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Dr. Filip Ionescu (hematology-oncology fellow at Moffitt Cancer Center in Tampa, FL), Dr. Teodora Donisan (cardiology fellow at the Mayo Clinic in Rochester, MN and CardioNerds House Thomas chief), Dr. Sarah Waliany (internal medicine chief resident at Stanford University in Palo Alto, CA), Dr. Dinu Balanescu (internal medicine chief resident at Beaumont Hospital in Royal Oak, MI) and Dr. Amit Goyal (structural interventional cardiology fellow at the Cleveland Clinic, in Cleveland, OH and CardioNerds Co-Founder), discuss the cardiotoxicities of common cancer treatments with Dr. Susan Dent, a medical oncologist and one of the founders of the field of Cardio-Oncology. Using the recently published ESC Guidelines on cardio-oncology, they cover cardiovascular risk stratification in oncology patients, pretreatment testing, as well as prevention and management of established cardiotoxicity resulting from anthracyclines, trastuzumab, and fluoropyrimidines. They touch on the unique aspects of cardio-oncology encountered in patients with breast cancer, rectal cancer, and lung cancer, who are frequently the recipients of multiple cardiotoxic treatments. Audio editing by CardioNerds Academy Intern, student doctor Chelsea Amo Tweneboah. Access the CardioNerds Cardiac Amyloidosis Series for a deep dive into this important topic. This episode is supported by a grant from Pfizer Inc. This CardioNerds Cardio-Oncology series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Giselle Suero Abreu, Dr. Dinu Balanescu, and Dr. Teodora Donisan.  Pearls • Notes • References • Production Team CardioNerds Cardio-Oncology PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls and Quotes - Cancer Therapy-Related Cardiac Dysfunction (CTRCD) – The Oncologist Perspective with Dr. Susan Dent Formal cardiovascular risk stratification must be performed prior to initiating a potentially cardiotoxic anticancer treatment regimen. Considering both drug toxicity and patient-related factors (e.g., age, smoking, hypertension etc) is important.  Anthracyclines affect the cardiomyocyte in complex ways which lead to a largely irreversible cardiomyopathy. All patients should have a pretreatment echocardiogram and ECG.  Trastuzumab cardiotoxicity, by contrast, is more like stunning the myocardium, which manifests as a reversible decrease in left ventricular ejection fraction which generally normalizes upon discontinuation of the drug.  The treatment of chemotherapy-induced cardiomyopathy should involve interdisciplinary discussions and shared decision making with the patient. Beyond guideline-directed medical therapy of heart failure with reduced ejection fraction, management can include temporarily holding or permanently discontinuing the offending agent.  Fluoropyrimidine-associated cardiotoxicity manifests as cardiac ischemia from coronary vasospasm. A 5FU infusion is essentially a stress test as it tends to unmask clinically silent atherosclerosis.  Show notes What is the basic pretreatment assessment of any oncology patient who is to receive a potentially cardiotoxic regimen?  Awareness and management of the cardiovascular toxicity of oncology treatments are of paramount importance to be able to deliver treatment safely and to achieve maximal efficacy guided by an expert multidisciplinary team. Thanks to Dr. Dent and her colleagues' work, this year we have seen the publication of the first Cardio-Oncology guideline (1). Perhaps the most important recommendation is that cancer patients about to start a cardiotoxic regimen should undergo formal cardiovascular risk stratification by considering both the adverse profile of the planned treatment...

