Clinical death: what it is and how it manifests itself

Clinical death is a condition in which blood circulation and breathing have ceased (usually due to sudden cardiac arrest), but reversibility remains possible with timely resuscitation. A person is outwardly unconscious, not breathing, and has no pulse in the major arteries—this is a "window of opportunity" that closes very quickly if chest compressions and defibrillation are not initiated when indicated. In modern classification, this is synonymous with cardiac arrest.

It's important to distinguish clinical death from biological death (irreversible) and brain death (legally equivalent to death due to the complete and irreversible cessation of brain function). Clinical death can progress to biological death if blood flow is not restored within minutes; brain death is diagnosed in a hospital according to strict criteria when reversibility is no longer possible. [2]

Modern rescue chains emphasize the role of the bystander: the sooner a cardiac arrest is recognized, emergency services are called, compressions are initiated, and an automated external defibrillator (AED) is connected, the higher the chances of survival and good neurological recovery. This is not dogma—it is the result of thousands of observations and randomized trials. [3]

Following successful restoration of spontaneous circulation (ROSC), the post-resuscitation phase is critical: protecting the brain, controlling temperature (preventing fever), ensuring adequate oxygenation/perfusion, early identification of the cause, and treating seizures. This phase often determines the survivor's quality of life. [4]

Epidemiology

Out-of-hospital cardiac arrest is one of the leading causes of sudden death in developed countries. The 2020 AHA guidelines note that survival rates after out-of-hospital cardiac arrest have increased compared to the past decade but have plateaued since 2012; in-hospital cardiac arrest offers better outcomes due to rapid team action. This explains the emphasis on bystander training and the availability of defibrillators. [5]

Most cardiac arrests in adults are cardiac in nature, and in approximately one-third to one-half of cases, the primary rhythm is fibrillation/nonsustained tachyarrhythmia, where early defibrillation is critical. In the remaining cases, shockless rhythms (PEA/asystole) predominate, where the outcome depends on the speed of compression initiation and the elimination of reversible causes. [6]

At the healthcare system level, outcomes are determined by the "survival formula": quality of recommendations → quality of training → quality of implementation. Cities and countries that widely educate their populations and provide AEDs demonstrate a significant advantage in survival. This is confirmed by European guidelines for resuscitation systems. [7]

After restoration of circulation, mortality remains high, with the primary cause being hypoxic-ischemic brain injury and multiorgan dysfunction of post-resuscitation syndrome. Standardized intensive care unit protocols are essential here. [8]

Reasons

In adults, the key causes are acute coronary syndrome, primary arrhythmias, cardiomyopathy, and severe heart failure. Non-cardiac causes include massive pulmonary embolism, hypoxia (asphyxiation, drowning), blood loss, cardiac tamponade, tension pneumothorax, and poisoning. Clinically, this is consolidated into the "4H + 4T" rule. [9]

In children, respiratory causes (asphyxia, inhalation), metabolic disorders, and congenital anomalies are more common, so primary ventilation plays a greater role here than in adults. The principles of recognition and algorithms remain the same—early initiation of CPR remains key. [10]

In-hospital cardiac arrests are often associated with the progression of severe somatic pathology or procedural complications. Prevention involves monitoring at-risk patients and rapid response teams. [11]

Finally, some cardiac arrests are associated with correctable acute factors: hypokalemia/hyperkalemia, acidosis, hypothermia/hyperthermia, and certain toxicants. Rapid recognition through bedside diagnostics and targeted treatment can dramatically change the outcome. [12]

Risk factors

The main risk factors include atherosclerosis and its "classic four": smoking, hypertension, dyslipidemia, and diabetes. They increase the likelihood of fatal arrhythmias due to ischemia. Risk factor control is the first level of prevention of clinical death. [13]

High-risk clinical conditions: previous myocardial infarction, reduced ejection fraction, severe heart failure, congenital arrhythmogenic syndromes (long QT, Brugada), hypertrophic cardiomyopathy. In these patients, the issue of an implantable cardioverter-defibrillator is considered. [14]

At home and at work, risks are increased by delays in calling an ambulance, the lack of trained bystanders, and the shortage of AEDs in public places. These factors affect not so much the likelihood of an accident as the chance of survival if one occurs. [15]

Separately, opioid overdoses: for these, the AHA emphasizes the role of early recognition and administration of naloxone in conjunction with basic CPR. This is a specific but important segment of the overall problem. [16]

Pathogenesis

After cardiac arrest, a "no-flow" phase (complete absence of perfusion) occurs, followed by "low-flow" (partial circulation due to compressions) during CPR. The brain is most vulnerable to ischemia: irreversible changes begin to form within 3-5 minutes at normal temperature, so every second before compressions begin is critical. Cooling, hypothermia, or rapid defibrillation can "lengthen" the window of reversibility.

