1 Year in Review. Airway management.

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Second step of 1 YEAR IN REVIEW, the classical end of year MEDEST appointment with all that matter in emergency medicine literature.

In this post we review the 2018 Airway management literature of note divided by topic.

So let’s start

  • Bag mask ventilation

Effect of Bag-Mask Ventilation vs Endotracheal Intubation During Cardiopulmonary Resuscitation on Neurological Outcome After Out-of-Hospital Cardiorespiratory Arrest. A Randomized Clinical Trial

  • Extraglottic Devices

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.

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.

Preliminary Report: Comparing Aspiration Rates between Prehospital Patients Managed with Extraglottic Airway Devices and Endotracheal Intubation.

Pre-hospital i-gel blind intubation for trauma: a simulation study.

Supraglottic airway devices: indications, contraindications and management.

Laryngeal mask airway versus bag-mask ventilation or endotracheal intubation for neonatal resuscitation.

Self-pressurized air-Q intubating laryngeal airway versus the LMA ClassicTM: a randomized clinical trial.

  • Intubation, Direct Laryngoscopy, Airway management

Endotracheal Intubation for Traumatic Cardiac Arrest by an Australian Air Medical Service.

Effect of Cricoid Pressure Compared With a Sham Procedure in the Rapid Sequence Induction of Anesthesia. The IRIS Randomized Clinical Trial.

Effect of Use of a Bougie vs Endotracheal Tube and Stylet on First-Attempt Intubation Success Among Patients With Difficult Airways Undergoing Emergency Intubation. A Randomized Clinical Trial.

Cardiac Arrest and Mortality Related to Intubation Procedure in Critically Ill Adult Patients: A Multicenter Cohort Study.

Tracheal intubation in critically ill patients: a comprehensive systematic review of randomized trials.

Cardiac Arrest and Mortality Related to Intubation Procedure in Critically Ill Adult Patients: A Multicenter Cohort Study.

Airway Management During Out-of-Hospital Cardiac Arrest

Assessing Advanced Airway Management Performance in a National Cohort of Emergency Medical Services Agencies

  • Video Laringoscopy, VL vs DL

Comparison of video laryngoscopy versus direct laryngoscopy for intubation in emergency department patients with cardiac arrest: A multicentre study.

First attempt success with a Macintosh-style video laryngoscope is high whether or not the video screen is viewed.

Should the Glidescope video laryngoscope be used first line for all oral intubations or only in those with a difficult airway? A review of current literature.

Comparison of King Vision video laryngoscope and Macintosh laryngoscope: a prospective randomized controlled clinical trial.

Interpreting the Cormack and Lehane classification during videolaryngoscopy.

Intubation with cervical spine immobilisation: a comparison between the KingVision videolaryngoscope and the Macintosh laryngoscope. A randomised controlled trial.

Videolaryngoscopy versus direct laryngoscopy for emergency orotracheal intubation outside the operating room: a systematic review and metaanalysis

  • Guidelines, clinical policies and more

Guidelines for the management of tracheal intubation in critically ill adults.

Airway Management for Trauma Patients

Pragmatic Airway Management in Out-of-Hospital Cardiac Arrest

Implementation of a Clinical Bundle to Reduce Out-of-Hospital Peri-intubation Hypoxia

The Vortex model: A different approach to the difficult airway

Airway management in critical illness: practice implications of new Difficult Airway Society guidelines

Airway Management Practice in Adults With an Unstable Cervical Spine: The Harborview Medical Center Experience

Defining the criteria for intubation of the patient with thermal burns

Shifting Priorities from Intubation to Circulation First in Hypotensive Trauma Patients

Airway and ventilation management strategies for haemorrhagic shock. To tube, or not to tube, that is the question!

Advanced airway management in hoist and longline operations in mountain HEMS. Considerations in austere environments: a narrative review This review is endorsed by the International Commission for Mountain Emergency Medicine (ICAR MEDCOM)

  • Pediatric

Pediatric airway management devices: an update on recent advances and future directions

Cricoid Pressure During Induction for Tracheal Intubation in Critically Ill Children: A Report From National Emergency Airway Registry for Children

  • Drugs

Emergency Department Intubation Success With Succinylcholine Versus Rocuronium: A National Emergency Airway Registry Study

Rapid Sequence Intubation in Traumatic Brain-injured Adults

  • The rest

How much experience do rescuers require to achieve successful tracheal intubation during cardiopulmonary resuscitation?


