Podcasts about do2

Hey There Listeners! This week's episode piggy backs off of last week's, where we talked about WHEN your child should be reading. This week, we are going to talk about WHAT your child should be reading. So many parents come to us and ask for great book recommendations. The market for children's books is incredibly saturated. How do you know what will be a stay-up-all-night-until-I-finish-it book versus a gather-dust-on-the-shelf book? We have read thousands of children's books, in the classroom, at home with our children, and in our Enriched offices with our students. We know what gets a little person's engine going and have culled together a list of best reads for ages 5-10…just in time for the holidays! Consider this our gift: You can give just the right book - the gift that keeps on giving - and put it into the hands of your little ones with just a few short clicks below. That's right, not only do we tell you about each read we recommend in the pod, but we've linked access to the books mentioned in this episode in our show notes. Yes, we love you that much.   Listen to find out about some amazing page turners!   Episode reading list:   Penguin Young Readers: https://www.penguin.com/static/pages/youngreaders/levels/ Henry and Mudge Series: https://www.simonandschuster.com/books/Henry-and-Mudge-The-Complete-Collection/Cynthia-Rylant/Henry-Mudge/9781534427136 James Marshall Fox Books: https://www.amazon.com/Friends-Penguin-Young-Readers-Level/dp/0140370072 Bunnicula Early Readers: https://www.amazon.com/Vampire-Bunny-Bunnicula-Friends/dp/0689857497 Oliver and Amanda Pig Series: https://www.penguinrandomhouse.com/series/DS1/oliver-and-amanda Froggy Series: https://www.penguinrandomhouse.com/series/DO2/froggy Cam Jansen Series: https://www.camjansen.com/ Cowgirl Kate and Cocoa Series: https://www.amazon.com/Cowgirl-Kate-Cocoa-Erica-Silverman/dp/0152056602 Frances Learn to Read Series: https://www.amazon.com/Bargain-Frances-Can-Read-Level/dp/006444001X Ivy and Bean Series: http://anniebarrows.com/kids-home/ivy-bean/ Heidi Hecklebeck Series: https://www.simonandschuster.com/series/Heidi-Heckelbeck Dory Fantasmagory Series: https://www.penguinrandomhouse.com/series/DYY/dory-fantasmagory Judy Moody Series: https://judymoody.com/ Mery Watson Series: https://www.mercywatson.com/ Roald Dahl Series: https://www.roalddahl.com/global/roald-dahl-titles Beverly Cleary Book List: https://www.bookseriesinorder.com/beverly-cleary/ Andrew Clements Series: https://www.andrewclements.com/books Louis Sacher Wayside School Books: https://www.amazon.com/Complete-Wayside-School-Set-Books/dp/B0164E33OU Who Was Book Series: https://www.whowasbookseries.com/who-was/

Freunde der Qualität, wir begrüßen Euch zu unserer 9. Podcast-Ausgabe! Christian Brandes, Team Lead Requirements Engineering bei QualityMinds, tauscht sich mit seiner Kollegin Rebecca Schönberger darüber aus, wie ein „agiles RE“ konkret aussehen könnte und sollte, was man damit erreichen kann und warum so viele Projekte und Unternehmen mit diesem Thema offenbar immer noch so große Schwierigkeiten haben. Viel Spaß dabei! Sprecher: Christian Brandes: www.xing.com/profile/Christian_Brandes11 Rebecca Schönberger: www.xing.com/profile/Rebecca_Schoenberger Ressourcen online: Christians Folien auf der ModernRE-Konferenz 2018: www.modern-re.de/files/modernre/site/vortraege2018/tag3/Do2.3_Christian_Brandes-ModernRE2018_Brandes_AgilesRE.pdf User Stories sind keine Requirements: www.scrumexpert.com/knowledge/user-stories-are-not-requirements/ https://jaxenter.de/scrum-user-stories-78154 Ron Jeffries’ CCC-Prinzip: http://ronjeffries.com/xprog/articles/expcardconversationconfirmation/ Product-Canvas-Beispiel: www.romanpichler.com/blog/the-product-canvas/ Agile Testing Quadrants: lisacrispin.com/2011/11/08/using-the-agile-testing-quadrants/ Über QualityMinds: www.qualityminds.de twitter.com/qualitymindsde Feedback & Themenwünsche an: Zu dieser Folge: requirements@qualityminds.de

In today's VETgirl online veterinary continuing education podcast, we review the incidence of hospital-acquired anemia in the hospitalized canine and feline patient. In the veterinary patient, the presence of anemia results in decreased oxygen carrying capacity, which directly affects all tissues by diminishing function and impairing tissue healing. It other words, it results in decreased oxygen deliver (DO2).

