maturner

Kaiser, UCSD, Balboa (Navy)-and yes they have civilian CRNAs, Paradise Valley, and possibly others about which I am not aware

You must be a Kaiser Grad!

I hope to get some of the folks in HI to buy into the block. I loved it @ Navy and IMHO found it easier and more reliable than interscalene. Bye the way, The Irishman and myself received the good word about our board results yesterday. It sure feels good to have that final hurdle out of the way. I haven't been this relaxed in 2+ years! The wife and I can now head off on our sailing vacation in the British Virgin Islands with no worries!!!

Congrats buddy! The Irishman and I took the quiz on wednesday. I was so nervous when I hit the enter button on that 90th question, and so relieved when it shutdown.

No where do I see an onset of 15 minutes! Interestingly the onset following deltoid injection falls right within the the onset of 3-5 minutes for Sux. Those darn pharmokinetics. So much for useless... Anesth Analg. 1997 Jan;84(1):54-8. Sullivan KJ, Berman LS, Koska J, Goodwin SR, Setzer N, White SE, Graves SA, Nall AV. Department of Anesthesiology, University of Florida College of Medicine, Gainesville 32610-0254, USA. In children undergoing inhaled induction of anesthesia with halothane who suffer bradycardia, submental glossal injection of atropine may result in more rapid onset of vagolysis than traditional intramuscular sites. We compared the intervals between injection and onset of heart rate acceleration (tHR increases) after intramuscular injection of atropine into the deltoid, vastus lateralis, and glossa in children between 1 mo and 10 yr of age scheduled for elective surgery. The tHR increases was determined by measuring the interval between atropine injection and the time point at which the slope of the heart rate curve initially became positive. To ensure that the drug had taken effect before surgical stimulation, heart rate observation was continued until it increased at least 5% above baseline with evidence of continuing acceleration. Anesthesia was induced in all subjects by mask with nitrous oxide and halothane. After tracheal intubation, constant inspired concentrations of the anesthetics were administered for 3 min. While heart rate was monitored, atropine (0.02 mg/kg) was injected into one of the three sites. Each patient's end-tidal anesthetic concentrations were recorded, and minimum alveolar anesthetic concentrations (MAC) were subsequently calculated and adjusted for age. The tHR increases was recorded and averaged for each group. The study groups did not differ by age, weight, end-tidal anesthetic concentrations, age-adjusted MAC, or heart rate at the time atropine was administered. After submental glossal injection (n = 11), tHR increases increase was fastest (3.0 +/- 1.1 min) and was significantly faster than that found with deltoid injection (n = 16; 4.4 +/- 1.1 min) or vastus lateralis injection (n = 8; 6.4 +/- 2.4 min) (P PMID: 8988999 [PubMed - indexed for MEDLINE]

Look MAN! I am not suggesting anyone to act on anything I have said. Looking up every bit of research to determine how to act and respond is great. However, this is nothing more than a chat room and I am simply sharing my experience and not writing a thesis. I have a life outside of healthcare and have bigger fish to fry. I have absolutely NOTHING TO PROVE TO YOU. I was simply stating what my experience has been thus far, what the practice is in my part of the country and what is in the texts. The people that I know who have used the dart have had good experience with it. There are Pros and cons to the administration of any medication by any route and each situation should be evaluated for the best course of action. If I encounter a laryngospasm that does not break with PPV and the patient has no IV I will administer a SUX/Atropine dart as is suggested by Morgan and Mickhail and what has been used successfully by people with whom I have practiced. Being that you are the one that has nothing better to do than argue online and look up research, why don't you provide EBP guidelines or research regarding the negative implications following the coadministration of IM SUX/ATROPINE for the abatement of Larygospasm in the pediatric population prior to establishment of an intravenous line? Mike

Is it better to give a drug to prevent or attenuate a bradycardic response or stand there like Gomer Pyle? PPV is always the first like offense to break a laryngospasm The first line defense is don't muck with the cords during stage II of anesthetic depth I have not used lidocaine directly on the cords (nor have I had to use the DART) PPV has worked thus far... knock on wood... I vaguely remember reading something somewhere about lidocaine on the cords to break a spasm but most texts discuss sux as the primary back up following PPV. M&M has a vignette about a pressure point behind the ear that can break a spasm but again I don't remember the details. Mike

IM Sux/atropine (a.k.a sux/atropine DART) in peds is for the purpose of breaking a laryngospasm in a patient without an IV. Which is frequently the case during mask inductions or short procedures such a PE tubes. The atropine is to off set the bradycardia frequently associated with sux administration in this population. Peds particularly small ones are PNS (vagal) dominant as their SNS system is immature. The dose per Nagelhoudt is sux 4mg/kg and atropine 0.03mg/kg. The sux/atropine dart is pretty much standard in the 10+ hospitals through which I have rotated in SoCal and HI.

