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Send us a textIn this special anniversary edition of the Journal Club, Ben and Daphna celebrate four years of The Incubator Podcast while diving into a compelling lineup of neonatal studies. The episode kicks off with a review of a phase 2 multicenter trial on the safety of furosemide in preterm infants at risk for BPD. Despite widespread Lasix use in NICUs, data on dosing and safety have been lacking—this study finds no significant increase in serious adverse events but emphasizes the need for larger trials to better define its role. The team then explores a study from India comparing 7- vs. 14-day antibiotic courses in culture-proven neonatal sepsis, showing that shorter courses may be safe and effective in select populations.Additional discussions include a randomized trial from Australia evaluating “sigh breaths” during high-frequency oscillatory ventilation and their effects on lung volume and oxygenation, a study examining how kangaroo mother care boosts breast milk intake, and a large Japanese cohort study detailing neurodevelopmental outcomes of infants born at 22–31 weeks. Finally, a meta-analysis on prenatal cannabis exposure underscores risks of low birth weight and preterm birth. With depth, humor, and clarity, Ben and Daphna guide listeners through evidence that shapes neonatal care. As always, feel free to send us questions, comments, or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through Instagram or Twitter, @nicupodcast. Or contact Ben and Daphna directly via their Twitter profiles: @drnicu and @doctordaphnamd. The papers discussed in today's episode are listed and timestamped on the webpage linked below. Enjoy!
PTF and Nick Tammaro kick off the show with a look back at stakes races from the weekend with a big focus on Santa Anita, as well as Gulfstream and a little Fair Grounds.Next, they take an initial dive into the Pegasus World Cup through the lens of the current international betting market.Last but not least, PTF welcomes in Spencer Luginbuhl as he discusses the past, present and future of Redboard Rewind.*Takeaways: The Pegasus World Cup Betting Championship offers a prize pool of $225,000, including NHC and BCBC seats. Santa Anita showcased some significant stakes races this weekend, making it a must-watch. PTF and Nick discussed the impact of Lasix on horse performances, particularly for Saudi Crown. The upcoming Pegasus race features a competitive field with no clear favorite emerging yet. Spencer Luginbuhl reflects on the evolution of his podcast, Redboard Rewind, over the years. Discussion on how weather conditions at Fairgrounds complicate the task of making accurate speed figures.
PTF and Nick Tammaro kick off the show with a look back at stakes races from the weekend with a big focus on Santa Anita, as well as Gulfstream and a little Fair Grounds.Next, they take an initial dive into the Pegasus World Cup through the lens of the current international betting market.Last but not least, PTF welcomes in Spencer Luginbuhl as he discusses the past, present and future of Redboard Rewind.*Takeaways: The Pegasus World Cup Betting Championship offers a prize pool of $225,000, including NHC and BCBC seats. Santa Anita showcased some significant stakes races this weekend, making it a must-watch. PTF and Nick discussed the impact of Lasix on horse performances, particularly for Saudi Crown. The upcoming Pegasus race features a competitive field with no clear favorite emerging yet. Spencer Luginbuhl reflects on the evolution of his podcast, Redboard Rewind, over the years. Discussion on how weather conditions at Fairgrounds complicate the task of making accurate speed figures.
Plus Vancouver Pro Review - It's Just Bodybuilding Big Ron Partlow, Dusty Hanshaw, Scott McNally - Time Stamps Below Chapters: 00:00:00 - Bodybuilding Expenses and Financial Advice 00:04:18 - The Terrible Business of Bodybuilding & Student Loans 00:08:15 - The Fashion of Bodybuilding 00:12:10 - The Joy of Buying New Clothes 00:16:12 - The Frustration of Bodybuilding Conversations 00:19:59 - Practicing Awareness in Conversation 00:23:26 - The Annoyance of Small Talk 00:27:06 - Vancouver Pro 00:31:04 - Impressive Physiques at the Competition 00:35:01 - Preparing for a Show a Week Apart 00:42:41 - The use of Lasix in bodybuilding 00:46:18 - Chris Aceto - New Rules Part 2 00:50:08 - The Flattery of Problem-Solving Abilities 00:54:21 - Prioritizing Home Gym Equipment 00:58:20 - Equipment for Legs in a Home Gym 01:02:23 - The Drive to Lift Heavy 01:10:15 - Intense Soccer Games and Feuds among Fans 01:14:30 - The Altitude of Skydiving and Airplanes 01:18:45 - Compartmentalization and Survival 01:23:04 - Helicopter ride in Hawaii 01:26:56 - Fashion Faux Pas 01:31:03 - Spectacular Female Listener
Though Karen did research and took birthing classes before her first baby, she didn't realize how much advocating for herself could change the course of her birth. She wanted to be the “good” patient and told herself she could do without the things her body told her she needed during labor. Karen ended up pushing for over four hours and consenting to what she was told was an emergency C-section, even though the actual surgery didn't happen until hours later.Karen had some serious postpartum symptoms of swelling and difficulty breathing that were dismissed and even laughed at until things came to a point where she knew something was very wrong. She was diagnosed with postpartum cardiomyopathy, admitted to the ICU, and transferred to cardiac care. Doctors told Karen very different things about her condition. She went from being told not to have any more children to hearing that VBAC was absolutely safe. Karen discusses how her gestational hypertension came into play with the different advice as well. Karen found her voice. She advocated for herself. She knew what her body was saying and what it was capable of. Her labor was so smooth and she WAS able to birth vaginally!Informed Pregnancy PlusNeeded WebsiteHow to VBAC: The Ultimate Prep Course for ParentsFull Transcript under Episode Details 3:46 Review of the Week06:27 Karen's stories08:50 First labor10:47 Pushing for four hours15:11 Karen's C-section17:43 Postpartum swelling and difficulty breathing21:03 Fluid in her lungs23:52 Moving to Florida and getting answers25:13 Getting pregnant again29:53 Advocating for a VBAC32:14 A spiritual dream34:34 Gestational hypertension39:36 Signing an AMA41:31 Going to the hospital45:20 Pushing for 20 minutes47:30 White coat syndrome51:59 Symptoms of hypertension and preeclampsia54:52 Tips for hypertension and preeclampsia 56:55 Karen's final tipsMeagan: Hello, hello. We are getting into almost our 300th episode, you guys. Every single time I'm recording and I'm looking at these numbers, I am blown away. I cannot believe that we have almost put out 300 episodes. Oh my goodness. I am so glad that you are here. I have this energy this year. I don't know what it is. You'll have to let me know if you notice it, but I have this energy every time I'm recording this podcast. 2024 is vibing. I'm vibing with it. I'm really liking it. We have our friend Karen and are you from Florida, Karen? Karen: Yep. I'm in Orlando, Florida. Meagan: Florida. That's what I was thinking. So if we have Florida mamas looking for providers, this is definitely an episode. I feel like probably weekly we would get 10 messages asking about providers and Florida is huge so Florida is actually one that is really common where we are getting messages for supportive providers. So Karen, along the way, if you feel to name-drop some providers that are supportive, feel free to do so but we are going to get into sharing her story in just one moment because we do have a Review of the Week. 3:46 Review of the Week Meagan: This is from louuuhuuuu. So louuuhuuuu, thank you for your review. They say that this is “very inspirational.” It says, “I knew I wanted a VBAC with my third pregnancy, but I wasn't sure if it was possible. However, I knew I didn't feel like being flat-out told, ‘No' at the first appointment. Listening to the podcast was definitely the start of me really researching birth and looking into my options. I ended up with a successful HBA2C and I definitely don't think I would have had the courage or believed it was possible without this podcast. Thank you, Meagan, for all of the work that you do to provide this information.” I love that review so much. I think that through time in my own research, I was told no. I wasn't told, “No, no.” I was told, “Sure, probably yeah. You could VBAC,” but I never really got that positive vibe. I feel like this community that we have created with all of the people on the podcast and all of the people in the community on Facebook truly is something that I lacked when I was preparing for my VBAC. I'm so grateful that we have this community for you today. Thank you, louuuuhuuuu, and huge congrats on your HBAC, your home birth after two Cesareans. If you didn't what HBA2C meant, that's home birth after two Cesareans. Just like louuuhuuuu, you can too. Make sure to follow us in our Facebook community. You can find it at The VBAC Link Community on Facebook. Answer all of the questions and we will let you in. You can find out as well that it is possible. VBAC is possible. 06:27 Karen's storiesMeagan: Okay, Karen. Welcome to the show and thank you so much for taking the time to share your story today, well your stories today. Karen: Yeah. Thank you for having me. It's a little wild actually being on your show. I've been thinking about what I was going to say even before you invited me like, “What would I say if I finally get my VBAC? It's crazy to actually be sharing my story now so I'm really excited to be talking to you today.” Meagan: Well I'm so excited that you are here and sharing your inspirational message. You know, going through your submission, it sounds so similar to so many of us. You went in for a totally planned unmedicated birth that switched to the complete opposite where you had a C-section. There are so many of us. When I was reading that, I was like, “I bet I could probably find hundreds of stories not even just in our own community that start out like that.” Karen: Yes. That's why I love listening to your podcast so much because for the first time, I didn't feel alone. But yeah. I can get into my story now if you'd like. Meagan: Yes. I would love it. Karen: Okay. So back in August– or, I'm sorry. My son was due in August 2023. This was our first baby and he was a little bit of a surprise baby, but he was very much welcome and we were excited for him. At the time, we were living in Virginia. My husband had just gotten out of the Navy and he was about to start law school. I did prepare for the birth but I don't think I prepared enough. I took a Hypnobirthing class and the doula who was leading the class was super supportive. She was just like, “You're just going to birth beautifully. I can just tell.” The midwives, the nurses at the practice were like, “Oh, you're going to birth beautifully. I can just tell.” I just kept hearing that over and over again. My ego was a little over-inflated and I was like, “I don't need to do much. I've got this.” I don't think I was prepared enough. I didn't know what I was really getting into. 08:50 First laborKaren: So when I actually started going into labor, I got there way too early. I got to the hospital too early. Like you mentioned, I wanted an unmedicated birth. I got there, I think my contractions were about every seven minutes. Now I know that I definitely should have waited at home longer. But everything seemed to be going well. I arrived. They admitted me. They seemed a little bit hesitant, but they were like, “Oh, well she's in labor. Let's just bring her in.” My water broke on its own that afternoon. Things seemed to be going well until the pain really started kicking in. I had a really hard time working through the pain even with everything I learned in HypnoBirthing. I still hadn't quite found my voice yet, my mama voice. I couldn't tell people, “Hey, you're distracting me. I'm trying to do HypnoBirthing.” I felt embarrassed about putting up the sign outside my door saying, “Hey, HypnoBirthing in progress. Please keep quiet.” I just didn't speak up. I was just trying to be a good girl and just listen to what everyone says. I heard so many times in different episodes being a good girl and just doing what I've been told. Meagan: Right. We are people pleasers. I think a lot of us are people pleasers. We don't want to ruffle feathers. We want to stay in line. We want to follow this path that we are being told we have to stay on. Karen: Yes. I mean, I just didn't realize it was something I needed to form as a mama to be able to stand up for myself because pretty soon there was going to be a baby that needed me to stand up for them. Like I said, during the birth, there were just so many distractions, people coming in and out, nurses, and visitors. It was too much. I did end up getting an epidural because I just couldn't hold out any longer. 10:47 Pushing for four hoursKaren: Around 2:00 AM, the labor and delivery nurse told me, “Oh, you need to start pushing.” I was on my back. I pushed for about two hours. I had some breaks but the baby was just stuck. For part of it, we could see that he was crowning but he just would not come out. During this entire time, no one really looked at me. I just had this one labor and delivery nurse. She was so sweet, but the midwife didn't come by. The OB didn't come by. No one really came by and I wanted to move into different positions. I felt my body telling me, “Hey, try this. Try this,” and they would tell me, “You can't move. You have to stay like that.” I pushed for four hours. Baby was in distress. I felt fine but the midwife came in and told me, “You're going to need a C-section.” This was the first time I had seen her. She told me. Meagan: Wow. Karen: Yeah. So she says, “You need a C-section. He's not going to come out vaginally.” I didn't know. I didn't know what to do. I mean, I felt that was my only option. I got really upset. I started crying. I felt like a failure. I know now that I'm not a failure. That wasn't it. But that's how I felt at the moment and my husband was devastated. He was such an amazing birth partner and he felt like he failed me. I was like, “No. You didn't fail either,” but at that moment, we just felt so let down that one, I had to ask for an epidural, and two that I was going to need a C-section. Karen: They told me. I don't remember if the word “emergency” was used or not, but they made me feel like it was an emergency and it needed to happen immediately. When I look at the paperwork and all of that stuff, I'm like, “Where was the urgency?” Because the C-section didn't happen until 10:00 AM. Meagan: Yeah. That's not an emergency. This is another thing that I'm going to be honest– it irks me because there are so many of us who are told it is an emergency. When we hear “emergency”, what do we think? Panic. Scary. Right? We divert into asking– divert. I don't know if that's the right word. We stop asking questions and we say, “Okay. Okay. Okay,” because it's an emergency and we are told that. Karen: Exactly. Meagan: I think a lot of times, truly that we are told it is an emergency and that offers some sort of– it's weird, but some sort of validation where it's like, “But it's an emergency, so okay.” We just agree and then we are grateful. We look at them in a way because it's an emergency so they are saving. Does this make sense? I don't know. Karen: No, it does. To me, when I think about it now, it feels like manipulation. Meagan: Okay, yeah. Yeah. Yeah. It can be. Truly, there are real emergent Cesareans. Karen: Agreed. Meagan: We are so grateful for Cesareans that can help us and those are real, true emergent situations, but so many of us are told it's an emergency and then like you said, it's 10:00 AM or they come in and they're like, “We need to shave you,” and it's like, “Okay, that's not an emergency.” If they have time to shave you, talk with you, and leave you for four hours, no. It's not an emergency. Karen: Exactly. So if I had known what I know now, I would have asked for my options, asked to push and change positions. There are so many things I would have done but like you said, I thought it was an emergency. I was treating my baby in danger. I need to do this now even though there was nothing wrong with the baby. There wasn't. Meagan: Or you. Karen: Mhmm, exactly. His heart was fine. Everything was fine as far as I could see as far as I remember, as far as the paperwork says, so it doesn't make sense anymore to me. But yeah. 15:11 Karen's C-sectionKaren: My husband was told to dress in scrubs while they prepped me and then I asked the nurse to make sure that no one was in the room when I got back. When we came back to surgery, they wheeled me over to the OR and they were just checking to see that the epidural was still good. I could feel them touching my belly. I told them and that's the last thing I remember. The next thing I know, I just hear a baby crying in the distance. I was waking up in a different room and there were just these two nurses chatting about their day. To me, it was traumatizing. I couldn't even process what was going on and what happened. That was just so, so scary. Meagan: I'm so sorry. Karen: Yeah. Sorry. So then they wheeled me out and that's where my husband and our whole family were waiting. I was so frustrated because I told the nurse I didn't want anyone here. I knew I would be upset after the C-section and there was everyone in the room waiting. I also found out that my baby got passed around so I didn't even get to be the first to hold him. That was so extremely upsetting. I told my husband, “I want everyone out.” Everyone left and it was just me and my husband and our baby, Luke. We were there for about 15 minutes before they started to prep me to move the recovery room and I was like, “Wait a minute. I thought I got a golden hour where I would get to be alone with the baby for an hour.” They were like, “Oh yeah, you can do that in the recovery room,” and they just wheeled me over. I get so sad when I look at pictures of that time because my baby is so beautiful. I love him so much, but I felt so drugged up that I couldn't connect with him. You can see it in the pictures. I just look like I don't know where I am. I'm in pain. It's just not what I imagined that experience to be. Meagan: Right. Karen: I definitely felt robbed of an experience. I felt extremely traumatized. That was hard in and of itself, but I was trying to come to terms with what happened. It was just a very rough time in the hospital. We had some family drama as well so that didn't help. Meagan: No. Karen: I was discharged less than 48 hours later which now I know is way too early considering the symptoms I was feeling. 17:43 Postpartum swelling and difficulty breathingKaren: My legs were extremely swollen. My whole body was extremely swollen. It didn't even look like I had given birth because I was just swollen all over. One nurse even made fun of my legs and she was like, “They look like baseball bats.” She was just tapping them.Meagan: That's a warning sign. That's something to think about. Karen: Well, I didn't know that. Meagan: Well, of course, you didn't, but as a professional, she shouldn't be tapping on your legs. She should be like, “Hmm, was this like this?” Karen: I've told other medical professionals that story and they are horrified. They are like, “That was a big warning sign something was wrong,” but they discharged me regardless. I felt so completely unprepared. It was just a very bad experience all around. They didn't have a lactation consultant working over the weekend so my baby was crying and crying and crying. He wasn't getting enough to eat when he was breastfeeding. They were just laughing and saying, “Oh, all moms feel like that. He's getting enough to eat.” Sure enough, my son was jaundiced and his pediatrician was like, “No, he needs formula. He's not getting enough to eat.” He had a significant tongue tie so he was not getting enough to eat. When I got home, like I said, baby was starving. I'm not getting any sleep. When he does fall asleep, I can't sleep. I remember explaining to different people like, “I'm having trouble breathing every time I lay down.” Everyone was just like, “Oh yeah. New mom, new baby. Totally normal.” Meagan: What? It is not normal to not feel like you can't breathe. Karen: You're going to love this then. At one point, I called the nurse hotline at the hospital because they gave it to me when I was discharged. I told the nurse, “When I lay down, I can't breathe. It feels like I can't breathe.” Her response was, “Oh, sometimes new moms don't know how pain feels like.” I was just like, “Okay, I guess this is just me.” She was like, “Technically, we're supposed to tell you to come to the hospital if you are having trouble breathing.” Meagan: Technically. Karen: Technically. So I was trying to be the good girl and trying not to ruffle any feathers and I was just like, “Okay. I'll keep pushing through,” but the moment I realized things were not good, I was extremely depressed. I thought that I was going to die and leave my child alone. I was having horrible thoughts like that. Then I realized, “I'm starting to hallucinate.” So after three days of not sleeping, there was one incident where I heard my baby crying and screaming. I went over to the bassinet to look at him and he's sleeping peacefully, but I can still hear him crying and screaming clearly. I'm like, “That's not normal.” 21:03 Fluid in her lungsKaren: Once he woke up because I was trying to be a good new mom, so once he woke up, I packed myself up and my mom and I went to the ER. I explained to them, “I'm not getting sleep. I can't sleep. Every time I lay down, I can't breathe.” They were like, “Okay. Maybe you have a blood clot.” They took me back. They did an MRI scan and when I was lying down for the scan, I started taking these small quick breaths and the nurse was like, “Are you having a panic attack? What's going on?” I go, “I can't breathe.” She finally was the one that was just like, “There is something deeply wrong here. This is not normal at all.” I loved her. She really pushed to make sure that I got seen quickly. They determined that I was experiencing congestive heart failure. The way they explained it is my heart was not pumping strong enough I guess. It wasn't pumping right so that's why I was having trouble breathing because my lungs were filling up with fluid. They were able to give me medication. It was Lasix to help push out all of the fluid. I was kept at the ICU for two nights then they transferred me to the cardiac wing of the hospital. I was there four nights total because they just wanted to keep an eye on my blood pressure and this obviously wasn't normal what was happening. My blood pressure was through the roof. That was a really, really difficult time because one, I was away from my new baby and then I had three different doctors tell me, “There is something wrong with your heart. You won't be able to have more children. Your heart can't handle it.” That was distressing because my husband and I dreamed of having a big family and we were thinking, “This might be our last child.” But weirdly enough, my OB– the one who performed the C-section– disagreed. I don't like how he said this, but he was like, “Oh, don't be dramatic. It was just a little extra fluid. You're fine.” I was like, “Okay.” He said, “You can have a VBAC. You can have as many children as you want. You're going to be fine.” I wasn't a fan of him but that was interesting that he had told me, “You're going to be a great VBAC candidate.” He kind of put that idea in my head. He said that the only reason my son got stuck was because he was 9 pounds, 15 ounces so basically a 10-pounder. I was like, “Okay.” I didn't know what I know now, but that's the reason they gave me. 23:52 Moving to Florida and getting answersKaren: Eventually, we moved to Florida because I'm from Florida so I felt more comfortable with the medical care there. I just kept finding out different ways that I was failed by the medical system back in Virginia. My primary doctor determined that I had postpartum depression. My son was already two years old when she discovered that. It was just like, “Oh, okay.” Here's some medication. Now I feel like myself again. It made me realize, “Okay, what else do I need to look into?” I got a cardiologist. She was saying, “There is nothing wrong with your heart.” She can't definitively say because she wasn't there, but she was like, “They put too many fluids in your body. You are fine. There is nothing wrong with your heart.” She was just like, “You're good to go. You can have a VBAC. You can have another C-section. You can do whatever you want. You're fine. We can keep an eye on you, but you're okay.” I started seeing an OB and I told her everything that happened and I was just like, “I want a VBAC.” I told her everything the cardiologist said, gave her all of the paperwork and she was like, “Yeah. You can totally have a VBAC.” So with both of their blessings, I was like, “Okay. Let's try for baby number two. I'm okay. I'm healthy. I'm fine.” 25:13 Getting pregnant againKaren: So I got pregnant with baby number two and that was very exciting. I thought everything was going well then at 20 weeks, my OB said, “Unfortunately, I can't be your doctor anymore. This practice cannot deliver you. You are too high of a risk for this office.” Meagan: For the office. Karen: Yes. Yes. They only delivered at these smaller boutique hospitals so they said that I needed to deliver at a high-risk hospital or a hospital that accepts high-risk patients. Meagan: Okay, got you. I got you. Karen: I got a little tongue-tied. They told me I needed to deliver at a different hospital that I didn't want to deliver at. I was like, “If I'm going to deliver at a big hospital, it's going to be Winnie Palmer in Orlando.” I'm a huge fan of theirs. So I was just like, “Okay. I can't deliver with this office even though they've been aware of all my situations for a while. I'll find a different office.” But I was already 20 weeks so it's really hard to find a provider at 20 weeks. Meagan: It can be, yeah. Karen: The other disappointing thing they told me is, “Oh, by the way, you can't have any more children. You really shouldn't because, with everything that is going on with you, your body can't handle it.” It was just like, I don't understand where this is coming from. You've been telling me I've been okay. My cardiologist says I've been okay. I didn't really get what was going on. Karen: I called around and only one clinic would take me when I was that far along with this high-risk label on me. Meagan: I was going to say the label. That's exactly the word I was going to say. Karen: Yeah. I didn't feel like it really fit, but that's what they said I was. I found a big practice that had lots of doctors. It is a very prominent practice here in Orlando and I felt like I just had to settle. The first doctor I met with I was already frustrated because I asked for a female doctor and they gave me a male doctor. I don't have anything against male doctors, I just feel more comfortable with a female doctor but he was just like, “Oh. You can't VBAC at all. You had a vertical incision so you have to have a repeat C-section.” I was like, “I don't– I've never heard anyone say that. Where does it say that in my medical records?” He was just like, “I don't see it in your records, but this other doctor said that you had a vertical incision.” I'm like, “Well, how does she know that?” So I had to go and start pulling all of these records and got the surgical notes for my C-section and everything and finally, I found something that said I did not have a vertical incision so once I showed it to him, he was just like, “Oh, okay. Well, you still can't VBAC. Your hips are too tiny. You can't deliver a baby.” Meagan: Oh my goodness, just pulling them all out. Let me just shift this jar around and pull out the next reason. Karen: Yes. I was just like, “Are you serious? Okay.” Meagan: Goodness. 29:53 Advocating for a VBACKaren: So me and my husband were like, “No. I want to try. We want to try.” I'm so glad my husband was there because he is always so good at being an advocate for me. He was just like, “No. She wants a VBAC. What can we do to make it happen?” So he said, “Well, your weight is one thing because your baby was so big the first time because you gained a lot of weight. We can help you try but if after two hours of pushing you can't get that baby out, we're going to give you a C-section.” It was very frustrating, but I felt like I really had no choice. Meagan: Yeah. Karen: I hadn't discovered you yet so I was just like, “Okay. I guess it is what it is. I will try my best to have a VBAC, but this guy's going to stop me.” So I was very blessed that due to a scheduling issue, I had an appointment with a totally different doctor. She was this young female doctor. She was around my age and I felt like I could relate to her. I just really enjoyed talking to her. I don't know if this has something to do with it, but my background is I am Japanese and Colombian and she was Asian, so it was just like, “Okay. I have someone else who is a person of color who understands at least the cultural differences.” So I don't know if that really had anything to do with anything, but it did make me feel more comfortable with her.Meagan: Which is important. Karen: Yes. After years of different doctors telling me there was something wrong with me, it was so nice to have her say to me, “Oh. You want a VBAC? Yeah. You are super healthy. You are going to be fine.” It was just like, “Oh my gosh. You think I'm healthy? Every doctor had been telling me that I'm overweight. There's something wrong with my heart. There's something wrong,” and she was telling me that I was healthy. That just made me so inspired and I just became a lot more proactive with my health. I didn't feel like things had to happen to me. I felt like I had a lot more control over my situation. 32:14 A spiritual dreamKaren: There was also one other event that happened and this was around Christmas. I'm a Christian, so we've been going to God a lot with prayers and I have been asking for a successful VBAC. So Christmas morning, I woke up to a dream but it didn't feel like a dream. It felt more like a vision and I was giving birth vaginally to a little girl. In the dream, I had the knowledge that this was going to be my third child. I was like, “Wait a second. But I'm pregnant right now with my second child. How did that birth go?” I just was told by God, “Oh, that birth went well too. You're going to be fine. You're going to be happy. You're going to have many children.” So I woke up so happy that Christmas morning. I told my husband with everything I've been battling and all of these negative thoughts, there is no way that this could have been something I produced myself or just dreamed of myself because it was such a positive, happy dream when before that, I had just been having constant nightmares about C-sections.It was just this moment of, “Okay. God really is with us and he's going to make sure everything is okay.” So yeah, between having this great doctor and then having that dream, I just was more motivated to really take control of the situation like, “Okay. I don't have to let things happen to me. What can I do?” Which actually led me to The VBAC Link. I was already 33 weeks pregnant when I found you guys so it was kind of late in the game, but I'm so glad I did. I listened to The VBAC Link obsessively in the car, when I was walking my dog, all the time and I would just hear these different stories and notate, “Okay. This is what she did. This is how she got results. This is what happened to her.” I started taking all of these notes about how I should respond in different situations and I'm so glad I did because I did use some of that later on. 34:34 Gestational hypertensionKaren: Unfortunately, I did develop gestational hypertension but I'm still not completely convinced that I actually had it. They diagnosed me the week I had to put down my dog and I had her since I was 15 so it was just devastating. I was under a lot of stress and I tried to explain that to them. They were like, “No. This is gestational hypertension.” I'm like, “Okay. Here is another label.” But I kept on top of my blood pressure readings. I never had high readings. I ate well. I tried to do exercise as much as you can when you are in your third trimester. Unfortunately, this practice had a policy that patients with gestational hypertension must deliver by 37 weeks. Meagan: Whoa. Karen: Yes. They said that if you are a VBAC patient, they won't induce you. So there's another timeline. I had to deliver by 37 weeks. But yeah, things seemed to be going really well. Once I reached around 36 weeks, I actually started having prodromal labor. I'm like, “Okay, yes. Things are going really well.” Because I had gestational hypertension, I was going 3-4 times a week to the doctor at that point. Meagan: For non-stress tests and stuff? Karen: Yes, exactly. They could see that I was already 3 centimeters dilated so I was like, “Great. Everything is going great.” At the 37-week appointment, there was a scheduling issue and instead of being able to see my regular doctor, they assigned me to a different doctor and that just made me really, really nervous. I was just like, “I don't want to go. I don't feel right. Something is going to go wrong. It's not my doctor. I don't want to go.” My husband was like, “No. It's going to be okay. It's going to be okay. Let's go.” He canceled work so he could go with me. He was like, “Everything is going to be okay.” The other thing that happened that morning was my sister who was going to be in the room with us woke up with strep throat. I was like, “This is not a good week. This is not a good day. I don't want to go in.” So when I went in, my blood pressure was 160/113 which was extremely high. This doctor told me, “You need to get a C-section today.” So I was just like, “Okay. I don't want to hurt my baby. That's fine.” I was really, really upset. I was crying and I told her I was scared and she was like, “Why are you scared?” My husband was pretty blunt and was like, “Because the doctors almost killed her last time.”She was like, “How did they almost kill her?” He was like, “They put too much fluid in her body and they caused heart failure.” She laughed and she said, “That's not a thing.” I was like, “Well, my cardiologist said it was a thing. How could you say it's not a thing?” I went to the hospital. I was really upset but the nurse there was amazing. She was like, “What happened?” I basically told her everything like my life story basically up until that point. She was like, “I checked your blood pressure when you came in. You are fine.” She was like, “This is ridiculous. It just sounds like you are stressed out.” At that point, my blood pressure was–Meagan: Reasonably so.Karen: She checked my blood pressure and it was 117/83 so it was great. It was so funny because she kept the blood pressure cuff on me and the doctor who was working that day was the same doctor who told me I'd never be able to VBAC and kept coming up with excuses. My nurse was just like, “Look, her blood pressure is fine.” Then she took my blood pressure again in front of him and it went back up. She was like, “Can you step out?” She took it again and then it was fine. She started advocating on my behalf. She was like, “You guys are causing her heart pressure to go up. You guys are stressing her out. She does not have high blood pressure because of herself. It's you guys.” The doctor was just like, “Oh, well I guess it's fine, but wouldn't you rather just have a birthday today?” I'm like, “No. I would not like to just have a C-section for no reason.” He's like, “I really don't want to send you home though,” but you really should consider this C-section just in case your blood pressure goes back up. I was like, “Look. I can check it repeatedly and if it goes up, I will come back. I'm not going to be stupid and put my son's life in danger. I will come back.” He just kept trying to convince me and finally, we were like, “No. We're leaving.” I told them, “If I'm going to have a C-section, it's going to be with my regular doctor. I trust her. I'm going to have control over this situation somehow. Even if I have to have a C-section, it's going to be by someone I trust. It's not going to be by you.” 39:36 Signing an AMAKaren: He was not thrilled about hearing that but he said, “Okay fine. You have to fill out this paperwork saying you're leaving against medical advice, but it will be fine.” I was like, “Okay, fine.” I filled out this paperwork. I was scared like, “They're probably going to kick me out afterward, but whatever.” I filled it out and I went home. They did make me schedule a C-section for two days later when my regular doctor was on call. I was like, “You know what? If it has to happen that day, it's fine. I did everything I could. I took control of whatever I could. It's my doctor.” She made me feel seen and heard and she had my best interest at heart, so we are going to pray and just do what we can. The next two days, I walked 10 miles. I drank raspberry leaf tea. We had sex. We did basically everything you can do to get labor going. I was still having prodromal labor so we would get our hopes up and then it would stop and then get our hopes up and then it would stop. Around midnight the night before I was supposed to get my C-section, I was so upset. I was just like, “It's not going to happen. I'm just going to have to get a C-section.” I just gave up completely. My husband was just like, “No. God told you this was going to be fine. You're going to be fine. Let's just get some rest because it's already midnight and we have to leave at 3:00 AM so let's just get a little bit of rest and it will be fine. We will talk to the doctor in the morning.” I was like, “Okay.” So we went to sleep at 1:00. The alarm rang at 3:00 and I was in labor. Meagan: Yay! Karen: I was so excited. 41:31 Going to the hospitalKaren: We went to the hospital. They still prepped me for a C-section. They were like, “Just in case,” but I was having regular contractions. It wasn't going away. My doctor came in. She checked me and she was like, “Okay. If you want to TOLAC, I'll send you over.” I was just like, “Oh my gosh, yes. This is my dream!” We were so happy. They wheeled us over and it just felt so surreal. We just kept waiting for the rug to be pulled out from under us and someone came in and was like, “No, you need a C-section now. You're not allowed to be over here,” or something. We were just waiting. I wanted this to be another unmedicated birth, but our midwife came in and she told me her plan. She said she wanted to try a small bit of Pitocin to see if I could make the contractions a little bit stronger and then she saw my hesitation and told me, “It's only a small amount to help move things along, but you are not on a time limit. You can take however long you need to labor. It's just to help move things along. The max is 10. We won't ever get to that point.” I was just like, “Okay. I'm going to put my trust in you because my doctor trusts you.” She also asked if she could break my water to help move things along and I felt at ease so I was just like, “Okay. That's fine.” My husband was really surprised I was consenting to the Pitocin and to the water breaking. I told him, “I don't know. All this time, I'm always fighting against my gut and my gut is telling me I can trust them fine and this is going to be okay.” I listened to her plan and I said, “Yeah, let's do it.” They also kept a really close eye on my fluid levels– the thing that the other doctor said was not a thing. It felt good to know that they were actually paying attention to me and listening to me. Karen: The other thing that happened was at 10:00 AM, my sister completed 48 hours of antibiotics so she was able to join us and I was like, “Okay. Everything is going to be okay.” My husband and I were finally able to relax. Meagan: Good. Karen: Yeah. Again, I wanted to go unmedicated but I noticed something about my body which was that I could not relax my pelvic floor. I was so tired. I was so exhausted from the last 48 hours, from the walking, from not sleeping, and from everything. I was just like, “I'm trying, but I cannot relax it.” I was just like, “I think I want an epidural. I think that will relax my pelvic floor and just relax in general.” They gave me the epidural so I was finally able to get some rest. Without even having to ask them, the midwife would come in, put me in different positions, and just do different things to help me get the baby down on its own instead of last time where they just left me lying in there with no instructions. Then around 4:00 PM, they told me I was fully dilated and they were like, “Let's do some practice pushes. Let's just make sure you know what you're doing with your body. We can troubleshoot and then when you're ready, you know what to do already.” I was like, “Yeah. That's fine.” They get everything ready, start doing some practice pushes, and the midwife goes, “Oh, these aren't practice pushes.” 