ACLS & Cardiac Arrest — Part 2: Cardiac Arrest Algorithms & ACLS Pharmacotherapy
VF/pVT and asystole/PEA algorithms, H's and T's reversible causes, epinephrine, amiodarone, lidocaine, sodium bicarbonate, calcium, magnesium, lipid emulsion, and advanced airway management during arrest.
1. Cardiac Arrest Algorithm — Overview
The cardiac arrest algorithm is initiated when a patient is confirmed to be in cardiac arrest (unresponsive, no normal breathing, no pulse). The algorithm immediately bifurcates based on whether the presenting rhythm is shockable (ventricular fibrillation or pulseless ventricular tachycardia) or non-shockable (asystole or pulseless electrical activity). The universal first step, regardless of rhythm, is the initiation of high-quality CPR.1 2 3
1.1 Initial Assessment Steps (All Rhythms)
- Confirm cardiac arrest: Unresponsive, no normal breathing (agonal gasps are NOT normal breathing), no definite pulse within 10 seconds
- Activate emergency response system (call code / call 911)
- Begin CPR: Start chest compressions immediately (push hard, push fast: 100–120/min, 5–6 cm depth, full recoil)
- Attach defibrillator/monitor: Apply pads; analyze rhythm as soon as possible
- Establish IV/IO access: Peripheral IV preferred; intraosseous (IO) if IV not rapidly obtainable (within 1–2 minutes)
- Apply waveform capnography if advanced airway is placed
2. Shockable Rhythms: VF/pVT Algorithm
Ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT) are the rhythms most amenable to treatment. Survival from witnessed VF/pVT with prompt defibrillation and high-quality CPR can exceed 50% in optimized systems.1 2 4
2.1 Step-by-Step VF/pVT Algorithm
| Step | Cycle | Action | Details |
|---|---|---|---|
| 1 | — | Identify VF/pVT on monitor | Disorganized high-frequency waveform (VF) or organized wide-complex tachycardia without pulse (pVT) |
| 2 | — | Deliver first shock | Biphasic: 120–200 J (device-specific); monophasic: 360 J |
| 3 | Cycle 1 | Immediately resume CPR for 2 minutes | Do NOT pause to recheck rhythm after shock; begin compressions within 5 seconds of shock |
| 4 | Cycle 1 | Establish IV/IO access | During CPR; do not interrupt compressions |
| 5 | — | Rhythm check at 2 minutes | Brief pause (<10 seconds); analyze rhythm |
| 6 | — | If still VF/pVT: Deliver second shock | Same or escalated energy |
| 7 | Cycle 2 | Immediately resume CPR for 2 minutes | |
| 8 | Cycle 2 | Epinephrine 1 mg IV/IO | Administer as soon as feasible after second shock (do not delay CPR); repeat every 3–5 minutes thereafter |
| 9 | — | Rhythm check at 2 minutes | Brief pause |
| 10 | — | If still VF/pVT: Deliver third shock | Same or escalated energy |
| 11 | Cycle 3 | Immediately resume CPR for 2 minutes | |
| 12 | Cycle 3 | Amiodarone 300 mg IV/IO bolus OR Lidocaine 1–1.5 mg/kg IV/IO | First dose of antiarrhythmic after third shock |
| 13 | — | Continue 2-minute cycles | Rhythm check → shock if VF/pVT → CPR → medications |
| 14 | Subsequent | Amiodarone 150 mg IV/IO (second dose) OR Lidocaine 0.5–0.75 mg/kg IV/IO (repeat) | May give one additional dose of amiodarone; lidocaine may be repeated every 5–10 minutes to max 3 mg/kg |
| 15 | All cycles | Search for and treat reversible causes (H’s and T’s) | Continuous reassessment throughout resuscitation |
2.2 Key Principles for VF/pVT Management
- Defibrillation is the definitive treatment — medications are adjuncts to defibrillation, not substitutes
- Minimize peri-shock pauses: Continue compressions while defibrillator charges; immediately resume after shock
- Epinephrine timing in VF/pVT: Give after the second shock (not immediately); early epinephrine in shockable rhythms has not shown benefit and may be harmful if given before the first defibrillation attempt
- Antiarrhythmics are given after the third shock: This reflects the evidence base from the ALPS trial (amiodarone vs lidocaine vs placebo) 5
- If rhythm becomes non-shockable at any point: Transition to the asystole/PEA algorithm
- If ROSC is achieved: Begin immediate post-cardiac arrest care
3. Non-Shockable Rhythms: Asystole/PEA Algorithm
Asystole and pulseless electrical activity (PEA) carry a worse prognosis than VF/pVT. Survival depends primarily on identification and treatment of the underlying reversible cause. Defibrillation has no role in these rhythms.1 2 3
3.1 Distinguishing Asystole from PEA
| Rhythm | ECG Appearance | Key Features |
|---|---|---|
| Asystole | Flat line (absence of discernible electrical activity) | Confirm in two leads; ensure leads are connected and gain is adequate; rule out fine VF |
| PEA | Organized electrical activity (may appear normal or abnormal) without a palpable pulse | Wide variety of ECG patterns possible; narrow-complex PEA has better prognosis than wide-complex PEA; organized PEA with higher rate has better prognosis |
Pseudo-PEA: Some patients in apparent PEA have detectable cardiac output on echocardiography or arterial line monitoring but insufficient blood pressure to generate a palpable pulse. This “pseudo-PEA” has a better prognosis and warrants aggressive treatment of underlying causes and vasopressor support.
