ACLS & Cardiac Arrest — Part 5: ECPR, CPR Quality Metrics, Pediatric Considerations & Termination of Resuscitation
Extracorporeal CPR indications and evidence, CPR quality metrics and physiologic targets, pediatric cardiac arrest differences with weight-based dosing, neonatal resuscitation overview, termination of resuscitation criteria, and post-arrest care cross-reference.
1. Extracorporeal CPR (ECPR)
Extracorporeal cardiopulmonary resuscitation (ECPR) refers to the emergent initiation of venoarterial extracorporeal membrane oxygenation (VA-ECMO) during cardiac arrest to provide mechanical circulatory support and gas exchange while the underlying cause of arrest is identified and treated. ECPR has emerged as a potentially transformative intervention for selected patients with refractory cardiac arrest.1 2 3
1.1 Mechanism and Rationale
During conventional CPR, even high-quality chest compressions generate only 25–33% of normal cardiac output. This is often insufficient to maintain end-organ perfusion during prolonged resuscitations. ECPR provides near-normal blood flow and oxygenation, potentially allowing:
- Maintenance of coronary and cerebral perfusion during ongoing arrest
- Time for treatment of the underlying cause (e.g., percutaneous coronary intervention for acute MI, thrombolysis for massive PE, rewarming for hypothermia)
- Bridge to recovery or definitive therapy
1.2 ECPR Cannulation
| Parameter | Detail |
|---|---|
| Configuration | Venoarterial (VA) ECMO: venous drainage cannula placed in the femoral vein (advanced to the right atrium) and arterial return cannula placed in the femoral artery |
| Cannulation technique | Percutaneous Seldinger technique under ultrasound guidance; performed during ongoing CPR (mechanical CPR device facilitates the procedure by keeping the field stable) |
| Circuit | Centrifugal pump + membrane oxygenator + heat exchanger; primed with crystalloid; target flow 3–5 L/min |
| Time to cannulation | Goal <60 minutes from arrest onset; centers with ECPR programs typically achieve cannulation in 20–40 minutes from arrival |
| Distal perfusion | An antegrade distal perfusion cannula (7–9 Fr) should be placed in the superficial femoral artery to prevent limb ischemia |
1.3 Patient Selection Criteria for ECPR
Selection criteria vary by institution, but the following general framework reflects the published evidence and expert consensus:1 2 3 4
Inclusion criteria (general):
| Criterion | Typical Threshold |
|---|---|
| Age | 18–75 years (some centers extend to 80 years) |
| Witnessed arrest | Yes (bystander witnessed or EMS witnessed) |
| Bystander CPR | Initiated within minutes of arrest; high-quality CPR ongoing |
| Initial rhythm | Shockable rhythm (VF/pVT) preferred; some centers include non-shockable rhythms with suspected reversible cause |
| Time from arrest | <60 minutes of total CPR time at the time of ECMO cannulation (shorter is better; strongest benefit when cannulation occurs within 30–60 minutes) |
| No ROSC | Despite ≥3 shocks and standard ACLS pharmacotherapy |
| Suspected reversible etiology | Acute MI, massive PE, hypothermia, refractory VF, drug toxicity |
Exclusion criteria (general):
| Criterion | Rationale |
|---|---|
| Unwitnessed arrest with unknown downtime | Poor neurologic prognosis |
| Prolonged no-flow time (>5 minutes without CPR) | Irreversible brain injury likely |
| Known terminal illness / DNR | Not appropriate for aggressive resuscitation |
| Active uncontrollable hemorrhage | ECMO requires anticoagulation; hemorrhage will worsen |
| Severe aortic insufficiency | VA-ECMO increases LV afterload; aortic insufficiency leads to LV distension and failure to decompressing the heart |
| Aortic dissection | Femoral arterial cannulation may extend dissection |
| ETCO2 persistently <10 mmHg | Suggests very poor CPR quality or prolonged arrest with poor prognosis (used by some protocols as exclusion criterion) |
| Arrest from clearly non-survivable cause | Massive intracranial hemorrhage, advanced metastatic disease, etc. |
1.4 Key Trials and Evidence for ECPR
| Trial | Design | Patients | Key Findings |
|---|---|---|---|
