Podcasts about Po2

Scott and Joris sit down to discuss all the latest news across Belgian football. Things are changing up in PO1, a funny red card in PO2, relegation looms closer for some, and they get excited by the impending wild climax to the season in the Challenger Pro League.

Normal 95 - 100% Indications Determine respiratory status Part of Arterial Blood Gas (ABG) testing Description Oxygen saturation (SaO2) is a measurement of the percentage of how much hemoglobin is saturated with oxygen. Oxygen is transported in the blood in two ways: oxygen dissolved in blood plasma (pO2) and oxygen bound to hemoglobin (SaO2). About 97% of oxygen is bound to hemoglobin while 3% is dissolved in plasma. SaO2 and pO2 have direct relationships, if one is decreased so is the other. The relationship between oxygen saturation (SaO2) and partial pressure O2 (PaO2) is referred to as the oxyhemoglobin (HbO2) dissociation curve. SaO2 of about 90% is associated with PaO2 of about 60 mmHg. What would cause increased levels? Polycythemia Increased inspired O2 Hyperventilation What would cause decreased levels? Anemia's Hypoventilation Bronchospasm Mucus plugs Atelectasis Pneumothorax Pulmonary edema Adult respiratory distress syndrome

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  

Club gaat naar PO1 en maakte indruk. Ook al was het tegen Eupen en Westerlo. Wat gaat Club doen tegen Antwerp, Genk en Union? Gent delft het onderspit, PO2 is hun lot. Het lot van Zulte Waregem is helemaal dramatisch, ze gaan naar 1B.

This edition features a story about how PRT Khost continues overseeing the transition of authority to the Afghan government in its area. They also work with a village who's traditions set the example for the country. Petty Officer Erick Holmes tells us more. Soundbite includes CDR. Bradley Brewer – Commanding Officer, Provincial Reconstruction Team Khost. Produced by PO2. Erick Holmes, Afghanistan and hosted by SSgt. Melissa Hay. Also available in High Definition.

Genk heeft verloren omdat het rond de tegendoelpunten het noorden kwijt was. Genk's rapport is gewoon slecht met 9 op 24. AA Gent lijkt zijn PO1-ticket niet meer uit handen te geven. Club Brugge is op z'n plaats in PO2. En Anderlecht is zijn goeie elan kwijt en zou wel eens PO2 kunnen missen.

Zeno Debast aborde son amour pour RSC Anderlecht, la Course au PO2 ainsi que ses premières sélections pour les Diables rouges Dans ce Eleven Insiders, Séverine Parlakou et Jérémie Baise sont accueillis au Lotto Park pour un entretien exclusif avec l'international belge. 

Get a free nursing lab values cheat sheet at NURSING.com/63labs   What is the Lab Name for Oxygen Saturation (SaO2) Lab Values? Oxygen Saturation   What is the Lab Abbreviation for Oxygen Saturation? SaO2   What is Oxygen Saturation in terms of Nursing Labs? Oxygen saturation (SaO2) is a measurement of the percentage of how much hemoglobin is saturated with oxygen. Oxygen is transported in the blood in two ways: oxygen dissolved in blood plasma (pO2) and oxygen bound to hemoglobin (SaO2). About 97% of oxygen is bound to hemoglobin while 3% is dissolved in plasma. SaO2 and pO2 have direct relationships, if one is decreased so is the other. The relationship between oxygen saturation (SaO2) and partial pressure O2 (PaO2) is referred to as the oxyhemoglobin (HbO2) dissociation curve. SaO2 of about 90% is associated with PaO2 of about 60 mmHg. For more information on PaO2, SaO2 and oxyhemoglobin dissociation curve visit this link HERE.   What is the Normal Range for Oxygen Saturation? 95 – 100%   What are the Indications for Oxygen Saturation? Determine respiratory status Part of Arterial Blood Gas (ABG) testing   What would cause Increased Levels of Oxygen Saturation? Polycythemia Increased inspired O2 Hyperventilation   What would cause Decreased Levels of Oxygen Saturation? Anemia's Hypoventilation Bronchospasm Mucus plugs Atelectasis Pneumothorax Pulmonary edema Adult respiratory distress syndrome

  Während der Covid-Pandemie ist es uns Primärversorgern sicher allen schon passiert. Aufnahme eines Patienten auf die Intensivstation, wegen „schlechten pO2“s. Patient wird vorgefahren, und es geht ihm subjektiv super. „Haben Sie Luftnot?“ – „Nö.“, und daddelt mit dem Handy. Klinisch einzig zu sehen ist eine deutlich erhöhte Atemfrequenz mit 20-30/min, ansonsten nichts. Sobald aber … Weiterlesen

Paul V. Abney STGCM(SW/IUSS) RetiredSenior Analyst American Systems Corporation (ASC)Retired Master Chief Petty Officer Paul Abney has 45 years of combined service to the navy from December 1976 to present. Thirty years of active-duty service followed by 15 years of support to the US Navy as a defense contractor. He began active-duty April 1977, following delayed entry from Dec 1976. His ship assignments were as a PO3/2 on USS Dale (CG 19), PO2/1 as a work center supervisor (WCS) on USS John Rodgers (DD 983), then commissioning leading Chief Petty Officer (LCPO) on USS Lake Champlain (CG 57), and finally as departmental LCPO & acting command master chief (CMC) abord USS Cole (DDG 67), until relieved by James Parlier, and surviving the terrorist attack onboard in Yemen October 12th, 2000. Personal decorations include the Meritorious Service Medal, Navy and Marine Corps Commendation Medal (4), Navy and Marine Corps Achievement Medal, the Combat Action Ribbon and various meritorious, service and campaign awards. A native of Apopka, Florida, he completed the Senior Enlisted Academy (SEA) 1995 in class 66 khaki. He earned his Associate of the Arts (AA) degree from St. Leo University in 1996 and his Bachelor of Science (BS) degree in interdisciplinary studies from Norfolk State University in 1997. After retiring from the Navy, he earned a Master's in Business Administration (MBA) degree from Regent University in 2015 and currently supports the Tactical Training Group Atlantic (TTGL) as a senior analyst and subject matter expert contracted with American Systems Corporation (ASC). He started at DDL OMNI after his navy retirement in April 2007; DDL OMNI was later purchased by ASC in 2018, giving him nearly 15 years of naval contractor support following his 30-year naval career.Links:https://www.facebook.com/iconutilityservices/photos/pcb.3282304212030773/3282304082030786/https://www.youtube.com/channel/UCqvd5sUEtC9xkm7ejGNK5Zw/featuredhttps://www.facebook.com/aqseiberthttps://www.facebook.com/CombatVetVisionEmail: Aqseibert@yahoo.comThe Warrior Built Foundation - https://warriorbuilt.org/The PTSD Foundation of America - https://ptsdusa.org/Virtual Office(Come see me) Virbella.comhttps://recon-chief-inc.business.site/?utm_source=gmb&utm_medium=referralSponsorsSitch Radio - https://sitchradio.com/If you would like to become a sponsor or advertiser Call Sitch Radio (714) 643-2500 X 1 I part of the solution or the problem.PTSD FOA Warrior Group Chaptershttps://ptsdusa.org/about-us/chapters/

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.

Second week of the play offs down, with PO2 stealing all the goals this weekend! PO1 had intrigue but no goals, while Seraing survive against RWDM for another year in 1A!

The play offs have started, and so has the drama! Joris returns to join Ben and Scott as they break down the relegation play off first leg and the first round of both PO1 and PO2. They also chat through the cup final from Easter Monday.

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.

Two match weeks have passed since our last episode, and plenty has happened! Scott, Joris and Ben discuss Club Brugge finally winning in the playoff round, Genk keeping the pressure on, Mechelen and Gent pushing to win PO2. They also discuss the new managers announced at Waasland-Beveren and Charleroi, as well as looking at the recently announced Red Devils squad for EURO2020.

  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

In this episode we talk about the main steps that facilitate gas exchange at the placenta. This is great applied respiratory physiology and a common question in the viva and SAQs!Double Bohr effectCheck out power and Kam chapter 3 - resp physiology or this great summaryhttp://www.anaesthesia.uct.ac.za/sites/default/files/image_tool/images/93/10-The%20Bohr%20and%20Haldane%20Effects%20%28K%20Bergh%29.pdfcheck out some model answers athttps://anaesthesiacollective.com/education/first-part-exam/Power and Kamhttps://www.amazon.com.au/Principles-Physiology-Anaesthetist-Peter-Kam-ebook/dp/B08GY1MXMH/ref=sr_1_1?crid=3B9KG9NMH60BU&dchild=1&keywords=principles+of+anatomy+and+physiology+for+the+anaesthetist&qid=1614831758&s=books&sprefix=principles+of+%2Cstripbooks%2C328&sr=1-1Table with approx valuesUterine Artery       pO2 100    100% sats      pCO2 32mmHgUterine Vein           pO2 40        80% sats         pCO2 46Umbilical Artery          pO2 20        60% sats         pCO2 50Umbilical Vein               pO2 30        80% sats         pCO2 40          Please rate, post a review and subscribe!Check out www.anaesthesiacollective.com and sign up to the ABCs of Anaesthesia facebook group https://www.facebook.com/groups/2082807131964430and check out the ABCs of Anaesthesia YouTube channel for more contenthttps://www.youtube.com/c/ABCsofAnaesthesiaIf you have any questions, please email Lahiruandstan@gmail.com  Disclaimer: The information contained in this podcast is for medical practitioner education only. It is not and will not be relevant for 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 viewing The 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 podcasts 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.  

