16 Replies to “Episode 97: Waking up”

  1. Something I have seen from time to time is the use of low dose ketamine, or dexmedetomidine infusions for waking up pediatric patients, and/or agitated patients. This is strictly observational and anecdotal, and I’m unsure of the current evidence. I know there has been literature for ICU patients and using dexmedetomidine (https://www.ncbi.nlm.nih.gov/m/pubmed/26975647/) but unsure how that translates to the OR.

    Great episode as always, thanks again for your work! Maybe an episode expanding this topic could be “delayed extubation” and a systematic algorithm for working through a diagnosis.

  2. Awesome episode as always!

    Though it may be blasphemy among some practitioners or institutions, if I’m using a volatile anesthetic, I’m personally a fan of finishing off a case with nitrous. I find that if a patient has enough analgesia on board, has been given appropriate antiemetics, and of course, it is timed correctly, emergence can be comparable in smoothness and clarity to to a “remi wake-up.”

    Another strategy I will sometimes utilize for emergence, that I believe to be reasonably common among anesthesia practitioners, is actually to do the opposite of trying to get the patient to breathe. That is, I will over-breathe the patient by increasing their minute ventilation in order to decrease their PaCO2, and therefore respiratory drive. This potentially accomplishes three goals:
    1. By decreasing the patient’s respiratory drive, they may not try to breath or move, and remain relatively motionless for the less stimulating final moments of a procedure.
    2. Increasing minute ventilation, (specifically by decreasing tidal volumes and increasing respiratory rate) in combination with increasing fresh gas flows, decreases the time constant of both the circuit and the lungs, and therefore a more rapid decrease in the concentration of volatile anesthesia remaining.
    3. The time it will take for a decrease in alveolar concentration of volatile agent is not especially predictable. However, the rate of rise of pCO2 in an apneic patient is quite predictable. The PaCO2 of an awake, preoxygenated adult with normal lungs rises 7 mm Hg/minute for the first 10 seconds, 2 mm Hg/min for the next 10 seconds, then 6 mm Hg/minute afterwards [Stock MC et. al. J Clin Anesth 1: 96, 1988], so essentially 6 mm Hg/min or 1 mm Hg every 10 seconds. With this knowledge in mind, I will attempt to rid the patient of the less predictable variable of decreasing volatile anesthetic concentration by driving the end-tidal volatile anesthetic concentration to zero. And then knowing that my patient will start to breath again in just 2-3 minutes (if they are not over narcotized or have residual neuromuscular blockade).

    I like to use this strategy in combination with nitrous, and I find it especially useful if I have somewhat mistimed my emergence, and am in a bit of a “hurry” to decrease the patient’s concentration of volatile anesthetic!

    I also like using dexmedetomidine for emergence for certain patients. I find it to be great to reduce agitation, and some bucking/coughing. I would describe the result as a calm and smooth emergence, but a little bit at the sacrifice of clarity and rapidity of meeting PACU discharge criteria.

    1. Great points Steven. The one thing I would slightly disagree with is the rate of rise of CO2. The study by Stock was in AWAKE apneic people. Under general anesthesia, the pCO2 increase is not as rapid because not as much CO2 is produced. However, your point is still valid. CO2 will always rise when you make a patient apneic, and it will rise reliably and relatively quickly. So breathing off anesthetic gas by hyperventilating and then allowing CO2 to rise is a perfectly reasonable approach.


  3. As always very interesting to hear other tactics.

    Totally concur with Dr Wolpaw about communication with the operators.

    Where I work the surgeons tend ( basically because I always asked) to give a heads up when they are getting near the finish and the estimated time to end of closing. It just makes life so much easier. While that is nice I try to basically know the steps of the all the procedures that are done.It’s a great help to know when the case is going to end so you can plan and work towards wake up, but also know when there will be major bleeding (spine cases come to mind that can have a very specific window of profuse bleeding) or when a more painful stimulus can expected .

