You hear the code call. The clock starts. In ninety seconds you need to know if you're treating a shockable rhythm, a pulseless rhythm with electrical activity, an unstable bradycardia, or something else entirely — and your hands need to move before your brain finishes the sentence. That's why the AHA built the ACLS algorithms the way it did. They aren't textbook pages. They're decision trees that survive panic.
This guide walks through every 2026 algorithm an ACLS provider is expected to know cold: adult cardiac arrest, the VF/pulseless VT pathway, asystole and PEA, post-cardiac-arrest care, symptomatic bradycardia, stable and unstable tachycardia, acute coronary syndromes, and the suspected stroke chain. We'll also cover the small but tested changes the AHA folded in for 2025–2026, the drug doses examiners actually quiz on, and the team-leader habits that turn a chaotic code into a clean run.
If you're studying for an AHA aha acls certification exam, prepping for renewal, or refreshing memory before a shift, treat this page as a working bench. Every section maps to the 2025 ECC Guidelines and reflects what shows up on the acls precourse self assessment answers. We mark the spots where students lose points and the rhythms that get mixed up under stress.
One more thing before we open the algorithms. The AHA describes the cardiac arrest chain of survival as five linked actions, and every algorithm assumes the earlier links are already happening: recognition, activation, high-quality CPR, defibrillation, and advanced care. If chest compressions are weak or interrupted, no algorithm in this guide will save the patient. Hands first, then drugs, then thinking.
Decades of resuscitation research kept showing the same uncomfortable pattern. Skilled providers, working alone, performed worse than less experienced providers working from a shared algorithm. The reason wasn't competence. It was cognitive load. A cardiac arrest fires a flood of decisions at the team in seconds, and the human brain isn't built to hold ten branching possibilities in working memory while also leading compressions.
So the AHA pulled the decisions out of memory and put them on paper. Each algorithm is a flowchart with one entry point and one or two branching questions per node. Is the rhythm shockable? Is the patient stable? Is the QRS narrow or wide? Each answer leads to one action, and each action loops back to the next decision. The provider's job stopped being to remember what to do next. The job became running the flowchart.
That's why ACLS exams test algorithm recognition more than rote facts. Examiners want to see if you can identify the entry point, follow the branch, and recognize when a patient has moved from one algorithm to another (bradycardia to cardiac arrest, for example, or tachycardia to ROSC).
The 2025 AHA Focused Update kept the core algorithms stable but adjusted a few specifics that show up on the exam:
The master algorithm. Branches at the first rhythm check into shockable (VF/pulseless VT) and non-shockable (asystole/PEA) pathways. Every other arrest decision flows from here.
Sequence: start CPR → attach monitor/defib → identify rhythm → shock or no shock → 2 minutes of CPR → recheck rhythm → cycle until ROSC or termination.
The shockable pathway. Defibrillate, immediately resume compressions, give epinephrine after the second shock, add amiodarone or lidocaine after the third. Search for reversible causes between rhythm checks.
The non-shockable pathway. CPR drives this entire algorithm — no shock is delivered. Epinephrine 1 mg IV as soon as access is available, then every 3–5 minutes. Aggressively pursue the Hs and Ts.
For symptomatic bradycardia with a pulse. Identify whether the patient is unstable (hypotension, altered mental status, signs of shock, ischemic chest pain, acute heart failure). Atropine first; if ineffective, move to transcutaneous pacing or a dopamine/epinephrine infusion.
Splits on stability and QRS width. Unstable + tachycardia → synchronized cardioversion. Stable narrow regular → vagal maneuvers, adenosine. Stable wide regular → adenosine or antiarrhythmic. Stable irregular → rate control or anticoagulation considerations.
After ROSC: airway and ventilation (avoid hyperventilation), maintain SBP ≥ 90 mmHg, obtain 12-lead ECG (consider PCI for STEMI), targeted temperature management, and neuroprognostication delayed at least 72 hours.
The acute coronary syndromes algorithm. Recognize symptoms, obtain 12-lead ECG within 10 minutes of arrival, classify as STEMI / NSTEMI / unstable angina, and start MONA-B selectively. STEMI patients route to PCI within 90 minutes if available, fibrinolytics within 30 minutes if not.
The suspected stroke algorithm. Recognize signs (FAST), transport to a stroke center, obtain non-contrast CT within 25 minutes of arrival, complete radiologist read within 45 minutes. Eligible patients get fibrinolytics within 60 minutes (door-to-needle).
This is the algorithm everything else hangs on. Whether the code is running in a hospital corridor or a parking lot, the structure is identical. Begin chest compressions immediately, attach the monitor/defibrillator the instant it arrives, and let the rhythm dictate the next move.
If the first analyzed rhythm is shockable, you're going down the VF/pVT branch. If not, you're treating asystole or PEA. Both branches loop back to the same two-minute cycle of compressions, rhythm check, drug, repeat.
The compressor switches every two minutes, no exceptions. Fatigue tanks compression depth faster than people admit, and depth correlates directly with survival. Use a metronome, a defib feedback pad, or a designated counter — anything that keeps the rate between 100 and 120 per minute.
The chest must fully recoil between compressions, and pauses (rhythm check, intubation attempt, pulse check) must stay under ten seconds whenever possible. End-tidal CO₂ readings above 10 mmHg are a quiet sign that compressions are perfusing; below that, suspect technique or fatigue.
Every algorithm tells you to identify and treat reversible causes, but the cue gets lost in the noise. Memorize them as a checklist your team runs out loud during the two-minute compression cycle.
The Hs are hypovolemia, hypoxia, hydrogen ion (acidosis), hypo/hyperkalemia, and hypothermia. The Ts are tension pneumothorax, tamponade (cardiac), toxins, thrombosis (pulmonary), and thrombosis (coronary). Strong teams assign one team member to call these out during every two-minute round.
Termination of resuscitation is one of the hardest decisions in medicine. The AHA doesn't set a strict time limit, but most teams discuss stopping after 20–30 minutes of asystole with no reversible cause identified.
The triggers for the conversation are no ROSC despite high-quality CPR and end-tidal CO₂ persistently below 10 mmHg after 20 minutes. For shockable rhythms, teams typically extend longer because the survival math is better and refractory VF sometimes converts after extended efforts.
If the first rhythm is ventricular fibrillation or pulseless ventricular tachycardia, defibrillate immediately at 120–200 J biphasic (or device-specific). Don't wait for IV access. Don't wait for an airway. Resume CPR the second the shock is delivered.
After two minutes, recheck the rhythm. If still shockable, shock again, then start epinephrine 1 mg IV every 3–5 minutes. After the third shock, give amiodarone 300 mg IV bolus (second dose 150 mg) or lidocaine 1–1.5 mg/kg.
The detailed shockable pathway is mapped out in the acls vf vt algorithm walkthrough. Refractory VF — VF that persists after three appropriately-delivered shocks — is where double sequential defibrillation may now be considered as a backup strategy.
True refractory VF often has a reversible driver: ongoing ischemia, electrolyte derangement (especially low magnesium or potassium), acidosis, hypothermia, or drug toxicity. While compressions continue, the team should be checking labs, reviewing the medication history, and considering whether the patient needs ECMO transfer if available locally.
≤10 seconds. Shock if shockable, then immediately resume compressions.
100–120/min, full recoil, depth 2–2.4 inches. Compressor #1 active.
Epinephrine 1 mg IV (if due). Amiodarone 300 mg after 3rd shock in VF/pVT.
Team leader runs the reversible-cause checklist out loud.
Next compressor positions hands. Swap occurs at the next rhythm check.
Cycle restarts. Total cycle ≤10-second pause.
No shock will fix asystole or PEA. Compressions and reversible-cause hunting are the entire treatment, with epinephrine 1 mg IV every 3–5 minutes layered on top. Confirm asystole in two leads — fine VF can masquerade as asystole on a single lead, especially with low monitor gain.
For PEA, the rhythm on the monitor is organized but the patient has no pulse. The diagnosis lives in the absent pulse, not in the QRS shape. PEA outcomes hinge almost entirely on finding the H or T that caused it.
A useful framing: narrow-complex PEA usually has a mechanical or volume cause (tamponade, tension pneumothorax, hypovolemia, PE). Wide-complex PEA leans toward metabolic causes (hyperkalemia, sodium-channel blocker toxicity, severe acidosis, MI). The QRS width can steer your H/T hunt.
The bradyarrhythmia acls algorithm starts with one question: is the patient unstable? Hypotension, acute altered mental status, signs of shock, ischemic chest discomfort, or acute heart failure earn the unstable label.
Unstable bradycardia gets atropine 1 mg IV (up to 3 mg total). If atropine fails or the patient is in second-degree type II or third-degree block, move to transcutaneous pacing or a dopamine (5–20 mcg/kg/min) or epinephrine (2–10 mcg/min) infusion.
Stable bradycardia gets monitoring and a workup for cause — drug effect, electrolyte derangement, ischemia, increased intracranial pressure, or hypothyroidism are the usual suspects.
Transcutaneous pacing fails more often than students expect. Capture isn't just a pacer spike on the monitor — it's a QRS that follows every spike and a palpable femoral pulse that matches the pacing rate.
Confirm both. Sedate the patient as soon as possible; conscious pacing is brutally uncomfortable. And don't delay transvenous pacing or chronotropic infusions while waiting on capture that isn't coming.
Tachycardia algorithms split on two questions: is the patient stable, and is the QRS narrow or wide? Unstable tachycardia (defined by the same criteria as unstable bradycardia) goes directly to synchronized cardioversion.
Stable narrow regular tachycardia gets vagal maneuvers first, then adenosine 6 mg rapid IV push (then 12 mg if needed). Stable wide regular tachycardia is treated as ventricular tachycardia until proven otherwise — adenosine, or an antiarrhythmic like amiodarone, procainamide, or sotalol.
