Podcast appearances and mentions of frank starling

What began as taking different life paths for both Laura Brown and Frank Starling has evolved into a shared mission: building inclusive spaces in the advertising industry. At just 21, Laura was made redundant with no savings, before she started temping as a receptionist at Cannes Lions. What seemed like a setback became a launchpad. Today, she is Cannes Lion's Head of Advancing Equitable Access and leads its See It Be It program — which builds inclusive spaces to help elevate women and nonbinary people's careers in advertising.  For Frank, entering the work force early with a passion for improving his community in East London forged a relentless drive to make workplaces more inclusive. Now as LION's Chief DEI Officer, he's using his platform to build belonging across the advertising and communication industries. Together, they unpack how See It Be It advances careers, focuses on retention just as much as recruitment, and how supporting regional communities play a vital role in sustaining inclusion efforts. The Cannes Lions festival will take place from June 16 through June 20, 2025. Founders International Network is the official media partner for Cannes Lions' See It Be It Program. This episode was produced by Hauwa Otori with help from Osheiza Otori. Music composed by Kevin Edwards. You can follow FIN on LinkedIn and BBP on Instagram.

Often when a patient's blood pressure has dropped, we administer fluids without truly knowing the exact reason for the change. Does the patient have low volume, were they vasodilating, or is their heart not squeezing effectively? Fluid resuscitation is not always the answer, but there's no clear guideline to assess patients without advanced tools that take time and specialists. Enter the FloPatch from Flosonics, an innovative device that quickly measures blood flow in real time.Fluids can cause damage when given in excess, so it's crucial for nurses to understand why blood pressure isn't an adequate indicator of fluid responsiveness, and how a patient can show signs of fluid responsiveness but cardiac output is not increasing. That's why host Sarah Lorenzini is speaking with Corinne RN to find out more about how Flosonics is helping nurses guide their fluid resuscitation using the portable FloPatch device.In this episode, Corinne shares patient stories to exhibit how FloPatch can improve patient outcomes, especially in those with sepsis. Corinne and Sarah also discuss the concept of Frank-Starling's law, the components of stroke volume, and MORE.FloPatch can help you assess patients and provide precise care. Tune in to find out how it works, the benefits of the product, and why you want to use it at your hospital!Topics discussed in this episode:How Corrine RN became so passionate about fluid resuscitationWhy blood pressure isn't the best tool for determining cardiac outputFactors that influence blood pressureThe relationship between preload, afterload, and contractilityThe consequences of fluid overloadExamples of how FloPatch can improve patient careFloPatch is a game-changing advancement in precision fluid management for critical care, particularly in the management of sepsis. As the world's first wireless, wearable Doppler ultrasound technology, it provides real-time, non-invasive assessments of arterial and venous blood flow. FloPatch empowers clinicians at the bedside to make rapid, data-driven decisions on fluid resuscitation, mitigating risks of complications such as pulmonary edema and acute kidney injury. FloPatch holds the potential to transform the way clinicians approach and manage hemodynamic assessments, paving the way for increased clinical confidence for more efficient, effective, and patient-centered care.Visit their website to learn more and request a demo: https://flosonicsmedical.com/Share this podcast episode with your colleagues to spread the word about FloPatch.Follow FloPatch on Instagram, Twitter and LinkedIn for the latest updates and clinical insight:Instagram: https://www.instagram.com/flopatch_/Twitter: https://twitter.com/Flosonics/LinkedIn: https://www.linkedin.com/company/flosonics-medicalHave questions for Corinn? Email her at czehner@flosonicsmedical.comJoin the Sepsis Alliance Summit 2023 during Sepsis Awareness Month! This virtual event is hosted on September 27th to 28th. Learn more here: https://learn.sepsis.org/virtual-conferenceMentioned in this episode:Rapid Response and Rescue Intro CourseIf you would...

