Cardiac Arrest: Causes, Recognition, and Resuscitation

Cardiac arrest is the sudden cessation of effective mechanical activity of the myocardium, leading to circulatory arrest and death without immediate assistance. Clinically, this condition is characterized by loss of consciousness, breathing (or agonal breathing), and pulses in the major arteries. Seconds can determine the outcome: early recognition by a bystander, immediate pressing of the 911/913 alarm, initiation of chest compressions, and early defibrillation of fibrillation/pulseless tachycardia significantly increase survival. Current AHA/ERC guidelines emphasize the "chain of survival": early call for help → high-performance CPR → defibrillation → advanced care → postresuscitation care. [1]

Today, we better understand that "quality CPR" is not a slogan, but a set of measurable parameters: a compression rate of 100-120/min, a depth of 5-6 cm in adults, full chest expansion, minimal pauses, and a compression:ventilation ratio of 30:2 in the absence of an advanced airway. Real-time feedback devices and teamwork improve these metrics and outcomes. [2]

A distinction is made between out-of-hospital cardiac arrest (OHCA) and in-hospital cardiac arrest (IHCA): the care pathways differ, but the principles are the same. The introduction of public automated external defibrillators (AEDs) and CPR training for the general population are key systemic measures. In hospitals, rapid recognition by a monitor, an ALS protocol, and a multidisciplinary post-resuscitation team are crucial. [3]

A separate area is the postresuscitation period. Following restoration of spontaneous circulation (ROSC), oxygen and carbon dioxide management, maintenance of perfusion pressure, temperature control, timely coronary management if an ischemic cause is suspected, and structured neuroprognostic assessment are required. The 2023-2024 updates (ERC/Resus Council UK, ILCOR) have clarified targets and approaches to temperature and neuroprognostic assessment. [4]

Code according to ICD-10 and ICD-11

In ICD-10-CM, cardiac arrest is coded in block I46:

• I46.0 - cardiac arrest with successful recovery,
• I46.1 - sudden cardiac death, described,
• I46.9 - Cardiac arrest, unspecified. These codes are often combined with the underlying cause (e.g., MI - I21 , PE - I26 ), which is important for surveillance and payment. [5]

ICD-11 introduces a separate, more detailed node MC82 "Cardiac arrest" with the following subtypes: MC82.0 (arrest in VT/VF), MC82.1 (bradiarrhea), MC82.2 (asystole), MC82.3 (PEA - pulseless electrical activity), MC82.4 (cardiopulmonary arrest), MC82.Z (unspecified). Post-coordination is recommended: a code for the etiology and circumstances (place, time) is added to the arrest, which improves the registry quality of the data. [6]

Table 1. Codes for cardiac arrest (practical minimum)

System	Block	Subtypes/examples
ICD-10-CM	I46.*	I46.0 (with recovery), I46.1 (sudden death), I46.9 (unspecified)
ICD-11	MC82.*	MC82.0 (VT/VF), MC82.1 (bradyarrest), MC82.2 (asystole), MC82.3 (PEA), MC82.4, MC82.Z
Etiology (both options)	-	Add the cause: MI (I21/BA40), PE (I26/BD71), intoxication, etc.

Epidemiology

The annual incidence of OHCA in countries with well-developed registries ranges from tens to hundreds of cases per 100,000 population. The proportion of patients discharged alive after OHCA varies but remains single-digit on average; it is significantly higher in cases of shockable primary rhythm (VF/VT) and early defibrillation. The updated Utstein 2024 reporting protocols standardized indicators (time to CPR/CF, compression quality, neurological outcomes), which will allow for more accurate comparisons of care systems. [7]

IHCA has better outcomes than OHCA due to monitoring and immediate access to a defibrillator: ROSC and survival rates in inpatients are higher, although much depends on the initial condition and cause of cardiac arrest. According to AHA reports, the trend toward improved IHCA outcomes continues with the implementation of modern algorithms. [8]

Key system-level factors include bystander training, AED availability, EMS arrival time, and CPR quality (compressions without pauses, rate and depth, minimization of pre- and post-shock interruptions). Real-time audio/video instruction by the dispatcher increases the rate of CPR initiation and survival. [9]

Interpretation of statistics is complicated by heterogeneity of coding; the transition to ICD-11 (MC82) and updated Utstein templates should improve data comparability and the accuracy of surveillance. [10]

Reasons

Causes are grouped into cardiac and non-cardiac. Cardiac: ischemic heart disease (acute coronary syndrome, infarction), primary rhythm disturbances (channelopathies, WPW with AF, etc.), cardiomyopathy, complications of myocarditis, mechanical accidents (tamponade, myocardial rupture), massive pulmonary embolism. [11]

