Podcasts about fio2

basic mechanical ventilation fio2

Play Episode Listen Later Oct 21, 2024 9:30

Hipoksinin zararlı etkilerini biliyoruz ve hepimiz bundan sıklıkla kaçınıyoruz. Peki mekanik ventilatör altında entübe şekilde takip ettiğimiz hastalarda aslında göz ardı ettiğimiz hiperoksi durumu masum mu? Mekanik ventilasyon modu ve oksijenasyon hedefleri hastalık seyrini etkileyebilir. Mekanik ventilasyonun, akut akciğer hasarı (ALI) veya akut solunum sıkıntısı sendromlu (ARDS) kritik hastalarda akciğer hasarına neden olabileceği veya bunu kötüleştirebileceği genel olarak kabul edilmektedir. Oksijenin yüksek miktarlarının toksik olabileceğinden hiperoksiden kaçınmak gerekir. İlk olarak, yüksek FiO2 değerlerinin akciğer için toksik olabileceği bilinmektedir. Hayvanlarda, uzun süreli hiperoksi ARDS'de görülenlere benzer histopatolojik değişikliklere neden olduğu görülmüştür (1). Sağlıklı insanlarda, %100 oksijene maruz kalma, atelektaziye, bozulmuş mukosiliyer klirense ve trakeobronşite ve alveolar nötrofillerde artışa yol açabilir (2). Akciğer üzerindeki etkilerinin yanı sıra oksijen, sistemik toksisiteye de yol açabilir. Vasküler dirençte artış ve kardiyak outputta azalma ile de ilişkilendirilmiştir (3). Hiperoksi, merkezi sinir sistemi, hepatik ve pulmoner serbest radikallerin oluşumuna neden olabilir. Hiperoksi ve HALI Oksijenin yüksek konsantrasyonlarda solunmasının akciğere zararlı olduğu bilgisi 1700'lü yılların sonlarına kadar dayanmaktadır. 1783 yılında Antoine Lavoisier'in bir çalışmasında FiO2'yi 1'den verdiği kobayların öldüğünü ve otopsilerinde sağ kalbin mavimsi ve genişlemiş şişkin, akciğerlerin ise kıpkırmızı sert ve kanla dolu olduğunu gözlemlemiş (4,5). FiO2'nin çok yüksek değerleri (FiO2 ≥ 0,9) ve uzun süre bu değerlerde kalması genellikle hiperoksik akut akciğer hasarına (HALI- Hiperoksik Acute Lung Injury) neden olur. HALI'nin şiddeti, PaO2 özellikle >450 mmHg, FIO2 >0,6 ve maruz kalma süresiyle doğru orantılıdır. Hiperoksi, doğal antioksidan savunmalarını alt üst eden ve hücresel yapıları birkaç yolla tahrip eden olağanüstü miktarda reaktif O2 türü üretir. Klinik olarak, HALI riski FiO2 0,7'yi aştığında ortaya çıkar. Hem yüksek gerilimli mekanik ventilasyon hem de hiperoksi, akciğer hasarını şiddetlendirir ve pulmoner enfeksiyonu teşvik edebilir. 1866'da Jean Baptiste Dumas, 1.0'lık bir FiO2'de uzun süreli solunum üzerine ilk çalışmayı yayınlamıştı. Köpeklerin toraksının "acı serum ve pıhtılaşmış kanla dolu olduğunu; bronşiyal tüplerin sıvıyla dolduğunu" ve "akciğerlerin bir süredir iltihaplı olan organlarda olduğu gibi önemli ölçüde katılaştığını" ortaya koymuştur (5). O zamandan beri yapılan tüm çalışmalarda uzun süreli FiO2'nin >0,8 olması ile çoğu hayvan birkaç gün sonra öldüğü gözlemlenmiştir. En etkili laboratuvar çalışmalarından biri ise 1899'da James Lorrain Smith tarafından yapılmış. Smith, bir haftadan uzun süreli 0,4 değerinde FiO2 soluyan farelerin toksisiteye dair hiçbir kanıt göstermediğini bulmuş. Buna karşılık, 0,7-0,8 değerinde FiO2'ye maruz kalan farelerin yarısı solunum yetmezliğinden öldüğünü göstermiş (6). Smith bu çalışmadan sonuçla 0,7'lik bir FiO2'ye uzun süreli maruz kalmanın muhtemelen önemli toksisite eşiğini temsil ettiği ve 0,8'lik bir FiO2'de oksijenin toksik etkilerinin hayvanın direncine göre değiştiği sonucuna varmıştır. 20. yüzyılın ilk yarısında yapılan çok sayıda deneyden elde edilen genel izlenim, FiO2 0,6'nın üzerine çıktıkça ve maruz kalma süresi uzadıkça toksisitenin daha hızlı artmasıdır (6). Uzun süreli hiperoksi; diffüz interstisyal ödem, kanama,nötrofil infiltrasyonu, trakeobronşit, atelektazi, mukosiliyer transport bozukluğu, bakteriyel klerensin azalması, alveolar makrofaj fonksiyon bozukluğu ve pnömoniye yol açar. Normal akciğerlere sahip insanlarda hiperoksi üzerine yapılan çalışmalar oldukça sınırlıdır. 20. yüzyılın başlarından ortalarına kadar yapılan birkaç küçük çalışma, 48 saat boyunca 0,96-1,0 FiO2 ile nefes almanın çoğu erkekte toksisite semptomları üretmediğini bulmuştur.

normal klinik o2 hem peki uzun ards buna akut akci mmhg vask fio2

Mechanical Ventilation Basic Part 3: Episode 8

Tracheostomy Education

Play Episode Listen Later Aug 23, 2024 23:15

The conversation focuses on the alarms set on mechanical ventilators. Dr. Jerry Gentile explains the general ventilator alarm guidelines, including apnea parameters, FIO2 settings, and pressure alarms. He emphasizes the importance of adhering to these guidelines and avoiding dangerous practices like setting high pressure limits too high. Jerry also discusses the reasons for alarms going off and highlights the need for a backup ventilator. The conversation concludes with a mention of ventilator-associated events and the importance of preventive measures.Support the Show.https://tracheostomyeducation.cominstagram.com/tracheostomyeducationlinkedin.com/in/nicole-de-palma-708b16blinkedin.com/in/dr-jerry-gentile

#224 - [Journal Club Shorts] -

The Incubator

Play Episode Listen Later Jul 7, 2024 15:13

Send us a Text Message.Initial Oxygen Concentration for the Resuscitation of Infants Born at Less Than 32 Weeks' Gestation: A Systematic Review and Individual Participant Data Network Meta-Analysis.Sotiropoulos JX, Oei JL, Schmölzer GM, Libesman S, Hunter KE, Williams JG, Webster AC, Vento M, Kapadia V, Rabi Y, Dekker J, Vermeulen MJ, Sundaram V, Kumar P, Kaban RK, Rohsiswatmo R, Saugstad OD, Seidler AL.JAMA Pediatr. 2024 Jun 24:e241848. doi: 10.1001/jamapediatrics.2024.1848. Online ahead of print.PMID: 38913382As always, feel free to send us questions, comments, or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through Instagram or Twitter, @nicupodcast. Or contact Ben and Daphna directly via their Twitter profiles: @drnicu and @doctordaphnamd. The papers discussed in today's episode are listed and timestamped on the webpage linked below. Enjoy!

#224 -

The Incubator

Play Episode Listen Later Jul 7, 2024 87:20 Transcription Available

Send us a Text Message.In this packed episode of Journal Club, Ben and Daphna review eleven recent papers covering a range of neonatology topics. They discuss a study on CRP use in early-onset sepsis evaluations, finding that high CRP use was associated with increased antibiotic administration. Another paper examined iron supplementation in healthy breastfed infants, showing no significant developmental benefits at 12-36 months.They review a JAMA Network Open study on the long term outcomes of infants enrolled in the umbilical cord milking study MINVI. They also cover a paper on cannabis use in pregnancy, noting a significantly increased risk of fetal death associated with maternal cannabis use.Other topics include antibiotic exposure and BPD risk in very preterm infants, comparisons of different BPD definitions, and the effects of phototherapy on plasma metabolites in preterm infants with hyperbilirubinemia.The episode features a special segment with Dr. James Sotiropoulos discussing his recent paper on initial oxygen concentrations for resuscitating extremely preterm infants. The study found a potential mortality benefit with higher initial FiO2, though more research is needed.Ben and Daphna also review papers on improving NICU communication and antenatal consultation practices. They close by welcoming new trainees starting in July and reminding listeners about The Incubator's board review resources for neonatology fellows.Overall, this comprehensive episode provides an excellent overview of recent impactful research across multiple areas of neonatology and perinatal medicine. As always, feel free to send us questions, comments, or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through Instagram or Twitter, @nicupodcast. Or contact Ben and Daphna directly via their Twitter profiles: @drnicu and @doctordaphnamd. The papers discussed in today's episode are listed and timestamped on the webpage linked below. Enjoy!

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Präklinischen NIV Profi: Mit effektiver Strategie zur Patiententoleranz

Rettungsdienst LUKS - Der Notfallmedizin Podcast

Play Episode Listen Later May 31, 2024 43:41

Mit der präklinischen NIV Therapie rettest du Leben. Das hört sich erstmal nach Clickbait an, ist aber ganz pragmatische Evidenz. Statistisch rettest du jeden 5. Patienten mit einer akuten, hyperkapnischen, respiratorischen Insuffizienz vor der Intubation und jeden 12.(!) vor dem Tod. Rettungsdienst LUKS - Der Notfallmedizin Podcast macht dich deswegen mit dieser Folge zum Präklinischen NIV Profi: Mit effektiver Strategie zur PatiententoleranzIn dieser Folge: - Die akute, respiratorische Insuffizienz erklärt.- Kontraindikationen der NIV Therapie ganz einfach merken mit dem Akronym SAFE- Darf ich vorstellen?: FiO2, PEEP, Pressure Support, Rampe und Flow Trigger- Mit Strategie zur Patiententoleranz. Vorbereiten, gewöhnen und therapieren.Das SAFE AkronymS - Schnappatmung, Apnoe, und KomaA - Verlegter AtemwegF - Fraktur (Schweres SHT oder Gesichtstrauma), PneumothoraxE - Erbrechen, Ileus oder GI-BlutungHomepage des Rettungsdienst LUKSLink zur letzten Folge zum Thema Notfall: Akut exazerbierte COPD - Obstruktion im Bronchialwald (und zu allen anderen Folgen)Aus den Rettungsdienst LUKS Nachrichten: SINNHAFT Übergabeschema: https://link.springer.com/article/10.1007/s10049-023-01167-4DSI von Dr. Daniel Freidorfer (Ab 32:38): https://www.youtube.com/watch?v=IKqM8BTrJJkDSI Kurzfassung von Fomamina: https://foamina.blog/2017/06/13/dsi/Kochrezept a la Nerdfallmedizin findest du unter diesem Link. Alle Evidenzen zu dieser Folge findest du hier: Ambühl, M. "Nicht-Invasive Ventilation - Ein praxisorientierter Ansatz für Präklinik und Schockraum" 20. Oktober 2023, https://www.youtube.com/watch?v=VG_aytxd7KEWesthoff, M., Neumann, P., Geisler, J., et. al. (2023). 10 Kernaussagen zur S2k-Leitlinie „Nichtinvasive Beatmung als Therapie der akuten respiratorischen Insuffizienz“. Abgerufen am 01. Januar 2024, von https://link.springer.com/article/10.1007/s00063-023-01017-8Scheschkowski, T., Budweiser, S. (2019). Akute respiratorische Insuffizienz bei chronischen Lungenerkrankungen. Nofallmedizin up2date, DOI: 10.1055/a-0868-2242Gruneberg, D., Schneider, N., Weilbacher, F., et. al. (2021). Nicht-invasive Beatmung in der Präklinik. Notarzt, DOI: 10.1055/a-1580-3036

PICU Doc on Call Shorts: Alveolar Gas Equation

Play Episode Listen Later Apr 28, 2024 20:06

Welcome to PICU Doc On Call, where Dr. Pradip Kamat from Children's Healthcare of Atlanta/Emory University School of Medicine and Dr. Rahul Damania from Cleveland Clinic Children's Hospital delve into the intricacies of Pediatric Intensive Care Medicine. In this special episode of PICU Doc on Call shorts, we dissect the Alveolar Gas Equation—a fundamental concept in respiratory physiology with significant clinical relevance.Key Concepts Covered:Alveolar Gas Equation Demystified: Dr. Rahul explains the Alveolar Gas Equation, which calculates the partial pressure of oxygen in the alveoli (PAO2). This equation, PAO2 = FiO2 (Patm - PH2O) - (PaCO2/R), is essential in understanding hypoxemia and the dynamics of gas exchange in the lungs.Calculating PAO2: Using the Alveolar Gas Equation, the hosts demonstrate how to calculate PAO2 at sea level, emphasizing the influence of atmospheric pressure, fraction of inspired oxygen (FiO2), water vapor pressure, arterial carbon dioxide pressure (PaCO2), and respiratory quotient (R) on oxygenation.A-a Gradient and Hypoxemia: The A-a gradient, derived from the Alveolar Gas Equation, is discussed in the context of hypoxemia evaluation. Understanding the causes of hypoxemia, including ventilation/perfusion (V/Q) mismatch, anatomical shunt, diffusion defects, and hypoventilation, is crucial for clinical diagnosis and management.Clinical Scenarios and A-a Gradient Interpretation: Through a clinical scenario, the hosts elucidate how different conditions affect the A-a gradient and oxygenation, providing insights into respiratory pathophysiology and differential diagnosis.Clinical Implications and Management Strategies: The hosts highlight the clinical significance of the Alveolar Gas Equation in assessing oxygenation status, diagnosing gas exchange abnormalities, and tailoring respiratory management strategies in the pediatric intensive care setting.Key Takeaways:Utility of the Alveolar Gas Equation: Understanding and applying the Alveolar Gas Equation is essential for evaluating oxygenation and diagnosing respiratory abnormalities.Interpreting A-a Gradient: A normal A-a gradient suggests alveolar hypoventilation as the likely cause of hypoxemia, whereas elevated gradients indicate other underlying pathologies.Clinical Relevance: Recognizing the clinical implications of the Alveolar Gas Equation aids in accurate diagnosis and optimal management of respiratory conditions in pediatric intensive care patients.Conclusion:Join Dr. Kamat and Dr. Damania as they unravel the complexities of the Alveolar Gas Equation, providing valuable insights into respiratory physiology and its clinical applications. Don't forget to subscribe, share your feedback, and visit picudoconcall.org for more educational content and resources.References:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter: Physiology of the respiratory system. Chapter 42. Khemani et al. Pages 470-481Rogers textbook of Pediatric intensive care: Chapter 44....