45:20 Pushing for 20 minutesKaren: She starts getting suited up and the room starts filling up with people and 20 minutes later, my baby was out. Meagan: 20 minutes! Karen: Yeah, 20 minutes of pushing. He was 9 pounds so he was still a big baby and perfectly healthy and beautiful. It was wonderful. One thing that my husband noticed was that the whole room was all women. It was such a cool girl power moment. They were all cheering and so happy for me getting my VBAC and it was just a total girl power that we were all like, “Yes. We did it. Girl power! The doctor is a woman. The pediatrician is a woman. We did this.” It was such a cool, surreal moment and then they had other nurses coming in and they were like, “We heard your story. That is so cool you got your VBAC.” It was so, so amazing. It was just such a huge difference having this supportive environment. I don't know. In that moment, it was like an instant feeling of relief because I felt like all of this trauma that I had been carrying with me for so long was just lifted. I felt like I was finally healed and I was able to forgive myself for the C-section and realize, “Okay. You didn't fail at anything. Things happen. You didn't know. It's okay.” Finally, I didn't have this label that I was defining myself with for so long which was traumatic birth. I finally just got to have the birth I wanted for it to be pretty smooth after the drama of the earlier morning. Everything just went perfectly and it was so, so beautiful. I was crying. We were all crying. The doctor was just like, “Okay, is this pain crying or is this happiness?” I'm like, “This is happiness!” Meagan: Pure joy.Karen: That's my story. 47:30 White coat syndromeMeagan: That is awesome. I love that you truly got to end that way surrounded with women and somebody that you really like and just having everyone rejoicing and happy and crying together and having that space be such a drastic change in your first birth. That is amazing. Thank you so much. Did you have any blood pressure issues during your labor at all? Karen: No. My blood pressure was fine. They were keeping an eye on it the entire time and I was getting nervous because I thought, maybe if it should up they would wheel me over to a C-section, but no. It was fine the entire time. Meagan: I love that. It's kind of interesting because there have been times where I've had clients where they don't have any signs of hypertension or preeclampsia or anything like that, but then they go to their visit and then they are like, “Oh my gosh. My blood pressure was just through the roof.” They go home and they are checking it at home and they are like, “It's fine.” But then they go and it's through the roof every time they go. We just had a client just the other day. She's 34 weeks and she went and her blood pressure was pretty high. It really was. It was high. The reading was high and they did a couple of readings. They said things like, “Well, we might have to go to an emergency C-section.” This and that. Anyway, she was like, “Whoa, whoa, whoa, whoa. Hold on.” She was like, “I want to go home.” She went home and relaxed and had food. Her blood pressure was fine. White coat syndrome is a real thing and it's something to take into consideration like, “I never have blood pressure issues. I don't have any signs. I don't have protein. I don't have these things. What may be going on?” I love how your nurse was like, “Hey, can you step out? Go out.” She was very able to relate to that. Then sometimes, we have it and we don't know why. With your first pregnancy, did you have any high blood pressure at all? Karen: No. It was just a very uneventful pregnancy. Everything was perfect. It was very strange for these blood pressure problems to happen afterward.Meagan: Yeah. I think it's called peripartum so it could happen before or postpartum cardiomyopathy. Karen: Yes. Yes. Meagan: That's what I was thinking it was going where the heart muscles weaken and can lead to heart failure progressively. The symptoms include fatigue, hard to breathe, and feeling your heart rush. Those are common. Karen: Yeah, so that's actually what is on my medical records is that I had peripartum cardiomyopathy but my cardiologist was just like, “I don't believe that for a second. Your heart is fine.” She kept an eye on my heart the entire pregnancy and after the pregnancy. Nothing else happened. Meagan: I almost wonder if your heart was under stress. You talked about fluids. We get an astronomical amount of fluids during a C-section too. I'm just wondering if your body just went under a lot with a Cesarean. There was a lot of shifting and a lot of things happening and then of course a Cesarean. It just made me curious because sometimes if you have hypertension before, it can be a risk factor in that. Interesting. Karen: Yeah. That's something that the cardiologist said is that sometimes it gets confused with fluid overload. She thinks that's what happened. Part of the labeling that was happening is throughout my second pregnancy, I kept having to tell people that I did not have blood pressure issues with the first because they kept going, “Oh yeah, well you had blood pressure issues with your first pregnancy,” and I'd be like, “No, I didn't. Stop assuming that.” Meagan: I mean, I am no medical professional by any means, but it makes me wonder if it could have been related to the birth itself. 51:59 Symptoms of hypertension and preeclampsiaMeagan: I'd love to talk about hypertension and preeclampsia and things like that because hypertension is something that happens during pregnancy and it can be associated with lots of different reasons, but sometimes hypertension during pregnancy can lead to preeclampsia or HELLP or things like that. I want to give a little educational tidbit here. Talking about just hypertension. High blood pressure or hypertension does not necessarily make us feel unwell all the time. You can have that and not know. So you walking into your visit and them being like, “You have hypertension.” You're like, “Oh.” It's not completely abnormal to just walk in, but sometimes we might have headaches or not feel super great. If you are feeling crummy or especially if you are feeling like you can't breathe when you lay down or have shortness of breath, do not think that those are all just normal pregnancy symptoms that people who told you, “Oh, yeah. It's a new mom.” You're like, “No.” So follow your body. Trust your body. Preeclampsia is a condition that does affect pregnant women and can sometimes come on after that 20-week mark where we are having some of that swelling. We are having the high blood pressure. We have protein in our urine. That's when it turns into that preeclampsia stage. It's really hard. It's still unknown exactly why preeclampsia or hypertension come, but it's believe to be placenta-related so sometimes our placenta doesn't attach in the full-on correct manner and our blood vessels are pumping differently so we can get high blood pressure. I want to note that if you are told that you have high blood pressure or if you have preeclampsia, that doesn't always mean you have to schedule a C-section. It just doesn't. It doesn't mean it's always the best decision to not schedule a C-section if that makes sense, but that doesn't mean you have to have a C-section because you have hypertension or blood pressure. I feel like time and time again, I do. I see these comments in our community where it's like, “I really wanted my VBAC, but I just got preeclampsia. The doctor says I have to have a C-section.” That just isn't necessarily true. They can be induced. I know you mentioned your one hospital was like, “No, we can't induce because you are a VBAC,” which also isn't necessarily true. 54:52 Tips for hypertension and preeclampsia Meagan: Sometimes we also want to be aware of hypertension or preeclampsia getting worse because labor can be stressful on our body and all of the things. I wanted to just give a couple of little tips. If you have high blood pressure, increase your hydration. Go for walks. Cut out a lot of salts so really eating healthy and then you can get good supplements to help. If you are in labor and you are getting induced or something like that, sometimes you may want to shift gears. Maybe an epidural can be a good thing to reduce stress or a provider may suggest that it's not abnormal. But know that if you were told you have hypertension or you have preeclampsia, it doesn't always mean it's a for sure absolutely have to have a C-section. Even your provider was like, “Oh yeah. We've got this high blood pressure stuff. I really wanted to keep you.” You were like, “No.” Then your other doctor was like, “We'll kick you over here to 38 weeks,” because everything really was looking okay. Yay for that doctor for not making you stay and have a C-section that day. Know that you do have options. Time and time we talk about this. Don't hesitate to ask questions. Ask questions. Can I get a second opinion? Can I go home and relax and take a reading there? Is there something I can take to help with my blood pressure? Those types of things and then following your heart. What does your heart say? That's just my little tidbit. Do you have anything to add? I know you didn't have high blood pressure in the first pregnancy and then you kind of did sort of maybe have white coat syndrome or blood pressure with the second but do you have any tips on this situation? You were exactly in that space of they are telling you you have blood pressure. He is telling you he doesn't want you to go home and that type of thing.Do you have any messages to the audience?56:55 Karen's final tipsKaren: One thing I started doing during this pregnancy was meditation and that helped a lot. Whenever I felt like, “Okay. I'm going to go into a stressful situation,” which was most doctor visits, I would meditate before the doctor came in and that would really help a lot. Meagan: Yes. Exercising, eating, hydrating, meditation, and doing something to bring yourself back down can help. It doesn't always help. Sometimes we have high blood pressure and we do not understand it. We cannot control it as much as we are trying to. It just doesn't want to listen to what we are trying to do or receive the things we are trying to do, but all of these things can help. I am just so happy for you that you found good support, that you found the true bubble of love in your hospital room at the very end, and that you were able to have your VBAC. Karen: Thank you. Yeah. I do want to make sure. I'm not trying to send a message of, “Ignore high blood pressure! Do what you want!” It absolutely can be a very scary thing. If you need to have a C-section because of it, totally understandable. It's just that my big message that I tell new moms is to listen to your body and you are allowed to say no. You are allowed to say no to people and ask for options. But the big one is to listen to your body. Listen to your gut. You know what is really, truly going on with your body. Meagan: Of course, right. And typically, birth is actually the full cure for things like preeclampsia. Getting baby earthside is typically the end of that preeclampsia and the stop. That doesn't mean you shouldn't say, “No, I'm not going to do anything,” but just know that you have options. Induction is still okay typically. Ask those providers about your individual needs. Talk about your individual case but yeah, I would agree. I'm not trying to say, “Don't listen to your provider.” I'm just saying that you have options and you often will have options if they say one thing or another. Don't hesitate to ask questions. Karen: Exactly. Exactly. ClosingWould you like to be a guest on the podcast? Tell us about your experience at thevbaclink.com/share. For more information on all things VBAC including online and in-person VBAC classes, The VBAC Link blog, and Meagan's bio, head over to thevbaclink.com. Congratulations on starting your journey of learning and discovery with The VBAC Link.Support this podcast at — https://redcircle.com/the-vbac-link/donationsAdvertising Inquiries: https://redcircle.com/brands
In this podcast episode, Dennis talks with Doug (an ICU doctor) about acute kidney injury. They discuss the causes and types of acute kidney injury, how to recognize it, and the treatment options available. They also cover the recovery and prognosis of acute kidney injury, as well as the crush injury protocol and managing potassium levels. The episode provides valuable insights for healthcare practitioners dealing with acute kidney injury in prolonged field care situations. Takeaways Acute kidney injury can be caused by a drop in perfusion to the kidneys, blockage of urine flow, or toxic injury to the kidneys. Recognizing acute kidney injury is important, and urine output and laboratory tests can help in the diagnosis. Treatment of acute kidney injury involves preventing further injury, ensuring adequate volume replacement, and adjusting medication dosages. Most young healthy kidneys will recover from a hypoxic type of injury, but toxic injuries may cause irreversible damage. The crush injury protocol includes bicarbonate, albuterol, insulin, and glucose to manage potassium levels. Monitoring and adjusting treatment is crucial, and Lasix may be used in certain cases of acute kidney injury. Thank you to Delta Development Team for in part, sponsoring this podcast. deltadevteam.com For more content go to www.prolongedfieldcare.org Consider supporting us: patreon.com/ProlongedFieldCareCollective
Glory to God! Great News! Followup Interview w/Little Girl Autumn's Mom: Released From Hospital Captivity!Big Pharma Must Fail Along With The Babylonian System!!!When doctor's saw Autumn's E. Coli infection as a case study, they began a series of drug concoctions that have only led to her decline, even to the point of vomiting blood. Using drugs such as Lasix, Diarel and Aminophalen has proven dangerous and reckless, yet doctors refuse to heed the pleas of Autumn's family to extubate her. Remnant Nursing's advocacy services were retained after multiple ethics violations by doctors and administrators. To exacerbate the situation, LPCH has called in Child Protective Services, a move typical of medical professionals attempting to intimidate families who don't agree with the dangerous methods being administered. This followup interview with Hope Schacter, Autumn's Mother, was conducted by our EA Truth Radio Host, Andrew Shecktor on January 29, 2024. In it Hope provides a remarkable, blessed update on her 4-year old's release from Corrupt Big Pharma Captivity, and how well she's improving after the traumatic event she should not have had to endure as a poor little child. Our prayers are with Autumn and the family during this difficult time. If you feel led to help them in anyway, please reach out to: Kimberly@nursefreedomnetwork.orgSupport the show
For almost 4 weeks, four-year-old Autumn Schall has been virtually trapped at Lucile Packard Children's Hospital, in Palo Alto, CA against the will of her parents. Today, mother Hope Schacter joins the program to discuss Autumn's situation. Autumn was admitted to the teaching hospital for an e-coli infection but within days, she became critically ill, receiving care in the ICU, being given intravenously a cocktail of risky drugs, and eventually put on a ventilator. When the parents questioned the treatment, the hospital reported them to Child Protective Services. They are working with advocates and a lawyer to have her moved to another hospital where their daughter won't be viewed as a “case study,” and the family is treated like an ally not an adversary. Autumn was referred to Lucile Packard Children's Hospital for a diagnostic work to examine her bowel after a week-long case of diarrhea. Her bowel was normal, but the hospital diagnosed an e-coli condition and wanted to admit her. After the parents agreed, the hospital proceeded with an aggressive treatment plan including powerful drugs such as Lasix, Diarel, and Aminophalen. “Their protocol was very aggressive. My daughter was never on Tylenol before. She was never really sick and when they're throwing all these diuretics at you, and given the side effects these can produce, I just thought it was a lot for her constitution,” said Hope Schacter. The family has been working with Remnant Nursing advocacy services which has identified multiple ethical and clinical lapses. Schacter believes the hospital is trying to cover up clinical errors at the beginning of care that damaged her daughter's kidneys and caused her to have a seizure. They complied with all treatment recommendations, even an MRI, which required intubation. Autumn has also had to undergo a blood transfusion. There was a hearing involving the CPS complaint. The hospital is trying to get the parents to sign off on all intervention deemed “emergency,” but the parents say it has been vaguely defined. Related Health Care News articles on patient advocacy in hospitals: Minnesota Legislature Considers ‘Trusted Doctor' Bill, May 3, 2023 Down Syndrome Patient's Family Sues Hospital for Do Not Resuscitate Order, June 20, 2023 Judge Plans Three Week Jury Trial in Do Not Resuscitate Case, August 1, 2023 Patient Takes Hospital to Court for Life-Saving COVID -19 Treatment, Feb. 12, 2021 Ivermectin obstacles during COVID
For almost 4 weeks, four-year-old Autumn Schall has been virtually trapped at Lucile Packard Children's Hospital, in Palo Alto, CA against the will of her parents. Today, mother Hope Schacter joins the program to discuss Autumn's situation. Autumn was admitted to the teaching hospital for an e-coli infection but within days, she became critically ill, receiving care in the ICU, being given intravenously a cocktail of risky drugs, and eventually put on a ventilator. When the parents questioned the treatment, the hospital reported them to Child Protective Services. They are working with advocates and a lawyer to have her moved to another hospital where their daughter won't be viewed as a “case study,” and the family is treated like an ally not an adversary. Autumn was referred to Lucile Packard Children's Hospital for a diagnostic work to examine her bowel after a week-long case of diarrhea. Her bowel was normal, but the hospital diagnosed an e-coli condition and wanted to admit her. After the parents agreed, the hospital proceeded with an aggressive treatment plan including powerful drugs such as Lasix, Diarel, and Aminophalen. “Their protocol was very aggressive. My daughter was never on Tylenol before. She was never really sick and when they're throwing all these diuretics at you, and given the side effects these can produce, I just thought it was a lot for her constitution,” said Hope Schacter. The family has been working with Remnant Nursing advocacy services which has identified multiple ethical and clinical lapses. Schacter believes the hospital is trying to cover up clinical errors at the beginning of care that damaged her daughter's kidneys and caused her to have a seizure. They complied with all treatment recommendations, even an MRI, which required intubation. Autumn has also had to undergo a blood transfusion. There was a hearing involving the CPS complaint. The hospital is trying to get the parents to sign off on all intervention deemed “emergency,” but the parents say it has been vaguely defined. Related Health Care News articles on patient advocacy in hospitals: Minnesota Legislature Considers ‘Trusted Doctor' Bill, May 3, 2023 Down Syndrome Patient's Family Sues Hospital for Do Not Resuscitate Order, June 20, 2023 Judge Plans Three Week Jury Trial in Do Not Resuscitate Case, August 1, 2023 Patient Takes Hospital to Court for Life-Saving COVID -19 Treatment, Feb. 12, 2021 Ivermectin obstacles during COVID
Which of the following adverse effects is the patient MOST likely to experience during exercise intervention as a result of the furosemide? Find it all out in the podcast! Be prepared for the NPTE so that you can pass with flying colors! Check out www.ptfinalexam.com/podcast for more information and to stay up-to-date with our latest courses and projects. Register for the FREE one-day event in Chicago, Nov. 18!
Health Hero Show: The official Chemical Free Body Lifestyle Podcast
Episode 191 - Hello Health Heroes! The family of 4-year-old Autumn Schall recently retained our advocacy services at Remnant Nursing after multiple ethics violations by the staff at Lucile Packard Children's Hospital in Palo Alto, CA left them feeling abandoned, alone, and frightened for the life of their child. Autumn was diagnosed with an E. coli infection at her local ER. They advised her parents that they did not treat pediatric e-coli infections at this hospital and that a transfer of care to Lucile Packard Children's Hospital for “Fluid Management" would be necessary. Upon arrival at LPCH, Autumn was labeled by physicians as a “case study.” Per Autumn's mother Hope, they then began an aggressive swarm of medications including Lasix and Diarel to force her kidneys to excrete more urine in an attempt to “mass flush” the infection byproducts. This just overwhelmed her system. Her mother attempted to advocate, demanding pacing, but physicians and hospital staff continued to fight her and ignore her pleas. Only when Autumn began vomiting blood, did they finally discontinue ONE of the medications. From here it has been a constant barrage of multiple interventions that many of the medical professionals we have consulted agreed were aggressive, unnecessary, and likely contributing factors to her declining health. When a blood transfusion was deemed necessary, the hospital staff fought any attempt by the family to facilitate a directed donation, to the point of threatening a court order to transfuse without parental consent. Autumn was placed on dialysis that included the use of Albumin, a human blood product. Her parents were not informed, nor did they consent to its use. This exposure has understandably caused her family a considerable amount of stress. The family was ready to remove Autumn from the hospital, but they have since placed her on a ventilator, impeding their ability to do so. A 22-year veteran Pediatric Respiratory Therapist whom we have consulted on this case, states that there is no justification for her prolonged intubation and that based on her numbers, she meets the standard criteria for extubation. Despite the parent's multiple requests to do so, they are refusing to extubate her. They are keeping her heavily sedated and blaming her mother's insistence on the use of a gentler diuretic as the reason for indefinite intubation, which carries a myriad of risks. The family feels as if they are being held hostage in this situation, with each additional intervention causing greater harm than the last. With time being of the essence, they feel that bringing their story to the media, may be the only chance they have to save their precious daughter from being the latest victim in a rash of medical kidnappings that we have seen around the country. I was just informed that Child Protective Services has arrived at the hospital. We know that this is a shameful tactic that is often used to gaslight parents and force compliance with hospital protocols. Please leave a comment and share this episode and remember you can always send us topics you're interested in knowing more about. Love & Light Coach Tim. Help Save Autumn, go to: https://www.remnantnursing.org/ or send and email to: clientservices@nursefreedomnetwork.org You can donate and also please call the Hospital and let them know in a nice way you are watching them. Lucile Packard Children's Hospital 650-736-4089 Tim's Favorite, HIGHEST QUALITY Health Product Recommendations: Best Detox & Nutrition Supplements: https://www.chemicalfreebody.com/ Best Hydrogen Machine: Tim's personal unit - CLICK HERE Best Infrared Saunas & Healing Lamps: Tim's personal unit - Save $100 CLICK HERE Water Purification/Restructuring System: Book FREE Consult CLICK HERE Best Home Air Purification Unit : Tim's personal unit CLICK HERE Best Non Toxic Home Building Materials: CLICK HERE See omnystudio.com/listener for privacy information.
Intensief de podcast is terug!En deze keer een aflevering over Asthma Cardiale, FOSPE en SCAPE.Wat kunnen we leren over de juiste behandeling om onze patiënten weg te krijgen van de IC en ze een intubatie te besparen?Veel luisterplezier :)Bronnen:Patterns of Weight Change Preceding Hospitalization for Heart Failure | Circulation (ahajournals.org)Transition From Chronic Compensated to Acute Decompensated Heart Failure | Circulation (ahajournals.org)Role of high-dose intravenous nitrates in hypertensive acute heart failure - PubMed (nih.gov)Sympathetic Crashing Acute Pulmonary Edema (SCAPE): Insight into Pathophysiology and the Role of High Dose Nitroglycerin in Treatment | RECAPEMSympathetic crashing acute pulmonary edema - PMC (nih.gov)Sympathetic Crashing Acute Pulmonary Edema (SCAPE) - EMCrit ProjectemDOCs.net – Emergency Medicine EducationFurosemide in the Treatment of Acute Pulmonary Edema - emDOCs.net - Emergency Medicine EducationemDOCs.net – Emergency Medicine EducationED Management of Heart Failure: Pearls and Pitfalls - emDOCs.net - Emergency Medicine EducationAcuut hartfalen - Het Acute BoekjeFurosemide: Venodilation - OpenAnesthesiaWhat is the evidence on the use of high-dose nitroglycerin for SCAPE? | Drug Information Group | University of Illinois Chicago (uic.edu)Use of nitroglycerin by bolus prevents intensive care unit admission in patients with acute hypertensive heart failure - ScienceDirectReview article: lack of effect of opiates in the treatment of acute cardiogenic pulmonary oedema - PubMed (nih.gov)Midazolam versus morphine in acute cardiogenic pulmonary oedema: results of a multicentre, open-label, randomized controlled trial - PubMed (nih.gov)Narrative review: the management of acute decompensated heart failureBedankt voor het luisteren!Volg @intensiefdepodcast op InstagramVragen? intensiefdepodcast@gmail.com
Most doctors don't use loop diuretics like lasix, bumex correctly. Here is why. And here is how to use them correctly. https://dralo.net/links
Explore why engaging in difficult conversations is a pivotal element for sustaining successful business partnerships. Lesley Logan and Brad Crowell share valuable insights and personal experiences, highlighting the importance of clear communication, commitment, and dealing with partnership red flags in today's recap episode. If you have any questions about this episode or want to get some of the resources we mentioned, head over to LesleyLogan.co/podcast. If you have any comments or questions about the Be It pod shoot us a message at beit@lesleylogan.co . And as always, if you're enjoying the show please share it with someone who you think would enjoy it as well. It is your continued support that will help us continue to help others. Thank you so much! Never miss another show by subscribing at LesleyLogan.co/subscribe.In this episode you will learn about:The importance of scheduling lunch breaks to ensure work-life balanceHow to leverage your strengths to propel your business forward. Why clear communication is key to a thriving business partnership.Learn how to redefine your brand by presenting your authentic self online. Why it's crucial to check back in with your actual goals regularly.Episode References/Links:OPC Tour Email ListGet on the waitlist for eLevate Round Four If you enjoyed this episode, make sure and give us a five star rating and leave us a review on iTunes, Podcast Addict, Podchaser or Castbox.Join us at our Cambodia Retreat - Oct. 8-13, 2023Get your free Athletic Greens 1 year supply of Vitamin D3+K2 and 5 free travel packsGet your discount for some Toe Sox using the code: LESLEYBe It Till You See It Podcast SurveyBe in the know with all the workshops at OPCBe a part of Lesley's Pilates MentorshipFREE Ditching Busy Webinar ResourcesWatch the Be It Till You See It podcast on YouTube!Lesley Logan websiteBe It Till You See It PodcastOnline Pilates Classes by Lesley LoganOnline Pilates Classes by Lesley Logan on YouTubeProfitable PilatesSocial MediaInstagramFacebookLinkedInEpisode Transcript:Lesley Logan [00:00:00]:It's all communication. This is why I keep saying it's a partnership and your business is like a marriage. You have to do the exact same thing before you marry someone. These are the exact same things you have to do. But I think so many people are afraid of looking dumb or like they know what they're doing, or they get caught up in the excitement of what the business could be. And it's like, you got to sit down and just go, okay, down and dirty. Like, how deep am I going to get into this? How deep are we both getting into this before, like, we go, this isn't working.Lesley Logan [00:00:30]:Welcome to the Be It Till You See It podcast, where we talk about taking messy action, knowing that perfect is boring. I'm Lesley Logan, Pilates instructor and fitness business coach. I've trained thousands of people around the world, and the number one thing I see stopping people from achieving anything is self-doubt. My friends, action brings clarity and it's the antidote to fear. Each week, my guests will bring bold, executable, intrinsic and targeted steps that you can use to put yourself first and be It till you see it. It's a practice, not a perfect. Let's get started.Lesley Logan [00:01:12]:Welcome back to the Be It Till You See It interview recap, where my co-host in life, Brad, and I are going to dig into the captivating convo I had with Kristen Crowley and Jill Bunny in our last episode. If you haven't yet listened to that interview, feel free to go back now and listen, or listen to this one and then listen to that one. You can go in any order you want. (Brad Crowell: You can.) You really can. It is your own adventure and we want to support that, but they're pretty bunch badass bitches, so you should listen to it. Today is October twelveth at the time that you're listening to this. We are in the midst of our retreat this year, so we are in Cambodia. We should be out at the temples today, like, living our best life up, (Brad: Loving it.) which is so exciting.Lesley Logan [00:01:51]:And that also means today is World Arthritis and World Sight Day, both important things you should know about. So, first of all, arthritis is real, so go get yourself checked out and do the things you can do to avoid the heck out of them, like getting stronger. And the World Sight Day, I didn't actually look up what that means, but make sure it's seeing well. Like, do I need to go to the eye doctor today? Is that what it's telling me to do?Brad Crowell [00:02:17]:World Sight Day.Lesley Logan [00:02:18]:You want to know something funny?Brad Crowell [00:02:22]:Observed every year. What's funny?Lesley Logan [00:02:23]:Well, I got lasix when I was 30 and everyone said, that's so dumb because at 40, you're going to need to have reading glasses. And I want to let you know right now, you guys, I'm 40 and I do not need reading glasses. So, go Lasix.Brad Crowell [00:02:37]:That's true. It is a day first initiated by Lions Club International Foundation during their site first campaign in an effort to spread awareness about preventable blindness and help people who are visually impaired.Lesley Logan [00:02:49]:Oh, well, then go to schedule your doctor's appointment to prevent blindness. I think that's genius. I didn't know that. That's great. Wonderful. Gaia, we think is probably blind. She did she did bark at a bolster. It's okay.Brad Crowell [00:03:06]:She just sat up. She can hear just fine.Lesley Logan [00:03:09]:She can hear just fine. It's believing. Here we go. So, yes, we are in Cambodia next year. We will be back here in Cambodia in October. So you'll want to be on the waitlist to make sure you get to sign up and get the Early Bird special. So you'll want to go to Lesleylogan.co/retreat to enjoy what's coming up in January. So in January, we'll open up the doors, but you want to be on the waitlist to hear about those doors.Lesley Logan [00:03:34]:Then I come back. I go to Chicago with Erika Quest to do a weekend of workshops at Club Pilates and St. Charles. St. George. St. Charles Street, I think.Lesley Logan [00:03:47]:Anyways, we're going to be in Chicago at a Club Pilates teaching some workshops. If you want to see if there's any spots left, DM me, because there's not a lot of spots ever. So you'll want to DM me to get that information. In December, Erika Quest and I will be back at a Club Pilates in Frisco, Texas. And then I come back, and then we pack up the van, and Brad takes me on a tour that he keeps threatening is not going to ever end. And I keep threatening to say, but I have a girl's date, so you got to get me back here in time for my New Year's Eve.Brad Crowell [00:04:16]:But we'll be back in Frisco, Texas.Lesley Logan [00:04:18]:We'll be back in Frisco, Texas, right after we've done this before. Frisco. You always bring it. And so (Brad: So fun.) We can't wait to celebrate the end of the year with you, as well as the beginning of the end of the year with you. So if you want to hear about the tour, make sure you get on our email list. Just in generalBrad Crowell [00:04:34]:Go to opc.me/tour.Lesley Logan [00:04:37]:Yeah and you'll hear all about the tour. (Brad: Oh, yeah) because it's epic, and there's, like, really cool things that are happening you wouldn't want to miss out on, because you'll miss out on those epic things. And then in January, I do kick off eLevate round four. And if there's any spots left, you are going to want to apply, because 2025 will be the next time that I run it, and that's a long ways away in my world. So go to lesleylogan.co/elevate. That'll get you on the waitlist. But if you actually want to get in on 2024, DM me and I will chat with you. We'll see if this is the right thing for you.Lesley Logan [00:05:11]:We are so, so excited. Some people, like I said last episode, call it a game changer. And those people would be eLevate members, multiple of them. They told me it's game changing. And I'm like, yeah, eLevate. Game changing. Love the tagline.Brad Crowell [00:05:24]:Love it.Lesley Logan [00:05:25]:Before we talk about Jill Bunny and Kristen Crowley. I just want Jill Bunny's name. I'm just going to be really honest. I want it. (Brad: It's a name.) I want to know. I have so many questions about that.Brad Crowell [00:05:36]:If it was like she nicknamed herself.Lesley Logan [00:05:38]:But I don't think I don't. I don't think so. Especially after my brother sat there and read every baseball player name off to us. And I was like, really? Someone named their kid that oil win something.Brad Crowell [00:05:52]:Anyways, what if she had a brother named Jack?Lesley Logan [00:05:56]:Jack Bunny and Jill bunny.Brad Crowell [00:05:58]:Yeah.Lesley Logan [00:05:59]:Well, like, just Jack and Jill.Brad Crowell [00:06:01]:Well, Jack Rabbit bunny.Lesley Logan [00:06:04]:Oh, I see. I was thinking of Jack and Jill. I wasn't thinking of Jack Rabbit.Brad Crowell [00:06:07]:I like the Jack and Jill, too.Lesley Logan [00:06:08]:Because also it makes me think of those houses where they have a bathroom in between, two bedrooms for siblings to share, but the sink is always too low.Brad Crowell [00:06:17]:I'm sure she's heard that before.Lesley Logan [00:06:19]:I'm sure she heard all of this. I'm sure she's like, can we get to talking about me? Yes, we will, in just a second, Jill Bunny, because you're a badass. But first, we have an audience question.Brad Crowell [00:06:27]:Yeah, we do. The question was, do you actually schedule your lunch break?Lesley Logan [00:06:33]:Fuck yes, we do.Brad Crowell [00:06:34]:Yeah.Lesley Logan [00:06:34]:Did we always?Brad Crowell [00:06:36]:No, we didn't always.Lesley Logan [00:06:37]:Well, I did. When I was teaching, I always had a break in the middle of the day.Brad Crowell [00:06:42]:I did not.Lesley Logan [00:06:43]:You've never ever.Brad Crowell [00:06:44]:I've never been good at this except for, well, the last couple of years.Lesley Logan [00:06:46]:Sometimes at 02:00. Brad's like, I haven't eaten yet today. And I'm like, are you an adult? Are you hungry? We need to have a reminder.Brad Crowell [00:06:57]:I don't usually eat breakfast.Lesley Logan [00:07:00]:I know you really don't. But at any rate, I have always had a lunch. Now I have scheduled lunch because we work at home together, and if it's not scheduled, then one of us will interrupt the other person's work break. So we just take at the same time.Brad Crowell [00:07:13]:Yeah. And that's nice, actually. It's a lot of fun.Lesley Logan [00:07:15]:Yeah. Sometimes you make me lunch.Brad Crowell [00:07:17]:It happens. Definitely. But the reason that we do that is because if I didn't put it in my calendar, it wouldn't happen. I would just never take a lunch.Lesley Logan [00:07:27]:That's everything, you guys. If you don't put it in your calendar, it doesn't get done, period.Brad Crowell [00:07:31]:Yeah. So that's legit. Definitely scheduling your lunch break. It's worth it. You'll enjoy it.Lesley Logan [00:07:37]:And look, even if you don't, you're like, guys, I'm not that hungry. I can eat when I'm on the road. Our doctor, Dr. Bender, shout out to her. She, with both of us, is like, you have to sit down and just eat your lunch. Like not be on your phone, don't listen to a podcast, which we still do, but just not reading something for work, but just sit and eat your lunch and let it digest. And so we have a whole hour blocked off for lunch, every workday, and we can do whatever we want in that hour.Lesley Logan [00:08:10]:We can play around for half an hour and then eat lunch. We can eat lunch and then walk around the block or whatever.Brad Crowell [00:08:16]:Or you can make a really extravagant lunch that takes 45 minutes to make.Lesley Logan [00:08:20]:He does that a lot. He does that a lot. Or you can go and go, you know what I'm going to do? I'm going to drive across town to get that coffee that would go great after this lunch right now, even though I can make that latte.Brad Crowell [00:08:33]:She does that a lot.Lesley Logan [00:08:34]:I do. But there's something luxurious about it. And here's the thing. There are times to hustle and to another shout out to Kareen until it comes a hassle. And you have got to take time for yourself and not just in the morning and not just at night, but different parts throughout the day. And lunch is very important. The only day we don't have lunch together is on Tuesdays because I have a fly session after my lunch, technically, so I have lunch after that. But you've made it for me before and we just put in the fridge and I'll eat it later.Lesley Logan [00:09:05]:So, yes, schedule your lunch break. You matter.Brad Crowell [00:09:09]:Okay, now let's talk about our guests,Kristen Crowley and Jill Bunny. As co-entrepreneurs I was just going to say copreneurs. As co-entrepreneurs, Jill and Kristen present a harmonious balance of analytical and creative approaches to business. Both promote building genuine online brands using their backgrounds to help women grow their brands. The name reFRAME became symbolic of their adaptability and resilience in the business landscape and they laughed and said the name just stuck. And that is like officially the name of their business. And what they actually focus on are events and retreats.Lesley Logan [00:09:49]:Yeah, I really loved a lot of what they said, it was actually a really fun conversation. They're really one of the few partnerships and I'm like, okay, they can work together as we've just seen too many partnerships not work out. They really understand each other and their strengths and everything. So I love this. Jill mentioned confidence comes over time and that just because you have a business doesn't actually mean you are a business owner. That kind of also comes with time. And I think that's really interesting because first of all, I think there's a lot of people going, oh my God, I don't want to be a business owner, but like fell into this business and also you don't know what you don't know. So you're kind of flying by the seat of your pant, moment to moment, trying to figure things out.Lesley Logan [00:10:33]:And then over time, you get confidence, like, oh, I've seen this problem before. And it's really like those after that first year or so, you really go, okay, I got this down, okay? It's not going to blow up on me. And I've got some ideas. So I think that that was really cool. So she said what we have to do is put the reps in and the time in and be proud of what you're good at. And I just thought, what a great thing to highlight, just be proud of what you're good at. Too often people are like, oh, I don't want to brag about what I'm good at because some people are going to think I'm overconfident or weird or whatever. And it's like, actually no, you should be really proud of what you're good at because we're not good at everything.Lesley Logan [00:11:10]:And so the things we're good at are like going to propel the business forward and the things we're not good at, we're going to hire out.Brad Crowell [00:11:15]:Yeah, I think that it was interesting just to hear them talk about how they connected with each other and how it became like obviously kindred spirits. And we often tell people not to partner up with people, but I know part of the conversation, you talked about it being like a marriage, which we've talked about here before on this pod, but they totally agreed and they both came from businesses before and partnerships before in different ways and it just seemed to make sense. It seemed to click for them. So I thought that was really interesting.Lesley Logan [00:11:56]:Yeah, well, I mean, just to jump into your side of things, they said you need to make sure that your partner has the same moral compass. And I think that is the same as your partner in life, but really that makes a big difference. And I think a lot of people partner up in business and they both want the thing to grow and they don't want to do all the work alone, which is why they do it, but they don't actually have the same moral compass. In fact, in Agency Mini, this one person was like, hey, should I partner up with this studio owner? And I'm like, you mean the studio owner who's illegally got you