Clinical Guides
Cardiac Arrest
An India-contextualised guide to adult cardiac-arrest recognition, high-quality CPR, AED and defibrillator use, rhythm-based advanced life support, reversible causes, transfer and evidence-based post-arrest care.
MedNext Academy | 14 min read
Cardiac Arrest
An India-contextualised guide to adult cardiac-arrest recognition, high-quality CPR, AED and defibrillator use, rhythm-based advanced life support, reversible causes, transfer and evidence-based post-arrest care.
Summary
Cardiac arrest is the abrupt loss of effective circulation. An adult who is unresponsive and absent or abnormally breathing, including only gasping, should be treated as being in cardiac arrest; a healthcare professional may check a pulse for no more than ten seconds and should start the arrest pathway if no definite pulse is felt. Activate the emergency response system, begin high-quality cardiopulmonary resuscitation and attach an automated external defibrillator or manual defibrillator as soon as available. These actions matter more than prolonged diagnostic discussion.
Adult chest compressions should be delivered at 100 to 120 per minute, at least 5 cm but not more than 6 cm deep, with complete recoil and the smallest possible interruption. Use a 30:2 compression-to-ventilation ratio before an advanced airway, unless an applicable special-circumstance protocol changes the approach. Ventilate only enough to produce visible chest rise and avoid excessive ventilation. Ventricular fibrillation and pulseless ventricular tachycardia are shockable; pulseless electrical activity and asystole are not. Defibrillation, epinephrine, selected antiarrhythmics and correction of reversible causes follow the current authenticated algorithm without displacing compressions.
Return of spontaneous circulation begins a second emergency. Secure oxygenation and ventilation, support perfusion, obtain a twelve-lead ECG, identify the cause, assess for coronary reperfusion, control temperature in an unresponsive survivor, detect seizures and delay neurological prognostication until confounders are addressed. Transfer to a facility capable of critical care and definitive cause treatment. Cardiac arrest is not synonymous with myocardial infarction, death or a do-not-resuscitate decision. This reviewed educational draft is has been reviewed by the MedNext Clinical Team and does not replace certified resuscitation training, local protocols or real-time clinical leadership.
How Common Is It?
Cardiac arrest occurs outside hospital and in every hospital environment, but useful Indian incidence and survival estimates remain incomplete because case capture, emergency-medical-service coverage, bystander recognition, registry definitions and neurological follow-up vary. Arrests that are unwitnessed, never reached by an ambulance or recorded only as death on arrival may be missed. Hospital series overrepresent centres with resuscitation teams and intensive care. International survival percentages therefore describe their own systems and should not be presented as national Indian outcomes.
Frequency is concentrated among people with coronary disease, cardiomyopathy and heart failure, yet non-cardiac causes are prominent: hypoxia, sepsis, trauma, pulmonary embolism, poisoning, metabolic disturbance, drowning, haemorrhage and pregnancy-related catastrophe can all culminate in arrest. Location, witness status, initial rhythm, bystander CPR, time to first shock, ambulance response and post-arrest capability influence survival. A witnessed ventricular-fibrillation arrest beside an AED is a different clinical population from unwitnessed asphyxial arrest after prolonged downtime.
Service measurement should capture recognition-to-compression time, bystander CPR, dispatcher-assisted CPR, AED availability, first monitored rhythm, time to defibrillation, ROSC, survival to discharge and function at follow-up. Counting only ROSC exaggerates meaningful recovery, while counting only deaths hides correct resuscitations in profoundly non-survivable disease. Facilities should audit equipment checks, team response, compression fraction, medication timing and debriefing. Community programmes should map AEDs and train likely responders. This guide avoids claiming that one device, drug or training course alone can overcome weaknesses across the entire chain of survival.
Risk Factors
Coronary artery disease, previous myocardial infarction, reduced left-ventricular function, cardiomyopathy, heart failure, inherited channelopathy, congenital heart disease and significant valvular disease increase the risk of sudden arrhythmic arrest. Prior ventricular tachycardia, unexplained syncope during exertion, a family history of young sudden death, prolonged QT, Brugada pattern and hypertrophic cardiomyopathy require specialist assessment before an event. Diabetes, hypertension, smoking, chronic kidney disease and dyslipidaemia contribute through structural and coronary disease rather than acting as immediate diagnoses during resuscitation.
