12 Ott

Should we withhold chest compressions in traumatic cardiac arrest. A (very) reasonable poin of view.

The Collective

‘Don’t compress the chest in traumatic arrest…’ That’s the narrative. But Alan Garner has questions.

Do you do chest compressions in traumatic cardiac arrest (TCA)?

Don’t be dopey, right? Compressions are not important compared with seeking and correcting reversible causes. Indeed you can just omit the compressions altogether and transport the patient without them as they are detrimental in hypovolaemia and obstructive causes of arrest, right?

I would like to work through the logic of this.  I think the nidus of an idea got dropped into a super saturated FOAMEd solution and Milton the Monster* precipitated out.  The end result might be an approach that got extrapolated way beyond the biologically plausible.

The Starting Point

First let’s try to step slowly through the logic…

  1. In hypovolaemia or obstructive causes of shock that are likely in the trauma patient (tension and tamponade) and where the patient is in PEA (preferably with good…

View original post 1.100 altre parole

The Never Ending Debate. Airway management in cardiac arrest.

22 Set

Yes we are talking about airway management in cardiac arrest.

Yes this is another blog post on that topic, and if you are leaving the blog cause you had enough of that topic you have all my comprehension!

Still there?

I ask you just a few minutes of your time and attention to review two new studies that are making so much noise in the FOAMED world.

Here is the first trial:

Effect of a Strategy of a Supraglottic Airway Device vs Tracheal Intubation During Out-of-Hospital Cardiac Arrest on Functional Outcome. The AIRWAYS-2 Randomized Clinical Trial.

Jonathan R. Benger, MD1; Kim Kirby, MRes1,2; Sarah Black, DClinRes2; et al

What kind of study is this:

This is a multicenter, cluster randomized clinical trial of paramedics from 4 ambulance services in England.

Inclusion criteria

  • 18 years or older
  • Non-traumatic OHCA

Exclusion criteria

  • Detained by Her Majesty’s Prison Service
  • Previously recruited to the trial (determined retrospectively);
  • Resuscitation deemed inappropriate (using guidelines from the Joint Royal Colleges Ambulance Liaison Committee)
  • Advanced airway already in place (inserted by another paramedic, physician, or nurse) when a paramedic participating in the trial arrived at the patient’s side;
  • Known to be enrolled in another prehospital RCT
  • The patient’s mouth opened less than 2 cm


  • Insertion of a second-generation supraglottic airway device with a soft non inflatable cuff (i-gel; Intersurgical) (759 paramedics)


  • Tracheal intubation using direct laryngoscopy (764 paramedics)

Main Outcome

  • Modified Rankin Scale score at hospital discharge or 30 days after out-of-hospital cardiac arrest
  • Secondary outcomes included ventilation success, regurgitation, and aspiration.


Sample population

  • 1523 paramedics involved
  • 95 hospitals
  • 13462 potentially eligible patients
  • 4166 (31%)excluded
  • 9296(69%) enrolled

Primary outcome

  • The primary outcome was available for 9289 of 9296 patients (99.9%).
  • In the supraglottic airway device group, 311 of 4882 patients (6.4%) had a good outcome (modified Rankin Scale score range, 0-3)
  • In the TI group 300 of 4407 patients (6.8% adjusted OR, 0.92 [95%CI, 0.77 to 1.09];

Secondary outcomes

  • The supraglottic airway device treatment strategy was significantly more successful in achieving ventilation after up to 2 attempts with tracheal intubation
  • Two of the secondary outcomes, regurgitation and aspiration, were not significantly different between groups
  • The median time to death was not significantly different between the groups
  • The compression fraction was not significantly different between the group but in a very small sample of 66 patients


Among patients with out-of-hospital cardiac arrest, randomization to a strategy of advanced airway management with a supraglottic airway device compared with tracheal intubation did not result in a favorable functional outcome at 30days.

