Podcasts about Ventricle

Do all hearts beat the same? We don't know…unless we listen to them. With the help of four well-informed hummingbirds and renowned muralist Ruben Rojas, Andrew & Polly explore what they know about hearts – biological and metaphorical! Our friends Maya, Anders, Jackson, and Emmet share about how their hearts feel when they give and receive Valentines. And Polly shares about the little robot in her chest (her pacemaker-defibrillator) and the way it keeps her heart dancing to a steady beat. Many thanks to artist, muralist, designer, entrepreneur and podcaster Ruben Rojas for talking with us. His podcast explores the emotional journeys of artists, athletes and other creators seeking to Live Through Love. You can find more of Reuben's work at rubenrojas.com – or if you walk around, you might just find it on GIANT WALLS. And thanks to Fyütch + Aura V for sharing their new single, I AM LOVE, I AM LIGHT, available wherever you get your affirmational bops! Vocabulary & Ideas in this episode include: Stethoscope Animal heart rates Aorta! Atrium! Ventricle! Arrhythmia Pacemaker-defibrillator Mural Electro-pounce Thanks to EVERYPLATE for sponsoring Ear Sncaks. Go to everyplate.com/podcast and enter code 49earsnacks for $1.49 per meal + $1 steaks for life. Subscription must be active to qualify and redeem $1 steak. Need more snacks? Connect with us on Instagram, Facebook, Twitter or TikTok! To learn more or to be on the show, visit earsnacks.org

This week we review the results of the latest update of the Single Ventricle Reconstruction trial, specifically SVR III. How are HLHS patients are faring post Norwood at age 12? What is the overall transplant-free survival rate in this group? Are there differences in survival seen at 12 years between BTTT shunt patients and RV-PA conduit shunt patients? How do they compare in exercise capabilities? What about rates of PLE or arrhythmias seen? Are there interventions that may improve outcomes going forward? These are amongst the questions reviewed this week with the first author, Dr. Caren Goldberg who is Professor of Pediatrics at the University of Michigan. DOI: https://doi.org/10.1161/circulationaha.123.065192

Commentary by Dr. Valentin Fuster

This podcast explains the pathophysiology of single ventricle cardiac lesions, and reviews the three-step surgical procedure used for palliation. 0:00 Introduction 1:55 Anatomy & Pathophysiology 3:56 Typical Palliation 8:50 Long Term Complications After Repair LEARNING OBJECTIVES After listening to this podcast, the learner should be able to: • Explain the pathophysiology of single ventricle heart disease • Discuss the different stages of palliation for single ventricle heart disease • Describe the physiological consequences of the Fontan circulation • Recognize long term problems associated with the Fontan circulation AUTHORS Madeleine Alvin, MD Pediatric Anesthesiology Fellow Boston Children's Hospital Annette Schure, MD Senior Associate in Cardiac Anesthesia Boston Children's Hospital DATES Initial publication: October 19, 2023 CITATION Alvin ML, Marcley S, Soohey R, McFee AM, Wolbrink TA, Schure AY. Surgical Palliation for Single Ventricle Lesions. 10/2023. OPENPediatrics. Online Course: https://learn.openpediatrics.org/learn/course/internal/view/elearning/5439/Surgical-Palliation-for-Single-Ventricle-Lesions. Video: https://youtu.be/zptfxT1pjxg. Podcast: https://soundcloud.com/openpediatrics/surgical-palliation-for-single-ventricle-lesions-by-madeleine-alvin-for-openpediatrics/s-j1wNCnQ9ZIX. Please visit: http://www.openpediatrics.org OPENPediatrics™ is an interactive digital learning platform for healthcare clinicians sponsored by Boston Children's Hospital and in collaboration with the World Federation of Pediatric Intensive and Critical Care Societies. It is designed to promote the exchange of knowledge between healthcare providers around the world caring for critically ill children in all resource settings. The content includes internationally recognized experts teaching the full range of topics on the care of critically ill children. All content is peer-reviewed and open access-and thus at no expense to the user. For further information on how to enroll, please email: openpediatrics@childrens.harvard.edu

Matt Siuba, DO, MS is an assistant professor of medicine in the department of critical care medicine at Cleveland Clinic. He is one of the authors of a recent review article on RV therapies in ARDS published in Critical Care. This is the topic of his lecture today. Ganeriwal S, ...

Adult with Systemic Right Ventricle Failure: Which Medications Work? Guest: Charles Jain, M.D. Hosts: Luke J. Burchill, M.B.B.S., Ph.D. In this Podcast, we will discuss which medications work and when these medications should be used in adults with systemic right ventricles. Topics Discussed: Systemic Right Ventricle Patients Congenitally Corrected Transposition (CCTGA) Medications Used for Care and Why They are Different Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. LinkedIn: Mayo Clinic Cardiovascular Services Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.

Commentary by Dr. Valentin Fuster

Our bodies depend on our hearts maintaining a steady beat, and increasing it appropriately in response to exercise. If the heart goes too fast, or too slowly, we have effects ranging from tiredness to unexpectedly passing out to death.This lecture will consider the normal heartbeat, the causes of the heart going too fast or slowly and how it is treated when it does.A lecture by Sir Chris Whitty recorded on 21 February 2023 at Barnard's Inn Hall, London.The transcript and downloadable versions of the lecture are available from the Gresham College website: https://www.gresham.ac.uk/watch-now/rhythm-heartGresham College has offered free public lectures for over 400 years, thanks to the generosity of our supporters. There are currently over 2,500 lectures free to access. We believe that everyone should have the opportunity to learn from some of the greatest minds. To support Gresham's mission, please consider making a donation: https://gresham.ac.uk/support/Website:  https://gresham.ac.ukTwitter:  https://twitter.com/greshamcollegeFacebook: https://facebook.com/greshamcollegeInstagram: https://instagram.com/greshamcollegeSupport the show

Interview with Dr. Katsuhide Maeda MD PhD (Children's Hospital of Philadelphia) and John Dykes MD (Lucile Packard Children's Hospital) about the history and current state of VAD support for single ventricle patients. Co-Hosts: Monica Mafla MS, PNP-AC (Lucile Packard Children's Hospital/Stanford) and Amy Romer MD (Children's Hospital of Philadelphia). Editors: Monica Mafla MS, PNP-AC, and Lillian Su, MD Producer: Lillian Su, MD (Phoenix Children's Hospital)

