eMedicine Specialties > Cardiology > Arrhythmias

Pulseless Electrical Activity

Author: Patrick O'Beirne, MD, Fellow in Cardiovascular Medicine, UMass Memorial Medical Center
Coauthor(s): Dionyssios A Robotis, MD, MPH, FACC, Assistant Professor of Medicine, University of Massachusetts; Consulting Staff Cardiologist/Electrophysiologist, University of Massachusetts Memorial Medical Center; Lawrence Rosenthal, MD, PhD, Associate Professor of Medicine, Director, Section of Cardiac Electrophysiology and Pacing, Fellowship Director of Clinical Cardiac Electrophysiology, Department of Internal Medicine, Division of Cardiovascular Medicine, University of Massachusetts Memorial Medical Center
Contributor Information and Disclosures

Updated: May 11, 2009

Introduction

Background

Pulseless electrical activity (PEA) is a clinical condition characterized by unresponsiveness and lack of palpable pulse in the presence of organized cardiac electrical activity. Pulseless electrical activity has previously been referred to as electromechanical dissociation (EMD).

While a lack of ventricular electrical activity always implies a lack of ventricular mechanical activity (asystole), the reverse is not always true. In a situation of cardiac arrest, the presence of organized ventricular electrical activity is not necessarily accompanied by meaningful ventricular mechanical activity. The latter clinical scenario has been called pulseless electrical activity or electromechanical dissociation. The qualifier “meaningful” is used to describe such a degree of ventricular mechanical activity that is sufficient to generate a palpable pulse. In other words, electrical activity is a necessary but not sufficient condition for mechanical activity.

Pulseless electrical activity does not mean mechanical quiescence. Patients may have weak ventricular contractions and recordable aortic pressure (pseudo-PEA). True pulseless electrical activity is a condition in which cardiac contractions are absent in the presence of coordinated electrical activity. Pulseless electrical activity encompasses a number of organized cardiac rhythms including supraventricular rhythms (sinus versus nonsinus) or ventricular rhythms (accelerated idioventricular or escape). The absence of peripheral pulses should not be equated with pulseless electrical activity as it may be due to severe peripheral vascular disease.

Pathophysiology

Pulseless electrical activity is the result of a major cardiovascular, respiratory, or metabolic derangement. Situations that cause sudden changes in preload, afterload, or contractility often result in PEA. 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, even though electrical activity is present. This event creates a vicious cycle, causing degeneration of the rhythm and subsequent death of the patient.

PEA is caused by the inability of cardiac muscle to generate sufficient force in response to electrical depolarization. This form of electromechanical decoupling may be the final result of many factors. PEA is always caused by a profound cardiovascular insult (eg, severe prolonged hypoxia or acidosis or extreme hypovolemia or flow-restricting pulmonary embolus). Transient coronary occlusion usually does not cause PEA, unless hypotension or other arrhythmias are involved. Hypoxia secondary to respiratory failure is probably the most common cause of PEA with respiratory insufficiency accompanying 40-50% of PEA cases. The common mechanisms involved are as follows:

• Decreased preload: Cardiac sarcomeres require an optimal length (ie, preload) for an efficient contraction. If this length is unattainable because of volume loss or pulmonary embolus (causing decreased venous return to the left atrium), the left ventricle is unable to generate sufficient pressure to overcome its afterload. Volume loss resulting in PEA is most likely to happen in cases of major trauma. In these situations, rapid blood loss and subsequent hypovolemia can exhaust cardiovascular compensatory mechanisms, culminating in PEA. Cardiac tamponade may also cause decreased ventricular filling. 
• Decreased contractility: Optimal myocardial contractility depends on optimal filling pressure, afterload, and the presence and availability of inotropic substances (eg, epinephrine, norepinephrine, or calcium). Calcium influx and binding to troponin C is essential for cardiac contraction. If calcium is not available (eg, calcium channel blocker overdose) or if calcium's affinity to troponin C is decreased (as in hypoxia), contractility suffers. Depletion of intracellular adenosine triphosphate (ATP) reserves causes an increase in adenosine diphosphate (ADP), which can bind calcium, further reducing energy reserves. Excess intracellular calcium can result in reperfusion injury by causing severe damage to the intracellular structures, predominantly the mitochondria.
• Afterload is inversely related to cardiac output. Severe increases in afterload pressure cause a decrease in cardiac output. However, this mechanism is rarely solely responsible for PEA.

