Ī priority in resuscitation is placement of an intravenous or intraosseous line for administration of medications. There is no evidence that external cardiac compression can increase cardiac output in any of the many scenarios of PEA, such as hemorrhage, in which impairment of cardiac filling is the underlying mechanism producing loss of a detectable pulse. Where an underlying cause for PEA cannot be determined and/or reversed, the treatment of pulseless electrical activity is similar to that for asystole. The approach in treatment of PEA is to treat the underlying cause, if known (e.g. Treatment Ĭardiac resuscitation guidelines (ACLS/BCLS) advise that cardiopulmonary resuscitation should be initiated promptly to maintain cardiac output until the PEA can be corrected. In PEA, there is organised or semi-organised electrical activity in the heart as opposed to asystole (flatline) or to the disorganised electrical activity of either ventricular fibrillation or ventricular tachycardia. The absence of a pulse confirms a clinical diagnosis of cardiac arrest, but PEA can only be distinguished from other causes of cardiac arrest with a device capable of electrocardiography (ECG/EKG). Pulseless electrical activity, it is possible to observe by invasive blood pressure (red) the transition from a normal mechanical activity of the heart, which progressively changes in rhythm and contractile quality to asystole, even in the presence of normal electrical activity (green), also confirmed by the pulse oximeter detection even if with artifacts (blue)
More than one mechanism may be involved in any given case. These are (1) impairment of cardiac filling, (2) impaired pumping effectiveness of the heart, (3) circulatory obstruction and (4) pathological vasodilation causing loss of vascular resistance and excess capacitance. The possible mechanisms by which the above conditions can cause pulseless in PEA are the same as those recognized as producing circulatory shock states. Trauma (e.g., hypovolemia from blood loss).Thrombosis (e.g., myocardial infarction, pulmonary embolism).These possible causes are remembered as the 6 Hs and the 6 Ts. This is confirmed by examining the airway for obstruction, observing the chest for respiratory movement, and feeling the pulse (usually at the carotid artery) for a period of 10 seconds. As a result, PEA is usually noticed when a person loses consciousness and stops breathing spontaneously. Pulseless electrical activity leads to a loss of cardiac output, and the blood supply to the brain is interrupted. Survival is about 20% if the event occurred while the patient was already in the hospital setting. The medication epinephrine (aka adrenaline) may be administered. While PEA is classified as a form of cardiac arrest, significant cardiac output may still be present, which may be determined and best visualized by bedside ultrasound ( echocardiography).Ĭardiopulmonary resuscitation (CPR) is the first treatment for PEA, while potential underlying causes are identified and treated. In PEA, there is electrical activity but insufficient cardiac output to generate a pulse and supply blood to the organs, whether the heart itself is failing to contract or otherwise. Under normal circumstances, electrical activation of muscle cells precedes mechanical contraction of the heart (known as electromechanical coupling).
Pulseless electrical activity is found initially in about 20% of out-of-hospital cardiac arrests and about 50% of in-hospital cardiac arrests. Pulseless electrical activity ( PEA) refers to cardiac arrest in which the electrocardiogram shows a heart rhythm that should produce a pulse, but does not. Medical condition Pulseless electrical activityĪ drawing of what a rhythm strip showing PEA could look like
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