In today's VETgirl online veterinary continuing education podcast, we review the incidence of hospital-acquired anemia in the hospitalized canine and feline patient. In the veterinary patient, the presence of anemia results in decreased oxygen carrying capacity, which directly affects all tissues by diminishing function and impairing tissue healing. It other words, it results in decreased oxygen deliver (DO2).

Danfoss ERC 213 Timestamps: 10:30 – Key Features 10:41 – Voltage Protection 10:56 – Compressor Protection 14:43 – Applications 15:15 – App 0 No predefined application 15:28 – App 1 Medium temperature ventilated refrigeration units with timed natural defrost 15:52 – App 2 Medium temperature ventilated refrigeration units with timed electrical defrost 16:03 – App 3 Low temperature ventilated refrigeration units with timed electrical defrost 16:13 – App 4 Medium temperature ventilated refrigeration units with electrical defrost (by temperature) 16:26 – App 5 Low temperature ventilated refrigeration units with electrical defrost (by temperature) 16:37 – App 6 No predefined application with simplified list of parameters 19:45 – Sensors 22:06 – Basic Groups of Parameters 23:09 – r-- Thermostat 23:12 – r00 Temperature setpoint 23:24 – r01 Differential 23:32 – r02 Min setpoint limitation and r03 Max setpoint limitation 24:02 – r04 Display offset 25:19 – r05 Display Unit (°C/°F) 25:33 – r09 Calibration of Sair 25:47 – r12 Main switch 27:17 – r13 Night set back 27:48 – r40 Thermostat reference displacement (offset temperature) 28:30 – r96 Pull-down duration and r97 Pull-down limit temperature 29:06 – A-- Alarms 29:13 – A03 Delay for temperature alarm during normal conditions 30:15 – A12 Delay for temperature alarm during pull-down/start-up/defrost 31:00 – A13 High temperature alarm limit (Cabinet/Room) 31:34 – A14 Low temperature alarm limit 31:55 – A27 DI1 delay and A28 DI2 delay 32:17 – A37 Condenser high alarm limit 32:41 – A54 Condenser high block limit 33:45 – A72 Voltage protection enable 34:03 – A73 Minimum cut-in voltage and A74 Minimum cut-out voltage 35:04 – A75 Maximum Voltage 37:37 – d-- Defrost 37:49 – d01 Defrost method 38:32 – d02 Defrost stop temperature 38:50 – d10 Defrost stop sensor 40:51 – d03 Defrost interval 41:16 – d04 Max defrost time 43:38 – d05 Defrost delay at power up (or DI signal) 44:29 – d06 Drip delay 44:49 – d07 Fan delay after defrost 45:49 – d08 Fan start temperature after defrost 47:21 – d09 Fan during defrost 47:40 – d10 Defrost stop sensor (part II) 48:16 – d18 Compressor accumulated runtime to start defrost 50:04 – d19 Defrost on demand 53:26 – d30 Defrost delay after pull-down 53:53 – F-- Fan control 54:03 – F01 Fan at compressor cutout 55:00 – F04 Fan stop evaporator temperature 55:51 – F07 Fan ON cycle and F08 Fan OFF cycle 56:28 – c-- Compressor 56:37 – c01 Compressor minimum ON time 56:47 – c02 Compressor minimum OFF time 57:01 – c04 Compressor OFF delay at door open 57:51 – c70 Zero crossing selection 58:22 – o-- Others 58:37 – o01 Delay of outputs at startup 59:11 – o02 DI1 configuration 1:01:36 – o05 Password 1:02:08 – o06 Sensor type selection 1:02:27 – 015 Display resolution 1:03:31 – o23 Relay 1 counter, o24 Relay 2 counter and 025 o24 Relay 3 counter 1:04:13 – o37 DI2 configuration 1:04:52 – o61 DI2 configuration 1:05:07 – o67 Save settings as factory 1:05:39 – o71 DO2 config 1:06:23 – o91 Display at defrost 1:07:04 – P-- Polarity 1:07:06 – P73 DI1 input polarity and P74 DI2 input polarity 1:07:32 – P75 Invert alarm relay 1:07:59 – P76 Keyboard lock enable 1:08:21 – u-- Readouts 1:08:30 – u00 Controller Status 1:09:37 – u01 Air temperature (Sair) 1:10:12 – u58 Compressor relay status, u59 Fan relay status, u60 Defrost relay status and u63 Light relay status

