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Adult cardiac arrest and advanced cardiovascular life support

Adult in-hospital and out-of-hospital cardiac arrest from recognition and high-quality CPR through defibrillation, drugs, airway, reversible causes, mechanical and extracorporeal CPR, termination of resuscitation, and the periarrest bradycardia and tachycardia algorithms.

Definitions and terminology in adult cardiac arrest

Cardiac arrest is the cessation of effective mechanical cardiac activity, recognized clinically by unresponsiveness, absent or abnormal (agonal) breathing, and the absence of a definite central pulse. Sudden cardiac arrest denotes an unexpected arrest in a person without a known terminal illness, and sudden cardiac death is the fatal outcome when resuscitation fails or is not attempted. Prevention of sudden cardiac death in patients at risk, and the evaluation of survivors for an arrhythmic substrate and a defibrillator, are covered in the ventricular tachycardia and sudden cardiac death hub; this page covers the arrest itself and the periarrest rhythms that precede or follow it.

The initial rhythm sorts every arrest into one of two management pathways. Shockable rhythms are ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT), which are terminated by defibrillation. Nonshockable rhythms are asystole and pulseless electrical activity (PEA, an organized electrical rhythm without a palpable pulse). A shock does not correct them, and they are treated by compressions, epinephrine, and correction of the cause. Pseudo-PEA describes organized electrical activity with cardiac wall motion on ultrasound or a measurable arterial waveform but no palpable pulse, a profound low-output state that behaves differently from true electromechanical dissociation.

Return of spontaneous circulation (ROSC) is the resumption of a sustained perfusing rhythm, usually defined in trials as a palpable pulse or measurable blood pressure for at least 20 minutes. The 2025 AHA guidelines use return of circulation (ROC) when circulation is restored by mechanical means such as extracorporeal membrane oxygenation (ECMO). Refractory VF has had many definitions. The 2025 AHA adult advanced life support (ALS) guideline adopts the term persisting VF/pVT for VF or pulseless VT that continues after 3 or more consecutive shocks. The mechanism (failure to terminate versus recurrence after successful termination) usually cannot be distinguished at the bedside. Most VF seen after a shock is recurrent fibrillation after successful defibrillation, not shock failure. Out-of-hospital cardiac arrest (OHCA) and in-hospital cardiac arrest (IHCA) differ in cause, rhythm, response time, and outcome, and registries report them separately using Utstein definitions.

What changed in the 2025 AHA adult resuscitation guidelines

The 2025 AHA guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care were published in October 2025 in 12 parts, with adult basic life support (BLS) in Part 7, adult ALS in Part 9, special circumstances in Part 10, and post-cardiac arrest care in Part 11. They draw on the 2025 International Liaison Committee on Resuscitation (ILCOR) consensus on science with treatment recommendations.

Principal 2025 AHA changes and confirmed positions for adult cardiac arrest, from Parts 1, 4, 7, 9, and 10. Class 1, strong; 2a, moderate; 2b, weak; 3, no benefit or harm. LOE, level of evidence: A, high-quality evidence from more than one randomized trial; B-R, randomized evidence; B-NR, nonrandomized evidence; C-LD, limited data; C-EO, expert opinion.

The 2023 AHA focused update on adult ALS addressed vasopressors and calcium, extracorporeal CPR (ECPR), coronary angiography after arrest, temperature control, seizure management, and organ donation. It contains the current AHA recommendation on ECPR in refractory arrest. The 2025 AHA systems-of-care guideline cites that recommendation and adds new recommendations on how ECPR programs are organized.

Epidemiology and survival of adult cardiac arrest

In the United States, emergency medical services (EMS) attend about 356,000 adults with OHCA each year, about 83 per 100,000 population. In the 2024 Cardiac Arrest Registry to Enhance Survival (CARES), survival to hospital discharge after OHCA was 10.5% and survival with favorable neurologic function about 8.2%. Most arrests occur in private residences, and 18% occur in public places. A bystander provided CPR in 47.7% of adult OHCA and applied an automated external defibrillator (AED) in 7.9%. IHCA affects an estimated 292,000 adults a year, about 60% in intensive care, emergency, and procedural areas and 40% on general wards. Adult survival to discharge after IHCA fell to 18.8% during the COVID-19 pandemic and recovered to 23.6% in 2023.

Adult OHCA and IHCA in the United States. Incidence and survival from the 2025 AHA adult basic life support guideline and systems-of-care guideline; rhythm distribution for IHCA from the 2019 JAMA review of in-hospital cardiac arrest.

Survival is strongly time dependent. In a survival model of witnessed VF, the probability of survival fell by roughly 7% to 10% for each minute without CPR or defibrillation and by about half that rate when bystander CPR was in progress. Survival after a shockable initial rhythm is several-fold higher than after asystole or PEA, both out of and in hospital. VF usually reflects a still-viable myocardium and a reversible electrical event, whereas nonshockable arrest more often reflects prolonged hypoxia, profound shock, or end-stage disease. Between 1 in 6 and 1 in 3 OHCAs in the United States are related to drug overdose, most often opioids. Survivors frequently have cognitive, psychological, and physical impairments, which is why recovery is the final link of the chain of survival.

Pathophysiology of cardiac arrest: electrical, circulatory, and metabolic phases

A three-phase model of VF arrest explains why the best first intervention changes with time. In the electrical phase, roughly the first 4 minutes, myocardial energy stores are relatively preserved and immediate defibrillation is the most effective treatment. In the circulatory phase, roughly 4 to 10 minutes, the fibrillating myocardium is depleted of high-energy phosphates, a shock without preceding compressions more often produces asystole or PEA, and a period of compressions that restores coronary perfusion before the shock improves the response. In the metabolic phase, after about 10 minutes, global ischemia and reperfusion injury dominate, and survival with ordinary CPR and defibrillation is low. This phase is the rationale for extracorporeal circulation in selected patients.

During chest compressions, forward flow is generated by direct cardiac compression and by changes in intrathoracic pressure. Cardiac output during well-performed manual CPR is a fraction of normal. Myocardial blood flow depends on the coronary perfusion pressure, which is the aortic diastolic (relaxation-phase) pressure minus the right atrial pressure. Every pause in compressions drops aortic pressure within seconds, and several compressions are needed to rebuild it. Incomplete chest recoil raises intrathoracic and right atrial pressure and lowers coronary perfusion pressure. Excessive ventilation raises mean intrathoracic pressure, impairs venous return, and lowers coronary and cerebral perfusion. In one EMS series, rescuers delivered a mean of 30 breaths a minute, and hyperventilation lowered survival in an animal model.

Epinephrine acts during CPR mainly through alpha-adrenergic vasoconstriction, which raises aortic diastolic pressure and coronary perfusion pressure. Its beta-adrenergic effects increase myocardial oxygen consumption and may promote recurrent ventricular arrhythmias after ROSC, and its microvascular vasoconstriction may reduce cerebral microcirculatory flow. These opposing effects explain why epinephrine increases ROSC and survival but has not clearly improved survival with good neurologic function.

