Intubations the shock pt

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bkell101

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http://emcrit.org/podcasts/intubation-patient-shock/

Came across the above podcast....very entertaining speaker

If you have the chance to listen to it...

Overall, what are your thoughts?

He doesn't seem to like etomidate ( more for dosing reasons than adrenal supp), do you share the same opinion?

He is a proponent of ketamine in this podcast.

Does anybody else routinely use ketamine for the shocked pt?

Is what he says regarding the dosing and the myocardial depression associated w/ketamine true?
 
Overall, what are your thoughts?

Good lecture. I agree with essentially everything he presented.


He doesn't seem to like etomidate ( more for dosing reasons than adrenal supp), do you share the same opinion?

I do not use much etomidate in septic shock patients. I favor greatly reduced doses of propofol, or ketamine if it's within arm's reach. The whole adrenal suppression thing probably doesn't matter, but I don't see a good reason to use etomidate in those cases.

I will say that in the last year, during a trauma sabbatical of sorts, I used a ton of etomidate in hypovolemic shock patients, for reasons mostly related to institutional inertia and availability in the trauma bays, and it was Just Fine.


He is a proponent of ketamine in this podcast.

Does anybody else routinely use ketamine for the shocked pt?

Is what he says regarding the dosing and the myocardial depression associated w/ketamine true?

I love ketamine.

I don't know if the exacerbated hypotension you will see using ketamine as an induction agent for very hypovolemic or septic patients is due to direct myocardial depression (doubt it) or a result of a reduction in circulating catecholamines from the brain going from freaked-out to asleep (probably), but it absolutely does happen. Any and every induction agent will worsen hypotension in a patient living at the edge of his physiologic reserve.

It was nice to hear him state unequivically that ketamine is OK in head injury patients who aren't in Cushing response territory (ie it's OK for patients who are hypo- or normo-tensive). I had this conversation with our neurosurgeon and the rest of my department over in traumaland but they were dubious, and I didn't care enough to press the issue. But ketamine is OK for head injuries, provided you're sane about keeping the patient's hemodynamics reasonable.


Concerning the specific case of hypovolemic shock, my $.02, having recently done a lot of trauma in a setting where anesthesia received and managed patients in the ER trauma bay, and many patients were deep into hypovolemic shock from blood loss -

It doesn't matter one little bit what induction agent you use (or even how you use it most of the time!), because the best course of action is almost always to wait to induce/intubate until after the Belmont has run in a bunch of blood and resuscitated the patient.

There's rarely a need to secure the airway immediately, the only real exceptions being combative/dangerous patients and those with oxygenation/ventilation problems. People are excitable and everyone's in a hurry, but we don't have to be. If bleeding is controlled, there's no rush. If bleeding is uncontrolled (ie chest/abd/pelvis), there's still no rush to intubate, and what you probably want to do is get to the OR, get on the table, get the patient prepped and the surgeon ready to cut, then everyone can rush to intubate/operate at the same time.

We routinely got adult patients with HR of 150+ and systolic BPs under 80 with 1-4 tourniquets in place, and/or ongoing internal bleeding from chest/abd/pelvic trauma. Even so, we were always able to get a line and resuscitate the patient prior to induction. 4-6 units of red cells and 4-6 of FFP through a Belmont and subclavian cordis made choice of induction agent almost moot. We sometimes had to tell people to just relax and WAIT in the trauma bay for a few minutes while the blood went in.

We usually used propofol or normal doses of etomidate, after resuscitation. For patients who were still unstable despite aggressive transfusion, ketamine ... or scopalamine.


Other good points from the podcast:
- the vasopressor to have in your pocket, diluted and ready to push, is epinephrine not phenylephrine
- be careful with vent settings after intubation
 
Trauma is one of my areas of interest because how we manage the patient can have a significant impact on how the patient ultimately does. I also practice at a pediatric level 1 trauma center, so we get some train wrecks.(literally)
This is how I've been doing trauma/septic patients forever. I'd give the same lecture. I wonder if we were trained by faculty that trained/practiced together.
It's worth noting that even low doses of ketamine (0.5mg/kg) can cause significant hypotension in the major trauma patients that are catecholamine depleted, and I avoid any opiates in that group until after securing the airway and seeing that they are stable on the vent. Unlike the cardiac and sick but stable NICU cases that get an opiate based anesthetic. A 0.5-1 mcg/kg epi kiss with induction and starting an infusion in these patients can make a big difference when there is no time to fluid resuscitate properly to normotension prior to securing the airway.
 
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I wanted to emphasize the no opioid until more stable one more time. You might be tempted to think, "what's the harm, a little fentanyl, I use it in my sick cardiac folks every day, no problem..."
It can be a BIG problem in the circling the drain septic folks and empty heart trauma guys. If they're a little tachy and hypertensive after intubation, GOOD!!
 
