Great post Scott!

I had a few thoughts:
1) What about topical lidocaine or IV lidocaine? The last hemodynamically unstable pt I intubated (critical AS with hypoxia/resp failure and hypotension) I only used lido spray and 0.1mg epinephrine to intubate. A quick topicalization and suction can smooth over some of the analgesic and lack of paralysis (laryngospasm) that may occur from underdosing.

Also, my limited experience with IV lidocaine is that it acts basically as a GA agent, and it reduces the dose of other induction agents you may need. It seems to be fairly cardiac stable, and may have some additional benefit in TBI/ICP patients.

2) If you are giving high-dose sux or high-dose roc, why not just give the roc? There is no chance of MH-reaction, and also less risk of masseter muscle spasm and sux is the most commonly implicated agent for histamine release or anaphylactoid reactions.

Question? Could you give a small dose push dose pressor epi since there is likely some hypotension to develop…working in small increments to prevent the hemodynamic instability before it actually occurs…

Hi Dr. Weingart,

Awesome podcast to listen to after intubating a septic patient last night. If patient does not have a central line, when they need to be intubated, do you suggest still having norepi at the bedside during peri-intubation? And giving it via peripheral line if necessary?
Do you give your push dose pressors via peripheral lines?
In the peri-intubation period, with the norepi at bedside, how long do you wait for fluid response before starting norepi? If MAP is not at 65 after intubation, are you just starting norepi along with keeping fluids going? Even if you have not given 2 liters of NS?
Thanks a million.
Awesome lecture.

Hi Dr. Weingart,
With Ketamine what is your middle ground dosing? I heard the dissociative dose of 1-2mg/kg but do not think you mentioned the middle groound dose. Thanks!

I’d like to say…thankyou

Wow. I thought I knew what to expect with this month’s cast but you went above and beyond my expectations. Additionally the graphics were a really cool treat. Thank you.

Hi Scott. I like you prioritizing life before awareness, but what is the difference between memory and awareness???

how you monitor blood pressure? we are used to go with 2.5 minutes interval. what do you think?

Ditto on the “Thank-you and cool graphics”.

Great lecture. An additional reason to not use etomidate is that it cannot be used as an infusion. There is a false sense of security in relying on a short acting hemodyndamically “inert” induction agent and then often having an intubated patient without adequate sedation/analgesia out of fear of other using other agents in an unstable patient. Makes more sense to go through the initial intellectual exercise of selecting appropriate analgesics and induction agents for a specific case that can be titrated after intubation for an adequate analgesia/sedation package.

Thanks Scott, Listening to this has given me alot more insight into a recent case. We had a 15month present to Janus Hospital in what looked like septic shock. She was RSI’d with ketamine and sux and promptly went into cardiac arrest requiring CPR. She had good CPR, and responded the the adrenaline, and went on to inotrope and vasopressor infusions. Turns out she had myocarditis. One of the discussions around this was that she already had a sympathetic overdrive, and the ketamine further pushed her sympathetic system, beyond its capacity and hence she arrested. And this was / is the main reason some of the intensivists I work with would not have used Ketamine. Realistically the dose of ketamine was more than you suggest and this is the likely mechanism. Do you think you would use ketamine in this situation? Is there basis to the above explanation?

Amazing podcast, thanks so much for putting it out.

I was intrigued by the 90% reduction in propofol dose for hemmorrhagic shock. Have you come across any studies looking at sedative dosing in other forms of shock? Sepsis for example? If not what does your experience tell you?

This is fantastic! We still use allot of “normal dose” thio around these parts, which, oddly enough, leads to quite a bit of hypotension.

I’ve finally gotten around to translating this into “Kiwi” It would be great to hear your comments.
http://www.thesharpend.org/eeacc-5-airway-pharmacology

Scott,
I love what you are doing, keep on doing it man! So as a third year at my program at henry ford, we do evidence based lectures. My topic is podcasts as teaching tools. Some push back I get from older attendings is “well they are not peer reviewed” and “how do you know they are evidence based?” One of my favorite ‘casts of yours is the hemodynamics kills (intubating the shock patient) one. So what I have chosen to do as part of my lecture is break down your podcast and look at the evidence you use to support this. Regarding this I have 2 specific questions:

1) You saw all induction agents will drop the pressure in shock patients. I love your analogy of NIN to bob marley! Theoretically, it makes sense. While you present evidence for and against this, it is by association. Do you have any direct causation evidence (i.e., looking at physiologically there is a loss of sympathetic surge once these patients are “induced”)?

2) your choice to use a lower dose of ketamine than the standard. any direct evidence or more anecdotal?

Thanks Scott!

Eric Einstein

What induction agent do you use for post cardiac arrest patients? Does the sympathetic surge from ketamine increase the risk of further dysrhythmia?

Hi Scott,

one issue with middle dose ketamine I experienced is that some patients are still awake during the intubation period. They eventually received an additional small dose of etomidate and are fine. I prefer Ket because I haven’t seen any periintubation hypotension patient since I started using it instead of eto.
But what is the issue here with patients receiving Ket at your recommended dose and being awake?