Podcasts about paco2

Listener discretion is advised (language). References: Abdo WF, Heunks LM. Oxygen-induced hypercapnia in COPD: myths and facts. Crit Care. 2012 Oct 29;16(5):323. Bonilla Arcos D, Krishnan JA, et al. High-Dose Versus Low-Dose Systemic Steroids in the Treatment of Acute Exacerbations of Chronic Obstructive Pulmonary Disease: Systematic Review. Chronic Obstr Pulm Dis. 2016 Feb 17;3(2):580-588. Fawzy A, Wise RA. Pulse Oximetry Misclassifies Need for Long-Term Oxygen Therapy in Chronic Obstructive Pulmonary Disease. Ann Am Thorac Soc. 2023 Nov;20(11):1556-1557. Goldberg P, Reissmann H, Maltais F, Ranieri M, Gottfried SB. Efficacy of noninvasive CPAP in COPD with acute respiratory failure. Eur Respir J. 1995 Nov;8(11):1894-900. Jennifer T. Thibodeau, Mark H. Drazner. The Role of the Clinical Examination in Patients With Heart Failure,JACC: Heart Failure, Volume 6, Issue 7, 2018, Pages 543-551. Kartal M, Goksu E, Eray O, et al. The value of ETCO2 measurement for COPD patients in the emergency department. Eur J Emerg Med. 2011 Feb;18(1):9-12. Ni, H., Aye, S., Naing, C. Magnesium sulfate for acute exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2022 May 26; 2022(5):CD013506. Pertzov, B., Ronen, M., Rosengarten, D. et al. Use of capnography for prediction of obstruction severity in non-intubated COPD and asthma patients. Respir Res 22, 154 (2021). Pu X, Liu L, Feng B, Wang M, Dong L, Zhang Z, Fan Q, Li Y, Wang G. Efficacy and Safety of Different Doses of Systemic Corticosteroids in COPD Exacerbation. Respir Care. 2021 Feb;66(2):316-326. Tyagi D, Govindagoudar MB, et al. Correlation of PaCO2 and ETCO2 in COPD Patients with Exacerbation on Mechanical Ventilation. Indian J Crit Care Med. 2021 Mar;25(3):305-309. van Gestel AJ, Steier J. Autonomic dysfunction in patients with chronic obstructive pulmonary disease (COPD). J Thorac Dis. 2010 Dec;2(4):215-22. doi: 10.3978/j.issn.2072-1439.2010.02.04.5.

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....

The ABC of ABG. Ph stat vs. Alpha stat ABG for Profound Hypothermia. Welcome to our upcoming webinar, a pivotal educational event tailored for perfusionists seeking to expand their knowledge and expertise in arterial blood gas (ABG) analysis and management during profound hypothermia. This webinar is part of our commitment to providing continuous education and valuable resources for perfusionists, enabling them to earn CEUs while enhancing their professional skills. Part 1: The ABC of ABG - Presented by J. Basha, CCP The first segment of our webinar, "The ABC of ABG," will be led by the esteemed J. Basha, CCP, a renowned expert in the field. This session aims to demystify the complexities of ABG analysis and provide a solid foundation for understanding its critical role in patient management. Understanding ABG: We begin with the basics, explaining the components of ABG, including pH, PaCO2, PaO2, HCO3-, and SaO2. This foundational knowledge is crucial for perfusionists to make informed decisions during cardiopulmonary bypass procedures. Clinical Relevance: The session will delve into the clinical significance of each component of ABG, illustrating how they directly impact patient outcomes. Real-world case studies will be used to demonstrate the practical application of ABG analysis in various clinical scenarios. Interpreting Results: A comprehensive guide on interpreting ABG results will be provided. This includes understanding acid-base balance, recognizing common disorders like acidosis and alkalosis, and applying this knowledge in clinical practice. Part 2: Ph Stat vs. Alpha Stat ABG for Profound Hypothermia - Presented by B. Bolkacav, CCP The second part of our webinar, led by B. Bolkacav, CCP, focuses on the critical decision-making process in managing ABG during profound hypothermia, a common scenario in cardiac surgeries. Ph Stat and Alpha Stat - A Comparative Overview: This session will offer an in-depth look at both Ph Stat and Alpha Stat strategies, discussing their principles, methodologies, and clinical implications. Impact on Perfusion Strategy during Hypothermia: The choice between Ph Stat and Alpha Stat management during profound hypothermia can significantly influence patient outcomes. We will explore how these strategies affect cerebral blood flow, oxygen delivery, and overall patient stability. Case Studies and Best Practices: Drawing from a wealth of experience, Bolkacav will present case studies highlighting the application of both strategies. This practical approach will help perfusionists understand the nuances and best practices for managing ABG during profound hypothermia. Interactive Q&A Sessions: Both sessions will conclude with a live Q&A segment, allowing participants to engage directly with our experts. This interactive component is designed to clarify doubts, discuss complex scenarios, and share experiences among peers. Why Attend This Webinar? Enhanced Knowledge: Gain an in-depth understanding of ABG analysis and its critical role in perfusion, along with specialized knowledge in managing ABG during profound hypothermia. Expert Insights: Learn from seasoned professionals who bring a wealth of experience and practical insights. Networking Opportunity: Connect with fellow perfusionists, fostering a community of learning and professional growth. Earn CEUs: This webinar is accredited by the ABCP, offering valuable CEUs to help meet your professional development requirements. Join Us: This webinar promises to be an enriching experience, combining theoretical knowledge with practical insights. It's an essential addition to the professional toolkit of every perfusionist who strives for excellence in patient care. We eagerly look forward to your participation in this enlightening and engaging session. Faculty: J. Basha, CCP B. Bolkacav, CCP