Psychotherapist Tracy Livecchi, LCSW, joins Paul Cardall to discuss healing hearts and minds of people born with an illness that requires a life time of medical care. Both Tracy and Paul were born with complex congenital heart defects. Although congenital heart disease or CHD is the least funded of all major illnesses, CHD remains the leading cause of infant related deaths. However, because of advancements in medicine and technology millions of people have survived and adapt to what would be considered a normal life, although their lives have required a life-time of medical care and surgical procedures. They swap stories and go into detail about the miracle of life and how Tracy's parents were instrumental in working with doctors to secure her survival. Because of the lack of information for lifelong patients, Tracy and her colleague Liza Morton, PhD have written "Healing Hearts and Minds: A Holistic Approach to Coping Well With Congenital Heart Disease." ABOUT TRACY LIVECCHI, LCSWTracy writes on her website: In terms of my training, I received my Masters Degree in Social Work from Rutgers University. I have worked in a variety of settings as a private therapist, a clinical director, as well as a consultant for long-term care and hospital settings. I have been working as a psychotherapist in private practice since 1998, and currently provide psychotherapy to individual adults, adolescents, and couples in my Westport practice. I work from an eclectic theoretical orientation and provide supportive counseling while also utilizing cognitive, behavioral, psychodynamic and trauma informed, mindfulness approaches, when appropriate. I am the Mental Health Consultant for the Adult Congenital Heart Association's Peer Mentorship Program and speak nationwide on the importance of addressing the psychosocial effects of heart disease. I am passionate about mental health access for all and have a special interest in working with individuals and their families dealing with serious and chronic illness. I live in CT with my husband and two daughters. Website: https://tracylivecchi.com/GET THE BOOK: Healing Hearts & MindsACHA or ADULT CONGENITAL HEART DISEASE ASSOCIATION  ABOUT THE HOST PAUL CARDALLhttp://www.paulcardall.comhttp://www.facebook.com/paulcardallmusichttp://www.youtube.com/cardallhttp://www.instagram.com/paulcardall LISTEN TO HIS MUSICAPPLE MUSIC - https://music.apple.com/us/artist/paul-cardall/4312819SPOTIFY - https://open.spotify.com/artist/7FQRbf8gbKw8KZQZAJWxH2AMAZON - Ask Alexa to play Peaceful Piano by Paul Cardall Paul Cardall is an artist who has given a new meaning to the phrase, a change of heart and how he used this radical change to take his music to an unexpected place.  Despite being born with a potentially life-threatening heart defect Paul Cardall has become a world recognized pianist. He is even endorsed by Steinway & Sons as one of the finest pianist of our time. A Dove award winner for his Christmas album, Paul's recordings have debuted on 11 No. 1 Billboard charts along with 46 other chart debuts. His music has 25 million monthly listeners with more than 3 billion lifetime streams and is often categorized as Classical, Christian, and Holiday. Although most of albums are instrumental, Paul has songs that feature Grammy winning gospel legend CeCe Winans, Matt Hammitt (Sanctus Real), Kristin Chenoweth, Country duo Thompson Square, David Archuleta, Tyler Glenn (Neon Trees), Audrey Assad, Steven Sharp Nelson (The Piano Guys), and more.    Paul has performed for audiences worldwide including the White House. Forbes, American Songwriter, Jesus Calling, Lifestyles Television, Mix Magazine, and countless other media outlets have share his remarkable journey of receiving a life changing heart transplant and using music as a tool to help God heal spiritual, mental, and emotional hearts.

This week we replay a 2020 episode in which we reviewed a then recent PCCC study assessing outcomes of single ventricle patients who have undergone replacement of the AV or semilunar valve. We speak with Professor Geetha Raghuveer of University of Missouri-Kansas City about this work she co-authored. Outcomes are generally poor in this patient group but are there lessons that can be gleaned from the data regarding optimal timing for repair or replacement of valves in this patient group? This is a great follow-up of episode # 58 from 3.5 years ago. See you next week with a brand new episode! doi: 10.1007/s00246-019-02234-9.

This week we review a recent report on the differences between pulse oximeter Sp02 and arterial Sa02. Are there patient specific factors that may result in inaccuracies of measurement? What single ventricular factors may also result in more significant inaccuracies and how should these data be used at the bedside when assessing a child who is cyanosed? We speak with Dr. Cara Pritchett, critical care fellow at Lurie Children's Hospital - Northwestern University about a recent work she co-authored on this important and practical topic. DOI: https://doi.org/10.1016/j.jscai.2022.100394

Recently-four-year-old Greyson Ouellette wasn't even born yet when his parents, Sarah and Brian, found out he had a heart defect. At her 20-week full anatomy scan, Sarah's care team determined that the ventricle of Greyson's heart was already significantly smaller than normal size, meaning that he would be born with Single Ventricle Disease (SVD), a rare congenital heart defect that affects just five out of every 100,000 newborns in America each year. Babies born with SVD require surgery immediately after birth, often one or more afterwards and, in some cases, need a heart transplant later in life. Today, Greyson has had two open-heart surgeries in his only four years of life but is doing well, playing with his older twin brothers and attending preschool. During all of Greyson's treatments, procedures, and inpatient stays, Sarah promised herself that once Greyson was stable, she would find a way to families struggling with this rare disease. She believed not enough was being done to advance new treatments and improve outcomes for these kids, so awareness and support of SVD families became her mission. She started putting together care packages for families who've just found out their baby will be born with SVD, including supplies necessary for long hospital stays and a heartfelt letter of her own story. She raises funds for this project by selling “Team Greyson” merchandise online.  As one of Bloodworks tiniest patients, Greyson is a reminder that anyone, at any time, might need blood to live. That's why donating blood is so important.   

Commentary by Dr. Valentin Fuster

This week we review a recent work on outcomes of univentricular adult patients who have not been palliated with a Fontan. Do these patients fare better than Fontan patients? What factors are associated with worse or better outcomes? How do these factors inform decision making for the single ventricle adult patient? We speak with adult congenital expert, Dr. Danielle Massarella of University of Toronto about her thoughts on this work and some of its important lessons. DOI: https://doi.org/10.1016/j.cjca.2021.06.001

Recently-four-year-old Greyson Ouellette wasn't even born yet when his parents, Sarah and Brian, found out he had a heart defect. At her 20-week full anatomy scan, Sarah's care team determined that the ventricle of Greyson's heart was already significantly smaller than normal size, meaning that he would be born with Single Ventricle Disease (SVD), a rare congenital heart defect that affects just five out of every 100,000 newborns in America each year. Babies born with SVD require surgery immediately after birth, often one or more afterwards and, in some cases, need a heart transplant later in life. Today, Greyson has had two open-heart surgeries in his only four years of life but is doing well, playing with his older twin brothers and attending preschool. During all of Greyson's treatments, procedures, and inpatient stays, Sarah promised herself that once Greyson was stable, she would find a way to families struggling with this rare disease. She believed not enough was being done to advance new treatments and improve outcomes for these kids, so awareness and support of SVD families became her mission. She started putting together care packages for families who've just found out their baby will be born with SVD, including supplies necessary for long hospital stays and a heartfelt letter of her own story. She raises funds for this project by selling “Team Greyson” merchandise online.  As one of Bloodworks tiniest patients, Greyson is a reminder that anyone, at any time, might need blood to live. That's why donating blood is so important.   

