Podcasts about pco2

This episode on Happy Hour with Bundle Birth Nurses, Sarah Lavonne is joined with Bundle Birth educator, Heidi Nielsen in this enlightening episode as they dive into the critical world of cord gas analysis. Understanding cord gas results is essential in guiding newborn care, particularly for identifying infants at risk of hypoxic ischemic encephalopathy (HIE) who may need therapeutic cooling.Sarah and Heidi break down the basics of interpreting arterial and venous cord gases, explaining why parameters like pH, PCO2, and base deficit matter so much. They discuss the signs of respiratory and metabolic acidosis, how each can impact a newborn's health, and why proper sample collection is so important—especially in settings without immediate NICU access.In this episode, you'll learn how these essential numbers reveal vital clues about a newborn's condition, empowering nurses to support and advocate for newborns from the very start.EDIT at 12:59: ACOG says 7.0 for pH, AWHONN says 7.1, What the research shows is that injury occurs at 7.18, and injury becomes more likely as you continue to move towards 7.0. Normal pH is actually considered to be 7.2.Helpful Links: Follow on Instagram and stay tuned Wednesday for Test Your Knowledge day.Join our Mentorship Program!RNC-OB Exam Prep Class

In today's episode, hosts Anna Madlener and Wil Burns are joined by Grace Andrews from Hourglass Climate. They discuss Hourglass' work on environmental monitoring and carbon removal quantification of Ocean Alkalinity Enhancement (OAE)  trials as a research non-profit.To view the Ocean Visions webinar referenced on the podcast, click here: LINK.Acronyms:MRV (1:42) mCDR (3:28)USGS (18:51)EPA (19:32)NOAA (20:51)LCA (23:09)pCO2 (25:02)Plan Sea is a semi-weekly podcast exploring ocean-based climate solutions, brought to you by the Carbon to Sea Initiative & the American University Institute for Responsible Carbon Removal.

In neurocritical care, the initial evaluation is often fast paced, and assessment and management go hand in hand. History, clinical examination, and workup should be obtained while considering therapeutic implications and the need for lifesaving interventions. In this episode, Aaron Berkowitz, MD, PhD FAAN, speaks with Sarah Wahlster, MD, an author of the article “The Neurocritical Care Examination and Workup,” in the Continuum June 2024 Neurocritical Care issue. Dr. Berkowitz is a Continuum® Audio interviewer and professor of neurology at the University of California San Francisco, Department of Neurology and a neurohospitalist, general neurologist, and a clinician educator at the San Francisco VA Medical Center and San Francisco General Hospital in San Francisco, California. Dr. Wahlster is an associate professor of neurology in the departments of neurology, neurological surgery, and anesthesiology and pain medicine at Harborview Medical Center, University of Washington in Seattle, Washington. Additional Resources Read the article: The Neurocritical Care Examination and Workup Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz Guest: @SWahlster Full Episode Transcript Sarah Wahlster, MD   Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, a companion podcast to the journal. Continuum Audio features conversations with the guest editors and authors of Continuum, who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article by clicking on the link in the Show Notes. Subscribers also have access to exclusive audio content not featured on the podcast. As an ad-free journal entirely supported by subscriptions, if you're not already a subscriber, we encourage you to become one. For more information on subscribing, please visit the link in the Show Notes. AAN members: stay tuned after the episode to hear how you can get CME for listening.  Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Sarah Wahlster about her article on examination and workup of the neurocritical care patient, which is part of the June 2024 Continuum issue on neurocritical care. Welcome to the podcast, Dr Wahlster. Can you please introduce yourself to the audience? Dr Wahlster: Thank you very much, Aaron. I'm Sarah Wahlster. I'm a neurologist and neurontensivist at Harborview Medical Center at the University of Washington. Dr Berkowitz: Well, Sarah and I know each other for many, many years. Sarah was my senior resident at Mass General and Brigham and Women's Hospital. Actually, Sarah was at my interview dinner for that program, and I remember meeting her and thinking, “If such brilliant, kind, talented people are in this program, I should try to see if I can find my way here so I can learn from them.” So, I learned a lot from Sarah as a resident, I learned a lot from this article, and excited for all of us to learn from Sarah, today, talking about this important topic. So, to start off, let's take a common scenario that we see often. We're called to the emergency room because a patient is found down, unresponsive, and neurology is called to see the patient. So, what's running through your mind? And then, walk us through your approach as you're getting to the bedside and as you're at the bedside. Dr Wahlster: Yeah, absolutely. This was a fun topic to write about because I think this initial kind of mystery of a patient and the initial approach is something that is one of the puzzles in neurology. And I think, especially if you're thinking about an emergency, the tricky part is that the evaluation and management go hand in hand. The thinking I've adapted as a neurointensivist is really thinking about “column A” (what is likely?) and “column B” (what are must-not-miss things?). It's actually something I learned from Steve Greenberg, who was a mutual mentor of us - but he always talked me through that. There's always things at the back of your head that you just want to rule out. I do think you evaluate the patient having in mind, “What are time-sensitive, critical interventions that this patient might need?” And so, I think that is usually my approach. Those things are usually anything with elevated intracranial pressure: Is the patient at risk of herniating imminently and would need a neurosurgical intervention, such as an EVD or decompression? Is there a neurovascular emergency, such as an acute ischemic stroke, a large-vessel occlusion, a subarachnoid hemorrhage that needs emergent intervention? And then other things you think about are seizures, convulsive/nonconvulsive status, CNS infection, spinal cord compression. But I think, just thinking about these pathologies somewhere and then really approaching the patient by just, very quickly, trying to gather as much possible information through a combination of exam and history. Dr Berkowitz: Great. So, you're thinking about all these not-to-miss diagnoses that would be life-threatening for the patient and you're getting to the bedside. So, how do you approach the exam? Often, this is a different scenario than usual, where the patient's not going to be able to give us a history or maybe necessarily even participate in the exam, and yet, as you said, the stakes are high to determine if there are neurologic conditions playing into this patient's status. So, how do you approach a patient at the bedside? Dr Wahlster: So, I think first step in an ICU setting (especially if the patient has a breathing tube) is you think about any confounders (especially sedation or metabolic confounders) - you want to remove as soon as possible, if able. I think as you do the exam, you try to kind of incorporate snippets of the history and really try to see - you know, localize the problem. And also kind of see, you know, what is the time course of the deterioration, what is the time course of the presentation. And that is something I actually learned from you. I know you've always had this framework of “what is it, where is it?” But I think in terms of just a clinical exam, I would look at localizing signs. I think, in the absence of being able to do the full head-to-toe neuro exam and interact with the patient, you really try to look at the brainstem findings. I always look at the eyes right away and look at, I think, just things like, you know, the gaze (how is it aligned? is there deviation? is there a skew? what do the pupils look like? [pupillary reactivity]). I think that's usually often a first step - that I just look at the patient's eyes. I think other objective findings, such as brainstem reflexes and motor responses, are also helpful. And then you just look whether there's any kind of focality in terms of - you know, is there any difference in size? But I think those are kind of the imminent things I look at quickly. Dr Berkowitz: Fantastic. Most of the time, this evaluation is happening kind of en route to the CT scanner or maybe a CT has already happened. So, let's say you're seeing a patient who's found down, the CT has either happened or you asked for it to happen somewhat quickly after you've done your exam, and let's say it's not particularly revealing early on. What are the sort things on your exam that would then push you to think about an MRI, a lumbar puncture, an EEG? You and I both spend time in large community hospitals, right, where “found down” is one of the most common chief concerns. In many cases, there isn't something to see on the CT or something obvious in the initial labs, and the question always comes up, “Who gets an MRI? Who gets an LP? Who gets an EEG?” - and I'm not sure I have a great framework for this. Obviously, you see focality on your exam, you know you need to look further. But, any factors in the history or exam that, even with a normal CT, raise your suspicion that you need to go further? Dr Wahlster: It's always a challenge, especially at a community hospital, because some of these patients come in at 1 AM where the EEG is not imminently available. But I think - let's say the CT scan is absolutely normal and doesn't give me a cause, but as an acute concerning deterioration, I think both EEG and LP would cross my mind. MRI I kind of see a little bit as a second-day test. I think there's very rare situation where an acute MRI would inform my imminent management. It's very informative, right, because you can see very small-vessel strokes. We had this patient that actually had this really bad vasculitis and we were able to see the small strokes everywhere on the MRI the day later, or sometimes helps you visualize acute brainstem pathology. But I think, even that - if you rule out a large-vessel occlusion on your CTA, there's brainstem pathology that is not imminently visible on the CT - it's nothing you need to go after. So, I do think the CT is a critical part of that initial eval, and whereas I always admire the neurological subspecialties, such as movements, where you just – like, your exam is everything. I think, to determine these acute time-sensitive interventions, the CT is key. And also, seeing a normal CT makes me a little less worried. You always look at these “four H” (they're big hypodensity, hyperdensity, any shift; is there hydrocephalus or herniation). I think if I don't have an explanation, my mind would imminently jump to seizure or CNS infection, or sometimes both. And I think then I would really kind of - to guide those decisions and whether I want to call in the EEG tech at 2 AM - I would, you know, again, look at the history and exam, see if there's any gaze deviation, tongue biting, incontinence - anything leading up towards seizure. I think, though, even if I didn't have any of those, those would strengthen my suspicion. If I really, absolutely don't have an explanation and the patient off sedation is just absolutely altered, I would still advocate for an EEG and maybe, in the meantime, do a small treatment trial. And I think with CNS infection - obviously, there are patients that are high risk for it - I would try to go back and get history about prodromes and, you know, look at things like the white count, fevers, and all of that. But again, I think if there's such a profound alteration in neurologic exam, there's nothing in the CT, and there's no other explanation, I would tend to do these things up front because, again, you don't want to miss them. Dr Berkowitz: Yeah, perfect. So many pearls in there, but one I just want to highlight because I'm not sure I've heard the mnemonic - can you tell us the four Hs again of sort of neurologic emergencies on CT? Dr Wahlster: Yeah. So, it's funny; for ages - I'm actually not sure where that's coming from, and I learned it from one of my fellows, one of our neurocritical care fellows - he's a fantastic teacher and he would teach our EM and anesthesia residents about it and his approach to CT. But yeah, the four H - he was always kind of like, “Look at the CT. Do you see any acute hypodensities, any hyperdensities?” And hypodensities would be involving infarct or edema; hyperdensities would be, most likely, hemorrhage (sometimes calcification or other things). Then, “Do you see hydrocephalus?” (because that needs an intervention). And, “Look at the midline structures and the ventricles.” And then, “Do you see any signs of herniation?” And he would go through the different types of herniation. But I thought that's a very good framework for looking at the “noncon” and just identifying critical pathology that needs some intervention. Dr Berkowitz: Yeah – so, hypodensity, hyperdensity, herniation, hydrocephalus. That's a good one – the four Hs; fantastic. Okay. So, a point that comes up a few times in your article - which I thought was very helpful to walk through and I'd love to pick your brain about a little bit – is, which patients need to be intubated for a neurologic indication? So, often we do consultations in medical, surgical ICUs; patients are intubated for medical respiratory reasons, but sometimes patients are intubated for neurologic reasons. So, can you walk us through your thinking on how to decide who needs to be intubated for the concern of depressed level of consciousness? Dr. Wahlster: It's an excellent question, and I think I would bet there's a lot of variation in practice and difference in opinion. There was actually the 2020 ESICM guidelines kind of commented on it, and those are great guidelines in terms of just intubation, mechanical ventilation of patients, and just acknowledging how there is a lack of really strong evidence. I would say the typical mantra (“GCS 8, intubate”) has been proposed in the trauma literature. And at some point, I actually dug into this to look behind the evidence, and there's actually not as much evidence as it's been put forth in guidelines and that kind of surprised me - that was just recently. I was like, “Actually, let me look this up.” I would say I didn't find a ton of strong evidence for it. I would say, as neurologist – you know, I'm amazed because GCS, I think is a - in some ways, a good tool to track things because it's so widely used across the board. But I would say, as neurologists, we all know that it sometimes doesn't account for some sort of nuances; you know, if a patient is aphasic, if a patient has an eyelid-opening apraxia - it can always be a little confounded. I'm amazed that GCS is still so widely used, to be frank. But I would say there is some literature - some school of thought - that maybe just blindly going by that mantra could be harmful or could not be ideal. I would say – I mean, I look at the two kind of functional things: oxygenation and ventilation. I think, in a neuro patient, you always think about airway protection or the decreased level of consciousness being a major issue (What is truly airway protection? Probably a mix of things). Then there's the issue of respiratory centers and respiratory drive - I think those are two issues you think about. But ultimately, if it leads to insufficient oxygenation - hypoxia early on is bad and that's been shown in several neurologic acute brain injuries. I think you also want to think about ventilation, especially if the mental status is poor to the point that the PCO2 elevates, that could also augment an ICP or exacerbate an ICP crisis. Or sometimes, I think there's just dysregulation of ventilation and there's hyperventilation to the point that the PCO2 is so low that I worry about cerebral vasoconstriction. So, I worry about these markers. I think, the oxygenation, I usually just kind of initially track on the sats. Sometimes, if the patient is profoundly altered, I do look at an arterial blood gas. And then there are things like breathing sounds (stridor, stertor [the work of breathing]). And I think something that also makes me have a lower threshold to intubate is if I'm worried and I want to scan, and I'm worried that the patient can't tolerate it - I want an imminent scan to just see why the patient is altered, or seizing, or presenting a certain way. Dr Berkowitz: All great pearls for how to think through this. Yeah - it's hard to think of hard and fast rules, and you can get to eight on the GCS in many different ways, as you said, some of which may not involve the respiratory mechanics at all. So, that's a helpful way of thinking about it that involves both the mental state, kind of the tracheal apparatus and how it's being managed by the neurologic system, and also the oxygen and carbon dioxide (sort of, respiratory parameters) – so, linking all those together; that's very helpful. And, related question – so, that's sort of for that patient with central nervous system pathology, who we're thinking about whether they need to be intubated for a primary neurologic indication. What about from the acute neuromuscular perspective (so, patients with Guillain-Barré syndrome or myasthenic crisis); how do you think about when to intubate those patients? Dr Wahlster: Yeah, absolutely - I think that's a really important one. And I think especially in a patient that is rapidly progressing, you always kind of think about that, and you want them in a supervised setting, either the ER or the ICU. I mean, there's some scores - I think there's the EGRIS score; there's some kind of models that predict it. I would say, the factors within that model, and based on my experience, often the pace of progression of reflex motor syndrome. I often see things like, kind of, changes in voice. You know, myasthenia, you look at things like head extension, flexion - those are the kind of factors. I would say there's this “20/30/40 rule” about various measures of, like, NIF and vital capacities, which is great. I would say in practice, I sometimes see that sometimes the participation in how the NIF is obtained is a little bit funky, so I wouldn't always blindly go by these numbers but sometimes it's helpful to track them. If you get a reliable kind of sixty and suddenly it drops to twenty, that makes me very concerned. But I would say, in general, it's really a little bit the work of breathing - looking at how the patient looks like. There's also (at some point) ABG abnormalities, but we always say, once those happen, you're kind of later in the game, so you should really - I think anyone that is in respiratory distress, you should think about it and have a low threshold to do it, and, at a minimum, monitor very closely. Dr Berkowitz: Yeah, we have those numbers, but so often, our patients who are weak, from a neuromuscular perspective, often have facial and other bulbar weakness and can't make a seal on the device that is used to check these numbers, and it can look very concerning when the patient may not, or can be a little bit difficult to interpret. So, I appreciate you giving us sort of the protocol and then the pearls of the caveats of how to interpret them and going sort of back to basics. So, just looking at the patient at the bedside and how hard they are working to breathe, or how difficult it is for them to clear their secretions from bulbar weakness. Moving on to another topic, you have a really wonderful section in your article on detecting clinical deterioration in patients in the neuro ICU. Many patients in the neuro ICU - for example, due to head trauma or large ischemic stroke or intracerebral hemorrhage, subarachnoid hemorrhage, or status epilepticus - they can't communicate with us to tell us something is getting worse, and they can't (in many cases) participate in the examination. They may be intubated, as you said, sedated or maybe even not sedated, and there's not necessarily much to follow on the exam to begin with if the GCS is very low. So, I'd love to hear your thoughts and your pearls, as someone who rounds in the neuro-ICU almost every day. What are you looking for at the bedside to try to detect sort of covert deterioration, if you will, in patients who already have major neurologic deficits, major neurologic injury or disease that we're aware of? I'm trying to see if there is some type of difference at the bedside that would lead you to be concerned for some underlying change and go back to the scanner or repeat EEG, LP, et cetera. Dr Wahlster: Yeah. I think that's an excellent question because that's a lot of what we do in the neuro ICU, right? And when you read your Clans, your residency, like, “Ah, QNR neuro checks, [IG1]  ” right? We often do that in many patients. But I think in the right patient, it can really be life or death a matter, and it is the exam that really then drives a whole cascade of changes in management and detects the need for lifesaving procedure. I would say it depends very much on the process and what you anticipate, right? If you have, for example, someone with a large ischemic stroke, large MCA stroke, especially, right, then there's sometimes conversations about doing a surgical procedure before they herniate. But let's say, kind of watch them and are worried that they will, you do worry about uncal herniation, and you pay attention to the pupil, because often, if the inferior division is infarcted, you know, you can see that kind of temporal tickling the uncus already. And so, I think those are patients that I torture with those NPi checks and checking the pupil very vigilantly. I would say, if it's a cerebellar stroke, for example, right, then you think about, you know, hydrocephalus. And often patients with cerebellar stroke - you know, the beauty of it is that if you detect it early, those patients can do so well, but they can die, and will die if they develop hydrocephalus start swelling. But I think, often something I always like to teach trainees is looking at the eye movements in upgaze and downgaze because, often, as the aqueduct, the third ventricle gets compressed and there's pressure on the colliculi – you kind of see vertical gaze get worse. But I would say I think it's always good to know what the process is and then what deterioration would look like. For example, in subarachnoid hemorrhage, where you talk about vasospasm - it's funny - I think a really good, experienced nurse is actually the best tool in this, but they will sometimes come to you and say, “I see this flavor,” and it's actually a constellation of symptoms, especially in the anterior ACA (ACom) aneurysms. You sometimes see patients suddenly, like, making funky jokes or saying really weird things. And then you see that in combination with, sometimes, a sodium drop, a little bit of subfebrile temperature; blood pressure shoot up sometimes, and that is a way the brain is sometimes regulating. But it's often a constellation of things, and I think it depends a little on the process that you're worried about. Dr Berkowitz: Yeah, that's very helpful. You just gave us some pearls for detecting deterioration related to vasospasm and subarachnoid hemorrhage; some pearls for detecting malignant edema in an MCA stroke or fourth ventricular compression in a large cerebellar stroke. Patients I find often very challenging to get a sense of what's going on and often get scanned over and over and back on EEG, not necessarily find something: patients with large intracerebral hemorrhage (particularly, in my experience, if the thalamus is involved) just can fluctuate a lot, and it's not clear to me actually what the fluctuation is. But you're looking for whether they're developing hydrocephalus from third ventricular compression with a thalamic hemorrhage (probably shouldn't be seizing from the thalamus, but if it's a large hemorrhage and cortical networks are disrupted and it's beyond sort of the subcortical gray matter, or has the hemorrhage expanded or ruptured it into the ventricular system?) And yet, you scan these patients over and over, sometimes, and just see it's the same thalamic hemorrhage and there's some, probably, just fluctuation level of arousal from the thalamic lesion. How do you, as someone who sees a lot of these patients, decide which patients with intracerebral hemorrhage - what are you looking for as far as deterioration? How do you decide who to keep scanning when you're seeing the same fluctuations? I find it so challenging - I'm curious to hear your perspective. Dr Wahlster: Yeah, no - that is a very tricky one. I mean, unfortunately, in patients with deeper hemorrhages or deeper lesions - you know, thalamic or then affecting brainstem - I think those are the ones that ultimately don't have good, consistent airway protection and do end up needing a trach, just because there's so much fluctuation. But I agree - it's so tricky, and I don't think I can give a perfect answer. I would say, a little bit I lean on the imaging. And for example - let's say there's a thalamic hemorrhage. We recently actually had a patient - I was on service last week - we had a thalamic hemorrhage with a fair amount of edema on it that was also kind of pressing on the aqueduct and didn't have a lot of IVH, right? But it was, like, from the outside pushing on it and where we ended up getting more scans. And I have to say, that patient actually just did fine and actually got the drain out and didn't need a shunt or anything, and actually never drained. We put an EVD and actually drained very little. So, I think we're still bad at gauging those. But I think, in general, my index of suspicion or threshold to scan would be lower if there was something, like, you know, a lot of IVH associated, if, you know, just kind of push on the aqueduct. It's very hard to say, I think. Sometimes, as you get to know your patients, you can get a little bit of a flavor of what is within normal fluctuation. I think it's probably true for every patient, right? - that there's always some fluctuation within the realm of like, “that's what he does,” and then there's something more profound. Yeah, sorry - I wish I could give a better answer, but I would say it's very tricky and requires experience and, ideally, you really taking the time to examine the patient yourself (ideally, several times). Sometimes, we see the patient - we get really worried. Or the typical thing we see the ICU is that the neurosurgeons walk around at 5 AM and say, like, “She's altered, she's different, she's changed.” And then the nurse will tell you at 8 AM, like, “No, they woke up and they ate their breakfast.” So, I think really working with your nurse and examining the patient yourself and just getting a flavor for what the realm of fluctuation is. Dr Berkowitz: Yeah - that's helpful to hear how challenging it is, even for a neurocritical care expert. I'm often taking care of these patients when they come out of the ICU and I'm thinking, “Am I scanning these patients too much?” Because I just don't sort of see the initial stage, and then, you know, you realize, “If I'm concerned and this is not fitting, then I should get a CT scan,” and sometimes you can't sort it out of the bedside. So, far from apologizing for your answer, it's reassuring, right, that sometimes you really can't tell at the bedside, as much as we value our exam. And the stakes are quite high if this patient's developed intraventricular hemorrhage or hydrocephalus, and these would change the management. Sometimes you have these patients the first few days in the ICU (for us, when they come out of the ICU) are getting scanned more often than you would like to. But then you get a sense of, “Oh, yeah - these times of day, they're hard to arouse,” or, “They're hard to arouse, but they are arousable this way,” and then, “When they are aroused, this is what they can do, and that's kind of what we saw yesterday.” And yet, as you said, if anyone on the team (the resident, the nurse, the student, our neurosurgery colleague) says, “I don't think this is how they were yesterday,” then, very low threshold to just go back and get a CT and make sure we're not missing something. Dr. Wahlster: Exactly. Yeah. I would say the other thing is also certain time intervals, right? If I'm seeing a patient that may be in vasospasm kind of around the days seven to ten, for the first fourteen day, I would be a little bit more nervous. Or with swelling - acute ischemic stroke says that could peak swelling, when knowing which [IG2]  , I would just be more anxious or have a lower threshold to scan. Yeah. Dr Berkowitz: Yeah - very helpful. Well, thank you so much for joining me today on Continuum Audio. Dr Wahlster: Thank you very much, Aaron. Dr Berkowitz: Again, today we've been interviewing Dr Sarah Wahlster, whose article, “Examination and Workup of the Neurocritical Care Patient” appears in the most recent issue of Continuum, on neurocritical care. Be sure to check out Continuum Audio episodes from this and other issues. And thank you so much to our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practice. And right now, during our Spring Special, all subscriptions are 15% off. Go to Continpub.com/Spring2024 or use the link in the episode notes to learn more and take advantage of this great discount. This offer ends June 30, 2024. AAN members: go to the link in the episode notes and complete the evaluation to get CME. Thank you for listening to Continuum Audio.