Immediate precipitants include acute coronary occlusion, profound hypoxaemia, massive pulmonary embolism, tension pneumothorax, cardiac tamponade, severe haemorrhage or dehydration, sepsis, electrolyte disturbance and toxin exposure. Dialysis interruption, potassium-altering medicines, QT-prolonging combinations, digoxin toxicity, tricyclic antidepressants, pesticides, opioids and local anaesthetic toxicity are examples requiring a targeted history and special-circumstance protocol. Trauma and drowning create different priorities. Pregnancy changes resuscitation positioning, cause profile and the threshold for resuscitative delivery; specialist algorithms apply.
Risk of poor outcome rises with unwitnessed collapse, absent bystander CPR, long no-flow or low-flow intervals and delayed defibrillation, but these are population associations rather than bedside permission to abandon care. Scene danger can create additional casualties, so rescuers first ensure safety. In hospital, deterioration commonly precedes arrest: escalating oxygen need, abnormal respiratory rate, hypotension, altered mentation, chest pain or worsening arrhythmia should activate rapid-response care. Prevention includes treating deterioration, appropriate implantable-defibrillator evaluation, medication reconciliation, electrolyte surveillance, resuscitation planning and ensuring that limitations of treatment are discussed before crisis rather than invented during it.
Diagnosis
History
Recognition precedes a detailed history. Establish responsiveness and breathing immediately; gasping is abnormal. Ask a witness what happened, the exact collapse time, whether CPR began, whether shocks were delivered and whether the person had chest pain, dyspnoea, seizure-like movements, choking, trauma, immersion, pregnancy, overdose or known disease. Obtain medicines, allergies, dialysis status, implanted-device history and any valid treatment-limitation document without stopping resuscitation. Brief tonic movement at collapse may reflect cerebral hypoperfusion rather than epilepsy.
Examination
A lay responder does not delay for pulse palpation. A healthcare professional checks for a definite central pulse for no more than ten seconds while assessing breathing. If absent or uncertain, start compressions. Expose the chest, attach pads and assess rhythm at scheduled pauses. Look rapidly for major haemorrhage, airway obstruction, pregnancy, trauma, temperature exposure and signs pointing to reversible causes. During CPR, evaluate compression quality, chest rise, pad contact, vascular access and team performance. Point-of-care ultrasound by an expert may investigate a reversible cause only if it does not prolong pauses.
Investigations
The defibrillator rhythm is the decisive immediate investigation: VF or pulseless VT is shocked; PEA or asystole receives CPR, epinephrine and cause treatment without shock. Confirm apparent asystole by checking leads, gain and connections. Capnography after advanced airway placement confirms ventilation and may help monitor CPR or detect ROSC; no single end-tidal value should end resuscitation. Obtain bedside glucose and targeted blood gas, electrolytes and toxin tests when feasible. After ROSC, perform ECG, blood tests, echocardiography and cause-directed CT or coronary imaging without destabilizing the patient. Arrest remains a clinical state; troponin elevation after CPR does not by itself prove acute coronary occlusion.
Differential Diagnosis
Syncope is a transient loss of consciousness with spontaneous recovery and maintained circulation; cardiac arrest has no effective pulse and requires immediate CPR. Seizure may cause unresponsiveness, cyanosis and jerking, but agonal movements also occur at the start of arrest. If normal breathing and circulation are not definite, do not wait for the movements to stop before activating emergency care. Opioid-related respiratory arrest may retain a pulse initially; provide ventilation, use naloxone according to protocol and monitor closely, while commencing full CPR if circulation is lost.
Profound shock can produce a barely palpable pulse. Healthcare professionals may use ECG, arterial waveform or focused ultrasound when immediately available, but none should create a long compression pause. Severe bradycardia with a pulse uses the peri-arrest bradycardia pathway, not the pulseless algorithm. An implanted ventricular-assist device can produce continuous flow with an absent palpable pulse; use device-specific assessment and specialist support. Hypothermia, pregnancy, trauma, drowning, electrocution, avalanche, asthma and poisoning require special-circumstance modifications.
The rhythm differential matters. Fine ventricular fibrillation can resemble asystole; check leads and seek expert rhythm interpretation without repeated prolonged pauses. Organised electrical activity without a pulse is PEA, not a perfusing rhythm. Movement or an abrupt sustained capnography rise can suggest ROSC and should prompt an efficient pulse and rhythm assessment. After ROSC, determine the underlying cause rather than labelling every collapse a primary arrhythmia. Acute coronary syndrome, pulmonary embolism, intracranial catastrophe, sepsis, hypoxia, electrolyte abnormality, tamponade and haemorrhage lead to different definitive treatments even though the initial CPR sequence is shared.