| ARREST (2020) | Single-center RCT; OHCA with refractory VF; ECPR vs standard ACLS | n=30 (stopped early by DSMB for efficacy) | Survival to hospital discharge: 43% ECPR vs 7% standard (p=0.006); all ECPR survivors had favorable neurologic outcome (CPC 1-2). Trial stopped early due to overwhelming benefit in ECPR arm 3 |
| Prague OHCA (2022) | Multicenter RCT; OHCA with refractory shockable or non-shockable rhythm; invasive strategy (including ECPR + PCI) vs standard ACLS | n=256 | 180-day survival with good neurologic outcome: 31.5% invasive vs 22.0% standard (p=0.09; not statistically significant). Subgroup analysis suggested benefit in shockable rhythms. 30-day survival: 32.0% vs 22.4% (borderline significant) 4 |
| INCEPTION (2023) | Multicenter RCT (Netherlands); OHCA with shockable rhythm refractory to ≥3 shocks; ECPR vs standard ACLS | n=160 | 30-day survival with good neurologic outcome: 20% ECPR vs 16% standard (p=0.52; not significant). High crossover rate and logistic challenges may have attenuated treatment effect 5 |
| Observational data | Multiple retrospective cohorts and propensity-matched studies | Various | Consistently show higher survival with ECPR in selected patients with refractory VF when implemented in experienced centers with established protocols; benefit most pronounced with short low-flow times and rapid cannulation |
1.5 Current Recommendations for ECPR
- ECPR may be considered for selected patients with cardiac arrest when conventional CPR is failing, the arrest has a suspected reversible etiology, and ECPR can be initiated within a timeframe and setting in which the institutional expertise supports its use 1 2
- ECPR requires a system-level protocol including pre-identified patient selection criteria, a trained cannulation team, mechanical CPR availability, and a post-cannulation care pathway
- The benefit of ECPR is most clearly established for refractory VF/pVT with suspected cardiac etiology
- ECPR for non-shockable rhythms remains an area of active investigation; may be considered when a clearly reversible cause is identified (massive PE, hypothermia, toxicologic)
1.6 ECPR in Specific Scenarios
| Scenario | Role of ECPR |
|---|---|
| Refractory VF | Most well-supported indication; provides circulatory support while treating underlying ischemia or arrhythmia substrate |
| Massive pulmonary embolism | ECPR as bridge to surgical or catheter-directed embolectomy; provides circulatory support while thrombolytics take effect |
| Accidental hypothermia | ECPR/ECMO is the gold standard for rewarming severe hypothermic cardiac arrest; provides both circulatory support and controlled rewarming |
| Toxic ingestion | ECPR may bridge patients through the period of drug effect; particularly relevant for massive sodium channel blocker, calcium channel blocker, or beta-blocker ingestion |
| Myocarditis | Fulminant myocarditis with refractory cardiogenic shock or cardiac arrest; ECPR as bridge to recovery |
| In-hospital cardiac arrest | Patients arresting in the cardiac catheterization laboratory, OR, or ICU may be ideal candidates for rapid ECPR |
2. CPR Quality Metrics — Comprehensive Reference
Systematic measurement and optimization of CPR quality metrics is the most impactful intervention for improving cardiac arrest outcomes at the institutional level. Every resuscitation team should track these metrics and use them for real-time feedback and post-event debriefing.1 6 7
2.1 Core CPR Quality Metrics
| Metric | Target | Measurement | Clinical Significance |
|---|---|---|---|
| Chest compression fraction (CCF) | >80% (minimum >60%) | Proportion of arrest time during which compressions are being performed; calculated from defibrillator accelerometer or impedance data | The single most important modifiable metric; each 10% increase in CCF is associated with improved survival; pauses for rhythm checks, intubation, and vascular access are the most common reasons for low CCF 7 |
| Compression rate | 100–120/min | Defibrillator sensor or CPR feedback device | Rates <100/min produce inadequate flow; rates >120/min are associated with inadequate depth (trade-off between speed and depth) |
| Compression depth | 5–6 cm (2–2.4 inches) | Accelerometer-based feedback device (note: mattress displacement can falsely inflate depth measurements on hospital beds — use a backboard or CPR mode on beds) | Depths <5 cm are associated with decreased ROSC and survival; depths >6 cm increase risk of chest injury |
