eMedicine Specialties > Cardiology > Arrhythmias

Pulseless Electrical Activity

Patrick O'Beirne, MD, Fellow in Cardiovascular Medicine, UMass Memorial Medical Center
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

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.

Differential Diagnoses

Accelerated Idioventricular Rhythm

Workup

Laboratory 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, serum electrolytes, and glucose may provide information regarding serum pH, oxygenation, serum potassium and glucose. 

Imaging Studies

Bedside echocardiography may rapidly identify reversible cardiac problems (eg, cardiac tamponade, rupture, massive myocardial infarction). Echocardiography also identifies patients with weak cardiac contractions who have pseudo-PEA. This group of patients is more likely to benefit from aggressive resuscitation.⁵

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; these patients are likely to have a better outcome if given aggressive resuscitation.

Treatment

Medical Care

• For a patient in whom PEA is suspected, the American Heart Association - Advanced Cardiac Life Support (AHA-ACLS) guidelines protocol recommends the following⁷ :
  • Initiate CPR.
  • Place an intravenous line.
  • Intubate the patient.
  • 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
  • Hypoxia
  • Acidosis  
  • Hypokalemia/hyperkalemia
  • Hypoglycemia
  • Hypothermia
  • Toxins (eg, tricyclic antidepressants, digoxin, calcium channel blocker, beta-blockers)
  • Cardiac tamponade
  • Tension pneumothorax
  • Massive pulmonary embolus
  • Acute myocardial infarction
• 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.⁸
• 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. Acute rightward axis shifts can suggest possible pulmonary embolus.
  • Invasive monitoring (eg, arterial line) may be placed if it does not cause a delay in delivering standard ACLS care.
  • 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,⁵ right ventricular enlargement, pulmonary hypertension suggestive of pulmonary emboli, 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, vasopressin, and atropine. 
  • Epinephrine should be administered in 1 mg doses IV/IO q3-5min during PEA arrest.
  • Higher doses of epinephrine have been studied and show no improvement in survival or neurologic outcomes in most patients.
  • Special populations of patients, such as those who have overdosed on beta-blockers and calcium channel blockers may benefit from higher dose epinephrine. 
  • Vasopressin 40 U IV/IO may replace either the first or second dose of epinephrine in patients with pulseless electrical activity.^9,10
• If the underlying rhythm is bradycardia (ie, heart rate <60 bpm) associated with hypotension, then atropine (1 mg IV q3-5min, up to 3 doses) should be administered. This is considered the total vagolytic dose, beyond which no further benefit will occur. Note that atropine may cause pupillary dilation, and this sign then cannot be used to assess neurologic 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 the 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 the incidence of mechanical contractions; hence, this procedure is not recommended.
• Near pulseless electrical activity, or a profound low output state, may also be addressed with different means of circulatory assist (eg, intra-aortic balloon pump, extracorporeal membrane oxygenation, cardiopulmonary bypass, ventricular assist device).

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 toxicology department or the local poison center may be useful after hemodynamic stability is restored.

Medication

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

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.

Epinephrine (Adrenalin)

Has alpha-agonist effects that include increased peripheral vascular resistance and reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist effects of epinephrine include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.

Dosing

Adult

1 mg IV q3-5min

Pediatric

Not established

Interactions

Increases toxicity of beta-blocking agents, alpha-blocking agents, and halogenated inhalational anesthetics

Contraindications

Documented hypersensitivity; cardiac arrhythmias; angle-closure glaucoma; during labor (may delay second stage of labor)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in elderly persons and in prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias; if ventricular tachycardia or fibrillation (recurrent or persistent) develops, may be caused by effects of epinephrine

Anticholinergic agents

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

Atropine (Atropair)

Used for treatment of bradyarrhythmias. Works to increase heart rate through vagolytic effects, causing increase in cardiac output. Total vagolytic dose is 2 mg; doses <0.5 mg may exacerbate bradycardia.

Dosing

Adult

0.5-1 mg IV q 3-5 min; not to exceed 2 mg

Pediatric

0.01 mg/kg IV, may repeat q5min; not to exceed 0.4 mg

Interactions

Other anticholinergics have additive effects; may increase pharmacologic effects of atenolol and digoxin; may decrease antipsychotic effects of phenothiazines; TCAs with anticholinergic activity may increase effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid in patients with Down syndrome and/or in children with brain damage to prevent hyperreactive response; avoid in coronary heart disease, thyrotoxicosis, narrow-angle glaucoma, CHF, cardiac arrhythmias, and hypertension; caution in peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in prostatic hypertrophy or prostatism, may cause dysuria requiring catheterization

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.

