Cardiac arrest

Cardiac arrest is the sudden loss of effective cardiac output, recognised by unresponsiveness, absent normal breathing and no central pulse. Survival depends on how fast compressions, defibrillation of a shockable rhythm and treatment of the cause begin. This article covers recognition, rhythm specific drugs, cause identification and post arrest decisions, and assumes basic life support and defibrillation are already running.

Rhythms. Shockable: ventricular fibrillation and pulseless ventricular tachycardia. Non-shockable: asystole and pulseless electrical activity. Shockable rhythms carry the best survival. Pulseless electrical activity and asystole usually reflect a reversible non-cardiac cause or advanced disease.

Settings. Out of hospital arrests are mostly cardiac in origin, with a shockable first rhythm in a minority. In hospital arrests are mostly non-shockable and follow hours of physiological deterioration that is often detectable.

Phases. Electrical (about the first 4 minutes): defibrillation is most effective. Circulatory (about 4 to 10 minutes): compressions before shock improve success. Metabolic (over 10 minutes): reperfusion injury dominates and outcomes fall steeply.

Reversible causes. Hypoxia, hypovolaemia, hyperkalaemia, hypokalaemia and other metabolic disturbance, hypothermia, hyperthermia, thrombosis (coronary or pulmonary), tension pneumothorax, cardiac tamponade and toxins.

Key distinctions. Agonal gasping is not normal breathing and is common in early arrest. A pulse check that is uncertain after 10 seconds counts as absent. Pulseless electrical activity means organised electrical activity with no palpable pulse, whereas profound shock has a faint pulse and a measurable pressure.

Recognition. Unresponsive, no normal breathing, and no definite central pulse within 10 seconds. Do not delay compressions to confirm.

Information from the team and bystanders.

• Time of collapse, whether witnessed, bystander resuscitation and its start time, first rhythm, and total no flow and low flow time.
• Prodrome: chest pain, palpitations, syncope, breathlessness, headache, seizure.
• Background: cardiac disease, family history of sudden death, diabetes, kidney disease (potassium), asthma, anaphylaxis exposure, pregnancy, recent surgery, immobility, long haul travel.
• Drugs and substances: QT prolonging agents, digoxin, beta blockers, calcium channel blockers, insulin, opioids, tricyclic antidepressants, cocaine, local anaesthetics, anticoagulants.
• Implanted devices, valid advance decisions, and the patient's wishes.

Examination during resuscitation. Pupils, skin colour and temperature, injuries, rash or urticaria, needle marks, jugular venous distension, tracheal deviation, unequal air entry, abdominal distension, signs of haemorrhage, and medical alert items. Pulses are checked only at planned rhythm checks.

Bedside tools.

• Waveform capnography: confirms tube position and compression quality. End tidal CO2 under 1.3 kPa (10 mmHg) after 20 minutes of resuscitation is associated with very poor outcome, and an abrupt rise to 5 kPa (35 mmHg) or more suggests return of spontaneous circulation. It informs but never alone decides termination.
• Point of care ultrasound at rhythm checks within a 10 second pause: pericardial effusion, right ventricular dilatation, hypovolaemia, lung sliding, and organised cardiac activity.

Red flags (imminent arrest).

• Heart rate under 40 or over 140 beats/min, systolic pressure under 90 mmHg, respiratory rate under 8 or over 30 breaths/min, saturation under 90% on oxygen.
• New fall in Glasgow Coma Scale of 2 or more, new ventricular arrhythmia, ST elevation, and lactate over 4 mmol/L.

Primary cardiac.

• Acute myocardial infarction, ventricular fibrillation, ventricular tachycardia, torsades de pointes, complete heart block.
• Long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, short QT syndrome, Wolff-Parkinson-White syndrome with atrial fibrillation.
• Hypertrophic cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, myocarditis, aortic stenosis, congenital heart disease, anomalous coronary artery, commotio cordis.
• Aortic dissection, cardiac tamponade, cardiogenic shock.

Respiratory and circulatory. Pulmonary embolism, tension pneumothorax, severe asthma, chronic obstructive pulmonary disease exacerbation, drowning, airway obstruction, haemorrhagic shock, anaphylaxis, sepsis.

Metabolic. Hyperkalaemia, hypokalaemia, hypomagnesaemia, hypocalcaemia, hypoglycaemia, severe metabolic acidosis.

Toxic. Opioid poisoning, tricyclic antidepressant poisoning, digoxin toxicity, beta blocker poisoning, calcium channel blocker poisoning, local anaesthetic systemic toxicity, cocaine toxicity, carbon monoxide poisoning, cyanide poisoning, organophosphate poisoning.