Management
Ensure scene safety, check response and breathing, call for help and activate the local emergency system. A lone lay responder with a mobile phone should use speaker mode where possible, follow dispatcher instructions and start compressions. Push hard and fast in the centre of the chest, switch compressor about every two minutes before fatigue degrades depth, and resume immediately after rhythm analysis or shock. Attach an AED as soon as it arrives, follow its prompts, clear the patient during analysis and shock, then restart compressions without checking a pulse unless signs of ROSC appear.
For trained teams, assign leadership, compressor, airway, defibrillator, access and recorder roles. Use 30 compressions to two breaths until an advanced airway is placed; thereafter provide continuous compressions with protocol-rate ventilation and avoid hyperventilation. Shock VF or pulseless VT promptly using the manufacturer's recommended biphasic energy and escalate according to the device or algorithm. PEA and asystole are never defibrillated. Establish intravenous access; intraosseous access is reasonable when intravenous access cannot be obtained promptly. Administer algorithm drugs without delaying shocks or compressions.
Search systematically for reversible causes: hypovolaemia, hypoxia, hydrogen-ion excess, hypo- or hyperkalaemia and other metabolic disturbance, hypothermia, tension pneumothorax, tamponade, toxins, pulmonary thrombosis and coronary thrombosis. Treat only supported causes; blind procedures consume time and cause harm. Consider extracorporeal CPR only for highly selected refractory arrests in systems able to initiate it rapidly within an established protocol. After ROSC, move into a coordinated bundle of airway, oxygen, ventilation, blood-pressure, ECG, temperature, seizure and cause management. Document timings, communicate with family compassionately, and conduct a structured team debrief after care is transferred.
Prescribing Information
Epinephrine is the standard vasopressor in adult cardiac arrest. The 2025 AHA advanced-life-support guidance retains 1 mg intravenously or intraosseously every three to five minutes. Give it as soon as feasible for PEA or asystole; in a shockable arrest, prioritize rapid defibrillation and give epinephrine after initial CPR and shock attempts have failed, following the current algorithm. Flush the access and account for circulation time. Do not substitute high-dose regimens or vasopressin combinations routinely, and never confuse the cardiac-arrest intravenous preparation with intramuscular adrenaline used for anaphylaxis.
For VF or pulseless VT that persists despite defibrillation, amiodarone or lidocaine may be considered. AHA algorithms commonly use amiodarone 300 mg IV or IO as the first bolus and 150 mg as a subsequent dose; local crash-cart labelling and current protocol must be checked. Neither drug should postpone a shock. Magnesium is not routine for all arrest but is used for torsades de pointes or documented hypomagnesaemia. Sodium bicarbonate, calcium, thrombolysis and antidotes are reserved for defined circumstances rather than indiscriminate administration. Dose selection in poisoning and pregnancy belongs to the relevant special-circumstance guidance.
Oxygen is delivered at maximal available concentration during CPR. After ROSC, use 100% oxygen only until saturation or arterial oxygen can be measured reliably, then titrate to avoid both hypoxaemia and hyperoxaemia; AHA gives an SpO2 target of 90% to 98%. Treat hypotension with cause-directed fluids and vasoactive support while avoiding reflex large-volume loading. Reconcile every administered medicine after ROSC, correct potassium and glucose carefully, and review QT-prolonging agents. Verbal orders should be closed-loop, concentrations read aloud and empty ampoules retained for reconciliation where local practice permits.
When to Refer
Cardiac arrest is an emergency activation, not a routine referral. Outside hospital, summon emergency medical services immediately through the locally operational number and continue CPR and AED use until the person moves, trained help assumes care, the scene becomes unsafe or the rescuer is physically unable to continue. Do not place an arrested patient in a private vehicle while effective CPR and defibrillation are available at the scene; movement commonly degrades compressions. The 2025 AHA BLS guidance generally supports resuscitating where the patient is found when high-quality CPR can be delivered safely.
After ROSC, transfer to a hospital able to provide continuous critical care, cause-specific treatment and neurological support. Pre-alert the receiving emergency department or cardiac-arrest centre with age, collapse and CPR timings, witness and bystander status, initial rhythm, shocks, drugs, airway, ROSC time, haemodynamics, ECG findings, suspected cause and ongoing infusions. A STEMI pattern, cardiogenic shock, recurrent ventricular arrhythmia or continuing ischaemia requires urgent coronary-team discussion. Suspected pulmonary embolism, aortic catastrophe, poisoning, pregnancy, trauma or intracranial disease requires the matching specialist pathway.