Download for FREE today -  special Mnemonics Cheatsheet - so you can be SURE that you have that Must Know information down:  bit.ly/nursing-memory   Outline ROME R-Respiratory O-Opposite M-Metabolic E-Equal Description First look at the pH: if it is low it is acidosis, high indicates alkalosis. Second use the ROME mnemonic to determine if you have respiratory vs. metabolic. For Metabolic look at HCO3. For Respiratory, look at pCO2. Metabolic Acidosis – pH Low, HCO3 Low. Metabolic Alkalosis – pH High, HCO3 High. Respiratory Acidosis – pH Low, pCO2 High. Respiratory Alkalosis – pH High, pCO2 Low.

Contributor: Aaron Lessen MD Educational Pearls: What is measured in an ABG/VBG? Blood values for oxygen tension (pO2), carbon dioxide tension (pCO2), acidity (pH), oxyhemoglobin saturation, and bicarbonate (HCO3) in either arterial or venous blood Other tests can measure methemoglobin, carboxyhemoglobin, hemoglobin levels, base excess, and lactate What are they used for? Identification of ventilation/acid-base disturbances. For example: if a patient is in septic shock, oxyhemoglobin saturation can be used to guide resuscitation efforts (early goal- directed therapy) What's the difference between an ABG and VBG? One of the main differences is how the blood samples are collected. Venous blood gas is normally collected from existing venous access such as a central venous catheter. Arterial blood gases must be drawn from an artery, such as the radial artery. Arterial blood draws can be difficult, painful, and contraindicated in many situations. ABGs have traditionally provided more accurate measurements for assessing oxygenation, ventilation, and acid-base status. However, several studies have found that VBGs can still be used to accurately assess pH, pCO2, HCO3, lactate, sodium, potassium, chloride, ionized calcium, blood urea nitrogen, base excess, and arterial/alveolar oxygen ratio. This is supported by a recent study in 2023 in the International Journal of Emergency Medicine which specifically studied patients with hypotension and use of VBGs for resuscitation guidance.  Are there other non-invasive methods that can be used to fill in the gaps to avoid ordering an ABG? Oxygenation can be measured by pulse oximetry Arterial carbon dioxide tension can be estimated by end-tidal carbon dioxide (PetCO2) Mixed venous blood gases are another alternative for patients who already have a pulmonary artery catheter References Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M; Early Goal-Directed Therapy Collaborative Group. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001 Nov 8;345(19):1368-77. doi: 10.1056/NEJMoa010307. PMID: 11794169. Prasad H, Vempalli N, Agrawal N, Ajun UN, Salam A, Subhra Datta S, Singhal A, Ranjan N, Shabeeba Sherin PP, Sundareshan G. Correlation and agreement between arterial and venous blood gas analysis in patients with hypotension-an emergency department-based cross-sectional study. Int J Emerg Med. 2023 Mar 10;16(1):18. doi: 10.1186/s12245-023-00486-0. PMID: 36899297; PMCID: PMC9999648. Summarized by Jeffrey Olson, MS2 | Edited by Jorge Chalit, OMSII  

In July 2023, the world experienced three consecutive days which were the hottest day on record. In fact, an interview with the Washington Post cited that it was the hottest day for 125,000 years. What does that mean? Well, today's episode will put that number into prehistorical and historical context, as well as compare our current global warming to an example of change from the Cretaceous. 1) Blum, M. G. B., and Jakobsson, M. (2010), Deep Divergence of Human Gene Trees and Models of Human Origins. Molecular Biology and Evolution 28(2): 889- 898. 2) Cavalheiro, L., Wagner, T., Steinig, S., Bottini, C., Dummann, W., Esegbue, O., Gambacorta, G., Giraldo-Gómez, V., Farnsworth, A., Flögel, S., Hofmann, P., Lunt, D. J., Rethemeyer, J., Torricelli, S. and Erba, E. (2021), Impact of global cooling on Early Cretaceous high pCO2 world during the Weissert event. Nature Communications 12: 5411. 3) Dee, M., Wengrow, D., Shortland, A., Stevenson, A., Brock, F., Flink, L. G. and Ramsey, C. B. (2013), An absolute chronology for early Egypt using radiocarbon dating and Bayesian statistical modelling. Proceedings of the Royal Society A 469: 20130395. 4) Gómez-Robles, A. (2019), Dental evolutionary rates and its implications for the Neanderthal–modern human divergence. Science Advances 5(5): eaaw1268. 5) Haber, M., Jones, A. L., Connell, B. A., Asan, E. A., Yang, H., Thomas, M. G., Xue Y. and Tyler-Smith, C. (2019), A Rare Deep-Rooting D0 African Y-Chromosomal Haplogroup and Its Implications for the Expansion of Modern Humans Out of Africa. Genetics 212(4): 1421-1428. 6) Hublin, J.-J. (2017), The last Neanderthal. Proceedings of the National Academy of Sciences of the United States of America 114(40): 10520- 10522. 7) Jones, D. (2007), The Neanderthal within. New Scientist 193(2593): 28-32. 8) Osborne, M., Smithsonian Magazine (2023), Earth Faces Hottest Day Ever Recorded- Three Days In A Row (online) [Accessed 07/07/2023]. 9) Pettitt, P. B. (1999) Disappearing from the World: An Archaeological Perspective on Neanderthal Extinction. Oxford Journal of Archaeology 18: 217-240. 10) Plant, V., Exeposé (2019), Things are Heating Up (online) [Accessed 07/07/2023]. 11) Sands, L., Washington Post (2023), This July 4 was hot. Earth's hottest day on record, in fact (online) [Accessed 07/07/2023]. 12) Stringer, C. (2012), The Status of Homo heidelbergensis (Shoetenstack 1908). Evolutionary Anthropology: Issues, News and Reviews 21(3): 87- 125. 13) Su, D., The Conversation (2022), How many ice ages has the Earth had, and could humans live through one? (online) [Accessed 07/07/2023]. 14) Zhang, S., truthout (2023), July 3 Was the Hottest Day on Record. Then July 4 Came Along. (online) [Accessed 07/07/2023]. 15) Author unknown, CNN (2023), Global temperatures break heat record (online) [Accessed 07/07/2023]. 16) Author unknown, Smithsonian Museum of Natural History (date unknown), Homo neanderthalensis (online) [Accessed 07/07/2023]. 17) Author unknown, Wikipedia (date unknown), Mesozoic (online) [Accessed 09/07/2023]. 18) Author unknown, Wikipedia (date unknown), Palaeogene (online) [Accessed 09/07/2023].

ReferencesWe considered the complexity of the machinery to excrete ammonium in the context of research on dietary protein and how high protein intake may increase glomerular pressure and contribute to progressive renal disease (many refer to this as the “Brenner hypothesis”). Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal diseaseA trial that studied low protein and progression of CKD The Effects of Dietary Protein Restriction and Blood-Pressure Control on the Progression of Chronic Renal Disease(and famously provided data for the MDRD eGFR equation A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study GroupWe wondered about dietary recommendations in CKD. of note, this is best done in the DKD guidelines from KDIGO Executive summary of the 2020 KDIGO Diabetes Management in CKD Guideline: evidence-based advances in monitoring and treatment.Joel mentioned this study on red meat and risk of ESKD. Red Meat Intake and Risk of ESRDWe referenced the notion of a plant-based diet. This is an excellent review by Deborah Clegg and Kathleen Hill Gallant. Plant-Based Diets in CKD : Clinical Journal of the American Society of NephrologyHere's the review that Josh mentioned on how the kidney appears to sense pH Molecular mechanisms of acid-base sensing by the kidneyRemarkably, Dr. Dale Dubin put a prize in his ECG book Free Car Prize Hidden in Textbook Read the fine print: Student wins T-birdA review of the role of the kidney in DKA: Diabetic ketoacidosis: Role of the kidney in the acid-base homeostasis re-evaluatedJosh mentioned the effects of infusing large amounts of bicarbonate The effect of prolonged administration of large doses of sodium bicarbonate in man and this study on the respiratory response to a bicarbonate infusion: The Acute Effects In Man Of A Rapid Intravenous Infusion Of Hypertonic Sodium Bicarbonate Solution. Ii. Changes In Respiration And Output Of Carbon DioxideThis is the study of acute respiratory alkalosis in dogs: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC293311/?page=1And this is the study of medical students who went to the High Alpine Research Station on the Jungfraujoch in the Swiss Alps https://www.nejm.org/doi/full/10.1056/nejm199105163242003Self explanatory! A group favorite! It Is Chloride Depletion Alkalosis, Not Contraction AlkalosisEffects of chloride and extracellular fluid volume on bicarbonate reabsorption along the nephron in metabolic alkalosis in the rat. Reassessment of the classical hypothesis of the pathogenesis of metabolic alkalosisA review of pendrin's role in volume homeostasis: The role of pendrin in blood pressure regulation | American Journal of Physiology-Renal PhysiologyInfusion of bicarbonate may lead to a decrease in respiratory stimulation but the shift of bicarbonate to the CSF may lag. Check out this review Neural Control of Breathing and CO2 Homeostasis and this classic paper Spinal-Fluid pH and Neurologic Symptoms in Systemic Acidosis.OutlineOutline: Chapter 11- Regulation of Acid-Base Balance- Introduction - Bicarb plus a proton in equilibrium with CO2 and water - Can be rearranged to HH - Importance of regulating pCO2 and HCO3 outside of this equation - Metabolism of carbs and fats results in the production of 15,000 mmol of CO2 per day - Metabolism of protein and other “substances” generates non-carbonic acids and bases - Mostly from sulfur containing methionine and cysteine - And cationic arginine and lysine - Hydrolysis of dietary phosphate that exists and H2PO4– - Source of base/alkali - Metabolism of an ionic amino acids - Glutamate and asparatate - Organic anions going through gluconeogenesis - Glutamate, Citrate and lactate - Net effect on a normal western diet 50-100 mEq of H+ per day - Homeostatic response to these acid-base loads has three stages: - Chemical buffering - Changes in ventilation - Changes in H+ excretion - Example of H2SO4 from oxidation of sulfur containing AA - Drop in bicarb will stimulate renal acid secretion - Nice table of normal cid-base values, arterial and venous- Great 6 bullet points of acid-base on page 328 - Kidneys must excrete 50-100 of non-carbonic acid daily - This occurs by H secretion, but mechanisms change by area of nephron - Not excreted as free H+ due to minimal urine pH being equivalent to 0.05 mmol/L - No H+ can be excreted until virtually all of th filtered bicarb is reabsorbed - Secreted H+ must bind buffers (phosphate, NH3, cr) - PH is main stimulus for H secretion, though K, aldo and volume can affect this.- Renal Hydrogen excretion - Critical to understand that loss of bicarb is like addition of hydrogen to the body - So all bicarb must be reabsorbed before dietary H load can be secreted - GFR of 125 and bicarb of 24 results in 4300 mEq of bicarb to be reabsorbed daily - Reabsorption of bicarb and secretion of H involve H secretion from tubular cells into the lumen. - Thee initial points need to be emphasized - Secreted H+ ion are generated from dissociation of H2O - Also creates OH ion - Which combine with CO2 to form HCO3 with the help of zinc containing intracellular carbonic anhydrase. - This is how the secretion of H+ which creates an OH ultimately produces HCO3 - Different mechanisms for proximal and distal acidification - NET ACID EXCRETION - Free H+ is negligible - So net H+ is TA + NH4 – HCO3 loss - Unusually equal to net H+ load, 50-100 mEq/day - Can bump up to 300 mEq/day if acid production is increased - Net acid excretion can go negative following a bicarb or citrate load - Proximal Acidification - Na-H antiporter (or exchanger) in luminal membrane - Basolateral membrane has a 3 HCO3 Na cotransporter - This is electrogenic with 3 anions going out and only one cation - The Na-H antiporter also works in the thick ascending limb of LOH - How about this, there is also a H-ATPase just like found in the intercalated cells in the proximal tubule and is responsible for about a third of H secretion - And similarly there is also. HCO3 Cl exchanger (pendrin-like) in the proximal tubule - Footnote says the Na- 3HCO3 cotransporter (which moves sodium against chemical gradient NS uses negative charge inside cell to power it) is important for sensing acid-base changes in the cell. - Distal acidification - Occurs in intercalated cells of of cortical and medullary collecting tubule - Three main characteristics - H secretion via active secretory pumps in the luminal membrane - Both H-ATPase and H-K ATPase - H- K ATPase is an exchange pump, k reabsorption - H-K exchange may be more important in hypokalemia rather than in acid-base balance - Whole paragraph on how a Na-H exchanger couldn't work because the gradient that H has to be pumped up is too big. - H-ATPase work like vasopressin with premise H-ATPase sitting on endocarditis vesicles a=which are then inserted into the membrane. Alkalosis causes them to be recycled out of the membrane. - H secretory cells do not transport Na since they have few luminal Na channels, but are assisted by the lumen negative tubule from eNaC. - Minimizes back diffusion of H+ and promotes bicarb resorption - Bicarbonate leaves the cell through HCO3-Cl exchanger which uses the low intracellular Cl concentration to power this process. - Same molecule is found on RBC where it is called band 3 protein - Figure 11-5 is interesting - Bicarbonate resorption - 90% in the first 1-22 mm of the proximal tubule (how long is the proximal tubule?) - Lots of Na-H exchangers and I handed permeability to HCO3 (permeability where?) - Last 10% happens distally mostly TAL LOH via Na-H exchange - And the last little bit int he outer medullary collecting duct. - Carbonic anhydrase and disequilibrium pH - CA plays central role in HCO3 reabsorption - After H is secreted in the proximal tubule it combines with HCO# to form carbonic acid. CA then dehydrates it to CO2 and H2O. (Step 2) - Constantly moving carbonic acid to CO2 and H2O keeps hydrogen combining with HCO3 since the product is rapidly consumed. - This can be demonstrated by the minimal fall in luminal pH - That is important so there is not a luminal gradient for H to overcome in the Na-H exchanger (this is why we need a H-ATPase later) - CA inhibitors that are limited tot he extracellular compartment can impair HCO3 reabsorption by 80%. - CA is found in S1, S2 but not S3 segment. See consequence in figure 11-6. - The disequilibrium comes from areas where there is no CA, the HH formula falls down because one of the assumptions of that formula is that H2CO3 (carbonic acid) is a transient actor, but without CA it is not and can accumulate, so the pKa is not 6.1. - Bicarbonate secretion - Type B intercalated cells - H-ATPase polarity reversed - HCO3 Cl exchanger faces the apical rather than basolateral membrane- Titratable acidity - Weak acids are filtered at the glom and act as buffers in the urine. - HPO4 has PKA of 6.8 making it ideal - Creatinine (pKa 4.97) and uric acid (pKa 5.75) also contribute - Under normal cinditions TA buffers 10-40 mEa of H per day - Does an example of HPO4(2-):H2PO4 (1-) which exists 4:1 at pH of 7.4 (glomerular filtrate) - So for 50 mEq of Phos 40 is HPO4 and 10 is H2PO4 - When pH drops to 6.8 then the ratio is 1:1 so for 50 - So the 50 mEq is 25 and 25, so this buffered an additional 15 mEq of H while the free H+ concentration increased from 40 to 160 nanomol/L so over 99.99% of secreted H was buffered - When pH drops to 4.8 ratio is 1:100 so almost all 50 mEq of phos is H2PO4 and 39.5 mEq of H are buffered. - Acid loading decreases phosphate reabsorption so more is there to act as TA. - Decreases activity of Na-phosphate cotransporter - DKA provides a novel weak acid/buffer beta-hydroxybutyrate (pKa 4.8) which buffers significant amount of acid (50 mEq/d).- Ammonium Excretion - Ability to excrete H+ as ammonium ions adds an important amount of flexibility to renal acid-base regulation - NH3 and NH4 production and excretion can be varied according to physiologic need. - Starts with NH3 production in tubular cells - NH3, since it is neutral then diffuses into the tubule where it is acidified by the low pH to NH4+ - NH4+ is ionized and cannot cross back into the tubule cells(it is trapped in the tubular fluid) - This is important for it acting as an important buffer eve though the pKa is 9.0 - At pH of 6.0 the ratio of NH3 to NH4 is 1:1000 - As the neutral NH3 is converted to NH4 more NH3 from theintracellular compartment flows into the tubular fluid replacing the lost NH3. Rinse wash repeat. - This is an over simplification and that there are threemajor steps - NH4 is produced in early proximal tubular cells - Luminal NH4 is partially reabsorbed in the TAL and theNH3 is then recycled within the renal medulla - The medullary interstitial NH3 reaches highconcentrations that allow NH3 to diffuse into the tubular lumen in the medullary collecting tubule where it is trapped as NH4 by secreted H+ - NH4 production from Glutamine which converts to NH4 and glutamate - Glutamate is converted to alpha-ketoglutarate - Alpha ketoglutarate is converted to 2 HCO3 ions - HCO3 sent to systemic circulation by Na-3 HCO3 transporter - NH4 then secreted via Na-H exchanger into the lumen - NH4 is then reabsorbed by NaK2Cl transporter in TAL - NH4 substitutes for K - Once reabsorbed the higher intracellular pH causes NH4 to convert to NH3 and the H that is removed is secreted through Na-H exchanger to scavenge the last of the filtered bicarb. - NH3 diffuses out of the tubular cells into the interstitium - NH4 reabsorption in the TAL is suppressed by hyperkalemia and stimulated by chronic metabolic acidosis - NH4 recycling promotes acid clearance - The collecting tubule has a very low NH3 concentration - This promotes diffusion of NH3 into the collecting duct - NH3 that goes there is rapidly converted to NH4 allowing more NH3 to diffuse in. - Response to changes in pH - Increased ammonium excretion with two processes - Increased proximal NH4 production - This is delayed 24 hours to 2-3 days depending on which enzyme you look at - Decreased urine pH increases diffusion of ammonia into the MCD - Occurs with in hours of an acid load - Peak ammonium excretion takes 5-6 days! (Fig 11-10) - Glutamine is picked up from tubular fluid but with acidosis get Na dependent peritublar capillary glutamine scavenging too - Glutamine metabolism is pH dependent with increase with academia and decrease with alkalemia - NH4 excretion can go from 30-40 mEq/day to > 300 with severe metabolic acidosis (38 NaBicarb tabs) - Says each NH4 produces equimolar generation of HCO3 but I thought it was two bicarb for every alpha ketoglutarate?- The importance of urine pH - Though the total amount of hydrogren cleared by urine pH is insignificant, an acidic urine pH is essential for driving the reactions of TA and NH4 forward.- Regulation of renal hydrogen excretion - Net acid excretion vary inverse with extracellular pH - Academia triggers proximal and distal acidification - Proximally this: - Increased Na-H exchange - Increased luminal H-ATPase activity - Increased Na:3HCO3 cotransporter on the basolateral membrane - Increased NH4 production from glutamine - In the collecting tubules - Increased H-ATPase - Reduction of tubular pH promotes diffusion of NH3 which gets converted to NH4…ION TRAPPING - Extracellular pH affects net acid excretion through its affect on intracellular pH - This happens directly with respiratory disorders due to movement of CO2 through the lipid bilayer - In metabolic disorders a low extracellular bicarb with cause bicarb to diffuse out of the cell passively, this lowers intracellular pH - If you manipulate both low pCO2 and low Bicarb to keep pH stable there will be no change in the intracellular pH and there is no change in renal handling of acid. It is intracellular pH dependent - Metabolic acidosis - Ramps up net acid secretion - Starts within 24 hours and peaks after 5-6 days - Increase net secretion comes from NH4 - Phosphate is generally limited by diet - in DKA titratable acid can be ramped up - Metabolic alkalosis - Alkaline extracellular pH - Increased bicarb excretion - Decrease reabsorption - HCO3 secretion (pendrin) in cortical collecting tubule - Occurs in cortical intercalated cells able to insert H-ATPase in basolateral cells (rather than luminal membrane) - Normal subjects are able to secrete 1000 mmol/day of bicarb - Maintenance of metabolic alkalosis requires a defect which forces the renal resorption of bicarb - This can be chloride/volume deficiency - Hypokalemia - Hyperaldosteronism - Respiratory acidosis and alkalosis - PCO2 via its effect on intracellular pH is an important determinant of renal acid handling - Ratios he uses: - 3.5 per 10 for respiratory acidosis - 5 per 10 for respiratory alkalosis - Interesting paragraph contrasting the response to chronic metabolic acidosis vs chronic respiratory acidosis - Less urinary ammonium in respiratory acidosis - Major differences in proximal tubule cell pH - In metabolic acidosis there is decreased bicarb load so less to be reabsorbed proximally - In respiratory acidosis the increased serum bicarb increases the amount of bicarb that must be reabsorbed proximally - The increased activity of Na-H antiporter returns tubular cell pH to normal and prevents it from creating increased urinary ammonium - Mentions that weirdly more mRNA for H-Na antiporter in metabolic acidosis than in respiratory acidosis - Net hydrogen excretion varies with effective circulating volume - Starts with bicarb infusions - Normally Tm at 26 - But if you volume deplete the patient with diuretics first this increases to 35+ - Four factors explain this increased Tm for bicarb with volume deficiency - Reduced GFR - Activation of RAAS - Ang2 stim H-Na antiporter proximally - Ang2 also stimulates Na-3HCO3 cotransporter on basolateral membrane - Aldosterone stimulates H-ATPase in distal nephron - ALdo stimulates Cl HCO3 exchanger on basolateral membrane - Aldo stimulates eNaC producing tubular lumen negative charge to allow H secretion to occur and prevents back diffusion - Hypochloremia - Increases H secretion by both Na-dependent and Na-independent methods - If Na is 140 and Cl is 115, only 115 of Na can be reabsorbed as NaCl, the remainder must be reabsorbed with HCO3 or associated with secretion of K or H to maintained electro neutrality - This is enhanced with hypochloridemia - Concurrent hypokalemia - Changes in K lead to trans cellular shifts that affect inctracellular pH - Hypokalemia causes K out, H in and in the tubular cell the cell acts if there is systemic acidosis and increases H secretion (and bicarbonate resorption) - PTH - Decreases proximal HCO3 resorption - Primary HyperCard as cause of type 2 RTA - Does acidosis stim PTH or does PTH stim net acid excretion

Nesse episódio do Journal Club, apresentamos artigos discutindo a o manejo da dor relacionada a enterocolite necrosante (ECN), a importância de um consenso de limiar de oxigênio para indicação de surfactante, a técnica de realimentação através de fístula mucosa para melhorar a nutrição de prematuros, a influência da frequência respiratória de ventilação não invasiva sobre os níveis de PCO2 e a oferta de leite posterior para aumentar o ritmo de crescimento de prematuros.Você pode ter acesso aos artigos na íntegra acessando nosso site: https://www.the-incubator.org/portuguese/Se quiser nos mandar sugestões, comentários, críticas e elogios, manda um e-mail pra gente: incubadora@the-incubator.orgNão esqueça: você pode ter acesso aos artigos do nosso Journal Club no nosso site: https://www.the-incubator.org/podcast-1 Se estiver gostando do nosso Podcast, por favor deixe sua avaliação no seu aplicativo favorito e compartilhe com seus colegas. O nosso objetivo é democratizar a informação. Se quiser entrar em contato, nos mandar sugestões, comentários, críticas e elogios, manda um e-mail pra gente: incubadora@the-incubator.org

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.I'm Pradip Kamat coming to you from Children's Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania from Cleveland Clinic Children's Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let's get into our episode.Here's the case of a 12-week-old girl old who is limp and seizing presented by Rahul.Chief Complaint: A 12-week-old previously healthy female infant was found limp in her crib and developed generalized tonic-clonic seizures on the way to the hospital.History of Present Illness: The mother returned from work on a Saturday to find her daughter unresponsive in her crib. The infant had been left in the care of her mother's boyfriend, who stated that the daughter had been sleeping all day and had a small spit up. As the patient continued to have low appetite throughout the day and continued to be unresponsive in her crib, mother called EMS to bring her to the emergency department. En route, the patient had tonic movement that did not resolve with intranasal benzodiazepines.ED Course: The infant presents to the ED being masked. Upon arrival at the ED, the infant was in respiratory distress, with a heart rate of 190 beats per minute, respiratory rate of 50 breaths per minute, and oxygen saturation of 85% with bagging. She was intubated for seizure control upon arrival at the ED. Physical examination in the ED revealed bruising on the right neck region but was otherwise unremarkable. A non-contrast head CT showed no acute intracranial abnormalities. The initial diagnostic workup revealed normal CBC, mildly elevated hepatic enzymes, and pancreatic enzymes which were within normal limits. The blood gas showed metabolic acidemia with PCO2 in the 60s.Admission to PICU: Upon admission to the PICU, neurosurgery and trauma teams were consulted. A skeletal survey and ophthalmology consult for a fundoscopic examination were ordered, as there were concerns of non-accidental trauma. Further investigation is underway to determine the cause of the infant's condition.To summarize key elements from this case, this patient has:Patient left with mother's boyfriendInfant found limp and had seizures requiring intubationNeck bruiseAll of these bring up a concern for Non-Accidental Trauma (NAT) the topic of our discussion.Let's start with a short multiple-choice question:Which imaging modality is the most appropriate for establishing a diagnosis of abusive head trauma (AHT) in a 12-week-old infant with an open fontanelle on the exam?A. CT scan of the brain without contrast B. MRI of the brain without contrast C. Skull X-ray D. Doppler ultrasound of the headRahul, the correct answer is A. Though

ReferencesWe considered the effect of a high protein diet and potential metabolic acidosis on kidney function. This review is of interest by Donald Wesson, a champion for addressing this issue and limiting animal protein: Mechanisms of Metabolic Acidosis-Induced Kidney Injury in Chronic Kidney DiseaseHostetter explored the effect of a high protein diet in the remnant kidney model with 1 ¾ nephrectomy. Rats with reduced dietary acid load (by bicarbonate supplementation) had less tubular damage. Chronic effects of dietary protein in the rat with intact and reduced renal massWesson explored treatment of metabolic acidosis in humans with stage 3 CKD in this study. Treatment of metabolic acidosis in patients with stage 3 chronic kidney disease with fruits and vegetables or oral bicarbonate reduces urine angiotensinogen and preserves glomerular filtration rateIn addition to the effect of metabolic acidosis from a diet high in animal protein, this diet also leads to hyperfiltration. This was demonstrated in normal subjects; ingesting a protein diet had a significantly higher creatinine clearance than a comparable group of normal subjects ingesting a vegetarian diet. Renal functional reserve in humans: Effect of protein intake on glomerular filtration rate.This finding has been implicated in Brenner's theory regarding hyperfiltration: The hyperfiltration theory: a paradigm shift in nephrologyOne of multiple publications from Dr. Nimrat Goraya whom Joel mentioned in the voice over: Dietary Protein as Kidney Protection: Quality or Quantity?We wondered about the time course in buffering a high protein meal (and its subsequent acid load on ventilation) and Amy found this report:Effect of Protein Intake on Ventilatory Drive | Anesthesiology | American Society of Anesthesiologists Roger mentioned that the need for acetate to balance the acid from amino acids in parenteral nutrition was identified in pediatrics perhaps because infants may have reduced ability to generate acid. Randomised controlled trial of acetate in preterm neonates receiving parenteral nutrition - PMCHe also recommended an excellent review on the complications of parenteral nutrition by Knochel https://www.kidney-international.org/action/showPdf?pii=S0085-2538%2815%2933384-6 which explained that when the infused amino acids disproportionately include cationic amino acids, metabolism led to H+ production. This is typically mitigated by preparing a solution that is balanced by acetate. Amy mentioned this study that explored the effect of protein intake on ventilation: Effect of Protein Intake on Ventilatory Drive | Anesthesiology | American Society of AnesthesiologistsAnna and Amy reminisced about a Skeleton Key Group Case from the renal fellow network Skeleton Key Group: Electrolyte Case #7JC wondered about isolated defects in the proximal tubule and an example is found here: Mutations in SLC4A4 cause permanent isolated proximal renal tubular acidosis with ocular abnormalitiesAnna's Voiceover re: Gastric neobladder → metabolic alkalosis and yes, dysuria. The physiology of gastrocystoplasty: once a stomach, always a stomach but not as common as you might think Gastrocystoplasty: long-term complications in 22 patientsSjögren's syndrome has been associated with acquired distal RTA and in some cases, an absence of the H+ ATPase, presumably from autoantibodies to this transporter. Here's a case report: Absence of H(+)-ATPase in cortical collecting tubules of a patient with Sjogren's syndrome and distal renal tubular acidosisCan't get enough disequilibrium pH? Check this out- Spontaneous luminal disequilibrium pH in S3 proximal tubules. Role in ammonia and bicarbonate transport.Acetazolamide secretion was studied in this report Concentration-dependent tubular secretion of acetazolamide and its inhibition by salicylic acid in the isolated perfused rat kidney. | Drug Metabolism & DispositionIn this excellent review, David Goldfarb tackles the challenging case of a A Woman with Recurrent Calcium Phosphate Kidney Stones (spoiler alert, many of these patients have incomplete distal RTA and this problem is hard to treat). Molecular mechanisms of renal ammonia transport excellent review from David Winer and Lee Hamm. OutlineOutline: Chapter 11- Regulation of Acid-Base Balance- Introduction - Bicarb plus a proton in equilibrium with CO2 and water - Can be rearranged to HH - Importance of regulating pCO2 and HCO3 outside of this equation - Metabolism of carbs and fats results in the production of 15,000 mmol of CO2 per day - Metabolism of protein and other “substances” generates non-carbonic acids and bases - Mostly from sulfur containing methionine and cysteine - And cationic arginine and lysine - Hydrolysis of dietary phosphate that exists and H2PO4– - Source of base/alkali - Metabolism of an ionic amino acids - Glutamate and asparatate - Organic anions going through gluconeogenesis - Glutamate, Citrate and lactate - Net effect on a normal western diet 50-100 mEq of H+ per day - Homeostatic response to these acid-base loads has three stages: - Chemical buffering - Changes in ventilation - Changes in H+ excretion - Example of H2SO4 from oxidation of sulfur containing AA - Drop in bicarb will stimulate renal acid secretion - Nice table of normal cid-base values, arterial and venous- Great 6 bullet points of acid-base on page 328 - Kidneys must excrete 50-100 of non-carbonic acid daily - This occurs by H secretion, but mechanisms change by area of nephron - Not excreted as free H+ due to minimal urine pH being equivalent to 0.05 mmol/L - No H+ can be excreted until virtually all of th filtered bicarb is reabsorbed - Secreted H+ must bind buffers (phosphate, NH3, cr) - PH is main stimulus for H secretion, though K, aldo and volume can affect this.- Renal Hydrogen excretion - Critical to understand that loss of bicarb is like addition of hydrogen to the body - So all bicarb must be reabsorbed before dietary H load can be secreted - GFR of 125 and bicarb of 24 results in 4300 mEq of bicarb to be reabsorbed daily - Reabsorption of bicarb and secretion of H involve H secretion from tubular cells into the lumen. - Thee initial points need to be emphasized - Secreted H+ ion are generated from dissociation of H2O - Also creates OH ion - Which combine with CO2 to form HCO3 with the help of zinc containing intracellular carbonic anhydrase. - This is how the secretion of H+ which creates an OH ultimately produces HCO3 - Different mechanisms for proximal and distal acidification - NET ACID EXCRETION - Free H+ is negligible - So net H+ is TA + NH4 – HCO3 loss - Unusually equal to net H+ load, 50-100 mEq/day - Can bump up to 300 mEq/day if acid production is increased - Net acid excretion can go negative following a bicarb or citrate load - Proximal Acidification - Na-H antiporter (or exchanger) in luminal membrane - Basolateral membrane has a 3 HCO3 Na cotransporter - This is electrogenic with 3 anions going out and only one cation - The Na-H antiporter also works in the thick ascending limb of LOH - How about this, there is also a H-ATPase just like found in the intercalated cells in the proximal tubule and is responsible for about a third of H secretion - And similarly there is also. HCO3 Cl exchanger (pendrin-like) in the proximal tubule - Footnote says the Na- 3HCO3 cotransporter (which moves sodium against chemical gradient NS uses negative charge inside cell to power it) is important for sensing acid-base changes in the cell. - Distal acidification - Occurs in intercalated cells of of cortical and medullary collecting tubule - Three main characteristics - H secretion via active secretory pumps in the luminal membrane - Both H-ATPase and H-K ATPase - H- K ATPase is an exchange pump, k reabsorption - H-K exchange may be more important in hypokalemia rather than in acid-base balance - Whole paragraph on how a Na-H exchanger couldn't work because the gradient that H has to be pumped up is too big. - H-ATPase work like vasopressin with premise H-ATPase sitting on endocarditis vesicles a=which are then inserted into the membrane. Alkalosis causes them to be recycled out of the membrane. - H secretory cells do not transport Na since they have few luminal Na channels, but are assisted by the lumen negative tubule from eNaC. - Minimizes back diffusion of H+ and promotes bicarb resorption - Bicarbonate leaves the cell through HCO3-Cl exchanger which uses the low intracellular Cl concentration to power this process. - Same molecule is found on RBC where it is called band 3 protein - Figure 11-5 is interesting - Bicarbonate resorption - 90% in the first 1-22 mm of the proximal tubule (how long is the proximal tubule?) - Lots of Na-H exchangers and I handed permeability to HCO3 (permeability where?) - Last 10% happens distally mostly TAL LOH via Na-H exchange - And the last little bit int he outer medullary collecting duct. - Carbonic anhydrase and disequilibrium pH - CA plays central role in HCO3 reabsorption - After H is secreted in the proximal tubule it combines with HCO# to form carbonic acid. CA then dehydrates it to CO2 and H2O. (Step 2) - Constantly moving carbonic acid to CO2 and H2O keeps hydrogen combining with HCO3 since the product is rapidly consumed. - This can be demonstrated by the minimal fall in luminal pH - That is important so there is not a luminal gradient for H to overcome in the Na-H exchanger (this is why we need a H-ATPase later) - CA inhibitors that are limited tot he extracellular compartment can impair HCO3 reabsorption by 80%. - CA is found in S1, S2 but not S3 segment. See consequence in figure 11-6. - The disequilibrium comes from areas where there is no CA, the HH formula falls down because one of the assumptions of that formula is that H2CO3 (carbonic acid) is a transient actor, but without CA it is not and can accumulate, so the pKa is not 6.1. - Bicarbonate secretion - Type B intercalated cells - H-ATPase polarity reversed - HCO3 Cl exchanger faces the apical rather than basolateral membrane- Titratable acidity - Weak acids are filtered at the glom and act as buffers in the urine. - HPO4 has PKA of 6.8 making it ideal - Creatinine (pKa 4.97) and uric acid (pKa 5.75) also contribute - Under normal cinditions TA buffers 10-40 mEa of H per day - Does an example of HPO4(2-):H2PO4 (1-) which exists 4:1 at pH of 7.4 (glomerular filtrate) - So for 50 mEq of Phos 40 is HPO4 and 10 is H2PO4 - When pH drops to 6.8 then the ratio is 1:1 so for 50 - So the 50 mEq is 25 and 25, so this buffered an additional 15 mEq of H while the free H+ concentration increased from 40 to 160 nanomol/L so over 99.99% of secreted H was buffered - When pH drops to 4.8 ratio is 1:100 so almost all 50 mEq of phos is H2PO4 and 39.5 mEq of H are buffered. - Acid loading decreases phosphate reabsorption so more is there to act as TA. - Decreases activity of Na-phosphate cotransporter - DKA provides a novel weak acid/buffer beta-hydroxybutyrate (pKa 4.8) which buffers significant amount of acid (50 mEq/d).- Ammonium Excretion - Ability to excrete H+ as ammonium ions adds an important amount of flexibility to renal acid-base regulation - NH3 and NH4 production and excretion can be varied according to physiologic need. - Starts with NH3 production in tubular cells - NH3, since it is neutral then diffuses into the tubule where it is acidified by the low pH to NH4+ - NH4+ is ionized and cannot cross back into the tubule cells(it is trapped in the tubular fluid) - This is important for it acting as an important buffer eve though the pKa is 9.0 - At pH of 6.0 the ratio of NH3 to NH4 is 1:1000 - As the neutral NH3 is converted to NH4 more NH3 from theintracellular compartment flows into the tubular fluid replacing the lost NH3. Rinse wash repeat. - This is an over simplification and that there are threemajor steps - NH4 is produced in early proximal tubular cells - Luminal NH4 is partially reabsorbed in the TAL and theNH3 is then recycled within the renal medulla - The medullary interstitial NH3 reaches highconcentrations that allow NH3 to diffuse into the tubular lumen in the medullary collecting tubule where it is trapped as NH4 by secreted H+ - NH4 production from Glutamine which converts to NH4 and glutamate - Glutamate is converted to alpha-ketoglutarate - Alpha ketoglutarate is converted to 2 HCO3 ions - HCO3 sent to systemic circulation by Na-3 HCO3 transporter - NH4 then secreted via Na-H exchanger into the lumen - NH4 is then reabsorbed by NaK2Cl transporter in TAL - NH4 substitutes for K - Once reabsorbed the higher intracellular pH causes NH4 to convert to NH3 and the H that is removed is secreted through Na-H exchanger to scavenge the last of the filtered bicarb. - NH3 diffuses out of the tubular cells into the interstitium - NH4 reabsorption in the TAL is suppressed by hyperkalemia and stimulated by chronic metabolic acidosis - NH4 recycling promotes acid clearance - The collecting tubule has a very low NH3 concentration - This promotes diffusion of NH3 into the collecting duct - NH3 that goes there is rapidly converted to NH4 allowing more NH3 to diffuse in. - Response to changes in pH - Increased ammonium excretion with two processes - Increased proximal NH4 production - This is delayed 24 hours to 2-3 days depending on which enzyme you look at - Decreased urine pH increases diffusion of ammonia into the MCD - Occurs with in hours of an acid load - Peak ammonium excretion takes 5-6 days! (Fig 11-10) - Glutamine is picked up from tubular fluid but with acidosis get Na dependent peritublar capillary glutamine scavenging too - Glutamine metabolism is pH dependent with increase with academia and decrease with alkalemia - NH4 excretion can go from 30-40 mEq/day to > 300 with severe metabolic acidosis (38 NaBicarb tabs) - Says each NH4 produces equimolar generation of HCO3 but I thought it was two bicarb for every alpha ketoglutarate?- The importance of urine pH - Though the total amount of hydrogren cleared by urine pH is insignificant, an acidic urine pH is essential for driving the reactions of TA and NH4 forward.- Regulation of renal hydrogen excretion - Net acid excretion vary inverse with extracellular pH - Academia triggers proximal and distal acidification - Proximally this: - Increased Na-H exchange - Increased luminal H-ATPase activity - Increased Na:3HCO3 cotransporter on the basolateral membrane - Increased NH4 production from glutamine - In the collecting tubules - Increased H-ATPase - Reduction of tubular pH promotes diffusion of NH3 which gets converted to NH4…ION TRAPPING - Extracellular pH affects net acid excretion through its affect on intracellular pH - This happens directly with respiratory disorders due to movement of CO2 through the lipid bilayer - In metabolic disorders a low extracellular bicarb with cause bicarb to diffuse out of the cell passively, this lowers intracellular pH - If you manipulate both low pCO2 and low Bicarb to keep pH stable there will be no change in the intracellular pH and there is no change in renal handling of acid. It is intracellular pH dependent - Metabolic acidosis - Ramps up net acid secretion - Starts within 24 hours and peaks after 5-6 days - Increase net secretion comes from NH4 - Phosphate is generally limited by diet - in DKA titratable acid can be ramped up - Metabolic alkalosis - Alkaline extracellular pH - Increased bicarb excretion - Decrease reabsorption - HCO3 secretion (pendrin) in cortical collecting tubule - Occurs in cortical intercalated cells able to insert H-ATPase in basolateral cells (rather than luminal membrane) - Normal subjects are able to secrete 1000 mmol/day of bicarb - Maintenance of metabolic alkalosis requires a defect which forces the renal resorption of bicarb - This can be chloride/volume deficiency - Hypokalemia - Hyperaldosteronism - Respiratory acidosis and alkalosis - PCO2 via its effect on intracellular pH is an important determinant of renal acid handling - Ratios he uses: - 3.5 per 10 for respiratory acidosis - 5 per 10 for respiratory alkalosis - Interesting paragraph contrasting the response to chronic metabolic acidosis vs chronic respiratory acidosis - Less urinary ammonium in respiratory acidosis - Major differences in proximal tubule cell pH - In metabolic acidosis there is decreased bicarb load so less to be reabsorbed proximally - In respiratory acidosis the increased serum bicarb increases the amount of bicarb that must be reabsorbed proximally - The increased activity of Na-H antiporter returns tubular cell pH to normal and prevents it from creating increased urinary ammonium - Mentions that weirdly more mRNA for H-Na antiporter in metabolic acidosis than in respiratory acidosis - Net hydrogen excretion varies with effective circulating volume - Starts with bicarb infusions - Normally Tm at 26 - But if you volume deplete the patient with diuretics first this increases to 35+ - Four factors explain this increased Tm for bicarb with volume deficiency - Reduced GFR - Activation of RAAS - Ang2 stim H-Na antiporter proximally - Ang2 also stimulates Na-3HCO3 cotransporter on basolateral membrane - Aldosterone stimulates H-ATPase in distal nephron - ALdo stimulates Cl HCO3 exchanger on basolateral membrane - Aldo stimulates eNaC producing tubular lumen negative charge to allow H secretion to occur and prevents back diffusion - Hypochloremia - Increases H secretion by both Na-dependent and Na-independent methods - If Na is 140 and Cl is 115, only 115 of Na can be reabsorbed as NaCl, the remainder must be reabsorbed with HCO3 or associated with secretion of K or H to maintained electro neutrality - This is enhanced with hypochloridemia - Concurrent hypokalemia - Changes in K lead to trans cellular shifts that affect inctracellular pH - Hypokalemia causes K out, H in and in the tubular cell the cell acts if there is systemic acidosis and increases H secretion (and bicarbonate resorption) - PTH - Decreases proximal HCO3 resorption - Primary HyperCard as cause of type 2 RTA - Does acidosis stim PTH or does PTH stim net acid excretion

References for Chapter 10We did not mention many references in our discussion today but our listeners may enjoy some of the references below. Effects of pH on Potassium: New Explanations for Old Observations - PMC although the focus of this article is on potassium, this elegant review by Aronson and Giebisch reviews intracellular shifts as it relates to pH and K+.Josh swooned for Figure 10-1 is this right? Which figure was it? which shows the relationship between [H+] and pH. You can find this figure in the original reference from Halperin ML and others, Figure 1 here. Factors That Control the Effect of pH on Glycolysis in Leukocytes Here's Leticia Rolon's favorite Henderson-Hasselbalch calculator website: ​​Henderson-Hasselbalch Calculator | Buffer Solutions [hint! for this site, use the bicarbonate (or “total CO2”) for A- and PCO2 for the HA] There's also a cooking tab for converting units! Fundamentals of Arterial Blood Gas Interpretation - PMC this review published posthumously from the late but beloved Jerry Yee and his group at Henry Ford Hospital, explores the details and underpinnings of our understandings of arterial blood gas interpretation (and this also addresses how our colleagues in clinical chemistry measure total CO2 - which JC referenced- but JC said “machine” and our colleagues prefer the word “instrument.”)Amy went deep on bicarbonate in respiratory acidosis. Here are her refs:Sodium bicarbonate therapy for acute respiratory acidosisSodium Bicarbonate in Respiratory AcidosisBicarbonate therapy in severe metabolic acidosisEffect of Intravenous Sodium Bicarbonate on Ventilation, Gas Exchange, and Acid-Base Balance in Patients with Chronic Pulmonary InsufficiencyBicarbonate Therapy in Severe Metabolic Acidosis | American Society of Nephrology this review article from Sabatini and Kurtzman addresses the issues regarding bicarbonate therapy including theoretical intracellular acidosis. Bicarbonate in DKA? Don't do it: Bicarbonate in diabetic ketoacidosis - a systematic review Here's a review from Bushinsky and Krieger on the effect acidosis on bone https://www.sciencedirect.com/science/article/abs/pii/S0085253822002174Here is the primary resource that Anna used in here investigation of meat replacements Nutritional Composition of Novel Plant-Based Meat Alternatives and Traditional Animal-Based MeatsWe enjoyed this paper that Dr. Rose references from the Journal of Clinical Investigation 1955 in which investigators infused HCl into nephrectomized dogs and observed changes in extracellular ions. https://www.jci.org/articles/view/103073/pdWe wondered about the amino acids/protein in some available meat alternatives they are explored in this article in the journal Amino Acids: Protein content and amino acid composition of commercially available plant-based protein isolates - PMC and you may enjoy this exploration of the nutritional value of these foods: Full article: Examination of the nutritional composition of alternative beef burgers available in the United StatesOutlineChapter 10: Acid-Base Physiology - H concentration regulated tightly - Normal H+ is 40 nm/L - This one millionth the concentration of Na and K - It needs to be this dilute because H+ fucks shit up - Especially proteins - Cool foot note H+ actually exists as H3O+ - Under normal conditions the H+ concentration varies little from normal due to three steps - Chemical buffering by extracellular and intracellular bufffers - Control of partial pressure of CO2 by alterations of alveolar ventilation - Control of plasma bicarbonate by changes in renal H+ excretion - Acid and bases - Use definition by Bronsted - Acid can donate protons - Base can accept protons - There are two classes of acids** - Carbonic acid H2CO3 - Each day 15000 mmol of CO2 are generated - CO2 not acid but combines with water to form carbonic acid H2CO3 - CO2 cleared by the lungs - Noncarbonic acid - Formed from metabolism of protein. Sulfur containing AA generate H2SO4. Only 50-100 mEq of acid produced from these sources. - Cleared by the kidneys - Law of Mass Action - Velocity of reaction proportional to the product of the concentrations of the reactants - Goes through mass action formula for water - Concludes that water has H of 155 nanoM/L, more than the 40 in plasma - Says you can do the same mass experiment for every acid in the body - Can do it also for bases but he is not going to. - Acids and Bases can be strong or weak - Strong acids completely dissociate - Weak acids not so much - H2PO4 is only 80% dissociated - Weak acids are the principle buffers in the body - Then he goes through how H is measured in the blood and it becomes clear why pH is a logical way to measure. - Then there is a lot of math - HH equation - Derives it - Then uses it to look at phos. Very interesting application - Buffers - Goes tot he phosphate well again. Amazing math describing how powerful buffers can be - Big picture the closer the pKa is to the starting pH the better buffer, i.e. it can absorb lots of OH or H without appreciably changing pH - HCO3 CO2 system - H2CO3 to H + HCO3 has a PKA of 2.72 but then lots of Math and the bicarb buffer system has a pKa of 6.1 - But the real power of the bicarb buffer is that it is not a sealed system. The ability to ventilate and keep CO2 constant increases the buffering efficiency by 11 fold and the ability to lower the CO2 below normal increases 18 fold. - Isohydric principle - There is only one hydrogen ion concentration and since that is a critical part of the buffer equation, all buffer eq are linked and you can understand all of them by understanding one of them. So we just can look at bicarb and understand the totality of acid base. - Bicarb is the most important buffer because - High concentration in plasma - Ability for CO2 to ventilate - Other buffers include - Bone - Bone is more than just inorganic reaction - Live bone releases more calcium in response to an acid load than dead bone - More effect with metabolic acidosis than respiratory acidosis - Hgb - Phosphate - Protein

Alkol kullanımına bağlı bir çok problemle acil servislerde karşılaşmaya alışığız. Görece nadir karşılaştığımız alkol yoksunluğu alkol ilişkili acil durumlardan birisi olmakla birlikte yönetimi kimi zaman zorlayıcı olabilmektedir. Bu yazımda alkol yoksunluk sendromu yönetimini geçen ay acilimize gelen bir vaka üzerinden anlatmaya çalışacağım. İyi okumalar dilerim. Vaka 34 yaşında erkek hasta ellerde titreme, konuşma güçlüğü ve istemsiz ekstremite hareketleri şikayeti ile getirildi. Vitallerde hipertansif, taşikardik, takipneik, oksijen saturasyonu normal ve ateşi yoktu. Hasta resüsitasyon alanına alındı ve monitorize edildi. Anamnezde 10 yılı aşkın süredir progresif artan miktarda ve son yıllarda günde 1 litre civarında viski içtiği fakat son 5 gündür yakınlarının teşviği ile alkol almadığı öğrenildi. 2 gün önce psikiyatra başvurmuş fakat yazılan ilaçları henüz kullanmamış. 1 gün önce sabah başlayan bulantı, kendini kötü hissetme hali akşam artmış. Sabah uyandığında konuşamama, kusma, ellerde titreme, baş dönmesi şikayetleri olması üzerine acil servise getirilmiş. Ek hastalığı veya kullandığı ilaç yokmuş. Muayenede GKS:14, motor komutlara uymaya çalışıyor, sözel oryantasyon bozuk. Kooperasyon kısıtlı ve ajite (RAS skoru 3). Pupiller izokorik, ışık refleksi doğal. Tüm ekstremitelerde belirgin tremor mevcut. Lateralize nörolojik bulgu yok. Solunum doğal, batın rahat. Periferik nabızlar açık. Hastada ön planda alkol yoksunluk sendromu ve buna bağlı deliryum tremens düşünüldü. Santral patolojilerin ekarte edilmesi ve hastanın metanol intoksikasyonu açısından değerlendirilmesi gerekmekteydi. Çekilen tomografide haliyle hareket artefaktı vardı. Suboptimal değerlendirmede patoloji saptanmadı. Hematolojik tetkiklerde 14.000 lökositoz ve AST 5 kat, ALT 2 kat, Kreatin Kinazın 6 kat artmış olduğu görüldü. Elektrolikter ve BFT normal bulundu. Kan gazında pH:7.10, pCO2:26, CHCO3:8 olacak şekilde anyon açığı artmış (+19) derin metabolik asidozu vardı. Etanol değeri sıfır ölçüldü. Hastanın oral alımı kapatıldı. Dekstroz ve SF ile hidrate edildi, tiamin verildi. Ajitasyonların tedavisi için diazem ile tedaviye başlanıldı. Asidozu devam eden hasta hemodiyalize alındı. Acil serviste geçen 10 saatlik süre boyunca toplamda 80 mg diazepam ve 20 mg midazolam verildi fakat hastanın ajitasyonu devam etti. Hasta üçüncü basamak yoğun bakıma devredildi. Hastanın tedavisine diazemle devam edildiğini, yatışın 24. saatlerinde ajitasyonun azaldığını ve 6. gün psikiyatri poliklinik önerisiyle taburcu edildiğini öğrendik. Tartışma Alkol kullanan kişiler tüketimi aniden bıraktıklarında yoksunluk sendromu yaşayabiliriler. Yoksunluk durumuna düşmek için ne kadar süre ve ne kadar miktarda alkol alınması gerektiği net değildir. Bunun yanı sıra yoksunluk yaşayanlar arasında da semptomların çeşitliliği ve ağırlığı kişiden kişiye göre değişmektedir. Yapılan çalışmalarda daha uzun süre ve sürekli alkol verilen gönüllülerin daha kısa süre alkol alanlara göre daha şiddetli yoksunluk yaşadıklarını göstermiştir.​1​ Minor yoksunluk belirtileri genellikle 6-24 saat içinde başlar ve kendiliğinden sonlanır. Bu semptomlar uykusuzluk, titreme, hafif kaygı, gastrointestinal rahatsızlık, baş ağrısı, terleme ve çarpıntı olarak sayılabilir. Fakat orta ve ileri yoksunluk durumlarında jeneralize tonik klonik nöbetler, alkolik halüsinoz, deliryum tremens, rabdomiyoliz ve mortalite görülebilmektedir.​2​ Yoksunluğun şiddetini belirleyebileceğimiz CIWA-Ar ölçeği 2014 yılında yayınlanmıştır. Hastanın semptomlarının şiddetine göre verilen puanlar toplanır. Bu ölçeğe göre 15 puan üzeri alan hastalara orta yoksunluk, 20 puan üzeri alanlar ise şiddetli yoksunluk olarak değerlendirilmektedir. Tablonun ayrıntılı versiyonu için bu linke tıklayabilirsiniz. CIWA-Ar Ölçeği Minor yoksunluk semptomları için ayaktan tedavi önerilmektedir. Genellikle psikiyatri polikliniklerinde hastalara oral benzodiazepinler başlanılmaktadır.

First look at the pH: if it is low it is acidosis, high indicates alkalosis. Second use the ROME mnemonic to determine if you have respiratory vs. metabolic. For Metabolic look at HCO3. For Respiratory, look at pCO2. Metabolic Acidosis – pH Low, HCO3 Low. Metabolic Alkalosis – pH High, HCO3 High. Respiratory Acidosis – pH Low, pCO2 High. Respiratory Alkalosis – pH High, pCO2 Low.  

Bu yazımda acil serviste takip ettiğimiz hastalarda sık karşılaştığımız bir durum olan metabolik asidoz sebepleri ve yönetimini özetlemeyi amaçladım. Ayrıca sık gözlenen klinik durumlardaki tedavi önerilerini derlemeye çalıştım. İyi okumalar dilerim. Metabolik asidoz vücuttaki hidrojen iyonlarının arttığı ve bikarbonatın azaldığı bir süreç olarak tabir edilebilir. Bu süreç sadece kan gazı sonuçlarında pH değerine bakarak açıklanmamalıdır. Metabolik asidozda vücuttaki kompansasyona bağlı olarak pH değeri düşük, normal veya yüksek saptanabilir. Kan pH değerinin

What an academic feast organized by the SEMI-WB on the weekend of 16-17th July 2022 for the academic residents of emergency medicine. I start of the episode by talking about the EZECON. Also the 24th Annual Conference of SEMI is happening in Kerala from 23-27th November. Do register for it. In this episode I give an insight towards dealing with acid base disorders using the modified stewart's approach. Following are the references you can go through to understand more and change your practice - 1. https://emcrit.org/wp-content/uploads/acid_base_sheet_2-2011.pdf 2. Story DA. Stewart Acid-Base: A Simplified Bedside Approach. Anesth Analg. 2016 Aug;123(2):511-5. doi: 10.1213/ANE.0000000000001261. PMID: 27140683. 3. Jones NL. A quantitative physicochemical approach to acid-base physiology. Clin Biochem. 1990 Jun;23(3):189-95. doi: 10.1016/0009-9120(90)90588-l. PMID: 2115411. 4. Mallat J, Michel D, Salaun P, Thevenin D, Tronchon L. Defining metabolic acidosis in patients with septic shock using Stewart approach. Am J Emerg Med. 2012 Mar;30(3):391-8. doi: 10.1016/j.ajem.2010.11.039. Epub 2011 Jan 28. PMID: 21277142. 5. Morgan TJ. The Stewart approach--one clinician's perspective. Clin Biochem Rev. 2009 May;30(2):41-54. PMID: 19565024; PMCID: PMC2702213. 6.Kaplan LJ, Kellum JA. Initial pH, base deficit, lactate, anion gap, strong ion difference, and strong ion gap predict outcome from major vascular injury. Crit Care Med. 2004 May;32(5):1120-4. doi: 10.1097/01.ccm.0000125517.28517.74. PMID: 15190960. 7. Malatesha G, Singh NK, Bharija A, Rehani B, Goel A. Comparison of arterial and venous pH, bicarbonate, PCO2 and PO2 in initial emergency department assessment. Emerg Med J. 2007 Aug;24(8):569-71. doi: 10.1136/emj.2007.046979. PMID: 17652681; PMCID: PMC2660085. 8. Kelly AM, McAlpine R, Kyle E. Venous pH can safely replace arterial pH in the initial evaluation of patients in the emergency department. Emerg Med J. 2001 Sep;18(5):340-2. doi: 10.1136/emj.18.5.340. PMID: 11559602; PMCID: PMC1725689. 9. Byrne AL, Bennett M, Chatterji R, Symons R, Pace NL, Thomas PS. Peripheral venous and arterial blood gas analysis in adults: are they comparable? A systematic review and meta-analysis. Respirology. 2014 Feb;19(2):168-175. doi: 10.1111/resp.12225. Epub 2014 Jan 3. PMID: 24383789.

Baz açığı (baz eksesi) ilk kez 1960 yılında Siggaard-Andersen tarafından; respiratuar durumdan bağımsız olarak metabolik asidoz/alkoloz varlığının değerlendirilebilmesi ve varsa ciddiyetinin tanımlanabilmesi amacıyla ortaya konmuştur. Aslında önceleri metabolik değişimleri değerlendirmek amaçlı ilk kullanılan parametre aktüel HCO3 (HCO3a) seviyesi olmuştur (plazma örneğinde ölçülen HCO3 değeri). Ancak HCO3 parsiyel CO2 basıncına oldukça bağımlı bir değişken olduğundan, respiratuar değişikliklerin etkisini nötralize etmek amaçlı standart HCO3 (HCO3st) tanımlanmıştır. Standart HCO3 değeri PCO2 40 mmHg olduğunda olması gereken HCO3 konsantrasyonudur. Dolayısıyla: HCO3a = HCO3st ise hastada solunumsal dengenin korunduğu düşünülür. HCO3a > HCO3st ise SOLUNUMSAL ASİDOZ vardır. HCO3a < HCO3st ise SOLUNUMSAL ALKOLAZ vardır. HCO3st değerlendirmeyi bir tık daha doğru hale getirmiş olsa da halen nonkarbonik asitlerin (albümin başta olmak üzere, sülfat, fosfat gibi)  zayıf tampon etkisi hesaba dahil edilmemektedir. Yani örneğin HCO3 seviyesi 24 mmol/L olan kana 10 mmol/L lik güçlü asit eklendiğinde HCO3st beklendiği gibi 14mmol/L (24-10) yerine 16 mmol/L olarak ölçülür çünkü eklenen asitin 2 mmol/L lik kısmı non-karbonik tamponlar ile nötrlenmiştir. Bu problemi çözmek için ise Singer ve Hastings buffer base (BB) (tampon bazı) nı tanımlamışlardır. BB tüm tampon anyonların toplamına eşittir. BB= HCO3- + A- Ancak her ne kadar teorikte BB CO2 bağımsız bir değer olsa da, pratikte non-karbonik tampon konsantrasyonlarındaki farklılıklara bağlı BB değerinin değişkenlik gösterdiği bulunmuştur. Bunun üzerine Siggaard- Andersan aktüel BB ile normal BB (NBB) arasındaki farkı alarak Baz açığını tanımlamıştır. NBB deneysel olarak elde edilen PH 7.40 ve PCO2 40 mmHg iken olması gereken BB değeridir. Bu durumda baz açığı (BE) PCO2 40 mmHg kabul edildiğinde kan örneğinin PH sını 7.40 yapmak için eklenmesi gereken kuvvetli asit veya baz değeridir. Normal değeri -2 +2 arasındadır. Teorikte metabolik bozukluğu değerlendirmede kullanılır ve < -2 olması metabolik asidozu, > +2 olması metabolik alkolozu gösterir.​1​ BE = ∆ BB = BB – NBB Klinik kullanımda direkt ölçümü zor olacağından belli formüller ile hesaplanır; bunlardan en sık kullanılanı: BE = (HCO3- - 24.8)  + ᵝ . (PH -7.40) dır. ᵝ değeri hemoglobin konsantrasyonuna dayalı bir formülle hesaplanabileceği gibi sabit olarak 16.2 mmol/L olarak da kabul edilebilir. Klinik uygulamada bu kısmın tampon etkisinin non-karbonik asitleri yansıttığı ve baz açığı üzerinde düşük bir etkisinin olduğu unutulmamalıdır.  Baz açığı tüm kan için ifade edilebilir. Bu durumda BE(B) olarak ifade edilir ve intersisyel aralık ile kanın etkileşimi hesaplamada dikkate alınmaz.  Standart baz açığı (SBE) ise ekstaselüler boşluğu hesaba katarak ulaşılan bir değerdir ve bu durumda hesaplamada kullanılan ᵝ değeri belirlenirken hemoglobin konsantrasyonu 1/3 ile çarpılır. Ancak zaten formülde bu kısmın etki değeri düşük olduğundan ciddi anemi veya polisitemi durumlarında bile klinik açıdan anlamlı bir fark oluşması beklenmez. Baz açığının dezavantajları neler? Baz açığı, her ne kadar metabolik bozuklukların değerlendirilmesinde faydalı bir parametre olsa da bazı dezavantajları mevcuttur. Bunlardan ilki altta yatan patolojik mekanizma hakkında bize bilgi vermez. Kompozit bir belirteç olduğundan son değer laktat, ketoasitler, albümin gibi birçok farklı değere bağlıdır. Örneğin hastada hem hiperkloremi (güçlü anyonlarda artış), hem de hipoalbuminemi (negatif yükte azalma) bir arada olabilir. Böyle bir durumda baz açığı 0 bulunabilir. Baz açığı değerlendirilmesiyle ilgili bazı klinik tablo örnekleri aşağıda verilmiştir. Ama daha iyi bir yorum yeteneği için kan gazı analizini ve Steward metodunu sindirmeniz gerekir ( ki bunun için Melis'in yazısına bakmanızı öneririm https://acilci.net/steward-metodu-ile-asit-baz-ve-kan-gazi-degerlendirmesi-kantitatif-teori/) . Durum A: Normal durum

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat coming to you from Children's Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania from Cleveland Clinic Children's Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let's get into our episode: In today's episode, we discuss about a 12-year-old male with lethargy after ingestion. Here's the case presented by Rahul: A 12-year-old male is found unresponsive at home. He was previously well and has no relevant past medical history. The mother states that he was recently in an argument with his sister and thought he was going into his room to “have some space.” The mother noticed the patient was in his room for about 1 hour. After coming into the room she noticed him drooling, minimally responsive, and cold to the touch. The patient was noted to be moaning in pain pointing to his abdomen and breathing fast. Dark red vomitus was surrounding the patient. The mother called 911 as she was concerned about his neurological state. With 911 on the way, the mother noticed a set of empty vitamins next to the patient. She noted that these were the iron pills the patient's sister was on for anemia. EMS arrives for acute stabilization, and the patient is brought to the ED. En route, serum glucose was normal. The patient presents to the ED with hypothermia, tachycardia, tachypnea, and hypertension. His GCS is 8, he has poor peripheral perfusion and a diffusely tender abdomen. He continues to have hematemesis and is intubated for airway protection along with declining neurological status. After resuscitation, he presents to the Pediatric ICU. Upon intubation, an arterial blood gas is drawn. His pH is 7.22/34/110/-6 — serum HCO3 is 16, and his AG is elevated. To summarize key elements from this case, this patient has: Lethargy and unresponsiveness after acute ingestion. His hematemesis is most likely related to his acute ingestion. And finally, he has an anion gap metabolic acidosis, as evidenced by his low pH and low HCO3. All of these salient factors bring up the concern for acute iron ingestion! In today's episode, we will not only go through acute management pearls for iron poisoning, but also go back to the fundamentals, and cover ACID BASE disorders. We will break this episode down into giving a broad overview of acid base, build a stepwise approach, and apply our knowledge with integrated cases. We will use a physiologic approach to cover this topic! Pradip, can you give us a quick overview of some general principles when it comes to tackling this high-yield critical care topic? Absolutely, internal acid base homeostasis is paramount for maintaining life. Moreover, we know that accurate and timely interpretation of an acid–base disorder can be lifesaving. When we conceptualize acid base today, we will focus on pH, HCO3, and CO2. As we go into each disorder keep in mind to always correlate your interpretation of blood gasses to the clinical status of the patient. Going back to basic chemistry, can you comment on the relationship between CO2 and HCO3? Yes, now this is a throwback. However, we have to review the Henderson–Hasselbalch equation. The equation has constants & logs involved, however in general this equation shows that the pH is determined by the ratio of the serum bicarbonate (HCO3) concentration and the PCO2, not by the value of either one alone. In general, an acid–base disorder is called “respiratory” when it is caused by a primary abnormality in respiratory function (i.e., a change in the PaCO2) and “metabolic” when the primary change is attributed to a variation in the bicarbonate concentration. Now that we have some fundamentals down, let's move into definitions. Can you define acidemia and alkalemia and comment on how...

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat My name is Rahul Damania, a current 3rd-year pediatric critical care fellow and we are coming to you from Children's Healthcare of Atlanta Emory University School of Medicine Today's episode is dedicated to the transition between NICU & PICU. We will focus on the ventilation of the ex-premature infant who graduated from NICU care and transitioned to the PICU. I will turn it over to Rahul to start with our patient case. Case: A 4-month-old ex-27 week baby boy is transferred to our PICU after an echo at an outside hospital showed elevated pulmonary pressures. The infant was born via a stat C-section due to maternal complications during pregnancy. His birth weight was 560 g. The patient was intubated shortly after delivery and had a protracted course in the NICU which included a sepsis rule out, increased ventilator settings, and a few weeks on inhaled nitric oxide (iNO). The intubation course was complicated pulmonary hemorrhage on day 1 after intubation. After such an extensive NICU course, thankfully, the infant survived & was sent home on 1/2 LPM NC, diuretics, albuterol, inhaled corticosteroids, Synthroid, multivitamin with iron as well as Vitamin D. The patient was able to tolerate breast milk via NG tube and had a home apnea monitor with pulse oximetry. After about a week's stay at home, the mother noted that the patient's SPO2 was in the low 80s. The mother took the patient to the local hospital, where the patient was started on HFNC which improved his saturations. An echo done at the OSH showed elevated RV pressures (higher than the prior echo). The patient was subsequently transferred to our hospital for further management. At our hospital, the patient presented hypoxemic, tachycardic, and tachypneic. On physical exam: Baby appeared well developed, had a systolic murmur heard throughout the precordium, and there was increased WOB with significant intercostal retraction. There was no hepatosplenomegaly. Due to worsening respiratory distress, and increasing FIO2 requirement despite maximum RAM cannula, the patient was intubated and placed on conventional MV. A blood gas prior to intubation revealed a pH of 7.1/PCO2 of 100. An arterial line and a central venous line were also placed for better access and monitoring. Initial vent settings post intubation PRVC ventilation: TV 32cc, (25/10), 0.7 time, rate 0 (patient sedated/paralyzed). To summarize, What are some of the features in H&P that are concerning for you in this case: Ex-27 week prematurity with a birth weight of 560 gms Prolonged MV in the NICU Home O2 requirement Abnormal echo showing high pulmonary pressures hypercarbia despite the use of RAM cannula As mentioned, our patient was intubated, can you tell us pertinent diagnostics which were obtained? CXR revealed: Hazy airspace opacification in the right upper lung concerning developing pneumonia. Streaky airspace opacity in the left lung base medially may represent atelectasis. I do want to highlight that the intubation of an ex-premie especially with elevated RV pressures is a high-risk scenario, it is best managed by a provider with experience, in a very controlled setting with optimal team dynamics. Adequate preparation to optimize the patient prior to the intubation as well as the knowledge to manage the post intubation cardiopulmonary interactions are essential. I would highly advise you to re-visit our previous podcast on intubation of the high-risk PICU patient by Dr. Heather Viamonte. Like many Peds ICU conditions, the management of the EX-NICU graduate in the PICU is a multidisciplinary team sport. Our patient likely has the diagnosis of Bronchopulmonary Dysplasia or BPD, Pradip, can you comment on the evolving definition of this diagnosis? Let me first define BPD — Clinically, BPD is defined by a requirement of oxygen supplementation either at...