The common causes of adult arrest include acute coronary occlusion and myocardial ischemia, scar-related VF in chronic coronary disease and cardiomyopathy, inherited arrhythmia syndromes, respiratory failure and hypoxia, hemorrhage and hypovolemia, pulmonary embolism, tamponade, tension pneumothorax, electrolyte disorders, drug toxicity, and hypothermia. These are organized for bedside use as the reversible causes in the Hs and Ts table.

The chain of survival and systems of care

The 2025 AHA guidelines describe a single chain of survival for in-hospital and out-of-hospital arrest, with six links: recognition and emergency activation, high-quality CPR, defibrillation, advanced resuscitation interventions, post-cardiac arrest care, and recovery. Prevention and preparedness are discussed in the guideline but were not added as a link.

Out of hospital, telecommunicators locate the event first and then instruct callers to begin CPR for suspected arrest (Class 1). Compression-only telecommunicator CPR is recommended for adult OHCA (Class 1, A); in pooled adult randomized trials it carried a risk ratio of 1.22 for survival. Two scripted questions about consciousness and normal breathing identify most OHCAs, but telecommunicator recognition varies between 46% and 98% across systems. Public access defibrillation programs are recommended in communities at high risk (Class 1). In the Public Access Defibrillation trial, 30 of 128 arrests in units trained in CPR plus AED use survived compared with 15 of 107 in units trained in CPR alone. Mobile technologies that summon nearby trained volunteers are reasonable (Class 2a), and AED delivery by drone is under evaluation. Within EMS, the presence of an ALS clinician during resuscitation can be beneficial (Class 2a), and on-scene resuscitation focused on sustained ROSC before transport is reasonable (Class 2a). Chest compressions during transport are of lower quality, and intra-arrest transport was associated with about half the survival to discharge in secondary analyses.

Organizations that treat cardiac arrest are expected to collect process and outcome data (Class 1), and resuscitated patients may be transported to specialized cardiac arrest centers when comprehensive post-arrest care is not available locally (Class 2b). Patients resuscitated from arrest who later meet neurologic criteria for death are evaluated for organ donation (Class 1).

Recognition of cardiac arrest and the pulse check

Lay rescuers who find an unresponsive adult with absent or abnormal breathing assume cardiac arrest (Class 1), activate the emergency response system, and begin compressions immediately. A lone rescuer with a mobile phone activates the system and begins CPR at the same time (Class 1). Agonal gasping is a sign of arrest, not of effective breathing. Health care professionals assess breathing and the central pulse simultaneously for no more than 10 seconds (Class 1). When a pulse is not definitely felt within 10 seconds, compressions begin. Manual pulse palpation is unreliable during low-output states. Starting compressions in a patient with a weak pulse costs far less than withholding them in a patient in arrest.

During resuscitation, the pulse check is combined with the rhythm check every 2 minutes and is limited to the same 10 seconds; a pulse is sought only when an organized rhythm is present. A lone health care professional begins with compressions, not ventilation (Class 1). Seizure-like activity at collapse is common in VF and does not exclude arrest. In monitored patients, the arrest is recognized from the monitor and the arterial or end-tidal CO2 waveform before any pulse check; a witnessed, monitored VF arrest with a defibrillator at hand is shocked immediately (Class 2a).

High-quality CPR: rate, depth, recoil, compression fraction, and ventilation

High-quality CPR is the intervention with the broadest effect on outcome in every rhythm, and the 2025 AHA adult basic life support guideline specifies its components.

Components of high-quality adult CPR in the 2025 AHA adult basic life support and advanced life support guidelines. Health care professionals may also use continuous compressions with asynchronous breaths before an advanced airway is placed (Class 2b).

Compression depth and rate interact: rates above 120 per minute are associated with shallower compressions, and depths beyond 6 cm are associated with injury and, in observational data, lower survival. Complete recoil allows venous return and a fall in intrathoracic pressure. Compressor fatigue reduces depth within 1 to 2 minutes, often without the compressor noticing, which is the basis for rotation at each rhythm check. Rescuers kneel beside a patient on the floor; in hospital, the bed is lowered or a step stool is used, and the mattress CPR setting is engaged. The 2025 guideline found no benefit from a partial backboard under a patient on a hospital mattress, and it recommends moving an obese patient to a firm surface only when the benefit outweighs the interruption.

Compression-only CPR by lay rescuers produces outcomes similar to CPR with breaths in the first minutes of witnessed adult cardiac arrest. Trained rescuers provide breaths with compressions (Class 2a), because oxygen stores fall as arrest continues and asphyxial causes such as drowning and overdose require ventilation. Cricoid pressure is not used routinely (Class 3: No Benefit).

Monitoring CPR quality: capnography, arterial pressure, and feedback

Physiologic monitoring during CPR serves three purposes: confirming and monitoring an advanced airway, assessing the quality of compressions, and detecting ROSC without a pause. The 2025 AHA ALS guideline states that physiologic parameters such as arterial blood pressure or end-tidal CO2 (ETCO2) may be used to monitor and optimize CPR quality (Class 2b).

Waveform capnography. ETCO2 during CPR reflects pulmonary blood flow, and therefore cardiac output generated by compressions, provided ventilation is constant. Values of at least 10 mm Hg, and ideally 20 mm Hg or greater, may indicate adequate compressions, while values persistently below 10 mm Hg are generally associated with poor outcome. A sudden sustained rise of more than 10 mm Hg may indicate ROSC (Class 2b) and allows the team to complete the 2-minute cycle and confirm a pulse at the rhythm check. ETCO2 is affected by factors other than flow. It rises transiently after sodium bicarbonate and falls after an epinephrine bolus because of increased pulmonary vascular resistance and shunting. It also falls with hyperventilation and is low in pulmonary embolism, severe bronchospasm, and an obstructed tube. Continuous waveform capnography is recommended to confirm and monitor tracheal tube placement during CPR (Class 1); a flat trace after intubation indicates esophageal placement or no pulmonary blood flow and is acted on immediately.

Arterial pressure. When an arterial line is already in place, as in intensive care, the operating room, and the catheterization laboratory, the relaxation-phase (diastolic) arterial pressure approximates coronary perfusion pressure. The 2025 AHA guideline states that adult data are inadequate to set a specific target pressure. An arterial waveform may also be used to detect ROSC during compressions (Class 2b, C-EO). Arterial line insertion does not interrupt compressions.

Feedback and other measures. Audiovisual feedback devices that report rate, depth, recoil, and pauses are reasonable (Class 2a), and defibrillator-recorded CPR data underpin quality review and debriefing. Arterial blood gas measurement during CPR has uncertain benefit (Class 2b), and a single gas obtained during low flow does not reflect tissue acid-base status. Artifact-filtering algorithms that allow rhythm analysis during compressions, and VF waveform analysis to guide timing of shocks, have not been shown to improve outcome (Class 2b).

The adult cardiac arrest algorithm: shockable and nonshockable pathways

The AHA adult cardiac arrest algorithm organizes resuscitation into 2-minute cycles of compressions separated by brief rhythm checks. The two pathways differ in the shock sequence, drug timing, and doses.

