official AHA Provider Manual. We also flag the five or six numbers students miss most often: the second dose of adenosine (12 mg, not 6 mg), the loading infusion of amiodarone after ROSC (1 mg/min for six hours), and the maximum atropine dose for symptomatic bradycardia (3 mg total). These small details account for a disproportionate share of failed exam attempts.
Whether you are recertifying or sitting for ACLS for the first time, plan to spend roughly eight to twelve hours specifically on pharmacology. Pair this guide with the official Provider Manual, the precourse self-assessment, and at least three full-length practice exams. Use spaced repetition for dose numbers and active recall for indications. By the end of this article, you will recognize every drug the megacode instructor can throw at you, know exactly when to call for it, and understand why it works at the cellular level.
Use the table of contents to jump to specific algorithms, and revisit the FAQ at the bottom for the questions students email us most often before exam day. ACLS pharmacology is finite, learnable, and ultimately one of the most rewarding clinical knowledge bases you will ever build.
Epinephrine remains the cornerstone vasopressor at 1 mg IV/IO every 3-5 minutes during cardiac arrest. Vasopressin was removed from the AHA algorithm in 2015 but may still appear on older exam banks.
Amiodarone 300 mg first dose then 150 mg, or lidocaine 1-1.5 mg/kg then 0.5-0.75 mg/kg, are used for shock-refractory VF/pVT. Magnesium sulfate 1-2 g is reserved for torsades de pointes.
Atropine 1 mg every 3-5 minutes (max 3 mg) treats symptomatic bradycardia. Dopamine 5-20 mcg/kg/min and epinephrine 2-10 mcg/min infusions serve as second-line agents when atropine fails.
Adenosine 6 mg then 12 mg rapid IV push terminates stable SVT. Diltiazem and beta-blockers control atrial fibrillation rate when the patient is hemodynamically stable.
Magnesium for torsades, calcium for hyperkalemia, sodium bicarbonate for TCA overdose, and naloxone 0.4-2 mg for opioid-induced respiratory arrest round out the cart.
Cardiac arrest pharmacology centers on two drugs that every ACLS provider must recite in their sleep: epinephrine and amiodarone. Epinephrine 1 mg (10 mL of 1:10,000 concentration) is given intravenously or intraosseously every three to five minutes during both shockable and non-shockable arrests. For shockable rhythms (VF/pVT), the first dose follows the second defibrillation; for non-shockable rhythms (asystole/PEA), it is given as soon as IV/IO access is established. The mechanism is alpha-1 mediated peripheral vasoconstriction, which raises coronary and cerebral perfusion pressure during chest compressions.
Amiodarone is the antiarrhythmic of choice for shock-refractory VF or pulseless VT. The first dose is 300 mg IV/IO push, followed by a second dose of 150 mg if the rhythm persists after additional shocks. Amiodarone works through multi-channel blockade — primarily potassium, but also sodium, calcium, and beta-adrenergic receptors — which makes it broadly effective but also raises the risk of hypotension and bradycardia after ROSC. After return of spontaneous circulation, a maintenance infusion of 1 mg/min for six hours, then 0.5 mg/min for eighteen hours, prevents recurrent arrhythmia.
Lidocaine is an acceptable alternative when amiodarone is unavailable. The initial dose is 1 to 1.5 mg/kg IV/IO push, followed by 0.5 to 0.75 mg/kg every five to ten minutes up to a maximum cumulative dose of 3 mg/kg. Lidocaine blocks sodium channels preferentially in ischemic tissue, making it particularly useful when the arrest is presumed to be ischemic in origin. The maintenance infusion runs at 1 to 4 mg/min after ROSC.
Magnesium sulfate 1 to 2 g diluted in 10 mL of D5W is reserved for torsades de pointes, a polymorphic ventricular tachycardia associated with prolonged QT interval. It is not recommended for routine VF or monomorphic VT. Hypomagnesemia is a known trigger for torsades, so magnesium replenishment serves both therapeutic and prophylactic roles. Push it slowly over five to twenty minutes in stable patients, or as a rapid IV push during arrest.
The 2020 AHA guidelines downgraded vasopressin and methylprednisolone from the standard arrest algorithm, though a recent VAM-IHCA trial has reopened interest in vasopressin plus steroids for in-hospital arrest. For the exam, do not give vasopressin unless a question stem explicitly references the combined protocol. Stick with epinephrine as your sole vasopressor and amiodarone or lidocaine as your sole antiarrhythmic during arrest.
