Cardiac arrest and post-resuscitation care

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

High-quality CPR, early defibrillation, effective ventilation and prompt treatment of reversible causes take priority over advanced procedures. Airway attempts, ultrasound and vascular access must not create long compression pauses.

The arrest algorithm divides shockable VF/pVT from non-shockable PEA/asystole, but both repeat in 2-minute cycles with rhythm review, drug timing and Hs-and-Ts treatment. A sudden rise in ETCO2 can suggest ROSC but is not enough alone to stop compressions.

ROSC starts a new resuscitation phase: controlled oxygen/ventilation and BP, ECG/coronary triage, cause-directed CT/echo, seizure and fever control, multimodal prognostication and survivor/co-survivor rehabilitation.

Key points

Agonal gasps, slow laboured breathing and brief seizure-like activity can be cardiac arrest; if unresponsive and not breathing normally, assume arrest and start CPR.
Compress the lower half of the sternum at 100–120/min to 5–6 cm with full recoil and minimal pauses; use 30:2 until an advanced airway permits continuous compressions with 10 breaths/min.
Defibrillate VF/pulseless VT early, resume CPR immediately for 2 minutes and keep peri-shock pauses under 5 seconds; the first biphasic shock is at least 150 J unless device guidance differs.
For shockable arrest, give adrenaline 1 mg and amiodarone 300 mg after the third shock; repeat adrenaline every 3–5 minutes and give amiodarone 150 mg after the fifth shock.
For PEA/asystole, give adrenaline 1 mg as soon as possible, repeat every 3–5 minutes and aggressively search for reversible causes.
Do not routinely give calcium, sodium bicarbonate, corticosteroids or fluid; fluid is for hypovolaemic arrest and thrombolysis is considered when PE is suspected/confirmed.
After ROSC, initially use 100% oxygen only until saturation is reliable, then titrate to SpO2 94–98% and target PaCO2 4.7–6.0 kPa; avoid hypoxaemia, hyperoxaemia and hypocapnia.
In comatose survivors actively prevent fever at ≤37.5°C, investigate the cause, and delay final poor-outcome conclusions until multimodal assessment at least 72 hours after ROSC without confounders.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Coronary thrombosis and ventricular arrhythmia

Acute coronary occlusion can trigger ventricular fibrillation or pulseless ventricular tachycardia by creating electrically unstable ischaemic myocardium. It may also cause severe pump failure and a non-shockable arrest.

Hypoxia or hypovolaemia

Respiratory failure deprives the myocardium of oxygen, while major fluid or blood loss prevents adequate ventricular filling. Both mechanisms reduce coronary perfusion and can culminate in pulseless electrical activity.

Metabolic, temperature and toxic causes

Severe electrolyte or acid–base disturbance, hypothermia and toxins can suppress myocardial contraction or destabilise conduction. Blood gas, glucose, electrolytes, temperature and exposure history guide specific reversal.

Obstructed circulation

Pulmonary thrombosis blocks flow through the lungs, tamponade restricts cardiac filling and tension pneumothorax impairs venous return. Each causes sudden mechanical failure despite potentially organised electrical activity.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Loss of effective cardiac output
Ventricular fibrillation abolishes coordinated ejection, while pulseless ventricular tachycardia produces no clinically effective output. Asystole has no ventricular electrical activity; pulseless electrical activity has organised electrical activity without a palpable pulse. Systemic blood flow therefore ceases.
2
Global ischaemia
Absent circulation rapidly deprives brain and myocardium of oxygen and prevents clearance of carbon dioxide and metabolites. Cellular energy failure and acidosis progress until blood flow is restored.
3
Artificial perfusion and rhythm restoration
Chest compressions provide limited cerebral and coronary flow, ventilation treats hypoxia, and defibrillation may terminate a shockable rhythm. Correcting the causal obstruction, deficit or toxin is essential for sustained circulation.
4
Return of spontaneous circulation
Successful resuscitation restores a pulse but leaves unstable myocardium and organs exposed to whole-body ischaemia and reperfusion. Oxygenation, ventilation, perfusion and the arrest cause require active control.
5
Post-arrest neurological injury
The brain may remain injured despite restored circulation, producing coma, seizures or myoclonus. Sedation, shock and temperature confound early signs, so prognosis requires delayed multimodal assessment.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Cardiac-arrest breathingRed flag

Unresponsiveness plus absent or abnormal breathing—including gasping or slow laboured breaths—means start CPR; do not wait for cyanosis or a lay pulse check.

Shockable rhythmRed flag

VF or pulseless VT requires immediate defibrillation with CPR resumed straight after each shock.

Non-shockable rhythmRed flag

PEA or asystole requires immediate CPR, early adrenaline and cause treatment; confirm true asystole and check leads/gain.

Reversible causeRed flag

Hypoxia, hypovolaemia, electrolyte/metabolic disorder, hypothermia, thrombosis, tamponade, tension pneumothorax and toxins are sought and treated without stopping CPR unnecessarily.

Return of spontaneous circulation

Purposeful movement, normal breathing, a pulsatile arterial waveform or a sharp sustained ETCO2 rise may indicate ROSC; confirm with combined clinical/physiological signs.