And here is the second trial:

Effect of a Strategy of Initial Laryngeal Tube Insertion vs Endotracheal Intubation on 72-Hour Survival in Adults With Out-of-Hospital Cardiac Arrest. A Randomized Clinical Trial

Henry E. Wang, MD, MS1,2; Robert H. Schmicker, MS3; Mohamud R. Daya, MD, MS4; et al

What kind of study is this:

Multicenter pragmatic cluster-crossover clinical trial involving 37 EMS agencies from the Resuscitation Outcomes Consortium Paramedics where Randomized in 13 clusters. Crossover of clusters to the alternate strategy at 3- to 5-month intervals.

Inclusion criteria:

Adults with OHCA and anticipated need for advanced airway management


  • LT insertion (n = 1505 patients)


  • ETI (n = 1499 patients)

Main Outcome

  • 72-hour survival

Secondary outcomes

  • Return of spontaneous circulation
  • Survival to hospital discharge
    Favorable neurological status at hospital discharge (Modified Rankin Scale score3)
  • Key adverse events



  • 3004 enrolled patients

Rates of initial airway success

  • 90.3%with LT
  • 51.6%with ET

Primary Outcome

  • Seventy-two hour survival was 18.3%in the LT group vs 15.4%in the ETI group

Secondary Outcomes

  • Return of spontaneous circulation in the LT group 27.9% vs 24.3% in ETI group
  • Hospital survival LT group 10.8%vs 8.1% in ET group
  • Favorable neurological status at discharge 7.1% in LT group vs 5.0% in ET group
  • No significant differences in oropharyngeal or hypopharyngeal injury airway swelling or pneumonia or pneumonitis


Among adults with OHCA, a strategy of initial LT insertion was associated with significantly greater 72-hour survival compared with a strategy of initial ETI. These findings suggest that LT insertion may be considered as an initial airway management strategy in patients with OHCA,


This is a well conducted study with a large population that investigated a relevant clinical  topic.


In the TI group the first passage success rate is particularly low (51%) and there is no mention on the percentage of reintubation. This makes the neurologic outcome of this group particularly subject to procedural bias.

In general there is no mention of the post resuscitation care protocol and we know how this period is important on neurological outcome and individual variation makes bias very likely on this particular end point.

Take home messages Airway.001Take home messages Airway.002Take home messages Airway.003Take home messages Airway.004



Epinephrine in cardiac arrest: the past, the present and the (im)possible future. Reflections after PARAMEDIC 2 trial.

23 Lug

The past (a brief history of epinephrine use in cardiac arrest)


In 1901 Jokichi Takamine (1854-1922) isolated the pure form of adrenaline, also known as epinephrine.

Routine use of adrenaline for cardiac arrest was first proposed in the 1960’s. Its inclusion within cardiac arrest management was based upon an understanding of the physiological role of adrenaline, and experimental data from animal research which showed that ROSC was more likely when the drug was used.

Epinephrine was not included in cardiac arrest protocols on the basis of evidence of benefit in humans.

Epinephrine remained, since today, a significant component of advanced life support despite minimal human data indicating beneficial effect .

The rationale for use of epinephrine in cardiac arrest was that, in animal studies, increases aortic blood pressure and thus coronary perfusion pressure during chest compressions.

IMPORTANT, brief reminder on epinephrine effect and Coronary Perfusion Pressure.
  • Coronary vessels are contained in epicardium and their flow is possible in the diastole when they are not compressed by myocardium during systolic contraction.coro-vessels
  • Coronary flow depends from the gradient between aortic diastolic (Ao) pressure and diastolic left ventricular (LV) pressure.acls3_3-1
  • Higher is the coronary pressure perfusion (CPP), greater is the chance of ROSC.


  • Epinephrine is a key determinant factor in maintaining diastolic aortic pressure in cardiac arrest; thanks to its interaction with alpha receptors, located on the endothelium of the arteries, produce generalized peripheral arterial vasoconstriction maintaining aortic diastolic pressure to a high level even during chest compressions.
  • The cut off value for ROSC is 15 mmHg of CPP, but more is better (at least 40 mmHg9.

