ACLS: Drugs, Defibrillators, and Monitors

Introduction

• Cardiac arrest continues to represent a major public health challenge, with survival highly dependent on early recognition and prompt initiation of CPR. Immediate interventions, including high-quality chest compressions and early defibrillation, have been shown to improve both survival and neurological outcomes.^1,2
• In-hospital cardiac arrest occurs in approximately 1 in 100 hospitalized adults, and data suggest that approximately 72.2% of these patients achieve return of spontaneous circulation (ROSC).¹
• Despite this, long-term outcomes remain poor, emphasizing the need for optimization of advanced cardiac life support (ACLS) interventions.^1,2

Defibrillators

• Defibrillation is the primary treatment for VF and pVT. It delivers controlled electrical energy across the thorax to depolarize myocardial cells and restore organized rhythm. Early defibrillation combined with high-quality CPR is critical, with over 75% of VF/pVT episodes terminating successfully when optimal technique is applied.^1,2
• Modern defibrillators use biphasic waveforms, which require less energy and achieve higher first-shock success rates than older monophasic devices. Shock strategies can be fixed-energy or escalating-energy, both effective in terminating VF/pVT.^1,3,4
• A single-shock strategy followed immediately by CPR is preferred, as stacked shocks reduce CPR quality and first-shock efficacy. Escalating energy may be used if multiple shocks are required, though no survival advantage has been shown.¹
• Pad placement and vector adjustments are important. Standard placement is anterior-lateral, but repositioning to anterior-posterior (vector change) can improve shock effectiveness when initial attempts fail. Double sequential defibrillation (two shocks from separate defibrillators) is not routinely recommended.^3,4
• Optimizing current delivery involves ensuring good pad-skin contact, removing hair or moisture, applying firm pressure, and adjusting pad placement or vector as needed.¹
• Please see the OA summary on cardioversion and defibrillation for more details. Link

Drugs

• Pharmacologic therapy is administered when ROSC has not been achieved after CPR and defibrillation.¹
• Peripheral intravenous (IV) access is commonly used but may be difficult to obtain; alternative routes include intraosseous (IO) access, central venous access, and, rarely, the endotracheal route.¹
• Intracardiac drug administration is no longer recommended due to risk and the availability of safer alternative.¹

Vasopressors

• Epinephrine is first-line for all cardiac arrest rhythms; it increases coronary perfusion pressure and the likelihood of ROSC. Dose 1mg IV/IO. Repeat every 3–5 min.¹ Please see the OA summary on epinephrine for more details. Link
• Vasopressin (20 IU IV, optional with methylprednisolone 40 mg) can be used in non-shockable rhythms but offers no survival advantage over epinephrine.^1,2 Please see the OA summary on vasopressin for more details. Link

Antiarrhythmic Drugs

• Amiodarone (Class III) prolongs repolarization and the refractory period; it is indicated for refractory VF/pVT. Dose: 300 mg IV/IO bolus, repeat 150 mg as needed. Improves short-term rhythm control but does not increase survival to discharge.⁵
• Lidocaine (Class Ib) blocks sodium channels and raises the ventricular fibrillatory threshold. Used for refractory VF/pVT. Dose: 1–1.5 mg/kg IV/IO, then 0.5–0.75 mg/kg every 5–10 min. Comparable to amiodarone; no proven survival benefit.⁶
  Other antiarrhythmics (bretylium, sotalol, procainamide, beta-blockers, nifekalant) have limited evidence and are rarely used.¹
• Please see the OA summary on antiarrhythmic drugs for more details. Link

Electrolytes/Adjuncts

• Magnesium: stabilizes cardiac membranes; reserved for torsades de pointes. Dose: 2 g IV/IO slow push.¹
• Calcium: indicated for hyperkalemia, calcium-channel blocker toxicity, and hypocalcemia. Dose 1 g IV. Routine use is not beneficial.¹
• Sodium bicarbonate: buffers acidosis; reserved for pre-existing metabolic acidosis or hyperkalemia. Dose 50–100 mEq IV as indicated. Meta-analyses (>20,000 patients) show no benefit of routine administration during CPR.³

Monitors

ECG Monitoring

• ECG is essential in ACLS for rapid assessment of rhythm and guidance of interventions. Correct interpretation determines whether the rhythm is shockable (VF/pVT) or nonshockable (asystole/pulseless electrical activity.¹

EtCO2

• EtCO₂ provides a reliable surrogate for cardiac output during CPR.¹ A sudden rise of more than 10 mmHg may indicate ROSC, though smaller rises can also be significant.¹

Real-Time CPR Feedback

• Real-time CPR feedback systems monitor chest compression rate, depth, recoil, and ventilation, providing instant guidance via tactile, visual, or audio cues. These systems, integrated into manikins, wearable devices, or automated external defibrillators (AEDs), help rescuers maintain high-quality compressions, enhance training and skill retention, track performance data, and increase confidence, ultimately improving resuscitation outcomes.³

Laboratory and Physiologic Monitoring2

• Rapid glucose and serum electrolytes (K⁺, Ca²⁺, Mg²⁺)
• Arterial or venous blood gas ± co-oximetry
• Core temperature monitoring
• CPR should not be interrupted to place arterial or central venous catheters.³ When an arterial line is present: Diastolic pressure >20 mm Hg is a reasonable goal for coronary perfusion.³ Development of an arterial waveform or sudden rise in diastolic pressure during an organized rhythm suggests ROSC.¹

Point-of-Care Ultrasound (POCUS)

• POCUS may identify reversible causes of cardiac arrest, but has been associated with longer interruptions in CPR.³
• Transesophageal echocardiography provides the highest diagnostic yield and enables real-time optimization of resuscitation without interrupting chest compressions.