Akut beyin hasarı (ABH), invaziv mekanik ventilasyon (MV) gerektirebilecek travmatik beyin hasarı (TBH), subaraknoid kanama (SAK), intraserebral kanama ve hipoksik iskemik beyin hasarı gibi farklı alt türleri kapsayan heterojen bir kliniktir. Her bir klinik senaryoda hasta için optimal MV ayarlarının yapılması bazı zorluklar içermektedir. ABH hastalarında genellikle ventilatör desteği için primer bir solunum endikasyonu olmaz ancak sıklıkla spontan soluyabilmelerine rağmen uzun süreli MV ihtiyacı gelişir. Beyin ve solunum/ventilasyon arasındaki karmaşık ilişkiyi daha iyi anlamak ve uygun solunum desteği sağlamak bu hastalarda kritik öneme sahiptir. Bu yazıda ABH hastalarında solunum problemlerinin patogenezi ve güncel literatür ışığında spesifik durumlarda önerilen yaklaşımların özetinin sunulması amaçlanmıştır. Ayrıca konu ile ilgili Sayın Haldun Akoğlu'nun “Travmatik Beyin Hasarında Entübasyon” yazısına da buradan ulaşabilirsiniz. 1. Akut Beyin Hasarında Solunum Problemleri Patogenezi Beyin sabit hacimli bir kemik yapı ile çevrilidir ve beyin hacmini etkileyen herhangi bir değişiklik, kafa içi basıncında bir artışa ve belli bir eşiğin üzerinde kan akışının bozulmasına yol açar. Beyin perfüzyonu, serebral kan akışını sistemik basınç ve metabolizmadaki değişikliklere karşı dengede tutan serebral otoregülasyon mekanizmaları tarafından sıkı bir şekilde düzenlenir. PaCO2 düzeyinde değişiklikler serebral otoregülasyonu etkiler. Hem hipokapni hem de hiperkapni, sırasıyla vazokonstriksiyon ve vazodilatasyon yoluyla perfüzyonda azalmaya yol açarak serebral iskemiyi indükleyebilir. Hiperkapni bu yolla intrakraniyal basınç artışına da yol açabilmektedir. 1.1. Disregüle Solunum Merkezi Fonksiyonları ABH'de solunum disfonksiyonu yaygındır ve solunum merkezlerinin bozulan işlevlerine bağlı solunum paternlerinin düzensizliğinden veya akut akciğer hasarından kaynaklanabilmektedir. Beyin sapı, solunumun düzenlenmesinden sorumlu solunum merkezlerini içerir. ABH'de solunum merkezleri beyin sapına doğrudan hasar yoluyla veya dolaylı olarak intrakraniyal basınçta artış ve serebral kanama veya ödem nedeniyle kitle etkileri yoluyla solunumu etkileyebilmektedir.   Beyin omurilik sıvısında veya beyin dokusunda PaCO2 artışı ve düşük pH CO2'yi stabilize etmek için solunum tepkisini düzenler. Karotid cisimde ve akciğerlerde bulunan periferik kemoreseptörler ise merkezi kemoreseptörlerin duyarlılığını ve eşiğini değiştirerek solunum dürtüsünü etkiler. Ek olarak, akciğer mekanoreseptörleri, akciğer şişmesi ile aktive olan gerilme reseptörleridir ve Hering-Breuer inhibitör refleksi sırasında inspirasyonu sonlandıran merkezi kemoreseptörleri inhibe eder. Bu solunum düzenleyici yolaklar yalnızca asidoz, hipoksemi, hiperkarbi ve/veya atelektazi gibi mekanik bir sebeple değil primer beyin hasarı nedeniyle de tehlikeye girebilmektedir.​1​ 1.2. Akut Akciğer Hasarı ABH, hasar görmüş solunum merkezi dışında, nörojenik pulmoner ödem (NPÖ), akciğerde inflamasyon, akut respiratuar distres sendromu (ARDS), aspirasyon pnömonisi, ventilatörle ilişkili pnömoni (VAP) ve kontüzyon gibi akut akciğer hasarı ile de solunum sıkıntısına yol açabilmektedir. NPÖ ile en sık ilişkili ABH; SAK, anevrizma rüptürü ve TBH olarak bilinmektedir. NPÖ tipik olarak başka herhangi bir solunum yetmezliği nedeni olmaksızın her iki akciğerde diffüz infiltratlarla solunum sıkıntısı, hipoksemi ve bilateral alveoler opasitelerin varlığı ile karakterize edilir Bu nedenle NPÖ, ARDS gibi akut hipoksemik solunum yetmezliğinin en şiddetli formuna benzer ancak farklı bir patofizyolojiye sahiptir.​2​ Tipik olarak, artmış intrakraniyal basınç varlığında, hipotalamus preoptik çekirdeğinin bazal kısmı ve periventriküler sistem gibi anatomik bölgelerden masif bir nöral sempatik deşarj meydana gelir. Bu merkezi sempatik deşarj pulmoner ve sistemik vazokonstriksiyona veya vasküler permeabilitede bozulmaya neden olarak pulmoner ödemi tetikler.

International guidelines recommend targeting normocapnia in adults with coma resuscitated after out-of-hospital cardiac arrest. However, normocapnia may be insufficient to restore and maintain adequate cerebral perfusion. Conversely, mild hypercapnia increases cerebral blood flow and may improve neurologic outcomes. Nevertheless, the most effective Paco2 target in adults with coma resuscitated after out-of-hospital cardiac arrest has not been well studied in randomized trials. Therefore, the Targeted Therapeutic Mild Hypercapnia After Resuscitated Cardiac Arrest (TAME) trial was conducted to test the hypothesis that targeted mild hypercapnia would improve neurologic outcomes at 6 months as compared with targeted normocapnia in adults with coma who had been resuscitated after out-of-hospital cardiac arrest.Listen to the podcast for more insight into the hypothesis, methodology and findings from the TAME study. Original paper: Mild Hypercapnia or Normocapnia after Out-of-Hospital Cardiac ArrestSpeakersClaudio SANDRONI. Policlinico Universitario Agostino Gemelli, Rome (IT). Markus SKRIFVARS. University of Helsinki (FI). Chair, ESICM Trauma & Emergency Medicine (TEM) Section. Chiara ROBBA. University of Genova (IT). ESICM Neuro-Intensive Care (NIC) Section.

In this episode, Maddi covers various factors affecting PaCO2 levels.  

