Cardiac Arrest: Definition and Management
Cardiac arrest is characterized by an abrupt loss of effective blood flow, sufficient to cause immediate loss of consciousness, leading immediately to death if untreated. 1
Definition of Cardiac Arrest
Cardiac arrest is defined as the sudden cessation of cardiac mechanical activity, confirmed by:
- Absence of a detectable pulse
- Unresponsiveness
- Apnea or agonal respirations 1
From a resuscitation perspective, sudden cardiac arrest (SCA) is defined as "malfunction or cessation of the electrical and mechanical activity of the heart, resulting in almost instantaneous loss of consciousness and collapse." 1
Pathophysiology
The pathophysiology of cardiac arrest is time-dependent and occurs in three phases:
Electrical phase (0-4 minutes):
- Characterized by shockable rhythms (VF/pVT)
- Heart is responsive to defibrillation
- Highest chance of survival 1
Circulatory phase (4-10 minutes):
- Characterized by tissue hypoxemia and emergence of asystole
- CPR is crucial during this phase
- Defibrillation is less effective 1
Metabolic phase (>10 minutes):
- Characterized by asystole, worsening hypoxia, and metabolic factors
- Survival is unlikely without advanced interventions
- Often associated with severe functional disability 1
Presenting Rhythms in Cardiac Arrest
The most common electrical mechanisms for cardiac arrest include:
- Ventricular fibrillation (VF)
- Pulseless ventricular tachycardia (pVT)
- Asystole
- Pulseless electrical activity (PEA) 1
In adults, VF is the most common primary rhythm in sudden cardiac death, especially in victims of sudden, unheralded death. However, substantial numbers of cardiac arrests begin as severe bradyarrhythmias, asystole, or PEA. 1
Management of Cardiac Arrest
Immediate Actions
Activation of response team:
- After establishing the presence of cardiac arrest, the first priority is activating a response team capable of identifying the specific mechanism and carrying out prompt intervention 1
High-quality CPR:
- Chest compressions generate forward blood flow (30-40% of normal cardiac output)
- Compression fraction should be >80% (minimize pauses)
- Allow complete chest recoil
- Avoid excessive compression rates 1
Early defibrillation (for shockable rhythms):
- Deliver shocks of 200J, 200J, and 360J quickly (within 30-45 seconds)
- Do not interrupt sequence with basic life support measures
- Check rhythm or pulse after each shock 1
Airway management and ventilation:
- Secure airway with endotracheal intubation if possible
- Avoid excessive ventilation (target 10-12 breaths/minute)
- Use highest available oxygen concentration initially 2
Vascular access and medication administration:
Identifying and Treating Reversible Causes
Systematically check for potentially reversible causes ("H's and T's") 2:
- Hypoxia: Ensure proper ventilation with 100% oxygen
- Hypovolemia: Rapid IV/IO fluid administration
- Hydrogen ion (acidosis): Ensure adequate ventilation
- Hypo/Hyperkalemia: Treat electrolyte imbalances
- Hypothermia: Active rewarming
- Toxins: Specific antidotes if available
- Cardiac tamponade: Pericardiocentesis
- Tension pneumothorax: Needle decompression
- Thrombosis (coronary): Consider emergent coronary angiography
- Thrombosis (pulmonary): Consider fibrinolytic therapy
Advanced Interventions
Point-of-care ultrasound:
- Identify reversible causes with minimal interruption to chest compressions
- Differentiate true PEA from pseudo-PEA 2
Mechanical CPR devices:
- Consider when manual CPR is difficult to maintain
- May provide more consistent compressions 3
Extracorporeal CPR (ECPR):
Post-Resuscitation Care
After return of spontaneous circulation (ROSC), focus on:
Targeted temperature management:
Hemodynamic optimization:
- Target MAP ≥65 mmHg
- Treat post-cardiac arrest myocardial dysfunction 1
Ventilation management:
- Avoid hyperoxia (target SpO₂ 94-98%)
- Avoid hyperventilation (target PaCO₂ 40-45 mmHg) 1
Coronary angiography:
- Emergency coronary angiography for patients with STEMI on ECG
- Consider for cardiac arrest of presumed cardiac origin 2
Neurological prognostication:
Pitfalls and Caveats
Assuming PEA is always non-cardiac: PEA can be caused by reversible conditions that require specific interventions beyond standard ACLS.
Excessive ventilation: Overzealous ventilation increases intrathoracic pressure, decreases venous return, and reduces cardiac output.
Prolonged interruptions in chest compressions: Even brief pauses significantly reduce coronary and cerebral perfusion pressures.
Delayed defibrillation: For shockable rhythms, early defibrillation is critical for survival.
Premature prognostication: Avoid withdrawal of care based on early clinical findings, as neurological recovery may continue for days to weeks.
Failure to identify and treat underlying cause: Cardiac arrest is often a symptom of an underlying condition that requires specific treatment.
Hyperoxia after ROSC: Excessive oxygen can cause oxidative stress and worsen neurological outcomes.