How can a 30-year-old Heart Warrior single ventricle survivor live without the Fontan? What special considerations need to be made when moving from Egypt to Canada? What are the biggest concerns when you fall out of cardiac care?Ellen Banoub was born in Egypt 30 years ago. She is a Heart Warrior, diagnosed with a hypoplastic left ventricle, transposition of the great arteries (TGA), pulmonary atresia, and dextrocardia. Ellen has had two surgeries, a shunt operation at one year of age, and a half-Fontan when she was 11 years old. She moved to Canada in 2013. She is studying social services and academic English and hopes to study social work to help others with social and medical problems. She has three heart-healthy siblings. Her older sister is a doctor who takes care of Ellen's health. Ellen recently became an aunt to Molly, who was born in early 2022. Aside from studying and spending time with family, Ellen enjoys acting, watching movies, listening to music, and reading.Ellen talks with Anna about how she was born with a single ventricle heart and had surgery abroad since she was unable to have the surgery in her homeland (Egypt). Ellen talks about how she eventually moved to Canada where she has been able to get the care she needed for her heart. She shares how she came to study social work and how working in this field is her new purpose in life.Please visit our Social Media and Podcast pages:Apple Podcasts: https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2Facebook: https://www.facebook.com/HearttoHeartwithAnna/Instagram: https://www.instagram.com/hearttoheartwithanna/MeWe: https://mewe.com/i/annajaworskiTwitter: https://twitter.com/AnnaJaworskiYouTube: https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5ZwWebsite: https://www.hug-podcastnetwork.com/Music thanks to the Baby Blue Sound Collective - https://music.apple.com/us/album/home-tonight-forever/1201349904If you enjoy this program and would like to be a Patron, please check out our Patreon page: https://www.patreon.com/HeartToHeartSupport the show

In this replay of episode 92 from 2019, we speak with cardiovascular surgeon Dr. Johann Brink about a recent work he co-authored from the Royal Children's Hospital in Melbourne, Australia about the team's experience with shunt malfunctions. Are there factors that are associated with shunt failure in this sometimes fragile patient group? Survival to Fontan in most series is roughly 70% - what, if anything, can 'move the needle' to higher levels of survival in this patient population? Dr. Brink offers some interesting and important insights this week. doi: 10.1016/j.jtcvs.2019.03.126