Environmental and neurological. Hypothermia, heat stroke, electrocution, subarachnoid haemorrhage, intracerebral haemorrhage, status epilepticus.

Obstetric. Amniotic fluid embolism, eclampsia, postpartum haemorrhage.

During resuscitation. Rhythm analysis every 2 minutes with pauses under 10 seconds. Tests that do not interrupt compressions:

• Capillary glucose, and arterial or venous blood gas with potassium, lactate, haemoglobin, pH and calcium from a bedside analyser.
• Point of care ultrasound, targeted at the reversible causes. Chest radiograph after airway placement.
• Medication, toxicology and history checks by a team member.

After return of spontaneous circulation.

• 12 lead ECG as soon as possible: ST elevation, new left bundle branch block, QTc (over 500 ms is high risk), Brugada pattern, delta wave, epsilon wave, tricyclic effect (QRS over 100 ms).
• Blood: full blood count, urea, creatinine, electrolytes, corrected calcium, magnesium, phosphate, liver tests, glucose, lactate, troponin (limited diagnostic value in the first hours), creatine kinase, coagulation, blood cultures if infection is suspected, pregnancy test, and drug levels or toxicology where relevant.
• Echocardiography, CT pulmonary angiography or CT head and spine directed by the suspected cause, once stable.
• Coronary angiography: immediately for ST elevation. For no ST elevation, consider urgent angiography with haemodynamic or electrical instability or ongoing ischaemia, and delayed angiography otherwise.

Prognostication. Not earlier than 72 hours after return to normothermia, and only once sedatives, neuromuscular blockers, hypothermia and metabolic disturbance are excluded as confounders. Use two or more concordant findings:

• Motor score 3 or less, absent bilateral pupillary and corneal reflexes at 72 hours or more.
• Bilaterally absent N20 somatosensory evoked potentials.
• Neuron specific enolase over 60 micrograms/L at 48 or 72 hours (assay variation limits use).
• Status myoclonus within 72 hours, highly malignant EEG patterns, and diffuse anoxic injury on CT or MRI at 2 to 7 days.

Limitations. Capnography is unreliable after bicarbonate or adrenaline boluses and in severe lung disease. Ultrasound pauses prolong no flow time if not disciplined. Early prognostic tests have false positive rates that make early withdrawal of care unsafe.

Key parameters. Compressions 100 to 120/min, depth 5 to 6 cm, full recoil, minimal interruption. Adult biphasic defibrillation 150 to 200 J, with the same or escalating energy for later shocks as the device directs.

Shockable rhythm drugs.

• Adrenaline: 1 mg IV or intraosseous after the third shock, then every 3 to 5 minutes (alternate cycles) until return of circulation or termination; no fixed maximum, stop once circulation returns; monitor rhythm, blood pressure and end tidal CO2; flush with 20 mL isotonic saline; no kidney or liver adjustment during arrest.
• Amiodarone: 300 mg IV or intraosseous after the third shock, then 150 mg after the fifth shock; maximum 450 mg as boluses; after return of circulation 900 mg IV over 24 hours (1 mg/min for 6 hours, then 0.5 mg/min); monitor QTc, blood pressure, heart rate, liver tests; no adjustment in arrest.
• Lidocaine if amiodarone is unavailable: 1 mg/kg IV (usual 100 mg), then 0.5 mg/kg after a further shock; maximum 3 mg/kg in the first hour; reduce in liver impairment and heart failure.

Non-shockable rhythm. Adrenaline 1 mg IV or intraosseous as soon as access is secured, then every 3 to 5 minutes, with no fixed maximum, stopping once circulation returns, and monitoring of rhythm, blood pressure and end tidal CO2. Atropine has no role.

Cause directed treatment.