Frequency

United States

The frequency of PEA varies among different patient populations. The condition accounts for approximately 20% of cardiac arrests that occur outside the hospital.

• Raizes et al found that PEA was responsible for 68% of monitored in-hospital deaths and 10% of all in-hospital deaths.¹ Because of the increased disease acuity observed in patients who are admitted, PEA may be more likely to occur in patients who are hospitalized. Also, these patients are more likely to have pulmonary emboli and such conditions as ventilator-induced auto–PEEP (positive–end-expiratory pressure).
• Nadkarni et al found that PEA was the first documented rhythm in 32% of adults with in-hospital cardiac arrest.²  
• The use of beta-blockers and calcium channel blockers may increase the frequency of PEA, presumably by interfering with cardiac contractility .

Mortality/Morbidity

The overall mortality rate is high in patients in whom PEA is the initial rhythm during cardiac arrest. In the study by Nadkarni et al, only 11.2% of patients who had PEA as their first documented rhythm survived to hospital discharge.² Given this grim outlook, the rapid initiation of advanced cardiac life support (ACLS) and identification of any reversible cause are critical. Initiation of ACLS may improve patient outcome if a reversible cause is identified and rapidly corrected.

Race

No data suggest any racial predilection.

Sex

Females are more likely to develop PEA than males. The reasons for this predilection are unclear but may relate to different etiologies of cardiac arrest. 

Age

The average patient age is 70 years. Older patients are more likely to have PEA as an etiology of cardiac arrest. Whether the patient outcome differs based on age is not known; however, advanced age is likely associated with a worse outcome.

Clinical

History

Knowledge of prior medical conditions allows prompt identification and correction of reversible causes. For example, a debilitated patient who develops acute respiratory failure and then manifests PEA may have a pulmonary embolus. If an elderly woman develops PEA 2-5 days after a myocardial infarction, a cardiac etiology should be considered (ie, cardiac rupture, recurrent infarction). History of prior drug intake is crucial, enabling prompt treatment of patients in whom drug overdose is suspected. The presence of PEA in the setting of trauma makes hemorrhage (hypovolemia), tension pneumothorax, and cardiac tamponade the more likely causes. 

Physical

By definition, patients with PEA have no pulses in the presence of organized electrical activity. The physical examination should focus on identification of reversible causes; for example, tracheal shift or unilateral absence of breath sounds indicates tension pneumothorax, while normal lung sounds and distended jugular veins point to cardiac tamponade.

Causes

Pulseless electrical activity can be classified by a number of criteria. While an exhaustive enumeration of causes has the advantage of completeness, it is not a convenient tool at the bedside.

The American Heart Association (AHA) and European Resuscitation Council favor the mnemonic of “Hs and Ts” as follows:

• Hypovolemia
• Hypoxia
• Hydrogen ion (acidosis)
• Hypokalemia/hyperkalemia
• Hypoglycemia
• Hypothermia
• Toxins
• Tamponade, cardiac
• Tension Pneumothorax
• Thrombosis (coronary or pulmonary)
• Trauma

• Severe hypovolemia
• Pump failure
• Obstruction to circulation: The 3 main causes of obstruction to circulation are as follows:
  • Tension pneumothorax⁴
  • Cardiac tamponade⁵
  • Massive pulmonary embolus⁶

Pump failure is the result of massive myocardial infarction, with or without cardiac rupture, and severe heart failure. Major trauma can be responsible for hypovolemia, tension pneumothorax, or cardiac tamponade.

Metabolic derangements (acidosis, hyperkalemia, hypokalemia), while rarely the initiators of PEA, are common contributing factors. Drug overdose (tricyclic antidepressants, digitalis, calcium channel and beta-blockers) or toxins are also rare causes of PEA. Hypothermia should be considered in the appropriate clinical context of out-of-hospital PEA.

Postdefibrillation PEA is characterized by the presence of organized electrical activity, occurring immediately after electrical cardioversion in the absence of palpable pulse. Postdefibrillation PEA may be associated with a better prognosis than continued ventricular fibrillation. A spontaneous return of pulse is likely, and cardiopulmonary resuscitation (CPR) should be continued for as long as 1 minute to allow for spontaneous recovery.

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