What is the immediate management for cardiac arrest using Advanced Cardiovascular Life Support (ACLS) protocol?

ACLS Management of Cardiac Arrest

Immediately begin high-quality chest compressions at a rate of 100-120/min with a depth of at least 2 inches (5 cm), attach a defibrillator/monitor to identify the rhythm, and prepare for rhythm-specific interventions—this is the foundation of ACLS that directly impacts survival. 1

Initial Response and Assessment

Upon recognizing cardiac arrest, activate the emergency response system, retrieve the AED/defibrillator, and simultaneously check for pulse and breathing within 10 seconds. 1, 2 If no pulse is detected, immediately initiate CPR without delay. 1

The critical first 30 seconds should focus on:

• Chest compressions (immediate initiation) 3
• Pad placement (defibrillator pads) 3
• Access (IV/IO line establishment) 3
• Drug preparation 3
• Scribe assignment (documentation) 3

High-Quality CPR: The Most Critical Intervention

CPR quality is the single most important determinant of survival—push hard (at least 2 inches/5 cm), push fast (100-120/min), allow complete chest recoil, minimize interruptions to less than 10 seconds, and rotate compressors every 2 minutes. 1, 2

Without Advanced Airway:

• Perform 30 compressions followed by 2 ventilations 1
• Maintain this 30:2 ratio continuously 1

With Advanced Airway:

• Provide continuous chest compressions without pauses 1
• Deliver 1 breath every 6 seconds (10 breaths/min) 1, 2
• Avoid excessive ventilation, which impairs cardiac output 1, 4

Common pitfall: Excessive ventilation is frequently observed and decreases venous return and cardiac output. 1, 4

Rhythm-Based Management

Shockable Rhythms (VF/Pulseless VT):

Deliver one shock immediately upon rhythm identification, then resume CPR for exactly 2 minutes before rechecking rhythm—early defibrillation is the only intervention besides CPR proven to improve survival in VF/pVT. 1

Defibrillation Energy:

• Biphasic: Use manufacturer recommendation (typically 120-200 Joules initially); if unknown, use maximum available 1
• Monophasic: 360 Joules 1
• Subsequent shocks should be equivalent or higher energy 1

Medication Protocol:

• Epinephrine 1 mg IV/IO every 3-5 minutes throughout the resuscitation 1, 2
• For refractory VF/pVT (after 2-3 shocks): Administer either amiodarone OR lidocaine 1, 4
  • Amiodarone: 300 mg IV/IO bolus first dose, then 150 mg second dose 1
  • Lidocaine: 1-1.5 mg/kg IV/IO first dose, then 0.5-0.75 mg/kg second dose 1

Important nuance: The 2018 AHA guidelines changed from favoring amiodarone to considering either amiodarone or lidocaine equally, as neither has demonstrated improved long-term survival or neurological outcomes. 1 Recent research suggests lidocaine may actually be associated with better outcomes for in-hospital cardiac arrest (higher ROSC, 24-hour survival, and favorable neurological outcomes), though this requires further validation. 5

Non-Shockable Rhythms (PEA/Asystole):

Focus on high-quality CPR, early epinephrine administration (1 mg IV/IO every 3-5 minutes), and aggressive identification/treatment of reversible causes—no shock is indicated. 1, 4

Vascular Access and Drug Administration

Establish IV or IO access without interrupting chest compressions. 1, 2 Attempt IV access first, but if unsuccessful or not feasible, proceed immediately to IO access. 4

Alternative route: Epinephrine, lidocaine, and atropine can be administered via endotracheal tube if IV/IO access is not established, though this is less preferred. 6

Advanced Airway Management

Consider endotracheal intubation or supraglottic airway placement only when it can be accomplished without prolonged interruption of chest compressions. 1, 4

Airway Confirmation and Monitoring:

• Mandatory: Use waveform capnography to confirm and continuously monitor tube placement 1, 2
• PETCO₂ < 10 mmHg indicates inadequate CPR quality—improve compressions 1, 4
• Abrupt sustained increase in PETCO₂ (typically ≥40 mmHg) suggests ROSC 1, 4

Critical caveat: PETCO₂ should NOT be used alone to predict mortality or terminate resuscitation efforts. 2

CPR Quality Monitoring

Use quantitative waveform capnography and, when available, arterial pressure monitoring to optimize CPR quality in real-time. 1, 4

• Target PETCO₂ > 10 mmHg 1
• Target arterial diastolic pressure > 20 mmHg during the relaxation phase 1, 4
• If these targets are not met, immediately improve compression technique 1

Reversible Causes (H's and T's)

Systematically evaluate and treat the reversible causes while maintaining high-quality CPR—failure to identify these causes is a common reason for unsuccessful resuscitation. 7

The H's:

• Hypovolemia: IV fluid boluses 7
• Hypoxia: Ensure adequate oxygenation 7
• Hydrogen ion (acidosis): Adequate ventilation 7
• Hypo/hyperkalemia: Check and correct electrolytes 7
• Hypothermia: Rewarm if accidental 7

The T's:

• Tension pneumothorax: Needle decompression 7
• Tamponade (cardiac): Pericardiocentesis 7
• Toxins: Specific antidotes 7
• Thrombosis (pulmonary): Consider thrombolytics 7
• Thrombosis (coronary): Emergent cardiac catheterization 7

Recognition of ROSC

Indicators of ROSC include palpable pulse with blood pressure, abrupt sustained increase in PETCO₂ (typically >40 mmHg), and spontaneous arterial pressure waves on invasive monitoring. 1, 7

Post-Resuscitation Care

Once ROSC is achieved:

• Maintain oxygenation: Target SpO₂ 94-98% (avoid both hypoxia and hyperoxia) 7
• Maintain normocapnia through appropriate ventilation 7
• Ensure hemodynamic stability with vasopressors as needed 7
• Obtain 12-lead ECG immediately to identify ST-elevation MI 7
• Consider emergent coronary angiography for suspected cardiac etiology, particularly with ST-elevation 7
• Initiate targeted temperature management for patients not following commands 7

Special Populations

• Pregnant patients: Perform manual left uterine displacement to relieve aortocaval compression 2
• Hypothermic patients: Continue resuscitation until rewarmed 2
• Refractory VF/pVT: Consider ECPR (extracorporeal CPR) in select witnessed arrests with shockable rhythms when conventional CPR fails—this has shown significant survival benefit (43% vs 7% survival to discharge in one trial) 2, 8

Key Evidence Limitations

No antiarrhythmic drug has been definitively shown to improve long-term survival or neurological outcomes—treatment recommendations are based on short-term outcomes like ROSC and survival to hospital admission. 1, 4 The optimal sequence and timing of ACLS interventions remain unknown and should be adapted based on the number of providers, their skill levels, and ability to establish vascular access. 1, 4