You arrive on the scene of a motorbike accident. The driver, a 50 years old male, at your arrival is in “Pain” state with eyes closed and you can hear just a “snoring” sound coming from his mouth. His vitals are: NIMBP 80 over 50, HR 110, A quick primary survey reveal a low level of consciousness (eyes closed no finalised arms movement) with restored airway patency that after basic airway manoeuvres and O2 therapy (SaO2 goes to 95%) no signs of tension pneumo. A quick look to the pelvis and legs reveal a suspected “open book” lesion and a bilateral femoral fracture. No PMH is available at the moment.
Physiological response to shock
From the primary survey and vitals you can understand the patient is compensating a state of profound (hypovolemic) shock and consequent organ low perfusion with a sympathetic activation. Endogenous adrenergic mediators are trying to restore organ perfusion by vasoconstriction and increase in cardiac output.
First do not harm
Can we kill a patient destroying the physiologic response to shock?
The answer is YES! The need to protect airway performing a rapid pharmacological assisted airway management (RSI), can lead to bad consequences, destroying the physiological response to a state of profound shock.
All sedative, analgesic and anaesthetic drugs in fact antagonise and depress the sympathetic adrenergic response physiologically targeted to restore perfusion to vital organs.
First do not harm and choose minimal emodynamic impact type and dose of drugs to perform sedation. As we know (till now) the better choice are Ketamine and Etomidate with no clear evidences on which one is preferable. We for sure know that Ketamine can be dangerous in cathecolamine depleted patients and that this effect is dose dependent. So consider using a lower dose to reach dissociative threshold being conscious that can lead to a non ideal intubation condition.
After a dissociative dose of Ketamine, our next clinical target is to reanimate the patient form an oxygenation and/or an organ perfusion point of view.
So we shift from a concept of Rapid Sequence Intubation to a more comprehensive plan of Delayed Sequence Airway Management. Delayed (Ketamine/Etomidate induced) to get time and reanimate, Airway Management intended as any plan (tracheal intubation, supraglottic airway) we can apply in that specific patient in the middle of the road or in other prehospital scenarios.
A properly performed pre-oxygenation with the adjunct of apneic oxygenation can restore O2 levels giving us also a good reserve for following apnea times.
Cautelative fluid administration (avoid fluids in trauma, use BLOOD) and, push dose (Epinephrine, Phenilephrine) or continuous infusion (Norepinephrine)vasopressors, can restore perfusion to abdominal and extra abdominal organs by increasing circulating volume and cardiac performance (Alfa and Beta agonist ).
Delayed paralytic administration give us the time to perform a proper reanimation reanimation and to check the effects of our interventions.
If everything goes well and the patient’s oxygenation and emodynamic state is compensated, we can administer paralytic, and go straight to perform tracheal intubation.
But if the patient remains uncompensated despite all our efforts to correct the potentially lethal cause, our last weapon can be to preserve spontaneous breathing.
Don’t live me breathless
WHY? During inspiratory phase of respiratory cycle the negative intrathoracic pressure favourites venous return and increase the telediastolic volume of the left ventricle. The augmented left ventricle end diastolic pressure (LVEDP) according to Frank-Starling law improves myocardial performance increasing stroke volume and consequently cardiac output.
The refractory shocked patient is heavily preload dependent and suppressing the inspiratory drive risk to worsen the already dramatic emodynamic state taking him on the irreversible part of the shock curve.
We’ve got a plan
We need to have a plan for high difficult physiological airways. This is just a small residual percentage of the airways we manage in our clinical practice, but can be dramatically catastrophic when we deal with those patients without a precise plan.
We’ve got a backup plan
But when intubation fails we need to have a backup plan!
Case conclusion
You understand the need to protect patient’s airways but also the extreme physiologic difficulty of this airway.
After administering a dissociative dose of Ketamine, due to the failure of any try to restore perfusion, you decide to perform a DISSOCIATIVE INTUBATION using a videolaryngoscope with a hyperangulated blade and a bougie, AVOIDING PARALYSIS.
Then you put the patient on ACV mechanical ventilation targeting a TV of 6 ml/kg and considering a “zero PEEP” strategy.
Special Thanks to Scott Weingart and Jim DuCanto for the kindness and fundamental mentorship on inspiring and peer reviewing the algorithm
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این سایت را به آن دکتوران و محصلین طب که شب و روز برای رفاه نوع انسان فداکاری می کنند ، جوانی و لذایذ زندگی را بدون چشمداشت به امتیاز و نفرین و آفرین قربان خدمت به بشر می کنند و بار سنگین خدمت و اصلاح را بدوش می کشند ، اهداء می کنم This site is dedicated to all Doctors and students that aver the great responsibility of People’s well-being upon their shoulders and carry on their onerous task with utmost dedication and Devotionاولین سایت و ژورنال انتــرنتی علـــمی ،تخـصصی ، پــژوهشــی و آمــوزشــی طبـــی در افغــانســـتان
Learning everything I can from everywhere I can. This is my little blog to keep track of new things medical, paramedical and pre-hospital from a student's perspective.
MEDEST 
Don’t live me Breathless
28 GenCase presentation
You arrive on the scene of a motorbike accident. The driver, a 50 years old male, at your arrival is in “Pain” state with eyes closed and you can hear just a “snoring” sound coming from his mouth. His vitals are: NIMBP 80 over 50, HR 110, A quick primary survey reveal a low level of consciousness (eyes closed no finalised arms movement) with restored airway patency that after basic airway manoeuvres and O2 therapy (SaO2 goes to 95%) no signs of tension pneumo. A quick look to the pelvis and legs reveal a suspected “open book” lesion and a bilateral femoral fracture. No PMH is available at the moment.