3.2 Step-by-Step Asystole/PEA Algorithm
| Step | Cycle | Action | Details |
|---|---|---|---|
| 1 | — | Identify asystole or PEA | No shockable rhythm identified |
| 2 | Cycle 1 | Begin/continue high-quality CPR | 30:2 with bag-mask or continuous compressions with advanced airway |
| 3 | Cycle 1 | Epinephrine 1 mg IV/IO as soon as possible | In non-shockable rhythms, epinephrine should be given as early as feasible; early administration is associated with improved ROSC and survival 6 |
| 4 | Cycle 1 | Establish IV/IO access if not already done | |
| 5 | Cycle 1 | Aggressively search for reversible causes (H’s and T’s) | This is the most critical step — survival depends on finding and treating the cause |
| 6 | — | Rhythm check at 2 minutes | Brief pause (<10 seconds) |
| 7 | — | If asystole/PEA continues: Resume CPR | |
| 8 | Cycle 2 | Epinephrine 1 mg IV/IO every 3–5 minutes | Continue throughout resuscitation |
| 9 | — | If rhythm changes to VF/pVT: Transition to shockable algorithm | Deliver shock, then resume CPR |
| 10 | All | Consider advanced airway | Endotracheal intubation or supraglottic airway; should not delay CPR or other critical interventions |
| 11 | All | Continuously reassess for reversible causes | Point-of-care ultrasound, laboratory values, history |
3.3 Key Principles for Asystole/PEA Management
- Epinephrine is given immediately (not delayed until after shocks, since there are no shocks to deliver) — the earlier epinephrine is given in non-shockable rhythms, the better the outcome 6
- Defibrillation is NOT indicated for asystole or PEA; shocking asystole is futile and delays CPR
- Do not treat fine VF as asystole: If there is any doubt about whether the rhythm is asystole vs fine VF, treat as VF (defibrillate)
- PEA with an organized, narrow-complex rhythm is more likely to have a treatable cause; intensify the search for H’s and T’s
- Antiarrhythmics have no role in asystole or PEA
4. Reversible Causes: The H’s and T’s
Identification and treatment of reversible causes is a critical component of every cardiac arrest resuscitation. The mnemonic “H’s and T’s” provides a systematic framework for this assessment. In PEA arrest especially, failure to identify the underlying cause is the most common reason for resuscitation failure.1 2 3
4.1 The H’s
| Cause | Clues to Diagnosis | Treatment During Arrest |
|---|---|---|
| Hypovolemia | History of bleeding, trauma, GI hemorrhage, ruptured AAA, ectopic pregnancy; flat neck veins; narrow-complex rapid PEA; ultrasound showing empty ventricles | Aggressive volume resuscitation with crystalloid and blood products; activate massive transfusion protocol if hemorrhagic; source control (surgery, IR) |
| Hypoxia | History of respiratory distress, airway obstruction, drowning, asthma; cyanosis | Secure airway with endotracheal intubation; confirm placement with capnography; provide 100% FiO2; ensure bilateral breath sounds (rule out right mainstem, pneumothorax) |
| Hydrogen ion excess (acidosis) | History of prolonged arrest, diabetes (DKA), renal failure, toxic ingestion (methanol, ethylene glycol); pre-existing metabolic acidosis | Ensure adequate ventilation; sodium bicarbonate 1 mEq/kg IV if severe preexisting metabolic acidosis, prolonged arrest, or specific toxicologic indications; do NOT use bicarbonate empirically |
| Hyperkalemia | History of renal failure, dialysis, potassium-sparing diuretics, ACE inhibitors, rhabdomyolysis; ECG showing peaked T waves, wide QRS, sine wave pattern | Calcium chloride 10% 1–2 g IV (or calcium gluconate 3 g IV) for membrane stabilization; sodium bicarbonate 50 mEq IV; insulin 10 units regular IV + dextrose 25 g IV; albuterol nebulized 10–20 mg; consider emergent dialysis |
| Hypokalemia | History of diuretics, GI losses, poor intake; ECG showing flattened T waves, U waves, prolonged QT | Potassium chloride 40 mEq IV over 10–20 minutes (faster infusion acceptable during arrest through central line); magnesium sulfate 2 g IV (hypokalemia is often accompanied by hypomagnesemia) |