In deze aflevering bespreken we de interpretatie van een bloedgas.- Waarom is de normale pH eigenlijk 7,4?- Waarom partiële compensatie niet bestaat.- Wanneer gebruik je de anion gap?- Wat is de functie van het base excess?- Kan je een veneus bloedgas net zo interpreteren als een arterieel bloedgas?- Wat is de Winters Formule?- Hoezo worden patiënten acidotisch van NaCl 0,9%?Buffer vergelijking:CO2 + H2O H2CO3 HCO3- + H+Bloedgas oefenen:Casus 1:Septische patiënt van de verpleegafdeling, flink gevuld aldaar.pH 7,30pCO2 26mmHg/3,5kPaHCO3 12,7 mmol/lCasus 2:Patiënt met gastro-enteritis en frequent braken.pH 7,56pCO2 37,5 mmHg/5,0kPaHCO3 31 mmol/lCasus 3:Hartpatiënt met forse benauwdheid en crepitaties en mogelijk NSTEMIpH 7,16pCO2 56mmHg/7,5kPaHCO3 19,5 mmol/lCasus 4:Patiënt in weantraject 1h na aanpassen PS naar CPAP.pH 7,48pCO2 29mmHg/3,8kPaHCO3 22 mmol/lCompensatie berekenen?We nemen als normaal waarden een pCO2 van 40mmHg en een HCO3 van 24 mmol/lVerwacht HCO3:Acute respiratoire acidose:  Elke 10mmHg (1,3 kPa) stijging van het pCO2 stijgt het HCO3 met 1mmol/lChronische respiratoire acidose:  Elke 10mmHg stijging van het pCO2 stijgt het HCO3 met 3,5mmol/lAcute respiratoire alkalose: Elke 10mmHg daling van het pCO2 daalt het HCO3 met 2mmol/l, voor chronisch 5mmol/lAcute respiratoire alkalose: Elke 10mmHg daling van het pCO2 daalt het HCO3 met 5mmol/lVerwacht pCO2Metabole acidose: 1,5 x (HCO3) + 8 (+-2mmHg range) (in mmHg of /7,5 in kPa) Metabole alkalose: 0,7 x (HCO3) + 21 (+-2mmHg range) (in mmHg of /7,5 in kPa)pCO2 | pH | Metabool of respiratoirHoog | Hoog | MetaboolNormaal | Hoog | MetaboolLaag | Hoog | RespiratoirHoog | Laag | RespiratoirNormaal | Laag | MetaboolLaag | Laag | MetaboolBronnen:Interpretation of arterial blood gasBase excess and standard base excessArterial blood gas interpretationBedankt voor het luisteren!Volg @intensiefdepodcast op InstagramVragen? intensiefdepodcast@gmail.com

Good morning and welcome to your Thursday dose of Your Daily Meds.Bonus Review: How is CSF different from Plasma?Answer: CSF is identical to brain ECF in composition. But the differences to plasma include - pCO2 is higher in CSF (about 50mmHg) resulting in lower pH (about 7.33)Very low protein content - so CSF has low acid-base buffering abilityLower glucose concentration[Cl-] is higher by about 10% and [K+] is lower by about 40%Very low cholesterol contentPsych Question:Which of the following does NOT contribute to the classification of anxiety as pathological?Fear greatly out of proportion to severity of risk or threatResponse continues until removal of the threatResponse becomes generalised to other similar or dissimilar situationsSocial or occupational function is impairedComorbid with substance use and depressionHave a think.Scroll for the chat.Surgery Question:A 49-year-old man underwent a complete thyroidectomy in the setting of papillary thyroid cancer. Which of the following would be the least likely complication of this surgery?Peri-oral paraesthesiaHoarsenessDysphagiaSeroma formationPtosisHave a think.Scroll for the chat.The Threat:Anxiety is a fearful response in the absence of a specific danger or threat, or in their anticipation. Anxiety is distinct from fear, which is a response to a realistic and immediate danger. Fear is adaptive in situations of stress or danger with priming of the physiological ‘fight or flight’ mechanism.Anxiety is more likely to diminish performance and is considered pathological when:Fear greatly out of proportion to severity of risk or threatResponse continues beyond existence of threatResponse becomes generalised to other similar or dissimilar situationsSocial or occupational function is impairedComorbid with substance use and depressionSo a response that continues until removal of the threat is least likely to contribute to the classification of anxiety as pathological, rather a response continuing beyond the existence of the threat would be indicative.Complications:Perioral paraesthesia is a symptom of hypocalcaemia. Hypocalcaemia as a result of hypoparathyroidism (parathyroid damage or removal in surgery) is the most common complication of thyroidectomy. This would be very bad.Hoarseness after thyroid surgery is common and can be due to a range of problems ranging from oedema to nerve injury, such as to the recurrent laryngeal nerve.Dysphagia, difficulty swallowing, post-thyroid surgery is common and may be due to adhesions, trauma, inflammation or nerve damage.Wound seromas post-operatively tend to resolve without intervention.Ptosis (as in part of Horner syndrome) is a very rare complication of thyroidectomy and results from disruption of the sympathetic supply to the head, eye and neck. Horner syndrome is most often associated with lateral neck dissection. (Or an apical lung cancer affecting the sympathetic trunk…)Bonus: Can substances pass freely from blood into the CSF?Answer in tomorrow’s dose.Closing:Thank you for taking your Meds and we will see you tomorrow for your MANE dose. As always, please contact us with any questions, concerns, tips or suggestions. Have a great day!Luke.Remember, you are free to rip these questions and answers and use them for your own flashcards, study and question banks. Just credit us where credit is due. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit yourdailymeds.substack.com

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat My name is Rahul Damania, a current 2nd year pediatric critical care fellow. We come to you from Emory University,School of Medicine, Children's Healthcare of Atlanta, Atlanta, GA. Today's episode is dedicated to O2 delivery in the PICU. We would like to highlight in this episode Stanford University School of Medicine Pediatric Critical Care's LearnPICU website. Thehttp://learnpicu.com ( LearnPICU.com) website Is dedicated to reviewing clinical topics related to pediatric critical care, and is an open access resources which Is widely accessed worldwide. The website has over 10,000 visits each month, and is managed by Dr. Kevin Kuo - Clinical associate professor of pediatrics pediatric critical care at Stanford University. Dr. Kuo has Been featured on our prior episode entitled seven habits of highly effective Picu fellows, and we are very excited to collaborate with his educational resources to provide you the listener a comprehensive educational experience. Rahul, let's go ahead and get into today's case. A 17-year old boy is admitted after he was struck by a car at slow speed while crossing the street. He is has SPO2 of 98%, HR 98 bpm with a normal capillary refill and perfusion. His blood gas at admission to the PICU reveals a ph of 7.3/PCO2 35/PaO2 196 mm Hg on 50% NRB with 100% O2 flowing at 12LPM. His admission hgb is 10.5 gm%. 4 hours post admission, the nurses noticed that the patient is tachycardic to 150s, with a drop in his BP, delayed capillary refill, with cool extremities and increased output from the chest tube. His SpO2 has decreased to 86% and PaO2 on his blood gas is now 65mm HG. He is found to have a POC Hgb of 6.8 mg/dL. Let's take this case and highlight key components of O2 delivery and O2 consumption. Lets focus on O2 delivery first. Rahul What are the components of O2 delivery ?  Pradip, O2 delivery is made of O2 content X Cardiac output Simply put, O2 content is the amount of blood present in 100ml of arterial or venous blood. Its is denoted by CaO2 or CvO2 and its unit is mL O2 / dL blood or mL O2 per 100 mL of blood. Before we introduce the complicated formula, let's just appreciate the variables within the equation. Oxygen content is going to be a function of three variables: This is going to be Hgb, Saturations on the hemoglobin also known as SaO2, and the amount of oxygen that is dissolved within the blood also known as your PaO2. Pradip, Can you elucidate further about O2 content? O2 content is given by the formula: CaO2 = (1.34X Hgb gm/dl X SaO2) + (0.003X PaO2) Important points to remember about above formula is that the constant 1.34 (or 1.36 as given by some textbooks) is the amount of O2 in mL bound by one gm of Hgb and is called as the O2 carrying capacity of Hgb. In a healthy person say with 15gm% of Hgb, the O2 carrying capacity is about 15X1.34 = 20gm%. Now many times amount of O2 bound to Hgb may not always reflect 100% saturation So we need to factor the % oxygen saturation into the oxygen carrying capacity of the Hgb. The final element is to understand that some oxygen is dissolved in the plasma and is calculated using a constant 0.003 X PaO2. Typically 100ml of arterial blood with a saturation of 100 will contain 100 X 0.003 = 0.30ml of dissolved oxygen. Rahul can you calculate the pre-decompensation oxygen content in the above case? The above patients hgb pre-decompensation = 10.5gm%. His room air saturation 98% and his PaO2 is 196. CaO2 = (1.34X10.5X0.98) + 0.003 X 196 = 13.7 + 0.58 = 14.2ml O2/dL blood. Great - what is the post decompensation CaO2.? The post decompensation CaO2 can be estimated using same formula as above: CaO2 = (1.34 X 6.8 X0.86) + (0.003 X 65) = 7.8 + 0.195 = 7.9 O2/dL blood. Exactly So if you see the pre and post bleed O2 content just with a drop in Hgb from 10.5 to 7.5gm/dL: There is almost a 38% decrease in...

Acute pulmonary Hypertensive Crises Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode a 7 month old boy ex-26 week premature infant with acute hypoxemia, bradycardia episodes, poor perfusion Here's the case: A 7 month old ex-26 week male was transferred from the outside hospital to our PICU for tracheostomy evaluation. Patient was intubated on second day of life. He had a prolonged course, on inhaled Nitric Oxide for first 2-3 months of life in the setting of severe pulmonary hypertension, requiring HFOV for a prolonged period of time. Failed extubation attempts multiple times. Received steroid burst x2. BPD settings trialed (lower rate, longer iTime, high PEEP, larger TV) without improvement. At time of transfer he was in PRVC mode on the ventilator — TV ~10ml/kg, 50%, PEEP 8, rate 28 (Peak pressures 27-32). Patient received albuterol Q4 for bronchospasm/wheezing and pulmicort BID. Patient was deeply sedated with morphine and midazolam. Interstitial lung disease panel was negative. ECHO showed: systolic septal flattening, moderate RV hypertrophy with normal systolic functioning. Patient was not on any PH medications at transfer. Patient is also on furosemide, hydrochlorothiazide and spironolactone. Patient has completed a course of antibiotics for klebsiella tracheitis from a ETT CX a week prior to admission to our picu. Patient tolerated feeds via an NJ tube. The team continues to evaluate his case as the Patient continues to have episodes of acute desaturation, tachycardia, cool extremities and poor perfusion. To summarize key elements from this case, we have a 7month old who is ex-26 week premie Patient has BPD and is on high vent settings and failing extubation Abnormal echocardiogram with flat septum and hypertrophied Right ventricle Episodes of cold shock-tachycardia, poor perfusion, and cool extremities Hypoxia All of which bring up a concern for acute pulmonary hypertensive crisis Rahul Let's transition into some history and physical exam components of this case? What are key history features in this infants who presents with an acute pulmonary hypertensive crisis Prematurity BPD Remember BPD is defined by a requirement of oxygen supplementation either at 28 days postnatal age or 36 weeks postmenstrual age. Are there some red-flag symptoms or physical exam components which you could highlight? Presence of cold shock: tachycardia, cool extremities and poor perfusion Hypoxia Cardiac exam will reveal a bounding right ventricle, prominent loud single S2 Although not obvious in this patient: some patients can have a palpable liver, cardiac gallop, peripheral edema and jugular venous distention S2 heart sound represents the closure of the PV very close to AV — In pulmonary hypertension this PE sign is seen with equal right and left ventricular pressures. To continue with our case, the patient's labs were consistent with: Respiratory acidosis (PCO2 > 100) CMP, CBC are normal BNP < 100, serum lactate normal Echocardiography findings in these patients can show tricuspid regurgitation. We can estimate right ventricular systolic pressure on echo and, by extension, systolic PAP (sPAP), by using tricuspid regurgitant (TR) jet velocity in combination with other echocardiographic findings. Using the modified bernoulli principle 4 x TR jet velocity squared, we can estimate the sPAP. If sPAP >2/3 systemic sBP with severe flattening or posterior bowing of the interventricular septum the patient can be diagnosed with severe pHTN. Pradip, what if the patient had a PDA on echo — what would you see? Rahul, when you see Predominantly right-to-left shunting across the PDA suggests suprasystemic sPAP. And as a result these patients can be hypoxemic Ok, to summarize, we have: A 7-month ex-26 week premie...

In this episode we delve into gravitational effects on the lung including ventilation aspects, pO2, pCO2, VQ matching and its effects and Wests Zones.The diagrams are from Respiratory Physiology by John B West.Please support us on our Patreonhttps://www.patreon.com/anaesthesiaAll proceeds will go to Fund a Fellow to help train anaesthetists in developing countries whilst acknowledging the work it takes to keep creating this educational resource.If you enjoyed this content please like and subscribePlease post any comments or questions below. Check out www.anaesthesiacollective.com and sign up to the ABCs of Anaesthesia facebook group for other content.Any questions please email lahiruandstan@gmail.comDisclaimer: The information contained in this video/audio/graphic is for medical practitioner education only. It is not and will not be relevant for the general public.Where applicable patients have given written informed consent to the use of their images in video/photography and aware that it will be published online and visible by medical practitioners and the general public.This contains general information about medical conditions and treatments. The information is not advice and should not be treated as such. The medical information is provided “as is” without any representations or warranties, express or implied. The presenter makes no representations or warranties in relation to the medical information on this video. You must not rely on the information as an alternative to assessing and managing your patient with your treating team and consultant. You should seek your own advice from your medical practitioner in relation to any of the topics discussed in this episode' Medical information can change rapidly, and the author/s make all reasonable attempts to provide accurate information at the time of filming. There is no guarantee that the information will be accurate at the time of viewingThe information provided is within the scope of a specialist anaesthetist (FANZCA) working in Australia.The information presented here does not represent the views of any hospital or ANZCA.These videos are solely for training and education of medical practitioners, and are not an advertisement. They were not sponsored and offer no discounts, gifts or other inducements. This disclaimer was created based on a Contractology template available at http://www.contractology.com.

Contributor:  Nick Tsipis, MD Educational Pearls: pH 7.45=alkalemia If pH low and pCO2 high, indicates a respiratory acidosis If pH low and pCO2 low, indicates metabolic acidosis After determining type of acidosis, check bicarb to determine compensation for acidosis and check electrolytes to calculate anion gap Metabolic acidosis can present with tachypnea (Kussmaul breathing) and hypotension due to loss of catecholamine function and suboptimal cardiac function at low pH Treat with IV fluids and address the underlying cause, limited role for bicarb References Burger MK, Schaller DJ. Metabolic Acidosis. [Updated 2020 Nov 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan. Cadogan M. Acid Base Disorders. Life in the Fast Lane • LITFL. https://litfl.com/acid-base-disorders/. Published November 3, 2020. Accessed June 23, 2021. Summarized by John Spartz, MS4 | Edited by Erik Verzemnieks, MD   The Emergency Medical Minute is excited to announce that we are now offering AMA PRA Category 1 credits™ via online course modules. To access these and for more information, visit our website at www.emergencymedicalminute.com/cme-courses/ and create an account.  Donate to EMM today!

Today's episode is dedicated to the differentiation and management of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) We are delighted to be joined by Dr. Eric Felner. Dr. Felner is a Professor of Pediatrics/Pediatric Endocrinology at the Emory University School of Medicine and is an Adjunct Professor of Chemical and Biomedical Engineering at Georgia Tech. Show Highlights: Our case, symptoms, and diagnosis: A 15-year-old male presents with a one-week history of increased urination. He is otherwise healthy except for a viral URI last week. He is found to be disoriented and tachycardic, with an exam notable for delayed peripheral capillary refill and cool extremities. The patient has deep, labored respirations upon examination, and labs confirm hyperglycemia with a serum glucose of 850, mild acidosis, and 2+ ketones. His CPK level is elevated, and a crystalloid fluid bolus is started.  Hyperosmolar hyperglycemic state is defined as a serum glucose greater than 600 mg/dL, serum osmolality of 330 mOsm/kg, and the absence of ketosis and acidosis. The key difference between HHS and DKA is that DKA is characterized by the presence of ketones in the blood and acidosis, but HHS means these are completely absent. Even though DKA and HHS are similar, their management strategies have their own nuances. In DKA, the lack of insulin leads to management strategies, while HHS is marked by complete dehydration and excessive urination.  Factors that point to HHS will be a very overweight child, family history, and ethnicity; Type-2 diabetes is much more common in African-American, Latin-American, and Native-American children, while Type-1 is more common in Caucasians.  Specific labs for patients with suspected DKA or HHS include a comprehensive metabolic panel (CMP), blood gas, and CPK for HHS. For both conditions, management strategies focus on insulin and fluid administration, but there are key differentiations: DKA is managed using the triple bag therapy that was pioneered by Dr. Felner. There is a risk for cerebral edema with administering fluid. The most important data relating to fluid administration with regard to neurological outcomes is what we have learned in calculating fluids with the “2x maintenance formula” to guard against mistakes that could result in cerebral edema. Key considerations regarding low-dose vs. standard-dose insulin therapy revolve around the weight and age of the pediatric patient. For HHS, the key is to manage fluids and give insulin; for Type-1 diabetics, the key is to eliminate acidosis. Key PICU management pearls in minimizing cerebral edema risks are to determine the level of sickness by the PCO2 level, high BUN, and by not giving bicarbonate. Remember that children under age 5 have a higher risk for cerebral edema. In the management of both DKA and HHS, remember that it comes down to how sick a patient is and not necessarily following the numbers.  In general pediatrics, managing a sick DKA patient means giving an IV, administer fluids, and call a specialist management team right away. Dr. Felner discusses the association between COVID-19 and Type 1 diabetes based on his experience.  As intensivists and endocrinology teams work together to transition patients to an intermittent insulin regimen, it's important to remember how to convert from IV insulin to subQ insulin.  Takeaway clinical pearls include the key diagnostic elements between DKA and HHS. In HHS, patients will have higher glucose levels, milder acidosis, mild ketosis, and increased dehydration. Both conditions will have insulin and fluid management, and HHS patients may require increased fluid resuscitation.   

Chapter Three: How the proximal tubule is like Elizabeth Warren and other truths my friends from Boston taught me References for Chapter 3: Faisy C, Meziani F, PLanquette B et al. Effect of Acetazolamide vs. Placebo on Duration of Invasive Mechanical Ventilation among patients with chronic obstructive pulmonary disease: a randomized clinical trial. JAMA 2016 https://pubmed.ncbi.nlm.nih.gov/26836730/This randomized controlled double blinded multi-center study of acetazolamide to shorten the duration of mechanical ventilation (known as DIABLO) there was no statistically significant difference (though it may have been underpowered to do so).Salazar H, Swanson J, Mozo K, White AC, Cabda MM Acute Mountain sickness impact among travelers to Cusco, Peru J Travel Med 2012 https://pubmed.ncbi.nlm.nih.gov/22776382/ Investigators found that altitude sickness is common and alters travel plans for 1 in 5 travelers but was prescribed infrequently.Buzas GM and Supuran CT. Journal of enzyme inhibition and medicinal chemistry 2015 https://www.tandfonline.com/doi/full/10.3109/14756366.2015.1051042This review describes the use of acetazolamide to treat peptic ulcers and how it was later learned that H. pylori have carbonic anhydrase NORDIC idiopathic intracranial Hypertension Study Writing Committee. The effect of acetazolamide on visual function in patients with idiopathic intracranial hypertension and mild visual loss: the idiopathic intracranial hypertension treatment trial. JAMA 2014 https://pubmed.ncbi.nlm.nih.gov/24756514/In this multi-centered trial, acetazolamide and low sodium weight reduction diet improved mild visual loss more than diet alone. Mullens W et al. Rationale and design of the ADVOR (acetazolamide in decompensated heart failure with volume overload trial) Eur J Heart Failure 2018 https://pubmed.ncbi.nlm.nih.gov/30238574/This reference explains the rationale for this ongoing trial.Gordon CE, Vantzelfde S and Francis JM. Acetazolamide in Lithium-induced nephrogenic diabetes insipidus NEJM 2016 https://www.nejm.org/doi/full/10.1056/NEJMc1609483A case report of efficacy of acetazolamide in a patient with severe polyuria.Zehnder D et al. Expression of 25-hydroxyvitamin D-1alpha hydroxylase in the human kidney. JASN 1999 This report explores the activity in the enzyme in nephron segments and suggests that the distal nephron may play an important part in the formation of 1,25 vitamin D https://jasn.asnjournals.org/content/10/12/2465Outline: Chapter 3 - This is chapter three, kind of the first real chapter of the book- Proximal Tubule- Reabsorbs 55-60% of the filtrate - Active sodium resorption - 65% of the sodium - 55% of the chloride - 90% of HCO3 - 100% glucose and amino acids - Passive water resorption - Water resorption is isosmotic - Secretion of - Hydrogen - Organic anions - Organic cations - Anatomy - S1, S2, S3 can be differentiated by peptidases - S1 more sodium resorption and hydrogen secretion, high capacity - S2 more organic ion secretion - Cell model - Basolateral membrane - Na-K-ATPase powers all the resorption - Luminal membrane - 100 liters a day crosses the proximal tubule cells - Microvilli to increase surface area - Microvilli has brush border which has carrier proteins as well as carbonic anhydrase - Water permeable, so sodium resorption leads to water resorption - Aquaporin-1 (sounds like this transporter is unique to the proximal tubule and RBC) - HCO3 is reabsorbed early, along with Na, resulting in increased chloride concentration which passively reabsorbed via paracellular route. - Tight junction has only one strand (on freeze fracture) as opposed to 8 in distal nephron - The Na-K-ATPase - Lower activity than in the LOH and distal nephron - Maintained intracellular Na at effective concentration of 30 mmol/L - Interior of the cell is negative due to 3 sodium out and 2 K in, then K leaks back out. - 3 Na out for 2 K in - An ATP sensitive K outflow channel on the basolateral membrane - Increased ATP slows potassium eflux - The idea is if Na-K slows, ATP will accumulate and this will slow K leaving, because there is less potassium entering. - K channel is ATP sensitive, ATP antagonizes K leak. - Highly favorable ELECTROCHEMICAL gradient for sodium to flow into the cell through the luminal membrane - Must be via a channel or carrier - Cotransporters - Amino acids - Phosphate - Glucose - Called secondary active transport - Countertransporters - Only example is H excretion - Basolateral membrane - Na-3HCO3 transporter - Powered by the negative charge in the cell- Chloride resorption - Formate chloride exchanger - Formate combines with hydrogen in the lumen, becomes neutral formic acid, and is reabsorbed where the higher pH causes it to dissociate and recycle again. - Dependent on continued H+ secretion - Chloride moves across basolateral membrane thanks to Cl and KCl transporters, taking advantage of negative intracellular charge- Passive mechanisms of proximal tubule transport - Accounts for one third of fluid resorption - Mechanism - Early proximal tubule resorts most of the bicarb and less of the chloride - Tubular fluid gets a high chloride concentration - Chloride flows through the tight junction down its concentration gradient - Sodium and water follow passively behind - Water moves osmotically into intercellular space from tubular fluid even though the osmolalities are equal since chloride is an ineffective osmole, so tonicity is not the same. ****** - Argues that bicarb is primarily important solute for passive resorbtion - Acetazolamide blocks Na and chloride resorption - Similar thing happens with metabolic acidosis where less bicarb is available to drive passive resorbtion of Na and Cl - Summary - Other than Na-K-ATPase Na-H antiporter main determinant of proximal Na and water resorption - 1. Direct bicarb resorption - Preferential bicarb resorbtion proximally drives passive chloride resorption - Drives active the formate exchanger for chloride resorption- Neurohormonal influence - AT2 drives a lot of Na resorption, primarily in S1 segment - Does not have a net effect on H-CO3 movement - Dopamine antagonizes sodium resorption - Blocks both Na-K-ATPase and - Na H antiporter- Capillary uptake - Starlings. Again - Low hydraulic pressure due to glomerular arteriole - High plasma on oncotic pressure from loss of the filtrate - The two together promote resorption - There maybe movement from interstitial back into tubular fluid (back diffusion) conflicting data- Glomerular tubular balance - The fractional tubular reabsorption remains constant despite changes in GFR (tubular load) - It is essential the GFR is matched by resorption - The rise in capillary osmotic pressure with increased GFR via increased filtration fraction is one mechanism of GT balance - Glomerular tubular balance os one of three mechanisms that prevents fluid delivery from exceeding the resorptive capacity of the tubules - GT balance - TG feedback - Autoregulation - GT balance can be altered if patients are volume overloaded or depleted - Closes this section with a story of a kid born without a brush border - Primacy of sodium in proximal tubule activity - Discusses bicarb resorbtion - There is no Tm for Bicarb as long as volume overload is prevented, in rats can rise over 60! - If you give NaHCO3 you get volume overload and the Tm I about 60 - Glucose - S1 and S2 have high capacity, low affinity glucose resorption - S3 has high affinity 2 Na fo every glucose - Tm glucose is 375 mg/min - For a GFR of 125t that comes out to 300mg/dL - 125 ml/min * 3mg/ml (300 mg/dL) = 375 mg/min - Functionally this is 200 mg/dL due to splay - Urea - Only 50-60 of filtered urea is excreted - Calcium Loop and distal tubule - Phosphate - 3Na-Phosphate high affinity transporters late in proximal tubule - three types of Na-Phos transporters, type 2 are the most important - regulated by PTH and plasma phosphate - PTH suppresses Phos resorption -Metabolic acidosis also reduces phosphate resorption (good to have phosphate in the tubule to soak up H+ - Decreased tubular pH converts HPO42- to H2PO4- which has lower affinity for phosphate binding site - Mg Loop and distal tubule - Uric AcidWhy do I love acetazolamide?- I love the proximal tubule- Many uses- Often forgottenMOA- Inhibit carbonic anhydraseMain effects- Renal: less bicarb reabsorption (ie less H secretion) à more distal Na/bicarb delivery à hypokalemic metabolic acidosis- Brain: reduce CSF production, reduce ICP/IOP, aqueous humor- Pulm: COPDNotes- Tolerance develops in 2-3 days- Sulfonamide derivative- Highly protein bound, eliminated by kidneys Source: Buzas and upuran, JEIMC, 2016S Data:1968 - High altitudeHigh altitude usually results in respiratory alkalosisAcetazolamide – lessens symptoms of altitude sickness (insomnia, headache) which occur because of periodic breathing/apnea1979- NEJM study took 9 mountaineers asleep at 5360 meters à improvement in sleep, improved SaO2 from 72 to 78.7 mmHg, reduce periodic breathing, increased alveolar ventilation (pCO2 change from 37 mmHg to 30.8mm Hg)1950s - Seizures/migrainesCAI reduces pH (more H intracellularly), K movement extracellularly à hyperpolarization and increase in seizure thresholdWeak CAI (Topamax, zonisamide) but not though to be important mechanism of antiseizure effect (topamax enhances inhibitory effect of GABA, block voltage dependent Na and Ca channels)Pulmonary/COPDThought to help with the metabolic alkalosis and as a respiratory stimulant to increase RR, TV, reduce ventilator timeIn 2001 Cochrane review – no difference in clinical outcomes, but did reduce pH and bicarb minimallyDIABLO study (RCT) on ventilated COPD patients – no difference in median duration of mechanical ventilation despite correction of metabolic alkalosisHigh altitude erythropoiesis (Monge disease)First described in 1925 via Dr. Carlos Monge Medrano (Peruvian doctor), seen in people living > 2500-3000 meters (more common in South America than other high altitude areas)Usually chronic altitude sickness with HgB > 21 g/dL + chronic hypoxemia, pHTNAcetazolamide – reduces polycythemia because induces a met acidosis à increases ventilation and arterial PPO2 and SaO2 à blunts erythropoiesis and reduces HCT and improves pulmonary vascular resistanceGI ulcersWhen H2 and PPI available, less useHistory: 1932 – observed alkaline tide, presumed existence of gastric CA (demonstrated in 1939)Acetazolamide was used to inhibit acid secretion in 1960s, ulcer symptoms, with reversible metabolic acidosis, BUT lots of SE (electrolyte losses, used Na/K/Mg salts to help, renal colic, headache, fatigue, etc)Later found H. Pylori encodes for two different CasHelps to acclimatize to acidic environmentBasically, the Ca changes CO2 into H+ and HCO3They also have a urease which produces NH3The NH3 binds with H+, leaving an alkaline environment for them to live inInhibition of CA with acetazolamide is lethal for pathogen in vitro1940sFound there was CA in pancreasThought acetazolamide to reduce volume of secretions from NGT (output from exocrine pancreas) Source: Human Anatomy at Colby Blog Diuretic resistanceIf develop hyperchloremic metabolic alkalosis, short course of acetazolamide + spironolactone (b/c need distal Na blockage) à can helpMay help with urine alkalization (ie uric acid stone) but increases risk of calcium phosphate stonesADVOR trial acetazolamide in HF exacerbation in Belgiumuse may help to prevent new episode, lower total diuretic doseCSF reduction (pseudotumor cerebri)Reduces CSF by as much as 48% when > 99.5% of CA in choroid plexus is inhibitedNORDIC trial (acetazolamide v. placebo) – improvement in visual symptoms especially if advanced papilledema, and reduced opening pressure)Side note also used off label to help with increased ICP and CSF leaks, as alternative to VP shunts, repeat LPs, etc Source: Eftekari et al, Fluid Barriers CNS, 2019.