Calcium chloride 1 g or calcium gluconate 3 g is indicated for known hyperkalemia, calcium channel blocker overdose, or magnesium toxicity. Sodium bicarbonate 1 mEq/kg is reserved for tricyclic antidepressant overdose, severe metabolic acidosis with prolonged arrest, or hyperkalemia. Routine bicarbonate during arrest is not recommended because it can worsen intracellular acidosis and shift the oxyhemoglobin dissociation curve unfavorably.
Always remember the five Hs and five Ts when no drug seems to work. Treating the underlying cause — hypoxia, hypovolemia, hydrogen ion (acidosis), hypo/hyperkalemia, hypothermia, tension pneumothorax, tamponade, toxins, thrombosis (pulmonary), and thrombosis (coronary) — is often more impactful than another round of epinephrine.
For symptomatic bradycardia with poor perfusion, atropine 1 mg IV every three to five minutes is the first-line intervention, up to a maximum cumulative dose of 3 mg. Atropine works by competitively blocking acetylcholine at muscarinic receptors, reducing vagal tone and increasing heart rate. It is unlikely to work in second-degree type II or third-degree AV block, and in those cases transcutaneous pacing should be initiated immediately while preparing for transvenous pacing.
If atropine fails or pacing is unavailable, start a dopamine infusion at 5 to 20 mcg/kg/min titrated to effect, or epinephrine infusion at 2 to 10 mcg/min. Both are beta-1 agonists that increase heart rate and contractility. Avoid these agents in patients with severe coronary disease where increased myocardial oxygen demand may precipitate ischemia. Always identify and treat reversible causes such as hyperkalemia, hypoxia, or beta-blocker overdose.
For stable narrow-complex tachycardia (likely SVT), attempt vagal maneuvers first, then give adenosine 6 mg rapid IV push followed by a 20 mL saline flush. If unsuccessful after one to two minutes, administer adenosine 12 mg rapid IV push, which may be repeated once. Adenosine works by transiently blocking AV nodal conduction, breaking the reentrant circuit. Warn the patient about brief chest discomfort and a feeling of impending doom — these sensations resolve within seconds.
For stable atrial fibrillation or flutter with rapid ventricular response, diltiazem 15 to 20 mg (0.25 mg/kg) IV over two minutes, followed by 20 to 25 mg if needed, controls rate effectively. Beta-blockers like metoprolol 5 mg IV every five minutes up to 15 mg are alternatives. For stable wide-complex tachycardia, procainamide 20-50 mg/min or amiodarone 150 mg over ten minutes are preferred over lidocaine.
Any tachycardia with serious signs and symptoms — hypotension, altered mental status, shock, chest pain, or acute heart failure — warrants immediate synchronized cardioversion rather than drugs. Sedate the conscious patient with midazolam 1-2 mg or etomidate 0.1-0.3 mg/kg before cardioversion when time permits. Energy doses are 50-100 J for narrow regular, 120-200 J biphasic for atrial fibrillation, and 100 J for stable monomorphic VT with pulse.
If polymorphic VT is suspected and not torsades, treat as VF with defibrillation at full energy. For torsades de pointes with a pulse, give magnesium sulfate 1-2 g IV over 15 minutes and correct underlying QT-prolonging factors. Overdrive pacing or isoproterenol may be required for recurrent torsades despite magnesium. Always check for QT-prolonging drugs, hypokalemia, and hypomagnesemia in these patients.
Over 40% of pharmacology questions on the ACLS exam involve sequencing — "what is the next intervention" or "the next dose." If you can recite the algorithm out loud while naming each drug, dose, and interval, you will outperform candidates who only memorize isolated drug facts. Pair every dose number with its algorithm position.
Post-ROSC care relies heavily on pharmacology to stabilize the patient and prevent re-arrest. The first priority is blood pressure: target a mean arterial pressure (MAP) above 65 mmHg, ideally 80-100 mmHg. If the patient is hypotensive after fluids, start norepinephrine 0.1-0.5 mcg/kg/min as the first-line vasopressor, or epinephrine infusion 2-10 mcg/min for combined inotropy and vasopressor support. Dopamine 5-20 mcg/kg/min is an alternative but is now considered second-line due to higher arrhythmia rates.