This month on Episode 35 of Discover CircRes, host Cynthia St. Hilaire highlights two original research articles featured in the April 1 issue of Circulation Research, as well as highlights from the Stroke and Neurocognitive Impairment Compendium in the April 15th issue.  This episode also features a conversation with Dr Shubing Chen and Dr Yuling Han from Weill Cornell Medical College to discuss their study, SARS-CoV-2 Infection Induces Ferroptosis of Sinoatrial Node Pacemaker Cells.   Article highlights:   Pabel, et al. Effects of Atrial Fibrillation on the Ventricle   Pattarabanjird, et al. P62-Mediated B1b Cell Atheroprotection   Iadecola, et al. Introduction to the Compendium on Stroke and Neurocognitive Impairment   Cindy St. Hilaire:        Hi and welcome to Discover CircRes, the podcast of the American Heart Association's Journal, Circulation Research. I'm your host, Dr Cindy St. Hilaire, from the Vascular Medicine Institute at the University of Pittsburgh. And today I'm going to be highlighting articles from our April issues of Circulation Research.                                     I'll also speak with Dr Shubing Chen and Dr Yuling Han from Weill Cornell Medical College, and they're with me to discuss their study, SARS-CoV-2 infection induces ferroptosis of Sinoatrial node pacemaker cells.   Cindy St. Hilaire:        The first article I want to share is titled, Effects of Atrial Fibrillation on the Human Ventricle. The first author is Steffen Pabel and the corresponding author is Samuel Sossalla and they're from Regensburg University. Atrial fibrillation, or AFib, is the most common form of heart arrhythmia. Patients with AFib may experience shortness of breath, dizziness and weakness. And they're also at risk for more life-threatening complications, such as clot-induced stroke and heart failure. Focusing on heart failure, this study investigated how disruptions to rhythm in the atria might lead to changes in the ventricular myocardium. The team studied ventricular muscle tissue from 24 patients with AFib and 31 without AFib. While the levels of fibrosis were equivalent in ventricular myocytes from both the AFib and the non AFib patients, other cellular features were distinct. For example, patients with AFib had reduced systolic calcium release, prolonged action potential duration and increased oxidative stress, compared with the non AFib patient controls. These differences were largely recapitulated in ventricular myocytes derived from human induced pluripotent stem cells that had been electrically stimulated to either mimic AFib or normal sinus rhythm. The results indicate that AFib affects the ventricles just as well as the atria and might therefore be best studied and treated with the whole heart in mind.   Cindy St. Hilaire:        The second article I want to share is titled B-1b Cells Possess Unique bHLH-Driven P62-Dependent Self-Renewal and Atheroprotection. The first author is Tanyaporn Pattarabanjird and the corresponding author is Colleen McNamara, from the University of Virginia.   Atherosclerosis is a complex and dynamic chronic inflammatory condition. However, not all immune cells exacerbate this disease. Some immune cells are actively dampening the inflammation. B-1 cells are such cells that do this, and they produce IgM antibodies that bind cholesterol, preventing its uptake into macrophages and therefore limiting macrophage driven inflammatory responses. Increased number of B1 cells, therefore, might be atheroprotective. In mice, deletion of the transcription factor ID3 leads to a boost in B-1 cell IgM production.   Cindy St. Hilaire:        In this work the authors investigated the molecular mechanism underlying this effect and found that upon deletion of ID3 in mice B-1b cells, the level of P62 protein was increased. B-1b cell proliferation was found to be dependent on P62 and over expression of P62 in mouse B-1b cells increased cell numbers, raised plasma IgM levels and importantly, ameliorated diet-induced atherosclerosis in animals. The team went on to show that people with an ID3 mutation had an unusually high level of serum IgM and B-1b cell P62. This suggests that results from mice may hold true for humans, and if so, could inform the development of immunomodulatory treatments for atherosclerosis.   Cindy St. Hilaire:        So the April 15th issue of Circulation Research is our Stroke And Neurocognitive Impairment Compendium. The last Circulation Research Compendium on Stroke was published about five years ago. In this year Dr Costantino Iadecola, Dr Mark Fisher and Dr Ralph Sacco focused this update on advances made over the past five years, with a focus on topics that were not addressed in the previous compendium, that best reflect the leading edge of basic in clinical science related to cerebral vascular diseases. Seemant Chaturvedi, Brian Mac Grory and colleagues provide an overview of preventative strategies according to stroke mechanism, including stroke of unknown cause. And the challenges of stroke prevention with antithrombotic therapy and subjects with increased hemorrhage risk are also considered.   Cindy St. Hilaire:        Stéphanie Debette and Hugh Markus provide an account of the most recent developments in the genetics of cerebrovascular diseases. The gut microbiota is another factor that has recently been linked to stroke risk and Pedram Honarpisheh, Louise McCullough and colleagues provide a comprehensive overview of the microbiology and the microbiota, and the influence that stroke risk factors exert on its composition and homeostatic relationship with mucosal surfaces. Karin Hochrainer and Wei Yang provide a systematic review of the large amount of data and stroke proteomic from animal models and human patients. Matthias Endres and colleagues cover the dramatic effect that innate and adaptive immunity exert on stroke risk and on acute brain damage and post stroke sequelae, such as post-stroke cognitive impairment and depression.                                     Cindy St. Hilaire:        Manuela De Michele, Alexander Merkler and colleagues discuss the cerebral vascular diseases that have emerged as a frequent manifestation of the maladaptive immune response to severe SARS-CoV-2 infection. Jessica Magid-Bernstein and Lauren Sansing review the current concepts on epidemiology, risk factors in etiology, clinical features, as well as the medical and surgical interventions for cerebral hemorrhage. Yunyun Xiong and Marc Fisher cover the progress that has been achieved in the treatment of acute ischemic stroke and Natalie Rost and Martin Dichgans and colleagues address the long term impact of stroke on cognitive function, which is becoming a significant healthcare challenge in the world's aging population.   Cindy St. Hilaire:        So today I have Dr Shubing Chen and Yuling Han from Weill Cornell Medical College. And they're with me to discuss their study SARS-CoV-2 infection induces ferroptosis of Sinoatrial node pacemaker cells. And this article is in our April 1st issue of Circulation Research. So thank you both for joining me today.   Shubing Chen:             Thank you. It's really nice to join the program, and it's really a great honor.   Cindy St. Hilaire:        It's a really great article. I'm so excited to talk about. So there's a lot of research happening regarding SARS-CoV-2 virus and the patients who are infected and have COVID-19. And this paper is focusing on the impact of viral infection on the heart and specifically on the sinoatrial node, which is the primary cardiac pacemaker that keeps our hearts beating. So I was wondering if you could tell us what led you to focus on this particular aspect of COVID-19 symptoms, and also how early in the pandemic did you start this?   Shubing Chen:             Yeah, so we started working on SARS-CoV-2 through back to early 2020 when very unfortunately, New York City was a pandemic center and we had a lot of patients in the hospital unit, and also postdoc students working very hard in the lab. So that's the time we start working on SARS-CoV-2. And I was trained as a stem cell biologist. And what we're really interest is to set up a platform to basically understand which type of cells can be infected by SARS-CoV-2 and if they can, how they respond to SARS-CoV-2 infection. Not only for SARS-CoV-2, we sent it as like a viral infection platform, but SARS-CoV-2 is one of the virus we study now. And it's kind of very surprising. We have a pretty broad platform. We have a lung organoid, we have colon organoids, we have pancreas, we have cardiomyocytes, pacemaker cells. And as expected, we see lung can be infected like colon and because patient had GI tract, liver can be infected, but very surprisingly we see very high cardiomyocytes infection as well as pacemakers.                                       So as we'll know that still big controversy in the field, whether we can detect SARS-CoV-2 like viral protein or viral RA in the heart, in particular, cardiomyocytes. But I think now everyone agree that the cardiomyocytes really can be very well infected actually. Because it's very difficult to get the pacemaker tissue and the sinoatrial tissue from the COVID patient. So we collaborate with Dr Ben Andora's lab at NYU to get this hamster model. So we basically take SA tissue from hamster and then other colleagues basically did the section imaging, and we confirm that the hC4 polymerase cells can be infected by SARS-CoV-2. And at that time we start to learn a more clinical studies they report the COVID patient, they develop arrhythmia, or some other problem, not only with cardiomyocyte, as well as the conduction system. So at that time, that's the time that we say maybe we should do something on the pacemaker and focus on that. So that's how the project was developed.   Cindy St. Hilaire:        That is so interesting. And so I know humans infected, like you just said with SARS-CoV-2, they can develop arrhythmias. What's that timeframe? Is there a common timeframe that this happens? Does it normally happen very close to the infection or only in later stage? What's that window of when these arrhythmias are happening?   Shubing Chen:             At least based on the clinical study we show right now, actually the patient can develop acute arrhythmia. So it can be very soon after they developed symptom for COVID.   Cindy St. Hilaire:        Wow. That's amazing. So you mentioned this, your study utilized a hamster model, which you actually don't see a lot of. Most studies use a lot of rats or most studies I'm familiar with, especially in Circulation Research, they use more rats or more mouse models. So what advantages does that hamster model have and why were you interested in using it?   Shubing Chen:             Yeah, that's actually really specific for SARS-CoV-2. As SARS-CoV-2 mainly use ACE2 as a key entry factor to enter the cells. Of course, there's additional receptor, like neutrophils is one. Like all this enzyme involved, but human and mouse ACE2, they have very different structure. So the SARS-CoV-2 virus combine with human ACE2 very well but not mouse ACE2. So from the beginning, the rat and mouse was not used as a very good model to study SARS-CoV-2 infection. Of course there are other models, like knockin human ACE2 in the mouse and also like ACE2 transgenic mice. That's how different mouse model use. But hamster you don't need any modification, but they are very promising to SARS-CoV-2 infection. And so that's a reason we decide to use that as an animal model to basically run in parallel with our human stem cell model.   Cindy St. Hilaire:        We joke in my lab, mice are not little humans, but it's really true in a lot of cases, they're beautiful models in so many ways, but then when they don't work, they really don't work.   Shubing Chen:             Yeah. Before COVID every time when we try to talk about our human stem cell, derived cells, organoids as a disease model. People always ask, why do you want to work on human organoids? Right? It's that we have all these beautiful animal models like as you mentioned, mouse or rats, that's very broadly used. And we have to find different reasons. And now when we start working on SARS-CoV-2, which is very clear example, that mouse are not identical to human. Yeah.   Cindy St. Hilaire:        Yeah. That's great. I love finding additional models to use that are the best one for the question. So in order to investigate, I guess kind of the mechanism of how this was happening in the SAN cells, the sinoatrial node cells, you had to develop a new differentiation protocol that took the human embryonic stem cells, I think it was the H9 line you used, and essentially differentiate that cell line into a sinoatrial node-like cell. So I was wondering if you could tell us a little bit about A) how did you figure out that protocol and B) how does it work?   