In this Episode of the Digital Insurance Podcast Alexander Tackenberg interviews relevant people in the insurtech industry at the 2023 Insurtech Insights Conference. One of the biggest challenges in the insurance industry are legacy systems. Especially an old core system presents a risk. Generally, legacy systems no longer have support and maintenance and they are limited in terms of growth. Transformational mind change needs to occure. Raphael Schmid adds that an event like the insurtech insights conference helps tremendously in inspiring eachother and moving the digitalisation process forward. Especially the service industry is highlited as an industry we can learn from. Because Customer centricity is the way to move forward. But also technologies and the work with ai is something we should learn from. By using technologies to automate manual processes such as underwriting and claims handeling, processes would become more efficient. A big thank you to all the interviewees who participated in this episode: Amit Batzir, co-founder of Spott, Monique Rodriguez, Revolut, CFO of Revolut Insurance, MBA Oxford, Danilo Raponi, Group Head of Innovation, Generali, Mark Klein, Chief Digital Officer at Ergo Group, Stefano Bison Group Head of Business Development & Partnerships at Generali, Esther Prax, Programme Director at ITHM, Raphael Schmid, Chief Specialty Officer at AON Switzerland, Sarah Wernér, Co- Founder & CEO, Husmus, Martin Micko, CEO & Founder of omni:us, Florian Graillot, Investor @ astorya.vc, Oliver Werneyer, VP of Strategy, Imburse, Merlin Beyts, Head of Content ITC Europe, Roman Rittweger, Aufsichtsrat, Ottonova, Michael Hubbard, Commercial Director at Freedom to insure, Tomer Kashi, Co-Founder & CEO at Voom Insurance, Janthana Kaenprakhamroy , Chief Executive Officer, Tapoly, Pierangelo Campopiano, CEO Smile Insurance, Frank Starling, CEO of Variety Pack, Susan Winkler, Vice President & Executive Director, Connecticut Insurance and Financial Services (CT IFS), and Selina Bilton from Lukango. Links in this issue Homepage of Jonas Piela LinkedIn-Profil of Jonas Piela LinkedIn-Profil of Alexander Tackenberg Vertrauen Sie auf Ihren guten Ruf? Er ist Ihr Versprechen an Ihre Kunden. Mit ProvenExpert bauen Sie online Vertrauen auf, indem Sie authentische Kundenstimmen nutzen und sichtbar werden. Für unsere Hörer gibt es hier alle Infos sowie ein exklusives Angebot, um eure Online Sichtbarkeit durch Kundenbewertungen auf ein neues Level zu heben! geht es zu Ihrem exklusiven Angebot als Zuhörer des Digital Insurance Podcasts. ProvenExpert – Für alle, die wissen, dass Vertrauen mehr wert ist als Gold KI, Dynamisches Pricing, Embedded Insurance, Nutzungsbasierte Versicherung – Keylane setzt diese Themen bereits seit Jahren erfolgreich mit ihren Kunden um. Willst Du wissen, wie das funktioniert? Folge oder schreibe Keylane bei LinkedIn. Keylane – Unlock tomorrow! Das Digital Insurance Job Board ist live! Du suchst einen Job im Versicherungsumfeld mit Perspektive, spannenden Themen und in einem innovativen Team? Hier findest du die aktuellsten Stellen rund um Digital Insurance im DACH Raum.

In this episode, Sacha chats with DEI practitioner and Founder of Variety Pack, Frank Starling. They discuss the challenges facing #dei practitioners in the UK and Europe - including classism, the link between allyship, psychological safety, and intersectionality, as well as how to support organizations as they move from awareness to action. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/deiafter5/support

In deze aflevering van Intensief de Podcast bespreek ik samen met Thomas Smits alles omtrent vocht toediening en fluid responsiveness. Thomas is IC-verpleegkundige en verplegingswetenschapper en heeft tijdens zijn studie veel expertise opgedaan over het bepalen van fluid responsiveness en zal deze expertise met ons delen. We bespreken de o.a. volgende onderwerpen:Wat is fluid responsiveness en het Frank-Starling principe?Waarom geven we vocht aan onze IC-patiënten?Waarom moeten we vocht als medicijn gaan zien?Waarom zijn tachycardie, hypotensie, een lage CVD en een hoog lactaat slechte tekenen  voor fluid responsiveness? En wat zijn dynamische en statische parameters?Wat is een fluid challenge en een passive leg raise?Hoe kan je de beademingsmachine gebruiken om fluid responsiveness te bepalen?Waarom moeten we vocht met een drukzak toedienen en niet met een infuuspomp?Wat zijn de nieuwste technieken en hoe ziet de toekomst eruit?Bronnen:CV Physiology | Frank-Starling MechanismFluid responsiveness in acute circulatory failure | Journal of Intensive CareFluid challenges in intensive care: the FENICE studyIV Fluid Overload: Don't Drown your Patients!Ventricular Pressure-Volume Relationship: Preload, Afterload, Stroke Volume, Wall Stress & Frank-Starling's law – ECG & ECHOHypotension: Differential Diagnosis – emupdatesTachycardia DDx • LITFL • CCC Differential DiagnosisWill This Hemodynamically Unstable Patient Respond to a Bolus of Intravenous Fluids? | Acid Base, Electrolytes, Fluids | JAMA | JAMA NetworkNoninterventional follow‐up vs fluid bolus in RESPONSE to oliguria—The RESPONSE trial protocol and statistical analysis plan Fluid Bolus in Resuscitation: Pressure Bag vs. 999ml/hr on the IV PumpPrediction of fluid responsiveness. What's new?Hoeveel zout mag ik eten? | VoedingscentrumBalanced Crystalloids Versus Saline in Critically Ill Adults: A Systematic Review and Meta-analysisEffect of a fluid bolus on cardiovascular collapse among critically ill adults undergoing tracheal intubation (PrePARE): a randomised controlled trial Effect of Fluid Bolus Administration on Cardiovascular Collapse Among Critically Ill Patients Undergoing Tracheal Intubation (PREPAREBedankt voor het luisteren!Volg @intensiefdepodcast op InstagramVragen? intensiefdepodcast@gmail.com

So many companies are reworking their relationship with diversity, equity and inclusion actions this year, as they should. But for affinity groups within companies, like ERGs or BRGs, developed to support underrepresented groups - what is the best role for leadership to play? Should they be the driving force, or take a backseat role? Join host Christine Dela Rosa and debaters Dominique Ward and Shannon Winter, as they consider the best ways management can support these internal groups. In this episode, you'll hear from DEI consultant Frank Starling on the opportunities for accountability when leadership drives ERGs; and the Surdna Foundation's Mekaelia Davis shares why ERG members ultimately benefit more when they are in the driver's seat themselves. For the transcript and downloadable takeaways, visit https://www.atlassian.com/blog/podcast/work-check.

