ACLS Exam Prep 9-Week Study Plan

Week 1 — Part I: Rhythm Recognition

Difficulty: Heavy — Foundation Critical

What it covers: Part I builds the rhythm-strip literacy that every other ACLS decision depends on. You will learn the conduction hierarchy from SA node to AV junction to ventricular escape pacemakers and the intrinsic rate ranges of each, the systematic 6-step rhythm interpretation method (rate, regularity, P waves, PR interval, QRS width, P–QRS relationship), the sinus rhythms (normal sinus, sinus brady, sinus tachy) and how to distinguish them from pathologic mimics, the atrial tachyarrhythmias including atrial flutter (sawtooth), atrial fibrillation (irregularly irregular, no discrete P waves), and supraventricular tachycardia (regular narrow-complex tachycardia with hidden P waves), the AV block spectrum from first-degree (prolonged PR, every beat conducts) through Mobitz I (Wenckebach — progressive PR lengthening with grouped beating), Mobitz II (sudden non-conducted P waves with fixed PR), and complete heart block (full AV dissociation), the ventricular tachyarrhythmias including monomorphic VT, polymorphic VT, torsades de pointes in the setting of long QT, ventricular fibrillation (coarse vs. fine), pulseless electrical activity, and asystole confirmation in two leads, the paced rhythms with capture and sensing patterns, and the high-yield artifact-versus-rhythm differentiation that prevents inappropriate shocks.

Print: 1 Mind Map, 4 Comparison Charts, 3 Cornell Notes pages

Study Tasks

☐ Read the Study Guide first — complete the High-Yield Objectives, Key Terms and Definitions, and Concept Overview sections before opening the chapter.

☐ Highlight as you read — follow the Made Easy Highlighting System exactly:

• Blue: Rhythm Recognition (What the Strip Looks Like) — "If I saw this on a monitor right now, what is it?" — Wenckebach (progressive PR lengthening) vs. Mobitz II (sudden dropped beat), monomorphic VT (uniform wide QRS) vs. polymorphic VT (twisting morphology), coarse VF vs. fine VF vs. asystole confirmation, atrial flutter (sawtooth) vs. atrial fibrillation (irregularly irregular), R-on-T phenomenon and paced rhythm spikes

• Orange: Drug Facts (Name, Dose, Push It Right) — "What drug, what dose, what route, what max?" — Drugs are minimal in this Part; flag any cross-references to amiodarone for VT/VF, adenosine for SVT, and atropine for bradycardia for full coverage in Part III

• Green: Algorithm Steps (What Comes Next in the Protocol) — "I'm in the middle of the code — what's my next move?" — The 6-step rhythm interpretation sequence (rate → regularity → P waves → PR → QRS → relationship), narrow vs. wide complex branch logic, regular vs. irregular branch logic, two-lead asystole confirmation

• Yellow: Critical Numbers & Time Windows (Memorize the Exact Value) — "This is a number I need to know cold." — SA node intrinsic rate 60–100 bpm, AV junctional 40–60 bpm, ventricular escape 20–40 bpm, normal PR 0.12–0.20 sec, normal QRS <0.12 sec, QTc upper limit ~0.44 sec (men) / 0.46 sec (women), small box = 0.04 sec, large box = 0.20 sec

• Red: Contraindications & Don't-Do's (Stop — This Will Harm the Patient) — "Doing this would make things worse, not better." — Never shock asystole, never shock PEA, never delay defibrillation in shockable rhythms to "look harder" at the strip, never call asystole from a single lead, never assume artifact without checking the patient

• Purple: Mnemonics & Memory Aids (The Trick That Unlocks Recall) — "There's a shortcut for this — use the acronym." — The 6-step interpretation order, "Longer, longer, longer, drop — that's a Wenckebach" (Mobitz I), "If some Ps don't get through, then you have a Mobitz II," "P and QRS don't agree — must be third-degree"

☐ Master the conduction hierarchy as your rhythm-naming engine. The SA node fires at 60–100 bpm and is the default pacemaker. When it fails, the AV junction takes over at 40–60 bpm, producing junctional rhythms with absent or inverted P waves and a narrow QRS. When the AV junction fails, ventricular escape pacemakers fire at 20–40 bpm with wide QRS complexes. Recognizing where the rhythm originated is the key to naming it correctly — and the slower the inherent rate, the lower in the hierarchy the impulse is being generated.

☐ Lock in the 6-step rhythm interpretation method as your default reflex. Step 1: rate — count R waves in a 6-second strip and multiply by 10. Step 2: regularity — march out the R-R intervals. Step 3: P waves — present, absent, inverted, multiple morphologies, or sawtooth. Step 4: PR interval — normal (0.12–0.20 sec), prolonged, or variable. Step 5: QRS width — narrow (<0.12 sec, supraventricular origin) or wide (≥0.12 sec, ventricular origin or aberrancy). Step 6: P–QRS relationship — 1:1, varying, or dissociated. Apply this same six-step sequence to every strip, every time.

☐ Own the atrial tachyarrhythmias and their distinguishing features. Atrial flutter shows organized sawtooth flutter waves at 250–350 bpm with a regular ventricular response (often 2:1 or 4:1 conduction). Atrial fibrillation shows a chaotic baseline with no discrete P waves and an irregularly irregular ventricular response. SVT shows a regular tachycardia at 150–250 bpm with hidden or buried P waves and a narrow QRS. The baseline pattern between QRS complexes is the diagnostic feature — read the gaps, not just the beats.

☐ Master the AV block spectrum and why Mobitz II changes management. First-degree block prolongs PR beyond 0.20 sec but every beat conducts — usually benign. Mobitz I (Wenckebach) shows progressive PR lengthening until a beat drops, producing grouped beating — usually stable. Mobitz II shows sudden non-conducted P waves with a fixed PR interval on conducted beats — unstable, usually requires pacing because it can progress without warning to complete block. Complete heart block (third-degree) shows full AV dissociation: P waves and QRS complexes march independently. Distinguishing Mobitz I from Mobitz II is one of the highest-yield distinctions on the exam because it changes management.

☐ Build ventricular tachyarrhythmia recognition for shock decisions. Wide-complex tachycardia is treated as ventricular in origin until proven otherwise. Monomorphic VT shows uniform wide QRS complexes; polymorphic VT shows changing morphology; torsades de pointes is polymorphic VT in the setting of a long QT interval. The decisive clinical question is always: pulse or no pulse — pulseless VT is treated like VF (shock), VT with a pulse goes into the tachycardia algorithm. VF appears as chaotic, disorganized electrical activity with no recognizable QRS complexes; coarse VF has high amplitude, fine VF has low amplitude (but both are shockable). Asystole is a flat line, must be confirmed in two leads, and is never shocked.

☐ Know PEA recognition — organized rhythm, no pulse. PEA is any organized electrical rhythm on the monitor without a palpable pulse. The rhythm strip looks like it should produce a cardiac output (sinus, junctional, or even narrow tachycardia patterns), but the patient has no pulse. Recognition relies on simultaneous monitor and pulse check — and the immediate priority shifts to high-quality CPR plus the H's and T's reversible-cause search.

☐ Build artifact-versus-rhythm differentiation. Lead disconnection mimics asystole, electrical interference mimics VF, and patient movement mimics tachycardia. Always check the patient before treating the strip — pulse first, monitor second. This single habit prevents inappropriate shocks and missed arrests.

☐ Complete the Practice Questions for Part I in your quiz bank. Review every rationale — correct and incorrect.

How to Use Your Templates

☐ Mind Map: Central node = ACLS Rhythm Recognition. Main branches: Conduction Hierarchy (SA → AV junction → ventricular escape rates) → 6-Step Interpretation Method (rate, regularity, P waves, PR, QRS, relationship) → Sinus Rhythms (normal, brady, tachy) → Atrial Tachyarrhythmias (flutter, fib, SVT) → AV Blocks (1st, Mobitz I, Mobitz II, 3rd) → Ventricular Rhythms (monomorphic VT, polymorphic VT/torsades, VF coarse/fine, PEA, asystole) → Paced Rhythms → Treat the Patient, Not the Strip (artifact vs. real rhythm).

Comparison Charts:

☐ Chart 1 — AV Block Spectrum: First-degree, Mobitz I (Wenckebach), Mobitz II, Complete Heart Block; PR pattern, QRS dropping pattern, ventricular rate, stability, management implications (observe vs. pace).

☐ Chart 2 — Tachyarrhythmia Differentiation: Sinus tachy, atrial flutter, atrial fibrillation, SVT, monomorphic VT, polymorphic VT, torsades; QRS width, regularity, P-wave appearance, baseline pattern, key distinguishing feature.

☐ Chart 3 — Cardiac Arrest Rhythms (Shockable vs. Non-Shockable): VF (coarse), VF (fine), pulseless VT, PEA, asystole; rhythm description, shockable status, immediate intervention, two-lead confirmation requirement.

☐ Chart 4 — Pacemaker Hierarchy: SA node, AV junction, ventricular escape; intrinsic rate, P-wave appearance, QRS width, when each takes over, clinical implications when a higher pacemaker fails.

Cornell Notes:

☐ Page 1 — Cue questions: What are the six steps of systematic rhythm interpretation, in order? What are the intrinsic rates of the SA node, AV junction, and ventricular escape pacemakers? How do you distinguish atrial flutter from atrial fibrillation from SVT on a strip?

☐ Page 2 — Cue questions: What distinguishes Mobitz I from Mobitz II, and why does that distinction change management? How do you tell monomorphic VT from polymorphic VT from torsades de pointes? What is the rule for confirming asystole, and why is it absolute?

☐ Page 3 — Cue questions: What is PEA, and how does its recognition differ from every other arrest rhythm? What are the most common artifacts that mimic dangerous rhythms, and what is the one habit that prevents inappropriate shocks? How does QRS width help you decide between supraventricular and ventricular origin?

Week 2 — Part II: Airway and Capnography

Difficulty: Moderate — Skills Critical

What it covers: Part II covers the airway management skills and waveform monitoring that determine ventilation quality during a code. You will learn the airway adjuncts and when to use each (oropharyngeal airway in the unresponsive patient without a gag reflex, nasopharyngeal airway when a gag is present), bag-valve-mask (BVM) technique including the E-C clamp seal, two-rescuer ventilation, and the importance of avoiding hyperventilation, the supraglottic airway options (laryngeal mask airway, i-gel, King LT, Combitube) and the clinical situations that favor each, endotracheal intubation indications, equipment, and the ACLS-relevant focus of placement confirmation rather than insertion technique, the gold-standard role of waveform capnography for confirming tube placement, monitoring CPR quality, and detecting ROSC, the specific ETCO2 thresholds that drive decisions during a code, ventilation rate targets in arrest (1 breath every 6 seconds with an advanced airway) and post-arrest, the DOPES mnemonic for troubleshooting sudden deterioration after intubation, and the integration of airway management into the broader cardiac arrest algorithm without interrupting compressions.