ECG normal x SCA by Cardiopapers

Please join author Subodh Verma and Guest Editor Christopher Granger as they discuss the article "Empagliflozin and Left Ventricular Remodeling in People Without Diabetes: Primary Results of the EMPA-HEART 2 CardioLink-7 Randomized Clinical Trial." 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-host. I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr. Peder Myhre: And I'm Dr. Peder Myhre, social media editor and doctor at Akershus University Hospital at University of Oslo in Norway. Dr. Carolyn Lam: Peder, I am so excited to be discussing this issue. So many great articles and a feature discussion coming up on the SGLT2 inhibitor, empagliflozin. And do you think it's got effects on left ventricular remodeling in people without diabetes? Very interesting question. Dr. Peder Myhre: That is so interesting, Carolyn. I can't wait to hear this discussion. Dr. Carolyn Lam: Yep, I agree, but we got to wait till we discuss the other papers in today's issue. I want to go first. So we know that non-vitamin K oral anticoagulants, or NOACs, they've become the standard therapy for preventing stroke and ischemic thromboembolism in most patients with atrial fibrillation. But, what is the effectiveness and safety of NOACs in patients on dialysis? That is hemodialysis. The AXADIA-AFNET 8 study sought to test the hypothesis that apixaban would be non-inferior to vitamin K antagonists in these very patients undergoing hemodialysis. Dr. Peder Myhre: Oh wow. This is really a gap of knowledge that we've been waiting to hear more about. NOACs in patients with hemodialysis. Tell us about this trial, Carolyn. Dr. Carolyn Lam: Sure. So this is from corresponding author, Dr. Reinecke, and colleagues, from University of Munster in Germany. And it's an investigator initiated prospective randomized open-blinded outcome assessment of 97 patients with atrial fibrillation on chronic hemodialysis randomized to either apixaban 2.5 mg BID, or a vitamin K antagonist, aiming for an INR between 2 and 3. Over a median follow-up time of 429 days for apixaban, and 506 days for the vitamin K antagonist, the composite primary safety outcome of first, major bleeding, clinically relevant, non-major bleeding, or all cause death, occurred in 46% of patients on apixaban, and 51% of patients on the vitamin K antagonist. That would be a hazard ratio of 0.91, with a p for non-inferiority being 0.157. How about the primary efficacy outcome? While this was a composite of ischemic stroke, all cause death, myocardial infarction, or deep vein thrombosis, and/or pulmonary embolism, and that occurred in 21% of patients on apixaban and 31% of patients on the vitamin K antagonists. Again, no difference when there was testing. So, in summary, Peder, there were no differences in the safety or efficacy observed between apixaban and vitamin K antagonists in patients with atrial fibrillation on chronic hemodialysis. Of note, however, even receiving oral anticoagulations, these patients remain at very high risk of cardiovascular events. So these data really support the consideration of apixaban for prevention of cardiovascular complications in patients with atrial fibrillation on chronic hemodialysis, but larger studies are definitely needed. Dr. Peder Myhre: Oh wow, Carolyn, that is so clinically relevant. And the next paper is also a clinically relevant paper. And it comes to us from the SPRINT authors. And to remind you, the SPRINT study was a study of intensive systolic blood pressure lowering compared to standard blood pressure lowering. And the results demonstrated that there was a robust reduction in both heart failure endpoints and all cause mortality. And in this sub-study that comes to us from corresponding author Jarett Berry from University of Texas Tyler School of Medicine, these authors look at the mechanisms through which intensive blood pressure lowering reduces the risk of these endpoints. And given the important role of cardiac injury and neurohormonal activation in the pathways leading from hypertension to heart failure, and strong association that has been observed between hypertension and levels of cardiac troponin and NT-proBNP, the authors hypothesized that intensive systolic blood pressure lowering would decrease levels of high sensitivity cardiac troponin T and NT-proBNP. Dr. Carolyn Lam: Cool. That's interesting. So how did they do this, and what did they find? Dr. Peder Myhre: So, as expected, Carolyn, the authors found that increases in troponin and NT-proBNP from baseline to 1 year were associated with a higher risk of heart failure and death. And there were really no significant interaction by treatment assignment. But let's look at the changes in troponin. And these results showed that randomization to intensive blood pressure lowering versus standard blood pressure lowering resulted in a significant 3% increase in cardiac troponin T level over 1 year follow up, and a higher proportion of participants with more than 50% increase, and that's with an odds ratio of 1.47. And Carolyn, in contrast, NT-proBNP decreased by 10% in intensive blood pressure arm. And these patients had substantially lower probability of increasing more than 50% in NT-proBNP, with an odds ratio of 0.57 compared to the standard arm. And now, to the most interesting part of this analysis, Carolyn, the association of randomized treatment assignment on changes in troponin was completely attenuated after accounting for changes in eGFR during the follow up, whereas the association of treatment with NT-proBNP changes were completely attenuated after adjusting for changes in systolic blood pressure. So Carolyn, the authors highlight in their discussion the importance of non-cardiac factors influencing variation in cardiac biomarkers, and raise questions about the potential role of cardiac troponin T as a surrogate marker for heart failure or death in blood pressure lowering studies. Dr. Carolyn Lam: Wow, very interesting. Thanks, Peder. Can I tell you now about a preclinical study? Very interesting, because it shows that cardiac inflammation and hypertrophy are regulated by a heart-brain interaction. Dr. Peder Myhre: Wow, Carolyn, a heart-brain interaction. I'm excited to hear more about this. Please explain. Dr. Carolyn Lam: I'd love to, but first some background. Interleukin-1 beta, now that is a pro-inflammatory cytokine that causes cardiac hypertrophy and heart failure. I need to familiarize you with this, the nucleotide-binding domain leucine-rich containing family, pyrin domain-containing-3, NLRP3 for short, which is an inflammasome, which is a cytosolic multiprotein complex that mediates active interleukin-1 beta production. Okay? So you know these terms, and now I want to tell you about the study. This is an elegant series of experiments performed by co-corresponding authors, Dr. Higashikuni, from University of Tokyo, and Dr. Sata, from Tokushima University Graduate School of Medicine, and their colleagues. They first showed that genetic disruption of the NLRP3 inflammasome resulted in significant loss of interleukin-1 beta production, cardiac hypertrophy, and contractile function during pressure overload. Next, a bone marrow transplantation experiment revealed an essential role of NLRP3 inflammasome in cardiac non-immune cells in myocardial interleukin-1 beta production and the cardiac phenotype. It was extracellular ATP released from sympathetic nerve terminals that induced the hypertrophic changes of cardiac cells in an NLRP3 and interleukin-1 beta dependent manner in vitro. And finally, depletion of ATP release from sympathetic efferent nerves, or ablation of cardiac afferent nerves, or a lipophilic beta-blocker, all reduced cardiac extracellular ATP, and inhibited the NLRP3 inflammasome activation, the interleukin-1 beta production, and the adaptive cardiac hypertrophy during pressure overload. So all of this suggests that controlling the neuronal brain signals might have therapeutic potential for the treatment of hypertensive heart disease. Neat, huh? Dr. Peder Myhre: Oh, that is so interesting. The heart and brain interaction. And, Carolyn, we're going to stay in the field of preclinical science. And now we're going to talk about another field that is really interesting, and that is regeneration of cardiomyocytes. Because, Carolyn, developmental cardiac tissue holds remarkable capacity to regenerate after injury, and consists of regenerative mononuclear and deployed cardiomyocytes. Whether reprogramming metabolism promotes persistence of these regenerative mononuclear and deployed cardiomyocytes that enhance cardiac function in repair after injury is unknown. Therefore, these researcher, led by corresponding author, Mohsin Khan, from Temple University School of Medicine, investigated whether the RNA binding protein, LIN28a, which is a master regulator of cellular metabolism, plays a role in cardiac repair following injury. Dr. Carolyn Lam: Wow. That is always, always interesting, regeneration and repair following injury. So what did the authors find? Dr. Peder Myhre: Well, Carolyn, through a number of elegant experiments, the authors made the following key findings. For the first time, they documented a role for RNA binding protein LIN28A in regulating cardiomyocyte turnover in the postnatal and adult heart. And LIN28a overexpression promotes cardiomyocyte cell cycle activity during postnatal development and extends cardiac regenerative ability of the mammalian heart to postnatal day 7. And in the adult heart, the authors could demonstrate that LIN28a drives new myocyte formation, augmenting cardiac structure and function after myocardial injury. And Carolyn, I'm sure you're going to ask the clinical implications of this study. Dr. Carolyn Lam: Indeed. Dr. Peder Myhre: And that is that these results may suggest a novel translational role for LIN28a based strategy to replenish cardiomyocytes in the adult heart after injury. Dr. Carolyn Lam: Very nice, Peder. Thank you. Also in the issue is a Research Letter by Dr. Bick on interleukin-6 receptor polymorphism attenuates clonal hematopoiesis mediated coronary artery disease risk among many individuals in the UK Biobank. There's also Cardiology News by Tracy Hampton, where she highlights few really interesting things, like aging cardiomyocytes accumulate new genetic mutations that was published in Nature Aging, cytokines promote tissue repair after a heart attack in mice, and that was published in Science, and scientists identifying molecular alterations in a failing heart at a single cell resolution, which was published in Nature. Dr. Peder Myhre: And there are a couple of other papers also in this issue, Carolyn. And there's first, an exchange of letters by Drs. Halushka, Lu, and Mayr, regarding the article "Circulating MicroRNA-122-5p is Associated with a Lack of Improvement in Left Ventricular Function after TAVR and Regulates Viability of Cardiomyocytes Through Extracellular Vesicles." And finally, we have an "On My Mind" piece by doctors Monda and Limongelli entitled "An Integrated Sudden Cardiac Risk Prediction Model for Patients with Hypertrophic Cardiomyopathy." Dr. Carolyn Lam: Oh, nice. Nice full issue. Thank you, Peder. Let's go to our feature discussion now. Shall we? Dr. Peder Myhre: Let's go. Dr. Greg Hundley: Welcome listeners to this feature discussion on January 24th. And we have with us Dr. Subodh Verma, from St. Michael's University in Toronto, Canada. And a guest editor, Dr. Christopher Granger, from Duke University in Durham, North Carolina. Welcome gentlemen. Well, Subodh, we will start with you. Can you describe for us some of the background information that went into the preparation of your study, and what was the hypothesis that you wanted to address? Dr. Subodh Verma: First, my great pleasure to be here, and thank you very much for the opportunity to discuss this paper with your viewers. As you know, SGLT2 inhibitors have been truly transformative therapies. From a heart failure perspective, we know that they prevent incident heart failure in people with diabetes who have vascular disease or risk factors. They also have been shown to treat prevalent heart failure in people with heart failure and either a reduced, mildly reduced, or preserved ejection fraction independent of glycemic status. And really, these have been the basis of very strong recommendations to use these agents in the prevention of heart failure in people with diabetes, and also in the treatment of prevalent heart failure in people with and without diabetes. Now, the fact that these drugs have such broad effects in people with heart failure has led to a theory that maybe these drugs could be introduced earlier on in the natural history of heart failure in people who neither have diabetes nor have significant heart failure, the so-called sort of stage A or stage B patient. But there really have been no clinical trials evaluating this question. There've been a lot of translational randomized trials that have provided some mechanistic insights about LV remodeling in people with diabetes or in people with prevalent heart failure. And we hypothesized that maybe the first step to evaluate whether SGLT2 inhibitors may have favorable effects on cardiac remodeling in people without diabetes or without heart failure would be to conduct a randomized double-blind control trial looking at indices of left ventricular remodeling in a population that I've just described. Dr. Greg Hundley: Very nice, Subodh. So you've started us into your study design. Maybe describe that a little more fully, and then who was included in your study population? Dr. Subodh Verma: So EMPA-HEART 2 CardioLink was a multi-center double-blind placebo control randomized trial in which we studied the effects of empagliflozin, an SGLT2 inhibitor, at a dose of 10 mg per day versus placebo in people who did not have type 2 diabetes or significant heart failure. We included people who were adults between the age of 40 and 80 who met 1 of 2 entry criteria. Either they had to have one major criteria, which was an increase in left ventricular mass index by specific echo criteria or MRI criteria, or they could have increased LVH as identified by ECG or by intraventricular septal or posterior wall thickness. They could also get in if they had resistant hypertension, hypertension despite being on 3 antihypertensive agents, or the second strata was entry through 2 minor criteria, which included a history of myocardial infarction, a GFR between 30 or 60, or evidence of overweight or obesity. Dr. Greg Hundley: And how many subjects did you randomize? Dr. Subodh Verma: So we randomized, of the 318 that we screened, 169 were randomized to receive empagliflozin 10 mg or a placebo. Patients had a baseline cardiac MRI done, and then the exposure was 6 months. They had a follow-up MRI at the end of 6 months. And the primary outcome measure was a 6-month change in left ventricular mass index from baseline to 6 months between the two groups. Dr. Greg Hundley: Very nice. And so , Subodh, can you describe for us now, what did you find? What were your study results? Dr. Subodh Verma: So, first and foremost, what we found in terms of baseline characteristics was that we enrolled a population of people with a mean age of around 60 with a BMI of around 30 kg/m2, predominantly men, about 80% or so were men. These were patients who did not have significant heart failure. The NT-proBNP at baseline was around 50 pg/mL. The eGFR was around 80 mL/minute, and the vast majority of these patients actually had a history of hypertension. Of course, none of them had diabetes by definition. The hemoglobin A1C was around 5.8%. Now what we found was, despite the fact that we went after patients who we thought would be enriched for a baseline increase in LV mass indices, the baseline LV mass index was mildly elevated, was around 63 g/m2. And over the course of 6 months, we did not find any significant difference in terms of LV mass regression between the placebo and empagliflozin groups. In fact, the adjusted treatment effect was minus 0.30 g/m2, which was not statistically significant. No other differences were found in terms of other indices of a remodeling, including left ventricular and diastolic or end systolic volume indices or in terms of left ventricular ejection fraction. There was a 2% increase in ejection fraction, and the p-value for that was 0.07, but really was not statistically significant. Dr. Greg Hundley: And very nice. And realizing that women may have smaller LV masses, any stratified analysis that evaluated effects on men versus women? And then what about, perhaps in the higher quartile versus lower quartile, of age? Dr. Subodh Verma: Right. So, Greg, we actually did look at various subgroups and covariates, including gender, including age. And age or gender did not really influence the overall result that we obtained. There was really a neutral result in empagliflozin, irrespective of these 2 covariates. We also looked at baseline blood pressure, baseline NT-proBNP, LV mass indices, the presence or absence of heart failure, chronic kidney disease. So for the covariates that we have evaluated over a short term of 6 months in this relatively low risk population, we did not find any heterogeneity the result, per se. Dr. Greg Hundley: Very good. Well, Subodh, thank you so much for that beautiful presentation. And listeners, now we're going to turn to our guest editor, Dr. Chris Granger. And Chris is an expert in the field of heart failure. Also, a lot of familiarity with HFpEF, which sounds a little bit, we're looking at precursors. We don't have HFpEF yet, but maybe trying to inhibit this from happening using empagliflozin. How do you put these results in the context with other studies that have emphasized utilizing SGLT2 inhibitors in patients with sort of a preserved ejection fraction and absence of diabetes? Dr. Christopher Granger: Yeah. Well thanks, Greg. And again, congratulations, Subodh, to your study. And I think you framed some of the context here as these drugs, the SGLT2 inhibitors, as being transformative, which I think is exactly right. And it's such a fascinating story. Right? These drugs, which we thought originally, with their cause of glucose spilling in the urine, and a modest decrease in blood glucose, might have a role for modestly improving glucose control in diabetes. And low and behold, they've turned out to be one of the great stories I think in recent, across all of medicine, in terms of their consistent and substantial improving clinical outcomes for patients with heart failure, with diabetes and cardiovascular disease, and now even kidney protection, and much broader implications. And their well tolerated, and they don't have dose titration. So there's some practical appeal to this class of drugs in terms of their benefits, in terms of clinical outcomes. But we're left with having this amazing evidence-based generated without really understanding why are these drugs so effective? And what are they doing? And you've provided, I think, an important piece to the puzzle. We did have the data from patients with diabetes and heart failure, with diabetes and left ventricular hypertrophy, that there is a modest reduce in LV mass with SGLT2 inhibitors. And what you've shown is that for patients that with mild LVH, with risk for LVH, that we simply don't see a substantial reduction in LV mass with the use of these drugs. So I think that provides this evidence that that's not a major cause of benefit, at least in this earlier phase of development of heart failure. And I think it really underscores the fact that there's a lot of work to do still to understand. We know that the renal effects are obvious place that these drugs have such an important benefit. And then the linkage of renal disease and cardiac performance is one of the areas, I think, that's a very exciting aspect of a probable contribution of the mechanism of these drugs. But I think in the end, we're left with still not really understanding why these drugs are so beneficial. But understanding that, I think, will be important, both for opening new avenues of targeting pathways, as well as being able to tell the clinical community, okay, you have these important benefits, but people do want to also know why are we seeing these benefits. Dr. Greg Hundley: Very nice. Well, listeners, we're going to turn back to Dr. Verma here. Subodh, what do you see is the next study to be performed in this sphere of research? Dr. Subodh Verma: Well, first, my thanks to Professor Granger, Chris, for handling this paper and for his very thoughtful comments. And he's absolutely right. We have such wonderful clinical data, and these results, of course, should not in any way take away from the importance of using empagliflozin or other SGLT2 inhibitors in the prevention of heart failure in people with diabetes, or in the treatment of HFpEF or HFrEF. But we're struggling with trying to understand what is the dominant mechanism of action here. And, in the previous precursor to EMPA-HEART 2, we did EMPA-HEART 1 in people with diabetes, and we saw a modest effect that was statistically significant of reduction in LV mass index. And we did not see this, of course, in a lower risk population without diabetes. And that tells me that remodeling may be occurring to a modest effect, it may require a longer time to actually show its benefits, but that this is unlikely a dominant sort of mechanism through which these drugs are working. And I do share Chris's thoughts that one of the key mechanisms of benefit that needs to be further explored is looking at the renal cardiac axes. We know that these drugs are profoundly renal protective, and that the benefits may actually be secondary to improvements in renal hemodynamics, improvements in renal function. And I think that is a population that needs to be, that's a mechanism that needs to be studied further. So I think the next generation of translational mechanistic studies need to really tease out the renal cardiac axes, maybe tease out populations that are at risk but have more significant left ventricular hypertrophy, maybe evaluate patients for a longer duration of treatment, or select people who truly have significant hypertension at baseline. I think those are groups and questions that need further exploration. And, of course, the translational science needs to be also studied in the context of larger completed clinical trials, where biomarkers are currently available and they can be linked, of course, to the outcomes in those trials. So those are some of my thoughts as to where the field could move towards. Dr. Greg Hundley: Very nice. And Chris, do you have anything to add? Dr. Christopher Granger: Subodh, I think that was a great summary. And I might just make a comment on the other end of the spectrum. That is, we have these drugs and the evidence of their benefit, and yet they're grossly underused in the populations that have proven to have benefit. Now it takes some time to educate, to get people familiar with, and get them to integrate these treatments into practice, but there's an enormous opportunity, and I think there is a linkage here. I think when people understand the mechanism, and when they're thoughtful about how these drugs may be working, that that really helps to make the case that the drug should be used, and that people are on board with using them. So I think there's this linkage here, there's the need to both better understand mechanism, and there's the need to have systems of care where these treatments are integrated to provide the benefit that's been so clearly shown in the randomized trials. Dr. Greg Hundley: Very nice. Well, listeners, we want to thank Dr. Subodh Verma, from St. Michael's University in Toronto, and our guest editor, Dr. Chris Granger, from Duke University in Durham, North Carolina, for bringing this paper highlighting that among people with neither diabetes nor significant heart failure but with risk factors for adverse cardiac remodeling, that SGLT2 inhibition with empagliflozin did not, did not, result in a meaningful reduction in LV mass index after 6 months. Well, on behalf of Carolyn, Peder, and myself, we want to wish you a great week, and we will catch you next week on the run. This program is copyright of the American Heart Association 2023. 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.

