chbare

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chbare last won the day on December 18 2016

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About chbare

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  1. Pathophysiology of cyanide poisioning

    Hi Kenny, the chief way cyanide antidotes work is not really centered around directly acting on cytochrome c oxidase, but rather haemoglobin; at least in the case of the traditional therapy (Nitrates + Methylene Blue). As I outlined in the video, the traditional therapy changes the oxidation state of the Iron atom in the porphyrin ring of the sub units of haemoglobin. Typically, the Iron will be in a default configuration of +2/Fe II/Ferrous. Nitrates and other substances can further oxidise the Iron into the +3/FeIII/Ferric state. For reasons that I cannot pull out of my head (I suspect it has to do with the fact that Fe III is a strong Lewis acid and would not be able to coordinate reversibly with the Oxygen molecule.) Fe III does not coordinate with the Oxygen molecule. It however does coordinate exceptionally well with cyanide. This will create a situation where kinetics and thermodynamics favour cyanide coordination with the haemoglobin as opposed to the Iron in the cytochrome c oxidase enzyme. However, this also means the patient has methaemoblobin toxicity and could develop histotoxic hypoxia due to ineffective haemoglobin function. Hence, the need to administer agents that can reduce haemoglobin such as methylene blue. However, the other antidote modality in the United States works very differently. Hydroxocobalamin is a vitamin B12 precursor that contains a Cobalt atom configured in a way that allows it to have a high affinity for the cyanide molecule. The high affinity favours the coordination of cyanide with the Cobalt as opposed to the Iron in cytochrome c oxidase. Again, the exact details are complex, but chemical kinetics and thermodynamics favour Cobalt coordination in this case. A relatively inert molecule known as cyanocobalamin is produced in a 1:1 manner (1 mole of hydroxocobalamin can coordinate with 1 mole of cyanide) that is easily eliminated in the urine. Hopefully that helps out a bit. No worries about being a student. Do not let anybody make you think humanity has developed a deep understand of these things. Much of the universe is a complete mystery to us and as you progress along your educational pathway, you will likely be disturbed from how inadequate and uncertain you feel at each step along the process. My experience has been that with every degree that I have obtained, I had the expectation that I would emerge with a more comprehensive understanding of the world. Every step left me lacking significantly. This was not due to lack of trying or failure of dedication, but a fundamental part of the uncertainty of being a human being attempting to understand a vast and complex universe. Point being, I do not want you to be discouraged.
  2. Pathophysiology of cyanide poisioning

    Good day. You are a bit off but the general reasoning in the the right direction. I will post a video that I filmed some years ago while I was in graduate school. It covers this topic, but I'd ask that you review the concepts of ferrous versus ferric Iron and ultimately, the concept of oxidation state. The Iron in Cytochrome c oxidase is in a similar configuration as haemoglobin but the enzyme dynamics dictate a narrative that is counter to the typical "blood poisoning" that sometimes surrounds a discussion of Cyanide Toxicity. I must warn you that I was grossly overweight and profoundly depressed when I made the video, so it's not super high fidelity, but the information is relevant nonetheless.
  3. CHF & Low BP

    Dobutamine is a tricky one. Like some of the other sympathomimetics, it comes as a racemic mixture. One isomer has very mild alpha 1 agonist effects while the other isomer has mild alpha 1 antagonising effects. This means it may not reliably support blood pressure, even if it does enhance contractility. In an already hypotensive patient, dobutamine may be problematic without the concomitant use of agents that are better at supporting blood pressure.
  4. 2015 ACLS updates

    Targeted temperature management in the ROSC patient is one of the bigger changes.
  5. Narcan at the EMT level.

    Again, I think it is important to emphasise a key point. ERdoc is not talking about "awaking" people up. I believe he and others are discussing this in terms of a much more nuanced approach. As already stated, anecdote is of limited value when attempting to generalise. Is there literature that looks at the issue at hand however?
  6. Thoughts on this? Uber style Narcan delivery!

    First, we need to be able to divorce human hubris and bias from the discussion. For example, I saw earlier comments go on about heroin. What does the data tell us about the types of opioid overdoses that are killing folks? In many cases, the substances involved were not illegally pulled from poppy fields in Afghsnistan, but rather were from prescription opioids. Once we start attaching emotions and using bias to conflate the picture, it is easy to make incorrect conclusions that can further reinforce prior assertions that may not accurately reflect the actual situation. With that said, I would ask to look at the evidence. What is the impact when naloxone programmes are used? Do they lead to increased abuse and more problems as some may assert? In general, how does education and risk reduction compare to the use of coercion (making drugs illegal and throwing people in prison) when combating the issue of opioid associated death via overdose? There is a base of literature out there that could allow us to make reasonable conclusions. Regarding this particular article and novel approaches it suggests, I'd ask if it was worth considering the author's thesis based on the current literature. I'm not entirely sure, but would it be worthwhile for somebody to develop a protocol, approach an IRB and gather some data?
  7. Pain Management

