Podcasts about pressors

We know what to do with the patient who is sick and hypotensive.  But what about the patient who is sick but not hypotensive?  Or the patient who is hypotensive but not sick?References for the papers mentioned in the podcast on use of midodrine in the ED:Puissant et al (2022). Wait, What? Oral Midodrine Instead of Pressors for Septic Shock? Annals of Emergency Medicine;80(4):S94Zada et al (2024). Midodrine in Early Septic Shock. Critical Care Medicine 52(1):S708Lal et al (2021). Oral Midodrine Administration During the First 24 Hours of Sepsis to Reduce the Need of Vasoactive Agents: Placebo-Controlled Feasibility Clinical Trial. Critical Care Explorations 3(5):e0382Additional content and educational resources at ICUedu.org

Episode 35! In this episode we talk about extubation practices with "Effect of aggressive vs conservative screening and confirmatory test on time to extubation among patients at low or intermediate risk: a randomized clinical trial" published in Intensive Care Medicine by Hernandez et al. We then talk about an observation study by Zarrabian et al published in the Blue Journal "Liberation from Invasive Mechanical Ventilation with Continued Receipt of Vasopressor Infusions".SPEED UP: https://pubmed.ncbi.nlm.nih.gov/38353714/Extubation on Pressors: https://pubmed.ncbi.nlm.nih.gov/35107416/If you enjoy the show be sure to like and subscribe, leave that 5 star review! Be sure to follow us on the social @icucast for the associated figures, comments, and other content not available in the audio format! Email us at icuedandtoddcast@gmail.com with any questions or suggestions! Thank you Mike Gannon for the intro and exit music!

In this episode we discuss whether the concept of having a "max dose" of your pressor has any evidence or physiological backing. Joining me in this discussion are Dan Rauh, Shane O'Donnell, and Shad Ruby.  

Episode 22! In this episode we talk about "Peripheral Administration of Norepinephrine: A Prospective Observational Study" published August 2023 by Yerke et al in CHEST. For our old article we talk about "Effect of midodrine versus placebo on time to vasopressor discontinuation in patients with persistent hypotension in the intensive care unit (MIDAS)" by Santer et al published October 2020 by Santer et al.No mailbag this time, we recorded this episode ahead of time to account for travel schedules.Peripheral Pressors: https://pubmed.ncbi.nlm.nih.gov/37611862/MIDAS: https://pubmed.ncbi.nlm.nih.gov/32885276/Be sure to follow us on the social @icucast for the associated figures, comments, and other content not available in the audio format! Email us at icuedandtoddcast@gmail.com with any questions or suggestions! Thank you Mike Gannon for the intro and exit music!

The JournalFeed podcast for the week of Oct 2-6, 2023.These are summaries from just 2 of the 5 article we cover every week! For access to more, please visit JournalFeed.org for details about becoming a member.Tuesday Spoon Feed:This prospective observational cohort study found implementing a protocol for peripheral norepinephrine (NE) decreased median number of central venous catheter (CVC) days per patient by one, and 51.6% avoided a CVC entirely. Wednesday Spoon Feed:Using intubation videos, this group identified 13 key performance errors that occur during laryngoscopy. Read more to see what the proceduralists did wrong.

In this episode, we sit down with emergency physician and EMS medical director, Dr. Jon Allen, and discuss the application of push dose pressors in the EMS setting, particularly regarding ground transport. For more info on Doc Allen, hit up our previous episode where we introduce him. 

Welcome to another insightful episode of The Nurse Dose Podcast! In this episode, we dive deep into the fascinating world of titrating pressors. Join us as we explore the critical role of nurses in managing patients requiring vasopressor support and unravel the intricacies involved in adjusting these medications to optimize patient outcomes. Critical Care Cheat sheets are available at: ⁠https://www.etsy.com/shop/NurseDose⁠ This podcast is intended for informational and educational purposes only. It is not intended to provide medical advice or to substitute for the advice provided by your own physician or other medical professionals. The information contained herein is not intended to diagnose, treat, cure, or prevent any disease. If you have any concerns or questions about your health, you should always consult with a physician or other healthcare professional. The opinions expressed in this podcast are those of the host and guests and do not necessarily reflect the views of any medical institution, organization, or employer. By listening to this podcast, you agree to hold harmless the host, guests, and any associated parties from any and all liability or damages arising from your use of the information provided.

Chapter 1: Why Start Vasoactives?Chapter 2: When Start Vasoactives?Chapter 3: Which Vasoactive to Start?Access to video version of lecture, supplemental materials & references at: https://www.icuedu.org/pressorsvasoactives

00:00 Pathophysiology13:27 Decision to initiate massive transfusion28:18 Massive transfusion product composition35:21 Metabolic derangements39:51 Pressors in hemorrhagic shock?47:54 Approach to refractory shock

After establishing return of spontaneous circulation (ROSC) we should assess the patient's O2, CO2, blood pressure, and level of consciousness to guide our next actions. Oxygen and CO2 is maintained by small adjustments to the FiO2, tidal volume, and ventilation rate. Small changes can have big effects so this is best left to respiratory (if you have them) and requires close monitoring. Blood pressure may be affected by administration of a fluid bolus or use of pressor medications such as Dopamine or an Epinephrine drip. Pressors should be started at the lowest suggested dose and titrated up until a systolic BP of 90 mmHg. If, after ensuring O2, CO2, and BP; the patient can't obey simple commands we should start targeted temperature management for 24 hours. CT, MRI, & PCI can be done while patients are being cooled. Connect with me: Website:  https://passacls.com (https://passacls.com) https://twitter.com/PassACLS (@PassACLS) on Twitter https://www.linkedin.com/company/pass-acls-podcast/ (@Pass-ACLS-Podcast) on LinkedIn Good luck with your ACLS class!