ECG characteristics of supraventricular tachycardia (SVT) vs. sinus tachycardia. Signs & symptoms that indicate a patient is unstable. Delivery of a synchronized shock for the treatment of unstable SVT using a biphasic vs monophasic defibrillator.Consideration for team safety while performing synchronized cardioversion.Management of stable patients in SVT.For more on narrow complex tachycardias, check out the pod resource page at passacls.com.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGive back & support the show:via PayPal Good luck with your ACLS class!

Challenges in Teaching ECG Interpretation Guest: Kevin E. O'Brien, M.D. Hosts: Anthony H. Kashou, M.D. (@anthonykashoumd) Joining us today to discuss the challenges in teaching ECG interpretation is Kevin O'Brien, M.D., professor of medicine at the University of South Florida Morsani College of Medicine. His research interests center around issues dealing with the evaluation and assessment, the learning environment, interpretation of common diagnostic studies, and physician and trainee wellness. Tune in to learn more about the education aspect of ECG interpretation. Specific topics discussed: What cardiology topics do you teach? To Whom? When? Where? How long have you been doing this? Who inspired you to teach electrocardiography? Why do you enjoy teaching about electrocardiography? Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. Facebook: MayoCVservices LinkedIn: Mayo Clinic Cardiovascular Services NEW Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.