• Torsades de pointes: magnesium sulphate 2 g IV over 1 to 2 minutes, repeat once; monitor reflexes, respiration, blood pressure; reduce in kidney impairment.
• Hyperkalaemia: calcium chloride 10% 10 mL IV over 2 to 5 minutes, repeated after 5 to 10 minutes if ECG changes persist (monitor ECG; do not mix with bicarbonate; extravasation injures tissue); soluble insulin 10 units IV with glucose 50% 50 mL over 5 to 15 minutes (use 5 units in kidney failure and check glucose hourly for 6 hours); sodium bicarbonate 8.4% 50 mmol IV over 5 minutes (directed by blood gas); salbutamol 10 to 20 mg nebulised.
• Sodium bicarbonate is not routine. Use it for tricyclic or sodium channel blocker toxicity, hyperkalaemia and severe acidosis, repeating as directed by the blood gas.
• Suspected or confirmed pulmonary embolism: alteplase 50 mg IV bolus, repeated once after 15 minutes if needed; maximum 100 mg; continue resuscitation for 60 to 90 minutes after the dose; follow with unfractionated heparin 80 units/kg IV bolus then 18 units/kg/hour; monitor bleeding and aPTT.
• Tension pneumothorax: immediate finger or needle decompression in the fifth intercostal space anterior to the mid axillary line, followed by a chest drain.
• Tamponade: pericardiocentesis under ultrasound direction, or resuscitative thoracotomy in trauma.
• Hypovolaemia: haemorrhage control and blood products, with calcium chloride 10% 10 mL IV after every 4 units of red cells; tranexamic acid 1 g IV over 10 minutes within 3 hours of injury, then 1 g over 8 hours.
• Opioid poisoning: ventilation first, then naloxone 0.4 mg IV, repeated every 2 to 3 minutes; use 0.04 to 0.1 mg increments in chronic opioid users; maximum about 10 mg before the diagnosis is reconsidered; naloxone lasts 20 to 90 minutes, so observe for resedation.
• Local anaesthetic toxicity: lipid emulsion 20% 1.5 mL/kg IV over 1 minute, then 15 mL/kg/hour; repeat the bolus twice at 5 minute intervals if circulation does not return; maximum 12 mL/kg in total; use adrenaline only in small boluses of 10 to 100 micrograms.
• Anaphylaxis: adrenaline 0.5 mg IM into the anterolateral mid thigh (0.5 mL of 1 mg/mL), repeated every 5 minutes if there is no improvement, with rapid isotonic crystalloid.
• Hypothermia under 30 °C: no more than 3 shocks and no adrenaline until the core temperature is over 30 °C; rewarm, preferably by extracorporeal methods; continue until rewarmed unless injuries are clearly fatal.

Special groups.

• Pregnancy (over 20 weeks): manual left uterine displacement, 100% oxygen, early airway control, and if there is no return of circulation within 4 minutes, emergency hysterotomy so the baby is delivered by 5 minutes. Eclampsia: magnesium sulphate 4 g IV over 5 to 15 minutes if the arrest is not yet established.
• Children: adrenaline 10 micrograms/kg IV or intraosseous (maximum 1 mg) every 3 to 5 minutes, amiodarone 5 mg/kg after the third and fifth shocks, defibrillation 4 J/kg, compression to one third of chest depth (about 4 cm in infants and 5 cm in children), five initial breaths, then 15 compressions to 2 breaths for two rescuers.
• Traumatic arrest: simultaneous haemorrhage control, bilateral chest decompression, airway and pericardial release take priority over adrenaline.

Return of circulation care. Oxygen titrated to saturation 94 to 98%, PaCO2 4.5 to 6.0 kPa, mean arterial pressure 65 mmHg or more with isotonic fluid and noradrenaline 0.05 to 0.5 micrograms/kg/min if needed (central line when possible; monitor rhythm, urine output and lactate).

Keep glucose 6 to 10 mmol/L and potassium 4.0 to 5.0 mmol/L. Treat seizures (levetiracetam or benzodiazepine, after EEG when possible). Give no prophylactic antibiotics or antiepileptics.

Temperature should be held steady between 32 and 37.5 °C for at least 24 hours with fever prevented (over 37.7 °C) for 72 hours. Evidence for cooling under 36 °C is limited.

Termination. Decided by the team leader. Consider stopping after 20 minutes of advanced life support with asystole, no reversible cause, an unwitnessed arrest and no return of circulation, with end tidal CO2 under 1.3 kPa as supporting data. Prolong resuscitation for hypothermia, drowning, drug toxicity, pregnancy, thrombolysed pulmonary embolism and young patients. Extracorporeal resuscitation is an option for selected refractory shockable arrests in capable centres.

Monitoring. Continuous ECG, arterial pressure, capnography, saturation, temperature, hourly urine output, glucose hourly, lactate and blood gas every 1 to 2 hours initially, electrolytes every 4 to 6 hours.

Referral and escalation. Critical care for every patient with return of circulation. Cardiology and the catheter laboratory for ST elevation or suspected coronary cause. Neurology for prognostication and seizures. Electrophysiology for inherited arrhythmia and implantable defibrillator decisions. Obstetrics and neonatology for pregnancy. Poison centre for toxic causes.

Admission criteria. All patients with return of circulation go to critical care. Patients who die are discussed with the family and referred to the coroner or medicolegal authority where local law requires.

Discharge and follow up. Before discharge: a cause identified or an inherited cause evaluated, an implantable defibrillator considered for arrest without a reversible cause, cardiac rehabilitation, cognitive and psychological follow up, driving restrictions, and family screening for inherited disease. Families are told to seek urgent review for syncope, palpitations or chest pain.