In this DEI Bucket List podcast episode, our host Magnus Okuonghae invites Frank Starling (Founder & Chief Diversity Officer at Variety Pack). He talks about tackling uncomfortable conversations, speaking to the truths of inclusion and embracing different lived experiences, and about what drives his passion for the impactful work that he does, with some insights into the early practical steps that can be taken to change behaviours.

Bom dia, boa tarde, boa noite! Esse é mais um podcast do Medicina do Conhecimento. Ciência e informação a qualquer momento, em todo lugar. Eu sou Pablo Gusman, o Anestesiador. E como compartilhar é multiplicar vamos juntos pelo mundo do conhecimento. Quanto custa hiperhidratar nossos pacientes? Temos idéia de que o custo dos líquidos administrados por nós de forma endovenosa em nossos pacientes não representa efetivamente grande porcentagem do que se gasta durante uma internação, mas o mais importante é saber que o gerenciamento adequado desses fluidos pode melhorar os resultados clínicos, potencialmente economizando milhões em custos operacionais. Em um estudo retrospectivo de quase 200 pacientes, pesquisadores da Universidade de Kansas avaliaram que a ressuscitação guiada por métodos não invasivos guiada pelo volume sistólico em pacientes de UTI com sepse e choque séptico mostraram redução de 2,8 dias na internação no CTI, 13,2% na terapia substitutiva renal, redução do risco de ventilação mecânica em 50% e um economia de mais de 14 mil dólares por paciente. Apenas 50% dos pacientes hemodinamicamente instáveis respondedores ao fluidos terão um aumento do débito cardíaco e da perfusão. O que nos interessa é saber se nossa microcirculação está satisfeita com nossa oferta! E podemos usar testes como a elevação passiva dos membros inferiores para nos orientar quanto a fluidorresponsividade. Apesar dos avanços tecnológicos no CC e UTI’s, a avaliação do estado de fluidos na sala de emergência depende principalmente do julgamento clínico à beira do leito usando parâmetros vitais pouco conclusivos como pulso, pressão arterial e diurese. Autores descobriram que a elevação dos membros medida pelo biorreatância é uma ferramenta promissora para a avaliação da responsividade do volume sistólico. Essa ação se torna viável na sala de emergência por ser mais reproduzível do que a técnica de bolus de fluido para avaliar capacidade de resposta ao volume. Isso provavelmente está relacionado mais aos desafios de reprodução do bolus de fluido e às mudanças irreversíveis feitas pela administração do primeiro bolus, que, como esperado, moveu os pacientes para cima da Curva de Frank Starling, limitando assim a aplicação para se guiar a ressuscitação. Em populações ainda mais sensíveis a volume como os pacientes portadores de falência renal, tem havido muito debate sobre a busca do equilíbrio do volume administrado com importantes implicações de tratamento. Um modelo multivariado foi construído para prever a mortalidade com um ajuste aplicado à gravidade da doença e avaliação da morbidade. O volume médio de fluidos no dia 1 foram 3,7L (mediana 3,1L), os mais baixos naqueles sem vasopressores (3,2L) e maiores naqueles com Ventilação Mecânica e choque séptico (5,4L). A mortalidade hospitalar foi de 16,5% para os sobreviventes do dia 1, variando de 7,8% naqueles sem ventilação mecânica e sem vasopressores, a 53% entre aqueles com ventilação e vasopressores. Houve associações significativas entre o volume de fluidos do dia 1 e sobrevivência hospitalar. A mortalidade geral foi de 29,3% para aqueles que recebem mais de 9 litros de fluidos. Naqueles que requereram vasopressores e suporte ventilatório, existiu uma associação clara entre o excesso de volume e os resultados, enfatizando uma melhor compreensão das necessidades individuais de fluidos neste população específica. Portanto, mesmo que por si só não representem grande parte da conta hospitalar, os fluídos merecem ser bem geridos. O excesso ou pelo menos a infusão maior do que o paciente necessita pode levar a um aumento significativo no tempo de internação, exacerbação de comorbidades e piora no prognóstico. Esse podcast tem o apoio científico da Baxter Hospitalar. Na intercessão entre salvar e prolongar vidas, com seu compromisso de nos ajudar a enfrentar os desafios e aproveitar as oportunidades cada vez maiores nos cuidados do paciente.