classified as not an employee and is, in your words, squandering? No, you should not. You should not because that's not the same role compass.Brad Crowell [00:12:40]:Right. Yeah, totally. I'm glad they talked about partnerships, like how that works because they said that the thing that was really important was sitting down and being crystal clear with each other about things. Like number one thing was money. Are we both putting our personal money into this? Are we raising money from somewhere else? Like, how are we doing this? What are our expectations and how is this going to work? And they both agreed on the way that it would work and effectively being transparent about their personal finances just in case something didn't go the way they expected, could they continue to keep it going? And they effectively made a financial commitment to each other, and then they agreed on they understood, okay, cool. This is where we're at. They said, specifically because at the end of the day, everyone has to be on the same page.Lesley Logan [00:13:34]:Well, here's what I love. It's all communication, and this is the same thing.Brad Crowell [00:13:37]:It really is.Lesley Logan [00:13:38]:This is why I keep saying it's a partnership and your business is like a marriage. You have to do the exact same thing before you marry someone. These are the exact same things you have to do. But I think so many people are afraid of looking dumb or like they know what they're doing, or they get caught up in the excitement of what the business could be. And it's like, you got to sit down and just go, okay, down and dirty. Like, how deep am I going to get into this? How deep are we both getting into this before we go? This isn't working. You have to have the exit strategy as well, because you do have to think, what if this doesn't go well? Who gets what? What happens here? And I learned that from oh, my gosh, a podcast I listened to ten years ago.Lesley Logan [00:14:19]:These two girls became friends on Facebook or whatever. They both did similar things. They partnered up and had an amazing podcast. It was one of the top podcasts at the time for women in business. And they decided to eventually actually make a membership together, which would be the first thing, except for the podcast, where they actually made money together. And they brought on their lawyer, and they said, we sat down with a lawyer and we said, what do we need to talk about before we do this? And she said, we should talk about what happens if one of you doesn't want to do this anymore. We have to talk about how this ends, what are the different ways it could end, and then what happens? And that was such an interesting thing to hear, because no one wants to talk about, like, well, how does it end? But you have to think about it so that if you do need to walk away, how much does each person get? How much do you have to pay to get out of it? Or how much should you get paid to get out of it? So I really enjoyed listening to the fact that they talked about the money. They were very clear on things, and they got very vulnerable about what the states of their personal lives were, because guess what? Your personal life comes into your business all the fucking time.Brad Crowell [00:15:30]:Yeah, totally.Lesley Logan [00:15:31]:All the time.Brad Crowell [00:15:32]:Totally.Lesley Logan [00:15:32]:If anything's going on with one of our family members and they call us the middle of a workday, you better believe it fucks the day up. So I just thought it was really nice, honest conversation.Brad Crowell [00:15:42]:Yeah. And they talked briefly about some red flags, and that was basically hiding things and not being communicative or not being as committed to the vision. And they said, definitely partnerships shouldn't be formed out of desperation. A good partner should push for growth and also keep one on track.Lesley Logan [00:16:08]:Can we just highlight, partnerships should not be put together out of desperation. So if you are having someone partner with you because you're desperate and you need help in your business, that is not the best time to get a partner. You need to take a pause and really understand what you're doing because you'll partner up with someone who you think is a lifeline, and then it just really changes the roles and you don't think through things clearly.Brad Crowell [00:16:34]:Yeah. I do think that if you are going to bring on a team member or a partner, it should be someone with complementary skills, skills that are not your own, so that you're not both trying to do the same things. But yeah, like making a partnership out of desperation is dangerous. (Lesley Logan: Yeah.) All right, so finally, let's talk about those Be It Action Items. What bold, executable, intrinsic or targeted action items can we take away from your convo with Kristen Crowley and Jill Bunny? They said when it came to understanding and presenting your authentic self online rather than imitating others. So this is actually really similar to what we were just talking about with a PR person in the last episode, because what their retreats are all about is rebranding your brand. So if you're stuck, you're not feeling like you know what you're doing with your brand, then they offer these events where you can dig in over a couple of days, or some of them are just day retreats and really analyze your social media presence and the way your brand looks and all these kinds of things. And so when they're talking about presenting yourself authentically we're reiterating this here, people, because they said building a brand is about knowing who you are and who you're serving, and then you're going to structure everything around it, around your story, and then the problems that you're solving for the people that you're serving.Lesley Logan [00:18:08]:I love this is back to back with Whitney Lee.Brad Crowell [00:18:09]:It's kind of crazy.Lesley Logan [00:18:10]:You did a good job there. So I actually really enjoyed the action items that Jill talked about because she's like, I'm Jill 2.0 and she is, like, checking in throughout the day if what she's doing is aligned with her, with the 2.0. So all these things that she wants are the actions that she's taking, align with that, not just writing them down and going off onto the day, but really checking back in. So it's not just about journaling, so you feel good about yourself, but actually going, okay, where am I at in alignment with what this is? Am I actually doing those steps that get through there. And it made me think of Alan Stein Jr. Jeez. His interview from the beginning of this year just keeps on giving, and his whole thing is he ends every single day. Like, am I 1% closer to the man I want to be? And it's like, how can you find time in your day to check back in with your actual goals and just really understand, like, okay, today I did these things, and they had nothing to do with 2.0, in fact, I like, went backwards, and just being honest with that.Brad Crowell [00:19:12]:Episode 167.Lesley Logan [00:19:13]:167. I was not going to get that because I don't remember what the year started. But that's my fault. Maybe I should study.Brad Crowell [00:19:20]:It's all good. You're fine.Lesley Logan [00:19:21]:I know, but I want to be like that guy who's uncrooked, who he can go Oscar winner director, 1973. And he's like, DA DA DA DA. And I'm like, no, maybe I don't have that skill. But be it till we see it. Right. So, anyways, I think it's really important to check back in, whether it's a vision board or a journal or a goal, just making sure each day it's like, look at that and go, yes, I'm still on track. Or go, oh, wow, I got a little derailed today. Little derailed.Lesley Logan [00:19:52]:And what can you do to just get back on that I just thought was a really fun way of reflecting on where we're trying to be so we can be it till we see it.Brad Crowell [00:20:01]:I love it.Lesley Logan [00:20:02]:Me too. I'm Lesley Logan.Brad Crowell [00:20:03]:And I'm Brad Crowell.Lesley Logan [00:20:04]:Thank you so much for listening to this amazing podcast. We couldn't do it without you. So what are you going to do with these tips? How are you going to use them? What was your favorite part? We want to know. Tag, jill Bunny and Kristen Crowley and the Be It pod. And let us know and share this with a friend who needs to hear that they can reframe, that they can start over. They can do awesome things. Maybe that friend is you. And until next time, Be It Till You See It.Brad Crowell [00:20:25]:Bye for now.Lesley Logan [00:20:26]:That's all I've got for this episode of the Be It Till You See It podcast. One thing that would help both myself and future listeners is for you to rate the show and leave a review and follow or subscribe for free wherever you listen to your podcast. Also, make sure to introduce yourself over at the Be It pod on Instagram. I would love to know more about you. Share this episode with whoever you think needs to hear it. Help us and others Be It Till You See It.Lesley Logan [00:20:50]:Have an awesome day. Be It Till You See It is a production of the Bloom Podcast Network.Brad Crowell [00:20:57]:It's written, filmed, and recorded by your hosts, Lesley Logan and me, Brad Crowell.Lesley Logan [00:21:02]:It is produced and edited by the epic team at Disenyo.Brad Crowell [00:21:04]:Our theme music is by Ali At Apex Production Music and our branding by designer and artist Gianfranco Cioffi.Lesley Logan [00:21:13]:Special thanks to Melissa Solomon for creating visuals and Ximena Velazquez for our transcriptions.Brad Crowell [00:21:18]:Also to Angelina Hiraco for adding all the content to our website. And finally to Meredith Crowell for keeping us all on point and on time.Support this podcast at — https://redcircle.com/be-it-till-you-see-it/donationsAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy
Christina Prevett // #GeriOnICE // www.ptonice.com In today's episode of the PT on ICE Daily Show, Modern Management of the Older Adult lead faculty Christina Prevett discusses the significance of research in the field of physical therapy is along with the importance of translating that research into evidence-informed practice. She acknowledges the substantial nature of their research and highlights the necessity for clinicians on the front line to have access to this valuable information. Staying up to date with available evidence and combining it with clinical expertise and patients' experiences and desires is emphasized as crucial for clinicians. The episode also addresses several gaps in research that need attention, including the need for rehab research for individuals in sitting positions, outcome measures for wheelchair users, and managing conditions in neurological populations. The host expresses frustration at the lack of clinically relevant outcome measures for wheelchair users and emphasizes the need for research to support the role of rehab in enhancing quality of life and managing various conditions. Overall, the episode underscores the importance of research in informing and improving physical therapy practice. Take a listen to learn how to better serve this population of patients & athletes. If you're looking to learn more about live courses designed to better serve older adults in physical therapy or our online physical therapy courses, check our entire list of continuing education courses for physical therapy including our physical therapy certifications by checking out our website. Don't forget about all of our FREE eBooks, prebuilt workshops, free CEUs, and other physical therapy continuing education on our Resources tab. EPISODE TRANSCRIPTION 00:00 INTRO What's up everybody, welcome back to the PT omn ICE Daily Show. Before we jump into today's episode, let's chat about Jane, our show sponsor. Jane makes the Daily Show possible and is the practice management software that so many folks here at ICE utilize. The team at Jane knows how important it is for your patients to get the care they need and with this in mind, they've made it really easy and convenient for patients to book online. One tip that has worked well for a lot of practices is to make the booking button on your website prominent so patients can't miss it. Once clicked, they get redirected to a beautifully branded online booking site and from there, the entire booking process only takes around two minutes. After booking an appointment, patients get access to a secure portal where they can conveniently manage their appointments and payment details, add themselves to a waitlist, opt in to text and email reminders and fill out their intake form. If you all are curious to learn more about online booking with Jane, head over to jane.app slash physical therapy, book their one-on-one demo with a member of their team and if you're sure to use the code ICEPT1MO when you sign up, that gives you a one-month grace period that gets applied to your new account. Thanks everybody.Enjoy today's show. 01:33 CHRISTINA PREVETT Hello everyone and welcome to the PT on ICE Daily Show. My name is Christina Prevett. I am one of the lead faculty in our geriatrics curriculum. So in our geriatrics curriculum, we have three courses in CertMMOA. We have our online eight-week essential foundations course, our online eight-week advanced concepts course and then we have our live course. We are on the road in the summer and into the end of 2023. So our books are closed for 2023. So we have all of the courses that are going to be on the 2023 calendar on the calendar. And so if you are looking to get into one of our courses, know that there isn't going to be an option for something closer until we're kind of booking for 2024. So this weekend, Julie is going to be in Watertown, Connecticut. And then the next weekend, 29th, I guess it will be two weekends, 29th, 30th, I'm in Watkinsville, Georgia. There's still some room in those courses. And so if you guys are interested, just let us know and come hang out with us for all of our geriatric research and all of our geriatric course material. Okay. In today's content, on Monday, I talked about gaps in pelvic health research. So I'm on our pelvic faculty as well. And so today I'm going to take the exact same approach and talk about gaps we see in the geriatric research. I am obviously in full blown research prep mode. I am defending my PhD on resistance training in older adults, at risk older adults at the end of July. So you're going to see me full blown in the research space. And so hence the topic of these podcast episodes. When we are comparing different areas of literature, and we're talking about geriatric rehab in particular, one of the things that I want to start out with is that the state of our research in geriatrics is actually pretty good. You know, we are pretty far ahead when it comes to comparing to other areas. Like when I compare to pelvic health research, there is no comparison. I can off the top of my head bring out 10 studies that have never actually even been done before in our pelvic health research, but I cannot say the same thing in geriatrics. I had to really, pardon me, I had to really think about where I thought our gaps were. And obviously I'm thinking about this around my contribution to the literature with respect to my PhD. So the first thing that I wanted to talk about is the fact that our research is pretty good. You know, we have a lot more in this space and now we're kind of going into the nuance of our rehab and how to translate the research that we do have so that clinicians who are on the front line have access to that research and can really truly embrace evidence informed practice where they are up to date with the evidence that is available. They're taking their clinical expertise, they're taking their patients experience and desires and kind of combining them together. So that's the first thing. So I'm going to be talking about four, three or four different gaps in the research that we have so far and what this means when we are making recommendations or we are thinking about them with respect to our plan of care for our older adults. So the first thing, and I'm on, this is my bias because this is where my PhD was, was we have very few studies that have looked at high load, low repetition weight schemas for resistance training with older adults. We have one that I can think of maybe two studies and the second study is kind of an ish because it had a descending rep scheme where they use less than five repetitions and higher loads. My PhD tried to change that. I did two pilot studies that looked at the safety and feasibility of a three sets of three to five repetition schema at an intensity of seven to eight out of 10. So that high vigorous intensity, high load, low repetition resistance training. And so it's important for us to know this, right? We don't have this research. And when it comes to the way that we work in geriatric literature is that we see what works in our younger or middle aged individuals. Then we push into our healthy older adults and then we push into pathology. Right. This is the story that we saw with high intensity interval training, for example. Right. We saw that it worked in athletic populations. We started pushing the intensity into HIIT training in middle age, healthy older adults. And now the state of the literature, we cannot even deny it because we have evidence for HIIT training in a variety of different pathologies, multimorbidity, obesity, different age groups, et cetera, which is great. We don't have that yet when it comes to geriatric literature in this high load schema. What we see from a muscle physiology perspective is that the magnitude of strength increase tends to bias heavily towards heavier weights. See the one that I did there versus lower weights, higher repetitions. When it comes to individuals who are doing nothing and they start doing something, of course, we're going to see improvements in strength at any set reps. But the magnitude of those differences tends to bias when our loads are heavier. Because we don't have anything in the under five repetition schema, we see this reflected in our exercise guidelines. Right. Why are our exercise guidelines the way they are? Right. Two to three sets, eight to twelve repetitions, 60. Now we're kind of pushing into that 70 to 79 percent of a person's one repetition maximum is the standard exercise prescription that we're seeing out of the American College of Sports Medicine. We saw it in the International Conference for Frality and Sarcopenia Research consensus statement. And this is because that is where the vast majority of the literature goes. And this is where this momentum can build around two to three sets of 10. Right. Because we've always done it this way. There's a good chunk of literature that's there and we don't have anything on the flanks. Right. We don't have anything in under five. We don't have a ton in the 20 plus. And when we get into the higher repetition ranges, now we have this interference that can happen between cardiovascular fitness and neuromuscular fatigue. And which one is the one that's breaking down first or is the limiting factor? All of this to say. When we don't have those discrepancies, we have to be mindful, one, about the strength of our recommendations, but number two, we have to be pushing towards trying to get studies that evaluate this type of loading schema so that we can take a big picture view and then really start to look at dose response data. So that's number one is that we don't really have a ton of studies that look at repetitions less than five and kind of my one B is that this influences things like our exercise guidelines and not in a good or bad way, just a we have to use what's available. And that's why things are the way that they are. The second one is going to kind of be a blend of pelvic health because we in advanced concepts, we go through in week five urinary incontinence and pelvic health issues and geriatrics. And I've talked about this a bunch on the podcast before. But we have very little evidence that's looking at conservative management of pelvic floor dysfunction for individuals over the age of 65. And we have almost nothing when we look at individuals over 75 or 80. Urinary incontinence is one of the leading causes of institutionalization. So where individuals need a higher level of care, end up in assisted living, end up in institutionalized setting is because of issues with urinary incontinence. That should be justification enough that that we need studies in this area and kind of this one B or two B to C type of step down is we don't really have a ton on pelvic floor muscle training in older adults. We have some. It's not a ton. Oftentimes, our older adults are giving are given medications that influence their urine flow rate, whether that's directly with medications being given to work towards helping with kidney function or things that are given as a consequence of having urinary incontinence that change urinary flow and urinary output. A big example that has nothing to do with either of those things, but is actually a side effect because this is the second classification is individuals are given a medication for one issue and side effects relate to urinary incontinence or other pelvic floor dysfunctions is Lasix or diuretics. Individuals who are on diuretics can have horrible, horrible problems with urinary urgency and urinary incontinence or both. And it has a huge impact on their quality of life. And right now, the only research we have is that it negatively impacts their quality of life. And the next step is to try and figure out what to do about it or what can we do about it conservatively? Can we change medication timing? Can we work on different things? Can we work on urge suppression techniques? Is that going to be relevant because urine outflow is higher because of the water pill? There are so many questions, but we have nothing like we have zero studies that have looked at how to help our clients with urinary urgency or urinary incontinence as a consequence of their medication regimens. This is important because the thing that happens is that people stop taking their meds because they literally cannot go out of their house or cannot be too far from a bathroom without not taking their pill. Because if they're on their pill, they're going to the bathroom all of the time for the five to six hours post taking their medication. And so this can essentially make a person homebound. That is important, right? In PT, that's a super big thing. In OT, it's a super big thing. In rehab in general, we are trying to discharge homebound status. And this is a big influence of that. Kind of in this urinary incontinence vein for the elderly, for our older adults, you know, we have conservative management in general. We have men management in combination with conservative management when there is a medical side effect because of the medication a person is on. And then the third one is some of the issues that we see post catheterization. So individuals who are placed with an indwelling catheter and then are removed from that get into this situation where they are in bed, they go to the bathroom whenever they need to because the catheter is there. And then once the catheter has been removed, sometimes there can be a disruption of pelvic floor musculature. There can potentially be damage to the urethral structures. And then you also have to try and work on those urge suppression techniques so that now you're not just going to the bathroom whenever you get the slightest urge to go to the bathroom, but you're holding it in order to go to the bathroom when it's convenient for your schedule or when you have the block of time within your day that you can go to the bathroom. We are now also seeing different types of catheters like periwicks, which are external catheters. And what do those do? All of these things that we're seeing hugely in acute care, we're seeing it in, you know, individuals going into home health. This kind of goes into neurological populations who may be doing self catheterization. All of these things and the role of rehab in managing these conditions to improve a person's function and quality of life really has been understudied and a big low hanging fruit that we could potentially be having huge impacts and potentially preventing transitions to institutionalized care is by being able to tackle some of these problems. But we need the research to back us up first. So that's number two and two A and two B. And then the third one that we're going to talk about, and I think this one is a frustration point for a lot of our clinicians, is clinically relevant outcome measures for our wheelchair users. So we have a ton of outcome measures in the geriatric space. One of the things that I think is actually really cool is that in our rehab space, our geriatric outcome measures are very strong. We have we have several options. We have good cutoff scores. We have reliability and validity data. We have minimally clinically important differences. All of these things. We have standardized protocols. We have different MCIDs, different reliability and validity data across different settings, which makes sense because our older adult population is extremely heterogeneous. All of that is good. You know, that is great. We touch on that a lot in MMOA about how we want to be leveraging our outcome measures and not just for the sake of doing outcome measures, but in order to guide our clinical reasoning and create risk stratification, which is what they're intended for. The problem becomes when we have a client who spends a good portion of their day in sitting. When it comes to our outcome measures, we have this Goldilocks type of scenario that we need to be mindful of. We are going to have a cohort of individuals who are going to experience a floor effect and a person who is a wheelchair user on a 30 second sit to stand test is a very good example of that. They are going to get zero and they are probably always going to get zero. And therefore using a 30 second sit to stand test for a person who spends the majority of their day in a wheelchair is not helpful. We also see that we're going to have some older adults who are going to have this ceiling effect where they are going to knock it out of the park and we're not getting any information. When I was working predominantly in outpatient, one of the first things that I would ask my older adults who walked in independently into my clinic was can you stand on one leg? I was not going to be wasting 15 minutes of my time doing a Berg on those individuals because it's a waste of their time. It's a waste of my time and it doesn't tell me anything. And so we have to kind of figure out we want this composite, we want these tools in our toolbox that we can pull and leverage based on our clinical impression after a person's subjective. But when we have individuals who are sitting, we have very, very few outcome measures. We have the function in sitting test, we have stuff like the FIM. We can maybe start using the Berg and look at some of their transfers, but our pool to try and fit this Goldilocks scenario is quite limited. And so we really do need to think about clinically relevant outcome measures for things like transfers or bed mobility or things that are relevant for them. And these things are starting to come out. We have some pilot research on different outcome measures. But what we try and leverage now with an MMOA is trying to get objective data for things like transfers. And what that can look like is instead of giving MinMondax assist, which is important, we're going to do that based on our clinical judgment, but also put a timer on it. And so if we can put a timer on it, then we can see the first time we did this sitting at the edge of the bed transfer, it took us five minutes from start to finish. And now it's taking you 30 seconds. Like that's a huge improvement or it's taking three minutes. That changes the flow of a person's day. It helps the caregiver a ton. It makes individuals feel more capable who are trying to help their caregivers with their care. And so we also need the research to back us up with that. And we need help to try and figure out how we can justify our rehab for individuals in sitting. If we can't use the outcome measures that are so commonly prescribed in different settings to try and see improvements over time. And we can make huge improvements in a person's function and a person's capacity who may not have the potential to get into standing and do more standing tasks, but still has an infinite amount of potential to improve their quality of life and the things that they're doing throughout their day. So those are kind of my big three areas in geriatric practice that I think we need to be focusing on that rep dose response data in resistance training, where we're looking at load under five repetitions and seeing, does that have any improvements or the magnitude of that improvement in strength with, with a direct influence on a person's physical function? When it comes to pelvic floor in the older adult space, we have a lot of work to do when it comes to just conservative management in general in our individuals over 75, anything with response to medication management, symptoms, side effect profiles of medications and their influence on the pelvic floor. And then post catheterization work, whether that's indwelling or external catheterization and what that does to things like urgent continents. And then our third is helping our individuals who are spending most of their day in sitting. How do we help our wheelchair users so that we can justify our care, have normative data and reliability and validity data of outcome measures to be able to speak to our insurance providers who are, you know, a lot of times we're trying to justify our treatment interventions and then make sure that we know when we're making clinically relevant changes in their quality of life, when the goal of getting them in standing is not the one that we're looking at. All right. I hope you found that helpful. If you have any other questions, just let me know. I'm going to be in the research space a lot in the next couple of weeks. I might be sick of it by the time I get to the end of the month with my defense. But let me know what your thoughts are. If you have any other questions, if you are not signed up for MMOA digest, that is our every two week newsletter where we bring all of that research to your inbox. So if we see any studies that are coming out that are filling in some of the gaps that we were talking about, you're going to know about it first. If you're signed up for MMOA digest, just head to ptnice.com slash resources. If you're looking for research in general, make sure you are following hump day hustling. All right. Have a great day everyone. And we'll talk soon. 20:07 OUTRO Hey, thanks for tuning into the PT on ice daily show. If you enjoyed this content, head on over to iTunes and leave us a review and be sure to check us out on Facebook and Instagram at the Institute of Clinical Excellence. If you're interested in getting plugged into more ice content on a weekly basis while earning CUs from home, check out our virtual ice online mentorship program at pt on ice.com. While you're there, sign up for our hump day hustling newsletter for a free email every Wednesday morning with our top five research articles and social media posts that we think are worth reading. Head over to pt on ice.com and scroll to the bottom of the page to sign up.
Visit: https://nursing.com/140meds to request your free copy of "140 Must Know Meds" Generic Name Furosemide Trade Name Lasix Indication Edema, hypertension Action Prevents reabsorption of sodium and chloride in the kidneys, increase excretion of water, sodium, chloride, magnesium, potassium Therapeutic Class Diuretics Pharmacologic Class Loop diuretics Nursing Considerations • Use caution with liver disease • May cause hypotension, dry mouth, excessive urination, dehydration, electrolyte abnormalities, metabolic alkalosis • Hypokalemia may lead to increase risk of digoxin toxicity • Monitor renal panel • Use caution with other antihypertensives • Causes arthritic symptoms/do not administer with aminoglycosides due to ototoxicity
Overview John Bruening is from Cleveland and writes a series of pulp fiction for his Flinch press publisher. These are modern books that have that pulp flair. This episode is also a cross-over episode with my Relentless Geekery podcast. The 3rd voice you hear is Alan Baltis, co-host on that podcast. Book YouTube https://youtu.be/1kaa7cO7Jkg Transcript Hey John. Hey, John. Okay, you got your Stephen: mic off? Let's see. Alan: How's that? There we go. John: There we go. Okay. How's the look, how's. Looks fine. I got that sort of shiny thing going on here. That's Alan: true. You got the, a little bit of glare from the window, but it casts your face in John: a heroic, it's a noir kinda thing there. Exactly. Yeah, I had a second. Stephen: All the radiation from his monitor and that's what makes him, John: yeah it's gonna turn me into some kind of a superhero or something. That's what we would hope. Try these, this boy. Okay, there we go. Exactly. These are for like, far away. And this screen is it's like my eyes have reached a point where there's no sweet spot. You just have to like, Stephen: to nerd it up there, my glasses so I had Lasix a couple years ago when I had cataract surgery, and so I can see far away. I can see things just fine, but up close I. Can't see. So I asked them specifically my glasses to tune them for how far away I normally sit to the computer. So these glasses, I can't really read with them, but at the computer it makes everything look perfect. So there's nerding it up. I think John: I followed that. Yes. I just had an high appointment in December. I had a, I had an appointment in December and I'm in the earl They told me early stage cataracts, which really sucks. I'll be 60 at the end of this year and I'm just I'm gonna need eight months. I'm gonna need the eight months between now and December to just get my head around that concept. But yes, yeah, we've Alan: actually talked about that before. I don't have any diagnosis of cataracts yet, but I'm really not looking forward to it because I'm really flinchy Ah-huh. We're gonna bring that in about things going near my eyes. I hate putting in eyedrops. I hate, like, when I get puffed at, when they're doing the they don't do that anymore. Test and stuff like that. It's just Stephen: they're modern now, Alan, they don't do the puff. They have a device. They actually stick on your eye and make everything go watery. Wavy Alan: I do have the new one, but even like that the little thing moving into my field of vision and getting uncomfortably close, I'm, there's. I know we always jump around in our discussions. There was a great book, great Books by Gene Wolf, the Shadow of the torturer books. Remember those? And one of the things they talked about how one of the most base human instincts is to protect your head. Like you, you react to stop an arrow sword, whatever might be coming at you before your thinking. Mine could do it, right? And one of the ways in which somebody gets dispatched is he's got two heads and they, he protects the one but the other one gets killed and that still kills him. So there's a science fiction fantasy reference that even that incredible base human thing of avoiding falling and keeping your temperature and. Protecting your head doesn't work if you're zab bile bro type where you've got two heads anyway, John: guys, I'm gonna go shut my door and hopefully my dog won't gimme one second, I'll be right. Sure. Stephen: Yeah, we're gonna talk Pulp Fiction. Hey, we got five minutes left, so let's mention Pulp Fiction a bit. That's how Alan: it goes. I really, I actually did, make some notes to try to get, I made notes as to good questions to ask and stuff. Here we go. Stephen: Here we go. Don't ruin things now. Good questions. Oh man, John, so John: we started yet, what are we doing here? Yeah, Stephen: we kinda roll and we,
When we released our Patreon subscriber exclusive episode a few months ago and asked our listeners what veterinary questions they wanted to have answered - there were countless questions about bleeding and Lasix usage. We decided to have an entire podcast focused on that topic alone for all of our listeners and here it is! Dr. Melissa Fenn is an internal medicine specialist at Littleton Equine Medical Center and we have personally had horses go through her treatment and knew she was the perfect person to discuss this topic with. Around the barn its called bleeding, but Exercise Induced Pulmonary Hemorrhage is a battle most barrel racers deal with and it's a hot topic on the best way to manage, treat and prevent it. We value and appreciate Dr. Fenn's time and sharing her knowledge with us on this episode and hope you learn as much as we did. As always with these types of episodes, our goal is to share education on the topic but please always refer to your veterinarian for treatment for your horses.
Spencer and Clay go over 3 races from this past Saturday at Oaklawn Park those races are 8-10-11 and some angles they talk about are Lasix on/off for stakes races and why its so important to have a fit horse with no layoff lines at Oaklawn
This week Alex and Mary discuss what it's like to travel with a chronic illness. They share tips for their preparation and planning for their upcoming trip to Germany. Listen on our website, www.downthereaware.com/podcast, or wherever you get your podcasts. #Podcast #Spotify #Anchor #research #advocacy #travel #Germany #medications #preparations #chronicillness #compressionsocks #Lasix #mobility #blood sugar #hcm #diabetes Stay Connected Email Us: downthereaware@gmail.com Instagram:@downthereaware Facebook: Down There Aware Twitter: @downthereaware Pinterest: Down There Aware TikTok: Down There Aware Episode Highlights Intro [0:13] Welcome Back! [1:24] Chronic illness travel prep [4:50] Checking in with the cardiologist [5:20] Compression socks [6:05] Lasix and frequent bathroom breaks [6:55] Restroom accessibility in Europe [8:00] Refrigerated medications [8:48] Upgraded to lie-flat accommodations [10:30] Mobility on airplane [11:45] Snacks to control blood sugar [12:22] Medications in carry-on luggage [12:55] Organization [14:10] Sadie Mae and Uncle Will [15:12] In USA docs limited in out of state RXs [15:45] Alex's travel packets [16:55] Shout out to Steve and Victoria [17:21] Dress for destination weather [17:55] Menstruating on a long trip [19:05] Flight Attendant requests, if needed [19:55] Atlanta airport [21:10] Think ahead [22:28] “Give yourself grace.” [22:42] Pace out the itinerary [23:40] 5-week series [23:54] Sadie Mae joins us [25:03] Thanks for listening! [25:39] Summary Keywords Podcast, Spotify, Anchor, research, travel, Germany, medications, preparations, chronic illness, compression socks, Lasix, mobility, blood sugar, HCM, diabetes --- Send in a voice message: https://anchor.fm/downthereaware/message
Show Notes: 00:00 If dogs can stretch in public, so should humans! 04:16 Crazy rain in California and eating Chipotle. 05:51 Mag scores BIG at the Rose Bowl Flea Market. 11:06 Unintended repercussions of Dan's comment response. 12:58 Dan and Shay learn about Chat GPT at Speakers Roundtable. 20:00 Maggie's stress about upcoming Lasix. 22:48 The cool new sweater that looks like a bathmat. 24:10 Pre-recording a speech. 25:16 Falling asleep during conversations. 27:34 Maggie's technique for stretching at a stop light. 31:00 Dan's technique for adjusting your back with a sneeze. 32:00 Shay watching “Emily in Paris” to deal with Europe withdrawal. 33:39 Writing in the style of Play Dough. 35:27 Obligatory pickleball shoutout.
Welcome to another episode of Past the Wire's podcast Gate to Wire.Bleeding in racehorses. What exactly is it and what causes it? Is Lasix the answer or the problem? Do other countries ban Lasix as is widespread believed. Do Horses bleed more today than in the past? Michael Wilson and Jonathan Stettin delve into this topic as well as the Jason Servis guilty plea and what it means to racing going forward.Last but certainly not least, we talk JJ Graci and his recent passing. JJ Graci had tremendous passion for the sport we love in addition to quite the resume.
Julie's beautiful mother, Stephanie, was murdered by a Washington State Hospital in December of 2021. Upon admission, the hospital confiscated her Ivermectin and vitamins. And then refused to give her food and water for NINE (9) DAYS and continuously turned up her oxygen higher and higher when she refused to be intubated, causing damage to her lungs. After starving and dehydrating her for over a week, the hospital then filled her so full of IV fluids that they put on 30+ pounds of water weight and refused to give Lasix to help take the water weight off.Julie was not going to let her mom die at the hospital--she did not want them to receive their federal Covid monies for killing her mom. So she demanded that she be discharged AMA (against medical advice). Stephanie passed away at home shortly after she was discharged. Her death certificate stated that Stephanie passed away at the hospital which was a fraud.Support Ask The Nurses Podcasthttps://www.patreon.com/AskTheNursesPodcastSupport the show
Host: Dr. Ritika Kompella, Internal Medicine PGY-2, UCONN Guest Speaker: Dr. Erika Faircloth, former Chief Medical Resident at UCONN and a second-year cardiology fellow at Hartford Hospital Editor: Dr. Alla Turshudzhyan, Chief Medical Resident at UCONN This week, let's discuss heart failure, its' etiologies, and approaches to management. More on cardiology to come... stay tuned. Thank you for listening.