Adult cardiac arrest algorithm, after the 2025 AHA adult advanced life support guideline and its algorithm. Epinephrine is reasonable every 3 to 5 minutes (Class 2a), as soon as feasible in nonshockable rhythms (Class 2a), and after initial defibrillation attempts fail in shockable rhythms (Class 2a). Amiodarone or lidocaine may be considered for VF or pVT unresponsive to defibrillation (Class 2b).

The sequence assumes high-quality compressions throughout. Drugs are drawn up and given during compressions, not during the rhythm check. The defibrillator is charged during the last seconds of each cycle so that the shock follows the rhythm analysis within a few seconds. Rhythm and pulse checks take no more than 10 seconds. An organized rhythm at a rhythm check prompts a pulse check; no pulse means PEA, and compressions resume at once.

The calculator derives the next shock, epinephrine, and antiarrhythmic step from the rhythm, the defibrillator type, the shocks and drugs already given, and body weight, using 2025 AHA algorithm doses and timing.

Epinephrine 1 mg IV or IO every 3–5 minutes; in shockable rhythms it is given after initial defibrillation attempts fail, which in the AHA algorithm is after the second shock. Amiodarone 300 mg then 150 mg, or lidocaine 1–1.5 mg/kg then 0.5–0.75 mg/kg, for VF or pVT persisting after the third shock. Doses apply to adults in arrest only.

Defibrillation: waveforms, energy, pad position, and the peri-shock pause

Defibrillation depolarizes a critical mass of myocardium so that organized activity can resume. Its success depends on the current that crosses the heart, which is determined by the selected energy, the waveform, transthoracic impedance, pad position, and the metabolic state of the myocardium. The 2025 AHA guideline recommends defibrillators with biphasic or monophasic waveforms for VF and pVT (Class 1) and prefers biphasic waveforms (Class 2a), which terminate VF at lower energy than monophasic waveforms.

Defibrillation energy by waveform. In the 2025 AHA guideline, the choice of fixed or escalating energy for subsequent shocks follows the manufacturer's instructions for that waveform (Class 2a, C-LD). Higher energy for second and later shocks on escalating devices may be considered (Class 2b, B-R). The manufacturer's recommended first-shock dose, or the maximal dose when that is unknown, may be reasonable (Class 2b, C-LD). The setting printed on the defibrillator governs.

In the BIPHASIC trial of OHCA, a fixed 150-J strategy and an escalating strategy of 200, 300, and 360 J had similar first-shock success, but escalating energy produced more conversion to an organized rhythm in patients who needed multiple shocks; survival did not differ. A single-shock strategy with immediate resumption of compressions is preferred over stacked shocks (Class 2a), because stacked shocks lengthen interruptions and the first-shock success of biphasic waveforms is high. The single-shock strategy improved survival to admission and discharge. The exception is a monitored arrest after cardiac surgery, where up to 3 stacked shocks are delivered immediately before compressions are started (Class 1).

Pad position. Adhesive pads are placed on bare skin in the anterolateral position (right infraclavicular and left midaxillary at the cardiac apex) or the anteroposterior position (left precordium and left infrascapular back) (Class 2a). The 2025 AHA guideline lists the optimal configuration as a knowledge gap. The apical pad is placed laterally enough that current traverses the left ventricle. A common error is a pad placed over the breast or too medially. Excess hair, sweat, transdermal patches, and poor pad adhesion increase impedance; a bra may be repositioned instead of removed (Class 2b). Pads are placed at least several centimeters from an implanted pacemaker or defibrillator generator, and a subsequent device check is performed. Manual pressure on a pad with appropriate insulation, and changing to a new pad vector, increase delivered current and are the first steps when shocks repeatedly fail.

The peri-shock pause. Longer pre-shock and peri-shock pauses are independently associated with lower survival to discharge after shockable OHCA. The pre-shock pause is shortened by charging the defibrillator during the final compressions of each cycle, analyzing the rhythm quickly, and delivering the shock as soon as the rhythm is confirmed; the post-shock pause is eliminated by resuming compressions immediately without a rhythm or pulse check. Rescuers are cleared from the patient by announcement while compressions continue until the moment of shock delivery. Hands-on defibrillation during compressions is not a standard technique.

Shock before or after CPR. For a witnessed or monitored VF arrest with a defibrillator attached or immediately available, immediate defibrillation is reasonable (Class 2a). For an unmonitored arrest, CPR is provided until the defibrillator or AED is applied (Class 1), and a brief period of CPR while it is obtained is reasonable (Class 2a); trials of a fixed period of CPR before the first shock showed no benefit. Electrical pacing has no role in established cardiac arrest, including asystole (Class 3: No Benefit).

Shockable rhythms: ventricular fibrillation, pulseless VT, and persisting VF

VF is chaotic ventricular electrical activity without organized QRS complexes or effective contraction; coarse VF has higher amplitude and a better response to defibrillation than fine VF, and very fine VF can be mistaken for asystole. Pulseless VT is a wide-complex tachycardia without a palpable pulse and is treated identically to VF with unsynchronized shocks. Polymorphic VT, including torsades de pointes, is always electrically and hemodynamically unstable in the 2025 AHA guideline and is treated with an immediate unsynchronized shock whether or not a pulse is present (Class 1), because synchronization to a varying QRS is unreliable.

Persisting VF. VF or pVT that continues or recurs after 3 or more shocks is common and carries a poor prognosis. The 2025 AHA approach is to review, in order, the factors that determine shock success and recurrence. Pad position, contact, and vector are verified. Pressure is applied to the anterior pad, and energy is escalated to the device maximum. Compression quality is confirmed by capnography or arterial pressure, and epinephrine and an antiarrhythmic are given at the recommended intervals. Causes that recreate the arrhythmic substrate are treated, above all acute coronary occlusion and also hyperkalemia, hypomagnesemia with torsades, drug toxicity, and excess endogenous or exogenous catecholamines.

The DOSE-VF cluster-randomized trial in Canadian OHCA compared standard defibrillation, vector change (anterior-posterior pads), and double sequential external defibrillation (two defibrillators fired in rapid sequence by one operator) after three failed shocks. Survival to discharge was 13.3% with standard defibrillation, 21.7% with vector change, and 30.4% with double sequential defibrillation. The 2025 AHA guideline grades the usefulness of both vector change and double sequential defibrillation as not established (Class 2b, B-R). The benefit was seen in the intention-to-treat analysis but not in the analysis by treatment actually received. In a secondary analysis, the double sequential benefit was confined to the 17% of patients with incessant VF. The 2025 ILCOR consensus, by contrast, suggests that either strategy may be considered after 3 or more consecutive shocks (weak recommendation), with a single operator activating both defibrillators if double sequential defibrillation is used.

Beta-blockade with esmolol or landiolol aims to blunt the adrenergic drive that sustains electrical storm; the 2025 AHA guideline grades beta-blockers, bretylium, procainamide, and sotalol for shock-refractory VF as of uncertain benefit (Class 2b). Persisting VF in a witnessed arrest with a presumed coronary cause is the principal indication for extracorporeal CPR and emergency angiography in centers with the capability, discussed in extracorporeal CPR.

