ONE PATIENT. ONE CHAIN.
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Megacode scenarios in clinical order: read the rhythm, commit to the action, give the right drug at the right dose, reassess.
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THE ALGORITHMS, PLAINLY
Field guide
Adult ACLS the way it is taught in Canadian practice (Heart and Stroke Foundation of Canada courses follow the same international science). Every section is backed by an open-source textbook — follow the source links to read the full text.
1 · Recognize the arrest, start perfect CPR
Unresponsive, not breathing normally, no definite pulse within 10 seconds → call for help, get the defibrillator, and start compressions. Compressions start within 10 seconds of recognition. Everything else in ACLS is built on top of uninterrupted, high-quality CPR:
- Rate 100–120/min, depth 5–6 cm (2–2.4 in) in adults, full chest recoil between compressions.
- Minimize interruptions — pause only for rhythm/pulse checks every 2 minutes, and keep every pause under 10 seconds.
- Without an advanced airway: 30 compressions : 2 breaths. Avoid excessive ventilation.
- Switch compressors every 2 minutes — quality fades before the compressor feels tired.
- If capnography is running, an EtCO₂ under 10 mmHg means flow is poor: push harder/deeper, check recoil, switch compressors. A sudden sustained rise in EtCO₂ is often the first sign of ROSC.
2 · Cardiac arrest — the shockable arm (VF / pulseless VT)
- CPR running. As soon as the defibrillator is ready: shock — biphasic 120–200 J (the manufacturer's setting; escalate for later shocks), monophasic 360 J. Unsynchronized.
- Immediately resume CPR for 2 minutes — do not stop to check the rhythm or a pulse first.
- Rhythm check. Still VF/pVT → shock again, resume CPR. Epinephrine 1 mg IV/IO after the initial shocks, then every 3–5 minutes.
- Still VF/pVT → shock again. Amiodarone 300 mg IV/IO for shock-refractory VF/pVT; a second dose of 150 mg may follow. (Lidocaine is the alternative antiarrhythmic.)
- Keep cycling: CPR 2 min → check → shock if still shockable → drugs on schedule — while hunting the H's & T's (section 7).
Defibrillation is the definitive treatment — its success falls by roughly 10% for every minute of delay. Never let IV access, intubation, or a drug round delay a shock.
📖 Sources: StatPearls — Defibrillation · StatPearls — Ventricular Fibrillation · StatPearls — Pulseless Ventricular Tachycardia
3 · Cardiac arrest — the non-shockable arm (PEA / asystole)
- Do not shock. Electricity does not fix PEA or asystole.
- High-quality CPR, continuously. Epinephrine 1 mg IV/IO as soon as possible, repeated every 3–5 minutes.
- Before calling asystole, confirm it: check the cables/gain and look in another lead — fine VF and a loose lead both impersonate a flat line. Never shock a "flat line" you have not confirmed.
- Spend every cycle hunting the cause (section 7). PEA is a symptom: a fast, narrow-complex PEA often means a flow problem (bleeding, tamponade, tension pneumothorax, massive PE); a slow, wide PEA points to metabolic causes like hyperkalemia or drug toxicity.
- Point-of-care ultrasound can help identify tamponade or a standstill heart — only if it never interrupts compressions.
Atropine has no role in cardiac arrest. It was removed from the arrest algorithm years ago; it belongs only in the bradycardia-with-a-pulse algorithm (section 4).
4 · Bradycardia with a pulse
Treat the patient, not the number: bradycardia needs treatment when it causes hypotension, altered mental status, signs of shock, ischemic chest pain, or acute heart failure.
- Airway and breathing, oxygen if hypoxemic, monitor, IV access, 12-lead ECG.
- Atropine 1 mg IV, repeat every 3–5 minutes to a maximum of 3 mg.
- Atropine ineffective → transcutaneous pacing (confirm electrical and mechanical capture — a pulse with every paced beat; give analgesia/sedation once capturing if the blood pressure allows) or an epinephrine infusion (2–10 mcg/min) or dopamine infusion (5–20 mcg/kg/min), titrated to response.
- Arrange transvenous pacing and expert consultation; treat the cause (beta-blocker or calcium-channel-blocker overdose, hyperkalemia, ischemia).
