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Confirming Tracheal Intubation: stop wasting your time!

2 Lug

Intro

The methods to confirm tracheal intubation (and exclude accidental oesophageal intubation) are classically divided in Techniques not requiring manual ventilation and Techniques requiring manual ventilation::

  1. Techniques not requiring manual ventilation
    • Inspection of the vocal cords: there should be visual confirm- ation that the tube lies surrounded by the glottic structures
    • Palpation of the trachea: an assistant palpating the external trachea may feel vibrations, corresponding to the tube passing the tracheal rings
    • Oesophageal detector device: Tracheal placement results in free aspiration of gas from the lungs; in oesophageal intubation, the walls of the oesophagus collapse around the tube lumen preventing gas flow
  2. Techniques requiring manual ventilation:
    • Sounds
    • Compliance: A ‘normal’ compliance during manual ventilation
    • Inspection of the chest: Good expansion of the chest on manual ventilation
    • Auscultation of the epigastrium
    • Auscultation of the chest
    • CO2 detection
      • Capnography – a normal capnogram for at least six breaths suggests tracheal intubation
      • Capnometry – a change in indicator to denote CO2 suggests tracheal intubation

Despite nowadays is evident that CO2 detection is the gold standard in terms of sensibility and specificity, our daily practice in managing airways still and strongly rely on clinical methods to confirm when the tube is correctly posed in the trachea and not in the oesophagus.

The article

Hansel, J., Law, J.A., Chrimes, N., Higgs, A. and Cook, T.M. (2023),

Clinical tests for confirming tracheal intubation or excluding oesophageal intubation: a diagnostic test accuracy systematic review and meta-analysis. Anaesthesia. https://doi.org/10.1111/anae.16059

In this meta-analysis the authors investigated the literature about the reliability of different methods to confirm tracheal intubation and exclude oesophageal intubation.

This is a clinically relevant point cause the unrecognised oesophageal intubation leads to catastrophic consequences on patients health.

Which Clinical test they evaluated:

How they presented the data

The false positive rate (FPR)

The FPR indicates how often any sign that is considered suggestive of successful tracheal intubation (for example chest rising or hearing breath sounds),might occur despite the tube is not in the trachea but in the oesophageal. Usually an acceptable number of FPR can be 0,1 (or the 10% (10 out of 100) of the total positive results) but you can understand how in this case, considered the high clinical relevance of the topic we have to reach for lower FPR the 1 out of 10.

The Likelihood Ratio (LR): positive (LR+) or negative (LR-)

The positive LR (LR+) indicates how many times is more probable that the tube is the trachea than in the oesophagus the investigated sign is present

A test with a LR+=10 (cut off value for reliability) means that there is 10 times more probability that the tube is really in the trachea than in the oesophagus

The negative LR (LR-) indicates how many times is more probable that the tube is the oesophagus han in the trachea if the investigated sign is present

A test with a LR- of 0.1 (cut off value for reliability) means that there is 1/10 times more probability that the tube is in the oesophagus than in the trachea.

What they found

Conclusion

The available data strongly suggest that clinical signs lack the discriminatory power to exclude oesophageal intubation to a sufficient degree to ensure patient safety when capnography is not available or doubted. The oesophageal detector device performs better than clinical examination, and in resource-limited environments with no access to capnography, may be sufficiently sensitive and specific to help guide decision-making.

Clinical Practice Take Home Message

Based on the result of this study when available use waveform capnography to confirm tracheal intubation and exclude oesophageal intubation. Clinical tests can be dangerously misleading and potentially a waste of precious time in difficult environments as emergency prehospital setting.

In poor resources systems if any form of ETCO2 is not available, the most reliable test to confirm tracheal intubation is the Oesophageal detector device.

God save the King!

27 Giu

Matthew E. Prekker, M.D., M.P.H.,  Brian E. Driver, Video versus Direct Laryngoscopy for Tracheal Intubation of Critically Ill Adults

The DirEct versus VIdeo LaryngosCopE (DEVICE) trial is a prospective, multicentre, non-blinded, randomised trial being conducted in 7 EDs and 10 ICUs in the USA

Critically ill adults undergoing tracheal intubation randomly assigned to the video-laryngoscope group or the direct-laryngoscope group

The primary outcome was successful intubation on the first attempt.

The secondary outcome was the occurrence of severe complications during intubation: severe hypoxemia, severe hypotension, new or increased vasopressor use, cardiac arrest, or death.