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Acute Bronchiolitis in the PICU

Extra to Love: A Trisomy Podcast

Play Episode Listen Later Feb 18, 2024 29:57

Hosts:Pradip Kamat, Children's Healthcare of Atlanta/Emory University School of MedicineRahul Damania, Cleveland Clinic Children's HospitalIntroductionToday, we discuss the case of an 8-month-old infant with severe bronchospasm and abnormal blood gas. We'll delve into the epidemiology, pathophysiology, and evidence-based management of acute bronchiolitis.Case SummaryAn 8-month-old infant presented to the ER with decreased alertness following worsening work of breathing, preceded by URI symptoms. The infant was intubated and transferred to the PICU, testing positive for RSV. Initial blood gas showed 6.8/125/-4, and CXR revealed massive hyperinflation. Vitals: HR 180, BP 75/45, SPO2 92% on 100% FIO2, RR 12 (prior to intubation), now around 16 on the ventilator, afebrile.Discussion PointsEtiology & Pathogenesis: Bronchiolitis is primarily caused by RSV, with other viruses and bacteria playing a role. RSV bronchiolitis is the most common cause of hospitalization in infants, particularly in winter months. Immuno-pathology involves an unbalanced immune response and can lead to various extra-pulmonary manifestations.Diagnosis: Diagnosis is clinical, based on history and examination. Key signs include upper respiratory symptoms followed by lower respiratory distress. Blood gas, chest radiography, and viral testing are generally not recommended unless warranted by severe symptoms or clinical deterioration.Management Framework: For patients requiring PICU admission, focus on oxygenation and hydration. High-flow therapy and nasal continuous positive airway pressure (CPAP) can be used. Hydration and feeding support are crucial. Antibiotics, steroids, and bronchodilators are generally not recommended. Mechanical ventilation and ECMO may be necessary in severe cases.Immunoprophylaxis & Nosocomial Infection Prevention: Palivizumab and nirsevimab are used for RSV prevention in high-risk infants. Strict infection control measures, including hand hygiene and isolation, are essential to prevent nosocomial infections.ConclusionRSV bronchiolitis is a common and potentially severe respiratory illness in infants. Management focuses on supportive care, with a careful balance between oxygenation and hydration. Immunoprophylaxis and infection control are crucial in preventing the spread of the virus.Thank you for listening to our episode on acute bronchiolitis. Please subscribe, share your feedback, and visit our website at picudoconcall.org for more resources. Stay tuned for our next episode!ReferencesRogers - Textbook of Pediatric Critical Care Chapter 49: Pneumonia and Bronchiolitis. De Carvalho et al. page 797-823Reference 1: Dalziel, Stuart R; Haskell, Libby; O'Brien, Sharon; Borland, Meredith L; Plint, Amy C; Babl, Franz E; Oakley, Ed. Bronchiolitis. The Lancet. , 2022, Vol.400(10349), p.392-406. DOI: 10.1016/S0140-6736(22)01016-9; PMID:...

Our Experience with Hospice/Comfort Care

Play Episode Listen Later Sep 13, 2023 48:33

Amber, Jenn, and Emma discuss their experience with "Hospice/Comfort Care" measures. One of us skipped over it, the other was not given a choice and the last of us chose it! In this episode we discuss our vastly different experiences and what lead us to make the decisions we did. We discuss the importance of titration of the FIO2 for your child. Disclaimer: "Amber here, in this episode we do discuss death, I want to put a quick disclaimer that my ease of using the word "dead" in the episode came from my own healing of trauma. I was at a beautiful retreat where I had the honor of hearing Bethany Bernard play her newest album. She discussed, there is a terrible stigma around using the words "death, and dead." It took me 9 months to be able to say that my own daughter had died and not using that verbiage for me, minimized her story."Our Website and Social's are listed Below!https://www.extratolove.org/https://www.facebook.com/ExtraToLove/https://www.instagram.com/Extratolove/

relationships social families hospice fio2 comfort care edwards syndrome

High-Flow Nasal Cannula: It's Not Just a Bunch of Hot Air!

EMS Today

Play Episode Listen Later Sep 11, 2023 8:04

Not every patient experiencing a moderate level of hypoxemic respiratory failure does well on a high-flow nasal cannula. (Photo courtesy Hamilton Medical AG)When I first started as a hospital respiratory therapist, the nasal cannula was our go-to low-flow (LFNC) device, designed to deliver an FiO2 of approximately 24 to 44% at flows of 1 to 6 liters per minute. When patients needed more oxygen, we would typically consider a face mask using a humidified large volume nebulizer to deliver 35-50%. A tandem setup could deliver upward of 80-90%. When more oxygen was necessary, we had the NRB (non-rebreather) mask. Read the full article here.

nasal hot air nrb fio2

Integrated PICU Journal Club: An Intubated, Febrile Toddler

PaperPlayer biorxiv neuroscience

Play Episode Listen Later May 21, 2023 19:55

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.I'm Pradip Kamat coming to you from Children's Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania from Cleveland Clinic Children's Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let's get into our episode.In today's episode, we're bringing together some of the best content from our previous podcasts to present a comprehensive clinical case. We're also excited to share with you some of the most highly cited articles from the past year, presented in a practical, case-based format. This episode will offer you valuable insights into the latest research findings while also highlighting the real-world application of this knowledge in a clinical setting.We'll start by presenting an interesting case of a toddler who was transferred to the PICU due to increasing respiratory distress:A 2-year-old male was brought to the emergency department with a chief complaint of increased work of breathing and URI symptoms, including a cough and runny nose. The child had no significant past medical history, was not taking any medications, and had no known allergies. The child was up-to-date on immunizations, and there were no significant sick contacts.The family brought the child to the emergency department after noticing a significant increase in work of breathing, including the use of accessory muscles, nasal flaring, and chest retractions. The initial physical exam revealed tachypnea and decreased breath sounds on the right side. The child's vital signs were concerning for respiratory distress, with a heart rate of 170 beats per minute, respiratory rate of 50 breaths per minute, and oxygen saturation of 85% on room air. Chest X-ray revealed right lower lobe pneumonia.The child was started on supplemental oxygen, and broad-spectrum antibiotics, and trialed with albuterol. Despite initial treatment, the child's respiratory distress worsened, and the decision was made to transfer the child to the PICU and place the patient on HFNC 1.5 L/kg. Upon admission to the PICU, the child's vital signs were still concerning, he was afebrile, with a heart rate of 180 beats per minute, respiratory rate of 60 breaths per minute, and oxygen saturation of 85% on 1.5L/kg HFNC at 75% FiO2. Given the persistent respiratory distress, the decision was made to intubate the child in the PICU for acute hypoxemic respiratory failure. Shortly after intubation, a central line is placed in the R internal jugular vein.To summarize key elements from this case:2-year-old with a prodrome of URI symptomsIs otherwise previously healthy with no significant medical history or allergiesDeveloped respiratory distress and diagnosed with pneumoniaTransferred to PICU, intubated for respiratory failureLet's fast forward in the case and talk about a scenario that frequently arises in the PICU. It's hospital day 2, and the patient's RSV swab is positive, and we're seeing some improvement on the X-ray....

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Ultrasound neuromodulation of an anti-inflammatory pathway at the spleen produces sustained improvement of experimental pulmonary hypertension

Play Episode Listen Later Mar 28, 2023

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.28.534567v1?rss=1 Authors: Zafeiropoulos, S., Ahmed, U., Mughrabi, I., Jayaprakash, N., Chadwick, C., Daytz, A., Bekiaridou, A., Saleknezhad, N., Atish-Fregoso, Y., Carroll, K., Giannakoulas, G., al-Abed, Y., Puleo, C., Nicolls, M. R., Diamond, B., Zanos, S. Abstract: Rationale: Chronic inflammation is pathogenically implicated in pulmonary arterial hypertension (PAH), however, it has not been adequately targeted therapeutically. Objectives: We investigated whether neuromodulation of an anti-inflammatory neuroimmune pathway using noninvasive, focused ultrasound stimulation of the spleen (sFUS) can improve experimental pulmonary hypertension (PH). Methods: PH was induced in rats by SU5416 (20 mg/kg SQ) injection, followed by 21 (or 35) days of hypoxia (10% FiO2). Animals were randomized to receive either daily, 12-min-long sessions of sFUS or sham-stimulation, for 14 days. Invasive hemodynamics, echocardiography, autonomic function parameters, lung and heart histology/immunohistochemistry, and lung single-cell-RNA sequencing were performed after treatment to assess effects of sFUS. Results: Compared to sham, sFUS treatment reduces right ventricular (RV) systolic pressure by 25-30%; it improves RV function and indices of autonomic function. sFUS treatment reduces wall thickness in small pulmonary arterioles, suppresses inflammatory cell infiltration in lungs and RV fibrosis and hypertrophy, and lowers serum levels of brain natriuretic peptide. Beneficial effects persist for weeks after sFUS treatment discontinuation and are more robust when treatment is initiated earlier and delivered for longer. Selective ablation of the splenic nerve abolishes the therapeutic benefits of sFUS. sFUS treatment downregulates several inflammatory genes and pathways in nonclassical and classical monocytes, and macrophages in the lung; differentially expressed genes in those cell types are significantly enriched for genes associated with human PAH. Conclusions: Noninvasive, sFUS treatment causes sustained improvement of hemodynamic, autonomic, laboratory and pathological manifestations of experimental PH, and downregulates inflammatory genes and pathways in the lung, many of which are relevant in human disease. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Low Flow Oxygen Systems

Respiratory Therapy Study Hall

Play Episode Listen Later Mar 14, 2023 11:20

This episode covers different types of nasal cannulas and how to estimate the FiO2. Low flow masks, including simple, non-rebreather, and partial rebreather. I talk about when to use each mask and the hazards that can potentially be associated with them. Find the Ultimate Oxygen Therapy Study Package on www.myvresp.com. You can search Respiratory Therapy Study Hall on Facebook and YouTube.

oxygen fio2

247. CCC: Biventricular Failure and the Use of VA-ECMO with Dr. Ann Gage

Cardionerds

Play Episode Listen Later Dec 5, 2022 54:56

In this episode, we discuss the utility of veno-arterial extra-corporeal membrane oxygenation (VA-ECMO) for the temporary management of biventricular failure and cardiogenic shock requiring full cardiopulmonary support. Here, we define the types of ECMO and describe the unique physiology of this mechanical circulatory support platform, as well as review the potential complications and management strategies. Most notably, we highlight indications for and contraindications to the use of VA-ECMO and review the importance of patient selection. Lastly, we discuss de-escalation and de-cannulation strategies for patients on VA-ECMO as a bridge to recovery. Join Dr. Amit Goyal (CardioNerds Cofounder and FIT at Cleveland Clinic), Dr. Yoav Karpenshif (Series Co-chair and FIT at University of Pennsylvania), and Dr. Megan Burke (Episode FIT Lead and FIT at University of Pennsylvania) as they learn about how to care for some of our sickest patients from Dr. Ann Gage, interventional and critical care cardiologist at Centennial Heart. At the beginning of the episode, enjoy a message from the very first CardioNerds Scholar, Dr. Katie Vaughan (Chief Resident and soon Cardiology Fellow at BIDMC). Episode notes were developed by Dr. Megan Burke. Audio editing by CardioNerds Academy Intern, Hirsh Elhence. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Biventricular Failure and the Use of VA-ECMO Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a form of temporary mechanical circulatory support that can do the work of both the heart and lungs. The ECMO circuit is a narcissist, i.e. cannulas are named in reference to the circuit and not the patient (“inflow” vs “outflow”). The decision to utilize ECMO should be made by a multidisciplinary shock team and patient selection is KEY! ECMO physiology rule #1: VA-ECMO increases LV afterload Patients on VA-ECMO should be monitored with a PA catheter and an arterial line in the right arm Show notes - Biventricular Failure and the Use of VA-ECMO Notes drafted by Dr. Megan Burke. 1. What is ECMO and what are the different types? Extracorporeal membrane oxygenation (ECMO) is a temporary form of mechanical life support that comes in two flavors: veno-arterial, or “VA” and veno-venous, or “VV.” VV-ECMO supports extracorporeal gas exchange in the setting of acute respiratory failure VA-ECMO provides full circulatory support in addition to gas exchange, doing the work of both the heart and lungs. 2. What are the components and “anatomy” of the VA-ECMO circuit? The circuit is made up of the following major components: Venous (inflow) cannula Centrifugal Pump Oxygenator (also responsible for CO2 removal) Arterial (outflow) cannula The cannulas are named in reference to the ECMO circuit, not the patient. Dr. Gage suggests that we think of the ECMO circuit (and mechanical circulatory support in general) as narcissistic, i.e. flow is always in reference to the device. Gas exchange happens in the oxygenator. In the oxygenator blood flows through thin filaments that allow for diffusion of oxygen and carbon dioxide. Gas flows in the opposite direction of blood flow to maximize diffusion through the countercurrent effect. Oxygenation is determined by rate of blood flow through the oxygenator and FiO2 delivered. Carbon dioxide removal is determined by rate of countercurrent gas flow,