In the first part of the Cardiology chapter, we cover: - Heart and Blood Vessels (Including anatomy of the heart as well as anatomy of the circulatory system)- Physiology (Cardiovascular terminology and formulas) - Electrophysiology (Including cardiac myocytes, Frank-Starling curve, cardiac cycle, and heart sounds & murmurs) Get a discount on best selling study resources from Elsevier ITB listeners can get 30% off of books like Crush Step 1, USMLE Step 2 Secrets, Netter’s Anatomy Coloring Book, and more! Head over to us.elsevierhealth.com/insidetheboards and use the code ITB30 at checkout.About the Crush Step 1 Podcast With a focus on teaching you to “think like a question writer”, InsideTheBoards is the leading producer of medical education podcasts. The Crush Step 1 podcast, the second collaboration between InsideTheBoards and Elsevier, features a totally free, audio optimized, complete narration of Crush Step 1: The Ultimate USMLE Step 1 Review by Ted O'Connell, Ryan Pedigo, and Thomas Blair. Crush Step 1 features up-to-date, easy-to-read (or listen to), high yield info on all the material tested on the exam with topics selected by a review board of current medical students and residents who scored in the 99th percentile on the USMLE Step 1. The Crush Step 1 podcast is the perfect companion for your dedicated prep time. InsideTheBoards Study Smarter Podcast Each year during the dedicated prep time we run a “Study Smarter Series for the USMLE Step 1 and COMLEX Level 1” on our Study Smarter Podcast with a focus exclusively on breaking down USMLE style questions. Click here to check it out on iTunes or visit our BRAND NEW Website ITB Audio Qbank and iOS Beta AppThe Audio Qbank by InsideTheBoards mobile app has both free and premium features and is available on both Android and iOS. To get started, first, create a Boardsinsider Account on our website insidetheboards.comFree Features All of our podcasts in one place organized into playlists for easy studying (also with less ads and exclusive content) Mindfulness meditations designed specifically for medical students A monthly offering of high yield content (questions dissections, audio qbank samples) available only on our mobile app. Early Access and exclusive content like a preview of the soon to be released "Crush Step 1" podcast and the "Inside ITB" podcast where we "get real" about the challenges of building ITB and the day to day behind the scenes stuff. Premium FeaturesSubscribe to an ITB premium account and get additional features Access to 500+ audio optimized board style practice questions in our Audio Qbank. The Step 1 version is powered by Exam Circle and the Step 2 Version is powered by OnlineMedEd. New questions added each month. High Yield Pharmacology (powered by Lecturio) with 100 of the top pharm questions you need to know for both Step 1 and Step 2 Audio Flashcards (coming soon) Our audio qbank is PERFECT for studying for the boards on the go. And we're adding content and improving it all the time. Learn more about the Audio Qbank by InsideTheBoards mobile app hereInsideTheBoards, Elsevier and their collaborators are not affiliated with the NBME, USMLE, COMLEX, NBOME or any professional licensing body. InsideTheBoards and its partners fully adhere to the policies on irregular conduct outlined by the aforementioned credentialing bodies.

Frank Starling

What does Frank Starling’s Law mean? How’s cardiac output affected? This podcast basically answers these questions. --- Support this podcast: https://anchor.fm/kamesa-anota/support

How do PV loops change with increased preload, contractility and afterload? Cardiac output | PV loops | Frank-Starling Curve or principle --- Support this podcast: https://anchor.fm/kamesa-anota/support