| Hypothermia | History of environmental exposure, submersion, intoxication with cold exposure; core temperature <30°C | Active external and internal rewarming; withhold medications and limit defibrillation attempts to one until core temperature >30°C; full resuscitation protocols once >30°C; extend resuscitation — “not dead until warm and dead”; ECMO/ECPR for severe hypothermia |
| Hypoglycemia | History of diabetes, insulin use, sepsis; point-of-care glucose | Dextrose 50% 25–50 g IV (D50W); recheck glucose |
4.2 The T’s
| Cause | Clues to Diagnosis | Treatment During Arrest |
|---|---|---|
| Tension pneumothorax | History of trauma, central line placement, positive-pressure ventilation, COPD, asthma; unilateral absent breath sounds; tracheal deviation (late sign); distended neck veins; difficulty ventilating; ultrasound showing absent lung sliding | Immediate needle decompression (14-gauge angiocatheter, 2nd intercostal space midclavicular line or 4th–5th intercostal space anterior axillary line) followed by finger/tube thoracostomy; do NOT delay treatment for imaging |
| Cardiac tamponade | History of penetrating trauma, pericarditis, malignancy, post-cardiac surgery, aortic dissection; distended neck veins; muffled heart sounds; ultrasound showing pericardial effusion with RV diastolic collapse | Emergency pericardiocentesis (ultrasound-guided subxiphoid approach preferred); emergency thoracotomy if traumatic etiology and available expertise |
| Toxins/tablets (poisoning) | History of ingestion, substance abuse, medication bottles; toxidromes; specific ECG patterns (wide QRS for sodium channel blockers, prolonged QT for various agents) | Specific antidotes (see Section 4.3 below); sodium bicarbonate for sodium channel blockade (TCA, flecainide); naloxone for opioids; lipid emulsion for local anesthetic toxicity; digoxin-specific antibodies for digoxin toxicity; glucagon/high-dose insulin for beta-blocker/CCB toxicity |
| Thrombosis — coronary | History suggestive of acute coronary syndrome; ST-segment changes on monitor; prior cardiac history; witnessed VF arrest | Treat per ACLS algorithm (VF is the most common initial rhythm in acute MI arrest); if ROSC achieved, emergent coronary angiography and PCI; consider fibrinolytics if PCI not available |
| Thrombosis — pulmonary (massive PE) | History of immobilization, recent surgery, malignancy, DVT, hormonal therapy; acute right heart failure signs; ultrasound showing RV dilation and septal bowing; sudden PEA with narrow complex; abrupt ETCO2 drop | Systemic thrombolysis during CPR: alteplase (tPA) 50 mg IV bolus (may repeat once); tenecteplase weight-based dosing is an alternative; continue CPR for at least 60–90 minutes after thrombolysis to allow drug effect; surgical embolectomy or catheter-directed therapy if available; ECPR as bridge |
4.3 Toxicologic Causes — Specific Antidotes During Cardiac Arrest
| Toxin/Drug Class | ECG/Clinical Features | Specific Treatment During Arrest |
|---|---|---|
| Tricyclic antidepressants (TCAs) | Wide QRS (>100 ms), rightward terminal 40-ms axis, sinus tachycardia, seizures | Sodium bicarbonate 1–2 mEq/kg IV bolus; repeat until QRS narrows; target serum pH 7.50–7.55; hypertonic saline 100 mL of 3% if refractory |
| Sodium channel blockers (flecainide, propafenone, cocaine) | Wide QRS, Brugada-pattern ECG | Sodium bicarbonate 1–2 mEq/kg IV bolus; repeat as needed; lipid emulsion for local anesthetic and some sodium channel blocker toxicity |
| Beta-blockers | Bradycardia, hypotension, wide QRS, cardiogenic shock | Glucagon 3–10 mg IV bolus, then 3–5 mg/hr infusion; high-dose insulin (1 unit/kg bolus + 1–10 units/kg/hr infusion with dextrose); vasopressors; consider lipid emulsion; IV calcium for concurrent calcium channel blocker ingestion |
| Calcium channel blockers | Bradycardia, hypotension, hyperglycemia | High-dose insulin (1 unit/kg bolus + 1–10 units/kg/hr) with dextrose and potassium monitoring; calcium chloride 1–2 g IV (or calcium gluconate 3–6 g IV); vasopressors; consider lipid emulsion; methylene blue for refractory vasoplegia |