Print: 1 Mind Map, 3 Comparison Charts, 2 Cornell Notes pages

Study Tasks

☐ Read the Study Guide first — complete the High-Yield Objectives, Key Terms and Definitions, and Concept Overview sections before opening the chapter.

☐ Highlight as you read — follow the Made Easy Highlighting System exactly:

• Blue: Rhythm Recognition — Capnography waveform shapes (normal box-shaped capnogram, low/flat ETCO2 during poor CPR, sudden ETCO2 spike with ROSC, shark-fin pattern with bronchospasm), tube-placement waveform vs. esophageal placement waveform

• Orange: Drug Facts — Cross-reference any medications mentioned in airway management (e.g., RSI agents, bronchodilators); full drug coverage in Part III

• Green: Algorithm Steps — BVM-first ventilation strategy, when to escalate to supraglottic, when to escalate to ET tube, two-rescuer BVM technique, post-intubation confirmation sequence (auscultation + waveform capnography + chest rise), DOPES sequence when ventilation fails after advanced airway

• Yellow: Critical Numbers & Time Windows — Ventilation rate with advanced airway: 1 breath every 6 seconds (10/min), tidal volume ~500–600 mL (just enough for visible chest rise), ETCO2 < 10 mmHg suggests poor CPR quality, ETCO2 sudden spike to ≥ 35–40 mmHg signals ROSC, normal ETCO2 35–45 mmHg, BVM seal achieved with E-C clamp technique

• Red: Contraindications & Don't-Do's — Don't hyperventilate (decreases venous return, worsens outcomes), don't interrupt compressions for intubation attempts beyond ~10 seconds, don't rely on auscultation alone for tube confirmation, don't continue ventilating if no waveform capnogram appears, don't use NPA in suspected basilar skull fracture

• Purple: Mnemonics & Memory Aids — DOPES (Displacement, Obstruction, Pneumothorax, Equipment, Stacked breaths) for sudden post-intubation deterioration, the E-C clamp shape for BVM seal

☐ Master BVM technique as your first-line ventilation skill. A good BVM seal beats a poorly placed ET tube every time. Use the E-C clamp: thumb and index finger form a "C" pressing the mask down onto the face, while the third, fourth, and fifth fingers form an "E" lifting the mandible up into the mask. In two-rescuer BVM, one rescuer maintains the seal with both hands while the second squeezes the bag — this is the highest-quality BVM ventilation. Deliver just enough volume to produce visible chest rise, no more.

☐ Lock in the airway adjunct decision rule. OPA (oropharyngeal airway) goes into the unresponsive patient without a gag reflex; sizing is from the corner of the mouth to the angle of the jaw. NPA (nasopharyngeal airway) is tolerated in patients with an intact gag reflex; sizing is from the tip of the nose to the earlobe. Avoid NPA in suspected basilar skull fracture (raccoon eyes, Battle's sign, CSF rhinorrhea) because of the risk of intracranial passage.

☐ Own the supraglottic airway role in modern ACLS. Supraglottic airways (LMA, i-gel, King LT) are now first-line advanced airways for cardiac arrest in most ACLS-style protocols because they can be placed quickly without interrupting compressions and don't require visualization of the cords. They are designed to sit above the glottis and provide ventilation without true intubation. Confirm placement with waveform capnography just as you would for an ET tube.

☐ Master waveform capnography as the single most informative monitor in a code. Waveform capnography does four things at once: confirms ET tube placement (a sustained, box-shaped waveform is your gold standard — esophageal placement gives no waveform), monitors CPR quality (ETCO2 < 10 mmHg means compressions are inadequate — push deeper, faster, or rotate compressors), detects ROSC (a sudden sustained jump from ~15 mmHg to ≥ 35–40 mmHg is the classic capnographic signature of return of spontaneous circulation), and warns of trouble (a falling ETCO2 trend signals tube displacement, circuit leak, or worsening cardiac output).

☐ Build the 1-breath-every-6-seconds ventilation discipline. Once an advanced airway is in place, compressions become continuous and ventilations are delivered asynchronously at 10 breaths per minute (one every six seconds). This is roughly half the rate that feels natural under stress. Hyperventilation increases intrathoracic pressure, decreases venous return, decreases coronary perfusion pressure, and worsens survival. Count out loud or use a metronome — the under-ventilation rule is non-negotiable.

☐ Know DOPES for sudden post-intubation deterioration. When a previously stable intubated patient suddenly deteriorates, work through DOPES in order: Displacement (tube migrated into the right mainstem bronchus or out of the trachea — check depth, recheck waveform, auscultate), Obstruction (mucus plug, kink, biting on the tube — suction, check for kinks), Pneumothorax (especially tension — needle decompress if hemodynamic collapse), Equipment (ventilator settings, oxygen source, BVM connection), Stacked breaths (auto-PEEP from inadequate exhalation time — disconnect from circuit and allow passive exhalation).

☐ Complete the Practice Questions for Part II in your quiz bank. Review every rationale — correct and incorrect.

How to Use Your Templates

☐ Mind Map: Central node = ACLS Airway Management. Main branches: Basic Adjuncts (OPA, NPA, sizing, contraindications) → BVM Technique (E-C clamp, two-rescuer) → Supraglottic Airways (LMA, i-gel, King LT, placement and confirmation) → Endotracheal Intubation (indications, confirmation requirements) → Waveform Capnography (placement, CPR quality, ROSC, trends) → Ventilation Rates (with and without advanced airway) → DOPES Troubleshooting → Integration with Compressions.

Comparison Charts:

☐ Chart 1 — Airway Adjuncts: OPA, NPA; indications, contraindications, sizing method, insertion technique, common errors.

☐ Chart 2 — Advanced Airway Options: Supraglottic (LMA/i-gel/King LT), endotracheal tube; speed of placement, training required, confirmation method, advantages, limitations, role in ACLS.

☐ Chart 3 — Capnography Waveforms and Their Meaning: Normal box-shaped, absent waveform, low ETCO2 (< 10 mmHg), sudden sustained spike (≥ 35–40 mmHg), gradual decline, shark-fin shape; clinical interpretation, immediate action, integration with the algorithm.

Cornell Notes:

☐ Page 1 — Cue questions: What is the proper E-C clamp BVM technique, and why is two-rescuer BVM superior to one-rescuer? What are the indications, contraindications, and sizing methods for OPA versus NPA? What is the recommended ventilation rate with and without an advanced airway, and what are the consequences of hyperventilation?

☐ Page 2 — Cue questions: What are the four roles of waveform capnography during a cardiac arrest? What are the specific ETCO2 thresholds that signal poor CPR quality, ROSC, and normal ventilation? What does DOPES stand for, and when do you run through it?

Week 3 — Part III: Pharmacology

Difficulty: Heavy — Memorization Critical

What it covers: Part III covers every ACLS medication you must know cold for the exam and the resuscitation bay. You will learn the cardiac arrest medications (epinephrine 1 mg IV/IO every 3–5 minutes for any arrest rhythm; amiodarone 300 mg first dose then 150 mg second dose for refractory VF/pVT; lidocaine as an alternative antiarrhythmic when amiodarone is unavailable), the bradycardia medications (atropine 1 mg every 3–5 minutes, max 3 mg total; dopamine and epinephrine infusions when atropine fails or pacing is unavailable), the tachycardia medications (adenosine 6 mg rapid IV push then 12 mg if needed for stable regular narrow-complex SVT; calcium channel blockers and beta-blockers for rate control; magnesium for torsades), the ACS medications (aspirin 162–325 mg chewed in suspected acute coronary syndrome; nitroglycerin for ongoing chest pain; oxygen only for hypoxia; morphine for refractory pain; heparin and fibrinolytics in their proper windows), the stroke medications (tPA/alteplase or tenecteplase within the appropriate window with strict inclusion/exclusion criteria), the routes of administration including IV (preferred), IO (when IV access is delayed), and the nuances of why endotracheal drug administration has fallen out of favor, the indications and contraindications that turn a helpful drug into a harmful one, and the dose-rate-route-max framework that lets you reproduce any drug card under exam pressure.

Print: 1 Mind Map, 4 Comparison Charts, 3 Cornell Notes pages

Study Tasks

☐ Read the Study Guide first — complete the High-Yield Objectives, Key Terms and Definitions, and Concept Overview sections before opening the chapter.

☐ Highlight as you read — follow the Made Easy Highlighting System exactly:

• Blue: Rhythm Recognition — Cross-reference the rhythm that triggers each drug (VF/pVT → epi + amio, asystole/PEA → epi only, symptomatic brady → atropine, stable SVT → adenosine, torsades → magnesium)

• Orange: Drug Facts (this is the central color of Part III) — Epinephrine 1 mg IV/IO every 3–5 minutes during arrest; Amiodarone 300 mg first dose, 150 mg second dose in VF/pVT; Lidocaine 1–1.5 mg/kg first dose, then 0.5–0.75 mg/kg as alternative antiarrhythmic; Atropine 1 mg every 3–5 minutes, max total 3 mg; Adenosine 6 mg rapid push, then 12 mg if needed; Aspirin 162–325 mg chewed in suspected ACS; Nitroglycerin SL 0.4 mg q5 min × 3; Magnesium 1–2 g IV for torsades; Dopamine infusion 5–20 mcg/kg/min for refractory bradycardia; Epinephrine infusion 2–10 mcg/min for refractory bradycardia or post-ROSC hypotension

• Green: Algorithm Steps — Where each drug enters its algorithm: epi early in any arrest, amio after second shock in VF/pVT, atropine first in symptomatic brady before pacing or pressors, adenosine after vagal maneuvers in stable regular SVT, fibrinolytics after exclusion criteria are cleared

• Yellow: Critical Numbers & Time Windows — Door-to-balloon ≤ 90 minutes for STEMI PCI, door-to-needle ≤ 60 minutes for STEMI fibrinolytics, fibrinolytic window for ischemic stroke 3–4.5 hours, thrombectomy window up to 24 hours in selected patients, atropine max total 3 mg, amiodarone max cumulative dose ~2.2 g/24 h

• Red: Contraindications & Don't-Do's — Don't give fibrinolytics with active bleeding, recent stroke, recent surgery, or known intracranial pathology; don't give nitroglycerin in RV infarct or after recent PDE-5 inhibitor (sildenafil/tadalafil); don't use adenosine in irregular wide-complex tachycardia (could be WPW with atrial fibrillation — risk of accelerating to VF); don't delay defibrillation in shockable rhythms — shock first, drugs second; avoid atropine in second-degree type II or third-degree block (won't work and may worsen by speeding sinus rate without improving conduction)

• Purple: Mnemonics & Memory Aids — "Epi every five, amio after the second shock, atropine three is the cap" — and any book-provided rhymes that distill dose-route-max into a recallable pattern

☐ Master the cardiac arrest pharmacology trio. Epinephrine 1 mg IV/IO every 3–5 minutes is given in every cardiac arrest rhythm — VF, pVT, asystole, and PEA. The mechanism is alpha-mediated vasoconstriction that raises coronary perfusion pressure during compressions. Amiodarone is added for refractory shockable rhythms only: 300 mg IV/IO bolus after the second shock + epi cycle, then 150 mg if a third antiarrhythmic dose is needed. Lidocaine (1–1.5 mg/kg first dose, 0.5–0.75 mg/kg subsequent) is the alternative antiarrhythmic when amiodarone is unavailable. None of these drugs replaces high-quality compressions and timely defibrillation.