The trial was stopped for efficacy at the time of the single preplanned interim analysis.

Conclusions: Among critically ill adults undergoing tracheal intubation in an emergency department or ICU, the use of a videolaryngoscope resulted in a higher incidence of successful intubation on the first attempt than the use of a direct laryngoscope.

Comment: This a long journey hopefully coming to an end. From 2022 we have clear evidences on the superiority of Video versus Direct laryngoscopy Hansel J, Rogers AM, Lewis SR, Cook TM, Smith AF. Videolaryngoscopy versus direct laryngoscopy for adults undergoing tracheal intubation. Cochrane Database Syst Rev. 2022 Apr 4;4(4):CD011136. doi: 10.1002/14651858.CD011136.pub3. PMID: 35373840; PMCID: PMC8978307.. Main airway management societies (Difficult Airway Society; Society for Airway Management; European Airway Management Society; All India Difficult Airway Society; Canadian Airway Focus Group; Safe Airway Society; and International Airway Management Society) recently updated their statements on preventing the accidental oesophageal intubation in that sense. Preventing unrecognised oesophageal intubation: a consensus guideline from the Project for Universal Management of Airways and international airway societies. The DEVICE trial is another brick in the wall of consciousness about superiority of VL vs DL despite some findings are not replicable ( ex. DL FPS 70,8%) in systems where airway management and expertise in DL is a longstanding tradition. But as said we didn’t need this trial to arrive at the conclusion of the journey.

Use the videolaryngoscope (VL) as first choice in emergent tracheal intubation to improve first passage success and prevent accidental oesophageal intubation.

Use direct laryngoscope (DL) just as rescue device in case of technical failure of the videolrayngoscope

All medical systems involved in airway management need to be aware of this. A videolaryngoscope is no longer an option but a standard equipment. The best choice is to have both, standard and hyperangulated geometry blades, in adult and paediatric sizes.

The first approach with a standard geometry blade permits to shift from VL to DL without changing device. The hyparangulated blade can be useful in selected cases even as first option..

We also consequently need to shift paradigm from classical way of teaching airway management, to a VL first approach as default method and simulating any tech failure during the practical training forcing the trainee to use the DL as rescue plan.

To let me know what is your opinion fill the survey at the link below:

VL first approach

Also read:

Beyond Guidelines: what’s new in OCHA management

6 Set

Chest compressions alternate to abdominal compression–decompression technique

Background

The abdominal compression–decompression technique is based on an “abdominal pump” model, which induces pressure changes within the abdominal cavity and promotes the return of blood from the abdominal cavity to fill the heart and be eventually pumped to the brain. A combination of abdominal compression–decompression and chest compression was previously shown to increase the venous refilling of the heart, which could generate increased coronary perfusion pressure and increase blood flow to vital organs . With this combination method, chest release during abdominal compression leads to increased venous return to the thorax by negative intrathoracic pressure. Moreover, abdominal decompression during chest compression may lead to increased blood flow via decreased afterload. In myocardial blood flow, a better 48-h outcome was documented with the combination method compared with STD-CPR

The study

Evaluation of abdominal compression– decompression combined with chest compression CP9R performed by a new device: Is the prognosis improved after this combination CPR technique?

This study was performed in China. It’s a single center, randomised, not blinded study.

The study aimed to compare the outcomes of standard cardiopulmonary resuscitation (STD- CPR) and combined chest compression and abdominal compression–decompression cardiopulmonary resuscitation (CO-CPR) following out-of-hospital cardiac arrest (OHCA).

Primary outcome ROSC. Secondary outcome hospital admission, hospital discharge and neurological outcome at hospital discharge.

Results

ROSC and survival to hospital admission: no statistical benefit

Survival at hospital discharge and neurological outcome: CO-CPR had statistical significant better outcome respect STD-CPR

Limitations

Single center, small sample size, no evaluation of possible abdominal injuries.

Bottom line

For prehospital use of combined chest compression and abdominal compression–decompression cardiopulmonary resuscitation we have first of all to account the need of an additional rescuer to perform abdominal compression-decompression. By the way the alternate chest/abdominal compression-decompression method is promising even if we need larger multicenter randomised trial for a more consistent evaluation of its efficacy.