Dr Carolyn Lam:                Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr Carolyn Lam, Associate Editor from the National Heart Center and Duke National University of Singapore.                                                 This week's feature discussion focuses on first and man pilot study results of pericardiotomy and its influence on left ventricular diastolic reserve with volume loading. Very fascinating implications for heart failure with reserved ejection fraction, coming right up after these summaries.                                                 Cardiac dysfunction is a major component of sepsis-induced multi-organ failure in critical care units. But what are the underlying mechanisms and potential therapeutic approaches to this? Well, in today's paper from co-first authors Drs Sun and Yao, corresponding author Dr Chang, and colleagues from UT Southwestern Medical Center, the authors examine the status of cardiac autophagy and its role during sepsis pathogenesis using a rodent lipopolysaccharide-induced sepsis model. They've found that forced overexpression of Beclin-1 in the heart promoted autophagy and mitophagy, protected mitochondria, improved cardiac function, and alleviated inflammation and fibrosis after a lipopolysaccharide challenge. Whereas, haplosufficiency for Beclin-1 resulted in the opposite effects. For the more injection of a cell permeable Tat-Beclin-1 peptide improved outcomes in lipopolysaccharide-challenged animals. Thus promoting Beclin-1-dependent signaling may be a novel and effective intervention to alleviate organ dysfunction caused by maladaptive autophagy during severe sepsis.                                                 The next paper presents important experimental data that causes us to consider the potential cardiovascular hazards of anti B-cell activating factor immunotherapy, which is currently approved for the treatment of autoimmune systemic lupus erythematosus. You see, genomic data has shown that B-cell activating factor receptor pathway is specifically essential for the survival of conventional B lymphocytes, which is a key driver of coronary heart disease. However, in today's paper from co-first authors, Drs Tsiantoulas and Sage, corresponding author Dr Binder and colleagues from Medical University of Vienna, the authors reported an unexpected finding that B-cell activating factor neutralization increased atherosclerotic plaque size and complexity despite efficient depletion of mature, conventional B lymphocytes. Furthermore, the authors provided evidence suggesting a novel B-cell independent anti-inflammatory property of B-cell activating factor. They showed that the expression of the alternative B-cell activating factor binding receptor, transmembrane activator and CAML interactor in myeloid cells limited atherosclerosis thus showing novel atheroprotective pathways. Thus, these results introduce a new perspective with respect to the potential cardiovascular hazards that may be associated with the long term blockade of B-cell activating factor in chronic inflammatory settings. There is a need for more refine therapeutic approaches targeting the B-cell activating factor pathway.                                                 Vascular smooth muscle cells are known to possess remarkable plasticity undergoing fundamental phenotypic switches from a differentiated to a dedifferentiated state in response to vascular injury or remodeling. However, what are the underlying cellular processes by which vascular smooth muscle cells maintain their cell identity? Well, in today's paper from co-first authors Dr Yao, Yu and Li, corresponding Dr Wang from Fu Wai Hospital National Center for Cardiovascular Diseases, Chinese Academy of Medical Science and Peking University Medical College. The authors applied single cell RNA sequencing to analyze disease human arteries and identified histone variant H2A.Z as a key histone signature that maintains vascular smooth muscle cell identity. H2A.Z occupied genomic regions near vascular smooth muscle cell marker genes and it's occupancy was decreased in vascular smooth muscle cells undergoing dedifferention. H2A.Z expression was dramatically reduced at both messenger RNA and protein levels in diseased human vascular tissues compared to those in normal arteries. Notably, in vivo overexpression of H2A.Z rescued injury-induced loss of vascular smooth muscle cells identity and new intima formation. Together, these data introduced dynamic occupancy of a histone variant as a novel regulatory basis contributing to cell fate decisions and implied that H2A.Z may be a potential intervention known for vascular diseases.                                                 What is the causal role of body mass index and cardiovascular health in young adults? In the next paper from first and corresponding author Dr Wade from University of Bristol in United Kingdom and her colleagues. The authors used a combination of conventional multivariable regression analyses, Mendelian randomization and subsample recall by genotype methodologies. Recall by genotype is a novel approach that exploits the random assortment of alleles through meiotic cell division at conception to inform genetically base recall and enables the collection of precise phenotypic measures in smaller studies while maintaining statistical power and ability for causal inference. The authors use these methods to estimate the causal effect of body mass index on gross level and detail cardiovascular health in healthy participants from the Avon longitudinal study of parents and children at age 17 years as well as in an independent sample from the same cohort study at age 21 years.                                                 Their results showed that higher body mass index was likely to cause worse cardiovascular health specifically higher blood pressure and higher left ventricular mass index even in youth. Higher body mass index also resulted in increased cardiac output in the recall by genotype study which appeared to be solely driven by stroke volume, as neither the Mendelian randomization nor the recall by genotype analyses suggested a causal effect of body mass index on heart rate. These consistent results support efforts to reduce body mass index from a young age to prevent later adverse cardiovascular health and illustrate the potential for phenotypic resolution with maintained analytical power using a recall by genotype methodology.                                                 Older adults undergoing aortic valve replacement are at risk for malnutrition, however, what is the association between pre-procedural nutritional status at midterm mortality? First author, Dr Goldfarb, corresponding author Dr Afilalo from McGill University in Montreal, Quebec, reported results of the FRAILTY-AVR prospective multicenter international cohort study conducted between 2012 and 2017 in 14 centers in three countries. This study included patients 70 years and older who underwent transcatheter aortic valve replacement or surgical aortic valve replacement. The mini nutritional assessment short form was assessed by trained observers pre procedure with scores seven or less out of 14 being considered to be malnourished. The short performance physical battery was simultaneously assessed to measure physical frailty. The authors found that malnutrition was associated with higher one-year mortality and 30-day adverse events following aortic valve replacement via a transcatheter or surgical approach. While malnutrition and frailty were interrelated, the integration of nutritional assessment resulted in improved predictive value for frail patients. Clinical trials are needed to determine whether pre and post procedural nutritional interventions can improve clinical outcomes in these vulnerable patients.                                                 Do newer generation ultra-thin strut drug-eluding stents improve clinical outcomes over contemporary thicker strut stents? First and corresponding author, Dr Bangalore from New York University's School of Medicine and colleagues search PubMed, Embase and Central and identified 10 trials that randomized more than 11,650 patients and evaluated three newer generation ultra-thin strut drug-eluding stents, that is defined as a strut thickness less than 70 microns, versus thicker strut second generation drug eluding stents and reported clinical outcomes. They found that newer generation ultra-thin strut drug-eluding stents were associated with a 16% reduction in target lesion failure, which was a composite of cardiovascular death, target vessel myocardial infarction or ischemia-driven target lesion revascularization evaluated at one year follow-up. Ultra-thin strut drug-eluding stents reduced the risk of target-lesion failure driven by a reduction in myocardial infarction and also a qualitatively lower rate of stent thrombosis compared to contemporary thicker strut second generation drug-eluding stents.                                                 Ambient air pollutants are known to be associated with increased cardiovascular morbidity and mortality, however, what is the association between air pollution and cardiac structure and function? First and corresponding author Dr Aung from Queen Mary University of London and colleagues performed a cross-sectional analysis of a large population free of preexisting cardiovascular disease in the UK Biobank population study. They found that higher past exposure to fine particulate matter and nitrogen dioxide were associated with larger cardiac biventricular volumes. Proximity to major roads, a surrogate for chronic air pollution exposure, was additionally associated with higher left ventricular mass. These associations between ambient air pollution and at first cardiac phenotypic changes, in individuals without prevalent cardiovascular disease, suggest that air pollution should be recognized as a major modifiable risk factor which needs to be targeted by a public health measures.                                                 The final original paper this week is the first study to demonstrate a causal link between atrial fibrillation and the NLRP3 inflammasome, which is an innate inflammation signaling complex. Co-first authors, Drs Yao and Veleva, corresponding author Dr Li from Baylor College of Medicine and colleagues assessed MLRP3 inflammasome activation by immunoblot in atrial whole tissue lysates and cardiomyocytes from patients with paroxysmal or long-standing persistent atrial fibrillation. They found that NLRP3 inflammasome activity was increased in these patients. To determine whether cardiomyocytes specific activation of NRLP3 was sufficient to promote atrial fibrillation, they established a cardiomyocyte specific knock in mouse model which expressed constitutively active NLRP3. These mice developed spontaneous premature atrial contractions, an inducible atrial fibrillation, which was attenuated by a specific NLRP3 inflammasome inhibitor. Cardiomyocyte-specific knockdown of NRLP3 suppressed atrial fibrillation development in these mice. Thus, these results establish a novel pathophysiological role for cardiomyocyte NLRP3 inflammasome signaling with a mechanistic link to the pathogenesis of atrial fibrillation, and suggests that inhibition of NLRP3 may be a potential novel atrial fibrillation therapy approach.                                                 And that brings us to the end of our summaries.                                                 Now for our feature discussion.                                                 