☐ Lock in the bradycardia ladder. Atropine 1 mg IV every 3–5 minutes (max 3 mg total) is the first-line drug for symptomatic bradycardia. If atropine fails — or if the block is below the AV node (Mobitz II, third-degree) where atropine is unreliable — escalate to transcutaneous pacing, dopamine infusion (5–20 mcg/kg/min), or epinephrine infusion (2–10 mcg/min). Pacing and pressors are functionally interchangeable as second-line; pacing is faster if pads are already on, infusions are faster if you have IV access and no pacer.

☐ Own adenosine for stable, regular, narrow-complex SVT. Vagal maneuvers first (Valsalva, modified Valsalva, carotid sinus massage in selected patients). If unsuccessful, adenosine 6 mg rapid IV push followed by a saline flush (it has a half-life under 10 seconds — must be pushed fast and as proximal as possible). If no conversion in 1–2 minutes, give adenosine 12 mg with the same technique; a third 12 mg dose may be given. Warn the patient about the brief sense of impending doom. Adenosine is contraindicated in irregular wide-complex tachycardia because of the risk of accelerating WPW-with-atrial-fibrillation to VF.

☐ Master magnesium for torsades. Polymorphic VT with a long QT interval (torsades de pointes) responds to magnesium sulfate 1–2 g IV/IO over 5–60 minutes depending on stability. Identify the long QT etiology (electrolyte abnormalities, QT-prolonging drugs, congenital long QT) and stop the offending agents.

☐ Build the ACS pharmacologic bundle. In suspected acute coronary syndrome the early bundle is: aspirin 162–325 mg chewed (faster onset than swallowed), nitroglycerin SL 0.4 mg every 5 minutes up to 3 doses for ongoing chest pain (avoid in suspected RV infarct or recent PDE-5 inhibitor use), oxygen only if SpO2 < 90% or respiratory distress, morphine for pain not relieved by nitrates. Heparin and a P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel) are added as STEMI/NSTEMI protocols dictate. Fibrinolytics enter the picture only when PCI is unavailable within the door-to-balloon window and contraindications are excluded.

☐ Know the time windows that drive everything. Door-to-balloon ≤ 90 minutes for STEMI primary PCI. Door-to-needle ≤ 60 minutes for STEMI fibrinolytics when PCI is unavailable. Fibrinolytic window for ischemic stroke 3–4.5 hours from last known well (with strict criteria for the 3–4.5 hour extension). Mechanical thrombectomy window up to 24 hours in selected stroke patients with large vessel occlusion. These numbers are the single highest-yield set of values in the back half of ACLS.

☐ Drill the dose-route-max framework on every drug. For every ACLS medication, you should be able to answer in one breath: drug name, indication, dose, route, frequency, max total dose, key contraindications. Build a personal drug card for each medication and review it daily. Under exam stress, the structure of this framework is what lets you reproduce a drug card you almost forgot.

☐ Complete the Practice Questions for Part III in your quiz bank. Review every rationale — correct and incorrect.

How to Use Your Templates

☐ Mind Map: Central node = ACLS Pharmacology. Main branches: Cardiac Arrest Drugs (epinephrine, amiodarone, lidocaine) → Bradycardia Drugs (atropine, dopamine infusion, epinephrine infusion) → Tachycardia Drugs (adenosine, calcium channel blockers, beta-blockers, magnesium) → ACS Bundle (aspirin, nitroglycerin, oxygen, morphine, heparin) → Stroke Pharmacology (tPA/alteplase, tenecteplase, criteria) → Routes (IV, IO, why ET fell out of favor) → Time Windows (door-to-balloon, door-to-needle, stroke windows) → Contraindications That Cause Harm.

Comparison Charts:

☐ Chart 1 — Cardiac Arrest Drug Card: Epinephrine, amiodarone, lidocaine; indication rhythm, dose, route, frequency, max, when in the algorithm to give it.

☐ Chart 2 — Bradycardia Ladder: Atropine, transcutaneous pacing, dopamine infusion, epinephrine infusion; mechanism, dose/range, when to escalate, contraindications, monitoring needs.

☐ Chart 3 — Tachycardia Drugs: Adenosine, calcium channel blockers, beta-blockers, magnesium, amiodarone; rhythm indication, dose, push speed, contraindications, pearls (e.g., transient asystole after adenosine, magnesium for torsades only).

☐ Chart 4 — Time Windows for ACS and Stroke: Door-to-balloon, door-to-needle (STEMI fibrinolytics), stroke fibrinolytic window (≤ 3 h, 3–4.5 h extended), thrombectomy window (≤ 24 h selected); cutoff, eligibility, key exclusion criteria.

Cornell Notes:

☐ Page 1 — Cue questions: What is the dose, route, frequency, and indication for epinephrine in cardiac arrest, and how does it differ from epinephrine infusion in bradycardia? What is the dosing scheme for amiodarone in refractory VF/pVT, and when does it enter the algorithm? What is the maximum cumulative atropine dose, and why does atropine often fail in Mobitz II and complete heart block?

☐ Page 2 — Cue questions: What are the dose, push technique, and contraindications for adenosine in stable SVT? What is the standard ACS pharmacologic bundle, and what are the contraindications to nitroglycerin? When is magnesium indicated in cardiac dysrhythmia, and what is the typical dose?

☐ Page 3 — Cue questions: What are the door-to-balloon and door-to-needle targets for STEMI care? What are the time windows for ischemic stroke fibrinolytics and mechanical thrombectomy? What are the absolute contraindications to fibrinolytic therapy in both ACS and stroke?

Week 4 — Part IV: Adult Cardiac Arrest Algorithms

Difficulty: Heavy — Algorithm Critical

What it covers: Part IV is the heart of ACLS — the integrated algorithms that combine rhythm recognition, airway, and pharmacology into a coordinated resuscitation. You will learn the BLS-to-ACLS handoff and how high-quality CPR underpins everything that follows, the universal cardiac arrest algorithm with its branch point at "Is the rhythm shockable?", the VF/pVT pathway including the immediate shock, the 2-minute compression cycle, the rhythm/pulse check, escalating energy levels, the timing and dose of epinephrine, and the entry point of amiodarone or lidocaine, the asystole/PEA pathway with its no-shock rule, the same epi-every-3-to-5 timing, and the parallel obligation to identify and treat reversible causes, the H's and T's framework as the single most important diagnostic checklist in a code (Hypoxia, Hypovolemia, Hydrogen ion/acidosis, Hypo/hyperkalemia, Hypothermia, Tension pneumothorax, Tamponade, Toxins, Thrombosis pulmonary, Thrombosis coronary), the role of high-quality CPR throughout (rate 100–120/min, depth ≥ 2 inches/5 cm in adults, full recoil, minimize interruptions, change compressors every 2 minutes), the criteria for terminating resuscitation, and the immediate post-ROSC priorities that hand off to Part VIII.

Print: 1 Mind Map, 4 Comparison Charts, 3 Cornell Notes pages

Study Tasks

☐ Read the Study Guide first — complete the High-Yield Objectives, Key Terms and Definitions, and Concept Overview sections before opening the chapter.

☐ Highlight as you read — follow the Made Easy Highlighting System exactly:

• Blue: Rhythm Recognition — The four arrest rhythms and their treatment branch (VF and pVT → shock pathway; asystole and PEA → no-shock pathway)

• Orange: Drug Facts — Cardiac arrest doses recurring across both pathways: epinephrine 1 mg IV/IO every 3–5 minutes (any arrest rhythm), amiodarone 300/150 mg or lidocaine 1–1.5 mg/kg then 0.5–0.75 mg/kg in VF/pVT only

• Green: Algorithm Steps — VF/pVT loop: CPR → shock → CPR + epi → shock → CPR + amiodarone (or lidocaine) → shock → continue cycles. Asystole/PEA loop: CPR + epi every 3–5 minutes, no shock, identify and treat reversible causes. Two-minute cycle structure: 2 min compressions → rhythm check → if shockable, shock → resume compressions immediately

• Yellow: Critical Numbers & Time Windows — Compression rate 100–120/min, depth ≥ 2 inches (5 cm) in adults but ≤ 2.4 inches (6 cm), full chest recoil, compressor change every 2 minutes, ETCO2 < 10 mmHg signals inadequate CPR, ETCO2 sudden spike to ≥ 35–40 mmHg signals ROSC, defibrillation energy biphasic 120–200 J (manufacturer specific) and monophasic 360 J, escalating shocks for refractory VF/pVT

• Red: Contraindications & Don't-Do's — Don't shock asystole or PEA, don't delay defibrillation in shockable rhythms (shock first, drugs second), don't interrupt compressions for more than 10 seconds for any reason except shock delivery, don't hyperventilate after advanced airway placement, don't stop CPR for pulse check until the rhythm check at the 2-minute mark

• Purple: Mnemonics & Memory Aids — H's and T's for reversible causes (Hypoxia, Hypovolemia, Hydrogen ion, Hypo/hyperkalemia, Hypothermia / Tension pneumothorax, Tamponade, Toxins, Thrombosis pulmonary, Thrombosis coronary), CAB sequence (Compressions, Airway, Breathing) for BLS startup

☐ Master the universal arrest algorithm branch point. Every cardiac arrest algorithm starts the same: recognize arrest, start CPR, attach monitor/defibrillator, identify rhythm. The single most important question follows: is the rhythm shockable? VF and pulseless VT go to the shock pathway; asystole and PEA go to the no-shock pathway. Both pathways share high-quality CPR, epinephrine every 3–5 minutes, advanced airway when feasible, and the H's and T's reversible-cause search. Only the rhythm-specific interventions differ.