By popular demand, here is the actual physiology and pharmacology viva that Stan was examined on for the part 1 ANZCA exam!Please rate, post a review and subscribe!Check out www.anaesthesiacollective.com and sign up to the ABCs of Anaesthesia facebook group and check you the ABCs of Anaesthesia YouTube channel for more contentAny questions please email Lahiruandstan@gmail.com Some links and formulas!How does it measure cardiac output?Using thermodilution and utilisation of Stewart Hamilton's equation of:(Tb-Ti)*Volume*k/intergration of change in TWhat is venous admixture?Venous admixture is the amount of mixed venous blood that needs to be added to end-capillary blood to account for the difference seen in pO2 between arterial blood and end-capillary blood.It is calculated using the equation:Qs/Qt = Cc'O2 – CaO2 / Cc'O2 – CvO2Alveolar gas equation.PAO2 = FiO2 (Patm – PH2O) – pCO2/R Is there anything else at the end?Yes there is a correction factor (+F) which is FiO2 * pCO2 * (1-R)/R and this is normally less than 2mmHg.O2 content = SaO2 * Hb * 1.34 (Huffner's constant which ideally is 1.39) + pO2 * 0.003the isoshunt diagram is figure 8 here: https://erj.ersjournals.com/content/44/4/1023.figures-onlyPlease rate, post a review and subscribe!Check out https://anaesthesiacollective.com/education/first-part-exam/ for general information and a collection of model answersand sign up to the ABCs of Anaesthesia facebook group https://www.facebook.com/groups/2082807131964430and check out the ABCs of Anaesthesia YouTube channel for more contenthttps://www.youtube.com/c/ABCsofAnaesthesiaIf you have any questions, please email Lahiruandstan@gmail.com  Disclaimer: The information contained in this podcast is for medical practitioner education only. It is not and will not be relevant for 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 viewing The 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 podcasts 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. 

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.21.255802v1?rss=1 Authors: Poublanc, J., Sobczyk, O., Shafi, R., Uludag, K., Wood, J., Vu, C., Dharmakumar, R., Fisher, J. A., Mikulis, D. J. Abstract: BACKGROUND: The paramagnetic properties of deoxyhemoglobin shorten T2* as do gadolinium based contrast agents. Induction of abrupt changes in arterial deoxyhemoglobin concentration ([dOHb]) can mimic the action of intra-vascular boluses of gadolinium based contrast agents (GBCAs) used for perfusion imaging. AIM: To demonstrate the feasibility of rapidly changing pulmonary venous hemoglobin saturation for generating boluses of blood with altered T2* properties for measuring flow metrics in the systemic circulation. METHODS: A gas blender with a sequential gas delivery breathing circuit and software enabling prospective arterial blood gas targeting was used to implement rapid lung changes in the partial pressure of blood oxygen (PaO2) while maintaining isocapnea. Lung PaO2 was initially lowered to induce a low baseline deoxyhemoglobin concentration [dOHb]. PaO2 was then rapidly raised to normal for 10 seconds and then rapidly lowered to the initial low baseline creating a oxyhemoglobin (OHb) bolus. R2* changes were measured using blood oxygenation dependent (BOLD) MRI signal changes in large arteries and veins as well as in the microcirculation. This enabled generation of the following maps: bolus arrival time delay (TD) cerebral blood volume (CBV), mean transit time (MTT) and cerebral blood flow (CBF). RESULTS: BOLD signal in the middle cerebral artery showed a sharp increase during the OHb bolus transit indicating minimal dispersion confirming effective rapid modulation of pulmonary venous PO2 with reasonable cortical contrast-to-noise ratio of 3. Signals sorted by amplitude of signal changes and arrival times enabled the visualization of major arteries and veins. Contrast to noise ratio was adequate for a single gas challenge to provide most of the contrast, little improved by averaging over the remaining set of challenges. Values of the flow metrics derived from the perfusion maps were within normal ranges from published literature values. CONCLUSION: Non-invasive induction of abrupt changes in OHb saturation can function as a novel non-invasive vascular contrast agent for use in perfusion imaging. Copy rights belong to original authors. Visit the link for more info

One of the central things we do for neuro patients in control their ICP. But, does tight control of ICP improve outcomes? Is ICP the best thing for us to be optimizing, especially if brain ischemia is what we're trying to avoid? What about brain tissue oxygenation? I'll quickly review the evidence, and you decide. Lundberg demonstrating ICP measured from an EVD in TBI patients. Lundberg, N., Troupp, H., Lorin, H. (1965). Continuous Recording of the Ventricular-Fluid Pressure in Patients with Severe Acute Traumatic Brain Injury Journal of Neurosurgery 22(6), 581-590. https://dx.doi.org/10.3171/jns.1965.22.6.0581 Model showing independent effects of ICP and blood pressure on TBI outcomes. Marmarou, A., Anderson, R., Ward, J., Choi, S., Young, H., Eisenberg, H., Foulkes, M., Marshall, L., Jane, J. (1991). Impact of ICP instability and hypotension on outcome in patients with severe head trauma Journal of Neurosurgery 75(Supplement), S59-S66. https://dx.doi.org/10.3171/sup.1991.75.1s.0s59 Mortality in TBI over the past 150 years (note the large decrease through the 70s and 80s). Stein, S., Georgoff, P., Meghan, S., Mizra, K., Sonnad, S. (2010). 150 Years of Treating Severe Traumatic Brain Injury: A Systematic Review of Progress in Mortality Journal of Neurotrauma 27(7), 1343-1353. https://dx.doi.org/10.1089/neu.2009.1206 BEST-TRIP trial comparing invasive ICP monitoring to clinical exam and CT. No difference in outcomes in severe TBI patients. Chesnut, R., Temkin, N., Carney, N., Dikmen, S., Rondina, C., Videtta, W., Petroni, G., Lujan, S., Pridgeon, J., Barber, J., Machamer, J., Chaddock, K., Celix, J., Cherner, M., Hendrix, T. (2012). A Trial of Intracranial-Pressure Monitoring in Traumatic Brain Injury The New England Journal of Medicine 367(26), 2471-2481. https://dx.doi.org/10.1056/NEJMoa1207363 Meta-analysis of invasive ICP studies. Observational studies consistently show a benefit to ICP monitoring. Shen, L., Wang, Z., Su, Z., Qiu, S., Xu, J., Zhou, Y., Yan, A., Yin, R., Lu, B., Nie, X., Zhao, S., Yan, R. (2016). Effects of Intracranial Pressure Monitoring on Mortality in Patients with Severe Traumatic Brain Injury: A Meta-Analysis PLOS ONE 11(12), e0168901. https://dx.doi.org/10.1371/journal.pone.0168901 Original Lancet article discussing secondary injury from ischemia in TBI. Graham, D., Adams, J. (1971). ISCHÆMIC BRAIN DAMAGE IN FATAL HEAD INJURIES The Lancet 297(7693), 265-266. https://dx.doi.org/10.1016/s0140-6736(71)91003-8 First studies to look at outcome in TBI patients using Licox Santbrink, H., Maas, A., Avezaat, C. (1996). Continuous Monitoring of Partial Pressure of Brain Tissue Oxygen in Patients with Severe Head Injury Neurosurgery 38(1), 21-31. https://dx.doi.org/10.1097/00006123-199601000-00007 Valadka, A., Gopinath, S., Contant, C., Uzura, M., Robertson, C. (1998). Relationship of brain tissue PO2 to outcome after severe head injury Critical Care Medicine 26(9), 1576-1581. https://dx.doi.org/10.1097/00003246-199809000-00029 BOOST-II trial. Respiratory interventions were able to improve PbO2 in TBI patients, and that group showed an improved outcome, including disability and mortality. Okonkwo, D., Shutter, L., Moore, C., Temkin, N., Puccio, A., Madden, C., Andaluz, N., Chesnut, R., Bullock, M., Grant, G., McGregor, J., Weaver, M., Jallo, J., LeRoux, P., Moberg, D., Barber, J., Lazaridis, C., Diaz-Arrastia, R. (2017). Brain Oxygen Optimization in Severe Traumatic Brain Injury Phase-II Critical Care Medicine 45(11), 1907. https://dx.doi.org/10.1097/CCM.0000000000002619

Anagha Arla and Caitlin Wonsowski sit down in this episode of Po2 to offer their different cultural perspectives on the topic of pop culture.

Anagha Arla and December graduate Caitlin Wonsowski sit down in this episode of Po2 to offer their different cultural perspectives on the topic of graduation.

