![]() ![]() 11 Pseudo-PEA is a form of severe shock in which diminished coronary perfusion leads to decreased myocardial function, thus further propagating hypotension. 14 In pseudo-PEA, cardiac electrical activity is present with myocardial contractions that are not adequate to produce a palpable pulse. 11 Pseudo-PEA has the presence of aortic pulse pressures with a perfusion pressure less than 60 mm Hg. Pseudo-PEA is a profound state of cardiogenic shock that is inadequate to maintain perfusion pressure (and thus a nondetectable pulse). ![]() 2,8,18,9Įven though most providers define PEA as an electrical rhythm with absent mechanical activity, Mehta further delineated PEA into pseudo-PEA and true PEA. Characteristics of the PEA arrest rhythm may help with determining who would benefit from aggressive postcardiac care interventions such as therapeutic hypothermia. Often, a standardized treatment algorithm is deployed that is the same for each patient in PEA regardless of the etiology, particularly in the prehospital setting, due to the time-critical nature of the disease and lack of a clear identifiable etiology during resuscitation 12. ![]() They are hypoxia, hypovolemia, hypothermia, hyper/hypokalemia, hydrogen ion (acidosis), tension pneumothorax, tamponade (cardiac), toxins, and thrombosis (cardiac/pulmonary). American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care list the “ 5 Hs and 5 Ts” that should be evaluated and treated when attempting to diagnose the cause(s) of PEA. Various causes of pulseless electrical activity include significant hypoxia, profound acidosis, severe hypovolemia, tension pneumothorax, electrolyte imbalance, drug overdose, sepsis, large myocardial infarction, massive pulmonary embolism, cardiac tamponade, hypoglycemia, hypothermia, and trauma. 14 All cardiac arrest rhythms-that is, pulseless rhythms-that fall outside the category of pulseless ventricular tachycardia, ventricular fibrillation, or asystole are considered pulseless electrical activity. 11 The absence of mechanical contractions is produced by factors that deplete myocyte high-energy phosphate stores and inhibit myocardial fiber shortening, including hypoxia, ischemia, metabolic acidosis, and ionic perturbations (particularly potassium and calcium changes). PEA, formerly known as electromechanical dissociation, occurs in patients who have organized cardiac electrical activity without a palpable pulse. 13 Furthermore, post-countershock PEA with a slow and wide complex rhythm is associated with a worsened prognosis compared to the rapid, narrow complex PEA. 17,3 In addition, pulseless electrical activity after countershock is correlated with a worse prognosis than PEA presenting as the initial rhythm, with 0% to 2% of patients in post-countershock PEA surviving to discharge. 5,6 PEA arrests are associated with a poor prognosis, with a survival to discharge rate between 2% and 5% for out-of-hospital cardiac arrest. 20,15 For out-of-hospital cardiac arrest, the incidence of PEA is 22% to 30%. Several studies have shown the incidence of PEA in-hospital to be approximately 35% to 40% of arrest events. 16 Two-thirds of OHCA has an initial non-shockable rhythm of PEA or asystole with an increasing incidence compared with initial shockable rhythms (ventricular fibrillation and pulseless ventricular tachycardia). 10 The initial rhythm may be ventricular fibrillation (VF), pulseless ventricular tachycardia (VT), asystole, or pulseless electrical activity (PEA). Approximately 300,000 out-of-hospital cardiac arrests (OHCA) occur annually in the United States, with survival around 8%. ![]()
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