Is pericardiotomy going to be our next treatment for heart failure with preserved ejection fraction or HFpEF? I have the first and corresponding author of a very intriguing research letter. Dr Barry Borlaug from Mayo Clinic in Rochester, Minnesota, joining me today to tell today about his great paper. Barry, welcome back to the show. You are amazing. Congratulations on yet another wonderful publication. So, could you set us up. Those of us who don't think about this every day. The hemodynamics of what pericardiotomy does. Tell us what was the rationale of doing this study? Dr Barry Borlaug:              You know, it's interesting. We think about intracavitary pressures on the left side ventricle and the left atrium causing congestion and pulmonary hypertension. We think that this is all related to left ventricular issues, but about 30 or 40% of the pressure is actually related to external restraint on the heart as mediated by the right ventricle across the septum and the pericardium and external pericardial contact restraints. In animals, we've known since back in the late 1970s, that with the chest open, if you open up the pericardium, which we know in HFpEF, on average, is shifted up and to the left. It's stiffer. This effect really comes into play more at higher heart volumes. It doesn't have as much of an affect at lower heart volumes like might be absorbed with rest. It's even been rumored that in some species like greyhounds, illicit dog racers, would actually cut away the pericardium so these dogs could race better. It's actually been shown that they can experimentally, in a paper in the 1980s, that they can exercise the higher peak VO2. They have a higher cardiac output response, because the heart is better able to utilize the Frank-Starling relationships to augment ventricular filling and ejection at fuller pressures. Dr Carolyn Lam:                Oh my goodness. I didn't know that latter fact about the racing dogs. Could I ask you something? We've talked about this before back in the day. When you say the left side the filling pressures go up when there's pericardial restraint, remember we used to talk about a parallel shift upwards versus true intrinsic stiffening ... diastolic stiffening. You still do mean that parallel shift upwards, right? Dr Barry Borlaug:              That's right. If it was purely an increase in stiffness, we would expect it to sort of rotate, pivot from the bottom left up, but what we see, and in human data, we published a number of years ago, most of the increase in LV end-diastolic pressure is a parallel shift upward in the diastolic pressure volume relationship. That really suggests that there's an increase in restraints on the heart. That's why we think that that's an important target and it's possibly more remediable to treatment since we're having such tough luck changing the viscoelastic properties of the left ventricle, not that we shouldn't be doing that, but this might be something different that we could do that might give us a little bit more of a benefit in terms of filling pressure reduction. Dr Carolyn Lam:                True. True. But the way you describe it too, it does mean that we may be talking about, I hate to say this but, specific subsets or types of HFpEF, where that may play a bigger role and I'd just like to bring the audience to your incredible paper that I think that I've cited a gazillion times already on the obese HFpEF phenotype. Do you want to remind everyone about that because I think there you really [inaudible 00:16:30], didn't you that ventricular interdependence played a big role. Dr Barry Borlaug:              So, in people with obese HFpEF, which is now becoming by far one of the most dominant. Oh God. We did a study that compared them to non-obese and we see that the obese patients have a bit more plasma volume expansion, a bit more cardiac remodeling, right heart enlargements, increase of LV mass and an increase in epicardial fat. What all this does is increases the total heart volume in the pericardial space. Because the pericardium doesn't appear to grow as much as the heart volume, this increases the coupling between the right and left heart. Some people, perhaps like the obese phenotype of HFpEF, might be more poised to derive benefit from approaches to therapeutically remove this excess pericardial restraint. Dr Carolyn Lam:                Okay, now you just have to get down to telling us what you did. This was a first in man pilot study. Drum roll everybody. You gotta listen up. This was so cool. Dr Barry Borlaug:              This physiology just got us thinking that maybe we could do this to help our patients with HFpEF. First we tested this in dogs, then with pigs with features of HFpEF and it seemed to work there so the next step was to show that it might work in people. We took people that were already going to get their pericardium open, so people that were referred for cardiac surgery. We wanted to choose people that had risk factors for HFpEF and diastolic dysfunction but maybe not necessarily diagnosed HFpEF. Dr Barry Borlaug:              We took people who were referred for aortic valve replacement for AS, coronary artery bypass grafting or both and consented them ahead of time, put catheters into them to measure hemodynamics and then we measured resting hemodynamics with the chest open, but pericardium intact, because the changes that we see occur predominantly when there's an increase in volume load to the heart, we then had to stress the system. Now we can't have them exercise cause they're under general anesthesia with an open chest. You achieve that by elevating their legs and giving them a little saline bolus, so we had a pressure at rest, pressure with saline load.                                                 Then we asked our surgeons to open the pericardium, which they do obviously to gain access to the heart for cardiac surgery and we repeated the same assessments and intervention. What we saw was that the resting filling pressures, again these people did have diastolic dysfunction, the resting pulmonary wedge pressure was about 16. With the volume load maneuver, it increased to 25 when the pericardium was intact. After we had opened the pericardium, the increase in wedge pressure, which was our primary endpoint, was reduced from an increase in nine millimeters of mercury down to an increase of only three millimeters of mercury. So that verified our hypothesis that the pericardium contributed and that we could prove total cardiac diastolic reserve, if you will, just by removing that pericardial restraints. Dr Carolyn Lam:                Wow. I love the figures, by the way, that you've drawn as always they illustrate that so beautifully. And listeners, this is a research letter, so there's that one central figure that you must get your hands on right away. Now Barry, I think the first question is this wasn't really HFpEF patients right? Let's be very clear with the audience who these were though and then you did a subset analyses though, a further analysis that showed this may apply more to people with higher wedge at rest. Could you elaborate? Dr Barry Borlaug:              Absolutely. While these people, and Carolyn, I think you know as well, I think a lot of people probably have HFpEF that they have a sort of occult HFpEF, that's not been diagnosed maybe because unfortunately, not everybody else thinks about this diagnosis. When you look at the charts very carefully, and found out about 13 of the 19 patients complained of significant dyspnea based on chart review. Of those 13, 10 had other indicators that according to current criteria would give them the diagnosis. When we looked at this at this very post hoc, sort of exploratory subset, we actually saw that these patients, even though they didn't necessarily have a clinic diagnosis of HFpEF, that these patients actually responded even more favorably to the effects of pericardiotomy in their greater reduction in the increase in wedge pressure. When we plotted in the figure that you mentioned, we plotted the change in the increase in wedge pressure, it was really the patients that had the greatest increase with volume loading initially that derived the most benefit. That makes sense because those were the people where the pericardium and the restraint is the becoming most operative, when the heart is most distended and congested. Dr Carolyn Lam                 Maybe one quick last question. What next Dr Borlaug? Gosh, you just keep coming up with one thing after another with the animals. I noticed that it was a non-invasive pericardiotomy. I'm reading between the lines here. What are you going to do next? Do you think this is ready for prime time? Dr Barry Borlaug:              As usual, you're reading correctly between the lines. We have filed a patent awhile back for this and we have a device that can achieve a pericardial modification or an anterior pericardiotomy without the need for open heart surgery, so that you don't crack the sternum. It's done from a subxiphoid approach and we've actually just received some funding to start doing this under an IDE, which we will need to work with the FDA. We hope to do and start testing this in patients that have HFpEF and then look at the acute hemodynamically affects. Then we'll also begin to explore the safety and potential efficacy using other indices like imaging, exercise capacity and things like that. Dr Carolyn Lam:                That is just so cool. I think that one of the immediate take home messages for me now though is when we see patients who we think have HFpEF, have a low threshold to look for evidence of constriction. I would say that we may miss the diagnosis of people who legitimately have constrictive pericarditis and may need to benefit from this. I think it's one of those hidden diagnosis, so that's one thing. And then the next thing, if I could just ask you, are there any patient populations that you say should not undergo this? And I say this because I remember back in the day again, when we were experimenting with dog models, this is just gestalt okay, but I thought that the dogs who had right-sided heart failure, severe right-sided heart failure, needed that pericardium to lean on, and if you released it, the dilatation on the right side would just be inexorable because there is no pericardium to rein them in. Do you get what I mean? I don't know. I'm just curious if you have any patient population right now that you're already thinking I'm not going to include in my trial. Dr Barry Borlaug:              Yeah. That's a very important point, Carolyn. We would not want to apply or test initially certainly this therapy where eccentric cardiac remodeling is a problem because we know that there is a little bit of eccentric dilatation even in people after a regular cardiac surgery with pericardiotomy. Marty Molenter showed that, in a paper back in the 1980s, you have a patient who already has some dysfunction, we would hypothesize that they may get a bit worse, so we would not want to test this in people with the right ventricular dysfunction, right ventricular enlargement phenotype of HFpEF. We would not want to give this to people with HFrEF. Remember with HFrEF, we wanted to do just the opposite. We tested this years ago with the ACORN trial or older studies wrapping the latissimus dorsi around the heart to cause reverse remodeling so this is really something that would maybe work more for people with smaller stiff hearts, HFpEF, where that concern that they're going to dilate and get low EF heart failure either on the left or on the right side. We would want to focus more on the small hearts and away from those people with dilation. Dr Carolyn Lam:                That is so great. Thanks so much Barry for letting us under the hood. Congratulations once again. These are just great papers. Keep them coming. Well listeners. I'm sure you enjoyed that as much as I did. Don't forget to tune in again next week.  

