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




Still not time! But we’re moving forward!

12 Giu
We launched several days ago the pool about which was the first choice when dealing with airways in a critical hill patient. Provocatively the pool was introduced by an announcement about the death of Direct Laringoscopy and the rising of Video Laryngoscopy as first choice. 


Here are the results!


So it’s stil not time? Yes, but we are moving toward an era where videolaryngoscopy will be the first choice.
Almost one third of the providers are already choosing video as the first choice in environments, prehospital, ER an critical care where this technology is still not widely available and where the classical airway management teaching is still dominated by direct laringoscopy. 
My personale thought is that direct laryngoscopy has to be part of the cultural and technical baggage of an emergency provider and has to be part of teaching courses but just as prelude to a clinical practice environment where technology and well trained professionals permit to use the best available device. 




It’s Time!

29 Mag


rising sunVL

And what about you?



Prehospital Emergency Medicine. We are different.

12 Mag


YES prehospital professionals are different from any other medical provider.
YES Prehospital Emergency Medicine is different because is not just clinical competence and technical skills. It’s much more.
WE are different because performing skills or procedures depends not just from the right patient and the right indication, but is heavily influenced by the environment where we work and the team we lead.
BUT despite this we perform complex procedures even in the hardest situations.
WE are different because we always deal with the “contro” of a possible failure in the middle of nowhere, and the “pro” of a probable success in a safe and warm environment (as the nearest emergency room).
BUT despite this we act, succeed and learn from our failures.
WE are lucky because often our patients don’t have life treating conditions, they just need to talk and we probably are their last chance. 
WE love our job.
WE love Prehospital Emergency Medicine.


Join us in Rome to share the same passion



La gestione del paziente critico in emergenza territoriale. Il corso.

8 Mag
Ci siamo! Manca pochissimo e noi siamo prontissimi ad accogliervi.
Federica Stella, Giacomo Magagnotti, Francesco Patrone ed io Mario Rugna saremo lieti di guidarvi attraverso l’affascinante mondo dell’emergenza territoriale.
Grazie a SIMEU abbiamo creato una faculty formata da professionisti sanitari provenienti dall’emergenza territoriale per un corso completamente dedicato alla gestione extraospedaliera del paziente critico.


Parleremo di gestione dell’arresto cardiaco, di gestione delle vie aeree di diagnosi e terapia delle maggiori emergenze extraospedlaiera attraverso la simulazione ad alta fedeltà e con l’utilizzo di modelli biologici. 
Saranno due giorni intensi, interattivi e speriamo divertenti. 
Per iscriversi andate sul sito del Congresso SIMEU 2018
Vi aspettiamo!



Articles at the Top. Take home messages from 2017 (part 3). Trauma.

1 Mag

Welcome to our review of the best articles from the last year.

This will be a weekly (or so..) appointment with the top articles from 2017 divided by topic and chosen by me.

Here is the best about:


Traumatic Cardiac Arrest

Fluid Therapy

Spinal Immobilisation

Field Triage


Prehospital blood

Massive transfusion protocol

Traumatic Brain Injury

The rest

If you are interested on a daily update about the best emergency medicine literature follow me on Facebook, Twitter or give your like to MEDEST Facebook page.



Don’t kill your patient with a probe! Welcome to UltraSound in Cardiac Arrest for (not so) Dummies!

8 Mar

A 2017 study about US and cardiac arrest aroused the debate about using POCUS during cardiac arrest . The authors concluded that:

“The use of POCUS during cardiac arrest resuscitation was associated with significantly increased duration of pulse checks, nearly doubling the 10-s maximum duration recommended in current guidelines.”


Is POCUS an unuseful loose of time and a potential KILLER when used on patients in Cardiac Arrest?


In my personal experience (and in the EMS where I work) we tried to give an answer to this question formulating a structured approach to use ultrasound during a code. The objective is to have vital information from the probe without delays or interruption in chest compressions. 


In WHICH cardiac arrest using POCUS really worths the price?