Her iki yatağa bir hemşirenin baktığı ve kontrollü hasta yatışı sağlanan yoğun bakımlara göre acil serviste mekanik ventilasyonda hasta izlemi önemli bir sorundur. Bugün birçok üçüncü basamak acil serviste kritik bakım alanları olmakla beraber, engellenemez hasta sirkülasyonu nedeniyle, hastanın yoğun bakım ünitesine hızlı nakli en uygun çözümdür. Buna karşılık günümüzde yoğun bakım gereksinimi olan çok sayıda hasta yoğun bakımların dışında takip edilmek zorunda kalınmaktadır. ABD'de yoğun bakıma yatırılan hasta sayısı %48.8 artmış bildirilmektedir.​1​ ABD'de her yıl 200 binden fazla hastaya acil serviste mekanik ventilasyon uygulanmaktadır ve üçte biri 5 saatten uzun süre acil serviste kalmaktadır. Üstelik mortaliteleri yoğun bakıma yatırılan diğer hastalara göre belirgin olarak daha yüksektir (%24'e %9.3). ​2​ Ülkemizde de acil servislerimizde her geçen gün daha fazla sayıda mekanik ventile hastayı acil serviste beklenenden uzun süre takip etmek zorunda kalıyoruz. Belki de bu nedenle daha fazla sayıda hekim konuya ilgi gösteriyor. Sitemizde invaziv mekanik ventilasyon konusunda çok sayıda yazı yazıldı. Uzun süredir kurslarda acil hekimleri için konuyu basitleştirmeye çalışsam da burada bu konuda az sayıda yazı yazmıştım. Bu nedenle bu yazıda ARDS(Acute Respiratory Distress Syndrome Akut Solunum Sıkıntısı Sendromu) hastasının acil serviste mekanik ventilasyonu konusunda yazmak istedim. Olgu AS'e nefes darlığı şikayeti ile getirilen 71 yaşında erkek hastanın son 3 gün içerisinde artan öksürük, balgam ve nefes darlığı şikayetleri mevcut. AS'e getirildiğinde GD kötü, nonkoopere olan hastanın ilk değerlendirilmesinde KB: 160/90 mmHg, KH: 128/dk, SS: 32/dk, Oksijen satürasyonu: %75 olarak saptanıyor. Fizik muayene akciğerde bilateral ralleri olan hastaya CPAP başlanıyor (CPAP: 8cmH2O ve %60 oksijenle). Arteriyel kan gazında pH:7.447, PaCO2: 46.1mmHg, PaO2: 43.2mmHg, HCO3: 29.8 mmol/L, Laktat: 1.4 mmol/L saptanıyor. İzlemde genel durumunda düzelme olmayan hasta RSI ile entübe ediliyor. Entübasyon sonrasında çekilen toraks BT'si aşağıda görülen hastanın mekanik ventilasyonunda nelere dikkat edelim? Öncelikle hastanın durumunun hızlı anlaşılması oksijen uygulamalarının yönteminde ilk adım olmalı. Bunun için yönettiğimiz bu hastada ARDS olduğunu anlamamız gerekiyor. ARDS tanısı için Berlin kriterlerini kullanıyoruz, bunu hatırlayalım; Son bir hafta içerisinde yeni ya da kötüleşen olunum etmezliği (Kalp yetmezliği veya Hipervolemiye bağlı değil !) Akciğer görüntülemesinde füzyon, kollapsların veya modülle açıklanamayan bilateral opasiteler Son olarak oksijenizasyon durumu PaO2/FiO2 oranı değerlendirilir. Hafif: 200-300 mmHg (PEEP veya CPAP ≥5 cm H₂O) Orta: 100-200 mmHg (PEEP ≥5 cm H₂O) Ciddi: ≤ 100 mmHg (PEEP ≥5 cm H₂O) Berlin kriterleri, PaO2/FiO2 oranının en az 5 cmH2O'luk pozitif ekspirasyon sonu basınç (PEEP) seviyesinde ölçülmesi gerektiğini belirtiyor. Yani en azından noninvaziv ventilasyon almayan bir hastada değerlendirme mümkün gözükmüyor. Bu hastalarda tanı izlemde konur. Bir çalışmada bilateral infiltrasyonları olan ve standart oksijen altında PaO2/FiO2≤300 mmHg olan hemen hemen tüm hastaların noninvaziv ventilasyon altında ilk 24 saat içinde ARDS kriterlerini karşıladığı ve ölüm oranlarının Berlin tanımlarında bildirilene benzer olduğu bildirildi.​3​ Bu nedenle, ARDS kriterlerine sahip spontan soluyan hastalar pozitif basınçlı ventilasyon olmadan erken tanımlanabilir. Tabi sadece bu kriterler yeterli olmayacak. Hastanın risk faktörlerini ( pnömoni, travma, sepsis, pankreatit vs); sorgulamalıyız. Hiçbir risk faktörü yoksa hidrostatik ödemi dışlamak için objektif değerlendirmeye (örn. ekokardiyografi) ihtiyaç vardır.​4​ NOT: Akut hipoksemik solunum yetmezliğinde hastada KOAH ve/veya hipoventilasyon düşünülüyorsa noninvaziv ventilasyon(NİV) veya yüksek akışlı nazal oksijen (YANO)tedavisi öncelikli düşünülür. Bunun dışındaki hastalarda entübasyon ihtiyacı yoksa yine NİV düşü...

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

Almost complete credit to Stan Tay at adrenaline memories.

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

Questa è la prima di due puntate sull'anidride carbonica e il controllo della ventilazione . I meccanismi che controllano la ventilazione richiedono l'integrazione di diverse strutture del sistema nervoso centrale e periferico. Nel sistema nervoso centrale è il midollo allungato, la sede dei principali centri nervosi che controllano la ventilazione. Tra questi c'è il complesso pre-Botzinger (pre-BotC), coinvolto nella generazione del ritmo inspiratorio e il nucleo retrotrapezoidale. Il nucleo retrotrapezoidale è caratterizzato da neuroni chemosensibili che si attivano in risposta all'aumento dei protoni e che una volta attivati trasmettono al complesso pre-Botzinger e al gruppo respiratorio ventrale rostrale (rVRG) per aumentare la frequenza e la profondità degli atti respiratori. L'aumento dei protoni, degli ioni idrogeno si verifica quando c'è ipercapnia ovvero quando la PaCO2 è al di sopra del range normale 34-46 mm Hg.Questa risposta ventilatoria alla CO2 viene definita risposta ventilatoria ipercapnica (HCVR).In Fisiologia la risposta ventilatoria ipercapnica è studiata con la curva ventilazione/pressione parziale arteriosa di CO2.In Anestesia la curva ventilatoria ipercapnica ha tutta una serie di ripercussioni pratiche, essendo influenzata dalla somministrazione dai più comuni farmaci anestetici: propofol, benzodiazepine, oppioidi e agenti inalatori e da varie condizioni patologiche , tra cui la più estrema è la morte cerebrale.

Idag presenterar jag VR, eller ventilatorisk kvot, som kan vara användbart som objektivt mått på svårighetsgraden av andningssvikt. PaCO2(predicted) = 5kPa VE(predicted) = PBW x 0,1 liter PBW (Predicted Body Weight) enligt ARDS Network: Vuxen man: 50 + 0.91 (längd i cm −152.4) Vuxen kvinna: 45 + 0.91 (längd i cm −152.4) Referenser: 1. Ursprungsartikeln […]