    In Germany it is very common to do arthroscopic surgery and all kinds of minor surgery under general anesthesia. So >50% of cases I run are short and use an lma whenever I can. In Europe the use of LMA’s is maybe a bit more liberal than in the US, but I like to use LMA’s even in morbidly obese patients. My experience with obese patients of around 100kg is absolutely unproblematic compared to normal weight patients (they work mostly better than on thin people) as they tend to seal very well. My heaviest patient I had so far was about 450 lbs and and needed a short 20 min general anesthesia which was just done on sevorane with relatively high mac and a tiny bit of remifentanyl with spontaneous breathing in half sitting position (I use extra restraints to keep the legs in check in case of unrest at emergence).

    Generally using an LMA makes wake up a lot less complicated as there is no relaxant and it tends to induce less bucking so you can stimulate them a bit and pull the LMA and say hello.

    Is there any upside of isoflurane vs sevoflurane outside of cost ?

    1. Thanks JM,

      One potential upside of iso compared to sevo: you can run very low flows with iso, so less waste, less cost, friendlier to the environment, keeps the air warmer that the patient is breathing, etc. Sevo, as you know, needs to be run at least 2L/min to prevent the development of compound A.

      1. I was unaware that compound A is deemded relevant in the US

        In Germany ( and Europe) it is routine to run 0.5 l/min (down to 0.35l) of O2 flow with Sevorane.The consensus is that compound A has no clinical significance as the levels for nephrotoxicity is 800 ppm/h is a factor 20 higher than what is encountered clinically regardless of flow.
        There has been pretty much no further research into the clinical effects since 2000.(I. Mazze et al. Anesthesia & Analgesia. 90(3):683–688, MAR 2000 (stanford) did a 22 center study. and stated that “Additionally, no trends specific to sevoflurane were observed with respect to postoperative serum creatinine concentration and fresh gas flow rate, concurrent treatment with nephrotoxic antibiotics, or type of carbon dioxide absorbent. Implications: Our data for changes in serum creatinine and blood urea nitrogen indicate that, for exposures of less than 4 minimum alveolar anesthetic conc”

        Given that this has been standard practice for about two decades in Europe (meaning several million cases) and we did no end up with droves of people on dialysis I think it might be time to re-assess this dogma for OR use.

        That said a more cautious approach in kidney transplants or people with marginal kidney function seems prudent although there is little data to support this practice.

        1. i the qoute is missing this: sevoflurane is not associated with an increased risk of renal toxicity compared with other commonly used anesthetics

    1. Hi Hosam,

      I’ve never used it and don’t think we have it here but I’d be interested to hear if anyone else has experience with it.


  4. Fantastic episode. Not only does a good wake up look slick, it dramatically improves safety immediately postop, upon transport, and in Pacu.
    To me, the Sedline is a must. You wouldn’t look at the HR without the EKG, so why look at a patient state index worjout the underlying waveform (both hemispheres)? Titrating to age and BP just isn’t going to get it done this day in age. There are plenty of times using EEG isn’t possible (crani, small surgery center); the info learned from hundreds of EEG-assisted anesthetic is invaluable, and helps guide anesthetics where use isn’t possible.
    Again, just a tool, but technology is getting better and better. We have to get better and better.

  5. Thank you for the episode. Would be better if a little more evidenced-based. Really good lecture for a junior resident I think. In this era of opioid-sparing ERAS protocols, I’d personally like to hear an updated podcast on wake-ups. One note: turning off lidocaine gtts completely an hour out is perhaps not ideal if the goal is a smooth wakeup. Thank you again.

  6. To make sure the patient is breathing on his own I don’t ever put him off the ventilator to the bag, and this is most important for COPD or obese patients who really benefit of uninterrupted PEEP ventilation. We use GE machines that instead allow us to turn the support to zero in pressure supporte mode, without modifying the PEEP setting; maybe other ventilators don’t allow this.

    1. I think that makes sense unless you are worried that the patient may not actually be breathing. If, for example, cardiac oscillations or surgeon motion is triggering the PSV breaths it may look like the patient is breathing when they aren’t. And by closing the pop off valve part way you can give peep while on “the bag”.

      1. No, with the support turned to zero there is no PSV to trigger, and all you see is the genuine patient activity above a fixed PEEP. Any variation in the circuit pressure due to other causes (heart beat or external compression) will trigger a zero pressure breath, so no flow at all given by the machine.

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