Shubing Chen:             So it's actually a long story to cell line.   Cindy St. Hilaire:        We can condense it. Let's get-   Shubing Chen:             At least based on the clinical study we show right now, actually the patient can. Let's condense it. But it's as you can imagine, we did not develop this cell line only for this particular project. Actually, we start working on this cell line back to maybe six, seven years ago. The first postdoc we have who basically knockin the mCherry, Myh6. Which basically label the atrial cardiomyocytes. And another postdoc, Zanir, he basically put a GFP in the SARS2 locus. So now we have this duel reporter line we can visualize the SA nodal cells. And we really spend a lot of time on that because we think that unfortunately in our hand, there is not really no good antibody for SARS2. We think it's very, very important that you can see these cells. So after developing these lines and because my lab run a lot of chemical screening, where we run Zanir, we run several chemical screening to develop the protocol.                                       And Jialing Zhu, another postdoc in the lab, also pick up the project to further develop the protocol. And there is several years' work. We do have this good protocol to make pretty efficiently to make the cells. And it's not only our work. I want to say that. For example, Dr Sean Wu from Stanford, they did this beautiful study on the single cell RNC mouse conduction system and Dr Gordon Keller and many other labs also basically published protocol in the field. We are very excited about this duel reporter line. I think they gave us a lot of new opportunity and we are very happy to share this line. Yeah. So if anyone in the field are interested in that, just contact us.   Cindy St. Hilaire:        Yeah. Anyone listening. That's great. So were you surprised to find the entry factors that SARS-CoV-2 uses to get into a cell, were you surprised to find them on these sinoatrial node cells? And I guess in the context of comparing these particular cells to other cells in the heart, are those entry factors higher in the sinoatrial node cells?   Shubing Chen:             So it can be either surprised or not surprised let's say this way. So because one, we see the cardiomyocytes that can be infected, we were kind of surprised. And then we find actually several type of cells in the heart can be infected, like endothelial cells. I will say that the ACE2 expression of like ACE2 aminophenol in pacemaker cell, it's not significantly higher than cardiomyocytes. So we are not really saying, or seeing that SA nodal cells are more permissive to SARS-CoV-2 infections compared to cardiomyocytes, even in the petri dish, but they can be infected.   Cindy St. Hilaire:        So you found SARS-CoV-2 infection in these sinoatrial nodal cells induces a process called ferroptosis. So Yuling, I was wondering if you could tell us what is ferroptosis and what is it doing in these pacemaker cells?   Yuling Han:                 For the ferroptosis, they was surprised so far that its by the RA sequencing of the SARS-CoV-2 infection make our cells. And the first process is mainly caused by the-   Shubing Chen:             Error in iron.   Yuling Han:                 Yes. So more intake of the iron error and induced the RA's pathway and caused the cell deaths. So by our RA sequencing, we found the key factor involved in ferroptosis pathway is the GPS score was checked after the SARS-CoV-2 infection. So we focused on the ferroptosis pathway and found other key factors or checked after the infection makes in the pacemaker cells.   Cindy St. Hilaire:        What is the ferroptosis doing that disrupts the SNA cells?   Shubing Chen:             Ferroptosis is a type of cell death mechanism. So eventually it will cause cell death. And we think something that is really surprising, but we think it's very interesting, is we only see ferroptosis in the SARS-CoV-2 infected general atrial cells. So SA cells, we actually, as Yuling mentioned, when we develop this platform, we see different type of cell can be affected. And we are very curious what happened. So we see that we run a sequence on each individual cells we can see infection and along, we can see cell death like apoptosis in cardiomyocytes. We see apoptosis and only in SA nodal cells, we actually see the ferroptosis pathway as we come up.   Cindy St. Hilaire:        Why do you think that is in that cell type versus in another? Do you have any ideas about why?   Shubing Chen:             No, we don't have any idea yet to be honest, but we are working on that. But at least I think that it gave us some clue that we really need to use different type of whole cells to study the whole cell response. Because traditionally when we study viral infection and when we see lung, we always say, oh, the cell died. It's fairly simple. But now if we really study the details and we think it's maybe over simplified way to think about how cells can respond to viral infection, not only to SARS-CoV-2 infection. So it gives us the motivation, very strong motivation to now really study how different host tissues response to viral infection.   Cindy St. Hilaire:        I thought that was really interesting, not all cell death is the same.   Shubing Chen:             Yeah. And another thing is kind of a little bit surprising is we actually did a very careful comparison between the SA nodal cells and the cardiomyocyte. We only see ferroptosis come up as SA nodal cell, but not cardiomyocyte. Again, we don't understand why as maybe some host factor that is specific, we're working on that.   Cindy St. Hilaire:        So in addition to working out this mechanism of what is going wrong when these cells are infected with the virus, you also used this embryonic stem cell like tool for a drug screen. So can you walk us through that process in terms of what you did to do that? Did you focus in on one specific type of drugs or was it just kind of an unbiased screen?   Yuling Han:                 For the sinoatrial pacemaker cells, we focus on the antiviral drugs screening. And we also did several other projects, like lot of night or some neuron cells. For the [they did drug screening to find some drugs to inhibit the SARS-CoV-2 entry. And for the dominic neuron, we found SARS-CoV-2 infection can cause neuro cells synapses. So we focus on the synapses associated drug screening, but for the pacemaker cells, they only did the antiviral drug screen.   Cindy St. Hilaire:        And you came up with two drugs that you wrote about in the paper, deferoxamine and imatinib. So what are the mechanisms of action of those drugs? Are they targeting the same thing or are they targeting slightly different things?   Yuling Han:                 For the imatinib, we also found this drug inhibit SARS-CoV-2 entry and we did several other screenings, like the lung organoids and neuro cells. We also found this drugs. And the six drug, the mechanism is kept and the spec protein of SARS-CoV-2. And this was found by several other groups and published some paper this year. And we found this in 2020 maybe. And we published this paper before and we found this mechanism. And for another drug, we checked the RA sequencing data of SARS-CoV-2 affect the peacemaker cells. And we did several run of RA sequencing. And we compared the key factors, involved in SARS-CoV-2 entry. Several key factors like CTSL and like TMPS2 and among several run of RA sequencing. We only found the drug can decrease the expression of CTSL. So we also did PTR immunostaining, and then we found the drug decrease the expression level of CTSL.   Shubing Chen:             Yeah. So actually the other drug, it's also an antiferroptosis drug. So we did the mechanism study and it's very nice to see, we also identify the drug from an unbiased chemical screen. And for the chemical screening, we actually have a pretty large platform and we have around 1200 FDA approved drugs. We have like a 2000 anatrofin amino acid that signal pathway regulators for most of the SARS-CoV-2 screening, as you did mention, we have multiple screening platform. We focus on FDA approved drug. So it's more like for the drug repurposing and for other screening we also write larger skills.   Cindy St. Hilaire:        So we got a mechanism, we got a super specific cell type and we now have some drugs. So what are the translational implications of these findings? And I guess I'm thinking about that in terms of the time course of when a patient gets infected, has symptoms, has arrhythmia, like where could you possibly target this ferroptosis pathway? Meaning if someone already is exhibiting AFib as a result of the infection, is that actually too late? Or can you start to treat it to reverse it or prevent it from getting worse? Like what do you see as a therapeutic potential for using these drugs?   Shubing Chen:             That's a very good question. I will say this way, I think when we identify all these drugs, it's very, very exciting. But for antiviral drug development perspective, we definitely want a drug that show broader spectrum. So for COVID patient, of course we want to protect their heart, but we also want to protect their lungs.   Cindy St. Hilaire:        Exactly. Protect everything.   Shubing Chen:             Exactly. Exactly. So for the real drug that can clinical use, I think the lack of broad spectrum antiviral drug, I think that will be the way to go for drug development and for the cardioprotective respective. So if the patient do have very severe cardio symptom, particularly like arrhythmia symptom, I think that can be considered. But I don't want to really say this is the drug to treat the COVID patient. I don't think that's a way to go, particularly for ferroptosis is a cell type. This is a phenotype, very specific for the pacemaker. And I think for us, as a basic scientist, is very, very important that we understand the biology and we can identify these normal chemical tools that we can manipulate the system that can facilitate the future drug development.   Cindy St. Hilaire:        So do you think your findings and I mean findings at multiple levels, that a viral infection can induce apoptosis in one cell, but ferroptosis in another cell, but also the findings of viral infection in general, sufficient enough to drives sinoatrial node cell dysfunction. Do you think this is specific to SARS-CoV-2 and corona viruses or do you think this is something that is more broad with other viruses that maybe we just haven't recognized possibly because we don't have the tools yet?   Shubing Chen:            That's a great question. I will say some other type of virus can also infect heart, at least cardiomyocyte, like a Coxsackie virus, regular virus three. And there's actually a lot of study on the viral infection on the cardiomyocytes. And for us, the most exciting part is we really have now in serious, limited starting materials to get these pacemaker cells. Like I SA nodal cells. So we can use this as a platform to study how other virus infect, how the viral infection in general cause cell dysfunction. Because in the study we also do the calcium blocks assay, we can monitor their beating and then we can do RN-seq to monitor their transcription changes. Because this we have this still reporting system, we can purify cells, we can even run larger scale, like epigenetic level, how they change. So that's a very useful tool to study how cell responds to viral infection. I'm very excited about that.   Cindy St. Hilaire:        That's great. Well, Dr Chen and Dr Han, thank you so much for joining me today. Congratulations on a beautiful story. And I look forward to hearing more out all these different organoid and cell models you have.   Shubing Chen:            Cindy, thank you. Thank you for so much for having us.   Cindy St. Hilaire:        That's it for the highlights from the April issues of Circulation Research. Thank you for listening. Please check out the CircRes Facebook page and follow us on Twitter and Instagram with the handle @CircRes and #DiscoverCircRes. Thank you to our guests, Dr Shubing Chen and Dr Yuling Han. This podcast was produced by Ishara Rantikac edited by Melissa Stoner and supported by the editorial team of Circulation Research. Some of the copy text for highlighted articles was provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire, and this is Discover CircRes, you're on the go source for the most exciting discoveries in basic cardiovascular research. This program is copyright of the American Heart Association, 2022. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American heart Association. For more our information visit ahajournals.org.  