Nonshockable rhythms: asystole and pulseless electrical activity

Asystole is the absence of ventricular electrical activity. Before asystole is accepted, lead connections, gain, and a second lead are confirmed, because fine VF and a disconnected lead can produce a flat line. Asystole is the terminal rhythm of prolonged arrest and carries the lowest survival of any initial rhythm. Atropine has had no place in the AHA arrest algorithm since 2010, and transcutaneous or transvenous pacing does not improve outcome in established asystolic arrest (Class 3: No Benefit). The exception is asystole or bradycardic arrest after cardiac surgery with epicardial pacing wires in place, in which immediate pacing is recommended, with compressions started if pacing does not restore circulation within 1 minute (Class 1).

Pulseless electrical activity covers a spectrum from true electromechanical dissociation to pseudo-PEA with weak contraction and an unpalpable pulse. The management is compressions, epinephrine as soon as feasible, and an urgent search for the cause, since PEA usually has one. A pragmatic bedside framework uses QRS width. Narrow-complex PEA more often reflects a mechanical cause with a structurally intact conduction system and right ventricular inflow or outflow obstruction: tamponade, tension pneumothorax, massive pulmonary embolism, hypovolemia, or mechanical complication of infarction. Wide-complex PEA more often reflects a metabolic or myocardial cause: severe hyperkalemia, sodium channel blocker toxicity, profound acidosis, or extensive myocardial ischemia. The distinction is a guide to the order of investigation, not a diagnosis.

Point-of-care ultrasound distinguishes PEA with no cardiac motion from pseudo-PEA with organized contraction, as described under point-of-care ultrasound during cardiac arrest. In pseudo-PEA, the circulation is supported with continuing compressions and vasopressors while the cause is treated. Time to epinephrine matters in nonshockable arrest: in a registry of IHCA with nonshockable rhythms, each successive 3-minute interval of delay to the first dose was associated with progressively lower survival to discharge, ROSC, and neurologically intact survival.

Vascular access during cardiac arrest: intravenous first, intraosseous second

Vascular access is obtained without interrupting compressions or delaying defibrillation. The 2025 AHA guideline recommends that clinicians first attempt peripheral intravenous access (Class 1, A). Intraosseous access is reasonable if initial intravenous attempts are unsuccessful or not feasible (Class 2a, A), and central venous access by trained clinicians may be considered after both fail (Class 2b). The ILCOR 2025 treatment recommendation adds a good practice statement that intraosseous access is reasonable if intravenous access cannot be achieved within two attempts. The endotracheal route was removed from the 2025 guideline because it produces low, unpredictable drug concentrations.

Randomized trials of intraosseous versus intravenous access in adult OHCA. The trials were designed for superiority, so the absence of a difference does not establish equivalence. In PARAMEDIC-3, enrollment stopped at about 6,000 of a planned 15,000 participants, and crossover between routes occurred in 8.7%.

Peripheral intravenous drugs reach the central circulation more slowly than central drugs, and each is followed by a 20-mL saline flush and elevation of the limb. Humeral and proximal tibial intraosseous sites are used, and a site distal to a suspected fracture or in an injured limb is avoided. Most resuscitation drugs and fluids can be given by the intraosseous route at the same doses. In patients with an existing central venous catheter, drugs are given centrally. Intracardiac injection has no role.

Epinephrine and other vasopressors during cardiac arrest

Epinephrine is recommended for adults in cardiac arrest (Class 1, B-R), at 1 mg intravenously or intraosseously every 3 to 5 minutes (Class 2a). In nonshockable rhythms, it is reasonable to give it as soon as feasible (Class 2a, B-NR); in shockable rhythms, after initial defibrillation attempts have failed (Class 2a, B-NR). High-dose epinephrine is not recommended (Class 3: No Benefit), and vasopressin alone or combined with epinephrine offers no advantage as a substitute for epinephrine (Class 3: No Benefit).

Randomized and registry evidence for vasopressors during cardiac arrest. In PARAMEDIC2, the median time from emergency call to drug was over 20 minutes, which limits inference about early administration.

Epinephrine's effect on ROSC is consistent and its effect on neurologically intact survival is small or uncertain, which explains the guideline's strong recommendation for use with weaker recommendations for timing. In shockable rhythms, early epinephrine before initial shocks offers little because defibrillation is the definitive treatment, and the drug may increase myocardial oxygen demand and recurrent VF. In nonshockable rhythms, where no shock is available, earlier administration is associated with better outcomes. Fixed intervals of about 4 minutes, timed to alternate rhythm checks, are a practical way to stay within the 3-to-5-minute window. The combination of vasopressin and corticosteroids increased ROSC in two Greek IHCA trials and in VAM-IHCA without improving survival. The 2025 AHA guideline grades steroids during arrest as of uncertain benefit (Class 2b), and ILCOR suggests against the combination in IHCA and OHCA.

Antiarrhythmic drugs for shock-refractory VF and pulseless VT

Amiodarone or lidocaine may be considered for VF or pVT unresponsive to defibrillation (Class 2b, B-R). Amiodarone is given as a 300-mg intravenous or intraosseous bolus, followed by 150 mg if VF persists; lidocaine is given as 1 to 1.5 mg/kg, followed by 0.5 to 0.75 mg/kg. The drugs are alternatives, not a combination.

In the Amiodarone, Lidocaine, or Placebo Study (ALPS), adults with OHCA and VF or pVT after at least one shock received amiodarone, lidocaine, or placebo. Survival to discharge was 24.4%, 23.7%, and 21.0%, respectively, a difference that was not significant. Both drugs improved survival to hospital admission, and in the prespecified subgroup with bystander-witnessed arrest, survival to discharge was higher with either drug than with placebo. A secondary analysis found that amiodarone given early after EMS arrival was associated with better outcomes, suggesting a time-dependent benefit. The data do not distinguish the two drugs.

Amiodarone causes hypotension and bradycardia after ROSC, more so with older formulations containing polysorbate. Lidocaine has a narrow therapeutic range in older adults and in hepatic and heart failure. Magnesium is not given routinely for VF (Class 3: No Benefit). It may be considered for recurrent torsades de pointes, which is polymorphic VT with a long QT interval (Class 2b); the European Resuscitation Council (ERC) regimen is 2 g (8 mmol) intravenously over about 10 minutes. For polymorphic VT with a normal QT interval, lidocaine, amiodarone, and treatment of myocardial ischemia may be considered (Class 2b), and routine magnesium has no benefit (Class 3: No Benefit). Antiarrhythmic infusions after ROSC, and the management of recurrent VF and electrical storm in survivors, are covered in the ventricular tachycardia and sudden cardiac death hub.

Calcium, sodium bicarbonate, fibrinolytics, and other drugs during arrest

Trials found no benefit from several drugs once given routinely during arrest, and these are now reserved for specific causes.

Drugs used during adult cardiac arrest, with the 2025 AHA class of recommendation. The 2025 AHA guideline does not specify calcium or bicarbonate doses for hyperkalemic arrest; calcium chloride 10% 10 mL and sodium bicarbonate 50 mmol are the ERC 2025 doses, and calcium gluconate 10% 30 mL delivers a similar amount of calcium. Management of these causes is detailed in the resuscitation in special circumstances hub.

