In Podcast 104, we discussed how to avoid killing hemodynamically unstable patients while intubating. Today's podcast takes that concept a step further to allow you achieve a hemodynamically neutral intubation.
The Pieces
Rapid Sequence Awake
Discussed in this podcast
or
Dissociated “Awake” Intubation
or
A Combination
then
you can consider a DSI for Hemodynamics, but only in non-tenuous patients
then
place the patients on CPAP/PSV mode with both set to zero
if the patient requires mechanical ventilatory support because they continue to decline, consider
Higher Vt/Lower Rate as per Davis et al.
and
Sedate with small hits of ketamine or fentanyl
Further Reading
Additional New Information
More on EMCrit
- Podcast 104 – Laryngoscope as a Murder Weapon (LAMW) Series – Hemodynamic Kills(Opens in a new browser tab)
- Podcast 173 – LaMW – Oxygenation Kills Part I(Opens in a new browser tab)
- Podcast 174 – LaMW – Oxygenation Kills Part II(Opens in a new browser tab)
- EMCrit 3 – Laryngoscope as a Murder Weapon (LAMW) Series – Ventilatory Kills – Intubating the patient with Severe Metabolic Acidosis(Opens in a new browser tab)
- Podcast 129 LAMW: The Neurocritical Care Intubation
Additional Resources
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- EMCrit 373 – Mike Weinstock with another Critical Care Bounceback: “Asymptomatic Hypertension” - April 18, 2024
- EMCrit Wee – Ross Prager on 10 Heuristics for the New ICU Attending - April 13, 2024
- EMCrit 372 – FoundStab Intubation SOP - April 5, 2024
Great great episode, Already commented on Twitter but I guess it is better to do it here.
Some topics that I would like to clarify:
– Remifentanil for sedation… I know you dont have it, but here in Argentina we do use it a lot.
– Impact of ket on very elderly / fragile folks, is it really so dangerous?
– Risk of adrenal supression with etomidate, real impact?
– In case I use a push dose pressor, what would be your choice and in which dose?
Again, congrats on a great work!
Best
Fede
no impact (neg impact) on anyone if they are hypotensive, when using doses I describe
etomidate’s adrenal suppression has not shown pt important outcomes, but i see very little use for this drug.
see the push-dose pressor update episode
Dr. Weingart, can you explain how CPAP and PS at Zero does anything? Does the ventilator provide any support?
With the PEEP & PS at 0, the vent would do exactly nothing, which is actually one of the big points in (an expert level player) using the approach described. As he explained in the beginning the 3 causes of peri-intubation hypotension are: vasodilatory effects of sedatives, loss of sympathetic drive with sedatives, and conversion to positive pressure ventilation, and this approach is designed to avoid them all to the degree possible. Any degree to which the ventilator supports the pt is positive pressure ventilation (whether a little w/ something like PEEP 0, PS 5 or a lot w/ something… Read more »
I understand WHY, I’m wondering what if anything the vent does. With Zero pressure support and PEEP, what does the ventilator do, if anything? Does it just open the valves to allow the flow of gas?
Gotcha. Yeah, it should just open the circuit (I’m sure there would be specifics for each particular vent that reps/RT’s might know). You could, of course, still control FiO2, and it would calculate VTe, minute ventilation, etc as normal with alarms/back up rates in the case of hypoventilation or apnea depending on the ventilator’s backup settings and your alarm settings. I’m sure it would still have all the same indicators of pt effort, too (familiar w/ LTV1200 which has a pt effort light, I know some hospital vents show that with different colors of waveform). I’m not an expert at… Read more »
I am not so sure this is correct. Setting a pressure support of 0 implies that a pressure of zero will be maintained in the airway circuit. Spontaneous breathing is performed by generating a negative pressure, not a zero pressure. That makes me think that a PS of 0 would actually be offering just enough pressure to “counter” the negative inspiratory force. It’s less impactful than having a positive pressure >0, but more than being open to air with something like T-piece.
that is not how Press Support Works.