For sure PEA and Asistoly are the the most relevant conditions to use a probe, on the contrary in defibrillating rhythms, defibrillation and anti-arythmic therapy is a priority, and no useful information can come from ultrasound.

So look at the monitor, if there is a defibrillating rhythm continue with classical ALS approach.

Use a probe only if Asystoly or a PEA are present.

WHEN we use the probe?

The right moment is during the 10 seconds pause indicated from guidelines to asses the rhythm.

Look at the monitor screen for rhythm check and place the probe on the patient for no longer than 10 seconds.

WHERE we place the probe.

  1. SubCOSTAL view of the heart for heart beating
  2. SubCOSTAL view of the heart pericardial effusion and VD>VS
  3. Left CHEST view for lung sliding
  4. Right CHEST view for lung slinging

WHAT  we can identify with ultrasound during Cardiac Arrest.

First thing is there any cardiac activity?

We no more check the pulse, but rely on indirect signs of cardiac arrest when starting chest compressions, but at the beginning of the code and during the reanimation, cardiac activity is a game changing information.

Second thing is does exists any reversible cause of Cardiac Arrest?

Addressing and treating those can really change the outcome of the patient. 

Pulmonary Embolism

Cardiac Tamponade

Tension Pneumo



Infogram ECOALS

The method

During the 10 sec pause asses the rhythm and place the probe .

During the following 2 min CPR think and address, when indicated, the reversible causes.














If heart is beating and the rhythm is Asystoly think to an equipment problem or to a very fine VF.


If the heart is beating and we have a PEA this is not a true PEA but a pseudo PEA so we have to treat this patient as a profound shock patient (POCUS differential diagnosis for shock) more than CA patient.


If heart is not beating, any rhythm, we look for reversible cause of CA.










Infogram ECOALS1

If pericardial effusion is present think at CARDIAC TAMPONADE


If no one of that are present go to the following step 





Lung Sliding





Infogram ECOALS1

If lung sliding is absent  think at a selective intubation of the right main bronchus or at a PNX. If lung sliding is present go to the following step.



IMG_2597Lung Sliding




Infogram ECOALS1

If lung sliding is absent  think at a PNX.

Can we scan more during 2 min CPR?

We can

Left flank and look for free fluid.


Right flank and look for free fluid.


If there is free fluid in the abdomen think and treat HYPOVOLEMIA.


REMEMBER! At any time during the code, if EtCO2 rises or a coordinated electric activity is present 






If no reversible cause are detected, and the patient is still in non defibrillating rhythm, check the heart and the EtCO2.

If heart is not beating and EtCO2 level is less than 10 mmHg. during good quality chest compressions, consider to call the code.










Fall and Rise of Morphine in ACS.

26 Feb

Yesterday the usual MEDEST letterature review was almost fully pointed on Morphine use in ACS. The cited articles talked about Morphine use and survival outcome or P2Y12 inhibitors absorption. The latest evidence pointed toward less survival and less PY12 absorption when Morphine is administered in patients that suffered of ACS.

First evidences about those effects can be dated to CRUSADE(1) study, but more recently other studies pointed in this direction (2,3, 4).

And what about using Fentanyl instead? Some authors compared Morphine to Fentanyl (4) finding no evidences about the superiority of one on another, and on a recent study (5) Fentanyl carried the same detrimental effect on Ticagrelor absorption.

So we really have to ban Morphine or Opiates in ACS?

In an interesting post (6) Rory Spiegel questioned about the basic assumption that P2Y12 benefits in ACS was never really proven and so, even if P2Y12 inhibition by Morphine was real, no damages derived from Opiates effects on them.

On the other hand Vince di Giulio on EMS 12 leads (7) criticised the methodology of most studies at the basis of the P2Y12 inhibition and detrimental effect on survival.

Are you enough confused? What you really do and what all of this matter for daily clinical practice?

In the meantime you decide this is my personal clinical behaviour on opiates and ACS.

  1. In general I limit Opiates use in ACS only when pain is really a problem for patients(VNS>7) and it was not relieved by NTS.
  2. I’m more concerned about emodynamic profile of opiates so I prefer Fentanyl over Morphine cause is more stable, has a better pharmacological profile and induce less histamine release.