Contributor: Aaron Lessen, MD Educational Pearls: Hypotension after cardiac arrest often requires a vasopressor to improve blood pressure Recent observational study from France examined outcomes of patients who received either epinephrine or norepinephrine for post-resuscitation shock Norepinephrine had significantly better outcomes  Death from shock was 35% in the epinephrine group vs. 9% in the norepinephrine group Recurrent cardiac arrest was 9% in epinephrine group vs. 3% in norepinephrine group For epinephrine: The all cause mortality was 2.5 times higher than norepinephrine Cardiovascular mortality was 5 times higher than norepinephrine Favorable neurological outcomes was 3 times worse than norepinephrine References Bougouin W, Slimani K, Renaudier M, Binois Y, Paul M, Dumas F, Lamhaut L, Loeb T, Ortuno S, Deye N, Voicu S, Beganton F, Jost D, Mekontso-Dessap A, Marijon E, Jouven X, Aissaoui N, Cariou A; Sudden Death Expertise Center Investigators. Epinephrine versus norepinephrine in cardiac arrest patients with post-resuscitation shock. Intensive Care Med. 2022 Mar;48(3):300-310. doi: 10.1007/s00134-021-06608-7. Epub 2022 Feb 7. PMID: 35129643. Summarized by John Spartz, MS4 | Edited by Erik Verzemnieks, MD   The Emergency Medical Minute is excited to announce that we are now offering AMA PRA Category 1 credits™ via online course modules. To access these and for more information, visit our website at https://emergencymedicalminute.org/cme-courses/ and create an account.  Donate to EMM today!

Sometimes a small dose of epinephrine or norepinephrine can keep a patient from becoming hypotensive during intubation, or may help bridge the patient to a continuous infusion. Dr. Pickett talks about simple methods for mixing and administering push doses of these pressors and how to administer the infusion. NOTE: It is ASSUMED you already know… Continue reading Push Dose Pressors for EMS: Epinephrine and Norepinephrine

In this episode we'll discuss tips and tricks for dominating your clinical interview. We'll cover Trauma, ABG's, Neuro Emergencies, Labs, RSI, Preoxygenation, DKA, and Pressors.

Dr. Brady, an ICU intensivist and the director of the critical care medicine clerkship at Beth Israel Deaconess Medical Center (BIDMC), discusses vasopressors and inotropes with RTL host, Dr. Navin Kumar. Together, they use the previous episode's (Ep. 71: Approach to Shock) case of an elderly patient with suspected distributive shock secondary to urosepsis as a framework to approach pressor requirements. Dr. Brady walks through establishing access, how to choose a pressor based on adrenergic physiology, and emphasizes when to take a diagnostic timeout in the ICU.

Dr. Engstrom lectures on pressors.

This episode of Inside EMS is sponsored by Eko. Learn how CORE stethoscope technology helps EMS providers make confident split-second decisions by clicking here. In this week's episode of Inside EMS, Kelly Grayson is joined by guest host Rob Lawrence. The subject of the week is trauma, and Rob and Kelly discuss the origins and meaning of the Trimodal Distribution of Death and the advances in trauma treatment. Kelly then answers the key trauma treatment question of fluids versus pressors.

It's the JournalFeed Podcast for the week of August 9-13, 2021. We cover frequent epinephrine dosing in pediatric arrest, pressors for trauma patients, CAM boot or cast for toddler's fracture, why PEM physicians are sued, and emergency cricothyrotomy anatomy and angles.

Please enjoy Episode 15.     Getting ready to record our next episode with Jake Good.  Get your questions in now!!   CLICK HERE to submit your question now!   1.  When should pressors be started?   2.  Do you always copy the facilities vent settings?   3.  Adjustments with the T1   4.  What do you think of Simone Biles' decision not to compete in the Olympics?   We are looking forward to hearing from you.  Design your own podcast next by sending us your questions today!

Drs. Pescatore and Raja talk about an unexpected effect of COVID-19 and why TXA doesn’t change the need for nasal packing in their latest podcast. Bonus! An interview with Daniel Boron-Brenner, DO, on push-dose pressors.

It’s the JournalFeed Podcast for the week of Dec 7-11, 2020. We cover tetracaine for corneal abrasion, peripheral vasopressor safety, personalized vasopressor management, cardiac arrest survival with PE, and intra-articular lidocaine for shoulder dislocation.

This episode continues our discussion of managing low blood pressure under anesthesia. Together, we lay out my 5 step approach to hypotension - 1) Evaluate the patient 2) Reduce the inhalant if possible 3) Normalize heart rate, 4) Fluid support, and lastly, 5) Pressors, and/or positive inotropes.

We discuss cardiogenic shock and decision making in the case of a young female presenting to the ER. We have a panel of cardiologists guide the discussion. Drs Rene Alvarez, Daniel Sims and Alec Vishnevski discuss the case presented by cardiology fellow Rachna Kataria, MD. Thanks for listening. Please like, subscribe and give us a rating.

We discuss the various aspects of cardiogenic shock including definition, heterogeneity, classification and management with an internationally renowned expert in the field Dr Navin Kapur. Dr Kapur is the Director of the Acute Mechanical Circulatory Support Program at Tufts University School of Medicine, Boston, MA. Listen, like, subscribe, and give us a high rating.

In this 5 minute bit, Ralph goes over a few options that you have for push dose pressors.Questions? Email us at ResusNowQuestions@gmail.comPlease click on the links below for evidence related to this topichttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5052865/pdf/ceem-15-010.pdfhttp://www.emdocs.net/push-dose-vasopressors-an-update-for-2019/https://www.tandfonline.com/doi/abs/10.1080/10903127.2019.1588443?journalCode=ipec20https://emcrit.org/wp-content/uploads/2017/08/holden-push-dose.pdfhttps://pubmed.ncbi.nlm.nih.gov/28248702/Below is a link to a printable mixing sheet courtesy of EmCrit.orghttps://emcrit.org/wp-content/uploads/push-dose-pressors.pdf

In this episode, we go through an approach to vasopressors. We talk about the physiology of the receptors they act on, and the scenarios in which we would use the 5 most common vasopressors: Norepinephrine, Vasopressin, Epinephrine, Dopamine and Phenylephrine. We also introduce our latest initiative Medicine Basecamp - which can be found here at www.theinternatwork.com/basecamp.

In this episode, we cover a core component of any resuscitationists tool kit: vasoactive agents. We've got your vasopressors, your inodilators, your inopressors, you oral cheat code and some hail merry approaches. Come listen for all things pressure and flow.

Pressors in trauma resuscitation? Heresy!  Or is it…?  Dr. Carrie Sims discusses her recently published study showing use of low-dose vasopressin in the trauma bay resulted in lower utilization of blood products, with equivalent outcomes.  Dr. Sims also discusses how she was able to get this study through the IRB with exception from informed consent (EFIC), a major hurdle for high-quality trauma research. Supplemental InformationEffect of low-dose supplementation of arginine vasopressin on need for blood product transfusions in patients with trauma and hemorrhagic shockArginine vasopressin, copeptin, and the development of relative AVP deficiency in hemorrhagic shockThe pathogenesis of vasodilatory shockEarly use of vasopressors after injury: caution before constriction

1.The 1st line agent for an exsanguinating patient is and always will be blood.   2.There may be circumstances in which MSFP needs to be adjusted in order to compensate for changes we cause through the process of intubation and PPV.   3. The only reason we have literature showing pressors associated with an increase in mortality in trauma is because this intervention is performed on a daily basis in emergency departments and operating rooms. We need a well designed study that reports dosing regimens, a control arm, and patients randomly allocated.    https://www.foamfrat.com/single-post/2019/09/19/If-I-Taught-Hemodynamics-Response-To-EricNaysayerBauer

A post arrest patient just got initiated on ECMO.  Do you give fluids, add pressors, or increase flow?  Marc Dickstein, an anesthesiologist from Columbia University and an expert in the physiology of ECMO, talks with Zack about how to manage these patients, what diagnostics we need and how to optimize your use of the machine.  This talk is a must for everyone starting ECPR in their departments. The post 56: Pressors, Fluid, or Flow – Optimizing ECMO Physiology appeared first on ED ECMO.

Scott Weingart and Amal Mattu are our guests as we break down the critical decision points in a case of a patient with an acute anterior STEMI and cardiogenic shock. Want weekly episodes, world class show notes, CME, and a super sweet app? Go to ercast.org and subscribe to the kit and caboodle.

Episode 110: Push Dose Pressors in the Crashing Patient

In part 2 of her interview with Dr. Haney Mallemat, Dr. Jessie Werner finds out how to manage the ventilator in the ED and reviews some real-life cases with Haney! Overview: As Emergency Medicine physicians we’re tasked with taking care of the sickest of the sick, often before we even have a diagnosis to clarify the clinical picture. Stabilizing critically ill patients may require placing a definitive airway and providing hemodynamic support with pressors. When faced with these challenging situations, what do you do? So you decide to intubate. Now what? What are the different ventilator modes and how do we choose? What does it mean when the vent is alarming? Find out how to select vent settings and troubleshoot problems in Part 2 on becoming a critical care beast in the ED!  Key Points There’s no difference between pressure and volume control If you’re giving a certain pressure, you monitor the volume, and vice-versa Remember 6-8cc/kg of volume (using ideal body weight) for lung protective strategy Peak pressure is the sum of resistance and compliance Plateau pressure measures compliance High peak pressure indicates a resistance problem High peak AND plateau pressure indicate the lungs are stiff To diagnose a ventilator problem think DOPES: D: displaced tube or cuff problem O: obstructed tube P: pneumothorax E: equipment problem S: breath stacking To fix a ventilator problem think DOTTS: D: disconnect from the ventilator and allow for full exhalation O: oxygenation - are they bagging okay? T: tube in the right place T: tweak the vent to prevent breath stacking S: ultraSound   References / Resources Weingart, Scott D. "Managing initial mechanical ventilation in the emergency department." Annals of emergency medicine68.5 (2016): 614-617.    