In this episode, we talk all things critical care the one and only, Dr. Jean-Louis Vincent aka. JLV. This episode is a MUST listen. We touch upon the evolution of early goal directed therapy, measures of fluid responsiveness, optimizing oxygen delivery, and the importance of integrating data points versus examining them in isolation when caring for our critically ill and injured patients. This and MUCH MUCH more in arguably one of my favorite episodes to date!!Timestamps00:00 Introduction01:21 What happened to SG catheters and should we use them?04:05 What decreases mortality in critical care patients?05:30 When to transfuse critical care patient? Use your brain! 08:55 Measures of tissue perfusion and fluid responsiveness09:36 JLV breaks down the Rivers trial10:36 Recent EGDT papers 10:54 How to optimize O2 delivery? Late ScVO2, dob challenge, and fluid challenges13:21 Dynamic measures of fluid responsiveness13:46 CVP as a relative value15:14 Passive leg raising (PLR) as a measure of fluid responsiveness21:20 JLV's take on therapeutic nihilism24:45 Don't isolate; integrate!26:46 Navigating the future of critical care – JLV's thoughts on AI in the ICU29:55 Rapid fire hot topics in the ICU – Yes or No -Metabolic cocktail-Corticosteroids for septic shock-Albumin and Lasix or Lasix alonePCT/CRP and sepsis/AbxResources:International Symposium on Intensive Care and Emergency Medicine (ISICEM):https://www.isicem.orgISICEM Chats Platform:https://www.isicem.org/e-chat/index.asp Articles:Passive leg raising:five rules, not a drop of fluid! https://ccforum.biomedcentral.com/articles/10.1186/s13054-014-0708-5The fluid challengehttps://ccforum.biomedcentral.com/articles/10.1186/s13054-020-03443-yBlood lactate levels in sepsis: 8 questionsVincent JL, Bakker J. Blood lactate levels in sepsis: in 8 questions. Curr Opin Crit Care. 2021 Jun 1;27(3):298-302. doi: 10.1097/MCC.0000000000000824. PMID: 33852499.We should avoid the term "fluid overload"https://ccforum.biomedcentral.com/articles/10.1186/s13054-018-2141-7EGDT in the Treatment of Severe Sepsis and Septic Shockhttps://www.nejm.org/doi/full/10.1056/nejmoa010307A Randomized Trial of Protocol-Based Care for Early Septic Shockhttps://www.nejm.org/doi/full/10.1056/nejmoa1401602Support the show
Download the cheat: https://bit.ly/50-meds View the lesson: https://bit.ly/FurosemideLasixNursingConsiderations Generic Name Furosemide Trade Name Lasix Indication Edema, hypertension Action Prevents reabsorption of sodium and chloride in the kidneys, increase excretion of water, sodium, chloride, magnesium, potassium Therapeutic Class Diuretics Pharmacologic Class Loop diuretics Nursing Considerations • Use caution with liver disease • May cause hypotension, dry mouth, excessive urination, dehydration, electrolyte abnormalities, metabolic alkalosis • Hypokalemia may lead to increase risk of digoxin toxicity • Monitor renal panel • Use caution with other antihypertensives • Causes arthritic symptoms/do not administer with aminoglycosides due to ototoxicity
This week, please join authors John McMurray and David Cherney, editorialist Kausik Umanath, as well as Associate Editors Ian Neeland and Brendan Everett as they discuss the original research articles "Initial Decline (Dip) in Estimated Glomerular Filtration Rate After Initiation of Dapagliflozin in Patients With Heart Failure and Reduced Ejection Fraction: Insights from DAPA-HF" and "Renal and Vascular Effects of Combined SGLT2 and Angiotensin-Converting Enzyme Inhibition" and editorial ""Dip" in eGFR: Stay the Course With SGLT-2 Inhibition." Dr. Carolyn Lam: Welcome to Circulation On the Run, your weekly podcast summary and backstage pass to the Journal and its editors. We're your co-hosts, I'm Dr. Carolyn Lam, Associate Editor from the National Heart Centre and Duke National University of Singapore. Dr. Greg Hundley: I'm Dr. Greg Hundley, Associate Editor and director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam: Greg, it's the season of double features. Except this time, we're having a forum discussion of two related articles and an editorial that discusses both. What is it on? SGLT2 inhibitors. In the first paper, an analysis from the DAPA-HF trial, looking specifically at that initial dip in GFR that follows initiation of dapagliflozin in patients with HFrEF. Then we will discuss further, in a mechanistic way, the renal and vascular effects of combining SGLT2 inhibition on top of ACE inhibition. Lots and lots of good learning and insights, but let's go on first to the other papers in today's issue. Shall we? Dr. Greg Hundley: You bet, Carolyn, and I'm going to grab a cup of coffee. Carolyn, in this issue, wow, so many exciting original articles. In fact, there are two more articles that were going to pair together, both clinical and pertaining to TAVR procedures. In the first one, it was a group of authors led by Dr. Duk-Woo Park from the Asan Medical Center at the University of Ulsan College of Medicine. They conducted a multicenter, open-label randomized trial comparing edoxaban with dual antiplatelet therapy or DAPT, aspirin plus clopidogrel, in patients who had undergone successful TAVR and did not have an indication for anticoagulation. Now in this study, Carolyn, the primary endpoint was an incidence of leaflet thrombosis on four-dimensional computed tomography, CT, performed at six months after the TAVR procedure. Key secondary endpoints were the number and volume of new cerebral lesions on brain magnetic resonance imaging or MRI and the serial changes of neurological and neurocognitive function between six months and that time immediately post the TAVR procedure. Dr. Carolyn Lam: Oh, interesting. What did they find? Dr. Greg Hundley: Right, Carolyn. In patients without an indication for long-term anticoagulation after successful TAVR, the incidence of leaflet thrombosis was numerically lower with edoxaban than with dual antiplatelet therapy, but this was not statistically significant. The effect on new cerebral thromboembolism and neurological or neurocognitive function were also not different between the two groups. Now because the study was underpowered, the results should be considered really as hypothesis generating, but do highlight the need for further research. Dr. Greg Hundley: Carolyn, there's a second paper pertaining to transcatheter aortic valve prosthesis. It's led by a group directed by Dr. Paul Sorajja from the Minneapolis Heart Institute Foundation and Abbott Northwestern Hospital. Carolyn, these authors prospectively examined 565 patients with cardiac CT screening for HALT, or what we would define as hypoattenuating leaflet thickening, at 30 days following balloon-expandable and self-expanding TAVR. Now, deformation of the TAVR prosthesis, asymmetric prosthesis leaflet expansion, prosthesis sinus volumes, and commissural alignment were analyzed on the post-procedural CT. For descriptive purposes, an index of prosthesis deformation was calculated, with values greater than 1 representing relative midsegment underexpansion. A time-to-event model was also performed to evaluate the association of HALT with the clinical outcomes. Dr. Carolyn Lam: Oh, interesting. What did they find? Dr. Greg Hundley: Right, Carolyn. Nonuniform expansion of TAVR prosthesis resulting in frame deformation, asymmetric leaflet, and smaller neosinus volume was related to the occurrence of HALT in patients who underwent TAVR. What's the take home here, Carolyn? These data may have implications for both prosthesis valve design and deployment techniques to improve clinical outcomes in these patients. Now, Carolyn, both of these articles are accompanied by an editorial from Dr. Raj Makkar from the Smidt Heart Institute at Cedars-Sinai's Medical Center. It's a very lovely piece entitled Missing Pieces of the TAVR Subclinical Leaflet Thrombosis Puzzle. Well, how about we check what else is in this issue? My goodness, this was a packed issue. First, Carolyn, there are three letters to the editor from Professors Ennezat, Dweck, and then a response from Dr. Banovic pertaining to a follow-up from a previously published study, the AVATAR study, in evaluating valve replacement in asymptomatic aortic stenosis. There's also a Perspective piece from Dr. Wells entitled “Treatment of Chronic Hypertension in Pregnancy: Is It Time For A Change?” There's a Global Rounds piece from Professor Berwanger entitled “Cardiovascular Care in Brazil: Current Status, Challenges, and Opportunities.” Then there's also a Research Letter from Professor Eikelboom entitled “Rivaroxaban 2.5 mg Twice Daily Plus Aspirin Reduces Venous Thromboembolism in Patients With Chronic Atherosclerosis.” Dr. Carolyn Lam: There's another Research letter by Dr. Borlaug on longitudinal evolution of cardiac dysfunction in heart failure with normal natriuretic peptide levels. There's also a beautiful Cardiology News piece by Bridget Kuehn on the post-COVID return to play guidelines and how they're evolving. Well, that was a great summary of today's issue. Let's hop on to our feature forum. Shall we? Dr. Greg Hundley: You bet, Carolyn. Can't wait. Dr. Carolyn Lam: Today's feature discussion is actually a forum because we have two feature papers in today's issue. They all surround the cardiorenal interaction, should I say, of the SGLT2 inhibitors. For the first paper, discussing that initial decline or that dip in the GFR following initiation of dapagliflozin would be Dr. John McMurray, who's the corresponding author of this paper from DAPA-HF. Dr. John McMurray's from the University of Glasgow. Now next, we have also the corresponding author of another paper, really going into the mechanistic insights of the renal and vascular effects of combined SGLT2 and ACE inhibition. Dr. David Cherney is from Toronto General Hospital, University of Toronto. Dr. Carolyn Lam: We have the editorial list of these two wonderful papers, Dr. Kausik Umanath from Henry Ford Health in Michigan. Finally, our beloved associate editors, Dr. Ian Neeland from Case Western Reserve and Dr. Brendan Everett from Brigham and Women's Hospital, Harvard Medical School. Thank you, gentlemen. Now with all of that, what an exciting forum we have in front of us. Could I start by asking, of course, the respective authors to talk a little bit about your papers? I think a good place to start would be with Dr. McMurray. John, please. Dr. John McMurray: Thanks, Carolyn. I think our paper had three key messages. The early dip in eGFR that we saw was, on average, very small in patients with heart failure, about 3 mLs/min or about 5%. Very few patients had a large reduction in the eGFR. It was around 3%. Dapagliflozin-treated patients had a 30% or greater decline compared to about 1% of placebo patients. Finally, very few of those patients had a decline in the eGFR below a critical threshold, which for cardiologists might be around 20 mLs/min. We saw that in only five patients; that's 0.2% of the dapagliflozin-treated patients. Second message was that that early decline partially reverses. The nadir in our study was about 14 days. But by 60 days, on average, eGFR had increased again. Hold your nerve if you see an early decline in eGFR. Dr. John McMurray: Maybe the most important message was that that decline in the eGFR is not associated with worse cardiovascular or renal outcomes. In fact, if anything, the opposite. If you look at the patients in the dapagliflozin group with a 10% or greater decline in eGFR, then compare it to patients who didn't have that decline, these individuals were about 27% less likely to experience the primary composite outcome of worsening heart failure and cardiovascular death. If you look at the placebo group, we saw exactly the opposite. Amongst those who had a greater than 10% decline in eGFR compared to those who didn't, those people with the early decline in eGFR were 45% more likely to experience the primary composite endpoint. The same is true for other cardiovascular outcomes for worsening kidney function. In the dapagliflozin group, decline in eGFR was not associated with more adverse events, not associated with more treatment discontinuation. That small decline in the eGFR is not a bad prognostic sign. If anything, it might be the opposite. Dr. Carolyn Lam: Thank you so much. That was really clear. David, are you going to tell us why this decline occurs? Dr. David Cherney: Yeah. Perhaps the paper that we published gives some insights into the mechanisms that are responsible for some of those changes in GFR that are thought to be acute hemodynamic effects. In the between trial, which is the trial that we published examining the effect of ACE inhibition followed by SGLT2 inhibition in patients with type 1 diabetes, we also saw that there was an expected effect of adding SGLT2 inhibition on top of an ACE inhibitor in people with uncomplicated type 1 diabetes. This acute dip in GFR was seen in this cohort of patients. We included only 30 patients in this small mechanistic study. At the same time, along with that dip in GFR, we also saw an increase in measures of proximal natriuresis. That proximal sodium loss is linked with changes in sodium handling in the kidney, which then causes changes in both probably afferent and efferent tone, which causes this dip in GFR primarily through natriuresis in this phenomenon called tubuloglomerular feedback. That was one major observation that gives insight into what we see in larger trials around the dip in GFR. Dr. David Cherney: In our mechanistic study, we also saw an additive effect on blood pressure. Blood pressure went down further with the addition of empagliflozin on top of an ACE inhibitor. In terms of the mechanisms that are responsible for the reduction in blood pressure, natriuresis certainly may be in part responsible, but we also saw a novel observation whereby there was a reduction in peripheral vascular resistance using noninvasive measures. There are likely several mechanisms that are responsible for the reduction in blood pressure. Then finally, we also saw reductions in markers of oxidative stress, which may also account for some of the effects that we see in blood pressure, as well as potentially some of the anti-inflammatory and anti-fibrotic effects that we see at least in experimental models that may have some clinical translatability to humans as well around the clinical benefits. I think the blood pressure, the renal hemodynamic effects, and some of the neurohormonal mechanisms are the major observations that we saw that may in part explain some of the really nice changes that were seen in Dr. McMurray's study. Dr. Carolyn Lam: Right. Thanks, David. But these were patients with type 1 diabetes and no heart failure. John, do you have any reflections or questions about how that may apply? By the way, what a beautiful study. Thank you, David. Dr. David Cherney: Pleasure. Thank you. Dr. John McMurray: Yes, David. I really enjoyed your study. In fact, I think, Carolyn, it does shed some insights perhaps to what's going on. As David pointed out, the reduction in peripheral arterial resistance, reduction in blood pressure, that may play some role in that early dip in eGFR as well as autoregulation in the kidney. Then the other interesting thing is that the distal nephron seems to adapt to that effect in the proximal tubule. Again, that may account for some of that recovery in eGFR, that reversal in the early dip that I spoke about, and which I think is very clinically important because, of course, physicians should make sure that they recheck eGFR if they see that early dip. Because they may find that few weeks later that that dip is much smaller and of much less concern. Dr. Carolyn Lam: Thank you, John. In fact, you're saying, stay the course, right- Dr. John McMurray: I have. Dr. Carolyn Lam: ... with the SGLT2 inhibitors. I'm actually stealing the words of the title of the editorial, a beautiful editorial by Kausik. I love that. Stay the course. Kausik, please, could you frame both papers and then with an important clinical take home message for our audience? Dr. Kausik Umanath: Sure. I think the analysis by John and his group was really relevant with the large sample size. What's impressive? Similar to a lot of these other SGLT2 studies that have come out, both in heart failure and in kidney disease progression and so on, it's remarkable how the other analysis, like the analysis of EMPA-REG and CREDENCE and so on, of similar dips. All show more or less the same magnitude, the same relative proportions of this GFR trajectory. I think the mechanistic study only highlights that though it's working with a slightly different population of type 1 patients and much earlier in their course in terms of where their GFRs are. Dr. Kausik Umanath: The other piece is that ultimately we need to understand this dip and know to monitor for it and so on. But I think the general clinician should really understand that a dip of greater than 10% really occurs in less than half the population that takes these agents. That dip, if it occurs, certainly doesn't do any harm. That said, if they see a bigger dip in the 30% range, monitor more closely and consider making sure that there aren't any other renal issues out there for that patient because they are a much smaller proportion of patients in these large trials that generate that level of dip. They should be monitored. Dr. Kausik Umanath: The other thought that we had, and thinking through this in a practical sense, is because you expect this dip, many of our cardiologists or even the nephrologists when we titrate these drugs, they're on a suite of other drugs. It's probably best to not adjust their Lasix or their loop diuretic, or their RAAS inhibitor at the same time as you're adjusting the SGLT2 inhibitor or starting it because then you may just introduce more noise into the GFR changes that you see over the next several weeks. It may be a sequential piece or at least holding those other agents constant while this gets titrated and introduced is a prudent course of action, so you don't misattribute changes. Dr. Carolyn Lam: Thanks so much. What clinically relevant points. In fact, that point about the diuretic especially applies in our heart failure world. You see the dip. Well, first, make sure the patient's not overdiuresed. Remember, there's more that the patient's taking. Thank you. That was a really great point. Brendan and Ian, I have to get you guys to share your views and questions right now. But before that, can I take a pause with you and just say, aren't you just so proud to be AEs of Circulation when we see papers like these and we just realize how incredible the data are and the clinical implications are? I just really had to say that. All right. But with that, please, what are your thoughts, Brendan? Dr. Brendan Everett: Yeah, sure. Thank you, Carolyn. Hats off to all three of our authors today for doing some amazing science. Thank you for sending it to Circulation. I think, in particular, I handled David's paper. I'm not a nephrologist and I'm probably the furthest thing from a nephrologist. Had to do my best to try and understand these concepts that I'm not sure I ever even was exposed to in medical school many years ago. I think it shows the breadth of the interest in our readership. The fact that these changes in eGFR have become a primary focus for our cardiovascular patients and that the clinical implications are really important. I guess my question, David, is... In your paper, you talked a little bit about this hypothesis of hyperfiltration and the role that hyperfiltration plays in setting patients with diabetes up for kidney disease. Is that playing a role in John's observation or not? Again, as a non-nephrologist, I have trouble connecting the dots in terms of that hypothesis and John's observation of the clinical benefit for patients that have a reduction in eGFR as opposed to no change. Dr. David Cherney: Yeah. It's a great question. It's very difficult to know with certainty in a human cohort because we can't measure the critical parameter, which is intraglomerular pressure, which we think these changes in GFR are a surrogate for. But if we go along with that train of thought, along reductions in glomerular hypertension, it very much makes sense that the patients who dip are those who have the... They're taking their medication, number one. Number two, they respond physiologically in the way that you expect them to, which is that their GFR dips at least transiently and then goes back up again through some of the compensatory mechanisms that John mentioned earlier. As was mentioned not only in this paper, but also in previous analyses from CREDENCE and previous analyses from VERTIS CV and others have shown that indeed that dip in GFR is linked with longer term renal benefits, at least. That is reflected in a reduction in the loss of kidney function over time. Dr. David Cherney: The patients who are on an SGLT2 inhibitor and those who dip by around 10% or less, those patients tend to do the best over time in terms of preserving GFR, not losing kidney function compared to patients who are on an SGLT2 inhibitor but do not dip, or those patients who actually have an increase in GFR. That is consistent with this idea that there may be a reduction in glomerular pressure, which is protective over the long term. That ties back into your question around hyperfiltration that this may indeed be due to a reduction in glomerular pressure, which is linked with risk over the long term. Dr. Carolyn Lam: Ian? Dr. Ian Neeland: I wanted to echo Brendan's comments about the excellent science. When I read these papers, it really speaks to the existential struggle that cardiologists have between kidney function and these medications that we know have cardiovascular benefits. How do we manage that practically? It's so clinically relevant, both the observation that John's paper made about the dip in the DAPA-HF trial as well as, David, your mechanistic insights. Dr. Ian Neeland: I wanted to ask John potentially about the most fascinating aspect to me of this paper was that patients with a dip of 10% or more actually ended up doing better in terms of cardiovascular outcomes, specifically hospital heart failure and hospitalizations than people on placebo with a greater than 10% dip. It speaks to the fact that... Is the physiology going on here different between those individuals whose GFR went down on placebo versus those who are on SGLT2 inhibitors? All the mechanistic insight that David's paper had in terms of blood pressure and intraglomerular pressure, how does that feedback and speak to why heart failure is strongly linked to this mechanism? We see this not just with SGLT2 inhibitors, but there are other medications now coming out showing that there's a relationship between this dip in GFR and heart failure. Can you speak to why this heart failure-kidney connection is so important and becoming greater and greater in terms of our understanding? Dr. John McMurray: Well, thank you for asking me the hardest question and one that I truly don't think I have a good answer to. I think it's obvious to all of us that the kidney is central in heart failure and perhaps cardiologists have neglected that fact, focusing more on the other organ. But by definition, almost the fluid retention that characterizes heart failure in terms of signs, and probably is the primary cause of symptoms, that clearly is a renally-mediated phenomenon. The kidney must be central to all of this. I think David right. I think the decline in eGFR that you see with this drug is simply a marker that the drug is having its physiological effect or effects. Whatever those are, they're beneficial. Clearly, patients who have an eGFR decline on placebo are different and they reflect, again, the patients that we see all the time. As our patients with heart failure deteriorate, one of the things that we commonly see, in fact becomes one of the biggest problems that we have to deal with, is that their kidney function declines. As their symptoms get worse, as their cardiac function gets worse, their kidney function also declines. Dr. John McMurray: I think you're seeing two contrasting effects here. One is the background change in eGFR, which is the placebo patients, and we've always known that that's a bad thing. Then we're seeing that early within 14 days marker of the pharmacological or physiological action of the drug. I hope you don't ask me how SGLT2 inhibitors work in heart failure. That's the other most difficult question I can think of, but I think this is just a marker of the fact that they are working. Dr. David Cherney: Yeah. Just to add to that briefly, there is this difficulty in sorting out the mechanisms that are relevant around the acute effects in the kidney that the dip in GFR reflects natriuresis that could keep patients out of heart failure; that the reduction in glomerular pressure reduces albuminuria. Albuminuria reduction is linked with kidney protection. It's linked with heart failure and ASCVD protection. Then there's also this concept of if you dip and then you stay stable afterwards, your GFR stays stable afterwards, those patients with stable kidney function that's not declining, the dippers in other words, those patients are probably able to maintain salt and water homeostasis better than someone who's declining more rapidly. All these things probably tie together in order to reflect, of course, there's a renal protective effect, but that some of those mechanisms may also tie into the heart failure mechanisms that John was mentioning. Dr. John McMurray: But, David, it's hard to imagine if we don't protect the kidney, we won't protect patients with heart failure given how fundamental, as I said, the kidney is, and how fundamentally important worsening kidney function is. Not only because it is a marker of things going badly, but also because it often results in discontinuation or reduction in dose of other life-saving treatments. To Kausik's point, it was very important about the risk of changing background life-saving disease modifying therapy. Actually, we didn't see that in DAPA-HF, which was very intriguing. There was no reduction in use of renin-angiotensin system blockers or mineralocorticoid receptor antagonists. Dr. Carolyn Lam: Thank you so much, gentlemen. Unfortunately, we are running out of time, but I would really like to ask one last question to the guests, if possible. Where do you think the field is heading? What next? What's the next most important thing we need to know? David, do you want to start? Then John, then Kausik. Dr. David Cherney: I think one of the aspects that we need to know in the future is where else can we extend these therapies into novel indications and extend the boundaries of where we currently work with these therapies. People with type 1 diabetes, for example, with either heart failure or with significant kidney disease, patients with kidney transplantation, is there a renal or cardiovascular protective effect? Then another high risk cohorts who have not been included in trials, those on immunosuppressants, for example, who were excluded from the trials. I think those are some of the areas that we need to extend into now that we understand how these therapies work in even very sick patients and that we also know that they likely have at least some benefit through suppressing inflammation, and possibly reducing infectious risks. That would provide a rationale for extending into some of these new areas. I think that's certainly, hopefully on the horizon for us. Dr. Carolyn Lam: John? Dr. John McMurray: Carolyn, obviously I think looking at post myocardial infarction population, that's an obvious place to go. There are a couple of trials there. I suppose the trial that I would love to see, and which I think would address the core question that we've been discussing today, which is: Is this all about the effect in the kidney and how important is the diuretic and natriuretic action of these drugs in heart failure? I think the key study that would address this would be doing a study in patients on dialysis. Because in those patients we could, I think, separate the issue of natriuresis, diuresis, and maybe even the dip in EGR that we've been talking about. If these drugs prove to be effective in end-stage kidney disease, patients on dialysis, that would be really fascinating. Dr. Carolyn Lam: Kausik? Dr. Kausik Umanath: That is a very interesting point. I don't know that we know necessarily outcomes, but I think from working with the DAPA-CKD, we do have a little bit of the safety data because we did continue it. I was the US MLI for that study and we did continue the SGLT2 passed into renal failure. There is a little bit of safety data there. But I don't think once you've declared an outcome, you're not collecting outcomes data after that point. That's a very interesting area to look into. Dr. Kausik Umanath: I also think the other place where this field's heading is trying to better tier and layer the multitude of agents. I think we've been waiting for about 20 to 30 years, at least in the kidney field, for something new to affect the progression of kidney disease after the ACE/ARB trials and so on. This one we've got SGLT2 inhibitors. We've got the new MRA, finerenone, and so on, which also have very beneficial cardiovascular effects. The question becomes: How do we layer these therapies? Which sequence to go in? Some of the others that are in pipeline as well that are out there that have very beneficial cardiovascular effects that may indeed also help kidney function and diabetes control, which do you go with first and so on? Dr. Carolyn Lam: Wow! Thank you so much. We really could go on forever on this topic, but it has been tremendous. Thank you once again. On behalf of Brendan, Ian, Greg, thank you so much for joining us today in the audience. You've been listening to Circulation On the Run. Don't forget to tune in again next week. Dr. Greg Hundley: 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, please visit ahajournals.org.
Alien prisoners Corporal Sergeant Aloysius Beauregard Abernathy (@necrobranson), Lasix (@intellegint), and Shakespeare (@charlesraustin) discuss their captivity and their pasts. E1 on Patreon: https://www.patreon.com/e1podcast
Alien prisoners Corporal Sergeant Aloysius Beauregard Abernathy (@necrobranson), Lasix (@intellegint), and Shakespeare (@charlesraustin) discuss their captivity and their pasts. E1 on Patreon: https://www.patreon.com/e1podcast
This week, please join author Ratika Parkash and Editorialist Sean D. Pokorney as they discuss the article "Randomized Ablation-Based Rhythm-Control Versus Rate-Control Trial in Patients with Heart Failure and Atrial Fibrillation: Results from the RAFT-AF trial" and the editorial "The Evidence Builds for Catheter Ablation for Atrial Fibrillation and Heart Failure." Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the Journal and its editors. We're your co-hosts. I'm Dr. Carolyn Lam, Associate Editor, from the National Heart Centre and Duke National University of Singapore. Dr. Greg Hundley: And I'm Dr. Greg Hundley, Associate Editor, Director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Well, Carolyn, this week's feature discussion, oh, so exciting. We enter the month of June, and it pertains to heart failure and atrial fibrillation. And we are going to learn a little bit more from the RAFT-AF trial, involving randomizing patients to ablation and rhythm control, as opposed to just settling for rate control for patients with AFib. But before we do that, how about we grab a cup of coffee and start with some of the other articles in the issue? Would you like to go first? Dr. Carolyn Lam: I absolutely would. And I will start by asking everyone a question. Could a single high-sensitivity cardiac troponin T level, below the limit of detection of six nanograms per liter, exclude an acute myocardial infarction? Well, you are going to find out because, remember that data for excluding AMI with a single high-sensitivity cardiac troponin level relies largely on the limit of detection, which is really a threshold of five nanograms per liter, which cannot be reported in the United States, per the FDA, because there, only the lowest reportable concentration is allowed, which is the limit of quantitation of six nanograms per liter. Dr. Carolyn Lam: So, today's authors Dr. Sandoval from Mayo Clinic and colleagues, very cleverly sought to determine whether a single high-sensitivity cardiac troponin T level below the limit of quantitation of six nanograms per liter could indeed identify patients at low risk for AMI. Dr. Greg Hundley: Very interesting, Carolyn. So we have the limit of quantitation and then the limit of detection. This is really intriguing. And of course, cardiac troponin T, as cardiologists, we receive a lot of requests for consults on this. So, what did this study find, Carolyn? Dr. Carolyn Lam: A total of over 85,000 patients were first evaluated in the CV data marked biomarker cohort, amongst which 29% had a baseline high-sensitivity cardiac troponin T level below this limit of quantitation of six nanograms per liter. Among 11,962 patients with this baseline high-sensitivity cardiac troponin below six nanogram per liter and serial measurements, only 1.2% developed acute myocardial injury, resulting in a negative predictive value of 98.8% and a sensitivity of 99.6%. Dr. Carolyn Lam: In an adjudicated cohort, among those with a non-ischemic electrocardiogram, only 0.2% had myocardial infarction or death at 30 days. So in summary, Greg, this is the largest study evaluating a single high-sensitivity cardiac troponin T level below this limit of quantitation of six nanograms per liter to identify patients at low risk for AMI. Dr. Carolyn Lam: And indeed, the present study demonstrates that a single high-sensitivity cardiac troponin level below six nanogram per litter is a safe and rapid method to identify a substantial number of patients at very low risk for acute myocardial injury and infarction. Dr. Greg Hundley: Oh wow, Carolyn, really informative study. Well, Carolyn, my next study comes from the world of preclinical science. And Carolyn, vascular smooth muscle cell phenotypic switching contributes to cardiovascular diseases. And epigenetic regulation is emerging as a key regulatory mechanism with the methylcytosine dioxygenase Tet2, acting as a master regulator of the smooth muscle cell phenotype. Dr. Greg Hundley: The histone acetyltransferases, HATs p300, and CBP are highly homologous and often considered to be interchangeable. And their roles in smooth muscle cell phenotypic regulation are not known. So Carolyn, these authors led by Dr. Kathleen Martin from Yale University School of Medicine assessed the roles of p300 and CBP in human vascular smooth muscle cells with knockdown in inducible, smooth muscle specific knockout mice, and in samples of human intimal hyperplasia. Dr. Carolyn Lam: Cool, Greg. So what did they find? Dr. Greg Hundley: Right, Carolyn. So, they found that p300 and CBP serve non-redundant and opposing function in vascular smooth muscle cell phenotypic switching and coordinately regulate chromatin modifications through distinct functional interactions with Tet2 or HDACs. And Carolyn, targeting specific histone acetyltransferases therefore may hold therapeutic promise for future cardiovascular disease interventions. Dr. Carolyn Lam: Oh, that's great, Greg. Well, to round it all up, there are some other papers in today's issue. There's a Research Letter from Professor Zhang, entitled “Single Nucleus Transcriptomics: Apical Resection in Newborn Pigs Extends the Time-Window of Cardiomyocyte Proliferation and Myocardial Regeneration.” There's also a Research Letter from Dr. Vaduganathan, entitled “Estimating the Benefits of Combination Medical Therapy in Heart Failure with Mildly Reduced and Preserved Ejection Fraction.” Ah, that's such a cool issue. Now, let's go on to our feature discussion. Shall we, Greg? Dr. Greg Hundley: You bet, and learn a little bit more about rhythm versus rate control in patients with heart failure and atrial fibrillation. Dr. Carolyn Lam: Our feature discussion today is about the long-awaited results of the RAFT-AF trial, and that is the randomized ablation-based rhythm control versus rate control trial in patients with heart failure and atrial fibrillation. Thank you so much, Dr. Ratika Parkash for joining us today as the first and corresponding author from Queen Elizabeth II Health Sciences Center in Canada, as well as Dr. Sean Pokorney, the editorialist from Duke University. Dr. Carolyn Lam: I am so, so excited to be discussing this paper. I really meant it. You know, as a heart failure cardiologist, we've been waiting for these results and trying to understand everything in context. So maybe, Ratika, could you please start off by telling us about the RAFT-AF trial and what you found? Dr. Ratika Parkash: Thank you, Carolyn. I'm happy to be able to talk about this study on behalf of the RAFT-AF investigators and my co-PI, Dr. Anthony Tang. So the trial... First of all, the rationale for the study, I think many of us, as heart failure or heart rhythm specialists, understand that in the past, we've done many trials looking at rate versus rhythm control, the AFFIRM trial being the largest, and then of course, specifically in heart failure patients, the AF-CHF trial, both of which were negative in reducing cardiovascular events and mortality in patients with or without heart failure, in terms of a rate to rhythm control. Dr. Ratika Parkash: One of the issues with those trials is that the form of rhythm control was antiarrhythmic drugs. So we have learned that catheter ablation is superior to antiarrhythmic drugs in maintaining sinus rhythm. And based on that premise, we decided to go forward with the RAFT-AF study. Dr. Carolyn Lam: That's great, Ratika, so thanks. And what were the results? Dr. Ratika Parkash: The main finding, so the primary outcome of the study was mortality and heart failure events. Heart failure events was defined as a heart failure hospitalization or any escalation of heart failure therapy that was done in the outpatient settings, including the use of intravenous Lasix in an emergency department setting. Dr. Ratika Parkash: So the main findings were that ablation-based rhythm control was not statistically significant in reducing mortality and heart failure events over rate control in patients with atrial fibrillation and heart failure. The study included patients both with preserved ejection fraction, as well as reduced eject fraction. And we did stratify based on ejection fraction at the entry point into the trial. The hazard ratio was 0.71 and the 95% confidence interval just crossed unity, ranging from 0.49 to 1.03 with a P value of 0.066. Dr. Carolyn Lam: Oh, ouch. So, thank you. And again, truly, congratulations on a very, very important trial. Sean, I said it before, I'll say it again, really, really loved your editorial. Could you put these findings in the context of... Maybe, start with even the most recent guidelines, the 2022 ACC/AHA/HFSA heart failure guidelines, which I believe gives catheter ablation a class 2A recommendation. Maybe, start from there, and how does this fall in place? Dr. Sean Pokorney: Yeah, no, absolutely. I think, first of all, it's a really important trial and it's great to have this additional data. I do think, as you said, that it's important to understand the context. We now have several recent guidelines that have commented on the role of catheter ablation in patients with heart failure. Dr. Sean Pokorney: You mentioned the most recent heart failure guidelines. We also have additional AFib guidelines and we have the 2019 AHA/ACC/HRS guidelines for atrial fibrillation that give catheter ablation a 2B recommendation in patients who have heart failure, to potentially lower mortality and reduce hospitalization. And it has a 2A indication in the 2020 ESC guidelines. And we're currently undergoing some revisions of the guidelines for atrial fibrillation, and there'll be new guidelines around atrial fibrillation coming out from AHA/ACC/HRS in the coming years. And so that will also be helpful, I think, to incorporate some of this additional data. Sean Pokorney: When you really look at the guidelines and see what's driving the guidelines, there are several trials now that are really driving the guidelines. And so I think, looking back on the data, we have the AATAC trial, which was a trial of 203 patients that looked at ablation versus amiodarone. And we have the CASTLE-AF trial, which had 363 patients in it and was looking at atrial fibrillation in patients with heart failure with reduced ejection fraction and defibrillators. Dr. Sean Pokorney: And when you put that data into context, the AATAC trial did find lower rates of death and hospitalization as a secondary outcome, and CASTLE-AF did identify a reduction in heart failure hospitalizations and death. At the three year follow-up, there was a statistically significant reduction, although the event number was lower than the previously sort of calculated target sample size. Dr. Sean Pokorney: And so in aggregate, these trials do show a modest evidence of benefit for clinical outcomes in this population. And that's where adding more data is really critical. Dr. Carolyn Lam: That's so true. And actually, Ratika, is there any plan for some meta-analysis or sort of adding the data? And if you could, also speak to, the trial was interrupted at some point, so how that may have impacted things as well. Dr. Ratika Parkash: Those are important questions. So, first of all, there is a planned longer term follow-up for the study, to look at whether or not following these patients out beyond our meeting follow-up of 37 months, it will actually produce a different result than what we observed in the current findings. Dr. Ratika Parkash: I think a meta-analysis is obviously going to show benefit for ablation-based rhythm control, based on the data that Sean had just described. One of the things that we'd need to keep in mind is that this trial, the RAFT-AF study really enrolled patients who were suitable for either ablation-based rhythm control or rate control. So it wasn't a study that looked at rhythm control only. Dr. Ratika Parkash: So, the CASTLE-AF trial had essentially two rhythm control arms. The medical therapy arm was, was amiodarone in that trial, versus catheter ablation. So patients could get rhythm control in both. And so, the types of patients that would've gotten into CASTLE-AF were different than the patients in our trial, even when you look at the reduced ejection fraction patients. Dr. Ratika Parkash: Having said that, our curves, when you look at the reduced ejection fraction group in our study does mirror what was observed in CASTLE-AF. So, even if a patient is not deteriorating initially with rate control, it appears that over time they begin to deteriorate. And that's what all of these trials have shown, is that patients do better with ablation-based rhythm control, the best form of sinus rhythm maintenance that we have. Dr. Ratika Parkash: And it takes time for them to deteriorate and it takes time to accrue those events. And this is evident in all trials of atrial fibrillation. You either need a very large sample size, like 15,000 patients, to look at heart failure in a short period of time, or you follow them longer, so that you can accrue those events. Dr. Ratika Parkash: In terms of the stopping of the trial, certainly, had we reached the sample size of 600, which was the intended sample size after recalculation during the study from 1000 down to 600, I believe we would have reached a positive outcome. But again, we hope that our longer term follow-up might shed some light on that. The interruption of the study was based on the DSMC decision and certainly could have affected the power of the study. Dr. Ratika Parkash: We have to remember that the other possibilities are that ablation-based rhythm control is not superior to rate control. And as someone who is pro-ablation, it's difficult to say that, but we see hints of benefit and we have to recognize that. Dr. Ratika Parkash: The other issue is that the secondary endpoints in our trial were all significant, as overall, it doesn't matter which group you looked at, NT-proBNP, six-minute walk test, quality of life, both for heart failure and atrial fibrillation, as well as ejection fraction, were all improved. And for many of the studies that have been done previously, those were the primary endpoints of those studies. Dr. Ratika Parkash: The idea of whether ablation-based rhythm control reduces heart failure per se, is from our study, purely from our study, we can't be a hundred percent certain. There's definitely a hint of clinical benefit there. From all the secondary endpoints, which are the current guidelines, is what they indicate ablation should be done for, is to improve quality of life. Our study was certainly supportive of that. Dr. Carolyn Lam: You know, Sean, I especially appreciated your discussion of these issues, the early stopping of the trial, the secondary endpoints. Could you know, share some of those thoughts? Dr. Sean Pokorney: I think it's really an important topic. I think that, again, as Ratika said, part of why this trial is so important is that many of the previous trials that have been published and many of the data sets have really looked at rhythm control versus rhythm control in this population, even including the analysis from CABANA, which included almost 780 patients from CABANA that had heart failure. And in that population, they did show a reduction in the composite primary endpoint of death, disabling stroke, serious bleeding, or cardiac arrest. And again, CABANA was, as well, a study of rhythm control with ablation versus medical therapy, most patients getting rhythm control in that medical therapy arm. Dr. Sean Pokorney: And so this data really is additive. I think that one of the challenges is always, how do we make sure to get the most information out of a clinical trial once we commit patients to that scientific process? And I think here, at least in retrospect, it's obviously unfortunate that the trial was stopped early. I think that more data would certainly be helpful. Dr. Sean Pokorney: I appreciate the fact that longer term data may help solve that gap and close that gap a little bit. I think that, I guess, it'd be interesting to hear from Ratika a little bit more about the process that was involved with interaction with the DSMC and stopping the trial. Dr. Ratika Parkash: Yeah. Thanks, Sean. That also is a very good question. The DSMC really evaluated the data, evaluated the progress of the trial, back in 2017. It had been six years since we'd started the study. The data they had, in fact, did not show any benefit to ablation-based rhythm control over rate control at the time. So the follow-up period at the time was around two years. Dr. Ratika Parkash: And again, if you look at our Kaplan-Meier curves, you can understand why they would have made that decision at the time, based on 363 patients for the data that was available to them. They had a futility index that they looked at. it was calculated. The cutoff for stopping of the study was 0.8, and it was 0.81. So, there was a 19% chance that the study was going to show any benefit. And based on that, plus the progress of the trial, they made a decision to stop the study. Dr. Sean Pokorney: Yeah. I think it's really important when we look at these decisions, that there was example when we talk about this in the editorial as well with the ISIS-2 trial, where early on in the data, ISIS-2 was a trial looking at aspirin versus placebo. And basically in that trial, when you looked early on at the events that were accumulating, there was really roughly no difference between aspirin and placebo. And ultimately, that trial became positive and was a really critical trial. And if it had been stopped at that point for futility, we wouldn't have had some really critical data. Dr. Sean Pokorney: So, it's always a challenging decision. And obviously, the decisions are trying to be made in the best interest of the patients. Here, it just shows how important this additional follow-up data is for this trial, for RAFT in particular. And ultimately, it'll be interesting to see, as you mentioned, as we add additional long-term follow-up, how that will affect the results. Dr. Ratika Parkash: Absolutely. So, we hope that our additional follow-up is of benefit to clarifying our results. The unfortunate issue, I agree, was the stopping of the study, but we do trust our DSMCs. We have them for a reason and they perform an important function. So, we have to pay attention of course, to how they see things and evaluate the... at the time. Dr. Ratika Parkash: The other thing we should keep in context is that ablation for those, that time period, is not the same as it is today. Our safety has improved. You may have noticed that there were some adverse events in the study with ablation, and we would expect it to actually be lower, but in this day and age, but at the time, contact force wasn't available. Dr. Ratika Parkash: There were some tools and techniques that we now have at our disposal, improved mapping systems and so on, that allow us to do a safer and more efficacious job. But even in the context of that, our sinus rhythm maintenance was almost 80 to 90% for patients that you wouldn't normally expect to have that much sinus rhythm. Dr. Sean Pokorney: Yeah. I think that's a really critical point. You made a lot of really important points there, actually. Obviously, the vision of the field of electrophysiology is shifting, as you mentioned. And with data from EAST-AFNET 4, we're really shifting towards earlier rhythm control, as well as additional ablation trials attest, stop AFib or stop AF. Dr. Sean Pokorney: So again, there have been several studies that have shown the benefits of earlier rhythm control, EAST-AFNET 4, I think, being obviously one of the most relevant, looking at addressing atrial fibrillation of population of patients who've been diagnosed within the last year, and showing that there was a benefit to rhythm control, although the majority of rhythm control in that study was antiarrhythmic medications. Dr. Sean Pokorney: I think in the heart failure population, the challenge with rhythm control is that we're a lot more limited in terms of the medical therapies that are available for these patients. And I think that's where ablation really plays in a more important role, because not only have you shown that it seems to be efficacious in this patient population, with a really high rate of rhythm control, but in a lot of these patients, it's often a safer alternative than antiarrhythmic therapy. Dr. Ratika Parkash: Absolutely. And we've already shown that amiodarone is ineffective in this population, in AF-CHF. So, using that drug does not seem to be, in a population that could go for an ablation, the appropriate approach. Dr. Sean Pokorney: Yeah. And as well, I think that's important. And when you look back at data from SCD-HeFT as well, there were some concerns with safety signals of amiodarone in patients with heart failure as well, from that study, again, likely related to the side effects of the medication itself. Dr. Sean Pokorney: So again, it is a complex patient population in terms of decision-making and management. And I do think, again, we talked a lot about the trial being stopped earlier than we would've ideally liked. I still think that the data that you guys produced is really important and critical and additive. Again, we're consistently seeing these modest treatment effects across multiple studies. And the fact that all the studies are pointing in the same direction is very reassuring. Dr. Ratika Parkash: Yeah. I was just going to comment on some of the points that Sean had raised, with respect to early rhythm control and the concept of atrial substrate, and how advanced atrial substrate with a negative remodeling effect in patients with heart failure or prolonged atrial fibrillation may not necessarily be in our patient's benefits to then try to intervene, and trying to get these patients early would be useful. Dr. Ratika Parkash: So in RAFT-AF, patients did not have to fail an antiarrhythmic drug in order to get into the study. So that, again, critical, very much along the lines of EAST-AFNET and EARLY-AF, which was also published, demonstrating benefit for early intervention. Dr. Carolyn Lam: Wow. Just, thank you so much, both of you. That was such a rich discussion, really, really unpacking very, very important elements of the trial, not just the trial results, but also the implications of what happens with trial conduct and execution and so on. Dr. Carolyn Lam: Again, thank you so much Ratika, for publishing this very important paper in circulation, Sean, for your beautiful editorial that put it all in context, the audience for listening today. From Greg and I, you've been listening to circulation on the run. Thank you for joining us today, and don't forget to tune in again next week. Dr. Greg Hundley: 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, please visit AHAJournals.org.
Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Here's the case: A 6-year-old child with a known h/o craniopharyngioma who has been endocrinologically intact with exception of needing thyroid replacement was admitted to the PICU prior to craniotomy to proceed with further tumor resection as well as the removal of a secondary cyst impacting his brainstem. The patient is receiving Keppra for seizures and per mother, he has recently been significantly more sleepy at school. On POD Op day 5: the PICU the bedside nurse notices increased urine output (6cc/kg/hr to as high as 10cc/kg/hr). Initially, there was an increase in Na to 157mEq/L within 48-72 hours the serum Na dropped to 128mEq/L To summarize key elements from this case, this patient has: Increase UOP Rapidly increasing Na initially followed by a drop All of which brings up a concern for Na abnormality post craniotomy In today's episode, we will be breaking down all things Sodium & the Brain. We will discuss diagnostic & management frameworks related to three pathologies: Central Diabetes Insipidus Syndrome of inappropriate Anti-Diuretic Hormone or SIADH Cerebral Salt Wasting These diagnoses can certainly be seen individually inpatients or as a spectrum of diseases — as we go through each of these diagnoses, pay particular attention to patient characteristics and lab abnormalities. Namely, serum sodium, serum osm, and urine osm. To build the fundamentals, lets first start with classic nephrology saying: Serum Na represents Hydration This takes us into a brief review of normal physiology — talking about three important hormones: ADH Aldosterone Atrial Natriuretic Peptide (ANP) Let's go through a quick multiple-choice question. A patient is recently started on DDAVP for pan-hypopituitarism. The medication acts similarly to a hormone that is physiologically synthesized in which of the following from which are in the body? A. Paraventricular Nucleus of the Hypothalamus B. Supraoptic Nucleus of the Hypothalamus C. Anterior Pituitary D. Vascular Endothelium The correct answer here is B the Supraoptic Nucleus of the Hypothalamus. Remember that ADH is synthesized in the hypothalamus and released from the posterior pituitary. What are the physiologic actions of ADH? ADH Increases H2O permeability by directing the insertion of aquaporin 2 (AQP2) H2O channels in the luminal membrane of the principal cells. Thus, as we will see with Central Diabetes insipidus, in the absence of ADH, the principal cells are virtually impermeable to water. Let's talk about our next hormone, aldosterone. What are the important physiologic considerations? Aldosterone is secreted from the adrenal cortex as a byproduct of the RAAS. Aldosterone increases Na+ reabsorption by the renal distal tubule, thereby increasing extracellular fluid (ECF) volume, blood volume, and arterial pressure. It also helps in secreting K and H. This physiology is applied directly at the bedside when we have patients in the ICU who have a contraction alkalosis secondary to diuretics. The increase in aldosterone as these patients lose free water from their Lasix administration results in hypokalemia and metabolic alkalosis. Alright, what about the third hormone, ANP? Atrial natriuretic peptide (ANP) is released from the atria in response to an increase in blood volume and atrial pressure. ANP causes relaxation of vascular smooth muscle, dilation of arterioles, and decreased TPR. causes increased excretion of Na+ and water by the kidney, which reduces blood volume and attempts to bring arterial pressure down to normal. As ANP causes natriuresis, diuresis, and inhibition of renin, you can consider this hormone as having a complementary & opposite effect to ADH and aldosterone. Alright, now that we...
As always, detailed Timestamps and Links follow! More #historyandscandals 00:28 Medina Spirit is Disqualified from his 2021 Kentucky Derby win by the state racing commission. 90-day suspension for trainer Bob Baffert. Purse to be redistributed with the title to Mandaloun** (Juddmonte stables, trainer Brad Cox, and jockey Florent Geroux) **We still LUV Medina Spirit, who gave everything and deserved far better. https://paulickreport.com/news/the-biz/medina-spirit-disqualified-from-2021-kentucky-derby-win-baffert-given-90-day-suspension/ 4:09 Baffert's horse Blackadder just won the El Camino Real Derby, a Preakness win-and-you're-in race. Will the Maryland uphold KY's ruling? UPDATE: YES! https://www.baltimoresun.com/sports/horse-racing/bs-sp-preakness-medina-spirit-disqualified-bob-baffert-suspended-20220221-7kblrvwf7bgfhltc6wltz2nt5i-story.html His 90 days end a week before the Belmont Stakes—will Baffert still be banned in NY? 7:40 One genuine 3 year-old Derby contender is Newgrange, currently scheduled for the Rebel Stakes G2 at this weekend. And what about Corniche?! 11:23 Besides the Medina Spirit tragedy, Baffert has plenty of questionable history 13:27 The Jockey Club has had its eyes on doping since its FIRST roundtable proceeding in 1953. The Horseracing Safety and Integrity Act (HISA) is the most recent legislative approach** to get at the issue. **The Jockey Club pulled strings with “policing” too. To learn a LOT more, listen to our podcast The Fishman Affair Parts 1 and 2 (Season 2, Episodes 5 & 6). 16:57 Weej finds eerie similarities in notes from the first roundtable. https://www.jockeyclub.com/Default.asp?section=Resources&area=14 19:37 “Hopping” was the old doping slang. Gray zone nutritional supplements always blur the lines and penalize the scrupulous. 22:08 After federal indictments of dopers, Mark Casse knew his horses would seem to “get faster.” HA! https://paulickreport.com/news/people/from-the-brink-of-retirement-federal-indictments-have-given-casse-renewed-hope/ 23:25 Could HISA really help us get data-driven analysis on issues like Lasix (furosemide)? 25:08 Back to 1953 and unfair competition. Arthur Hancock, JUNIOR is mentioned. A generation later, in 1991, it's Arthur Hancock III (TREY!) who will still be talking about “drugs and thugs” at the racing symposium at the University of AZ. 28:46 Jockey Club rule against abuse and substances. http://www.registry.jockeyclub.com/registry.cfm?Page=tjcRuleBook#nineteen 31:07 Vet Michael Posner rented his prescription pad (cheaply!) to pharmacist-compounder Scott Mangini. https://paulickreport.com/news/the-biz/trial-date-set-for-vet-connected-with-federal-doping-case/ 32:24 Trainer Marcus Vitali flitted between state jurisdictions to avoid consequences https://paulickreport.com/news/the-biz/vitali-suspended-one-year-after-meth-positive-in-pennsylvania-appeal-ongoing/ 39:35 Bettors should demand better and withhold support from corrupt operations and actors, because horse racing ISN'T DYING! 43:45 Adverse incentives work! People shouldn't have to turn a blind eye to have careers or enjoy the sport. We love making jokes, but love
Dog lovers frequently wonder if there is a more natural option that could be used instead of pharmaceuticals to treat their dogs. The answer is… sometimes! Bam Bam has elevated calcium levels in his blood, and his human wants to know if she can swap out some of his medications. Dr. Nancy Reese breaks down how the medications prednisone, Lasix, and Palladia work and why they might have been chosen to be part of the treatment plan, as well as some natural options that might work to help out a bit. Although a pharmaceutical may be just what your pet needs for the best results, there are often natural remedies that can help to support conventional treatments. Links Mentioned in Today's Show: Vitamin C for Dogs with Cancer podcast episode Related Links: DogCancer.TV: Palladia™ and Dog Cancer- What You Need to Know Prednisone for Dogs: Uses for Dog Cancer and Other Medical Conditions, Side Effects, Alternative Options, and More About Today's Guest, Dr. Nancy Reese: Dr. Nancy Reese is a small animal veterinarian with over 30 years of clinical experience taking care of cats and dogs and other critters in the Sierra Nevada foothills. She is also a perpetual student and researcher, as evidenced by her many degrees. In addition to her Doctor of Veterinary Medicine from the University of California, Davis, she earned a Masters in Preventive Veterinary Medicine at UC Davis and then a Ph.D. in Epidemiology at UC Davis. If you string all her letters out after her name it looks like this: Nancy Reese, DVM, MPVM, PhD. In her spare time, she volunteers to help evacuate and shelter animals caught up in disasters, and she's currently training to help in human search and rescue efforts. Dr. Reese lives in a log cabin with her husband, her 13-year-old golden retriever, and her two 13-year-old cats. Her hobbies include boosting the quality of life and longevity for all animals in her care, hiking, travelling, and cross-country skiing. Oh, and lots of dog walking. degree from the University of California at Davis before earning his Doctorate in Veterinary Medicine from Cornell University. Other Links: To join the private Facebook group for readers of Dr. Dressler's book “The Dog Cancer Survival Guide,” go to https://www.facebook.com/groups/dogcancersupport/ Dog Cancer Answers is a Maui Media production in association with Dog Podcast Network This episode is sponsored by the best-selling animal health book The Dog Cancer Survival Guide: Full Spectrum Treatments to Optimize Your Dog's Life Quality and Longevity by Dr. Demian Dressler and Dr. Susan Ettinger. Available everywhere fine books are sold. Have a guest you think would be great for our show? Contact our producers at DogCancerAnswers.com Have an inspiring True Tail about your own dog's cancer journey you think would help other dog lovers? Share your true tail with our producers. If you would like to ask a dog cancer related question for one of our expert veterinarians to answer on a future Q&A episode, call our Listener Line at 808-868-3200 www.dogcanceransers.com. Dog Cancer News is a free weekly newsletter that contains useful information designed to help your dog with cancer. To sign up, please visit: www.dogcancernews.com
La tertulia favorita de los hípicos de habla hispana, Ramon Brito y ElPotroRoberto comentan sobre los finalistas a los premios Eclipse, Fausto Gutierrez nos habla sobre el futuro de Letruska, ejercicios de Life Is Good y Knicks Go, Lasix, posible plan del entrenador Kenny McPeeck con los potros Tiz the Bomb, Smile Happy, y Dash Attack, todo esto y mucho más. Síguenos para más contenido en https://www.drf.com/espanol https://twitter.com/DRFenEspanol https://www.instagram.com/drfenespanol/ https://www.facebook.com/drfenespanol #DRFenEspanol “La casa de los hípicos de habla hispana”
José Francisco Rivera y el miembro del Salón de la fama Ramón Alfredo Domínguez conversan con Ramón Morales y Marc Tacher, entrenador y propietario respectivamente de TAMBORERO, ganador del https://www.youtube.com/hashtag/cl%C3%A1sicodelcaribe (#ClásicoDelCaribe) 2021 celebrado en https://www.youtube.com/hashtag/puertorico (#PuertoRico). En una amena conversación se abordaron varios temas de interés para la Serie hípica del Caribe. Se habló sobre el triunfo de su ejemplar, el espectáculo musical antes del Clásico, la administración del medicamento Lasix, la próxima edición de la cita caribeña, la rivalidad hípica entre Puerto Rico y Venezuela, y mucho más. Síguenos en las redes sociales. Twitter: Exacta_Box Instagram: exacta_box Facebook: Exacta Box Suscríbete a nuestro canal de YouTube EXACTA BOX y disfruta con los profesionales y los protagonistas lo mejor del https://www.youtube.com/hashtag/hipismo (#hipismo).
Hello everyone! Welcome to the WPB Health Consulting Podcast. Where we bring clarity to coaching. In 2017, the mission to bring clarity to evidence-based health coaching was created. WPB Health Consulting's mission is to bring clarity to coaching and consulting practice. WPB stands for Wellness, Performance, and Bodybuilding. How is by developing and elevating health coaches and clients education and practical application. This is done by our coaching service and podcast! Our coaching service: Will empower you and be in constant contact to uplift you toward your goals. Our podcast: Will provide FREE evidence-based coaches in all areas of life. By doing so, coaches and clients will bring clarity on how to communicate and elevate their health habits through evidence-based practice. The information on this site is not intended or implied to be a substitute for professional medical advice, diagnosis or treatment. All content, including text, graphics, images and information, contained on or available through this website is for general information purposes only. WPB Health Consulting makes no representation and assumes no responsibility for the accuracy of the information contained on or available through this website, and such information is subject to change without notice. You are encouraged to confirm any information obtained from or through this website with other sources and review all information regarding any medical condition or treatment with your physician. NEVER DISREGARD PROFESSIONAL MEDICAL ADVICE OR DELAY SEEKING MEDICAL TREATMENT BECAUSE OF SOMETHING YOU HAVE READ ON OR ACCESSED THROUGH THIS WEBSITE. On Today's podcast: 1. Dominic Kuza's journey with competitors this year. 2. Common themes of diuretic use you are seeing within the competition community 3. Defining Diuretics and their mechanism of action: The three types of diuretic medications are called thiazide, loop, and potassium-sparing diuretics. All of them make your body excrete more fluids via urine. Understanding Thiazide diuretics: Thiazides are the most commonly prescribed diuretics. They're most often used to treat high blood pressure. These drugs not only decrease fluids, they also cause your blood vessels to relax. 4. Thiazides are sometimes taken with other medications used to lower blood pressure. Examples of thiazides include: chlorthalidone Hydrochlorothiazide (Microzide) metolazone indapamide 5. Understanding Loop diuretics Loop diuretics are often used to treat heart failure. Examples of these drugs include: torsemide (Demadex) furosemide (Lasix) bumetanide Bumex 6. Potassium-sparing diuretics Potassium-sparing diuretics reduce fluid levels in your body without causing you to lose potassium, an important nutrient. The other types of diuretics cause you to lose potassium, which can lead to health problems such as arrhythmia. Potassium-sparing diuretics may be prescribed for people at risk of low potassium levels, such as those who take other medications that deplete potassium. Potassium-sparing diuretics don't reduce blood pressure as well as the other types of diuretics do. Therefore, your doctor may prescribe a potassium-sparing diuretic with another medication that also lowers blood pressure. Examples of potassium-sparing diuretics include: Amiloride Triamterene (Dyrenium) Spironolactone (Aldactone) Eplerenone (Inspra) 7. Discussing the dangers of nutrition and monitoring potassium intake with diuretic use 8. Discuss the effects of the longevity of bodybuilding and diuretic use
A retrospective cohort study published in Cardiology Research questions the need to transition heart failure patients to oral diuretics before discharge. Trial of Oral Diuretics Prior to Discharge Is Not Associated With Improved Outcomes in Decompensated Heart Failure | Hospital Medicine Virtual Journal Club
Timestamped topics below. 1:30 Big Dreaming scratches, the luck of the draw. 2:31 Strong Tide, solid horse at first post, why aren't we more in love? 2:56 Glynn County, decent late speed, but also feeling lukewarm? 3:25 Domestic Spending, superhero! At the Manhattan Stakes, showed off from ten lengths out! Flavien Prat keeps the band together for this big 2021 earner, who may be our turf equivalent of Knicks Go or Essential Quality. 6:06 Two Emmys, in a strange twist of nomenclature, apparently loves second place. Underbet? 6:54 Zulu Alpha, 8 year-old gelding to be ridden by Luis Saez, Saratoga's winningest jockey, has already finished behind three of this race's contenders earlier in the year. 8:49 Another Mystery, late speed amid undistinguised company? This may be our unpredictable long shot, as opposed to… 9:54 Space Traveller, British import who's been losing in G1s and G2s, but winning in G3s. During this strange return-season of racing, have Del Mar and Saratoga left the rest of the fields too thin? 11:35 Bizzee Channel, spotty, but perhaps a decent undercard pick? 12:43 Armory, strong contender who's raced in good company, but our attraction may be too great for the stats to justify. Poor last race in late July (too-recent?) may be worth noting for this kid of Galileo. 15:30 Is Space Traveller really a “live long shot?” Ummm. 17:00 Our racing tour's next weekend stops are Del Mar's Pacific Classic and Saratoga's 141st running of the Alabama. See our whole schedule of races preceding the Breeders Cup at www.33xpl.com and bet-a-long! No Sleep ‘Til Del Mar! 17:47 The “All-Drug Olympics” for horses, Lasix for everybody?! 18:22 Brief description of Lasix use in horse racing. Another quick summary of the state of its use is here: https://www.courier-journal.com/story/sports/horses/horse-racing/2019/04/18/horse-racing-doping-what-lasix-and-how-used/3495967002/ 19:05 Space Traveller skips the lotus-eating party. Can he win without the sauce? JUST FOR THE RECORD: We love making jokes, but love horses more. We encourage and support widespread reform with regard to doping, medical care, and equine treatment. We want sparkling ethics, so we can enjoy the sport happily and encourage others to become fans, too! Enjoy more from us, the team behind 33xpl, at your favorite podcasting platform or posted at our You Tube channel along with other informational vids. You can also check us out at Instagram, Pinterest, and our own site, www.33xpl.com, where you can download our racing “tour schedule” to bet-a-long and sign up for our very-occasional newsletter with goodies for subscribers. Please Like, Comment, and Subscribe, and until next time, HAPPY RACING, YA'LL! Trixie and Weej
Our first guest will be trainer Elizabeth Lizzie Merryman. After two consecutive stakes triumphs at five furlongs, her homebred Caravel carried her winning form into graded-stakes company, following a torrid pace and gunning down frontrunner Robin Sparkles in mid-stretch to conquer the G3, $200,000 Caress for older fillies and mares contesting 5 1/2 furlongs over Saratoga Race Course's Mellon turf. It was the first graded stakes win for Caravel and her owner/breeder/trainer. Caravel is now co-owned by Elizabeth Merryman in partnership with celebrity chef Bobby Flay who recently purchased 75% of the filly. Following the Caress, Caravel will be transferred to the barn of fellow Fair Hill based trainer Graham Motion, with eyes set on the G1, $1 million Breeders' Cup Turf Sprint on November 6 at Del Mar. Merryman will remain a part owner. We have talked for weeks about her. He's watched her train pretty much every day, Merryman said. He's just been so nice and classy and sweet about her. He was very much laying low today, but we talked a lot about her and we'll continue to talk about her. And we'll be talking with Lizzie about what it was like to raise a foal from birth and train her through a graded stakes victory at Saratoga. We'll also address her mixed feelings about watching her homebred success being led from her stall to the shed row of a new trainer. Terry Hill will be our guest handicapper for Whitney Weekend at Saratoga. Hill has been a writer all his life, first in advertising and later as the the co-author of the Two Guys series of books (Two Guys Read Moby-Dick, Two Guys Read the Obituaries, Two Guys Read the Box Scores, etc.). For the last three years he has been working for the Saratoga Special as a horse racing writer and columnist. Simultaneously he has been forging a career out of being old. His ambition is to live forever. So far, so good. Looking for his first Grade 1 win since the Pegasus World Cup Invitational last winter, Knicks Go drew post 4 on Wednesday and was made the 6-5 morning-line favorite against Maxfield, Silver State, By My Standards and champion filly Swiss Skydiver in Saturday's $1 million Whitney Stakes at Saratoga. The 1 1/8-mile, no-Lasix race is an automatic qualifier for the Breeders' Cup Classic. Swiss Skydiver (6-1) was drawn into post 3. Originally scheduled to race July 25 against fillies and mares in the Shuvee Stakes, she was forced to wait through a quarantine brought on by a positive equine-herpesvirus test in a nearby barn stall at Saratoga. Forced into an alternative plan, trainer Kenny McPeek decided to give his 2020 Preakness victor a chance to become the seventh filly ever to win the Whitney, and the first in 33 years. She is 1-for-1 at Saratoga, having won last year in the Alabama (G1). The Whitney is the only $1 million race on Saturday at the Spa. Terry and John will also analyze the Saratoga Derby Invitational on the turf and the G1, $500,000 Longines Test
Furosemide is an antihypertensive loop diuretic drug. The main indications are for edema and hypertension with an off-label use for hypercalcemia. The general dosing range is between 40-120 mg per day with a max of 600 mg per day. The mechanism of action is it interferes with the chloride-binding co-transport system causing a natriuretic effect. It inhibits sodium and chloride resorption in the ascending Loop of Henle and the proximal and distal renal tubules. The onset of action for diuresis is around 30-60 minutes with symptomatic improvement of acute pulmonary edema occurs within 15-20 minutes. Caution should be observed in patients with electrolyte imbalances, the elderly, premature neonates, patients with gout, lupus, and diabetes. There is a black box warning for fluid and electrolyte loss if excessive amounts are used. When considering the drug interactions one should consider that furosemide is an OAT1 and OAT3 substrate, it may cause hypocalcemia, hypokalemia, hyponatremia, ototoxicity, and others. Go to DrugCardsDaily.com for episode show notes which consist of the drug summary, quiz, and link to the drug card for FREE! Please SUBSCRIBE, FOLLOW, and RATE on Spotify, Apple Podcasts, or wherever your favorite place to listen to podcasts are. The main goal is to go over the Top 200 Drugs with the occasional drug of interest. Also, if you'd like to say hello, suggest a drug, or leave some feedback I'd really appreciate hearing from you! Leave a voice message at anchor.fm/drugcardsdaily or find me on twitter @drugcardsdaily --- Send in a voice message: https://anchor.fm/drugcardsdaily/message
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
We are back with another great episode of Past the Wire TV and our Gate to Wire podcast, brought to you by Spendthrift Farm. Yes, once again we take you Past the Wire!Besides being a true horseman, lover of the sport and animal, great trainer, Graham Motion is also a delightful guy and a total pleasure to talk with.We were fortunate to have Graham join Jonathan Stettin on this episode of Past the Wire TV for a chat about several topics in horse racing. Graham and Jonathan are both extremely passionate about racing and the current state of the sport and share a deep concern about its future.Graham and Jon talk about everything from horse individuality to training on a farm as opposed to at the racetrack. Lasix, race day medications, HISA, shipping, and on track pharmacies work their way into the discussion. The show ends with Graham talking about Mean Mary who we are scheduled to see in the Grade 2 New York Handicap on Friday. Wanna know if Mean Mary is mean which could be a good thing for a mare or if it is just a name? You'll have to listen to learn that and how Graham points for the races he is after. Graham Motion has reached the pinnacle of the sport. With wins in the Breeders' Cup, Kentucky Derby, Dubai World Cup and many other graded stakes Graham was kind enough to share his opinions and some of the vast wealth of knowledge he brings to the table. If you're a student of the game like we are you will soak it up like a sponge. Once again thank you for tuning in and we hope you enjoy the show:
Ralph Siraco is no stranger to Winningponies and even covered some racing events with “The Regular Guy.” Never short on an honest opinion, John will check his views of such topics as Jockey Whip Restrictions, the Medina Spirit wailings, the Lasix debates and Saturday’s three graded races at Santa Anita. Featured are the Gr. 2 $200,000 Charles Whittingham on the turf; Gr. 2 $200,000 Triple Bend and the Gr. 3 $100,000 Daytona Stakes over the greensward. Jason Beem, who has been a guest on Winningponies over the years will join us in the second segment. Jason and John worked together when he started calling the races at River Downs in 2006. Since that stepping off point in his career, he has called races at numerous Thoroughbred tracks. It was announced last week that Jason has been hired as the announcer at Tampa Bay Downs. He will begin on June 30, the first day of the track's two-day Summer Festival of Racing. The 41-year-old University of Washington graduate currently announces at Grants Pass Downs in Oregon and will begin his third season at Colonial Downs in New Kent, Va., on July 19. At Tampa Bay Downs, he replaces Richard Grunder, who retired on May 2 after 37 years and more than 37,000 races at the Oldsmar oval. “I love the racing there and am excited to become a part of it,” said Beem, who hosts an hour-long podcast each Monday through Friday – the Jason Beem Horse Racing Podcast sponsored by Twinspires – on which he interviews many of the sport's leading figures. Margo Flynn, the Vice President of Marketing and Publicity at Tampa Bay Downs, believes Beem will be embraced by listeners accustomed to Grunder's energetic, fan-friendly style, while attracting new followers through his social-media platforms. In addition to his podcast, Beem is active on Twitter ( @BeemieAwards ) and Instagram ( @jasonbeemracing ) and has a YouTube channel. Beem knows it is a next-to-impossible task replacing Grunder, who is a jockey's agent at Canterbury Park in Shakopee, Minn. In an almost-eerie coincidence, both called races at since-closed Portland Meadows in Oregon at similar stages of their careers, with Beem working there from 2006-2014. “I don't look at it as trying to replace him, because he is a legend,” Beem said. “I just want to be a great member of the Tampa Bay Downs team, get to know the horse-playing community and get a lot of people excited about horse racing.
A career dedicated to the improvement of horse health, welfare, and performance all started with a $300 bet, or investment if you will in a bucket of stuff. Justin Sallusto has a good heart, and that heart prompted him to feel for an older salesman trying to sell a bag of stuff he claimed was all natural and could help a horse. The rest has become horse health history and led Justin, a Grade 1 winning trainer into a venture that led him on a path to improve horse health and performance through nutrition and without the use of drugs.On this episode of Past the Wire's podcast, Gate to Wire, brought to you by Spendthrift Farm you will meet Justin and hear how it all started. Justin has been around the racetrack a long time and has his share of racetrack tales and he did share a few with us.Hear Justin's take on bleeding, Lasix, race day medications and a variety of other horse health and welfare topics including what constitutes a performance enhancer. We'll go back in time and explore horse health and how the thoroughbred of today is different from the thoroughbred of yesterday. You'll also hear about some of the Kingdom Nutrition Company products and what Justin claims they can do, and the examples of when and how they worked at every level of the game. This is an interesting show not only for owners, trainers, and breeders, but also fans and handicappers as there is a lot of knowledge and experience shared. Thank you for tuning in. You can listen to the podcast below or watch the Past the Wire TV YouTube version as well. Whatever works:
The Past the Wire clan welcomes retired trainer Chuck Simon, who hosts his own podcast Going in Circles, along with renowned Veterinarians Dr. Kathryn Papp and Dr. Bryan Langlois to this episode of Past the Wire's podcast, Gate to Wire brought to you by Spendthrift Farm. On the heels of trainer Joe Orseno's comments about Lasix following Imprimis bleeding at Keeneland, and Hidden Scroll bleeding following a race on the same card the panel sat down to discuss Lasix. Sure we know the topic has been debated many times in the past, but now a federal law exists that will ultimately ban the drug from race day use in the United States, or at least in the states which opt in to the Horse Racing safety and Integrity Act. There is so much to work out and the panel starts by exploring what has changed in racing creating an environment where over 90% of our horses race with the drug, and how much it helps as opposed to whether it hurts the horses both short and long term. As with many aspects of the Sport of Kings, Thoroughbred Horse Racing one issue ties into another which ties into another and it almost seems endless. This is a video and podcast you won't want to miss as the panel brings so much to the table and hits on so many topics and issues hindering the success and growth let alone the survival of the sport we love. With a panel like this you can expect solutions offered with their opinions. This is an outspoken and passionate bunch who may differ in thoughts and views but share a commonality in their love for the horse and the animals well being put first before the business of racing and breeding. Lasix as a mask for other substances is debunked but the use of other substances is explored along with policies of racetrack management and state governing bodies on doing what is necessary to create a level playing field for healthy and sound horses. If you care about the horses and the sport this is a show you will wamt to check out. What would racing be without the bettor? Nothing, the bettor is the customer with no voice in the game, well not one that anyone hears or listens to anyway. Our panel tackles that issue as well realizing the bettor is an integral and vital piece of the equation. This reminds us of Jonathan Stettin's Who Yields the Power article and it is always the one with the checkbook or money. Sit back and enjoy the show.