Clinal Myths and Scientific Truth about heart failure/pulmonary edema management in prehospital setting.

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Clinical Myth #1. All heart failure/cardiogenic pulmonary edema (HF/CPE) patients are fluid overladed .

Scientific Truth #1: Just a small part of heart failure/ cariogenic pulmonary edema (HF/CPE) patients are fluid overloaded. Most (>50%) patients are redistributed (from splanchnic circulation and lover limb to pulmonary circle). Use your clinical judgement (poor sensitivity and specificity) or ultrasound (lung US for the presence of ≥3 B lines in ≥2 bilateral thoracic lung zones is reliable and sensitive for pulmonary edema) to establish which kind of patient you are dealing with: Overloaded or Redistributed. That makes the difference.

Clinical Myth #2. All HF/CP patients benefit from diuretic ( Furosemide or other diuretics) therapy.

Scientific Truth #2: Just normotensive overloaded HF/CPE patients can benefit from diuretic ( Furosemide or other diuretics) therapy.

Furosemide can be detrimental on short and long term outcome because:

  • decreases LV function, increasing ventricular filling pressure 

  • increases systemic vascular resistance through activation of the renin-angiothensyn system

  • decreases glomerular filtration rate

Clinical Myth #3. Nitrates small doses continuous infusion is the right strategy in HF/CP patients.

Scientific Truth #3: Nitrates and Non Invasive Positive Pressure Ventilation are effective first line interventions in hypertensive HF/CPE patients.

High doses Nitrates administration is safe. 2 mg bolus of nitrates every 3 min in hypertensive patients (with close blood pressure check) are safe and faster in achieving clinical targets and symptoms relief. 

Clinical Myth #4. Morphine is safe and effective in HF/CP patients because relief anxiety and reduce preload, and has to be part of first line interventions.

Scientific Truth #4: Morphine administration has no evidences of clinical benefit in HF/CPE patients and is not part of first line treatment for HF/CPE patients. Low quality evidence suggests that morphine is associated with worse outcomes when compared to patients not receiving opioids.

Clinical Myth #5. In hypotensive (cariogenic shock) HF/CP patients Dopamine is the first choice vasopressor.

Scientific Truth #5: Norepinephrine is the first line medication to reach target mean arterial pressure and achieve organ perfusion, rather than Dopamine. Evidence suggests that norepinephrine is associated with improved outcomes including
lower mortality and lower risk of dysrhythmia when compared with Dopamine.

Bottom Line Clinical Pearl: Use ultrasound during every step of your clinical pathway in HF/CPE patients.

  • US detection of B-lines for diagnosis in undifferentiated dyspneic patients

  • US of IVC to discriminate between fluid overloaded or redistributed patients

  • Pump/Tank/Pipes US approach for differential diagnosis in undifferentiated shock patients


Liberally adapted from:

Brit Long MD, Alex Koyfman, MD,  Eric J. Chin, MD. Misconceptions in acute heart failure diagnosis and Management in theEmergency Department. American Journal of Emergency Medicine. 2018 Sep;36(9):1666-1673. doi: 10.1016/j.ajem.2018.05.077. Epub 2018 Jun 1


Myth #1

  • Fallick C, Sobotka PA, Dunlap ME. Sympathetically mediated changes in capacitance: redistribution of the venous reservoir as a cause of decompensation. Circ Heart Fail 2011;4:669–75.
  • Zile MR, Bennett TD, St John Sutton M, et al. Transition from chronic compensated to acute decompensated heart failure: pathophysiological insights obtained from continuous monitoring of intracardiac pressures. Circulation 2008 Sep 30;118 (14):1433–41.
  • Chaudhry SI,Wang Y, Concato J, Gill TM, Krumholz HM. Patterns of weight change preceding hospitalization for heart failure. Circulation 2007;116:1549–54
  • Viau DM, Sala-Mercado JA, Spranger MD, et al. The pathophysiology of hypertensive acute heart failure. Heart 2015;101:1861–7.
  • Jambrik Z, Monti S, Coppola V, et al. Usefulness of ultrasound lung comets as a non radiologic sign of extravascular lung water. Am J Cardiol 2004;93(10):1265–70.
  • Mallamaci F, Benedetto FA, Tripepi R, et al. Detection of pulmonary congestion by chest ultrasound in dialysis patients. JACC Cardiovasc Imaging 2010;3(6):586–94.
  • Anderson KL, Fields JM, Panebianco NL, et al. Inter-rater reliability of quantifying pleural B-lines using multiple counting methods. J Ultrasound Med 2013;32(1):115-20.