Post-cardiac-arrest brain injury

Persistent coma, seizures/myoclonus and imaging/EEG abnormalities need controlled ICU assessment; early single signs must not trigger premature prognostication.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Defibrillator rhythm analysis every 2 minutesFirst step
Why
Separate VF/pVT from PEA/asystole and time shocks/drugs.
Interpretation and limitations
Minimise pauses; shock VF of any amplitude and immediately resume compressions without a routine post-shock pulse check.
02
Waveform capnography
Why
Confirm tracheal-tube placement, monitor CPR quality and identify possible ROSC.
Interpretation and limitations
A sustained trace is mandatory after intubation; a low ETCO2 value alone must never decide termination.
03
Blood gas, glucose and urgent electrolytes
Why
Find hypoxia, acidosis, potassium disturbance and metabolic/toxic causes.
Interpretation and limitations
Treat actionable abnormalities but do not routinely give bicarbonate or calcium without a specific indication.
04
Intra-arrest point-of-care ultrasound
Why
Find tamponade, tension pneumothorax or selected reversible pathology.
Interpretation and limitations
Skilled operators only during planned pauses; RV dilation alone does not diagnose PE and myocardial standstill alone must not terminate CPR.
05
Post-ROSC 12-lead ECG, echocardiography and coronary angiography
Why
Identify coronary occlusion and cardiac cause/complications.
Interpretation and limitations
Prioritise immediate angiography for clear ST elevation or high suspicion such as electrical/haemodynamic instability; without ST elevation, delay routine cath unless acute occlusion remains likely.
06
Cause-directed whole-body CT plus EEG/SSEP, biomarkers and brain imaging
Why
Find non-coronary cause and support seizure detection/prognosis.
Interpretation and limitations
Use multimodal neurological assessment without confounders; final poor-outcome assessment is at ≥72 hours and generally needs at least two concordant predictors.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Syncope

Syncope is usually brief, with normal breathing and clear signs of circulation returning promptly when the person is supine. Persistent unresponsiveness or abnormal breathing should be treated as cardiac arrest.

Generalised seizure

Tonic–clonic activity followed by post-ictal confusion, normal breathing and clear signs of circulation supports seizure. Cardiac arrest can begin with brief seizure-like movements, so unresponsiveness with abnormal breathing still warrants immediate CPR.

Respiratory arrest with a pulse

Profound hypoventilation from airway obstruction, opioids or neurological disease may leave a definite central pulse initially. Immediate ventilation and repeated circulation checks are required because cardiac arrest can follow.

Severe bradycardia with circulation

An organised slow rhythm accompanied by a palpable pulse or pulsatile arterial waveform is a peri-arrest bradyarrhythmia rather than established arrest. Treat adverse features while preparing for deterioration.

Monitor artefact

Movement or poor electrode contact can resemble ventricular fibrillation. Patient responsiveness, breathing, pulse, an arterial waveform and a rapid lead check distinguish artefact without delaying treatment of genuine arrest.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-lineBLS and defibrillatorFirst stepFirst lineUnresponsive adult with abnormal breathing

1Ensure safety, call 999 or the hospital arrest number 2222, start chest compressions immediately and send for an AED/defibrillator.
2Compress 100–120/min to 5–6 cm with full recoil; give 30:2 if trained/able, otherwise continuous compression following dispatcher advice.
3Attach the AED as soon as available, follow prompts, deliver an advised shock and resume CPR immediately.
4Change compressor before fatigue while minimising every interruption.

02Second-lineShockable ALSSecond lineVF or pulseless VT

1Defibrillate with at least 150 J biphasic for the first shock (or device-recommended/highest setting if unknown) and resume CPR for 2 minutes.
2EscalationContinue 2-minute cycles, escalating energy where possible; after the third shock give adrenaline 1 mg and amiodarone 300 mg IV/IO.
3Repeat adrenaline every 3–5 minutes and give amiodarone 150 mg after the fifth shock; correct reversible causes throughout.
4For refractory VF after three shocks, confirm pad position and consider antero-posterior vector change; routine dual sequential defibrillation is not recommended.

03Third-lineNon-shockable ALS and special causeThird linePEA or asystole

1Start/continue CPR, give adrenaline 1 mg as soon as possible and repeat every 3–5 minutes.
2Confirm airway/ventilation and IV access (use IO if IV cannot be achieved rapidly within two attempts); reassess rhythm every 2 minutes.
3Identify and treat Hs and Ts; use fluid only for hypovolaemia and consider immediate thrombolysis if PE is suspected or confirmed.
4In selected suspected PE after thrombolysis, consider continuing CPR for 60–90 minutes; selected refractory arrests may enter an ECPR pathway where implemented.

04EscalationPost-ROSC careEscalationSustained spontaneous circulation

1Secure airway/ventilation as needed; titrate oxygen to SpO2 94–98%, target PaCO2 4.7–6.0 kPa and support perfusion while avoiding hypotension.
2Obtain ECG and urgent cause imaging; prioritise cath lab for ST elevation or high suspicion of coronary occlusion.
3In comatose patients prevent fever at ≤37.5°C, treat seizures when present, avoid routine seizure prophylaxis and use structured ICU care.
4Delay final neurological prognostication until ≥72 hours without confounders, then provide functional assessment, rehabilitation and follow-up within 3 months for survivor and co-survivor needs.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

ALS vasopressor in both non-shockable and shockable arrest at rhythm-specific timing.

