Pseudo PEA? When, How, What?

17 Lug

Clinical Scenario

55 years old male arrested in front of the ACLS team in prehospital setting.

The call was due to hypotension and cold sweeting. The team found the patient conscious and responding to their answers. He denied chest pain or dyspnea, referring just dizziness and profound astenia.

No time to put him on monitor and BOOM! Cardiac arrest occurred. PEA. Narrow organised EKG activity, no carotid pulse no indirect signs of circulation. 

Mechanical CPR and standard ACLS started. First rhythm control, probe on the chest (subxifoid view)

HEART IS MOVING! NO CAROTID PULSE YET. This is not a cardiac arrest, but it’s not ROSC either!

What’s this condition? For standard ACLS it doesn’t exists, it’s not mentioned and there are no practice guidelines to follow.

But beyond ACLS this is a well recognised situation and is called PSEUDO PEA.

Pseudo PEA

In a recent trial (Focused echocardiographic evaluation in life support and peri-resuscitation of emergency patients: a prospective trial link in the referencesevaluating the use of POCUS in extreme shock and cardiac arrest in prehospital setting the investigators found that, examining with ultrasound patients in cardiac arrest, 74,5% and 35% of PEA and Asystole respectively had cardiac wall motion and a rate of survival significatively higher than “no cardiac activity patients” (55% vs 8% in PEA and 24% vs 11% in Asystole)


Image attribution How Do You FEEL About Echo in Cardiac Arrest? 

Three simple steps to manage pseudo PEA

Let’s go back to the clinical case (just to mention this is not a simulated scenario, the patient was real  and the team was not from another part of the planet but was my team) How you manage this patient beyond and in absence of clear guidelines?

  1. Looking for reversible causes
  2. Monitoring perfusion
  3. Supporting circulation

Looking for reversible causes

Searching for reversible causes of PEA is a mix between clinical history, physical exams and instrumental findings. I’m not a great fan of H’s and T’s approach. 

I use ultrasound!

If you can find the cause, treat it right away, other ways go to next steps monitoring perfusion and supporting circulation.

Monitoring perfusion

Monitoring perfusion in an arrested (technically but not practically) patient on the field (where you don’t have the chance to insert an arterial line to have invasive determination of arterial blood pressure) is a matter of indirect  signs and numbers.

“The digitomer” for sure is the worst way to do it. So forget the central pulse it’s subjective and not reliable, as any BLS provider knows.

EtCO2 and pletismographic waveform of capillary pulse are both crucial elements to decide when stopping (or not stopping) CPR and starting vasopressors.

We alla know almost everything about EtCO2 and its value to show perfusion, so I want just to spend some words on a less famous, and widely underestimated, method of monitoring distal perfusion: capillary pulse waveform. We all have pulse ox, few of us consider it’s waveform at all, and certainly not as indicator of perfusion. But a wide range of recent letterature indicates a good correlation between arterial pressure and capillary pressure.

Below you can see the an analysis of the arterial pressure waveform.

Art wave

Image attribution University College London (UCL)

and this below is the waveform recorded from a human photoplethysmogram (in other words the waveform shown from any pulse ox) at the capillary level


Image attribution

We don’t need much of evidences to understand how the two waveforms correlates.

So pulse ox waveform can be used as good estimation of arterial pressure and distal perfusion even if  we know its often influenced by artefacts expecially in low flow conditions.

I personally consider the EKG trace also a useful tool. An organised electric activity with narrow complexes at a normal rate is more probable to give a perfusing flow than a bradicardic, wide QRS one.

But let’s go back to practical. Which one is the best method to use in prehospital? I personally use all the information, cause in a difficult setting relying on just one of them is dangerous.

So a pseudo PEA condition with narrow complexes electric activity at a rate above 60 bpm,  EtCO2 around 35-40 mmHg a good shaped capillary waveform in absence of chest compressions for me is grant of perfusion.

A non organised or wide complexes low rate ekg trace, low EtCO2 and no capillary waveform is a non perfusing state.

Supporting circulation

What to do in those cases?

In the case of “non perfusing” pseudo PEA, no doubt, you need to continue chest compressions to sustain circulatory state. 

In the case of “perfusing” pseudo PEA, use vasopressors.

My favourite way to give them, and the more reliable in prehospital environment, is push dose.

My favorite vasopressor is Epinephrine.


Other acceptable alternative is Phenylephrine.


I don’t believe that administering vasopressors in continuous infusion on the field is a good idea. For me is dangerous and not practical. Most of the times we don’t have volumetric or infusion pump ready available so we are not sure about the exact dose administered easily loosing control of the situation.

But in case you intend to give continuous infusion vasopressors use Norepinephrine.




When you have a pseudo PEA patient, the crucial decision is if the present cardiac activity is perfusing (the brain and the other vital organs or not) even in absence of a palpable carotid central pulse. 

To understand how is the perfusion going use EtCO2, waveform pulse oximetry and EKG. 

If the signs of perfusion are not good continue with chest compressions 

If you have good signs of perfusion start vasopressors to sustain circulation. 

Remember: This is not an arrested patient! Needs to be in the hospital ASAP to start ECMO, PCA or other definitive care.

Take home points about pseudo PEA:

  1. ALWAYS use ultrasound to determine cardiac activity in cardiac arrest patients
  2. Don’t trust central pulse palpation
  3. Pseudo PEA is an ultrasound evident cardiac activity without carotid pulse
  4. Pseudo PEA is a big clinical reality beyond ACLS mantras
  5. Use ultrasound to look for reversible causes of pseudo PEA.
  6. Use waveform EtCO2 and waveform Pulse Oximetry to monitor perfusion
  7. Continue CHEST COMPRESSIONS in pseudo PEA with bad perfusion state indicators:
    • Wide bradycardic electric activity
    • Low EtCO2 (below 20 mmHg)
    • No waveform on Pulse ox
  8. Use VASOPRESSORS in pseudo PEA with good perfusion state indicators:
    • Narrow normofrequent electric activity
    • EtCO2 above 35-40
    • Good waveform on Pulse ox




2 Risposte a “Pseudo PEA? When, How, What?”

  1. paoloff 17 luglio 2018 a 3:49 PM #

    great article Mario! Now I’ve revalued the Pulsoxy…(and I’d like to have a portable eco in ambulance…) do you think EtCO2 waveform can help us in the pre hospital care in this case and for the outcome of the Patient? thanks. P.F.

    • medest118 17 luglio 2018 a 4:01 PM #

      For sure Paolo EtCO2 is still the more reliable method to predict outcome and circulatory status on this kind of patients. A square waveform with physiological values (above 30 mmHg) is a crucial determination to support out clinical decision.


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