Discover common practices that persist in the hospital wards despite no proven benefit! We review how potassium replacement goals should not drive you bananas, extra oxygen should not give you comfort, and how you should maybe calm down with antipsychotics for delirium. Join returning guests: high-value care specialist Dr. Lenny Feldman (@DocLennyF, Johns Hopkins) and tweetorialist Dr. Tony Breu (@tony_breu, Harvard) as they walk us through round 3 of “Things We Do for No ReasonTM. SHM members can claim CME-MOC credit at https://www.shmlearningportal.org/curbsiders (CME goes live at 0900 ET on the episode’s release date). Note: The planners and faculty for this activity have no relevant relationships or conflicts to disclose. Show Notes | Subscribe | Spotify | Swag! | Top Picks | Mailing List | thecurbsiders@gmail.com Credits Written and Produced by: Burton H. Shen MD, Justin Berk, MD MPH MBA Infographic: Cover Art: Hosts: Justin Berk MD MPH MBA; Stuart Brigham MD; Matthew Watto MD, FACP; Paul Williams MD, FaCP Editor: Matthew Watto MD, FACP (written materials); Clair Morgan of Nodderly.com (audio) Guest: Lenny Feldman MD, Tony Breu MD Sponsors The Society of Hospital Medicine Hospital Medicine 2020 (HM20) is the Society of Hospital Medicine’s Annual Conference April 15th through the 18th in sunny San Diego. Don’t miss the largest hospital medicine meeting. Register now at https://shmannualconference.org/ and use the code CURBSIDERS to receive a $50 discount. Primary Care Internal Medicine of Ithaca Join a well established practice in beautiful upstate New York near the finger lakes and wine country! You'll have flexible hours and the ability to take the time you need with patients! Contact Dr. Ann Costello arcostello@gmail.com to find out more about this incredible opportunity to join the team at Primary Care Internal Medicine of Ithaca https://www.primarycareinternalmedicineofithaca.com/.  Time Stamps 00:00 Sponsors -SHM’s Annual Conference, HM20 (use code CURBSIDERS) and Primary Care Internal Medicine of Ithaca (email: arcostello@gmail.com) 00:38 Intro, disclaimer, guest bio 02:10 Guest one-liners 03:35 Picks of the Week*: Knives Out (film), Priced Out by Uwe E. Reinhardt; Crisis in the Red Zone by Richard Preston; CardioNerds podcast; Outbreak (film); Teaching Physiology on the Fly (faculty development course) 07:55 Sponsors -SHM’s Annual Conference, HM20 (use code CURBSIDERS) and Primary Care Internal Medicine of Ithaca (email: arcostello@gmail.com) 09:30 Case of Eric Lokay; Repleting potassium. Is it necessary to “buff the lytes” 20:30 Pathophysiology of hypokalemia; Final recommendations on potassium repletion 24:30 Supplemental oxygen; pO2 vs total oxygen content; Oxygen, vasoconstriction and potential harms 30:33 Evidence of harm from supplemental O2 35:00 Tony’s recommendations for use of supplemental O2 41:55 Case of delirium; Definition and diagnosis 46:20 Can we prevent delirium? Melatonin and ramelteon 50:33 Should we use antipsychotics? Benzodiazepines?; What should we do instead? 58:25 Take home points, Outro and a terrible pun *The Curbsiders participates in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising commissions by linking to Amazon. Simply put, if you click on our Amazon.com links and buy something we earn a (very) small commission, yet you don’t pay any extra. Disclosures Dr. Feldman and Dr. Breu report no relevant financial disclosures. The Curbsiders report no relevant financial disclosures.  Citation Feldman L, Breu T, Shen BH, Berk JL, Williams PN, Brigham SK, Watto MF. “#195 TWDFNRTM 3: Potassium, Oxygen, and antipsychotics”. The Curbsiders Internal Medicine Podcast. https://thecurbsiders.com/episode-list. February 17, 2020.

Guillaume ontdekt het geluid van de Croky Cup-mascotte, terwijl Gert luistert naar PO2, Lars zich ontpopt als echte quizmaster en Nederlandse gast Neal Petersen het Play-offsysteem probeert uit te leggen.

In this third episode of 40 and 20 Everett and Andrew change pace, and discuss some "reach" watches, or watches on the more expensive side of their comfort zone. Along the way we talk about what reaching means for each of us, how we save for watches, and what we look for in a reach watch. We even talk about donuts and duck calls! Show Notes: Seiko Turtle SRP777: https://www.amazon.com/Seiko-SRP773-Prospex-Automatic-Stainless/dp/B01N95N8AR Citizen Nighthawk BJ7000-52E https://www.jomashop.com/citizen-bj7000-52e.html Timex Waterbury: https://www.amazon.com/Timex-Waterbury-Quartz-Stainless-Leather/dp/B019FELCFI?tag=vs-watchuseek-convert-20 Victorinox 241291: https://www.ashford.com/us/watches/victorinox-swiss-army/classic/classic-infantry/241291-PO2.pid?source=370000001&s_kwcid=PTC!pla!!!557647480271!g!!54906151765&CAWELAID=120016340000161014&CAGPSPN=pla&CAAGID=14374508125&CATCI=pla-557647480271&CATARGETID=120016340000157923&CADevice=c&gclid=CjwKCAiAiarfBRASEiwAw1tYv-H6SPv22zphJr5J3Ur5_Qe-G6XpT3GsHLikflS_WTikN-GJsPf6VhoCATEQAvD_BwE Phoibos PX002B: https://www.amazon.com/Phoibos-PX002B-Watch-Swiss-Quartz/dp/B01N6KIO7Z G Shock DW 5750: https://www.jomashop.com/casio-watch-dw-5750e-1bcr.html Strela Cosmos CO38LAS: https://strela-watch.de/product/co38las/ Stova Marine Classic: https://www.stowa.de/en/Marine+Klassik+40+hite.htm Shinola Runwell: https://www.shinola.com/mens/watches/all/the-runwell-chrono/therunwell41-chrono-s0198.html Nomos Club Campus: https://nomos-glashuette.com/en/watches/series/campus Monta Triumph: https://montawatch.com/products/triumph Orion Calamity: https://orionwatch.com/calamity/ Haveston Heavy Watch Straps: http://haveston.com Royal Crown Cola: https://www.drpeppersnapplegroup.com/brands/rc-cola Intro/Outro Music: Bummin on Tremelo Kevin MacLeod (incompetech.com) Licensed under Creative Commons: By Attribution 3.0 License creativecommons.org/licenses/by/3.0/

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).