Please join author Pieter Martens and Associate Editor Justin Grodin as they discuss the article "Decongestion With Acetazolamide in Acute Decompensated Heart Failure Across the Spectrum of Left Ventricular Ejection Fraction: A Prespecified Analysis From the ADVOR Trial." Dr. Greg Hundley: Welcome listeners to this January 17th issue of Circulation on the Run. And I am Dr. Greg Hundley, Director at the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Peder Myhre: And I'm Dr. Peder Myhre from Akershus University Hospital and University of Oslo, in Norway. And today, Greg, we have such an exciting feature paper. It comes to us from the ADVOR trialists. And the ADVOR trial examined the effect of acetazolamide in acute decompensated heart failure. And in this paper we're going to discuss how that treatment effect was across the left ventricular ejection fraction, across the spectrum. Greg, what do you think? Dr. Greg Hundley: Oh, wow. Sounds very interesting. But we might have some other articles in the issue. How about we grab a cup of coffee and Peder maybe this week, I'll go first and we'll start with preclinical science. How about that? Dr. Peder Myhre: Let's do preclinical science, Greg. Dr. Greg Hundley: Well, Peder, this particular paper focuses on the relationship between cardiac fibroblasts and cardiomyocytes. Remember that myocytes sit on a lattice of network of fibroblasts. And when the myocytes die, the fibroblasts then proliferates, secrete collagen and form this thick scar. Now, if we're going to try to regenerate, how are we going to get myocytes to get back into that thick scar when there's really a complete absence? And so as adult cardiomyocytes have little regenerative capacity, resident cardiac fibroblasts synthesize extracellular matrix, post myocardial infarction to form fibrosis, leading to cardiac dysfunction and heart failure. And therapies that can regenerate the myocardium and reverse fibrosis in the setting of a chronic myocardial infarction are lacking. Now, these investigators led by Professor Masaki Ieda from University of Tsukuba, were going to evaluate this process. The overexpression of cardiac transcription factors, including Mef2c, Gata4, Tbx5, Han2, all combined as MGTH. They can directly reprogram cardiac fibroblasts into induced cardiomyocytes and improve cardiac function in and under the setting of an acute myocardial infarction. However, the ability of an in vivo cardiac reprogramming to repair chronic myocardial infarction with established scars, well, that is really undetermined. Dr. Peder Myhre: Oh, what a wonderful introduction, Greg. And the way you described to us how cardiomyocytes and fibroblasts interact was really fascinating. Thank you. And now let's hear what the authors found and don't forget the clinical implications. Dr. Greg Hundley: Thanks, Peder. So these authors developed a novel transgenic mouse system where cardiac reprogramming and fibroblasts lineage tracing could be regulated spatiotemporally with tamoxifen treatment to analyze in vivo cardiac reprogramming in the setting of chronic MI. Then with this new model, the authors found in vivo cardiac reprogramming generates new induced cardiomyocytes from resident cardiac fibroblasts that improves cardiac function and reduces fibrosis in chronic myocardial infarction in mice. Wow. And additionally, they found that overexpression of cardiac reprogramming factors converts profibrotic cardio fibroblasts to a quiescent state, and that reverses fibrosis in chronic myocardial infarction. And therefore, Peder, direct cardiac reprogramming may be a promising therapy for chronic ischemic cardiomyopathies and heart failure. Really exciting work, converting scar tissue to actual functional cardiomyocytes. Dr. Peder Myhre: That was such a fantastic summary, Greg, and a very interesting paper. And I'm now going to take us back to clinical science and epidemiology. Because Greg, we all know that social and psychosocial factors are associated with cardiovascular disease risk. But the relative contributions of these factors to racial and ethnic differences in cardiovascular health has not been quantified. So these authors, led by the corresponding author, Nilay Shah from Northwestern University Feinberg School of Medicine in Chicago, used data from NHANES to examine the contributions of individual level social and psychosocial factors to racial and ethnic differences in population cardiovascular health. And that was measured by something called the cardiovascular health score, CVH score, which ranges from zero to 14, and it counts for diet, smoking, physical activity, body mass index, blood pressure, cholesterol, and blood glucose. Dr. Greg Hundley: Wow, really interesting, Peder. So what did they find here? Dr. Peder Myhre: So Greg, among males, the mean cardiovascular health score was 7.5 in Hispanic, 8.7 in non-Hispanic Asian, 7.5 in non-Hispanic black, and 7.6 in non-Hispanic white adults. And the authors found that the education explained the largest component of cardiovascular health differences among males. And now what about females? In females, the mean score was 8.0 in Hispanic, 9.3 in non-Hispanic Asian, 7.4 in non-Hispanic black, and 8.0 in non-Hispanic white adults. And for women, education explained the largest competence of cardiovascular health difference in non-Hispanic black. And place of birth, and that is US born versus born outside the US, explained the largest component of cardiovascular health difference in Hispanic and non-Hispanic Asian females. So Greg, the authors conclude that education and place of birth conferred the largest statistical contributions to the racial and ethnic differences in cardiovascular health among US adults. Dr. Greg Hundley: Very nice, Peder. What a beautiful description and outline that so well highlighting the differences in men versus women. Well, now we're going to turn back to the world of preclinical science, listeners. And we will continue with the paper by Dr. Amit Khera from Verve Therapeutics. Now, Peder, VERVE-101, this is an investigational in vivo CRISPR base editing medicine designed to alter a single DNA base in the PCSK9 gene. And that permanently turns off hepatic protein production and thereby, durably lowers LDL cholesterol. In this study, the investigators tested the efficacy, durability, tolerability, and potential for germline editing of VERVE-101 in studies of non-human primates and also in a murine F1 progeny study. Dr. Peder Myhre: So more on PCSK9s, and this time CRISPR technology. Very exciting. Greg, what did they find? Dr. Greg Hundley: Right, Peder. So VERVE-101 was well tolerated in non-human primates and led to, listen to this, an 83% lower blood PCSK9 protein and 69% lowering of LDL-C with durable effects up to 476 days following the dosing. These results have supported initiation of a first inhuman clinical trial. That's what needs to come next in patients with heterozygous familial hypercholesterolemia and atherosclerotic cardiovascular disease. Wow. Dr. Peder Myhre: Even greater reductions from this therapy on PCSK9 than the previous PCSK9 inhibitor therapies. Wow. Okay, Greg, and now we go from one fascinating study to another. And this time we actually have the primary results from a large randomized clinical trial, Greg. Isn't that exciting? Dr. Greg Hundley: Yes. Dr. Peder Myhre: And this paper describes the primary results of a trial testing in Indobufen versus aspirin on top of clopidogrel in patients undergoing PCI with drug-eluting stent DES who did not have elevated troponin. So that is patients without mycardial infarction. And in fact, fact, this is the first large randomized control trial to explore the efficacy and safety of aspirin replacement on top of P2Y12 inhibitor in patients receiving PCI with death. And Greg, I suppose you like I wonder what Indobufen is, and I just learned that that is a reversible inhibitor of platelet Cox-1 activity and it has comparable biochemical and functional effects to dose of aspirin. And previous data indicate that Indobufen could lessen the unwanted side effects of aspirin and that includes allergy intolerance and most importantly, aspirin resistance, while it retains the antithrombotic efficacy. Dr. Greg Hundley: Wow, Peder. Really interesting and great explanation. Indobufen. So how did they design this trial and what were the primary results? Dr. Peder Myhre: So Greg, the investigators of this trial, called OPTION, led by corresponding authors, Drs. Ge, Quian, and Wu from Fudan University in Shanghai, randomized 4,551 patients from 103 center to either indobufen based DAPT or conventional, and that is aspirin based DAPT for 12 months after DES implementation. And the trial was open label and with a non-inferiority design, which is important to keep in mind. And the primary endpoint was a one year composite of cardiovascular death, non-fatal MI, ischemic stroke, definite or probable stent thrombosis or bleeding, defined as BARC criteria type 2, 3, or 5. And now Greg, the primary endpoint occurred in 101, that is 4.5% of patients in the indobufen based DAPT group compared to 140, that is 6.1% patients, in the conventional DAPT group. And that yields an absolute difference of 1.6%. And the P for non-inferiority was less than 0.01. And the hazard ratio was 0.73 with confidence intervals ranging from 0.56 to 0.94. And Greg, the occurrence of bleeding was particularly interesting and that was also lower in the indobufen based DAPT group compared to the conventional DAPT group. And that was 3.0% versus 4.0% with the hazard ratio of 0.63. And that was primarily driven by a decrease in BARC type two bleeding. So Greg, the authors conclude that in Chinese patients with negative cardiac troponin undergoing DES implementation, indobufen plus clopidogrel DAPT compared with aspirin plus clopidogrel DAPT significantly reduced the risk of one year net clinical outcomes, which was mainly driven by reduction in bleeding events without an increase in ischemic events. Dr. Greg Hundley: Very nice, Peder. So another reversible inhibitor of platelet COX-1 activity, indobufen. And seems to be very, have high utility in individuals of Chinese ethnicity and Asian race. Well, perhaps more to come on that particular drug. Peder, how about we dive into some of the other articles in the issue? And I'll go first. So first, there's a Frontiers article by Professor Beatty entitled “A New Era and Cardiac Rehabilitation Delivery: Research Gaps, Questions, Strategies and Priorities.” And then there's a Research Letter by Professor Zuurbier entitled, “SGLT-2 inhibitor, Empagliflozin, reduces Infarct Size Independent of SGLT-2.” Dr. Peder Myhre: And then Greg, we have a new ECG challenge by Drs. Haghighat, Goldschlager and Oesterle entitled, “AV Block or Something Else?” And then there is a Perspective piece by Dr. Patrick Lawler entitled, “Models for Evidence Generation During the COVID-19 Pandemic: New Opportunities for Clinical Trials in Cardiovascular Medicine.” And Greg, there's definitely so much to learn from all the research that has been done through the pandemic. And finally, we have our own Molly Robbins giving us Highlights from the Circulation Family of Journals. And first, there is a paper describing the characteristics of postoperative heart block in patients undergoing congenital heart surgery described in Circulation: Arrhythmia Electrophysiology. Next, the impact of socioeconomic disadvantages on heart failure outcomes reported in Circulation: Heart Failure. Then there is social and physical barriers to healthy food explored in circulation, cardiovascular quality and outcomes. And then there is the association of culprit-plaque morphology with varying degrees of infarct, myocardial injury size reported in Circulation: Cardiovascular Imaging. And finally, the impact of optical coherence tomography on PCI decisions reported in circulation cardiovascular interventions. Dr. Greg Hundley: Fantastic, Peder. Well, how about we get off to that feature discussion? Dr. Peder Myhre: Let's go. Dr. Mercedes Carnethon: Well, thank you and welcome to this episode of the Circulation on the Run Podcast. I'm really excited today to host this show. My name is Mercedes Carnethon. I'm an associate editor at Circulation and Professor and Vice Chair of Preventive Medicine at the Northwestern University Feinberg School of Medicine. I'm really excited to learn from the lead author of a new study on decongestion with Acetazolamide and acute decompensated heart failure across the spectrum of LV ejection fraction. And I've got the lead author with me today, Pieter Martens, as well as my colleague and associate editor Justin Grodin, who handled the paper. So I'd love to start off with just welcoming you, Dr. Martens. Dr. Pieter Martens: Thank you for having me. It's a pleasure to be here today. Dr. Mercedes Carnethon: Yes. And thank you so much for submitting your important work to the journal, Circulation. I'd love to start to hear a little bit about what was your rationale for carrying out this trial and tell us a little bit about what you found. Dr. Pieter Martens: So the ADVOR trial was a double blind placebo controlled randomized trial, which was performed in Belgium. And it set out to assess the effect of acetazolamide in acute decompensated heart failure and this on top of standardized loop diuretic therapy and patients with heart failure. And the goal of the current analysis was to assess whether the treatment effect of acetazolamide in acute heart failure differs amongst patients with a different ejection fraction at baseline at randomization. So we looked specifically at patients with heart failure, reduced, mildly reduced and preserved ejection fraction to determine whether acetazolamide works equally well in those patients. Dr. Mercedes Carnethon: Well, thank you so much. Tell me a little more. What did you find? Did your findings surprise you? Dr. Pieter Martens: All patients that were randomized in the ADVOR trial, we registered a baseline left ventricular ejection fraction at baseline. And what we saw was at the multiple endpoints that we collected in the ADVOR trial, that randomization towards acetazolamide was associated with a pronounced and preserved treatment effect. And different endpoints that we looked at was a primary endpoint which was successful, which is an important endpoint, which we all strive towards in acute decompensated heart failure. And we saw that irrespective of what your baseline ejection fraction was, that randomization towards acetazolamide was associated with a higher odds ratio for having successful decongestion. And also looking at other endpoints which we find important in the treatment of patients with acute compensated heart failure, such as renal endpoints such as the diuresis, the amount of urine that they make, or the natruresis, the amount of sodium that they excrete, we again saw that randomization towards acetazolamide was associated with a higher treatment effect, so more diuresis, more natruresis, which was not effective, whether you had heart failure, reduced, mildly reduced or preserved eject fraction. We did see a slight increase in the creatinine, which was a little bit more pronounced in patients with heart failure with reduced ejection fraction. Dr. Mercedes Carnethon: Thank you so much for that excellent summary. I'm an epidemiologist, so I'm certainly aware that of the cardiovascular diseases and their changes over time, heart failure is one that is going up over time and affecting more of the population. So I know I really enjoyed hearing about an additional therapy that helps to improve quality of life and improve clinical outcomes in individuals who are experiencing heart failure. And I'm really curious as I turn to you, Justin, what attracted you to this particular article and why did you find it to be such a good fit for our audience here at Circulation? Dr. Justin Grodin: Well, Mercedes, I mean, I think you hit the nail on the head with your comment. And clearly when we look at Medicare beneficiaries in the United States, hospitalization for decompensated heart failure is the number one or most common cause for hospitalization. And up to this time, we really haven't had any multi-center randomized control clinical trials that have really informed clinical care with a positive result or a novel strategy that says, "Hey, this might be a better way to treat someone in comparison with something else." And so when we have a clinical trial like ADVOR, one of the crucial things that we want to understand is how does this work and does it work for everybody? And now when we look at the population hospitalized with heart failure, we know that approximately half of them have a weak heart or low ejection fraction, and the other half have a stiff heart, a normal ejection fraction. And so since we've got this 50/50 makeup, it is a crucially important question to understand if we have an important study like ADVOR, does this apply? Are these benefits enjoyed by all these individuals across the spectrum? Dr. Mercedes Carnethon: Thank you so much for really putting that in context. And I believe you had some additional questions for Dr. Martens. Dr. Justin Grodin: Yes. Yeah, thank you. So Pieter, I mean obviously this was a terrific study. One question I had for you guys is, you and your colleagues and the ADVOR research team is whether you had expected these results. Because we know at least historically, that there might be different cardiorenal implications for individuals that have a weak heart or heart failure with reduced ejection fraction in comparison with a stiff heart or heart failure with preserved ejection fraction. Dr. Pieter Martens: Thank you for that comment. And thank you also for the nice feedback on the paper. I think we were not really completely surprised by the results. I think from a pathophysiologic perspective, we do wonder whether heart failure with reduced ejection fraction from a kind of renal perspective is different from heart failure with preserved ejection fraction. Clearly, there are a lot of pathophysiological differences between heart failure with reduced, mildly reduced and preserved ejection fraction. But when it comes to congestion and acute heart failure, they seem to behave, or at least similarly in terms of response to acetazolamide, which was very interesting. We do think there are neurohormonal differences between heart failure reduced ejection fraction, preserved ejection fraction. But at least how acetazolamide works seems relatively unaffected by the ejection fraction. Dr. Justin Grodin: And Pieter, another question that comes to mind, and this is getting a little bit technical, but there have been studies that have shown that people that present to the hospital with decompensated heart failure, that have HFpEF, have a very different perhaps congestion phenotype where they might not have as much blood volume expansion. And so I, for one, was pretty curious as to how these results were going to play out. And I wonder what your thoughts are on that, or maybe that's perhaps more niche and less widely applicable than what you observed. Dr. Pieter Martens: Now, I can completely agree that when we are thinking about congestion, the congestion itself is a sort of pressure based phenomenon. And the pressure based phenomenon is based on what your volume is and the compliance within your cardiovascular system. But I think one of the important things to remember is that how we enrolled patients in the ADVOR trial was that we enrolled patients who had clear signs of volume overload. Remember, we used a volume score to assess clinical decongestion or actually getting rid of the volume. Volume assessment isn't really necessarily a pressure based assessment. And pressures might be the genesis of elevated pressures might be different amongst heart failure with reduced versus preserved ejection fraction. But what was really clear was that all these patients were volume overloaded. And when you think about the volume axis, then it's really about getting rid of that additional sodium, water, and that's where really acetazolamide works. So I do think we differ a little bit from historical acute decompensated heart failure trials in which they sometimes use signs and symptoms of more congestion, a pressure based phenomenon, where our endpoint was truly at volume endpoint. And we do believe that diuretics work really on a volume component of heart failure. Dr. Mercedes Carnethon: Thank you so much, especially for explaining that in a way that even non-clinicians such as myself can understand the potential implications. A big picture question that I have, and I really enjoy these discussions because they give us an opportunity to speculate beyond what we read in the paper. And that question is we do clinical trials and we identify effective therapies. And one of the bigger challenges we often face is getting those therapies out to the people who need them. Do you perceive any barriers in uptake of the use of acetazolamide in clinical practice? Dr. Pieter Martens: That's an excellent question. So one of the, I think beauties about acetazolamide is that this drug has been on the market for about 70 years. So I think everybody has access to it. This is not a novel compound which needs to go through different steps of getting marketing approval and getting a sort of reimbursement before it becomes available in clinical practice. And in theory, everybody should have access to this relatively cheap agent and can use it in its clinical practice. And I think it was very interested when we came out with the initial paper. I think already the day afterwards, we were getting messages from across the world that people have been using acetazolamide. So I think it is an agent which is available in current clinical practice and should not be too many barriers to its current implementation and clinical practice. Dr. Mercedes Carnethon: Well, that's fantastic to hear. So I hope Justin, that you will certainly help to ring the bell to get the information out about this wonderful study. I do want to turn to you, Pieter, to find out whether or not there are any final points that you didn't have an opportunity to discuss with us today. Dr. Pieter Martens: Think some of the other end points we didn't discuss were the effect, for instance, on length of stay. I think length of stay is a very important endpoint because hospital admissions, like Justin said, heart failure is the number one reason why elderly patients are being admitted. And just shortening the length of stay from a financial perspective might be important. So it was also very interesting to see that the use of acetazolamide in the study also translated into a shorter length of stay, which was also was unaffected, whether you had heart failure, reduced, mildly reduced or preserved ejection fraction, Dr. Mercedes Carnethon: Well, I certainly know people appreciate being in their own homes and being able to discharge is certainly a major benefit. So thank you so much for sharing that final point. I really want to thank you so much for a stimulating discussion today. I know that I learned a lot from you, Pieter, and the hard work of your research team as well as from you, Justin, for putting these findings in context and really helping our listeners and the readers of our journal understand why this paper is so important and how it's really moving the field forward for a clinically important problem. So thank you both so much for joining us here today on Circulation on the Run. Dr. Justin Grodin: Thank you. Dr. Pieter Martens: Thank you for having me. Dr. Mercedes Carnethon: I really want to thank our listeners for joining us today for this episode of Circulation on the Run. I hope you will join us again next week for more exciting discussions with our authors. Dr. Greg Hundley: This program is copyright of the American Heart Association 2023. 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.