Calcium. In the Danish COCA trial, calcium chloride given after the first dose of epinephrine in OHCA was stopped early for a signal of harm: sustained ROSC occurred in 19% with calcium and 27% with saline (RR 0.72, 95% CI 0.49–1.03), and survival and neurologic outcome did not favor calcium. Routine calcium is not recommended (Class 3: No Benefit, B-R). In hyperkalemic arrest, the effectiveness of calcium is not well established (Class 2b), but it is given because it stabilizes the myocardial membrane.

Sodium bicarbonate. Bicarbonate generates carbon dioxide that diffuses into cells and worsens intracellular acidosis unless ventilation is increased, causes hypernatremia and hyperosmolality, and shifts the oxyhemoglobin curve. Observational associations with outcome are confounded by resuscitation time bias, because bicarbonate is given late in long resuscitations. Routine use is not recommended (Class 3: No Benefit), and ILCOR suggests against buffering agents in IHCA and OHCA unless a special circumstance is present.

Fibrinolysis. In the TROICA trial of OHCA with presumed cardiac cause, tenecteplase during CPR did not improve 30-day survival (14.7% vs 17.0%) and increased intracranial hemorrhage. Routine fibrinolysis is therefore not used. Fibrinolysis is reasonable for arrest from confirmed pulmonary embolism (Class 2a) and may be considered for suspected pulmonary embolism (Class 2b), as discussed in cardiac causes of arrest.

Airway management and ventilation during cardiac arrest

Airway management during arrest balances oxygenation and ventilation against interruptions in compressions, aspiration, and unrecognized misplacement. Bag-mask ventilation or an advanced airway strategy may be used for adults in arrest in any setting (Class 2b, B-R). Bag-mask ventilation is most effective with two rescuers, one holding the mask with two hands and the other squeezing the bag (Class 2a), with oropharyngeal or nasopharyngeal adjuncts. Each breath produces visible chest rise over about 1 second; large, fast breaths cause gastric insufflation and raise intrathoracic pressure.

Randomized trials of airway strategy in adult OHCA. Outcomes depend on intubation success rates, which differ widely between systems.

The 2025 AHA guideline states that a supraglottic airway can be acceptable in settings with a low intubation success rate (Class 2a), that either a supraglottic airway or an endotracheal tube can be used for OHCA in systems with high success rates or skilled clinicians (Class 2a), and that either can be used for IHCA managed by expert clinicians (Class 2a). Clinicians who intubate need frequent experience or retraining (Class 1). If placement of an advanced airway would interrupt compressions, it is deferred until the patient fails to respond to initial CPR and defibrillation attempts or until ROSC (Class 1). Intubation is performed with compressions continuing; a pause, if needed, is limited to passage of the tube through the cords.

Tube position is confirmed by continuous waveform capnography in addition to clinical assessment (Class 1); auscultation, chest rise, and tube misting are unreliable, and colorimetric detectors are a fallback when waveform capnography is not available. With an advanced airway in place, ventilation is delivered at 1 breath every 6 seconds (10 per minute) without pausing compressions (Class 2b). The maximal feasible inspired oxygen concentration is reasonable during CPR (Class 2b); oxygen titration begins only after ROSC. Front-of-neck access by cricothyroidotomy is reasonable for trained rescuers when standard airway strategies have failed (ILCOR good practice statement).

Reversible causes of cardiac arrest: the Hs and Ts

The reversible causes are reviewed at every arrest and are the main determinant of outcome in nonshockable and persisting shockable rhythms. The history from witnesses, the setting, the preceding vital signs and laboratory values, the ECG before the arrest, and the bedside examination usually point to one or two causes before any test is available.

Reversible causes of adult cardiac arrest with the findings that suggest each one and the corresponding treatment. Hyperkalemia, poisoning, hypothermia, drowning, anaphylaxis, and arrest in pregnancy are covered in detail in the resuscitation in special circumstances hub.

Some causes call for resuscitation well beyond the usual duration because the cause can be reversed and neurologic recovery is possible after long low-flow periods: accidental hypothermia, many poisonings, hyperkalemia, pulmonary embolism treated with fibrinolysis, and refractory VF bridged to extracorporeal support. Profound hypothermia in particular is not treated as death until the patient is rewarmed, except with an obviously lethal injury.

Point-of-care ultrasound during cardiac arrest

Focused cardiac ultrasound during arrest can show pericardial effusion with tamponade, right ventricular dilation suggesting pulmonary embolism, an empty hyperdynamic ventricle in hypovolemia, absent lung sliding in pneumothorax, and the presence or absence of organized cardiac motion. The 2025 AHA guideline states that its use by experienced clinicians to diagnose reversible causes is not well established (Class 2b), and that it is acceptable only when it does not interrupt compressions. The 2025 ILCOR consensus suggests against routine ultrasound during CPR to diagnose reversible causes, and supports it as an additional tool when a specific reversible cause is suspected and experienced personnel can perform it without interrupting CPR.

The main harm is interruption: in a prospective cohort, pauses in compressions were significantly longer when ultrasound was performed during the rhythm check. Interruptions are minimized by obtaining the image with a subxiphoid or parasternal view during the rhythm check, recording a clip, and resuming compressions before the clip is interpreted. Transesophageal echocardiography, available in some emergency departments and catheterization laboratories, images the heart during compressions without pauses and shows the area of maximal compression.

Prognosis from ultrasound. In the REASON study, absence of cardiac activity during arrest was associated with low but not zero survival, and the presence of cardiac activity, including in patients with PEA, with higher rates of ROSC and survival. Interobserver agreement on cardiac standstill is imperfect, and fibrillation can be misread as standstill. The 2025 AHA guideline grades echocardiography for prognostication during CPR as not well established (Class 2b), and ILCOR suggests against it; absent cardiac motion is therefore not used alone to stop resuscitation.

Coronary occlusion, pulmonary embolism, and tamponade as causes of arrest

Acute coronary occlusion. Acute coronary occlusion causes a large share of OHCA with a shockable rhythm, and unstable coronary disease is present in most patients with refractory VF who undergo extracorporeal CPR and angiography. During ongoing arrest, coronary angiography is feasible only with mechanical CPR or extracorporeal support. After ROSC, emergent angiography is recommended for suspected cardiac cause with persistent ST elevation (Class 1), and the selection of patients without ST elevation is discussed in the post-cardiac arrest care hub. Arrest complicating acute myocardial infarction is covered in the ST-elevation myocardial infarction hub.

Arrest in the catheterization laboratory. Arrest during PCI or structural intervention is usually witnessed and monitored, often shockable, and often due to a mechanical problem the operator can correct. The 2025 AHA special circumstances guideline states that mechanical CPR devices are reasonable to provide compressions in the cardiac intervention laboratory (Class 2a) and that extracorporeal life support is reasonable when initial therapy fails (Class 2a). Intracoronary epinephrine may be reasonable (Class 2b). Causes specific to the laboratory include coronary dissection or no-reflow, air embolism, perforation with tamponade, acute stent thrombosis, vasovagal reactions and contrast reactions, and vascular access bleeding. Fluoroscopy confirms tamponade or a new occlusion within seconds, and a temporary pacing wire treats sudden complete heart block.