Good lecture. I agree with essentially everything he presented.




I do not use much etomidate in septic shock patients. I favor greatly reduced doses of propofol, or ketamine if it's within arm's reach. The whole adrenal suppression thing probably doesn't matter, but I don't see a good reason to use etomidate in those cases.

I will say that in the last year, during a trauma sabbatical of sorts, I used a ton of etomidate in hypovolemic shock patients, for reasons mostly related to institutional inertia and availability in the trauma bays, and it was Just Fine.




I love ketamine.

I don't know if the exacerbated hypotension you will see using ketamine as an induction agent for very hypovolemic or septic patients is due to direct myocardial depression (doubt it) or a result of a reduction in circulating catecholamines from the brain going from freaked-out to asleep (probably), but it absolutely does happen. Any and every induction agent will worsen hypotension in a patient living at the edge of his physiologic reserve.

It was nice to hear him state unequivically that ketamine is OK in head injury patients who aren't in Cushing response territory (ie it's OK for patients who are hypo- or normo-tensive). I had this conversation with our neurosurgeon and the rest of my department over in traumaland but they were dubious, and I didn't care enough to press the issue. But ketamine is OK for head injuries, provided you're sane about keeping the patient's hemodynamics reasonable.


Concerning the specific case of hypovolemic shock, my $.02, having recently done a lot of trauma in a setting where anesthesia received and managed patients in the ER trauma bay, and many patients were deep into hypovolemic shock from blood loss -

It doesn't matter one little bit what induction agent you use (or even how you use it most of the time!), because the best course of action is almost always to wait to induce/intubate until after the Belmont has run in a bunch of blood and resuscitated the patient.

There's rarely a need to secure the airway immediately, the only real exceptions being combative/dangerous patients and those with oxygenation/ventilation problems. People are excitable and everyone's in a hurry, but we don't have to be. If bleeding is controlled, there's no rush. If bleeding is uncontrolled (ie chest/abd/pelvis), there's still no rush to intubate, and what you probably want to do is get to the OR, get on the table, get the patient prepped and the surgeon ready to cut, then everyone can rush to intubate/operate at the same time.

We routinely got adult patients with HR of 150+ and systolic BPs under 80 with 1-4 tourniquets in place, and/or ongoing internal bleeding from chest/abd/pelvic trauma. Even so, we were always able to get a line and resuscitate the patient prior to induction. 4-6 units of red cells and 4-6 of FFP through a Belmont and subclavian cordis made choice of induction agent almost moot. We sometimes had to tell people to just relax and WAIT in the trauma bay for a few minutes while the blood went in.

We usually used propofol or normal doses of etomidate, after resuscitation. For patients who were still unstable despite aggressive transfusion, ketamine ... or scopalamine.


Other good points from the podcast:
- the vasopressor to have in your pocket, diluted and ready to push, is epinephrine not phenylephrine
- be careful with vent settings after intubation


Thank you for the awesome response.

I was able to see the Belmont yesterday in action for the first time while on one of my last "shadow calls" As a ca-1...really impressive

We took the same approach you described...patience with the airway...we put in a ton of volume before inducing

Epinephrine over neo because of the beta/improvement in cardiac output?

Also, at my institution we use either push dose neo or ephedrine on a routine basis....I understand basic miller type stuff about ephedrine, but why not use a diluted eppi?
 
Epinephrine over neo because of the beta/improvement in cardiac output?

Yes, in a hypovolemic patient, you want the tachycardia and extra inotropy. Assuming they were previously healthy they're already nearly maximally vasoconstricted, not vasodilated. In those cases the pure alpha from phenylephrine isn't as helpful, and might not perfuse the brain as well as something with some beta effects.


Also, at my institution we use either push dose neo or ephedrine on a routine basis....I understand basic miller type stuff about ephedrine, but why not use a diluted eppi?

Neo is a great choice in the normal anesthesia/OR world, because almost all of the hypotension we see in the OR is iatrogenic, and most anesthesia-related hypotension is vasodilation. Volatiles cause it, so do sympathectomies from spinals and epidurals. A pure alpha vasoconstrictor makes a lot of sense there.

But there is nothing inherently wrong with diluting epi down to 10 mcg/mL and giving a cc or two at a time instead of ephedrine. It won't last as long, and the double-dilution is an extra step, so generally there's not much reason to do so. But I think residents should get comfortable with using small doses of epi, if for no other reason than to break themselves of the feeling that epi is a 'big gun' to only use when the case is going to hell.

Next time you're about to give some young healthy outpatient 5 mg of ephedrine, try 10 mcg of epi just to see what happens. (You should generally make a habit of trying different stuff all throughout residency.)
 
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