If the patient was successfully resuscitated from VF/pVT with amiodarone, continue the amiodarone maintenance infusion at 1 mg/min for the first six hours, then drop to 0.5 mg/min for the next eighteen hours, for a 24-hour cumulative dose around 1 g. This prevents recurrent ventricular arrhythmia during the vulnerable post-arrest window. Monitor for hypotension, bradycardia, and infusion-site phlebitis — central access is preferred for prolonged amiodarone.
Targeted temperature management (TTM) at 32-36°C for 24 hours is standard for comatose post-arrest patients. Shivering must be controlled with adequate sedation (propofol 5-50 mcg/kg/min or midazolam 0.02-0.1 mg/kg/hr) and analgesia (fentanyl 25-100 mcg/hr). Neuromuscular blockade with cisatracurium may be needed for refractory shivering. Avoid hyperthermia at all costs in the first 72 hours, as it worsens neurologic outcomes.
For acute coronary syndrome identified on post-arrest ECG, the standard combination is aspirin 162-325 mg chewed, a P2Y12 inhibitor (ticagrelor 180 mg, clopidogrel 300-600 mg, or prasugrel 60 mg), and anticoagulation with heparin or enoxaparin. Time to PCI matters more than any specific drug — door-to-balloon should be under 90 minutes. Nitrates and morphine provide symptom relief but have not been shown to reduce mortality.
Acute ischemic stroke pharmacology centers on thrombolytics. Alteplase 0.9 mg/kg (max 90 mg) is given as 10% bolus over one minute and the remaining 90% over 60 minutes, within 4.5 hours of symptom onset. Tenecteplase 0.25 mg/kg single bolus is an emerging alternative. Strict blood pressure control below 185/110 mmHg before thrombolytics and below 180/105 mmHg for 24 hours afterward is required to prevent hemorrhagic conversion.
Opioid-induced respiratory arrest is increasingly common given the ongoing fentanyl crisis. Naloxone 0.4-2 mg IV/IM/IN is repeated every 2-3 minutes until adequate respirations return. For chronic opioid users, start with lower doses (0.04-0.1 mg) to avoid precipitous withdrawal. Long-acting opioids like methadone or fentanyl patches may require continuous naloxone infusion at two-thirds of the effective wake-up dose per hour.
Anaphylaxis with cardiovascular collapse is treated with epinephrine 0.3-0.5 mg IM (1:1,000) into the lateral thigh, repeated every 5-15 minutes. If shock persists, transition to an epinephrine infusion 1-10 mcg/min. Adjuncts include diphenhydramine 25-50 mg IV, methylprednisolone 125 mg IV, and aggressive fluid resuscitation. Glucagon 1-5 mg IV is reserved for beta-blocked patients who do not respond to epinephrine.
Effective exam preparation for ACLS pharmacology requires structured study rather than passive reading. Begin by downloading the official AHA Provider Manual and the 2025 Focused Update on Adult Advanced Cardiovascular Life Support. Read the pharmacology sections twice — once for orientation and once for active note-taking. Create flashcards for every drug with dose, indication, contraindication, and mechanism on separate sides. Spaced repetition apps like Anki are particularly effective because pharmacology recall is the highest-yield testable knowledge on the exam.
Next, integrate pharmacology with each algorithm. Print the AHA algorithm cards and rewrite them from memory, inserting the exact drug and dose at each branch point. Practice this on a whiteboard until you can reconstruct any algorithm — arrest, bradycardia, tachycardia, ACS, stroke, post-arrest — without prompts. The exam frequently presents a rhythm strip and asks for the next intervention, so muscle memory between rhythm recognition and drug selection is essential.
Take at least three full-length practice exams under timed conditions. Many candidates score 90% on individual chapter quizzes but drop to 75% on integrated exams because they cannot context-switch between algorithms. After each practice test, review every missed question — not just the correct answer, but why the other options were wrong. This metacognitive review builds the discrimination skills the AHA examiners test.
