What is the pathophysiology of cardiac arrest?

Pathophysiology of Cardiac Arrest

Cardiac arrest is defined as the malfunction or cessation of the electrical and mechanical activity of the heart, resulting in almost instantaneous loss of consciousness and collapse, with the pathophysiology following a time-dependent progression through three distinct phases: electrical, circulatory, and metabolic. 1

Three-Phase Model of Cardiac Arrest

Electrical Phase (0-4 minutes)

• Occurs during the first approximately 4 minutes after cardiac arrest
• Characterized by the presence of shockable rhythms (ventricular fibrillation/pulseless ventricular tachycardia)
• The heart remains responsive to defibrillation during this phase
• Early defibrillation is the most effective intervention during this phase 1

Circulatory Phase (4-10 minutes)

• Begins approximately 4 minutes after cardiac arrest
• Characterized by onset of tissue hypoxemia and emergence of asystole
• Cardiopulmonary resuscitation (CPR) to provide oxygen delivery becomes crucial
• Defibrillation is less effective but may be enhanced by pre-shock epinephrine administration and effective CPR 1
• Bystander CPR shows increasing benefit during this phase compared to the electrical phase 2

Metabolic Phase (>10 minutes)

• Begins approximately 10 minutes after cardiac arrest
• Distinguished by asystole, worsening hypoxia, and circulating metabolic factors
• Results in cell death and end-organ dysfunction
• Survival during this phase is unlikely and often associated with severe functional disability 1

Primary Cardiac Arrest Rhythms

• Ventricular fibrillation (VF) - common in primary cardiac arrests, especially in young people without comorbidities 1
• Pulseless ventricular tachycardia (pVT) 1
• Asystole - often represents end-stage rhythm following prolonged VF or PEA 3
• Pulseless electrical activity (PEA) 1

Pathophysiological Consequences

Hemodynamic Effects

• Complete cessation of cardiac output results in no blood flow to vital organs 3
• Standard CPR produces only 30-40% of normal cardiac output 1
• Cerebral blood flow may reach 60% of normal with effective CPR, but myocardial flow is substantially lower at 10-30% 1, 3

Post-Cardiac Arrest Syndrome

• Develops after return of spontaneous circulation (ROSC) 1
• Consists of four key components:
  1. Post-cardiac arrest brain injury
  2. Post-cardiac arrest myocardial dysfunction
  3. Systemic ischemia/reperfusion response
  4. Persistent precipitating pathology 1

Post-Cardiac Arrest Brain Injury

• Manifests as coma, seizures, myoclonus, varying degrees of neurocognitive dysfunction, and brain death 1
• May be exacerbated by microcirculatory failure, impaired autoregulation, hypotension, hypercarbia, hypoxemia, hyperoxemia, pyrexia, hypoglycemia, hyperglycemia, and seizures 1

Post-Cardiac Arrest Myocardial Dysfunction

• Begins within hours of the arrest
• Peaks at approximately 8 hours
• Begins to improve at 24 hours
• Typically resolves within 48-72 hours
• Associated with cardiovascular ischemia/reperfusion 1

Systemic Ischemia/Reperfusion Response

• Produces a state similar to sepsis syndrome
• Characterized by elevated cytokines, presence of endotoxin in plasma, activation of coagulation pathways, and inhibition of anticoagulant pathways 1
• Activates immune and coagulation pathways, contributing to multiple organ failure and increasing risk of infection 1
• Shares features with sepsis, including intravascular volume depletion, vasodilation, endothelial injury, and microcirculation abnormalities 1

Special Considerations

Pediatric Cardiac Arrest

• In pediatric out-of-hospital cardiac arrest (OHCA), asystole is more common than ventricular arrhythmias 1
• However, in young people without comorbidities, the primary arrhythmia is often VF 1
• Post-cardiac arrest care must be tailored to address specific pediatric considerations 1

Reversible Causes

• Potentially reversible causes of cardiac arrest are clustered into four Hs and four Ts:
  • Hypoxia, Hypovolemia, Hyperkalemia/other electrolyte disorders, Hypothermia
  • Thrombosis, Tamponade, Tension pneumothorax, Toxic agents 4
• Early identification and treatment of these causes is critical for improving outcomes 4

Implications for Management

• High-quality chest compressions and early defibrillation remain the cornerstone of cardiac arrest management 1
• The phase of cardiac arrest should guide therapeutic interventions:
  • Electrical phase: prioritize immediate defibrillation
  • Circulatory phase: emphasize high-quality CPR before defibrillation
  • Metabolic phase: consider advanced therapies and address post-arrest syndrome 1, 2
• Post-cardiac arrest care should focus on identifying and treating the underlying cause, mitigating ischemia-reperfusion injury, preventing secondary organ injury, and making accurate prognostic assessments 1

Understanding the time-dependent pathophysiology of cardiac arrest is crucial for optimizing resuscitation strategies and improving survival outcomes.