Ignoring the very strong anti-CRNA bias that seems to be the main point of the article (the author probably doesn't know any different and was clearly spoon fed by highly political anti-CRNA anesthesiologists).......FWIW I actually did 6 EGD's this morning, without an anesthesiologist within 30 miles.....remarkably, everybody survived.
The first case illustrates a couple important things that do relate to prehospital airway management:
1. The hazards of sedation cases. Many people have the attitude that "it's just a sedation case - no big deal - it isn't like you are going all the way to sleep" but a higher rate of anesthesia related complications happen during sedation than during general anesthesia. EGD's can be especially difficult because you often don't have immediate access to the airway, and because the scope can stimulate the lower pharynx (or even the glottis itself, if the endoscopist is sloppy) causing airway irritation leading to laryngospasm and bronchospasm.
2. The challenge of managing morbidly obese patients during anesthesia, especially sedation cases. Everything that makes sedation cases challenging is made several times more challenging when someone is really heavy. Giving a person just enough propofol to keep them from gagging and hacking on the endoscope but still breathing can be tricky in a healthy person, but it is much harder in a really heavy person. Partly because of the way that morbid obesity affects pharmacokinetics, but also because of passive airway obstruction, which I can guarantee was pretty severe in this patient, with a BMI of 52.
There was nothing wrong with the doses of drugs mentioned in the article. Whoever thinks that 100mg of propofol is excessive for an EGD has no business speaking about the topic because they clearly have never done an EGD themselves. Same with the 200mg of sux. Perfect dose when you have to rescue an airway NOW.
It seems unlikely that 4mg of zofran would cause torsades, and if it did, I probably wouldn't expect it to take over 20 minutes to do so. Maybe she got other QT-lengthening drugs that just weren't mentioned in the article. Many drugs have the potential to lengthen the QT.
It sounds like a primary respiratory issue, though. As someone who does a lot of these cases in a part of the country where BMI's (and rates of smoking, and COPD) are much higher than average, my guess would be that the patient's obese airway completely obstructed when the propofol made her relax, and because of her size she had very poor respiratory reserve coupled with a high oxygen demand, so she de-satted quickly. Because of the pathological changes that occur secondary to OSA, it took her longer to recover from the propofol than would a healthier person. She was then hard to ventilate and intubate and even when good air exchange was finally established, atelectasis and greater oxygen demand kept her Sp02 from recovering.
But of course none of that would have happened if an anesthesiologist had been in the room. Just ask Joan Rivers.