Atropine works at the AV node — so it rarely works in Mobitz II or complete heart block, where no impulse crosses the node. In high-grade block, do not waste time on repeated atropine: pace.
📖 Sources: StatPearls — Transcutaneous Pacing · StatPearls — Third-Degree Atrioventricular Block · Medical-Surgical Nursing (OpenStax) — 12.2 Dysrhythmia
5 · Tachycardia with a pulse
The one question that runs this algorithm: is the patient unstable? (hypotension, altered mental status, shock, ischemic chest pain, acute heart failure).
- Unstable → synchronized cardioversion, now. Sedate first only if it costs no time. Starting energies (biphasic): narrow regular (SVT/flutter) 50–100 J; narrow irregular (AF) 120–200 J; wide regular (VT with a pulse) 100 J. If it fails, re-sync, step the energy up, and shock again. Synchronization times the shock to the R wave so it cannot land on the vulnerable T wave.
- Stable narrow regular (SVT) → vagal maneuvers first, then adenosine 6 mg rapid IV push chased by a saline flush; if it persists, 12 mg, and a second 12 mg dose may follow. Warn the patient: a few seconds of flushing and chest pressure are normal — the half-life is under 10 seconds.
- Stable wide complex → treat as VT (about 9 in 10 wide-complex tachycardias are VT): antiarrhythmic infusion such as amiodarone 150 mg IV over 10 minutes plus urgent expert consultation. If the patient deteriorates at any point, cardiovert.
- Stable AF with a rapid response → rate control with an AV-nodal blocker (beta blocker or diltiazem) per orders, and treat the driver (sepsis, pain, fever, hypovolemia). If AF has lasted >48 h or the duration is unknown, elective cardioversion waits for anticoagulation or exclusion of atrial clot — a shock can embolize it.
- Torsades de pointes (twisting polymorphic VT, usually with a long QT): stop every QT-prolonging drug, give magnesium sulfate 2 g IV first-line (then an infusion), and replete potassium to about 4.5–5.0 mmol/L. Pulseless torsades is defibrillated like VF — never give amiodarone, which prolongs the QT further.
📖 Sources: StatPearls — Synchronized Electrical Cardioversion · StatPearls — Adenosine · StatPearls — Supraventricular Tachycardia · StatPearls — Torsade de Pointes
6 · After ROSC — post-cardiac-arrest care
- 12-lead ECG immediately. STEMI (or a strongly suspected coronary cause) → emergent coronary angiography / PCI. Do not let cooling delay the cath lab.
- Oxygen: titrate FiO₂ down to keep SpO₂ 92–98% — both hypoxia and prolonged hyperoxia harm the injured brain.
- Blood pressure: keep SBP above 90 mmHg and MAP ≥ 65 mmHg with fluids and vasopressors as needed.
- Ventilation: normocapnia — target PaCO₂ 35–45 mmHg; avoid hyperventilation.
- Temperature: if the patient is comatose, start targeted temperature management — select and maintain a constant target between 32 °C and 36 °C for at least 24 hours, and actively prevent fever.
- Glucose: check it; treat hypoglycemia and avoid extremes.
- ICU admission, continuous monitoring, seizure watch, and a cause workup. Do not attempt neurological prognostication in the first hours — reliable assessment comes days later, after rewarming and clearing confounders.