S2E8: Don't Leave Money on the Table with Sandra Myerson, Assoc Principal & Nate McCarthy, Partner at ECG with host Dr. Nick. In general, everything around us is something of a gamble and everything we do is essentially a gamble and consists of weighing up odds. Life is but a series of gambles. Everything has risks. And our best bet is to learn how to make good bets. This is true in healthcare. Healthcare leaders are gambling on a daily basis as they try to navigate the long list of variables and changing demands of our health systems. Compelling evidence and data tells us that the fee-for-service model may have worked in the past but is no longer serving us. Fee for service should be a waning system being replaced by value-based care that as you will hear has and is delivering value to institutions. Your better pill to swallow is not to leave money on the healthcare table by leading your whole organization to commit to value-based care. To stream our Station live 24/7 visit www.HealthcareNOWRadio.com or ask your Smart Device to “….Play Healthcare NOW Radio”. Find all of our network podcasts on your favorite podcast platforms and be sure to subscribe and like us. Learn more at www.healthcarenowradio.com/listen

For apneic patients without a carotid pulse or pulseless patients with only gasping/agonal respirations, we will follow the Adult Cardiac Arrest algorithm. For pulseless patients that the AED doesn't advise a shock, the patient's ECG shows asystole, or a non-perfusing organized rhythm (PEA), we will follow the right side of the algorithm.Initial steps are aimed at delivery of high-quality CPR to keep the brain and vital organs alive. Epinephrine administration.Placement of an advanced airway.Considering possible reversible H & T causes of cardiac arrest including three common causes of PEA and their emergent interventions.When we should discontinue resuscitation efforts and call the code.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGive back & support the show:via PayPal Good luck with your ACLS class!

Although magnesium can be used in the treatment of other medical conditions such as eclampsia, asthma, & digitalis toxicity; for ACLS, magnesium is primarily used to treat Torsades de Pointes. Identification of Torsades on the ECG.Administration of a magnesium infusion for stable patients vs slow IV push for patients in cardiac arrest.Procainamide use for stable patients with a monomorphic wide-complex tachycardia. Procainamide dosing and when to stop the infusion. Tip for determining whether magnesium or Procainamide should be used when treating stable patients with V-Tach.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGive back & support the show:via PayPal Good luck with your ACLS class!

Why do cardio machines require you to put two hands on them to measure your heart beat when a wrist watch can do it just with one wrist? What's the difference between an ECG and EKG? Which types of monitor is most accurate? ... we explain like I'm five Thank you to the r/explainlikeimfive community and in particular the following users whose questions and comments formed the basis of this discussion: saltyson32, internetboyfriend666, blindedbythesight, iuse2bgood, vexx_nl, angryocelot and notwearingatie To the ELI5 community that has supported us so far, thanks for all your feedback and comments. Join us on Twitter: https://www.twitter.com/eli5ThePodcast/ or send us an e-mail: ELI5ThePodcast@gmail.com

In atrial fibrillation (A-Fib) and atrial flutter (A-Flutter) the electrical impulse for cardiac contraction is in the atria but isn't the normal pacemaker of the heart, the SA node. The ECG characteristics of A-Fib and A-Flutter. Recognition and treatment of unstable patients in A-Fib/Flutter with rapid ventricular response (RVR).Suggested energy settings for synchronized cardioversion of stable patients with a narrow complex tachycardia. Team safety when cardioverting an unstable patient in A-FIB.Adenosine's role for stable SVT patients with atrial rhythms.Treatment of stable patients in A-Fib/Flutter with RVR.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGood luck with your ACLS class!

For most MedTech devices, the path to development starts with defining a market need, then creating a technology to fill that need. But sometimes innovation lies in finding a new application for an existing technology. And sometimes the inspiration can come from a totally unexpected place.Such was the case for Venk Varadan, indie film producer-turned MedTech CEO of Nanowear, a wearable diagnostic device for cardiac patients. Nanowear adapted a unique sensor technology originally designed to provide data-rich sonar for submarines and high-flying aircraft, to create a cloth nanotechnology, which captures and transmits 85+ dimensions of clinical-grade biomarker data from basic skin contact. The fabric has a suede-like texture, which comes from billions of tiny vertical sensors.Nanowear's SimpleSense™ is an FDA-cleared wearable A.I.-based remote diagnostic platform.  The non-invasive smart fabric collects a variety of metrics including ECG, heart rate variability, respiratory rate, actigraphy, impedance cardiography, thoracic impedance, and cardio-phonography. Nanowear is one of a handful of ways to track heart rate, blood pressure, and other vital signs for long periods of time. But the big plus is that it's non-invasive and can be used at home, facilitating patient compliance and, through telehealth, expanding the geography of high-quality care in rural markets. Andy Rogers of Key Tech gets to the heart of the matter as he talks with Venk about the journey from lab to marketplace.Need to know: Decide who you're going to be. Early on, Nanowear chose to go into MedTech, when they could have easily applied their technology to sports or wellness markets.  Don't be afraid to re-think. Nanowear was originally two products: a tank top for men and a bra for women. The realities of sizing and inventory forced a change to a unisex shoulder sash. Know what you don't know. Become an information sponge. Start small, stay small. After seven years, the Nanowear team is still only 30 people, recruited mainly from family (Venk's father, Vijay, developed the fundamental technology), friends, and colleagues. Look at the angles. Consider the viewpoints of all your stakeholders: investors, clinicians, patients, and your own staff.  The nitty-grittyThe primary factors that drive the application of nanosensors in healthcare are their non-invasive ease of use, high signal fidelity, and continuous monitoring capability.  Nanowear's shoulder sash is an easy-to-use multi-metric diagnostic system with state-of-the-art embedded wireless network devices that feeds data to a smartphone, a laptop, or directly to a remote server. This in turn enables a closed-loop digital system for specific machine-learning algorithms built on terabytes of patient data.Right now, Nanowear is focusing on monitoring congestive heart failure, which affects over 5 million patients in the U.S. With this versatile undergarment, doctors can remotely monitor patients and hopefully reduce expensive hospital visits. For patients, it's a comfortable, easy way to stay on top of their condition. The SimpleSense™ fabric is the first cloth that's FDA 510-cleared, but pioneering the cloth technology was only the beginning. The next challenge was dealing with the “firehose of data” that it generated.Collecting more data. Nanowear sensors capture 85+ medical grade biomarkers directly from the skin and provide accurate, continuous, real-time assessment of the heart, lungs, and upper vascular system: a more comprehensive picture of patient health. Managing more data. The cloth technology produces exceptionally high-quality raw signal data. To analyze millions of data points per patient per day, Nanowear had to create proprietary software. Retaining more data. With machine learning algorithms, Nanowear can track trends in a patient's cardiovascular health over time, providing clinicians with a tool that enables much more accurate decision-making.

Listen to a recap of the top stories of the day from 9to5Mac. 9to5Mac Daily is available on iTunes and Apple's Podcasts app, Stitcher, TuneIn, Google Play, or through our dedicated RSS feed for Overcast and other podcast players. Sponsored by SecuritySpy: Check out SecuritySpy CCTV video surveillance software for macOS. SecuritySpy allows customers to easily set up CCTV systems in their home or business, with just a Mac and some IP cameras. iTunes/Apple Podcast or your favorite podcast player to guarantee new episodes are delivered as soon as they're available. Stories discussed in this episode: Tesla announces its own AirPower-like Qi charger that works with up to three devices simultaneously Netflix hiding its cheapest ad-free plan, new ad tier still doesn't work on Apple TV ITC rules that Apple Watch infringed AliveCor's ECG patent, US sales potentially threatened Report: Apple axed plans for next-generation GPU in iPhone 14 Pro after rare engineering blunder Update from Chance Enjoy the podcast? Shop Apple at Amazon to support 9to5Mac Daily! Follow Zac: Twitter: @apollozac Mastodon: @zac@home.social Follow Seth: Twitter: @SethKurk Post: @sethkurk Listen & Subscribe: Apple Podcasts Overcast RSS Spotify TuneIn Google Play Catch up on 9to5Mac Daily episodes! Don't miss out on our other daily podcasts: Quick Charge 9to5Toys Daily Share your thoughts! Drop us a line at happyhour@9to5mac.com. You can also rate us in Apple Podcasts or recommend us in Overcast to help more people discover the show!