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Dr. Bharath Srivatsa, Neonatologist at Pediatrix Neonatology Associates of Atlanta

Becker’s Healthcare Podcast

Play Episode Listen Later Oct 27, 2022 16:51

In this episode we unpack and discuss recent neonatal research published in The Journal of Pediatrics. Tune in to hear from Dr. Bharath Srivatsa on what he and the research team aimed to learn about the effect of a novel oxygen saturation targeting strategy for extremely preterm neonates. We talk about the findings, a solution on how NICUs can incorporate simultaneous SpO2 and FiO2 monitoring, and more.This episode is sponsored by Pediatrix.

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227. CCC: Positive Pressure Ventilation in the CICU with Dr. Sam Brusca, Dr. Chris Barnett, and Dr. Burton Lee

Cardionerds

Play Episode Listen Later Aug 14, 2022 65:40

The modern CICU has evolved to include patients with complex pulmonary mechanics requiring more non-invasive and mechanical ventilation. Series co-chairs Dr. Eunice Dugan and Dr. Karan Desai along with CardioNerds Co-founder Dr. Amit Goyal were joined by FIT lead, Dr. Sam Brusca, who has completed his NIH Critical Care and UCSF Cardiology fellow and currently faculty at USCF. We were fortunate enough to have two expert discussants: Dr. Burton Lee, Head of Medical Education and Global Critical Care within the National Institutes of Health Critical Care Medicine Department and master clinician educator with the ATS Scholar's Critical Care for Non-Intensivists program, and Dr. Chris Barnett, ACC Critical Care Cardiology council member and Section Chair of Critical Care Cardiology at UCSF. In this episode, these experts discuss the basics of mechanical ventilation, including the physiology/pathophysiology of negative and positive pressure breathing, a review of ventilator modes, and a framework for outlining the goals of mechanical ventilation. They proceed to apply these principles to patients in the CICU, specifically focusing on patients with RV predominant failure due to pulmonary hypertension and patients with LV predominant failure. Audio editing by CardioNerds Academy Intern, student doctor, Shivani Reddy. The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif. Pearls • Notes • References • Production Team CardioNerds Cardiac Critical Care PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Positive Pressure Ventilation in the CICU Respiratory distress, during spontaneous negative pressure breathing can lead to high transpulmonary pressures and potentially large tidal volumes. This will increase both RV afterload (by increasing pulmonary vascular resistance) and LV afterload (by increasing LV wall stress). An analogy for the impact of negative pleural pressure during spontaneous respiration on LV function is that of a person jumping over a hurdle. The height of the hurdle does not increase, but the ground starts to sink, so it is still harder to jump over. Intubation in patients with right ventricular failure is a tenuous situation, especially in patients with chronic RV failure and remodeling (increased RV thickness, perfusion predominantly during diastole, RV pressure near or higher than systemic pressure). The key tenant to safe intubation is avoiding hypotension, utilizing induction agents such as ketamine or etomidate, infusing pressors, and potentially even performing awake intubations. Non-invasive positive pressure ventilation in HFrEF has hemodynamic effects similar to a cocktail of IV inotropes, dilators, and diuretics. CPAP decreases pulmonary capillary wedge pressure (LV preload), decreases systemic vascular resistance (afterload), and increases cardiac output. Airway pressure during mechanical ventilation is based on the “equation of motion”: Pressure = Volume/Compliance + Flow*Resistance + PEEP. Our goals of oxygenation on mechanical ventilation include achieving acceptable PaO2/Sat with the lowest FiO2 possible (avoiding oxygen toxicity) and optimal PEEP (which increases oxygenation but can have detrimental impact on cardiac output) Our goals of ventilation on mechanical ventilation include achieving acceptable pH and PaCO2 while preventing ventilator induced lung injury and avoiding auto-PEEP. We prevent lung injury by reducing tidal volume (ideally

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77: ECMO in Trauma with Justyna Swol

ED ECMO

Play Episode Listen Later Jul 13, 2022 35:48

Using ECMO for traumatic patients has had some promising papers through the years, but the data overall is still poor. Justyna Swol has teamed up with ELSO to improve this deficiency by making a trauma carve out of the ELSO registry. In this episode, Zack discusses with Justyna the many facets of ECMO in trauma. A few pearls and references are below: Anticoagulation in ECMO is not mandatory. A reasonable strategy is heparinized circuit with a titrating dose of systemic heparin as necessary in the trauma patient. This includes everyone from isolated pulmonary contusions to intracranial hemorrhage. VV-ECMO similar to ARDS in medical causes can be used and likely offers survival benefit to those patients with post traumatic lung injury. Initiating early (maybe PaO2 of 80 on 100% FiO2) is likely best. ECPR can be done in the traumatic arrest. Best when done in parallel to the other resuscitative needs of the patient. Data is promising in case series. Need for bigger data sets is clear.

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Pulmonary Hemorrhage

Play Episode Listen Later Jul 10, 2022 17:21

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. Welcome to our Episode a 16-year-old who is coughing up blood. Here's the case: A 16-year-old female with h/o SLE was transferred to the PICU due to hypoxia requiring increasing FIO2. A few hours prior to admission to the PICU patient also started coughing up blood and had difficulty breathing. The patient was admitted to the general pediatric floor 2 days earlier for pneumonia requiring an IV antibiotic and O2 via NC. Once transferred to the PICU, she had a rapid deterioration with progressive hematemesis, worsening respiratory distress, and saturations in the low 70s requiring escalating FIO2. The patient was emergently intubated using ketamine + fentanyl and rocuronium. Chest radiograph showed: Worsening bibasilar alveolar and interstitial airspace disease concerning pulmonary hemorrhage. The patient was initially placed on HFOV Paw 26, FIO2 70%, Hz 8, Dp 70, and later transitioned to airway pressure release ventilation or APRV. The patient was also started on inhaled tranexamic acid or TXA and high-dose pulse steroids. The patient initially continued to have some blood coming out from the ETT with suctioning but secretions became clear in ~24 hours. The mother reported that the patient has never had hematemesis/hemoptysis before, or bleeding from any site in the past. Denied history of frequent respiratory infections or recent URI symptoms. The patient has been vaccinated/boosted x3 vs covid. Her COVID PCR is negative. The mother states that she does not engage in tobacco products or alcohol. A physical exam revealed a well-developed teenage girl laying supine in bed deeply sedated and mechanically ventilated. There was decreased AE at lung bases and coarse breath sounds throughout. There was no hepatosplenomegaly and exams of the heart, abdomen and other systems were normal. There was no skin rash and extremities were well perfused with no clubbing in the fingers. The pulmonary team was consulted and a workup was started for pulmonary hemorrhage. To summarize key elements from this case, this patient has: Autoimmune disease: Systemic lupus erythematosus Respiratory Failure warranting MV 2/2 Pulmonary hemorrhage Her presentation and deterioration bring up a concern for diffuse alveolar hemorrhage our topic of discussion for today. This episode will be organized… Definition Etiology Pathophysiology Diagnosis Management Rahul: How do we define pulmonary hemorrhage (PH): PH is defined as the extravasation of blood into airways and/or lung parenchyma. Blood in the airways produces a diffusion barrier resulting in hypoxemia. Due to the reduction of airway diameter from accumulated blood, there is increased airway resistance and even airway obstruction. Subsequently, ventilation can be impaired leading to increased WOB as well as myocardial work required for O2 delivery. Repeated episodes of PH can result in interstitial fibrosis thus changing lung compliance. Hemoptysis by definition is any bleeding from below the vocal cords. PH can be classified as focal or diffuse. Diffuse is further classified as diffuse immune or diffuse nonimmune. Loss of 10% of a patient's circulating blood volume into the lungs, regardless of age, causes a significant alteration in cardiorespiratory function and should be considered massive. In adults, massive pulmonary hemorrhage is defined as blood loss of 600mL or more in 24 hours. In infants, the involvement of at least two pulmonary lobes by confluent foci of extravasated RBCs constitutes as massive PH. “Enough bleeding to make one nervous is probably massive.” Let's pivot and talk about etiologies. Pradip, What are some of the causes of pulmonary hemorrhage in the PICU? Non-immune diffuse PH is usually seen in patients with congenital heart disease (TAPVR, pulmonary atresia, mitral stenosis, hypoplastic left heart syndrome to name a few) neonates (secondary to sepsis, HIE, BW < 1500...

Post Cardiac Arrest Care

Pass ACLS Tip of the Day

Play Episode Listen Later Jun 7, 2022 4:59

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!

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Ventilation of the Ex-premie in the PICU

Play Episode Listen Later Jun 5, 2022 28:17

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

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Necrotizing Enterocolitis (NEC)

children babies medicine current healthcare ga echo improved nicu sma preventative nec bpd npo bw prematurity necrotizing podcast dedicated fio2 necrotizing enterocolitis

Play Episode Listen Later Apr 10, 2022 16:07

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat. I'm Dr. Ali Towne, a rising 3rd-year pediatrics resident interested in a neonatology fellowship, and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode a 5-month-old, ex-28 week female with abdominal distention. Here's the case: A 5-month-old, ex 28 week, female with a past medical history of severe BPD, pulmonary hypertension, home oxygen requirement, and G-tube dependence presents with hypoxemia and increased work of breathing. The patient has a history of prolonged NICU stay with 8 weeks of intubation. The patient developed worsening respiratory distress requiring increased support and eventual intubation for hypoxemic respiratory failure. Echo showed worsened pulmonary hypertension with severe systolic flattening of the ventricular septum and a markedly elevated TR jet. The patient had poor peripheral perfusion, and upon intubation was started on milrinone and epinephrine. The patient improved, but the patient then developed abdominal distention and increasing FiO2 requirements prompting an abdominal x-ray. X-ray showed diffuse pneumatosis with portal venous gas. The patient was made NPO and antibiotic therapy was initiated. To summarize key elements from this case, this patient has NEC. NEC is not a homogenous disease, but rather a collection of diseases with similar phenotypes. Some people split NEC into two categories: Cardiac NEC and Inflammatory NEC. Babies who develop cardiac NEC tend to be significantly older than babies who develop inflammatory NEC (about 1 month vs 2 weeks). There are three main contributory factors to the development of NEC: gut prematurity, abnormal bacterial colonization, and ischemia-reperfusion injury. Many cases result from an ischemic insult to the bowel, resulting in translocation of intra-luminal bacteria into the wall of the bowel, but the etiology and course of NEC can be very variable. This translocation can cause sepsis and death; the ischemia of the bowel can result in intestinal perforation and/or necrosis. Necrotizing enterocolitis (NEC) is one of the most common gastrointestinal emergencies in the newborn infant. It is estimated to occur in 1 to 3 per 1000 live births. More than 90 percent of cases occur in very low birth weight (VLBW) infants (BW