Merhabalar. Gebe hasta geldiğinde tedirgin olmayan acil servis hekimi var mı? Sanıyorum ki yoktur :) Tanıda, ayırıcı tanıda, tetkikte, tedavide, taburculukta defalarca düşünürüz. Bugün de, acil hekimini son derece tedirgin edici bir klinik durum olan gebelerde akut solunum yetmezliğinden bahsedeceğiz. İyi okumalar. Gebelerde fizyolojik mekanizma Biliyoruz ki gebelik sürecinde organizma, kardiyopulmoner sistemde önemli fizyolojik adaptasyonlar geliştirmektedir. Gebelik kesesinin büyümesiyle birlikte diyafram yüksekliği artar, total akciğer kapasitesi azalır, rezidü volüm azalır. Artmış progesteron etkisiyle alveolar ventilasyon artar. Diğer taraftan üst solunum yolu mukozasında glandüler hiperaktivite gelişir. Bununla birlikte özellikle son haftalarda pulmoner arter basıncında artış ve az da olsa diyastolik disfonksiyon gözlenebilir. ​1​ Bu değişiklikler doğrultusunda gebeler ilerleyen gebelik haftalarında gündelik yaşamı kısıtlamayan takipne ve efor kapasitesinde azalma yaşarlar. Nasıl ayırt edelim? Nefes darlığı şikayeti ile acil servise başvuran bir gebedeki bu durumun progesteron ilişkili hiperventilasyon mu, gebelik kesesinin büyüklüğüne bağlı fizyolojik bir nefes darlığı mı veya altta yatan bir patolojinin bulgusu mu olduğunu ayırt etmek bazı zamanlarda zorlayıcı olabilir. Bunun için ayrıntılı bir anamnez alınmalı ve detaylı fizik muayene yapılmalıdır. Nefes darlığının ne süredir olduğu, akut başlangıçlı olup olmadığı, eşlik eden öksürük, balgam, ateş, göğüs ağrısı veya hemoptizi varlığı sorgulanmalıdır. Altta yatan yapısal (myokardiyal veya valvüler) kalp hastalıkları, koroner arter hastalığı, aritmiler, astım hastalığı olup olmadığı, rutin kullandığı ilaçlar ve sigara öyküsü detaylandırılmalıdır. Hastanın solunum yoluyla bulaşan bir enfeksiyona maruz kalma ihtimali düşünülerek, tüberküloz ve Covid-19 hastalıkları başta olmak üzere temas öyküsü sorgulanmalıdır. Kistik fibrozis, alfa-1 antitripsin eksikliği gibi genetik geçişli bazı hastalıklar gebelik döneminde ortaya çıkabilir. Dikkat! Gebelikte mekanik ventilatör desteği gerektiren akut solunum yetmezliği durumları nadir görülmekle birlikte anne ve bebek için mortal seyredebilir. ​2​ Vital bulgular ; >120 atım/dk taşikardi, >24/dk takipne,

In this episode we talk about this very common phenomenon in anaesthesia, the difference between ETCO2 and PaCO2.Essentially this all comes down to patient and equipment factors.BUT the essential element that makes the largest difference is DEAD SPACE.we discuss the factors effecting it, and the Bohr equation that measures dead space.Please support us on our Patreonhttps://www.patreon.com/anaesthesiaAll proceeds will go to Fund a Fellow to help train anaesthetists in developing countries whilst acknowledging the work it takes to keep creating this educational resource.If you enjoyed this content please like and subscribePlease post any comments or questions below. Check out www.anaesthesiacollective.com and sign up to the ABCs of Anaesthesia facebook group for other content.Any questions please email lahiruandstan@gmail.comDisclaimer: The information contained in this video/audio/graphic is for medical practitioner education only. It is not and will not be relevant for the general public.Where applicable patients have given written informed consent to the use of their images in video/photography and aware that it will be published online and visible by medical practitioners and the general public.This contains general information about medical conditions and treatments. The information is not advice and should not be treated as such. The medical information is provided “as is” without any representations or warranties, express or implied. The presenter makes no representations or warranties in relation to the medical information on this video. You must not rely on the information as an alternative to assessing and managing your patient with your treating team and consultant. You should seek your own advice from your medical practitioner in relation to any of the topics discussed in this episode' Medical information can change rapidly, and the author/s make all reasonable attempts to provide accurate information at the time of filming. There is no guarantee that the information will be accurate at the time of viewingThe information provided is within the scope of a specialist anaesthetist (FANZCA) working in Australia.The information presented here does not represent the views of any hospital or ANZCA.These videos are solely for training and education of medical practitioners, and are not an advertisement. They were not sponsored and offer no discounts, gifts or other inducements. This disclaimer was created based on a Contractology template available at http://www.contractology.com.

The manipulation of arterial carbon dioxide levels (PaCO2) is easy, and hyperventilation (HV) has been a common ICP-lowering strategy for over half a century. However, hyperventilation-induced vasoconstriction is a double-edged sword. It reduces cerebral blood volume and intracranial volume, and therefore, lowers ICP. We observed huge variability among centres in PaCO2 values and use of HV. Although causal inferences cannot be drawn from these observational data, our results suggest that, in patients with severe intracranial hypertension, HV is not associated with worse long-term clinical outcomes. Original article: https://rdcu.be/cyz40 (Management of arterial partial pressure of carbon dioxide in the first week after traumatic brain injury: results from the Center-TBI study) Speakers: David K. MENON. Neurocritical Care Unit, Addenbrooke's Hospital, Cambridge, UK Laura BORGSTEDT. Clinic for Anaesthesiology and Intensive Care Medicine - Klinikum rechts der Isar of the Technical University of Munich

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 buradan​1​ 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:​2​Enfeksiyon: 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

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 buradan​1​ 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:​2​Enfeksiyon: 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