Do we recognize shock early enough? How do we prioritize our interventions? How can we tell whether we’re making our patient better or worse?   World wide, shock is a leading cause of morbidity and mortality in children, mostly for failure to recognize or to treat adequately. So, what is shock? Simply put, shock is the inadequate delivery of oxygen to your tissues.  That’s it.  Our main focus is on improving our patient’s perfusion. Oxygen delivery to the tissues depends on cardiac output, hemoglobin concentration, the oxygen saturation of the hemoglobin you have, and the environmental partial pressure of oxygen. At the bedside, we can measure some of these things, directly or indirectly.  But did you notice that blood pressure is not part of the equation?  The reason for that is that blood pressure is really an indirect proxy for perfusion – it’s not necessary the ultimate goal. The equation here is a formality: DO2 = (cardiac output) x [(hemoglobin concentration) x SaO2 x 1.39] + (PaO2  x 0.003)     Shock CAN be associated with a low blood pressure, but shock is not DEFINED by a low blood pressure.     Compensated Shock: tachycardia with poor perfusion.  A child compensates for low cardiac output with tachycardia and a increase in systemic vascular resistance.     Decompensated Shock: frank hypotension, an ominous, pre-arrest phenomenon.   Shock is multifactorial, but we need to identify a primary cause to prioritize interventions.     How they "COHDe": Cardiogenic, Obstructive, Hypovolemic, and Distributive.   Cardiogenic Shock All will present with tachycardia out of proportion to exam, and sometimes with unexplained belly pain, usually due to hepatic congestion.  The typical scenario in myocarditis is a precipitous decline after what seemed like a run-of-the-mill URI. Cardiogenic shock in children can be from congenital heart disease or from acquired etiologies, such as myocarditis.  Children, like adults, present in cardiogenic shock in any four of the following combinations: warm, cold, wet, or dry. "Warm and Dry" A child with heart failure is “warm and dry” when he has heart failure signs (weight gain, mild hepatomegaly), but has enough forward flow that he has not developed pulmonary venous congestion.  A warm and dry presentation is typically early in the course, and presents with tachycardia only. "Warm and Wet" If he worsens, he becomes “warm and wet” with pulmonary congestion – you’ll hear crackles and see some respiratory distress.  Infants with a “warm and wet” cardiac presentation sometimes show sacral edema – it is their dependent region, equivalent to peripheral edema as we see in adults with right-sided failure. “Warm” patients – both warm and dry and warm and wet -- typically have had a slower onset of their symptoms, and time to compensate partially. Cool patients are much sicker. "Cold and Dry” A patient with poor cardiac output; he is doing everything he can to compensate with increased peripheral vascular resistance, which will only worsen forward flow.  Children who have a “cold and dry” cardiac presentation may have oliguria, and are often very ill appearing, with altered mental status. "Cold and Wet" The sickest of the group, this patient is so clamped down peripherally that it is now hindering forward flow, causing acute congestion, and pulmonary venous back-up.  You will see cool, mottled extremities. Cardiogenic Shock: Act Use point-of-care cardiac ultrasound: Good Squeeze? M-mode to measure fractional shortening of the myocardium or anterior mitral leaflet excursion. Pericardial Effusion? Get ready to aspirate. Ventricle Size? Collapsed, Dilated, Careful with fluids -- patients in cardiogenic shock may need small aliquots, but go quickly to a pressor to support perfusion Pressor of choice: epinephrine, continuous IV infusion: 0.1 to 1 mcg/kg/minute.  