Ace844

Seems to me we recently had the definitive care debate ing the 'Is EMS Definitive care Thread'; Is EMS definative care?....hmmmmm..Guess are going to end up going back there. A furthere reply will be forthcoming. ACE844

"aussiephil", We actually agree on a lot of points and it’s the semantics where we disagree.[/font:73f20e37a3] I would agree that it does take tests to narrow you DDX list down, but your DDX list should only be at max about 5 things anyway. This is done most often without the use of that equipment which you are touting as necessary to do so. This is done using physical exam and history skills as well as ‘tests’ within that realm to narrow it down further. A good diagnostician can narrow the list down and in some cases often nail the DX with out those tests. Yes, training, education and experience have a role here. [/font:73f20e37a3] Actually this statement makes it sound like you are using the ‘monitor’ to make the diagnosis for you. Here’s another key factor where we differ. The monitor and those other tools are used to CONFIRM what you have already as your narrowed DX. This is the case with the majority of the tests which you are tough ting as the things which would replace your H&P. This is in fact against the ‘standard of care and teaching’ in medicine. I have provided ample evidence to ‘prove’ my point, now lets see yours..[/font:73f20e37a3] If by initial observation you mean a full physical exam and history than yes, that is so, but to use the machine to cover the fact that you didn’t do something or don’t have a clear picture of what’s going on and are merely using it ‘to tell you’. That is wrong. You should not be performing an intervention, or a test, or labs…to give you an answer. You are doing so to CONFIRM what you already know and suspect. A subtle but important point.[/font:73f20e37a3] The days of just doing O2 and transport are gone. Long gone. The reality is you do a full H&P, assessment, identify life threats and treat-correct them, re-assess, treat and correct potential life threats and continuously provide treatment and care for your patient on a continuous basis. While doing this, you also work towards transport to the hospital and are thus ensuring their appropriate timely access to continual and in some cases specialized care. In doing so though it is important to note that you are not neglecting the aforementioned things like you are insinuating. [/font:73f20e37a3] That is correct, it doesn’t say that. It does say in effect that not every patient should get all the lab studies and tests available, radiological imaging, and a full workup and evaluation by every piece of equipment to determine what is wrong. It is doen how I stated above.[/font:73f20e37a3] Correct, note the word CONFIRM. They had already arrived at a diagnosis clinically and used the test, to PROVE what they knew. A subtle but important distinction and point.[/font:73f20e37a3] Please see my responses above and I will add another point which you seem to have missed as well. DIAGNOSIS is an object of exclusion in all settings. You arrive at your diagnosis through the H&P because in the course of doing it you have ruled out all those other things and you are left with your DX![/font:73f20e37a3] Again, the days of just doing O2 and transport are gone. Long gone. The reality is you do a full H&P, assessment, identify life threats and treat-correct them, re-assess, treat and correct potential life threats and continuously provide treatment and care for your patient on a continuous basis. While doing this, you also work towards transport to the hospital and are thus ensuring their appropriate timely access to continual and in some cases specialized care. In doing so though it is important to note that you are not neglecting the aforementioned things like you are insinuating. No where has anyone said you shouldn’t do any talking or providing of comfort. [/font:73f20e37a3] Fact is often times with some education, training and experience we are often able to arrive at the same place. Further this with the point that you can’t ever progress to treatment without a diagnosis. PERIOD! Additionally, your statement of we are “just EMERGENCY MEDICAL SERVICE” is another point I disagree with. Especially in this era, where we are seeing more chronic illness and issues related to that than life threatening etiologies…in the large majority of the cases you are dealing with are general internal medicine issues. Yes, there are EMERGENCY situations we encounter, but they are a rarity. Out Here, ACE844[/font:73f20e37a3]

For those who are interested, this is the closest I could to the info. I posted earlier. HTH, ACE844

(Avian influenza transition to pandemic virus may be complex process August 1 @ 2006 NEW YORK (Reuters Health)) A simple exchange of genes between the H5N1 avian influenza virus and a human influenza virus appears to be insufficient to cause efficient person-to-person transmissibility that could lead to a pandemic outbreak, scientists report in the early online edition of the Proceedings of the National Academy of Science. Nevertheless, "these findings do not mean that the H5N1 avian influenza virus cannot become a pandemic strain," Dr. Julie Gerberding, director of the US Centers for Disease Control and Prevention (CDC) in Atlanta, warned at a media briefing. "It just means that such a transition will be more complicated than a simple one-to-one genetic transfer." "We cannot become complacent about pandemic preparedness," she emphasized. Dr. Gerberding explained that there are three requirements necessary for a pandemic virus to develop: The virus must have a new surface protein to which humans have no immunity; it must be able to cause infection and disease; and it must be able to move easily from one person to another. "Two of those three conditions have been met," she continued, as evidenced by the facts that 231 humans have been infected with the H5N1 virus since 1997, of whom 133 have died. "The missing component is efficient transmissibility." To better understand the molecular and biologic requirements for H5N1 viruses to confer efficient transmissibility among humans, Dr. Jacqueline M. Katz, from the CDC and an international team of scientists, developed an animal model of disease using the ferret, which is similar to humans in its susceptibility to influenza. They used data from the 1957 and 1968 influenza pandemics, which were caused by a virus that had suddenly become more transmissible by combining genes from avian and human viruses. Influenza is spread primarily through droplets expelled when infected persons cough or sneeze. Dr. Katz and her colleagues therefore developed a "specialized caging system" designed to study transmission between ferrets in close contact with each other, but could only transmit the infection through respiratory droplets. They also used "reverse genetics to make hybrid viruses containing genes from both," she said. The reassortant viruses contained a surface glycoprotein gene of an H5N1 avian viral strain that had infected a human in 1997, and an internal gene from the H3N2 virus, the most common strain that circulates from season to season in humans. Some of the strains were viable and could replicate after infecting a ferret. However, they were not efficiently transmitted and were less virulent than the original avian strain. When nasal secretions from an infected ferret were transferred to healthy ferrets, "the virus did not acquire any additional capacity to transmit efficiently," Dr. Katz said. "That told us we have a good research tool to assess ongoing genetic changes that H5N1 may acquire that would enhance its ability to transmit efficiently." However, she stressed that these results are only relevant to the specific viruses used in the study and cannot be generalized. The team now plans to repeat their experiments using more recent avian and human influenza strains to generate reassortant virus in the lab, and assess their transmissibility. They will also take another approach with the ferret model, "to look at viruses in the field that are naturally acquiring genetic changes over time," Dr. Katz noted, "and see if they develop an enhanced ability to transmit from animal to animal." "That way, we should be able to identify critical changes that enhance this essential property of a pandemic strain," she added. In conclusion, Dr. Gerberding commented, "We know that the H5N1 virus continues to undergo microevolution, through a series of subtle genetic changes." As a result, "the virus is constantly evolving" in ways that are not predictable "So there is a lot of work to do to prepare for a future pandemic," she stressed, which history shows is inevitable, whether or not it involves the H5N1 virus. "Every community in every part of the world needs to be as prepared as possible." Proc Natl Acad Sci USA 2006.