Return of blood circulation is accompanied by reperfusion syndrome, activation of inflammation and coagulation, myocardial dysfunction (often resolving by days 2-3), and microcirculatory disturbances. This post-resuscitation syndrome resembles sepsis and requires targeted intensive care management. [18]

Neurological outcome is influenced by: total no-flow/low-flow time, compression quality, time to first defibrillation in shockable rhythm, oxygen/carbon dioxide management, temperature, and seizure activity after ROSC. Management of these variables is the subject of modern protocols. [19]

From a systems medicine perspective, outcome is the product of three factors: quality of science → quality of training → local implementation (the ERC's "survival formula"). A weak link in any of these factors dramatically reduces the patient's chances. [20]

Symptoms (how to recognize clinical death)

The main signs are: no consciousness, no normal breathing (or rare convulsive "sighs" appear - agonal breathing, which should not be considered normal), no signs of circulation. Pulse checks by non-specialists are unreliable, so emphasis is placed on the absence of breathing and response to handling/shaking. [21]

The bystander algorithm is simple: ensure safety, assess response/breathing for ≤10 seconds, call 911, turn on the speakerphone, begin compressions (rate 100-120/min, depth 5-6 cm, full chest return), connect an AED as soon as possible, and follow voice prompts. This is basic CPR (hands-only is acceptable for those who cannot listen for breathing). [22]

In hospital, monitoring is added to the recognition process: absence of a pulse on the arterial line, pulseless ECG rhythms, apnea by capnography. Low end-tidal CO₂ values during CPR are associated with poor blood flow; a sharp rise is an early sign of ROSC. [23]

If suffocation/drowning/infantile arrest is suspected, ventilation is added (30:2 or "2 breaths after 30 compressions"), but compressions are not withheld. In cases of drug overdose, naloxone should be administered as soon as possible, without stopping compressions. [24]

Table 1. "Chain of Survival" (ERC/AHA)

Link	What to do immediately	Why is this important?
Early recognition and calling for help	Reaction/breathing test ≤10 sec, call 112/103/911	Reduces no-flow
Early CPR	Compressions 100-120/min, 5-6 cm, minimize pauses	Supports brain/heart
Early defibrillation	Connect the AED and follow the prompts.	"Treats" fibrillation/TVZ
Effective IT assistance	ALS, eliminating the causes	Increases the chance of ROSC
Post-resuscitation stage	Brain protection, temperature control, IT support	Determines the quality of survival [25]

Forms and stages

It's more accurate to talk about stages of clinical death and its management. Stage 1 - arrest and recognition; Stage 2 - basic CPR/defibrillation; Stage 3 - advanced life support (ALS) with drugs and an advanced airway if indicated; Stage 4 - post-resuscitation care. Skipping any stage reduces the overall chance. [26]

Based on rhythm, shockable (fibrillation/pulseless tachycardia) and non-shockable (asystole/PEA) arrests are distinguished – this determines the priority of defibrillation. The patient may appear identical, but the monitor shows different tactics in the first minutes. [27]

Regarding reversibility, arrests due to 4H+4T are often "treated" by eliminating the cause (oxygen, fluids/blood, needle decompression, thrombolysis, antidotes). In shock rhythm, defibrillation is a key step. [28]

Refractory arrest (no ROSC after optimal CPR/defibrillation) is considered separately - for selected patients, extracorporeal CPR (ECPR) is discussed in centers ready for this technology. [29]

Table 2. Time windows (guidelines for practice)

Event	Critical time
The onset of compressions from the moment of collapse	≤ 1 min (witness)
First defibrillation for shockable rhythm	≤ 3-5 min
"Safe" pause of compressions	No more than 5-10 seconds (breaks are minimal)
Primary neuroprognosis after ROSC	Not earlier than 72 hours and after eliminating the influence of temperature/sedation [30]

Complications and consequences

Even with ROSC, the patient experiences post-resuscitation syndrome: myocardial dysfunction, vasoplegia, immune and coagulation changes, and pulmonary and renal dysfunction. Hypotension, hypoxemia, hyperoxemia, fever, and seizures worsen neurological outcome; their prevention and correction are essential. [31]