45: Pediatric Post Cardiac Arrest Syndrome (PCAS) Part 1

Play Episode Listen Later Mar 13, 2022 21:38

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat. My name is Rahul Damania, a current 2nd-year pediatric critical care fellow. We come to you from Children's Healthcare of Atlanta-Emory University School of Medicine. Today's episode is dedicated to pediatric post-cardiac arrest care. We are going to split this topic into two episodes, part one of pediatric post-cardiac arrest syndrome will address the epidemiology, causes, and pathophysiology. I will turn it over to Rahul to start with our patient case... 11 yo previously healthy M who is admitted to the PICU after cardiac arrest. The patient was noted to be found unresponsive and submerged in a neighborhood pool. He was pulled out by bystanders and CPR was started for 5 minutes with two rounds of epinephrine prior to achieving ROSC. During transport to the OSH, the patient developed hypotension requiring a continuous epinephrine infusion. His initial blood gas was notable for a mixed respiratory and metabolic acidosis: 7.0/60/-20 His initial serum lactate was 6.8 mmol/L. He presents to the PICU with a temperature of 36.6, HR 130s, MAPs 50s on Epinephrine infusion at 0.03mcg/kg/min He is mechanically ventilated with notable settings PEEP of 10, FiO2 65%. The patient is taken to head CT which shows diffuse cerebral edema and diffusely diminished grey-white differentiation most pronounced in the basal ganglia. Great Rahul, can you please comment on his physical exam & PMH? Important physical exam findings include an unresponsive intubated patient with a cervical collar and bilateral non-reactive pupils at 4mm. The patient received mechanical ventilation with coarse breath sounds. A heart exam revealed tachycardia with no murmur or gallop. The patient does not respond to stimuli, intermittent jerking movements of arms and legs were observed. There was no evidence of rash or trauma. No past medical history of seizures or any heart disease. No home medications or toxic ingestions are suspected. So now he is transferred to the ICU, what did we do? An arterial line, central venous line, urinary catheter, esophageal temperature probe was placed. The patient was ventilated using a TV of 6cc/kg and a PEEP of 10 (FIO2 ~65%) to keep SPO2 >94%. The patient initially had runs of ventricular tachycardia for which lidocaine was used. Although the initial EKG showed mild QTc prolongation, it subsequently normalized and was considered to be due to his cardiac arrest and resuscitation. An echocardiogram revealed normal biventricular systolic function (on epinephrine) and also showed normal origins of the coronary arteries. Comprehensive Arrhythmia Panel did not identify a specific genetic cause for the patient's sudden cardiac arrest. The patient was placed on continuous EEG, which demonstrated severe diffuse encephalopathy with myoclonic status likely from anoxic brain injury Patient was also started on Levetiracetam and valproic acid. Initial portable CT scan done on day # of admission showed diffuse cerebral edema and diffusely diminished gray-white differentiation (most pronounced in the basal ganglia). MRI was deferred due to patient instability. The case we talked about highlights a patient who had a trigger that then resulted in cardiac arrest is common is one of the common reasons for admission to the PICU at Children's hospitals whether from submersion injury, trauma, ingestion, cardiac arrhythmia, sepsis, etc. Can we start by defining post-cardiac arrest syndrome? Successful resuscitation from cardiac arrest results in a post-cardiac arrest syndrome, which can evolve in the days to weeks after the return of spontaneous circulation. The components of post-cardiac arrest syndrome are brain injury, myocardial dysfunction, systemic ischemia/reperfusion response, and persistent precipitating pathophysiology. Prior to 2008, the AHA pediatric advanced life support (PALS) guidelines...

Siyanozla Gelen Çocuk Hastaya Yaklaşım

Play Episode Listen Later Jan 28, 2022 12:50

Bu yazımda acile başvurduğunda hepimiz için endişeli bir sürecin başladığı bir tablodan bahsedeceğim: çocuk hasta ve siyanoz. Kimi zaman temizlemekle geçen bir gıda boyası kadar basitçe çözülse de, bir çok durumda yönetilmesi zorlu bir süreç olarak karşımıza çıkmaktadır. Bu hastalarda dakikalar içinde yapılacak müdahaleler hayat kurtarıcı olacaktır. Hiç bir çocuğun hasta olmadığı bir dünya dileyerek tanımlarla başlayalım. İyi okumalar. Tanımlar Siyanoz, kılcal yatakta deoksijenize hemoglobinin artmasıyla dokunun mavi-mora doğru renk değiştirmesidir. Aydınlatma koşulları, gölgelenme, ciltteki pigmentasyonlara bağlı ilk bakışta gözlenmesi kimi zaman zor olsa da tırnak yatakları, dudaklar, müköz membranlar ve derinin ince olduğu bölgelerde tanınması daha kolaydır. Çocuklarda yaşamı tehdit eden siyanoz çoğunlukla solunumsal hastalıklardan kaynaklanmaktadır. Santral ve periferik olmak üzere iki çeşit siyanoz görülür. Santral siyanozda kandaki deoksijenize hemoglobin konsantrasyonu 5 g/dL'nin üzerindedir.1 Periferik siyanozlu hastalarda ise kan oksijen saturasyonu normaldir fakat, cilt ve ciltaltı damar yatağındaki vazokonstruksiyon morarmaya neden olmuştur. Tek bir ekstremitede gözlenen periferik siyanoz ise arteriyel veya venöz dolaşımın lokalize kesintiye uğradığını düşündürür. 2,3 Yaşamı Tehdit Eden Durumlar Öncesinde sağlıklı olan bir çocukta yeni gelişen santral siyanoz sıklıkla solunumsal nedenlerden kaynaklanır. Küçük bebeklerde kardiyak ve pulmoner vasküler sebepler de etyolojide önemli yer turar. Solunumsal Nedenler Oksijenin alveollere ulaşmasını engelleyen veya alveoler oksijen geçirgenliğini bozan aşağıda ayrıntılandırılmış herhangi bir sebep siyanoza neden olabilir. Azalmış FiO2 İnspire edilen havadaki oksijen konsantrasyonunun düşük olması siyanoza sebep olabilir. Çocuklarda bu durum sıklıkla yangınlarda gözlenir. Yangınlarda çocuklarda karbon monoksit ve siyanid intoksikasyonu ve termal yanıklar ve partikül solumaya bağlı hava yolu obstrüksiyonlarına da dikkat etmek gerekir. Nadiren çocuklar boğucu gazlara maruz kalabilirler. Örneğin propan, bütan gibi yanıcı gazlara mutfak tüpü ve ocaklardan sızmalarda maruz kalınabilir. Bu durumlarda da azalmış FiO2 ye bağlı hipoksemi ve siyanoz gözlenir. Boğucu gaz ortamdan uzaklaştırılmalı ve derhal çocuğa %100 oksijen vermelidir. Üst hava yolu obstrüksiyonu Bu başlıkta etyolojide yabancı cisim obstrüksiyonu yanı sıra, krup, bakteriyel trakeit, epiglottit, termal yaralanma, trakeobronşiyal ağaç yaralanması ve konjenital anomaliler yer alır. Obstrüksiyona bağlı alveolar ventilasyon azalır ve hipoksemiye bağlı santral siyanoz gözlenir. Bu hastalarda tedavi ilgili uzman tarafından derhal başlatılmalıdır, tıkanıklığın giderilememesi durumunda çocuğun durumu hızla kötüleşir. Altı aydan küçük zorunlu burun solunumu yapan bebeklerde burun salgıları da tıkanıklığa neden olabilir ve siyanoz gözlenebilir. Salgıların aspire edilmesi durumu hızlıca geri çevirir. Göğüs duvarı bozuklukları veya yetersiz akciğer ekspansiyonu Bu durumla genellikle yüksek enerjili toraks travmaları sonrasında karşılaşılır. Yelken göğüs, hemopnömotoraks, tansiyon pnömotoraks ile birlikteliği sıktır. Klinikte göğüs duvarında deformiteler, ekimozlar, palpasyonda ciltaltında ve kotlarda krepitasyonlar ve hassasiyet yer alabilir. Bu yaralanmalar hızlıca tanınmalı ve iğne veya tüp torakostomi uygulanmalıdır. Ayrıca siyanoz solunum sıkıntısı yaşayan bebeklerde ve çocuklarda göğüs duvarı kas yorgunluğuna bağlı da gözlenebilir. Bu durumda noninvaziv ve gerektiğinde invaziv mekanik ventilasyon ile solunum desteklenmelidir. İntrinsik akciğer hastalıkları Şiddetli pnömoni, astım, boğmaca, bronşiolit, ampiyem, nonkardiyak pulmoner ödem, kistik fibrozis siyanoza neden olan en sık intrinsik akciğer hastalıklarıdır. Bu etyolojiler hem küçük hava yollarının obstrüksiyonuna hem dealveollerde oksijen değişiminin bozulmasına neden olarak siyanoz yapabilirler.

alt yang bu dl kimi ayr tek salg yakla gelen ayd fio2 santral

41: Airway Clearance Techniques in the PICU

Play Episode Listen Later Jan 23, 2022 28:19

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our discussion today on airway clearance in the critically-ill patient in the PICU. We will focus on the use of pharmacological as well as non-pharmacological techniques in critically ill children admitted to the ICU. This episode will be a general overview as specific clinical scenarios such as NM disease may warrant specific therapeutics. Let's get started with the case: We have an 8-month old ex-34 week premie intubated for acute respiratory failure secondary to RSV bronchiolitis. The patient is on a conventional mechanical ventilator receiving a TV of 6ml/kg, rate of 20, PEEP 6, 40% FiO2 inspiratory time of 0.7 CXR shows a pattern suggestive of viral pneumonia with minimal hyperinflation and atelectasis of the right middle lobe. The patient has excessive secretions when the suction catheter is assessed. The patient is hemodynamically stable and is on feeds via a NG tube. Rahul, Can you comment on how a child clears his/her pulmonary secretions normally when not ill? That's an excellent question. Normally some baseline secretions are produced by all humans. Normal bronchial secretions are made up of contributions from mucus-secreting (goblet)cells as well as cells secreting serous fluid. The ciliary epithelium made of columnar cells line the entire tracheobronchial tree up to the alveolar ducts. This ciliary epithelium provides the coordinated rhythmic force that propels the overlying “mucus blanket” towards the central airways and upper respiratory tract. Primary mechanisms of tracheobronchial clearance of these secretions consist of (1) The mucociliary (MC) escalator in the smaller airways and (2) Cough in central and larger airways. The co-ordinating activity of the beating cilia and their interaction with the overlying viscoelastic layer of mucus makes up the mucociliary escalator. The MC escalator helps remove both healthy and pathologic secretions from the airways as well as the removal of inhaled particles. This MC transport can be affected by mycoplasma, influenza and other viruses as well as exposure to toxins (cigarette smoke, vaping) as well as in CF, asthma, COPD, and ciliary dyskinesia just to name a few. Once the secretions are in large or central airways they are coughed out or swallowed. Let's transition and talk a little on how one generates an effective cough: For an effective cough one needs firstly to take a sufficiently deep breath in. The glottis needs to close briefly to allow an increase in intrathoracic pressure This is followed by expulsive glottic opening together with abdominal contraction, which results in air being forcibly expelled. Individuals with neuromuscular disease, bulbar insufficiency, obtunded patients, those on MV with chemical neuromuscular blockade, severe skeletal deformity may have decreased cough expiratory airflow. Reduced ability to cough results in secretion retention, mucus plugging, atelectasis and pre-disposition to infection even if the MC escalator function is normal. Q2. Pradip can you tell us about atelectasis This is a great question. The term atelectasis means “imperfect expansion” and indicates reversible loss of aerated lung with otherwise normal lung parenchyma. Thats a nice concise definition, so if atelectasis reperesents imperfect expansion, what are mechanisms which keep our lungs open? There are three major mechanisms: 1. Pulmonary Surfactant 2. Collateral Ventilation 3. Lung & Chest Wall Balance Let's go into each of these in more detail: A pulmonary surfactant that covers the large alveolar surface is composed of phospholipids (mostly phosphatidylcholine), neutral lipids, and surfactant-specific apoproteins (termed surfactant proteins A , B , C , and D ). By reducing...

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40: Toddler with Cough and Difficulty Breathing

breathing mechanical rr modes critically optimising roadside ventilation resus rob james fio2

Play Episode Listen Later Jan 16, 2022 30:50

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our episode of a three-year-old girl presenting with a cough and difficulty breathing Here's the case presented by Rahul: A previously healthy 3-year-old girl presented to the OSH for difficulty breathing. She had a two-day h/o of cough (worse at night) and congestion but no fever. She has no h/o of emesis, h/o recent travel, or exposure to some/toxins. Initially, she received steroids, albuterol, and O2 but due to continued worsening of breathing and hypoxia-She was transferred to our PICU for initiation of High Flow Nasal Cannula. She has no allergies and her immunizations are up to date. There is a strong family history of asthma and atopic dermatitis. The mother also noted that the patient has h/o of coughing episodes while playing outside with her siblings. Initial Vitals: Temp 37.9, HR 100, BP 97/73, respiratory rate 49, SPO2 98% on 15LPM HFNC at 60% FIO2 , weight 17.5kg On PE: The child is awake, playful. she is tachycardic with no murmur. She has subcostal, intercostal, supra-sternal retractions. There is bilateral symmetric chest expansion. The air entry is decreased with diffuse (B) wheeze. There is atopic dermatitis in the flexor areas of the elbows/knees. The rest of the physical examination was normal. No hepatosplenomegaly. Viral panel: positive for HMP, SARS COV-2 negative CXR: Atelectasis superimposed upon viral pneumonitis versus multifocal bronchopneumonia. No evidence of parapneumonic effusion or air leak. CBC and BMP are normal. To summarize key elements from this case, this 3-year-old girl has: Cough and congestion Increased WOB and difficulty breathing Hypoxia No fever or rash No recent ingestions or exposure to tobacco smoke All of which brings up a concern for a lower airway obstructive process most likely acute asthma Let's transition into some history and physical exam components of this case? Rahul, what are key history features in this child who presents with increased work of breathing? Cough and congestion Difficulty breathing No h/o suggestive of atopic dermatitis Increased WOB: retractions (subcostal, intercostal, suprasternal). Important to note there is no nasal flaring, head bobbing or grunting. Decreased AE Diffuse (B) wheezing. No subcutaneous emphysema on palpation of the chest or cervical region. Hypoxia needing oxygen Atopic dermatitis No crackles No hepatomegaly No altered mental status Not all respiratory distress arises within the respiratory tract. Important physical examination to note in any infant or toddler with increased work of breathing is to palpate for hepatomegaly as well as carefully listen for bilateral inspiratory crackles. The presence of hepatomegaly or (B) crackles should raise concern for myocarditis or congestive heart failure. In Newborns with respiratory distress-always make a habit to feel femoral pulses. Acidosis, intracranial hemorrhage, foreign body, panic attacks can also present as respiratory distress. To continue with our case, Pradip, the patient's labs/diagnostic were consistent with: CBC, BMP were normal Respiratory viral panel positive for HMP virus, Negative for SARS-COV-2 Chest radiograph: Atelectasis superimposed upon viral pneumonitis versus multifocal bronchopneumonia OK, to summarize, we have: A 3-year-old with acute respiratory distress, wheezing, hypoxia after 2 days h/o of cough/congestion. Rahul, let's start with a short multiple-choice question: A 15-year-old teenager with know h/o asthma presents to the ED in severe respiratory distress, increased work of breathing, hypoxia, and diffuse wheezing. Of the following the presentation that would most likely require intubation in this teenager include- A) Inability to talk in complete sentences B) A blood gas that shows...