    Oh, pain meds were given, but the patient was pretty messed up and giving more than 100 mcg of fentanyl will apparently result in a patient's head spinning around a couple of times, falling off, rolling down the hallway and spontaneously combusting in the Pyxis room.
  8. Pain Management

    Man, just had a rough one in the ER. Older patient fell down and sustained multiple fractures. Screaming in pain, couldn't get orders. It sucks seeing people needlessly suffer. Rather happy my hospital shifts are limited by educational duties these days. It can be a pretty nihilistic environment as far as providers are concerned. Some days are a constant fight against people who just don't care or are really good at making up reasons not to care. Even worse not having any power to facilitate comfort. Don't take the autonomy you have to make more independant decisions out in the field lightly folks.
  9. Pain Management

    [Citation needed].
  10. Pain Management

    Pain is a pretty subjective experience and addicts also experience pain. I ended up in the hospital last year with a prostate infection, in terrible pain. Because I appeared calm and collected I was not given pain medications. I was able to convince a PA to write me a script for a few tablets of pyridium however. Don't assume you know how to weed out fakers, you may very well be incorrect. Fentanyl is certainly not a "lower level" medication than morphine. Neither is Toradol. Also remember fentanyl is an opioid analgesic like morphine. Twenty minutes of severe pain is twenty minutes of suffering. The evidence is rather weak in supporting the life saving potential of EMS, but being able to respond to pain and suffering is actually something that we have a bit of control over. If anything, managing pain is a primary indication for ALS care.
  11. Oxygen causing harm?

    There is actually a fair amount of literature about this issue. I am not sure how much physical science you have but Oxygen at "normal" levels is harmful. Mammals have evolved complex enzyme systems to deal with the consequences of Oxygen and highly reactive molecules and forms of Oxygen known as reactive Oxygen species or ROS. These are a natural consequence of normal cellular respiration. Heck, our immune system sometimes makes use of ROS as part of the inflammatory response and when attacking pathogens. While mammalian physiology is generally good at dealing with ROS, many situations can markedly increase the amount of ROS being produced. This is known as oxidative stress. Good luck looking for literature. It's certainly out there but a perfectly clear and concise picture has not been completely developed.
  12. Stump the Chump/medic: IV Opioids AND IV Alcohol

    1) I would assume the area under the concentration/time curve would be larger as is the case for other substances that are given in a way that bypasses first pass. Ethanol already has a high bioavailability, but I would anticipate a bioavailability approaching 1.0 and a very rapid peak in plasma concentration. As far as metabolism and elimination, ethanol quickly reaches saturation kinetics and as such follows 0 order elimination kinetics even at low concentrations. I would not anticipate this to change. Ethanol is metabolised via three pathways: ADH enzyme, catalase enzymes and CYP2E1. Normally, catalase and CYP2E1 are minor pathways, but with chronic ethanol exposure, CYP2E1 is inducible. I'd expect that to occur with chronic ethanol exposure at sufficiently high enough concentrations regardless of the route. 2) Reasonably high with enough use. 3) Not sure, but I'm not surprised by the story.
  13. EMT to Advanced EMT

    I completed an EMT-I/85 to AEMT transition class and took the national exam and I currently teach AEMT classes. It will be roughly similar to EMT. You can expect an additional 200-300 hours of lab, lecture and clinical experience. You will dive into some concepts such as pharmacology and the human body in more detail and learn about a few new interventions, interventions you probably have a basic understanding of, being an Army medic. The registry exam is interesting, long and much more complex than the EMT exam. Good luck.
  14. Septic Shock Management

    Unfortunately, medicine is not nearly as evidence based as we often like to profess. There are many interesting situations. Think about "coma cocktails," tissue plasminogen activator for ischaemic stroke and others that are based on evidence that is perhaps not as robust as we would like. Fortunately, we can have dialogue and discuss some of these issues. With that, I still believe general guidelines are still generally good and can act as a starting point or a place to run back home to mom when we are completely lost. They also help to put everybody on the same page in critical situations. However, sometimes our care may not be in perfect alignment with guidelines and guidelines can also change. It's so important to look at the evidence as we are doing here. It's also possible for two very qualified people to come of with different conclusions and that discourse is interesting, relevant and hopefully, productive to discuss.
  15. Septic Shock Management

    I recently had a discussion with a friend who turned me onto to some new material out of our friends at emcrit (Thanks Ronel!). The original podcast with Dr. Marik's conclusions can be found here: http://emcrit.org/po...-fluids-sepsis/ The response to Dr. Marik's lecture can be found here: http://emcrit.org/po...-severe-sepsis/ I would strongly suggest people go through both the initial lecture and response before replying, but I would love to get every bodies take on this interesting issue.