Read more about this topic. Explore the References:

  1. Meine TJ, Roe MT, Chen AY, Patel MR, Washam JB, Ohman EM, Peacock WF, Pollack CV Jr, Gibler WB, Peterson ED; CRUSADE Investigators. Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative. Am Heart J. 2005 Jun;149(6):1043-9. doi: 10.1016/j.ahj.2005.02.010. PMID: 15976786.
  2. Parodi G et al. Morphine is Associated with a Delayed Activity of Oral Antiplatelet Agents in Patients with ST-Elevation Acute Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention. Circ Cardiovasc Interv. 2014. PMID: 25552565
  3. Puymirat E et al. Correlates of Pre-Hospital Morphine Use in ST-Elevation Myocardial Infartion Patients and its Association with In-Hospital Outcomes and Long-Term Mortality: The FAST-MI (French Registry of Acute ST-Hobl EL et al. Morphine Interaction with Prasugrel: A Double-Blind Cross-Over Trial in Healthy Volunteers. Clin Res Cardiol. 2016. PMCID: PMC4805697Elevation and Non-ST-Elevation Myocardial Infarction) Programme. Eur Heart J 2016. PMID: 26578201
  4. Hobl EL et al. Morphine Interaction with Prasugrel: A Double-Blind Cross-Over Trial in Healthy Volunteers. Clin Res Cardiol. 2016. PMCID: PMC4805697
  5. McEvoy JW, Ibrahim K, Kickler TS, Clarke WA, Hasan RK, Czarny MJ, Keramati AR, Goli RR, Gratton TP, Brinker JA, Chacko M, Hwang CW, Johnston PV, Miller JM, Trost JC, Herzog WR, Blumenthal RS, Thiemann DR, Resar JR, Schulman SP. Effect of Intravenous Fentanyl on Ticagrelor Absorption and Platelet Inhibition Among Patients Undergoing Percutaneous Coronary Intervention: The PACIFY Randomized Clinical Trial. Circulation. 2018 Jan 16;137(3):307-309. Epub 2017 Oct 18. doi: 10.1161/CIRCULATIONAHA.117.031678. PMID: 29046319.
  6. Weldon ER et al. Comparison of Fentanyl and Morphine in the Prehospital Treatment of Ischemic Type Chest Pain. Prehosp Emerg Care 2016. PMID: 26727338
  7. Rory Spiegel at EM NERD (EMCrit): The Case of the Inconsequential Truth
  8. In defense of Morphine part 1
  9. In defense of Morphine part 2


Articles at the Top. Take home messages from 2017 (part 2).

19 Gen

Welcome to our annual review of the best articles from the finishing year.

This will be a weekly (or so..) appointment with the top (or so…) articles of 2017 divided by topic and chosen by me.

Here is the best (for me) about:

 Advanced Life Support

Here are the best 2017 articles:

My take home messages:

Pathophysiological bases in experimental swine models

  • In a swine model following primary cardiac arrest the respiration continues at least for 1 minute. and after that Gasping starts lasting for another minute.
  • In a swine model following primary cardiac arrest the blood shifts from high pressure compartment (arteries) to low pressure compartment (veins). 
  • In a swine model the PaO2 following primary cardiac untreated VF arrests PaO2 results 70 mmHg after 9 min with a saturation of 93% and decrease at 44 mmHg with a saturation of 61% after 14 min of CPR. In this period airway management with possible interruption of chest compressions and starting positive pressure ventilation (with decreased return to the thorax end depression of cardiac output) is not mandatory due to the low cost/beneficial ratio and the potential detrimental effect. 

Chest compressions

  • Chest compressione only CPR is associated with worst outcome in children under 8 yers. Always perform chest compression/ventilation (ratio 15:2) in children <8 years of age (only exception if the cardiac arrest is due to primitive cardiac causes). 
  • Chest compressione only CPR can be a valuable option in adult witnessed VF/pulseless VT primary cardiac arrest (delayed airway management and passive O2 administration is reasonable).
  • Mechanical chest compression (MCC) is the future of CPR. They still do not demonstrated evident superiority in terms of outcome respect to manual chest compressions, but are evidently not inferior with a similar rate of life treating lesions. For sure MCC avoid variability in quality and allows good quality CC during transport. 