(*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

Summary: In 2004 Barbara Currier and her husband Michael were relocated to Richmond, VA, where she began teaching agility at All Dog Adventures. It was there that Barbara was introduced to Susan Garrett and her amazing foundation-based training, centered around impulse control and relationship building with your dog.   She continues to train with some of the best handlers in the world and has implemented what she has learned from each of them into her training program. She became heavily involved in the OneMind Dogs handling method in 2014. She has successfully competed in agility with over 10 different breeds of dogs. Along the way, she started her own in home training and behavioral rehabilitation business. She was the trainer for Richmond Boxer Rescue and also assisted Southeastern Virginia Golden Retriever Rescue in assessing some of their dogs. Over the years, Barbara has worked extensively with many rescue organizations in numerous states. Barbara has also worked as an animal wrangler for Marvel's Ant-Man, 90 Minutes in Heaven, the TV series Satisfaction and various commercials. Today Barbara is the head dog trainer for the F.I.D.O Program run at Georgia Tech which creates wearable computing for military, SAR and service dogs. Links Party of 2 (PO2) - Barbara's Website F.I.D.O at Georgia Tech Next Episode:  To be released 10/13/2017, featuring Loretta Mueller to talk about managing a multi-dog household. TRANSCRIPTION: Melissa Breau: This is Melissa Breau, and you're listening to the Fenzi Dog Sports podcast, brought to you by the Fenzi Dog Sports Academy, an online school dedicated to providing high quality instruction for competitive dog sports, using only the most current and progressive training methods. Today I'll be talking to Barbara Currier. In 2004, Barbara and her husband, Michael, were relocated to Richmond, VA, where she began teaching agility at All Dog Adventures. It was there that Barbara was introduced to Susan Garrett and her amazing foundation based training centered around impulse control and relationship building with your dog. She continues to train with some of the best handlers in the world and has implemented what she has learned, from each of them, into her training program. She became heavily involved in the OneMind Dogs handling method, in 2014. She successfully competed in agility with over ten different breeds of dogs. Along the way, she started her own in-home training and behavioral rehabilitation business. She was the trainer for Richmond Boxer Rescue, and also assisted Southeastern Virginia Golden Retriever Rescue and assessing some of their dogs. Over the years, Barbara has worked extensively with many rescue organizations in numerous states. Barbara has also worked as an animal wrangler for Marvel's Ant-Man, 90 Minutes in Heaven, the TV series, Satisfaction, and various commercials. Today Barbara is the head dog trainer for the FIDO Program, run at Georgia Tech, which creates wearable computing for military search and rescue service dogs. Hi, Barbara. Welcome to the podcast. Barbara Currier: Thanks for having me, Melissa. I'm really happy to be here. Melissa Breau: As a new FDSA instructor, I'm looking forward to getting to know you a little bit. Barbara Currier: Thank you. Melissa Breau: To start us out, do you want to just tell us a little bit about the dogs that you have now and what you're working on with them? Barbara Currier: Sure. I have four dogs, currently, two Border Collies, a Parson Russell Terrier, and a Miniature Poodle. My oldest is Piper. She is the Parson Russell Terrier. She's 8 years old. I got her when she was 2 years old. She belonged to a friend of mine, who passed away unexpectedly. We tried agility with her, but she didn't love it. She loved it when there was cheese around, but the moment the treats went away, it was more of, okay, I'll do it, but the love clearly wasn't there. She's also built like a typical terrier, so she's very front-end heavy. She's really straight in the shoulder, and I really struggled with keeping her sound. I specifically thought, when we would work weave poles and when we would do A-frame stuff, she was constantly coming up lame, and so I decided since she didn't particularly love it, and I, you know, didn't want to keep injuring her, that I would just find something else that she would like better, so one of the things that she's always loved is swimming, so I decided to try dock diving with her, and that is, truly, her love. We don't need to have cheese, or any type of treat, within a 50-mile radius and she will happily do her dock diving all day long, so that's been really fun. I have a Border Collie, Brazen. I have two Border Collies. Brazen is the oldest of the two, by a few months. She's 8 years old. I got her from a breeder, in Virginia, when she was 8 weeks old. Unfortunately, she has a lot of health problems, so she has not really been able to do any type of sport. She has some minor brain damage. The best way to describe her is, basically, she's like autistic. She doesn't deal well with any types of changes in her environment. She tends to be a self-mutilator, so when anything changes, like my neighbor parks his truck in a different part of his driveway, she'll rip the hair out of her body, so we've gotten that under control. It was really bad, when she was a puppy, but we've gotten it under control, but she doesn't handle any types of changes well, so she's happiest when she can just be at home, on the property, so we let her just do that. She also has a very severe case of Border Collie collapse, so she passes out whenever she has any type of hard exercise, even just playing frisbee, so we have to, kind of, keep that managed too, so unfortunately, she never really got to do any type of performance, but she's happy being at home and chilling and getting out and playing. We have five acres, completely fenced, so she gets plenty of room to run around, so that's, kind of, what she does. Blitz is my other Border Collie. He is also 8. I adopted him from Bimmer's Border Collie Rescue, in Virginia, when he was 10 months old. He just recently retired from agility due to, at 7, he tore his psoas and we rehabbed that for a year, and then, when he came back, he was sound for about two months, and then he injured his flexor tendon, and I felt like we were having progressive injuries, and that was not the way I wanted him to be in his later years. I wanted him to be able to enjoy life and do all of the things that he loves to do without constant rehabbing, so I made the decision to retire him from agility, about three months ago. It just seemed like that was the thing that kept injuring him, but everything else, in life, wasn't, so it just seemed like it was the right choice, and he's loving retirement. He's doing dock diving now. He's also my service dog. I am hypoglycemic, and he actually detects it about 30 minutes before I know anything is going to happen, and if I eat, then I don't have any episodes, so he is, kind of, my other half. He's just amazing.   Then my youngest is Miso. She is a Miniature Poodle. She is 3 years old, and I got her from a breeder in Florida, when she was 8 weeks, and actually waited for 10 years to get a puppy from her line, and she was worth every year I waited because she has been perfect since the moment she came home. She's been competing for about a year and a half now, in agility, and in her first year, of competing, she actually qualified for AKC Nationals, and she's, actually, the seventh ranking dog in the 12-inch division, in the country, and she's already been to two world team tryouts, and won round one of the FCI World Team tryout. She's already qualified for her second AKC Nationals. She's qualified for USDAA Cynosport, and she is one double q away from her MACH, and at this point she's only been trialing a year and a half, and I actually only trial about once a month because I am so busy, so she is pretty remarkable. Melissa Breau: Wow. That's impressive. Barbara Currier: Yeah. Yes. She is a super impressive little girl, so she's been really, really fun and we have a new puppy coming, in the fall, hopefully. Melissa Breau: Fingers crossed. Barbara Currier: Yeah. Yeah. It's all good. Melissa Breau: Yeah. So, how did you originally get started in all of this, in dog training and agility. I mentioned a little bit, kind of in the bio, I think 2004, right, so what kind of kicked things off? Barbara Currier: Well, in the late ‘90s, I adopted a 9 month old Chihuahua, named Cabal, from Chihuahua Rescue, and he was my first dog, as an adult, you know, we had dogs growing up, but he was my very first dog, and at the time I was technician at a veterinarian hospital and one of the technicians that I worked with, there, she bred and trained Belgian Tervurens and competed them in obedience and tracking, and so she started working with me on training dogs, and training for obedience and tracking, and I started, kind of, assisting with her and learning, kind of, the trade, and during our training we discovered that Cabal had a chemical imbalance, which made him, sort of, a challenge to train, so I'm kind of obsessive in anything I do, and I have to learn everything I can and be the best at everything I can, and so I became obsessive on learning about behavior training and how everything I could do to make him have the happiest, most well rounded, stable life, which we were quite successful at. He went on to compete in agility, and he did obedience and carting and climbed mountains all over the White Mountains, in New Hampshire, and taught me so much about dog training, and he really is what opened up the whole world of dog sports for me. Melissa Breau: So, what got you started, kind of, training positively? Was it that way from the beginning? What got you started on that part of your journey? Barbara Currier: Well, again, it kind of stemmed back to Cabal. When I started training him, it was, kind of, the old school method of the collar corrections, and there was always this nagging, in the back of my head of, you know, I'm collar correcting a six-pound Chihuahua. There's got to be a better way, and my background is in equestrian show jumping, and I trained horses for many years, and I was never a harsh physical trainer with my horses either, and I feel like training dogs and training horses is not entirely different, and agility and show jumping are not a lot different, in the way things need to be trained except agility is far less dangerous than show jumping, so that's always fun. So, I've always, kind of, wanted to have a bond with my animals and train my animals through trust and mutual respect. I don't want a relationship built out of fear and pain, so that's when I started looking into, you know, there's got to be more positive ways that I can train this dog without having to collar correct and do those types of physical corrections. Melissa Breau: How would you describe your training philosophy these days? Barbara Currier: I really like for my dogs to think of training as lots of games. So, again, I want my relationship to be, with them, a partnership that's based completely on trust, and so I want them to understand that, you know, if they get something wrong, not to shut down. You know, a mistake is just that didn't work, try something else, and so, to them, it's just a big puzzle that they're trying to figure out, so they never have a fear of, I'm going to be angry, or you know, they're going to get hurt in any way. It's just a big game, and it's a puzzle they're trying to figure out with lots of rewards throughout it. You know, every time I bring them out for any type of training, they're just all thinking that it's the most wonderful thing in the world, and that's how, I think, it should be, with any animal that you're training.    Melissa Breau: So, I have to say, kind of working on your bio, it seems like you've had the opportunity to do lots of different really interesting things, in the world of dogs, from animal wrangling to working on wearable computing, so I wanted to ask a little more about what you do now. Can you tell us just a little bit about the FIDO Program there, at Georgia Tech, and what you're working on with the dogs there? Barbara Currier: Sure. So, FIDO stands for Facilitating Interactions for Dogs with Occupations. My best friend, Dr. Melody Jackson, she's a professor there, at Georgia Tech, and she runs the brain lab and the animal computer interaction lab. She came up with the idea of creating wearable computing for service dogs, military dogs, police, search and rescue, any type of working dog, and she asked me to come on to oversee the dog training aspects of the work. Within the last year, I've been really busy with travel, and so I, actually, haven't been working a lot with them, on the project, and she's actually taking over most of the dog training aspect, the pilot testing, with her dog, but up to this point, a lot of the stuff that they've created, it's kind of funny, when I tell people what I do there, the team that creates all the stuff, it's Melody Jackson and her lab partner Thad Starner, they're brilliant people, and the students that all work there are super brilliant. I am not a techy person. I'm lucky if I can turn my computer on, I just train dogs, so I kind of compare it to like the big bang theory, and I'm Penny amongst all of these brilliant people, and they just say stuff and I'm like, that's great, just tell me what you want the dogs to do. That's, kind of, where my expertise is, and I don't have any idea what the technical aspect of it is, but we've, actually, created some really cool things. They've created a vest that a service dog is trained to activate that has a tug sensor on it, and so we had a woman come to us that had a speech problem where she doesn't have, she can't project her voice out very loudly, and she's also wheelchair bound, and she was at the dog park, one day, with her dog, and her wheelchair got stuck in some mud, and she couldn't holler to anybody because her voice just didn't project like that, and she really needed, like, a way that she could send her service dog to get help to come back, and you know, but a dog running up to somebody, at a dog park, barking, nobody is going to think that's anything unusual. So, they created a vest that has a computer on it, and the dog has a tug sensor, on the vest, so she can direct the dog to go to somebody, and the dog can go up and it will pull a tug sensor and the vest will actually say, excuse me, my handler needs assistance, please follow me, and the dog can bring that person back to the handler.   