Sodium bicarbonate (Neut)

Used only when patient is diagnosed with bicarbonate-responsive acidosis, hyperkalemia, or TCA or phenobarbital overdose. Routine use not recommended.

Dosing

Adult

Initial: 1 mEq/kg IV; depending on results of ABGs, additional doses of 0.5 mEq/kg may be given q10min (usual concentration is 7.5%)

Pediatric

Not established

Interactions

Induces urinary alkalinization, which may decrease levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; increases levels of amphetamines, pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine

Contraindications

Documented hypersensitivity; alkalosis; hypernatremia; hypocalcemia; severe pulmonary edema; abdominal pain of unknown cause

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Can cause alkalosis, decreased plasma potassium, hypocalcemia, and hypernatremia; caution in electrolyte imbalances (eg, CHF, cirrhosis, edema, corticosteroid use, renal failure); avoid extravasation since can cause tissue necrosis; may cause precipitation of calcium salts if admixed

Follow-up

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 pulseless electrical activity.

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 pulseless electrical activity:

• 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 pulseless electrical activity 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 pulseless electrical activity; patients with a wider QRS (>0.2 s) fare worse.
• Interestingly, patients with out-of-hospital pulseless electrical activity 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 pulseless electrical activity. 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, pulseless electrical activity 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

Medicolegal Pitfalls

Failure to obtain appropriate documentation during and after advanced cardiac life support procedures.

References

1. Raizes G, Wagner GS, Hackel DB. Instantaneous nonarrhythmic cardiac death in acute myocardial infarction. Am J Cardiol. Jan 1977;39(1):1-6. [Medline].

2. Nadkarni VM, Larkin GL, Peberdy MA, Carey SM, Kaye W, Mancini ME. First documented rhythm and clinical outcome from in-hospital cardiac arrest among children and adults. JAMA. Jan 4 2006;295(1):50-7. [Medline].

3. Desbiens NA. Simplifying the diagnosis and management of pulseless electrical activity in adults: a qualitative review. Crit Care Med. Feb 2008;36(2):391-6. [Medline].

4. Hutchings AC, Darcy KJ, Cumberbatch GL. Tension pneumothorax secondary to automatic mechanical compression decompression device. Emerg Med J. Feb 2009;26(2):145-6. [Medline].

5. Steiger HV, Rimbach K, Müller E, Breitkreutz R. Focused emergency echocardiography: lifesaving tool for a 14-year-old girl suffering out-of-hospital pulseless electrical activity arrest because of cardiac tamponade. Eur J Emerg Med. Apr 2009;16(2):103-5. [Medline].

6. Fuzaylov G, Woods B, Driscoll W. Documentation of resuscitation of an infant with pulseless electrical activity because of venous air embolism. Paediatr Anaesth. Nov 2008;18(11):1121-3. [Medline].

7. Hazinski MF, Nadkarni VM, Hickey RW, O'Connor R, Becker LB, Zaritsky A. Major changes in the 2005 AHA Guidelines for CPR and ECC: reaching the tipping point for change. Circulation. Dec 13 2005;112(24 Suppl):IV206-11. [Medline].

8. Nichols R, Zawada E. A case study in therapeutic hypothermia treatment post-cardiac arrest in a 56-year-old male. S D Med. Oct 2008;61(10):371-3. [Medline].

9. Kotak D. Comment on Grmec et al.: A treatment protocol including vasopressin and hydroxyethyl starch solution is associated with increased rate of return of spontaneous circulation in blunt trauma patients with pulseless electrical activity. Int J Emerg Med. Apr 2009;2(1):57-8. [Medline].

10. Grmec S, Strnad M, Cander D, Mally S. A treatment protocol including vasopressin and hydroxyethyl starch solution is associated with increased rate of return of spontaneous circulation in blunt trauma patients with pulseless electrical activity. Int J Emerg Med. Dec 2008;1(4):311-6. [Medline].

11. Aufderheide TP, Thakur RK, Stueven HA. Electrocardiographic characteristics in EMD. Resuscitation. Apr 1989;17(2):183-93. [Medline].

12. Berenyi KJ, Wolk M, Killip T. Cerebrospinal fluid acidosis complicating therapy of experimental cardiopulmonary arrest. Circulation. Aug 1975;52(2):319-24. [Medline].

13. 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].

14. Colwell C, Murphy P, Bryan T. Pulseless electrical activity. Emerg Med Serv. Sep 2004;33(9):63-6, 68. [Medline].

15. Herlitz J, Rundqvist S, Bang A, Aune S, Lundstrom G, Ekstrom L, et al. Is there a difference between women and men in characteristics and outcome after in hospital cardiac arrest?. Resuscitation. Apr 2001;49(1):15-23. [Medline].