Pay special attention to dose ranges versus single numbers. Atropine is 1 mg per dose with a maximum of 3 mg total. Amiodarone is 300 mg first, then 150 mg, then 1 mg/min for six hours. Dopamine is a range (5-20 mcg/kg/min). Confusing a range for a fixed dose is a classic exam trap. Make a one-page dosing cheat sheet that distinguishes single doses, maximums, and infusion ranges, and review it daily for two weeks before the exam.
Megacode preparation requires verbal practice, not just silent reading. Recruit a study partner or use video simulations to call out drugs and doses in real time. Say "epinephrine 1 milligram IV push, repeat every three to five minutes" out loud. The pressure of verbal recall reveals weaknesses that silent study hides. Many testing centers now include observed megacode stations, where the examiner expects rapid, confident verbal orders.
Do not neglect the precourse self-assessment — it accurately predicts your actual exam performance. A score below 84% on the precourse test suggests you need additional pharmacology review before sitting for the official exam. Use that self-assessment as a diagnostic tool to identify weak chapters, then circle back to focused study before retesting. The AHA requires at least 70% on the precourse self-assessment for course entry at many sites.
Finally, the night before the exam, get adequate sleep rather than cramming. Pharmacology recall depends on consolidated memory, which is impaired by sleep deprivation. Review your one-page dose cheat sheet briefly that evening, then close the books. On exam day, eat a moderate breakfast, arrive early, and approach each question methodically — read the stem twice, eliminate clearly wrong answers, and trust the dosing knowledge you have built.
The final week before your ACLS exam is best spent in deliberate practice rather than new learning. By this point you should be comfortable with the core drugs; what remains is converting recognition into rapid recall. Set aside two 30-minute sessions per day for active dose recitation — once in the morning and once before bed. The morning session reinforces working memory; the evening session leverages sleep consolidation. Speak the doses aloud, including units and routes, to engage auditory and motor memory pathways.
Build a personal megacode script. Imagine yourself as the team leader during a witnessed VF arrest: "Begin high-quality CPR, attach defibrillator, shock at 200 joules biphasic, resume CPR for two minutes, establish IV/IO access, epinephrine 1 milligram IV push and repeat every three to five minutes, after second shock consider amiodarone 300 milligrams IV push." Rehearsing this script ten times builds the verbal fluency examiners look for during practical stations.
Address common knowledge gaps that trip up candidates. Many students forget that epinephrine concentration differs by indication: 1:10,000 (0.1 mg/mL) for IV arrest dosing, but 1:1,000 (1 mg/mL) for IM anaphylaxis. Push-dose epinephrine for post-intubation hypotension is 10-20 mcg every 2-5 minutes, made by mixing 1 mL of 1:10,000 into 9 mL of saline. These nuances appear in scenario-based questions and reflect real ICU practice.
Review reversible causes with their specific antidotes. Opioid overdose responds to naloxone, benzodiazepine overdose to flumazenil (rarely used in ACLS), beta-blocker overdose to glucagon and high-dose insulin/dextrose, calcium channel blocker overdose to calcium and high-dose insulin, and tricyclic antidepressant overdose to sodium bicarbonate. Knowing antidotes signals advanced clinical reasoning, which examiners reward in scenario questions.
Refresh your understanding of pediatric considerations if your course covers PALS overlap. ACLS is adult-focused, but some questions reference dose-by-weight calculations. Epinephrine pediatric arrest dose is 0.01 mg/kg of the 1:10,000 concentration, atropine pediatric dose is 0.02 mg/kg (minimum 0.1 mg), and amiodarone is 5 mg/kg. While not the focus of ACLS, occasional crossover questions appear, especially on combined ACLS/PALS programs.
Master the timing rules. Epinephrine is given every three to five minutes during arrest — not after every shock, not every cycle, but on the time clock. Adenosine is pushed rapidly and flushed immediately because its half-life is under ten seconds. Amiodarone is pushed during arrest but infused slowly over ten minutes for stable wide-complex tachycardia. Timing errors are a frequent reason candidates miss otherwise straightforward questions.
On exam day morning, eat a protein-rich breakfast, hydrate appropriately, and arrive at the testing center fifteen minutes early. Bring your AHA student ID, a watch (most centers prohibit phones), and a calm mindset. Read each question stem twice, identify the key clinical clue, eliminate distractors, and commit to your answer. If you have prepared with this guide and the recommended practice tests, you will pass with confidence and walk away with knowledge that will serve real patients for years to come.