Passin' Gas

can't answer most of your question, not involved with the navy. however, i would like to mention in may 2003, at the height of the military effort in iraq, 364 crnas and 77 anesthesiologists were deployed as part of operation iraqi freedom. aana website. pg

I remember hearing voices sing "Hallelujah" choruses with the first few intubations! I was so excited to see the 'pearly gates' and have the tube go into the light....I was gently brought back to earth by the CRNA whispering 'you're not finished, inflate the cuff, connect the circuit, make sure it's in the CORRECT hole!' I have to admit I still hear the Hallelujah choruses after difficult intubations. Have a great time on your first day and all that follow, PG

I sent a PM suggesting these very same groups! PG

Best of luck to you!! Congratulations and welcome to the ranks of CRNAs (I have no doubt you will sail through the certification exam!) Any thought of returning to your blog?.... PG

Thanks for the response, heartICU. PTO...PAID time off?? Was that a Freudian slip?

When are classes and exams scheduled? Is there consideration of clinical scheduling and exams, i.e. day 'off' from clinical day before exam? Do you have to go to class at 1600 for three hours after being in clinical since 0600? How difficult is it to study pain pathways, pulmonary physiology, and pharmacology after a 10-12h day in clinical? And what about call schedules...how soon do you take call? Are you required to be in class at 0800 after getting off a 16h clinical shift from 1500-0700 (and, of course, you never even saw the call room)? Both ways are challenging...just trying to bring in some other issues to the discussion. PG

FYI COA (Council on Accreditation) requires an ethics course in nurse anesthesia curricula. Nursing theory, however, (thankfully) is NOT required. PG

Just FYI, there's a few AAs and MDAs who read and post on this CRNA forum. jwk is an AA.PG

Yep, you're right. I stand corrected (and I corrected my post). I know the hypotension is more profound with propofol and knew it had arteriolar vasodilation. Somewhere in time I deleted the myocardial depression. PG

1. IMHO: In my humble opinion2. Propofol does cause myocardial depression, it also causes arteriolar vasodilation reducing SVR. Sympathetic activity is also diminished, damped baroreflex in response to decreased MAP. 3. Highly lipid soluble, fat accumulation occurs with long-term infusions i.e. 10 days in the ICU, not bolus dosing for a short procedure. In fact, the lipid solubility accounts for fast onset, the drug is then redistributed by CO to skeletal muscle and fat, decreasing the levels in CNS and this accounts for rapid awakening. 4. Anyone, I mean anyone, who administers this drug needs to be facile in airway management. None of this "I'm BLS and ACLS certified and can intubate the mannequin 1 out of 3 tries every two years." This drug needs to be administered in persons skilled in airway management including oral airways, nasal trumpets, bag-mask ventilation, and intubation. If you give the drug you need to be able to handle the effects of it. Quote from package insert for propofol: WARNINGS For general anesthesia or monitored anesthesia care (MAC) sedation, propofol should be administered only by persons trained in the administration of general anesthesia and not involved in the conduct of the surgical/diagnostic procedure. Patients should be continuously monitored, and facilities for maintenance of a patent airway, airtificial ventilation, and oxygen enrichment and circulatory resuscitation must be immediately available. For sedation of intubated, mechanically ventilated adult patients in the ICU propofol should be administered only by persons skilled in the management of critically ill patients and trained in CV resuscitation and airway management. 5. 51 year old male for colonoscopy. Receding chin, full beard/mustache, moderately obese gets a 'little too much' propofol goes apneic. Patient becomes apneic, can't ventilate, no one in the room able to intubate since the 'bad airway' was not picked up by MD screening the patient nor by the RN 'knowledgable' in the administration of propofol. Anesthesia's all tied up in the OR (remember they're not needed). Hypoxia leading to a vegetative state in a 51 year old male with wife, two kids, and CEO of a financial firm will pay for all the anesthesia providers to cover the GI lab. 6. Proper training for RNs is called nurse anesthesia school. PG

Been in anesthesia for over ten years. I very rarely sit during cases. Enhances my sense of alertness, I'm watching the surgery, keeping up with the progress/complications/completion of procedure. Surgeons and other personnel take note of who is paying attention (if standing is a measure of attention). Yeah, I can pay attention from the stool behind the drapes but I am much more involved in the case when I'm standing, watching actively, and participating in the entire surgical procedure. On the other hand, one CRNA intoned the following advice: Never stand when you can sit, never sit when you can lie down, and never just lie down when you can actually sleep! Now, this individual did a LOT of 16 and 24h call shifts in a trauma center. Hence, conservation of energy was paramount. My current practice setting runs to 10-12h days. Usually 4-8 cases a day. Frankly, I'm too busy to sit. PG

