Pulseless electrical activity (PEA), also known as electromechanical dissociation, is a clinical condition characterized by unresponsiveness and impalpable pulse in the presence of sufficient electrical discharge. A lack of ventricular impulse often points to the absence of ventricular contraction, but the contrary is not always true. It means that the electrical activity is pertinent, but not sufficient, condition for contraction. In the case of cardiac arrest, the organized ventricular electrical activity does not usually follow sufficient ventricular response. This activity reviews pulseless electrical activity, its causes, its pathophysiology, management, and prognosis of this entity.
pulseless electrical activity pdf free
Objectives:Describe the etiology of pulseless electrical activity.Explain the pathophysiology of pulseless electrical activity.Review the diagnosis and management of pulseless electrical activity.Explain the importance of interprofessional team effort in the successful resuscitation of a patient with pulseless electrical activity.Access free multiple choice questions on this topic.
Pulseless electrical activity does not necessarily mean the lack of mechanical activity. There can be ventricular contractions and detectable pressures in the aorta, which are also known as pseudo-PEA.[1] True pulseless electrical activity is a state in which cardiac contractions are lacking in the presence of coordinated electrical impulses. Pulseless electrical activity can include a number of organized cardiac rhythms that may be supraventricular in origin, sinus versus non sinus, or ventricular in origin such as accelerated idioventricular or escape. An impalpable pulse should not always be taken as a pulseless electrical activity because it may be due to severe peripheral vascular abnormality.[2][3][4]
The incidence of pulseless electrical activity varies among different the United States patient populations. It accounts for approximately 20% of sudden cardiac deaths outside of the hospital setting.[8][9]
A study found that 68% of the recorded in-hospital deaths and 10% of all in-hospital deaths were attributed to pulseless electrical activity. In addition, hospitalized patients are more likely to have a pulmonary embolism, among other complications. Pulseless electrical activity is the first documented rhythm in 30 to 38% of adults with in-hospital cardiac arrest. Beta-blockers and calcium channel blockers may alter contractility, leading to increased susceptibility and resistance to treatment.[10] Women are more likely to develop pulseless electrical activity as compared to the male population. The risk of pulseless electrical activity increases over the age of 70, especially in the female population.
Pulseless electrical activity occurs when an insult involving the cardiovascular, gastrointestinal, or respiratory system results in the inability of the cardiac muscle to generate adequate force in response to electrical depolarization. This adverse event decreases cardiac contractility, and the situation gets severe by potential acidosis, hypoxia, and worsening vagal tone. More compromise of the inotropic state of the cardiac muscle leads to insufficient mechanical activity, despite the presence of electrical activity. It causes degeneration of cardiac rhythm, and eventually, death follows.[11]
Transient coronary occlusion usually does not cause pulseless electrical activity unless hypotension or other arrhythmias are involved. Respiratory failure leading to hypoxia is one of the most common causes of pulseless electrical activity, responsible for about half of the PEA cases. The following are other mechanisms for pulseless electrical activity:
Decreased cardiac contractility has been related to changes in intracellular calcium levels, which explains why patients with beta-blockers or calcium channel blockers are more prone to developing pulseless electrical activity and may become unresponsive to therapy.[12][13][14]
The first step in managing pulseless electrical activity is to begin chest compressions according to the advanced cardiac life support (ACLS) protocol followed by administrating epinephrine every 3 to 5 minutes, while simultaneously looking for any reversible causes. Once a diagnosis is made, begin immediate, specific management, i.e., decompression of pneumothorax, pericardial drain for tamponade, fluids infusion for hypovolemia, correction of body temperature for hypothermia, administration of thrombolytics for myocardial infarction or pulmonary embolism. An arterial blood gas and serum electrolytes should be obtained during the resuscitation process.
Epinephrine should be administered in 1 mg doses intravenously (IV)/intraosseously (IO) every 3 to 5 minutes during pulseless electrical activity arrest. Each dose should be followed by 20 ml of flush and elevating the arm for 10 to 20 seconds for better perfusion. Higher doses of epinephrine have not been shown to improve survival or neurologic outcomes in most patients. Selected patients, like those with beta-blockers or calcium channel blockers overdose, may benefit from higher-dose epinephrine. It can also be given via an endotracheal tube after mixing 2 mg in 10 ml of normal saline.[17]
Pericardial drainage and emergent surgery may be lifesaving in appropriate patients with pulseless electrical activity. In a patient with a refractory case and chest trauma, a thoracotomy may be performed. Near pulseless electrical activity or a very low-output state may also be managed with circulatory assistance (e.g., intra-aortic balloon pump, extracorporeal membrane oxygenation, cardiopulmonary bypass, and ventricular assist device).