Head and thorax elevation during cardiopulmonary resuscitation

Background

Gradual elevation of the head and thorax enhances venous return from the head and neck to the thorax and further lowers intracranial pressure. This automated controlled elevation (ACE) CPR strategy consists of: (1) manual active compression decompression (ACD)-CPR and/or suction cup-based automated (LUCAS 3) CPR; (2) an impedance threshold device (ITD); and (3) an automated controlled head and thorax patient positioning device (APPD).

The study

Head and thorax elevation during cardiopulmonary resuscitation using circulatory adjuncts is associated with improved survival

Observational, prospective study. The Objectives of the study was to assess the probability of OHCA survival to hospital discharge after ACE-CPR versus C-CPR. ACE-CPR data were collected from a dedicated registry implemented by 10 EMS Agencies. Conventional (C) CPR data were collected from 3 large historical randomized controlled OHCA resuscitation trials.

NB: for ACE-CPR only 6/10 agencies data were evaluated.

The primary outcome was survival to hospital discharge. Secondary outcomes included ROSC at any time, and survival to hospital dis- charge with favorable neurological function.

Results

Cumulative results on primary and secondary outcome before taking into consideration the time from 911 call to ACE-CPR were not statistically significative differences. The statistical significance of ACE-CPR was reached only when time from 911 call to ACE-CPR initiation was considered.

Limitations

Observational study. Participating personnel form EMS agencies were highly motivated about ACE-CPR. 165 patients excluded with no clear explanation (generally didn’t meet inclusion criteria) from 4 EMS participating agencies. Statistical significance on primary and secondary outcome was reached after surrogate secondary analysis that considered time form 911 call to ACE-CPR start.

Bottom line

There are still insufficient historical data to understand the benefit of automated controlled elevation (ACE) CPR and this study doesn’t clear any doubt about it’s efficacies on clinical oriented outcomes.

Aortic occlusion during cardiac arrest. Mechanical adrenaline?

Background

Thoracic aortic occlusion during chest compressions limits the vascular bed for the generated cardiac output. This may increase the aortic pressure and subsequently the coronary perfusion pressure (CPP).

The coronary perfusion pressure (CPP), the pressure gradient between the aorta and right atrium, is a major determinant of the myocardial blood flow. Consequently, generating a high CPP by providing high-quality chest compression during CPR is one of the most critical factors for achieving ROSC in cardiac arrest patients.

It is uncontroversial to state that the desired effect of adrenaline in CPR is the potential increase in CPP. The potential detrimental effects of adrenaline, such as decreased cerebral blood flow, increased myocardial oxygen consumption or recurrent ventricular tachycardias after ROSC, is yet to be found with REBOA. However, adverse effects of REBOA are not reported in the limited human data published, nor has this been an endpoint in the studies conducted so far.

The study

Resuscitative endovascular occlusion of the aorta (REBOA) as a mechanical method for increasing the coronary perfusion pressure in non-traumatic out-of-hospital cardiac arrest patients

This is a pilot study. The aim of the study was to calculate the CPP before and after REBOA balloon inflation. EtCO2 and median aortic pressure before and after balloon inflating were also measured.

Results

CPP, MAP and EtCO2 significative increased after REBOA placement in Zone 1 and balloon inflation

Limitations

Single center, small numbers, need of a large number of operators to insert the REBOA and to obtain the measurements.

Bottom line

REBOA in Cardiac Arrest is potentially useful to increase CPP and less dangerous than epinephrine administration.

It’s feasibility in emergency (in-hospital and out of hospital) settings in a timely manner and with a small number of medical personnel needs to be demonstrated.

By Mario Rugna

In case of oesophageal intubation

19 Ago

Just published Preventing unrecognised oesophageal intubation: a consensus guideline from the Project for Universal Management of Airways and international airway societies

Thanks to a prestigious panel of international authors. Great job and definitely solid indication about how to prevent and recognise accidental oesophageal intubation.

Just some of the key recommendations

  • Exhaled carbon dioxide monitoring and pulse oximetry should be available and used for all episodes of airway management.
  • Routine use of a videolaryngoscope is recommended whenever feasible.
  • Inability to detect sustained exhaled carbon dioxide requires oesophageal intubation to be actively excluded.
  • Tube removal should be undertaken if any of the following are true:
    • Oesophageal placement cannot be excluded
    • Sustained exhaled carbon dioxide cannot be restored
    • Oxygen saturation deteriorates at any point before restoring sustained exhaled carbon dioxide

Refer to the full text guidelines for more.
Here is the link to Safe Airway Society livestream event.
Must read, must follow. Free open access.