In part 1 of her interview with Dr. Haney Mallemat, Dr. Jessie Werner discusses using pressors in the ED. Stay tuned for part 2 on managing the ventilator! Overview: As Emergency Medicine physicians we’re tasked with taking care of the sickest of the sick, often before we even have a diagnosis to clarify the clinical picture. Stabilizing critically ill patients may require placing a definitive airway and providing hemodynamic support with pressors. When faced with these challenging situations, how do you choose the right pressor? What’s the dose? When do you add another agent? What about fluids? We answer all these questions and more in this episode of EMRA CAST. Also, stay tuned for the follow-up to this episode which covers vent management in ED.  We’ve got you covered with all the tips you need to become a critical care beast in the ED! Key Resources: The RUSH protocol (which includes the HI-MAP technique Dr. Mallemat mentions) – Rapid Ultrasound for Shock and Hypotension.  Key Points Perfusion is composed of the tank (preload), the pump (cardiac output), and the pipes (systemic vascular resistance).  Hypotension or shock can be caused by ANY of these, so consider performing ultrasound using the HIMAP protocol: HEART, IVC, MORISON’S POUCH, AORTA, and PULMONARY to determine the cause of the hypotension and tailor your resuscitation. Pressor Algorithm: As long as there is not evidence of a decreased EF or another cause of hypotension, Haney recommends starting with fluids to resuscitate a hypotensive patient. If a patient is critically ill and/or not responsive to fluids, consider starting norepinephrine. It’s okay to start it peripherally! If the patient is profoundly vasoplegic and norepinephrine is not working, consider adding vasopressin at a dose of 0.03 mg/kg. After that point, you can consider starting epinephrine at a higher dose, or greater than 0.05 mcg/kg/min to get the most vasopressive effect. There is no known maximum dosing, but organ ischemia - particularly gut ischemia - can occur.   Dopamine has fallen out of favor due to concern over arrhythmogenic properties; however, you could consider using dopamine if a patient is bradycardic AND hypotensive (for example, if they’re beta-blocked). If a patient has a “pump” problem with a significantly reduced EF, you should consider dobutamine in conjunction with cardiology or an intensive care specialist. References / Resources Rezaie S. RUSH protocol: Rapid Ultrasound for Shock and Hypotension. ALiEM Website. https://www.aliem.com/2013/06/rush-protocol-rapid-ultrasound-shock-hypotension/. Updated 6/1/2013. Accessed 12/13/2018.   Host Jessie Werner, MD Alpert Medical at Brown University PGY3 @JessWernerMDEMRA Cast Episodes Guest Haney Mallemat, MD Associate Professor of Emergency Medicine at Cooper Medical School Triple boarded in EM, IM, CritCare Medicine.  Internationally recognized educator in CC Medicine. Hospital Affiliation: Cooper Medical School @CriticalCareNowEMResident Articles

Descrição, indicações e considerações práticas sobre o uso de vasopressores em bolus no manejo do paciente com hipotensão.

I will openly admit that when Dr. Weingart first coined the term "Push Dose Pressor," I drank the Kool Aid.. I remember pitching it to my organization and discussing the concept with the guys at my station. I think the early adoption was due to: 1. Cool Name 2. Easy To Mix 3. Weingart  4. Was better than pushing 500 mcg of cardiac epi when the patient starts circling the drain.   Now I'm questioning this techniques application in EMS.   Join Michael Perlmutter, Bryan Winchell, and myself as we discuss the finer points of PDP.   www.FOAMfrat.com

Hypotension is one of our number one enemies in prehospital care. In this episode, Dr. Patrick and Dickson begin with a review of vasopressor physiology and then they dive into the evidence and rationale behind push dose epinephrine use. References: https://emcrit.org/emcrit/push-dose-pressor-update/ https://www.nejm.org/doi/full/10.1056/NEJMoa0907118

Author: Nick Hatch, MD. Educational Pearls:   A common concern using vasopressors is the risk of digital and mesenteric ischemia. The absolute risk of digital ischemia and/or mesenteric ischemia is pretty low. Norepinephrine at its highest doses carries a 5% digital ischemia rate and a 2% mesenteric ischemia rate. The studies demonstrating this complication were predominately patients with pre-existing liver disease. Providers commonly mistake purpura fulminans, a common complication of sepsis, for digital ischemia.   References Brown, SM. et al.  Survival After Shock Requiring High-Dose Vasopressor Therapy. Chest. 2013. 143(3), 664–671. http://doi.org/10.1378/chest.12-1106. Malay MB et al. Heterogeneity of the vasoconstrictor effect of vasopressin in septic shock. Critical Care Medicine. 2004. 32(6), 1327-31.

PDP is the cool kid on the block these days, but it is a bridge to an infusion. 

ACEP-EQUAL webinar podcast on sepsis and the management dilemmas with intravenous fluid resuscitation and vasopressors. Featured Experts: Dr. Tiffany Osborn (Washington University at St. Louis) and Dr. Laurence Dubensky (Aventura) Podcast Host: Dr. Jason Woods Podcast Editor/Engineer: James Ede

  I’m not a powerful Jedi Master with Force Visions and frankly, unable to see into the future. Hello Star Wars fans!   This is a follow-up bonus episode in response to Episode 5 Push Dose Pressors, listeners' questions, and also in light of recent journal articles that recently got published. Timing was completely coincidental when Episode 5 Push Dose Pressor podcast episode was released.   Although I’ve been using push dose pressors for years now, I still researched the topic awhile ago. Frankly, there wasn’t much out there - and there still isn’t. Why? Because it’s not standard of care. But I suspect it will be once there are RCTs and more research and we all know that takes time. Meanwhile, this is a practice that is happening in our Emergency Departments and as ED nurses, we definitely should know about them.   This is the initial reason for a push dose pressor episode on this podcast. Nurses, we are going to be the ones mixing and preparing the push dose pressors, and a good chance we will be administering it. These medications, epinephrine and phenylephrine, are extremely potent and should be highly respected when used.  It also warrants an increased awareness of the entire process - including when to use them, and what safety measures we can use to prevent medication errors.   So let’s go over some safety measures that will ensure the correct utilization of push dose pressors.    1. Mixing/Preparing Epinephrine Push Dose Pressor Let’s start with preparing an epinephrine push dose pressor - After I had released my podcast, a nurse listener, immediately brought to my attention that using pre-filled saline flushes to prepare the epinephrine push dose concentration is bad because it can lead to medication errors. I definitely argued that I don’t see the difference between using a pre-filled saline flush for a push dose pressor versus a pre-filled saline bag for a drip - as long as it is labeled properly (use concentration doses).   More responses came and a major safety issue came up that health care providers are NOT labeling their syringes after mixing - why??!!  And there has been reported errors in medication where health care providers are mistakenly pushing what they think is a NS flush syringe - but it actually has medication in them (epinephrine or other medications).   This gave me a heavy heart - and you know, I wanted to puke a little bit. I hope you all can forgive me. The last thing I would ever want to endorse is an unsafe practice, or a practice that can lead to even more errors. That being said, I will change my own practice to draw up epinephrine in an empty syringe and dilute it to a proper push dose concentration - and immediately label the syringe afterwards.   Never let that syringe out of your hands or eyesight until the label is securely on the syringe.   Epinephrine is a medication that is prone to errors to begin with.   Some additional tips on mixing:   Labeling Always label where you can still see your mL markings on the syringe - it’s important that way you know how much you are giving! This also applies to other medications like your intubation meds..   Why Use Cardiac Pre-filled Syringes? You may wonder why it is recommended to mix from a cardiac pre-filled syringe - it’s because you can guarantee the concentration (1:10000 with 10mL). Many medication rooms will have different concentrations stocked 1:1000 for anaphylaxis or 1:10000 for cardiac arrest - but both are in 1mL vials. If you were to grab the vial of Epinephrine 1:10000 in 1mL - you are supposed to further dilute that before administering.   So when your patient is crashing, to prevent thinking it even further, it’s easier to grab the cardiac pre-filled syringe because you know it will have a concentration of 1:10000 in 10mL.   Maintain Sterility When mixing, try to maintain sterility as much as possible. Remember all medications will go into the blood stream, we do not want to introduce more problems.