☐ Lock in the VF/pVT loop as your most-tested algorithm. Cycle: CPR → shock → CPR + epi → shock → CPR + amiodarone (or lidocaine) → shock → continue. The 2-minute compression cycle is the structural unit — every cycle ends with a rhythm check, and a shock is delivered immediately if VF/pVT persists. Epinephrine enters as soon as IV/IO access is obtained (the early-epi principle for non-shockable rhythms; in shockable rhythms epi is given after the second shock if access is in place). Amiodarone enters after the second or third shock if the rhythm remains refractory. Each shock is followed by immediate resumption of compressions — do not pause for pulse check after defibrillation.

☐ Own the asystole/PEA loop and the parallel reversible-cause search. No shock, ever. CPR is continuous, with a brief rhythm check every 2 minutes. Epinephrine 1 mg IV/IO every 3–5 minutes from the moment access is obtained. The other engine running in parallel is the H's and T's: every PEA arrest needs an active search for the underlying cause, because PEA without a corrected cause does not survive. PEA from hypovolemia responds to fluids; PEA from tension pneumothorax responds to needle decompression; PEA from massive PE responds to fibrinolysis; PEA from hyperkalemia responds to calcium and shifters.

☐ Master the H's and T's as a real-time diagnostic engine. Hypoxia — confirm advanced airway placement, ensure oxygenation. Hypovolemia — bolus crystalloid; consider hemorrhage. Hydrogen ion (acidosis) — quality ventilation, consider bicarb in specific cases (TCA overdose, severe hyperkalemia). Hypo/hyperkalemia — point-of-care K+; treat hyperkalemia with calcium, insulin/dextrose, bicarb. Hypothermia — core temp, active rewarming, prolonged resuscitation. Tension pneumothorax — needle decompression, then chest tube. Tamponade — pericardiocentesis. Toxins — toxidrome recognition, specific antidotes (naloxone for opioid arrest, intralipid for local anesthetic systemic toxicity). Thrombosis pulmonary (massive PE) — fibrinolytics during arrest in suspected PE. Thrombosis coronary — proceed to PCI/cath lab post-ROSC.

☐ Build the high-quality CPR habits that drive survival. Compression rate 100–120/min — fast enough to maintain cardiac output, slow enough to allow filling. Depth at least 2 inches (5 cm) but not more than 2.4 inches (6 cm) in adults. Full chest recoil between compressions — leaning on the chest reduces venous return. Minimize interruptions — chest compression fraction should be ≥ 60% (ideally ≥ 80%) of total code time. Rotate compressors every 2 minutes to prevent fatigue-driven shallowing. Use waveform capnography and arterial line tracings if available to titrate compression quality in real time.

☐ Know defibrillation mechanics that change outcomes. Biphasic devices (the standard now) use 120–200 J per manufacturer specifications for the first shock; subsequent shocks use the same or escalating energy. Monophasic devices use 360 J for all shocks. Apply pads in the anterolateral or anteroposterior position. Clear the patient and the oxygen source. Resume compressions immediately after the shock — no pulse check, no rhythm check, no hesitation. The pulse and rhythm check come at the next 2-minute interval.

☐ Own the criteria for resuscitation termination. Termination is considered when there is no ROSC after a sustained, high-quality resuscitation effort with all reversible causes addressed and ongoing asystole. Field termination protocols vary by EMS system; in-hospital, the team leader weighs duration, reversibility, ETCO2 trend (sustained < 10 mmHg despite quality CPR carries a poor prognostic signal), patient wishes (advance directives, code status), and family presence. ROSC handoff goes immediately to the post-arrest care bundle (Part VIII).

☐ Complete the Practice Questions for Part IV in your quiz bank. Review every rationale — correct and incorrect.

How to Use Your Templates

☐ Mind Map: Central node = Adult Cardiac Arrest Algorithm. Main branches: BLS Foundation (CAB, high-quality CPR) → Rhythm Identification → Shockable Pathway (VF/pVT loop with shocks, epi, amio) → Non-Shockable Pathway (asystole/PEA loop with epi, no shocks) → H's and T's (reversible-cause search) → Defibrillation Mechanics (energy, pad placement, immediate resumption of CPR) → Compression Quality Metrics (rate, depth, recoil, fraction) → Termination Criteria → ROSC Handoff to Post-Arrest Care.

Comparison Charts:

☐ Chart 1 — Shockable vs. Non-Shockable Arrest Pathways: VF/pVT vs. asystole/PEA; rhythm characteristics, shock decision, epinephrine timing, antiarrhythmic role, special diagnostic emphasis, prognostic implications.

☐ Chart 2 — High-Quality CPR Metrics: Rate, depth, recoil, chest compression fraction, compressor rotation, ETCO2 monitoring; target value, common errors, real-time corrective actions.

☐ Chart 3 — H's and T's Reversible Causes: All 10 causes; rapid clinical clues, point-of-care test or maneuver, immediate intervention, prognostic implications if missed.

☐ Chart 4 — Defibrillation Energy Levels: Biphasic (first shock and subsequent), monophasic; manufacturer-recommended ranges, escalation strategy in refractory cases, pad placement options, common pitfalls (oxygen near pads, wet skin, missed contact).

Cornell Notes:

☐ Page 1 — Cue questions: What is the universal cardiac arrest algorithm branch point, and what determines which pathway you take? Walk through one full VF/pVT cycle, naming the order of shock, CPR, epinephrine, and amiodarone. Walk through one full asystole/PEA cycle, naming what is given and what is not given.

☐ Page 2 — Cue questions: Name all 10 H's and T's, and for each, give one rapid clinical clue and one immediate intervention. What are the high-quality CPR metrics (rate, depth, recoil, fraction, rotation), and what consequences follow when each is missed? What are the ETCO2 thresholds during resuscitation that signal poor CPR quality and ROSC?

☐ Page 3 — Cue questions: What is the proper sequence after defibrillation — pulse check first, or compressions first, and why? What are the energy levels for biphasic vs. monophasic defibrillation, and how do you decide on escalation? What are the criteria and considerations for terminating resuscitation in the field versus the hospital?

Week 5 — Part V: Bradycardia and Tachycardia Algorithms

Difficulty: Heavy — Decision Critical

What it covers: Part V covers the algorithms for the patient who has a pulse but a dangerous rhythm. You will learn the symptomatic bradycardia algorithm with its central question — is the patient stable or unstable? — the bradycardia ladder (atropine 1 mg every 3–5 minutes max 3 mg → transcutaneous pacing → dopamine infusion → epinephrine infusion), the special note that atropine often fails in Mobitz II and complete heart block because the block is below the AV node, the tachycardia algorithm with its first branch (stable vs. unstable) and second branch (narrow vs. wide complex, regular vs. irregular), the unstable tachycardia path that goes directly to synchronized cardioversion (with the energy levels that vary by rhythm), the stable narrow-complex regular path (vagal maneuvers → adenosine → rate-control agents), the stable narrow-complex irregular path (rate control with calcium channel blocker or beta-blocker for atrial fibrillation/flutter, with anticoagulation considerations), the stable wide-complex regular path (treat as VT — amiodarone, procainamide, or sotalol), the stable wide-complex irregular path (assume polymorphic VT or pre-excited atrial fibrillation — adenosine is contraindicated here), the recognition and management of torsades de pointes (magnesium plus QT-prolonging-agent removal), and the pacing modalities (transcutaneous as the default emergent option, transvenous as the more reliable bridge).

Print: 1 Mind Map, 4 Comparison Charts, 3 Cornell Notes pages

Study Tasks

☐ Read the Study Guide first — complete the High-Yield Objectives, Key Terms and Definitions, and Concept Overview sections before opening the chapter.

☐ Highlight as you read — follow the Made Easy Highlighting System exactly:

• Blue: Rhythm Recognition — Sinus brady vs. junctional rhythm vs. AV blocks (Mobitz I, Mobitz II, third-degree); narrow vs. wide complex tachycardia; regular vs. irregular; monomorphic VT vs. polymorphic VT vs. torsades; pre-excited atrial fibrillation (irregular wide-complex with varying QRS morphology — WPW with afib)

• Orange: Drug Facts — Atropine 1 mg every 3–5 minutes, max 3 mg; dopamine infusion 5–20 mcg/kg/min; epinephrine infusion 2–10 mcg/min; adenosine 6 mg → 12 mg → 12 mg; amiodarone 150 mg over 10 minutes for stable wide-complex tachycardia; procainamide; magnesium 1–2 g for torsades; diltiazem and metoprolol for rate control in stable atrial fibrillation/flutter

• Green: Algorithm Steps — Bradycardia ladder: identify symptomatic → atropine → pacing or pressor infusion. Tachycardia decision tree: stable or unstable → if unstable, synchronized cardioversion → if stable, narrow vs. wide and regular vs. irregular → branch-specific therapy

• Yellow: Critical Numbers & Time Windows — Symptomatic bradycardia threshold (HR < 50 with symptoms, not just a number), stable vs. unstable cutoffs (altered mental status, ischemic chest pain, hypotension/shock, acute heart failure), synchronized cardioversion energy: regular narrow-complex 50–100 J biphasic, irregular narrow-complex (afib) 120–200 J biphasic, regular wide-complex (monomorphic VT with pulse) 100 J biphasic, polymorphic VT — defibrillation (unsynchronized) at full energy

• Red: Contraindications & Don't-Do's — Don't give atropine in Mobitz II or third-degree block expecting it to work — pace early; don't push adenosine in irregular wide-complex tachycardia (could be WPW with afib — risk of accelerating to VF); don't synchronize-cardiovert polymorphic VT (the sync function can't lock onto the chaotic morphology — defibrillate); don't use AV nodal blockers (CCB, beta-blocker, digoxin, adenosine) in known WPW with atrial fibrillation; don't delay cardioversion for IV access in the unstable patient

• Purple: Mnemonics & Memory Aids — "Stable, narrow, regular — vagal then adenosine," "Wide and regular, treat like VT," "Wide and irregular, don't be a hero" (avoid AV nodal blockers and adenosine), "If unstable, shock 'em" (synchronized for organized rhythm with pulse, defib for polymorphic VT/pulseless)

☐ Master the symptomatic bradycardia decision rule. Bradycardia is symptomatic when the slow rate produces signs of poor perfusion: altered mental status, ischemic chest pain, hypotension, acute heart failure, or other shock signs. Asymptomatic bradycardia — even at rates well under 50 — does not require ACLS intervention. The ladder for the symptomatic patient: atropine 1 mg IV every 3–5 minutes, max total 3 mg → if atropine fails or is unlikely to work (Mobitz II, third-degree block), move to transcutaneous pacing or pressor infusion (dopamine 5–20 mcg/kg/min or epinephrine 2–10 mcg/min). Transvenous pacing is the definitive bridge to permanent pacemaker placement for high-degree blocks.