| Full chest recoil | Complete release between compressions; no residual leaning force | Force-sensing device | Incomplete recoil (leaning) increases intrathoracic pressure, reduces venous return, and decreases coronary perfusion pressure; common with rescuer fatigue |
| Pre-shock pause | <10 seconds | Time from last compression to shock delivery | Prolonged pre-shock pauses reduce defibrillation success; hands-on defibrillation techniques or compressions during charging can minimize this |
| Post-shock pause | <5 seconds | Time from shock delivery to first post-shock compression | Immediately resume compressions after shock; do not pause to check rhythm (next check is at 2 minutes) |
| Peri-shock pause | <10 seconds total | Combined pre- and post-shock pauses | The total pause around defibrillation should be minimized to maintain coronary perfusion |
| Ventilation rate | 10/min (with advanced airway) | Capnography waveform counting; team member coaching | Hyperventilation is the most common ventilation error; rates >12/min impair hemodynamics |
| First shock time (IHCA) | <2 minutes from arrest recognition | Code response timestamps | Directly correlated with survival from shockable rhythms; system-level process metric |
2.2 Physiologic Targets During CPR
| Physiologic Parameter | Target | Measurement Method | Interpretation |
|---|---|---|---|
| End-tidal CO2 (ETCO2) | >20 mmHg (minimum >10 mmHg) | Continuous waveform capnography via advanced airway | Surrogate for cardiac output during CPR; values <10 mmHg suggest inadequate compression quality or irreversible arrest; abrupt rise to >35 mmHg suggests ROSC 6 |
| Arterial diastolic blood pressure (if arterial line in place) | >25 mmHg | Invasive arterial monitoring | Correlates with coronary perfusion pressure; can guide compression quality and vasopressor timing |
| Coronary perfusion pressure (CPP) | >15 mmHg (ideally >20 mmHg) | Aortic diastolic pressure minus right atrial diastolic pressure (requires both arterial and central venous lines) | The physiologic determinant of myocardial blood flow during CPR; values >15 mmHg are associated with ROSC; this is the gold standard hemodynamic target during CPR but rarely measured in real-time outside research settings 7 |
| Central venous oxygen saturation (ScvO2) | >30% (if central line in place) | Central venous blood gas | Low values indicate very poor cardiac output from CPR; may guide compression optimization |
| Cerebral oximetry (regional brain tissue oxygen saturation) | >40% (if NIRS monitoring available) | Near-infrared spectroscopy (NIRS) | Used in some ECPR programs; low values suggest inadequate cerebral perfusion; trending may guide interventions |
2.3 Systems-Level Quality Improvement
| Element | Description |
|---|---|
| Post-event debriefing | Review CPR performance data within 24 hours of every cardiac arrest; identify specific quality gaps; celebrate successes; use objective data (compression rate, depth, fraction, pause durations) to ground the discussion |
| Mock code drills | Regular simulation-based resuscitation training; focus on team dynamics, communication, and CPR quality; data show that institutions with regular mock codes have better cardiac arrest outcomes |
| CPR dashboard | Institutional tracking of aggregate CPR quality metrics, time to first shock, survival rates, and neurologic outcomes; benchmark against national registries |
| Rapid response systems | Early identification of deteriorating patients prevents some cardiac arrests entirely; track rapid response team activation rates and outcomes |
| Code team composition | Designated team roles (team leader, compressor, airway manager, medication nurse, recorder, CPR coach); clear communication protocols (closed-loop communication) |
3. Pediatric Cardiac Arrest — Key Differences from Adult ACLS
Pediatric cardiac arrest differs fundamentally from adult cardiac arrest in etiology, presentation, and management. While adult cardiac arrest is most often cardiac in origin (VF/pVT from acute MI), pediatric cardiac arrest is most commonly caused by respiratory failure or shock leading to hypoxia and subsequent bradycardic arrest progressing to asystole or PEA.1 8 9
3.1 Pediatric CPR Parameters