I could be wrong; tell me how! I think it is a common misperception that pressure modes on the vent (or even on a non-invasive device, other than very simple ones such as those sometimes used by EMS) generate some sort of fixed pressure head at the inlet. But in my understanding this is wrong, because the actual pressure created in the airway would then be arbitrary. In reality, pressure modes adjust the flow rate until the pressure within in the circuit reaches the target pressure, then hold it for the set inspiratory time (or in pressure support, hold it… Read more »
Well the main way is regarding a setting of zero on PS. If you set it to zero, the system doesn’t attempt to maintain a Paw of zero, it actually deactivates PSV. A vent set to PSV 0 and CPAP 5 becomes a pure CPAP mode–there is no alteration of what happens during the insp. phase through PSV. As to the rest of your description of PSV, yes–accurate, but non-germane. Not sure what any of that has to do with the ? at hand. Discussion was what happens when you set PS to 0. Perhaps to reinforce this, a setting… Read more »
Just trying to make sure we’re on the same page. I guess the crucial question is how the vent behaves specifically with a PS and a PEEP both set to zero. I agree that there is utility to a mode that actually “opens” the circuit and turns it into a virtual T-piece, but that would be a qualitative difference in behavior compared to how PS works in all other situations — in other words, changing the PS from 2 to 1 would mean something very different from changing it from 1 to 0. And it may be. If you’ve looked… Read more »
Great stuff, Scott.
I am sceptical about the point you make around 18:40-1855, if you are talking about patients with massive PE. These folks have high pco2 (because they have high dead space) and resp acidosis will make their pulmonary hypertension worse if you pay no attention to the pco2 with you mechanical ventilation strategy
Petros,
If you parse your comments you will see they are self-contradictory
As always, fantastic post. I had a comment in general to a somewhat common theme in your podcasts when you talk about an “evidence-free zone” or are talking about “studies” on a particular intervention without direct conduct in an RCT. You’ve said before “I don’t want to do the trial unless no one else will” and something *loosely* to the effect of “I’d rather evaluate someone else’s trial and make my own judgement on how to adapt my practice”. In fact, in one of your episodes you openly responded to critiques from a Letter to the Editor about one of… Read more »
Dave,
I think you will be very happy with the KeyLIME podcast from the ICE folks.
Anyone using IV scopolamine as a sedative for these types of intubations? I’ve also seen some of my mentors trial their push dose pressers before intubating. On patients who are on the borderline and not on pressors yet we’ll give a 100mcg of phenylephrine — if it works ,great, if not, we’ll prepare another press or infusion and have it running before the intubation.
mentioned during the original hemodynamic kills podcast
An interesting post about a very common but least discussed issue. My query is how do u use ketamine even in the low dose that u describe in a patient whose heart rate is already around 150 beats / min. I have precipitated arrhythmias in a few patients. I use fentanyl alone along with topical lido.
What is the blood pressure or another marker based on which u switch in r initial ventilation settings
HI Scott
I’d not intubate the crashing PE ( Even the presumptive crashing PE), with RV dilation on bedside scan – I’d push tenecteplase, yes the next 2-3 minutes are a little tense – especially convincing , junior’s to wait, but generally their saturations and BP improve after that.. Likewise with a tamponade, they don’t need an airway, they need the tamponade drained, and if too unstable to go to the lab then that’s done in the resus room.
However for severe crashing sepsis this is a useful approach
Thanks for the podcast Scott, intriguing topic. Lignocaine topicalisation of the airway is very effective for removing the gag/cough reflex to an ETT in-situ. We do it all the time for awake fibre-optic intubation. But I don’t believe having insensate mucous membranes around the larynx/pharynx will ablate the sympathetic response to laryngoscopy. The difference being that laryngoscopy causes subluxation of the mandible and significant pressure on the hyo-epiglottic ligament. Just like the mandibular movement from an aggressive jaw thrust is stimulating enough to wake up a sedated patient, even though there is nothing in their pharynx/larynx. It may be possible… Read more »
Daniel–I’m not sure I understand your intent. This is a post on hypotensive/shocked patients,why would you want to avoid sympathetic stimulation?
extraordinary, scott.
thank you
You’ve mentioned dexmedetomidine in previous airway lectures. Would you consider that to provide patient comfort once the tube is in, +/- additional topicalization down the bronch? I wonder if this would avoid any potential hypotension issues associated with opiates, although I think highly of Dutton’s fentanyl-based approach.
i still like ketamine initially. once you stabilize them then give them what you want–and that is the goal-fix the reason for the hypotension