| Digoxin | Bidirectional VT, atrial tachycardia with block, regularized atrial fibrillation, bradyarrhythmias, hyperkalemia | Digoxin-specific antibody fragments (Fab): 10–20 vials IV for acute life-threatening ingestion (each vial binds 0.5 mg digoxin); magnesium sulfate 2 g IV; avoid calcium (controversial — traditional teaching advises against calcium in digoxin toxicity due to risk of “stone heart,” but recent evidence suggests calcium may be safer than previously believed; use only if concurrent hyperkalemia is immediately life-threatening) |
| Local anesthetics (bupivacaine, ropivacaine) | Rapid CNS toxicity → seizures → cardiovascular collapse → cardiac arrest; wide QRS; VF or asystole | Lipid emulsion therapy (20% Intralipid): 1.5 mL/kg IV bolus over 1 minute, followed by 0.25 mL/kg/min infusion; may repeat bolus 1–2 times at 5-minute intervals; maximum total dose 12 mL/kg; continue infusion for at least 10 minutes after hemodynamic stability; avoid propofol (also a lipid but insufficient lipid load and added cardiac depressant) |
| Opioids | Respiratory depression → hypoxia → arrest; miosis; history of opioid use | Naloxone 2 mg IV/IO/IM/IN; may repeat; during cardiac arrest, naloxone is an adjunct — high-quality CPR and standard ACLS remain the priority; naloxone alone does not reverse cardiac arrest |
| Organophosphates/nerve agents | Cholinergic toxidrome (SLUDGE/DUMBELS); bradycardia; bronchospasm; bronchorrhea | Atropine 2–4 mg IV (much higher doses than standard ACLS); repeat every 3–5 minutes; pralidoxime 1–2 g IV over 15–30 minutes; aggressive airway suctioning |
5. ACLS Pharmacotherapy — Detailed Drug Reference
5.1 Epinephrine
Epinephrine is the cornerstone vasopressor in cardiac arrest, recommended for all cardiac arrest rhythms.1 2 6 7
| Parameter | Detail |
|---|---|
| Mechanism | Alpha-1 adrenergic effects increase systemic vascular resistance, augmenting aortic diastolic pressure and coronary perfusion pressure during CPR; beta-1 effects increase myocardial contractility and heart rate |
| Dose — cardiac arrest | 1 mg (1 mL of 1:1,000 or 10 mL of 1:10,000 or 1 mg/mL) IV/IO every 3–5 minutes |
| Route | IV or IO; endotracheal administration is no longer recommended (unreliable absorption) |
| Timing — shockable rhythms (VF/pVT) | Administer after the second shock (during or after CPR cycle 2); then every 3–5 minutes |
| Timing — non-shockable rhythms (asystole/PEA) | Administer as early as possible; early epinephrine in non-shockable rhythms improves ROSC and survival to discharge |
| Key trial — PARAMEDIC2 | Randomized, double-blind, placebo-controlled trial (n=8,014); epinephrine vs placebo for OHCA. Epinephrine significantly improved 30-day survival (3.2% vs 2.4%; OR 1.39; p=0.02) but no significant difference in survival with favorable neurologic outcome (2.2% vs 1.9%). Confirmed that epinephrine improves ROSC rates (36.3% vs 11.7%) 7 |
| Concerns | Beta-adrenergic effects may increase myocardial oxygen demand and worsen post-ROSC myocardial dysfunction; may impair cerebral microcirculation; PARAMEDIC2 showed trend toward more survivors with poor neurologic outcomes in epinephrine group |
| High-dose epinephrine | NOT recommended; multiple trials showed no survival benefit and potential harm from high-dose (0.1–0.2 mg/kg) epinephrine 1 |
5.2 Vasopressin
| Parameter | Detail |
|---|---|
| Mechanism | Non-adrenergic peripheral vasoconstrictor (V1 receptor agonist); increases coronary and cerebral perfusion pressure |
| Historical dose | 40 units IV, single dose, as alternative to first or second dose of epinephrine |
| Current recommendation | No longer recommended as a replacement for epinephrine in cardiac arrest. Removed from the cardiac arrest algorithm based on evidence showing no advantage over epinephrine. May be combined with epinephrine, but this has not demonstrated superiority over epinephrine alone 1 2 |
5.3 Amiodarone
