PULSELESS ELECTRICAL ACTIVITY

Pulseless electrical activity refers to a cardiac arrest situation in which a heart rhythm is observed on the electrocardiogram that should be producing a pulse but is not. Under normal circumstances, electrical activation of the cardiac muscle cells precedes mechanical contraction of the heart. Pulseless electrical activity is also referred to as PEA or, by the older term, electromechanical dissociation. Pulseless electrical activity is the clinical condition characterized by unresponsive and lack of a palpable pulse in the presence of organized cardiac electrical activity. Electrical activity is a necessary but not sufficient condition for mechanical activity. In pulseless electrical activity, the heart either does not contract or there are other reasons why this results in an insufficient cardiac output to generate a pulse and supply blood to vital organs. This condition is usually noticed because a person loses consciousness and stops breathing spontaneously. This is confirmed by examining the airway for obstructions, observing the chest for airway movement (rise and fall, and feeling a pulse (which is usually the carotid pulse) for a ten second period. The possible causes of pulseless electrical activity is remembered as the six Hs and the six Ts. The six Hs are as followed: hypovolemia, hypoxia, hydrogen ions (acidosis), hyperkalemia/hypokalemia, hypoglycemia, and hypothermia. The six Ts are also as followed: toxins (drug overdose), cardiac tamponade, tension pneumothorax, thrombosis (myocardial infarction, pulmonary embolism), tachycardia, and trauma (hypovolemia due to blood loss). The diagnosis of pulseless electrical activity comes when you see electrical activity on the device capable of electrocardiography but the person does not produce a pulse. Cardiopulmonary resuscitation is initiated immediately, although this may not take place if there has been a decision made not to resuscitate. The main approach in treatment of pulseless electrical activity is to treat the underlying cause, if it is known. The treatment of pulseless electrical activity is similar to that of asystole in situation where an underlying cause cannot be determined and/or reversed. The mainstay of drug therapy for pulseless electrical activity is epinephrine 1mg every 3 to 5 minutes. Previously the use of atropine was recommended in the treatment of pulseless electrical activity/ asystole. This recommendation was withdrawn in 2010 by the American Heart Association due to the lack of evidence for therapeutic benefit. Sodium Bicarbonate 1mcq per kilogram may be considered in this rhythm as well, although there is little evidence to support this practice. Its routine use is not recommended for patients in this context, except in special situations. All of these drugs should be administered along with appropriate cardiopulmonary resuscitation techniques. Defibrillators are not used for this rhythm, as the problem lies in the response of the myocardial tissue to electrical impulses. It is becoming increasingly common for emergency medical service providers to encounter patients with pulseless electrical activity. In the United States, it is currently estimated the pulseless electrical activity may occur in as many as thirty-five percent of prehospital cardiac arrests. Different form of pulseless electrical activity may be identified. Pulseless electrical activity may be referred to as primary pulseless electrical activity if identified as the first rhythm. In cases where pulseless electrical activity is defined as the rhythm after a patient has been defibrillated from ventricular fibrillation or ventricular tachycardia, it is referred to as post defibrillation pulseless electrical activity. This helps to clarify the type of pulseless electrical activity that is involved. It may potentially be used when trying to predict patient outcomes. If pulseless electrical activity is identified as the first rhythm that is managed in the prehospital environment, it is reported the patient will have a greater rate of restored spontaneous circulation. Knowing this may prove useful in managing patient immediate and long term care needs. It is appropriate to review the pathology that may be involved along with defining pulseless electrical activity. When an event such as significant cardiac insult occurs, pulseless electrical activity develops followed by a decrease in cardiac contractility. Contractility can be influenced by hypoxia, acidosis, increased vagal tone, and a medical condition that influences preload and afterload. Impaired myocardial inotropy may then result and lead to inadequate mechanical activity. This is a very unique situation when this occurs. Outcomes of pulseless electrical activity are foreshadowed by several factors. For instance, a narrow QRS complex and a faster rate has been associated with improved patient outcomes. A fast, narrow complex rhythm may indicate a relatively normal heart responding to a severe clinical condition such as hypovolemia or cardiac tamponade. These severe clinical conditions may improve with a specific intervention. In other cases, a better outcome may be obtained if the cause of pulseless electrical activity is identified and treated appropriately. On the other hand, if pulseless electrical activity involves a wide QRS complex and a slow rate may represent a dying myocardium or indicate a specific critical rhythm disturbance. Hyperkalemia can cause this situation. Pulseless electrical activity, in many cases, is a terminal rhythm associated with a high mortality rate. Some people argue that they are seeing less ventricular fibrillation and more pulseless electrical activity. This is due to the attention that has been focused on prevention and care of coronary artery disease. Regardless, of which is correct, emergency medical providers should still strive to determine the cause of the patient’s cardiac arrest and pay attention to potentially reversible causes. The patient will benefit and have a better outcome if the cause of the cardiac arrest is identified and treated appropriately. By ensuring that we as emergency medical providers are aware of the possible causes of pulseless electrical activity, we can reduce prehospital morbidity and mortality.