Ventilation; Roadside to Resus

The Resus Room

Play Episode Listen Later Dec 15, 2021 58:32

Critically unwell patients often present with inadequate oxygenation and ventilation, in this episode we're going to explore some of the physiology of critical illness, look at how we can improve oxygenation and ventilation, take a look mechanical ventilation and have a think about how we can deliver this to a really high level. We'll be covering the following; Type 1 & 2 respiratory failure Breathing assessment Optimising patients own ventilation Mechanical ventilation Modes of ventilation Setting up a ventilator; tidal volume, RR, FiO2, I:E ratios, dead space End tidal CO2 Optimising oxygenation & ventilation Hand ventilation Ventilation in cardiac arrest Once again we'd love to hear any thoughts or feedback either on the website or via twitter @TheResusRoom. Enjoy! Simon, Rob & James

Intro to Mechanical Ventilation

Pharmacy to Dose: The Critical Care Podcast

Play Episode Listen Later Nov 15, 2021 72:31

Introduction to Mechanical Ventilation Special Guests: Andrea Sikora Newsome, PharmD, BCPS, BCCCP, FCCM Reference List: https://pharmacytodose.files.wordpress.com/2021/11/mechanical-ventilation-references.pdf 05:49 – Indications for mechanical ventilation; 12:45 – Principles of critical care; 16:40 – Review of respiratory cycle; 20:04 – Common terminology (Tidal volume, FiO2, PEEP); 32:01 – Ventilator modes; 39:15 – Pressure v. volume control; 47:00 – Inspiratory pressure, plateau pressure, and autoPEEP; 51:50 – Ventilator weaning; 61:00 – Take-home points PharmacyToDose.Com @PharmacyToDose on Twitter PharmacyToDose@Gmail.com

pressure principles tidal peep pharmd indications ventilator bcps mechanical ventilation fio2 bcccp

Podcast 715: Heated High Flow O2

Emergency Medical Minute

Play Episode Listen Later Sep 27, 2021 4:59

Contributor: Nick Hatch, MD Educational Pearls: High flow nasal cannula (HFNC) or “heated high flow” can deliver higher oxygen levels than nasal cannula It typically is used as an “intermediate” between oxygen via nasal cannula and other non-invasive positive pressure devices, such as BiPAP Can modify both the FiO2 and flow rate Maximum flow rate is typically 60 liters per minute (compare that to a typical breath that is 30-40 L/min) Humidification of HFNC is important due to risk of epistaxis from drying out the nasal mucosa Large energy expenditure to humidify airflow by a patient in respiratory distress, so humidified oxygen may help decrease this metabolic demand References Nishimura M. High-Flow Nasal Cannula Oxygen Therapy in Adults: Physiological Benefits, Indication, Clinical Benefits, and Adverse Effects. Respir Care. 2016;61(4):529-541. doi:10.4187/respcare.04577 Hacquin A, Perret M, Manckoundia P, et al. High-Flow Nasal Cannula Oxygenation in Older Patients with SARS-CoV-2-Related Acute Respiratory Failure. J Clin Med. 2021;10(16):3515. Published 2021 Aug 10. doi:10.3390/jcm10163515 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!

md large published maximum sars cov heated indication summarized emm adverse effects ama pra category fio2 respir care

Oksijenasyon Yöntemleri

Play Episode Listen Later Aug 20, 2021 8:21

Oksijenasyon acil servislerin ve hastane öncesi sağlık hizmetlerinde günlük klinik pratiğinin en sık uygulanan ve en önemli parçalarından biri1, peki hastalara her gün uyguladığımız oksijen terapisini yeterince tanıyor muyuz? Pandemi sürecinde hastaları oksijenize etmek için mekanik ventilasyondan bahsettik ama her gün uyguladığımız oksijen terapisini yeterince irdelemediğimizi düşünerek bu konuyu tartışalım istedim. Bu yazıda günlük klinik pratiğimizde sıklıkla kullandığımız yöntemleri ve özelliklerini ele alacağız. Ancak başlamadan önce oksijenin bir ilaç olduğunu hatırlatmak gerekli! Yani uygun doz, uygun süre, uygun sıklık ve uygun yöntem kullanılmalı! Her ilaçta olduğu gibi azı yetersiz, fazlası zararlı2 Oksijenasyon Hastaların havayolu yönetiminde temel amacımız hastalara yeterli ventilasyon ve oksijenizasyon sağlamaktır.2 Oksijen hipoksemi üzerine etkili ancak hipoksemik olmayan nefes darlığında kandaki yeterli O2 düzeylerini sağlamak, miyokard iş yükünü azaltmak, hipoksemiyi önlemek/mevcutsa tedavi etmek temel amaçlarımız arasında yer alıyor. Bu yazımızda kullandığımız yöntemler ve özellikleri ele alınacak. Bu konuda kullanılan yöntemlerin temel çerçevesi ve hangi hastalara nasıl oksijen verilmesi gerektiğine yönelik Başak Bayram'ın yazısına buradan ulaşabilirsiniz. Orta ve ciddi hipokseminin acil servislere solunum yetmezliği ile başvurduğunu göz önüne alırsak temel sınıflandırmayı gözden geçirmek gerekli. SınıflamaPaO2Normal80-100 mm HgHafif Hipoksemi60-80 mm HgOrta Hipoksemi40-60 mm HgCiddi Hipoksemi< 40 mm HgOksijenasyon için hipoksi sınıflaması Oksijenasyon Temel Tanımlar Hastalara oksijen tedavisi sürecinde temel parametrelere hakimiyet, ekipmanı tanımak, hastanın ihtiyacını belirlemek ve uygun şekilde takip edebilmek başarılı bir oksijenasyon sürecinin temellerini oluşturuyor. Bu temel tanımlar arasında anlamamız gereken başlıklar; Akım (low flow-high flow) O2 konsantrasyonu Tepe inspiratuar akım (peak inspiratory flow) FiO2 (İnspire edilen oksijen fraksiyonu) Akım (düşük ve yüksek akım) Kullandığımız yöntemler verdiğimiz akım hızlarına göre sınıflandırılmaktadır. Bu sınıflamada dikkati çeken venturi maskelerini yüksek akımlı yöntemlere dahil edilmesidir. Belirlenmiş FiO2 sağlama özellikleri nedeniyle diğer geleneksel yöntemlerden farklı sınıflanmıştır. Düşük Akımlı Yöntemler (FiO2 düzeyi kontrol edilemez.)Nasal KanülBasit Yüz MaskesiNon-Rebreather MaskelerDiffüzör maskeYüksek Akımlı Yöntemler (FiO2 düzeyi kontrol edilebilir.)Ventüri MaskeYüksek Akımlı Nasal KanülNon-invaziv mekanik ventilasyonİnvaziv mekanik ventilasyon Temel tanımları anlamak için verdiğimiz oksijenin konsantrasyonunu ve hastanın aldığı oksijenin düzeyini anlamak için kısa bir monolog yapalım: Soru: Normalde oda havasında (atmosfer) O2 düzeyleri ne kadar?Cevap: %21Soru: Peki oksijen tüpü yada hastanelerdeki santral oksijen kaynaklarından çıkan oksijen düzeyi nedir? (Diğer bir söylemle, oksijeni açtığınız anda akış ölçerden çıkan oksijenin FiO2'si nedir?)Cevap: %100Soru: Peki oksijen akış hızı, oksijen akış ölçerden iletilen saf oksijenin FiO2'sini gerçekten değiştirir mi?Cevap: HayırSoru: Peki nasıl oluyorda saf oksijeni hastaya başlamamıza rağmen çoğu yöntemde %100 FiO2'ye ulaşamıyoruz?Cevap: Peak inspiratory flowSoru: Yani hastalarımızın inspirium akım düzeyleri bizim sağladığımız oksijen akımından daha fazla olduğunda oda havasıyla karışarak inhale edilmiş oluyor.Cevap: Örnek verecek olursak; 10 lt/dk ile O2 başladık. Peak inspiratory flow 30 lt/dk olsunSoru: FiO2 nedir?Cevap: 10lt/dk maskedense, 20lt/dk odadan hava inspire edilecek. (10 x 100) + (20 x 21) = 1420%. 1420 ÷ 30 = 47% Yöntemlerin Gözden Geçirilmesi Verdiğimiz FiO2 kullandığımız yöntemlere göre, yada diğer bir söylemler hastanın inspire ettiği akıma ne kadar oksijen koyabildiğimize göre çeşitli farklılıklar gösterebiliyor. En sık kullandığımız yöntemleri gözden geçirelim. Nazal Kanül

peak bu ak vent pandemi o2 orta yani tepe bayram ancak cevap fio2

21: Extubation Readiness in the PICU

Play Episode Listen Later Jul 18, 2021 27:08

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our PICU Mini-Series Episode a 10 month old who is intubated for acute respiratory failure secondary to RSV bronchiolitis. Here's the case: A 10-month-old full-term infant girl old is intubated for acute respiratory failure secondary to RSV bronchiolitis. Patient was brought to the ED by parents on day 3 of her illness with h/o cough, congestion and worsening respiratory distress. She has had increasing WOB and grunting. After assessment in the ED where the patient had a brief trial of HFNC, she was intubated with a 4.0 ETT due to persistent hypoxemia. Pertinently, her viral panel was positive for RSV, and the patient was transferred to the PICU. In the PICU, patient was ventilated using PRVC: Set TV of 90cc (patient is 11KG), PEEP 6, PS 10, and FIO2 40%. Throughout her course, she was mechanically ventilated and sedated for about a week. She required a continuous infusion of rocuronium due to decreased lung compliance and high peak pressures. Patient weaned on her ventilator settings by ICU day 7 and the decision to move towards extubation was made. To summarize key elements from this case, this patient has: 10 month old with acute respiratory failure secondary to RSV infection and with a secondary bacterial infection due to H.Influenza. Had about a six day course on the ventilator requiring sedation and NMB and now we are at the discussion of extubation readiness.Rahul, do you mind summarizing the patient's peri-extubation course? Sure Pradip, so on day 6 of hospitalization our patient was weaned to low mechanical ventilator settings. The chest radiograph, which initially showed evidence of interstitial pneumonitis and atelectasis now improved and the patient had improved secretion burden. The patient was on ceftriaxone throughout the hospital course as her ETT cx with which grew Hemophilus Influenzae. What about the patient's neurological status? The patient was initially on fentanyl, dexmedetomidine and a rocuronium infusion — a day prior to considering extubation, the patient was off of the continuous rocuronium infusion oxygenating and ventilating well. The patient prior to extubation was wide awake and appropriate during the morning sedation holiday. Any other important clinical markers? Yes, the patient's clinical exam including lung exam was reassuring. The patient underwent a pressure support trial PEEP 5, CPAP 10 and had a normal respiratory effort with exhaled of about 5 mL/kg. The RT, however mentioned that the patient did not have a "leak" when performing the leak test. The finally the patient was given a few doses of furosemide for diuresis prior to extubation. Awesome, today's episode we really want to focus on extubation readiness however prior to this discussion, can we take a step back and talk about some red-flag symptoms which led to intubation for this patient? This patient had severe respiratory distress which progressed to failure. The tachypnea, decreased mentation, and grunting were key signs that the patient was progressing to endotracheal intubation. Grunting is important to highlight as this refers to the child generating auto-PEEP to combat the atelectasis present in bronchiolitis. Remember that a child's chest wall has a high compliance and a decreased propensity for outward elastic recoil — this in essence reduces FRC and thus there is a more balance towards the inward recoil of the long (closing capacity). The highly compliant chest wall and the natural inward recoil of the infant lung creates a propensity towards atelectasis and subsequent impairments in breathing. Low FRC can also create increase PVR which can thus imbalance optimal cardiopulmonary interactions. OK let's transition to our topic of discussion by a quick summary: A 10...