"Paramedic mike," Just soem thoughts from 'street level' first. It strikes me that there is no stability in this system in that the full timers may not have the ability to get all their 'full time' hours in depending on the staffing and schedule of the service. This is further complicate dby the fact that one cannot plan or have any kind of social life because you have no 'expectation' of working. I would not work under a system such as this for long. ACE

"AZCEP," Thanks for the info., I asked because I have been unable to find any source which quantifies the class 1 properties versus the others in any of the usual places. So I was curious if you had any info. in that realm of it's mechanisim. Thanks for the help, and additional info above., and the explanation on preciptiatory effects. ACE844

Hello Everyone, After a recent discussion with a colleague here over whether technology, and fancy hospital tests{alone} = accurate diagnosis; as oppossed to pertinent thorough H&P-P/E alone to arrive at your diagnosis. After our discussion of this issue I decided to do some research and here is just one of the studies that show this. It was also done at the MD level so thus taking away the 'prehospital vs. hospital educational and capability' portion of the debate. (Ann Neurol. 1990 Jul;28(1):86-7. The accuracy of bedside neurological diagnoses. Chimowitz MI @ Logigian EL, Caplan LR. Department of Neurology, New England Medical Center, Boston, MA.) The accuracy of bedside diagnoses was prospectively studied in 100 consecutive patients admitted to the neurology service at New England Medical Center, Boston. Each patient was evaluated independently by a junior resident, a senior resident, and a staff neurologist, who were required to make an anatomical and etiological diagnosis based solely on the history and physical examination.[/font:559bdc54a9] Fourteen patients were excluded because their diagnoses were known before admission. Of the remaining 86 patients, it was possible to confirm anatomical and etiological diagnoses in 40 by matching the clinical syndromes with highly specific laboratory findings. In the other 46 patients, the diagnoses could not be confirmed because the laboratory studies (including magnetic resonance imaging) were negative or nondiagnostic. In the 40 patients with laboratory confirmed final diagnoses, the clinical diagnoses of the junior residents, senior residents, and staff neurologists were correct in 26 (65%), 30 (75%), and 31 (77%), respectively. There was a trend for error rates to be higher among junior residents than staff (p = 0.06). The errors by the junior residents, [senior residents], (staff) were attributed to incomplete history and examination in 4 [1] (0), inadequate fund of knowledge in 4 [3] (3), and poor diagnostic reasoning in 6 [6] (6). These results indicate that technology is not a panacea for our diagnostic difficulties and that there is room for improvement in our clinical skills, especially diagnostic reasoning. (Good diagnostic skills should begin at the bedside Improving physical exams and history-taking can help you become more efficient and compassionate From the February 2001 ACP-ASIM Observer @ copyright © 2001 by the American College of Physicians-American Society of Internal Medicine. By Christine Kuehn Kelly Improve your auscultation skills) A University of Miami patient had experienced chronic undulating fevers for six months, but tests continued to be inconclusive. It wasn't until an infectious disease specialist asked him about his hobbies that the diagnosis became obvious. An avid hunter, the patient spent most of his vacations in the Southwest, hunting and skinning the animals he killed. The diagnosis: brucellosis. Echocardiograms, CT scans, ultrasound—there's no question that imaging and lab tests play a key role in making the difficult diagnosis. But it's the physical exam and history that account for 80% of diagnoses, experts point out. "The labs and imaging studies complement the picture of the patient created by a good history and physical exam," said Kavita Patel, ACP-ASIM Associate, a second-year internal medicine resident at Oregon Health Sciences University in Portland. That's why educators and residents alike say it's essential that residents learn how to conduct effective physical exams and practice on patients. "Don't let your residency go by without learning all you can about the physical exam and history," emphasized ACP-ASIM Associate Max Brito, a fellow in infectious disease at the University of Miami Jackson Memorial Hospital. Physical diagnosis is an important therapeutic instrument, noted Faith Fitzgerald, MACP, professor of medicine at University of California, Davis, School of Medicine. Physical examination and bedside diagnosis put the patient at the center of the physician's attention. "The physical exam is gratifying to doctors," she said. "It gives you a chance to get to know the patient, satisfy your basic impulse to make a diagnosis and make the patient feel better." Furthermore, the bedside exam gives attendings the best chance to teach intuitive diagnostic skills and therapeutic techniques that make a patient feel better, Dr. Fitzgerald said. Ten minutes with a patient will teach you more than 20 pages with a textbook, added Dr. Brito. And once you reach private practice, physical diagnosis skills can help you practice more efficiently. Expert diagnosticians point out that when you're pressed for time, it's important to maximize your face-to-face time with patients. Knowing what to look for—and how to rank a patient's symptoms—comes from experience and bedside teaching. As you become more experienced, for example, you aren't likely to routinely do certain maneuvers when examining a heart patient who complains of a sore knee, and not shortness of breath. While first-year residents will think of dozens of possible diagnoses, third-year residents can zero in on the top five or six possibilities. With experience, you will learn which questions you can safely rule out when you take a history. Physical diagnosis skills also serve as a filter for more intelligent use of diagnostic testing, according to Sal Mangione, MD, associate professor of medicine and director of the physical diagnosis curriculum at Jefferson Medical College in Philadelphia. Because unnecessary tests beget more tests (you usually find something unexpected), the lack of any filtering can increase costs and perhaps even harm the patient. Take evaluation of a systolic murmur, a very common and usually benign finding. Studies indicate that an accurate physical examination can usually separate innocent from pathologic murmurs, thus leading to more intelligent, cost-effective use of technology. Building your skills Here are some tips to help you get through the bedside physical diagnosis more efficiently—and compassionately: Control the environment. The noisy hospital room, with its ever-present television, dim lights and busy corridor sounds is not conducive to an accurate examination. Draw the curtain, turn up the lights and find a comfortable position to begin the physical exam. Build rapport. Know the patient's name when you walk into a hospital or exam room. Always ask patients' permission before you begin the exam. Then ask questions and listen. If you're visiting for just five minutes, try to spend at least three minutes listening to the patient. Start at the top. When performing the physical exam, start with the eyes and hands, and work your way down. You can learn a lot from visible signs such as clubbed fingers (possible respiratory disease) or a crease in the earlobe (possible cardiovascular problems). Consider environmental factors. Asking about hobbies, sports activities, travel, country of origin, family history, pets and diet can help pinpoint genetic conditions or disease vectors you might not otherwise consider. Look for mentors. Ask your program director about attendings or faculty who are expert at physical diagnosis, and round with them. A mentor is especially important when learning auscultation skills. Get help from journals. A large body of evidence-based medicine can help you pinpoint the most effective physical maneuvers to help you diagnose. A frequently cited series of articles that has been published in The Journal of the American Medical Association (JAMA) called "The Rational Physical Exam" discusses key physical signs and diagnostic maneuvers for major conditions. Take the long view. Honing physical diagnosis skills is a lifelong process. Building these skills in the hospital will ease the transition to an office or clinic setting, where patients want an immediate diagnosis and you generally cannot rely on a technological quick fix for the answer. Challenges Although there are many benefits to knowing how to do a good physical exam and history, said Dr. Mangione from Jefferson, most physicians still spend too little time during residency and medical school teaching these skills. "Bedside rounds are often not at the bedside at all," he explained. "Surveys have indicated that less than 16% of attending time may be spent at a patient's side." Another study showed that residents on rounds spent a median of nine minutes per patient at the bedside, compared to 32 minutes spent elsewhere on the floor. The constraints of managed care also affect how attendings and residents interact with patients. With outpatient visits limited to an average of 15 minutes and hospital encounters growing shorter all the time, residents have less time to interact with patients. Faculty also face increasing constraints on their bedside teaching time as they are required to take on more patients. Another reason educators are not teaching physical exam skills may be that many faculty simply lack confidence in their bedside diagnostic skills, pointed out Herbert S. Waxman, FACP, the College's Senior Vice President for Education. "Teachers put themselves on the line when they teach," he said, "and the greatest vulnerability is at the bedside." But faculty must make the effort to do more bedside teaching because it pays off for residents. Studies have shown that residents' skills in physical examination correlate with estimates of relative time spent by attending physicians at the bedside. Auscultatory proficiency is one major area where skills are lacking. This may stem in part from the lack of structured teaching of cardiac and pulmonary auscultation. (For more on auscultation tips, see Improve your auscultation skills, this page.) As a result, residents are often inaccurate. In one study conducted by Dr. Mangione, residents were incorrect four out of five times when they identified 12 commonly encountered cardiac auscultatory events. The rate did not improve throughout training: Residents were not significantly better than third-year medical students. That's why we need the return to formal training in the physical exam, said cardiologist Howard Weitz, FACP, deputy chairman of the Jefferson Medical College department of medicine and co-author with Dr. Mangione of an editorial on the value of beside skills in JAMA (Sept. 3, 1997). Fortunately, internal medicine programs are beginning to see the value of the physical exam. After years of absence in the curriculum, the physical exam is being taught in a structured way in more programs, according