PEA and Pseudo PEA: A Proposed Algorithm

 We do have a very powerful tool at our disposal that can help quickly identify possible causes of profound shock as well as PREM and PRES, ultrasound. The HIMAP version of the Rush Exam protocol is extremely helpful in identifying causes of shock and should be utilized in these cases (6).PEA and PseudoPEA: A Proposed new Algorithm 

In this post, we’ll talk about PEA, Pseudo PEA, and why we should look beyond the ACLS algorithm. 

• True PEA, once known as electro-mechanical dissociation is the presents of an organized electrical cardiac rhythm without cardiac muscle activity (cardiac standstill).
• Pseudo-PEA is an organized electrical cardiac rhythm and it has cardiac muscle activity (found on POCUS echo) however, there may not be a palpable pulse due to profound shock.

The important first point to recognize the differences between PEA and Pseudo-PEA is the echocardiographic findings. Terms coined by Scott Weingart may be better descriptors of this entity (1):

1. PRES (Pulseless with a Rhythm and Echocardiographic Standstill)
2. PREM (Pulseless with a Rhythm and Echocardiographic Motion) 

In reality, these two entities are really quite different from each other, yet in ACLS the algorithm it is more of a “one size fits all.” The ACLS protocol for PEA includes the ABCs, CPR, Epi  1 mg every 3-5 minutes IVP, and consideration of the reversible causes by reviewing the H’s and T’s with no mention of looking for a cardiac activity with POCUS echo. The heterogeneity of PRES and PREM makes this algorithm inappropriate and antiquated. 

The prognosis of PRES is really quite dismal at 5.9% survival to discharge (2). PREM on the other hand has a much more favorable prognosis with some papers showing as high as 70-94% rate of ROSC and about 50% had a good neurological outcome (3,4). 

Beyond the prognostic difference in PRES and PREM, the management of the two entities is really quite different. PRES is true cardiac arrest, having no cardiac activity found on POCUS echo during the resuscitation, CPR and epinephrine make sense by compressing on the heart to generate an artificial perfusing pressure and using epinephrine to increase vascular tone, cardiac rate, contractility, and automaticity.

However, in the case of PREM, the heart is generating rhythm and cardiac activity, but the pulse may be too weak to appreciate due to profound shock. Here, the early recognition of cardiac activity with POCUS echo is crucial. Doing chest compressions, in this case, has shown to be deleterious in animal models as it may interfere with cardiac filling. Additionally, too much epinephrine may also be detrimental. In the case of PREM, it would be better managed as a profound shock with vasopressors to support and investigate the causes of shock. 

In both PREM and PRES, the H’s and T’s should be investigated as potential causes and with prompt treatment (5).

• Hypovolemia – fluid, blood products, stop bleeding, clamp vessels
• Hypoxia – intubation, and ventilation (FiO2 1.0)
• Hypokalemia – K+ replacement
• Hyperkalemia – treat cause, Ca2+ gluconate 10mL 10%, insulin-dextrose, salbutamol, NaHCO3
• Metabolic disorders – Mg2+ if low, Ca2+ if low, consider bicarbonate for acidemia (e.g. with normal anion gap)
• Hyperthermia – cool, dantrolene for malignant hyperthermia
• Hypothermia– warm

• Toxicity – stop absorption, increase elimination, an antidote to a specific drug
• Tension pneumothorax – decompress (needle or finger thoracostomy prior to the intercostal catheter)
• Tamponade – pericardiocentesis, open chest
• Thromboembolism – thrombolysis (proven or suspected pulmonary embolus) +/- surgical embolectomy