| Parameter | Infant (<1 year) | Child (1 year to puberty) | Adolescent (puberty+) |
|---|---|---|---|
| Compression technique | Two-thumb encircling technique (preferred for two-rescuer); two-finger technique (lone rescuer) | Heel of one hand or two hands (depending on child size) | Two-hand technique (same as adult) |
| Compression depth | At least 1.5 inches (4 cm) — approximately 1/3 AP diameter of chest | At least 2 inches (5 cm) — approximately 1/3 AP diameter of chest | At least 2 inches (5 cm), not more than 2.4 inches (6 cm) — same as adult |
| Compression rate | 100–120/min | 100–120/min | 100–120/min |
| Compression-to-ventilation ratio (2 rescuers) | 15:2 | 15:2 | 30:2 (adult ratio) |
| Compression-to-ventilation ratio (lone rescuer) | 30:2 | 30:2 | 30:2 |
| Ventilation with advanced airway | 1 breath every 2–3 seconds (20–30/min) for infants; 1 breath every 3–5 seconds (12–20/min) for children | 1 breath every 3–5 seconds (12–20/min) | 1 breath every 6 seconds (10/min) — same as adult |
| Emphasis on ventilation | High priority — pediatric arrest is most often respiratory in origin; early ventilation is critical | High priority | Standard ACLS approach |
3.2 Pediatric Defibrillation
| Parameter | Recommendation |
|---|---|
| First shock | 2 J/kg |
| Second shock | 4 J/kg |
| Subsequent shocks | 4–10 J/kg (not to exceed adult maximum energy — typically 200–360 J) |
| Pad size | Use pediatric pads/paddles for children <25 kg (approximately <8 years); use adult pads for children ≥25 kg; if only adult pads are available for a small child, use anterior-posterior placement to avoid overlap |
| AED use | Use pediatric dose-attenuator system if available (for children 1–8 years); if not available, standard adult AED is acceptable |
| AED in infants | Manual defibrillator preferred; AED with dose attenuator acceptable; adult AED without attenuator is a last resort |
3.3 Pediatric ACLS Medications — Weight-Based Dosing
| Medication | Dose | Route | Notes |
|---|---|---|---|
| Epinephrine | 0.01 mg/kg (0.1 mL/kg of 1:10,000 or 0.1 mg/mL) IV/IO every 3–5 minutes | IV/IO | Maximum single dose: 1 mg; first dose in non-shockable rhythms as soon as possible; in shockable rhythms after second shock |
| Amiodarone | 5 mg/kg IV/IO bolus; may repeat twice up to max 15 mg/kg/day | IV/IO | For shock-refractory VF/pVT after 3rd shock; maximum single dose 300 mg |
| Lidocaine | 1 mg/kg IV/IO loading dose; may repeat at 20-minute intervals | IV/IO | Alternative to amiodarone; maintenance infusion 20–50 mcg/kg/min |
| Atropine | 0.02 mg/kg IV/IO (minimum dose 0.1 mg; maximum single dose 0.5 mg) | IV/IO | For bradycardia with poor perfusion; may repeat once; total maximum dose in child: 1 mg; in adolescent: 3 mg |
| Adenosine | 0.1 mg/kg (max first dose 6 mg) rapid IV push; second dose 0.2 mg/kg (max 12 mg) | IV (proximal site) | For SVT; rapid push with immediate flush |
| Calcium chloride 10% | 20 mg/kg (0.2 mL/kg) IV slow push | IV/IO (central line preferred) | For hyperkalemia, hypocalcemia, calcium channel blocker toxicity, hypermagnesemia |
| Sodium bicarbonate | 1 mEq/kg IV slow push | IV/IO | For hyperkalemia, severe metabolic acidosis, sodium channel blocker toxicity; use 4.2% (0.5 mEq/mL) concentration in neonates |
| Magnesium sulfate | 25–50 mg/kg IV/IO (max 2 g) over 10–20 minutes (push during arrest) | IV/IO | For torsades de pointes, documented hypomagnesemia |
| Glucose (dextrose) | 0.5–1 g/kg IV: D10W 5–10 mL/kg (neonates/infants); D25W 2–4 mL/kg (children); D50W 1–2 mL/kg (adolescents) | IV/IO | Check point-of-care glucose in all pediatric arrests; hypoglycemia is common and treatable |
3.4 Pediatric Reversible Causes
The H’s and T’s apply to pediatric patients with additional emphasis on:
| Cause | Pediatric Considerations |
|---|---|
| Hypoxia | The most common cause of pediatric cardiac arrest; aggressively manage airway and ventilation |
| Hypovolemia | Septic shock, hemorrhage (trauma, GI), dehydration; fluid bolus 20 mL/kg NS; may repeat up to 60 mL/kg |
| Hypothermia | Accidental hypothermia, cold water drowning; active rewarming |
| Congenital heart disease | Complex physiology (single ventricle, ductal-dependent lesions); prostaglandin E1 for ductal-dependent lesions in neonates (0.05–0.1 mcg/kg/min) |