Arrest after cardiac surgery. VF witnessed after cardiac surgery is treated with up to 3 immediate stacked shocks, with compressions started if defibrillation does not succeed within 1 minute (Class 1). Rapid resternotomy in an appropriately staffed and equipped intensive care unit is reasonable (Class 2a), and the capability is kept for at least 10 days after surgery; external compressions are given when resternotomy is not immediately available (Class 1). Asystole or bradycardic arrest with epicardial wires is paced immediately (Class 1).

Pulmonary embolism. Arrest from massive pulmonary embolism often presents as PEA with a low ETCO2 and a dilated right ventricle. In a retrospective multicenter study of patients given systemic fibrinolysis during arrest, cited in the 2025 AHA guideline, survival to discharge was 26% when pulmonary embolism was confirmed and 4% when it was presumed. Systemic fibrinolysis, surgical embolectomy, and percutaneous mechanical embolectomy are reasonable for confirmed pulmonary embolism (Class 2a). Fibrinolysis may be considered when pulmonary embolism is suspected (Class 2b), and extracorporeal life support is reasonable for arrest from confirmed or suspected pulmonary embolism (Class 2a). The optimal duration of CPR after systemic fibrinolysis is unclear (Class 2b); European guidance advises at least 60 to 90 minutes. Diagnosis, risk categories, and reperfusion outside arrest are covered in the pulmonary embolism hub.

Tamponade. Tamponade is a mechanical cause of PEA that compressions do not correct, because they have limited effect against a compressed heart. Ultrasound-guided pericardiocentesis, or surgical drainage after cardiac surgery, trauma, and aortic dissection, is the definitive treatment. Hemopericardium from type A dissection or free wall rupture requires surgery, and pericardiocentesis is a temporizing measure.

Mechanical CPR devices and head-up CPR

Mechanical CPR devices deliver compressions of consistent rate and depth without fatigue, using either a piston with a suction cup (active compression-decompression) or a load-distributing band around the chest. Routine use of mechanical CPR devices does not improve outcome and is not recommended (Class 3: No Benefit, B-R). Use may be considered in specific settings where high-quality manual compressions are challenging or dangerous for the rescuer (Class 2b): ambulance transport, prolonged resuscitation, the catheterization laboratory, imaging suites, and during cannulation for extracorporeal support. The 2025 ILCOR systematic review of 11 trials reached the same conclusion and noted that systems already using devices need not stop.

Randomized trials of mechanical CPR in adult OHCA. Deployment pauses, delayed first shocks, and training determined results; device-related injuries include rib and sternal fractures and, less often, visceral and vascular injury.

The device is applied after the first shock, if indicated, to avoid delaying defibrillation, and deployment pauses are rehearsed so that they stay short. Defibrillation can be delivered during mechanical compressions with the pads in place. Mechanical CPR allows coronary angiography and PCI during ongoing arrest, which is the basis of its role in the catheterization laboratory and in extracorporeal CPR pathways.

Head-up CPR. Controlled elevation of the head and thorax, combined with active compression-decompression and an impedance threshold device, improves cerebral perfusion pressure in animal models. The 2025 AHA guideline identified no randomized trials and only 3 observational studies and recommends against head-up CPR except in clinical trials (Class 3: No Benefit). Impedance threshold devices used alone did not improve survival in a large randomized trial and are not used routinely.

Extracorporeal CPR for refractory cardiac arrest

Extracorporeal CPR (ECPR) is the initiation of venoarterial ECMO during cardiac arrest refractory to conventional ALS, restoring circulation and oxygenation while the cause is treated. It is used in less than 1% of all cardiac arrests. The 2023 AHA focused update states that ECPR is reasonable for selected patients with arrest refractory to standard ALS when provided within an appropriately trained and equipped system of care (Class 2a, B-R). The 2025 AHA systems-of-care guideline adds that centers with ECPR programs develop and regularly reassess selection criteria (Class 2a) and that clinicians performing adult peripheral cannulation have percutaneous cannulation experience (Class 2a). A regionalized approach is reasonable (Class 2a), and intra-arrest transport to an ECPR center may be considered for limited, highly selected adult OHCA patients (Class 2b). ILCOR suggests that ECPR may be considered as rescue therapy for selected adults with OHCA and IHCA when conventional CPR is failing, in settings where it can be implemented (weak recommendations).

Randomized trials of extracorporeal CPR in adult OHCA. Results were best in a single highly experienced system with short times to flow.

Outcome after ECPR depends on the low-flow interval from collapse to extracorporeal flow, which in successful programs is under about 60 minutes, and on case selection. Selection criteria in the trials and in established programs include younger age, witnessed arrest with bystander CPR, an initial shockable rhythm or another presumed reversible cause, ETCO2 and other signs of effective CPR during transport, and the absence of severe comorbidity or a terminal illness. The decision to proceed is made early, because the low-flow interval continues to lengthen during transport and cannulation. In ARREST the trigger was 3 failed shocks, and in Prague OHCA randomization followed a minimum of 5 minutes of ALS without ROSC. Arrest from massive pulmonary embolism, accidental hypothermia, and some poisonings are additional indications. Cannulation is femoral-femoral under ultrasound or fluoroscopic guidance with mechanical compressions continuing. Left ventricular distension, limb ischemia, bleeding, and differential hypoxemia are the principal complications; device management is covered in the venoarterial ECMO hub.

Termination of resuscitation and prognostication during arrest

Resuscitation is stopped when ROSC is very unlikely and no reversible cause remains to be treated, or when continued efforts are inconsistent with the patient's known wishes. The 2025 AHA guideline recommends validated termination of resuscitation (TOR) rules for EMS, matched to the scope of practice of the crew that uses them, and it emphasizes that TOR rules are conservative and apply only to the populations in which they were validated.

Prehospital termination of resuscitation rules for adult OHCA in the 2025 AHA guideline. In the original validation of the BLS rule, fewer than 1% of patients who met the criteria survived to discharge.

End-tidal CO2. In intubated patients, failure to achieve an ETCO2 greater than 10 mm Hg by waveform capnography after 20 minutes of ALS resuscitation may be considered as one component of a multimodal decision to stop (Class 2b). It is not used alone, and in nonintubated patients a specific ETCO2 cutoff at any time is not used to stop resuscitation (Class 3: Harm), because a supraglottic or bag-mask airway leak gives falsely low values. Low ETCO2 also reflects poor compressions, hyperventilation, and pulmonary embolism, each of which can be corrected.

In hospital. No validated TOR rule exists for IHCA. Decisions incorporate the arrest duration, the initial and subsequent rhythms, witnessed status, ETCO2 and arterial pressure trends, ultrasound findings, the treated and untreated reversible causes, comorbidity, and the patient's goals. No single intra-arrest finding is a reliable predictor of death, and the 2025 AHA ethics guideline cautions that predictions made before, during, and after CPR are particularly susceptible to self-fulfilling prophecy. Arrest duration alone is not a criterion; some causes justify prolonged resuscitation, as noted under reversible causes.

