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, MRes^1,2; 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

Intervention

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

Control

• 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.

Results

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

Image attribution https://twitter.com/AIRWAYS_2/status/1034456519369256960

Image attribution https://twitter.com/AIRWAYS_2/status/1034456519369256960

Conclusions

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, MS^1,2; 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

Intervention

• LT insertion (n = 1505 patients)

Control

• 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

Results

Population

• 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

Image attribution https://jamanetwork.com/data/Journals/JAMA/937477/joi180058va.png

Conclusions

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,

Strength:

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

Limitations:

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.

References: 

• Henry E. Wang et al. Effect of a Strategy of Initial Laryngeal Tube Insertion vs Endotracheal Intubation on 72-Hour Survival in Adults With Out-of-Hospital Cardiac ArrestA Randomized Clinical Trial. 
• Jonathan R. Benger et al Effect of a Strategy of a Supraglottic Airway Device vs Tracheal Intubation During Out-of-Hospital Cardiac Arrest on Functional OutcomeThe AIRWAYS-2 Randomized Clinical Trial
• Lars W. Andersen et al. Pragmatic Airway Management in Out-of-Hospital Cardiac Arrest

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 references) evaluating 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.

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.

Conclusions

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

References

• Breitkreutz R et al. Focused echocardiographic evaluation in life support and peri-resuscitation of emergency patients: a prospective trial.Resuscitation 2010; 81: 1527-33. PMID: 20801576
• Nina Sviridova, Kenshi Sakai, Human photoplethysmogram: new insight into chaotic characteristics,Chaos, Solitons & Fractals, Volume 77, 2015, Pages 53-63,
  ISSN 0960-0779, https://doi.org/10.1016/j.chaos.2015.05.005 (http://www.sciencedirect.com/science/article/pii/S0960077915001344)
• Section 3: Cardiovascular physiology Chapter 33 Arterial pressure waveforms

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. 

And what about you?

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!

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

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

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

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

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

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

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

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

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

Read more about this topic. Explore the References:

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