ECG Diagnosis of Left Ventricular Hypertrophy Guest: Ljuba Bacharova, M.D., D.Sc, M.B.A. Hosts: Anthony H. Kashou, M.D. (@anthonykashoumd) Joining us today to discuss the diagnosis of left ventricular hypertrophy (LVH) by means of the ECG is Ljuba Bacharova, senior researcher in the International Laser Centre, CVTI, in Bratislava, Slovakia and instructor at Comenius University's Medical School. Dr. Bacharova's main focus in research has been in the evaluation of the cardiac electric field with a special interest in left ventricular hypertrophy. Tune in today to learn more about the ECG and LVH. Specific topics discussed: What do you see as the major problem in ECG-LVH diagnosis? And why is it still interesting/ actual? What are other key factors influencing the resultant QRS voltage in LVH? Thoughts around relative high specificity in ECG diagnosis of LVH. How to escape from the mental high-QRS-voltage trap in LVH diagnosis. Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. Facebook: MayoCVservices LinkedIn: Mayo Clinic Cardiovascular Services NEW Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.

Our primary focus immediately following return of spontaneous circulation (ROSC) is aimed at ensuring adequate perfusion of the patient's vital organs and decreasing cerebral damage.After we have assessed and addressed O2 saturation, ETCO2, and BP, we may consider the use of an antiarrhythmic infusion if the patient has ventricular ectopy on the ECG. Indications for use of an antiarrhythmic after ROSC.Determining which antiarrhythmic to use post cardiac arrest. Administration of Amiodarone or Lidocaine to control ventricular ectopy after ROSC. The use of Amiodarone post arrest if no antiarrhythmics were administered prior to obtaining ROSC. Links to other medical podcasts that cover antiarrhythmics and other ACLS-related topics are on the Pod Resource page at PassACLS.com.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGood luck with your ACLS class!

Support Topic Lords on Patreon and get episodes a week early! (https://www.patreon.com/topiclords) Lords: * Mark * Shirley Topics: * What would you do if you came downstairs and all of my clothes and my glasses were on the floor in a heap in a puddle of water? * Aphasia: What doesn't it mean? * Dr. Icecreamwala * https://www.icecreamderm.com/ * Eternal Champion - I Am The Hammer * https://eternalchampion.bandcamp.com/track/i-am-the-hammer * Teen Censorship (what to restrict, if anything?) * SCA stuff: social skills in the SCA, thrown weapons, and winter camping! Microtopics: * EEG, EKG and ECG. * Dogs and video games. * Kingdom: Two Crowns. * Whoops, I'm Dead! * Borker and Starina. * Waking up in the morning and telling your wife "and we're back!" * Sleeping with the Shirley-cicle. * When your wife turns into a puddle of water and you have to get a hot water bottle shaped like your wife to sleep with every night. * Hedge witches. * An Alex Mack situation. * Turning yourself into a goo accidentally vs. on purpose. * A dog athletic enough to pee on your glasses while you're wearing them. * Figuring out what muscle to flex to telepathically communicate as a glass of water. * Believing things you see written in an authoritative voice. * The kind of movies Bruce Willis has been making lately. * Aphasia vs. Primary Progressive Aphasia. * The four primary modalities of human language. * Figuring out how to hang out with someone you can't talk to. * Decoupling the word "yes" from its literal meaning. * Apraxia of speech. * Thanking colonialism for this moment of delight. * Serving your patients their prescription in a waffle cone. * Flying to the Bay Area to get some light dermatology done. * The battle-starved riders of Tarsul. * The demon priests of ill Nitaar. * Nolan Bushnell receiving feedback about the name Atari. * The God Blade. * Fist-pumpin', sword-swingin' heavy metal. * A good source of lore. * Cosmologies where god is a species. * Drinking his blood to see what happens. * Heavy metal bands fronted by blacksmiths. * Wanting your teenager to feel safe listening to fascist heavy metal in front of you so that you can talk to them about it. * Installing a web filter so that your child doesn't accidentally stumble into gross abusive porn. * Opinions about parent-child relationships from someone who was once a child. * Heavy metal bands who write music about white nationalism vs. heavy metal bands who are just white nationalist without writing about it. * Deliberately not separating the art from the artist so you get the extra enjoyment out of musicians who are cool people. * Videos of common household items being crushed under the wheels of a car. * Videos of people building things in the woods. * Devil's toothpaste. * Reacting to the sugar tax by angrily boycotting soda. * The Society for Creative Anachronism kicking you out if you dress up as a time traveler from the future or a 1950s greaser. * The SCA re-enacting the before-times, when morning zoo radio didn't exist yet. * Apex Nerds. * Geniuses above petty squabbling. * A better system of chilling out. * Going into the woods with your friend who likes building stuff in the woods and watching him build stuff in the woods. * Movies set in the 80s that have absolutely nothing from the 70s in them because everybody threw all that shit away on January 1st, 1980. * Handing out arm rings to your sworn men. * Instituting a buddy system where you buy each other awards. * Happy baby cow.

Being the team leader during a cardiac arrest is challenging. Using an algorithm helps by standardizing & prioritizing our interventions using an If/Then methodology. Review of BLS steps for determining if rescue breathing or CPR is needed and use of an AED for patients in cardiac arrest. If the patient is in a non-shockable rhythm on the ECG such as PEA or asystole, we will go down the right side of the Adult Cardiac Arrest Algorithm. If the patient is in a shockable rhythm on the ECG such as V-Fib or V-Tach, we will go down the left side of the Adult Cardiac Arrest Algorithm. An example of a code's flow for shockable rhythms when an antiarrhythmic such as Amiodarone or Lidocaine is administered. We will follow the algorithm until the patient has ROSC or we call the code.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGood luck with your ACLS class!

To pass ACLS, you will need to be able to identify common rhythms on a monitor during your mega code and ECG strips on your written exam.If you don't normally monitor patients as part of your job, I suggest two things:1. Find a system for ECG interpretation that works well for you; and2. Practice reading ECGs every day for a few weeks before your class.Review of normal ECG morphology of P wave, QRS complex, and T wave in lead II.Characteristics of first degree heart block.Characteristics of third degree (complete) AV block.Treatment of unstable patients in third degree block following the ACLS Bradycardia algorithm. Special considerations for use of Atropine when patients are in a third degree heart block.The use of TCP, Dopamine, & Epinephrine drip for unstable bradycardic patients refractory to Atropine.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGood luck with your ACLS class!

Bienvenue dans cet épisode 115 d'iWeek (la semaine Apple), le podcast. Apple Car, une voiture presque comme les autres à 100.000 $ ? Enregistré (exceptionnellement) le mercredi 7 décembre à 18h. Présentation : Benjamin Vincent. Intervenants : Elie Abitbol, Fabrice Neuman, Gilles Dounès. Invité : Frédéric Crassat, spécialiste des processeurs. Production : OUATCH Audio. Pour soutenir iWeek : patreon.com/iweek. Cette semaine : Apple aurait abandonné l'idée d'une voiture 100% autonome pour l'Apple Car, selon Mark Gurman de Bloomberg qui prédit une sortie en 2026 d'une voiture Apple capable de conduire seule, uniquement sur autoroute, pour un prix qui ne dépassera pas... 100.000 $. Cette 1ère Apple Car embarquerait 4 fois la puissance informatique de nos appareils d'aujourd'hui. Une raison largement suffisante pour proposer à Frédéric Crassat, spécialiste des processeurs, de revenir dans iWeek ! L'inauguration du site des futures usines TSMC à Phoenix dans l'Arizona, par Joe Biden et Tim Cook notamment, cette semaine, était une deuxième excellente raison de discuter finesse de gravure, du 5 au... 1 nanomètre. La mise au point de Gilles (Dounès) est consacrée aux nouveaux paliers tarifaires sur l'App Store. Des prix qui peuvent désormais aller jusqu'à 10.000 € pour une app... et sur lesquels Apple continue de toucher sa commission de 30 %. En réponse à une question de @StoffMac sur Twitter avec le hashtag #iweekLSA, nous consacrons un moment à discuter du suivi du rythme cardiaque sur Apple Watch. Et puis, ne manquez pas le bonus hebdo exclusif qui vous est réservé, à vous, nos soutiens Patreon : un bonus... vidéo, désormais. Cette semaine : ChatGPT, le chatbot phénomène qui a réponse à tout... ou presque ! Rendez-vous mercredi 14 décembre au soir, pour l'épisode 116 d'iWeek (la semaine Apple) ! Par ailleurs, retrouvez la version vidéo du podcast en avant-première sur Patreon, puis, à partir du dimanche, sur la chaîne YouTube d'iWeek ! Abonnez-vous à la chaîne YouTube d'iWeek et cliquez sur la cloche pour être alerté dès qu'un nouvel épisode est disponible en vidéo. Si l'actualité Apple vous passionne, abonnez-vous gratuitement à "la quotidienne iWeek", le 1er podcast quotidien sur l'actu Apple : 5 minutes par jour, 5 jours par semaine, du lundi au vendredi, avec l'essentiel de l'info Apple quotidienne. la quotidienne iWeek sur Apple Podcasts : https://apple.co/3lTrLe6 (nouveau lien) la quotidienne iWeek sur Spotify : https://sptfy.com/iweekLQI (nouveau lien) Pour avoir les dernières nouvelles d'iWeek, suivez notre compte Twitter : @iweeknewset notre compte Instagram : @iweek.news !

Episode: 2430 How we equipped today's medical clinics in 1915.  Today, your doctor's office comes into being.

Two things have changed in recent years to aid students that don't use ACLS in their daily practice1. The role of the team leader; and2. The ability to use your quick reference cards.The team leader is responsible for assigning tasks and overall direction of the team but may ask team members for help to confirm the ECG, suggest medications, identify possible reversible causes of cardiac arrest, and to speak up if they identify something that's unsafe.Students may use their book and quick reference cards during the mega code as well as the written exam.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGood luck with your ACLS class!