In hospital, activate the resuscitation team and critical care early; do not wait for arrest when a deteriorating patient already meets escalation criteria. Survivors need cardiology or other cause-specific evaluation, rehabilitation, cognitive and psychological screening, implantable-defibrillator assessment when indicated, driving and occupational advice, and family education. Unexplained young arrest or a family history of sudden death should prompt inherited-cardiac-condition assessment. Referral also includes bereavement support and transparent review when the patient dies. Decisions about stopping resuscitation must follow applicable law, policy, reliable information and senior clinical judgement; a single rhythm, duration or capnography value is not sufficient in isolation.
Red Flags
Unresponsiveness with absent or abnormal breathing is itself the critical red flag: activate help and begin CPR. Agonal gasps are not normal breathing. Do not delay for a lay pulse check, a blood-pressure machine, glucose result or search for medical records. In hospital, abrupt loss of consciousness, loss of a central pulse or a monitored transition to VF, pulseless VT, PEA or asystole demands the same immediate response. Any pause that lengthens while staff intubate, obtain access, perform ultrasound or discuss the rhythm is a safety failure.
During resuscitation, recurrent VF, inability to deliver a shock, poor pad contact, compressor fatigue, absent chest rise, suspected tension pneumothorax, massive haemorrhage, severe hyperkalaemia or toxin exposure requires targeted correction without abandoning core CPR. A sudden capnography rise, purposeful movement or return of a pulse suggests ROSC; stop only long enough to confirm. Mechanical CPR is not routine and should not be used merely because staff are tired; if a system uses it for transport or a special procedure, minimize deployment interruption.
After ROSC, rearrest, hypotension, recurrent ventricular arrhythmia, ST-segment elevation, ongoing chest pain, severe hypoxaemia, rising carbon dioxide, coma, seizures, fever, oliguria or worsening lactate demands immediate escalation. Myoclonus alone does not establish irreversible neurological injury. Sedation, paralysis, temperature treatment, shock and metabolic disturbance confound examination. Avoid early definitive prognostic statements. During transfer, secure the airway and all lines, carry defibrillation capability and emergency drugs, use continuous ECG and saturation monitoring, and ensure personnel can treat rearrest. A nominally stable pulse after ROSC does not make an unmonitored transfer safe.
Indian Clinical Context
India's Emergency Response Support System provides the integrated number 112, and the 2026 National Ambulance Service operational guidance recognises 108, 102 and 112 as access routes across states and Union Territories. Actual dispatch arrangements, ambulance staffing and equipment vary locally. Bystanders should be told the number that works in their area and use speakerphone instructions while CPR continues. Facility teams should not assume that every arriving ambulance has a manual defibrillator, advanced airway capability or vasoactive infusions; communicate requirements at dispatch and prepare an alternative escalation plan.
Crowded homes, public places, long transport times and limited AED density make immediate hands-only CPR by witnesses particularly important when rescuers cannot provide breaths. Hospitals and colleges should place clearly marked AEDs in high-footfall locations, register responsibility for pad and battery checks, and drill security, nursing and medical teams together. Training must include recognising gasping, overcoming fear of harm, switching compressors and providing privacy without obstructing care. Rural and district facilities need functioning oxygen, bag-mask devices, suction, defibrillation, intraosseous capability, emergency medicines and an explicit referral map, not a paper policy unsupported by equipment.
Resource limitation does not justify unsafe improvisation. If advanced airway expertise is absent, effective bag-mask ventilation with high-quality compressions is preferable to repeated failed intubation. If post-arrest coronary intervention, CT, targeted temperature control, EEG or critical care is unavailable, stabilize and arrange monitored interfacility transfer with an accepting clinician. Record downtime honestly; do not invent favourable timings for referral acceptance. International AHA recommendations guide the clinical sequence but require adaptation to Indian laws, formularies, training scope and state emergency systems. Data quality should improve through Utstein-style local registries while protecting privacy and avoiding public claims based on a single tertiary centre.
NMC Competency Mapping
The NMC CBME 2024 framework integrates physiology of circulation and ventilation with medicine, anaesthesiology, emergency care, pharmacology, forensic and communication competencies. A learner should recognise adult cardiac arrest, activate help, demonstrate chest compressions and ventilation on a manikin, and explain why early CPR and defibrillation improve the chance of survival. They should distinguish shockable from non-shockable rhythms and connect PEA with a search for reversible pathology rather than treating the tracing as a diagnosis.