16. Hoffman JR, Stevenson LW. Postdefibrillation idioventricular rhythm--a salvageable condition. West J Med. Feb 1987;146(2):188-91. [Medline].

17. Kim C, Fahrenbruch CE, Cobb LA, Eisenberg MS. Out-of-hospital cardiac arrest in men and women. Circulation. Nov 27 2001;104(22):2699-703. [Medline].

18. 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].

19. 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].

20. Stueven HA, Aufderheide T, Waite EM. Electromechanical dissociation: six years prehospital experience. Resuscitation. Apr 1989;17(2):173-82. [Medline].

21. Vincent JL, Thijs L, Weil MH. Clinical and experimental studies on electromechanical dissociation. Circulation. Jul 1981;64(1):18-27. [Medline].

22. 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].

23. Youngquist ST, Kaji AH, Niemann JT. Beta-blocker use and the changing epidemiology of out-of-hospital cardiac arrest rhythms. Resuscitation. Mar 2008;76(3):376-80. [Medline].

Keywords

pulseless electrical activity, electromechanical dissociation, cardiopulmonary resuscitation, CPR, advanced cardiac life support, ACLS, cardia arrest, treatment, symptoms, cardiac arrhythmia, cardiac contractions, ventricular mechanical activity, ventricular electrical activity, EMD, PEA, pseudo-PEA

Contributor Information and Disclosures

Author

Patrick O'Beirne, MD, Fellow in Cardiovascular Medicine, UMass Memorial Medical Center
Patrick O'Beirne, MD is a member of the following medical societies: American College of Cardiology, American Medical Association, Massachusetts Medical Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

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
Dionyssios A Robotis, MD, MPH, FACC is a member of the following medical societies: American College of Cardiology, Cardiac Electrophysiology Society, Heart Rhythm Society, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

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
Lawrence Rosenthal, MD, PhD is a member of the following medical societies: American College of Cardiology, American Heart Association, Heart Rhythm Society, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Eric Vanderbush, MD, FACC, MD, Chief, Department of Internal Medicine, Division of Cardiology, Clinical Assistant Professor, Harlem Hospital Center and Columbia University
Eric Vanderbush, MD, FACC, MD is a member of the following medical societies: American College of Cardiology and American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Steven J Compton, MD, FACC, FACP, Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals
Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, and Heart Rhythm Society
Disclosure: Nothing to disclose.

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD, Professor of Medicine and Pharmacology, Director, Clinical Cardiac Electrophysiology Fellowship Program, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center
Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Sumit Verma, MD, FACC and David S Marks, MD to the development and writing of this article.

Clinical guidelines

(1) ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to revise the 1999 guidelines for the Management of Acute Myocardial Infarction). (2) 2007 focused update of the ACC/AHA 2004 guidelines for the management of patients with ST-elevation myocardial infarction. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.
American College of Cardiology Foundation - Medical Specialty Society
American Heart Association - Professional Association.  1996 Nov 1 (revised 2004 Jul; addendum released 2008 Jan).  Original guideline: 211 pages; Focused update: 38.  NGC:006289

Cardiac arrhythmias in coronary heart disease. A national clinical guideline.
Scottish Intercollegiate Guidelines Network - National Government Agency [Non-U.S.].  2007 Feb.  40 pages.  NGC:005528
 
ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death).
American College of Cardiology Foundation - Medical Specialty Society
American Heart Association - Professional Association
European Heart Rhythm Association - Professional Association
European Society of Cardiology - Medical Specialty Society
Heart Rhythm Society - Professional Association.  2006 Sep 5.  100 pages.  NGC:005208

Resuscitation and defibrillation in the health care setting — 2004 revision & update.
American Association for Respiratory Care - Professional Association.  1993 Dec (revised 2004 Sep).  15 pages.  NGC:004081

Clinical trials

SmartCPR Trial: An Analysis of a Waveform-Based Automated External Defibrillation (AED) Algorithm on Survival From Out-of-Hospital Ventricular Fibrillation

Pre-Shock Cardiopulmonary Resuscitation to Patients With Out-of-Hospital Resuscitation, A Randomised Clinical Trial

Efficacy of Methylprednisolone for Hantavirus Cardiopulmonary Syndrome

Related eMedicine topics

Asystole (Emergency Medicine)

Ventricular Fibrillation (Cardiology)

Ventricular Fibrillation (Emergency Medicine)

Ventricular Fibrillation (Pediatrics)

Cardiopulmonary Resuscitation (CPR) (Procedures)

Therapeutic Hypothermia (Procedures)

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