An update on push-dose pressors

Why Use Push Dose Pressors? To buy yourself some time with your super hypotensive patients!! Ensure your patient's perfusion status while you are trying to: intubate managing transient hypotension preparing a drip preparing a central line Know which medication to use based on clinical presentation of patient. Dr. Scott Weingart's Easy Push Dose Printout (It has photos!) Epinephrine alpha 1&2, beta 1&2 agonist = inopressor (Increase in myocardial contraction, heart rate, and peripheral vascular resistance) Epinephrine Push Dose Concentration 10mcg/mL (1:100,000) vs. cardiac dose (1:10,000) Onset Immediate - 1 minute Duration 5-10 minutes Dose 5-20mcg every 2-5 minutes (0.5-2mL)   Preparation Draw up 9mL of Normal Saline in an empty 10mL syringe (updated - see below) Attach a syringe and draw up 1mL of epinephrine from the pre-filled cardiac dose amp (Epinephrine 100mcg/mL) Shake a little, Place a label: Epinephrine 10mcg/mL Phenylephrine alpha 1 agonist = increase in peripheral vascular resistance Heart rate remains the same. Watch out for reflex bradycardia.   Phenyelphrine Push Dose Concentration 100mcg/mL   Onset Immediate - 1 minute Duration 10-20 minutes Dose 50-200mcg every 2-5 minutes (0.5-2mL)   Preparation Draw up 1mL of phenylephrine (10mg/mL concentration vial) Inject into NS 100mL bag Shake a little, Place a label: Phenylephrine 100mcg/mL Use as a drip or draw up in a syringe. Super Nerdy Receptor Information Beta Receptors Tissue Receptor Subtype Heart beta1 Adipose Tissue beta1, beta3? Vascular Smooth Muscle beta2 Airway Smooth Muscle beta2 Beta1 Agonist Increases contractile force & HR. Activation of beta1 receptors in the atria and ventricles but the ventricles are really effected - thus increasing myocardial contraction. HR increases because SA node, AV node and the His-Purkinjie system are activated.   Beta 2 Agonist Relaxes smooth muscles   Alpha1 & Alpha 2 Agonist Constriction of vascular smooth muscle. Myocardial Alpha 1 may have a positive inotropic effect. No clear understanding on Alpha 2 receptors at this moment. Epinephrine & NE has equal affinity to both alpha 1 and alpha 2 receptors.  However, Epinephrine has a higher affinity to beta 2 receptors. So effects are dose dependent. Initially will activate beta 2 receptors so relaxes vascular smooth muscle and decrease peripheral resistance, but at higher doses, epinephrine will also bind to alpha 1 receptors which is a potent vasoconstrictor and will dominate as epinephrine concentrations are higher.   Phenylephrine is a pure alpha 1 agonist. Vasoconstriction of both arterial and venous vessels. Great for someone who has tachycardia/tachyarrhythmia but also hypotensive. Can cause reflex bradycardia. Update 8/6/2017 "Concentration" used to differentiate final concentration versus dosing, to have clear language. Update 8/8/2017 Brought to my attention by Craig Button, RN - There have been reported cases of serious medication errors due to mixing medications using pre-filled saline flushes and not labeling them. Therefore, I am going to change the recommended preparation of mixing epinephrine push dose concentrations. The LAST thing I want is to hear about unlabeled saline flushes with epinephrine lying around, and/or causing harm to patients. These medications should be respected so PLEASE LABEL ALL PREPARATIONS!! Original text is here. Blog post has been updated above. Original Text: Epinephrine Push Dose Concentration Preparation Take a NS 10mL flush and squeeze out air bubbles and saline so 9mL remains Attach a syringe and draw up 1mL of epinephrine from the pre-filled cardiac dose amp (Epinephrine 100mcg/mL) Shake a little, Place a label: Epinephrine 10mcg/mL Now listen to the episode.... References: Scott Weingart. EMCrit Podcast 6 – Push-Dose Pressors. EMCrit Blog. Published on July 10, 2009. Accessed on August 3rd 2017. Available at [https://emcrit.