Amiodarone is the first-line antiarrhythmic for shock-refractory VF/pVT.1 2 5
| Parameter | Detail |
|---|---|
| Mechanism | Class III antiarrhythmic (potassium channel blocker) with additional sodium channel, calcium channel, and beta-blocking properties |
| First dose | 300 mg IV/IO bolus (may be diluted in 20 mL D5W or given undiluted) |
| Second dose | 150 mg IV/IO bolus |
| Timing | First dose after third shock (during CPR cycle 3); second dose may be given in a subsequent cycle |
| Maximum dose during arrest | 450 mg total (300 mg + 150 mg) |
| Post-ROSC infusion | If amiodarone was effective during arrest: 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours (total 150 mg over first 6 hours + 540 mg over next 18 hours = 690 mg/24 hours) |
| Key trial — ALPS | Amiodarone, Lidocaine, or Placebo in OHCA (n=3,026). Amiodarone and lidocaine did not significantly improve overall survival to hospital discharge compared with placebo. In the pre-specified subgroup of witnessed arrests (bystander-witnessed VF/pVT), amiodarone showed improved survival to hospital discharge (27.7% vs 24.4% vs 16.6% for placebo) 5 |
| Adverse effects | Hypotension (from vasodilation and negative inotropy — mainly with the older IV formulation containing polysorbate 80; the newer aqueous formulation has fewer hemodynamic effects); bradycardia; QT prolongation |
5.4 Lidocaine
Lidocaine is an acceptable alternative to amiodarone for shock-refractory VF/pVT.1 5
| Parameter | Detail |
|---|---|
| Mechanism | Class IB antiarrhythmic (sodium channel blocker); suppresses ventricular ectopy and raises VF threshold |
| First dose | 1–1.5 mg/kg IV/IO |
| Repeat doses | 0.5–0.75 mg/kg IV/IO every 5–10 minutes |
| Maximum dose | 3 mg/kg total |
| Post-ROSC infusion | 1–4 mg/min (if lidocaine was effective during arrest) |
| Key evidence | ALPS trial showed lidocaine was comparable to amiodarone for survival to hospital discharge. Some EMS systems prefer lidocaine due to familiarity and lower cost. Lidocaine may be preferred in prolonged arrests where amiodarone’s negative hemodynamic effects are a concern 5 |
| Adverse effects | Seizures (at toxic levels >5 mcg/mL); altered mental status; bradycardia; avoid in patients with high-degree AV block |
5.5 Sodium Bicarbonate
| Parameter | Detail |
|---|---|
| Mechanism | Alkalinizing agent; buffers hydrogen ions; provides sodium load |
| Dose | 1 mEq/kg (typically 50 mEq = 1 ampule of 8.4% solution) IV slow push |
| Repeat | 0.5 mEq/kg every 10 minutes as needed, guided by arterial blood gas when available |
| Specific indications during arrest | Hyperkalemia (shifts potassium intracellularly); tricyclic antidepressant/sodium channel blocker overdose (sodium load overcomes sodium channel blockade + alkalinization enhances protein binding); preexisting metabolic acidosis (known preexisting non-anion gap acidosis, renal tubular acidosis); prolonged arrest (after extended resuscitation, only after ensuring adequate ventilation) |
| NOT routinely indicated | Routine use in cardiac arrest is NOT recommended; the primary treatment for acidosis during arrest is adequate ventilation and restoration of perfusion (via high-quality CPR and ROSC) 1 2 |
| Cautions | Produces CO2 (which freely crosses cell membranes and may paradoxically worsen intracellular acidosis if ventilation is inadequate); inactivates catecholamines and calcium if administered through the same line; may cause hypernatremia and hyperosmolality |
5.6 Calcium
| Parameter | Detail |
|---|---|
| Formulations and doses | Calcium chloride 10%: 1–2 g (10–20 mL) IV slow push over 2–5 minutes (preferred in cardiac arrest — provides 3x more elemental calcium per volume); Calcium gluconate 10%: 3–6 g (30–60 mL) IV — requires hepatic metabolism to release ionized calcium, slower onset |
| Specific indications during arrest | Hyperkalemia (membrane stabilization — first-line treatment along with defibrillation); calcium channel blocker overdose (overcomes receptor blockade; may require high-dose calcium — up to 5–10 g CaCl2); hypermagnesemia (reverses neuromuscular blockade); hypocalcemia (post-massive transfusion, citrate toxicity) |