children medicine current healthcare patients ps icu ett ml rt readiness influenza rsv peep rahul cpap frc picu grunting pvr wob podcast dedicated extubation fio2

94-INDICE DE ROX COMO PREDICTOR DE NECESIDAD DE VENTILACIÓN MECÁNICA.

cardiology expressed abg congenital heart disease vsd fio2 cyanotic

Play Episode Listen Later Jun 20, 2021 6:35

El Índice ROX fue desarrollado por el Dr. Roca y Col. para ayudar en la predicción de resultados clínicos de pacientes tratados con cánula nasal de alto flujo (CNAF). Este se calcula por la dividiendo la saturación de oxígeno (SatO2) con el oxímetro de pulso y la fracción inspirada de oxígeno (FiO2) y este resultado lo dividimos por la frecuencia respiratoria (FR). IROX = [SpO2/FiO2]/FR Este fue un estudio de cohorte observacional prospectivo multicéntrico de 2 años que incluyó pacientes con neumonía tratados con cánula nasal de alto flujo. Se evaluó el punto de corte más específico del índice ROX para predecir el fracaso y el éxito de la necesidad o no de intubación. 1. ROX mayor o igual a 4,88 después del inicio de la cánula nasal de alto flujo se asoció sistemáticamente con un menor riesgo de intubación. 2. Un ROX menor de 2,85, menor de 3,47 y menor de 3,85 a las 2, 6 y 12 horas de iniciación de la con cánula nasal de alto flujo, respectivamente, fueron predictores de falla de la cánula nasal de alto flujo. 3. Los pacientes que fracasaron presentaron un menor aumento de los valores del índice ROX a lo largo de las 12 horas. Entre los componentes del índice, la saturación de oxígeno medida por oximetría de pulso / FiO2 tuvo un peso mayor que la frecuencia respiratoria. Un buen resumen de información práctica para quedaros después de la revisión de la literatura seria: 1. Un índice de ROX ≥4,88 a las 2, 6 y 12 horas es un buen predictor de que el paciente no necesitará intubación orotraqueal. 2. Un índice de ROX entre 3,85-4,87 requiere monitoreo estrecho. 3. Un índice de ROX

col medicina recuerden roca predictors aprenderemos conducci tamayo indice rox epidemi z39 ventilaci fio2

Cardiology- Cyanotic Congenital Heart Disease (CHD)

Portable Peds

Play Episode Listen Later Jun 12, 2021 7:46

Today we'll be covering Cyanotic Congenital Heart Disease (CHD), going along with this month's theme, Cardiology. If you haven't listened to our podcast before, each week we have a case-based discussion about a medical topic to help you study for the pediatric medicine board exam. Episodes are released every weekend, and the case is then reviewed and reinforced on social media throughout the week. Follow the podcast on social media: Facebook- @portablepeds (www.facebook.com/portablepeds) Twitter- @portablepeds (www.twitter.com/portablepeds) We'd love to hear from you via email at portablepeds@gmail.com! Also, feel free to visit our website, www.portablepeds.com, for more content. Today's Case: A mother with scant prenatal care gives birth. Almost immediately following delivery, the infant is cyanotic. An ABG is obtained, and the PaO2 is 35mmHg. The infant is exposed to 100% FiO2 for 10 minutes, and a repeat ABG is obtained. The PaO2 remains at 35mmHg. A chest x-ray is obtained and demonstrates an “egg on a string” appearance. An echocardiogram confirms the diagnosis, and the patient is taken emergently for an atrial balloon septostomy until definitive surgical correction can be prepared. What is the most likely underlying lesion/lesions? A VSD, an overriding aorta, right ventricular outflow obstruction, and right ventricular hypertrophy Parallel pulmonary and systemic circulation A common truncal outflow tract and truncal valve Abnormal return of the pulmonary veins Absence of the tricuspid valve We would like to give an enormous thank you to Zack Goldmann for designing this podcast's logo and accompanying artwork. You can find more of his work at www.zackgoldmann.com. The intro and outro of this podcast is a public domain song obtained from scottholmesmusic.com. Intro/Outro- Hotshot by Scott Holmes Disclaimer: This podcast is intended for healthcare professionals. The information presented is for general educational purposes only and should NOT be used as professional medical advice or for the diagnosis or treatment of medical conditions. The views and opinions expressed do not represent the views and opinions of our employer or any affiliated institution. Expressed opinions are based on specific facts, under certain conditions, and subject to certain assumptions and should not be used or relied upon for any other purpose, including, but not limited to, the diagnosis or treatment of medical conditions or in any legal proceeding. Full terms and conditions can be found at portablepeds.com. Thanks for listening! As always, please Rate and Review this podcast on Apple Podcasts, Facebook, or your favorite podcasting platform. Also, Subscribe to get all the latest episodes, and Share this episode with someone you think would enjoy it! Hope to see you real soon!

86-OXIGENOTERAPIA EN COVID-19: VELOCIDAD DE OXÍGENO VERSUS FIO2 QUE RECIBE EL PACIENTE. GUÍA SIMPLE.

Play Episode Listen Later May 20, 2021 6:41

Oxigenoterapia La administración de oxígeno (O2) suplementario es una de las estrategias terapéuticas más utilizadas en el mundo, para el tratamiento primario de la hipoxemia. Su administración se cuantifica en porcentaje de la fracción de oxígeno (FiO2). El objetivo de la terapia con O2 es mantener los niveles de saturación arterial de O2 alrededor del 90-96%; en casos excepcionales como la enfermedad pulmonar obstructiva crónica, se permiten saturaciones alrededor del 88%. Durante la terapia con O2 se debe evitar de hiperoxemia, debido a que altos niveles en la presión arterial de oxígeno (PaO2) aumentan la toxicidad relacionada con la liberación de especies reactivas de O2, provocando lesión en el pulmón, la retina o en el sistema nervioso central; además, altos valores de FiO2 por un tiempo prolongado pueden generar atelectasias por absorción. Esquema de titulación de los métodos de oxígeno suplementario. ¿Cuál es la FiO2 que está recibiendo el paciente? 1-Cánula nasal 1 Lt/min FiO2(%) 24 2 Lt/min FiO2(%) 28 3 Lt/min FiO2(%) 32 4 Lt/min FiO2(%) 36 5 Lt/min FiO2(%) 40 NO USAR EN PACIENTE COVID-19 2-Mascarilla Simple 5-6 Lt/min FiO2(%) 40 NO USAR EN PACIENTE COVID-19 6-7 Lt/min FiO2(%) 50 NO USAR EN PACIENTE COVID-19 7-8 Lt/min FiO2(%) 60 NO USAR EN PACIENTE COVID-19 3-Máscara Venturi 3 Lt/min FiO2(%) 24 NO USAR EN PACIENTE COVID-19 6 Lt/min FiO2(%) 28 NO USAR EN PACIENTE COVID-19 9 Lt/min FiO2(%) 35 NO USAR EN PACIENTE COVID-19 12 Lt/min FiO2(%) 40 NO USAR EN PACIENTE COVID-19 15 Lt/min FiO2(%) 50 NO USAR EN PACIENTE COVID-19 4-Máscara de no-inhalación 6-7 Lt/min FiO2(%) 55-60 8-10 Lt/min FiO2(%) 70-90 5-Cánula de alto flujo 10-60 FiO2(%) 21-100 6-Ventilación mecánica no invasiva y Ventilación mecánica invasiva FiO2(%) 90-100 Recuerden como conclusión en pacientes covid-19- no usar oxigeno por Cánula Nasal desde 5 litros en adelante, con Mascara Sencilla o con Mascara Venturi. Por riesgo de aerolización al personal de la salud. REFERENCIA https://revistas.ces.edu.co/index.php/medicina/issue/view/304 https://revistas.ces.edu.co/index.php/medicina/article/download/5652/3196/29234 https://www.elsevier.es/es-revista-acta-colombiana-cuidado-intensivo-101-pdf-S0122726220300318 ADAPTACION PARA AUDIO-OYENTES: Medicina en una página. ================================================ PODCAST CORONAVIRUS. COVID-19 Este es un podcast en el que desde el ojo de la ciencia. Aprenderemos del coronavirus y de la enfermedad covid-19. Recuerden al enemigo es mejor conocerlo. Para acabarlo. Esta es una producción de: Medicina en una página. medicinaenunapagina@gmail.com Dirección y Conducción: John Jarbis García Tamayo. Médico y cirujano, Epidemiólogo y Pedagogo Universitario.

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Part 2 Final Exam Viva Demonstration - Airway surgery with Rachel

ABCs of Anaesthesia

Play Episode Listen Later May 7, 2021 32:25

Thanks Rachel for your great work at this exam!50yo Male (80kg) presents for your ENT list for a biopsy +/- removal of vocal cord tumour. What specifics would you like to know on assessment? Hx of lesion includesDiagnosisMass effect Critical structure effects - effects on the airway, symptoms, positional and rapidity of progressionMetsMetabolic effects of mass meds and treatmentsCauseand complications How do you prepare/mitigate the risk of laser ? Patient: low fiO2. Wet gauze. Saline bucket. ETT, matt instrumentsSafety officers. Laser testing. Goggles. 1 footplate. Warning signs, mask for plumeAirway optionsClosed systems: ETT/MLT/Laserflex Advantages are: Familiarity, Protects airway, Control of ventilation, Minimal pollution Open systems: intermittent apnoea, Jet ventilation via hunsaker, benjet, suspension laryngscope, transcricoid puncture.Advantages are: Better view of larynx. Laser safe if no ignition source Please rate, post a review and subscribe!Check out https://anaesthesiacollective.com/ for more useful information and dates for the Viva Boot Camp course for the part 2 ANZCA exam.and check out the ABCs of Anaesthesia YouTube channel for more contenthttps://www.youtube.com/c/ABCsofAnaesthesiaIf you have any questions, please email anaesthesiapodcast@gmail.com Andrew Heards fantastic Youtube resource! https://youtu.be/SbhEyGIf9Y4Disclaimer: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 episode. 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 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.

80-OXIGENOTERAPIA EN COVID-19: MONITORIZACIÓN. GUÍA SIMPLE.

Empowering NICU Parents Podcast

Play Episode Listen Later May 3, 2021 5:20

Los pacientes con síndrome de dificultad respiratoria aguda secundario a COVID-19, tienen una forma de presentación atípica, con una discrepancia entre una mecánica pulmonar aceptable y una hipoxia marcada. Las metas de saturación de oxígeno son, en general 90- 96 %, y no se debe retrasar la intubación y la ventilación mecánica en caso de tener la indicación. En el tratamiento de estos pacientes se deben tener en cuenta las siguientes 9 consideraciones con respecto a la monitorización: 1. Saturación de oxígeno • Si se usa oxímetro digital se deben despintar las uñas de los pacientes, para una adecuada medición. o Meta ≥ 90 % • A partir de la saturación se puede encontrar un equivalente de la PaO2 /FiO2 -> SO2 /FiO2. -Se calcula a partir de la relación entre la saturación periférica de O2 y la FiO2. -Meta ≥ 300 o Alerta, si ≤ 200. 2. Cardioscopio 3. Presión arterial no invasiva 4. Frecuencia respiratoria (FR) . Meta < 24 respiraciones por minuto. 5. Signos de distrés respiratorio • Uso de músculos accesorios. • Fatiga. • Aleteo nasal. • Retracciones. • Dificultad para completar frases. 6. Examen físico para la detección de hipoperfusión 7. Examen de piel: 8. Saturación venosa mixta de oxígeno (SVO2) 9. Gases arteriales La PaO2 /FiO2 es un indicador preciso del estado de oxigenación, la monitorización de esta es necesaria, sobre todo en pacientes con valores menores de 300, para ver la progresión de la enfermedad. REFERENCIA https://revistas.ces.edu.co/index.php/medicina/issue/view/304 https://revistas.ces.edu.co/index.php/medicina/article/download/5652/3196/29234 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7709579/pdf/main.pdf ADAPTACION PARA AUDIO-OYENTES: Medicina en una página. ================================================ PODCAST CORONAVIRUS. COVID-19 Este es un podcast en el que desde el ojo de la ciencia. Aprenderemos del coronavirus y de la enfermedad covid-19. Recuerden al enemigo es mejor conocerlo. Para acabarlo. Esta es una producción de: Medicina en una página. medicinaenunapagina@gmail.com Dirección y Conducción: John Jarbis García Tamayo. Médico y cirujano, Epidemiólogo y Pedagogo Universitario. Portada: Gracias a Sam Balye por compartir su trabajo (foto-portada) en https://unsplash.com/. Música: https://www.youtube.com/audiolibrary/music?nv=1

covid-19 simple medicina alerta uso examen recuerden o2 presi signos frecuencia dificultad aprenderemos conducci tamayo fatiga epidemi saturaci monitorizaci fio2

Non-Invasive Ventilation in the NICU - A Review of NIPPV, CPAP, HFNC, and LFNC too