Nick is joined by Lee Mottershead, senior writer from the Racing Post, to discuss all the day's horseracing news. With the weather still playing havoc in the UK, Nick brings breaking news that the fixture at Newbury this Saturday will likely move in its entirety to Sunday February 21st and feature the Betfair Hurdle, the UK's second richest hurdle race this season. Drew Fleming, President and CEO of Breeders' Cup, joins the conversation to discuss the ban on raceday Lasix for all BC Challenge Races, while sports psychologist Michael Caulfield talks about the added pressures on elite sport competitors during lockdown, and owner Brett Graham talks about his rollercoaster ride with Irish Gold Cup winner Kemboy.
Nick is joined by Lee Mottershead, senior writer from the Racing Post, to discuss all the day's horseracing news. With the weather still playing havoc in the UK, Nick brings breaking news that the fixture at Newbury this Saturday will likely move in its entirety to Sunday February 21st and feature the Betfair Hurdle, the UK's second richest hurdle race this season. Drew Fleming, President and CEO of Breeders' Cup, joins the conversation to discuss the ban on raceday Lasix for all BC Challenge Races, while sports psychologist Michael Caulfield talks about the added pressures on elite sport competitors during lockdown, and owner Brett Graham talks about his rollercoaster ride with Irish Gold Cup winner Kemboy.
See all the Healthcast's at https://www.biobalancehealth.com/healthcast-blog/ Painful intercourse is a common problem that OBGYNs diagnose and treat every day, but it is often a very upsetting problem that women don't like to talk about with their doctor, so they often live with it, silently. I want to encourage those of you who are experiencing this problem to talk to your doctor about it so you can receive treatment. It is important for women to ask their doctor about their pain with intercourse so they can have a fulfilling sex life. Most causes of painful intercourse are not “in your head” or psychological. I want to concentrate on the physical causes of painful intercourse and not psychological or couple issues, because frankly the psychological causes are not my area of expertise and I always ask my patients to see a counselor or psychiatrist to manage those causes. There are many physical reasons a woman may experience painful intercourse that prevents them from enjoying the benefits of a good sexual relationship, and today I will discuss the causes and treatments for physical causes of painful intercourse. At BioBalance Health® I concentrate on the hormonal deficiencies that can cause painful intercourse. For women before and after menopause, having enough testosterone and estrogen is key to lubrication and skin that is thick enough to have comfortable intercourse. Without these hormones the vagina cannot lubricate, the skin “shrinks around the vagina and clitoris and the vagina is no longer stretchy and pliable enough to dilate to accommodate a penis. The outcome of intercourse without enough estrogen and testosterone (called vaginal atrophy) is lack of orgasm, tearing of the vaginal opening, accompanied by pain and bleeding, and the feeling of being rubbed with “sandpaper” when having intercourse. Within 3 weeks of replacing testosterone and estradiol with bio-identical pellets brings women back to health in many ways and relieving the pain and agony of sex from low hormone levels brings the joy of sex back to my patients. Because of testosterone and estradiol deficiencies many of my patients have stopped having sex because it is too painful. We will talk about menopausal women who have hormone deficiencies first and then we will discuss painful intercourse in pre-menopausal women, what causes this problem and how to remedy this common problem. A wonderful example of vaginal dryness that caused painful intercourse was embodied in one of my recent patients who looked at the floor while she told me that she just “could not” have sex because her vagina was too small. This woman was 59 and she had been divorced for over 10 years by the time she came to my office for the first time. She had many other symptoms of estrogen and testosterone deficiency, and she had seen her gynecologist to ask for help. She had given her lubricant first and that did nothing for the size or stretchiness of my patient's vagina. She was still unable to have sex. I don't know why OBGYNs are afraid of using estrogen cream, estradiol in patch or pellet form or testosterone is any form, but they are! When she got to me the simplest answer was estrogen cream to put on and in her vagina. From experience I know that this doesn't fully bring a woman back to sexual wholeness, so I also gave her estradiol and testosterone pellets, and she was able to stop the cream after one month. Voila!! She was healed and her new relationship blossomed into marriage! With testosterone and estradiol her vagina was once again back to normal premenopausal shape and her sex life was not only possible, but wonderful! To summarize the effects one by one of replacing both testosterone and estradiol in women with painful intercourse I will list the post-menopausal effects of testosterone and estradiol attributed to each hormone deficiency. What Testosterone does for sex: Improves Libido Brings blood flow to the pelvis Makes orgasm possible Improves the wetness and stretchy ness of the vagina Lengthens the vagina Increases the size of the clitoris so it can be stimulated Allows the vagina to stretch to accommodate a penis of any size Labia around the vaginal opening enlarge and the skin of the whole vulva thickens Improves the sensitivity of the vagina, clitoris and G spot stradiol's function in sexual health: Increases wetness in the vagina Increases the thickness of the vaginal wall and vaginal opening Improves the sensitivity of the vulva Helps prevent recurrent bladder infections from having sex The quality of vaginal wetness and elasticity is vital to a satisfying sex life. The necessary hormones must be replaced to achieve the same level of sexual satisfaction as you had before your hormone loss, menopause In this area of concern, most women are not willing to settle for second best! There are other causes of painful intercourse that are not from a lack of hormones, but the previous causes and treatments for painful sex treat over 95% of my patients. Vaginal dryness can also be caused by dermatologic and medical disorders such as autoimmune diseases, vaginal infections and dehydration usually from diuretics like Lasix®. The other causes of a dry vagina, vaginal infections, are listed below. The one cause that will require antibiotic or yeast treatment is vaginal infection. Let me expand on that. Usually, bacteria from the rectum is pushed into the vagina from wiping the wrong way (the right way is front to back), sex, or underwear. This is hard to avoid and is from yeast, the bacteria called Gardnerella, Strep, Staph, or Ecoli. These are NOT necessarily a sexually transmitted disease; however any bacteria can be transmitted through intercourse. The sexually transmitted disease such as Chlamydia and Gonorrhea generally cause a vaginal discharge but create pelvic scarring and infertility and have delayed pain and pain when the infection is active in the pelvis causing adhesions and scarring of the tubes. Both of these sexually transmitted diseases can leave scars and cause pain during and after the infection. If you want to do a simple and crude test at home to determine whether your vaginal pain is from a yeast or a bacteria, you can use litmus paper and it if turns blue, it is usually Gardnerella and needs an antibiotic cream or oral prescription. If it turns yellow, it is generally yeast and requires over the counter yeast medicine. The discharge for Gardnerella usually smells like “fish” and the discharge for yeast may or may not smell like bread baking. The sexually transmitted disease is not generally those that change the pH so don't be fooled by a negative litmus test. To be completely safe you should have a vaginal exam by a gynecologist or family physician or their nurse practitioner who can culture your vagina to find out exactly which bacteria or yeast is the cause, and she will prescribe the right kind of antibiotics for you. Remember if it is rectal bacteria, it will turn the litmus paper blue, but you still need a doctor to prescribe your antibiotic and they will want to see you before writing the script! In the world of post-menopausal women, pelvic pain can rarely be caused by Pelvic abnormalities. This pain is usually not from the area around and in the vagina itself but deep in the pelvis when the penis thrusts against the vagina or cervix. This is usually cause by one of the following problems, most of which can be seen on ultrasound, with the exception being adhesions. Pelvic abnormalities causing painful intercourse after menopause Pelvic masses: fibroids, ovarian cysts, retroflexed uterus, Old Endometriosis Adhesions Colon mass or masses Cervical scarring from a difficult childbirth Uterine Prolapse The anatomy requirements for intercourse are that the vagina must be stretchy and elastic, it must be able to lengthen which means it requires hormones and cannot be tethered by adhesions in the pelvis, and the uterus if you have not had a hysterectomy must also be freely moving and not folded on itself in the front or back which is called anterior flexion or retroflexion. Sometimes the uterus “falls down” (uterine prolapse) into the vagina and the act of intercourse pushing it out of the pelvis is painful. The diagnosis of these problems must be made by a physician or nurse practitioner who specializes in women's health. First a physical and vaginal exam can find ovarian, colon and uterine masses like fibroids or ovarian cysts, and uterine prolapse. The vaginal exam can rule out vaginal atrophy and infection. Lastly, a vaginal or abdominal ultrasound or both can be ordered to “see” what is in the pelvis. We require these on every menopausal woman to make sure they don't get too much estradiol to stimulate their pre-existing problem (like fibroids). Some problems can only be diagnosed surgically. Uterine and pelvic adhesions can only be seen by doing a laparoscope under anesthesia. Fortunately, they can also be treated by cutting the adhesions and placing an antiadhesion fabric around the uterus or ovaries. Sometimes the adhesions are to the bowel and the treatment requires a hysterectomy only or with the removal of the ovaries. Fibroids can grow under the influence of estrogen, and endometriosis can be active pre-menopause and make long lasting adhesions, however if the ovaries are removed or a woman has been in menopause it rarely reawakens to cause trouble. The adhesions it made before menopause still remain unless they are surgically removed. It is important that a GYN or FP Doctor rule out the presence of ovarian, uterine and colon masses because rarely they can be precancer or cancer. Your doctor will usually order the for no other reason than to rule these problems out, but they can see many other things that a patient has in the same test. We have talked about several causative issues that result in painful intercourse, the diagnosis method and the treatments for them. There are many possible causes and many appropriate treatments. Sexual Pain is a very serious issue which is often under recognized and under treated by gynecologists. In order to be an informed consumer and participate in good medical decision making, a woman must know about their body and the malfunction thereof enough to ask (or even challenge) her physician to help her treat these very fixable problems. It is not “destiny” for a woman to be dry and have painful intercourse. The goal is to have pleasurable sex, it is good medicine and good treatment you can enjoy privately which can restore a happy satisfied mood, and the natural sexual abilities and climaxes you had in your youth!
Trainer Graham Motion joins the show to discuss Lasix and give his thoughts on this polarizing and sometimes confusing topic.
New month but staying boring with training and dashing. Lasix and DoorDashing add a twist to my morning workouts but as Ann Trason said “ultras are about problem solving”. This Vlog is documenting my journey from my first injury in 40 plus years of Endurance Training. On March 9th 2020, I was out walking in the pre dawn hours like I have done for decades... Then I ended up on my back and my left leg was killing me. John's Burger washed their cooking grease on to the sidewalk and I fell like they do in the movies on the banana peel. For the next 6 weeks, I could barely walk around the house and then when I could walk, I could barely breathe. On April 25th 2020, I was admitted to the hospital for the first time in my life (I was born in 1963) and three cardiologist told me I had Congestive Heart Failure. This is my journey back to Endurance Sports... Endurance News & Random Musings https://andynoise.com/ Andy Noise Gear https://andynoise.com/gear Andy Noise Experience Stay Healthy. Be Boring. Not Epic. --- Send in a voice message: https://anchor.fm/andy-noise/message Support this podcast: https://anchor.fm/andy-noise/support
As 2021 nears, so does the expanded commitment by many major racetracks - including the three Triple Crown tracks - to ban Lasix from horses competing in stakes races. Plus, will winter racing soon be coming to the island of Antigua?
Today’s episode is an interview with Nancy Globus, a pharmacist who uses her voice to advocate for medication safety. I really enjoyed this interview because two of Nancy’s passions overlap with mine: medication safety and poisoning prevention. Nancy Globus started in the pharmacy business at a young age. Her father opened his community pharmacy the year before she was born. Nancy began “counting pills” at her father’s side and eventually earned a Bachelor of Science Degree in Pharmacy from Rutgers College of Pharmacy. Then, she earned her PharmD from Philadelphia College of Pharmacy and Science and completed a one-year residency in a unique hospital, where most of the drugs were ordered and monitored by clinical pharmacists. Nancy has worked in a number of practice settings. She honed her clinical skills in hospital practice, served roles in medical affairs, and eventually worked a number of years in the Med-ERRS subsidiary of ISMP (the Institute for Safe Medication Practices). There, she became proficient in all areas of medication safety, especially as error prevention applies to assisting the pharmaceutical and biotech industries in trademark safety testing, package label assessments, and other risk-management and regulatory issues. When she is not saving humanity from confusing drug names and hard-to-read product labels, Nancy can be found translating “medicalese” for family members and friends and obsessing over her nail polish and cosmetics collection. She remains passionate about community pharmacy and has a strong interest in patient advocacy. Nancy Globus LinkedIn Profile Nancy’s Twitter Link Highlights from the interview Nancy has a passion for medication safety and poisoning prevention. She feels pharmacists are well-positioned to communicate important safety messages. Drug names are unique for safety reasons. Medication safety officers are important. They can prevent safety issues. Nancy talked about the confusion between Losec and Lasix and how Losec became Prilosec. There is not a clearly-defined path for a pharmacist to do what Nancy does. It’s a very niche job. All her professional experiences led her to medication safety roles. “We don’t lose. We win, or we learn.” Good advice from Nancy for new grads or pharmacists early in their careers. Nancy’s dream job would be naming nail polish colors for OPI or being a medical reporter on the TV news.
Proudly brought to you by the Breeders' Cup World Championships: Emmet Kennedy is joined by NBCSN's Nick Luck and American Expert Peter T. Fornatale to review an epic weekend of Horse Racing, as the Americans took on the UK and Ireland at Keeneland. The Team review every race from Future Stars Friday and all nine races on Championship Saturday, starting with all the Turf Races, where Kevin Ryan made history with Glass Slippers, Dermot Weld adds to his Group/Grade 1 CV with Tarnawa in the Turf and Aidan O'Brien landing the Breeders Cup Mile with a 1, 2, 3 led by the Notorious PCB! We then move onto the Classic where Authentic landed the Baffert Team the $1million bonus and the rest of the Dirt Races. Some strong opinions from the lads on how the races panned out, the use of Lasix, while picking Horses to back next time. Head to breederscup.com/2020 and enjoy all the races from the Breeders' Cup again. Likes & Shares on Twitter, Instagram and Facebook appreciated
BREEDERS CUP Podcast: Hot dogs, Budweiser and YEEHAAA'S, with John Leng, Cathryn Fry and myself all macheted up with Lasix, and hopefully some BIG WINNERS for you.
Vitals & Useful Links: Learn about one important way to evaluate ankle injuries (see spoilers below if you want to know more) MD Calc: Ottawa Ankle Rules Clinical Reference: The Ottawa Ankle Rules, ft a great demonstration by Dr. Ian Stiell Podcast: EM Cases - Commonly Missed Ankle Injuries Fun Facts about Ottawa EMJC's October twist is MS2s! Let's learn about how to approach ankle injuries and a few fun facts about Canada along the way. This week Charlie (MS4) leads Arman (MS4), Kyle (MS4), and special guests Chris (MS2) and Vera (MS2) through a case of a stuntman-level ankle injury (and some poutine). How would you approach this case? As always, we learn a couple very important points about evaluating ankle injuries. You can check out a simple description of the Ottawa Ankle Rules at MD Calc, and here's a great reference with a video of Dr. Stiell performing the Ottawa Ankle Rule maneuvers. If you have any questions, concerns, or comments, please email us at emjccast@gmail.com *EPISODE SPOILERS BELOW* Here's one article we presented today Shell, I. G., Greenberg, G. H., McKnight, R. D., Nair, R. C., McDowell, I., Reardon, M., ... & Maloney, J. (1993). Decision rules for the use of radiography in acute ankle injuries: refinement and prospective validation. Jama, 269(9), 1127-1132. Here's a paper on the accuracy of the Ottawa Ankle Rules Bachmann, L. M., Kolb, E., Koller, M. T., Steurer, J., & ter Riet, G. (2003). Accuracy of Ottawa ankle rules to exclude fractures of the ankle and mid-foot: systematic review. Bmj, 326(7386), 417. And don't forget about the effects of Lasix on shark rectal glands Kinne, R., & Kinne-Saffran, E. (1979). Effect of ‘loop diuretics' on the salt secretion in shark rectal gland. Mar. Ecol, 1, 129-132. DISCLAIMER: The views/opinions expressed in this podcast are that of the hosts/guests and do not reflect their respective institutions. This is NOT a medical advice podcast, if you are having a medical emergency you should call 911 and get help. This is an educational podcast, and as such, sometimes we get things wrong - if you notice this, please email us at emjccast@gmail.com.
Vitals & Useful Links: Learn about one important cause of lower extremity edema (see spoilers below if you want to know which one) Podcast: BNP for Diagnosis of Acute CHF - EM Cases Podcast, a great discussion of BNP in the diagnosis of CHF Clinical Reference: ACC Guidelines for Management of Heart Failure Time to learn about some puffy legs! This week Kyle (MS4) leads Arman (MS4) and Abby (MS4) through a case he had of a 56-year old male with a swollen legs. How would approach this case? As always, we learn a couple very important points about one etiology of lower extremity edema. You can check out a great discussion about the use of BNP in diagnosing CHF on the EM Cases Podcast, and here's a great reference for headaches from ACC's guidelines on CHF management. If you have any questions, concerns, or comments, please email us at emjccast@gmail.com *EPISODE SPOILERS BELOW* Here's the article we presented today Daniels, L. B., Clopton, P., Bhalla, V., Krishnaswamy, P., Nowak, R. M., McCord, J., ... & Abraham, W. T. (2006). How obesity affects the cut-points for B-type natriuretic peptide in the diagnosis of acute heart failure: results from the Breathing Not Properly Multinational Study. American heart journal, 151(5), 999-1005. Here's the ACC's Guideline on CHF Management Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Colvin, M. M., ... & Hollenberg, S. M. (2017). 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. Journal of the American College of Cardiology, 70(6), 776-803. How Salt Affects BNP Levels Morten Damgaard, Jens Peter Goetze, Peter Norsk, Niels Gadsbøll, Altered sodium intake affects plasma concentrations of BNP but not proBNP in healthy individuals and patients with compensated heart failure, European Heart Journal, Volume 28, Issue 22, November 2007, Pages 2726–2731. We briefly mentioned Lasix dosing in CKD, here's an article describing various dosage considerations Oh, S. W., & Han, S. Y. (2015). Loop Diuretics in Clinical Practice. Electrolyte & blood pressure : E & BP, 13(1), 17–21. DISCLAIMER: The views/opinions expressed in this podcast are that of the hosts/guests and do not reflect their respective institutions. This is NOT a medical advice podcast, if you are having a medical emergency you should call 911 and get help. This is an educational podcast, and as such, sometimes we get things wrong - if you notice this, please email us at emjccast@gmail.com.
One theory behind elevated post-partum blood pressure is that there is a large volume of sodium mobilized into the intravascular compartment in the post-partum period. Loop diuretics have been suggested as methods to accelerate post-partum blood pressure recovery due to their ability to mobilize sodium and fluid excretions. Is there level I data on the use of furosemide for postpartum preeclampsia/hypertension management? Does the use of Lasix affect serum magnesium levels? In this session, we will review 2 recent RCTs on the use of furosemide for Postpartum hypertension management and briefly review the pharmacology of furosemide.
When 3 Heart doctors diagnosis Congestive Heart Failure, I guess i have to accept that #CHF put me in the hospital for the first time in 56 years. The Lasix made me pee away 21 pounds of fluid so I could breathe again. The left leg that was severly injured in the John's Burger grease fall did not hurt any more so the day before my 57th birthday I set off to complete the Great Virtural Race Across Tennesse. From May 1st to August 31st, I walked over 2000 KMs and got my RAT (Race Across Tennesse) buckle and then my BAT (Back Across Tennesse) banner. So why not use the fitness and try to finish my 20th Hundred mile or longer race at: The Ride To Walk 100 Mile Endurance Race September 19th - 20th, 2020 Lincoln, CA Endurance Noise & Random Musings Please Subscribe to my YouTube Channel! Stay Healthy. Be Boring. Not Epic. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/andy-noise/message Support this podcast: https://anchor.fm/andy-noise/support
This week’s episode includes author Jeffrey Testani and Associate Editor Justin Grodin as they discuss empagliflozin heart failure, including diuretic and cardio-renal effects. TRANSCRIPT: 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 Centre and Duke National University of Singapore. Dr Greg Hundley: And I'm Greg. I'm the director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr Carolyn Lam: Greg, the SGLT-2 inhibitors have really revolutionized heart failure treatment, but we still need to understand a bit better how they work. And today's feature paper is so important, talking about diuretic and cardio-renal effects of Empagliflozin. That's all I'm going to tell you though, because I want to talk about another paper in the issue very related. And it's from John McMurray from the University of Glasgow with insights from DAPA-HF. But maybe a question for you first. Have you ever wondered what to do about loop diuretics doses in patients with heart failure and whom you're thinking of initiating an SGLT-2 inhibitor, Greg? Dr Greg Hundley: Absolutely, Carolyn. That comes up all the time and how do you make that transition. Dr Carolyn Lam: Exactly. And so this paper is just so important, and Dr McMurray and his colleagues showed that in the DAPA-HF trial, the SGLT-2 inhibitor, dapagliflozin, first, just as a reminder, reduce the risk of worsening heart failure and death in patients with heart failure and reduced ejection fraction. And in the current paper, they examined the efficacy and tolerability that dapagliflozin falls in relation to background diuretic treatment and change in diuretic therapy, following randomization to dapagliflozin or placebo. They found that 84% of patients randomized were treated with a conventional diuretic, such as the loop or thiazides diuretic. The majority of patients did not change their diuretic dose throughout follow-up. And the mean diuretic dose did not differ between the dapagliflozin and placebo group after randomization. Although a decrease in diuretic dose was more frequent with dapagliflozin than with placebo, the between-group differences were small. So treatment with dapagliflozin is safe and effective regardless of diuretic dose or diuretic use. Dr Greg Hundley: Very nice, Carolyn. That's such a nice practical article. I really enjoyed your presentation of that. My next article comes from Professor Karlheinz Peter, and it's investigating the reduction of shear stress and how that might impact monocyte activation in patients that undergo TAVI. So this group hypothesized that the large shear forces exerted on circulating cells, particularly in the largest circulating cells, monocytes, while passing through stenotic aortic valves results in pro-inflammatory effects that could be resolved with TAVI. So to address this, the investigative team implemented functional essays, calcium imaging, RNA gene silencing and pharmacologic agonist and antagonist to identify the key mechanical- receptor mediating the shear stress sensitivity of the monocytes. In addition, they stained for monocytes in explanted, stenotic, aortic human valves. Dr Carolyn Lam: Lots of work done in a very translational study. So what did they find Greg? Dr Greg Hundley: They found monocyte accumulation at the aortic side of the leaflets in the explanted aortic valves. That was the human subject study. In addition, they demonstrated that high shear stress activates multiple monocyte functions and identify PZ1 as the main responsible mechanoreceptors representing, therefore, a potentially druggable target. So reducing the shear stress from a stenotic valve promotes an anti-inflammatory effect and, therefore, could serve as a novel therapeutic benefit of those undergoing TAVI procedures. Dr Carolyn Lam: Really nice, Greg. Thanks. We're going to switch tracks a bit, Greg. What do you remember about Noonan's syndrome? Dr Greg Hundley: Oh boy. Impactful, congenital disease for both the probands, as well as the family. Dr Carolyn Lam: That's truly beautifully put and you're right. Noonan syndrome is a multisystemic developmental disorder characterized by common clinically variable symptoms, such as typical facial dysmorphism, short stature, developmental delay, intellectual disability, as well as cardiac hypertrophy. Now the underlying mechanism is a gain of function of the RAs MAPK signaling pathway, kinase signaling pathway. However, our understanding of the pathophysiological alterations and mechanisms, especially of the associated cardiomyopathy, really remains limited. So today's paper contributes significantly to our understanding and is also notable for the methods that these authors use to uncover this novel potential therapeutic approaches. The paper is from Dr Cyganek and Wollnik as co-corresponding authors from the University Medical Center Göttingen in Germany. And they presented a family with two siblings, displaying an autosomal recessive form of Noonan syndrome with massive hypertrophic cardiomyopathy. As the clinically most prevalent symptom caused by allelic mutations within the leucine zipper like transcription regulator 1. They generated induced pluripotent STEM cell derived cardiomyocytes of the effected siblings and investigated the patient-specific cardiomyocytes on the molecular and functional level. Dr Greg Hundley: Carolyn, is such a thorough investigative initiative. So what did they find? Dr Carolyn Lam: They found that the patients induced, pluripotent STEM cell cardiomyocytes recapitulated the hypertrophic phenotype and uncovered, a so far not described, causal link between this leucine zipper like transcription regulator 1 dysfunction and ras map, kinase signaling hyperactivity, as well as, the hypertrophic gene response and cellular hypertrophy. Calcium channel blockade and MEK inhibition could prevent some of the disease characteristics providing a molecular underpinning for the clinical use of these drugs in patients with Noonan syndrome. In a proof of concept approach, they further explored a clinically translatable intronic CRISPR repair and demonstrated a rescue of the hypertrophic phenotype. Massive amount of work in a beautiful paper. Dr Greg Hundley: You bet, Carolyn, and boy giving hope to address some of that adverse phenotype in the heart. What an outstanding job. Dr Carolyn Lam: You're right, Greg. But now switching tracks a yet again. What do you know about ischemic preconditioning? Ischemic preconditioning refers to the process in which non-lethal ischemic stress of the heart prevents subsequent lethal ischemia reperfusion injury and provides important intrinsic protection against ischemia reperfusion injury of the heart, as well as other organs. So in this paper co-corresponding authors, Doctors, Zhang, Xiao and Cao from Peking University and colleagues provided multiple lines of evidence that a multifunctional TRIM family protein, the Mitsugumin-53 or MG53 is secreted from the heart in rodents in response to ischemic, preconditioning or oxidative stress. Now this secreted MG53 protected the heart against ischemia reperfusion injury. In the human heart, MG53 was expressed at a level about 1/10th of its skeletal muscle counterpart. And MG53 secretion was triggered by oxidative stress and human embryonic STEM cell derived cardiomyocytes, while deficiency exacerbated oxidative injury in these cells. Dr Greg Hundley: Very nice, Caroline. Tell me the take home message. How do I incorporate this information, maybe even clinically? Dr Carolyn Lam: Well, these results really defines secreted MG53 as an essential factor, conveying ischemic preconditioning induced cardioprotection. Now, since systemic delivery of MG53 protein restored ischemic preconditioning mediated cardioprotection in deficient mice, recombinant human MG53 protein could perhaps, or potentially be developed, into a novel treatment for various diseases of the human heart in which indigenous MG53 may be low. Dr Greg Hundley: All right, Carolyn. I'm going to tell you about a couple of letters in the mailbag. First, there's a research letter from Richard Vander Heide regarding unexpected feathers in cardiac pathology in COVID-19. And then, there's a large exchange of letters between Dr Yuji MIura, Chuanli Ren and Laurent Azoulay regarding a prior publication, entitled "Aromatase Inhibitors and the Risk of Cardiovascular Outcomes in Women With Breast Cancer, A Population-Based Cohort Study." And then finally, Carolyn, there's another research letter from professor, Nilesh Samani, entitled "Genetic Associations with Plasma ACE2 Concentration: Potential Relevance to COVID-19 Risk." Dr Carolyn Lam: Wow, interesting. There's also an "On My Mind" paper by Dr Kimura on "contextual imaging, a requisite concept for the emergence of point-of-care ultrasound." There's an ECG challenge, by Dr Dewland, with a case of an intermittent -wide QRS complexes. There's a cardiovascular case series presentation by Dr Nijjar on "a solitary left ventricular septal mass and amaurosis fugax." Dr Greg Hundley: That's great, Carolyn. How about we move on to the feature discussion. Dr Carolyn Lam: Let's do that. Dr Greg Hundley: Well listeners, we are here to discuss again, another important paper related to SGLT-2 inhibition. And we have with us, Dr Jeff Testani from Yale New Haven and our own associate editor, Dr Justin Grodin from University of Texas Southwestern Medical Center. Welcome gentlemen. Jeff let's start with you. Can you describe for us some of the background behind this study, and then also the hypothesis that you wanted to address? Dr Jeffrey Testani: Our lab is very interested in understanding volume overload and heart failure, why does the kidney retain sodium and why it stops responding to loop diuretics. Several years ago, when the SGLT-2 first came out, we saw them as a diuretic with the side effect of glucosuria. Back when they were still being thought of as primarily diabetes medications. But as the story unfolded and we saw that the SGLT-2 seemed to be doing something much more than just control blood glucose in diabetics and was demonstrating, particularly, a pronounced effect on heart failure outcomes, we got very interested in, better understanding this. We know that loop diuretics, they're really a double-edged sword. Loop diuretics are our mainstay of therapy to relieve congestion and heart failure patients, but they do so at the expense of quite a bit of toxicity. And we know that the loop diuretics directly cause neuronal activation, elaboration of rennin, norepinephrine, etc. through their effects directly on the kidney. In addition to causing normal moral activation through the volume depletion they cause. And as we all know, blocking the neurohormonal activation is one of the primary therapies we use in heart failure. So even though it helps our patients keep the fluid off, it does that at an expense of potentially some very negative effects. The interesting thing with the SGLT-2 inhibitors is, we've seen that in the diabetic populations, that they seem to actually improve volume status in diabetics, more so than one would really expect by the week diuretics that they are. And by and large, they were doing that without a pronounced activation of the neurohormonal system. So this led us to the conclusion that we really need to rigorously study this in heart theory and see what exactly are these effects of diuretics volume status and how much negative impact will any of those effects bring towards normal activation, kidney dysfunction, etc. Dr Greg Hundley: Very clever, Jeff. How did you go about addressing this question? What was your study design and what was your study population? Who did you enroll? Dr Jeffrey Testani: We wanted to have a pretty clean mechanistic study here. We weren't looking at ethnicity. We were really trying to understand a mechanism here and what are these agents doing to sodium handling in the kidney, etc. We enrolled diabetic patients that were stable. Per their advanced heart failure position, they were at added at a stable volume status. They hadn't had recent changes in medications diuretics, and we use the crossover design where we brought the patient in for about an eight-hour rigorous GCRT type study where we administered empagliflozin in 10 milligrams and then did some pretty rigorous characterization of them. As far as body fluids spaces, renal function, normal activation, your sodium excretion. Then they would continue that therapy for two weeks, come in for a terminal visit, that was a very similar protocol. Then we'd wash them out for two weeks and cross them over to the alternative therapy. And they were randomized whether they had placebo or epilobium first in order. Dr Greg Hundley: Very good. So a crossover design. And what were your study results, Jeff? Dr Jeffrey Testani: We were quite interested in the overall effects and it was actually quite surprising. We know the loop diuretic resistance is common and when physicians and patients are not responding well enough, oftentimes we add thiazides. And thiazides waste potassium. They waste magnesium. They increase uric acid. They usually cause renal dysfunction and significant normal activation. That was the default hypothesis that we would see that. And to the contrary, we pretty much saw the opposite of what a thiazide did. We saw a modest, but clinically significant natriuresis. So as a monotherapy, these drugs are quite weak. Although we saw a doubling of a baseline level of sodium excretion, that's sort of a clinically irrelevant amount as an acute diarrheic. However, when we added the eplerenone to a loop diuretic, we got a 30, 40% increase in sodium excretion. And just to benchmark that, if you look at the dose trial where they compared low dose to high dose Lasix, which were one X versus two and a half X, their home loop diuretic, they got a similar increase in sodium excretion. So even though 30, 40% increase in sodium excretion doesn't sound like a lot, it's all of our normal interventions. It's actually a pretty significant increase. We found that happened acutely. And to our surprise, that natriuretic effect had not completely gone away by two weeks. So the patient was still in a negative sodium balance at the two-week time point. And they actually had a reduction in their blood volume, in their total body water, in their weight, as a result of that kind of slow persistent, natriuresis that had happened over those two weeks. We were unable to detect any signs of normal MAL activation with this. There was actually a statistically significant better change in norepinephrine during the dapagliflozin period versus placebo. And there's some evidence that, that might be an actual finding of saccharolytic effect of these drugs. As in many of the other trials we've seen no, despite a reduction of blood pressure and probably volume status, heart rate stays the same or even goes down. And we saw an improvement in uric acid. We saw no additional potassium wasting. We saw an improvement in serum magnesium levels. So really kind of like I started this way is the opposite, in many ways of what we see, side effect wise, with the diuretic is what we saw with addition of an SGLT-2 inhibitor. Dr Greg Hundley: Listeners, we're going to turn now to Dr Justin Grodin, who's one of our associate editors and is also an editorialist for this paper. And Justin, we've heard some really exciting results here. The addition of a dapagliflozin to a loop diuretic enhancing the neurohormonal access and receiving some unexpected benefits on the electrolyte portfolio. Can you tell us a little bit about how you put this work in the context of everything else that we have been reading about this exciting new class of drug therapy? Dr Justin Grodin: This certainly is exciting because with the release of the DAPA-HF clinical trial, just about a year ago, we've really come to recognize that there really are substantial, long-term beneficial effects with SGLT-2 inhibition in patients with heart failure, and as Jeff alluded to, a lot of these effects, we saw that they were beneficial in individuals that are high risk or who already had heart disease and diabetes. And we weren't sure if that was going to translate to individuals with heart failure. We really saw beneficial effects in both, individuals with heart failure, with or without diabetes. So this is an interesting paradigm because, although we saw dramatic effects in long-term survival quality of life, the mechanism was actually somewhat murky. And a lot of this was transitive based on prior works. We obviously had a strong hypothesis that they would work through reducing incident heart failure and diabetics, but then we were left questioning what is the mechanism? And I think Jeff highlighted it quite well. There was the early thought that this was perhaps just a weak diuretic and that it was additive, and these patients were just getting long-term natiurer recess. And then others thought that there might've been, perhaps, some positive influence by some very low level, blood pressure reduction with these therapies. So in that sense, I think Jeff's paper really is put in context and when we reviewed it, we thought it was quite fascinating because I think as Jeff showed in his paper quite elegantly and actually in a very, very careful study, which the reviewers and your editorial staff appreciated, we really saw that there was a probably more robust response to natriuresis than we had anticipated. And importantly, this was independent of glycosuria, which is a very important observation. And if I might take a 10,000-foot view of at least this therapy and how we might think about it as an incremental therapy in heart failure, it's really doing something else. So we thought that with SGLT-2 inhibition, you get a little sodium and a little natriuresis, maybe perhaps a little bit extra, as it complexes with glucose. I think if you look at what the potential physiology would be with this therapy is that it's doing far more than that. And I think Jeff's study at least supports some of the speculation. And again, I'm going to perhaps look beyond SGLP-2 inhibitor, and then more so focus on the physiology of the proximal convoluted tubule. And given the location of the blockade, this is really priming the kidney, or at least Jeff's manuscript, and Jeff's analysis, supports the hypothesis that SGLT-2 inhibitors influence the proximal tubule environment, such that the kidney is ready to reset in natriuresis. And I think Jeff's data it at. least supports that because if we look at the proximal tubule physiology, there's really a lot more going on, then SGLT-2 inhibition. There are other receptors that it can influence that might also promote natriuresis. It can also promote increased distal sodium delivery to other areas of the nephron. And in essence, this almost, and in Jeff has put it this way before, which I totally agree. This gives the opportunity for the kidney to taste the salt, as opposed to the more common state that we have in somebody with heart failure and congestion, where, and I talk about this on rounds all the time, the kidney's response to a failing heart is to retain salt and water. So this kidney is in this perpetual state of dehydration. And I think the idea that Jeff's analysis is at least supporting, is that somehow, we were influencing the physiology in the proximal convoluted tubule, we are actually priming the kidney and readying it. We're almost hitting reset, where the kidneys may lose this physiology, thinking that the body is dehydrated and in essence, really readying it to assist with decongestion. Dr Greg Hundley: I love the way you explained that. It's almost as if I'm on ward rounds with you that just knocks home a lot of the message here, and the importance of Jeff's work. Understanding the physiology of the proximal tubule and then readying the kidney, instead of moving into a mode of retaining salt and water, actually allowing that to flow and facilitating a diaresis. I'll start with you, Jeff, and then come back to Justin. You might have unlocked a really special key here. What do you see as the next steps in research in this particular field? Dr Jeffrey Testani: I think Justin really, really captured the essence of what excites us so much about this is, most diuretics are a brute force sort of approach to getting salt out of the body. They are a stick, not a carrot and SGLT-2 inhibitors, when you look at them as how they would work as a brute force diarrheic, they are really wimpy and there is every opportunity for the kidney to defeat the of a SGLT-2 inhibitor, if it wanted to buy where they work and what they block. But the reality is, is that they really seem to be the carrot almost. if you think of resetting the sodium set point of the kidney, kind of quenching some of that salt first or sodium humidity that Justin was referring to. And the thing that's really interesting is when we look at trials like DAPA-HF. So despite the fact that they do seem to have this natural effect in blood pressure lowering effect and these different effects, they don't tend to cause hypertension, over diaresis, it's a much more of a natural, where the kidneys regulatory mechanisms are still operative. we have this duality of not causing over diaresis but causing diaresis. So it's really when the body needs to get rid of salt, it helps it do that. And so I think the next steps, at least for our research program is, we want to understand taking these drugs out of the context of stable, relatively euvolemic chronic heart failure patients. And when we put them into the acute setting of actual volume overload, do we see more robust diathesis and that natriuresis in that setting. The second thing is we want to dig into what is the internal mechanisms that are allowing the kidney to do these things. How is it that it's able to dump out salt when it's beneficial, but not leaked over to uresis. Since we're digging into those mechanisms, I think will give us some additional insight into this class. Dr Greg Hundley: Justin. Dr Justin Grodin: I think Jeff really encapsulated, or at least certainly highlighted some very important points, that are largely in parallel with where I foresee this. Because really, if you look at just study, a lot of these patients were quite stable. So the questions that come along are whether or not that this synergistic effect number one, is sustained long-term. Because there are some data, at least in diabetic individuals, that this might not be the case. So Jeff's paper elegantly highlights the influence of these therapies in two weeks. Now, whether that's sustained is certainly unclear. I think the logical next step is, "Okay. We show that we have a therapy that might prime the kidney for increased natriuresis" what are its effects and individuals that might need the natriuresis even more. So as Jeff highlighted individuals with more decompensated heart failure, that are more congested and more hypervolemic. And then obviously individuals that might be quite diarrheic resistant. This is something that I think Jeff and I have given talks on. And Jeff is clearly one of the world's experts in this space, but it's obviously a very attractive possibility that this might influence individuals whose kidneys are teased or trained into just holding onto sodium, no matter what. Or really no matter what therapies we give the kidney. I don't know if Jeff mentioned this, but at least in his analysis, they also showed through indicator dilution methods that there was a reduction in plasma volume in these individuals. And I think that's really important because we at least hypothesize that in many heart failure phenotypes, plasma volume is certainly a component of decompensation. So whether these kidneys have a more pleiotropic effect on the fluid balance from your status between the interstitium and the vascular space, long-term is really unknown. Dr Greg Hundley: I want to thank both Jeff and Justin. What an incredible, exciting discussion. And this paper, Jeff, were so thrilled to have the opportunity to publish it in circulation. And the clarity, helping us understand some of the mechanism of the efficacy of SGLT-2 inhibition. And then this unique combination of SGLT-2 with loop diuretics, potentiating, dieresis natriuresis without some of the harmful effects on serum electrolytes. And then I really appreciate both of you giving us an insight into the future where more work is needed to understand, is this a sustainable beyond two-week effect? And then, can these therapies, this combination, be helpful in those with decompensated heart failure. On behalf of Carolyn and myself, we wish you a great week and we look forward to catching you next week on the Run. This program is copyright, the American Heart Association 2020.