CineECG for ECG Analysis Guest: Peter van Dam Ph.D. Hosts: Anthony H. Kashou, M.D. (@anthonykashoumd) Joining us today to discuss CineECG for ECG Analysis is Peter van Dam, Ph.D., co-founder and chief scientific officer of ECG Excellence, a Dutch company specialized in developing solutions to make 12-lead ECG interpretation better and easier for both non expert ECG physicians and expert ECG readers. CineECG is the first product of ECG Excellence, which is a software designed to support physicians in ECG interpretation. Tune in to learn more about this innovative topic. Specific topics discussed: What is CineECG? How does CineECG differs from 12 lead ECG What is the main advantage of using CineECG compared to the current standards? How we explore the advantages of CineECG ourselves? Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. Facebook: MayoCVservices LinkedIn: Mayo Clinic Cardiovascular Services NEW Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.

Part 2 of a 4 part series on  syncope.Syncope is one of the top reasons why a rapid response is called... but the question is, what precipitated the syncope?In this episode we discuss a classic case of vasovagal syncope, in which Annie's patient had a six second pause on his ECG in response to some overwhelming news.  We break down why atropine might not be the best intervention for this patient and some of the treatment options for bradycardia. 

 In this podcast, enneagram expert Dr. Baruch HaLevi and financial expert Michael Finer explore Enneagram 4, The Alternative Investor, and how they relate to money, finances, and investments. This is an investor who can open all our eyes to the deeper aspects of investing such as impact investing or ECG stocks.

David Albert is a physician, inventor, and serial entrepreneur. He is the Founder and Chief Medical Officer of Alivecor, the leading company in personal ECG technology. He has founded 5 companies, and sold two – one to Arrhythmia Research Technology and one to GE which he joined as Chief Scientist of GE Cardiology. David has 32 issued US patents and has authored or co-authored over 50 scientific abstracts and publications. In this episode David shares what makes ECG such useful tool, how the idea for personalized ECG came about, ECG regulatory strategy, technology development, the importance of robust clinical data, and the challenge of managing massive amounts of data.  Links from this episode:David Albert LinkedInAliveCorMastering Medical Device:WebsitePat Kothe LinkedIn

The chain of survival for ACLS is the same as was learned in your BLS class.The beginning steps of the Cardiac Emergency and Stroke chain of survival are the same.1. Recognizing the symptoms of a cardiac emergency or stroke;2. Activating an emergency response by calling 9-1-1, or a specialized code team if in the healthcare setting;3. Rapid assessment including 12 lead ECG for cardiac patients or FAST assessment for suspected stroke emergencies; 4. Provide ALS care and transport to the most appropriate facility; for5. Early reperfusion.ACLS's timed goals for first medical contact to PCI for STEMI and door-to-needle for ischemic stroke.Areas with strong EMS relationships, well-defined transport protocols, andspecialized teams that care for the patient in the hospital have significantlybetter patient outcomes. The cardiac arrest chain of survival adds: high quality CPR, early defibrillation, and advanced resuscitation as the next critical links followed by post arrest care and recovery.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGood luck with your ACLS class!

Heart muscle contraction and repolarization is dependent on Sodium, Calcium, Magnesium, and Potassium ions crossing cellular membranes.When a patient's potassium levels get too low or too high hypokalemia or hyperkalemia results respectively.Two things that may lead us to suspect hypo or hyperkalemia include:the patient's medical history; and changes to the T wave on the ECG.Medical conditions that cause potassium imbalance.ECG changes seen in hypo and hyperkalemia.Critical lab values that would indicate a need for treatment.Emergent, ACLS interventions for hypokalemia and hyperkalemia.Additional information on hypo and hyperkalemia can be found on Ninja Nerd podcast. Check out the pod resources page at passacls.com.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGood luck with your ACLS class!

Ventricular Tachycardia Database Development and Detection Guest: Michele Pelter, R.N., Ph.D. Hosts: Anthony H. Kashou, M.D. (@anthonykashoumd) Joining us today to discuss Ventricular Tachycardia Database Development and Detection designed to improve hospital-based ECG monitoring is Michele Pelter, R.N., Ph.D., associate professor in the School of Nursing at the University of California San Francisco. Her current work has focused on improving the detection of transient myocardial ischemia and most recently understanding false ECG alarms that might contribute to alarm fatigue in nurses. Specific topics discussed: Why is identifying ventricular tachycardia during hospital-based ECG monitoring a problem? Why is ventricular tachycardia the focus? What are some algorithm deficiencies? How might the annotated ventricular tachycardia database help improve the problem of false ventricular tachycardia alarms? Other projects that Dr. Pelter is working on related to hospital-based ECG monitoring. Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. Facebook: MayoCVservices LinkedIn: Mayo Clinic Cardiovascular Services NEW Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.

To pass the written ACLS exam and mega code, students need to be able to identify basic ECG dysrhythmias, including the two types of second-degree heart block.One method of ECG rhythm identification is to ask a series of questions such as: What's the rate (150);Is the rhythm regular or irregular;What's the shape and frequency of P waves and QRS complexes; andWhat's the P-R interval and is it constant?ECG characteristics of a second-degree Mobitz type I (Wenckebach).Identification of unstable bradycardia and it's treatment with Atropine.ECG characteristics of a second-degree Mobitz type II.Possible effect of using Atropine on patients with a second-degree type II AV block. Treatment of unstable patients refractory to Atropine using TCP, Dopamine, or Epinephrine drip.Starting dose and titration of Dopamine and Epinephrine drips.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGood luck with your ACLS class!

On this week's episode of The Tech Leader's podcast, Gareth is joined by Adrian Condon, the CTO of B-Secur, a company that creates cutting-edge, heart health technology that is used in some of our favourite tech wearables. In this episode, the topic of discussion centres around how technology can be used to understand the human body, exemplified by the life-saving heart rate variability monitors that Condon himself has helped create.  In understanding our connection to machinery, we also find out how our stress levels mirror that of a car in first gear, and how to avoid a subsequent tech-induced burnout. However, at a time where there is frequent talk about ‘cyborgs' replacing the organic human body, Adrian Condon discusses how technology should be used as a way of ‘aiding humans, not replacing them'. 02:16 – What does good leadership mean to Adrian?04:00 – What did Adrian want to be when he grew up?05:14 – Where B-Secur started08:20 – Information we can receive from ECG signals 10:20 – Where this technology is going in terms of clinical usage 11:30 – What does HRV (heart rate variability) mean?15:00 - Stress in relation to cardiovascular disease16:33 - Next wave of heart problems and “Athletes Heart”21:30 – Lifestyle impact of these wearable technologies23:40 – Is implantable technology the future?26:10 – Sports performance and how this technology assists athletes.29:40 – Alcohol, drinking and seeing the changes in HRV32:00 – What is Adrian most excited about in the world in terms of technology innovation?36:00 – How does Adrian stay healthy working in this field? 40:00 – Adrian's productivity advice41:00 – If Adrian could have a coffee with anyone in the world, who would it be?41:54 – What advice would you give to your 21-year-old self?43:10 - Encouraging start-ups and teaching schools about tech and money

Biotricity creates leading-edge professional and personal remote medical monitoring technology engineered to improve people's lives. Biotricity listed on the Nasdaq only 5 years into their journey. Biotricity Inc. (NASDAQ:BTCY) ("Biotricity" or the "Company"), a medical diagnostic and consumer healthcare technology company, has surpassed $10 million in annual revenue run rate. Biotricity boasts multiple ground-breaking products including Bioflux®, Biotres, and Bioheart which won TIME's Best Inventions of 2022. Bioflux: a high-precision, single-unit mobile cardiac telemetry (MCT) device that provides real-time monitoring and transmission of your ECG information to your doctor Biotres: an easy to wear, rechargeable device with wireless capability, utilizing the advanced technology of the Bioflux® for more active days Bioheart: a consumer-targeted continuous heart rhythm monitor that uses the most advanced heart technology to deliver unlimited heart data insights with three views of your heartGet interviewed on the Matt Brown Show: www.mattbrownshow.com

The 2020 ACLS guidelines updated the dose for administration of Atropine and Dopamine for the treatment of unstable bradycardia. The signs & symptoms of unstable bradycardia.Atropine's new dose and maximum.The use of atropine when a patient is in a second degree type II or third degree heart block.ECG changes that indicate subsequent doses of atropine are likely to be ineffective.The 2020 update to the starting dose of Dopamine.The use of Dopamine for bradycardia as an interim until TCP vs hypotension.The use of Atropine and Dopamine in patients with myocardial ischemia.Podcasts with additional (advanced-provider level) information about Atropine, Dopamine, and bradycardia can be found on the Pass ACLS pod resources page.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGood luck with your ACLS class!

CardioNerds (Dan Ambinder), episode lead Dr. Sarah Fahnhorst (ACHD Cardiologist at Spectrum Health in Grand Rapids, Michigan), and series co-chair Dr. Agnes Koczo (fellow at UPMC) learn about ASD from Dr. Richard Krasuski (ACHD Cardiologist and Director of ACHD at Duke University). Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares An atrial septal defect (ASD) is a common congenital heart disease most often diagnosed in childhood, but initial presentation can be in adulthood. ASDs are abnormal communications between the left and the right atrium.  There are four types of ASDs with different embryologic origins. If the defects are large, they will require percutaneous or surgical closure. Unrepaired defects can lead to symptoms of shortness of breath, exercise intolerance, recurrent chest infections, or pulmonary hypertension. This episode of CardioNerds will review the natural history, embryologic origin, diagnostic modalities/findings, indication for closure and long term complications of repaired and unrepaired atrial septal defects.  The CardioNerds Adult Congenital Heart Disease (ACHD) series provides a comprehensive curriculum to dive deep into the labyrinthine world of congenital heart disease with the aim of empowering every CardioNerd to help improve the lives of people living with congenital heart disease. This series is multi-institutional collaborative project made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Josh Saef, Dr. Agnes Koczo, and Dr. Dan Clark. The CardioNerds Adult Congenital Heart Disease Series is developed in collaboration with the Adult Congenital Heart Association, The CHiP Network, and Heart University. See more Disclosures: None Pearls • Notes • References • Guest Profiles • Production Team CardioNerds Adult Congenital Heart Disease PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Atrial Septal Defects It's a CLASSIC! – On physical exam a wide fixed split S2 along with a systolic ejection murmur due to increased blood flow across the pulmonary valve and potentially a diastolic rumble across the tricuspid valve are CLASSIC findings with atrial septal defects. Atrial septal defects are not all the same. There are four types of atrial septal defects: secundum ASD, primum ASD, sinus venosus and coronary sinus defects (NOTE – the latter are atrial level defects which actually do not involve the interatrial septum). The different types warrant a different approach to closure. Use your tools and if your suspicion is high for an atrial septal defect, keep looking. Sinus venosus defects can easily be missed since the superior vena cava is difficult to image in adults. Diagnostic tools include: history and physical exam (USE the stethoscope), ECG, echocardiogram, cardiac MRI, cardiac CT, and cardiac catheterization.Not all defects NEED to be closed immediately. Moderate-large defects with a shunt greater than 1.5:1 should be closed due to increased risk of pulmonary hypertension and arrhythmias, barring contraindications. Surgery was previously the gold standard for closure of ASDs, but many defects especially secundum atrial septal defects are closed in the cath lab.    Show notes - Atrial Septal Defects Notes (developed by Dr. Sarah Fahnhorst What are the four different types of atrial level defects?Secundum atrial septal defectMost common type of atrial septal defect (75%)Located in the center of the atrial septum (fossa ovalis)Hole in the primum septum due to deficiency of the septum secundumPrimum atrial septal defectAccounts for 15-20% of ASDLocated at the inferior portion of the atrial septumIn the spectrum of atrioventricular septal defects/endocardial cushion defectsDefect in the developme...