Adrenaline (cardiac arrest)

1 mg IV/IO as soon as possible for PEA/asystole, or after the third shock for VF/pVT; repeat 1 mg every 3–5 minutes while ALS continues.

Use the cardiac-arrest preparation/concentration and closed-loop documentation. Do not delay CPR/defibrillation or confuse with anaphylaxis dosing.

Antiarrhythmic for refractory or recurrent VF/pulseless VT.

Amiodarone (VF/pVT arrest)

300 mg IV/IO after a total of three shocks, then 150 mg after a total of five shocks.

Does not replace defibrillation or cause correction; timing counts total shocks even if VF/pVT is intermittent.

Alternative antiarrhythmic if amiodarone is unavailable or the resuscitation service has explicitly selected lidocaine.

Lidocaine (alternative to amiodarone)

100 mg IV after three shocks; an additional 50 mg may be given after five shocks when lidocaine is the selected RCUK alternative.

Do not combine routinely with amiodarone; account for severe liver disease or low body mass where relevant and document total shocks/doses.

Cause-specific reperfusion when PE is suspected or confirmed as the arrest cause.

Fibrinolytic for suspected/confirmed PE arrest

RCUK 2025 recommends immediate fibrinolytic therapy for suspected or confirmed PE arrest but does not specify one universal agent or dose. Use the pre-agreed emergency arrest regimen for the selected fibrinolytic; do not infer it from alteplase's licensed 100 mg over 2 hours regimen for non-arrest massive PE.

Major bleeding remains possible, but PE arrest is immediately fatal without reperfusion; after administration, consider 60–90 minutes of CPR in selected patients.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Hypoxic–ischaemic brain injury

Interrupted cerebral blood flow may cause persistent coma, cognitive impairment, seizures or myoclonus. Premature conclusions are unsafe because sedation, paralysis, shock and temperature can obscure neurological recovery.

Post-arrest myocardial dysfunction

Global ischaemia and the underlying cardiac cause can leave impaired contraction, hypotension and electrical instability after circulation returns. Continuous haemodynamic and rhythm monitoring guides support and coronary assessment.

Recurrent cardiac arrest

An untreated coronary, thrombotic, metabolic, toxic or mechanical cause can provoke recurrent arrhythmia or circulatory collapse. Cause-directed imaging and treatment remain urgent after the first return of circulation.

Multiorgan dysfunction

Whole-body ischaemia and shock can impair renal, hepatic and respiratory function, disturb glucose and electrolytes, and reduce urine output. Serial physiological and laboratory assessment identifies evolving injury.

Long-term functional and psychological effects

Survivors may experience impaired cognition, fatigue, mood disturbance and reduced physical function, while relatives and co-survivors can also be affected. Structured rehabilitation and follow-up are part of recovery.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Compression rate/depth, recoil, interruptions and compressor fatigue; use data-driven debriefing after the event.
Rhythm every 2 minutes, shock/drug times and continuous waveform capnography after an advanced airway.
Post-ROSC SpO2 94–98%, arterial gases and PaCO2 4.7–6.0 kPa; avoid hypoxaemia and hyperoxaemia.
Post-ROSC ECG/rhythm, BP/perfusion, lactate, urine output, glucose, electrolytes and organ function.
Core temperature with active fever prevention at ≤37.5°C for 36–72 hours in survivors who remain comatose.
Neurological examination with sedation/temperature confounders, EEG from day 1 where comatose, and multimodal prognostication at ≥72 hours.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Gasping is not normal breathing

Misreading agonal breaths is a major cause of delayed CPR; uncertainty favours starting compressions.

Shock then compress

Do not pause to look for a pulse after a shock; resume CPR immediately unless combined signs clearly indicate ROSC.

Airway skill determines airway choice

A supraglottic airway is safer than repeated failed intubation; intubation should be by a high-success operator with capnography and <5-second pause.

Ultrasound can harm through delay

POCUS is useful only when it fits inside the rhythm pause and does not prolong hands-off time.

Prognosis is deliberately late and multimodal

Sedation, paralysis, shock and temperature confound early signs; no single early test justifies a poor-outcome conclusion.

Survival includes rehabilitation

Cognition, fatigue, mood, physical function and family/co-survivor impact should be screened before discharge and again within three months.

11Common pitfallsFrequent interpretation and management errors.

01
Treating agonal gasps or a brief seizure-like onset as evidence against cardiac arrest.
02
Interrupting compressions for intubation, ultrasound, vascular access or a prolonged pulse check.
03
Giving adrenaline before the third shock in routine VF/pVT arrest or delaying it in PEA/asystole.
04
Routine calcium, bicarbonate, corticosteroid, fluid or post-ROSC antiarrhythmic prophylaxis without an indication.
05
Making a neurological prognosis before 72 hours from ROSC on one sign while confounders remain.