Play Episode Listen Later Apr 29, 2021 30:56

In this episode, we review non-invasive ventilation in the NICU, respiratory support without an endotracheal tube, but rather with a nasal cannula or face mask. If your baby currently has or had Respiratory Distress Syndrome, the chances are quite high that they are currently or were previously on at least one of the different modes of non-invasive ventilation, either nIMV or NIPPV, CPAP, HFNC, LFNC. This is a topic, I know so many of you will benefit from hearing. After listening, you will walk away with a much better understanding of the different options of non-invasive ventilation, why one method may be chosen over another, how they will be beneficial to your baby, and some of the potential complications. Tune in to gain a better understanding of the parameters set on each of the different modes of non-invasive ventilation including but not limited to rate, PIP, PEEP, i-time, L/min and FiO2. Grab your free graphics that correlate with the episode at: http://empoweringnicuparents.com/rds/https://empoweringnicuparents.com/nicuimage/Empowering NICU Parents Show Notes:https://empoweringnicuparents.com/episode11/Empowering NICU Parents Instagram: https://www.instagram.com/empoweringnicuparents/Empowering NICU Parents FB Group:https://www.facebook.com/groups/empoweringnicuparents

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73-PAFI. USO EN LA INSUFICIENCIA RESPIRATORIA AGUDA CAUSADA POR EL VIRUS DEL COVID-19

Play Episode Listen Later Apr 12, 2021 8:19

¿Qué es la PaFi, Índice de oxigenación tisular (IOT) o también llamado índice de kirby? Es un parámetro que se utiliza para medir el intercambio gaseoso y la gravedad de la insuficiencia respiratoria. Se calcula a partir de la fórmula: presión arterial de oxígeno arterial entre fracción inspirada de oxígeno (PaO2 / FiO2). y tiene utilidad en pacientes críticos para poder tomar decisiones en el tratamiento. ¿Cuál es el valor normal de la PAFI? Puede emplearse cuando la FIO2>0,4. Cuanto menor es el PAFI, quiere decir que hay un peor intercambio gaseoso. En general, se considera que por debajo de 300 puede haber una lesión aguda pulmonar y por debajo de 200 un síndrome de distrés respiratorio agudo. El síndrome de insuficiencia respiratoria aguda (SIRA) es una entidad clínica bien reconocida en las unidades de terapia intensiva. En 1967 Ashbaugh y Petty describieron, de donde derivaron los 3 criterios utilizados en la actualidad. Todos tomados con una presión positiva al final de la espiración dividido por la presión positiva continua en la vía aérea con un valor mayor o igual a 5 cm H2O. 1-SIRA leve PaO/FiO2 menor o igual a 300 mmHg pero mayor de 200 mmHg 2-SIRA moderado PaO/FiO2 menor o igual a 200 mmHg pero mayor de 100 mmHg 3-SIRA grave PaO/FiO2 menor de 100 Puntaje o escala de Murray En 1988 Murray desarrolla un sistema de puntuación para establecer la existencia de lesión pulmonar aguda o síndrome de insuficiencia respiratoria aguda, y su probabilidad de muerte, así. 1-PaO/FiO2 > 300 MORTALIDAD 0% 2-PaO/FiO2 225-299 MORTALIDAD 25% 3-PaO/FiO2 175-224 MORTALIDAD 50% 4-PaO/FiO2 100-174 MORTALIDAD 75% 5-PaO /FiO2

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Will you increase PEEP or FiO2 if the oxygen saturation drops?

advt7

Play Episode Listen Later Mar 28, 2021 3:24

Here is the brief review of ARDS management --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/snapmd/message

drops oxygen peep saturation ards fio2

How do you PREVENT HYPOXAEMIA when performing a rapid sequence induction (RSI)?

Anaesthesia Coffee Break

Play Episode Listen Later Jan 24, 2021 38:11

You've probably performed a few RSIs in your anaesthesia practice. But have you though about all the techniques you do to make this inherently risky technique safer?In this episode we chat about the approach to the question from the April 2014 and September 2013 SAQ paperDescribe the physiological basis of methods used to prevent hypoxaemia prior to intubation in a rapid sequence induction. Include any adverse effects of these methods. The exam paperhttps://networks.anzca.edu.au/d2l/le/content/7669/Home?itemIdentifier=D2L.LE.Content.ContentObject.ModuleCO-86745Atomic Habits summary by James Clearhttps://www.samuelthomasdavies.com/book-summaries/self-help/atomic-habits/The bookhttps://jamesclear.com/atomic-habitsInterview with James Clear on Making Sense Podcast with Sam Harrishttps://samharris.org/subscriber-extras/200-creatures-habit/Plateau of Latent potentialhttps://i0.wp.com/www.samuelthomasdavies.com/wp-content/uploads/2019/01/The-Plateau-of-Latent-Potential-1.png?w=2000&ssl=1Bleomycin and oxygen toxicityhttps://www.mayoclinicproceedings.org/article/S0025-6196(12)60489-3/fulltextOxygen therapy for sats

Çocuklarda Septik Şok ve Sepsis İlişkili Organ Disfonksiyonu

Play Episode Listen Later Jan 11, 2021 18:15

Acil Bakışıyla Surviving Sepsis Campaign Pediatrik Kılavuzu Sepsis, pediatrik yaş grubunda, tanınmasının oldukça önemli olduğu bir klinik durumdur. SSC tarafından Şubat 2020’de yayımlanan, çocuklarda sepsis ve septik şok yönetimine kanıta dayalı öneriler getiren bu kılavuzu acilci bakışıyla gözden geçirmek istedim. Kılavuzun tamamına buradan1 ulaşabilirsiniz. İyi okumalar. Sepsis, dünya genelinde pediatrik popülasyon için önde gelen bir morbidite ve mortalite nedenidir. Dünya çapında yılda 22/100000 çocuk sepsis vakası ve 100000 canlı doğumda 2202 yenidoğan sepsis vakası görülmektedir, bu sayılar toplamda 1,2 milyon/yıl çocukluk çağı sepsis vakasına tekabül etmektedir. 18 yaşın altında hastanede yatan tüm hastaların %4'ünden fazlasında ve çocuk yoğun bakım ünitelerine kabul edilen hastaların yaklaşık %8'inde sepsis görülür ve mortalite hastalığın şiddetine ve çocuğun risk faktörlerine bağlı olarak %4 ila %50 arasında değişmektedir. Sepsise bağlı ölümlerin çoğu ilk 48 ila 72 saat içinde meydana gelmektedir, birçoğu refrakter şok ve/veya çoklu organ disfonksiyonu ile ilişkilidir. Sepsis Tanımı Burada çocuklarda sepsis tanımıyla ilgili bir parantez açmamız gerekiyor. 2016’da Sepsis 3.0 ile erişkinlerde sepsis tanımında sepsis ve septik şok tanımları geçerliliğini korurken SIRS (Sistemik İnflamatuvar Yanıt Sendromu) ile ciddi sepsis tanımları günlük pratiğimizden çıkmıştı. Ancak bu değişiklikler şimdilik erişkin hastalar için geçerlidir. Çocuklar için mevcut tanımlar ise şu şekildedir:2Enfeksiyon: Herhangi bir patojen ile gelişen şüpheli ya da kanıtlanmış enfeksiyon durumu ya da yüksek olasılıkla enfeksiyon ilişkili gelişen bir klinik sendromSIRS: Aşağıdakilerden 2 ya da daha fazlasının olması (biri beyaz küre sayısı ya da ateş olmalı)1. Ateş >38,5 oC ya da 19,5 ya da 17,5 ya da 22>15,5 ya da 18>13,5 ya da 14>11,5 ya da

iv oc sd organ kb o2 yan sepsis ate sirs ssc ards ancak beyaz kili burada mmhg gks meq fio2 paco2

Çocuklarda Septik Şok ve Sepsis İlişkili Organ Disfonksiyonu

Nermana's Anesthesia Minute

Play Episode Listen Later Jan 11, 2021 18:15

Acil Bakışıyla Surviving Sepsis Campaign Pediatrik Kılavuzu Sepsis, pediatrik yaş grubunda, tanınmasının oldukça önemli olduğu bir klinik durumdur. SSC tarafından Şubat 2020’de yayımlanan, çocuklarda sepsis ve septik şok yönetimine kanıta dayalı öneriler getiren bu kılavuzu acilci bakışıyla gözden geçirmek istedim. Kılavuzun tamamına buradan1 ulaşabilirsiniz. İyi okumalar. Sepsis, dünya genelinde pediatrik popülasyon için önde gelen bir morbidite ve mortalite nedenidir. Dünya çapında yılda 22/100000 çocuk sepsis vakası ve 100000 canlı doğumda 2202 yenidoğan sepsis vakası görülmektedir, bu sayılar toplamda 1,2 milyon/yıl çocukluk çağı sepsis vakasına tekabül etmektedir. 18 yaşın altında hastanede yatan tüm hastaların %4'ünden fazlasında ve çocuk yoğun bakım ünitelerine kabul edilen hastaların yaklaşık %8'inde sepsis görülür ve mortalite hastalığın şiddetine ve çocuğun risk faktörlerine bağlı olarak %4 ila %50 arasında değişmektedir. Sepsise bağlı ölümlerin çoğu ilk 48 ila 72 saat içinde meydana gelmektedir, birçoğu refrakter şok ve/veya çoklu organ disfonksiyonu ile ilişkilidir. Sepsis Tanımı Burada çocuklarda sepsis tanımıyla ilgili bir parantez açmamız gerekiyor. 2016’da Sepsis 3.0 ile erişkinlerde sepsis tanımında sepsis ve septik şok tanımları geçerliliğini korurken SIRS (Sistemik İnflamatuvar Yanıt Sendromu) ile ciddi sepsis tanımları günlük pratiğimizden çıkmıştı. Ancak bu değişiklikler şimdilik erişkin hastalar için geçerlidir. Çocuklar için mevcut tanımlar ise şu şekildedir:2Enfeksiyon: Herhangi bir patojen ile gelişen şüpheli ya da kanıtlanmış enfeksiyon durumu ya da yüksek olasılıkla enfeksiyon ilişkili gelişen bir klinik sendromSIRS: Aşağıdakilerden 2 ya da daha fazlasının olması (biri beyaz küre sayısı ya da ateş olmalı)1. Ateş >38,5 oC ya da 19,5 ya da 17,5 ya da 22>15,5 ya da 18>13,5 ya da 14>11,5 ya da

iv oc sd organ kb o2 yan sepsis ate sirs ssc ards ancak beyaz kili burada mmhg gks meq fio2 paco2

FiO2. Is it really that big of a deal?

Play Episode Listen Later Nov 6, 2020 10:33

FiO2 selection in anesthesia often doesn't get a much thought as it probably deserves. Here I will discuss the shortcomings of the WHO recommendations, some of the drawbacks to high FiO2, and what you can do.