Stable irregular tachycardia (often atrial fibrillation with rapid ventricular response) typically gets rate control with a beta blocker or calcium channel blocker. If rapid AF is associated with pre-excitation (Wolff-Parkinson-White), nodal blockers are dangerous and procainamide or cardioversion is preferred.
Energy levels matter because they're tested constantly. Narrow regular: 50–100 J. Narrow irregular: 120–200 J biphasic. Wide regular: 100 J. Wide irregular: defibrillation dose (unsynchronized) because synchronizing on polymorphic rhythms is unreliable.
Always sedate the patient if conscious, and always confirm the synchronizer is engaged before pressing shock. A common test trap is the candidate who forgets to re-enable sync after an earlier defibrillation in the same case.
Adenosine is unique. It's pushed fast — true rapid push, followed immediately by a 20 mL saline flush — because its half-life is under ten seconds. Patients almost always describe a few seconds of chest pressure or impending doom.
Warn them. Have the defibrillator pads on, sync mode ready, just in case. If 6 mg fails, give 12 mg. If still no conversion, the rhythm probably isn't classic AVNRT/AVRT and a different drug is appropriate.
ROSC is the start of a new algorithm, not the end of the code. The post-arrest priorities are airway optimization with appropriate oxygenation (target SpO₂ 92–98%, not 100% — hyperoxia worsens outcomes).
Hemodynamic support keeps systolic blood pressure at or above 90 mmHg. Obtain a 12-lead ECG to identify STEMI candidates for cath lab activation. Targeted temperature management runs between 32 and 37.5°C for at least 24 hours.
Neurologic prognostication should be delayed at least 72 hours after ROSC (longer if the patient was cooled) because early exams under-predict good outcomes. Pupillary response, motor exam, and EEG patterns all become more reliable once sedation and hypothermia have worn off.
The ACS algorithm is a clock from the moment the patient hits the door. Twelve-lead ECG within 10 minutes. STEMI identified → cath lab activation, PCI within 90 minutes (or fibrinolytics within 30 if PCI is not available within 120).
Aspirin 162–325 mg chewed as early as possible. Beta blockers, statins, and anticoagulation per local protocol. The drugs and doses examiners love to test are summarized in our acls algorithms reference. NSTEMI patients still require urgent risk stratification — they're not low priority.
Stroke care lives or dies on door-to-needle time. CT within 25 minutes of arrival. Radiologist read within 45 minutes. Fibrinolytic decision within 60 minutes (door-to-needle). Door-to-device for thrombectomy candidates within 90 minutes.
Pre-hospital, the priority is recognizing FAST signs (face droop, arm weakness, speech difficulty, time to call) and transporting to a stroke-capable center. Blood pressure has to be under 185/110 before fibrinolytics — if it isn't, treat with labetalol or nicardipine first.
Examiners test the same doses every cycle. Epinephrine 1 mg IV/IO every 3–5 minutes in arrest. Amiodarone 300 mg IV first dose, 150 mg second dose, max 2.2 g over 24 hours.
Lidocaine 1–1.5 mg/kg first, 0.5–0.75 mg/kg second. Atropine 1 mg IV every 3–5 minutes, max 3 mg. Adenosine 6 mg rapid IV push, then 12 mg if needed. Magnesium sulfate 1–2 g IV for torsades de pointes.
Naloxone 0.4–2 mg IM/IN for suspected opioid overdose. Calcium chloride 1 g IV for hyperkalemia or calcium-channel-blocker toxicity. Sodium bicarbonate 1 mEq/kg for severe metabolic acidosis or tricyclic overdose.
Every published study on resuscitation outcomes points to the same conclusion: team performance matters more than any single drug or maneuver. The AHA codifies this with team-leader and team-member roles, closed-loop communication, clear role assignments, and constructive intervention.
The leader stays hands-off the compressions, keeps the algorithm in their head, calls drug orders by name and dose, and rotates compressors before fatigue degrades depth. Team members repeat orders back, announce when interventions are complete, and speak up if they see something wrong.
Closed loop sounds bureaucratic on paper. In a real code it's the only thing that prevents the wrong drug, the wrong dose, or the same drug given twice. The leader says: "Give 1 mg of epinephrine IV."
The team member says: "1 mg of epinephrine IV, giving now." When the push is done: "1 mg of epinephrine IV, given." Three sentences. Every order. Every time. It feels theatrical for thirty seconds, then the structure carries the room.
Watch for these failure modes during megacode and in real arrests: confusing PEA with asystole (and skipping the second-lead confirmation), failing to switch the compressor at the two-minute mark, and giving epinephrine too early in a shockable rhythm (it goes after the second shock, not the first).
Also: forgetting to engage sync mode after an earlier defibrillation, mismanaging the bradycardia pacing transition, and skipping the Hs and Ts huddle because the team is focused on the monitor. Strong teams build these checks into the cycle so they happen even when attention is exhausted.
The fastest way to internalize the algorithms isn't to read flashcards. It's to draw them. Get a blank piece of paper, pick a rhythm — say, refractory VF — and write out every step, every drug, every energy, every reversible cause check from memory. Then compare against the official flowchart and circle the gaps. Repeat tomorrow.