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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Sara Zand, M.D.[2] Edzel Lorraine Co, DMD, MD[3] Nehal Eid, M.D.[4]

Overview

The mainstay of therapy for patients with cardiac arrest is starting cardiopulmonary resuscitation (CPR) with minimizing interruption in chest compression. The rhythm should be reassessed. If the rhythm is ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), the shock should be delivered immediately. If the rhythm is asystole or pulseless electrical activity (PEA), CPR should be resumed. Advanced life support (ALS) should be kept with minimizing interruption in chest compression including: advanced airway, continuous chest compressions, capnography, intravenous (IV) intraosseous/ (IO) access, vasopressors, and antiarrhythmic therapy. This can address reversible causes such as hypoxia, hypovolemia,hypothermia, hyperkalemia, hypokalemia,acidosis, tension pneumothorax, tamponade, toxins (benzodiazepines, alcohol, opiates, tricyclics, barbiturates, betablockers, calcium channel blockers), thrombosis ST elevation myocardial infarction (STEMI, and massive pulmonary thromboembolism). The following should be considered immediately in post cardiac arrest patients: 12–lead electrocardiogram (ECG) ,perfusion/reperfusion in patients with acute myocardial infarction,(AMI), oxygenation and ventilation, temperature controlling, and treatment of reversible causes. Management of patients in post-cardiac arrest status include treatment of the underlying disorder, hemodynamic stability, respiratory support, and control of neurologic complications.


Urgent Treatment

Medical Therapy

A critical component of therapy for patients with cardiac arrest is starting cardiopulmonary resuscitation (CPR) with minimizing interruption in chest compression.[1][2] The 2025 AHA Guidelines reaffirm that high-quality CPR is the single most critical intervention for a patient in cardiac arrest, with a chest compression rate of 100 to 120 compressions per minute and a compression depth of at least 5 cm (2 inches) but not greater than 6 cm (2.4 inches) in adults.[3]

CPR and use of automated external defibrillators (AED) increase the chances of survival with improved neurological and functional outcomes [4] [5] [6] [7] [8] [9] [10]. Bystander CPR is provided in approximately 47.7% of adult out-of-hospital cardiac arrests (OHCA), and an AED is applied by a bystander in approximately 7.9% of cases. Survival to hospital discharge for OHCA is approximately 10.5%, with favorable neurological outcome in approximately 8.2%.[3]

Acute termination of acute coronary syndrome (ACS)-related arrhythmias can be achieved through defibrillation or electrical cardioversion [11] [12].

2025 AHA Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

The 2025 American Heart Association (AHA) Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care provide comprehensive, updated recommendations for the resuscitation and management of adults experiencing cardiac arrest, respiratory arrest, and life-threatening cardiovascular emergencies.[13][14] These guidelines supersede the 2020 AHA Guidelines and the 2023 AHA Focused Update on Adult Advanced Cardiovascular Life Support.[15]

Vasopressor Therapy (2025 AHA)

Recommendations for vasopressor medications in adult cardiac arrest (2025 AHA)
Class 1 (Level of Evidence: B-R)

Epinephrine 1 mg IV/IO every 3 to 5 minutes is recommended for patients in cardiac arrest.[13]

Class 1 (Level of Evidence: B-R)

For patients with nonshockable rhythms (asystole/pulseless electrical activity), epinephrine 1 mg should be administered as soon as feasible.[13]

Class 1 (Level of Evidence: B-R)

For patients with shockable rhythms (VF/pulseless VT), epinephrine should be administered if initial CPR and defibrillation are unsuccessful. Rapid defibrillation should be prioritized.[13]

Class III: No Benefit (Level of Evidence: A)

High-dose epinephrine (>1 mg boluses) compared with standard doses is not beneficial.[13][2]

Key updates regarding vasopressor therapy (2025 AHA):

Epinephrine has been upgraded from Class 2b (2020 AHA) to Class 1 (2025 AHA) based on consistent and compelling evidence from previous RCTs, cohort, and registry studies supporting a potent effect on ROSC, survival to hospital admission, and survival to hospital discharge.[13]

Earlier administration of epinephrine is associated with improved ROSC. A post-hoc analysis of the PARAMEDIC2 trial found that the effectiveness of epinephrine, compared to placebo, converges at approximately 20 minutes of pulselessness.[13]

Multiple systematic reviews and meta-analyses have found no difference in survival outcomes when comparing vasopressin alone or vasopressin combined with epinephrine versus epinephrine alone.[13]

Vascular Access (2025 AHA)

Recommendations for vascular access in cardiac arrest management (2025 AHA)
Class 2a (Level of Evidence: B-NR)

It is reasonable for providers to first attempt establishing intravenous (IV) access for drug administration in cardiac arrest.[13]

Class 2b (Level of Evidence: B-NR)

Intraosseous (IO) access may be considered if attempts at IV access are unsuccessful or not feasible.[13]

