More on EMCrit
Now on to the Grilling
Editor-in-Chief, at EMCrit.org
An ED Intensivist from NY.
Professor
Nassau University Medical Center
No conflicts of interest (coi).
Professor
Nassau University Medical Center
No conflicts of interest (coi).
Latest posts by Scott Weingart, MD FCCM (see all)
- EMCrit 363 – Retrograde Intubation - December 2, 2023
- ODR 013 – Should, Must, & Won't - November 25, 2023
- EMCrit Shadowboxing Case 6 – A Respiratory Case along with Extra Commentary from Mae West - November 23, 2023
Fascinating discussion. How obtruded or to what GCS (fully aware how limited the GCS is as a scoring tool on this setting) do u need this pt to avoid post intubation awareness? How do u decide ongoing management strategies for anaesthesia/ sedation until surgery is about to begin?
I just noticed the auto correction! Obtunded not obtruded!
IMO best option (if needed) in this scenario until OR is small aliquots of Ketamine
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Use clinical judgements for intubating rather than using blood gas values and also if the predicted course of the pathology is expected to worsen rather intubate after proper resuscitation with use of blood products before use of pressors…
Brilliant discussion there,few points since iv been caught many tyms between ED/OR for hemorrhagic cases and intubations 1. Ketamine is best way to go but it can have cardiodepressant effect in grade 3 to 4 hem shocks where there is catecholamine depletion setting in 2.already lactates high, u dont want to wait and let respirstory muscles fatugue causing further resp( co2 accum) plus muscle fatigue lactate ( metabolic) acidosis 3.RSI is best ,i want airway secure, aspiratiin from full stomach & altered mentation of shock 4. Id require direct vasopressors than indirect ones cuz cats already depleting. Ketamine needs catecholamines… Read more »
appreciate your comments!!! I have a review of the putative cardiodepressant effects of ketamine in the works–I have reviewed all of the extant literature for this work. I have yet to find any clinical evidence of the oft stated idea of negative inotropy at commonly used doses. At the doses that are actually required to dissociate patients in the midst of critical illness, I cannot imagine any cardiodepressant effect. We now have RCTs demonstrating hemodynamic stability in very sick patients–I predict, the catechol depletion unmasking neg inotropy idea will fall away just like the increased ICP myth, For #5–that was… Read more »
I’d like to thank you guys for this post—it makes me think about the various tools/meds/methods to handle these cases. I’ll add this. I want monitoring. I want an arterial line. I want an IV larger than an 18 gauge or the IO. Of course, I want it all!! (JK). Charge ahead without proper IV access and monitoring and you’re off to the races with CPR. With ultrasound, this should not be such an obstacle to obtain appropriate IV access and an arterial line. Nice blog entry—thanks again!
Hey Jim! Thanks for listening and for your comments brother. Agree and in general if there is time Arterial Lines are invaluable in these patients. By the way we did place a femoral A-line in the patient that sparked this discussion. Yup need bigger than 18’s and IOs just simply do not cut it for these patients at all. Blood is just far too viscous to flow through the bone marrow with any reasonable alacrity. I’m with you 100% re: US-guided lines but just to be clear for the readers bc I think this needs to be said (I know… Read more »
Given resuscitation with blood products, which pressors are you choosing in a RSI scenario? Vasopressin? Push Phenyl?
Hi, Peter. Neither of those options although we do have decent evidence that these patients probably eventually become catecholamine depleted and Vasopressin in particular may be a good choice later on. But in this ultra acute phase I think Epinephrine probably has the best overall physiologic profile for the purposes of RSI.
Thank you for a great post, and an interesting discussion. I have long taught trainees (and been taught at LAC) that RSI should occur in OT, so it was interesting to get some different insights. I work in Sydney where the experience of large volumes of patients in haemorrhagic shock patients is low (in comparison to other busy places) per centre. So therefore I often encounter anaesthetists using quite liberal amounts of metaraminol (alpha agonist sim to phenylephrine) to counter the effects of their choice of anaesthetic, usually propofol (!!) plus inhaled gas. I have mentioned considering these patients similar… Read more »
Matt, see the old podcasts with Rick Dutton on the site–they discuss this intensely. TLDR-avoidance of vasopressors in young patients with intact catechol system is the way to go. In fact, gently shedding their endogenous catechols is the goal. In older pts, things may shift as they may have a vasodilated milieu.
Thanks for the great discussion! Just one thought on the point that forceful inspiration helps venous return. I’ve come across some animal studies & clinical trials showing higher BP with the use of ITD, but I doubt how much those results can apply to the patient population you’re discussing i.e. a young & fit patient in extremis struggling to compensate for the exsanguination. No doubt if the patient is only moderately hypovolemic then forceful inspiration may help by lowering RAP. However if the patient is already in extremis from hemorrhage, his Guyton’s venous return curve is likely very downshifted that… Read more »
v. nice comment! would agree in isolation. but remember, we are not just sitting there. this patient would be receiving large volumes of blood product and will be constantly shifting from severe to moderate hypovolemia. the functional blood volume of these patients given their enormous endogenous catechol surge can be shifted with even a unit or two. we see this consistently when pts vacillate between 60/40 to 130/100 back and forth with each unit and then further rebleeding
I believe the transient improvement in BP reflects a different part of the physiology. When a patient actively inspires, the cardiac function curve shifts leftwards. So if you aren’t breathing hard enough then adding an ITD moves the CF curve more to the left so it intersects VR curve at a point with higher CO. However, if the young patient is already in extremis he’s likely maxing out his resp effort (red dotted line) so any additional resistance likely only increases WOB but does not increase CO as it’s on the flat part of VR curve already (purple dotted line).… Read more »
based on that logic, the ITD would never help a young patient then, which goes against the evidence we actually have on ITD in which all of the patients were young. They still must be somewhere on the up slope of the CO part of the curve not the plateau despite their bodies maximal efforts at respiration
withdrawn
Hi Emily. Sorry, no idea what that means! 🙂
Great discussion! I wonder how feasible an fiberoptic awake intubation is in an hemodynamically unstable patient. Everyone would be busy enough putting in IVs, getting the Ranger high flow setup and resuscitate. At my clinic an awake intubation is an whole endeavour with preparations and we don’t have a fiberscope in the ER. Is there an Emcrit podcast of urgent awake intubation?
Yes, just search for Kovacs and awake intubation and you will find. Takes less than 2 minutes prep. But in these circumstances I would much rather do video laryngoscope awake rather than bronchoscopic
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If this patient (as you described) has a cardiac arrest, as a direct result of their severe hemorrhagic shock, would you expect to see an ETC02 during CPR? If not, would you expect there to be a critical threshold for which you would need to transfuse in order to use ETC02 to guide resuscitative efforts? ( I understand the utility of cpr in traumatic cardiac arrest is controversial and I’m not looking to open up that can of worms). Thanks!
During cardiac arrest as long as your equipment is functioning and your tube is in the airway you should theoretically get ETCO2 whether CPR is ongoing or not (several studies showing that even cadavers will register end-tidal). Having said that I have seen scenarios where end-tidal ceases to register when compressions are held–so I think that depends on your specific equipment. But the answer to your question is definitively yes you should see ETCO2 during CPR.
There are situations of exsanguination so severe that there is no blood flow even with compressions–in this case there is no ETCO2–those patients are irreparably dead.