  Beim BGA-Automaten kann eine Temperaturkorrektur angewandt werden. Wunderbar. Aber ist sie auch sinnvoll? Die Antwort darauf ist tatsächlich vielschichtiger, als man vielleicht zunächst glauben mag. Interessanterweise gibt es auch in großen Lehrbüchern keine eindeutigen Aussagen zu dem Thema (z.B. „Oh’s Intensive Care Manual“, oder „Intensivmedizin“). Bei ersterem heißt es lapidar (achte Aufl., S. 164): … Weiterlesen

A wide range of interesting things this week - most of the links are below. Please send any comments and ideas to reviewer2geo@gmail.com or tweet us @reviewer2geo or me Clare @clare_nomad_geo or @geoengineering1 Intervention in the Earth's systems: Geoengineering https://diplomacy21-adelphi.wilsoncenter.org/geoengineering-intervention-atmosphere A report by Delphi and the Wilson centre with essays on solar geoengineering from Simon Nicholson https://twitter.com/simonnicholson4 and Oliver Morton https://twitter.com/Eaterofsun Oliver Morton Article https://diplomacy21-adelphi.wilsoncenter.org/article/geopolitical-challenges-geoengineering-and-geoengineerings-challenge-geopolitics "Foreign Policy IS Climate Policy" https://www.wilsoncenter.org/sites/default/files/media/uploads/documents/21st_century_diplomacy_report_spread.pdf Scientists are exploring ways to use mineral waste from mines to pull huge amounts of carbon dioxide out of the air. https://www.technologyreview.com/2020/10/06/1009374/asbestos-could-be-a-powerful-weapon-against-climate-change-you-read-that-right/ CO2 Sequestration in Mine Tailings https://www.mdru.ubc.ca/projects/co2-sequestration/ Eruptions & Emissions cause changes in ocean carbon sinks A new model explains why the ocean’s capacity to take up carbon was reduced on a decadal scale, by accounting for reduced pCO2 emissions and ocean state changes due to the eruption of Mt. Pinatubo. https://eos.org/editor-highlights/eruption-and-emissions-take-credit-for-ocean-carbon-sink-changes#.X3yG88CrTDY.twitter Using CaO- and MgO-rich Industrial Waste Streams for Carbon Sequestration Joshuah Stolaroff, Gregory Lowry, and David Keith. 2005. “Using CaO- and MgO-rich Industrial Waste Streams for Carbon Sequestration.” Energy Conversion and Management, 46, Pp. 687-699. -David keith commenting that theya re worth pursuing but not huge Unnatural climate solutions? Nature Climate Change volume 10, pages98–99(2020) Rob Bellamy on why the hype around ‘natural’ climate solutions threatens us all. His new paper is with Shannon Osaka. Abstract: Framing solutions to climate change as natural strongly influences their acceptability, but what constitutes a ‘natural’ climate solution is selected, not self-evident. We suggest that the current, narrow formulation of natural climate solutions risks constraining what are thought of as desirable policy options. https://www.nature.com/articles/s41558-019-0661-z

Dr RR Baliga's Internal Medicine "Got Knowledge Doc" Podcasts for Physicians. Not Medical Advice or opinion    

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.11.243964v1?rss=1 Authors: Brotherton, D. H., Savva, C., Ragan, T., Linthwaite, V., Cann, M., Dale, N., Cameron, A. D. Abstract: CO2 is the inevitable by-product of oxidative metabolism. Many physiological processes such as breathing and cerebral blood flow are sensitive to CO2. Historically, the physiological actions of CO2 have been regarded as being mediated exclusively via changes in pH. Here, we change this consensus by showing that the gap junction protein Connexin26 (Cx26) acts as a receptor for CO2 showing sensitivity to modest changes in PCO2 around the physiological norm. Mass spectrometry analysis shows that CO2 carbamylates specific lysines on a regulatory loop of Cx26 at high, but not at low levels of PCO2. By means of high resolution cryo-EM, we have solved structures of Cx26 gap junctions at 1.9, 2.2 and 2.1 [A] for PCO2 of 90, 55 and 20 mmHg respectively, all at pH 7.4. Classification of the particles at each level of PCO2, shows the transmembrane helices and N-terminal helix flexing at the dynamic cytoplasmic side of the protein. Gating of Cx26 gap junctions by CO2 involves movements of the N-terminus to plug the channel at high PCO2. We therefore provide mechanistic detail for a new paradigm by which CO2 can directly control breathing8 and other key physiological functions. Copy rights belong to original authors. Visit the link for more info

Hey everyone, today we'll be discussing the proper way to both treat and transport a pediatric DKA patient. We'll go over the treatments and why they matter, and talk about the dangers of inappropriate management in pediatrics with a diagnosis of DKA. Some visual info for you is below: Sample IV fluid maintenance schedule for pediatrics • 20kg = (1500ml + 20ml/kg) / day Labs for Case 1: • pH 7.11, PCO2 17, HCO3 9, BE -19, Lactate 2.7 • Na 132, K 5.2, Cl 95, CO2 8, glucose 540 • Urine: positive for glucose and ketones And don't forget! If you like this podcast, please give us a 5-Star rating, it helps us to be found by others! You can always reach me at: kisercpr@gmail.com #HEMS #criticalcare #flightparamedic #flightnurse #coffeebreakhems #FOAMed

Dr Biykem Bozkurt: I am Biykem Bozkurt, Professor of Medicine from Baylor College of Medicine, Senior Associate Editor for Circulation and today, I'm joined with Sana Al-Khatib, Professor of Medicine from Duke University, Senior Associate Editor of Circulation, for the podcast for the fourth annual Go Red for Women issue for Circulation. As all our listeners are aware, cardiovascular disease is a leading cause of death among women, but we have significant gaps in our awareness and treatments, and with a recognition of these disparities for cardiovascular care in women, AHA has launched a Go Red for Women campaign back in 2004. We have made great strides, and despite the improvement in awareness, significant gaps persist and adverse trends are emerging for cardiovascular disease in women. With such recognition, in 2017, Circulation launched the annual Go Red for Women issue, dedicated to cover transformative science, exciting new treatment strategies, recent epidemiological trends, and with an intent to close the gaps and eliminate the disparities for cardiovascular care in women. This is the fourth Go Red for Women issue and we have an exciting portfolio that we'd like to share with our readers and listeners. In this issue, we have quite a few important papers. The first two that we would like to start with are going over the epidemiologic trends. Sana, do you want to walk us through the two papers that we have on myocardial infarction and sudden cardiac death? Dr Sana Al-Khatib: I would love to start with the paper on sudden cardiac death, which is very fitting. That's what I focus most of my work on. This particular paper actually looked at sudden cardiac death as the first manifestation of heart disease in women, and it was focused on the Oregon sudden unexpected death study, the timeframe for which was between 2004 and 2016 and what they really wanted to do is to assess sex specific trends in sudden cardiac death incidence. And so they focused on out of hospital, sudden cardiac death cases among adults during that time period. And they divided that 12-year period from February 2004 to January 2016 into three four-year intervals, 2004 to 2007, 2008 to 2011 and 2012 to 2015. And they really looked at these trends among women and men and they found that there were 2,938 sudden cardiac deaths, 37% of who were women. And they found an interesting U-shaped pattern of risk of sudden cardiac death with Anader in 2011. An increase in the years that followed 2011 so regarding that rebound, the rates really increased in 2013 and 2015. And when they specifically looked at women, they found that the rates of sudden cardiac death declined by 30% between the first and second four year time period and increased by 27% between the second and third period. Interestingly, the subsets with sudden cardiac death as the first manifestation of heart disease, accounted for 58% of the total rebound in sudden cardiac death incidence from period two to three but there was no change in the incidence over time for sudden cardiac death occurring among people with preexisting heart disease. For men actually sudden cardiac death also declined from the first to the second period, but not as much as in women and also increased between the second and third periods. Again, not as much as we saw in women. Subsets of sudden cardiac death occurring in the setting of identifiable heart disease was responsible for 55% of the rebound in overall sudden cardiac deaths incidence. Certainly some significant differences between men and women. Very exciting findings. Then if we actually turn our attention to the second study looking at sex specific trends in acute myocardial infarction, this particular analysis, Biykem, was done within an integrated healthcare network between 2000 and 2014 and they picked the Kaiser Permanente Southern California network. They were able to identify 45,000 plus acute MI hospitalizations between 2000 and 2014 and they found that age and sex standardized incident rates of AMI declined from 2000 to 2014. And they found that a decline for women was actually more so than in men. And in fact for men it was pretty much stable. And they found that the incidence of hospitalized MI had declined, however, declines are slowing among women compared with men in recent years. That's actually identified some unmet care needs among women that hopefully can meet people and investigators to tailor their approaches to try to close those gaps and disparities in care. With that, let me actually turn it back to you to potentially talk about to cardiovascular risk assessments in women. Dr Biykem Bozkurt: With the recognition of the disparities and the recent emerging trends of adverse outcomes, especially in younger women, there has been a focused attention in how to assess risk, cardiovascular risk in women. There is a very comprehensive review by Salim Virani and colleagues who's addressing the cardiovascular risk assessment for women. As our listeners will recall in 2018, ACC/AHA cholesterol professional guidelines specified risk enhancing factors such as premature menopause or preeclampsia for women. And if present, in borderline or intermediate risk patients, would elevate the 10 year risk to a higher category. But now with a recognition of many more risk factors, Virani and colleagues are proposing a more comprehensive cardiovascular risk assessment for women. And these include the risk factors that are not only identified in the 2018 ACC/AHA cholesterol guidelines, but additional such as gestational hypertension and diabetes or adverse pregnancy outcomes such as preterm delivery, small birth for gestational age or placental abruption or infarct or premature menarche or premature menopause, primary ovarian failure or pregnancy loss and additionally inflammatory disorders such as lupus, rheumatoid arthritis, psoriasis and history of cancer and cancer related therapies. And they formulate this in a nice and well tabulated fashion. And all these risk factors are summarized table one which I think most of our listeners and readers will refer to. And they also come up with a nice approach. What shall we do? And how shall we detect that risk? First recommendation they have is that we should obtain a comprehensive obstetric and gynecological history from all women. And if these risk factors are present, then we should then screen for other traditional risk factors early and frequently and then treat for modifiable risk factors such as hypertension, hyperlipidemia, diabetes, metabolic syndrome, and also implement aggressive lifestyle modification with strategies such as management of blood pressure control, reduction of blood sugars, remaining active eating, healthy, losing weight, and not smoking. Which is summarized as life's simple seven which is an AHA initiative that summarizes healthy lifestyle as life's simple seven. And very complimentary to Virani’s review paper, we had another wonderful paper that is titled Life's Simple Seven and health by Jacqueline Kulinski who reminds us that not only these seven factors but breastfeeding for postpartum mothers is an important approach to reduce cardiovascular risk. Breastfeeding is not only beneficial for the newborn infants but for the mother as it's been associated with reduction in risk of myocardial infarction, stroke, cardiovascular disease hospitalization rates, future development of diabetes, hypertension, and even mortality. And this paper elaborates on potential mechanisms such as increases in metabolic expenditure, enhancement of insulin sensitivity, reduction in cholesterol, greater mobilization of fat stores and reversal of elevated triglycerides and cholesterol that's seen during pregnancy. It also emphasizes the importance of recognition and education of women because currently only about 25% of women are exclusively breastfeeding at six months and US has one of the lowest breastfeeding rates among industrialized countries. And we do have disparities according to race and income and black infants and infants living in rural areas in Southeast USA are less likely to be breastfed. And there is definitely increased recognition for importance and but it's also important to be able to accommodate and facilitate breastfeeding for mothers. Currently the paper emphasize that all 50 states now have laws allowing women to be able to breastfeed in public or private locations. But again, there definitely is a necessity for increased awareness and education. On that end, there is also a great paper covering the news release announcing the partnership between American Heart Association and American College of Gynecology and Obstetricians in promoting risk identification and reduction of cardiovascular disease in women through collaboration between obstetricians and gynecologists. In 2018, AHA and American College of Gynecology issued a call for action for both specialists to team up and increase screening for cardiovascular disease by obstetricians and provide education and appropriate referrals. And I think this initiative is going to increase the opportunities for young women whose primary care provider solely could be an obstetrician, who potentially will get screened for cardiovascular disease and if they have these risk factors, will potentially be able to be offered lifestyle modification, message and intervention strategies. These, I think, three very complimentary papers are enhancing our recognition for the new risk profile that needs to entail getting a comprehensive obstetric and gynecological history in all women. And in the event we recognize either of these risk factors including the traditional risk factors or obstetric and gynecological risk factors such as pregnancy related complications or preeclampsia or other additional special risk factors such as autoimmune disorders and cancer, then we will need to heighten our awareness for lifestyle modification, risk management, and earlier treatment and closer monitoring. That brings us to another important risk profile, which is cancer for women. And Sana, I know we do have two great papers related to cancer topic. If you could elaborate on those. Dr Sana Al-Khatib: I'm really excited about these papers. As you pointed out, Biykem, that cardio oncology is a field that is really expanding and so it was really very gratifying to get these two papers. The first paper had to do with a comparison between aromatase inhibitors and Tamoxifen in women with breast cancer in terms of their association with the risk of cardiovascular outcome. And this particular study was done in the United Kingdom and they studied women though with newly diagnosed breast cancer initiating hormonal therapy, either with everyone at aromatase inhibitors or Tamoxifen between 1998 and 2016. And the study outcomes that they were interested in included myocardial infarction, ischemic stroke, heart failure, and cardiovascular mortality. And they actually had a sizable patient population with 23,000 plus patients included in this analysis of whom close to 18,000 initiated treatment with either an aromatase inhibitor or Tamoxifen. And they found that the use of aromatase inhibitors was associated with a significantly increased risk of heart failure and cardiovascular mortality compared with Tamoxifen and that aromatase inhibitors seemed to have a trend towards increased risk of myocardial infarction, ischemic stroke. Although those differences were not statistically significant. They actually concluded that aromatase inhibitors were associated with an increased risk of heart failure and cardiovascular mortality compared with Tamoxifen and that there were trends toward increased risks also of MI and ischemic stroke. And so they really want clinicians and patients to be aware of these findings when they are trying to make decisions about treatment for breast cancer. We have another really interesting study, Biykem, that was actually a randomized control trial that studied the effect of exercise therapy dosing schedule on impaired cardiorespiratory fitness in patients with primary breast cancer. And so this randomized trial enrolled 174 post-menopausal patients who were randomly allocated to one of two supervised exercise training interventions, delivered either using a standard linear test or nonlinear test. And they had a control group of just stretching. They did some stretching. And they did the trial over at periods of 16 consecutive weeks and the primary endpoint was change in the VO2 level, PCO2 level from baseline to post intervention. They had a couple of other secondary endpoints and their results were interesting. They found no serious adverse events during the trial, but they actually found that 40% of patients in both exercise dosing regimens were classified as responders. And they concluded that short term exercise training independent of dosing schedule was associated with modest improvements in cardiorespiratory fitness in patients previously treated for early stage breast cancer. Really interesting, a smaller study, not really looking at hard endpoints yet. It's still important because I believe that it is going to form the basis for more studies and more research in this important field, Biykem. With this, I'd like to turn it over to you to talk about elevated body mass index in young women. Dr Biykem Bozkurt: And this is another fascinating study, a large study from Sweden. It involved more than 1.3 million young women. Average age was 27. It was a national prospective cohort. The recruitment was between 1982 and 2014. What they did was they measured the baseline of weight of women in early pregnancy in the first trimester, actually the first antenatal visit before they could gain any weight related to the pregnancy. With their BMI measurement at baseline, then they followed these patients for approximately 30 years and associated this baseline BMI with future developments or dilated cardiomyopathy or any cardiomyopathy. They looked at that dilated cardiomyopathies, hypertrophic cardiomyopathies, these other cardiomyopathies such as alcoholic cardiomyopathy and others. Interestingly, elevated body mass was associated with future development of dilated cardiomyopathy. A very similar finding was reported in former studies for adolescent men, but we didn't have this finding for young women. This study provides evidence that elevated BMI, even if it is only in the overweight range, is associated with future development of dilated cardiomyopathy. In the past we had numerous studies demonstrating overweight or obesity status being associated with future development of clinical heart failure, clinical symptoms of heart failure, but this is one of the largest scale population based cohorts demonstrating the association with dilated cardiomyopathy. And interestingly, these women at baseline did not have the usual other confounders or comorbidities associated with future development of cardiomyopathy. The risk of diabetes and hypertension was less than 1% at baseline. Very interestingly, BMI by itself, independent of all these other variables was associated with future risk. And of course the higher the BMI was, the higher the risk was. The highest risk was for those with morbid obesity or BMI over 35 and in those patients the risk was increased by about five fold. Sana, we talked about the disparities for women. Where are we with women participation in cardiovascular trials? And how do we looked globally overall regarding the disparity of cardiovascular diseases in woman? Dr Sana Al-Khatib: These are really important questions, Biykem. Let me first start with a study that will be in the Go Red for Women issue on women's participation in cardiovascular clinical trials. They looked at that. Between 2010 and 2017, which is a very important topic as you know, Biykem. And so what they did here is they actually assessed the participation of women in completed cardiovascular trials that were registered in clinical trials between 2010 and 2017. And they parked calculated the female to male ratio for each trial to determine the prevalence adjusted estimates for participation of women. And so they kind of defined it as participation prevalence ratio. And so they said that they were able to identify 740 completed cardiovascular trials including more than 860,000 adults of whom 38% were women. And they talked about how the median female to male ratio of each trial was 0.501 overall and varied by age group and type of intervention and region and trial size and funding sponsors. Actually, these are really interesting findings. In the interest of time, I'm not going to delve into all those details, but I think it would be really interesting for people to read that and look at this more carefully. But they found that relative to their presence in the disease population, the participation prevalence ratio of women versus men actually was a higher than 0.8 for hypertension, pulmonary arterial hypertension and lower for arrhythmia, coronary artery disease, acute coronary syndromes and heart failure trials. And they found that in the most recent time period, that they defined between 2013 and 2017, they saw a significant increase in the participation and prevalence ratios for stroke and heart failure trials compared to other periods. They concluded, not surprisingly, that among cardiovascular trials in the current decade, men still predominate overall, but that the representation of women actually is improving, especially when it comes to studies related to stroke and heart failure. That's what's really interesting, Biykem. The other point that you were very nicely raised had to do with sex differences in primary and secondary prevention of cardiovascular disease. And the one study that we have in our issue, Biykem, was actually done in China. I really like this global reach of our issue. I presented a study that was done in the UK. You presented a study done in Sweden. This particular one was done in China and they conducted a community based survey of adults in seven geographic regions of China between 2014 and 2016. They really wanted to determine sex differences in the primary and secondary prevention of cardiovascular disease. And they looked at different factors in terms of age, education level, area of residence. And they had more than 47,000 participants of whom 61% were women. And they found that 5,454 had established cardiovascular disease, 57% of whom were women and 9,532 had a high estimated 10 year cardiovascular disease risk. And of those, 71% were women. And they found that only about 49% of women versus 39%, 60% of men were on any kind of blood pressure lowering medications, lipid lowering medications, antiplatelet therapy for primary and secondary prevention. And they found that women with established cardiovascular disease were significantly less likely than men to receive blood pressure lowering medications, lipid lowering medications, antiplatelet therapy, so on, so forth. And that woman with established cardiovascular disease had better blood pressure control but less well controlled NVM cholesterol, were less likely to smoke and achieve physical activity targets. Conversely, women at high risk of cardiovascular disease were less likely than men to have their blood pressure LDL cholesterol, body weight controlled, despite the higher use of blood pressure lowering medication. Really interesting gaps in care that this study highlights that hopefully can form the basis for interventions to try to address those disparities. And then as you know, we actually have a couple of research letters on the representation of women in editorial boards of major general and subspecialty cardiology journals, publishing clinical research. In this particular study, they actually found significant disparities where women were less represented among deputy associate editors and more so in European journals compared with US journals, general cardiology journals. Although editorial board membership was actually similar between Europe and the US, and they found that over 20 years, women deputy associate editors representation increased significantly for our journal, Biykem, Circulation. That was really very encouraging to see. And women editorial board membership increased for Circulation and for JACC without a significant change for the American Journal of Cardiology. That was really nice to see. The one thing that was notable was in terms of women serving as editors-in-chief, we're still lagging behind in a big way, but I'm hoping that this particular study and several other studies that may get published in the future, will highlight these gaps and hopefully will lead to increased representation of women on editorial boards. And finally we have an interesting study looking at the representation of women and men among training programs where they looked at the AAMC data and they were interested in looking at training in general cardiovascular disease medicine as well as for adult cardiology sub-specialties. And they also looked at pediatric cardiology by the way. And they found that in 2017 to 2018, among all adult cardiology trainees, only 21% were women. 79% were men. And among trainees in the different adult cardiology subspecialties, the representation was actually pretty poor in interventional cardiology, where only 10% of the trainees were women. And for electrophysiology, my own sub specialty, were only 11.6% of the trainees were women. Really interesting findings, the representation for advanced heart failure and transplant like your specialty, Biykem, women constituted 31% of the trainees and women did better when it came to adult congenital heart disease representing 47% of the training. Really interesting trends and they concluded that in this review of ACG and the accredited training program, they found that cardiology ranked second for the most under representation of women, preceded as only by orthopedic surgery. And the sub specialty trends that I shared with you were really interesting. Hopefully as we see more of these publications, we'll be able to as a community come together and think about what are the barriers to more representation of women in these training programs? And how can we overcome these failures to encourage more women to go into this wonderful specialty of cardiology and the different sub-specialties, including procedural sub-specialties? Back to you, Biykem. Dr Biykem Bozkurt: Thank you Sana. Very interesting findings indeed. Another fascinating study that we have in our issue is a study that provides us some insights on peripartive cardiomyopathy and potentially the role of natriuretic peptides during pregnancy. This is an experimental study that involved natriuretic peptide receptor knockout in mice in which natriuretic peptides would not work. And the investigators demonstrated that these mice, during the postpartum lactation period, had elevated aldosterone levels, evidence of expression of pro inflammatory mediators such as IL-6, cardiac hypertrophy, fibrosis, left ventricular dysfunction, and even increased mortality. And interestingly, they were able to abrogate the effects of the lactation by use of mineralocorticoid receptor antagonists. With MRA use, there was evidence of reduction in LVH and reduction in inflammatory mediators. There is a great editorial by Denise Hilfiker-Kleiner, who addresses the potential hypothesis of the role of unbalanced oxidative stress with prolactin in peripartum cardiomyopathy. And that the natriuretic peptides can be protected. And raises the question whether there could be a role for augmenting the natriuretic peptides further by use of sacubitril/valsartan. Or as was demonstrated in this study by you as a mineralocorticoid receptor antagonists in the postpartum period. And she also questions why in this experimental model, the detrimental effects were not seen during pregnancy but only in the postpartum lactation period. Overall, very interesting papers. And finally we have an inspiring piece in our past or discovery section. It's an interview with Barbara Casadei, the President of European Society of Cardiology. She goes in a very detailed fashion over her career path, what she considers as the critical reasons for her success and how she envisions to shape the future of women in cardiology. Dr Sana Al-Khatib: We would like to thank everyone who submitted their research and their work for this issue and congratulate the authors and investigators who were successful in getting their work published. Thank you very much. Dr Biykem Bozkurt: We thank you for tuning in to our podcast. We hope that you'll enjoy our fourth issue for the Go Red for Women as we continue to highlight some of the best science for cardiovascular disease in women. Thank you. This program is copyright, the American Heart Association 2020.  