☐ Lock in the tachycardia decision tree. First branch: stable or unstable? Unstable patients (altered mental status, ischemic chest pain, hypotension, signs of shock, acute heart failure) go directly to electrical therapy — synchronized cardioversion for organized rhythms with a pulse, defibrillation for polymorphic VT. Don't delay cardioversion for IV access or pre-medication if the patient is crashing. Stable patients enter the second branch — narrow vs. wide and regular vs. irregular — for drug therapy.

☐ Own the four stable-tachycardia branches.

• Stable, narrow, regular (likely SVT): vagal maneuvers → adenosine 6 mg → 12 mg → 12 mg.

• Stable, narrow, irregular (likely atrial fibrillation or flutter with variable conduction): rate control with diltiazem or beta-blocker; consider rhythm control and anticoagulation per guidelines if duration < 48 hours or after appropriate workup.

• Stable, wide, regular (treat as VT until proven otherwise): amiodarone 150 mg IV over 10 minutes (may repeat), procainamide, or sotalol; expert consultation; cardioversion if deteriorating.

• Stable, wide, irregular (assume polymorphic VT or pre-excited atrial fibrillation — WPW with afib): avoid AV nodal blockers (CCB, beta-blocker, digoxin, adenosine); expert consultation, magnesium if torsades pattern, cardioversion or defibrillation as the patient evolves.

☐ Master synchronized cardioversion mechanics. Synchronization times the shock to the R wave to avoid the relative refractory period (R-on-T → VF). Energy levels: regular narrow-complex tachycardia (SVT, atrial flutter) 50–100 J biphasic; irregular narrow-complex (atrial fibrillation) 120–200 J biphasic; regular wide-complex (monomorphic VT with pulse) 100 J biphasic. Polymorphic VT cannot be reliably synchronized — defibrillate (unsynchronized) at full energy. Sedate before cardioversion when time permits; do not delay in the truly crashing patient.

☐ Build torsades-specific recognition and management. Torsades de pointes is polymorphic VT in the setting of a long QT interval. Identification on the strip: undulating QRS amplitude that "twists around the baseline" with a long preceding QT. Treatment: magnesium 1–2 g IV/IO. Search for and remove the QT-prolonging cause (hypomagnesemia, hypokalemia, QT-prolonging drugs — many antiemetics, antibiotics, antipsychotics). Pulseless torsades is defibrillated as VF; torsades with a pulse gets magnesium plus the polymorphic VT pathway.

☐ Know the WPW-with-atrial-fibrillation trap. Pre-excited atrial fibrillation (WPW with afib) shows an irregular, wide-complex tachycardia with varying QRS morphology — sometimes very fast (>250). AV nodal blockers (calcium channel blockers, beta-blockers, digoxin, adenosine) preferentially block the AV node and increase conduction down the accessory pathway, which can accelerate the rhythm into VF. Avoid these agents. Procainamide is the classic safer choice; cardioversion is the answer if the patient deteriorates.

☐ Own pacing modalities. Transcutaneous pacing (TCP) is the emergent default — fast to set up using the defibrillator's pacing function and large adhesive pads. Set rate ~ 60–80 bpm, increase output (mA) until electrical capture (pacer spike followed by wide QRS) and then mechanical capture (palpable pulse matching the pacer rate). Sedate the awake patient — TCP is uncomfortable. Transvenous pacing is the more reliable bridge to permanent pacemaker placement, but requires more time, training, and a procedural setting.

☐ Complete the Practice Questions for Part V in your quiz bank. Review every rationale — correct and incorrect.

How to Use Your Templates

☐ Mind Map: Central node = Bradycardia and Tachycardia Algorithms. Main branches: Symptomatic Bradycardia Decision (symptomatic vs. asymptomatic) → Bradycardia Ladder (atropine, pacing, dopamine, epinephrine) → Stable vs. Unstable Tachycardia → Unstable → Synchronized Cardioversion (or defib for polymorphic VT) → Stable, Narrow, Regular (vagal/adenosine) → Stable, Narrow, Irregular (rate control, anticoag) → Stable, Wide, Regular (treat as VT) → Stable, Wide, Irregular (avoid AV nodal blockers) → Torsades (magnesium, QT removal) → Pacing Modalities (TCP, TV).

Comparison Charts:

☐ Chart 1 — Bradycardia Ladder: Atropine, transcutaneous pacing, dopamine infusion, epinephrine infusion; mechanism, dose/range, reliability in Mobitz II and third-degree block, when to escalate, sedation considerations.

☐ Chart 2 — Tachycardia Decision Tree: Stable/unstable, narrow/wide, regular/irregular; first-line therapy in each cell of the matrix, drug doses, electrical alternatives, contraindications.

☐ Chart 3 — Synchronized Cardioversion vs. Defibrillation: Sync (regular SVT, atrial flutter, atrial fibrillation, monomorphic VT with pulse), defib (polymorphic VT, pulseless VT, VF); energy level, when to use which, why polymorphic VT can't be synced, sedation expectations.

☐ Chart 4 — WPW and Pre-Excited Atrial Fibrillation: Recognition (irregular wide-complex with varying morphology), drugs to avoid (CCB, beta-blocker, digoxin, adenosine), drugs/strategies that are safe (procainamide, cardioversion), why AV nodal blockers cause harm.

Cornell Notes:

☐ Page 1 — Cue questions: What is the difference between symptomatic and asymptomatic bradycardia, and what determines treatment? What is the bradycardia ladder, and why does atropine often fail in Mobitz II and third-degree block? What are the energy levels and indications for transcutaneous pacing?

☐ Page 2 — Cue questions: What are the first and second branch points of the tachycardia algorithm, and what therapy follows each path? What are the synchronized cardioversion energy levels for regular narrow-complex, irregular narrow-complex, and regular wide-complex tachycardia? Why is defibrillation rather than synchronized cardioversion used for polymorphic VT?

☐ Page 3 — Cue questions: How do you recognize torsades de pointes, and what is the first-line treatment? Why is adenosine contraindicated in irregular wide-complex tachycardia, and what alternative agents or strategies are safer? Walk through one full SVT scenario from vagal maneuvers through adenosine to electrical therapy.

Week 6 — Part VI: Special Situations

Difficulty: Moderate — Context Critical

What it covers: Part VI covers the cardiac arrest situations that modify the standard algorithm. You will learn the management of cardiac arrest in pregnancy, including left uterine displacement during compressions, the modified hand position (slightly higher on the sternum), the urgent indication for resuscitative hysterotomy (perimortem C-section) by the 4-minute mark if ROSC has not been achieved, and the full ACLS toolkit applied without modification — all the standard drugs and shock energies are used at standard doses, opioid-associated cardiac arrest with the role of naloxone (up to 4 mg IN or 0.4–2 mg IV, repeated as needed) when there is a pulse but no breathing, while standard CPR and the universal arrest algorithm continue if the patient is pulseless, hypothermic cardiac arrest with the principles of "not dead until warm and dead," prolonged resuscitation efforts, withholding additional drug doses and shocks until core temperature rises above ~30 °C, and active rewarming strategies (warm IV fluids, warmed humidified oxygen, ECMO/cardiopulmonary bypass), drowning arrest with the priority of ventilation/oxygenation as the first reversible cause to address, severe asthma arrest with attention to dynamic hyperinflation (auto-PEEP — disconnect from circuit and allow exhalation), tension pneumothorax (needle decompress), and ventilator strategy modifications, anaphylaxis with epinephrine IM 0.3–0.5 mg as the first move (and IV epi infusion in arrest), local anesthetic systemic toxicity (LAST) with intravenous lipid emulsion (intralipid) therapy, electrolyte emergencies including hyperkalemic arrest (calcium, insulin/dextrose, bicarbonate, and dialysis) and the cardiac toxicity patterns (peaked T waves, widened QRS, sine wave), and the integration of these special situations back into the standard algorithm without losing the universal principles.

Print: 1 Mind Map, 3 Comparison Charts, 2 Cornell Notes pages

Study Tasks

☐ Read the Study Guide first — complete the High-Yield Objectives, Key Terms and Definitions, and Concept Overview sections before opening the chapter.

