pulseless electrical activity

PEA occurs when the heart shows organized (non-shockable) electrical activity but fails to generate effective mechanical contraction sufficient to produce a palpable pulse. It is one of the four ACLS cardiac arrest rhythms, alongside asystole, ventricular fibrillation (VF), and pulseless ventricular tachycardia (VT). Unlike VF/VT, PEA is not treated with defibrillation; management centers on high-quality chest compressions, ventilation, IV/IO epinephrine (1 mg every 3-5 minutes), and rapid identification/treatment of the underlying reversible cause.

Common reversible causes are remembered via the 'Hs and Ts' mnemonic: - Hypovolemia - Hypoxia - Hydrogen ion (acidosis) - Hypo-/Hyperkalemia - Hypothermia - Tension pneumothorax - Tamponade (cardiac) - Toxins - Thrombosis (pulmonary or coronary)

Clinically, PEA can result from primary cardiac dysfunction (e.g., massive MI causing profound pump failure despite electrical activity) or from a non-cardiac cause preventing adequate cardiac filling or output (e.g., tension pneumothorax obstructing venous return, cardiac tamponade restricting ventricular filling, massive PE obstructing right ventricular outflow, or severe hypovolemia from hemorrhage). Point-of-care ultrasound (POCUS) is increasingly used during resuscitation to help identify causes such as tamponade, pneumothorax, or right heart strain from PE, and to assess for cardiac standstill (a poor prognostic sign).

Prognosis in PEA arrest is generally poor and closely tied to how quickly the underlying cause is identified and reversed. Pseudo-PEA (a subset where some mechanical contraction exists but is too weak to produce a peripheral pulse, often detectable by ultrasound or arterial line) tends to have a better prognosis than true PEA (complete absence of mechanical activity).