The IVIO trial (2025) compared initial intraosseous versus intravenous vascular access in 1479 adults with out-of-hospital cardiac arrest and found no significant difference in sustained ROSC (30% vs. 29%; risk ratio 1.06; 95% CI, 0.90–1.24; P=0.49), 30-day survival (12% vs. 10%), or 30-day survival with favorable neurologic outcome (9% vs. 8%).[16]

Antiarrhythmic Therapy (2025 AHA)

Recommendations for nonvasopressor medications during cardiac arrest (2025 AHA)
Class 2b (Level of Evidence: B-R)

Amiodarone or lidocaine may be considered for VF/pulseless VT that is unresponsive to defibrillation. These drugs may be particularly useful for patients with witnessed arrest, for whom time to drug administration may be shorter.[13][17]

Class III: No Benefit (Level of Evidence: A)

Routine calcium administration during cardiac arrest is not recommended, as it has not been shown to improve survival to hospital discharge or neurological outcome.[13][15]

Class III: No Benefit (Level of Evidence: C-LD)

Routine sodium bicarbonate administration in cardiac arrest is not recommended. However, sodium bicarbonate may be considered in specific circumstances such as hyperkalemia.[13][15]

Drug Indication Dose Class of Recommendation / LOE (2025 AHA)
Amiodarone Shock-refractory VF/pVT 300 mg IV/IO bolus (first dose); 150 mg IV/IO (second dose) Class 2b, LOE B-R[13]
Lidocaine Shock-refractory VF/pVT (alternative to amiodarone) 1.0 to 1.5 mg/kg IV/IO (first dose); 0.5 to 0.75 mg/kg IV/IO (second dose) Class 2b, LOE B-R[13][17]
Magnesium sulfate Torsades de pointes 1 to 2 g IV over 5 to 20 minutes Indicated for torsades de pointes; not beneficial for refractory VF not related to torsades de pointes (Class III: No Benefit)[2]

Key points regarding antiarrhythmic therapy (2025 AHA):

In the ROC-ALPS trial, amiodarone and lidocaine each improved survival to hospital admission over placebo, but there was no difference in survival to hospital discharge. In the subset of patients with witnessed cardiac arrest, survival to hospital discharge was higher with amiodarone or lidocaine compared with placebo.[17]

Data are insufficient to definitively distinguish between the effectiveness of lidocaine and amiodarone, nor their benefit when given in combination.[13]

No new evidence emerged from a 2025 ILCOR evidence update regarding the use of other parenteral antiarrhythmic agents in cardiac arrest, including bretylium, sotalol, procainamide, and beta blockers (for which ILCOR found insufficient evidence to recommend for or against use).[13]

A large multicenter, blinded, placebo-controlled randomized trial of in-hospital cardiac arrest deploying corticosteroids bundled with a vasopressor agent found an improved rate of ROSC but not survival to hospital discharge or neurological outcome.[13]

Defibrillation (2025 AHA)

Recommendations for defibrillation in adult cardiac arrest (2025 AHA)
Class 1 (Level of Evidence: B-NR)

Early defibrillation is critical to survival when sudden cardiac arrest is caused by ventricular fibrillation or pulseless ventricular tachycardia. Defibrillation is most successful when administered as soon as possible after the onset of VF/pVT.[3]

Class 2b (Level of Evidence: C-LD)

The usefulness of double sequential defibrillation (shock delivery by 2 defibrillators nearly simultaneously) for refractory shockable rhythm has not been established.[14]

Extracorporeal CPR (2025 AHA)

Recommendations for extracorporeal CPR systems of care (2025 AHA)
Class 2a (Level of Evidence: C-LD)

ECPR may be considered for select cardiac arrest patients for whom the suspected cause of the cardiac arrest is potentially reversible during a limited period of mechanical circulatory support, when provided within an appropriately trained and equipped system of care.[15][14]

Class 2a (Level of Evidence: C-LD)

Patient selection for ECPR with defined inclusion criteria, cannulation strategies, and regionalization of ECPR to specialized, experienced centers should be considered.[18]

Class 2b (Level of Evidence: B-R)

Intra-arrest transport to regionalized ECPR centers may be considered.[14]

Key ECPR trial data:

The ARREST trial (single-center) was stopped early for benefit favoring ECPR.[18]

The INCEPTION trial (2023) compared ECPR with conventional CPR in patients with refractory OHCA due to ventricular arrhythmia across 10 Dutch centers and did not demonstrate a statistically significant difference in survival with favorable neurologic outcome.[19]

Post-Cardiac Arrest Care (2025 AHA)

Recommendations for temperature control after cardiac arrest (2025 AHA)
Class 1 (Level of Evidence: B-R)

All adults who do not follow commands after ROSC, regardless of arrest location or presenting rhythm, should receive treatment that includes a deliberate strategy for temperature control. A constant temperature between 32°C and 37.5°C should be selected and maintained.[14][20]

Class 2a (Level of Evidence: B-R)

A minimum of 36 hours of total temperature control is the shortest recommended duration.[14][20]

2022 ESC Guidelines for the management of patients with ventricular arrythymias and the prevention of sudden cardiac death [21]