☐ Highlight as you read — follow the Made Easy Highlighting System exactly:

• Blue: Rhythm Recognition — Hyperkalemia ECG progression (peaked T waves → prolonged PR → widened QRS → sine wave), hypothermia ECG (Osborn/J waves at the J point), digoxin toxicity patterns (atrial tachycardia with block, bidirectional VT)

• Orange: Drug Facts — Naloxone 0.4–2 mg IV or 4 mg IN; epinephrine IM 0.3–0.5 mg in anaphylaxis; intralipid (20% lipid emulsion) for LAST — bolus 1.5 mL/kg then infusion 0.25 mL/kg/min; calcium chloride 1 g (or calcium gluconate 3 g) for hyperkalemia or calcium-channel-blocker toxicity; sodium bicarbonate 1 mEq/kg in TCA overdose with QRS widening or in severe acidosis/hyperkalemia; magnesium 2 g in torsades and severe asthma

• Green: Algorithm Steps — Pregnancy: standard ACLS + LUD + 4-minute hysterotomy decision; hypothermia: prolonged CPR, withhold drugs/shocks below ~30 °C, rewarm; opioid: naloxone if breathing absent but pulse present, otherwise standard ACLS with naloxone as adjunct; asthma: disconnect circuit for auto-PEEP, decompress for pneumothorax; anaphylaxis: IM epi first, then airway and IV access; LAST: stop the local anesthetic, intralipid, modified resuscitation

• Yellow: Critical Numbers & Time Windows — Perimortem C-section by 4 minutes from arrest if no ROSC, hypothermia drug-and-shock threshold ~30 °C, naloxone 4 mg IN or 0.4–2 mg IV, epinephrine IM in anaphylaxis 0.3–0.5 mg, intralipid bolus 1.5 mL/kg then 0.25 mL/kg/min, hyperkalemic arrest calcium 1 g chloride / 3 g gluconate, perimortem fundus position at uterine displacement

• Red: Contraindications & Don't-Do's — Don't delay perimortem C-section beyond 4 minutes if standard resuscitation hasn't produced ROSC, don't withhold standard ACLS drugs in pregnancy (they are given at standard doses), don't continue giving epi/shocks in profound hypothermia (let rewarming work first), don't treat opioid arrest with naloxone alone if pulseless — run the standard algorithm with naloxone as adjunct, don't skip needle decompression in suspected tension pneumothorax during asthma arrest

• Purple: Mnemonics & Memory Aids — "Not dead until warm and dead" for hypothermia, "DOPES" (recapped from Part II) for asthma post-intubation deterioration, the perimortem 4-minute rule, "shock first, drugs second" remains true in special situations

☐ Master cardiac-arrest-in-pregnancy modifications. Standard ACLS drugs and shock energies are used at standard doses in pregnancy — there is no dose modification for any ACLS medication. The modifications are mechanical: perform left uterine displacement (manually shift the gravid uterus to the patient's left) to relieve aortocaval compression and improve venous return; place hands slightly higher on the sternum if the gravid uterus distorts the usual landmarks; intubate early (pregnancy is associated with rapid desaturation and difficult airway). The single highest-yield decision is the 4-minute mark: if there is no ROSC by 4 minutes of high-quality resuscitation, prepare for resuscitative hysterotomy (perimortem C-section). Delivering the fetus offloads aortocaval compression, improves maternal venous return, and may produce ROSC.

☐ Lock in opioid-associated cardiac arrest management. The decision rule turns on the pulse. If the patient has a pulse but is not breathing or is hypoventilating, give naloxone (0.4–2 mg IV or 4 mg IN, repeat as needed) and provide ventilation. If the patient is pulseless, run the standard cardiac arrest algorithm with high-quality CPR and the H's and T's; naloxone may be given as an adjunct but does not replace compressions or shocks. Half-life mismatch matters — naloxone is shorter-acting than many opioids, so re-sedation is possible and the patient may need repeat dosing or a continuous infusion.

☐ Own hypothermia resuscitation principles. Severe hypothermia profoundly suppresses metabolism, including the metabolism of resuscitation drugs and the responsiveness of the myocardium to defibrillation. The "not dead until warm and dead" principle drives prolonged resuscitation efforts. Below ~30 °C core temperature, defer additional drug doses and limit defibrillation attempts (often to a single attempt) until rewarming begins. Active core rewarming options include warm IV fluids, warm humidified oxygen, body cavity lavage, and — for the most severe cases — ECMO or cardiopulmonary bypass. Above 30 °C, drug intervals may be extended and shocks resumed; above ~35 °C, full standard ACLS resumes.

☐ Master the asthma-arrest-specific moves. Severe asthma arrest is dominated by air trapping (auto-PEEP) and the risk of tension pneumothorax. If a previously stable intubated asthma patient deteriorates suddenly: disconnect from the ventilator/BVM circuit and allow passive exhalation (releases stacked breaths and auto-PEEP); reassess for tension pneumothorax and decompress with a needle if hemodynamic collapse persists; consider permissive hypercapnia ventilator strategy with low rate and prolonged exhalation time; magnesium 2 g IV may help bronchospasm.

☐ Build anaphylaxis recognition and IM epi as a reflex. Anaphylaxis is suspected with rapid onset of multi-system symptoms after exposure (skin, respiratory, cardiovascular, GI). The first move in any anaphylactic reaction is IM epinephrine 0.3–0.5 mg in the lateral thigh — not IV bolus epi (which is reserved for arrest or refractory shock with appropriate dilution and infusion). Adjuncts: airway management (early intubation if angioedema is progressing), IV fluids, antihistamines, glucocorticoids, and beta-agonists. If the patient progresses to arrest, run the standard algorithm with epinephrine infusion.

☐ Know LAST recognition and intralipid therapy. Local anesthetic systemic toxicity (LAST) presents with neurologic prodrome (perioral numbness, tinnitus, dysarthria, agitation, seizures) followed by cardiovascular collapse (arrhythmias, hypotension, cardiac arrest). Stop the offending local anesthetic. Give 20% intravenous lipid emulsion (intralipid): bolus 1.5 mL/kg over 1 minute, then infusion at 0.25 mL/kg/min. Modify resuscitation by reducing epinephrine doses (high-dose epi may worsen outcomes in LAST); avoid vasopressin, calcium-channel blockers, beta-blockers, and additional local anesthetics. Run prolonged resuscitation — LAST patients can recover after extended efforts.

☐ Own electrolyte-emergency cardiac arrest. Hyperkalemic arrest is the highest-yield: ECG progression peaked T waves → prolonged PR → widened QRS → sine wave → arrest. Treatment: calcium (chloride 1 g IV or gluconate 3 g IV) to stabilize the membrane, insulin (10 units regular IV) plus dextrose to shift K+ intracellularly, sodium bicarbonate in severe acidosis, and definitive removal via dialysis. In active arrest from suspected hyperkalemia, give calcium and bicarb during the resuscitation. Hypokalemia and hypomagnesemia predispose to torsades — replete aggressively.

☐ Complete the Practice Questions for Part VI in your quiz bank. Review every rationale — correct and incorrect.

How to Use Your Templates

☐ Mind Map: Central node = Special Situations in ACLS. Main branches: Pregnancy (LUD, hand position, 4-minute hysterotomy) → Opioid Arrest (pulse-based decision, naloxone vs. standard algorithm) → Hypothermia (prolonged effort, rewarming, drug/shock thresholds) → Drowning (ventilation priority) → Severe Asthma (auto-PEEP disconnect, pneumothorax, magnesium) → Anaphylaxis (IM epi first) → LAST (intralipid, modified resuscitation) → Electrolyte Emergencies (hyperkalemia ECG progression, calcium/insulin/bicarb) → Integration with Standard Algorithm.

Comparison Charts:

☐ Chart 1 — Modifications to Standard Algorithm by Special Situation: Pregnancy, hypothermia, opioid, asthma, anaphylaxis, LAST, hyperkalemia; what stays the same (standard doses, standard shock energies, high-quality CPR), what changes (mechanical adjustments, drug dose modifications, timing thresholds, addition of specific antidotes).

☐ Chart 2 — Antidote/Adjunct Drugs by Scenario: Naloxone (opioid), IM epi (anaphylaxis), intralipid (LAST), calcium/insulin/bicarb (hyperkalemia), magnesium (torsades, severe asthma); dose, route, when to give in the algorithm sequence.

☐ Chart 3 — Hyperkalemia ECG Progression: Peaked T → prolonged PR → widened QRS → sine wave → arrest; recognition at each stage, urgency of treatment, what to give first, when to escalate to dialysis.

Cornell Notes:

☐ Page 1 — Cue questions: What modifications to the standard algorithm are required in cardiac arrest in pregnancy, and what is the 4-minute rule? How does opioid arrest management differ based on whether the patient has a pulse, and why does naloxone alone not replace standard ACLS in the pulseless patient? What are the rewarming and drug/shock thresholds in hypothermic cardiac arrest, and why does "warm and dead" apply?

☐ Page 2 — Cue questions: What is the first move in anaphylaxis, and what is the route, dose, and site? What are the recognition features and treatment of LAST, including the intralipid dose? Walk through the hyperkalemia ECG progression and the four pharmacologic moves (stabilize, shift, remove, dialyze) with their specific drugs.

Week 7 — Part VII: ACS and Stroke

Difficulty: Moderate — Time Critical

What it covers: Part VII covers the time-critical non-arrest emergencies that ACLS-trained providers must recognize and act on within precise time windows. You will learn the recognition of acute coronary syndrome (chest pain or anginal-equivalent symptoms, typical and atypical presentations, populations more likely to present atypically — women, older adults, diabetics), the role of the 12-lead ECG within 10 minutes of arrival, the STEMI recognition criteria (≥ 1 mm ST elevation in 2 contiguous limb leads, or ≥ 2 mm in 2 contiguous precordial leads V2–V3 with sex/age cutoffs, plus new LBBB in the appropriate clinical context), the early ACS bundle (aspirin, nitroglycerin, oxygen if hypoxic, morphine for refractory pain) with the contraindications, the door-to-balloon ≤ 90 minutes target for primary PCI and door-to-needle ≤ 60 minutes for fibrinolytics when PCI is unavailable, the absolute and relative contraindications to fibrinolytic therapy in STEMI, the recognition of acute ischemic stroke using FAST and the more sensitive BEFAST mnemonic (Balance, Eyes, Face, Arms, Speech, Time), the determination of "last known well" time as the single most important historical question, the stroke fibrinolytic windows (≤ 3 hours universal eligibility, 3–4.5 hours extended window with stricter criteria), the mechanical thrombectomy window up to 24 hours in selected patients with large vessel occlusion, the absolute and relative contraindications to stroke fibrinolytics, the role of imaging (non-contrast CT first, CT angiography for LVO selection, CT/MR perfusion for extended-window selection), and the ACLS provider's role in the prehospital and ED phases of these time-critical workflows.

Print: 1 Mind Map, 3 Comparison Charts, 2 Cornell Notes pages

Study Tasks

☐ Read the Study Guide first — complete the High-Yield Objectives, Key Terms and Definitions, and Concept Overview sections before opening the chapter.