At the brain level, the main risk is hypoxic-ischemic injury and secondary strokes/seizures. Seizure activity during the first 72 hours is an unfavorable sign; seizure control is preferable with levetiracetam/valproate rather than phenytoin. [32]

Prolonged CPR is associated with rib/sternum injuries, bleeding, and pneumothorax—a cost that can be minimized with proper technique. In the hospital, prevention of thrombosis, infection, and stress ulcers is important. [33]

Psychological consequences affect both the patient (PTSD, cognitive complaints) and loved ones. Current protocols recommend post-intensive rehabilitation, neuropsychological assessment, and family-centered communication. [34]

Diagnostics

At the scene, diagnostics are minimal: no consciousness, no normal breathing, begin CPR, connect the AED. Any "diagnosis" that delays compressions/defibrillation worsens the outcome. The exception is immediately treatable causes (choking → airway clearance). [35]

In the emergency department/intensive care unit, in parallel with ALS, the following are sought: ECG (ischemia/block/electrolytes), blood gas composition, electrolytes, glucose, troponin, and toxicology as indicated. On-site ultrasound (FoCUS) helps identify tamponade, thromboembolism (indirect signs), hypovolemia, and pneumothorax. [36]

After ROSC, a CT scan of the brain is performed as indicated (to rule out hemorrhage), and a coronary assessment (invasive - in patients with shockable rhythms and signs of ischemia - according to the updated AHA focus updates) is performed. Outcome prediction is performed multimodally after ≥72 hours (clinical presentation, EEG patterns, background response, somatosensory evoked potentials, biomarkers), and only after temperature normalization and sedative withdrawal. [37]

Temperature management: Current guidelines support active fever prevention in comatose patients after ROSC rather than mandatory deep cooling for everyone. Decisions were influenced by data from large trials (including TTM2) and follow-up reviews in 2023–2025. [38]

Table 3. "4H + 4T": reversible causes of cardiac arrest

4H	Examples	4T	Examples
Hypoxia	Airway obstruction, aspiration	Tamponade	Trauma, infarction → effusion
Hypovolaemia (hypovolemia)	Blood loss, dehydration	Tension pneumothorax	Trauma, mechanical ventilation
Hypo/Hyperkalemia + Metab. Disorders	DKA, renal failure	Thrombosis	pulmonary embolism, coronary
Hypo/Hyperthermia	Hypothermia/overheating	Toxins	Opioids, TCAs, etc. [39]

Differential diagnosis

Sometimes witnesses confuse agonal breathing with normal breathing—these are rare, convulsive breaths; in this situation, CPR should be initiated. A normal fainting reaction (syncope) is accompanied by a rapid recovery of consciousness and breathing—this is not clinical death. [40]

A seizure in an adult may appear to be cardiac arrest, but breathing and consciousness return after the postictal period. If in doubt, it's best to begin chest compressions: the harm from brief CPR while the heart is still working is minimal, but in the case of true cardiac arrest, it's vital. [41]

Severe hypoglycemia, intoxication, and hypothermia are conditions where a person is unconscious and breathing is shallow or slow. In these situations, specific measures (dextrose, naloxone, and rewarming) are required in addition to CPR and oxygen. [42]

A separate category is brain death. In everyday life, it is sometimes confused with coma or clinical death. However, brain death is an irreversible condition, determined by strict protocols; resuscitation measures at the stage of brain death do not lead to recovery. [43]

Table 4. "Is this really a stop?" - quick reference points

Sign	More like a stop	There is probably no stop
No consciousness	Yes	It may occur with fainting or convulsions.
Breath	No/agonal sighs	There is regular breathing
Response to treatment/pain	No	Yes, even weak
Actions	Immediately CPR + AED	Assessment of causes, assistance without CPR [44]

Treatment

Basic CPR (BLS): for adults without breathing - compressions 100-120/min, depth 5-6 cm, full chest return, minimal pauses (less than 10 s), early defibrillation of shockable rhythms via an AED. Ventilation (30:2) is added by trained rescuers or if there is an obvious respiratory cause/in children. [45]

Advanced CPR (ALS): continuous compressions, monitoring/ECG, defibrillations according to protocol, adrenaline as early as possible for non-shockable rhythms, and after the second defibrillation for shockable rhythms; amidaron/lidocaine for refractory fibrillation, airway patency (with priority on minimizing compression-free intervals). In parallel, targeted search and correction of "4H+4T". [46]