https://ampa.org/   Happy Friday of #EMSWeek2017! https://emcrit.org/wp-content/uploads/push-dose-pressors.pdf    Resuscitation - beginning from initial patient contact to the emergency department to the intensive care unit is a continuun of care - though the first few minutes of patient contact with a critically ill patient can have tremendous repercussions on the patient's ultimate outcome.  Whether in critical care transport or in 911 emergency response, patient's may require a medication in small aliquots immediately that would be either unfeasible or cumbersome to administer via infusion on a dedicated pump.  While circumstances in which a patient needs a push dose medication may be uncommon, the administration of these drugs can be potentially lifesaving.  There are two prehospital scenarios in which the paramedic carries the necessary medication in their armamentariam and with appropriate instruction and training can safely reconstitute into an appropriate dose for use in out-of-hospital resuscitation for the critically ill patient.  Push dose pressors are often employed in profoundly hypotensive patients that will require endotracheal intubation.  Rapid Sequence Intubation and Positive Pressure Ventilation are both associated with hypotension, thus in the patient that requires advanced airway and is hypotensive upon EMS arrival, push dose pressors may be employed to effectively "resuscitate before you intubate".  Typically Epinephrine is diluted to an appropriate dose and adminstered in small aliquots (10mcg/ml) for inotropoic support to optimize hemodynamics prior to RSI or intubation.  There is also anaesthesia literature supporting the use of neosynephrine as well as phenylephrine for this purpose, though these medications are less readily available prehospitally.  Even brief episodes of relative hypotension can cause effects seen days later; in critically hypotensive patients these may be even more pronounced.  By using push dose pressors, a field provider can safely and effectively resuscitate their patient in order to mitigate the risks associated with endotracheal intubation prior to securing an advance airway. Conversely, a separate and distinct class of patients who suffer from decompensated heart failure may present with respiratory distress due to volume overload with pathophysiology associated with marked systemic hypertension. While CPAP is the mainstay of therapy for these patients prehospitally and has significantly reduced intubation of the CHF patient over the past several years, IV Lasix and topical Nitroglycerin play little role in the EMS management of the decompensated heart failure patient.  Nevertheless, these patients often require preload and afterload reduction to manage their symptomatology; it is common to initiate nitroglycerin infusions in critical care transport as well as in the emergency department for management of this hypertension.  Nitroglycerin lowers preload via venous vasodilation at low doses and lowers after load via arterial vasodilation at higher doses, making the patient's vascular container larger lowering the systemic pressure. Aggressive, high dose NTG paired with the recruitment of the alveoli using CPAP & PEEP make up the mainstay of pre-hospital treatment of APE and decompensated heart failure. Bolus doses as high as 2 mg (2000 mcg) of nitroglycerin have been given safely and effectively in previous studies.  In emergent resuscitations we need to focus on bolus dose medications in the acute phase versus starting and titrating critical care infusions while a patient is in extremis. The goal is to achieve clinical end points of treatment faster with bolus dosing at the bedside and then begin maintenance infusions once resuscitation goals are met and the hemodynamics are stable.  Similar to push dose pressors in the acutely hypotensive EMS patient requiring resuscitation, patients with decompensated heart failure may benefit acutely with push dose nitroglycerin, a potent vasodilator.   @AmpaDocs #CCTMC17 Mark your calendars for #CCTMC18 April 9-11th 2018 Wyndham Riverwalk - San Antonio Texas     Query us on Twitter: www.twitter.com/EMS_Nation Like us on Facebook: www.facebook.com/prehospitalnation   Wishing Everyone a safe tour! ~Faizan H. Arshad, MD @emscritcare www.emsnation.org

What are push dose pressors, and how do they work? When we have a patient who is hypotensive, either in the peri-intubation period or post-cardiac arrest, one of the primary things we need to manage is blood pressure. When a patient is hypotensive (SBP

A follow-up to our previous push-dose pressor podcast. Even though there is substantial evidence for push-dose pressors in certain situations, the air medical industry as a whole has yet to embrace them. It is important for us to be responsible in our care and with our knowledge and work hand-in-hand with our medical directors and with our patient care protocols. Having said this, it is also up to us to shape the care we give by influencing the folks that make decisions in our individual institutions. Join with Eric as he discusses push-dose pressors and their future in our practice.

A follow-up to our previous push-dose pressor podcast. Even though there is substantial evidence for push-dose pressors in certain situations, the air medical industry as a whole has yet to embrace them. It is important for us to be responsible in our care and with our knowledge and work hand-in-hand with our medical directors and with our patient care protocols. Having said this, it is also up to us to shape the care we give by influencing the folks that make decisions in our individual institutions. Join with Eric as he discusses push-dose pressors and their future in our practice.See omnystudio.com/listener for privacy information.

In this episode of the FlightBridgeED Podcast, we discuss how to use push dose pressors to offset the effects caused by sedation and paralysis on hemodynamically unstable patients requiring RSI.