  • Lower Tidal volumes following OHCA is independently associated with favourable neurocognitive outcome
  • Weak evidences demonstrate that the ideal rate for ventilation of intubated patients  during CPR is 10/min

Airway management

  • There is not beneficial effect on outcome with early intubation in Cardiac Arrest (CA)
  • Privilege High Quality CPR and Defibrillation (if needed).
  • Use Supraglottic Airway Devices (SAD) in first part (15 min) of resuscitation 
  • If Mechanical Chest Compressions is used, to optimise ventilation with SAD, use 30:2 ratio (because the intrathoracic pressure generated during MCC overrules that generated from SAD and impaires ventilation).
  • In prolonged Cardiac Arrest management converting SAD to Endotracheal Tube can be considered.
  • Experience provider only can perform endotracheal intubation in CA. They have a better chance of first passage rate, without interruption in chest compressions. First pass success rate is positively associated to survival and good neurological outcome.


  • Escalating bilevel energy (150-200-360 Joule) is associated with more efficacy in termination of shock resistant VF/pulselessVT cardiac arrest
  • Dual Sequential Defibrillation is feasible and safe. Although the evidences on its beneficial effect on outcome are still lacking it has to be considered in case of CA with refractory shockable rhythm. 

Antiarrhythmics drugs

  • There has been no conclusive evidence that any antiarrhythmic agents improve rates of ROSC, survival to admission, survival to discharge or neurological outcomes.


  • Ultrasound in PEA is a key tool to detect CA causes improving survivival.

Post Resuscitation Care

  • In post resuscitation phase avoid any arterial oxygen and carbon dioxide abnormality because are associated to increased mortality.
  • Centralisation of resuscitated patients toward an acute PCI/CABG capable Center  is associated to better outcome.

Targeted Temperature Management

  • Prehospital cooling does not improve faster in-hospital target temperature achieving and due to its costs is not recommended.
If you are interested on a daily update about the best emergency medicine literature follow me on Facebook, Twitter or give your like to MEDEST Facebook page.



Articles at the Top. Take home messages from 2017 (part 1).

25 Dic

Welcome to our annual review of the best articles from the past year.

This will be a weekly (or so..) appointment with the top (or so…) articles of 2017 divided by topic and chosen by me.

At the end of the post I will also mention some take home points as summary of the evidences emerged from the articles. 

And now here is the best (for me) about:

 Airway management

Here are the best articles of the past year about Airway Management:

My take home messages about airway management:

  1. Risk factors for intubation related cardiac arrest are: overweight or obesity, age more than 75 years old, low SBP prior to intubation, hypoxemia prior to intubation, and absence of preoxygenation before intubation procedure.
  2. Preoxygenation is crucial (at least 2 minutes), before paralysing, to extend safe apnea time.
  3. Use apneic oxygenation during intubation attempts.
  4. Tracheal intubation is good in the hands of very well skilled professionals. Otherwise can improve mortality rate.
  5. Supraglottic devices perform well in cardiac arrest and are a valuable option for airway management. 
  6. Videolaryngoscopy improve glottic view but need training to improve first pass success.
  7. Always use paralytics when intubating a non cardiac arrest patient. It improves the chances fo first pass success.
  8. Rocuronium and Succynocholine are both valuable options for paralysis in airway management. 
  9. Dose Succynocholine, and other depolarising neuromuscular blockade drugs, based on actual body weight. Dose Rocuronium or Vecuronium based on ideal body weight.
  10. Use cuffed tracheal tubes even in paediatric patients. They perform well and  complications rate is the same. 
  11. The difficult airway is a myth. It’s not  a matter of technique but of decision making.
If you are interested on a daily update about the best emergency medicine literature follow me on Facebook, Twitter or give your like to MEDEST Facebook page.




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