Melissa Breau: That's pretty cool. Barbara Currier: Yeah. It's super cool. So, my dog, Blitz, my Border Collie, Blitz, and Melody's Border Collie, Sky, are the two main test subjects for all of the stuff that we create. We have a few other dogs that we use consistently, but most of these things, like, we just bring in random people, and their dogs, to train everything, but Sky and Blitz, kind of, go through everything first, and we work all the bugs out on them. They've created a haptic bodysuit that allows handlers to communicate with SAR dogs from a distance, so, for instance, if a SAR dog is looking for a child with down syndrome, or autism, where they may be afraid of dogs, so a lot of times the SAR dogs will work at a very far distance from the handler, and they don't want the dogs to scare the person into running more. So, the SAR dogs can have like a camera on their vest, so when they find, whatever they're looking for, we have a computer that's on their vest that they can activate their GPS, so it sends out exactly where their location is, but then the owner can give the dog commands through this haptic vest that has vibrating sensors, in different parts of the dog's bodies, and each sensor vibrating, on a certain part of the body, means something, so, like, when the sensor vibrates on the back, that means lie down, so the handler can then vibrate the back sensor that tells the dog to lie down and stay, but the handler can be, you know, 20, 30, 40 feet away, so that's been really fun to work with that. We've taught dogs how to use large touchscreens, so for like hearing dogs, in the house, a lot of times, they don't wear vests, and so when a hearing dog hears something, they just go to their handler and they need to take them to the source of the sound, but sometimes we don't want them to take them to the source of the sound, like a tornado siren or a fire alarm, so we've created a large touchscreen that the dogs can differentiate the sounds, and they can actually go to the touch screen and detect fire alarm, and hit that, and like if the handler is wearing something that's called Google Glass, it will show up in the Google Glass that the fire alarm is going off, or if the doorbell is ringing, maybe the handler just doesn't want to get up and answer it, so the dog can actually differentiate the sounds and tell them, by using, it's like a giant iPad, exactly what sensor is going off. Melissa Breau: Interesting. Barbara Currier: Yeah. It's been really fun to watch the dogs be able to do all of these amazing things, and it's been really fun to watch the students say, do you think a dog can do this? I'm like, sure they can, and they do. I mean, it's just amazing what dogs can do. Melissa Breau: So, what about your experience animal wrangling? Do you want to share a little bit about that work? Barbara Currier: Yeah. I don't do it anymore. It's, honestly, not as glamourous as it sounds. Some of it's fun, some of it, not so much. It depends on, you know, the set you're working on, like the TV series, Satisfaction was super fun to work on, the people were really great. That was with my friend's dog. The producers were really great, but like the movies aren't always so fun to work on because the days are really, really long, and a lot of these people have no idea what it means to train animals, and so they, kind of, think that they're little computers and you can just program in whatever you want, and just change it, on the fly, and the dogs should just automatically know how to do it. It just can be a little frustrating sometimes, and so I did it for about two years and got burned out pretty quickly. Melissa Breau: Fair enough. Now I know that, I kind of mentioned, in the bio, a little bit about Susan Garrett, and I know that you have been able to work with a lot of different excellent handlers, in the agility world, so I wanted to ask a little bit about how working with those professionals has experienced and shaped your training. Barbara Currier: Well I have been lucky to work with some of the most amazing dog trainers, in the world, and I have to say, I've learned something from every trainer I've ever worked with. I'm a firm believer that there's always somebody out there that can teach us something, and the day that we feel that people don't know more than we do, then our education stops, and so I, for one, always want to keep learning and evolving, in my dog training, so even if I go and I take away one thing, from a weekend seminar, well that's one thing that I didn't have going into it, so, to me, it's just worth it. Melissa Breau: For those not familiar with OneMind Dog handling, specifically, do you mind just briefly, kind of, explaining what it is? Barbara Currier: Sure. The OneMind Dog handling, it's a handling method that's based on how dogs naturally respond to our physical cues, and what works best, from the dog's perspective, so it basically teaches us to speak the dog language instead of trying to force dogs to understand us, so a lot of the handling comes very, very natural to the dogs and takes little to no training. It's mostly just training the humans to learn how to speak to the dog, but the dog's, right from the beginning, really understand it quite well. I love when I'm working with a student, and I tell them to do something, and they're like, I don't think my dog's going to do that, and I say, if you do this, they will, and then the dogs do, and they're like, wow. I didn't know my dog could do that. Melissa Breau: So, the real question is, who's harder to train, the students or the dogs? Barbara Currier: Always the students. The dogs are easy. Melissa Breau: What was it that, kind of, originally attracted you to OMD? Barbara Currier: Well Blitz was 4 years old, when I got introduced to OneMind, and I was really struggling with Blitz, and I was having a very hard time. Our cue rate was extremely low. He was a very, very fast dog. He was very obstacle focused, and I just was really, really struggling with him, and I had never had a dog that I struggled that hard with. I've always been a very successful agility handler, and I was just really starting to doubt myself, and then I was introduced, I went to a seminar, I was introduced into the OneMind system, and immediately it was like Blitz was saying, oh, thank you. Finally, somebody is going to help her. It kind of just like came into place, and after one seminar, I went to a trial, that weekend, wear we hadn't cued in months, I think we came home with four cues, in one weekend, which was unheard of, for us, and that was after one seminar, so then I was really hooked, and then Jaakko and Janita, who are the founders, of OneMind, they did a tour, in the United States, a few years back, and they asked to come to my school, and so we hosted them, and they ended up staying with us. We hosted them for a weekend, and then they had like three weeks off between our place and where they were going next, and so we said, why don't you just stay here, and we'll show you around Georgia, and take you hiking, so they stayed and insisted on working with us every day to thank us for our hospitality, and so having three weeks of pure immersion into the OneMind system, I was completely hooked, and the difference that it made, in Blitz, was just out of control, and Miso is the first dog I've ever had that was trained, from day one, with the OneMind handling system, and the difference in her skill level, going out to start competing and the difference in any dog that I've ever had, has been night and day, and so I just was hook, line, and sinker sucked in. Melissa Breau: So, I want to talk a little bit about the class you have coming up, that kind of include some of those handling methods, so it's called Making It Easy, 12 Commonly Used OneMind Dog Inspired Techniques. Can you just share a little bit about what you will cover in that class? Barbara Currier: Sure. So, the OneMind handling system has 30 different handling techniques, and for the average person, who does AKC, USDAA, you're not going to use all 30 handling techniques. You'll use a lot more as you start getting into the international type handling, but this course will cover the 12 most commonly used techniques that people are going to use weekend to weekend, at their local trials. Melissa Breau: So, what are some of the, I guess, the common sticking points, for handlers, looking to teach those skills. How do you problem solve for some of those issues? Barbara Currier: Basically, one of the things that I see handlers struggle with the most is maintaining connection with their dogs while looking where they need to be going. So, dogs seek out connection with our face, when we're running, and if they can't find that connection, with our face, depending on the dog, they can have different reactions. Some dogs will just stop running through the obstacles and just try to drive around and curl in front of you, to search for your face, some will start dropping bars, some will just find a line and take it, so if we're not connected with our dogs, we also can't see whether they're committing to the correct obstacles and when we need to execute their turn signals, but our body wants us to, through self-preservation, look where we're going, so the hardest thing, for students, is to learn how to run forward, with your head looking back, and be connected with your dog, and see where you're going out of your peripheral vision, so I teach my students to basically go out and get used to running a course while looking behind you, and using your peripheral vision, because everybody has it, but again, it's kind of a brain training thing that the more you use it, the stronger it gets. When I first started doing it, I kind of saw blurry objects, in my peripheral, but I was never comfortable to run a whole course that way, where the more I went out and just practiced running a course, without my dog, and the stronger my peripheral vision got, so I can run full courses now and not worry about running into things, while staying strongly connected to my dogs, so that's probably the thing that I see most people struggle with, and my little games that I've created to help that seems to really help them with that. Melissa Breau: Do you want to talk just, maybe, a little more about which of the OneMind Dog handling techniques are, kind of, included in your class? I know you said the 12 most commonly used ones, but what are some of those? Barbara Currier: So, in the first week, we're going to start off with the most common handling technique that everybody knows, but a lot of people, actually, execute incorrectly, which is the front cross, so everybody probably knows that, but it's also one of the most commonly misused and done incorrectly, so we're tackling that right off the bat, and then we'll move into the forced front cross. Then, into week two, we address the Jaakko Turn and the reverse spin. Melissa Breau: So, for somebody not agility, like, savvy, what is that, the Jaakko turn? Barbara Currier: The Jaakko turn kind of takes the place of the traditional Post Turn, so in the traditional Post Turn as we're rotating around. Our chest laser is opened up to tall of these obstacles that we don't want our dog to take, so as we're rotating our dog, saying, is it that obstacle, is it that obstacle, is it that obstacle, and it's not until we actually get to where we want to go that we say, no, no, it's this one. Where the Jaakko Turn, we get the collection, at the jump, but the dog actually goes around behind our back, so our chest never opens up to all the obstacles we don't want, it's only going to be driving straight to the one obstacle we do want, so it's a really good technique for dogs that are super obstacle focused and really like to scope out lines on their own.   Then the next technique we'll tackle, in week two, is the Reverse Spin, which is, basically, it, sort of, looks like a Jaakko, but it doesn't get you as tight collection as a Jaakko. Your exit line is different, but it's a really good handling move to use if you, say your dog is on a pinwheel, and you want the first and the third jump but not the second jump, out on the pinwheel. By doing a reverse spin, you're going to change the dog's exit line and it's going to create collection for the dog, so you will not get that jump out on their natural path because you created a turn with more collection. It's kind of hard to explain without looking at a map, but. Melissa Breau: Yeah, but still. Barbara Currier: Then, in week three, we're going to look at the Reverse Wrap, which is a tight turn off of the backside of a jump, and Rear Cross, which is another one most everybody is familiar with but often done incorrectly. Week four we will look at a Lap Turn, which is a U-shaped turn that the dog turn happens on the flat, and I use Lap Turns so often, in pulling my dog to, if we're on a course, and the course is sending the dog to the tunnel, but the judge has nicely picked the offside tunnel, for the opening, Lap Turns work so great for that. I also, often, Lap Turn my dog into weave poles, on AKC courses, so that's a great one, and then we're going to move into the Double Lap, which is a Lap Turn to a Front Cross, and create the very tight O-shape turn, on a wing, for a dog. Week five we'll look at the Whisky Turn, which is a very shallow Rear Cross, and we are going to work on the Blind Cross, which I think is one of the most fantastic moves ever, for so many people, especially people that have knee issues because you don't have to deal with rotation, and it keeps you going forward on the line, but there are appropriate places to put Blind Crosses and places where a Front Cross would be a better choice, but not a lot of people understand. Then, week six, we'll work on the German Turn, which is a backside, it's a little hard to explain, it's a backside, almost like to a Serpentine into a Blind Cross, and that's a really fun one to do, and I actually use that one quite a bit, in premiere courses, and kind of the tournament classes in the USDAA classes. Then the Tandem Turn, which is a turn away from the handler, for the dog, on the flat, and that's a really good turn to have if you are on a straightway and you're having trouble getting down, in front of your dog, to do a turn, a Tandem Turn is a really, really handy move to have, especially when it's a straight line to a back side and you just know you're not beating your dog down that line. Melissa Breau: So, it sounds like you're definitely going to cover, kind of, the how to do all of these things. Are you also talking a little bit about when to use each of them, in the course? Barbara Currier: Yes. So, the course will be broken down to, step by step, how to train, on one jump, and then I'm giving them short sequences of three to eight obstacles, where they're going to see where this could fit into a course. Melissa Breau: Is there anything else you think the students, who are kind of trying to decide their classes, because this will go out during October registration, so anything else that students should, maybe, know if they're considering the class? Barbara Currier: Well I think it's important that, you know, and I put in there the pre-requisite for Loretta's class, because this isn't going to be the class where you are going to learn how to sequence one or two obstacles. The dogs, coming in, should know how to do, you know, at least eight obstacles in a row, just meaning jumps and a tunnel, so as long as they have a firm understanding of that, and I would assume that, coming in, they know what a Front Cross is and they know what a Rear Cross is. Beyond that, the other ones are all, you know, not ones that I would expect them to know coming in. Some people may know them, the other stuff, but I would, kind of, hope that everybody knows what a Front Cross and a Rear Cross is because those are the basics and everything, kind of, builds off of those. Melissa Breau: Okay. Excellent. We're getting close to, kind of, the end here, so I want to ask you the three questions that I always as, at the end of an interview. The first one, and I think some of my guests would say this is, probably, the hardest question, but what is the dog related accomplishment that you are proudest of? Barbara Currier: You know, I'm probably proudest of my school, Party of 2. I have a really large student base, here in Georgia, and I am so lucky to have the best students. They are just the greatest group of people, and they always want to push themselves to be better. I throw the craziest stuff at them. If I find a comfort level, I'm always looking how to push people out of it, and they are always willing to rise to the challenge, and they are so supportive of each other. We're like a big, giant family, and everybody is always willing to help anyone out, and I just love it. I'm just super proud of all of my students, at my school. Melissa Breau: Excellent. What is the best piece of training advice that you've ever heard? Barbara Currier: Oh, that's easy. Comparison is the thief of joy, is the best training advice I have ever had, and I remind myself that often. So, basically, not compare yourself to other dog trainers, your dog to other dogs, your dog to your dog's litter mates, or your friend's dog, or your trainer's dogs because, then, it overshadows any progress or triumphs that you made because you're always comparing it to somebody else, and it never feels like enough. Melissa Breau: Then, our last one, here, is who is someone else, in the dog world, that you look up to? Barbara Currier: That's a tough one. I'm not sure I can only pick one. I've have the longest training relationship with my mentor and coach, Tracy Sklenar. She's been my coach for over 10 years, but since I've become involved with OneMind, Jen Pinder and Mary Ellen Barry have been instrumental in my progression and mastering the OneMind handling system, so I would have to say it would be those three amazing, talented ladies that are at the top of my list. Melissa Breau:  Fair enough. Well thank you, so much, for coming on the podcast, Barbara. This has been great. Barbara Currier: Thank you, so much, for having me. I really enjoyed myself. Melissa Breau: Good. Thank you, so much, to our listeners, for tuning in. We'll be back next week, with Loretta Mueller to talk about managing a multi-dog household. As someone who just brought home dog number two, I'm looking forward to talking about skills we can learn and teach our dogs to make life go a little smoother. Don't miss it. If you haven't already, subscribe to our podcast in iTunes, or the podcast app of your choice, to have our next episode automatically downloaded to your phone, as soon as it becomes available. CREDITS: Today's show is brought to you by the Fenzi Dog Sports Academy. Special thanks to Denise Fenzi for supporting this podcast. Music provided royalty-free by BenSound.com; the track featured here is called “Buddy.” Audio editing provided by Chris Lang and transcription written by CLK Transcription Services.

