AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Pulseless electrical activity (PEA) is a clinical condition characterized by loss of palpable pulse in the presence of recordable cardiac electrical activity. PEA also is referred to as electromechanical dissociation (EMD).

PEA may result from various etiologies and has a spectrum of manifestations. Patients may present with recordable aortic pressures and absent peripheral pulses from weak cardiac contractions or severe peripheral vascular disease. These patients are classified as having pseudo-PEA. True PEA is a condition in which cardiac contractions are absent in the presence of coordinated electrical activity.

Pathophysiology

PEA is most frequently the end result of a major cardiac insult and commonly is caused by respiratory failure with hypoxia. Situations that cause sudden changes in preload or afterload (eg, massive pulmonary embolus) often result in PEA. The initial insult weakens cardiac contractions, and this situation is exacerbated by worsening acidosis, hypoxia, and increasing vagal tone. Further compromise of the inotropic state of 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 a sufficient force despite an electrical depolarization. This form of electromechanical decoupling may be the final result of many factors. PEA is always caused by a profound global cardiac insult (eg, severe prolonged hypoxia, acidosis). 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, comprising about 20-53% of cases. The common mechanisms involved are as follows:

• Decreased preload: Cardiac sarcomeres require an optimal length prior to contraction (ie, preload). If this length is not available 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 contract. Cardiac tamponade also may cause decreased ventricular filling.
• Decreased contractility: Optimal myocardial contractility is determined by optimal filling pressure, afterload, and the presence and availability of inotropic substances (eg, epinephrine, norepinephrine, digoxin, calcium). Calcium influx and binding to troponin C is essential for cardiac contraction. If calcium is not available (eg, with calcium channel blocker overdose) or if calcium's affinity to troponin C is decreased (as in hypoxia), contractility suffers. Depletion of intracellular ATP reserves causes an increase in 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 related inversely to cardiac output. Severe increases in afterload pressure cause a decrease in cardiac output. This mechanism is rarely solely responsible for PEA, however.

Frequency

United States

Frequency varies among different patient populations and reports. 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. In another study, PEA was responsible for approximately 66% of in-hospital deaths. 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 (post–end-expiratory pressure).
• The use of beta-blockers and calcium channel blockers may increase the frequency of PEA, presumably by interfering with cardiac contractility and depressing the conduction system.

Mortality/Morbidity

The overall mortality rate is high in patients in whom PEA is the initial rhythm during cardiac arrest. Rapid initiation of advanced cardiac life support (ACLS) is paramount. Initiation of ACLS may improve patient outcome if a reversible cause is identified and rapidly reversed. For this reason, PEA is considered a "rhythm of survival."

Race

No data suggest any racial predilection.

Sex

Females are more likely to be affected 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 on the basis of age is not known; however, advanced age likely produces a worse outcome.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

History of prior illnesses is crucial in guiding the treatment of patients with PEA. Knowledge of prior medical conditions allows identification of reversible conditions. For example, a debilitated patient who develops acute onset of respiratory failure and then develops PEA may have a pulmonary embolus. If an elderly woman develops PEA 2-5 days after a myocardial infarction, a cardiac etiology is immediately suspected (ie, cardiac rupture, recurrent infarction). History of prior drug intake is crucial, enabling prompt treatment of patients in whom drug overdose is suspected.

Physical

By definition, patients with PEA have an absence of palpable pulses in the presence of organized electrical activity. The patient should be examined promptly for some findings to identify reversible causes; for example, rectal temperature readings may identify hypothermia, and tracheal shift or unilateral absence of breath sounds may identify tension pneumothorax.

Causes

PEA is classified on the basis of etiology. It also may be classified by the presence or absence of aortic pressure. This differentiation is more practical because the etiology often is unclear. Occasionally, an aortic pressure may be recorded by invasive monitoring (ie, in pseudo-PEA), or cardiac contractions may be found by echocardiography (ie, normotensive PEA). Peripheral pulses may be absent because of very low aortic pressures or peripheral vascular disease. Approximately half of all patients may have an aortic pressure detectable by invasive monitoring. Also, patients with pseudo-PEA usually are younger, have a normal QRS interval, and are more likely to respond to epinephrine than patients with no aortic pressure. In one study, 77% (14/18) of patients with pseudo-PEA responded to epinephrine.

• Pulmonary - Respiratory arrest
• Mechanical - Cardiac tamponade, massive myocardial infarction, cardiac rupture, tension pneumothorax, auto-PEEP, severe congestive heart failure (CHF)
• Preload and afterload changes - Severe hypovolemia, massive pulmonary embolus, sepsis
• Metabolic changes - Hyperkalemia, hypothermia, drug ingestion (tricyclic antidepressant overdose, digitalis overdose, calcium channel and beta-blockers)
• Postdefibrillation PEA after prolonged ventricular fibrillation and electrical cardioversion
  • Postdefibrillation PEA is characterized by the presence of organized electrical activity, occurring immediately after electrical cardioversion and in the absence of palpable pulse. This may be the cause in as many as 60% of patients who experience PEA after defibrillation.
  • Postdefibrillation PEA may be associated with 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.
  • A further recommendation is to discontinue administration of epinephrine at this time to avoid precipitating ventricular fibrillation.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Because of the emergent nature of the problem, lab tests are not likely to be helpful in the immediate management of the patient.
• If available rapidly, arterial blood gases and serum electrolytes may provide information regarding serum pH, oxygenation, and serum potassium.

Imaging Studies

• Bedside echocardiography may rapidly identify reversible cardiac problems (eg, cardiac tamponade, rupture). Echocardiography also identifies patients with weak cardiac contractions who have pseudo-PEA. This group of patients is more likely to benefit from aggressive resuscitation.

Other Tests

• A 12-lead ECG is difficult to obtain during ongoing resuscitation but, if available, can provide clues to the presence of hyperkalemia (eg, peaked T waves, complete heart block, ventricular escape rhythm) or acute myocardial infarction. Hypothermia, if not already diagnosed, may be suspected by the presence of Osborne waves. Certain drug overdoses (eg, tricyclic antidepressants) prolong QRS duration.

Procedures

• Placement of an arterial line may identify patients with a recordable (but very low) blood pressure; however, these patients are likely to have a better outcome if given aggressive resuscitation.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• For a patient in whom PEA is suspected, the American Heart Association - Advanced Cardiac Life Support (AHA-ACLS) guidelines protocol recommends the following:
  • Initiate CPR.
  • Place an intravenous line.
  • Intubate the patient.
  • Assess blood flow using Doppler ultrasound.
  • Correct hypoxia by administering 100% oxygen.
• Once these basic measures are in place, reversible causes should be sought and corrected, which include the following:
  • Hypovolemia
  • Hypothermia
  • Hypoxia
  • Acidosis
  • Hypokalemia/hyperkalemia
  • Cardiac tamponade
  • Tension pneumothorax
  • Massive pulmonary embolus
  • Acute myocardial infarction
  • Drug overdose (eg, tricyclic antidepressants, digoxin, calcium channel blockers, beta-blockers)
• The clinical scenario usually provides useful information. Some examples include the following:
  • In a previously intubated patient, tension pneumothorax and auto-PEEP are more likely to occur.
  • In a patient on dialysis, consider hyperkalemia.
  • In a patient with prior myocardial infarction or CHF, myocardial dysfunction is likely.
  • A core temperature should always be obtained if the patient is thought to have hypothermia.
  • In patients diagnosed with hypothermia, resuscitative efforts should be continued at least until the patient is rewarmed because patient survival is possible even after prolonged resuscitation.
• Other components of the evaluation include the following:
  • Measure QRS duration since it has prognostic significance. Patients with QRS duration of less than 0.2 second are more likely to recover, and high-dose epinephrine may be administered.
  • Invasive monitoring (eg, arterial line) may be placed if it does not cause a delay in delivering standard ACLS care.
  • Absence of pulses should be confirmed by Doppler examination.
  • Echocardiography, if available, may assist with identifying the presence of cardiac contractions (pseudo-PEA). Patients with pseudo-PEA may have a rapidly reversible cause (eg, auto-PEEP, hypovolemia). Echocardiography also is invaluable in identifying cardiac tamponade, right ventricular enlargement, myocardial dysfunction, cardiorrhexis, or ventricular septal rupture.
  • In refractory cases, if the patient has suffered chest trauma, a thoracotomy may be performed, provided adequate expertise is available.
• Once reversible causes are identified, they should be corrected immediately. This process involves needle decompression of pneumothorax, pericardiocentesis for tamponade, volume infusion, correction of body temperature, and administration of thrombolytics or surgical embolectomy for pulmonary embolus.
• Resuscitative pharmacology includes epinephrine (1 mg IV q3-5min). If this therapy fails, a class IIb (acceptable, possibly helpful) regimen is to administer higher doses of epinephrine. Little data strongly recommends one regimen over the other. Higher doses include the following:
  • Intermediate - Epinephrine (2-5 mg q3-5min)
  • Escalating - Epinephrine (1 mg, 3 mg, or 5 mg q3min)
  • High dose - Epinephrine (0.1 mg/kg IV push q3-5min)
• If the underlying rhythm is bradycardiac (ie, heart rate <60 beats per min) associated with hypotension, then atropine (1 mg IV q3-5min, not to exceed 0.4 mg/kg) should be administered. This is considered the total vagolytic dose, beyond which no further benefit will occur. Note that atropine may cause papillary dilation, and this sign then cannot be used to assess neurological function.
• Sodium bicarbonate may be administered only in patients with severe systemic acidosis, hyperkalemia, or a tricyclic antidepressant overdose. The dose is 1 mEq/kg. Routine administration is discouraged because it worsens intracellular and intracerebral acidosis and does not appear to alter mortality rate.
• Prompt initiation of a cardiopulmonary bypass may have a role in carefully selected patients. This maneuver requires availability of expertise and support services. Patient selection is paramount because it should be used only in patients who have an easily reversible etiology of cardiac dysfunction. In an animal model, initiation of prompt cardiopulmonary bypass resulted in a higher rate of success in returning circulation than administration of high- or standard-dose epinephrine. Cardiac pacing can result in electrical capture but does not necessarily increase incidence of mechanical contractions; hence, this procedure is not recommended.

Surgical Care

Pericardiocentesis, chest tube thoracostomy, and even emergent cardiac surgery may be lifesaving procedures in appropriate patients.

Consultations

Once the cause of PEA is identified and the patient's condition is stabilized, consultation with appropriate services may be obtained.

• A cardiothoracic surgery consult may be appropriate for a pulmonary embolectomy in patients with large pulmonary embolus.
• In patients with drug overdoses, consultation with the local poison center may be useful after hemodynamic stability is restored.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Inotropic agents

Increase the central aortic pressure and counter myocardial depression. Their main therapeutic effects are cardiac stimulation, bronchial smooth muscle relaxation, and dilatation of skeletal muscle vasculature.

Drug Category: Anticholinergic agents

Improve conduction through the atrioventricular (AV) node by reducing vagal tone via muscarinic receptor blockade.

Drug Category: Alkalinizing agents

Are useful in alkalinization of urine. Routine administration of sodium bicarbonate is discouraged because it worsens intracellular and intracerebral acidosis and is not proven to reduce mortality rate.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Once resuscitation is successful, provide general care based on individual needs. Special care should be taken to adequately treat the initial problem that led to PEA.

Transfer

• Some institutions may not have the capability to provide specialized care (eg, cardiac surgery, pulmonary embolectomy). Once stabilized, patients in these centers may be transferred to tertiary care centers for definitive care.

Deterrence/Prevention

• The following measures may prevent some cases of in-hospital PEA:
• • Patients who have been on prolonged bed rest should receive deep venous thrombosis (DVT) prophylaxis.
  • Patients who are on ventilators should be monitored carefully for auto-PEEP development.
  • Hypovolemia should be treated aggressively, especially in patients with active bleeding.

Prognosis

• The overall prognosis for patients with PEA is poor, unless a rapidly reversible cause is identified and corrected. Evidence suggests that 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 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).
• 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.

Patient Education

• For excellent patient education resources, visit eMedicine's Public Health Center. Also, see eMedicine's patient education article Cardiopulmonary Resuscitation (CPR).

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to obtain appropriate documentation during and after ACLS procedure

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Aufderheide TP, Thakur RK, Stueven HA. Electrocardiographic characteristics in EMD. Resuscitation. Apr 1989;17(2):183-93. [Medline].
• Berenyi KJ, Wolk M, Killip T. Cerebrospinal fluid acidosis complicating therapy of experimental cardiopulmonary arrest. Circulation. Aug 1975;52(2):319-24. [Medline].
• Chen Q, Scott BH, Bilfinger TV, et al. Pulseless electrical activity after induction of anesthesia: A witnessed cardiac rupture. J Cardiothorac Vasc Anesth. Dec 2004;18(6):767-8. [Medline].
• Colwell C, Murphy P, Bryan T. Pulseless electrical activity. Emerg Med Serv. Sep 2004;33(9):63-6, 68. [Medline].
• Hoffman JR, Stevenson LW. Postdefibrillation idioventricular rhythm--a salvageable condition. West J Med. Feb 1987;146(2):188-91. [Medline].
• Paradis NA, Martin GB, Goetting MG. Aortic pressure during human cardiac arrest. Identification of pseudo- electromechanical dissociation. Chest. Jan 1992;101(1):123-8. [Medline].
• Parish DC, Dinesh Chandra KM, Dane FC. Success changes the problem: why ventricular fibrillation is declining, why pulseless electrical activity is emerging, and what to do about it. Resuscitation. Jul 2003;58(1):31-5. [Medline].
• Raizes G, Wagner GS, Hackel DB. Instantaneous nonarrhythmic cardiac death in acute myocardial infarction. Am J Cardiol. Jan 1977;39(1):1-6. [Medline].
• Stueven HA, Aufderheide T, Waite EM. Electromechanical dissociation: six years prehospital experience. Resuscitation. Apr 1989;17(2):173-82. [Medline].
• Vincent JL, Thijs L, Weil MH. Clinical and experimental studies on electromechanical dissociation. Circulation. Jul 1981;64(1):18-27. [Medline].
• Warner LL, Hoffman JR, Baraff LJ. Prognostic significance of field response in out-of-hospital ventricular fibrillation. Chest. Jan 1985;87(1):22-8. [Medline].

Article Last Updated: Mar 6, 2005