Vea la parte 1 aquí. Taquicardias El algoritmo de taquicardias de la actualización 2020 de ACLS es, en esencia, el mismo algoritmo anterior. Aunque no hay cambios en las recomendaciones, el algoritmo aclara algunas situaciones, y complica otras. Existen diferentes tipos de desfibriladores bifásicos que pueden administrar diferentes niveles de energía logrando el mismo resultado. Aunque 100 J sean un punto común de partida para la cardioversión sincronizada de la mayoría de las arritmias, algunas tecnologías específicas pueden lograr lo mismo con menos energía. Un aspecto relevante a recordar es que: El beneficio de cardiovertir una arritmia hemodinámicamente inestable es mayor que el potencial daño al músculo cardiaco, aún con niveles altos de energía. Si no convierte, aumente la energía para la segunda dosis. Algunas arritmias son notables porque NO convierten con dosis bajas de energía. Por ejemplo, es relativamente común tener que cardiovertir una fibrilación atrial con niveles altos. Si se comenzara inadvertidamente con una dosis baja, simplemente se aumenta la energía en una descarga subsiguiente. El algoritmo anterior reflejaba esto diciendo que la primera descarga debía ser entre 120 J y 200 J bifásicos (que equivalen a 360 J monofásicos). El algoritmo nuevo no hace esta aclaración o distinción debido a la variación que puede haber entre una marca de  equipo y otro. Por ejemplo, puede ver aquí el protocolo de desfibrilación de ZOLL. Este otro documento habla de las diferencias entre la energía bifásica y la bifásica truncada. Por otro lado, el otro cambio que el algoritmo tiene es precisamente diciendo lo mismo que acabo de mencionar. El algoritmo tiene un nuevo segmento que dice qué hacer cuando la cardioversión no funciona. Si la cardioversión no funciona, ¡aumenta la dosis de energía! En adición, sugiere identificar la causa de la taquicardia y/o añadir un antiarrítimico al manejo. Sonografía durante el paro cardiaco En este episodio previo del ECCpodcast hablamos sobre el rol de la sonografía para entender lo que ocurre con el paciente en paro cardiaco. Es importante señalar que el rol de la sonografía en este momento no es el pronosticar el éxito del intento de reanimación y/o decidir que se debe detener la reanimación basado en ausencia de signos alentadores a través de la sonografía (ausencia de movimiento de la pared ventricular, etc.). El rol de la sonografía en este momento debe ser en ayudarnos a entender la causa del paro cardiaco e identificar qué acciones pueden tener la mayor oportunidad de éxito. Situaciones especiales: intoxicación con opioides La intoxicación con opioides provoca depresión respiratoria. La depresión respiratoria puede ser desde leve hasta  provocar apnea. Aunque la naloxona (IN, IM o IV) es el antídoto a la intoxicación con opioides, lo primero que debe ser obvio es la necesidad de mantener la vía aérea abierta y una ventilación adecuada. No ignore la posibilidad de que el paciente esté en paro cardiaco por otra razón. Puede ver el algoritmo de paro cardiaco por intoxicación con opioides aquí. Situaciones especiales: Paro cardiaco en mujeres embarazadas Vea el algoritmo de cuidado a mujeres embarazadas en paro cardiaco aquí. Debido a que las pacientes embarazadas son más propensas a sufrir hipoxia, se debe priorizar la oxigenación y el manejo de la vía aérea durante la reanimación del paro cardíaco. (Clase de Recomendación: 1, Nivel de Evidencia: C-LD) Debido a la posible interferencia con la reanimación materna, no se debe llevar a cabo el monitoreo fetal durante el paro cardíaco en embarazadas. (Clase de Recomendación: 1, Nivel de Evidencia: C-EO) Recomendamos un manejo específico de la temperatura para embarazadas que permanecen en estado comatoso después de la reanimación del paro cardíaco. (Clase de Recomendación: 1, Nivel de Evidencia: C-EO) Durante el manejo específico de la temperatura de la paciente embarazada, se recomienda supervisar continuamente al feto para detectar bradicardia como una posible complicación, y se debe realizar una consulta obstétrica y neonatal. (Clase de Recomendación: 1, Nivel de Evidencia: C-EO) Cuidado médico pos-paro Vea el algoritmo de cuidado posparo aquí. El algoritmo de las guías 2015 presentaba cuatro aspectos importantes. Los cuatro elementos importantes que el paciente posparo necesita son: Mantener una oxigenación adecuada Mantener una perfusión adecuada Corregir la causa (en adultos, sospechar el SCA) Proteger el cerebro Esta lista no es exhaustiva. El curso PALS provee una lista de cotejo mucho más detallada que incluye otros aspectos a considerar. Cuidado médico pos-paro: Mantenerlo vivo El algoritmo muestra dos pasos iniciales muy importantes: mantener una ventilación y circulación adecuada. Estos dos pasos se enseñan secuencialmente pero se hacen simultáneamente. La frecuencia respiratoria debe ser lo suficiente para mantener un PaCO2 entre 35 mmHg y 45 mmHg y una oxigenación entre 92% a 98%. Anteriormente la recomendación era simplemente mantener la saturación sobre 94%. El monitorear los niveles de CO2 puede ser importante en pacientes que tengan presión intracranial elevada ya que la circulación cerebral responde a los niveles de CO2. Si el PaCO2 disminuye de 35 mmHg, ocurre vasoconstricción en la circulación cerebral. Vice versa, cuando los niveles de CO2 aumentan sobre 45 mmHg, ocurre vasodilatación en la circulación cerebral. Bajo condiciones normales, el cuerpo humano puede autorregular el flujo sanguíneo para mantener una presión intracranial aceptable. En pacientes cuyo problema incluya un problema de aumento en la presión intracranial, previo al cuidado definitivo, es importante proteger al cerebro de una lesión secundaria si los niveles de CO2 cambian y la circulación cerebral se disminuye o aumenta inapropiadamente. Colocación temprana del tubo endotraqueal Primum non nocere. Primero, no cause más daño. La intubación endotraqueal y ventilación mecánica en pacientes posparo es común. A no ser que el paciente recupere consciencia inmediatamente ocurra el retorno de circulación espontánea, el paciente posparo está inconsciente y por lo tanto no puede confiársele proteger su propia vía aérea. También pudiera ser que recupere pulso, pero no recupere respiración inmediatamente y requiera ser ventilado. La causa del paro cardiaco pudiera incluir alguna etiología que trastoque el equilibrio ácido-base y la ventilación del CO2 excesivo pudiera ser esencial para corregir la acidosis. Sin embargo, en otros episodios del ECCpodcast hemos discutido la importancia de cómo prevenir el paro cardiaco peri-intubación. El paciente en paro cardiaco puede estar hipoxémico, hipotenso y acidótico. Cada uno de estos tres factores pueden provocar hipotensión y/o un colapso circulatorio inmediatamente antes, durante o después de la intubación endotraqueal. Entonces, primero resucite y oxigene el paciente... luego lo intuba. Eso nos lleva al siguiente punto, corregir la hipotensión, lo cual pudiera ser necesario realizar concurrentemente mientras se prepara al paciente y al personal para la intubación. La presión arterial sistólica mínima debe ser 90 mmHg (presión arterial media de 65 mmHg). Es importante considerar mejorar la precarga para subir la presión, pero debemos dejar de pensar solamente en los fluidos como herramienta para mejorar la presión. Es necesario tener una cantidad adecuada de fluidos. Si la causa de la hipotensión es hipovolemia, el administrar fluidos puede ser útil. Sin embargo, si la causa no es hipovolemia, darle más fluido no debe ser la única estrategia. En este caso, el uso temprano de vasopresores puede ser útil. En este otro episodio del ECCpodcast se discute el uso de vasopresores en bolo para el manejo de hipotensión temporal, por ejemplo, secundaria al manejo de la vía aérea en un paciente susceptible. Cuidado médico pos-paro: Neuropronóstico Se teoriza que una de las posibles causas de malos resultados por paro cardiaco pudiera ser el retirar el cuidado médico demasiado temprano. A veces puede ser que algunos cerebros simplemente necesiten más tiempo. La actualización 2020 de ACLS provee una referencia más tangible de qué herramientas pueden servir para evaluar el paciente que tuvo un insulto cerebral anóxico y está comatoso posterior al retorno de circulación espontánea. Como parte de la evaluación en la unidad de cuidados intensivos. es importante medir inmediatamente el nivel de glucosa, electrolitos, y considerar los medicamentos de sedación, anestesia o bloqueo neuromuscular que pueden alterar el nivel de consciencia posterior al retorno de circulación espontánea, pero esto ya es valorado en el cuidado posparo en toda unidad de cuidados intensivos. La actualización 2020 de ACLS hacen referencia al uso de pruebas multimodales solamente luego de las primeras 72 horas posterior al retorno de circulación espontánea. Rehabilitación y recuperación Recomendamos que los sobrevivientes de un paro cardíaco tengan una evaluación y un tratamiento de rehabilitación multimodales para trastornos físicos, neurológicos, cardiopulmonares y cognitivos antes del alta hospitalaria. (Clase de Recomendación: I, Nivel de Evidencia: C-LD) Recomendamos que los sobrevivientes de un paro cardíaco y sus cuidadores reciban una planificación del alta integral y multidisciplinaria que incluya recomendaciones de tratamiento médico y de rehabilitación y las expectativas de regreso a la actividad / trabajo. (Clase  de Recomendación: I, Nivel de Evidencia: C-LD) Recomendamos realizar una evaluación estructurada de la ansiedad, la depresión, el estrés postraumático y la fatiga de los sobrevivientes de paro cardíaco y sus cuidadores. (Clase  de Recomendación: I, Nivel de Evidencia: B-NR) Los pacientes necesitan apoyo para entender la causa por la cual tuvieron el evento, y cómo prevenir una nueva ocurrencia. Esto puede inclusive incluir apoyo para el regreso a actividad niveles normales pre-evento. Debido a la importancia que tiene la rehabilitación y recuperación, la AHA ha añadido un eslabón más a la icónica "cadena de sobrevivencia" que ilustra los elementos en el sistema de cuidado para el éxito del paciente con paro cardiaco. Debriefing para los respondedores Pueden ser beneficiosos los debriefings y las derivaciones para dar apoyo emocional a reanimadores legos, proveedores de SEM y trabajadores de la salud hospitalarios después de un paro cardíaco. (Clase de Recomendación: IIb, Nivel de Evidencia: C-LD) Conclusión de la actualización 2020 de ACLS La siguiente infográfica ayuda a resumir algunos de los aspectos claves de la actualización. La actualización 2020 de ACLS provee cambios importantes en el manejo del paciente. El adiestramiento completo, prácticas frecuentes y retroalimentación efectiva salva vidas. Referencias Panchal AR, Bartos JA, Cabañas JG, Donnino MW, Drennan IR, Hirsch KG, Kudenchuk PJ, Kurz MC, Lavonas EJ, Morley PT, O’Neil BJ, Peberdy MA, Rittenberger JC, Rodriguez AJ, Sawyer KN, Berg KM; on behalf of the Adult Basic and Advanced Life Support Writing Group. Part 3: adult basic and advanced life support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020;142(suppl 2):S366–S468. doi: 10.1161/CIR.0000000000000916 Virani SS, Alonso A, Benjamin EJ, Bittencourt MS, Callaway CW, Carson AP, Chamberlain AM, Chang AR, Cheng S, Delling FN, et al: on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2020 update: a report from the American Heart Association. Circulation. 2020;141:e139–e596. doi: 10.1161/CIR.0000000000000757