1 app. 1 school best of luck

LMAO

If the blocked worked initially then there was no problem with the block or the marcaine. The bolus placed through the catheter did not work; therefore, the catheter was the problem. If the initial marcaine was placed via the catheter and the block worked then the problem is that the catheter migrated away from the nerve and the subsequent lidocaine bolus never reached its intended site of action.

Ditto. I initially started missing IVs that would have never missed, without the LA in the way, but with practice and improved technique no worries.

Look man, I just read it right from the source in Barash. Morgan and Mickhail shows the same thing. Nagelhout is brilliant, has a PhD. in pharmacology, and I have heard it repeatedly right from his mouth. Mike you are clearly very intelligent and have nearly single handedly revived this web site, now chill out. Keep posting the controversal stuff, I love it, just strap your muzzle on a little tighter before you respond. Like you and many others I was on the top of my game before school, in retrospect I had no idea how much I simply didn't know and you will find the same to be true.

Did the blocks work at all or did they simply not last beyond the duration of the surgery? Did both blocks have catheters? If so, I would say you had a catheter issue most likely from migration of the catheter away from proximity to the nerve. All of the local anesthetics work the same way, lidocaine, marcaine, ropivicaine etc.. Therefore it is not the marcaine that was the problem. Catheters in peripheral nerve blocks can be technically challenging to place.

WRONG! PROPOFOL has the most cardiac and respiratory depressant effects of any of the induction agents. Per BARASH, NAGELHOUT, and no doubtedly any other text comparing induction agents. I am not trying to insult you. I am simply pointing out your sophemoric attitude and the fact that you have much to learn. Y O U D O N O T K N O W, W H A T Y O U DO N O T K N O W !

well said! Hey mike, I don't want to harp but I have one question. What intravenous induction agent (propofol, pentothol, ketamine, etc.) given in equipotent doses has the greatest cardiac and respiratory depressive effects? Priority number one is not absence of personal liability but the presence of patient safety.

Were the two previous blocks administered at the same time? i.e. Fem and sciatic More details please.

Sigma, you are killing me dude.

WHAT the ... four pages of this thread are devoted to your whining about dead horses and now you have something valuable to add? Apparently, the horse isn't dead. Thanks for contributing to the discussion. And by the way, you did bring up the sevo vs. des question.

Wow, that is some great clinical debate. So you want to discuss whether Sevo or des is better for the obese pt. Okay, you start... ...waiting ...waiting ...oh yea, you would have no idea given the fact that you have NEVER used either one! So much for the discussion.

This website has seen more traffic with controversial topics than without and as a result more people as responding to other threads as well. So quit whining about the topic, stop reading the thread if you don't like it, and start taking advantage of the greater input to other threads as a result of this one.

Increasingly strong backing! Who do you think created AAs? They have always had the strong backing of MDs. AAs were created to limit the power of CRNAs, see proposed NC legistlation. AA practice is CONTROLLED by anesthesiologists, not ours. MDAs and AAs sell AAs as a God send and the equivalent to CRNAs. Afterall, they make the same money. If the MDA must supervise AAs, well then shouldn't they have to supervise CRNAs? They're the functional equivalent afterall, they do make the same money. THe ASA wants the lines blurred between the two. Don't buy into it. As a result of AAs the ASA can push their agenda from two fronts. The AAs have 100k+ "anesthetist jobs" and families to feed and will fight to preserve "their profession" kind of like a mercenary for the ASA. While the ASA fights from its own front that includes fighting all legistlation to expand the practice of all APRNs. Leaving CRNAs in the middle to fight a two front war. Georgia and JWK, are without a doubt good at what they do and I respect they're knowledge about anesthesia. However; they're agenda is to increase AA practice and by de facto the ASA agenda which runs contrary to the practice most CRNAs enjoy today.

Docs use Lidocaine 2%, anywhere from 60-100ml's volume, instilling the tissue involved with the generator pocket and obtaining venous access. YIKES! 1200-2000 mg of lidocaine! Max dose in 70 Kg individual 4.5 mg/kg 315mg sans epi; 7 mg/kg with epi 490mg Nevermind emaciated little old ladies! How much does an emaciated old lady weigh? maybe 50 Kg with their hair wet. Even 0.5% lido with epi at those volumes would be near toxic at 60cc and clearly toxic above that.

Dave -you're a wild man, you can do my anesthesia anytime.

The valsalva in anesthesia is actually generally applied during spinal cases to confirm that the dura has not been punctured or that the closure of dura is complete after it was intentionally opened. The pop off valve is closed and an inspiratory pressure of about 30 is held while the surgeon inspects the integrity of the dura. The increased thoracic pressure decreases venous return-> increasing venous dilation within the brain-> increased icp-> deceased CSF in cranial vault-> increased CSF in spinal column-> dural stretch = leak or no leak. Several other physiologic responses occur as a result of a valsalva; however, in anesthesia the above is the response for which we are generally looking.