Usual adult starting range will end up being 1 to 10 mcg/min. Avoid norepinephrine, as it increases systemic vascular resistance, may affect afterload Just say no to dopamine: increased mortality when compared to epinephrine   Obstructive Shock Mostly one of two entities: pulmonary embolism or cardiac tamponade. Pulmonary embolism in children is uncommon – when children have PE, there is almost always a reason for it – it just does not happen in normal, healthy children without risk factors. Children with PE will either have a major thrombophilic comorbidity, or they are generously sized teenage girls on estrogen therapy. Tamponade -- can be infectious, rheumotologic, oncologic, or traumatic.  It’s seen easily enough on point of care ultrasound.  If there is non-traumatic tamponade physiology, get that spinal needle and get to aspirating. Obstructive Shock: Act Pulmonary embolism (PE) with overt shock: thrombolyse; otherwise controversial.  PE with symptoms: heparin. Tamponade: if any sign of shock, pericardiocentesis, preferentially ultrasound-guided.   Hypovolemic Shock The most common presentation of pediatric shock; look for decreased activity, decreased urine output, absence of tears, dry mucous membranes, sunken fontanelle.  May be due to obvious GI losses or simply poor intake. Rapid reversal of hypovolemic shock: may need multiple sequential boluses of isotonic solutions. Use 10 mL/kg in neonates and young infants, and 20 mL/kg thereafter. Hypovolemic Shock: Act Tip: in infants, use pre-filled sterile flushes to push fluids quickly.  In older children, use a 3-way stop cock in line with your fluids and a 30 mL syringe to "pull" fluids, turn the stop cock, and "push them into the patient. Titrate to signs of perfusion, such as an improvement in mental status, heart rate, capillary refill, and urine output. When concerned about balancing between osmolality, acid-base status, and volume status, volume always wins.  Our kidneys are smarter than we are, but they need to be perfused first.   Distributive Shock The most common cause of distributive shock is sepsis, followed by anaphylactic, toxicologic, adrenal, and neurogenic causes.  Septic shock is multifactorial, with hypovolemic, cardiogenic, and distributive components. Children with sepsis come in two varieties: warm shock and cold shock. Distributive Shock: Act Warm shock is due to peripheral vascular dilation, and is best treated with norepinephrine. Cold shock is due to a child’s extreme vasoconstriction in an attempt to compensate.  Cold shock is the most common presentation in pediatric septic shock, and is treated with epinephrine. Early antibiotics are crucial, and culture everything that seems appropriate.   Shock: A Practical Approach   "How FAST you FILL the PUMP and SQUEEZE" Sometimes things are not so cut-and-dried.  We'll use a practical approach to diagnose and intervene simultaneously. Look at 4 key players in shock: heart rate, volume status, contractility, and systemic vascular resistance. How FAST you FILL the PUMP and SQUEEZE First, we look at heart rate -- how FAST? Look at the heart rate – is it sinus?  Could this be a supraventricular tachycardia that does not allow for enough diastolic filling, leading to poor cardiac output?  If so, use 1 J/kg to synchronize cardiovert.  Conversely, is the heart rate too slow – even if the stroke volume is sufficient, if there is severe bradycardia, then cardiac output  -- which is in liters/min – is decreased.  Chemically pace with atropine, 0.01 mg/kg up to 0.5 mg, or use transcutaneous pacing. If the heart rate is what is causing the shock, address that first. Next, we look at volume status. How FAST you FILL the PUMP and SQUEEZE Look to FILL the tank if necessary.  Does the patient appear volume depleted?  