(*Hypothetical Case) A woman is brought into your emergency dept by her husband at 14 weeks gestation. He tells you that she has been "really sick" for almost two months now. He states that they have seen their GP multiple times and have "tried almost everything". This is the second time they are presenting to your ED - they came 2 weeks ago where he recounts she was given some IV fluids and antiemetics before going home - but they were reluctant to come back because a member of staff was quite dismissive to them last time apparently she told them that if she ate ginger and sipped water she should be fine and "it all stops at 15 weeks anyway so not to worry it will be over soon". This time he tells you that she has practically eaten nothing in the last 4 weeks and she is now having trouble getting out of bed, because of almost 4 weeks of continuous vomiting. He thinks she has probably lost at least 8-10kg since becoming pregnant. He is "super-worried" and "she is just not herself anymore - please do something". She appears listless, drowsy and distracted when you try to question her directly, and she tells you she is thirsty, nauseated and has had enough - she even asks you as you take some bloods and place an iv whether it is permissible to get a termination for untreatable nausea. Bloods: pH 7.58 HCO3 28, PCO2 56, Na 126, K2.3, Gluc 8, LFTs normal Urinary Ketones +++, no glucose How would you approach the management of this woman? Join Graeme and I as we discuss this under appreciated & poorly understood yet potentially catastrophic condition...... USEFUL TREATMENT GUIDELINE https://www.rcog.org.uk/globalassets/documents/guidelines/green-top-guidelines/gtg69-hyperemesis.pdf LINKS Profound Hypokalaemia Resulting in Maternal Cardiac Arrest: A Catastrophic Complication of Hyperemesis Gravidarum? Wernicke's encephalopathy in hyperemesis gravidarum: A systematic review. http://www.hyperemesis.org/ Pregnancy sickness can kill – why are doctors so uninformed about it? Why are Women Still Dying from Nausea and Vomiting of Pregnancy? http://theconversation.com/when-nausea-from-pregnancy-is-life-threatening-46709

Kontakt: ivajuntan@gmail.com    Musik: Blind Love Dub by Jeris (c) copyright 2017 Licensed under a Creative Commons Attribution (3.0) license. http://dig.ccmixter.org/files/VJ_Memes/55416 Ft: Kara Square (mindmapthat)    Om du gillar du det vi gör - stöd Life Support Foundation! www.lifesupportfoundation.org     Bli månadsgivare eller används Swish: 1234610804    - Dagens artiklar: https://www.ncbi.nlm.nih.gov/pubmed/29860705   https://www.ncbi.nlm.nih.gov/pubmed/29854752 Kilgannon et al 2019  

Today, we'll be going over part 2 of 4 of the acid base disorders.  As a recap, what is normal?  Well, a normal pH is 7.35 - 7.45 If the pH is 7.45 then we have alkalemia. A normal bicarbonate is 22-26 and a normal pCO2 is 35-45.  In today's podcast we are going to tackle respiratory acidosis, partial vs complete compensation, and we'll show you what to look for to see if there is a co-existing acid/base disorder.  - Subscribe to our YouTube channel here: https://www.youtube.com/medgeeks - Follow us on Instagram here: https://www.instagram.com/medgeeksinc - Ace your exams: https://learn.medgeeks.co/ - We'd love to hear your feedback: team@medgeeks.co - This podcast should not be used in any legal capacity whatsoever, including but not limited to establishing standard of care in a legal sense or as a basis for expert witness testimony. No guarantee is given regarding the accuracy of any statements or opinions made on the podcast, video, or blog.  

Intro In this episode we dissect the following practice question with Dr. Brian Radvansky from MedSchoolTutors.  Question Stem A 67-year old man presents to the Emergency Department with a 2-day history of progressively worsening cough. He has a history of poorly-controlled hypertension, 30 pack-year smoking history, well-controlled diabetes, and a STEMI 4 years prior. He complains of mild sharp chest pain while coughing, some shortness of breath while walking around his apartment, and lightheadedness when standing up. Vital signs on arrival are HR 114, BP 100/55, RR 26, T 101.9 ℉, SpO2 86% on 4 L nasal cannula. Physical exam is significant for general ill appearance, decreased breath sounds in the right lower chest, tachypnea, tachycardia, and use of accessory muscles of breathing. His is somewhat alert and oriented only to person and place. ABG shows pH 7.29/pCO2 60/pO2 69. EKG shows Q-waves in the inferior leads. Which of the following is most likely to improve the patient’s clinical status? Dobutamine Furosemide Doxycycline Vancomycin and Piperacillin-Tazobactam Pleurocentesis Aspirin and Heparin The full post is not yet published. But you can read more high-yield question breakfowns on the MedSchoolTutors excellent blog.  ITB Audio Qbank and iOS Beta App The Audio Qbank by InsideTheBoards mobile app has both free and premium features and is available on both Android and iOS.  To get started, first, create a Boardsinsider Account on our website insidetheboards.com Free Features  All of our podcasts in one place organized into playlists for easy studying (also with less ads and exclusive content)  Mindfulness meditations designed specifically for medical students  A monthly offering of high yield content (questions dissections, audio qbank samples) available only on our mobile app.  Premium Features Subscribe to an ITB premium account and get additional features  Access to 500+ audio optimized board style practice questions in our Audio Qbank. The Step 1 version is powered by Exam Circle and the Step 2 Version is powered by OnlineMedEd. New questions added each month.  High Yield Pharmacology (powered by Lecturio) with 100 of the top pharm questions you need to know for both Step 1 and Step 2  Audio Flashcards (coming soon)  Our audio qbank is THE PERFECT companion for studying for the boards on the go. And we're adding content and improving it all the time.   Learn more about the Audio Qbank by InsideTheBoards mobile app here Legal Stuff InsideTheBoards is not affiliated with the NBME, USMLE, COMLEX, NBOME or any professional licensing body. InsideTheBoards fully adheres to the policies on irregular conduct outlined by the aforementioned credentialing bodies.  Music: "Anaesthetist" off The Mindsweep by Enter Shikari (used with permission).

In last weeks episode, we discussed the differences between DKA and HHS. Today, we'll be sharing how to manage these two diseases. If you missed last weeks episode, you can listen to that here: https://medgeeks.co/podcast/ We had that 35 year old female with type 1 DM on insulin complaining of burning with urination, followed by a few days of nausea, vomiting, abdominal pain, and poor PO intake.  Labs revealed DKA: glucose 480, HA1c 10.5%, positive urine/serum ketones, creatinine 1.6, and anion gap of 25. ABG showed ph of 7.25, PCO2 of 28, bicarb of 12, and O2 of 90 on room air. This is a metabolic acidosis with respiratory compensation. (We'll also show you a shortcut on how to calculate the expected compensation). Sodium was 136. UA was positive for infection. Vitals: BP 83/45 - MAP of 58, HR 110, 100.8 F.  Management can be grouped into 3 categories: 1. fluids and electrolytes 2. insulin 3. monitor Today, we'll break this all down for you. Enjoy! - Subscribe to our YouTube channel here: https://www.youtube.com/medgeeks - Follow us on Instagram here: https://www.instagram.com/medgeeksinc - Ace your exams: https://learn.medgeeks.co/ - We'd love to hear your feedback: team@medgeeks.co - This podcast should not be used in any legal capacity whatsoever, including but not limited to establishing standard of care in a legal sense or as a basis for expert witness testimony. No guarantee is given regarding the accuracy of any statements or opinions made on the podcast, video, or blog.

Dominate acid-base disturbances with the wisdom of @kidney_boy aka Joel Topf, MD, Chief of Nephrology at Kashlak Memorial Hospital.  Master his 5 key steps for interpreting acid-base disorders and decode any ABG, VBG, and BMP to find the primary disorder, and any other disorders tucked away in the ABG! Plus: Henderson-Hasselbach and pH simplified; the anion gap, should your correct it?; choice of IV fluid; osmolar gaps, methanol, ethylene glycol, isopropyl alcohol; and how metabolic disorders are like a boy band. Be sure to follow along the Dr. Topf’s brilliant acid-base powerpoint. Written and produced by Joel Topf MD, Shreya Trivedi MD, Xavi Jimenez MD; Images by Hannah Abrams; Edited by Matthew Watto MD Full show notes available at http://thecurbsiders.com/podcast Join our mailing list and receive a PDF copy of our show notes every Monday. Rate us on iTunes, recommend a guest or topic and give feedback at thecurbsiders@gmail.com.  Time Stamps 00:00 Announcement 01:00 Disclaimer 01:34 Intro 02:45 The setup and guest bio 03:15 How does Dr Topf compensate for difficulty 07:10 What has helped Dr Topf become successful as an educator 10:40 With which electrolyte do you most closely identify? 14:05 Picks of the week 16:05 Nephmadness explained 19:50 Joel’s big picture look at acid base 22:17 Acid base and logorhythmic scale 24:28 A caution about ABGs 27:23 Clinical case from Kashlak Memorial Hospital 28:05 Misinterpretation of low bicarb on a metabolic panel 29:20 Step 1 of acid base 32:00 Metabolic disorders and One Direction 35:15 Acidemia vs acidosis; alkalemia vs alkalosis 37:52 Compensation for acid base disorders 40:45 ABG apps and analyzers 42:40 Step 2 Is there a second primary disorder? Use equations for determining if compensation is appropriate. 51:31 How to determine if respiratory compensation is acute or chronic 54:26 Step 3 The anion gap 57:21 Correcting the anion gap 60:33 What causes a low anion gap? 63:58 Anion gap acidosis 66:05 GOLDMARK 69:15 Step 4 Is there an osmolar gap? 71:48 Toxic ingestions: Methanol, ethylene glycol, and isopropyl alcohol 76:15 Calculating the osmolar gap 79:08 Step 5 Gap-gap calculation aka “the bicarbonate before” 85:05 Choice of IV crystalloid fluid and when to use a bicarbonate drip 88:15 Bicarbonate in DKA 90:18 NephMadness plug 91:10 Outro Tags: acid, base, anion gap, metabolic, respiratory, toxic alcohol, goldmark, mudpiles, albumin, acidosis, alkalosis, compensation, nephrology,  Henderson-Hasselbalch, equation, ABG, VBG, bicarbonate, pCO2, assistant, care, doctor, education, family, foam, foamed, health, hospitalist, hospital, internal, internist, meded, medical, medicine, nurse, practitioner, professional, primary, physician, resident, student

Professor Ulrich Thome, Division of Neonatology, University Hospital for Children and Adolescents, University of Leipzig, Germany, joins Jonathan Davis to discuss the paper "Neurodevelopmental outcomes of extremely low birthweight infants randomised to different PCO2 targets: the PHELBI follow-up study". The Associate Editor of ADC Fetal and Neonatal edition spoke with the author at the Joint European Neonatal Societies meeting in Venice. Read the paper included in the September's 2017 edition of the journal here: http://fn.bmj.com/content/102/5/F376.

(*Fictitious case) A 32 yr old pregnant woman with insulin dependent diabetes presents to a regional hospital in WA at 27 weeks gestation, with probable premature rupture of her membranes, threatened preterm labour and a low grade fever. She is given a dose of celestone (betamethasone) intramuscularly, some nifedipine for tocoloysis and has an urgent areomedical transfer organised. During the flight she has a salbutamol infusion to provide further tocolysis and minimise the risk of delivery of a 27 week foetus in the back of the plane which the retrieval team are very keen to avoid! On arrival at your tertiary hospital she is febrile (T 38.4) but the most striking thing noted is the fact she is breathing very heavily but yet has clear lungs and normal SpO2 of 99%. The team assessing her do some blood tests including an arterial blood gas and obtain the following results: pH 7.26, pCO2 16, pO2 128, HCO3 7.5, Na 141, K 4.8, Cl 101, Gluc 19.0, Urea 8.1, Crn 0.09 Urine analysis: Glucose 4+, Ketones 1+ What is going on? How are you going to manage this patient? This week I am joined by my colleague Dr Graeme Johnson and we discuss the ins / outs of DKA during pregnancy. Diabetes is an increasingly common condition both in the general population but also in pregnancy. DKA is an important and life threatening critical illness which can develop in any pregnant unwell diabetic patient. All healthcare workers who may be involved in the care of a diabetic pregnant patient will benefit from understanding the basic physiological process which leads to DKA, how to recognise it, and the principles of management. Join Graeme and I as we discuss a hypothetical case. You can listen to the audio only on the blubrry podcast or if you prefer follow along with us watching the screencast which has the slides containing visual aids & diagrams. This does probably make it somewhat easier to follow the discussions we have about the metabolic pathways & ketone production. Screencast: https://youtu.be/dAGb6lEgsnk Here are the links to the two main articles used in putting together this weeks podcast: The Management of DKA References A Hallett, A Modi, N Levy; Developments in the management of diabetic ketoacidosis in adults: implications for anaesthetists, BJA Education, Volume 16, Issue 1, 1 January 2016, Pages 8–14, https://doi.org/10.1093/bjaceaccp/mkv006 Mohan M, Baagar KAM, Lindow S. Management of diabetic ketoacidosis in pregnancy. The Obstetrician & Gynaecologist 2017;19: 55–62. http://onlinelibrary.wiley.com/doi/10.1111/tog.12344/pdf   Want to Brush up on Arterial Blood Gas Analysis? Check out these amazing sites: 1 - Kerry Brandis' amazing Acid Base textbook available here on the anaesthesiamcq site: http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.php 2 - For those of you who like the super deep dive into a topic, I recommend Alex Yartsev's super detailed discussions on metabolic syndromes and blood gas analysis on his great ICU website below: http://www.derangedphysiology.com/main/core-topics-intensive-care/arterial-blood-gas-interpretation  

Merry Xmas! This weeks post was inspired by a recent unexpected case of severe hyperkalaemia in a severe pre-eclamptic - I have put together a fictitious case which is a little more severe in order to illustrate the principles of managing hyperkalaemia - I hope you enjoy & take it easy over Xmas! CASE HISTORY (*A fictitious patient history ) Your pager goes off - code blue medical labour ward! On arrival you are told the patient for whom the code was called has just arrived following an urgent transfer from another hospital. She presented to their service at 31 weeks with a headache, BP 190/100, proteinuria and mildly raised creatinine. She was diagnosed with severe pre-eclampsia, given labetalol, nifedipine and then transferred. She now appears confused with the following vital signs: HR 33/min, BP 74/55, SpO2 92%, RR 17/min (*Image courtesy www.lifeinthefastlane ) An immediate venous blood gas shows the following result: Na 139, K 8.4, pH 7.23, pCO2 37, pO2 63, Lactate 1.8 How are you going to manage this patient?   Immediate Standard Mgmt 1 - Is it real? Common causes of high potassium includes hemolysis of red cells from the sampling and handling process.  Always do an ECG whilst awaiting a repeat result - if the patient is compromised and the ECG is abnormal / consistent with hyperkalaemia then assume it is real and don't delay your treatment! The quickest way to get a repeat sample is usually a VBG this usually only takes a few minutes and will also give you the glucose and pH - important values to know for both mgmt and diagnosis. 2 - Prevent an arrhthymia Immediate mgmt - stabilise the cardiac membrane with intravenous calcium. Most guidelines recommend calcium if there are ECG changes or the absolute K level is over 7mmol/L. *Calcium chloride has 3 times more calcium than calcium gluconate. 3 - Shift K intracellularly a) Insulin / Glucose. Usual dose 10units actrapid + 25-50ml 50% Dextrose Stimulates Na/K/ATPase Give glucose to prevent hypoglycaemia' Lowers K by 0.5 -1 mmol/L per hour b) Salbutamol 20mg neb Good choice if the patient is bradycardic (common in severe hyperK) Stimulates Na/K/ATPase also c) NaHCO3 (if acidotic) When acidosis exists H+ is exchanged for intracellular K+ Makes sense to consider NaHCO3 if acidosis is present 50-100ml of NaHCO3 8.4% 4 - Eliminate K from the body (usually renal) - Enhance renal elimination - diuretics (e.g. frusemide), K free crystalloid (if indicated - saline) or both! - Dialysis - institute early in patients with complete renal failure -  GI exchange resins (eg resonium) most guidelines now consider they have no role in the acute management. 5 - Identify and treat the cause! - You need to address this issue to stop if from recurring! Usually multiple factors combine to lead to hyperkalaemia. Fix reversible causes especially drugs! Don't rely on your memory - get their medication chart out then google all the known drugs that can cause hyperkalaemia! Drugs Known to Cause / Contribute to hyperkalaemia (either impair excretion or promote transcellular shift) ACE inhibitors / AT2 antagonists Spironolactone / Amiloride NSAIDs Beta blockers (see discussion below) Trimethoprim Heparin Pentamidine Suxamethonium Renal dysfunction - almost always there is a degree of renal impairment preventing excretion of the excess K load. Make sure you aren't missing important reversible causes - e.g. obstruction (consider USS renal tract urgently).  Cell release (eg hemolysis, tumour lysis, trauma or extensive surgical injury). In our O& G patients this includes widespread tissue injury especially after major surgery or perhaps chemotherapy. BUT This is a pregnant woman with PET - renal impairment, acidosis, hemolysis, transfusion - these are common events in our pregnant patients. Cardiac Arrest Secondary to Hyperkalaemia

Chief Complaint Pt comes in with a heart rate of 170-200. Complains of palpitations/sob/chest pain/dizziness/or nothing.  Is this SVT or A-Fib? Hint! Today we are talking about SVT. Bedside Checklist Take off clothing waist up. Put on a hospital gown. Immediately place pulse ox, leads, and bp cuff - in that order. If oxygenation is poor with good waveform - address this first. Start with a nasal cannula, if that doesn't give your pt relief. Apply NRM, while you set up BIPAP. Find out if they have COPD or emphysema or a chronic smoker - oxygen saturation requirements are less for this population. High flow nasal cannula may be an option. Keep hob elevated to min. 30 degrees. 45-90 better. Watch the position that your patient is sitting. If they are leaning forward or sitting up straight - Put the hob at 90 degeees and ask them, is it easier for you to breathe sitting up. Obese patients may prefer to have legs over the side of the stretcher due to abdominal girth. Get an EKG stat. After you get the 12 lead - keep the EKG leads on pt Is this an atrial or ventricular rhythm? Today it’s an atrial rhythm. It’s so fast, we don’t know if it’s SVT or A Fib! Get 1-2 iv access. Preferably 2. Labs now or later? This is controversial. If the pt looks like they are a hard stick, I get labs so I can at least run a venous panel to get a baseline pCO2 level. If the pt goes on BIPAP or high flow nasal cannula - you can trend this along with other values to direct the oxygen needs. Look at your pt. If they are talking to you and appear somewhat calm - you have the time to get labs off that first iv line. If the pt looks really bad, just get the iv access and you can get the labs later. Ideally you have a 2nd nurse who is putting in the IV line while the EKG is in progress so you can get the labs right away. While you are doing this - examine your patient: Mental status - hello sir! Can you tell me your name? Do you know where you are? What day is it? If you know the pt has dementia, what year or who's the president seems to work better. Work of breath - are they gasping for air? What is the respiratory rate? Do they look tired? - worried about losing compensatory drive? Auscultate the lungs. Wheezing - inspiratory or expiratory or both? Upper or throughout the lungs? Crackles? Decreased air movement? Trick question - are they coming in with multiple problems? Yes, sometimes that happens. Get the story as the above is happening: What happened? When did this happen? Were you sitting, walking, lying down? SOB/Chest pain/Palpitations/Dizziness or Lightheadedness/Nausea/Vomiting/LOC? If BIBEMS, Ask EMS how did they find the patient and where, what interventions (oxygen, iv line, meds), do they look better now? Has this ever happened to you before? Any fevers or recent illness? Do you have a pacemaker or defibrillator? What medications are you on? Do you have any allergies to medications? SVT Treatment First line of treatment: Vagal Maneuvers. Ice to face Carotid massage Tell the pt to bear down Modified Valsalva Maneuver Technique Second line of treatment: Adenosine In 2015 the Lancet published the REVERT trial and the findings were pretty impressive. The REVERT trial created another vagal maneuver that actually works!  It’s called a Modified Valsalva Maneuver Technique.  I’ve tried this out myself and it works pretty well. You just have to make sure your technique is good and you have 2 people at the bedside. Modified Valsalva Maneuver Technique: Have the pt sit down on the stretcher with HOB elevated at 45 degrees (semi-recumbent) or the pt can just sit up straight. Use a 10mL syringe (pressure of 40mmHg) and have them blow into it for 15 seconds (creating the Valsalva strain) Immediately afterwards, place the pt in a supine position and passive leg raise 45-90 degrees for 45 seconds. (Increases the relaxation phase of venous return and vagal stimulation). This is the modification.