Author: Gretchen Hinson, M.D. Educational Pearls High-Altitude Pulmonary Edema (HAPE) is caused when hypoxemia due to low ambient pO2 leads to breakdown and constriction of the pulmonary vasculature leading to edema. HAPE is very rare under 8000 ft, but common over 10000 ft (6%). Over 18,000 ft the incidence is very high (12-15%). Symptoms include dyspnea, cough, weakness and chest tightness. Signs include hypoxemia, crackles, wheezing, central cyanosis, tachypnea and tachycardia. Drugs that reduce pulmonary resistance have been shown to help, but increased oxygenation and descent are the best treatments. References: http://emedicine.medscape.com/article/300716-overview

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  

De tweede gast van Jelle Tack is de kersvers met Antwerp naar eerste gepromoveerde Tuur Dierckx. Hij laat z'n licht schijnen op zowel PO1 als PO2, maar ook de Europa League en z'n eigen seizoen passeren de revue.

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?

Hey URR Friends! this is the link to my last YouTube video: https://www.youtube.com/watch?v=ZkrMf2wacJE I show evidence that The Clinton's show signs of being under MK Ultra mind control (a satanic ritualistic abuse program that leaves the victims full of demons). Bill once started blankly for an extended period of time ... showing a hypnotic state of mind! You need to realise that the elite use mind control victims in entertainment and politics. It's the easier ways to maintain full control of their puppets! Please share this video! God Bless, STAY VIGILANT & FEAR NO EVIL !!! WATCH MY LATEST BIBLE STUDIES: DO NOT CONFORM TO THIS WORLD !!! https://www.youtube.com/watch?v=PO2-2... How to Draw Near to God https://www.youtube.com/watch?v=VV4-x... WE ARE CALLED TO BE HOLY! SET APART FROM THIS WORLD! https://www.youtube.com/watch?v=Irq1s... TEST YOURSELF TO SEE IF YOU'RE A REAL CHRISTIAN (2 Corinthians 13:5) https://www.youtube.com/watch?v=y8_vn... (NO SEXUAL IMMORALITY, GREED OR IMPURITY) LIVING IN THE LIGHT & FOLLOWING GOD'S EXAMPLE https://www.youtube.com/watch?v=k0ZvZ... The Race War & The Bible (Mark 3:25) https://www.youtube.com/watch?v=ctwR2... Check out My Website - www.TVCFearNoEvil.com SUBSCRIBE TO TVC YouTube Channels: TVC Backup Channel https://www.youtube.com/channel/UCHKH... TVC Biblical Studies Channel Please Subscribe and Join us! https://www.youtube.com/channel/UCPgt... TVC Healthy Living - https://www.youtube.com/channel/UCsjq... Vigilant Christian Music - https://www.youtube.com/channel/UCuzx... The Godly Bros https://www.youtube.com/channel/UCfxy... Come and like us on Facebook @ www.facebook.com/thevigilantchristianmario Follow on Twitter - www.twitter.com/vigilantchrist Instagram @vigilantchristmario URR Radio