Extracorporeal cardiac resuscitation (ECPR) is a life-saving strategy for highly selected patients with refractory cardiac arrest (usually bystander-induced, rapid CPR, and a probable correctable cause), where the center is prepared to provide rapid cannulation and subsequent correction of the cause (e.g., percutaneous coronary artery bypass grafting). It is not a "universal" method, but its role is growing. [47]

After ROSC: maintenance of MAP (usually aim ≥65 mmHg with individualization), oxygen titration (avoid hypoxemia and hyperoxemia), ventilation with normocapnia, treatment of the coronary bed if an ischemic cause is suspected, active fever prophylaxis for at least 72 hours in comatose patients (deep cooling is not mandatory for everyone), prevention/treatment of seizures with modern anticonvulsants, multidomain rehabilitation. [48]

Table 5. BLS algorithm for a witness (in 8 lines)

Step	Action
1	Make sure it's safe
2	Check reaction/breathing ≤10 sec
3	Call 112/103/911, turn on speakerphone
4	Place your hands in the center of your chest and begin compressions.
5	Frequency 100-120/min, depth 5-6 cm, full return
6	Bring/connect the AED, follow the prompts
7	Change every ~2 minutes, do not delay defibrillation
8	Continue until help arrives or signs of life appear [49]

Table 6. Post-resuscitation care: key goals of the first hours

Target	Range/approach
Oxygenation	SpO₂ ~94-98%, avoid hyperoxemia
Ventilation	Normocapnia (EtCO₂ ~35-45 mmHg)
Perfusion	MAP ≥65 mmHg (individual)
Temperature	Actively prevent fever for ≥72 h
Cause	Early coronary assessment according to indications
Convulsions	Treatment with levetiracetam/valproate is preferred [50]

Table 7. Neuroprediction after ROSC (when and how)

Principle	Explanation
Term	Not earlier than 72 hours, after normothermia and withdrawal of sedatives
Approach	Only multimodal (clinical + EEG + evoked potentials + biomarkers + visualization)
"It is forbidden"	Drawing conclusions based on one sign/ahead of schedule
Communication	Discuss the uncertainty and assessment steps transparently with the family [51]

Prevention

Primary prevention includes control of cardiovascular risk factors (blood pressure, lipids, sugar, weight, and smoking cessation), physical activity, treatment of coronary heart disease and heart failure, and monitoring by a cardiologist for cardiomyopathy/arrhythmia. This reduces the likelihood of cardiac arrest. [52]

Secondary prevention of death includes training loved ones in CPR and AED use, home action plans for at-risk patients, naloxone in households where opioids are available, and widespread use of community AEDs. The more people who have these skills, the lower the community mortality rate. [53]

Forecast

The prognosis for clinical death is variable and depends on timing: early initiation of CPR and defibrillation, brief no-flow, shockable rhythm, and high-quality post-resuscitation care improve the chances. Even with an unfavorable start, competent actions by bystanders and the team can change the trajectory of events. [54]

Neurological outcome is determined by total cerebral ischemia and the quality of intensive care. Current data support a strategy of temperature control (fever prevention), normoxia/normocapnia, and delayed, multimodal prognosis after 72 hours. This reduces the risk of premature decisions and increases the proportion of patients with an acceptable quality of life. [55]

FAQ

• How much time is there to “return” a person?

Minutes. At normal temperature, 3-5 minutes without blood flow is already dangerous for the brain. But this is no reason to do nothing: compressions and defibrillation prolong the "window," and certain factors (cooling, rapid defibrillation) widen it.

• Should artificial respiration be performed?

For adults, "compressions only" is acceptable for bystanders unless you are trained in ventilation or are unwilling to administer it. For children, drowning, and suffocation, it's more important to add breaths. The key is to not delay compressions and connect an AED as soon as possible. [57]

• How is clinical death different from brain death?

Clinical death is sometimes reversible (if blood flow is quickly restored). Brain death is irreversible and legally equivalent to death; it is diagnosed in a hospital according to strict protocols. [58]

• Do everyone need to be cooled down after ROSC?

No. Current guidelines emphasize fever prevention in comatose patients, rather than mandatory deep cooling for everyone. The decision is individualized based on clinical and resource needs. [59]

• When can we talk about a forecast?

Not earlier than 72 hours after ROSC, at normal temperature, without the influence of sedatives and only multimodally - combining clinical, EEG, evoked potentials, biomarkers and imaging. [60]