Pulseless electrical activity
|Pulseless electrical activity|
|Classification and external resources|
Pulseless electrical activity or PEA (also known by the older term electromechanical dissociation) refers to a cardiac arrest situation in which a heart rhythm is observed on the electrocardiogram that should be producing a pulse, but is not. Under normal circumstances, electrical activation of muscle cells precedes mechanical contraction of the heart (known as electromechanical coupling). In PEA, there is electrical activity, but the heart either does not contract or there are other reasons why this results in an insufficient cardiac output to generate a pulse and supply blood to the organs.
Signs and symptoms
Pulseless electrical activity leads to a loss of cardiac output, and the blood supply to the brain is interrupted. As a result, PEA is usually noticed when a person loses consciousness and stops breathing spontaneously. This is confirmed by examining the airway for obstruction, observing the chest for respiratory movement, and feeling the pulse (usually at the carotid artery) for a period of 10 seconds.
- Hydrogen ions (Acidosis)
- Hyperkalemia or Hypokalemia
- Tablets or Toxins (Drug overdose)
- Cardiac Tamponade
- Tension pneumothorax
- Thrombosis (Myocardial infarction)(Pulmonary embolism)
- Trauma (Hypovolemia from blood loss)
The absence of a pulse confirms cardiac arrest, but PEA can only be distinguished from other causes of cardiac arrest with a device capable of electrocardiography (ECG/EKG). In PEA, there is electrical activity in the heart (as opposed to asystole), but not compatible with either ventricular fibrillation or ventricular tachycardia.
Cardiopulmonary resuscitation should be initiated promptly to maintain cardiac output until the PEA can be corrected. The approach in treatment of PEA is to treat the underlying cause, if known (e.g. relieving a tension pneumothorax). Where an underlying cause for PEA cannot be determined and/or reversed, the treatment of pulseless electrical activity is similar to that for asystole.
An intravenous or intraosseous line should be started to provide medications through. The mainstay of drug therapy for PEA is epinephrine 1 mg every 3–5 minutes. Although previously the use of atropine was recommended in the treatment of PEA/asystole, this recommendation was withdrawn in 2010 by the American Heart Association due to lack of evidence for therapeutic benefit.
Sodium bicarbonate 1meq per kilogram may be considered in this rhythm as well, although there is little evidence to support this practice. Its routine use is not recommended for patients in this context, except in special situations (e.g. preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdose).
All of these drugs should be administered along with appropriate CPR techniques. Defibrillators cannot be used to correct this rhythm, as the problem lies in the response of the myocardial tissue to electrical impulses.
- 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (November 2010). "Part 8: Adult Advanced Cardiovascular Life Support". Circulation 122 (18 Suppl): S729–S767. doi:10.1161/CIRCULATIONAHA.110.970988. PMID 20956224.
- Mazur, Glen (2003). Acls: Principles And Practice. [Dallas, TX]: Amer Heart Assn. pp. 71–87. ISBN 0-87493-341-2.
- Barnes, Thomas Garden; Cummins, Richard O.; Field, John; Hazinski, Mary Fran (2003). ACLS for experienced providers. [Dallas, TX]: American Heart Association. pp. 3–5. ISBN 0-87493-424-9.
- 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (December 2005). "Part 7.2: Management of Cardiac Arrest". Circulation 112 (24 Suppl): IV 58–66. doi:10.1161/CIRCULATIONAHA.105.166557.