| Hyperkalemia | Particularly in patients with renal disease; treatment same as adults but weight-based |
| Cardiac tamponade | Post-cardiac surgery, oncologic (mediastinal mass), trauma |
| Tension pneumothorax | Trauma, mechanical ventilation; needle decompression with appropriately sized angiocatheter (18–20 gauge in infants/small children) |
| Toxins | Accidental ingestion is common in toddlers; consider all age-appropriate toxins |
| Sepsis | Leading cause of non-respiratory pediatric cardiac arrest; aggressive fluid resuscitation and early antibiotics |
3.5 Pediatric Bradycardia Algorithm
Bradycardia with poor perfusion (HR <60 bpm with signs of shock) is the most common pre-arrest rhythm in children:
| Step | Action | Details |
|---|---|---|
| 1 | Support ABCs | Provide oxygen; assist ventilation with bag-mask if needed |
| 2 | If HR <60 with poor perfusion despite adequate oxygenation and ventilation | Begin CPR — this is a critical threshold in pediatrics; a heart rate <60 bpm with poor perfusion is treated as cardiac arrest |
| 3 | Epinephrine | 0.01 mg/kg IV/IO every 3–5 minutes |
| 4 | Atropine | 0.02 mg/kg IV/IO if increased vagal tone or primary AV block is suspected (min dose 0.1 mg, max single dose 0.5 mg) |
| 5 | Transcutaneous pacing | Consider if no response to medications; especially for AV block |
| 6 | Identify and treat cause | Hypoxia (most common), acidosis, hypothermia, drug effect, congenital heart block |
4. Neonatal Resuscitation — Brief Overview
Neonatal resuscitation follows a distinct algorithm from pediatric and adult ACLS, reflecting the unique physiology of the transition from fetal to extrauterine life.10
4.1 Key Differences from Pediatric/Adult Resuscitation
| Feature | Neonatal Approach |
|---|---|
| Primary focus | Ventilation and oxygenation (the vast majority of neonates who need resuscitation respond to effective ventilation alone) |
| Initial steps | Warm, dry, stimulate; position airway (sniffing position); suction if needed; assess breathing and heart rate |
| Ventilation | Positive-pressure ventilation (PPV) at 40–60 breaths/min; initial FiO2 21–30% for term neonates (titrate by SpO2); 21–30% for preterm; corrective steps if HR does not improve (MR SOPA: Mask adjustment, Reposition, Suction, Open mouth, Pressure increase, Alternative airway) |
| Compression-to-ventilation ratio | 3:1 (3 compressions followed by 1 breath); this 3:1 ratio is unique to neonates; delivery rate is approximately 120 events/min (90 compressions + 30 breaths) |
| Compression technique | Two-thumb encircling technique preferred; compress lower 1/3 of sternum; depth approximately 1/3 AP chest diameter |
| Epinephrine | 0.01–0.03 mg/kg (0.1–0.3 mL/kg of 1:10,000) IV/UVC; may give 0.05–0.1 mg/kg via ETT (higher dose for ETT route — this is the one remaining indication where ETT drug administration is accepted) |
| Volume expansion | 10 mL/kg NS or O-negative pRBCs if hypovolemia suspected |
| Umbilical venous catheter (UVC) | Preferred emergency vascular access in the delivery room; inserted into the umbilical vein to a depth where blood can be freely aspirated (approximately 2–4 cm beyond the skin in term neonates) |
5. Termination of Resuscitation
The decision to terminate resuscitative efforts is one of the most difficult in clinical medicine. It requires a systematic approach that balances the obligation to preserve life with the recognition that some patients cannot be resuscitated and that prolonged futile resuscitation has costs — both for the patient and for healthcare providers.1 2 11
5.1 BLS Termination of Resuscitation Rule (Out-of-Hospital)
This validated clinical decision rule helps EMS providers identify patients who are extremely unlikely to survive, allowing field termination rather than transport with ongoing CPR:11
| Criterion | Requirement |
|---|---|
| Arrest NOT witnessed by EMS personnel | Yes |
| No bystander CPR was provided | Yes |
| No AED shock was delivered | Yes |
| No ROSC achieved in the field | Yes |
Interpretation: If ALL four criteria are met, the specificity for death approaches 100%. Field termination of resuscitation is recommended. If ANY criterion is not met (e.g., arrest was witnessed, bystander CPR was given, a shock was delivered, or ROSC occurred), transport with ongoing resuscitation is warranted.