Ethics, goals of care, and family presence. The 2025 AHA ethics guideline describes portable orders for life-sustaining treatment (POLST), available throughout the United States, as the best method to document advance care plans specific to CPR. It holds that deliberately ineffective CPR (a slow code) is deceptive and not ethically sound. When uncertainty exists, resuscitation is generally started, because it can be stopped later while withholding it is irreversible. The ethics guideline calls family presence during resuscitation the recommended approach in most situations. In a randomized trial in France, relatives offered the opportunity to witness CPR at home had fewer symptoms of post-traumatic stress at 90 days than relatives in the control group, without interference with resuscitation. A staff member is assigned to support the family and explain events.

In-hospital arrest systems, team dynamics, and debriefing

Prevention of IHCA. Most IHCA is preceded by hours of physiologic deterioration. Early warning score systems that aggregate vital signs and mental status can be beneficial to detect deterioration (Class 2a), although observational studies conflict on whether they reduce arrest. Rapid response or medical emergency teams can be effective in reducing arrest, particularly on general wards (Class 2a), with mixed evidence for hospital mortality. Unit safety huddles can reduce arrest rates (Class 2a). Goals-of-care discussions during deterioration prevent resuscitation that patients would not want.

The code team. In-hospital code teams are composed of members with ALS training (Class 1), and designated or dedicated teams with clearly defined roles, diverse expertise, and adequate training are reasonable (Class 2a). The team leader stands back from procedures, assigns roles by name, maintains the 2-minute cycle and drug timing, summarizes at intervals, and invites input. Closed-loop communication, in which an order is repeated back and its completion reported, prevents omitted or duplicated drugs. A recorder documents rhythm, shocks, drugs, airway events, and times, and a timer announces each cycle. Cognitive aids and checklists reduce omissions in rare situations such as arrest in pregnancy, local anesthetic toxicity, and hyperkalemia.

Debriefing and quality improvement. Performance-focused debriefing of rescuers after cardiac arrest can be effective (Class 2a). It is particularly useful when it reviews objective data recorded by the defibrillator, such as compression rate, depth, fraction, and pause duration (Class 2a), is facilitated by trained clinicians (Class 2a), and includes both immediate and delayed sessions (Class 2a). Resuscitation programs report process and outcome measures in the Utstein format, which standardizes definitions of witnessed status, bystander CPR, initial rhythm, ROSC, and survival, and allows comparison between systems. Neurologic outcome in registries and trials is reported with the cerebral performance category from CPC 1 (good function) to CPC 5 (death or brain death), in which CPC 1 or 2 is considered favorable. The modified Rankin scale is also used, in which scores of 0 to 3 are commonly considered favorable after arrest.

Resuscitation skills decay within months of training and are maintained by frequent brief practice, simulation, and feedback.

Periarrest bradycardia: atropine, pacing, and chronotropic infusions

Bradycardia becomes a periarrest emergency when the slow rate causes hypotension, acutely altered mental status, signs of shock, ischemic chest discomfort, or acute heart failure. The 2025 AHA guideline places the emphasis on rapid assessment of clinical stability and on the proximate cause. The usual threshold is a heart rate below 50 per minute, although symptoms, not the number, define the emergency. Reversible causes include myocardial ischemia, hypoxemia, hypothyroidism, infection, increased vagal tone, metabolic and electrolyte disorders (particularly hyperkalemia), and drugs and toxins such as beta-blockers, calcium channel blockers, digoxin, and antiarrhythmics.

Periarrest bradycardia with a pulse. Classes from the 2025 AHA adult advanced life support guideline; atropine, dopamine, and epinephrine doses from the AHA adult bradycardia algorithm and the 2018 American College of Cardiology (ACC)/AHA/Heart Rhythm Society (HRS) bradycardia guideline.

Atropine is unlikely to work in Mobitz II and third-degree block with a wide escape rhythm, which reflect infranodal disease, and pacing is prepared without waiting for a response. Transcutaneous pacing is uncomfortable and capture can be unreliable, so it serves as a bridge to transvenous pacing. Bradycardia from beta-blocker or calcium channel blocker toxicity responds to glucagon, calcium, and high-dose insulin, digoxin toxicity to digoxin immune Fab, and hyperkalemic bradycardia to calcium and potassium-lowering therapy. Pacing frequently fails to capture in severe hyperkalemia until the potassium is lowered. Bradycardia with inferior myocardial infarction is usually vagal and responds to atropine. Indications for permanent pacing and the evaluation of conduction disease are covered in the bradycardia and atrioventricular block hub.

Periarrest tachycardia with a pulse: cardioversion and drug therapy

The first question in tachycardia with a pulse is whether the tachycardia is causing instability or is a response to another illness. Sinus tachycardia from hypovolemia, sepsis, pain, or pulmonary embolism is not cardioverted, and rates below about 150 per minute rarely cause instability unless ventricular function is poor. Tachycardia that is causing hypotension, altered mental status, shock, ischemic chest discomfort, or acute heart failure is treated with synchronized cardioversion (Class 1); the supporting text of the 2025 AHA guideline describes instability in wide-complex tachycardia as a systolic pressure below 80 mm Hg or altered mentation. Stable tachycardia is classified by QRS width (narrow below 120 ms) and regularity on a 12-lead ECG.

Periarrest tachycardia with a pulse in the 2025 AHA adult advanced life support guideline. Adenosine dosing follows the AHA adult tachycardia algorithm. The AHA reduces the initial dose to 3 mg when adenosine is given through a central venous line, after heart transplant, and in patients taking dipyridamole or carbamazepine. The drug label notes that central venous administration has not been systematically studied. The 2025 AHA tachyarrhythmia algorithm specifies the device's recommended energy for synchronized cardioversion, or the maximum setting when that is not known. The electrical cardioversion algorithm lists starting energies of 200 J for atrial fibrillation and flutter and 100 J for narrow-complex tachycardia and monomorphic VT, with an unsynchronized high-energy shock for polymorphic VT.

Narrow-complex tachycardia. The Valsalva maneuver terminates about 20% to 30% of regular narrow-complex tachycardias, and modified techniques such as a strain followed by supine repositioning with passive leg raise, or blowing into a 10-mL syringe, reach up to about 50%. Adenosine is given as a rapid push into a large proximal vein followed by a saline flush, with a continuous ECG recording, because transient AV block can unmask flutter waves or atrial tachycardia. Intravenous diltiazem or verapamil terminates 64% to 98% of these tachycardias and is avoided in hypotension and ventricular dysfunction. Recurrent and refractory supraventricular tachycardia is managed as in the 2015 ACC/AHA/HRS guideline.

Atrial fibrillation and flutter. Synchronized cardioversion is used immediately for instability, and urgent cardioversion is used for new-onset atrial fibrillation or flutter with acute coronary syndrome and ongoing ischemia, instability, or inadequate rate control (Class 1). In a network meta-analysis cited by the 2025 AHA guideline, an initial energy of 200 J achieved cumulative success above 90% across the three US biphasic platforms, and starting energies up to 360 J were not associated with myocardial injury; for flutter, success is about 50% to 75% at 50 J, 85% to 90% at 100 J, and approaching 100% at 200 J. Double synchronized cardioversion, as an initial or rescue strategy, is of uncertain usefulness (Class 2b). Thromboembolic risk from cardioversion of atrial fibrillation lasting more than 48 hours without anticoagulation is accepted only when instability leaves no alternative; anticoagulation and rhythm strategy are covered in the atrial fibrillation hub.