Non-cardiac: hypoxia (aspiration, drowning), trauma, blood loss/shock, metabolic disturbances (hypo-/hyperkalemia, acidosis), hypothermia/hyperthermia, anaphylaxis, toxic influences (opioids, other depressants), electrical injury. It is these “reversible causes” that are structured in the ERC section “special circumstances”. [12]

For practice, it is convenient to remember the mnemonic “H's & T's” (Hypoxia, Hypovolemia, Hydrogen ions/Acidosis, Hypo-/Hyperkalemia, etc.; Tension pneumothorax, Tamponade, Toxins, Thrombosis coronary/pulmonary) - a targeted search and elimination of these causes increases the chances of ROSC and survival. [13]

Risk factors

Cardiac factors include: age, male gender, coronary artery disease/previous MI, heart failure, cardiomyopathy, long QT/channelopathy, diabetes mellitus, hypertension, dyslipidemia, and smoking. Non-cardiac factors include COPD/bronchial asthma, sleep apnea, renal failure (electrolyte imbalances), and alcohol and substance abuse. [14]

Systemic risk factors for death in OHCA include lack of bystanders, lack of early CPR, delayed defibrillation, and lack of AEDs in public places. "Public access to defibrillation" programs and CPR training for schoolchildren reduce mortality. [15]

Pathogenesis

Pathophysiology is determined by the "primary rhythm." In VF/pulseless VT, chaotic or rapid ventricular electrical activity occurs without mechanical ejection; early shock restores perfusion. In PEA, electrical activity is present but pulseless due to mechanical obstruction or severe pump failure; management focuses on identifying H's and T's. In asystole, there is no electrical activity; the prognosis is worse, and the quality of CPR and correctability of the cause determine the outcome. [16]

The key mechanism of organ damage is global ischemia during cardiac arrest and reperfusion injury after ROSC. In the postresuscitation period, neuroinflammation, myocardial dysfunction, and endothelial and coagulation dysregulation are activated, which justifies a multimodal approach to therapy (pressure/oxygen/CO₂/temperature/correction of causes). [17]

Symptoms

Cardiac arrest is often preceded by sudden weakness, chest pain, shortness of breath, and dizziness. Cardiac arrest itself is characterized by loss of consciousness, absence of normal breathing (possibly rare, agonal gasps), and absence of a pulse. It is critical for bystanders to quickly recognize the absence of normal breathing and responsiveness and begin CPR with chest compressions. [18]

For medical personnel, triggers for initiating ALS include: confirmed circulatory arrest, identification of rhythm (shockable/non-shockable), immediate defibrillation in case of VF/VT, securing airway and vascular access, and drug therapy according to the algorithm. [19]

Forms and stages

There are four "primary" rhythms of cardiac arrest: VF, pulseless VT (shockable), and PEA, asystole (non-shockable). Depending on the location, they are OHCA and IHCA. It is useful to remember the phases of the resuscitation process: recognition → basic CPR (BLS) → advanced life support (ALS) → ROSC → post-resuscitation care. [20]

Table 2. Classification of cardiac arrest

Base	Categories	Practical tactics
Rhythm	VF/VT (shock); PEA/asystole (non-shock)	Shock immediately if shockable rhythm; if PEA/asystole - CPR and elimination of causes
Place	OHCA / IHCA	AED/Bystander CPR vs. Instant ALS
Phase	Pre-resuscitation / CPR / ROSC / post-resuscitation	Corresponding AHA/ERC algorithms

Complications and consequences

Even with ROSC, neurological damage, cardiac dysfunction, respiratory failure, and renal and hepatic dysfunction are possible. The risk of recurrent arrhythmia, hemodynamic instability, and multiple organ failure is highest in the first 24 hours. Transition to a structured post-resuscitation protocol is a mandatory continuation of resuscitation. [21]

In the long-term, cognitive impairment, PTSD in the patient and witnesses, and depression are important. Rehabilitation and family support are part of evidence-based care. [22]

Diagnostics

During cardiac arrest, diagnosis is extremely pragmatic: confirm the absence of breathing and pulse, start the timer, and activate the BLS/ALS algorithm. The monitor/defibrillator determines the rhythm and indicates the next step (shock/no shock). The sooner the AED is connected, the better the chances. [23]

In parallel, a search for reversible causes (H's & T's) is conducted. Clues: sudden dyspnea/cyanosis (PE, tension pneumothorax), trauma/bleeding (hypovolemia), anaphylaxis (cutaneous manifestations, hypotension), electrolyte disturbances (dialysis history, toxicology). Point-of-care ultrasound (POCUS) in short "safe windows" helps confirm tamponade, tension pneumothorax, massive PE (signs of RV overload). [24]