What is New York City style resuscitation? Reuben Strayer and Scott Weingart honed their chops in public hospitals in America’s largest city, where patients come from every country, speak every language, and manifest every physiologic derangement on earth. Preferring to ask neither permission nor forgiveness, Reuben and Scott have long challenged emergency medicine and critical care orthodoxy and developed lateral (though sometimes divergent) strategies in their approach to problems that arise in the care of the sometimes unwashed masses who tend to avoid presenting to medical attention until they’ve fallen off the Frank-Starling curve. Topics that may be discussed (or argued) include the use of epinephrine, the use of noninvasive ventilation, the management of recently intubated patients, the use of ketamine as an induction agent with and without a paralytic, and decision-making in badly injured trauma patients. Ad hominem attacks will be defined and probably employed. Though Weingart has a physical and intellectual disadvantage against the bigger, stronger, quicker, younger, and better-looking Strayer, these disparities will be muted by Natalie May’s capable moderation.

In this episode, I finished covering the basics of cardiovascular topics. I discussed Frank-Starling mechanics, high-yield cardio equations, determinants of blood pressure and flow, smooth muscle contraction, heart failure, and more. Enjoy!The Med School Phys podcast discusses topics in human physiology. Our primary aim is to help medical students learn/review high yield material for their classes and board exams. Hopefully listeners find that this alternative audio-based learning format works for them. This podcast is intended to be educational and all the information shared herein is publicly available through the internet. Med School Phys is an independent project and currently shares no affiliation with other organizations, companies, or academic institutions.-You can email me questions or constructive feedback at medschoolphys@gmail.com -Check out my book, Read This Before Medical School: https://www.amazon.com/dp/B07YCXZM3X/ref=docs-os-doi_0 -Episode transcriptions can be found at: https://drive.google.com/drive/folders/12QQSFho-ThIIeZuulsblGSnnNL8oJ7ag?usp=sharingDISCLAIMER: All information, content, and materials published by the Med School Phys podcast are for informational purposes only and are NOT intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified healthcare provider. Please consult your healthcare provider regarding personal medical decisions.