5.2 ALS Termination of Resuscitation Rule (Out-of-Hospital)
The ALS termination rule adds to the BLS rule:11
| Criterion | Requirement |
|---|---|
| All BLS criteria met | Yes |
| No ROSC despite complete ALS interventions | Yes |
| Arrest was not witnessed by a first responder or bystander | Yes |
5.3 In-Hospital Termination of Resuscitation Considerations
There is no single validated termination rule for IHCA. The decision to terminate in-hospital resuscitation is a clinical judgment that incorporates multiple factors:1
| Factor | Favorable for Continued Resuscitation | Favorable for Termination |
|---|---|---|
| Initial rhythm | Shockable (VF/pVT) | Non-shockable (asystole/PEA) |
| Duration of resuscitation | <20 minutes | >30–40 minutes without ROSC (though no absolute time cutoff exists) |
| ETCO2 | >10 mmHg, trending upward | Persistently <10 mmHg after 20 minutes of high-quality CPR |
| Reversible cause identified | Yes — and treatable | No reversible cause identified despite thorough evaluation |
| Intermittent ROSC | Yes (suggests a potentially recoverable rhythm) | No ROSC at any point |
| CPR quality | Confirmed high-quality | Quality in question |
| Patient factors | Young, previously healthy, no comorbidities | Advanced age, multiple comorbidities, terminal illness |
| Witnessed arrest | Yes | No |
| Hypothermia | Present (neuroprotective) | Normothermic arrest |
| Thrombolysis given | Yes — continue for at least 60–90 minutes after administration | — |
| ECPR candidacy | Patient meets ECPR criteria and ECPR is available | Not an ECPR candidate |
5.4 Duration of Resuscitation
- There is no universally agreed-upon maximum duration of resuscitation
- Evidence suggests that survival is rare after 20 minutes of resuscitation for non-shockable rhythms with persistently low ETCO2 (<10 mmHg) and no reversible cause
- For shockable rhythms, survival has been reported with extended resuscitations (>30–60 minutes), particularly when intervals of ROSC occur or the rhythm oscillates between VF and organized rhythms
- Special circumstances warrant prolonged resuscitation: hypothermia, pediatric patients, drug overdose/toxicity, lightning strike/electrocution, pregnancy (perimortem C-section may produce ROSC), submersion in cold water
- Average resuscitation duration for IHCA in national registry data is approximately 20 minutes for non-survivors and 12 minutes for survivors
5.5 Communication of Termination
| Element | Recommendation |
|---|---|
| Team leader authority | The team leader makes the final decision to terminate, ideally with input from the resuscitation team |
| Documentation of decision | Document all clinical findings that support the decision: duration of arrest, rhythm history, interventions performed, ETCO2 values, reversible causes assessed and addressed, patient factors |
| Time of death | Document the time at which resuscitative efforts are officially ceased; this is the recorded time of death |
| Family communication | If family members are present (increasingly common and encouraged by guidelines), the team leader or a designated member should provide clear, compassionate communication about what occurred and why efforts are being ceased |
| Organ donation | Consider referral to organ procurement organization; time-sensitive protocols may apply for donation after circulatory death (DCD) |
| Team support | Post-event debriefing should address both clinical performance and emotional well-being of team members; critical incident stress debriefing may be appropriate |
6. Post-Cardiac Arrest Care — Cross-Reference
Patients who achieve ROSC after cardiac arrest require immediate and sustained critical care management. Post-cardiac arrest care is addressed in a dedicated companion guideline:
See: Post-Cardiac Arrest Care and Targeted Temperature Management
Key post-arrest care elements include:
| Domain | Key Interventions |
|---|---|
| Oxygenation | Titrate FiO2 to SpO2 92–98%; avoid hyperoxia (PaO2 >300 mmHg is associated with worse outcomes); avoid hypoxemia |
| Ventilation | Target normocapnia (PaCO2 35–45 mmHg); avoid hyperventilation; lung-protective ventilation (6–8 mL/kg IBW) |
| Hemodynamics | Target MAP ≥65–80 mmHg (some evidence supports higher targets of ≥80 mmHg for cerebral perfusion); vasopressors (norepinephrine first-line); echocardiography to assess myocardial function; consider inotropes (dobutamine, milrinone) for post-arrest myocardial dysfunction |
| Temperature management | Actively prevent fever (≥37.7°C); consider targeted temperature management to 32–36°C for 24 hours (TTM2 trial showed no benefit of 33°C vs normothermia with active fever prevention); strict avoidance of hyperthermia for at least 72 hours after ROSC |
| Coronary angiography | Emergent angiography for STEMI or strong suspicion of acute coronary etiology; timing for non-STEMI indications is guided by the COACT and TOMAHAWK trials (early angiography within 24 hours is reasonable but immediate angiography is not required without STEMI) |
| Seizure management | Continuous EEG monitoring for 24–72+ hours; treat electrographic seizures and status epilepticus; levetiracetam and valproate are first-line; avoid aggressive sedation that confounds neuroprognostication |
| Neuroprognostication | Multimodal assessment no earlier than 72 hours after ROSC (or after rewarming and elimination of sedation); includes clinical examination, EEG, somatosensory evoked potentials (SSEPs), biomarkers (NSE), and neuroimaging (CT, MRI DWI) |
| Glucose management | Treat hyperglycemia (target <180 mg/dL); avoid hypoglycemia |
| Mechanical circulatory support | Consider IABP, Impella, or ECMO for refractory cardiogenic shock; consult cardiology/cardiac surgery |
7. ACLS Medications — Comprehensive Quick Reference Table
| Medication | Indication | Dose | Route | Frequency | Maximum | Key Notes |
|---|---|---|---|---|---|---|
| Epinephrine | All cardiac arrest rhythms | 1 mg | IV/IO | Every 3–5 min | No max in arrest | After 2nd shock in VF/pVT; ASAP in asystole/PEA |
| Amiodarone | Shock-refractory VF/pVT | 300 mg 1st dose; 150 mg 2nd dose | IV/IO | After 3rd shock; one additional dose | 450 mg in arrest | Post-ROSC: 1 mg/min x 6hr, then 0.5 mg/min x 18hr |
| Lidocaine | Shock-refractory VF/pVT (alternative to amiodarone) | 1–1.5 mg/kg 1st dose; 0.5–0.75 mg/kg repeat | IV/IO | Every 5–10 min | 3 mg/kg total | Post-ROSC: 1–4 mg/min infusion |
| Atropine | Symptomatic bradycardia | 1 mg | IV/IO | Every 3–5 min | 3 mg (0.04 mg/kg) | Ineffective for Mobitz II and complete heart block |
| Adenosine | Regular narrow-complex SVT | 6 mg 1st; 12 mg 2nd; 12 mg 3rd | Rapid IV push + flush | 1–2 min between doses | 36 mg total | Reduce dose if via central line or on dipyridamole |
| Diltiazem | AF/flutter rate control; SVT | 0.25 mg/kg (15–20 mg) then 0.35 mg/kg | IV over 2 min | 15 min between boluses | — | Infusion: 5–15 mg/hr; avoid in HFrEF |
| Metoprolol | AF/flutter rate control; SVT | 5 mg | IV over 2–5 min | Every 5 min | 15 mg total | Avoid in decompensated HF, severe bronchospasm |
| Procainamide | Wide complex tachycardia; pre-excited AF | 20–50 mg/min | IV infusion | Continuous until converted | 17 mg/kg | Stop if: QRS widens >50%, hypotension, conversion |
| Magnesium sulfate | Torsades de pointes | 1–2 g in 10 mL D5W | IV push/IO | May repeat once | 4 g | Also for refractory VF (empiric), hypomagnesemia |
| Calcium chloride 10% | Hyperkalemia, Ca-blocker OD, hypermagnesemia | 1–2 g (10–20 mL) | IV slow push | May repeat | — | Severe vesicant; prefer central line; 3x more Ca²⁺ than gluconate |