After ROSC, the following are required: blood gases (PaO₂, PaCO₂, pH), lactate, electrolytes (K⁺, Ca²⁺, Mg²⁺), troponin (MI context), glucose, ECG (ST elevation?), head CT (if an intracranial cause is suspected), and coronary strategy if ACS is suspected. Postresuscitation echocardiography helps to assess contractility and mechanical causes. [25]

Table 3. Diagnostic "minimums" by phases

Phase	What is required	For what
BLS	Determine absence of breathing/pulse, call for help/AED	Launching the chain of survival
ALS	Determine the rhythm, defibrillation/adrenaline/amiodaron according to the algorithm, POCUS in the "windows"	ROSC Probability ↑
ROSC	ECG, gases, lactate, electrolytes, echocardiography	Reason/severity/plan
Post-resuscitation	Neuroassessment, temperature, hemodynamics, CAG/CT as indicated	Reducing secondary damage
Sources: AHA 2020/2023, ERC 2021, Resus UK 2023. [26]

Differential diagnostics (popular science)

The main task is to distinguish true circulatory arrest from situations that mimic it: severe syncope/seizures/metabolic coma, deep hypothermia, severe poisoning with rare breaths. The rule is simple: no normal breathing or pulse → CPR; attempts to "drag out a diagnosis" are dangerous. [27]

Already at the medical facility, they differentiate between shockable and non-shockable rhythms, PEA versus "very small ejection fraction" (ultrasound helps to see pulseless heartbeats), and simultaneously search for a reversible cause (tamponade vs. massive PE vs. tension pneumothorax, etc.). The ERC identifies "special circumstances" requiring modifications to the algorithms (hypothermia, hyperkalemia, drowning, pregnancy, trauma). [28]

Table 4. What often mimics cardiac arrest - and clues

Situation	Hints/Check
Seizures/postictal coma	Breathing and pulse are maintained; recovery occurs within minutes
Deep hypothermia	Slow pulse, miosis, cold skin; special ERC protocol
Depressant poisoning	Miosis, slow breathing; benefit from naloxone (if opioids)
Pseudo-PEA	The ultrasound shows contractions, but no pulse → maintain perfusion, eliminate the cause

Treatment

Bystander and paramedic support: immediate compressions of 100-120/min, depth of 5-6 cm, minimal pauses, early defibrillation if shockable (connect an AED). Oral ventilation is acceptable, but if the rescuer is unprepared, focus on Hands-Only CPR until an AED/EMS arrives. Dispatch support increases the rate of CPR initiated. [29]

ALS (team/hospital):

• Shockable rhythm (VF/pulseless VT): immediate shock, 2-minute CPR cycles, then rhythm check; epinephrine (1 mg IV every 3-5 min after the second shock), amidaron (300 mg, then 150 mg) for refractory shockable rhythm; minimizing pauses before and immediately after the shock. The use of double sequential defibrillation for refractory shockable rhythm is being considered in centers with experience, taking into account ILCOR data (not standard, possible in protocols). [30]
• Non-shockable rhythm (PEA/asystole): continuous compressions, epinephrine as early as possible, active search for and immediate elimination of reversible causes (H's & T's). Ultrasound - only in short "windows" without reducing the compression fraction. [31]

Airway and ventilation: in the absence of an advanced airway, 30:2; after placement of an SAVD/tube, continuous compressions and ventilation at 10 breaths/min without hyperventilation. The choice of method (supraglottic vs. intubation) depends on the experience of the team; the focus is to minimize interruptions of compressions. [32]

ECPR (extracorporeal CPR): ILCOR 2024 allows for consideration of ECPR as a life-saving strategy in highly selected adults with out-of-hospital cardiac arrest and ongoing refractory VF/VT with a short collapse-to-cannulation time and a center-based protocol (weak recommendation, low-moderate evidence). This is not a universal standard, but an option for specialized teams. [33]

Postresuscitation care: after ROSC, target SpO₂ 94-98%, avoid hyperoxia; PaCO₂ in the normal range; maintain MAP ≥65 mmHg (personalized); temperature control (prevent hyperthermia; choice of target temperature and duration - according to the local protocol and the latest ERC/Resus UK 2023 updates); early coronary assessment if ACS is suspected (immediate CAG - in case of ST elevation or high clinical and electrocardiographic probability of ischemia); multimodal neuroprognostics after 72 h (or later with sedation/hypothermia). [34]

Table 5. “Short” ALS algorithm (adults)

Step	Shock Rhythm	Not a shock rhythm
1	Shock immediately, then CPR for 2 minutes	CPR 2 min, adrenaline as soon as possible
2	Rhythm check → shock in case of VF/VT	Rhythm check → continue CPR
Medicines	Adrenaline through 2nd shock; amidarone 300 mg	Adrenaline every 3-5 minutes
Special	Consideration of DSD/ECPR in centers	Active search for H's & T's
Sources: AHA 2020/Focus Update 2023; ILCOR 2024. [35]