In this episode we talk with Dr. Roham Zamanian about the use of Nitric Oxide as an outpatient treatment in a patient with PAH and COVID-19. We also discuss 3 articles on HRQOL questionnaires and outcomes in PAH, PaCO2 association with mortality risk in PAH and urban-rural disparities in the outcomes of patient with PAH.

PaCO2

Benvenuti sul primo podcast italiano che parla di anestesia e rianimazione, prodotto dalla Dr.ssa Maria Luisa Ruberto.La puntata del giorno parla di ....L'equazione della ventilazione alveolare descrive il rapporto tra la ventilazione, ed in particolare la ventilazione alveolare, e la pressione parziale di anidride carbonica alveolare, la PACO2.L'anestesista di sala che utilizza i ventilatori per ventilare in maniera controllata i pazienti in anestesia generale fa sempre riferimento alla pressione parziale dell'anidride carbonica di fine espirazione per capire quanto sta ventilando il paziente...se lo sta ipoventilando o lo sta iperventilando.L'equazione della ventilazione alveolare descrive anche come nell'apparato respiratorio umano le strutture anatomiche deputate alle ventilazione siano pressoché le stesse strutture deputate invece alla scambio gassoso.L'elaborazione dell'equazione della ventilazione alveolare è dipesa da necessità belliche durante la II Guerra Mondiale.L'equazione della ventilazione alveolare, insieme all'equazione dei gas alveolari è una delle equazioni fondamentali della fisiologia respiratoria.

Author: Peter Bakes, MD Educational Pearls: The differential diagnosis for pedal edema includes issues in the heart, kidney, and liver Obesity hypoventilation syndrome (OHS) is an important and common cause of right heart failure. Nighttime hypoventilation leads to pulmonary hypertension, causing right heart strain followed by right heart failure OHS criteria includes obesity, sleep disordered breathing, and alveolar hypoventilation (PaCO2 > 45 mmHg) The causes of OHS are multifactorial, and include mechanical problems with breathing and hormonal changes References Balachandran JS, Masa JF, Mokhlesi B. Obesity Hypoventilation Syndrome Epidemiology and Diagnosis. Sleep Med Clin. 2014;9(3):341–347. doi:10.1016/j.jsmc.2014.05.007 Summarized by Will Dewispelaere, MS3 | Edited by Erik Verzemnieks, MD

Core Questions: What is cerebral autoregulation? Describe your parameters for post-arrest care of a brain injured patient. List 7 interventions for management of a patient with elevated ICP. What are the equations for cerebral blood flow and cerebral perfusion pressure? Describe a protocol for induced hypothermia after cardiac arrest. In the patient with a traumatic brain injury, what is the optimal drug for and duration of seizure prophylaxis?   Wisecracks: What are Lundberg A waves? What is the relationship between PaCO2 and CBF? What is the Monro-Kellie hypothesis?    How do these values change in patients with severe coma? What is the probability that a survivor of cardiac arrest has a full neurologic recovery?

Core Questions: What is cerebral autoregulation? Describe your parameters for post-arrest care of a brain injured patient. List 7 interventions for management of a patient with elevated ICP. What are the equations for cerebral blood flow and cerebral perfusion pressure? Describe a protocol for induced hypothermia after cardiac arrest. In the patient with a traumatic brain injury, what is the optimal drug for and duration of seizure prophylaxis?   Wisecracks: What are Lundberg A waves? What is the relationship between PaCO2 and CBF? What is the Monro-Kellie hypothesis?    How do these values change in patients with severe coma? What is the probability that a survivor of cardiac arrest has a full neurologic recovery?

Podcast 75 är en inspelning av Johan Petersson, funktionsenhetschef CIVA Karolinska Solna, som föreläser om hyperkapni under ventilatorbehandling. Titeln var "Högt PaCO2 – vad beror det på, vad gör vi?"