to Dr. Mangione. "There's a beauty in the physical exam," said Dr. Weitz. "The laying on of hands creates a tangible connection with the patient. The physician who relies on technology only approaches patients from a distance." Christine Kuehn Kelly is a Philadelphia-based freelance writer specializing in health care. Improve your auscultation skills "The Auscultation Assistant," available online at www.med.ucla.edu/wilkes/intro.html, teaches heart and lung sounds. It was created by Chris Cable, ACP-ASIM Associate, a clinician teaching fellow at Seattle VA Medical Center. "Residents could improve their auscultation skills," Dr. Cable said, "and the best way to learn is to hear the sounds repeated." An annotated bibliography of literature on physical examination and interviewing is available from ACP-ASIM at www.acponline.org/public/bedside/index.html. Auscultation case studies from Agilent Technologies, a medical equipment manufacturer, are available at www.healthcare.agilent.com/ medical_supplies/education/toolbox/. The RALE Repository contains a collection of respiratory and heart sounds on the Web at www.rale.ca. "Physiological Origins of Heart Sounds and Murmurs" by J. Michael Criley, FACP. For information go to the Lippincott Williams & Wilkins Web site at http://lww.com/home/, or call 800-638-3030. The Rational Clinical Exam series, published from 1992 to present in The Journal of the American Medical Association, presents evidence-based approaches for more than 30 conditions. (Editorials Physical examination: bewitched @ bothered and bewildered Brendan M Reilly, Christopher A Smith and Brian P Lucas MJA 2005; 182 (8): 375-376) Young physicians today seem confused about physical examination. In the United States, many of them do not know how to do it and do not see why they should. Asymptomatic patients do not seem to need it; the US Preventive Services Task Force found insufficient evidence to recommend periodic physical examination of the breast, prostate, heart or anything else. Sick patients do not seem to benefit much from it either, most of them tested to death regardless of their physical findings. It is hard to say which is the chicken or the egg here, but physical diagnosis instruction in many US medical schools now is either out of date (emeritus faculty members teaching useless arcana like percussion of Traube’s space), out of touch (junior faculty members making rounds in a conference room, not at the bedside), or both. Young physicians trained outside the US are bewildered about this, too. Many of them, meticulously trained in physical examination, are appalled upon first encountering the “hands off” culture of US medicine. But they learn quickly, in the process often unlearning much of what they had learned before. The pace and clinical impact of this remarkable phenomenon is unknown because no one has studied it, a bewildering thing in itself. Many medical professionals claim to be bothered by this trend, but you would not know it from reading the medical literature. Although laudable research has clarified the accuracy (likelihood ratios) and reliability (kappa statistics) of particular physical findings,1 next to nothing is known about physical findings’ impact on patient care.2 In fact, you can count on one hand the number of studies ever published about this issue, not one of them large, controlled or externally funded.2-6 This inattention by researchers to medicine’s core clinical skills seems especially striking in this era of evidence-based medicine, in sharp contrast to the glut of acronymic mega-trials funded by “Big Pharma” to achieve statistically significant (but often clinically trivial) results. Some say not to worry about the lack of published evidence, the clinical value of physical examination is self-evident. To these true believers, we recommend a brief visit to any US teaching hospital today. The National Board of Medical Examiners, not so sanguine, plans to test the bedside skill of US medical students as a new requirement for graduation. This is a wise plan — in part because it has worked well in other countries — but not worth the bother if it ends there. What more can we do? In addition to evaluating how well our physicians learn the basics,7 we must continuously question what we teach them and why. For example, which physical findings have clinical utility in which clinical contexts? Palpating the carotid artery is essential in a patient with angina and a systolic murmur,1 less important in a patient with neck pain. Which physical findings, when shared with radiologists or pathologists, improve interpretation of diagnostic images or biopsies? Contrary to popular belief, the sensitivity and specificity of technological diagnostic tests may not be independent of patients’ clinical findings, knowledge of which may improve test performance.8 Conversely, which aspects of physical examination are useless (inaccurate, unreliable, redundant) or cost-inefficient when compared with technological testing? Thus, the real dilemma today is uncertainty about the “value added” by particular aspects of physical examination to the quality of patient care. If more attention were paid to this issue, more effort could be devoted to maintaining and improving particular bedside skills throughout physicians’ professional careers. Instead, the strongest praise many observers can offer is their feeling that the “laying on of hands” improves communication and trust between doctors and patients, somehow “connecting” them better, not just physically but otherwise. Despite its New Age vibrations, this feeling rings true to us, at least in the sense that careful physical examination focuses the physician, intently and singularly, on this patient now. (As one expert examiner put it, “The stethoscope allows you to connect not only your ears, but also your mind, to the patient.”9) This phenomenon is notable, and deserves further study, but it is not enough to convince the bewildered or sceptical among us about the value of physical examination. Proving scientifically physical examination’s clinical utility is difficult because this requires strict control of potential confounders. But to “isolate” the contribution of physical examination to diagnosis or prognosis — controlling methodologically and analytically for the patient’s history, test results and other confounders — makes little sense clinically. Physical findings add value precisely because they interact with and complement these other sources of information.3-6 For this reason, clinical epidemiologists commonly describe physical findings as “tests” whose result, when combined with a pre-test probability (based on prevalence, the clinical history or both), generates a post-test probability.1 This Bayesian approach makes it easier to describe the accuracy of physical findings, but there is scant evidence that physicians use this kind of reasoning when making clinical decisions. More promising, in our view, are clinical decision rules which, based on multivariate analysis of all potential clinical predictors (including physical findings), quantify the predictive power of the few key determinants of the outcome of interest.10 When impact analysis of such decision rules demonstrates that particular physical findings help to improve patient outcomes (for example, in the management of suspected pulmonary embolism or acute cardiac ischaemia),11,12 sceptics best take heed: these are things we all need to know. Much more research is needed in this area. In the end, we find ourselves bewildered by the need to say these things, bothered by the medical profession’s reticence about them. Together with the history, physical examination is the doctor’s best kept secret — powerful, portable, fast, cheap, durable, reproducible and fun — but it must be allowed out of the closet. We admit we are biased about this, perhaps even bewitched. How could we not be? Like other experienced clinicians, we cannot forget those memorable moments when a careful physical examination yielded magical results: neck veins that resurrected a young mother, moribund from pericardial constriction; a tender temple that rejuvenated an octogenarian, wasted by months of fever; a Babinski reflex that saved an Olympian, his brain tumor too early to see. And more, many more. Such anecdotes prove nothing, of course, but they are . . . bewitching. Modern medicine — bewitched by technology, bothered by its cost, bewildered by those who need it but cannot afford it — would do well to step back, re-examine itself. We recommend a thorough check-up. Preferably by a doctor who takes the time to look, listen, even touch. This should not be difficult to arrange. There are many such doctors out there. Good ones. For now, anyway. McGee S. Evidence-based physical diagnosis. Philadelphia: WB Saunders, 2001. Reilly BM. Physical examination in the care of medical inpatients. Lancet 2003; 362: 1100-1105. <PubMed> Crombie DL. Diagnostic process. J Coll Gen Pract 1963; 6: 579-589. Hampton JR, Harrison MJG, Mitchell JRA, et al. Relative contributions of history-taking, physical examination and laboratory investigation to diagnosis and management of medical outpatients. BMJ 1975; 2: 486-489. <PubMed> Peterson MC, Holbrook JH, Hales DV, et al. Contributions of the history, physical examination, and laboratory investigation in making medical diagnoses. West J Med 1992; 156: 163-165. <PubMed> Roshan M, Rao AP. A study on the relative contributions of the history, physical examination and investigations in making medical diagnosis. J Assoc Physicians India 2000; 48: 771-775. <PubMed> Holmboe ES. Faculty and the observation of trainees’ clinical skills: problems and opportunities. Acad Med 2004; 79: 16-22. <PubMed> Loy CT, Irwig L. Accuracy of diagnostic tests read with and without clinical information. A systematic review. JAMA 2004; 292: 1602-1609. <PubMed> Smith DS. Field guide to bedside diagnosis. Philadelphia: Lippincott Williams and Wilkins, 1999. Laupacis A, Sekar N, Stiell IG. Clinical prediction rules. A review and suggested modifications of methodological standards. JAMA 1997; 277: 488-494. <PubMed> Wells PS, Anderson DR, Rodger M. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and D-dimer. Ann Intern Med 2001; 135: 98-107. <PubMed> Reilly BM, Evans AT, Schaider JJ, et al. Impact of a clinical decision rule on hospital triage of patients with suspected acute cardiac ischemia in the emergency department. JAMA 2002; 288: 342-350. <PubMed> (Received 16 Dec 2004, accepted 31 Jan 2005) Department of Medicine, Cook County Hospital, Chicago, USA. Brendan M Reilly, MD; Christopher A Smith, MD; Brian P Lucas, MD. Now what do you all think? Out Here, ACE844 For those who are interested in evidenced based Dx, H&P, P/E here's a great link: http://depts.washington.edu/physdx/pulmonary/evidence.html http://www.carestudy.com/CareStudy/Default.asp http://www.sgim.org/clinexam.cfm http://www.dartmouth.edu/~biomed/resources...diagnosis.shtml http://www.acponline.org/public/bedside/index.html http://www.meddean.luc.edu/lumen/meded/med...pd/contents.htm http://www.rale.ca/Recordings.htm http://www.neuroexam.com/ http://araw.mede.uic.edu/cgi-bin/testcalc.pl http://www.medal.org/visitor/login.aspx http://members.tripod.com/~LouCaru/index-5.html http://www.saem.org/download/part1c.pdf