Table 6. "H's & T's": Reversible Causes and Effects

Cause	Tips	What to do immediately
Hypoxia	Cyanosis, hypoxemia	Oxygen/ventilation, patency of the respiratory tract
Hypovolemia	Blood loss, trauma	Fluids/blood, surgical control
Hydrogen ions (Acidosis)	Acidosis according to the gas analysis	Ventilation, correction of the cause
Hypo/Hyperkalemia	Dialysis, ECG signs	Ca²⁺, insulin/glucose, bicarbonate as indicated
Tension pneumothorax	Unilateral "silent" hemithorax	Immediate decompression
Tamponade	POCUS signs, trauma	Pericardiocentesis
Toxins	Poisoning/history	Antidotes (naloxone, etc.)
Thrombosis (coronary/pulmonary)	ST-elevation/PE scenario	CAG/reperfusion; thrombolysis/thrombextraction
Sources: ERC 2021; AHA 2020. [36]

Prevention

Community and systemic: distribution of AEDs in public places, mandatory Hands-Only CPR training in schools and workplaces, "dispatch CPR" scenarios, and navigation to the nearest AED in mobile services. These measures have been proven to increase the rate of CPR initiation and reduce the time to defibrillation. [37]

Clinical: monitoring of cardiometabolic factors (blood pressure, lipids, sugar), treatment of coronary heart disease, ICD in patients with a high risk of life-threatening arrhythmias (according to guidelines), correction of electrolytes, polypharmacy and drug interactions, prevention of pulmonary embolism. In hospitals - early escalation in case of deterioration, clear "Rapid Response" commands. [38]

Forecast

Prognosis is determined by the time to initiation of CPR, the time to the first shock in a shockable rhythm, and the quality of CPR. A favorable neurological outcome is achievable with early ROSC and a well-designed post-resuscitation strategy; hyperoxia and hypocapnia are associated with worse outcomes and should be avoided. [39]

Systemic improvements (community education, AED, well-established hospital algorithms) demonstrate sustained improvements in IHCA survival and local successes in OHCA, confirming the importance of not only clinical but also organizational interventions. [40]

FAQ

• Should I do artificial respiration if I don’t know how?

No. Current recommendations only allow for compressions until help arrives. If a second rescuer and a mask-valve are available, increase the ventilation ratio to 30:2. [41]

• After how many shocks should amidaron be administered?

In refractory VF/VT - after the second shock (300 mg), then 150 mg later, while continuing CPR and adrenaline. [42]

• Should everyone have ECPR for refractory VF?

No. ILCOR 2024 recommends that ECPR be considered only in highly selected patients in centers with an established protocol and short delays. [43]

• How to manage temperature after ROSC?

Avoid hyperthermia, maintain controlled temperature according to local protocol (target and duration chosen by the team based on the latest ERC/Resus UK guidelines). [44]

Additional tables (for quick layout/memos)

Table 7. CPR Quality: Numerical Goals

Parameter	Target
Compression frequency	100-120/min
Depth	5-6 cm for adults
Pauses	Minimize breaks ≤10 sec
Compression fraction	>60-80% of cycle time
Ventilation with advanced DP	~10/min, without hyperventilation
Source: AHA 2020, ERC 2021. [45]

Table 8. Postresuscitation goals (first 24 hours)

Parameter	Recommended range
SpO₂	94-98%
PaCO₂	Normacapnia (≈35-45 mmHg)
Mean arterial pressure	≥65 mmHg Art. (personalization)
Temperature	Avoid hyperthermia; monitor according to protocol
Glucose	Avoid hypo- and severe hyperglycemia
Sources: ERC/Resus UK 2023; AHA. [46]

Table 9. When to consider emergency CAG after ROSC

Situation	Tactics
ST elevation on ECG	Immediate CAG/revascularization
Without ST elevation, but high probability of ACS (shock, life-threatening arrhythmias, ischemic changes)	Early invasive assessment as decided by the team
Low probability of ACS	Individually, after stabilization
Source: AHA/ILCOR postresuscitation guidelines. [47]

Table 10. The role of technologies in resuscitation

Technology	What does it give?	Comment
Feedback sensors	Depth/frequency/fraction control	Improve the quality of CPR
AED card/mobile alerts	Reduces the time to shock	Element of public programs
POCUS	Quick search for reversible causes	Only during short windows
Mechanical compressors	Stable compressions during transport/catheter lab.	According to indications, not for everyone
Sources: ILCOR/AHA reviews. [48]