Basic Science Clinic by Steve Morgan & Sophie Connolly In the words of the canonical Roman poet Ovid: “Sickness seizes the body from bad ventilation”. Welcome to Basic Science Clinic Raw Science 9. Convective gas flow provides the substrate to interface with alveolar structural and functional adaptation in orchestrating gas exchange. Gas exchange is the serial interconnection of ventilation, diffusion and perfusion. Alveolar gas composition is determined by amount and type of gases delivered by ventilation, the rate and direction of gas diffusion, and the pulmonary blood flow which continuously recalibrates partial pressure gradients to direct oxygen and carbon dioxide movement. Bulk gas volume displacement is the mechanism of ventilation, but how do we conceptualise and quantify its contribution to gas exchange and its associated abnormalities? In this pod we will examine the quantification of ventilation and parse its correspondence with variance in the dead space volume and central role in carbon dioxide homeostasis. In this podcast we will cover: How do we define pulmonary ventilation? What is the relationship between alveolar minute ventilation and alveolar gas composition? What are the determinants of arterial carbon dioxide partial pressure? What are the physiological sequelae of hypercapnia? What is permissive hypercarpnia? What is dead space? How do we quantify dead space volume? What are the factors that affect dead space?   Here are your Raw Science factoids: Morphological dead space estimates give us volumes of 150mls for dogs, 380mls for cows and 150-300L for whales. In 1986 in Cameroon a paroxysmal expulsion of carbon dioxide from the volcanic lake Nyos resulted in the asphyxiation of 1700 people and 8000 animals. The highest documented PaCO2 to be measured in a subsequent survivor weighed in at 501 mmHg in a 16 year old boy swallowed, sequestered and asphyxiated by a rapidly filling grain truck. For feedback, corrections and suggestions find us on the twitter handles @falconzao and @sophmconnolly or alternatively post on ICN. Check out our new website basicscienceclinic.com where you can access the back catalogue and peruse the real brains behind our elaborate plagiarism by checking out the reference page to go direct to the source material. Thanks for listening. Next up we’ll consummate the journey of inspirate atmospheric gas into the blood phase, as we appraise gas diffusion across the alveolar-capillary membrane and dissect the pulmonary vasculature.  

FOAMcast is bringing you pearls from conferences we attend and, first up, the American College of Emergency Physicians annual meeting, ACEP14.   Today's Pearls: Emergency Physicians are like economists (We're more probalisticians than diagnosticians). Cardiology pearls from Dr. Slovis - TTM to 36 Celsius post-arrest should be standard. Many people probably could benefit from caths after arrest, we're not sure exactly who at this point. Patients returning from West Africa with fever probably have a regular virus, maybe malaria, but probably not ebola. There's really not much use for glucagon in calcium channel blocker toxicity. Think supportive care, insulin-dextrose. ETCO2 - it doesn't equal PaCO2 and it depends on cardiac output and alveolar ventilation   For updates, follow #ACEP14   Thanks for listening, y'all! Jeremy Faust and Lauren Westafer

In part 1 of this 3 episode series, we lay the foundation of Dominating Acid Base Balance. Included will be philosophical and clinical exploration of pH, PaCO2, HCO3, base deficits and how acid-base affects critical systems in the body.

In part 1 of this 3 episode series, we lay the foundation of Dominating Acid Base Balance. Included will be philosophical and clinical exploration of pH, PaCO2, HCO3, base deficits and how acid-base affects critical systems in the body.See omnystudio.com/listener for privacy information.

Background: Refinement of ventilatory techniques remains a challenge given the persistence of chronic lung disease of preterm infants. Objective: To test the hypothesis that proportional assist ventilation ( PAV) will allow to lower the ventilator pressure at equivalent fractions of inspiratory oxygen (FiO(2)) and arterial hemoglobin oxygen saturation in ventilator-dependent extremely low birth weight infants in comparison with standard patient-triggered ventilation ( PTV). Methods: Design: Randomized crossover design. Setting: Two level-3 university perinatal centers. Patients: 22 infants ( mean (SD): birth weight, 705 g ( 215); gestational age, 25.6 weeks ( 2.0); age at study, 22.9 days ( 15.6)). Interventions: One 4- hour period of PAV was applied on each of 2 consecutive days and compared with epochs of standard PTV. Results: Mean airway pressure was 5.64 ( SD, 0.81) cm H2O during PAV and 6.59 ( SD, 1.26) cm H2O during PTV ( p < 0.0001), the mean peak inspiratory pressure was 10.3 ( SD, 2.48) cm H2O and 15.1 ( SD, 3.64) cm H2O ( p < 0.001), respectively. The FiO(2) ( 0.34 (0.13) vs. 0.34 ( 0.14)) and pulse oximetry readings were not significantly different. The incidence of arterial oxygen desaturations was not different ( 3.48 ( 3.2) vs. 3.34 ( 3.0) episodes/ h) but desaturations lasted longer during PAV ( 2.60 ( 2.8) vs. 1.85 ( 2.2) min of desaturation/ h, p = 0.049). PaCO2 measured transcutaneously in a subgroup of 12 infants was similar. One infant met prespecified PAV failure criteria. No adverse events occurred during the 164 cumulative hours of PAV application. Conclusions: PAV safely maintains gas exchange at lower mean airway pressures compared with PTV without adverse effects in this population. Backup conventional ventilation breaths must be provided to prevent apnea-related desaturations. Copyright (c) 2007 S. Karger AG, Basel

Background: Inspiratory activity is a prerequisite for successful application of patient triggered ventilation such as proportional assist ventilation (PAV). It has recently been reported that surfactant instillation increases the activity of slowly adapting pulmonary stretch receptors (PSRs) followed by a shorter inspiratory time (Sindelar et al, J Appl Physiol, 2005 [Epub ahead of print]). Changes in lung mechanics, as observed in preterm infants with respiratory distress syndrome and after surfactant treatment, might therefore influence the inspiratory activity when applying PAV early after surfactant treatment. Objective: To investigate the regulation of breathing and ventilatory response in surfactant-depleted young cats during PAV and during continuous positive airway pressure ( CPAP) early after surfactant instillation in relation to phrenic nerve activity (PNA) and the activity of PSRs. Methods: Seven anesthetized, endotracheally intubated young cats were exposed to periods of CPAP and PAV with the same end-expiratory pressure (0.2 - 0.5 kPa) before and after lung lavage and after surfactant instillation. PAV was set to compensate for 75% of the lung elastic recoil. Results: Tidal volume and respiratory rate were higher with lower PaCO2 and higher PaO2 during PAV than during CPAP both before and after surfactant instillation ( p < 0.05; both conditions). As an indicator of breathing effort, esophageal deflection pressure and PNA were lower during PAV than during CPAP in both conditions ( p < 0.02). Peak PSR activity was higher and occurred earlier during PAV than during CPAP ( p < 0.01), and correlated linearly with PNA duration in all conditions studied ( p < 0.001). The inspiratory time decreased as tidal volume increased when CPAP was changed to PAV, with the highest correlation observed after surfactant instillation ( r = - 0.769). No apneic periods could be observed. Conclusion: PSR activity and the control of breathing are maintained during PAV in surfactant-depleted cats early after surfactant instillation, with a higher ventilatory response and a lower breathing effort than during CPAP.