☐ Highlight as you read — follow the Made Easy Highlighting System exactly:

• Blue: Rhythm Recognition — STEMI ECG patterns by territory: anterior (V1–V4, LAD), inferior (II, III, aVF, RCA), lateral (I, aVL, V5–V6, LCx), posterior (tall R in V1–V2, ST depression in V1–V3 — confirm with posterior leads), new LBBB in the appropriate clinical context; arrhythmias common in MI (sinus brady in inferior, AV block in inferior, VT/VF in any infarct)

• Orange: Drug Facts — Aspirin 162–325 mg chewed, nitroglycerin SL 0.4 mg q5 min × 3 (avoid in RV infarct or recent PDE-5 inhibitor), morphine for refractory chest pain, heparin per institutional protocol, P2Y12 inhibitor (clopidogrel/ticagrelor/prasugrel) per protocol; tPA/alteplase 0.9 mg/kg (max 90 mg, 10% bolus, 90% over 60 min) for stroke; tenecteplase as alternative

• Green: Algorithm Steps — ACS sequence: symptoms → 12-lead ≤ 10 min → STEMI recognition → bundle (ASA, nitro, O2 if hypoxic, morphine) → reperfusion decision (PCI vs. fibrinolytics) → cath lab. Stroke sequence: BEFAST → last known well → CT non-contrast → fibrinolytic vs. thrombectomy decision → reperfusion

• Yellow: Critical Numbers & Time Windows — Door-to-balloon ≤ 90 minutes for STEMI primary PCI, door-to-needle ≤ 60 minutes for STEMI fibrinolytics, 12-lead ECG within 10 minutes of arrival, fibrinolytic window for ischemic stroke ≤ 3 hours universally, 3–4.5 hours with stricter criteria, mechanical thrombectomy up to 24 hours in selected LVO patients, STEMI ECG criteria ≥ 1 mm in 2 contiguous limb leads or ≥ 2 mm in 2 contiguous precordial leads (V2–V3 with sex/age cutoffs)

• Red: Contraindications & Don't-Do's — Don't give nitroglycerin in RV infarct (right-sided ECG with ST elevation in V4R) or after recent PDE-5 inhibitor; don't give fibrinolytics with active bleeding, recent stroke, recent surgery, or known intracranial pathology; don't give aspirin in true allergy; don't give stroke fibrinolytics outside the time window or with contraindicated comorbidities (recent intracranial hemorrhage, active internal bleeding, recent major surgery, severe uncontrolled hypertension); don't delay stroke imaging beyond door-to-CT targets; don't give oxygen in normoxic ACS (can worsen outcomes)

• Purple: Mnemonics & Memory Aids — FAST (Face, Arms, Speech, Time) — and the more sensitive BEFAST (Balance, Eyes, Face, Arms, Speech, Time) which catches posterior circulation strokes; "Time is muscle" (ACS), "Time is brain" (stroke); MONA was a legacy mnemonic for ACS — current practice is selective and order matters less than indication and timing

☐ Master STEMI recognition. STEMI is defined by ≥ 1 mm ST elevation in two contiguous limb leads, or ≥ 2 mm in two contiguous precordial leads V2–V3 (with sex- and age-specific lower cutoffs in some criteria), or new LBBB in the appropriate clinical context. Anatomic territories: anterior (V1–V4, LAD), inferior (II, III, aVF, RCA), lateral (I, aVL, V5–V6, LCx), posterior (tall R waves in V1–V2 with ST depression — confirmed by posterior leads V7–V9 showing ST elevation). Inferior MI often involves the right ventricle — get a right-sided 12-lead (V4R) and avoid nitroglycerin if RV infarct is present.

☐ Lock in the early ACS bundle and its contraindications. Aspirin 162–325 mg chewed (faster absorption than swallowed) — withhold only in true allergy. Nitroglycerin SL 0.4 mg every 5 minutes up to 3 doses for ongoing chest pain — withhold in suspected RV infarct or recent PDE-5 inhibitor (sildenafil within 24 h, tadalafil within 48 h). Oxygen only if SpO2 < 90% or respiratory distress (routine oxygen in normoxic ACS may worsen outcomes). Morphine for refractory pain. Heparin and a P2Y12 inhibitor per institutional STEMI/NSTEMI protocol.

☐ Own the door-to-balloon and door-to-needle targets. STEMI primary PCI is the preferred reperfusion strategy when door-to-balloon ≤ 90 minutes can be achieved (≤ 120 minutes if transferring from a non-PCI center). When PCI is not available within these windows, fibrinolytic therapy is given with door-to-needle ≤ 60 minutes — assuming no contraindications. The fastest reperfusion wins; the institutional STEMI protocol exists to compress every step from EMS contact through cath lab activation.

☐ Master stroke recognition with FAST and BEFAST. FAST: Face droop, Arm drift, Speech slurred, Time to call. BEFAST adds Balance and Eyes — catching posterior circulation strokes (cerebellar/brainstem) that don't always show face/arm/speech findings. Establish "last known well" — the most recent time the patient was at neurologic baseline. This is the single most important historical question because it sets the eligibility window for fibrinolytics and thrombectomy.

☐ Build the stroke imaging and reperfusion decision. Non-contrast CT first to rule out hemorrhage. CT angiography (CTA) to identify large vessel occlusion (LVO) for thrombectomy candidacy. CT/MR perfusion in the extended window (6–24 hours) to identify salvageable penumbra in selected LVO patients. Fibrinolytic windows: ≤ 3 hours from last known well universally eligible; 3–4.5 hours eligible with stricter exclusion criteria. Mechanical thrombectomy windows up to 24 hours in selected LVO patients meeting perfusion imaging criteria. Match the right intervention to the right window with the right imaging.

☐ Know the absolute contraindications to stroke fibrinolytics. Active bleeding, recent intracranial hemorrhage, recent intracranial or spinal surgery, recent major head trauma, intracranial neoplasm/AVM/aneurysm, severe uncontrolled hypertension (typically > 185/110 mm Hg despite treatment), known bleeding diathesis, active anticoagulation outside the lab thresholds. The relative contraindications expand the list — review them once and revisit them in your final week.

☐ Own the ACLS provider's role in these workflows. Recognize early. Activate STEMI or stroke alert. Capture and transmit the 12-lead ECG within 10 minutes. Establish IV access, draw labs, complete the contraindication checklist. Don't delay imaging or transport. The provider closest to the patient is often the one who saves the most time — and time is muscle and brain.

☐ Complete the Practice Questions for Part VII in your quiz bank. Review every rationale — correct and incorrect.

How to Use Your Templates

☐ Mind Map: Central node = ACS and Stroke. Main branches: ACS Recognition (typical, atypical, populations) → 12-Lead ≤ 10 min → STEMI Criteria and Territories → Early Bundle (ASA, nitro, O2 conditional, morphine) → Reperfusion Decision (PCI vs. fibrinolytics) → Time Windows (door-to-balloon 90 min, door-to-needle 60 min) → Stroke Recognition (FAST/BEFAST) → Last Known Well → Imaging (non-contrast CT, CTA, perfusion) → Reperfusion (fibrinolytics ≤ 3 h universal, ≤ 4.5 h extended; thrombectomy up to 24 h) → Contraindications.

Comparison Charts:

☐ Chart 1 — STEMI Territories and Their Pearls: Anterior (LAD, V1–V4), inferior (RCA, II, III, aVF — watch for RV involvement and nitro caution), lateral (LCx, I, aVL, V5–V6), posterior (tall R V1–V2 with ST depression — confirm with posterior leads); typical complications (e.g., AV block in inferior MI), management nuances.

☐ Chart 2 — Reperfusion Time Windows: Door-to-balloon (STEMI PCI) ≤ 90 minutes, door-to-needle (STEMI fibrinolytics) ≤ 60 minutes, ischemic stroke fibrinolytics ≤ 3 hours universal and ≤ 4.5 hours extended, mechanical thrombectomy up to 24 hours; eligibility criteria, key exclusions, decision triggers.

☐ Chart 3 — Fibrinolytic Contraindications (ACS and Stroke): Absolute (active bleeding, recent ICH, recent major surgery, intracranial pathology, severe HTN), relative (recent minor surgery, anticoagulation, age, BP); how to apply the checklist quickly under time pressure.

Cornell Notes: 

☐ Page 1 — Cue questions: What are the ECG criteria for STEMI in limb leads, precordial leads, and new LBBB? What is the early ACS bundle, what are the doses, and what are the contraindications to nitroglycerin? What are the door-to-balloon and door-to-needle targets, and how do they drive the choice between PCI and fibrinolytics? 

☐ Page 2 — Cue questions: What does BEFAST stand for, and why is it more sensitive than FAST? What are the time windows for ischemic stroke fibrinolytic therapy and mechanical thrombectomy, and what imaging supports each decision? List the absolute contraindications to fibrinolytic therapy in stroke.

Week 8 — Part VIII: Post-ROSC, Termination, and Team Dynamics

Difficulty: Moderate — Outcome Critical

What it covers: Part VIII covers what happens after ROSC and how to lead a code well. You will learn the immediate post-ROSC priorities (airway secured and confirmed, oxygenation/ventilation targets, hemodynamic stabilization, 12-lead ECG, identification of arrest etiology, transport to definitive care), the post-ROSC oxygenation target (SpO2 92–98%, avoid hyperoxia which worsens neurologic outcomes; avoid hypoxia), the post-ROSC ventilation target (normocapnia ETCO2 35–45 mmHg, avoid hyperventilation), the post-ROSC hemodynamic targets (MAP ≥ 65 mmHg, treat hypotension with fluids and vasopressors as needed), the targeted temperature management (TTM) range of 32–36 °C maintained for 24 hours in comatose post-arrest patients with no contraindications, the role of urgent coronary angiography in post-ROSC patients with suspected ACS etiology or STEMI, the criteria for terminating resuscitation in the field and in the hospital and the prognostic role of sustained ETCO2 < 10 mmHg despite quality CPR, the team dynamics framework (clear role assignment, closed-loop communication, knowledge sharing, mutual respect, constructive intervention), the closed-loop communication pattern (order → repeat-back → confirm → report-completion), the importance of avoiding hyperventilation post-ROSC, the family presence and post-event debriefing principles, and the integration of the entire ACLS curriculum into a coordinated team performance under pressure.

Print: 1 Mind Map, 3 Comparison Charts, 2 Cornell Notes pages

Study Tasks

☐ Read the Study Guide first — complete the High-Yield Objectives, Key Terms and Definitions, and Concept Overview sections before opening the chapter.

