eMedicine Specialties > Cardiology > Arrhythmias

Pulseless Electrical Activity: Treatment & Medication

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

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.

Adult

1 mg IV q3-5min

Pediatric

Not established

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

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

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.

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

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

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.

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

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

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

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

More on Pulseless Electrical Activity

Overview: Pulseless Electrical Activity
Differential Diagnoses & Workup: Pulseless Electrical Activity
Treatment & Medication: Pulseless Electrical Activity
Follow-up: Pulseless Electrical Activity
References
Further Reading
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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].

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Further Reading

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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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

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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.

 
 
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