Many and strong recent evidences demonstrates that “Among patients with OHCA, use of prehospital epinephrine was significantly associated with increased chance of return of spontaneous circulation before hospital arrival but decreased chance of survival and good functional outcomes Screen-Shot-2015-03-11-at-8.38.35-PM

The Present: PARAMEDIC 2 trial.

G.D. Perkins, C. Ji, C.D. Deakin, et al. A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest. 

What kind of study is this:

Randomized, double-blind, multicentric.


8014 patients with out-of-hospital cardiac arrest in the United Kingdom

  • Inclusion Criteria

Adult (>16 years) patients, transported by five National Health Service ambulance services in the United Kingdom, who had sustained an out-of-hospital cardiac arrest for which advanced life support was provided by trial-trained paramedics.

  • Exclusion criteria

Apparent pregnancy, age of less than 16 years, cardiac arrest from anaphylaxis or asthma, administration of epinephrine before the arrival of the trial-trained paramedic.


Paramedics administered either IV epinephrine 1mg every 3 – 5min + standard care  or IV 0.9% normal saline bolus + standard care.


Placebo (IV 0.9% normal saline bolus) + standard care


Primary outcome:
  • Rate of survival at 30 days.
Secondary outcomes:
  • Rate of survival until hospital discharge with a favorable neurologic outcome, as indicated by a score of 3 or less on the modified Rankin scale. 
  • Lengths of stay in the hospital and in the intensive care unit
  • Rates of survival at hospital discharge and at 3 months
  • Neurologic outcomes at hospital discharge and at 3 months


  • Patients who received epinephrine had a higher rate of 30-day survival than those who received placebo.
  • No clear improvement in functional recovery among the survivors in the epinephrine group.
  • The proportion of survivors with severe neurologic impairment was higher in the epinephrine group (31.0% vs. 17.8%)
  • Epinephrine NNT of 112 patients to prevent 1 death at 30-days (Early defibrillation NNT = 5, CPR performed by a bystander NNT = 15 )

Image attribution: REBEL Cast Ep56 – PARAMEDIC-2: Time to Abandon Epinephrine in OHCA?


In adults with out-of-hospital cardiac arrest, the use of epinephrine resulted in a significantly higher rate of 30-day survival than the use of placebo, but there was no significant between-group difference in the rate of a favorable neurologic outcome because more survivors had severe neurologic impairment in the epinephrine group.


  • Randomized, multicenter, double blind, placebo controlled
  • 8014 patients randomised.
  • Well balanced characteristics at baseline of the two groups
  • Concurrent treatments were similar
  • Median time from the emergency call to ambulance arrival was 6.6 minutes
  • Patient oriented outcomes



  • Overall survival rate in this trial was disappointingly small (3.2% and 2.4%, respectively)
    • 615 patients where excluded because had return of spontaneous circulation before paramedics can open the trial pack. Of these 615 patients of which we don’t know the clinical outcome but including the survivors overall survival rate is similar to other EMS in Europe.
  • Median time from the emergency call until administration of the trial agent 21 min and we know (according the other studies) that cardiac arrest has 3 phases (Electrical Phase, first 5 min (Defib), Circulatory Phase next 10 – 15min (Chest compressions), Metabolic Phase 10-20min) and epinephrin is effective if administered in the first 20 min of the cardiac arrest.
  • Information about the quality of CPR was limited to the first 5 minutes of cardiac arrest and involved <5% of enrolled patients 
  • The protocol neither controlled nor measured in-hospital treatments and we know that the most common cause of in-hospital death is iatrogenic limitation of life support, which may result in the death of potentially viable patients.

What we know till today

  • Epinephrine in cardiac arrest improve ROSC and patients alive.
  • The improved survival is mostly due to patients with bad (<3 MRS) neurological outcome.