Try a standard bolus – if this improves his status, you are on the right track. Now, we look at contractility. How FAST you FILL the PUMP and SQUEEZE Is there a problem with the PUMP?  That is, with contractility?  Is this in an infarction, an infection, a poisoning?  Look for signs of cardiac congestion on physical exam.  Put the probe on the patient’s chest, and look for effusion.  Look to see if there is mild, moderate, or severe decrease in cardiac contractility.  If this is cardiogenic shock – a problem with the pump itself -- begin pressors. And finally, we look to the peripheral vascular resistance. How FAST you FILL the PUMP and SQUEEZE Is there a problem with systemic vascular resistance – the SQUEEZE? Look for signs of changes in temperature – is the patient flushed?  Is this an infectious etiology?  Are there neurogenic or anaphylactic concerns?  After assessing the heart rate, optimizing volume status, evaluating contractility, is the cause of the shock peripheral vasodilation?  If so, treat the cause – perhaps this is a distributive problem due to anaphylaxis.  Treat with epinephrine. The diagnosis of exclusion in trauma is neurogenic shock.  Perhaps this is warm shock, both are supported with norepinephrine.  All of these affect systemic vascular resistance – and the shock won’t be reversed until you optimize the peripheral squeeze.   Summary The four take-home points in the approach to shock in children To prioritize your innterventions, remember how patients COHDe: Cardiogenic, Obstructive, Hypovolemic, and Distributive. Your patient's shock may be multifactorial, but mentally prioritize what you think is the MAIN case of the shock, and deal with that first. To treat shock, remember: How FAST You FILL The PUMP and SQUEEZE: Look at the heart rate – how FAST.  Look at the volume status – the FILL.  Assess cardiac contractility – the PUMP, and evaluate the peripheral vascular tone – the SQUEEZE. In pediatric sepsis, the most common type is cold shock – use epinephrine (adrenaline) to get that heart to increase the cardiac output. In adolescents and adults, they more often present in warm shock, use norepinephrine (noradrenaline) for its peripheral squeeze to counteract this distributive type of shock. Rapid-fire word association: Epinephrine for cardiogenic shock Intervention for obstructive shock Fluids for hypovolemic shock Norepinephrine for distributive shock References Agha BS, Sturm JJ, Simon HK, Hirsh DA. Pulmonary embolism in the pediatric emergency department. Pediatrics. 2013 Oct;132(4):663-7. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013; 41:580-637. Jaff MR et al. for the American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; American Heart Association Council on Peripheral Vascular Disease; American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011; Apr 26;123(16):1788-830. Levy B et al. Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study. Crit Care Med. 2011; 39:450. Micek ST, McEvoy C, McKenzie M, Hampton N, Doherty JA, Kollef MH. Fluid balance and cardiac function in septic shock as predictors of hospital mortality. Crit Care. 2013; 17:R246. Osman D, Ridel C, Ray P, et al. Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge. Crit Care Med. 2007; 35:64-8. Ventura AM, Shieh HH, Bousso A, Góes PF, de Cássia F O Fernandes I, de Souza DC, Paulo RL, Chagas F, Gilio AE. Double-Blind Prospective Randomized Controlled Trial of Dopamine Versus Epinephrine as First-Line Vasoactive Drugs in Pediatric Septic Shock. Crit Care Med. 2015;43(11):2292-302. This post and podcast are dedicated to Natalie May, MBChB, MPHe, MCEM, FCEM for her collaborative spirit, expertise, and her super-charged support of #FOAMed.  You make a difference.  Thank you. Undifferentiated Shock Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP