Cardiac arrest and advanced life support

Cardiac arrest is the sudden cessation of effective cardiac mechanical activity, and its management — advanced life support — is the archetype of the time-critical, team-based emergency. Survival to a good neurological outcome depends on a small number of things done well and without delay: the immediate initiation of high-quality chest compressions, the rapid defibrillation of a shockable rhythm, the identification and reversal of the cause, and the high-quality post-resuscitation care. The algorithm is universal, it is rehearsed, and it is built to be executed under stress; the Fellowship candidate must know it cold, including the regional variations and the evidence behind each drug. [1]

The chain of survival and high-quality CPR

The chain of survival — early recognition and call for help, early high-quality cardiopulmonary resuscitation, early defibrillation, and high-quality post-resuscitation care — frames the whole effort, and the two pre-hospital links (CPR and defibrillation) are the ones that determine good survival. The quality of the CPR is decisive. The compressions are delivered at a rate of 100 to 120 per minute, to a depth of 5 to 6 centimetres in the adult, with full chest recoil between compressions and minimal interruption (pauses kept below 5 seconds and confined to the rhythm check and the shock). The compressor is rotated every two minutes to prevent fatigue, and excessive ventilation is avoided because it raises intrathoracic pressure and reduces coronary and cerebral perfusion. The compression-to-ventilation ratio for the adult with an unprotected airway is 30 to 2; once the airway is secured with a cuffed tracheal tube, compressions continue uninterrupted at 100 to 120 per minute with around 10 breaths per minute. High-quality CPR is the foundation on which everything else is built, and no intervention should be allowed to compromise it.[1]

The ALS algorithm and rhythm analysis

On recognising the arrest, help is summoned, CPR is begun, and the defibrillator is attached. The rhythm is analysed at the two-minute mark (the cycle length) and classified as shockable — ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT) — or non-shockable — asystole or pulseless electrical activity (PEA). The two rhythms are managed in two parallel loops, each built around two-minute cycles of CPR with a rhythm analysis and a drug at each cycle, and each interrupted by the search for and treatment of a reversible cause.[1][1]

Shockable rhythms: VF and pulseless VT

VF and pVT are the rhythms for which defibrillation is the definitive treatment, and the sooner the shock the better. The shock is delivered (a biphasic shock at the manufacturer-recommended energy, commonly 150 to 200 joules, escalating for subsequent shocks), CPR is resumed immediately for two minutes without pausing to check a rhythm or a pulse, and the rhythm is then reassessed. If VF or pVT persists, a second shock is given and CPR resumed. After the third shock, adrenaline 1 milligram intravenously or intraosseously is given every three to five minutes (every cycle) thereafter, and amiodarone 300 milligrams is given after the third shock with a further 150 milligrams after the fifth shock if needed (lidocaine is an alternative). The cycle of CPR, rhythm check and shock continues, with the drugs, until a stable rhythm returns or the decision is made to stop. The presence of a shockable rhythm is a good prognostic sign, and the energy of the resuscitation goes into minimising the time to the shock.[1][1]

Non-shockable rhythms: asystole and PEA

Asystole and PEA are not treated with a shock; they are managed with continuous CPR and adrenaline, and an unremitting search for a reversible cause. Adrenaline 1 milligram is given intravenously or intraosseously as soon as IV or IO access is available, and repeated every three to five minutes (every cycle). PEA — organised electrical activity without a pulse — is almost always a manifestation of a reversible cause (a tamponade, a tension pneumothorax, a massive thrombosis, hypovolaemia, or a toxin), and the survival of the PEA arrest turns on identifying and treating that cause; bedside ultrasound during the rhythm check is invaluable. Asystole carries the worst prognosis, but it too may reflect a reversible cause or a correctable profound bradycardia, and atropine is no longer recommended routinely.[1][1]

Differential diagnosis — the reversible causes

• Hypoxia — the asphyxial arrest, the drowning, the hanging; give the oxygen, the ventilation.
• Hypovolaemia — the haemorrhage, the sepsis; give the fluid, the blood.
• Hypo- or hyperkalaemia — the renal failure, the dialysis; give the calcium chloride 10 mL of 10 per cent, the insulin-dextrose, the bicarbonate.
• Hypothermia — the exposure, the immersion; rewarm slowly, do not declare death until warm and dead.
• Thrombosis (coronary) — the STEMI; consider the thrombolysis or the PCI.
• Thrombosis (pulmonary) — the massive PE; give the thrombolysis, continue the CPR for 60 minutes.
• Tension pneumothorax — the trauma; the needle decompression, the finger thoracostomy.
• Tamponade — the trauma, the post-MI; the pericardiocentesis, the resuscitative thoracotomy.
• Toxins — the TCA, the opioid, the beta-blocker; give the specific antidote (the sodium bicarbonate, the naloxone, the glucagon).

Adrenaline [1]

Adrenaline is the vasoconstrictor that raises the aortic and the coronary perfusion pressure during CPR, improving the return of spontaneous circulation. It is given at 1 milligram intravenously or intraosseously every three to five minutes, in both the shockable and the non-shockable loops, the timing of the first dose differing slightly between the regional guidelines (after the third shock in the United Kingdom algorithm, after the second in the Australasian). The large PARAMEDIC2 trial established that adrenaline improves survival to hospital discharge after out-of-hospital cardiac arrest — but it did not improve the rate of survival with a favourable neurological outcome, because some of the additional survivors survived with neurological injury.[1][4] The practical message is that adrenaline is given, but it is not allowed to delay or interrupt the high-quality CPR and the early defibrillation on which good outcome truly depends.

Antiarrhythmics and defibrillation

The antiarrhythmic is given for the refractory shockable rhythm. Amiodarone 300 milligrams after the third shock, with 150 milligrams after the fifth, is the standard; lidocaine (1 to 1.5 milligrams per kilogram) is an alternative. The ROC-ALPS trial found that neither amiodarone nor lidocaine produced a significant improvement in survival to discharge compared with placebo for out-of-hospital cardiac arrest overall, though a signal of benefit in the witnessed, monitored subgroup has kept the drugs in the algorithm.[3] Defibrillation itself is delivered with self-adhesive pads placed in the anterolateral (and, where available, anteroposterior) position, with a brief safety check and immediate resumption of CPR; the modern practice is a single shock followed by CPR rather than stacked shocks, because the heart is refractory and the CPR is more valuable in the immediate post-shock period. Hands-on defibrillation (with the compressor pausing only for the shock) is an emerging technique to reduce interruptions.[1]

The shockable versus non-shockable decision — the fork in the algorithm

The first rhythm analysis is the fork in the algorithm: the shockable rhythm (VF or pulseless VT) enters the defibrillation loop, and the non-shockable rhythm (asystole or PEA) enters the adrenaline-and-search loop. The distinction is made on the monitor within seconds and is re-checked every two-minute cycle, because the rhythm may change — the VF may degenerate to the asystole, and a fine VF masquerading as the asystole may be revealed by turning the gain up. The Fellowship candidate must recognise both the canonical rhythms and the pitfalls (the fine VF, the artefact, the disconnected lead).[1][1]

The reversible causes: the four Hs and four Ts

The search for a reversible cause runs through every arrest and is the key to the resuscitation that is failing. The four Hs are hypoxia (give oxygen, ventilate), hypovolaemia (give fluid or blood), hypo- or hyperkalaemia and the other metabolic derangements (treat with glucose, bicarbonate or electrolyte correction), and hypo- or hyperthermia. The four Ts are thrombosis (coronary or pulmonary — consider thrombolysis or thrombectomy), tension pneumothorax (decompress), tamponade (drain), and toxins (give the antidote).[1]

The Fellowship candidate must not only recall the list but know the bedside clue, the rapid diagnostic test and the immediate corrective action for each cause — this is the substance of the reversible-cause viva.[1][1]

Other arrest drugs

Beyond adrenaline and amiodarone, the other drugs are situation-specific. Sodium bicarbonate 50 mL of 8.4 per cent (50 mmol) IV is given for the arrest caused by hyperkalaemia or tricyclic antidepressant toxicity and in the prolonged arrest with a profound acidosis, but it is not given routinely. Magnesium 2 g (10 mL of 20 per cent) IV is given for torsades de pointes, hypomagnesaemia, and polymorphic VT. Calcium chloride 10 mL of 10 per cent IV is given in hyperkalaemia, hypocalcaemia, and calcium-channel-blocker toxicity. A thrombolytic (alteplase 50 mg IV or tenecteplase as weight-based) is given when a pulmonary embolism is the suspected cause of the arrest, with CPR continued for up to an hour. Glucose 25 g IV (50 mL of 50 per cent) is given for hypoglycaemia. The bedside blood gas, the electrolytes and the glucose taken early guide the targeted therapy. [1]

The team and human factors

The arrest is managed by a team with allocated roles — the team leader, the compressor, the airway operator, the person at the defibrillator, the drugs, the timekeeper and the scribe — and the quality of the resuscitation depends on the leadership and the communication as much as on the algorithm. Closed-loop communication, the structured handover, and the willingness to call for senior or critical-care help early are the components. The cognitive aids (the algorithm itself, the reversible-causes list) are displayed and followed. Fixation on the rhythm at the expense of the reversible-cause search, and the failure to rotate the compressor, are the common human-factor failures. [1]

The immediate post-ROSC period

The return of spontaneous circulation is not the end of the resuscitation; the post-arrest care determines the neurological outcome, and it begins in the emergency department. The airway and the breathing are managed with a target oxygen saturation of 94 to 98 per cent (avoiding both hypoxia and hyperoxia) and a normocapnic ventilation. The circulation is supported to a mean arterial pressure of 65 mmHg or more, with the cause investigated and, where cardiac, reperfused. The targeted temperature is managed at normothermia, actively avoiding fever — the TTM2 trial found that targeting hypothermia at 33 degrees did not improve outcome over normothermia, and the contemporary practice is to maintain a normothermic, fever-free state. Seizures are treated, glucose is controlled, and the prognostication is deferred. These elements are explored in the post-cardiac-arrest-care topic.[2][1]