What that means

  • Administering the current recommended dose of Epinephrine we have to choose between numbers and quality of life.
  • Patients clearly said quality of life is more important
  • Epinephrine is anyway important because having bigger numbers of ROSC give the chance to improve neurological outcomes.

Future challenges

  • Understanding why epinephrine doesn’t work and can be detrimental on long term neurological outcome.
  • Obtaining more ROSC and better neurological outcomes in Cardiac Arrest

The (im)possible future

I think there are two key factors, in the actual way to use Epinephrine, that determine its failure:

The wrong administration route

When epinephrine is administered intravenously in a low flow state patient (as is a patient during cardiac arrest, even if proper chest compressions are performed), the amount of drug that arrives to perform the “local” alpha effect on arteries is just a minimal quantity of the (high!!!) dose. The major part rely in the venous circulation and is mobilized in great quantity only when ROSC happens determining a widespread vasoconstriction and a consequent “overdose” effect (think just at the “stunned” myocardium that has to overwhelm such ha great post-load work).

The wrong dose to the wrong patient

From the coronary perfusion pressure (CPP) point of view, every cardiac arrest patient is different: some patients have a (relative) good aortic pressure and a (relative) good  coronary perfusione comparing to others.

When we administer the same amount of epinephrine to each of them this takes to an underdose in some patients (with low flow state) and an overdose in others (with good or high flow state).

So now what?

The right administration route

Probably the best route to administer epinephrine is not the vein but the artery.

It allows, even in a low flow state patient, a better chance to reach the vasoconstrictor effect maintaining a good aortic diastolic pressure and a consequent good coronary flow.

The right dose to the right patient

Giving epinephrine (standard dose) to a patient who has a low flow state (patients who need it more) make epinephrine usefulness (underdose) because just a little part of it circulate.

Giving  epinephrine to patients in a good or high flow state (patients that need it less or don’t need epi at all) is detrimental and can cause overdose effect.

We need to know wich is the circulatory state of the patients to administer the right dose avoiding the “overdose” effect.

The only way to do this is monitoring aortic diastolic pressure through an arterial catheter. We can target Epinephrine dosage to reach a good aortic pressure maintaining a good CPP (achieving ROSC) and avoiding overdose.


Take home messages for future improvements in cardiac arrest management 

  1. Obtain an arterial line

  2. Give Adrenaline intrarterially

  3. Check blood pressure via arterial line

  4. Target Adrenaline (doses and times) to maintain at least 40 mmHg of diastolic arterial pressure




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) https://doi.org/10.1017/CBO9781139226394.035

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 https://www.sciencedirect.com/science/article/pii/S0960077915001344

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.











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Learning everything I can from everywhere I can. This is my little blog to keep track of new things medical, paramedical and pre-hospital from a student's perspective.

Prehospital Emergency Medicine Blog

All you want to know about prehospital emergency medicine

Italy Customized Travel Blog

Local Travel Agent, sommelier, food & wine expert in Florence, Italy


The FOAM Search Engine

EM Lyceum

where everything is up for debate . . .


Free Open Access Medical Education for Paramedics


Free Open Access Meducation 4 General Practice

Rural Doctors Net

useful resources for rural clinicians

Auckland HEMS

Unofficial site for prehospital care providers of the Auckland HEMS service




Prehospital Emergency Medicine


Just another WordPress.com site

EM Basic

Your Boot Camp Guide to Emergency Medicine

KI Doc


Emergency Live

Prehospital Emergency Medicine


Academic Medicine Pearls in Emergency Medicine from THE Ohio State University Residency Program

Prehospital Emergency Medicine

 Academic Life in Emergency Medicine

Prehospital Emergency Medicine

Comments on: Homepage

Prehospital Emergency Medicine

Greater Sydney Area HEMS

The Pre-hospital & Retrieval Medicine Team of NSW Ambulance

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