The Vanderbilt Faculty team will discuss Single Ventricle physiology and how this affects perfusion technique during surgical correction. Matt Warhoover, CCP is your host.

CardioNerds (Amit Goyal and Daniel Ambinder), ACHD series co-chair Dr. Daniel Clark (Vanderbilt University), and ACHD FIT lead Dr. Danielle Massarella (Toronto University Health Network) join ACHD expert Dr. Yuli Kim (Associated Professor of Medicine & Pediatrics at the University of Pennsylvania), to discuss single ventricular heart disease and Fontan palliation. They cover the varied anatomical conditions that can require 3-step surgical palliation culminating in the Fontan circulation, which is characterized by passive pulmonary blood flow, high venous pressures, and low cardiac output. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship and CardioNerds Academy Fellow).  The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Claim free CME for enjoying this episode! Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls There are various forms of unpalliated ‘single ventricle' congenital heart disease. The three main hemodynamic issues that need to be addressed in any form are unbalanced flow, pulmonary over-circulation, and blood mixing.  The Fontan palliation is a series of operations for congenital heart disease patients in whom biventricular repair is not feasible.  In the completed Fontan circulation, systemic venous blood is surgically routed directly to the lungs, effectively bypassing the heart, and creating passive pulmonary blood flow.  The hallmarks of the Fontan circulation (and Fontan failure) are elevated central venous pressure and low cardiac output.  Patients with Fontan circulation may experience significant morbidity in the long term from both cardiac and non-cardiac sequelae, and require lifelong specialist care.  Show notes 1. Why do some patients require Fontan palliation?  Many different types of anatomies may ultimately require single ventricular palliation via the Fontan procedure due to inadequate biventricular function to support both pulmonary and systemic circulations. Some examples include Tricuspid Atresia (hypoplastic RV), Double Inlet Left Ventricle (DILV; hypoplastic RV), Hypoplastic Left Heart Syndrome (HLHS; hypoplastic LV), and atrioventricular septal defects (AVSD; either RV or LV may be inadequate based on “commitment” of the common AV valve). The Fontan procedure was first described in 1971; at this time, mortality of single ventricular patients exceeded 90% in the first year of life.  2. What are the stages of Fontan palliation?  Effective pulmonary blood flow/balancing flow to the pulmonary and systemic circulations: for many conditions, this involves retrograde pulmonary blood flow from a systemic -> PA shunt (i.e. Blalock-Taussig-Thomas “BTT” shunt in which the subclavian artery is turned down and anastomosed to the pulmonary artery). In infants, the pulmonary vascular resistance (PVR) is high perinatally and gradually lowers over the first 3 months of life to adult levels with exposure to the atmosphere's natural pulmonary vasodilator: oxygen. Thus, in the first 3 months of life babies have an intri...

Wait for it....Dr Joseph Poku talks about issues of dizziness,fainting,shocking a pregnant woman back to life and wait for it he has the happiest laugh ever! Dr. Joseph Poku #electricity #HeartBLOCK #GrinchSyndrome #ExecriseIsKey #HeartArrythmia #StraightFromtheHeart #HeartBeat #BPM #SVT #EKG Clinical Electrophysiologist discusses the cardiothoracic and vascular issues that pregnant women experience and laughs at his own brief tangent as he presents ways to decrease risks and treat heart problems in pregnant women. Our guest cardiologist specializing in electrophysiology gave the true breakdown of the heart and he defined the heart muscle as a pump that is driven by electricity. The electricity supply from the top part of the heart travels through the AV node (the middle toll booth) to the Ventricle (or bottom chamber). When heart is beating too fast or firing extra beats from other parts of the heart then the toll booth can get overloaded and cause the electric signals to bypass the normal toll booth (AV node) and goes down via another toll booth in the heart and this could affect blood pressure and potentially compromise the gas, nutrient, and waste exchange for the fetus that occurs via the placenta. In cases like this it may call for the mother's heart to be shocked back into normal rhythm. Dr. Poku consistently emphasized the need for the electrical wiring to be in sync. For informational reference, the normal heart rate for an adult was established to be anywhere between 60 and 100 beats per minute, but it was also made known to be on guard for a heart rate that is above 130 beats per minutes when resting because that is a problem. Dr. Poku provides the Cocoa Pods audience with a heart arrythmia perspective and focused on the issues of dizziness, fainting, and shocking a pregnant woman back to life. He designated dizziness as cardiac rhythm disturbances, and during pregnancy it is common to see an exacerbation of arrythmia symptoms which lead to some people coming to the cardiologist for the first time. Fainting spells usually only occur when there has been a history of fainting before getting pregnant, but the fainting becomes more frequent when pregnant perhaps because the increase in volume when the body gets bigger makes one prone to passing out.