| Calcium gluconate 10% | Same as CaCl (when CaCl unavailable) | 3–6 g (30–60 mL) | IV slow push | May repeat | — | Safer peripherally; slower onset |
| Sodium bicarbonate | Hyperkalemia, TCA OD, known acidosis | 1 mEq/kg (50 mEq) | IV slow push | 0.5 mEq/kg q10min | Guided by ABG | Not routine in arrest; ensure adequate ventilation |
| Lipid emulsion 20% | LAST, lipophilic drug toxicity | 1.5 mL/kg bolus then 0.25 mL/kg/min | IV | Repeat bolus x1–2 at 5min | 12 mL/kg total | Do not substitute propofol |
| Naloxone | Opioid-associated arrest/respiratory depression | 0.4–2 mg (up to 2 mg during arrest) | IV/IO/IM/IN | Every 2–3 min | No absolute max | Adjunct only; standard ACLS is primary |
| Dopamine | Symptomatic bradycardia (bridge) | 5–20 mcg/kg/min | IV infusion | Titrate | — | Chronotropic doses: >5 mcg/kg/min |
| Epinephrine infusion | Symptomatic bradycardia (bridge) | 2–10 mcg/min | IV infusion | Titrate | — | Bridge to transvenous pacing |
| Isoproterenol | Refractory bradycardia; torsades | 2–10 mcg/min | IV infusion | Titrate | — | Pure beta-agonist; may cause hypotension |
References
Panchal AR, Bartos JA, Cabanas JG, et al. “Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.” Circulation. 2020;142(16_suppl_2):S366-S468. DOI: 10.1161/CIR.0000000000000916 ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎ ↩︎
Soar J, Bottiger BW, Carli P, et al. “European Resuscitation Council Guidelines 2021: Adult Advanced Life Support.” Resuscitation. 2021;161:115-151. DOI: 10.1016/j.resuscitation.2021.02.010 ↩︎ ↩︎ ↩︎ ↩︎
Yannopoulos D, Bartos JA, Raveendran G, et al. “Advanced Reperfusion Strategies for Patients with Out-of-Hospital Cardiac Arrest and Refractory Ventricular Fibrillation (ARREST): A Phase 2, Single Centre, Open-Label, Randomised Controlled Trial.” Lancet. 2020;396(10265):1807-1816. DOI: 10.1016/S0140-6736(20)32338-2 ↩︎ ↩︎ ↩︎
Belohlavek J, Smalcova J, Rob D, et al. “Effect of Intra-arrest Transport, Extracorporeal Cardiopulmonary Resuscitation, and Immediate Invasive Assessment and Treatment on Functional Neurologic Outcome in Refractory Out-of-Hospital Cardiac Arrest: A Randomized Clinical Trial.” JAMA. 2022;327(8):737-747. DOI: 10.1001/jama.2022.1025 ↩︎ ↩︎
Suverein MM, Delecroix B, Lorusso R, et al. “Early Extracorporeal CPR for Refractory Out-of-Hospital Cardiac Arrest.” N Engl J Med. 2023;388(4):299-309. DOI: 10.1056/NEJMoa2204511 ↩︎
Meaney PA, Bobrow BJ, Mancini ME, et al. “Cardiopulmonary Resuscitation Quality: Improving Cardiac Resuscitation Outcomes Both Inside and Outside the Hospital: A Consensus Statement From the American Heart Association.” Circulation. 2013;128(4):417-435. DOI: 10.1161/CIR.0b013e31829d8654 ↩︎ ↩︎
Christenson J, Andrusiek D, Everson-Stewart S, et al. “Chest Compression Fraction Determines Survival in Patients with Out-of-Hospital Ventricular Fibrillation.” Circulation. 2009;120(13):1241-1247. DOI: 10.1161/CIRCULATIONAHA.109.852202 ↩︎ ↩︎ ↩︎
Topjian AA, Raymond TT, Atkins D, et al. “Part 4: Pediatric Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.” Circulation. 2020;142(16_suppl_2):S469-S523. DOI: 10.1161/CIR.0000000000000901 ↩︎
Van de Voorde P, Turner NM, Djakow J, et al. “European Resuscitation Council Guidelines 2021: Paediatric Life Support.” Resuscitation. 2021;161:327-387. DOI: 10.1016/j.resuscitation.2021.02.015 ↩︎
Aziz K, Lee HC, Escobedo MB, et al. “Part 5: Neonatal Resuscitation: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.” Circulation. 2020;142(16_suppl_2):S524-S550. DOI: 10.1161/CIR.0000000000000902 ↩︎
Morrison LJ, Verbeek PR, Vermeulen MJ, et al. “Derivation and Evaluation of a Termination of Resuscitation Clinical Prediction Rule for Advanced Life Support Providers.” Resuscitation. 2007;74(2):266-275. DOI: 10.1016/j.resuscitation.2007.01.013 ↩︎ ↩︎ ↩︎