fio2

Kar Kazaları

Play Episode Listen Later Oct 25, 2020 26:17

Giriş Dünyanın dağlık bölgelerinde kar ve buz çığları sık görülmektedir. Pek çok ülkenin bildirim sistemlerindeki eksiklikler nedeniyle çığ ilişkili morbidite ve mortaliteyi tam tahmin etmek oldukça güçtür. Avrupa ve Kuzey Amerika, çığ ilişkili ölümleri bildirmede oldukça iyi bir sisteme sahiptir. Her yıl Kuzey Amerika ve Avrupa’da ortalama olarak 150 kadar çığ ilişkili ölüm gerçekleşmektedir. 1983 ve 2015 yılları arasındaki 31 kış sezonunda, Avrupa ve Kuzey Amerika’da 5123 çığ ilişkili ölüm rapor edilmiştir. Ortalama olarak her yıl gerçekleşen 165 ölümün 130’unun Avrupa ülkelerinden olduğu bildirilmiştir. Aynı dönemde, ortalama olarak her sene Amerika’da 24, Kanada’da ise 12 kişi çığ nedeniyle hayatını kaybetmiştir. Belgelenen Kuzey Amerika ve Avrupa'daki çığ ölümlerinin çoğu, kar motosikletleri, kayakçılar, snowboardcular, dağcılar ve kar ayakkabıcıları gibi eğlence amaçlı aktivitelerde meydana gelmektedir. Yaralanma ve ölüm riskini azaltmanın ilk yöntemi çığdan kaçınma olmalıdır. Bir çığ olayı meydana gelirse, çığ altında kalan kişinin yakınındakilerin uyguladığı doğru resüsitasyon teknikleri ve ileri yaşam desteği, çığ ilişkili morbidite ve mortalitenin azalması için kritik öneme sahiptir. Bu sebeple Wilderness Medical Society tarafından, "Çığ İlişkili ve İlişkisiz Kar Altında Kalma Kazaları" ile ilgili kanıta dayalı öneriler geliştirmek için bir çalışma grubu oluşturularak bu kılavuz hazırlanmıştır. Öneri sınıfları ve kanıt düzeyleri yine American College of Chest Physicians şemasına göre belirlenmiştir1. Oldukça uzun olan bu kılavuzu2, çığ kazalarında mortalite ve morbiditeye neden olan patofizyoloji ve arama kurtarma tekniklerinden oluşan birinci kısım ve resüsitasyondan oluşan ikinci kısım olarak iki aşamada anlatmayı uygun bulduk. 1.PATOFİZYOLOJİ Çığ ilişkili olmayan derin kar altına gömülme durumunun patofizyolojisi de çığ gömülmesine benzer olarak birlikte anlatılmıştır. Çığ yaralanmalarının morbiditesi ve mortalitesi büyük ölçüde gömme süresine, hava yolunun açıklığına, hava cebi hacmine, gömülme derinliğine ve travmatik yaralanmalara bağlıdır. Hava cebi terimi, açık hava yolu ve ağız ve burun önündeki herhangi bir boşluk olarak tanımlanır. Yaralanmamış bir kurban için tam gömüldükten sonra (baş ve göğüs karın altında) hayatta kalma şansı yaklaşık % 50'dir. Yalnızca kısmen gömülmüşse (baş ve göğüs karın dışında), travma katkıda bulunan bir faktör değilse hayatta kalma şansı neredeyse % 100'dür. Asfiksi, çığ gömülmesi sırasında en yaygın ölüm nedenidir. Çığ ölümlerinin yaklaşık %75'i asfiksiye, % 25'i travmaya ve çok azı hipotermiye bağlıdır. 1.A. Asfiksi Çığa gömülme sırasında asfiksi 3 ana mekanizma ile gerçekleşir: üst solunum yolunun kar ile tıkanması, buz maskesi oluşumu ve verilen havanın yeniden solunması nedeniyle gelişen oksijen yoksunluğu. Çığ altında kalan hastalarda kar ile üst hava yolunun tamamen tıkanması sonucunda 10 dakika içinde hipoksi gerçekleşir. Asfiksi ise ilk 30 ile 60 dakikada gerçekleşir.Hava yolu açık ise, solunan havadaki su buharı yoğunlaşıp yüzün önündeki karda donarak hava akışını engelleyen bir “buz maskesi” meydana getirir. Çığa gömülme sırasında asfiksi başlıca ölüm nedeni olduğundan, kurtarılma zamanı hayatta kalmanın en önemli belirleyicisidir. Gömülü bir hastanın 30 dakikadan fazla bir süre sonra hayatta kalması için açık hava yolu ve bir hava cebi olması gerekir. Hava cebinin hacmi ne kadar büyükse, gömüldükten sonra olası hayatta kalma süresi o kadar uzun olur. Solunan hava %21 oksijen (O2) ve %0,03'ten az karbondioksit (CO2) içerir. Yeniden solunan havada ise yaklaşık %16 O2 ve %5 CO2 bulunur. Çığa gömülme sırasında verilen havanın yeniden solunması, solunan oksijen fraksiyonunda (FIO2) kademeli bir düşüşe ve solunan karbondioksit fraksiyonunda (FICO2) kademeli bir artışa neden olur. Hipoksi ve hiperkapni, yeterli bir hava cebi olmadığında asfiksi yoluyla ölüme neden olur. Daha büyük bir hava cebi,

co2 amerika bu american colleges kanada o2 bir daha pek hava avrupa yaln yeniden olduk chest physicians fio2 kuzey amerika

Kar Kazaları

Play Episode Listen Later Oct 25, 2020 26:17

Giriş Dünyanın dağlık bölgelerinde kar ve buz çığları sık görülmektedir. Pek çok ülkenin bildirim sistemlerindeki eksiklikler nedeniyle çığ ilişkili morbidite ve mortaliteyi tam tahmin etmek oldukça güçtür. Avrupa ve Kuzey Amerika, çığ ilişkili ölümleri bildirmede oldukça iyi bir sisteme sahiptir. Her yıl Kuzey Amerika ve Avrupa’da ortalama olarak 150 kadar çığ ilişkili ölüm gerçekleşmektedir. 1983 ve 2015 yılları arasındaki 31 kış sezonunda, Avrupa ve Kuzey Amerika’da 5123 çığ ilişkili ölüm rapor edilmiştir. Ortalama olarak her yıl gerçekleşen 165 ölümün 130’unun Avrupa ülkelerinden olduğu bildirilmiştir. Aynı dönemde, ortalama olarak her sene Amerika’da 24, Kanada’da ise 12 kişi çığ nedeniyle hayatını kaybetmiştir. Belgelenen Kuzey Amerika ve Avrupa'daki çığ ölümlerinin çoğu, kar motosikletleri, kayakçılar, snowboardcular, dağcılar ve kar ayakkabıcıları gibi eğlence amaçlı aktivitelerde meydana gelmektedir. Yaralanma ve ölüm riskini azaltmanın ilk yöntemi çığdan kaçınma olmalıdır. Bir çığ olayı meydana gelirse, çığ altında kalan kişinin yakınındakilerin uyguladığı doğru resüsitasyon teknikleri ve ileri yaşam desteği, çığ ilişkili morbidite ve mortalitenin azalması için kritik öneme sahiptir. Bu sebeple Wilderness Medical Society tarafından, "Çığ İlişkili ve İlişkisiz Kar Altında Kalma Kazaları" ile ilgili kanıta dayalı öneriler geliştirmek için bir çalışma grubu oluşturularak bu kılavuz hazırlanmıştır. Öneri sınıfları ve kanıt düzeyleri yine American College of Chest Physicians şemasına göre belirlenmiştir1. Oldukça uzun olan bu kılavuzu2, çığ kazalarında mortalite ve morbiditeye neden olan patofizyoloji ve arama kurtarma tekniklerinden oluşan birinci kısım ve resüsitasyondan oluşan ikinci kısım olarak iki aşamada anlatmayı uygun bulduk. 1.PATOFİZYOLOJİ Çığ ilişkili olmayan derin kar altına gömülme durumunun patofizyolojisi de çığ gömülmesine benzer olarak birlikte anlatılmıştır. Çığ yaralanmalarının morbiditesi ve mortalitesi büyük ölçüde gömme süresine, hava yolunun açıklığına, hava cebi hacmine, gömülme derinliğine ve travmatik yaralanmalara bağlıdır. Hava cebi terimi, açık hava yolu ve ağız ve burun önündeki herhangi bir boşluk olarak tanımlanır. Yaralanmamış bir kurban için tam gömüldükten sonra (baş ve göğüs karın altında) hayatta kalma şansı yaklaşık % 50'dir. Yalnızca kısmen gömülmüşse (baş ve göğüs karın dışında), travma katkıda bulunan bir faktör değilse hayatta kalma şansı neredeyse % 100'dür. Asfiksi, çığ gömülmesi sırasında en yaygın ölüm nedenidir. Çığ ölümlerinin yaklaşık %75'i asfiksiye, % 25'i travmaya ve çok azı hipotermiye bağlıdır. 1.A. Asfiksi Çığa gömülme sırasında asfiksi 3 ana mekanizma ile gerçekleşir: üst solunum yolunun kar ile tıkanması, buz maskesi oluşumu ve verilen havanın yeniden solunması nedeniyle gelişen oksijen yoksunluğu. Çığ altında kalan hastalarda kar ile üst hava yolunun tamamen tıkanması sonucunda 10 dakika içinde hipoksi gerçekleşir. Asfiksi ise ilk 30 ile 60 dakikada gerçekleşir.Hava yolu açık ise, solunan havadaki su buharı yoğunlaşıp yüzün önündeki karda donarak hava akışını engelleyen bir “buz maskesi” meydana getirir. Çığa gömülme sırasında asfiksi başlıca ölüm nedeni olduğundan, kurtarılma zamanı hayatta kalmanın en önemli belirleyicisidir. Gömülü bir hastanın 30 dakikadan fazla bir süre sonra hayatta kalması için açık hava yolu ve bir hava cebi olması gerekir. Hava cebinin hacmi ne kadar büyükse, gömüldükten sonra olası hayatta kalma süresi o kadar uzun olur. Solunan hava %21 oksijen (O2) ve %0,03'ten az karbondioksit (CO2) içerir. Yeniden solunan havada ise yaklaşık %16 O2 ve %5 CO2 bulunur. Çığa gömülme sırasında verilen havanın yeniden solunması, solunan oksijen fraksiyonunda (FIO2) kademeli bir düşüşe ve solunan karbondioksit fraksiyonunda (FICO2) kademeli bir artışa neden olur. Hipoksi ve hiperkapni, yeterli bir hava cebi olmadığında asfiksi yoluyla ölüme neden olur. Daha büyük bir hava cebi,

co2 amerika bu american colleges kanada o2 bir daha pek hava avrupa yaln yeniden olduk chest physicians fio2 kuzey amerika

Acil Serviste İnvaziv Mekanik Ventilasyon Yazı Serisi – 1

Play Episode Listen Later Oct 3, 2020 8:52

İnvaziv mekanik ventilasyon (IMV), endotrakeal entübasyon, acil trakeostomi vb. prosedürler ile havayolu güvenliği sağlandıktan sonra solunum dinamiklerinin ventilatör aracılığı ile yönetimidir.Bu yazı serisinin ilk kısmında mekanik ventilasyonun temel parametreleri değerlendireceğiz. IMV desteği alan hastaların acil serviste uzun dönem yönetimi temel bir hedef olmasa da, son dönemlerde yoğun bakımların doluluk oranlarının artması, hastaların yoğun bakımlara transport öncesi acil servislerde hatırı sayılır uzunlukta kalma süreleri ve acillerimizde kritik bakım gerektiren hastaların artması nedeniyle günlük klinik pratiğimizde daha fazla yer almaya başladı. Acil serviste IMV yapılan hastaların acil serviste kalış süreleri sağkalım için önemli bir faktör, aynı zamanda sağladığımız bu solunum desteğinin hastaların erken dönem mortaliteleri ve geç dönem nörokognitif sonlanımları içinde kritik olduğunu göz önünde bulundurmalıyız. IMV'nin zor ve karmaşık olarak adledilmesindeki en önemli faktör, solunum dinamiğinde yönetilmesi gereken çok fazla parametre olması ve hastanın klinik durumlarına göre farklı modlar ve farklı parametre ayarları gerekmesi sayılabilir. Tüm bunlar yetmezmiş gibi farklı firmaların cihazlarında kendilerine has farklı modlar ve arayüzler kullanması işi biraz daha karmaşık hale getirebiliyor. Ancak hastanın nasıl bir solunum desteği ihtiyacının olduğunun belirlenmesi ve temel ilkelere hakimiyet bu 'zor ve karmaşık' prosedürün rahatlıkla yönetilmesini sağlayabilir. İnvaziv Mekanik Ventilasyonda Solunum Yetmezlikleri İnvaziv mekanik ventilasyon gereken hastaların solunum dinamiklerinde 2 temel sınıflandırma yer alır ve bu farklılıkları anlamak, birazdan bahsedeceğimiz tüm parametreleri nasıl kullanmamız gerektiğine dair yolumuzu belirler. Ventilasyon Yetmezliği Karbondioksit atılımındaki yetersizlik Oksijenizasyon Yetmezliği Oksijen, alımındaki / dağılımındaki yetersizlik. Oksijenizasyon ve Ventilasyon yetmezlikleri ile ilgili detaylı bilgi için Ersin Fırıncıoğlu'nun yazısına buradan ulaşabilirsiniz. Peki bu temel parametreler nedir? Her konuda olduğu gibi temel parametrelere hakim olmak önemli, ama IMV da temel parametrelere hakimiyet, hangi cihazı yada modu kullanırsak kullanalım bir ön şart ve aslında prosedürün en önemli kısmı diyebiliriz. Frekans (Solunum hızı) Hastanın dakikada kaç kere soluyacağını belirlediğimiz parametre. Adı üstünde bir parametre olmasına rağmen ayarladığımız hızın mutlak solunum sayısı olmayacağını akılda tutmak gerekir. Hastanın tetiklemesine izin vermeyen modlarda, hasta ayarlanan freakans kadar solurken , hastanın kendi solunumuna izin veren yada kendi solunumlarını başlattığında destek yapan modlar için bu hız aslında dakikada minimum kaç soluk verileceğini belirler. Yazarın notu: Acil serviste entübe, obstrüktif tip solunum yetmezliği olan desature hastalarda O2 saturasyonun artması için solunum sayısını ve FiO2 yi arttırma refleksi gözlemlediğim en büyük hata. Solunum hızının gereksiz arttırılması ekspirium süresini kısaltarak, hastaların kötüleşmesine neden olacağı akılda tutulmalı. İnspire edilen O2 konsantrasyonu (FiO2) Tüm ventilatörlerde bu parametre oda havasındaki oksijen oranı olan %21 ile %100 arasında ayarlanabilmektedir. Sıklıkla entübasyon sonrasında %100 O2 ile başlanıp daha sonrasında güvenli sınır kabul edilen %60 altına çekilmesi önerilir. Ancak alt sınırdan başlayıp hastanın ihtiyacına göre titre edilerek arttırılmasını öneren otörler/çalışmalar mevcuttur. Acil servis hastaları için tek bir hedef değerden bahsetmek olanaksızdır ancak, medikal nedene göre değişse de, oksijen satürasyonu %88-94’ ve PaO2>60mmHg olmalıdır. Hastalara liberal oksijen verilmesi zararlıdır1 ve mekanik ventilasyonda ilk 24 saatte yüksek FiO2, düşük ya da yüksek PaO2’nin mortaliteyi artırdığı bildirilmiştir2. Yazarın notu: Farklı görüşler olmasına rağmen kişisel tercihim,

bu o2 peki farkl ancak yazar acil fio2

Acil Serviste İnvaziv Mekanik Ventilasyon Yazı Serisi – 1