"AZCEP," I thought Amiodarone is a Vaughn-Williams class 3 anti-arrythmic is it not? If so, wouldn't that make it a potassium channel blocker, and if so how then would it relate to the mechanisim you mentioned? I know it has class 1-1a-2 properties, but how great is the class 1 effects versus the class 3? Just curious, ACE844

I had a similar situation in one of my clinical rotations as well. I did the 'scut,' and kept my mouth shut..until it got to the point where I was delivering interdept. mail and messages-belongings from nurse to nurse in addition to everything else. Then i went to my program director with the issue and after he suffered a major hypertensive crisis, he straightened it out. Another thing that helped is I worked with the docs as much as possible and once they got comfortable with my abilities and knowledge, they would turn to me instead of the nurse and say..Why don't you go ahead and do the ETI, Cric, ...... It didn't take long before the nurses smartened up, and started to play along as well. Another thing you should be aware of is the fact that when its any nurse vs. you in a disagreement or whatever, your the outsider and the nurses will band together even if they dont agree with or like the nursing party involved, just my .02, and HLO, food for thought, ACE844

Come on guys, there are nearly 9000 members here, Here's your chance to be heard, Vote the poll....Post your opinion and make a difference!!!! ACE844

No tetracaine?!?!?!? 'ASYS,' what did you do to the nurses to induce this sadism? I hope your Ok, and no complications arise from this. It sounds like our luck is similar... Take care, and be sure to watch out for that fickled finger, ACE844