In this episode, I finished covering the basics of cardiovascular topics. I discussed Frank-Starling mechanics, high-yield cardio equations, determinants of blood pressure and flow, smooth muscle contraction, heart failure, and more. Enjoy!The Med School Phys podcast discusses topics in human physiology. Our primary aim is to help medical students learn/review high yield material for their classes and board exams. Hopefully listeners find that this alternative audio-based learning format works for them. This podcast is intended to be educational and all the information shared herein is publicly available through the internet. Med School Phys is an independent project and currently shares no affiliation with other organizations, companies, or academic institutions.You can email me questions or constructive feedback at medschoolphys@gmail.comYou can share a link to our episodes via Spreaker or encourage others to listen on their podcasting app of choice: https://www.spreaker.com/user/medschoolphysFind our Youtube channel at: https://www.youtube.com/channel/UCXEEgC1JZysYsKy9NRYisEQEpisode transcriptions can be found at: https://drive.google.com/drive/folders/12QQSFho-ThIIeZuulsblGSnnNL8oJ7ag?usp=sharingDISCLAIMER: All information, content, and materials published by the Med School Phys podcast are for informational purposes only and are NOT intended to serve as a substitute for the consultation, diagnosis, and/or medical treatment of a qualified healthcare provider. Please consult your healthcare provider regarding personal medical decisions.

This episode covers Chapter 81 of Rosen’s Emergency Medicine. This one is mint! Heart failure is one of those must-know-about presentations, you WILL see this in the ED.   Define Cardiac index Preload Afterload Describe: How compliance changes the relationship between end diastolic pressures and volume the Frank-Starling relationship Pousseils Law and LaPlaces Law List 3 CV and 4 Neurohormonal physiologic compensatory mechanisms in CHF List the 5 most common disease processes resulting in HF and briefly describe the contribution of each Describe the different classifications of heart failure: Acute vs. Chronic HF Systolic vs. Diastolic dysfunction Right vs. Left sided HF High-output vs. Low-output HF Describe the NYHA function HF Classes and the Killip Classification List 10 common precipitants of acute HF List 6 historical predictors of acute HF and 6 clinical features of acute HF List 5 CXR and 5 ECG findings of HF What is the role of BNP in HF? Describe the primary management goals in acute HF Describe the mechanism of action of NIPPV in HF. Who needs to be intubated? When is it contraindicated? Describe the pharmacologic treatment strategy for: Acute pulmonary edema + adequate perfusion Acute pulmonary edema + hypotension How do nitrates work in acute pulmonary edema? What is the dose? List 10 treatment options for chronic HF

This episode covers Chapter 81 of Rosen’s Emergency Medicine. This one is mint! Heart failure is one of those must-know-about presentations, you WILL see this in the ED.   Define Cardiac index Preload Afterload Describe: How compliance changes the relationship between end diastolic pressures and volume the Frank-Starling relationship Pousseils Law and LaPlaces Law List 3 CV and 4 Neurohormonal physiologic compensatory mechanisms in CHF List the 5 most common disease processes resulting in HF and briefly describe the contribution of each Describe the different classifications of heart failure: Acute vs. Chronic HF Systolic vs. Diastolic dysfunction Right vs. Left sided HF High-output vs. Low-output HF Describe the NYHA function HF Classes and the Killip Classification List 10 common precipitants of acute HF List 6 historical predictors of acute HF and 6 clinical features of acute HF List 5 CXR and 5 ECG findings of HF What is the role of BNP in HF? Describe the primary management goals in acute HF Describe the mechanism of action of NIPPV in HF. Who needs to be intubated? When is it contraindicated? Describe the pharmacologic treatment strategy for: Acute pulmonary edema + adequate perfusion Acute pulmonary edema + hypotension How do nitrates work in acute pulmonary edema? What is the dose? List 10 treatment options for chronic HF

Rob MacSweeney and Paul Marik debate whether the assessment of fluid responsiveness in the resuscitation of patients with shock a waste of time? Both Marik and MacSweeney agree that many of the traditional methods of assessing patients volume status are flawed and of no value. Marik goes on to argue that the only clinically meaningful outcome that we should measure in response to a fluid challenge is Stoke Volume. In at least 50% of patients there is no improvement in stroke volume and further treatment with fluid boluses will only likely cause harm. Marik goes on to argue that we must know where our patients are position on their Frank-Starling curve to predict whether they are fluid responsive and we can assess this with passive led raise.