📖 Sources: StatPearls — Cardiopulmonary Arrest in Adults (post-resuscitation care) · StatPearls — Ventricular Fibrillation (emergent angiography) · StatPearls — Targeted Temperature Management
7 · The reversible causes — H's & T's
| Cause | Clues during the code | The fix |
|---|---|---|
| Hypovolemia | Bleeding, trauma, flat neck veins, narrow-complex fast PEA | Volume / blood products, stop the bleeding |
| Hypoxia | Airway problem, low SpO₂ before arrest, no EtCO₂ waveform | Patent airway, ventilate with 100% O₂, confirm with capnography |
| Hydrogen ion (acidosis) | Prolonged arrest, sepsis, renal failure | Effective CPR and ventilation; bicarbonate only for specific indications |
| Hypo / hyperkalemia | HyperK: peaked T waves, wide slow PEA, dialysis patient | HyperK: IV calcium first (membrane stabilization), then insulin/dextrose and K removal |
| Hypothermia | Cold exposure, cold to touch | Rewarming is definitive; resuscitation may be prolonged |
| Tamponade | Trauma, post-cardiac surgery, distended neck veins, muffled sounds | Pericardiocentesis / surgical drainage; fluids as a bridge |
| Toxins | Overdose history, pinpoint pupils (opioids), wide QRS (TCA) | Specific antidotes (e.g. naloxone for opioids) — never instead of CPR |
| Tension pneumothorax | Ventilated/trauma patient, absent breath sounds one side, rising airway pressures | Immediate decompression, then a chest tube — do not wait for imaging |
| Thrombosis — pulmonary | Sudden dyspnea before arrest, post-op, very low EtCO₂ with good CPR | Thrombolysis discussion / PE-directed therapy with the team |
| Thrombosis — coronary | Chest pain before arrest, STEMI | Post-ROSC emergent angiography / PCI |
📖 Source: StatPearls — Cardiopulmonary Arrest in Adults (Hs and Ts)
8 · Drug table
| Drug | Where it fits | Dose |
|---|---|---|
| Epinephrine | Any cardiac arrest | 1 mg IV/IO every 3–5 min |
| Epinephrine (infusion) | Bradycardia unresponsive to atropine | 2–10 mcg/min, titrated to response |
| Amiodarone | Shock-refractory VF / pulseless VT | 300 mg IV/IO bolus; second dose 150 mg |
| Amiodarone (infusion) | Stable wide-complex tachycardia / post-arrest | 150 mg IV over 10 min, then 1 mg/min × 6 h, then 0.5 mg/min |
| Lidocaine | Alternative antiarrhythmic in arrest | 1–1.5 mg/kg IV/IO, then 0.5–0.75 mg/kg |
| Adenosine | Stable regular SVT (after vagal maneuvers) | 6 mg rapid IV push + flush; then 12 mg; may repeat 12 mg |
| Atropine | Symptomatic bradycardia ONLY — not in arrest | 1 mg IV every 3–5 min, max 3 mg |
| Dopamine (infusion) | Bradycardia unresponsive to atropine | 5–20 mcg/kg/min, titrated to response |
| Magnesium sulfate | Torsades de pointes | 2 g IV, then an infusion; replete K⁺ to ~4.5–5.0 mmol/L |
| Calcium | Hyperkalemia, hypocalcemia, calcium-channel-blocker overdose ONLY | IV per protocol — never routine in arrest |
| Sodium bicarbonate | Severe metabolic acidosis, hyperkalemia, TCA overdose | Per protocol — never routine in arrest |
📖 Sources: StatPearls — Defibrillation · StatPearls — Transcutaneous Pacing · StatPearls — Adenosine · StatPearls — Torsade de Pointes
9 · Airway & capnography
- Bag-mask ventilation with an oral airway is a perfectly good start — an advanced airway (supraglottic device or endotracheal tube) is placed by the most experienced operator without long pauses in compressions.
- Continuous waveform capnography plus clinical assessment is the most reliable way to confirm and monitor tube placement. No sustained CO₂ waveform after intubation during CPR → assume the tube is displaced or esophageal until proven otherwise (remember flow is low in arrest, so interpret with compressions running).
- With an advanced airway in place: continuous compressions with about one breath every 6 seconds — and never hyperventilate, which raises intrathoracic pressure and steals venous return.
- Capnography also grades your CPR (target EtCO₂ above 10 mmHg) and is usually the first place ROSC shows up.
📖 Sources: StatPearls — Carbon Dioxide Detector · StatPearls — Cardiopulmonary Arrest in Adults
10 · Team dynamics — the quiet half of ACLS
- One leader, clear roles: compressor, airway, monitor/defibrillator, medications, recorder. Nobody freelances.
- Closed-loop communication: an order is repeated back, and its completion is announced ("Epinephrine 1 mg is in").
- Protect the compressions: choreograph rhythm checks to stay under 10 seconds; charge the defibrillator during CPR; hover, don't lean.
- Say what you see: EtCO₂ trends, rhythm changes, elapsed time and drug times are called out loud so the whole team shares one picture.
📖 Sources: StatPearls — Defibrillation (team outcomes) · Medical-Surgical Nursing (OpenStax) — 12.2 Dysrhythmia (roles during cardiac arrest)