'Tis the ART of anesthesia...Give them what they need, not necessarily what the books say. This skill takes time to hone and read patient's responses to different anesthetic agents and techniques. Good point.PG

Aaahhh, grasshopper, (rather, gaspassah), you learn well...Next, we catch flies with chopsticks.... PG

Help. I got lost with this statement. For starters, I'm assuming you are referring to sevo and des as the more modern agents. These have LOW blood:gas and brain:blood partition coefficients. Hence, they are LESS soluble in fat, so when the gas is turned off they are rapidly excreted via the lungs. On the other hand, halothane has a high blood:gas partition coefficient, a high brain:blood partition coefficient, so when this gas is turned off it is continually taken up by the fat PLUS undergoes liver metabolism, therefore leading to faster than expected awakening with such a fat soluble agent. Sevo and des do not undergo significant metabolism, the rapid awakening is accredited to their low solubilities. Numbers from Barash: (I couldn't post the table as I desired, the numbers are in order of the agents listed first) sevoflurane desflurane isoflurane halothane oil:gas partition coefficient 47 19 91 224 blood:gas part coefficient 0.65 0.42 1.46 2.5 brain:blood part coefficient 1.7 1.3 1.6 1.9 fat:blood part coefficient 47.5 27.2 44.9 51.1

First off, there isn't a truly 'right or wrong' answer. This question is intended to gain insight how you will respond in difficult situations. It's also one of those 'depends on the situation' type questions. This could go either way. Hypothetical example: You are three weeks into clinical and dutifully look up and compose the optimal care plan for a 58 year old male for transverse colon resection, hx of diverticulitis and recently discovered colon CA. Otherwise, fairly healthy, actually ht/wt proportionate. You want to use propofol, cisatracurium, sufenta infusion (case expected to last 3h, slow surgeon), desflurane in air 2L flow and oxygen 2L flow rate. The MDA decides to use pentothal, pancuronium, fentanyl, isoflurane in 1L air and oxygen 1L flow rate. Both are acceptable techniques. The MDA's plan will be less expensive for the patient who is going to be 'in-house' for a few days and for the underfunded county hospital. Propofol? Great, but he's not heading home after surgery; pancuronium, need muscle relaxation for the whole case; fentanyl is less expensive than sufenta; running lower gas flow rates reduces loss of body heat plus,you guessed it, isoflurane is cheaper. Again, patient ain't going home in three hours postop. So, I wouldn't have a great heartache with the change in plans. But say the patient had chronic renal insufficiency, elevated BUN and Cr plus a history of CAD and the doc still wanted to use pancuronium. In that situation, I would defend the use of cisatracurium. Pick your battles wisely. PG

What would you do?

Alpha-2 receptors function to reduce release of NE into presynaptic ending. They function as autoreceptors, when NE is present, binds to receptor, and in effect, reduces further release of NE. An antagonist at an alpha-2 receptors would actually ENHANCE further release of NE. Using a selective alpha-1 antagonist will prevent NE from binding to the post-synaptic receptor, decrease vascular contractility on the venous and arteriolar beds, thereby reducing preload and SVR. Plus by using a competetive antagonist, the alpha-1 effects of e.g. prazosin (alpha-1 selective antagonist) can be overcome by phenylephrine. I.e. get the 'squeeze' back once the offending tumor is excised and the source of excess NE removed. The venous vascular beds have a high density of alpha-1 receptors. Blocking these will increase capacitance and allow 'tank refilling' since these patients are really intravascular volume depleted. PG

I've taken care of ruptured abdominal aortic aneurysms, MVAs with multiple wounds, fractured limbs, head injuries, burn victims, the list goes on... I have never witnessed anything so brutal in my life. Words will not do justice to the visceral upheaval I felt, and still feel. There is no comparison between the OR and what I just witnessed. Absolutely none. PG

Interpretation: A courtesy letter to let you know your application is complete, all parts and pieces are here. Now we're going to look at it to see if you qualify for an interview. PG

Welcome to anesthesia school! No matter what people tell you, yeah, it's hard, it's the hardest thing I've ever done, yeah, I REALLY had to study....never hits home until YOU are the recipient of the mountain of information to understand, assimilate, and retain not only for the exam but for future use, i.e. not bump off a patient Hang in there! Over time you will develop more effective study skills and methods. I strongly recommend studying with one or two classmates and go over every detail together. What one doesn't understand, another will catch on and be able to explain. Then there's always some things despite all the books and references, no one can see the light...then there's the instructor. Don't be shy in consulting for things that you don't understand. That's their job. The first round of exams tends to be a real eye-opener! Obviously, you have had this experience. Yeah, this ain't undergrad. Stick it out, it's definitely worth it! Good luck and get back to the books.... PG

http://www.sahp.vcu.edu/nrsa/ Check out Medical College of Virginia. Although this looks like post master's work. PG

I knew that didn't sound right. Self-employed so don't get employer contributions. Thanks for the correction.PG

Research this forum for other threads regarding contracts. Basically most will recommend sucking up loans and other financial aid vs signing your soul away to a group at this early stage of the game. Personal opinion, depending on where you are located, it's not a bad overall package, I've seen better. If you're locked in to living in X city, period, end of discussion and it's the only game in town, that might sway my decision. If you are mobile and can move after school, I'd definitely leave my options open. The LAST thing you should consider is "I'll take the money, get through school, and if something better comes along towards graduation, I'll pay this back and take the 'better' job." DO NOT DO THIS! Ethically wrong, sponsors will have this happen once or twice and decide supporting other students not worth the trouble so you ruin opportunities for others who will follow. IMHO, take out loans today, see where life takes you in the next 2-3 years, negotiate for loan repayment with future employers. Realistically, with incomes exceeding $120,000 and more, you can afford to pay for your own education. You will reap the benefits for many years to come. Just looking at the break down: 15 days vacation 12 sick days 5 days and $1500 for education 9 paid holidays... How many days have you missed per year for the past few years due to illness? That's one day a month. Are you compensated for days NOT TAKEN? Or is it beneficial to call in 0600 for a 'mental health' day? I"M NOT advocating the practice, just trying to point out finer details of pros and cons of contracts. Some practices give 35 paid 'off' days per year. Equivalent outcome. If you don't need the sick days, tack them on to the vacation time! i.e. scheduled mental health days! The 6% matching is ok. Say you contribute $12,000, which I believe is max for 2004. The employer matches 6% which is $720 for the year. The real benefit will come from reducing your tax liability by investing in your own retirement account. And most important for me, is who does what in the practice. How is the workload divided in an anesthesia care setting? Your best bet is to talk with several CRNAs with the group and get their input. Best of luck, PG

Appropriate professional etiquette. Do it. PG PS good luck!

Here's your articles. Two support benefits of renal dose dopamine, the third disputes this. PubMed is an easy tool to use for accessing current research articles. Most have links to the publisher to obtain the full article. Some of the most recent published articles will have only the abstract available. A trip to your friendly, local library is the only energy expenditure required to obtain the latest information. Increasing renal blood flow: low-dose dopamine or medium-dose norepinephrine. Chest. 2004 Jun;125(6):2260-7. Di Giantomasso D, Morimatsu H, May CN, Bellomo R. Department of Intensive Care, Austin and Repatriation Medical Centre, Heidelberg, Germany. BACKGROUND AND OBJECTIVES: Many clinicians believe that low-dose dopamine (LDD) [2 micro g/kg/min] increases renal blood flow (RBF) and medium-dose norepinephrine (MD-NE) [0.4 micro g/kg/min] decreases RBF. They also believe that MD-NE might induce mesenteric and/or coronary ischemia. In fact, the effects of these drugs on renal and vital organ blood flow are poorly understood. The aim of this study was to compare the effects of 6 h of IV LDD and MD-NE infusion on mammalian renal, coronary, mesenteric, and sagittal blood flow. DESIGN: Randomized, controlled, experimental animal study. SETTING: Animal laboratory of tertiary physiology institute. SUBJECTS: Seven Merino cross sheep were studied. MEASUREMENTS AND RESULTS: We performed a staged insertion of transit-time flow probes around ascending aorta, sagittal sinus and circumflex coronary, superior mesenteric, and left renal arteries. We then randomized these animal with long-term embedded flow probes to either 6 h of placebo (saline solution) or drugs (MD-NE at 0.4 micro g/kg/min or LDD at 2 micro g/kg/min), and performed continuous measurement of systemic pressures, cardiac output (CO), and flow to vital organs. We also sampled blood and urine for the measurement of lactate, creatinine, and creatinine clearances at preset intervals. RESULTS: Compared to placebo, LDD did not affect systemic hemodynamics. However, it increased mean RBF by 20% (267.3 +/- 87.6 mL/min vs 222.0 +/- 74.4 mL/min, p = 0.028) without a detectable effect on other vital regional circulations. MD-NE, however, increased mean arterial pressure (101.0 +/- 8.3 mL/min vs 84.2 +/- 5.2 mL/min, p = 0.018) [mean +/- SD] and CO (4.93 +/- 1.45 L/min vs 3.81 +/- 0.57 L/min, p = 0.028). It also increased coronary blood flow (36.0 +/- 15.7 mL/min vs 23.0 +/- 10.7 mL/min, p = 0.018) and RBF (286.5 +/- 79.0 mL/min vs 222.0 +/- 74.4 mL/min, p = 0.018). MD-NE had no detectable effect on mesenteric or sagittal sinus flow. LDD infusion increased urine output, but did not change creatinine clearance. MD-NE infusion increased urine output significantly more than LDD but not creatinine clearance. CONCLUSIONS: Both LDD (2 micro g/kg/min) and MD-NE (0.4 micro g/kg/min) increased RBF and urine output. However, the effect of MD-NE was more pronounced. LDD did not affect other vital organ flows, but MD-NE increased coronary blood flow without any changes in mesenteric and sagittal sinus blood flow. Should we give prophylactic renal-dose dopamine after coronary artery bypass surgery? J Card Surg. 2004 Mar-Apr;19(2):128-33. Gatot I, Abramov D, Tsodikov V, Yeshaaiahu M, Orman S, Gavriel A, Chorni I, Tuvbin D, Tager S, Apelbom A. Department of Cardiothoracic Surgery, Soroka Medical Center, Beer Sheva, Israel. OBJECTIVE: A prospective double-blind randomized study undertaken to assess the effect of postoperative prophylactic "renal-dose" dopamine on post-coronary artery bypass grafting surgery's clinical outcome. METHODS: Eighty-five consecutive patients undergoing CABG operation were randomized to receive either 3-5 microg/kg/min dopamine (group D, n = 41) or saline as placebo (group P, n = 45) for 48 postoperative hours. Clinical outcome parameters were collected for four postoperative days. RESULTS: Preoperative and operative parameters were similar in both groups. Four patients from group P and none from group D reached an end-point of the study (oliguria, renal dysfunction) and received dopamine. Two patients from group P and none from group D needed an additional inotropic support. Mean arterial pressure values were similar during the first 24 hours after operation, but left atrial pressure values tended to be higher in group P (10 +/- 4 vs 7 +/- 3 mmH2O, p = 0.18). The mean pH was higher in group D at 8 hours after operation (7.38 +/- 0.2 vs 7.36 +/- 0.3, p = NS), due to higher bicarbonate levels (23 +/- 2 mmol/l vs 21 +/- 2, p = 0.49). The incidence of lung congestion in chest X-rays and CT scans was significantly higher in group P (50% vs 29%, p = 0.073 at 48 hours postoperatively). Room air blood O2 saturation and maximal expiratory volume tended to be higher in group D (at 72 hours after operation- 92 +/- 4 vs 90%+/- 5, p = 0.29 and 646 +/- 276 vs 485 ml +/- 206, p = 0.16, respectively). There was no statistical difference in urine output but the amount of furosemide given to patients in group P was significantly higher (during the first 8 hours 2.5 +/- 0.5 vs. 0.3 mg +/- 1.6, p = 0.07). Plasma creatinine levels were significantly lower in group D (at 24 hours 0.93 +/- 0.02 vs 1.05 mg/dL +/- 0.02, p = 0.02). Mobilization after surgery was faster in group D. CONCLUSIONS: Prophylactic dopamine administration after coronary artery bypass grafting surgery improves patient hemodynamic and renal status, reduces the need for additional medical support (inotropes and furosemide) and thus, provides stable postoperative course. Is there still a place for dopamine in the modern intensive care unit? Anesth Analg. 2004 Feb;98(2):461-8. Debaveye YA, Van den Berghe GH. Department of Intensive Care Medicine, Catholic University of Leuven, Leuven, Belgium. For many years, dopamine was considered an essential drug in the intensive care unit (ICU) for its cardiovascular effects and, even more, for its supposedly protective effects on renal function and splanchnic mucosal perfusion. There is now ample scientific evidence that low dose dopamine is ineffective for prevention and treatment of acute renal failure and for protection of the gut. Until recently, low-dose dopamine was considered to be relatively free of side effects. However, it is now clear that low-dose dopamine, besides not achieving the preset goal of organ protection, may also be deleterious because it can induce renal failure in normo- and hypovolemic patients. Furthermore, dopamine may cause harm by impairing mucosal blood flow and by aggravating reduced gastric motility. Dopamine also suppresses the secretion and function of anterior pituitary hormones, thereby aggravating catabolism and cellular immune dysfunction and inducing central hypothyroidism. In addition, dopamine blunts the ventilatory drive, increasing the risk of respiratory failure in patients who are being weaned from mechanical ventilation. We conclude that there is no longer a place for low-dose dopamine in the ICU and that, in view of its side effects, its extended use as a vasopressor may also be questioned.