Pediatric airway management is a skill that integrates the three types of knowledge as described by the ancient Greeks: episteme, or theoretical knowledge, techne, or technical knowledge, and phronesis, or practical wisdom, also called prudence. Here we’ll invoke each type of knowledge and understanding as we go beyond the anatomical issues in pediatric airway management – to the advanced decision-making aspect of RSI and the what-to-do-when the rubber-hits-the road. Case 1: Sepsis Laura is a 2-month-old baby girl born at 32 weeks gestational age who today has been “breathing fast” per mother.  On arrival she is in severe respiratory distress with nasal flaring and intercostal retractions.   Her heart rate is 160, RR 50, oxygen saturation is 88% on RA.  She has fine tissue-paper like rales throughout her lung fields.  Despite a trial of a bronchodilator, supplemental oxygen, even nasal CPAP and fluids, she becomes less responsive and her heart rate begins to drop relatively in the 80s to 90s – this is not a sign of improvement, but of impending cardiovascular collapse. She is in respiratory failure from bronchiolitis and likely viral sepsis.  She needs her airway taken over. Is this child stable enough for intubation? We have a few minutes to optimize, to resuscitate before we intubate. Here’s an easy tip: use the sterile flushes in your IV cart and push in 20, 40, or 60 mL/kg NS.  Just keep track of the number of syringes you use – it is the fastest way to get a meaningful bolus in a small child. Alternatively, if you put a 3-way stop-cock in the IV line and attach a 30 mL syringe, you can turn the stop cock, draw up stream from the IV bag into the syringe, turn te stop cock, and push the fluid in the IV. Induction Agent in Sepsis The consensus recommendation for the induction agent of choice for sepsis in children is ketamine. Etomidate is perfectly acceptable, but ketamine is actually a superior drug to etomidate in the rapid sequence intubation of children in septic shock.  It rapidly provides sedation and analgesia, and supports hemodynamic stability by blocking the reuptake of catecholamines. Paralytic Agent in Sepsis The succinylcholine versus rocuronium debate… Succinylcholine and its PROS 82% of RSI in the ED used succinylcholine (According to the National Emergency Airway Registry, in 2005).  We know it, we are comfortable with it. Succinylcholine produces superior intubating conditions when comparing 1 mg/kg succinylcholine versus 0.6 mg/kg rocuronium, succinylcholine is that at 45 seconds. Succinylcholine and its CONs Raises serum potassium in everyone, typically 0.5 to 1 mEq/L.  That is not usually a problem, but for those with preexisting or inducible hyperkalemia, it can precipitate an arrest, as in renal failure, underlying neurologic or myopathic conditions like multiple sclerosis, muscular dystrophy, ALS, or those who had a stroke or a burn more than 72 hours prior. We often have limited information in critical situations. Succinylcholine gives us a false sense of security.  In children, there really is no “safe apnea” period. Succinylcholine’s effect on the nicotinic receptors results in mydriasis, tachycardia, weakness, twitching and hypertension, and fasciculations (Think nicotine overdose: M/T/W/Th/F). Succinylcholine’s effect on muscarinic receptors manifest (as in organophosphate overdose): SLUDGE – salivation, lacrimation, urination, defecation, GI upset or more apropos here: DUMBBELLS – diarrhea, urination, miosis, bradycardia, emesis, lacrimation, lethargy, salivation. Second dose of succinylcholine – beware of the muscarinic effects and bradycardia. Co-administer atropine, 0.01 mg/kg, up to 0.5 mg IV. Coda: succinylcholine is not that bad – we would not have had such great success with it during the early years of our specialty if it were such a terrible drug.  The side effects are rare, but they can be deadly.  So, what’s the alternative? Rocuronium and its PROs It has none of the side-effects of succinylcholine Rocuronium and its CONs Argument 1: the duration is too long if there is a difficult airway, since rocuronium can last over an hour. Still need to intubate, and now your patient is potentially worse. Argument 2: succinylcholine produces better intubating conditions at 45 seconds compared to rocuronium. At 0.6 mg/kg, rocuronium is inferior to succinylcholine at all time intervals. At 1.0 mg/kg, rocuronium is still inferior at 45 seconds.  At 1.2 mg/kg rocuronium – the dose now commonly recommended – there was no difference in intubating conditions, per a study by Heier et al. in Anethesia and Analgesia in 2000. Case 2: Multitrauma Joseph is a 3-year-old boy who is excited that there are so many guests at his house for a family party and when it’s starting to wind down and the guests begin to leave, he is unaccounted for. An unsuspecting driver of a mini-van backs over him. He is brought in by paramedics, who are now bagging him. Induction Agent in Trauma Need something that is hemodynamically stable – agents such as midazolam or propofol would cause too many problems. Etomidate is a short-acting imidazole derivative that acts on GABA-A receptors to induce loss of consciousness in 5-15 seconds. It can cause apnea, pain on injection, and myoclonus. Etomidate reduces cerebral blood flow, reduces intracranial pressure, and reduces cerebral oxygen consumption, all while maintaining arterial blood pressure and cerebral perfusion pressure. Ketamine is reasonable as well: there is no contraindication to ketamine except for known hydrocephalus. It is safe in head trauma. It is a good choice for the hypotensive trauma patient.  TBI is not a contraindication. In the case of the critically injured child who is normotensive, ketamine will raise his blood pressure and perhaps foster further bleeding.  The goal is a good general perfusion and a balanced resuscitation, ensuring enough cerebral perfusion without disrupting nascent clots.  On the other side of the spectrum, permissive hypotension is not described in children, as hypotension is a late and dangerous sign of shock. Paralytic Agent in Trauma Are your surgeons in an uproar about a long-acting agent and the pupillary response?  Relax, it’s a myth. Caro et al in Annals in 2011 reported that the majority of patients undergoing RSI preserved their pupillary response.  Succinylcholine actually performed worse than rocuronium. In the rocuronium group, all patients preserved their pupillary response. In the critically ill, we rethink your dosing of both the sedative and the paralytic. In a critically ill child or adult, perfusion suffers and it affects how we administer medications.  The patient’s arm-brain time or vein-to-brain time is less efficient; additionally, as the patient’s hemodynamic status softens, he becomes very sensitive to the effects of sedatives. We need to adjust our dosing for a critically ill patient: Decrease the sedative to avoid falling over the hemodynamic compensation cliff. Increase the paralytic to account for prolonged arm-brain time. Case 3: Cardiac/myocarditis/congenital heart disease Jacob is a 6-year-old-boy with tricuspid atresia s/p Fontan procedure who’s had one week of runny nose, cough, and now 2 days of high fever, vomiting, and difficulty breathing. The Fontan procedure is the last in a series of three palliative procedures in a child with complex cyanotic congenital heart disease with a single-ventricle physiology. The procedure reroutes venous blood to flow passively into the pulmonary arteries, because the right ventricle has been surgically repurposed to be the systemic pump.  The other most common defect with an indication for a Fontan is hypoplastic left heart syndrome. Typical “normal” saturations are 75 and 85% on RA.  Ask the parents or caregiver. Complications of the Fontan procedure include heart failure, superior vena cava syndrome, and hypercoagulable state, and others. A patient with a Fontan can present in cardiogenic shock from heart failure, distributive shock from an increased risk of infection, hypovolemic shock from over-diuresis or insensible fluid loss – or just a functional hypovolemia from the fact that his venous return is all passive – and finally obstructive shock due to a pulmonary thromboembolism. Types of shock mnemonic: this is how people COHDe – Cardiogenic, Obstructive, Hypovolemic, Distributive. Do we give fluids? Children after palliative surgery for cyanotic heart disease are volume-dependent.  Even if there is a component of cardiogenic shock, they need volume to drive their circuit.  Give a test dose of 10 mL/kg NS. Pressors in Pediatric Shock Children compensate their shock state early by increasing their SVR. Epinephrine (adrenaline) is great at increasing the cardiac output (with minimal increase in systemic vascular resistance; tachycardia)  In children the cardiac deleterious effects are not pronounced as in adults.  Later when the child is stabilized, other medication such as milrinone (ionotrope and venodilator) can be used. Epinephrine is also fantastic for cold shock when the patient is clamped down with cold extremities – the most common presentation in pediatric septic shock. Norepinephrine (noradrenaline) is best used when you need to augment systemic vascular resistance, such as in warm shock, where the patient has loss of peripheral vascular tone. Induction Agent in Cardiogenic Shock A blue baby – with a R –> L shunt – needs some pinking up with ketamine A pink baby – with a L –> R shunt – is already doing ok – don’t rock the boat – give a neutral agent like etomidate. Myocarditis or other acquired causes of cardiogenic shock – etomidate. Case 4: Status Epilepticus Jessica is a 10-year-old girl with Lennox-Gastaut syndrome who arrives to your ED in status epilepticus. She had been reasonably controlled on valproic acid, clonazepam, and a ketogenic diet, but yesterday she went to a birthday party, got into some cake, and has had stomach aches – she’s been refusing to take her medications today. On arrival, she is hypoventilating, with HR 130s, BP 140/70, SPO2 92% on face mask. She now becomes apneic. Induction Agent in Status Epilepticus Many choices, but we can use the properties of a given agent to our advantage. She is normo-to-hypertensive and tachycardic. She has been vomiting. A nice choice here would be propofol. Propofol as both a sedative and anti-epileptic agent works primarily on GABA-A and endocannabinoid receptors to provide a brief, but deep hypnotic sedation.  Side effects can include hypotension, which is often transient and resolves without treatment.  Apnea is the most common side-effect. Ketamine would be another good choice here, for its anti-epileptic activity. Paralytic Agent in Status Epilepticus Rocuronium (in general), as there are concerns of a neurologic comorbidity. Housekeeping in RSI What size catheter doe I use?  If you know your ETT size, then it is just a matter of multiplication by 2, 3, 4, or 5. Remember this: 2, 3, 4 – Tube, Tape, Tap The NG/OG/Foley is 2 x the ETT – tube The ETT should be taped at a depth of 3 x the ETT size – tape A chest tube size 4 x the ETT – tap In summary, in these cases of sepsis, multitrauma, cardiogenic shock, and status epilepticus: Resuscitate before you intubate Use the agent’s specific properties and talents to your benefit Adjust the dose in critically ill patients: decrease the sedative, increase the paralytic Have post-intubation care ready: sedation, verification, NG/OG/foley