Physiological response to shock
From the primary survey and vitals you can understand the patient is compensating a state of profound (hypovolemic) shock and consequent organ low perfusion with a sympathetic activation. Endogenous adrenergic mediators are trying to restore organ perfusion by vasoconstriction and increase in cardiac output.
First do not harm
Can we kill a patient destroying the physiologic response to shock?
The answer is YES! The need to protect airway performing a rapid pharmacological assisted airway management (RSI), can lead to bad consequences, destroying the physiological response to a state of profound shock.
All sedative, analgesic and anaesthetic drugs in fact antagonise and depress the sympathetic adrenergic response physiologically targeted to restore perfusion to vital organs.
First do not harm and choose minimal emodynamic impact type and dose of drugs to perform sedation. As we know (till now) the better choice are Ketamine and Etomidate with no clear evidences on which one is preferable. We for sure know that Ketamine can be dangerous in cathecolamine depleted patients and that this effect is dose dependent. So consider using a lower dose to reach dissociative threshold being conscious that can lead to a non ideal intubation condition.
Reanimate first intubate later (aka DSI)
After a dissociative dose of Ketamine, our next clinical target is to reanimate the patient form an oxygenation and/or an organ perfusion point of view.
So we shift from a concept of Rapid Sequence Intubation to a more comprehensive plan of Delayed Sequence Airway Management. Delayed (Ketamine/Etomidate induced) to get time and reanimate, Airway Management intended as any plan (tracheal intubation, supraglottic airway) we can apply in that specific patient in the middle of the road or in other prehospital scenarios.
A properly performed pre-oxygenation with the adjunct of apneic oxygenation can restore O2 levels giving us also a good reserve for following apnea times.
Cautelative fluid administration (avoid fluids in trauma, use BLOOD) and, push dose (Epinephrine, Phenilephrine) or continuous infusion (Norepinephrine) vasopressors, can restore perfusion to abdominal and extra abdominal organs by increasing circulating volume and cardiac performance (Alfa and Beta agonist ).
Delayed paralytic administration give us the time to perform a proper reanimation reanimation and to check the effects of our interventions.
If everything goes well and the patient’s oxygenation and emodynamic state is compensated, we can administer paralytic, and go straight to perform tracheal intubation.
But if the patient remains uncompensated despite all our efforts to correct the potentially lethal cause, our last weapon can be to preserve spontaneous breathing.
Don’t live me breathless
WHY? During inspiratory phase of respiratory cycle the negative intrathoracic pressure favourites venous return and increase the telediastolic volume of the left ventricle. The augmented left ventricle end diastolic pressure (LVEDP) according to Frank-Starling law improves myocardial performance increasing stroke volume and consequently cardiac output.
The refractory shocked patient is heavily preload dependent and suppressing the inspiratory drive risk to worsen the already dramatic emodynamic state taking him on the irreversible part of the shock curve.
We’ve got a plan
We need to have a plan for high difficult physiological airways. This is just a small residual percentage of the airways we manage in our clinical practice, but can be dramatically catastrophic when we deal with those patients without a precise plan.
We’ve got a backup plan
But when intubation fails we need to have a backup plan!
Case conclusion
You understand the need to protect patient’s airways but also the extreme physiologic difficulty of this airway.
After administering a dissociative dose of Ketamine, due to the failure of any try to restore perfusion, you decide to perform a DISSOCIATIVE INTUBATION using a videolaryngoscope with a hyperangulated blade and a bougie, AVOIDING PARALYSIS.
Then you put the patient on ACV mechanical ventilation targeting a TV of 6 ml/kg and considering a “zero PEEP” strategy.
Special Thanks to Scott Weingart and Jim DuCanto for the kindness and fundamental mentorship on inspiring and peer reviewing the algorithm
References
Brian E. Driver, Matthew E. Prekker, Robert F. Reardon, Benjamin J. Sandefur, Michael D. April, Ron M. Walls, Calvin A. Brown,
Success and Complications of the Ketamine-Only Intubation Method in the Emergency Department,
The Journal of Emergency Medicine
Weingart SD, Trueger NS, Wong N, Scofi J, Singh N, Rudolph SS. Delayed sequence intubation: a prospective observational study. Ann Emerg Med. 2015 Apr;65(4):349-55. doi: 10.1016/j.annemergmed.2014.09.025. Epub 2014 Oct 23. PMID: 25447559.
Merelman AH, Perlmutter MC, Strayer RJ. Alternatives to Rapid Sequence Intubation: Contemporary Airway Management with Ketamine. West J Emerg Med. 2019 May;20(3):466-471. doi: 10.5811/westjem.2019.4.42753. Epub 2019 Apr 26. PMID: 31123547; PMCID: PMC6526883.
Ko BS, Ahn R, Ryoo SM, et al. Prevalence and outcomes of endotracheal intubation–related cardiac arrest in the ED. Am J Emerg Med. 2015;33(11):1642-5.
Mort TC. Complications of emergency tracheal intubation: hemodynamic alterations – part I. J Intensive Care Med. 2007;22(3):157-65.
Jarvis JL, Gonzales J, Johns D, et al. Implementation of a clinical bundle to reduce out-of-pospital peri-intubation hypoxia. Ann Emerg Med.2018;72(3):272-279.e1.
Roantree RAG, Goldstein S. (2018). EMS, Facilitated Intubation Without 36.Paralytics. Treasure Island, Florida: StatPearls Publishing.
Braude D, Palomo O, Beamsley A. Sedation only intubation. EM:RAP. 39.2013.
Miller M, Kruit N, Heldreich C, et al. Hemodynamic response afterrapid sequence induction with ketamine in out-of-hospital patients 50. at risk of shock as defined by the shock index. Ann Emerg Med. 2016;68(2):181-8.e2.
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