☐ Highlight as you read — follow the Made Easy Highlighting System exactly:

• Blue: Rhythm Recognition — Post-ROSC 12-lead findings: STEMI patterns triggering urgent cath, arrhythmias common after ROSC (VT/VF, AV block), telemetry vigilance for re-arrest

• Orange: Drug Facts — Vasopressors for post-ROSC hypotension: norepinephrine 0.1–0.5 mcg/kg/min, epinephrine 2–10 mcg/min, dopamine 5–20 mcg/kg/min; antiarrhythmic continuation (amiodarone or lidocaine drip after VF/pVT arrest); sedation/neuromuscular blockade for TTM

• Green: Algorithm Steps — Post-ROSC bundle sequence: airway/oxygenation/ventilation → BP/MAP → 12-lead → identify cause → reperfusion if indicated → TTM if comatose → ICU disposition; closed-loop communication: order → repeat-back → confirm → report-completion

• Yellow: Critical Numbers & Time Windows — Post-ROSC oxygen target SpO2 92–98%, ventilation target ETCO2 35–45 mmHg, MAP target ≥ 65 mmHg, TTM range 32–36 °C for 24 hours, sustained ETCO2 < 10 mmHg despite quality CPR is a poor prognostic sign, debrief best done within hours of the event

• Red: Contraindications & Don't-Do's — Don't hyperventilate post-ROSC (drops cerebral perfusion), don't hyperoxygenate post-ROSC (oxidative neurologic injury), don't accept hypotension below MAP 65, don't skip the post-ROSC 12-lead, don't delay TTM in the comatose post-arrest patient without a contraindication, don't run a code without explicit role assignment

• Purple: Mnemonics & Memory Aids — Closed-loop communication (order → repeat-back → confirm → report-completion), the post-ROSC bundle in order (airway, oxygenation, ventilation, BP, 12-lead, cause, reperfusion, TTM)

☐ Master the post-ROSC bundle in sequence. First: airway secured and confirmed with waveform capnography. Second: oxygenation titrated to SpO2 92–98% — avoid hyperoxia (worsens neurologic outcomes via oxidative injury) and hypoxia. Third: ventilation titrated to normocapnia ETCO2 35–45 mmHg — avoid hyperventilation (cerebral vasoconstriction worsens perfusion). Fourth: hemodynamic stabilization with MAP target ≥ 65 mmHg using fluids and vasopressors (norepinephrine, epinephrine, or dopamine). Fifth: 12-lead ECG to identify acute coronary syndrome and direct urgent cath if STEMI. Sixth: identify and address the precipitating cause from the H's and T's that you started in the arrest. Seventh: targeted temperature management for comatose patients without contraindications. Eighth: ICU disposition.

☐ Lock in TTM principles. Targeted temperature management at 32–36 °C for 24 hours is offered to comatose post-arrest patients without contraindications (e.g., active bleeding, severe coagulopathy, advance directives against). The exact target temperature within the range is institution-specific. Initiate cooling early; maintain steady temperature with active cooling devices; manage shivering with sedation and neuromuscular blockade as needed; rewarm slowly and avoid rebound hyperthermia. The neurologic exam is unreliable during TTM and for at least 72 hours after rewarming — defer prognostication.

☐ Own the post-ROSC reperfusion decision. Post-ROSC patients with STEMI on the 12-lead go to urgent coronary angiography. Patients without STEMI but with high suspicion for an ACS etiology (e.g., shockable initial rhythm, no clear non-cardiac cause) are also typically considered for early angiography. The exact threshold is institutional, but the principle is unchanged: a coronary cause that can be reperfused is the single highest-impact post-ROSC intervention.

☐ Master termination-of-resuscitation considerations. Termination is considered when ROSC has not been achieved despite a sustained, high-quality resuscitation with all reversible causes addressed. Prognostically poor signs include sustained ETCO2 < 10 mmHg despite quality CPR, prolonged downtime without bystander CPR, and unwitnessed arrest. Field termination protocols vary by EMS system; in-hospital termination weighs duration, reversibility, ETCO2 trend, advance directives/code status, and family presence. The decision belongs to the team leader with team input — it is rarely a sole-actor call.

☐ Build team dynamics as a learnable skill. Effective resuscitation teams share five behaviors: clear role assignment (compressor, airway, IV/IO, drugs, recorder, leader), closed-loop communication (order → repeat-back → confirm → report-completion), knowledge sharing (anyone can voice concerns or new information), mutual respect (no shaming, no shouting), and constructive intervention (graded assertiveness when something is wrong — start with a question, escalate to a statement, then a directive). The team leader stays out of hands-on tasks when possible to maintain situational awareness.

☐ Own closed-loop communication as a habit. The four-step pattern: the leader gives a clear, specific order ("Give epi 1 mg IV now"); the receiver repeats it back ("Epi 1 mg IV now"); the leader confirms ("Yes"); the receiver reports completion ("Epi 1 mg IV in"). This loop catches mishearings, dose errors, and missed orders. Build it as muscle memory in low-stakes moments so it survives high-stakes ones.

☐ Know the family presence and debriefing principles. Family presence during resuscitation is supported by current evidence and policy in most settings — when staff are available to support the family and the team can continue without distraction. Post-event debriefing (within hours, ideally) reviews what went well, what could improve, and the emotional impact on the team. Debriefing is a learning tool, not a blame session.

☐ Complete the Practice Questions for Part VIII in your quiz bank. Review every rationale — correct and incorrect.

How to Use Your Templates

☐ Mind Map: Central node = Post-ROSC Care, Termination, and Team Dynamics. Main branches: Post-ROSC Bundle (airway, oxygenation, ventilation, BP, 12-lead, cause, reperfusion, TTM, ICU) → Oxygenation/Ventilation Targets (SpO2 92–98%, ETCO2 35–45) → Hemodynamic Targets (MAP ≥ 65) → TTM (32–36 °C × 24 h, contraindications) → Reperfusion (STEMI → cath) → Termination Criteria (ETCO2 trend, downtime, advance directives) → Team Dynamics (roles, closed-loop, knowledge sharing, mutual respect, constructive intervention) → Family Presence and Debriefing.

Comparison Charts:

☐ Chart 1 — Post-ROSC Targets: SpO2, ETCO2, MAP, temperature; target value, why it matters, monitoring tool, intervention if outside target.

☐ Chart 2 — Code Team Roles: Team leader, compressor, airway, IV/IO/drugs, recorder, defibrillator operator, family liaison; primary tasks, communication expectations, when to rotate.

☐ Chart 3 — Closed-Loop Communication vs. Open-Loop: Order, repeat-back, confirm, report-completion; common errors when steps are skipped, examples in code situations, why each step prevents specific errors.

Cornell Notes:

☐ Page 1 — Cue questions: What is the post-ROSC bundle in sequence, and what are the specific targets for oxygenation, ventilation, and MAP? What is targeted temperature management — the range, duration, and contraindications? When and why does post-ROSC patient go to urgent coronary angiography?

☐ Page 2 — Cue questions: What are the criteria for terminating resuscitation, and what role does ETCO2 trend play in the decision? What are the four steps of closed-loop communication, and what error does each step prevent? Name the five team behaviors that distinguish high-performing resuscitation teams.

Week 9 — Final Review & Exam Simulation

Your final week is not about learning new material — it is about consolidating everything you have built and proving it under exam conditions. Work through the days in order; if a topic feels solid on its scheduled day, move forward — do not skip ahead.

Day 1 — Rhythm Recognition Drill

☐ Re-draw the Part I Mind Map from memory. Check it against your original.

☐ Pull up 30+ rhythm strips (from your quiz bank, the book, or any rhythm-strip drill source) and run the 6-step interpretation method on each: rate → regularity → P waves → PR → QRS → relationship. Time yourself: target ≤ 15 seconds per strip.

☐ Drill the highest-yield rhythm distinctions: Wenckebach vs. Mobitz II, monomorphic VT vs. polymorphic VT vs. torsades, coarse VF vs. fine VF vs. asystole, atrial flutter vs. atrial fibrillation vs. SVT.

Day 2 — Pharmacology Drill

☐ Re-draw the Part III Mind Map from memory.

☐ Build a personal drug card from memory for every ACLS medication: name, indication, dose, route, frequency, max, key contraindication. Compare against your Part III chart.

☐ Drill the four highest-yield drugs out loud: epinephrine (every cardiac arrest, 1 mg q3–5 min), amiodarone (300 mg → 150 mg in refractory VF/pVT), atropine (1 mg q3–5 min, max 3 mg in symptomatic bradycardia), adenosine (6 mg → 12 mg → 12 mg in stable regular SVT).

☐ Quiz yourself on time windows: door-to-balloon, door-to-needle, stroke fibrinolytic windows, thrombectomy window.

Day 3 — Algorithm Walk-Through

☐ Walk through the VF/pVT algorithm from start through three full cycles, naming every action: shock, CPR, drug, energy level, when amiodarone enters.

☐ Walk through the asystole/PEA algorithm naming every action and the H's and T's reversible-cause search.

☐ Walk through the symptomatic bradycardia ladder: atropine → pacing → dopamine or epi infusion.

☐ Walk through the tachycardia decision tree: stable vs. unstable, then narrow vs. wide and regular vs. irregular, with the first-line agent or electrical therapy in each cell.

Day 4 — Special Situations and Scenario Drills

☐ Re-do any quiz bank questions you got wrong across Parts IV, V, and VI. Focus on the rationales.

☐ Drill the special-situations modifications: pregnancy 4-minute rule, hypothermia "warm and dead," opioid pulse-based decision, anaphylaxis IM epi first, LAST intralipid, hyperkalemia ECG progression and treatment.

☐ Run three scenario simulations from start to finish, talking yourself through each: a witnessed VF arrest, an inferior STEMI with bradycardia, an acute ischemic stroke at 2 hours from last known well.

Day 5 — ACS, Stroke, and Post-ROSC

☐ Re-do any quiz bank questions you got wrong from Parts VII and VIII.

☐ Drill STEMI territories and contraindications to nitroglycerin and fibrinolytics.

☐ Drill BEFAST recognition, last known well, fibrinolytic windows (≤ 3 h universal, ≤ 4.5 h extended), thrombectomy window (up to 24 h).

☐ Walk through the post-ROSC bundle in order and name every target: SpO2 92–98%, ETCO2 35–45, MAP ≥ 65, TTM 32–36 °C × 24 h.

☐ Practice closed-loop communication out loud with a study partner or in front of a mirror: order → repeat-back → confirm → report-completion.

Day 6 — Common Mistakes and Self-Assessment

☐ Review the Common Mistakes, Rapid Review, and Self-Assessment Checklist sections for your two weakest Parts.

☐ Re-do the Cornell Notes cue columns for your two weakest Parts — cover the right-hand notes and answer from memory.

☐ Drill the three highest-yield decision points one more time: shockable vs. non-shockable arrest pathway, stable vs. unstable in tachycardia, contraindications to fibrinolytic therapy.

Day 7 — Full-Length Exam Simulation

☐ Take the full-length ACLS practice exam included with this book. Complete it in one sitting, timed, as close to real exam conditions as possible.

☐ Review your emailed score report. Identify which Parts you missed most and spend any remaining time on those Parts' Rapid Review and application scenarios only.