You have all of the skills you need to care for an acutely ill infant.  Learn a few pearls to make this a smoother endeavor. The Pediatric Assessment Triangle is a rapid, global assessment tool using only visual and auditory clues to make determinations on three key domains: appearance, work of breathing, and circulation to the skin.  The combination of abnormalities determines the category of pathophysiology: respiratory distress, respiratory failure, CNS or metabolic problem, shock, or cardiopulmonary failure. Appearance "TICLS"Tone - the newborn should have a normal flexed tone; the 6 month old baby who sits up and controls her head; the toddler cruises around the room. Interactiveness - Does the 2 month old have a social smile?  Is the toddler interested in what is going on in the room?  Consolability - A child who cannot be consoled at some point by his mother is experiencing a medical emergency until proven otherwise.  Look/gaze - Does the child track or fix his gaze on you, or is there the "1000-yard stare"? Speech/cry - A vigorously crying baby can be a good sign, when consolable - when the cry is high-pitched, blood-curling, or even a soft whimper, something is wrong.  If the child fails any of the TICLS, then his appearance is abnormal. Work of Breathing Children are respiratory creatures - they are hypermetabolic - we need to key in on any respiratory embarrassment. Look for nasal flaring.   Uncover the chest and abdomen and look for retractions.  Listen - even without a stethoscope - for abnormal airway sounds like grunting or stridor.  Grunting is the child's last-ditch effort to produce auto-PEEP.  Stridor is a sign of critical upper airway narrowing.Look for abnormal positioning, like tripodding, or head bobbing Circulation to the skin Infants and children are vasospastic - they can change their vascular tone quickly, depending on their volume status or environment.  Without even having to touch the child, you can see signs of pallor, cyanosis, or mottling.  If any of these is present, this is an abnormal circulation to the skin. Pattern of Abnormal Arms = Category of Pathophysiology Differential Diagnosis in a Sick Infant: "THE MISFITS"     Trauma - birth trauma, non-accidental - check for a cephalohematoma which does not cross suture lines and feels like a ballotable balloon, as well as for subgaleal hemorrhage, which is just an amorphous bogginess that represents a dangerous bleed.  Do a total body check.     Heart disease or Hypovolemia - is there a history of congenital heart disease? Was there any prenatal care or ultrasound done?  Does this child look volume depleted?     Endocrine Emergencies - Could this be congenital adrenal hyperplasia with low sodium, high potassium, and shock? Look for clitoromegaly in girls, or hyperpigmented scrotum in boys.  Could this be congenital hypothyroidism with poor tone and poor feeding?  Any history of maternal illness or medications? Congenital hyperthyroidism with high output failure?     Metabolic - What electrolyte abnormality could be causing this presentation? Perhaps diGeorge syndrome with hypocalcemia and seizures?      Inborn Errors of Metabolism - there are over 200 inborn errors of metabolism, but only four common metabolic pathways that cause a child to be critically ill.  Searching for an inborn error of metabolism is like looking for A UFO - amino acids, uric acids, fatty acids, organic acids.  If the child's ammonia, glucose, ketones, and lactate are all normal in the ED, then his presentation to the ED should not be explained by a decompensation of an inborn error of metabolism.        Seizures - Neonatal seizures can be notoriously subtle - look for little repetitive movements of the arms, called "boxing" or of the legs, called "bicycling"     Formula problems - Hard times sometimes prompt parents to dilute formula, causing a dangerous hyponatremia, altered mental status, and seizures.  Conversely, concentrated formula can cause hypovolemia     Intestinal disasters - 10% of necrotizing enterocolitis occurs in full-term babies - look for pneumatosis intestinalis on abdominal XR; also think about aganglionic colon or Hirschprung disease; 80% of cases of volvulus occur within the 1st month of life     Toxins - was there some maternal medication or ingestion?  Is there some home remedy or medication used on the baby?  Check a glucose ad drug screen     Sepsis - Saved for last - You'll almost always treat the sick neonate empirically for sepsis - think of congenital and acquired etiologies. Hyperoxia TestThe hyperoxia test is the single most important initial test in suspected congenital heart disease - we can test the child's circulation by his reaction to oxygen on an arterial blood gas.  Place the child on a non-rebreather mask, and after several minutes, perform an ABG.  (Ideally you obtain a preductal ABG in the right upper extremity, and compare that with one on the lower extremity, but this may not be practical.) In a normal circulatory system, the pO2 should be high - in the hundreds - and certainly over 250 torr. This effectively excludes congenital heart disease as a factor.  If the pO2 on supplemental oxygen is less than 100, then this is extremely predictive of hemodynamically significant congenital heart disease.  Between 100 and 250, you have to make a judgement call, and I would side on worst first. If you are giving this child 100% O2, and he doesn't improve 100% -- that is, his ABG is not at least 100 - then he has congenital heart disease until proven otherwise.  Give prostaglandin if the patient is less than 4 weeks old (typical presentation is within the first 1-2 weeks of life).  Start at 0.05 mcg/kg/min.  PGE keep the systemic circulation supplied with some mixed venous blood until either surgery or palliation is decided.  Summary Points* When you see a sick infant, keep THE MISFITS around to keep you out of trouble.* Before you decide on sepsis, ask yourself, could this be a cardiac problem?* When in doubt, perform the hyperoxia test.* All the rest, you have time to look up. Before You Go: The Availability HeuristicSelected References Brousseau T, Sharieff GQ. Newborn Emergencies: The First 30 Days of Life. Pediatr Clin N Am. 2006; 53:69-84. Cloherty JP, Eichenwald EC, Stark AR: Manual of Neonatal Care, 5th edition. Philadelphia, PA, Lipincott Williams & Wilkins, 2004. Horeczko T, Young K: Congenital Heart Disease, in Pediatric Emergency Medicine-A Comprehensive Study Guide, 4th Ed. ACEP/McGraw-Hill, 2013. McGowan et al. Part 15: Neonatal Resuscitation: 2010 American Heart Association Guidelines. Circulation. 2010;122:S909-S919. Okada PJ, Hicks B. Neonatal Surgical Emergencies. Clin Ped Emerg Med. 2002; 3:3-13.

Click to Subscribe to All Ben's Fitness & Get A Free Surprise Gift from Ben. Click here for the full written transcript of this podcast episode. Do you have a future podcast question for Ben? Call toll free to 1-877-209-9439, Skype to "pacificfit" or scroll down on this post to access the free "Ask Ben" form...   In this October 19, 2011 free audio episode: Why fat is good, how to exhale when swimming, preventing cramps in high school athletes, are boot camps enough for strength, DMAE supplements, what happens when you taper, the difference between prebiotics and probiotics, is it normal to gain weight in the winter?, what should your partial pressure of oxygen be? Remember, if you have any trouble listening, downloading, or transferring to your mp3 player just e-mail ben@bengreenfieldfitness.com And don't forget to leave the podcast a ranking in iTunes - it only takes 2 minutes of your time and helps grow our healthy community! Just click here to go to our iTunes page and leave feedback. ----------------------------------------------------- Special Announcements: -New Podcast Hashtag contest! Get your tweet read on the next podcast episode with our new Fitness Hashtag contest! Just use Twitter to tell me who I should interview on the show and why, in 140 characters or less. To have your Hashtag read on the show, you need to use this format: @bengreenfield ________________________________________ #podcastguest -Vote for the BenGreenfieldFitness podcast for the Podcast Awards at http://www.podcastawards.com -The BenGreenfieldFitness gear and clothing store is now LIVE! Click here to get triathlon uniforms, tech pants and coat, hats and more - all emblazoned with Ben Greenfield's "Fire & Water" tattoo! -Click here to donate $1 to keep this podcast going! -Wed, November 2, noon Pacific time: Live Q&A With Ben, during which you can ask any of your questions about Ben's consulting services. Just come right back here at 12:00PST on Wednesday: http://InstantTeleseminar.com/?eventid=23580678 -BenGreenfieldFitness Inner Circle is now just $1 for a 14 Day Sneak Peek! Click here to join now. - Get insider VIP tips and discounts from Ben - conveniently delivered directly to your phone! Just complete the information below... First Name Last Name Email Cell # (1+area code) --------------------------------------------------------------- Featured Topic: Why Fat Is Good, How We've Been Lied To About The Obesity Epidemic, And How To Be A Fat Head. Have you seen the news stories about fat in fast food and the obesity epidemic? Did you see Morgan Spurlock's movie "Super Size Me"? Then guess what ... You've been fed a load of bologna. In this interview, comedian, author and speaker  Tom Naughton replies to the Super Size Me crowd by talking about how he lost weight on a fat-laden fast-food diet that included double quarter-pounders and fried chicken. He points out that nearly everything we've been told about obesity and healthy eating is wrong, and why fat is good. Here's a link to Fat Head on Hulu - or you can buy the Fat Head DVD on Amazon. --------------------------------------------------------------- Listener Q&A: Prior to asking your question, PLEASE be considerate and do a search in upper right hand corner of this website for the keywords associated with your question. 90% of the questions we receive have already been asked and answered here at BenGreenfieldFitness.com! ====================================== [contact-form-7 id="6222" title="Ask Ben"]====================================== Jeff has a call-in question about how to exhale when swimming. A listener has a call-in question about cramping in highschool football players. In my response, I recommend listening to this episode about muscle cramping with David Warden from TriTalk. Marcy asks: I just started a boot camp class 3 days a week. It's very hard. I'm not sure I've ever sweat that much. It's showing me that I'm not in as good shape as I thought. But I'm hanging in there. Would you say that that is enough resistance training. There are days that I am quite sore. Or should I add some gym days in between. Lia Marley asks: What are your thoughts on taking the supplement, DMAE? What are the benefits? I've heard that it can help with soreness and stiffness after working out. Glenn asks: Ben, i am training for my first marathon in 3 weeks. I understand some thing about the taper period, but i think i have heard you talk about the loss in fitness level during the taper. What really is going on physiologically during a proper taper? Surely it is more than "rest"? and, more importantly, what kind of GAINS are still available (strength, time to exhaustion, fat burning efficiency, etc.) to me in the next 2 weeks? Alex asks: Hi Ben. I heard you mention pro-biotics a few times but there's this supplement I was planing on buying that contains pre-biotics and they expressly mention it's not pro-biotics. What is the difference and which one is the preferred one? In my response to Alex, I mention Enerprime and Caprobiotics. Paul asks: I'm 5-foot-6 and weight about 150 pounds and I'd like to drop about five pounds by the time the next tri season rolls around. I've found it difficult to drop weight during the tri season, mostly because I don't want to short-change my nutrition while training hard. Now that the tri season is over, do you think it's a better idea to give my body a break and let it naturally pack on a couple of extra pounds over the winter (as it generally would) and then slim down to my new race weight as the next tri season approaches? Or would it be more effective to start slimming down now when I don't have the same nutritional needs as when I'm gearing up for a new season (or in the middle of the season)? Dave asks: I have been using the Restwise software that you discussed. My PO2 is usually in the 94-95% range. Recently had an unplanned ambulance ride and they measured PO2 @ 93. They were very surprised that it was that low. What do the numbers mean and is there an effective way to increase them. The EMT, knowing that I am a competitive athlete, thought it should be around 98%. In my response to Dave, I mention "Floradix" and also this episode with Restwise. -------------------------------------------- Remember, if you have any trouble listening, downloading, or transferring to your mp3 player just e-mail ben@bengreenfieldfitness.com And don't forget to leave the podcast a ranking in iTunes - it only takes 2 minutes of your time and helps grow our healthy community! 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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.