| NOT routinely indicated | Routine calcium administration in cardiac arrest has NOT been shown to improve outcomes and is not recommended 1 |
| Cautions | Calcium chloride is a severe vesicant — ideally given through a central line or large-bore peripheral IV; calcium chloride should not be mixed with sodium bicarbonate (precipitation); in digoxin toxicity, calcium administration is controversial (see toxicology section) |
5.7 Magnesium Sulfate
| Parameter | Detail |
|---|---|
| Dose | 1–2 g IV/IO diluted in 10 mL D5W, administered over 5–20 minutes (during arrest, may be given as rapid IV push) |
| Primary indication | Torsades de pointes (polymorphic VT with prolonged QT): Magnesium is the first-line treatment; administer 1–2 g IV push; highly effective |
| Other indications | Documented or suspected hypomagnesemia; refractory VF (empiric use is reasonable); accompaniment to potassium replacement in hypokalemia |
| NOT effective for | Magnesium does not terminate monomorphic VT or standard VF; routine empiric use in cardiac arrest is not recommended 1 |
5.8 Lipid Emulsion Therapy (Intralipid)
| Parameter | Detail |
|---|---|
| Formulation | 20% lipid emulsion (e.g., Intralipid 20%) |
| Mechanism | “Lipid sink” — sequesters lipophilic toxins from tissue binding sites; also provides fatty acid substrate for myocardial metabolism; may reverse mitochondrial dysfunction |
| Bolus dose | 1.5 mL/kg IV over 1 minute (approximately 100 mL for a 70-kg adult) |
| Infusion | 0.25 mL/kg/min after bolus |
| Repeat bolus | May repeat bolus 1–2 times at 5-minute intervals if cardiovascular instability persists |
| Maximum total dose | Approximately 12 mL/kg (approximately 840 mL for a 70-kg adult) |
| Primary indication | Local anesthetic systemic toxicity (LAST): bupivacaine, ropivacaine, lidocaine toxicity causing cardiovascular collapse or cardiac arrest; this is the most evidence-supported indication 8 |
| Extended indications | Case reports and series support use in overdose from other lipophilic drugs: tricyclic antidepressants, calcium channel blockers (verapamil, diltiazem), beta-blockers (propranolol), and other lipophilic xenobiotics |
| Cautions | Do NOT use propofol as a substitute for lipid emulsion (propofol contains lipid but in insufficient quantity and adds cardiac depressant effects); lipid emulsion may interfere with laboratory assays; may cause pancreatitis at high doses |
6. Advanced Airway Management During Cardiac Arrest
6.1 Timing of Advanced Airway Placement
The optimal timing of advanced airway placement during cardiac arrest remains debated. Current evidence and consensus recommendations:1 2 9
- Bag-mask ventilation is a reasonable initial airway strategy and may be continued throughout the resuscitation
- Advanced airway placement (endotracheal intubation or supraglottic airway) should NOT take priority over high-quality CPR and defibrillation
- If bag-mask ventilation is adequate, deferring advanced airway placement is reasonable
- If advanced airway placement is pursued, it should be performed by experienced providers with minimal interruption to compressions
6.2 Supraglottic Airway vs Endotracheal Intubation
| Feature | Supraglottic Airway (SGA) | Endotracheal Tube (ETT) |
|---|---|---|
| Ease of placement | Easier; higher first-pass success rate; less training required | More difficult; requires direct or video laryngoscopy; skill-dependent |
| Interruption to CPR | Minimal (can be placed during compressions) | May require brief pause in compressions for visualization |
| Airway protection | Incomplete seal; does not fully protect against aspiration | Cuffed tube provides definitive airway protection |
| Ventilation reliability | Adequate in most cases; some air leak at high airway pressures | Most reliable ventilation with cuffed seal |
| ETCO2 reliability | Less reliable (air leak around device may lower measured ETCO2) | Most reliable ETCO2 measurement |
