Weingart on hemodynamic assassination due to intubation
- preintubation hypotension = primary risk factor
- primary physiology = loss of catechols & transition from negative to positive pressure (reduces preload)
- @emcrit at #HRreloaded
Protective pathway for intubation
- separate out dissociation vs. paralysis
- 1st titrate ketamine to unawareness (ensures adequate dose but not too much)
- 2nd paralyze with high dose (2 mg/kg roc!) - ensures rapid onset
- @emcrit at #HRreloaded
Hemodynamically *neutral* path avoids rapid transition from negative --> positive pressure
- Purest form = awake intubation
- Addition of ketamine may facilitate in agitated pt
- Bronchoscopic intubation may involve least stimulation
- @emcrit at #HRreloaded
Hemodynamically neutral pathway 2/3 - key is after intubation do *not* put paralyze & place them on positive pressure ventilation. Allow patient to continue breathing on their own! Ongoing negative-pressure ventilation on the ventilator 🤯
- @emcrit at #HRreloaded
Hemodynamically neutral pathway 3/3 - Drawback of not providing vent support is that patient is doing the work of breathing. So as the patient stabilizes over time, you may *gradually* up-titrate the amount of positive pressure and ventilator support.
- @emcrit at #HRreloaded
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how to place a consult: you MUST understand the five stages of consultant grief.
once you can understand this painful and natural process, requesting consults will make a LOT more sense
buckle up, it can be a little rough…
🧵 1/6…
stage 1: denial
- You dont need a consult.
- You called the wrong service.
- 18 years old? consult pediatrics
- I’m not actually on call now
- Everything’s fine, just walk it off…
stage 2: anger
- you should have consulted us earlier/later
- you should have checked this test before calling us
- you’re a terrible doctor/student/human being
this is much better than MINDS (which contained ~90% hypoactive), but probably still not ideal.
(at this point, does anyone actually think that haloperidol helps with hypoactive delirium ??)
other than dilution of the patient population by patients with hypoactive delirium (who are unlikely to benefit & might conceivably be harmed by over-sedation), the methodology seems pretty solid.
I think it's time for a difficult discussion, folks.
Let's talk about CSF lactate 🫣
CSF lactate has been shown to be *superior* to traditional CSF studies in sorting out viral vs. bacterial meningitis in several studies & meta-analyses...
a subset of patients with viral meningitis will initially have a *neutrophilic* pleocytosis.
this can lead to unnecessary admissions & antibiotics
some patients are subjected to repeat LPs 😩
a low CSF lactate could avoid all of this, allowing patients to go home from the ED
CSF lactate measurement is recommended in guidelines from the United Kingdom, Europe, and France.
(it's not recommended in the ID society of America guidelines, but they're from *2004* and require revisions)