Diver Deaths on USCGC HEALY. In August of  2006, the US Coast Guard Cutter Healy (WAGB-20) was on Arctic Patrol. Military divers. Lt. Jessica Hill and  PO2 Stephen Duque died during Arctic Ocean diving operations. After reading the after action reports, Joe Cocozza gives his expert opinion and analysis of the incident. The USCG report is here for download http://www.uscg.mil/foia/Healy/HealyFDL.pdf

In der vorliegenden, randomisierten und verblindeten Studie wurden die Effekte von PerflubronTM 60% als Supplement zur konventionellen Volumentherapie des hämorrhagischen Schocks auf Sauerstofftransport und Gewebeoxygenierung untersucht. Die Studie wurde am experimentellen Modell des splenektomierten, narkotisierten Hundes durchgeführt. Nach der chirurgischen Präparation und einer Stabilisierungsphase erfolgte die Induktion eines hämorrhagischen Schocks mittels Blutentzug bis zu einem Mittleren Arteriellen Druck von 45 mmHg. Das Modell war über die im Verlauf der Hypotension eingegangene Sauerstoffschuld standardisiert, die definierte Schocktiefe war mit 120 ml/kg KG eingegangener Sauerstoffschuld erreicht. Durch Randomisierung erfolgte die Zuordnung der Tiere in zwei Gruppen. In der HES-Gruppe wurde das entzogene Blutvolumen normovolämisch mit 6% HES 200000 ersetzt. In der PFC-Gruppe wurden 2,7 g/kg KG PerflubronTM 60% infundiert und die verbleibende Differenz zum entzogenen Blutvolumen mit 6% HES 200000 ersetzt. Ab dem Therapiezeitpunkt wurden die Tiere beider Gruppen mit 100% O2 beatmet. Messungen fanden nach der Stabilisierungsphase, im Schock, direkt nach Therapie, sowie 30, 60 und 180 Minuten nach Therapie statt. Für die vorliegende Arbeit wurden die Parameter des systemischen Sauerstofftransportes und der Gewebeoxygenierung unter besonderer Berücksichtigung der regionalen, intestinal-mukosalen Situation untersucht. Weiterhin umfaßten die Messungen hämodynamische Werte, sowie Parameter zu Myokardfunktion und –oxygenierung. Die Ergebnisse der vorliegenden Arbeit lassen sich wie folgt zusammenfassen: Die Messungen zu systemischem Sauerstofftransport und Gewebeoxygenierung zeigten, daß der arterielle Sauerstoffpartialdruck in der PFC-Gruppe aufgrund der verbesserten Löslichkeit von Sauerstoff in Plasma signifikant stärker anstieg als in der HES-Gruppe. Der Plasmaanteil am Sauerstoffangebot war in der PFC-Gruppe um 20% höher als in der HES-Gruppe und führte zu einem höheren systemischen Sauerstoffangebot. Dies ermöglichte in der PFC-Gruppe einen höheren Sauerstoffverbrauch der Tiere und als Zeichen einer verbesserten Gewebeoxygenierung eine temporäre Senkung der Sauerstoffschuld. Die Messung des Gewebesauerstoffpartialdruckes auf der intestinalen Mukosaoberfläche ergab in der PFC-Gruppe einen um 4-8 mmHg höheren Medianwert des PO2 als in der HES-Gruppe bis 60 Minuten nach Therapie. Insbesondere fanden sich in der PFC-Gruppe signifikant weniger hypoxische Werte. Die PFC-Supplementierung führte in der vorliegenden Studie zu keinem relevanten Unterschied in der Überlebenszeit. Aufgrund der nur initial durchgeführten Therapie starben alle Tiere als Folge von kapillären Flüssigkeitsverlusten im kardialen Versagen. Unsere Studie zeigt, daß durch die Supplementierung der konventionellen Volumentherapie des hämorrhagischen Schocks mit PerflubronTM 60% eine temporäre Verbesserung des Sauerstofftransportes und der Gewebeoxygenierung erzielt werden kann. Durch den Einsatz von PerflubronTM 60% in der prähospitalen Therapie könnten daher theoretisch die Letalität und die Spätfolgen des hämorrhagischen Schocks gesenkt werden.

Die vorliegende Arbeit ist Teil eines wissenschaftlichen Kooperationsprojektes zwischen der Frauenklinik vom Roten Kreuz in München und der Klinik für Strahlentherapie und radiologische Onkologie am Klinikum rechts der Isar der Technischen Universität München. Ziel des Gesamtprojektes ist es den prädiktiven Wert für das Tumoransprechen auf primär systemische Chemotherapie von pO2 in malignen Mammatumoren zu bestimmen und seine Abhängigkeit von Serumhämoglobin, dem p53-Status und dem VEGF-Status zu untersuchen. In dieser Arbeit wurde der Zusammenhang zwischen dem intratumoralen Sauerstoffpartialdruck und dem VEGF-Status untersucht. Hierzu wurde das von 95 primären Mammakarzinomen stanzbiobtisch gewonnene Gewebe immunhistochemisch untersucht und die VEGF-Gewebeexpression bestimmt. Schließlich konnte, aus 109 ausgewerteten Sauerstoffmessungen und aus 95 bestimmten VEGF-Gewebeexpression, bei 77 Patientinnen sowohl Ergebnisse der Sauerstoffmessungen als auch der VEGF-Bestimmung zueinander in Beziehung gesetzt und statistisch ausgewertet werden. Zusätzlich wurden sowohl die pO2-Werte als auch der VEGF-Status mit den sog. klassischen Prognosefaktoren des Mammakarzinoms in Relation gesetzt. Hier wurden die gewonnen Werte mit dem Alter, der Tumorgröße, dem Nodalstatus, dem Grading und dem Hormonrezeptorstatus des untersuchten Patientinnenkollektivs zu einander in Beziehung gesetzt. Die der Arbeit zugrunde liegende Annahme war, dass, durch die Gewebehypoxie induzierte Hif-1 alpha Protein-Ausschüttung bedingte Steigerung der VEGF-Gewebeexpression, hypoxische Tumore einen gegenüber normoxischen Geweben erhöhten VEGF-Status haben müssten. Es konnte jedoch kein statistisch signifikanter Zusammenhang zwischen dem Oxygenierungsstatus und der VEGF-Gewebeexpression bei primären Mammakarzinomen nachgewiesen werden. Lediglich wurde eine statistisch nicht signifikante Verminderung in anoxischen Geweben von VEGF-positiven Tumoren nachgewiesen. Die erziehlten Ergebnisse entsprechen zwar nicht den Erwartungen, dennoch kann gefolgert werden, dass der intratumorale pO2 und die VEGF-Gewebeexpression voneinander unabhängige Faktoren sind, von denen jeder für sich, wie aus der Literatur bekannt ist, mit einer schlechten Prognose vergesellschaftet ist. Auch konnte keine Assoziation mit den klassischen Prognosefaktoren nachgewiesen werden.

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.

The contrast between resistance to ischemia and ischemic lesions in peripheral nerves of diabetic patients was explored by in vitro experiments. Isolated and desheathed rat peroneal nerves were incubated in the following solutions with different glucose availability: 1) 25 mM glucose, 2) 2.5 mM glucose, and 3) 2.5 mM glucose plus 10 mM 2-deoxy-D-glucose. Additionally, the buffering power of all of these solutions was modified. Compound nerve action potential (CNAP), extracellular pH, and extracellular potassium activity (aKe) were measured simultaneously before, during, and after a period of 30 min of anoxia. An increase in glucose availability led to a slower decline in CNAP and to a smaller rise in aKe during anoxia. This resistance to anoxia was accompanied by an enhanced extracellular acidosis. Postanoxic recovery of CNAP was always complete in 25 mM HCO3(-)-buffered solutions. In 5 mM HCO3- and in HCO3(-)-free solutions, however, nerves incubated in 25 mM glucose did not recover functionally after anoxia, whereas nerves bathed in solutions 2 or 3 showed a complete restitution of CNAP. We conclude that high glucose availability and low PO2 in the combination with decreased buffering power and/or inhibition of HCO3(-)-dependent pH regulation mechanisms may damage peripheral mammalian nerves due to a pronounced intracellular acidosis.