Pulseless electrical activity
Pulseless electrical activity | |
---|---|
Other names | Electromechanical dissociation |
A drawing of what a rhythm strip showing PEA could look like | |
Specialty | Cardiology |
Pulseless electrical activity (PEA) is a form of
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 insufficient cardiac output to generate a pulse and supply blood to the organs, whether the heart itself is failing to contract or otherwise.[3] While PEA is classified as a form of cardiac arrest, significant cardiac output may still be present, which may be determined and best visualized by bedside ultrasound (echocardiography).
Signs and symptoms
Pulseless electrical activity leads to a loss of cardiac output, and the blood supply to the
Causes
These possible causes are remembered as the 6 Hs and the 6 Ts.[5][6][7] See Hs and Ts
- Hypovolemia
- Hypoxia
- Hydrogen ions (Acidosis)
- Hyperkalemia or Hypokalemia
- Hypoglycemia
- Hypothermia
- Toxins
- Cardiac Tamponade
- Tension pneumothorax
- Thrombosis (e.g., myocardial infarction, pulmonary embolism)
- Tachycardia
- Trauma (e.g., hypovolemiafrom blood loss)
The possible mechanisms by which the above conditions can cause pulseless in PEA are the same as those recognized as producing circulatory shock states. These are (1) impairment of cardiac filling, (2) impaired pumping effectiveness of the heart, (3) circulatory obstruction and (4) pathological vasodilation causing loss of vascular resistance and excess capacitance. More than one mechanism may be involved in any given case.[citation needed]
Diagnosis
The absence of a pulse confirms a clinical diagnosis of 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 organised or semi-organised electrical activity in the heart as opposed to asystole (flatline) or to the disorganised electrical activity of either ventricular fibrillation or ventricular tachycardia.[3]
Treatment
Cardiac resuscitation guidelines (ACLS/BCLS) advise that 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.[3] There is no evidence that external cardiac compression can increase cardiac output in any of the many scenarios of PEA, such as hemorrhage, in which impairment of cardiac filling is the underlying mechanism producing loss of a detectable pulse.[citation needed]
A priority in resuscitation is placement of an intravenous or
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).[3]
All of these drugs should be administered along with appropriate CPR techniques.
References
- S2CID 53025153.
- PMID 35490937.
- ^ PMID 20956224.)
{{cite journal}}
: CS1 maint: numeric names: authors list (link - PMID 27484660.
- ISBN 0-87493-341-2.
- ISBN 0-87493-424-9.
- doi:10.1161/CIRCULATIONAHA.105.166557.)
{{cite journal}}
: CS1 maint: numeric names: authors list (link