Intravenous rate-control drugs for atrial fibrillation or flutter with rapid ventricular response in the periarrest setting, from Table 2 of the 2025 AHA adult advanced life support guideline.

Wide-complex tachycardia. A regular wide-complex tachycardia in an adult with structural heart disease is treated as VT, and stability does not exclude VT. When the patient is stable, a 12-lead ECG is obtained, and procainamide (20–50 mg/min until the arrhythmia is suppressed, hypotension develops, the QRS widens by more than 50%, or 17 mg/kg is given; avoided in prolonged QT and heart failure) or amiodarone (150 mg over 10 minutes, repeated as needed, then 1 mg/min for the first 6 hours) may be considered, with doses from the 2025 AHA tachyarrhythmia algorithm; IV sotalol is an alternative of the same class (Class 2b) and is avoided in prolonged QT. Electrocardiographic criteria that distinguish VT from aberrant conduction, and long-term management, are covered in the ventricular tachycardia and sudden cardiac death hub. Electrical storm, in which VT or VF recurs 3 or more times in 24 hours, is treated with sedation, beta-blockade, antiarrhythmic drugs, and ablation, as described in that hub.

Synchronized cardioversion technique. The patient is sedated whenever circumstances allow. The synchronization mode is selected and the marker is confirmed on each QRS complex, not on tall T waves; the mode must be reselected on many devices after each shock. If synchronization fails in an unstable patient, or the rhythm is polymorphic, an unsynchronized shock is delivered. An anteroposterior pad position, firm pad pressure, and escalating energy improve success in atrial fibrillation.

Immediate care after return of spontaneous circulation

ROSC is recognized by a palpable pulse and measurable blood pressure, an abrupt sustained rise in ETCO2, or spontaneous arterial pulsations, and it is confirmed at the rhythm check. The first minutes after ROSC carry a high risk of rearrest, and the team leader keeps the defibrillator attached, prepares epinephrine or norepinephrine infusions, and secures the airway. The 2025 AHA post-cardiac arrest care guideline recommends 100% inspired oxygen until oxygen saturation or arterial oxygen tension can be measured reliably, then a saturation target of 90% to 98% (Class 2a). It recommends a normal arterial carbon dioxide tension of 35 to 45 mm Hg in comatose patients (Class 1) and a mean arterial pressure of at least 65 mm Hg (Class 1). A 12-lead ECG is obtained as soon as possible, and emergent coronary angiography is recommended for suspected cardiac cause with persistent ST elevation (Class 1). Adults who do not follow commands after ROSC receive protocolized temperature control between 32 °C and 37.5 °C (Class 1) for at least 36 hours (Class 2a), and neurologic prognostication is multimodal and delayed until at least 72 hours after normothermia and the end of sedation (Class 2a). The management of the post-arrest syndrome, temperature control, angiography without ST elevation, seizures, and prognostication is covered in the post-cardiac arrest care hub, and cardiogenic shock after arrest in the cardiogenic shock hub.

Arrest in pregnancy, poisoning, hyperkalemia, hypothermia, and drowning

Several causes of arrest change the standard algorithm, and each has its own section in the 2025 AHA special circumstances guideline and the resuscitation in special circumstances hub.

• Pregnancy: high-quality CPR and defibrillation are unchanged, manual left uterine displacement relieves aortocaval compression when the uterus is at or above the umbilicus, and the team prepares for resuscitative delivery from the start of the arrest.
• Hyperkalemia: calcium, insulin with glucose, and sodium bicarbonate are given during arrest, each graded Class 2b (effectiveness not well established), with prolonged resuscitation and dialysis after ROSC; inhaled beta-agonists have no role during arrest (Class 3: No Benefit).
• Opioid overdose: rescue breathing and naloxone for respiratory arrest with a pulse (Class 1), and naloxone in arrest when it does not interrupt CPR (Class 2b).
• Local anesthetic systemic toxicity: intravenous lipid emulsion (Class 1), with benzodiazepines for seizures.
• Accidental hypothermia: full resuscitation with rewarming (Class 1), extracorporeal rewarming (Class 2a), one shock with further shocks deferred until the core temperature reaches 30 °C (Class 2b), and transport to an extracorporeal-capable center if reachable within 6 hours (Class 2b).
• Drowning: CPR with ventilation, which may begin with breaths, before the AED is applied (Class 1).

US, European, and international guidance compared

The AHA guidelines and the ERC guidelines are both based on the ILCOR consensus on science, and their core algorithm is the same. In shockable rhythms, the ERC 2025 adult ALS guideline gives the first dose of epinephrine (adrenaline) after the third shock, together with amiodarone 300 mg, whereas the AHA algorithm gives epinephrine after the second shock and the antiarrhythmic after the third. ILCOR and the ERC treat vector change and double sequential defibrillation as options that may be considered after 3 or more failed shocks, whereas the AHA grades their usefulness as not established.

Adult advanced life support recommendations in the 2025 AHA guideline and the 2025 ILCOR consensus on science with treatment recommendations. ILCOR uses strong and weak recommendations with certainty graded by Grading of Recommendations Assessment, Development and Evaluation (GRADE) in place of class and level.

Sources of error in adult resuscitation

• Prolonged pulse checks and pauses: pulse and rhythm checks that exceed 10 seconds, pauses for intubation or ultrasound, and post-shock rhythm checks lower coronary perfusion pressure and survival. Compressions resume immediately after a shock.
• Delayed first shock in a witnessed shockable arrest: a monitored VF arrest with pads in place is shocked immediately, without a preceding period of CPR or a search for a pulse.
• Hyperventilation: rates well above 10 per minute with an advanced airway, and large tidal volumes, raise intrathoracic pressure and reduce venous return. A ventilation timer or capnography-guided rate helps prevent it.
• Shallow, fast, or leaning compressions: depth falls with fatigue and with rates above 120 per minute. Compressors rotate every 2 minutes, and feedback devices make the problem visible.
• Misread asystole: fine VF on a low-gain or disconnected lead is mistaken for asystole. Gain and a second lead are checked before accepting asystole.
• Misplaced pads: an apical pad placed medially or over breast tissue shunts current away from the ventricles. Pad position, contact, and vector are reviewed after repeated shock failure.
• Epinephrine given at the wrong time: in shockable rhythms, epinephrine before the initial shocks adds risk without benefit; in nonshockable rhythms, delay lowers survival.
• Unrecognized esophageal intubation: a flat capnography trace after intubation indicates esophageal placement until proved otherwise, even during low-flow CPR.
• Termination based on a single finding: a low ETCO2 in a patient with a supraglottic airway, or absent cardiac motion on one ultrasound view, does not justify stopping; neither does duration alone in hypothermia, poisoning, or pulmonary embolism.
• Adenosine or calcium channel blockers in pre-excited atrial fibrillation, and calcium channel blockers in an undifferentiated wide-complex tachycardia: both can precipitate VF or collapse.

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