Cardiology

 
Background 

Pulseless Electrical Activity (PEA) is a clinical condition characterized by the presence of organized electrical activity on electrocardiogram (ECG) without a corresponding palpable pulse or effective cardiac output. It is one of the non-shockable rhythms in cardiac arrest and represents a state of electromechanical dissociation. Despite electrical activity, the heart is unable to generate sufficient mechanical force to produce a detectable pulse. 

II) Classification/Types 

By ECG Pattern: 

• Narrow complex PEA: Typically suggests a mechanical problem (e.g., tamponade, pneumothorax). 

• Wide complex PEA: Often associated with metabolic or toxic causes (e.g., hyperkalemia, drug overdose). 

By Underlying Cause (Hs and Ts): 

• Hypovolemia 

• Hypoxia 

• Hydrogen ion (acidosis) 

• Hyperkalemia/Hypokalemia 

• Hypoglycemia 

• Hypothermia 

• Tension pneumothorax 

• Tamponade (cardiac) 

• Toxins (e.g., digoxin, tricyclics) 

• Thrombosis (pulmonary or coronary) 

• Trauma 

Pathophysiology 

PEA occurs when the electrical system of the heart remains intact but the myocardial muscle is unable to contract effectively or at all, due to a lack of preload, obstruction, or intrinsic muscle dysfunction. It represents a mismatch between electrical excitation and mechanical contraction—termed electromechanical dissociation. Causes include severe hypovolemia, cardiac tamponade, tension pneumothorax, massive pulmonary embolism, profound acidosis, and electrolyte imbalances. 

Epidemiology 

• PEA accounts for approximately 20–30% of in-hospital cardiac arrests. 

• More common in older adults and critically ill patients. 

• Less favorable outcomes than ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT). 

• Survival rates vary widely (2–10%), largely depending on the underlying cause and time to intervention. 

Etiology 

I) Causes 

• Cardiac causes: Myocardial infarction, tamponade, massive pulmonary embolism 

• Non-cardiac causes: Hypoxia, severe acidosis, hypovolemia, electrolyte imbalances 

• Toxicologic: Drug overdose, poisoning 

• Mechanical: Tension pneumothorax, cardiac rupture, aortic dissection 

II) Risk Factors 

• Advanced age 

• Pre-existing heart disease 

• Severe infection or sepsis 

• Chronic renal failure (risk of electrolyte disturbances) 

• Recent surgery or trauma 

Clinical Presentation 

I) History (Symptoms) 

• Often sudden collapse with no warning 

• May be preceded by symptoms of hypoxia (e.g., dyspnea), chest pain, or hypotension 

• History may point to underlying cause (e.g., trauma, dialysis, medication use) 

II) Physical Exam (Signs) 

• Unresponsive and pulseless 

• Apneic or agonal respirations 

• Electrical activity seen on monitor but no palpable pulse or signs of perfusion 

• Signs of potential causes (e.g., distended neck veins in tamponade, unilateral breath sounds in pneumothorax) 

Differential Diagnosis (DDx) 

• Ventricular fibrillation 

• Pulseless VT 

• Asystole 

• Severe bradycardia 

• Artifact on ECG (e.g., muscle tremor) 

Diagnostic Tests 

Initial Work-Up (performed during CPR) 

• ECG: Shows organized rhythm (often sinus or junctional) without pulse 

• Bedside ultrasound (POCUS): Assess cardiac motion, tamponade, pneumothorax, PE 

• Arterial blood gas (ABG): Acidosis, hyperkalemia, hypoxia 

• Electrolyte panel: Potassium, calcium, glucose 

• Capnography: ETCO₂ <10 mmHg suggests poor perfusion and poor prognosis 

Advanced Testing 

Done after ROSC (Return of Spontaneous Circulation) 

• Echocardiogram: Assess structural heart issues 

• CT angiography: Rule out pulmonary embolism or aortic dissection 

• Toxicology screen: If overdose suspected 

Treatment 

I) Acute Management 

(Follow ACLS Protocol for Non-Shockable Rhythm) 

• High-quality CPR: Priority intervention 

• Epinephrine 1 mg IV/IO every 3–5 minutes 

• Identify and treat reversible causes (Hs & Ts) 

• Airway management: Intubation as needed 

• Volume resuscitation: If hypovolemia suspected 

• Targeted therapy: (e.g., needle decompression for tension pneumothorax, pericardiocentesis for tamponade) 

II) Chronic/Post-Resuscitation Management (after ROSC) 

• Hemodynamic stabilization (fluids, pressors) 

• Temperature management: Therapeutic hypothermia in comatose patients 

• Ongoing diagnostics to determine and treat underlying cause 

• ICU admission for close monitoring 

• Neurologic evaluation for anoxic brain injury 

Medications 

Device Therapy 

• Mechanical circulatory support (e.g., ECMO): Consider in select cases of refractory cardiac arrest 

• Defibrillation is not indicated unless rhythm changes to a shockable one (e.g., VT/VF) 

Patient Education, Screening, Vaccines 

• Education: Directed at prevention in high-risk individuals 

• Control chronic conditions (e.g., CHF, renal disease) 

• Medication adherence and regular monitoring 

• Screening/Prevention: 

• Monitor electrolytes in high-risk patients 

• Medication reconciliation to avoid proarrhythmic agents 

• Vaccines: Encourage routine vaccinations (influenza, pneumococcus) in chronic illness to prevent complications 

Consults/Referrals 

• Cardiology: For post-resuscitation care and cardiac evaluation 

• Critical Care/Intensivist: For post-arrest management 

• Toxicology: If overdose is suspected 

• Pulmonology/Thoracic Surgery: If PE or pneumothorax suspected 

• Nephrology: For dialysis-related electrolyte derangements 

Follow-Up 

Short-Term 

• Monitor for hemodynamic stability and neurologic recovery 

• Repeat labs (electrolytes, ABG, cardiac markers) 

• Post-resuscitation ECG and imaging 

Long-Term 

• Ongoing cardiac evaluation 

• ICD consideration if structural or electrical abnormalities found 

• Physical rehabilitation if anoxic brain injury occurred 

• Psychological support for patient and family 

Prognosis 

• Prognosis is poor without rapid identification and correction of underlying cause 

• Favorable if PEA is caused by a reversible condition and high-quality CPR is delivered promptly 

• Neurologic outcomes depend heavily on duration of arrest and effectiveness of resuscitation