Patients who have sudden cardiac arrest due to pulseless electrical activity have a poor outcome. In one study of 150 such patients, 23% were resuscitated and survived until hospital admission; only 11% survived until hospital discharge.
All healthcare workers, especially emergency department physicians, nurses, urgent care workers, internists, intensivists, and trauma specialists, must be certified in ACLS. While there are many causes of cardiac arrest, one needs to be aware of pulseless electrical activity, which carries a high mortality rate.
The first step in managing pulseless electrical activity is to start chest compressions according to the ACLS protocol along with using epinephrine, while simultaneously looking for any reversible causes. Once a diagnosis is made, begin immediate management, i.e., decompression of pneumothorax, pericardial drain for tamponade, fluids infusion, correction of body temperature, administration of thrombolytics, or surgical embolectomy for pulmonary embolus. A successful outcome very much depends on the combined efforts of an interprofessional team.
Cardiac arrest victims who present with pulseless electrical activity (PEA) usually have a grave prognosis. Several conditions, however, have cause-specific treatments which, if applied immediately, can lead to quick and sustained recovery. Current teaching focuses on recollection of numerous conditions that start with the letters H or T as potential causes of PEA. This teaching method is too complex, difficult to recall during resuscitation, and does not provide guidance to the most effective initial interventions. This review proposes a structured algorithm that is based on the differentiation of the PEA rhythm into narrow- or wide-complex subcategories, which simplifies the working differential and initial treatment approach. This, in conjunction with bedside ultrasound, can quickly point towards the most likely cause of PEA and thus guide resuscitation.
processing.... Drugs & Diseases > Cardiology Pulseless Electrical Activity Updated: Mar 27, 2018 Author: Sandy N Shah, DO, MBA, FACC, FACP, FACOI; Chief Editor: Jose M Dizon, MD more...
Share Email Print Feedback Close Facebook Twitter LinkedIn WhatsApp webmd.ads2.defineAd(id: 'ads-pos-421-sfp',pos: 421); Sections Pulseless Electrical Activity Sections Pulseless Electrical Activity Overview Background
Etiology Epidemiology Prognosis Show All Presentation DDx Workup Approach Considerations
Echocardiography Show All Treatment Approach Considerations
Pharmacologic Therapy Surgical Care Show All Guidelines Medication Medication Summary
Inotropic Agents Anticholinergic Agents Alkalinizing Agents Show All Questions & Answers References Overview Background Pulseless electrical activity (PEA) is a clinical condition characterized by unresponsiveness and the lack of a palpable pulse in the presence of organized cardiac electrical activity. Pulseless electrical activity has previously been referred to as electromechanical dissociation (EMD). (See Etiology.)
PEA does not mean mechanical quiescence. Patients may have weak ventricular contractions and recordable aortic pressure ("pseudo-PEA"). True PEA is a condition in which cardiac contractions are absent in the presence of coordinated electrical activity. PEA encompasses a number of organized cardiac rhythms, including supraventricular rhythms (sinus versus nonsinus) and ventricular rhythms (accelerated idioventricular or escape). The absence of peripheral pulses should not be equated with PEA, as it may be due to severe peripheral vascular disease. (See Etiology, Presentation, and Workup.)
Pulseless electrical activity (PEA) occurs when a major cardiovascular, respiratory, or metabolic derangement results in the inability of cardiac muscle to generate sufficient force in response to electrical depolarization. PEA is always caused by a profound cardiovascular insult (eg, severe prolonged hypoxia or acidosis or extreme hypovolemia or flow-restricting pulmonary embolus).
The initial insult weakens cardiac contraction, and this situation is exacerbated by worsening acidosis, hypoxia, and increasing vagal tone. Further compromise of the inotropic state of the cardiac muscle leads to inadequate mechanical activity, despite the presence of electrical activity. This event creates a vicious cycle, causing degeneration of the rhythm and subsequent death of the patient. 2ff7e9595c
Commenti