Let’s go outside

The following are personal considerations on peculiar aspects about management of accidental oesophageal intubation in prehospital environment and come from my personal clinical experience.

Beware they are just personal considerations and practical tricks and tips and are not intended to substitute the above guidelines. 

They are intended to suggest an alternative mental and technical approach when dealing with oesophageal intubation on uncontrolled patients in difficult environment.

Some general considerations

  1. Prehospital uncontrolled patients are not on empty stomach so are at high risk of regurgitation/inhalation
  2. Even few ventilation efforts in case of oesophageal intubation pone the patient at high risk of regurgitation/inhalation 
  3. Suctioning in prehospital setting is not always ready avalliate (mind your environment) or maximally performant (mind your equipment) 
  4. First attempt in prehospital setting must be always the best one. Think before trying a second attempt in case of failure. Implement your plan or change plan.
  5. Apply the Indication, Suitability, Feasibility approach while supporting oxygenation, ventilation and protection.

DO NOT REMOVE THE OT TUBE STRAIGHT FORWARD IN CASE OF ACCIDENTAL OESOPHAGEAL INTUBATION IN PREHOSPITAL ENVIRONMENT.

The way I like it. The way I do it.

  1. Live the “oesophageal” OT tube in (overcuffed) and if it’s possible apply a continuous suctioning to exclude the oesophagus and protect the airways 
  2. Place a SGA to restore oxygenation and ventilation (trough BMV or NIV)
  3. After restoring oxygenation (SaO2 >94%) and ventilation (EtCO2 40 mmHg) if suitable and feasible (see below) proceed to a second attempt of tracheal intubation (must be videolaryngoscope+bougie)
  4. If the second attempt succeeds remove the “oesophageal” OT
  5. If the second attempt is not suitable or feasible transport to nearest hospital (patient is well oxygenated and ventilated via SGA and protected via oesophageal exclusion) for further stabilisation (you can replace the oesophageal OT tube with a large bore oro-gastric tube or insert the orogastric tube trough the SGA dedicated channel)
  6. If you can’t restore oxygenation and ventilation via SGA or you can’t place a SGA remove the oesophageal OT tube and try to oxygenate and ventilate (remember patient is not protected) via BVM and NC (double oxygenation) 
  7. If even BVM fails declare CICO 
Suitability 
  • Do I have a plan to implement regarding the  first attempt
  • Can I improve my environment (Setting) moving the patient to a more comfortable place/position 
  • Is the time to nearest hospital short/long 
Feasibility 
  • Am I in the right mental mood after 1st attempt (me) to try a better second one
  • Is my team ready for a second attempt (team) 
  • Do I have the right equipment to implement my second attempt (Equipment)

The visual algorithm

The Video

By Mario Rugna

Pulseless electrical activity following traumatic cardiac arrest: Sign of life or death?

11 Giu

On May 2019 was published an article we review today, cause the authors conclusions are pretty astonishing and worth a deeper look.

Israr, S & Cook, AD & Chapple, KM & Jacobs, JV & McGeever, KP & Tiffany, BR & Schultz, SP & Petersen, SR & Weinberg, JA. (2019). Pulseless electrical activity following traumatic cardiac arrest: Sign of life or death?. Injury. 10.1016/j.injury.2019.05.025.

Authors Conclusions: Following pre-hospital traumatic cardiac arrest, PEA on arrival portends death. Although Cardiac Wall Motion (CWM) is associated with survival to admission, it is not associated with meaningful survival. Heroic resuscitative measures may be unwarranted for PEA following pre-hospital traumatic arrest, regardless of CWM.Trauma death 2.jpg

What kind of study is this?

retrospective, cohort study consisting of adult trauma patients (n. 277 patients ≥18 years of age) admitted to one of two American College of Surgeons verified level 1 trauma centers in Maricopa County, Arizona within the same hospital system between February 2013 to September 2017 and January 2015 to December 2017.

Pre-hospital management by emergency medical transport services was guided by advanced life support protocols. 

Both hospitals for management of Traumatic Cardiac Arrest (TCA) followed the Western Trauma Association Guidelines

The following variables were collected from each patient:

  • Age
  • Gender
  • Duration of pre-hospital CPR
  • Survival to admission vs. pronouncement of death in ED
  • Disposition at hospital discharge

Results

  • 277 trauma patients that underwent pre-hospital CPR for TCA
  • Mean patient age was 43.1
  • Mechanism of injury was penetrating in 99 patients (35.7%), the most common of which was due to ballistic injuries, the rest where blunt trauma.
  • 52.0% of the patients were intubated prior to hospital arrival
  • 235 patients received epinephrine in route (84.8%)
  • Pre-hospital resuscitation duration, 20.0 (15.0 – 25.0) minutes

Outcomes

20 patients were identified on arrival to have had ROSC. 18 of these patients survived to hospital admission and 4 of them were discharged alive from hospital

147 patients were identified on arrival in asystole. Among these patients none were discharged alive from hospital.

The remaining 110 patients presented with PEA. 10 patients survived to admission, 9.1%, but only one, 0.9% was discharged from alive from hospital.

P-FAST was performed in 79 of the 110 patients with PEA (71.8%)

Presence of CWM was significantly associated with survival to hospital admission (2 but not to hospital discharge (zero with or without CWM).

Authors conclusions

  • Resuscitative efforts are unlikely to reverse the course of this pathophysiology, warranting sound clinical judgement from the treating physician concerning the decision to continue or desist, relative to mechanism of injury and clinical presentation.
  • CWM (signifying a beating heart and thereby pseudo PEA) was not associated with meaningful survival.
  • Nonetheless, we conclude that P-FAST is a useful tool for distinguishing PEA with cardiac standstill, which is in all likelihood terminal (and continued resuscitation would become an attempt at reanimation), versus pseudo PEA, whereby the heart is actually still beating, representative of a veritable sign of life, and ongoing resuscitative attempts may be considered appropriate despite the unfavorable prognosis.

My considerations on methodology and results

  1. Conventional ACLS protocol, as performed in the study, IS NOT the standard of care in TCA.
  2. No clinical intervention to address reversible causes where performed (or mentioned) in the field.
  3. The only clinically oriented manoeuvre performed in the field was tracheal intubation in just half of the patients (52.0% of the patients were intubated).
  4. Prehospital resuscitation time (20 minutes mean time) was spent performing non useful and potentially  dangerous interventions (closed chest compressions, epinephrine administration) for TCA.
  5. Patients with PEA and documented CWM (but not only them) at their arrival in ED has been hypo perfused during the entire pre-hospital resuscitation time and lost most of their chances for good clinical outcome.

So in my opinion this study and it’s conclusions are biased by a wrong approach to Traumatica Cardiac Arrest in the prehospital phase.

Emergency providers, when treating patients in traumatic cardiac arrest, need to perform interventions addressing the possible REVERSIBLE causes:

  1. Exanguination/Massive Hemorrage (Pelvic Binding, TXA administration, Tourniquet or direct compression)
  2. Hypoxia (Tracheal Intubation)
  3. Tension Pneumo (Double Thoracostomy)
  4. Hypovolemia (Blood or fluid resuscitation)

Emergency providers need to rely on direct (central pulse palpation, Ultrasuond) or indirect (EtCO2, Plethysmography) signs of perfusion to guide their clinical interventions.

Resuscitation of Traumatic Cardiac Arrest patients in not futile just need to be performed in the right way.

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References

Israr, S & Cook, AD & Chapple, KM & Jacobs, JV & McGeever, KP & Tiffany, BR & Schultz, SP & Petersen, SR & Weinberg, JA. (2019). Pulseless electrical activity following traumatic cardiac arrest: Sign of life or death?. Injury. 10.1016/j.injury.2019.05.025.

 

 

1 Year in Review. 2018 Guidelines you must know.

13 Dic

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

 

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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)

19489_eb_adrenaline_molecule

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.

circ1

  • 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.

Population

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.

Intervention

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

Comparison

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

Outcome

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
Description-of-the-modified-Rankin-Scale.ppm

Results

  • 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 )

PARAMEDIC-2-Results-1024x255

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

Conclusions

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.

Strengths

  • 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

Paramedic

Limitations

  • 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.

evolution

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

References

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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:

 Trauma

Traumatic Cardiac Arrest

Fluid Therapy

Spinal Immobilisation

Field Triage

Antifibrinolytics

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.

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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. 

Ventilation

  • 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.

Defibrillation

  • 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

  • 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.

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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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