Recommendations for public basic life support and access to automated external defibrillators
Class I (Level of Evidence: B)
Class I (Level of Evidence: B)
  • Prompt CPR by bystanders is recommended at out-of-hospital cardiac arrest.
Class I (Level of Evidence: B)
Class IIa (Level of Evidence: B)
  • Mobile phone-based alerting of basic life support-trained bystander volunteers to assist nearby out-of-hospital cardiac arrest victims should be considered.
Recommendations for treatment of sudden cardiac death in patients with coronary anomalies
Class I (Level of Evidence: C)
Class IIa (Level of Evidence: C)
Recommendations for the management of patients with idiopathic premature ventricular complexes/ ventricular tachycardia
Class I (Level of Evidence: B)
Class I (Level of Evidence: C)
Class IIa (Level of Evidence: B)
Class IIa (Level of Evidence: C)
Class IIb (Level of Evidence: B)
Class III (Level of Evidence: C)
Class III (Level of Evidence: C)
Class III (Level of Evidence: C)
Recommendations for the management of patients with premature ventricular complex-induced or premature ventricular complex-aggravated cardiomyopathy
Class I (Level of Evidence: C)
Class IIa (Level of Evidence: C)
Class IIa (Level of Evidence: B)
Class IIa (Level of Evidence: C)
Recommendations for diagnosis of ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy
Class IIb (Level of Evidence: C)

2017AHA/ACC/HRS Guideline for management of sudden cardiac arrest and ventricular arrhythmia

[2]

Recommendations for management of cardiac arrest
CPR (Class I, Level of Evidence A):

CPR should be done according to basic and advanced cardiovascular life support algorithms

Amiodarone (Class I, Level of Evidence A) :

❑ In the recurrence of ventricular arrhythmia after maximum energy shock delivery and unstable hemodynamic, amiodarone should de infused

Direct current cardioversion : (Class I, Level of Evidence A)

❑ In ventricular arrhythmia and unstable hemodynamic, direct current cardioversion should be delivered

Revascularization:(Class I, Level of Evidence B)

❑ In patients with polymorphic VT and VF and evidence of acute STEMI in ECG, coronary angiography and emergency revascularization is advised

Wide QRS tachycardia: (Class I, Level of Evidence C)

Wide QRS tachycardia should be considered as VT if the diagnosis is unclear

Intravenous procainamide (Class 2a, Level of Evidence A):

❑ In hemodynamically stable VT, intravenous procainamide is recommended

Intravenous lidocaine : (Class 2a, Level of Evidence B)

Lidocaine is recommended in witness cardiac arrest due to polymorphic VT, VF unresponsed to CPR, defibrillation or vasopressor therapy

Intravenous betablocker : (Class 2a, Level of Evidence B)

❑ In polymorphic VT due to myocardial ischemia, intravenous betablocker maybe helpful

Intravenous Epinephrine : (Class 2b, Level of Evidence A)

❑ In cardiac arrest administration of 1 mg epinephrine every 3-5 minutes during CPR is recommended

Intravenous amiodarone : (Class 2b, Level of Evidence B)

❑ In hemodynamic stable VT, infusion of amiodarone or sotalole maybe considered

High dose of intravenous epinephrine : (Class III , Level of Evidence A)

❑ In cardiac arrest, administration of high dose epinephrine>1 mg bolouses is not beneficial
❑ In refractory VF not related to torsades de pointes, administration of intravenous magnesium is not beneficial

Intravenous amiodarone : (Class III , Level of Evidence B)

❑In acute myocardial infarction, prophylactic administration of lidocaine or amiodarone for prevention of VT is harmful

Intravenous verapamil, diltiazem : (Class III , Level of Evidence C)

❑ In a wide QRS tachycardia with unknown origin, administration of verapamil and diltiazem is harmful


 
 
 
 
 
 
 
 
 
 
Sustained monomorphic VT
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hemodynamic stability
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Stable
 
 
 
 
 
 
 
 
 
 
 
Unstable
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
12-Lead ECG, history, physical exam
 
 
 
 
 
 
 
 
 
 
 
Dirrect current cardioversion,ACLS
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Notifying disease causing VT
 
 
 
Cardioversion(class1)
 
 
 
 
 
 
 
VT termination
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Structural heart disease
 
 
 
Intravenous procainamide (class2a)
 
 
 
 
 
Yes, therapy of underlying heart disease
 
NO, cardioversion (class1)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
NO, Ideopathic VT
 
 
 
Intravenous amiodarone or sotalole (class2b)
 
 
 
 
 
 
 
 
VT termination
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Verapamil sensitive VT: Verapamil outflow tract VT: betablocker (class2a)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Effective
 
Non effective: cardioversion
 
 
 
 
 
 
 
 
Yes,therapy of underlying heart disease
 
NO, Sedation ,anesthesia, reassessing antiarrhythmic therapy, repeating cardioversion
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Therapy to prevent recurrence of VT
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
No VT termination
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Catheter ablation (class1)
 
 
Catheter ablation (class1)
 
Verapamil , betablocker (class2a)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 


Intervention

Catheter ablation can only be performed for patients with sustained monomorphic ventricular tachycardia based on these characteristics:

References

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