When 3 Heart doctors diagnosis Congestive Heart Failure, I guess i have to accept that #CHF put me in the hospital for the first time in 56 years. The Lasix made me pee away 21 pounds of fluid so I could breathe again. The left leg that was severly injured in the John's Burger grease fall did not hurt any more so the day before my 57th birthday I set off to complete the Great Virtural Race Across Tennesse. From May 1st to August 31st, I walked over 2000 KMs and got my RAT (Race Across Tennesse) buckle and then my BAT (Back Across Tennesse) banner. So why not use the fitness and try to finish my 20th Hundred mile or longer race at: The Ride To Walk 100 Mile Endurance Race September 19th - 20th, 2020 Lincoln, CA Endurance Noise & Random Musings Please Subscribe to my YouTube Channel! Stay Healthy. Be Boring. Not Epic. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/andy-noise/message Support this podcast: https://anchor.fm/andy-noise/support
People get cramps for all sorts of reasons, including underlying injury, disease, and medication side effects. The exercise-associated cramps you get during a running race may be influenced by some of these secondary factors. They may also be influenced by your genes: one of the best predictors of cramping is whether you’ve cramped in the past. The best way to avoid falling while trail running is to study the trail for hazards well in advance. But if you run, you will fall. When you’re going down, throw your hands out to protect your head and face, but don’t stiffen your elbows. With pools closed likely for the foreseeable future. Swim in the Wild! One of the main differences with Open Water Swimming is the need for safety, which features heavily below. Make sure that any race-specific workouts are done only when safety is taken care of! When 3 Heart doctors diagnosis Congestive Heart Failure, I guess i have to accept that #CHF put me in the hospital for the first time in 56 years. The Lasix made me pee away 21 pounds of fluid so I could breathe again. The left leg that was severly injured in the John's Burger grease fall did not hurt any more so the day before my 57th birthday I set off to complete the Great Virtural Race Across Tennesse. From May 1st to August 31st, I walked over 2000 KMs and got my RAT (Race Across Tennesse) buckle and then my BAT (Back Across Tennesse) banner. So why not use the fitness and try to finish my 20th Hundred mile or longer race at: The Ride To Walk 100 Mile Endurance Race September 19th - 20th, 2020 Lincoln, CA Endurance Noise & Random Musings Please Subscribe to my YouTube Channel! Stay Healthy. Be Boring. Not Epic. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/andy-noise/message Support this podcast: https://anchor.fm/andy-noise/support
Today on @MedTwitThisWeek, Dr. Avi Cooper (@AvrahamCooperMD) discusses his recent tweetorial on furosemide and the proposed mechanisms on how it works to improve symptoms in CHF. #MedTTW Published August 14, 2020 Host: Chris "The Chiu Man" Chiu Guest: Avraham Cooper @AvrahamCooperMD's #Tweetorial on how furosemide improves dyspnea in CHF. It's a venodilator and a bronchodilator? https://twitter.com/AvrahamCooperMD/status/1292134482812604418?s=20 @MedCrisis asks us, “Does furosemide save lives?” (48% says yes) https://twitter.com/MedCrisis/status/1292427000586567684?s=20 @CPSolvers and @kamal_mz with a beautiful schema on lactic acidosis.. https://twitter.com/CPSolvers/status/1293487391227994113 @GStetsonMD and the @MedEdTwagTeam (new twitter handle!) are at it again with their discussion on #HierarchyOfTeachingSkills and how their focus is now shifting to #ClinicalTeaching https://twitter.com/GStetsonMD/status/1293237368531480577 @laxswamy brings us @CritCareGame! Check out his pitch! https://twitter.com/CritCareGame/status/1293351706508566528?s=20 @BenSchwartz_MD gives us #OrthoTwitter tips… https://twitter.com/BenSchwartz_MD/status/1292971193407086595?s=20 @ID_fellows bring us their first #IDtweetorial which centers on the importance of Source Control when managing persistent bactermia: https://twitter.com/ID_fellows/status/1292815194037661697 @eemoin introduces a new phrase into my vocabulary: https://twitter.com/eemoin/status/1293373515513520128?s=21 If you want to get a head start on the next episode of @CuriousClinPod then reread @AvrahamCooperMD's thread from last year about “Abnormal Saline” https://twitter.com/avrahamcoopermd/status/1212040361188573185?s=21 Looking for #MedTTW on other platforms? YouTube: https://www.youtube.com/channel/UCzqsMnQAkVCTd0I5DuUzTfA Facebook: https://www.facebook.com/MedTwitThisWeek/ Twitter: https://twitter.com/MedTwitThisWeek Podcast Links: https://anchor.fm/MedTTW Apple Podcast: https://podcasts.apple.com/us/podcast/med-twitter-this-week/id1516685985?uo=4
This is in reference to State v Jennifer J Shipon, Burlington County NJ Prosecutor Scott A. Cofina prosecuting, court date Aug 3, 2020. The truth is never libel or slander. I am asking the State of NJ and the FBI to charge both my brother Theodore L Shipon and my sister-in-law Jennifer J. Rogers Shipon with the attempted murder by medication of my mother Laura Shipon, who is irrevocably injured with a Plavix poisoning stroke; and my father Stanley H Shipon, who survived but has his Lasix taken out of his medication regimen for 4 days by Jennifer Rogers and Ted Shipon. This was a double assassination attempt and the investigating detective hasn’t convinced the Prosecutor yet in case 2020-9956. Time to speed up the work of our civil servants. We don’t need less law enforcement. We need it to be swift as the angels. I hereby certify that everything represented here is true to the best of my knowledge. I know my Miranda rights and submit it into evidence for Burlington County NJ Prosecutor’s file 2000-1893. My electronic signature is my sworn testimony in a court of law — The Truth. Signed, sincerely, so help me God. Dr Randolph Shipon, licensed psychologist and Freemason, raised in Columbia Lodge No. 91 F&AM. The Nazis are all around us. Let’s fight them. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app · Charity Promotion: Democracy Works: This advertisement is part of a charitable initiative in partnership with Democracy Works. howto.vote
Sid Gustafson veterinarian speaks bluntly about Lasix, Clenbuterol etc
Lasix For More Endurance Noise & Random Musings! Become a Patreon! --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/andy-noise/message Support this podcast: https://anchor.fm/andy-noise/support
Fascinating discussion this week on the Can Do podcast with previous guest and award winning author Bill Heller. We talk about the microscope our sport is under and continue the debate about the use of Lasix on our athletes.
Gulfstream’s Mike Lakow joins the TDN Writers on the podcast to talk about the upcoming Pegasus Stakes and the rest of the Gulfstream meeting. Lasix, safety, Thoroughbred retirement and more on this week’s TDN podcast.
Winnie and Ashley chat about their 2019 highs and lows and how they dealt with them. Winnie and her daughters have spent a week at the AQHA Congress while Ashley wraps up her 2019 NBHA NJ01 barrel racing season. Winnie fills us in on her Congress trip and her bump in the road getting JayZ sound. Ashley is Breeders' Crown bound with her fingers crossed! Both girls chat about how the Congress and Breeders's Crown are the pinnacle of their sports and how honored they are to be apart of it. Emma is busy working, so we missed her this week, but she will be back next week with her full on Canadian accent!!!! ay
Sista anhalten på Sverigeturnén och så kul vi har haft det! Idag stannar vi till i Örebro och pratar om relativt gammal forskning om behandlingsresistent gonorré, smärta efter tonsilloperationer och en olyckligt döpt gen. Dessutom i slutet ett litet quiz om läkemedelsnamn - varför döptes Lasix till Lasix? Hör av er på @medforfattarna!
Megan Tones is a woman who was born with multiple congenital heart defects and who has undergone multiple medical procedures. In this episode of Heart to Heart with Anna, Megan details special considerations and precautions she underwent before (and during!) her travels to China, Egypt, and Japan. A native Australian, Megan has appreciated the beauty and majesty of these other countries and doesn't believe her heart defect should hold her back from the travel she and her husband so enjoy.Please take a moment to follow us on your preferred social media platforms:iTunes: https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2Facebook: https://www.facebook.com/HearttoHeartwithAnna/YouTube: https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5ZwInstagram: https://www.instagram.com/hugpodcastnetwork/If you enjoy this program and would like to be a Patron, please check out our Patreon page: https://www.patreon.com/HeartToHeartSupport the show (https://www.patreon.com/HearttoHeart)
This week we review 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
This week we review 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
He will ride the favorite Omaha Beach in next week's Kentucky Derby, and Hall of Famer Mike Smith is the featured guest from Santa Anita on the Ron Flatter Racing Pod. From Las Vegas, former National Horseplayers Championship Tour winner Jonathon Kinchen of Fox Sports Net offers his opinions about modern betting angles that are popular in racing. The Racehorses by the Letters feature looks at the best ever starting with “Y,” and Ron has a comment about the push to ban race-day Lasix across the nation. Learn more about your ad-choices at https://www.iheartpodcastnetwork.com
Emery Songer and John Hernandez go over the coalition of tracks in the United States that will phase out the use of Lasix. They also talk about the result of the Arkansas Derby. Laffit Pincay III from NBC Sports jumps on to talk about all things Kentucky Derby and where he believes the main contenders stand. Triple Crown winning trainer Bob Baffert calls in to detail his thoughts on his trio of Kentucky Derby runners: Roadster, Game Winner, and Improbable. He also talks about Triple Crown winning jockey Mike Smith electing to ride favorite Omaha Beach over Roadster.
TOTAL EM - Tools Of the Trade and Academic Learning in Emergency Medicine
Furosemide (frusemide) is a commonly used loop diuretic. Also known by the commercial name, Lasix, it is well established drug but is prone to some common myths. To help kill the dogma, we review a recently published paper discussing 10 myths regarding this frequently used medication.
How to go about breaking down some condition claiming ranks. Opinion on Lasix.
On Episode 9 of The Horse Racing Show, Kenny Rice talks March Madness in basketball and horse racing. Kenny also discusses the situation at the Santa Anita racetrack with his guests and previews some of the horses to watch for. Trainer Mark Casse speaks with Kenny about his Kentucky Derby hopeful War of Will, his preparation for the upcoming Louisiana Derby, and reminisces about growing up on the same street as the legendary Churchill Downs racetrack. Veterinarian Dr. Bonnie Barr explains her background in internal and pediatric medicine, how caring for foals is similar to caring for human babies, and provides insight for what the medication Lasix is and how it is used by trainers. Bloodhorse senior writer Steve Haskin tells us all about his Derby Dozen watch, and what to look for in the coming weeks leading up to the most exciting two minutes in sports. Connect with Us on Social Media! Twitter - @HorseRacingShow Youtube - https://www.youtube.com/c/TheHorseRacingShow Facebook - fb.me/TheHorseRacingShow Instagram - thehorseracingshow
In association with At The Races: Emmet Kennedy talks to NBC's Nick Luck to get the latest Breeders Cup info live Stateside. Then Kevin joins Emmet as the lads have a discussion on the Irish and British raiders and the complex issue that is Lasix! More to come tomorrow as we do an in-depth preview of the Breeders Cup exclusively live on At The Races. Subscribe for free on Apple Podcast's, SoundCloud, Podcast Republic, Google Play and Android Podcast apps. If you're listening on an Apple device, we'd really appreciate a Five Star Rating on Apple Podcast's to help spread the word about the show. www.attheraces.com/finalfurlongpodcast Download on iTunes itunes.apple.com/ie/podcast/the-f…id601526577?mt=2
Will the ashes of the late, great entertainer David Cassidy be spread over the grounds at Saratoga? Plus, a new study aims to find out exactly how Lasix works in horses.
In this weeks episode of the Ask Jim & Jay Podcast, hosted by Joshua Smith, the crew dives into the Golden Rules of Testosterone Optimization Therapy. Jim Brown & Jay Campbell are EXPERTS on the subject and have just released their new book which you can find a link to below! Get your notepads out and click play because there is a ton of knowledge about TOT, testosterone optimization therapy, in here waiting to be absorbed! The Golden Rules of TOT 10-15: 10) Your physician should know how to quickly alleviate common TOT side effects. These effects include high or low estrogen readings, itchy nipples (gynecomastia), water retention, lack of erectile strength, and mood imbalances. The potential side effects of TOT are minimal in scope, simple to detect and easy to safely correct when managed by a qualified TOT physician. Front-line treatment options should first involve changing the dose of testosterone(usually lowering) and the frequency of said doses before introducing medications that are specifically used for alleviating side effects. This rule is especially important when it comes to introducing AI medications into one’s TOT regime, which can cause terrible bone mineral density issues over time. 11) Therapeutic dosages of testosterone can completely change your physique by decreasing body fat and increasing muscle mass, but ONLY when living a dialed-in lifestyle. This lifestyle MUST CONSIST of a clean insulin-controlled diet, in combination with productive resistance and cardiovascular training. If you think you can hack life with TOT while eating Cheetos and laying down on the couch all day, you are DEAD WRONG!. TOT is NOT a magic bullet. Also, if you think you can get away with skipping cardio and doing nothing else but train with weights, think again. You’ll end up getting average to below average results at best. You must do cardio on a regular basis to keep your blood supply oxygenated, and decreasing the thickening of blood (via increased red blood cell counts) often caused when using injectable testosterone. 12) If Your body fat is over 30% (i.e. you are obese) and you start TOT without a FIRM COMMITMENT to getting rid of it, you will fail miserably. There are too many biological systems that are not functioning properly when you are obese. As a result, using testosterone in isolation can create additional problems. As discussed in the book, obesity and high aromatase levels go hand in hand with low testosterone levels. Dr. Rob Kominiarek says that when you are a ‘metabolic emergency’ due to things like insulin resistance and metabolic disorder, nothing will work ‘as expected’ until all systems are operating normally. Therefore, GET RID OF YOUR BODY FAT or accept inevitable failure as the likely result. 13) Almost every single “testosterone boosting” supplement sold today is a complete scam. The cold hard truth is that there’s little to NO SCIENTIFIC EVIDENCE which supports the claims made by supplement companies about their testosterone boosters actually raising testosterone levels. The only proven way to raise and optimize testosterone levels is through pharmaceutical means (i.e. utilizing TOT). This is because powerful factors in our modern-day environment are constantly placing our endocrine systems under siege. This environmental assault overshadows most men’s natural ability to produce testosterone, and their efforts to fix low testosterone levels. It is the opinion of the most advanced and progressive physicians, that only Type A personality types can fix their issues naturally, due to their commitment and their militant attention to detail. 14) There is nothing morally wrong, unethical or illegal about optimizing your body’s testosterone levels. It’s the exact same thing as having Lasix, or an artificial hip replacement surgery. Using TOT productively is a lifelong strategy, and so you need to be financially stable in order to start therapy. . Being able to pay for your treatment and any additional medications (when necessary) MUST BE factored into your daily expenses. 15) When using injectable testosterone as a delivery system, the optimal protocols to choose from in order are as follows: Option 1A: 10-30 mg of testosterone injected daily. This provides the most stable testosterone levels (i.e. mimicking endogenous production of testosterone as closely as possible), and it will also help to minimize aromatization (thereby minimizing side effects) and erythrocytosis (blood thickening). Normally, this type of protocol works well for individuals with a Type A personality. Option 1B: 50-70mg of testosterone injected every other day (EOD). This is a nice compromise between injecting yourself daily and injecting yourself twice a week. This protocol is best for individuals who cannot bring themselves to administer daily injections. Option 2: 50-100 mg of testosterone injected twice a week (preferably every 3rd day). This option is the MOST POPULAR CHOICE, and is preferred by most patients because they don’t have to inject themselves too often.Additionally, this protocol is still more advantageous than once per week therapy. To Get on the Waiting List for The TOT Bible! http://TOTBible.com http://metabolicblowtorchdiet.com/ https://www.amazon.com/exec/obidos/ASIN/B079JVH28N/trtrev71-20 Thanks for watching don’t forget to subscribe for daily content! https://www.youtube.com/subscription_center?add_user=joshuasmithaz Join the Free Private GSD Mode Facebook Group - http://www.facebook.com/groups/gsdmode iTunes - https://itunes.apple.com/us/podcast/gsd-mode/id964583650?mt=2 Full Website - http://www.gsdmode.com SUPPORTED BY: Perfect Storm - http://www.perfectstormnow.com 90 Day Mastery - http://www.90daymastery.com TRT Revolution - http://www.TRTrevolution.com GSD Shirts - http://www.gsdmode.com/gsd-mode-apparel CONNECT WITH US http://facebook.com/joshuasmithGSD http://instagram.com/joshuasmithgsd http://twitter.com/joshuasmithGSD
The post Furosemide (Lasix) Nursing Pharmacology Considerations appeared first on NURSING.com.
Speaker 1: Hi everyone. As a quick introduction, this is the full length recording of Anwar Chahal's interview with Calum MacRae from August 2017. A portion of this interview was included in episode seven of the Circulation Cardiovascular Genetics podcast "Getting Personal: Omics of the Heart". As we couldn't fit everything into that regular podcast episode, we've released the unedited version as a special, feature-length podcast. Enjoy. Dr Anwar Chahal: My name is Dr. Anwar Chahal. I'm a Cardiology Fellow in Training from London, U.K., and I'm doing my research fellowship here at the Mayo Clinic, and I'm very honored and delighted to have our guest, Dr. Calum MacRae. I searched for Dr. Calum MacRae's biography online and it came up with a Wikipedia page talking about somebody who's a rugby coach. So, Dr. MacRae, I hope that's not another one of strings to your bow, that's something else that you manage to squeeze in amongst everything else that you do in your busy and punishing schedule. Dr Calum MacRae: I did play a little rugby in my day, but I haven't coached any, I can assure you. Dr Anwar Chahal: So, you are the Chief of Cardiovascular Medicine, you are an MD, PhD by training, and you are Associate Professor at Harvard Medical School, and your expertise, amongst many other things, internal medicine, cardiovascular diseases, but in particular, inherited cardiovascular conditions. Is there anything else that you would add to that? Dr Calum MacRae: No, I'm a big fan of generalism, and I am quite interested in cardiovascular involvement in systemic disease as well, but largely as a means of keeping myself abreast with the biological mechanisms in every system that seems to be relevant to cardiovascular disease. Dr Anwar Chahal: So, that reminds me. Once I heard you talk, and you mentioned to all those people that were considering cardiovascular genetics the importance of phenotype and actually how people have become increasingly super-super-specialized, becoming the bundle branch block experts or the world's authority on the right coronary cusp of the aortic valve, and how things were now going full-circle as people actually need better and better, more general understanding so that we can accurately phenotype. And you once joked that you'd actually done residency three times, so you know the importance of having a good generalist base, so could you expand a little bit on that? Dr Calum MacRae: Well, I have to tell you, it wasn't a joke. I did actually do residency three times. But, I think the most important element of that theme is that biological processes do not, unfortunately, obey the silos in which medical subspecialists operate. So it is increasingly important to have a broad-based vision of how phenotypes might actually impact the whole organism. That's particularly true because it helps us ratify disease, so that there are mechanistic insights that come from the different cell types and tissues and biological processes that are affected. I think, in general, that is something that we've all appreciated, but as time goes by and people become more and more specialized, it's less regularly implemented in day to day clinical practice. And so, particularly as molecular medicine becomes more and more penetrant in clinical disease management, I think you're going to see a return toward some generalism. Obviously, procedural specialties are the exception in many ways in this setting, because you need concentrated procedural skill. But in general, particularly for translational scientists or scientists who are interested in the underlying mechanisms of disease I think, I see a general movement towards a degree of generalism. Dr Anwar Chahal: Indeed, and in terms of, as you say, trying to understand those disease processes and trying to, let's say for example, make sense of the incredible amounts of information that can now be gathered with genomics and high throughput omics, you believe that it is actually more of a requirement to be able to understand that now that we can gather this high resolution and broad depth of data? Dr Calum MacRae: Yes, I agree. I think one of the core elements of modern clinical medicine is that the phenotypes have, in the last 50 to 100 years, we've really focused more on improving the resolution of existing phenotypes than expanding the phenotypic space. To be completely frank, I think we've extracted a lot of the information content that we can from the phenotypic space that we've explored, and what we need to begin to do is to find ways to systematically expand that phenotypic space. I think there are a lot of reasonable ways of doing it just by thinking about other subspecialties. So, for example, in cardiovascular disease, we've focused very heavily on anatomy and physiology, but we haven't really done much in the way of cell biology. Whereas, in immunology, partly because there's access to those cell types, it's possible to do much more detailed cellular phenotyping. In neuroscience, we're now doing functional MRI, and looking at individual subsets of cells in the brain, and their function in the context of particular challenges. My general thesis would be that the type of strategy would serve us well and that there's also, I think, an important mismatch between the dimensionality of phenotyping that we currently undertake and the scale of the genome and epigenome, transcriptome, et cetera. So, it's not surprising that we can't be convoluted genome of 10 to the nine variants with a phenome that are present only really has about a 10 to the four phenotypes. And so, I think some systematic right-sizing of that balance will be necessary. There are lots of things that we record that we don't even think of as phenotypes, and there are phenotypes that we record that we don't really think about how to optimize the information of content. And so that's one of the things that we have begun to invest time and energy in. And thanks to the support of the American Heart Association, Verily, and AstraZeneca, as part of the One Brave Idea, we have elected to fully focus on that area in particular in coronary disease. But I think it's a generalizable problem with much of modern medicine that we tend to have focus on phenotypes that, in many instances, date back to the turn of the last century rather than to modern molecular and cellular biology. Dr Anwar Chahal: So, you beautifully brought us to the first question, which was to ask you about One Brave Idea. Could you just, for our listeners who aren't familiar with that, just give a little bit of a background on One Brave Idea, and you've already thanked the people who have funded that, but how did you actually reach the point where you thought that this is something that really, really needs to be done? What's the process of reaching that point of bringing this idea to fruition? Dr Calum MacRae: I think we had recognized in many instances that the families that we were seeing in cardiovascular genetics clinics were much smaller, the diseases appeared to be less penetrant than the original families that we studied when we cloned many of the disease genes. This was work that I did as a post-doctoral fellow in John and Christine Simons lab many years ago. One of the things that was pretty obvious was that there were subtle pre-clinically or sub-clinically affected individuals in almost every family. And that made me ... That implies that the average family is so different from the extreme family. Is it something to do with either the resolution with which we were assessing disease or are we actually just measuring the wrong elements of the underlying genetic trait? So that, for example, is a dilated cardiomyopathy family actually a family that is susceptible to dilated cardiomyopathy in the context of some unmeasured conditioning variable, maybe a viral infection or an exposure. And because we're not measuring the exposure, or we're not measuring the underlying diaphysis, we're only measuring the final state, so we only classify people as being affected if they actually have an extreme phenotype. Are we, therefore, missing the core elements of the biology? As part of doing that, we began to look outside the heart for other phenotypes, and one of the things we recognized ... This was in cardiomyopathy ... Was that different cardiac phenotypes were really aggregates of much more granular, multi-system phenotypes. So there would be families who would have dilated cardiomyopathy, but they would also actually have abnormalities, for example, of the distal interruptus muscles, and no other muscle group in their entire body. And in fact, the distal interruptus muscle phenotype was much more obvious than any cardiomyopathic phenotype. So you start to understand that either other extra cardiac or electrical phenotypes, or maybe even sometimes neurofunction phenotypes are more penitent features of some of these disorders, albeit rare disorders. And so that immediately leads you to think are most of the common traits that we look after really aggregates of things that really only share the relative frequency of the core phenotype, which often dates back to decades earlier when phenotyping was at a much more superficial level. So that vicious cycle perpetuates itself if we never look more deeply or look outside the constraints of a particular subspecialty. And so we have begun many, probably almost four years ago, to build a sort of next generation phenotyping clinic where we tried to bring either cell biology or molecular biology from outside the heart into phenotyping patients in a cardiovascular clinic. That idea was in our DNA, that's probably not the right way to say it, but it's something that we had worked on in a cardiomyopathy setting. Dr Anwar Chahal: Right. Dr Calum MacRae: And so then when the RFP for One Brave Idea came out, it seemed like a natural expansion of that to try and think about how you could apply new phenotyping in current disease. One of the inferences from that line of thought is to move, essentially, beyond ideally much upstream of the shared final common pathway so that you can begin to identify discreet underlying mechanisms. And then, given the success of cardiologists, and cardiology in general, in prevention, it became obvious that really what we wanted to do was to try and understand not just disease, but also wellness. And to do that in a way where we could potentially detect the transition from wellness to the very first stages of the disease or the diseases that we have labeled as atherosclerosis or coronary artery disease. That was the genesis of the central idea of the application and something that, obviously, we were excited to get the chance to pursue as a result of the generosity of the funders, and the vision of Nancy Brown at AHA and Andy Conrad at Verily, to not only award funding in a different way, but to also really try and drive us to think differently about how we executed on a research product. How we move forward, not with a five-year plan, but with a rapid cycle early hypothesis testing, fail fast and fail early, if you are going to fail, strategy. Rethink not just the focus of the research project, but the mechanisms by which you execute on it. I think one of the core elements of this is, obviously, we want to make sure in doing this that we build on all of the incredible work that's been done in the last 25 or 30 years in coronary disease, whether it's the pharmacologic work, or the genetics work that has emerged in the last few years. Those are all important building blocks, and what can you do that leverages all of that existing data and adds to it? Phenotype is obviously one of the most important areas where you can bring something to the table that add to existing genotypes and also layers in on top of existing pathophysiologic models. From my standpoint, it was an efficient strategy, and one that we hoped would also help us engage the people throughout the community in different ways of using data that might already have been collected or we were going to be able to collect for the first time. Dr Anwar Chahal: In terms of One Brave Idea, where is that right now in terms of execution, as you mentioned? What's the progress so far, and is anything that's come out already that you can share with us? Dr Calum MacRae: Yeah, of course. So we have begun a variety of different approaches to thinking through the best way of exploring this phenotypic space. One of the obvious things is you can take a couple of strategies to move into this unknown unknown. One of them is to take an incremental approach to move slowly from the areas where we have already established knowledge, and to move into new areas from that home base. And the other is to take a more agnostic strategy, which is to say are there orthogonal ways of thinking where you could look at a particular type of biology in a very focused way in coronary disease. You can define that in lots of different ways. You can say maybe we do it at an organelle level, or maybe we do it at some orthogonal component. The microbiome might be an obvious one. Another one that has been considered would be nutritional or other common environmental exposures. The nice thing about the flexibility of the funding is that we can afford to test multiple different hypotheses early on, see which of them has the best signal, and then invest more deeply in those that have shown early signal. At the moment, we have multiple active projects that are really testing those initial hypotheses. Is there a way of moving from the known genes that cause coronary artery disease and trying to understand are there novel phenotypes that are associated with those. And then another approach would be to take people with very early or pre-clinical disease and test areas of biology that have never been tested in atherosclerosis or in coronary disease in a systematic way. We could imagine lots of ways of doing it, but you might think about, lets say, looking at endocytosis, a process that we know already is affected by the core genes in familial hypoglycemia, but we've never really found ways to measure that in a rigorous fashion. In large populations of individuals, are there different ... Well, we know already there are different forms endocytosis, but are there discreet port ablations that might affect those. Another way of looking this might be to pick an organelle. Pick the peroxisome, or pick the nucleolus, pick some other element and ask how does the function of this organelle change in individuals who have early coronary disease. Where its boring each of these types of things systematically, and trying to learn not just which are the most important areas to focus on, but also trying to learn are there strategies that are useful that you could use in another disease. In other words, are there generalizable approaches to expanding phenotypic space that makes sense. I think one of the things that perhaps we underestimate about a genome is that it is the only bounded dataset in all of biology at the moment. There are no other bounded datasets. There is an infinite number of potential exposures. There's an infinite number of potential phenotypes that we could record, or at least as far as we know, are there ways of beginning to establish the boundaries of the phenome, the boundaries of the exposure or the exposal and how do we begin to do that in a way that efficiently yields new information. That's where we, as a consortium, have focused in the last few months. We're also, obviously, investing time and energy in thinking how do we begin to remodel the way in which research is evaluated and funded. The strategy that we've taken there is almost like a not-for-profit venture fund where we try and bring in ideas that we think might be able to leverage what's known already and move the field faster towards new pathways or new approaches to prevention, which are the core deliverables of the One Brave Idea award. As part of doing that, we obviously get the chance to interact with lots of exciting and creative scientists and that's something we're looking forward to doing in lots of different venues. We're reaching out to lots of people and lots of people are reaching out to us. We're trying to find ways to evaluate and prioritize science and then bring that science to fruition through novel approaches to funding it, either directly or as a joint venture with a foundation or some other funding source, or even as a joint venture with a commercial partner to try and move the field forward as efficiently as possible. Dr Anwar Chahal: Thank you very much for that, and I'm sure we all eagerly look forward to the results that are going to be coming out from One Brave Idea over the next few years. I'd like to now move on to genomic medicine training and you were involved in a statement that was put out regarding this. I think training across the world has increasingly recognized the importance of genetics and genomics, but I just want to share one little anecdote. My wife is a primary care physician, and I was visiting the GP practice where she works, and she'd mentioned that I had an interest in genetics and genomics. One of the partners came out with one of these reports that a patient had sent their sample to a private company, got this analyzed, brought it in to the clinic appointment and asked for an interpretation. The GP partner said to me, "I've absolutely no idea what any of these numbers, values, et cetera, mean, and I actually am looking forward to my retirement, because I really don't want to have to cover all this. Can you help me with it?" I sort of remember hearing Dr. Weinshilboum talk here at Mayo Clinic, who's really pushed forward pharmacogenomics, and he's been arguing for quite some time, as I've heard you say as well, that genomics and genetics is just going to be a part of the medical record in the same way that hemoglobin or a chest x-ray is. People better catch on because it's here, it's available commercially. People can send their samples directly, without the doctor's involvement, and then it's trying to make sense of all of that. I think, as a community, research and clinical, we have to take this very seriously. I'd be grateful for your insights on that, and then if you could then tell us what would be the best way for the up and coming generation and for programs to incorporate that into their training? Dr Calum MacRae: So, I think you're right. There is a general tendency in the public domain to test a variety of different genotypes. And in many instances, I think, the key elements are how do we as a profession, conceive of these tests? I think one of the things that we forget, perhaps at our peril, is that many of these things are problems that we've encountered before. There's a natural cycle of different tests in medicine where they start off in the academic medical centers, they propagate into the periphery, and then eventually they're assimilated as part of internal medicine. I think the scale of genomics is obviously somewhat broader than many individuals have seen in the types of data that they deal with on a day to day basis. But I think that's something that's happening in everybody's life. In every aspect of your life, you have many more channels to deal with. You have many more choices in the supermarket to deal with. So, I don't see this as a sort of existential challenge to medicine. Quite the opposite. In my experience, the core things that we need to remember is that DNA is no different from any other assay except for the fact that it's relatively straightforward to do DNA diagnostics. It's technically not as sensitive a set of biochemical issues, as are many other assays that we use in day to day clinical practice. The other thing that I think is perhaps a key element is it, as I said a few minutes ago, it's a bounded dataset, and it's stable for your whole life. You only need to have it tested once. So, to sort of invert the typical diagnostic paradigms, instead of a primary test being interpreted in the context of an ongoing clinical event, the test may have been present for decades, and the result will evolve over time, in light of the changing phenotype or some new information with respect to that genotype. What I've actually looked on genomics as is almost an organizing principle for the way that you build care. In fact, I see quite frequently, we now probably have an average one or two new patients a month in my clinic who bring their entire whole genome with them, either an axiom or a whole genome. And so, we've begun to really get to know quite well how to manage patients. Obviously, there are a selective of patients. But one of the things that I have found is that patients are really quite astute in understanding that genotype and phenotype are not deterministic relationships. What you have to do is always interpret these things in context of a probabilistic understanding. Most patients, I think, when they're told this, understand that we're going to learn much more about genomics going forward than we will ever imagine we could know at the present. That will involve lots of different things. It will involve new ways of displaying data, new ways of thinking about the data in the clinical context. I actually think one of the most interesting things about genomics, and to be honest, any assay is that they rarely reach any form of maturity until they are used in the clinic, until they are actually used in implementation. For example, many genetic tests at the moment, don't change therapy and they don't change outcomes. But partly, that's because they've never been studied in that context. One of the things that I think Glen [inaudible 00:26:58] has to be really congratulated for is his focus on pharmacogenomics as being one of the early areas in which this will really move forward. I believe that by immersing ourselves in it, by actually trying it in the clinic, we're going to learn much more. Part of that gets back to the original topic that we spoke about, which is phenotype. The