Pulseless Electrical Activity

Updated: Jan 03, 2016
  • Author: Sandy N Shah, DO, MBA, FACC, FACP, FACOI; Chief Editor: Jeffrey N Rottman, MD  more...
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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). (See Etiology.)

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

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, Clinical, 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, even though electrical activity is present. This event creates a vicious cycle, causing degeneration of the rhythm and subsequent death of the patient.

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. Situations that cause sudden changes in preload, afterload, or contractility often result in PEA.

The use of antipsychotic agents has been found to be a significant and independent predictor of PEA. [1]

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.

Increased afterload

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.

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.

Additional etiologic factors

PEA 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:

The above enumeration of causes does not offer any cues regarding the frequency or reversibility of each cause. As such, it may be not particularly useful, even for those who have committed it to memory. [2]

The "3 and 3 rule" of Desbiens [3] is more practical, because it allows easy recall of the most common correctable causes of PEA. It organizes PEA causes into 3 major ones:

  • Severe hypovolemia
  • Pump failure
  • Obstruction to circulation

The 3 main causes of obstruction to circulation are as follows:

  • Tension pneumothorax [4]
  • Cardiac tamponade [5]
  • Massive pulmonary embolus [6]

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. [7] 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.



Occurrence in the United States

The frequency of pulseless electrical activity (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. [8] 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). PEA is the first documented rhythm in 32-37% of adults with inhospital cardiac arrest. [9, 10]

The use of beta-blockers and calcium channel blockers may increase the frequency of PEA, presumably by interfering with cardiac contractility.

Sex- and age-related demographics

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

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.



The overall prognosis for patients with pulseless electrical activity (PEA) is poor unless a rapidly reversible cause is identified and corrected. Evidence suggests that electrocardiogram (ECG) characteristics are related to the patient's prognosis. The more abnormal the ECG characteristics, the less likely the patient is to recover from PEA; patients with a wider QRS (>0.2 s) fare worse.

Interestingly, patients with out-of-hospital PEA are more likely to recover than are patients who develop this condition in the hospital. In one study, 98 of 503 (19.5%) patients survived out-of-hospital PEA. This difference is likely because of different etiologies and severity of illness. Patients who are not in the hospital are more likely to have reversible etiologies (eg, hypothermia).

In addition, the rate of electrical activity and QRS width do not appear to correlate with survival or neurologic outcome in patients who present with PEA out-of-hospital cardiac arrest. [11]

Overall, PEA remains a poorly understood entity with a dismal prognosis. Reversing this otherwise lethal condition may be possible by aggressively seeking and promptly correcting reversible causes.

The Oregon Sudden Unexpected Death Study, which included more than 1,000 cases of patients who presented with PEA (vs ventricular fibrillation), indicated a significantly higher prevalence of syncope that was distinct from cases of ventricular fibrillation. Potential links between future manifestations of PEA and syncope should be investigated further. [12]


The overall mortality rate is high in patients in whom PEA is the initial rhythm during cardiac arrest. In a study by Nadkarni et al, only 11.2% of patients who had PEA as their first documented rhythm survived to hospital discharge. [9] In a study by Meaney et al, patients with PEA as the first documented rhythm had a lower rate of survival to discharge than did patients who had ventricular fibrillation or ventricular tachycardia as their first documented rhythm. [10]

Given this grim outlook, the rapid initiation of advanced cardiac life support (ACLS) and identification of a reversible cause are critical. Initiation of ACLS may improve patient outcome if a reversible cause is identified and rapidly corrected.