Oxygen is probably the drug that we give the most but possibly has the least governance over.  More has got to be good except in those at high risk of type II respiratory failure right?? Well as we know the evidence base has swung to challenge that idea in recent years and the new BTS guidelines for Oxygen use in Healthcare and Emergency Settings has just been published with a few things that are worth reviewing since the original publication in 2008. No apologies that this may be predominantly old ground here, this is an area we're all involved with day in and day out that is simple to correct and affects mortality Historically oxygen has been given without prescription; 42% of patients in the 2015 BTS audit had no accompanying prescription When it is prescribed this doesn't always correlate with delivery 1/3 of patients were outside of target SpO2 range (10% below & 22% above) If nothing else is taken from this document then reinforcement of the fact that we need to keep oxygen saturations normal/near normal for all patients, except groups at risk of type II respiratory failure Prescribe and delivery oxygen by target oxygen saturations What is normal? Normal Oxygen saturations for healthy young adults is approximately 96-98%, there is minor decrease with increasing age. Healthy subjects desaturate to 90% SpO2 during night time; be cautious interpreting a single oximetry reading from a sleeping patient, short duration overnight dips are normal   Will mental status give me an early indication of hypoxaemia? No, impaired mental function at a mean value of SaO2 64%, no evidence above SaO2 84% Loss of consciousness at a mean SaO2 56%   Aims of oxygen therapy Correct potentially harmful hypoxia Alleviate breathlessness only in those hypoxic   Why the fuss about hyperoxia? Hyperoxia has been shown to be associated with Risk to COPD patients and those at risk of type II respiratory failure Increased CK level in STEMI and increased infarct size on MR scan at 3 months Association of hyperoxaemia with increased mortality in several ITU studies Worsens systolic myocardial performance Absorption Atelectasis even at FIO2 30-50% Intrapulmonary shunting Post-operative hypoxaemia Coronary vasoconstriction Increased Systemic Vascular Resistance Reduced Cardiac Index Possible reperfusion injury post MI In patients with COPD studies have showed most hypercapnia patients arriving at hospital with the equivalent of SpO2 > 92% were acidotic, high concentration O2has been associated with more than double the mortality rate in those with acute exacerbations of COPD. Titrate O2 delivery down smoothly   Which patients are at risk of CO2 retention and acidosis if given high dose oxygen? Chronic hypoxic lung disease COPD/CF/Bronchiectasis Chest wall disease Kyphoscoliosis Thoracoplasty Neuromuscular disease Morbid obesity with hypo ventilatory syndrome   What is the oxygen target? Oxygen titrated to an SpO2 of 94-98% Except in those at risk of hypercapnia respiratory failure, then 88-92%(or specific SpO2 on patient's alert card)   What about in Palliative Care? Most breathlessness in cancer patients is caused by airflow obstruction, infections or pleural effusions and in these cases the issues need to be addressed. Oxygen does relieve breathlessness in hyperaemic cancer patients but not if SpO2 >90%. Midazolam and morphine also relieve breathlessness and are more likely to be effective.   Delivery Devices Reservior masks can deliver O2 concentrations between 60-80% Nasal cannualae at 1-6L/min can deliver 24-50% Venturi masks allow accurate delivery of O2 If tachypnoeic over 30 breaths per minute an increase over the marked flow rate should be delivered, note this won't increase the FiO2! Equivalent doses of O2 24% venturi = 1L O2 28 % venturi = 2L O2 35% venturi = 4L O2 40% venturi = nasal/facemask 5-6LO2 60% venturi = 7-10L simple face mask   Approach to oxygen delivery Firstly determine if at risk of type II respiratory failure If not; SpO2 < 94%, deliver oxygen Perform an ABG If high PCO2 consider invasive ventilation, in the interim aim SpO2 94-98% If PCO2 normal or low aim SpO2 94-98% and repeat ABG in 30-60 minutes If at risk of type II respiratory failure Obtain ABG if hypoxic or already on oxygen If a respiratory acidosis consider NIV, address medical condition and senior review. Treat with the lowest FiO2 via venturi or nasal specs to maintain an SpO2 88-92% If hypercapnia but not acidotic, titrate the lowest FiO2 via venturi or nasal specs to maintain an SpO2 88-92%. Repeat ABG after change of treatment/deterioration. Consider reducing FiO2 if PO2 on ABG >8kPa If PCO2 < 6 (normal or low) aim to keep SpO2 94-98% and repeat the ABG in 30-60 minutes Points specific to prehospital oxygen use A sudden reduction in 3% of SpO2 within the target range should prompt a fuller assessment of the patient Pulse oximetry must be available in all locations in which oxygen is being used Some patients over the age of 70 when clinically stable may have SpO2 between 92-94%, these patients don't require O2 therapy unless the SpO2 falls below the level that is known to be normal for that individual Patients with COPD should initially be given oxygen via 24% venturi at 2-4L/min or 28% mask at a flow rate 4L/min, or nasal cannulae at 1-2L/min aiming for 88-92% Patients over 50 years of age and long term smoker with a history of SOB on exertion and no other cause for their breathlessness should be treated as having COPD. Limit O2 driven nebs, if no air driven nebs available, to 6 minutes in duration in patients known to have COPD In summary.... So the bottom line? Well just like Goldielock's porridge, with oxygen we don't want too little, we don't want too much but we want just the right amount! There is no doubt that hypoxia kills but beware that too much of anything is bad for you and in the same way we need to be vigilant to targeting oxygen delivery to our patients target SpO2   References BTS Guideline for oxygen use in healthcare and emergency settings  

This episode covers Chapter 41 of Rosen’s Emergency Medicine. 1) list 7 causes of altered LOC in the trauma patient 2)  List four herniation syndromes. Describe the pathophysiology of uncal herniation and the typical presentation. Describe the presentation of central herniation. 3)  Describe how cerebral blood flow in relationship to the following parameters: PO2 , PCO2 , MAP and ICP. What are the indications for ICP monitoring?   4) What is the Canadian CT head rule? What are the inclusion criteria. What is the New Orleans CT head rule? What are the inclusion criteria? Which test is more sensitive? More specific? 5)  What is a concussion? How is a concussion managed? What are potential complications? Define second impact syndrome & return to play 6) Outline the ED management goals of TBI.   differentiated between direct and indirect TBI What are the indications for seizure prophylaxis following TBI? What are the indications for antibiotics in TBI? Complications of TBI? 7)  7 clinical features of basal skull #   Wisecracks CT tips: 3 signs of cerebral edema on CT,  5 differences on CT between SDH And EDH, List 3 CT findings in DAI What are: the Monroe-Kellie doctrine, the Cushing’s reflex, What is kernihan’s notch, and how does this syndrome present?

This episode covers Chapter 41 of Rosen’s Emergency Medicine. 1) list 7 causes of altered LOC in the trauma patient 2)  List four herniation syndromes. Describe the pathophysiology of uncal herniation and the typical presentation. Describe the presentation of central herniation. 3)  Describe how cerebral blood flow in relationship to the following parameters: PO2 , PCO2 , MAP and ICP. What are the indications for ICP monitoring?   4) What is the Canadian CT head rule? What are the inclusion criteria. What is the New Orleans CT head rule? What are the inclusion criteria? Which test is more sensitive? More specific? 5)  What is a concussion? How is a concussion managed? What are potential complications? Define second impact syndrome & return to play 6) Outline the ED management goals of TBI.   differentiated between direct and indirect TBI What are the indications for seizure prophylaxis following TBI? What are the indications for antibiotics in TBI? Complications of TBI? 7)  7 clinical features of basal skull #   Wisecracks CT tips: 3 signs of cerebral edema on CT,  5 differences on CT between SDH And EDH, List 3 CT findings in DAI What are: the Monroe-Kellie doctrine, the Cushing’s reflex, What is kernihan’s notch, and how does this syndrome present?

Pearls from a core content talk on adrenal emergencies, a journal update looking at D-dimer in aortic dissection and some acid/base cases. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_15_0_Final.m4a Download Leave a Comment Tags: Acid Base, Adrenal Gland, Adrenal Insufficiency, Aortic Dissection, Congenital Adrenal Hyperplasia, D-dimer Show Notes Shownotes Asha SE, Miers JW. A systematic review and meta-analysis of D-dimer as a rule-out test for suspected acute aortic dissection. Ann Emerg Med 2015. PMID: 25805111 Dierks DB et al. Clinical policy: critical issues in the evaluation and management of adult patients with suspected acute nontraumatic thoracic aortic dissection. Ann Emerg Med 2015; 65: 32-42. PMID: 25529153 Acid-Base Cases   Quick questions & answers: For acute respiratory acidosis or alkalosis, how much does the pH change for every 10mm change of PCO2? What is the Winter's formula? For stable chronic respiratory acidosis, for every 10 mm increase in PCO2, how much should the pH decrease by? For each of the following cases, please analyze the acid-base status (i.e. anion gap metabolic acidosis, respiratory alkalosis,

Pearls from a core content talk on adrenal emergencies, a journal update looking at D-dimer in aortic dissection and some acid/base cases. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_15_0_Final.m4a Download Leave a Comment Tags: Acid Base, Adrenal Gland, Adrenal Insufficiency, Aortic Dissection, Congenital Adrenal Hyperplasia, D-dimer Show Notes Shownotes Asha SE, Miers JW. A systematic review and meta-analysis of D-dimer as a rule-out test for suspected acute aortic dissection. Ann Emerg Med 2015. PMID: 25805111 Dierks DB et al. Clinical policy: critical issues in the evaluation and management of adult patients with suspected acute nontraumatic thoracic aortic dissection. Ann Emerg Med 2015; 65: 32-42. PMID: 25529153 Acid-Base Cases   Quick questions & answers: For acute respiratory acidosis or alkalosis, how much does the pH change for every 10mm change of PCO2? What is the Winter's formula? For stable chronic respiratory acidosis, for every 10 mm increase in PCO2, how much should the pH decrease by? For each of the following cases, please analyze the acid-base status (i.e. anion gap metabolic acidosis, respiratory alkalosis,

Pearls from a core content talk on adrenal emergencies, a journal update looking at D-dimer in aortic dissection and some acid/base cases. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_15_0_Final.m4a Download Leave a Comment Tags: Acid Base, Adrenal Gland, Adrenal Insufficiency, Aortic Dissection, Congenital Adrenal Hyperplasia, D-dimer Show Notes Shownotes Asha SE, Miers JW. A systematic review and meta-analysis of D-dimer as a rule-out test for suspected acute aortic dissection. Ann Emerg Med 2015. PMID: 25805111 Dierks DB et al. Clinical policy: critical issues in the evaluation and management of adult patients with suspected acute nontraumatic thoracic aortic dissection. Ann Emerg Med 2015; 65: 32-42. PMID: 25529153 Acid-Base Cases   Quick questions & answers: For acute respiratory acidosis or alkalosis, how much does the pH change for every 10mm change of PCO2? What is the Winter’s formula? For stable chronic respiratory acidosis, for every 10 mm increase in PCO2, how much should the pH decrease by? For each of the following cases, please analyze the acid-base status (i.e. anion gap metabolic acidosis, respiratory alkalosis,

Investigations about the isoflurane anaesthesia in swine Compared to other animal species, swine show typical defensive behaviour towards any kind of physical manipulation. Anaesthesia is thus not only indicated for surgical interventions but for diagnostic and therapeutic measures as well. This study evaluates whether inhalational anaesthesia with isoflurane via facemask can serve as a potential alternative to regular intramuscular or intravenous anaesthesia. Two different apparati are compared: the first one disperses medical oxygen (O2), the second filtered compartment air (CA), both in conjunction with isoflurane. Animals with a body weight (BW) up to 20 kg receive simply an inhalational anaesthesia, patients weighing more than 20 kg in addition to that an intramuscular pre-medication 10 minutes earlier with ketamine (10 mg/kg BW) and azaperone (2 mg/kg BW). The survey examines 156 normal pigs and 19 statistically non-evaluated miniature pigs. Animals with more than 10 kg BW in particular show vehement physical reactions to the basal anaesthesia. Pre-medicated test animals are immobilized after ten minutes and the anaesthesia can be deepened with isoflurane. Animals receiving pure inhalational anaesthesia show ataxia after 29 to 34 seconds. After 48 to 60 seconds the probands are in prone position and after 65 to 89 seconds in lateral position. The pre-medicated animals on the other hand are significantly slower to show ataxia (after 1,4 minutes), prone position (after 1,8 to 1,9 minutes) and lateral position (4,3 to 4,4 minutes). The hypnosis and surgical tolerance stage of anaesthesia are reached significantly faster with isoflurane in CA than with isoflurane in O2. Test animals with isoflurane/O2 require an isoflurane-vaporiser position of 2,24 to 3,38 Vol% during the whole intervention, those with isoflurane/CA 2,17 to 2,88 Vol%. Compared to that, the premedicated animals need significantly less isoflurane with 1,5 to 2,38 Vol% (O2) and 1,52 to 2,08 Vol% (CA). Probands with O2 as carrier gas show a significantly better oxygen saturation (94-95%) than test subjects with CA (78%). The measured arterial pH value of 7,27 to 7,34 indicates a low acidosis; a partial pressure of carbon dioxide of 49,7 to 65,7 mmHg exceeds the reference values. The partial oxygen pressure is significantly better with O2 (190,0 to 266,2 mmHg) than with CA (57,4 to 65,7 mmHg). During the recovery phase, all animals exhibit the reappearance of the claw reflex, the dewclaw reflex, the muscle tension and positive skin sensibility in consecutive order. Somewhat later they raise their heads, get into the prone position and try to rise. Given several more minutes, they manage to stand. Probands receiving pure inhalation anaesthesia are significantly faster (1,3 to 9,8 minutes) to reach the waking stage than animals with a combination of ketamine, azaperone and isoflurane (2,1 to 24,4 minutes). The average blood pressure during the basal narcosis is 128/71 mmHg (systole/diastole) and 130/72 mmHg during the maintenance stage. Body weight and premedication apparently play no significant role. Miniature pigs deliver similar results as the premedicated pigs, but need remarkably less isoflurane (1,10 to 1,58 Vol%). Conclusion: a pure inhalation anaesthesia with isoflurane in swine can only be recommended for animals with a body weight up to 10 kg (O2-apparatus: 2,24 to 3,38 Vol% for surgical tolerance, CA-apparatus: 2,17 to 2,88 Vol% for surgical tolerance); rapid drifting off and rapid waking are the obvious advantages. A premedication with ketamine (10 mg/kg BW) and azaperone (2mg/kg BW) reduces the dose of isoflurane significantly (O2-apparatus: 1,5 to 2,38 Vol%, CA-apparatus: 1,52 to 2,08 Vol%). The use of O2 as carrier gas allows an optimal anaesthesia with optimal O2 - saturation for every animal weight and size (94 to 95%). CA as carrier gas can cause hypoxia and acidosis (O2-saturation: 78%, pH: 7,31 to 7,33, pCO2: 53,0 to 60,4 mmHg, pO2: 57,4 to 65,7 mmHg) during longer interventions. Miniature pigs need considerably less isoflurane, though this cannot result solely from the pre-medication and needs to be examined further.

Die nekrotisierende Enterokolitis (NEC) wird als häufigste Ursache gastrointestinaler Notfallsituationen beim Früh- und Neugeborenen angesehen. Sie ist eine akut auftretende inflammatorische Erkrankung des Dünn- und Dickdarms, welche im Verlauf zu einem septischen Krankheitsbild führen kann. Das Ziel der vorliegenden Arbeit bestand darin, Daten einer großen Anzahl betroffener Kinder in einer matched pair Analyse retrospektiv im Hinblick auf mögliche Risikofaktoren für die Entstehung der NEC auszuwerten. Es wurden Patientendaten von 59 Kindern ausgewertet, die zwischen Januar 1994 und Dezember 1999 in München geboren und an einer histopathologisch gesicherten NEC operiert wurden. Diese Daten wurden mit denen einer Kontrollgruppe verglichen. Es ergaben sich keine statistisch signifikanten Unterschiede in den beiden Gruppen. Bei der vorliegenden Studie handelt es sich um die zweitumfangreichste matched pair Analyse von Ursachen der NEC. Es wurde bestätigt, daß die NEC hauptsächlich Frühgeborene trifft, wobei die Erkrankungswahrscheinlichkeit mit fallendem Geburtsgewicht und sinkender Schwangerschaftswoche steigt. Eine perinatale Darmischämie scheint ohne Bedeutung zu sein, da ein deutlicher zeitlicher Abstand zwischen Geburt und operationsbedürftiger NEC bestand. Risikofaktoren, die eine Minderdurchblutung im Splanchnikusbereich auslösen können, wie Viskositätsänderungen des Blutes (gemessen am Hämatokrit-Wert oder ausgelöst durch Gabe von Erythrozytenkonzentrat), eine erhöhte diastolische Strömungsumkehr (ausgelöst durch einen PDA) oder auch eine Gefäßengstellung (verursacht durch Gabe von Katecholaminen bzw. Indometacin oder durch eine erniedrigtes pCO2 ) konnten vermehrt bei den Kindern der NEC-Gruppe festgestellt werden. Es war jedoch in dieser retrospektiven Studie nicht möglich herauszufinden, ob diese Veränderungen als erste Manifestationszeichen der in der Entstehung begriffenen NEC oder aber als die Ursache für die Erkrankung anzunehmen sind. Eine Minderversorgung mit Sauerstoff, hervorgerufen durch vermehrte Apnoen und Bradykardien, oder auch die Gabe hyperosmolarer Präparate, die Darmwandnekrosen verursachen können, hatten keinen erkennbaren Einfluss auf die Häufigkeit der NEC, dies galt auch für CPAP-Beatmung. Bezüglich des Keimspektrums ließ sich bei den NEC-Kindern kein Unterschied zur Kontrollgruppe nachweisen. Trotz der relativ großen Zahl an betroffenen Kindern in der vorlegenden Studie konnte kein einzelner Risikofaktor als Ursache für die NEC gefunden werden. Reife und Gewicht sind weiterhin die entscheidenden Einflussfaktoren bei diesem multifaktoriell bedingten Geschehen. Die Senkung der Frühgeburtsrate ist damit momentan die effektivste Maßnahme zur Vermeidung der NEC.

Background: Inhibition of phrenic nerve activity (PNA) can be achieved when alveolar ventilation is adequate and when stretching of lung tissue stimulates mechanoreceptors to inhibit inspiratory activity. During mechanical ventilation under different lung conditions, inhibition of PNA can provide a physiological setting at which ventilatory parameters can be compared and related to arterial blood gases and pH. Objective: To study lung mechanics and gas exchange at inhibition of PNA during controlled gas ventilation (GV) and during partial liquid ventilation (PLV) before and after lung lavage. Methods: Nine anaesthetised, mechanically ventilated young cats ( age 3.8 +/- 0.5 months, weight 2.3 +/- 0.1 kg) ( mean +/- SD) were studied with stepwise increases in peak inspiratory pressure ( PIP) until total inhibition of PNA was attained before lavage ( with GV) and after lavage ( GV and PLV). Tidal volume (V-t), PIP, oesophageal pressure and arterial blood gases were measured at inhibition of PNA. One way repeated measures analysis of variance and Student Newman Keuls-tests were used for statistical analysis. Results: During GV, inhibition of PNA occurred at lower PIP, transpulmonary pressure (Ptp) and Vt before than after lung lavage. After lavage, inhibition of inspiratory activity was achieved at the same PIP, Ptp and Vt during GV and PLV, but occurred at a higher PaCO2 during PLV. After lavage compliance at inhibition was almost the same during GV and PLV and resistance was lower during GV than during PLV. Conclusion: Inhibition of inspiratory activity occurs at a higher PaCO2 during PLV than during GV in cats with surfactant-depleted lungs. This could indicate that PLV induces better recruitment of mechanoreceptors than GV.

Comparative studies on strain in avalanche- and rescue-dogs during running and searching 22 dogs of the “Lawinenhundestaffel Bergwacht Bayern” (avalanche rescue dog unit of Bavarian Mountain Rescue) were subjected to a series of tests on the strain exerted upon rescue dogs. In total, every dog underwent four different types of strain with a duration of 2 x 20 minutes each and a 20-minute break in between the two cycles. In the summer, the strain of running beside a bicycle was analyzed at a height of 700 metres above sea-level, and a combined area and alpine rubble search was carried out. Ambient temperature was between 9°C and 26°C in summer. In the winter, the strains of running beside skis and of an avalanche search were analyzed at a height of 2600 metres above sea-level and ambient temperatures between –3°C and –17°C. In order to be able to capture the influence of the nose´s activity as a strain factor, physiological values during and up to 2 hours after search strain were compared to those of pure running strain. In particular the clinical parameters yielded significant variations during the four types of strain. The heart rate reacted to all four types of strain with a marked increase. The continuously recorded heart rate increased to mean values of up to 164-176 beats per minute (bpm) (physiological: 70-160 bpm) during the four types of strain and returned to normal within 20-30 minutes after the end of strain. The body temperature was measured at six points in time prior to and after strain. After strain the body temperature rose to means between 39.0 and 39.7°C (physiological: 37.5-39.0°C) and returned to the initial values within 20-60 minutes after the end of strain. The venous blood parameters hardly showed any significant changes upon strain. All blood values were determined prior to and immediately after the second strain cycle as well as 2 hours after the end of strain. Blood gas pH increased after strain, reaching means of 7.40-7.43 (physiological: 7.30-7.40). In addition, there was a decrease in means of pCO2 to 30-31 mm Hg (physiological: 36-40 mm Hg) and in bikarbonate to 19-20 mmol/l (physiological: up to 24.2 mmol/l), whereas pO2 increased to up to 58 mm Hg (physiological: 34-54 mm Hg). In the muscle metabolism there was a continuous increase in creatine kinase activity after strain, with means up to 105 IU/l (physiological: up to 90 IU/l) after 2 hours in recovery. The plasma lactate concentration of the rescue dogs underwent no major changes in any of the four types of strain and never exceeded 2.3 mmol/l (physiological: 0.22-4.40 mmol/l). The renal (bounded urea nitrogen, creatinine), the hematological (hematocrit, hemoglobin) and the hepatic parameters (alkaline phosphatase, alanine transaminase, total bilirubin, cholesterol) as well as the proteins measured (total protein, albumin, globulin) did not change significantly under any of the four types of strain. In all strain types, blood glucose varied to a relatively small degree ranging between 5.4 mmol/l and 5.8 mmol/l (physiological: 3.9-6.7 mmol/l). As regards salivary cortisol, there was a delayed increase in the cortisol concentration during recovery. Means of salivary cortisol values reached 5.5 nmol/l in maximum (resting value: 1.5-2.3 nmol/l). Observation of behaviour yielded signs of fatigue during avalanche search in winter and in the rubble search in summer during the second strain phase in the form of a reduced activity index. Area search in the summer was generally associated with the highest activity level, and only in this type of search there was no decrease in the activity index during the second strain phase. Dividing the participating rescue dogs in three age-classes (up to 4 years, 4-7 years, over 7 years) age dependent differences could be seen. During the whole observation the older dogs showed significant higher heart rates and significant lower body temperatures. Compared to the other two age-classes the older dogs also had significant higher lactate concentrations and a obvious higher creatinkinase activity after strain. Dogs under 4 years of age showed constantly higher body temperatures and activity indices in comparison to the two older age-classes. After strain highest blood glucose levels could be found in the young dogs up to 4 years. The salivary cortisol concentration was significant lower in the dogs from 4-7 years of age. In summary, the parameters investigated did not indicate any differences in the strain physiology between the strain during search and the mere strain due to running. However, based on heart rate, body temperature, blood gas parameters, blood glucose and salivary cortisol values significant differences were found between the strain of search in summer and the strain of search in winter.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.04.16.042440v1?rss=1 Authors: van de Weil, J., Meigh, L., Bhandare, A., Cook, J., Huckstepp, R. T., Dale, N. Abstract: Breathing is highly sensitive to the PCO2 of arterial blood. Although CO2 is detected via the proxy of pH, CO2 acting directly via Cx26 may also contribute to the regulation of breathing. Here we exploit our knowledge of the structural motif of CO2-binding to Cx26 to devise a dominant negative subunit (Cx26DN) that removes the CO2-sensitivity from endogenously expressed wild type Cx26. Expression of Cx26DN in glial cells of a circumscribed region of the medulla - the caudal parapyramidal area - reduced the adaptive change in tidal volume and minute ventilation by approximately 30%. As central chemosensors mediate about 70% of the total response to hypercapnia, CO2-sensing via Cx26 contributed about 45% of the centrally-mediated ventilatory response to CO2. Our data unequivocally links the direct sensing of CO2 to the chemosensory control of breathing and demonstrates that CO2-binding to Cx26 is a key transduction step in this fundamental process. Copy rights belong to original authors. Visit the link for more info