Myth #2

  • Francis GS, Siegel RM, Goldsmith SR, et al. Acute vasoconstrictor response to intravenous furosemide in patients with chronic congestive heart failure. Ann Intern Med 1985;103(1):1–6.
  • Kraus PA, Lipman J, Becker PJ. Acute preload effects of furosemide. Chest 1990;98:124–8.

Myth #3

  • Cotter G, Metzkor E, Kaluski E, et al. Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet 1998;351:389–93.
  • Sharon A, Shpirer I, Kaluski E, et al. High-dose intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema. J Am Coll Cardiol 2000;36:832–7.
  • Sharon A, Shpirer I, Kaluski E, et al. High-dose intravenous isosorbide-dinitrate i safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema. J Am Coll Cardiol 2000;36:832–7.

Myth #4

  • Sosnowski MA. Review article: lack of effect of opiates in the treatment of acute cardiogenic pulmonary oedema. Emerg Med Australas 2008;20:384–90.
  • Vasko JS, Henney RP, Oldham HN. Mechanisms of action of morphine in the treatment of experimental pulmonary edema. Am J Cardiol 1966;18:876–83.
  • Kaye AD, Hoover JM, Kaye AJ, et al. Morphine, opioids, and the feline pulmonary vascular bed. Acta Anaesthesiol Scand 2008;52:931–7.
  • Riggs TR, Yano Y, Vargish T. Morphine depression of myocardial function. Circ Shock 1986;19:31–8.
  • Miró Ò, Gil V,Martín-Sánchez  FJ, et al.Morphine use in the ED and outcomes of patients with acute heart failure: a propensity score-matching analysis based on the EAHFE registry. Chest 2017 Oct;152(4):821–32.

Myth #5

  • Rui Q, Jiang Y, Chen M, et al. Dopamine versus norepinephrine in the treatment of cardiogenic shock: a PRISMA-compliant meta-analysis. Medicine 2017;96(43):e8402.



1 Year in Review. 2018 Guidelines you must know.

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So 2018 is at the end and we give, as every year, a look back to literature and articles of this finishing year.

This is the first step of 1 YEAR IN REVIEW the classical MEDEST appointment with all that matter in emergency medicine literature.

So let’s start with Guidelines but first I want to cite an important point of view about Clinical practice Guidelines and they future development:

Clinical practice guidelines will remain an important part of medicine. Trustworthy guidelines not only contain an important review and assessment of the medical literature but establish norms of practice. Ensuring that guidelines are up-to-date and that the development process minimizes the risk of bias are critical to their validity. Reconciling the differences in major guidelines is an important unresolved challenge.”

Paul G. Shekelle, MD, PhD. Clinical Practice Guidelines What’s Next?

And now here it is, divided by topics, the most important new 2018 Guidelines. Click on the link to read more.
  • Airway management

Guidelines for the management of tracheal intubation in critically ill adults
Guidelines for the management of tracheal intubation in critically ill adults PP presentation

  • Trauma

Management of severe traumatic brain injury (first 24 hours)
Spinal Motion Restriction in the Trauma Patient –A Joint Position Statement
Guidelines for Prehospital Fluid Resuscitation in the Injured Patient
Re-thinking resuscitation: leaving blood pressure cosmetics behind and moving forward to permissive hypotension and a tissue perfusion-based approach
  • Cardiac

2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay

  •  Stroke

2018 Guidelines for the Early Management of Patients with acute ischemic stroke.A Guideline for Healthcare Professionals From the American HeartAssociation/American Stroke Association

  • Others

Health Professions Council of South Africa. Clinical Practice Guidelines





Social media & aggiornamento. Dacci il tuo parere!

18 Ott

banner survey SoMe

Medici e infermieri d’emergenza-urgenza e area critica, come usate i #SocialMedia per aggiornarvi?

Rispondi a questa breve survey ➡️ bit.ly/2yiVXXI ⬅️per contribuire a delineare la realta’ italiana #FOAMed #FOANed #FOAMcc #AreaCritica #Emergenza




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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.

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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.

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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!

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