charles-thor

did anyone read the reports of brain death during the beach chair position in the apsa newsletter? one lady was in her mid 40's and healthy. controlled hypotenion (sbp also, vision loss should be a concern in long prone cases. johns hopkins looked at this and found several factors in common when this horrific event occurred: hypotension, anemia, long surgical cases, fluid overload.

One should raise the obvious question of whether or not the hospital houses a large anesthesiology residency program. I suspect that any institution that runs 2:1 is, in fact, an academic and not private practice, otherwise this is a really poor model for making any real money for the group.

I passed too! I found out this afternoon. I had heard rumors that the envelope comes addressed as "your name" CRNA, however when I didn't see those 4 very important letters after my name on the envelope, I was a bit worried. I just held it in my hand for a minute or so contemplating what I would tell my wife if the news wasn't so good...

I took the big quiz on Jan. 28, but still have not heard anything yet. A friend in my program took it on Jan. 12'ish, and found out in 20 days. Sprout - any word???

i'm taking it too at 8am. wish me luck.

Most ett cuffs utilized today employ low pressure and high volume balloons. The appropriate question should have been, "what is the maximum PRESSURE that is acceptable in an ett balloon - as pressure will change according to both the volume of the tracheal lumen and compliance of tracheal tissues. Put another way, the same volume will result in different pressures according to the two variables mentioned above. Furthermore, these variables are not static (i.e. lumenal diameter may be reduced over time secondary to edema from prolonged intubation). Tracheal capillary hydrostatic pressure is approximately 25-35 mmHg, so exceeding this pressure will severely diminish or even eliminate flow distal to the occlusion. Bottom line - the pressure in the ett balloon should not exceed ~25 mmHg (play it safe) or else perfusion to the surrounding tissues will be in jeopardy. What is better than contemplating Boyal's law when inflating an ett balloon? I hope this helps.

How to give anestheisa. You ready??? Induction - Give a syring of anestheisa. Give just enough, but certainly not too much! Maintance - Cuddle up to a good book, and try to stay warm. Emergence - Turn anestheisa off. PACU - Pretend to finish your charting while you snicker and discretly watch the PACU RN hook-up to monitors and deal with the patient who got just a wee too much ketamine. So what do you mean you're not trained in anesthesia reversal??? :chuckle :roll :chuckle Sorry folks, I just couldn't help myself. In all honesty, inadaquate training only leads down one road - the bad one. Insist that you are propertly trained how to recover post-op pts. And now, back to the books and only one more study day until the "big quiz"...

hi all. with a week until ANESTHEISA boards, i was wondering what everyone's suggestions are with respect to getting the most out of the next several days of studying. thanks in advance. sorry - i edited the heading to avoid confusion.

sounds like a lot of vec after a sux induction for a hip debriedment??? there are, however, many ways to skin the commonly quoted cat...

Spinal for C-section means you’ve got at least a T4 level. It’s probably fairly safe to assume that some, if not all, of her cardiac accelerators are blocked, thus beta blockade wouldn’t be my first choice. Sounds like she might be experiencing some sort of irritable focus or re-entry phenomenon, but obviously I’d have to know more about the pt. If I didn’t have anything more, I’d probably reach for verapamil. I would think that if her tachycardia subsided, as it often does at home, that I might hose myself giving a cholinergic agonist. If she was really worked up over the dyspnea, I’d talk her through it and, if I truly believed that her cogitative state might be contributing to the rhythm, I’d consider some fentanyl. So, how’d you handle it?

Not to confuse things further, but a relationship does exist between MAC and potency, in that the two are inversely related. MAC is how we compare potency amongst the inhalation agents. Agents in order from least to most potent and respective MAC values: N2O (104%), Des (6.0%), Sevo (2.0%), Enf (1.6%), Iso (1.2%), and Hal (0.75%) Notice that the more potent the agent, the lower its MAC value. Also, there is a rough parallel between oil solubility and potency (and thus MAC) shared between the agents, however Enf is the exception being slightly more lipid soluble than Iso, but a little less potent.

This is such a great topic, but I’m probably bias as this was the focus of my research requirement for school. Bradycardia leading to cardiac arrest with spinal anesthesia is probably a more common problem than many people believe with an estimated incidence of somewhere between around 7/10,000 spinal anesthetics. Originally bradycardia and subsequent cardiac arrest during sab was believed to be directly related to over sedation leading to hypoxia and cardiovascular instability. Today, however, we know this in fact not the case. Although there is no universally agreed upon answer as to why this occurs, its mechanism is believed to originate from 2 sources: 1.) An unopposed vagal tone secondary to sympathectomy. This sympathectomy occurs 2-6 dermatomes higher than sensory block, so that a sensory block of T6 can conceivably inhibit all of the sympathetic innervation to the heart. 2.) The Bezold-Jarisch reflex – which may be widely under appreciated phenomenon. You’ll be surprised how many clinicians are not well versed in this essential physiology. Sympathectomy → reductions in venous tone → profound decreased venous return. This activates mechanoreceptors embedded within the walls of the myocardium → stimulating vagal afferents → vasomotor center of medulla → increased vagal tone to the heart, thus slowing or stopping the heart entirely to allow enough filling time to generate an effective stroke volume. At first glance, this point seems counter intuitive, however ask yourself -what good is reflexively increasing HR in the relative absence of blood to pump forward? I could go on and on here, but I’ll stop and answer Kat’s questions. Atropine is largely ineffective for bradycardia in this situation, as it removes parasympathetic tone, but has no DIRECT action on the myocardium. If you have chemically dennervated the heart, than you have little to no (depending on the level of block and dose of atropine) autonomic influence to the heart. This does not necessarily result in asystole, because the SA node and the rest of the conduction system demonstrate automaticity. Think of the heart transplant patient. Many will argue the early use of atropine (glycopyrolate is a much weaker chronotrope) or ephedrine, but if these don’t work VERY EARLY, you should promptly switch to epinephrine. This will offer ino/chronotropic support and more importantly restore venous tone/return and support, which was the original cause of the problem. Here are 2 great articles: Caplan et al. Unexpected cardiac arrest during spinal anesthesia. Anesthesiology. 1988;68:5-11. Campagna JA, Carter C. Clinical relevance of the Bezold-Jarisch reflex. Anesthesiology. 2003 May;98(5):1250-60. Appreciating the potential height of the sympathectomy, maintaining preload, and prompt intervention with epinephrine for bradycardia during sab are thus essential to prevent ensuing cardiac arrest.

I'd imagine that this stuff is going to be quite expensive, so I wouldn't count on sux going anywhere anytime soon.

Hemodilution affects both hgb and hct. Imagine a set volume (the patient's blood volume) in which hgb is in solution - say a blood volume of 50 dl and a hgb concentration of 14 g/dl. If you add volume to the solution (giving crystalloid), but the amount of red cells is unchanged, then both the hgb and hct will decrease. In the case of surgical blood loss, you're giving fluid to maintain volume status, however this is doing nothing to preserve oxygen content. In essence, you can attempt to maintain the patient's volume status roughly similar to how they started out, but you've now diluted them with additional crystalloid. Transfusion is then considered when the patient's risk for ischemia outweighs risks of transfusion. I hope this helps.

the prospect of the unantisipated difficult airway, albeit a pretty rare event, is something the anesthesia provider must have tucked away in the back of his/her mind in order to best prevent a bad outcome