Welcome to the DAILY DROP from The New Science of Physical Health.Today's episode is all about the language of LIFE INSIDE YOUR BODY. Left Ventricle Volume. We know the language of our favourite obsession (mine is the Olympics) - but not life inside our body. Let's change this now!The first mini-series is called: THE THOMAS EDISON OF HEALTH TECHNOLOGY  IN THE 2020'S.  It will be ready very soon for those who self-select and want to deep dive into Life Inside Your Body. CLICK THE LINK BELOWhttps://forms.gle/tdqUPskRCEosZiXG7 (THIS IS THE THOMAS EDISON MINI-SERIES LINK)To access our brand new book and a special offer for listeners to this show: click here:https://go.expertroadmaps.com/entry-pager568o5dv To get access to TURN BACK YOUR BODY CLOCK - click this link.https://forms.gle/HgAGFbMxMkxUCeQ58To get access to THE PERFECT HEALTH LESSON  web class - click this linkhttps://forms.gle/hG2KZUZcndBu15dJ8

This week we replay an episode that reviews a critically important neurodevelopmental issue affecting infants who have single ventricle palliation - namely hearing loss. How common is hearing loss seen and what role does IV furosemide play in this finding amongst single ventricle patients? Are there techniques to avoid this complication and yet still use this commonly used diuretic agent? We discuss this important issue and study with Dr. Ari Joffe, Professor of Pediatrics University of Alberta - Stollery Children's Hospital who is the senior author of this week's work. doi: 10.1097/PCC.0000000000001807

Commentary by Dr. Valentin Fuster

This is the final episode of a three episode podcast series on single ventricle physiology. In this episode, we discuss the long-term management and complications associated with the Fontan circulation. We revisit the two hypothetical patients starring in the first two episodes and using their cases, we will cover the main long-term management considerations and complications associated with the Fontan circulation. This episode was created by Dr. Sabine Laguë, a first-year pediatrics resident at the University of British Columbia, in conjunction with Dr. Shreya Moodley, a pediatric cardiologist at BC Children's Hospital.

Happy birthday to us! A whole year since that first episode dropped. What a year it's been! Callum's taking the lead on our birthday special this May, with a great episode all about The People's Ventricle! He joins Mohammed in resus, where we'll meet Eoghan, our AP colleague who's brought us in a bit of a handful. Thankfully our Adult in The Room Dr Andy Neill is there to lend us a dig out. What does RVF mean for our POCUS assessment? Dr Nicolas Lim joins Callum in The Echo Chamber to discuss this. Finally, Callum sits down with Dr Pun Tong who gives us his perspective on how to go about honing your clinical acumen. Alright, let's get to it!

This podcast is the second part of a three-part series on single-ventricle physiology and focuses on hypoplastic left heart syndrome (HLHS). In this episode, the listener will learn the definition and pathophysiology of HLHS, its presentation, diagnostic modalities, and initial management recommendations. This episode was created by Dr. Sabine Lague, a first-year pediatrics resident at the University of British Columbia, in conjunction with Dr. Shreya Moodley, a pediatric cardiologist at BC Children's Hospital.

In this episode, Dr Asha Pavithran discusses key points from a recent case report published in EHJ – Case Reports.

This week we review a recent survey study on the topic of aortopulmonary collaterals in single ventricle patients. How often are these occluded in the single ventricle patient and when this is performed, how do interventionalists decide? How should they be occluded? Are there guidelines regarding this? We speak with Professor Ziyad Hijazi of Sidra Cardiovascular Center in Doha, Qatar about this recent work and also briefly discuss the PICS Society for pediatric and adult interventional cardiologists with Dr. Hijazi and Dr. Damien Kenny. doi: 10.1007/s00246-020-02418-8

Part 1 of this 3-part series on single ventricle physiology presents an approach to the management of tricuspid atresia in a neonate. In this episode, listeners will learn about the anatomy-associated anomalies, pathophysiology, and clinical presentation of tricuspid atresia as well as an approach to its diagnosis and management.

5th regular episode of Pediatrica Intensiva with Peta Alexander from Boston Children's, Mike Clifford from Royal Children's Melbourne & Greg Kelly from Westmead Children's Sydney. The interstage is a time of incredibly high mortality despite the fact it only lasts a few months. These patients can get sick for a variety of reasons between the mundane and the catastrophic - management is tricky and varies between centers. Follow Pediatrica Intensiva on Twitter here: https://twitter.com/PedsIntensiva Let us know what you think about the podcast with this survey: https://tinyurl.com/PedsIntensivaFeedback Hosts: Dr Greg Kelly (Westmead Children's Hospital, Sydney, Australia), Peta Alexander (Boston Children's Hospital), Mike Clifford (Royal Children's Hospital, Melbourne). Produced & edited by Caitlin Gibson, special thanks to Maya Newell.

Pediatricians must know a lot about immunology. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/maximumpodcast/support

Host: Grace Bichara, MD Guests: Joseph Forbess, MD, MBA & Can Yerebakan, MD Editor/Producer: David Werho, MD Drs. Joseph Forbess and Can Yerebakan discuss their philosophies and approaches to the high-risk single ventricle neonate.

BBC, NY Times, Match (詞組搭配) 每月開班！ 請私訊林威老師 lineID: linwayet 耳朵學英文 心房心室 atrium, ventricle 中譯誤導 The right ventricle uses the pulmonary valve to help move blood into the pulmonary arteries. 右心室使用肺動脈瓣幫助將血液移入肺動脈。 Atrium, in vertebrates and the higher invertebrates, heart chamber that receives blood into the heart and drives it into a ventricle, or chamber, for pumping blood away from the heart. 在脊椎動物和較高的無脊椎動物中，心房將心臟腔室吸收到心臟中並將血液驅入心室或腔室，以將血液從心臟中泵出。 .... The two atria are thin-walled chambers that receive blood from the veins. The two ventricles are thick-walled chambers that forcefully pump blood out of the heart. 兩個心房是從靜脈接收血液的薄壁腔室。這兩個心室是厚壁的腔室，有力地將血液泵出心臟。 ..... vent (v.) (常指不公地)發泄(負面情緒) The meeting will be an opportunity for everyone to give vent to their feelings. 這次會議將給每個人一吐為快的機會。 .... ventilation (n.) 通風(設備)；空氣流通(系統) Her room had poor ventilation and in summer it became unbearably stuffy. 她的房間通風非常不好，到了夏天就悶得要命。 a ventilation system 通風系統 .... ventilator (n.) 人工呼吸器 He was brought into intensive care shortly after the accident and immediately put on a ventilator. 車禍發生後不久，他就被送進了加護病房，並且馬上戴上了人工呼吸器。 ..... The medical instruments, such as ventilators, patient monitors, heart pacemakers, and dentistry chairs, etc. , imported by medical colleges and universities shall not be exempt from taxes. 醫學院校所進口的呼吸機，病人監護儀，心臟起搏器和牙科椅等醫療器械，應免稅。 .... le vent (法語) = the wind Il y a du vent . 有風。在颳風。 Il fait grand vent . 風很大。颳大風。 Le vent souffle depuis six jours. 已經颳了六天風了。