| Key trial evidence | AIRWAYS-2 trial (n=9,296): SGA (i-gel) vs ETT for OHCA showed no significant difference in 30-day functional outcome (supraglottic airway non-inferior); PART trial (n=3,004): laryngeal tube vs ETT for OHCA showed significantly better 72-hour survival with laryngeal tube 9 | |
| Current recommendation | Either SGA or ETT is acceptable; SGA may be preferred when intubation expertise is limited or when intubation would cause prolonged interruption to CPR 1 2 |
6.3 Ventilation After Advanced Airway Placement
| Parameter | Recommendation |
|---|---|
| Rate | 1 breath every 6 seconds (10 breaths/min) |
| Tidal volume | Sufficient to produce visible chest rise (approximately 500–600 mL; avoid excessive volumes) |
| Compression coordination | Continuous chest compressions; ventilations are delivered asynchronously (no pause for breaths) |
| FiO2 | 100% during arrest; titrate to SpO2 92–98% after ROSC |
| ETCO2 monitoring | Continuous waveform capnography for all patients with an advanced airway; confirms placement and monitors CPR quality |
| Hyperventilation avoidance | A designated team member should coach the ventilator operator; use a timing device if available; hyperventilation is consistently the most common ventilation error during resuscitation |
6.4 Confirmation of Advanced Airway Placement
| Method | Reliability | Notes |
|---|---|---|
| Waveform capnography (ETCO2) | Gold standard | Persistent waveform confirms tracheal placement; note: during cardiac arrest, ETCO2 may be very low (<10 mmHg) even with correct placement due to low pulmonary blood flow — absence of waveform does not always indicate esophageal placement |
| Direct visualization | Reliable (for ETT) | Visualize tube passing through vocal cords |
| Bilateral breath sounds | Supportive | Auscultate bilateral axillae and epigastrium; absence of epigastric sounds supports tracheal placement |
| Chest rise | Supportive | Bilateral symmetric chest rise with ventilation |
| Tube misting | Unreliable | Condensation in tube; neither sensitive nor specific |
| Esophageal detector device | Supportive | Bulb or syringe aspiration test; less reliable during cardiac arrest |
7. Vascular Access During Cardiac Arrest
7.1 IV vs IO Access
| Feature | Peripheral IV | Intraosseous (IO) |
|---|---|---|
| First-line | Yes — attempt peripheral IV first if rapidly obtainable | Second-line — use if IV access cannot be established within 1–2 minutes |
| Common IO sites | — | Proximal tibia (most common); proximal humerus (faster drug delivery to central circulation); distal tibia; sternum (sternal IO devices) |
| Onset of action | Rapid | Comparable to peripheral IV for most medications; humeral IO may have faster central drug delivery than tibial IO |
| Drug delivery | Standard | All ACLS medications can be administered IO; flush with 10–20 mL normal saline bolus after each medication |
| Complications | Extravasation, phlebitis | Extravasation, osteomyelitis (rare), fracture (rare), compartment syndrome (if needle misplaced), fat embolism (theoretical) |
7.2 Central Venous Access During Arrest
- Central venous access is NOT typically obtained during active cardiac arrest resuscitation (requires interruption of CPR, time-consuming, higher complication rate during compressions)
- If a central line is already in place (IHCA), it provides the fastest drug delivery to the central circulation
- If a central line is needed post-ROSC for vasopressor infusions, it should be placed after stabilization
7.3 Endotracheal Drug Administration
- No longer recommended for any ACLS medications 1 2
- Absorption via the endotracheal route is unreliable and unpredictable
- If IV/IO access cannot be established, continued attempts at IV/IO access are preferred over endotracheal drug administration
- Historical dose recommendations (2–2.5x the IV dose diluted in 5–10 mL normal saline or sterile water) should no longer be used
References
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