only way to really begin to understand collection of phenotype is if you do it in the context of existing genotype, I think. And so, as we move into new phenotypic areas, we're not going to be able to test everything and everybody. I think there, the genome will end up being an important framework, lifelong framework for the management of a patient's diagnosis, prognostication, and then therapy, potentially in that order. I think you need a whole different set of skills. You need a whole different set of technologies. But most importantly, you need information that you can interpret in the context of the person in front of you. Until you can make mechanistically important insights with one person, it's going to be very difficult for genomics to really change medical care. That's something that I think we should be focusing on. I think we've tended to have an associate of strategy for genetics. We haven't driven it into the clinic. As we drive tests into the clinic, whether it's troponin T or whatever, you begin to understand much better how to use them. Although, sometimes, that can also go in quite extreme directions that you may not necessarily anticipate. Troponin originally was a stratification tool for acute coronary syndromes, and now it's virtually a diagnosis in its own right. And I think you'll see that tendency revert over time as people begin to understand the biology of troponin, of isoform switching, and peripheral tissues of the way in which troponin may represent very different disease biologies. At the moment, it seems like it's a very simple and straightforward yes/no type of test. There's no such thing in medicine, and I think that's what we're learning about genomics. Instead of conceiving it as a series of ten to the nine yes/no tests, we're going to end up with a very different vision and view of how it can be implemented in clinical practice. And that can only come from having clinicians and geneticists work together on this. In fact, one of the things that we've been doing in the partners environment with some of our colleagues, and I have NIH funding to do this with Heidi Rehm, with Sandy Aronson, and with Sean Murphy, is to think about how we display data, but also how we collect information in light of that genomic data that helps in an iterative way and a learning fashion, informed genotype/phenotype relationships in a much more probabilistic manner than we have done to date. There are lots of efforts in that space, that just happens to be one that I'm involved in. But I think it's a generalizable approach that you're going to see moving into the clinic in the next few years. From the standpoint of training, I think what you want to do is to get exposure to all types of genetic information so you understand common alleles, rare alleles, genomics, and individual panels. I think the best way of doing that is to have that be part of training programs. In fact, with one of my junior colleagues, Dr. Aaron Aday, we recently wrote a short piece highlighting how important it will be for all of us to come together to think about how do we start to introduce the concepts of genomics into standard clinical training programs. And that's something we're working on fairly avidly at the Brigham, and I'm sure there are ... I know there are efforts at many other institutions to do similar things. Dr Anwar Chahal: That article was published in Circulation in July of this year, if anybody wants to download that. I think if we talk to clinical trainees and ask them what are their concerns about training, as you know, training can be very long in cardiology, which is a procedurally based specialty, whether or not you become an invasive proceduralist at the end of it, there is that component at the beginning. Do you think a standard, in the U.S. a standard three-year program with two years of clinical and one year of research, can incorporate that at a sound enough level to allow somebody to practice? Do you think we're going to look at increasingly a one-year, or a six-month, sort of add-on fellowship for those interested more on the inherited side or more on the genomic side? I, like yourself, trained in London, and the training programs are longer in the U.K. It was probably six years when you were there, it shortened to five, and now increasingly, it's going to become six and maybe even more with a general fellowship for five years, and then a super-advanced fellowship. Inherited cardiovascular conditions, certainly there, has become a module that is encouraged for people to take and then become somewhat certified in inherited cardiovascular conditions. What do you think there, in terms of incorporating all of that as well as learning basics of echo, and device therapy, and catheterization, what are your thoughts? Dr Calum MacRae: Again, I look at this as a spectrum. There's a trajectory for all of these types of innovation and knowledge. It starts off being super-specialized, it goes into a more general location, and then eventually, it's an integral part of everybody's clinical practice. I do think that what you're going to see is rather than, and this is already, I think, the case in many elements of medicine. Medicine has already exceeded the knowledge base, even when I was training, by probably a log order in terms of the complexity and extent of content, not that I trained that long ago. One of the core elements that I think that we're seeing is that we need to move medicine from what I believe has become somewhat deprofessionalized state, to one where you're actually focusing not on the actual core knowledge that you bring with you to the table, but actually the way in which you integrate knowledge. So, I think the focus of training is going to change somewhat. It has had to change in other fields. Medicine, I think, for a long time favored that sort of single, comprehensive approach in one mind. And medicine is going to become more of a team sport, and it's also going to become more of a knowledge integrator profession that it has been for some time. It's interesting, when medicine started, there was so little knowledge that you really had to have almost every physician be an experimentalist using [inaudible 00:34:48] of one experiments in front of them. I think the way that I see medicine evolving is that as the knowledge base and the rigor of that knowledge base improves, many of the things that we think of as professional activity today, will actually devolve through primary care and, to be honest, into the community. There are many things where the rigor of the underlying [inaudible 00:35:12] are as such that there's no reason for a licensed provider to be involved. We allow our patients to install their own wireless networks without a technician. I'm sure most of them could look after their own lipids pretty effectively if they were given the right information. So, a lot of stuff will begin to move in that direction. And as that happens, I think the way in which information is displayed, the way in which data are collected, and the workflow around integrating information will change. That doesn't get past the point that you brought up, which is that that will probably take a couple of decades, and in the interim, I think people are going to end up training in modules of subspecialty, but I think one of the things that I sometimes like to ask myself is what's the end game? Where is this going to end up? And can we build systems that train directly for that end game, rather than going through these intermediate steps. I think that's something where I think we tried, in the short piece that we wrote in Circulation, to argue that everybody should have some exposure, and that that exposure can change over time. We should be equipping people, not to know genomics, but to be able to learn how genomics is impacting their patients for the next 50 years. That model of professional training is actually the one that really was the dominant model until maybe 100 years ago. And then, for reasons that don't quite seem obvious to me at least at the moment, we sort of tended to slowly move to more of a learned knowledge base that was then applied. Physicians sort of steadily got to the point where we're now data entry clerks. The actual amount of professional and intellectual engagement has, I think, slowly diminished in many medical subspecialties and medical specialties. The opportunity that genomics and other advancements in technology in medicine bring is the chance to, I think, reprofessionalize ourselves to move from just simply defining ourselves in terms of the knowledge base that we each bring to the table, but defining ourselves rather in terms of how we put the knowledge together around individual problems and individual patients. It's a very much more patient-centered biological approach than perhaps we've had over the last couple of decades. I think these are ... I'm obviously stating a lot of this somewhat in extremes, but I think that these are general trends that you see in medicine. They've happened in other fields as well, and people have overcome them. It's usually a function of changing the workflow itself, of changing the way in which the information ends up in the professional's hands and how you collect the data that you use, then, to interpret the existing knowledge. That, I believe, we haven't really reworked probably since Ozler's time. It is amazing that we still have workflow ... I mean, it's amazing in lots of ways. It's an amazing tradition, but it is quite interesting that we still have workflow that is probably largely dependent on what Ozler liked to do when he was growing up in terms of the times of day that he got up and his workflow. That's sort of instantiated in many ways in everything that we do. Nothing entirely wrong with it, but there's a lot happened since then that we haven't really changed. Medicine is not yet, in many instances, a 24/7 profession, and yet most other things that have much less in the way of impact on society, are already 24/7 professions in many settings. So, I think you're going to see a lot of demographic changes in medicine that come from the advent of technology and other industries. And I think those will all transform the way that we imagine training in medicine, along the same sort of timeline as some of the traditional approaches that you described, building out a training module and then having a subgroup of people do a six-month or a year of extra training. I see that as a short-term solution. I think, ultimately, longer term solutions are changing the whole workflow of medicine. Dr Anwar Chahal: What have you done in your own program at the Brigham to introduce genomic medicine training for fellows? Dr Calum MacRae: We are building out ... Obviously we have a fairly large cardiovascular genetics clinic. I think probably the largest in the world. We have now seven, soon to be eight, providers working only and wholly in cardiovascular genetics. We therefore have the ability to have our fellows rotate through our genetics clinic. We have inpatient and outpatient genetics services. And we also, obviously, involve our fellows in a lot of the academic pursuits going on in both our genetics and genomics programs in the cardiovascular clinic. As we do, our colleagues are no longer in training. We have regular, in our clinical conference slot, we have, several times a year, a genetics component. And then, what we have also, is an integrated training program with clinicians and pathologists that is really bringing the individuals who are understanding the technical aspects of the genetic testing with the individuals who are learning and understanding the clinical aspects of that testing. And so, we imagine over time that this will evolve into potentially the type of specialist module that you described. But also, into a fixture that goes all the way through our two-year clinical training program. We've sort of taken the point of view that we probably need to do a bit of both. We need to, given what I've said in the last few minutes, that we need to take a thread that recognizes a short term and intermediate term need for specialization, but also recognizes that we have to equip every one of our trainees, and every one of our physicians with the ability to begin to learn the underlying sides of genomics, and the underlying approaches to using genomics in every aspect of clinical cardiology. And so, we're doing both of those things, and have active efforts in both. Dr Anwar Chahal: You mentioned integration with pathologists, but for our colleagues who are not clinicians, what about the research angle, and the scientists, when they're in training? Is that integrated so that we are getting this meeting of minds that is essential? Dr Calum MacRae: Absolutely. In fact we, thanks to a variety of efforts at Brigham Women's, we have now at least three separate venues in which this occurs. I mentioned cardiovascular genetics clinic. We also have a genomic medicine clinic, which I'm one of the clinical co-directors for, where we actually have cases that come through routine clinical care that seem as if they would benefit from whole genome or whole axiom sequencing. And then we have a weekly conference that's actually led by Dick Maas and Shamil Sunyaev, two of our genetics colleagues, and taped in specialists from Althrop Medicine as well as scientists from the entire Harvard Medical School environment. So we bring everybody together around mechanistically solving individual clinical cases. And then the third venue is one that's part of a national network, the Undiagnosed Diseases Network. We are one of the sites on the national NIH-funded UDN network. And there again, one of the themes is identifying individuals or families who would benefit from both rigorous genomic analyses as well as much deeper phenotyping. That's been a program that I think has been very exciting, and one that we, again, have learned a huge amount from in terms of how do you begin to build the infrastructure that brings, not just the fresh clinician to see the patient, but somebody who ... A whole team of people, who understand and can evaluate all the biological aspects that are relevant in that patient. It also brings to bear the scientific expertise that you might need in order to make a mechanistic connection between genotype and phenotype in that one individual. And some of that involves animal remodeling. In cancer, for example, there's a concept that has emerged over the last two to three years of what's called co-clinical modeling. Once you've identified some of the genomic features, it allows you to begin to model in an animal, in parallel with the trajectory of the patient, and individual [crosstalk 00:44:54]- Dr Anwar Chahal: As some people call them. Dr Calum MacRae: Exactly. Creating an avatar. And in many instances, that's an avatar that includes multiple different disease models. We have begun to do that in the cardiovascular space. I think, obviously it's early days yet, but I think there are lessons to be learned about how you build the types of infrastructure that allow people to move beyond this state where a patient's outcome is dependent on him seeing the right doctor, on the right day, at the right time. There are actually systems that funnel the patients into the right venue based on objective criteria at every stage. I think that's the type of reorganization, re imagination of the medical system that we need. We sort of duplicate things in lots of different areas, and you're still dependent on hitting the right specialist, on the right day, at the right time. Or not seeing a specialist. Seeing a generalist on the right day, at the right time, who is able to put everything together. Or even hitting somebody who has the time to listen to your story in a way that helps you identify the exposure or the genetic basis of your condition. If we recreate the professional environment that I talked about earlier, I think in ways that are both traditional and novel at the same time, I think we will do ourselves a great service and build a platform that lets all of the technologies, including genomics that we've talked about today, begin to impact patients in a real way on a regular basis. Dr Anwar Chahal: Thank you for that. One question I think is important to look at from the other side, you've gone from One Brave Idea to one revolution in medicine if I can be so bold. You mentioned so many other services are 24/7. You give an example, you can book your hotel in Shanghai sat in the Midwest, and you can change your booking on an app on a phone, and yet in medicine, it's so difficult to arrange an appointment. We have resisted that 24/7 service, aside from the acutes. But for the sort of chronic workload that we have, the 24/7 model has been resisted. What do you think are some of the challenges? Because I can almost hear members of our profession saying, "Well, who wants a 24/7 service and who wants to provide that 24/7 service?", and is it always necessary to have that 24/7 service? As you say, so many things, such as hypertension treatment, you mentioned lipid management, could actually be done reasonably well by patients who are well trained. And certainly in heart failure, you can teach patients to take their Furosemide or their Lasix by weighing themselves and adjusting it, and can do it relatively well, and relatively safely. What do you think are the challenges to get the profession to realize that this is what's going to happen, and they've got to get on board? Dr Calum MacRae: Well, I don't think you want to make it somehow mandatory. I think there are elements. Every patient is different. I think that's something we've used as a chivalrous for many decades as a profession. The reality is that we don't do very well. It takes, from the time a medication hits the guidelines, not the trials are finished, but the time that it gets accepted into the guidelines, let's say as a Class I recommendation. The average time to reaching equilibrium in the population is 12 to 15 years in cardiovascular disease. So you'd hate to be the person who got that drug in the 11th year, if you actually end up having your event in year three or four. And yet you can upgrade software for your phone, and hundreds of millions people upgrade it in the first couple of days after a release. So, we have to build systems that allow us to be as efficient as every other element of our lives, and yet don't, in any way, diminish the importance of the personal interaction, the healing interaction that comes from a patient provider encounter. I think we do ourselves a disservice if we just imagine everything in exactly the same way as it's always been. A lot of it just requires us to make relatively modest changes to the types of things that we do, and to cede some control over some elements of it. People are not dependent on making cyclical appointments to have doses of drugs tritrated. But once we've identified that a drug needs to be on board as a result of a primary indication, that we allow the titration to take place in an efficient and cost-effective manner. I think a lot of what we do is driven by how we get paid. A lot of ... And that's not criticism, it's natural in every single profession on the planet. You do things the way that the system is set up to have them be done. And so, I think with relatively little in the way of systems engineering, you can have a 24/7 system without having 24/7 physicians. There are some areas, obviously intensive care units, where you do have 24/7 coverage already, but people are so used to having asynchronous care that being able to literally come home after a night shift and make their reservation for a restaurant the following evening, on their phone, often on another continent, it is a little bit strange that we literally can't book patients into your own clinic without calling up a couple of people. I just think that some of this is resistance for resistance's sake. Some of it is people actually simply restating the things that we all believe are important parts of medical encounters. I think we just have to be creative about how we move from here to there. I think the thing that I find perhaps most interesting is that somehow the creativity of physicians is not fully exploited. We haven't really asked doctors and patients to come up with new approaches to how care is delivered, to how patients are seen. But I think if we allowed venues where that could happen, that would be actually the way in which we would evolve a very different system. I think some of that, as I said, just goes back to the way in which everything is structured. All of the payment models, all of the ... Even the types of places that we see patients, are very much anchored in history. They're legacy items and there are lots of reasons why that's the case. Medicine, you can't show up with a minimally viable product. You need something that works perfectly day one, because of the liability. And so, what we need are just to rethink the way in which we even move medicine forward. What we know we can't do is just keep doing what we're doing, and changing modestly, rearrange the deck chairs. What we need to actually be able to do is find places where we can actually, or venues where we can change things and test new models of care in a relatively low risk situation. I think you already see lots of payers, the federal government, and the NIH all thinking about how you can do that. Some of the [inaudible 00:52:55] efforts, some of the ... Even the NHGRI efforts in genomics. One of the nice things about genomics is because it's a new tool, it allows you to reinvent the way in which medicine is delivered. And so, I believe things as diverse as the precision medicine initiative, and as some of the most fundamental ways in which NIH funding is being restructured, will all potentially impact the way in which creativity and innovation start to evolve within the healthcare system. I don't want to sound revolutionary. We're all doing all of this, all of the time. It's just not structured in a way that seems to very efficiently reach reduction to practice across the entire medical ecosystem. Part of what I think we need to do is, as a profession, build better ways of identifying where the innovation is occurring, and I will tell you I think it's occurring almost evenly across the entire medical universe, it's just that it doesn't propagate. All medicine, at the moment, is quite local. I think the things that you start to see happening in the industry that will change it are the fact that medicine is becoming much more like every other area of endeavor. It's becoming linked by technology. And once information flows more efficiently, I think a lot of the things that sound as if they're revolutionary, will end up actually just seeming like a series of obvious conclusions, based on the information that we've gleaned from early outlets or success stories. Many of the things that I've mentioned today, they're not revolutionary at all. There are entire healthcare systems that use these approaches. But they just haven't become generalized because of the way that medicine works. And so, I think that's one of the reasons that I'm a believer that technology in particular will have a transformative effect, just on the way that doctors talk to other doctors or relate to their patients, and the way in which creativity and innovation propagate through the medical system will change very rapidly as a result of that. And that's one of the great benefits of the electronic health record. I don't think EHR's now are perfect. In fact, in many ways, they're where other industries were 15 or 20 years ago. The supply chain in many large retail organizations was much more sophisticated in the mid-80s than the average EHR is. But what they've done is begin to collect the data in the right place, and in the right way, in a structured format. But as technology begins to cut across different EHR's and across different healthcare network, you'll see things, synergies begin to emerge that will accelerate the pace of change. It's not by chance alone that medicine has attracted different types of people over the last 50 or 100 years. I think they'll just see the types of individuals that come to medicine be more diverse and more distinctive, and that also I think will help. More distinctive in their skillset, and that will help accelerate change in ways that again, will seem far from revolutionary fairly quickly. Dr Anwar Chahal: Thank you for that. I wanted to come to the last section of the podcast, and sort of back to where I said it was joking, and you said I wasn't joking about doing three residencies. So, could you tell us a little bit about your own training and your own path? Originally from Scotland, through to London, and then over to the U.S. And also, if you could share some of those pearls that you've picked up that aren't obvious to us in books, or sometimes are so obvious that they're elusive and not always apparent to young, up and coming trainees, both on the research side as well as the clinical. Dr Calum MacRae: Yeah, sure. I trained in [inaudible 00:57:15] which had I think a very healthy attitude to specialism and generalism, and the relationship between them, and instilled in all of the specialists the need to always maintain some general medical capability. To this day, I still intend on general medicine for that reason. I then moved, I did cardiology training in London, and was fortunate to work in a couple of hospitals, one of which had a very interesting, I supposed, quaternary care clinic which had extremely complicated patients. That's where I did my second internship, at the Ross Graduate Medical School in Hammersmith. And everybody who was an intern in that setting had already basically been board certified in internal medicine, so they'd all finished their medical training, come back to do an internship in that setting. And there, I saw some amazing cases. There was an entire service for carcinoids, there was an entire service for many rare and wonderful diseases. At that point, you began to see how super-specialist knowledge can be incredibly helpful. But it can also be restrictive if it's not applied in the right way. And then I did cardiology training at St. George's Hospital in London with some amazing mentors. John Camm, who many people will know from his work in atrial fibrillation and sudden death. David Warr, another very well known electrophysiologist, one of the early pioneers. Bill McKenna was my primary mentor, and he was somebody who had worked on the very earliest descriptions of hypertrophic cardiomyopathy when he had originally been at the Hammersmith, and then moved to St. George's. He taught me a lot about, well many things. First of all, focus in your career, understanding the skillsets that you needed to accumulate in order to a) build a distinctive portfolio and b) to maintain your relevance by accumulating new skillsets as you move forward. And he had actually established a collaboration with Simon's. That was one of the reasons that I ended up moving to the U.S., and had a fantastic time with John and Cricket, at one of the earliest times in genetics moving into cardiovascular disease. I learned a huge amount from colleagues, at that stage, both at the bench. Hugh Watkins is now chair of cardiology and lecturer of medicine now in Oxford, was a bay mate who was there a couple of years ahead of me and I learned a huge amount from him. I realized ... My wife is from New York City, from Long Island rather, and I realized I had to probably stay in the U.S. for those reasons, and I retrained at that stage in internal medicine again at the Brigham where mentors such as Marshall Wolf and, actually cardiology mentors at that stage were people like Punky Mudge and Pat O'Gara, who then helped me to adapt to the U.S. system. The only thing I will tell you is that I don't think I ever learned as much as I did in each of my internships. I think the learning curve is incredibly steep. I'd been out of clinical medicine for four or five years, focusing on the lab, before I went back to my third internship. But I still think it was one of the most amazing experiences, largely because of the fact that you learn from every colleague, and you learn from every patient. I think if you go through most of your life thinking like that, I think you can end up doing very well. Actually, one of the other things that's really important is actually emphasizing those personal connections. The first fellow I had at Brigham and Women's when I was an intern was Joe Hill, who's now the editor of Circulation, the chair of cardiology at UT Southwestern. Almost everybody that I know in cardiovascular medicine, I've encountered in those types of settings. Either in training settings, or in research collaborations, or at research meetings. You just begin to see a whole list of people that have worked together in different ways, and have learned from each other. I think that's one of the most powerful things to take away from research or clinical training. I then was fortunate enough to get the chance to do a second cardiology fellowship at Mass General. There, I went to Mass General actually because of the focus on zebra fish genetics. I realized at that stage to really be able to study things at the scale that I thought was going to be necessary, I needed a high [inaudible 01:02:40] system, and Mark Schwartz, before he went to Novardis, on the zebra fish and the cardiovascular system, was very inspiring and I had a great time there. And then, ended up spending some fantastic years at Mass General where I eventually became the program director. But again, there I learned an incredible amount from people like Bill Dec, from Roman Desanctis, from Dolph Hutter. All of whom had very strong clinical presence, as well as from the researchers. Mark Fishman, the late Ken Bloch, and many others. And then also, perhaps one of the most important people in my long term training was Peter Yurchak, who had been ... He had actually defined, I think, the training programs in U.S. cardiology about 35 years earlier. He had been the program director since its inception in the 50s until he retired in 2005 I think it was. And then I became the program director and was there until I moved back to the Brigham in 2009, and became chief in 2014. I think the trajectory is really, I outline it only to highlight the fact that it took me a long time to get where I was going, but that I spent most of my life enjoying the journey. And I think that's actually one of the most important lessons I took away from it. You can end up finding situations where you feel like you might become frustrated, but in fact, if you go into them with the right attitude, and not only that, if you do it with the right people, you can take a huge amount out of it. I was incredibly fortunate in the fellowship class that I had at Mass General. Mark Sabatine is now the chair of TIMI, Patrick Ellinor, who is the head of EP and a pioneer in atrial fibrillation genetics. Stan Shaw, who is now the chief scientific officer with me in One Brave Idea. Danita Yoerger, who's the head of ECHO, and an outstanding ECHO researcher at Mass General. Mark Rubenstein, who's a very successful cardiologist, and a fabulous clinician. That group of people actually, I think, together helped me realize how much you could take from training no matter how old you are, and no matter how grumpy you seem when you don't get the full nights sleep. In the research side, I think the other thing that was obvious was that so many people bring so many different things to the table in research that you should never over or underestimate any aspect of the entire profession. I think I still get remarkable insights into research questions from colleagues who are clinicians, who've never done any research, just from astute observation and declaring a problem in a way that encourages investigation. I think that's one of the most important elements of training is how do you work out what you need to do, and how do you make sure that everything that you do between the start and the finish of that journey is used to help and to improve the way in which you end up doing what you ultimately find as your sort of settling point in your career. I think the other thing that I will say from the standpoint of research is it's always best to try and think about blending different fields together. What you don't want to do is end up being a clone of one of your supervisors or your mentors. It's really an important thing, and I encourage this in all of our trainees the importance of being a bridge between different disciplines. I think that's something that requires real emphasis. And then, finally, never ever forget that the single most important thing in all of this, whether it's the reorganization of clinical care or the core research environments, is the biology in the patients in front of you. And so, one of the things that I'm particularly and acutely aware of almost every time I see patients is that the patients often know much more about the condition that they have than you ever will. Listening to them is actually very important piece of everything that you do. In fact, one of the reasons that we began to move outside the heart in our heart failure research was talking to patients about their pre-clinical elements that they found in their families. So, often, when you see a family with inherited heart disease, before the gene is identified, before anybody has a phenotype that you recognize, the patients themselves can assess who's likely to develop the disease from their intrinsic knowledge of their siblings, and their cousins, and their other family members. So, for example, one of the families that I've worked on intensely, there's a anxiety disorder that is a much more stable and much more specific part of the phenotype than any of the cardiac arrhythmias, and it's actually turned out to be quite a difficult anxiety disorder to define using even DFM criteria. But when we asked the family, they were very able to tell the people in the family who just were at the normal edge of neurotic from those who truly had the anxiety disorder that co-segregated eventually with the arrhythmia. The lesson I've learned time and time again is that patients always are a vital and central part of the answer. And it's a pride thing to say, but particularly in genetics and genomics, I think, and particularly with the reemphasis on phenotype, that I believe is necessary, I think we do well to try and make sure our research and our clinical care, our discovery, and our disease management are very tightly aligned. And I think technology is one of the ways that will help that happen. That actually is part of what being a professional really is. If you go back to the early professional guilds, that's exactly how they were formed. It was groups of experimentalists who were interested in particular problems that formed the original professions in European cities during the Renaissance. I think that's something that we would do well to think about as we continue to remodel medicine in the 21st century. Dr Anwar Chahal: Thank you for that. Lots of important points there, and I guess your emphasis that enjoying the journey rather than thinking about the destination, but did you always know where your destination would be? And, in fact, that brings me to another question. Have you actually reached your destination, or is your journey still ongoing? Dr Calum MacRae: So, exactly. I think that's the key thing. You don't need to necessarily know where you're going to stop. You just need to know where you're headed. That's something I actually tell people as they're interviewing for fellowship or residency, that part of what people are looking for when they talk to you is that you have thought through and organized your life around your goals. And those goals can change. Nobody's going to hold you ...
Jockey Javier Castellano reflects on being elected to the Hall of Fame. Plus, Teresa Genaro of the Brooklyn Backstretch blog on NY state's considering a partial Lasix ban.
Eye Conditions in ABC order Your eyes work together so that the line of focus for each eye cross, and that is your most in focus image. So as your eyes make tiny adjustments, you can focus on things close up or far away. Amblyopia If you have a lazy eye, the muscles don't allow the eye to focus and coordinate with the strong eye. This can lead to double vision or blurry vision. I remember it because it sounds like "ambling" which can mean to meander or wander around. Versions of this can be caused by torticollis, where a baby's head is tilted or twisted due to positioning in the womb. The eye can either compensate for the difference or it'll just give up and let the dominant eye do all the work. Correction of this issue usually involves patching the strong eye and making the weak eye do all the work. The blurry or double vision can lead to headaches. Overuse and fatigue (like long days at work) can make it worse. Astigmatism An astigmatism no a stigmatism. It's an irregularly-shaped cornea; think baseball vs football. A circular lens (baseball) focuses light to a single point. A football-shaped lens focuses light to a line, so that makes the vision blurry. This is why people with astigmatism will squint. Squinting is a way for your eyes to manipulate the amount of light coming in and alter the shape of the eye to clear up the image of what they're looking at. Lasix procedures can correct astigmatism - the laser does micro-damage to the eye and it heals more circular in the eye. Blepharitis Inflammation of eye lids. Can result in dry eye. It can affect the outside (eye lashes side) or the inside (lubrication gland size). This is NOT a stye. Caused by a chronic build-up of bacteria, skin flakes, dried eye lubrication. Some skin conditions can make a person more susceptible to blepharitis - Rosacea (overgrowth of skin bacteria), severe dermatitis, including psoriasis. It's recommended to use really good eye hygiene before having a doctor intervene. Using warm compresses to keep dried skin and "eye crusties" soft and glands open so they don't get clogged. Using clean cotton swabs or clothes instead of your hands to touch or wipe things out of your eyes, so you don't transfer bacteria. Doctor's can insert a catheter into the tear ducts to keep it open and less likely to keep it clogged. There's not a cure to make it go away for good. Cataracts The lens of the eye gets cloudy due to proteins clumping up. People have described trying to see with cataracts like trying to look through wax paper. Risk of cataracts normally increases with age. The risk for cataracts can be increased even more by chronic diseases (diabetes, high blood pressure), poor health habits (obesity, smoking, alcohol use), long-term use of certain medications (steroids, hormone replacement therapy). The current treatment for cataracts is lens replacement. The old treatment would be just removing the proteins, but depending on a person's longevity, they may get cataracts again in their lifetime. Connect with me Support us on Patreon *NEW* Join the Pharmacist Answers Podcast Community on Facebook Subscribe: iTunes, Stitcher, GooglePlay, TuneIn Radio Like the Facebook page Music Credits: “Radio Martini” Kevin MacLeod (incompetech.com) Licensed under Creative Commons: By Attribution 3.0 http://creativecommons.org/licenses/by/3.0/
Generic Name Furosemide Trade Name Lasix Indication edema, hypertension Action prevents reabsorption of sodium and chloride in the kidneys, increase excretion of water, sodium, chloride, magnesium, potassium Therapeutic Class diuretics Pharmacologic Class loop diuretics Nursing Considerations use caution with liver… The post Furosemide: Lasix (diuretics) appeared first on NURSING.com.
TwinSpires.com How to Bet the Belmont Stakes podcast presented by Brisnet.com
In the News & Notes segment, Derek Simon of TwinSpires.com and Ed DeRosa of Brisnet.com discuss a recent study on Lasix in the Breeders’ Cup and opine on the merits of juvenile sensation Shared Belief. In the U. of Bet segment, Derek and Dave “The Horse Handicapping Authority” Schwartz gives his thoughts on “pro” vs. “casual” players. Lastly, the “Wizard of Odds,” Michael Shackleford, a professional actuary who has made a career of analyzing casino games, helps to explain the role of mathematics in gambling.
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