Single Ventricle Stage I Palliation Procedures by Dot Beke by OPENPediatrics

Surgery is on tap this week as we discuss a recent paper from the team at Children's Hospital LA about diaphragm plication in the single ventricle patient. What impact did this intervention have on outcomes? How were hemodynamics impacted and did this change outcomes of the bidirectional Glenn or Fontan? What percentage of patients recovered diaphragm function? Professor S. Ram Kumar of USC shares his insights into his recent work with his team. DOI: 10.1016/j.jtcvs.2020.06.007

"Single Ventricle Home Monitoring Program" by Margaret Schoeder by OPENPediatrics

Commentary by Dr. Valentin Fuster

4th regular episode of Pediatrica Intensiva with Liz Crowe - Senior PICU Social Worker Having a child with single ventricle disease is an extraordinarily stressful time for the child, the family, and the staff who are involved. Liz is a world expert on these matters with over 20 years experience clinical work and a near completed PhD on grief, resilience and wellbeing. Follow Pediatrica Intensiva on Twitter here: https://twitter.com/PedsIntensiva Let us know what you think about the podcast with this survey: https://tinyurl.com/PedsIntensivaFeedback Hosts: Dr Greg Kelly (Westmead Children's Hospital, Sydney, Australia), Peta Alexander (Boston Children's Hospital), Mike Clifford (Royal Children's Hospital, Melbourne). Produced & edited by Caitlin Gibson, special thanks to Maya Newell.

This week we delve into the liver once more to review an intriguing report from the group at Johns Hopkins regarding hepatic stiffness in the 2 ventricle congenital heart patient. We know from prior works that single ventricle patients have enhanced liver stiffness but this work suggests that some 2 ventricle patients are also similarly affected. We speak with Professor Ari Cedars of Johns Hopkins University for his insights into these findings and who he thinks might warrant routine liver follow-up in the ACHD patient following congenital heart surgery. doi: 10.1016/j.athoracsur.2020

This week we delve into the liver once more to review an intriguing report from the group at Johns Hopkins regarding hepatic stiffness in the 2 ventricle congenital heart patient. We know from prior works that single ventricle patients have enhanced liver stiffness but this work suggests that some 2 ventricle patients are also similarly affected. We speak with Professor Ari Cedars of Johns Hopkins University for his insights into these findings and who he thinks might warrant routine liver follow-up in the ACHD patient following congenital heart surgery. doi: 10.1016/j.athoracsur.2020

3rd regular episode of Pediatrica Intensiva with Dr Ravi Thiagarajan - Division Chief of Cardiovascular Critical Care at Boston Children's Hospital Patients with single ventricle heart disease are a very high risk group for cardiopulmonary arrest and requirement for ECMO support. Arrest and CPR is not inevitable and we are increasingly finding ways to prevent it, as well as manage the CPR and ECMO period with more nuance and better outcomes. Tweetorial with written summary of podcast here (& link to PDF with references): Follow Pediatrica Intensiva on Twitter here: https://twitter.com/PedsIntensiva Let us know what you think about the podcast with this survey: https://tinyurl.com/PedsIntensivaFeedback Hosts: Dr Greg Kelly (Westmead Children's Hospital, Sydney, Australia), Peta Alexander (Boston Children's Hospital), Mike Clifford (Royal Children's Hospital, Melbourne). Produced & edited by Caitlin Gibson, special thanks to Maya Newell.  

Hypothetical case: You are called to a code blue medical on the gynaecology ward. A patient in her late 60s has collapsed in the bathroom. You are told she was admitted earlier that day for investigation of a probable pelvic cancer. She is conscious, has a heart rate 130/min, NIBP 90/45, SPO2 94% on hudson mask, and is mildly SOB with a respiratory rate 30/min. This patient undergoes investigation and is diagnosed with a large pulmonary embolism. She deteriorates suddenly with the following vitals: groaning, HR 145/min, NIBP 60/35, SpO2 85%, Respiratory rate 35/min. What is the physiology and what are the principles behind the resuscitation of a patient with an acute right ventricular emergency like this? Fluids? Vasopressors? Inotropes? Thrombolysis? Intubation? Pulmonary vasodilators? Join Graeme and I as we discuss this particularly challenging scenario which can be both hard to diagnose and resuscitate. There are some important and critical differences to other common causes of deterioration, and serious traps to be aware of and avoid. Whilst educating myself on this topic I realised that I wasn't as up to speed on this as I thought I was! Thanks to the following resources which I have listed below which I strongly recommend: USEFUL LINKS EMCrit 272 – Right Heart Failure with Sara Crager PulmCrit- Nebulized nitroglycerin: The stealth pulmonary vasodilator hiding under your nose?

2nd regular episode of Pediatrica Intensiva with Dr Mike Seed, division head of cardiology from Sick Kids and also a fully qualified cardiac radiologist. Patients with otherwise normal hearts can tolerate single residual lesions fairly well, but in single ventricle patients they are often associated with major adverse outcomes. Modern management involves aggressive monitoring for and intervention on residual lesions, though interventions must be seen in the context of the whole patient. Tweetorial with written summary of podcast here (& link to PDF with references): https://drive.google.com/file/d/1S8xqQTdAYaxk6mk_O4O3EvrSMDHgdMro/view?usp=sharing Follow Pediatrica Intensiva on Twitter here: https://twitter.com/PedsIntensiva Let us know what you think about the podcast with this survey: https://tinyurl.com/PedsIntensivaFeedback Hosts: Dr Greg Kelly (Westmead Children's Hospital, Sydney, Australia), Peta Alexander (Boston Children's Hospital), Mike Clifford (Royal Children's Hospital, Melbourne). Produced & edited by Caitlin Gibson, special thanks to Maya Newell.

This week we speak with the incredible Heart Doctor, Dr. Carley Saelinger about the physiological functions of the heart and all the intricacies of this organ. We learn about the symptoms, causes and medications for different diseases and more specifically about Pulmonary Hypertension, the one that stole our heart, Freddie. 

On this weeks episode we discuss the ins and outs of pulmonary hypertension- from the WHO 5 classifications of pulmonary hypertension, what to look out for on physical exam, diagnostic considerations and new guideline updates in the field. Written by: Sameer Kushwaha (Internal Medicine Resident)Reviewed by: Dr. John Thenganatt (Respirology)Dr. Gillian Spiegle (General Internal Medicine)Infographic by: Caitlyn Vlasschaert (Internal Medicine Resident)