What are the causes of pulseless electrical activity (PEA) arrest?

Causes of Pulseless Electrical Activity (PEA) Arrest

PEA arrest is most commonly caused by reversible conditions that must be systematically identified and treated during resuscitation, with the "H's and T's" serving as the primary framework: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo/Hyperkalemia, Hypothermia, Toxins, Tamponade (cardiac), Tension pneumothorax, Thrombosis (pulmonary or coronary), and Trauma. 1, 2

Primary Reversible Causes (The H's and T's)

The H's

• Hypovolemia: Severe blood loss or fluid depletion leading to inadequate preload and cardiac output 1, 2
• Hypoxia: Inadequate oxygenation from respiratory failure, airway obstruction, or severe lung disease—notably the most frequent cause at 23.6% in one registry 3
• Hydrogen ion (acidosis): Severe metabolic acidosis from any cause disrupting cardiac electrical-mechanical coupling 1, 2
• Hypo/Hyperkalemia: Electrolyte abnormalities, particularly elevated potassium, causing cardiac arrest 1, 2
• Hypothermia: Core body temperature depression affecting cardiac function 1, 2

The T's

• Tension pneumothorax: Air accumulation in pleural space causing mediastinal shift and impaired venous return 1, 2
• Tamponade (cardiac): Pericardial fluid accumulation restricting cardiac filling 1, 2
• Toxins: Drug overdoses or poisonings, particularly beta-blockers, calcium channel blockers, and other cardiotoxic agents 1, 2
• Thrombosis (pulmonary): Massive pulmonary embolism causing acute right heart failure—PEA is the presenting rhythm in 36-53% of PE-related arrests 4
• Thrombosis (coronary): Acute coronary occlusion causing myocardial infarction, accounting for 12.5% of PEA cases 3
• Trauma: Severe injuries causing hemorrhage, tension pneumothorax, or cardiac injury 1, 2

Additional Important Causes Beyond the Traditional Mnemonic

Recent evidence reveals that the traditional "4H&4T" mnemonic is incomplete:

• Acute coronary syndrome: Represents 12.5% of PEA arrests, particularly in patients with preexisting severe left ventricular dysfunction where acute coronary occlusion produces PEA within 2 minutes rather than ventricular fibrillation 5, 3
• Nonischemic cardiac disorders: Account for 8.3% of cases, including cardiomyopathies and valvular emergencies 3
• Intracranial hemorrhage: Represents 6.9% of PEA arrests, a frequently overlooked cause 3
• Sepsis/distributive shock: Can present as PEA from profound vasodilation and cardiac depression 1

Diagnostic Approach During Resuscitation

During each 2-minute CPR cycle, systematically recall the H's and T's while performing bedside cardiac ultrasound to identify reversible causes. 1, 6

Immediate Bedside Ultrasound Protocol

• Perform focused cardiac ultrasound immediately without interrupting chest compressions for more than 10 seconds 6
• Pulmonary views: Identify pneumothorax, pleural effusion, and assess lung pathology 7
• Cardiac views: Detect pericardial effusion/tamponade, assess ventricular contractility and size, identify right heart strain from PE 6, 7
• IVC assessment: Evaluate volume status (collapsed IVC suggests hypovolemia) 7
• Abdominal views: Identify free fluid from hemorrhage, aortic aneurysm 7

Point-of-care ultrasound demonstrates 100% sensitivity for cardiac tamponade, 100% sensitivity with 97% specificity for pulmonary embolism, and 86% sensitivity with 94% specificity for myocardial infarction 2

Clinical Context and Risk Factors

• Pulmonary embolism: Consider in patients with conventional thromboembolism risk factors, prodromal dyspnea or respiratory distress, and witnessed arrest 4
• Severe left ventricular dysfunction: Patients with baseline poor LV function and suspected coronary disease who develop PEA should be immediately evaluated for acute coronary occlusion, as ischemia produces PEA within 2 minutes in this population 5
• Trauma patients: High likelihood of tension pneumothorax, hemorrhage, or cardiac tamponade 3

Critical Management Implications

• Hypoxia management: Given its high frequency (23.6%), placement of an advanced airway is theoretically more important in PEA than in VF/pulseless VT arrests 1
• Pulmonary embolism: Early systemic thrombolysis (alteplase 50 mg IV bolus) is associated with improved outcomes compared to use after failure of conventional ACLS 4, 1
• Tension pneumothorax: Immediate needle decompression at 2nd intercostal space, mid-clavicular line if clinically suspected 2
• Hypovolemia/sepsis: Empirical IV/IO crystalloid administration is potentially beneficial 1

Common Pitfall to Avoid

Do not delay treatment while exhaustively searching for causes—continue high-quality CPR with minimal interruptions while systematically evaluating for reversible conditions. 2 Any pause in chest compressions reduces coronary perfusion pressure and decreases likelihood of return of spontaneous circulation. 2