Applied learning includes safe AED operation, bag-mask ventilation, airway adjunct principles, closed-loop communication, role allocation and documentation. Pharmacology links epinephrine and selected antiarrhythmics with indications, timing, route, concentration safety and limitations of evidence. Pathophysiology links coronary thrombosis, hypoxia, electrolyte disturbance, tamponade, tension pneumothorax, pulmonary embolism, toxins and hypovolaemia to arrest. Post-arrest competencies include interpreting the ECG, titrating oxygen after reliable measurement, supporting pressure, recognizing seizures and arranging definitive care. Communication includes family updates, consent where relevant, bereavement and respectful handling after death.
Competence must be assessed in simulation and supervised practice, not inferred from reading. This guide does not certify manual-defibrillator operation, advanced airway placement, intraosseous access, ultrasound during CPR, prescribing, termination decisions or team leadership. Students should renew practical training because psychomotor performance decays. They must also understand scope: a trained lay rescuer follows AED prompts, while advanced interventions belong to appropriately trained clinicians. Audit and debriefing should focus on system improvement rather than blame, while genuine unsafe deviation is addressed. The educational endpoint is a dependable first response and timely escalation, not memorisation of an algorithm detached from equipment and teamwork.
Key Exam Pearls for NEET PG
An unresponsive adult with absent or abnormal breathing, including gasping, is presumed to be in cardiac arrest. Healthcare professionals limit the pulse check to ten seconds. High-quality adult CPR uses a compression rate of 100 to 120 per minute, depth of at least 5 cm while avoiding more than 6 cm, full recoil and minimal interruptions. Before an advanced airway, use 30:2. With an advanced airway, compress continuously and ventilate at the protocol rate without hyperventilation. The AED analyses rhythm; rescuers must clear the patient and resume CPR immediately after a shock.
VF and pulseless VT are shockable. Asystole and PEA are not. Confirm apparent asystole by leads and gain. Defibrillation has priority in shockable arrest. Epinephrine 1 mg IV or IO every three to five minutes is standard: early for non-shockable arrest, after initial unsuccessful CPR and shocks in shockable arrest. Amiodarone or lidocaine may be considered for refractory VF or pulseless VT. Routine bicarbonate, calcium, magnesium or thrombolysis is wrong without a specific indication; magnesium is classically used for torsades de pointes.
Remember the reversible causes as hypovolaemia, hypoxia, hydrogen-ion excess, hypo- or hyperkalaemia and metabolic disturbance, hypothermia, tension pneumothorax, tamponade, toxins, pulmonary thrombosis and coronary thrombosis. After ROSC, obtain an ECG, treat the cause, support ventilation and pressure, and titrate oxygen to SpO2 90% to 98% once reliable measurement is available. An unresponsive survivor requires protocolized temperature control for at least 36 hours under 2025 AHA guidance. Emergency coronary angiography is indicated for appropriate post-arrest STEMI and selected unstable patients; routine immediate angiography is not beneficial for every stable comatose survivor without ST elevation, shock, electrical instability or ongoing ischaemia.
Frequently Asked Questions
Should a bystander check the pulse before starting adult CPR?
No. A lay rescuer should treat an unresponsive adult with absent or abnormal breathing, including gasping, as cardiac arrest, activate emergency response and begin compressions. Pulse checks are unreliable and delay treatment. A healthcare professional may check a central pulse, but for no longer than ten seconds.
Can an automated external defibrillator shock every cardiac-arrest rhythm?
No. An AED shocks ventricular fibrillation or pulseless ventricular tachycardia when its analysis identifies a shockable rhythm. It will advise no shock for asystole or pulseless electrical activity. In either case, rescuers follow its prompt and immediately resume CPR while trained teams treat reversible causes.
When is epinephrine given during adult cardiac arrest?
Current AHA guidance uses epinephrine 1 mg intravenously or intraosseously every three to five minutes. It is given as soon as feasible in non-shockable arrest. In shockable arrest, rapid defibrillation is prioritized and epinephrine follows initial unsuccessful CPR and shock attempts according to the authenticated algorithm.
Does return of a pulse mean the emergency is over?
No. Return of spontaneous circulation is followed by substantial risks of rearrest, shock, hypoxic brain injury, seizures and untreated underlying disease. The patient needs continuous monitoring, controlled oxygenation and ventilation, perfusion support, ECG and cause evaluation, temperature management when unresponsive, and monitored transfer to definitive critical care.
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