This is a discussion on the use of early, peripheral vasopressors in patients with septic shock. The core messages:  - limit fluids - use vasopressors earlier / synergistically with IV fluids - Use Noradrenaline - use it peripherally (ie. through a good, watched, flowing IVC - idealaly proxiaml to the elbow. - think about the use of CVCs and potential harms / benefits in small hospitals.

In this episode of the FlightBridgeED Podcast, we discuss how to use push dose pressors to offset the effects caused by sedation and paralysis on hemodynamically unstable patients requiring RSI.See omnystudio.com/listener for privacy information.

Psychic Terror as an Effective Pressor

Mohamed, a listener from Sudan, emailed asking about the treatment of acute pulmonary edema in patients with low blood pressure. This is in distinction to SCAPE patients (see podcast 1). If the patients have pulmonary edema and low BP from a cardiac cause, then they are in Cardiogenic shock. First, consider the etiology: Rate-related Valve Disorder Ischemic (Right sided infarct, STEMI, NSTEMI) Cardiomyopathy Toxicologic At the same time, you are treating the patient with: Inotropes (dobutamine, milrinone, calcium) Pressors to achieve a MAP > 65 (allows coronary perfusion) (Meta-Analysis demonstrates norepi superior to dopamine Medicine. 96(43):e8402, OCT 2017) Oxygenation support, most likely with intubation Optimize O2 carrying capacity (Hb>10) Here is a fantastic set of guidelines to manage these patients Update: Contemporary Management of Cardiogenic Shock Circulation 2017;136:e232 Journal Feed Summary