http://www.novalung.com/eng/medical_profes...iLA_therapy.asp

For those who are interested... Here's the 'full-text,' [web:00c7a44ea8]http://sas.epnet.com/externalframe.asp?tb=0&_ug=sid+9E699AFE%2D6895%2D437C%2DA6A6%2D7C2AE7692699%40sessionmgr5+4768&_us=SLsrc+ext+or+Date+034D&_usmtl=ftv+True+137E&_uso=hd+False+db%5B0+%2Dbyh+B26E&fi=byh_18826225_AN&lpdf=true&pdfs=&tn=&tp=PC&es=cs%5Fclient%2Easp%3FT%3DP%26P%3DAN%26K%3D18826225%26rn%3D1%26db%3Dbyh%26is%3D0267%2D6591%26sc%3D%26S%3D%26D%3Dbyh%26title%3DPerfusion%26year%3D2005%26bk%3DS&fn=1&rn=1&bk=S&EBSCOContent=ZWJjY8Pr5HePprBrsOvma6Gmr4GPp7WFpK65faWWxpjDpfS40OnssNOk7KzY5K2 w1+XyvwAA&an=18826225&db=byh&[/web:00c7a44ea8] [web:00c7a44ea8]http://weblinks3.epnet.com/externalframe.asp?tb=1&_ua=bt+TD++%2231J%22+shn+1+db+byhjnh+bo+B%5F+1EDC&_ug=sid+E093B59F%2D885D%2D490A%2D8C22%2DCEB34FB59780%40sessionmgr2+dbs+byh+cp+1+61EA&_us=hd+False+fcl+Aut+sm+ES+or+Date+frn+1+mdbs+byh+sl+%2D1+dstb+ES+sel+False+ri+KAAACB2D00081095+90F4&_uh=btn+N+6C9C&_uso=st%5B0+%2DJN++%22Perfusion%22++and++DT++20051101+tg%5B0+%2D+db%5B0+%2Dbyh+op%5B0+%2D+hd+False+ED7C&fi=byh_18826225_AN&lpdf=true&pdfs=489K&bk=H&tn=11&tp=CP&es=cs%5Fclient%2Easp%3FT%3DP%26P%3DAN%26K%3D18826225%26rn%3D2%26db%3Dbyh%26is%3D02676591%26sc%3DR%26S%3DR%26D%3Dbyh%26title%3DPerfusion%26year%3D2005%26bk%3DH&fn=1&rn=2&[/web:00c7a44ea8] (Seventy-two hour gas exchange performance and hemodynamic properties of NOVALUNG†iLA as a gas exchanger for arteriovenous carbon dioxide removal Xiaoqin Zhou @ David B Loran, Dongfang Wang, Brannon R Hyde, Scott D Lick and Joseph B Zwischenberger Department of Surgery, The University of Texas Medical Branch, Galveston, Texas, USA University Boulevard, Galveston, 77551-0528, Texas.Address for correspondence: Joseph B Zwischenberger, M.D., Division of Cardiothoracic Surgery, Department of Surgery, 301 E-mail: jzwische@utmb.edu Supported in part by Novalung GmBH. Perfusion 2005; 20: 303/308 # 2005 Edward Arnold (Publishers) Ltd 10.1191/0267659105pf838oa) Objective: Acute respiratory failure is complicated by acidosis and altered end-organ perfusion. NOVALUNG† iLA is an interventional lung assist (ILA) device for arteriovenous carbon dioxide removal (AVCO2R). The present study was conducted to evaluate the device for short-term CO2 removal performance and hemodynamic response. Methods: Six adult sheep received cannulation of the jugular vein and carotid artery. The ILA-AVCO2R circuit was placed on the sheep for 72 hours. Hemodynamics and PaCO2 were measured; CO2 removal was calculated while varying sweep gas flow rates (Qg), device blood flow rates (Qb), and PaCO2. Results: Hemodynamic variables remained normal throughout the 72 hour study. CO2 removal increased with increases in Qg or Qb. Mean CO2 removal was 119.3 ml/min for Qb 1 L/ min, Qg 5 L/min, and PaCO2 40/50 mmHg. PaCO2 was directly proportional to CO2 clearance (R/0.72, pB/0.001). Conclusion: NOVALUNG†iLA can provide near total CO2 removal with Qb 1/2 L/min, Qg 5 L/min, and minimal flow resistance (3.889/0.82 mmHg/L/min). PaCO2 correlates with CO2 removal and is dependent on Qb and Qg. Perfusion (2005) 20, 303/308. Introduction Extracorporeal membrane oxygenation (ECMO) may offer life-saving treatment of acute respiratory distress syndrome (ARDS) when conventional therapies have failed.1 ECMO, however, demands sophisticated equipment, well-trained bedside technicians, and is complex and expensive. Blood cell trauma from the pump and blood/surface interactions requires frequent blood transfusions and may augment the systemic inflammatory response.2,3 After animal trials establishing the feasibility of pumpless lung assist, an alternative approach has been developed primarily to remove carbon dioxide (CO2) by a membrane gas exchanger placed in a simple arteriovenous shunt while blood is oxygenated by the native lung.4 12 Arteriovenous carbon dioxide removal (AVCO2R) achieves near total CO2 clearance while allowing oxygenation by native apneic lungs in both sheep models1320 and adult humans with ARDS.19,21,22 Currently, in the United States, there is no FDAapproved, commercially available AVCO2R-specific CO2 removal device. NovaLungTM GmbH (Hechingen, Germany) has developed a small (1.3 m2 polyuropentene-fiber surface area), low-resistance gas exchanger for pumpless interventional lung assist (ILA). The NOVALUNG†iLA system (a photo is available at http://www.novalung.com) consists of a gas exchanger specifically designed for a percutaneous arteriovenous circuit. This gas exchanger’s small size, low resistance, and efficient gas exchange properties are ideal for AVCO2R. The arteriovenous pressure gradient drives blood through the device. Clinical use of NOVALUNG† iLA in Europe has demonstrated efficient oxygenation and CO2 removal in patients with acute respiratory failure.21,23 25 However, there is little large-animal data describing the ability of NOVALUNG† iLA to remove CO2 and maintain hemodynamic stability. Our present study aimed to systematically test the CO2 exchange capacity of the NOVALUNG†iLA and assess hemodynamic response in large animals (sheep) over a 72-hour study period. Materials and Methods Animals All animals received care according to the ‘Guide for the Care and Use of Laboratory Animals (1985)’ prepared by the US Department of Health and Human Services and published by the National Institutes of Health (NIH). The study was approved by the Institutional Animal Care and Use Committee (IACUC) of the University of Texas Medical Branch, Galveston, with strict adherence to the IACUC guidelines regarding humane use of animals. Our management of the sheep parallels our standards for patient care. Our team, including a faculty veterinary anesthesiologist, provides bedside care 24 hours per day. Animal Resource Center personnel make daily rounds to insure animal management protocol adherence. Surgical procedure Adult female sheep (n/6, 3/4 years old, 35/45 kg) were given ketamine (12.5 mg/kg intramuscular, 9/5 mg/kg intravenous titrated to effect) for initial sedation. The sheep were then orally intubated with an endotracheal tube and placement was confirmed by capnometry. Three percent halothane was administered via the anesthesia ventilator (Ohmeda 7000, BOC Health Care, Liberty Corner, NJ). Anesthesia was maintained during the surgical procedures with 1/2.5% isoflurane in 2/3 L/min oxygen titrated to a heart rate of 75/120 beats per minute. The sheep were prepped at the neck and groin and draped in the supine position. Using the Seldinger technique, a pulmonary artery/thermal dilution cardiac output catheter (Swan-Ganz, Baxter Healthcare Corp., Edwards Critical-Care Division, Irvine, CA) was introduced into the right external jugular vein. The right femoral artery and vein then were each cannulated with 16 gauge, 60-cm catheters (Intracath, Becton-Dickinson, Sandy, UT) via a sterile cut-down for blood gas sampling, hemodynamic monitoring and intravenous infusion. Equipment procedure All animals initially received a tracheostomy for further anesthesia administration and ventilator assistance in recovery. All sheep were anticoagulated with intravenous heparin (initial dose 100 units/kg bovine lung heparin, Upjohn, Kalamazoo, MI) for an activated clotting time (ACT, measured with Hemochron 400, International Technidyne, Edison, NJ) between 180/300 s. Sterile incision and cannulation (BIO-MEDICUS@ Pediatric venous cannula, Medtronic Inc., Minneapolis, MN) in the left carotid artery (12 Fr.) and left internal jugular vein (14 Fr.) was performed. The common carotid artery was ligated distal to the cannula. The NOVALUNG† iLA was primed with 240 mL of normal saline, de-aired, and connected to the vascular cannulae. Once the AVCO2R circuit was secured to the sheep, isoflurane was discontinued. The animals were transported to the ICU for recovery, connected to a volume-controlled ventilator (Servo 900C; Siemens- Elema SoPna, Sweden) and allowed access to food and water. Gas exchange with the native lung and the ILA device was observed for 72 hours. The fraction of inspired oxygen (FiO2) was titrated between 0.4 and 1.0 and the positive end-expiratory pressures (PEEP) between 5 and 10 mmHg to maintain adequate PaO2 levels (/80 mmHg). A HP 78534B Monitor continuously monitored systemic hemodynamic variables which included heat rate (HR), mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP) and cardiac output (CO). AVCO2R circuit blood flow was measured by a real-time flow meter (HT109, Transonic Systems, Ithaca, NY) with full continuous flow as determined by the size of the arterial cannula.26 Blood flow could be regulated by a C clamp on inlet blood tubing. Mean arterial pressures in the device inflow and outflow were measured intermittently. Partial pressures of gases in device inflow and outflow tubing were measured by the Synthesis 15 blood gas analysis system (Instrumentation Laboratory, Lexington, MA). During the 72-hour study, hemodynamic parameters, blood gases, and CO2 removal were evaluated and recorded at 0, 24, 48 and 72 hours. Prior to measuring CO2 removal at indicated timepoints, spontaneous breathing was suppressed by boluses of intravenous pentobarbital (180/200 mg/kg) to allow for a fixed respiratory rate of 4 breaths per minute. Tidal volume was adjusted between 2 and 8 mL/kg to maintain PaCO2 between 20 and 80 mmHg to observe the effects of PaCO2 on CO2 removal. The NOVALUNG†iLA sweep gas was 100% oxygen and the flow rate was controlled by an in-line flow regulator. Exhaust sweep gas CO2 concentration was measured in-line. Carbon dioxide clearance was calculated based on sweep gas flow and exhaust gas CO2 concentrations. Resistance was calculated as the quotient of the pressure drop and device flow. Statistical analysis All data were reported as mean value9/standard deviation. The relationships between dependent and independent variables were evaluated by one way ANOVA on rank and linear regression analysis. NOVALUNG†iLA for AVCO2R Results During the 72-hour observation course, hemodynamic parameters (MAP, MPAP, PCWP, CVP and CO) remained within normal limits and unchanged (p/0.05, Figure 1). Mean resistance through the lung assist device was 3.889/0.82 mmHg/L/min and independent of blood flow (Qb) and sweep gas flow (Qg). There was no device thrombosis, leakage, or other complications noted. Effect of sweep gas flow on CO2 removal With constant Qb and PaCO2, CO2 removal increased with Qg (1/15 L/min) directly and significantly (pB/0.001), but nonlinearly. With constant Qb (1 L/min), CO2 clearance was 60.039/4.43 mL/min with 1 L/min Qg, 92.909/14.70 mL/min with 2 L/min Qg, and 120.749/26.98 mL/min with 5 L/min Qg. Only a small increase in CO2 clearance was observed (133.599/24.63 mL/min for 10 L/min Qg and 140.259/34.10 mL/min for 15 L/min Qg) for further increases in sweep gas (Figure 2). Effect of Qb on CO2 removal With constant Qg (5 L/min) and PaCO2 (40/50mmHg), Qb was incrementally increased from 0.5L/min to 1.5 L/min while measuring CO2 removal.CO2 clearance increased from 84.049/25.01 mL/min to 139.409/27.61 mL/min (pB/0.05, Figure 3). For the 72-hour period (except for temporary experimental adjustments), we set Qb (1 L/min) and Qg (5 L/min) constant. Mean CO2 clearance was 119.39/25.1 mL/min (range, 57.6 to 174.5 mL/min).The quantity of CO2 removal did not significantly change with time (Figure 4). Effect of PaCO2 on CO2 removal With a constant Qb (1 L/min) and Qg (5 L/min), CO2 clearance was directly proportional to PaCO2 as it was increased from 20 to 80 mmHg by hypoventilation. A significant correlation between CO2 clearance and PaCO2 was expressed as: CO2 Removal14:9PaCO2 2:65 (R0:72; pB0:001; Figure 5): Discussion The NOVALUNG†iLA system removed CO2 efficiently with a simple arteriovenous shunt. Carbon dioxide clearance was influenced by the following factors: device blood flow, sweep gas flow and arterial PCO2. At PaCO2 between 40/50 mmHg, an increase in CO2 removal was seen as the sweep gas flow varied from 1 L/min to 15 L/min with a constant blood flow of 1 L/min. This increase became relatively less when sweep gas flow was above 5 L/min. Likewise, enhanced CO2 removal Figure 1 Hemodynamic response with time. p/0.05 (one-way ANOVA) at each time point. Figure 2 Relationship of sweep gas flow and CO2 removal. pB/0.001 (one-way ANOVA on rank) at each time point. NOVALUNG†iLA for AVCO2R was shown as blood flow varied from 0.5 L/min to 1.5 L/min with a constant sweep gas flow rate of 5 L/ min. When blood flow and sweep gas flow rates were held constant at 1 L/min and 5 L/min, respectively, CO2 removal varied directly with PaCO2 (20/80 mmHg). These results show the PaCO2 level and subsequent respiratory acidosis could be controlled over a wide range of arterial PaCO2 by adjusting the sweep gas flow or blood flow rate through the device. In addition, there was no evidence of hemodynamic instability for the 72-hour duration. Previous AVCO2R circuits have utilized commercially available gas exchange devices or ‘‘oxygenators’’ originally designed for cardiopulmonary bypass during cardiac surgery. The commercially available Affinity† (Medtronic Minneapolis, MN) device is an oxygenator with a conjoined heat exchanger. The Affinity† oxygenator consists of hollow polypropylene micropore fibers with total gas exchange surface area of 2.5 m2 and 270 ml of priming volume. AVCO2R utilizing the Affinity† has shown total removal of CO2 during acute respiratory failure and hypercapnea, normalization of arterial PCO2 and pH, and significant reductions in the level of mechanical ventilation required in both animal models4,5,7,8,10,18 and phase I clinical trials in adults with severe ARDS.19,22 The mean or median CO2 removal rates were in excess of 100 mL/min in both phase I studies. In large animal ARDS models, AVCO2R allows for decreased peak airway pressures resulting in reduced alveolar stretch, lower expression of interleukin-8, and lower rate of neutrophil translocation across damaged alveolar basement membranes.27 Decreased ventilator pressures might also ameliorate apoptosis of lung cells by down-regulating expression of tumor necrosis factor alpha (TNF-a) and proapoptotic factor.28 By providing control of PaCO2 and arterial pH, AVCO2R can attenuate the inflammatory response in ARDS and the iatrogenic damage caused by high ventilatory pressures. Clinically, these effects are manifested in patients with severe respiratory failure as an improvement in the PaO2/FiO2 ratio and reversal of CO2 retention.19 Compared to the Affinity†, the NOVALUNG†iLA has a smaller surface area (1.3 m2) of biocompatible hollow polymethylpentene fibers and smaller priming volume (240 mL) that theoretically minimizes blood trauma while maintaining an appropriate flow (around 1/2 L/ min) to surface area ratio. This smaller surface area allows near-total CO2 clearance through an arterialvenous shunt flow of only 10 to 15% of cardiac output, a flow rate we have previously shown not to affect distal organ perfusion.6 More recently, a hollow-fiber gas exchanger29,30 was designed with 1 m2 surface area that enables CO2 removal of 41 mL/min with 1 L/min blood flow Figure 4 CO2 removal over 72 hours at blood flow of 1 L/min, sweep gas of 5 L/min, and PaCO2 of 40/50 mmHg. Figure 5 CO2 removal as a function of PaCO2 at blood flow of 1 L/min and sweep gas flow of 5 L/min; pB/0.001. Figure 3 Relationship of blood flow and CO2 removal. pB/0.05 (one-way ANOVA on rank) at each time point. NOVALUNG†iLA for AVCO2R and 3 L/min sweep gas flow. However, the higher resistance of 20/40 mmHg/L/min may limit use without the addition of a pump.31 An ambulatory AVCO2R prototype from our group is composed of ultra tight polymethylpentene hollow fibers with 2m2 surface area and removes CO2 at 104.89/14.0 mL/min for 0.9 L/min blood flow and 2 L/min sweep gas flow with a mean resistance of 2.89/0.8 mmHg/L/min.32 The NOVALUNG†iLA device compares favorably with these alternative designs with a CO2 removal rate of 119.39/25.1 mL/min at 1 L/min blood flow and 5 L/min sweep gas flow with resistance as low as 3.889/0.82 mmHg/L/min. Recently, the NOVALUNG†iLA was utilized in an arterio-venous circuit for a case of ARDS refractory to high frequency oscillatory ventilation. PaCO2 was improved from 13.3 to 9.3 KPa and pH (baseline 7.14) was normalized within 4 hours at 2.1 L/min blood flow and 12 L/min sweep gas flow.25 Based on our 72-hour study, we conclude that the NOVALUNG†iLA AVCO2R circuit achieves predictable CO2 elimination via the small and ultra lowresistance gas exchanger without hemodynamic compromise. Carbon dioxide removal increases with increased arterial PCO2 gradient and can be augmented by increasing sweep gas flow and/or blood flow rates. Use of NOVALUNG†iLA in the management of acute respiratory failure is promising and demands further clinical application and outcomes determination. References 1 O’Rourke PP, Stolar CJ, Zwischenberger JB, Snedecor SM, Bartlett RH. Extracorporeal membrane oxygenation: support for overwhelming pulmonary failure in the pediatric population. Collective experience from the extracorporeal life support organization. J Pediatr Surg 1993; 28: 523/9. 2 Upp JR, Jr., Bush PE, Zwischenberger JB. Complications of neonatal extracorporeal membrane oxygenation. Perfusion 1994; 9: 241/56. 3 Zwischenberger JB, Cox CS, Jr., Minifee PK, et al. Pathophysiology of ovine smoke inhalation injury treated with extracorporeal membrane oxygenation. Chest 1993; 103: 1582/6. 4 Brunston RL, Jr., Tao W, Bidani A, et al. Prolonged hemodynamic stability during arteriovenous carbon dioxide removal for severe respiratory failure. J Thorac Cardiovasc Surg 1997; 114: 1107/14. 5 Brunston RL, Jr., Tao W, Bidani A, et al. Determination of low blood flow limits for arteriovenous carbon dioxide removal. Asaio J 1996; 42: M845/9. 6 Brunston RL, Jr., Tao W, Bidani A, Traber DL, Zwischenberger JB. Organ blood flow during arteriovenous carbon dioxide removal. Asaio J 1997; 43: M821/4. 7 Brunston RL, Jr., Zwischenberger JB, Tao W, et al. Total arteriovenous CO2 removal: simplifying extracorporeal support for respiratory failure. Ann Thorac Surg 1997; 64: 1599/605. 8 Alpard SK, Zwischenberger JB, Tao W, Deyo DJ, Bidani A. Reduced ventilator pressure and improved P/F ratio during percutaneous arteriovenous carbon dioxide removal for severe respiratory failure. Ann Surg 1999; 230: 215/24. 9 Conrad SA, Brown EG, Grier LR, et al. Arteriovenous extracorporeal carbon dioxide removal: a mathematical model and experimental evaluation. Asaio J 1998; 44: 267/77. 10 Jayroe JB, Alpard SK, Wang D, et al. Hemodynamic stability during arteriovenous carbon dioxide removal for adult respiratory distress syndrome: a prospective randomized outcomes study in adult sheep. Asaio J 2001; 47: 211/4. 11 Jayroe JB, Wang D, Deyo DJ, et al. The effect of augmented hemodynamics on blood flow during arteriovenous carbon dioxide removal. Asaio J 2003; 49: 30/4. 12 De Somer F, Van Belleghem Y, Foubert L, et al. Feasibility of a pumpless extracorporeal respiratory assist device. J Heart Lung Transplant 1999; 18: 1014/ 7. 13 Murphy JA, Savage CM, Alpard SK, et al. Low-dose versus high-dose heparinization during arteriovenous carbon dioxide removal. Perfusion 2001; 16: 460/8. 14 Pierre EJ, Zwischenberger JB, Angel C, et al. Extracorporeal membrane oxygenation in the treatment of respiratory failure in pediatric patients with burns. J Burn Care Rehabil 1998; 19: 131/4. 15 Tao W, Brunston RL, Jr., Bidani A, et al. Significant reduction in minute ventilation and peak inspiratory pressures with arteriovenous CO2 removal during severe respiratory failure. Crit Care Med 1997; 25: 689/95. 16 Wildin SR, Landry SH, Zwischenberger JB. Prospective, controlled study of developmental outcome in survivors of extracorporeal membrane oxygenation: the first 24 months. Pediatrics 1994; 93: 404/8. 17 Zwischenberger JB, Alpard SK, Conrad SA, Johnigan RH, Bidani A. Arteriovenous carbon dioxide removal: development and impact on ventilator management and survival during severe respiratory failure. Perfusion 1999; 14: 299/310. 18 Zwischenberger JB, Alpard SK, Tao W, Deyo DJ, Bidani A. Percutaneous extracorporeal arteriovenous carbon dioxide removal improves survival in respiratory distress syndrome: a prospective randomized outcomes study in adult sheep. J Thorac Cardiovasc Surg 2001; 121: 542/51. 19 Zwischenberger JB, Conrad SA, Alpard SK, Grier LR, Bidani A. Percutaneous extracorporeal arteriovenous CO2 removal for severe respiratory failure. Ann Thorac Surg 1999; 68: 181/7. 20 Zwischenberger JB, Nguyen TT, Upp JR, Jr., et al. Complications of neonatal extracorporeal membrane oxygenation. Collective experience from the Extracorporeal Life Support Organization. J Thorac Cardiovasc Surg 1994; 107: 838/49. NOVALUNG†iLA for AVCO2R X. Zhou et al.307 21 Reng M, Philipp A, Kaiser M, et al. Pumpless extracorporeal lung assist and adult respiratory distress syndrome. Lancet 2000; 356: 219/20. 22 Conrad SA, Zwischenberger JB, Grier LR, Alpard SK, Bidani A. Total extracorporeal arteriovenous carbon dioxide removal in acute respiratory failure: a phase I clinical study. Inten Care Med 2001; 27: 1340/51. 23 Liebold A, Reng CM, Philipp A, Pfeifer M, Birnbaum DE. Pumpless extracorporeal lung assist - experience with the first 20 cases. Eur J Cardiothorac Surg 2000;17: 608/13 24 Bein T, Prasser C, Philipp A, et al. Pumpless extracorporeal lung assist using arterio-venous shunt in severe ARDS. Experience with 30 cases. Anaesthesist 2004; 53: 813/9. 25 David M, Heinrichs W. High-frequency oscillatory ventilation and an interventional lung assist device to treat hypoxaemia and hypercapnia. Br J Anaesth 2004; 93: 582/6. 26 Frank BR, Tao W, Brunston RL, Jr., et al. High flow/low resistance cannulas for percutaneous arteriovenous carbon dioxide removal. Asaio J 1997; 43: M817/20. 27 Schmalstieg FC, Chow J, Savage C, et al. Interleukin-8, aquaporin-1, and inducible nitric oxide synthase in smoke and burn injured sheep treated with percutaneous carbon dioxide removal. Asaio J 2001; 47: 365/71 28 Vertrees RA, Nason R, Hold MD, et al. Smoke/burn injury-induced respiratory failure elicits apoptosis in bovine lungs and cultured lung cells, ameliorated with arteriovenous CO2 removal. Chest 2004; 125: 1472/82. 29 Kawahito S, Motomura T, Glueck J, Nose Y. Development of a new hollow fiber silicone membrane oxygenator for ECMO: the recent progress. Ann Thorac Cardiovasc Surg 2002; 8: 268/74. 30 Kawahito S, Haraguchi S, Maeda T, et al. Preclinical evaluation of a new hollow fiber silicone membrane oxygenator for pediatric cardiopulmonary bypass: exvivo study. Ann Thorac Cardiovasc Surg 2002; 8: 7/ 11. 31 Kawahito S, Maeda T, Motomura T, et al. Feasibility of a new hollow fiber silicone membrane oxygenator for long-term ECMO application. J Med Invest 2002; 49:156/62. 32 Wang D, Lick S, Alpard SK, et al. Toward ambulatory arteriovenous CO2 removal: initial studies and prototype development. Asaio J 2003; 49: 564/7.

"Asys," I'm going to have to disagree with you on this one and refer you to the article I posted on the previous page. Versed is an amnestic...So just because you got it, and then later can't remember that you had the pain, doesn't mean you and your body weren't still at the time experiencing the cruel, and undesirable physiologic side effects which can be very underirable in a patient population which is already physiologically compromised enough to warrant RSI-ETI emergently..Food for thought, Stay safe in the jungle, ACE844

which is purportedly speculation as no one has actually had discourse with him as far as we are able to ascertain.

That was rough I am sure...I am also sure finding that must have been worse...I'm glad it wasn't me, and I am quite sure Rykers is too nice a place for that trash, especially with his history. I heard a rumor your boys in blue tuned him up... good.... Hope all is well in your neck of the woods, I amy be down in the bronx in a few months.. Hope to run into you and Richard in the city. Also, I agree with your statements above! Be safe, ACE

Well I know for the long term part of why they mix it that way are for the reasons I mention above. Also considerations are 'compatibility' issues like the 'amiodarone'. Also, sometimes they use it with chemo drugs because they non-vessicant, and vessicant, so it is bad if they extravasate from a vessel. Out Here, ACE844

Some information related to what you requested can be found here: http://www.squidoo.com/hybridcarhazards/ http://www.emtcity.com/phpBB2/viewtopic.php?t=2479 http://www.emtcity.com/phpBB2/viewtopic.php?t=1499 ACE844

"FL_Medic," Are you asking if they use D5W in an amiodorance drip to 'ward off' Hyperchloremic acidosis and or hypernatremia? Just trying to understand your question more clearly. ACE844

Seems to me the victim of that was from up this way....If we are talking the same case..Night club bouncer the perp?

Nope...

No problem

Here are some links on documentatiopn and soem other aspects of it:: http://www.emtcity.com/phpBB2/viewtopic.php?t=561 http://www.emtcity.com/phpBB2/viewtopic.php?t=3560 http://www.emtcity.com/phpBB2/viewtopic.php?t=4431 http://www.emtcity.com/phpBB2/viewtopic.php?t=2342 http://www.emtcity.com/phpBB2/viewtopic.php?t=1305 http://www.emtcity.com/phpBB2/viewtopic.php?t=2414 http://www.emtcity.com/phpBB2/viewtopic.php?t=2471 http://www.emtcity.com/phpBB2/viewtopic.php?t=1482 http://www.emtcity.com/phpBB2/viewtopic.php?t=1069 Hope this helps, ACE844

good guess but no..

DWPA: Dead With Paramedic Assistance.. :wink: :shock: 8) hahahahaha,..... just kidding