The Effect of Hyperventilation on Cognitive Performance, Motor Functions and Lesion Volume after Controlled Cortical Impact in the Rat Introduction: We investigated the effects of short-term moderate hyperventilation on neurocognitive and motor functions as well as lesion volume in rats subjected to focal traumatic brain injury. Thereby the model of controlled cortical impact (CCI) was established associated with the evaluation of a battery of behavioral tests. Methode: 21 male Sprague-Dawley rats (369±15 g) were trained to achieve the modified Hole-Board Test (mHB-Test) for a period of 14 days and some more behavioral tests (Beam Walking, Beam Balance, neurologic score) for 3 days. After completion of specific baseline parameters of the mHB-Test rats were anesthetized with 1.0-1.5 Vol% halothane in O2/N2O (FiO2=0,33), intubated and mechanically ventilated for surgical preparation. After cranio-tomy CCI was induced using a pneumatic pistol (Ø 5 mm, 1,75 mm depth, 200 ms, 4 m/s). Animals were then randomly assigned to one of two groups for four hours post-traumatic ventilation with Halothan (0,8-1,0 Vol%): group 1=normoventilation (n=10; PaCO2=38-42 mmHg); group 2=hyperventilation (n=11; PaCO2=28-32 mmHg). During the entire study, brain temperature and mean arterial blood pressure were kept at normal physiological levels. Additionally breathing and heart rate, PaO2, pH, glucose and heamoglobin were messured. Upon recovery all behavioral tests were continued to euthanasia on the 20th day. During deep anesthesia rats were decapitated and their brains were sampled, frozen and then cut in 10 µm thick sections to evaluate lesion volume after cresyl violet staining. Results are tabu-lar shown Mean+/-SD and graphical Mean+/-SEM (statistic: ANOVA and post hoc t-test). Results: Hyperventilated rats developed a significant deficit in declarative memory (mHB-Test), with variances especially on days 1-2 after trauma associated with a decreased neuro-logical score on days 1-3 compared to normoventilated animals which had a decrease only on day 1. For motor impairments after CCI the Beam Walking and Beam Balance were most sensitive with deficits in both groups and a significant disability of hyperventilated rats. All impairments were just transient after the traumatic brain injury and adjusted to baseline pa-rameters on day 6. Bodyweight measurements, time of food intake or inactivity (mHB-Test) and all several motoric parameters show a marginal reduction of constitution in the rats after CCI. Exploration parameters of mHB-Test demonstrate that normoventilated rats are more active and explorativ following the CCI in comparison to hyperventilated rats. On day 20 after injury, lesion volume was significant larger in the hyperventilated group (69,7±13,0 mm3) versus the normoventilated group (48,3±15,6 mm3). Discussion: We evaluated a model of CCI, that is inducing a standardized and reproduce-able traumatic brain injury. Four hours of post-traumatic hyperventilation transiently impairs hippocampus-dependent declarative memory as well as neurocognitive and motor functions. Hyperventilation also enhances long-term histological damage. These data suggest, that hyperventilation without controlling intracranial pressure is able to deteriorate primary lesion and should be used with caution after acute head trauma.

Bei der Anästhesie mit Medetomidin, Midazolam und Fentanyl (MMF) wird stets ca. 3 Minuten nach Gabe der entsprechenden Antagonisten ein massiver Blutdruckabfall beobachtet. Daher sollte in der vorliegenden Studie der Einfluss der Antagonisierung auf die Hämodynamik, die Atmung und den Glukosestoffwechsel von Ratten im Volumenmangelschock an 145 männlichen Wistar-Ratten mit einem durchschnittlichen Körpergewicht von 359 g untersucht werden. Die Tiere wurden hierzu in drei Hauptgruppen mit unterschiedlichen vorgegebenen Blutdruckwerten, welche durch Blutentzug erzielt wurden, eingeteilt: Die Versuchsreihe Kontrolle (VR K) ohne Blutentzug. Die Versuchsreihen 70 (VR 70) und 40 (VR 40) mit einem Blutentzug bis zu einem mittleren arteriellen Blutdruck von 70 mmHg (VR 70) bzw. 40 mmHg (VR 40). Jede der VRn wurde wiederum in je 5 Behandlungsgruppen unterteilt, in denen durch prophylaktische i.v., i.p. oder s.c. Flüssigkeitsgabe vor bzw. durch therapeutische s.c. Substitution nach der Antagonisierung verschiedene Therapie- bzw . Prophylaxemöglichkeiten geprüft wurden. Es wurden nicht invasiv Temperatur, Atmung und Puls und invasiv die Parameter mittlerer arterieller Blutdruck, arterielle Blutgase, Säure-Basen-Status, Glukose und Hämatokrit in regelmäßigen Zeitabständen bestimmt und das Rate Pressure Product errechnet. Vor Euthanasie der Tiere zum Zeitpunkt t=130 wurden die Ratten zusätzlich klinisch an Hand verschiedener Bewertungsparameter beurteilt. Mit der Varianzanalyse (Repeated Measures ANOVA) wurde überprüft, ob signifikante Unterschiede zwischen den einzelnen Gruppen, im Kurvenverlauf oder zu bestimmten Zeitpunkten bestehen. Hierbei wurde ein Signifikanzniveau von p  0,05 angenommen. Auch unter der MMF-Narkose konnten die für den Volumenmangelschock typischen Veränderungen wie Anstieg der Herz- und Atemfrequenz mit nachfolgendem Abfall und Absinken des Rate Pressure Productes beobachtet werden. Zudem kam es durch den Blutentzug zu einer alveolären Hyperventilation mit sinkendem PaCO2 und dadurch abfallender HCO3- und BE, die kompensatorisch zur eintretenden metabolischen Azidose wirkte. Die Gruppen mit prophylaktischer Flüssigkeitssubstitution zeigten bereits in der Narkosephase einen weniger starken Herzfrequenzabfall und eine Erhöhung des mittleren arteriellen Blutdruckes und des Rate Pressure Productes. Nach der Antagonisierung trat erwartungsgemäß in allen Versuchsreihen ein kurzzeitiger, massiver Blutdruckabfall auf, der seinen Tiefststand nach ca. 3 Minuten hatte. Selbst bei den hypotensiven Ratten im schweren hämorrhagischen Schock kam es dabei jedoch zu keiner lebensbedrohlichen Situation. Bei den Untersuchungen zu den Therapie- bzw. Prophylaxemöglichkeiten wiesen die Ratten, denen 10 Minuten vor ihrer Antagonisierung 30 ml warme Ringer-Lösung s.c. verabreicht wurde, gute Endergebnisse auf, weshalb eine routinemäßige prophylaktische s.c. Volumensubstitution vor OP-Beginn erfolgen sollte. Die Ergebnisse zeigen weiter, dass die Antagonisierung der MMF-Narkose zu einer Verbesserung sowohl der Atemfrequenz als auch der Herz- und Kreislaufwerte und der Blutgase führt und daher trotz des vorübergehenden, massiven Blutdruckabfalles auch bei Risikopatienten im Volumenmangelschock empfehlenswert ist.

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