Special arrests

The cause and the context modify the resuscitation. The asphyxial arrest (drowning, hanging) prioritises oxygenation and ventilation. The anaphylactic arrest is treated with intramuscular adrenaline and fluid. The asthma arrest benefits from ventilation with a small tidal volume and a prolonged expiratory time, and from bronchodilators. The pulmonary embolism arrest is treated with thrombolysis. The traumatic arrest is managed with simultaneous resuscitation and the control of catastrophic haemorrhage, and adrenaline is not routinely effective in the hypovolaemic traumatic arrest.[4] The pregnant arrest is resuscitated with manual left uterine displacement, and a perimortem caesarean section is begun at four minutes of arrest in the pregnancy beyond 20 weeks to relieve aortocaval compression and to resuscitate mother and fetus. The hypothermic arrest is prolonged and resistant, and is resuscitated to normothermia with active rewarming (and, where available, extracorporeal) before the arrest is called. The drug-overdose arrest is treated with the antidote and the prolonged resuscitation that the reversibility warrants. Paediatric arrest is managed with age-appropriate compressions and ventilations (15 to 2 with two rescuers), a lower defibrillation energy, and an emphasis on the respiratory cause.

Termination, the refractory arrest, and regional practice

The decision to terminate the resuscitation is clinical, made by the team leader, and considers the downtime, the rhythm, the reversible causes, the comorbidity, and the response. The refractory arrest — VF or pVT that will not terminate despite the full algorithm — is an indication, in a suitable patient, for extracorporeal CPR as a bridge to recovery or to a definitive intervention. The guidelines are regional: the ARC/NZCOR guidelines govern the Australasian practice, the Resuscitation Council UK guidelines the United Kingdom practice, and the ILCOR Consensus on Science integrates the global evidence; the algorithm is the same in outline and differs in small details (the timing of the first adrenaline, the antiarrhythmic), which the candidate knows for the local exam.[1][1][1]

Post-ROSC care — the resuscitation that begins with the pulse

The return of spontaneous circulation is the beginning, not the end, of the resuscitation that determines the neurological outcome. The post-arrest patient is admitted to the ICU for the systematic bundle — the oxygenation, the ventilation, the haemodynamics, the temperature, the cause, the seizure, the glucose, the prognostication — and the emergency department initiates every element of it.[2][1]

Targeted temperature management (TTM)

The TTM2 trial (Dankiewicz, 2021) settled the long debate: targeting the hypothermia at 33 degrees C did not improve the outcome over the normothermia in the comatose survivor of the out-of-hospital cardiac arrest.[2] The contemporary practice is to maintain a normothermic, fever-free state — a target temperature of 36 to 37.5 degrees C with the active prevention of the fever (37.7 degrees C or more in the first 72 hours) using the cooling devices, the antipyretics and the sedation. The hypothermia at 32 to 36 degrees C is retained for the specific indications (the refractory status epilepticus, the malignant hyperthermia) and is not the routine post-arrest target. The Hyperion trial (the non-shockable arrest) is the exception — it showed a benefit of the 33-degree-C hypothermia in the non-shockable subgroup, and the cautious candidate keeps the option open for that context. The hypothermia itself has the predictable physiological effects — the bradycardia, the coagulopathy, the impaired clearance of the sedatives, the insulin resistance — and these are weighed when the lower target is chosen.

Coronary angiography after the ROSC

The early coronary angiography — and the percutaneous coronary intervention of the culprit lesion — improves the outcome of the comatose survivor of the out-of-hospital cardiac arrest with the suspected cardiac cause, regardless of the ST elevation on the post-ROSC ECG. The ST-elevation post-arrest patient goes to the angiography as the emergency; the non-ST-elevation patient with the high clinical suspicion (the witnessed collapse, the initial shockable rhythm, the older patient) is also referred for the early angiography. The decision is made jointly with the interventional cardiology in the first hours. The shockable-rhythm arrest without an obvious non-cardiac cause is, by default, a cardiac cause until proven otherwise. [1]

When to stop the resuscitation

The decision to terminate the resuscitation is clinical, made by the senior team leader, and it weighs the downtime, the rhythm, the reversible causes, the comorbidity, the baseline function and the response to the full algorithm. The termination is not the failure — it is the recognition that the resuscitation will not restore a meaningful life. The Fellowship candidate must know the criteria that support, but do not mandate, the termination.[1][1][1]

ECPR — the extracorporeal cardiopulmonary resuscitation in the ED

The extracorporeal CPR is the veno-arterial extracorporeal membrane oxygenation (the VA-ECMO) instituted during the ongoing CPR as the bridge to the recovery or the definitive intervention. It is the salvage therapy for the refractory in-hospital or the out-of-hospital arrest in the selected patient, and its role is expanding as the ED-based cannulation programmes mature. The candidate must know the indications, the contraindications and the timing.[1]

Clinical pearls — the high-yield viva answers

The landmark arrest trials — the evidence the candidate must know

Red flags

The following features identify the arrest at risk of a poor outcome or the resuscitation that is failing, in which the high-yield interventions are intensified: [1]