ECG characteristics of supraventricular tachycardia (SVT) vs. sinus tachycardia. Signs & symptoms that indicate a patient is unstable. Treatment of unstable SVT using a biphasic vs monophasic defibrillator. Consideration for team safety while performing synchronized cardioversion. Stable patients in SVT.For more on narrow complex tachycardias, check out the pod resource page at passacls.com.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGood luck with your ACLS class!

For apneic patients without a carotid pulse or pulseless patients with only gasping/agonal respirations, we will follow the Adult Cardiac Arrest algorithm. For pulseless patients that the AED doesn't advise a shock, the patient's ECG shows asystole, or a non-perfusing organized rhythm (PEA), we will follow the right side of the algorithm. Initial steps are aimed at delivery of high quality CPR to keep the brain and vital organs alive. Epinephrine administration.Placement of an advanced airway. Considering possible reversible H & T causes of cardiac arrest including three common causes of PEA and their emergent interventions. When we should discontinue resuscitation efforts and call the code.Connect with me:Website: https://passacls.com@PassACLS on Twitter@Pass-ACLS-Podcast on LinkedInGood luck with your ACLS class!

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 cohosts. I'm Dr. Carolyn Lam, Associate Editor from the National Heart Center, and Duke National University of Singapore. And... Dr. Peder Myhre: I'm Dr. Peder Myhre from Akershus University Hospital, and University of Oslo in Norway. Dr. Carolyn Lam: Peder, I'm so excited about our future discussion. It's about a very important topic of detecting atrial fibrillation in the population using wearable devices. It talks about the Fitbit Heart Study. So exciting, but we're going to keep the audience waiting a bit, because we're going to talk about some other things in the issue. And I would love to start with this now. We know that fulminant myocarditis presentation is a rare and severe presentation of myocarditis. But, what is its natural history, and clinical features associated with poor outcomes? Peder, what do you think? Dr. Peder Myhre: Oh, that's a great question. We really don't know, because prior studies have been relatively small and selected. So Carolyn, let me know. Dr. Carolyn Lam: You're absolutely right. But today's paper from Professor Saito, from Nara Medical University in Japan and colleagues, is the largest nationwide cohort study of patients with histologically proven fulminant myocarditis presentation. They study 344 patients, hospitalized with histologically proven myocarditis, who underwent catecholamine and/or mechanical support from 235 cardiovascular training hospitals across Japan, between 2012 and 2017, and here's what they found. Over a median follow up of 600 days, the accumulative risk of death or heart transplantation at 90 days was 29%. So, really high. These were the risk factors associated with a higher risk of death or heart transplantation, and they were non-sinus rhythm, older age, ventricular tachyarrhythmia, lower left ventricular ejection fraction. Severe histological damage was also associated with a worse 90 day outcome in lymphocytic myocarditis. Cool, huh? Dr. Peder Myhre: Oh wow. That was some really solid data. And now Carolyn, I'm going to take us over to the world of preclinical science. And the next paper entitled at “APIC Associated De Novo Purine Synthesis is Critically Involved in Proliferative Arterial Disease” by Yuqing Huo from Augusta University in Georgia. Dr. Carolyn Lam: Cool. Dr. Peder Myhre: And as you know, Carolyn, vascular smooth muscle cells are extremely important in vascular health. They're located in the medial layers of arteries, and normally exhibit a contractile phenotype that contributes to the regulation of blood vessel tone, blood flow distribution, and blood pressure in normal mature blood vessels. And in response to disease processes, the vascular smooth muscle cells are switched to an activated synthetic and proliferative phenotype, that contribute to the development of a variety of arterial diseases, including atherosclerosis, in-stent restenosis, and bypass graft occlusion. And nucleotides that we are familiar with, such as ATP and GTP, are essential for a large number of biological processes in cells, including proliferation. And Carolyn, the previous studies have demonstrated that de novo synthesis of purine is a critical pathway for nucleotide synthesis. And in this study, the authors assessed the role of de novo synthesis of purine in vascular smooth muscle cells by using knockout mice. Dr. Carolyn Lam: Oh, that was beautifully explained. Thanks, Peder. So what did they find? Dr. Peder Myhre: So the authors found that the de novo purine synthesis was increased in proliferative vascular smooth muscle cells. Moreover, they identified an important enzyme in the process called A-P-I-C, APIC. Which was observed in the neointima of the injured vessels, and atherosclerotic lesions in both mice and humans. Finally, they showed that in a mouse model with knocked out APIC, the atherosclerosis and arterial restenosis was attenuated. Dr. Carolyn Lam: Cool. So tell us what the clinical implications are. Dr. Peder Myhre: So these findings provide novel insights into the reprogramming of purine metabolism underlying vascular smooth muscle cells proliferation in the development of arterial disease. And that targeting APIC may be a promising therapeutic approach to combat arterial diseases. So Carolyn, please tell me about your next paper. Dr. Carolyn Lam: Ah, thanks, Peder. Well, back to the clinical world, this time, talking about arrhythmogenic right ventricular cardiomyopathy. We know that is characterized by progressive cardiomyocyte loss and fibro fatty replacement. And we know that patients with this a ARVC are at risk for life-threatening ventricular arrhythmias and sudden cardiac death. The placement of an ICD is a crucial component of ARVC management. But arrhythmic risk stratification and the selection of the optimal candidates for ICD, especially for primary prevention of sudden cardiac death, has, of course, been challenging. As background, a ventricular arrhythmia risk calculator, in patients without previous sustained ventricular arrhythmias, has been proposed, and includes seven clinical variables derived from non-invasive tests that are routinely performed in these patients. However, the possibility of integrating additional parameters, such as ventricular tachycardia inducibility on programmed ventricular stimulation, with this risk calculator, has been suggested, but not conclusively investigated in a large cohort. And so, here comes corresponding author, Dr. Cadrin-Tourigny, from Montreal Heart Institute and colleagues, who studied 288 patients with a definite ARVC diagnosis, no history of ventricular arrhythmias at diagnosis, and programmed ventricular stimulation performed at baseline. And these patients were identified from six international ARVC registries. Dr. Peder Myhre: Oh wow. So we're talking risk stratification for patients with ARVC. Such an interesting topic, Carolyn. So please tell me, what did they find? Dr. Carolyn Lam: So, programmed ventricular stimulation significantly improved risk stratification, above and beyond the calculator predicted risk of ventricular arrhythmias, in a primary prevention cohort of patients with ARVC. And this was mainly for patients considered to be at low and intermediate risk by the clinical risk calculator. If negative, its high negative predictive value of 93% in low and intermediate risk patients, may support the decision to forego ICD use in some patients. So, programmed ventricular stimulation results may be applied to the non-invasive ARVC risk calculator, in a two step approach to facilitate personalized decision making for ICD in such patients. Dr. Peder Myhre: Thank you, Carolyn. That was a great summary and a great paper. So we're going to move in to see what else is in the mail bag, Carolyn. Dr. Carolyn Lam: You bet. There's a letter by Dr. Agirbasli regarding the article, “Coronary Artery and Cardiac Disease in Patients with Type Two Myocardial Infarction, A Prospective Cohort Study,” and this, followed by a response by Dr. Chapman. There's an ECG Challenge by Dr. [Jingnan] Han, entitled, “Tachycardia Associated with Pacing.” From our own Molly Robbins, we have highlights from the Circulation Family of Journals. And she covers the experience with stereotactic radio ablation and electrical storm, reported in Circulation: Arrhythmia and Electrophysiology. The impact of accessibility to primary care on hypertension awareness and control is reported in Circulation: CV Quality and Outcomes. There's an analysis of lifestyle factors and their impact on the risk of heart failure by background genetic risk, and that's in Circulation: Heart Failure. There's a deep learning model of PET scans and coronary flow reserve reported in Circulation: CV Imaging. And finally, OCT based measurement of stent expansion and associations with outcomes are presented in Circulation: CV Interventions. A lot. Dr. Peder Myhre: Yeah, and there's more, Carolyn. In this issue, there is an extensive Frontiers review by the AF-SCREEN International Collaboration, entitled, “Consumer LED Screening for Atrial Fibrillation.” There is also a Research Letter by corresponding author Qi Fu, from University of Texas Southwestern Medical Center entitled, “Neuro Cardiovascular Dysregulation During Orthostasis in Women with Posttraumatic Stress Disorder.” And finally, a Research Letter by Pankaj Arora from University of Alabama entitled, “Mechanical Circulatory Support Devices Among Patients with Familial Dilated Cardiomyopathy, Insights from the INTERMACS.” Dr. Carolyn Lam: That's awesome, Peder. Thank you. Now let's go onto our feature discussion on atrial fibrillation detection and the Fitbit Heart Study, shall we? Today's feature discussion is about the Fitbit Heart Study, and none other than the first and corresponding author Dr. Steven Lubitz, from Massachusetts General Hospital in Boston to join us today. Steve, welcome. Congratulations. Am I right to say, this is the largest study of its kind to look at the detection of atrial fibrillation using wearable devices? Dr. Steven Lubitz: Thanks for having me, Carolyn. And that's right, this is. Dr. Carolyn Lam: Oh my gosh. Okay. Tell us all about it, what you did, what you found. Dr. Steven Lubitz: Well, thanks, Carolyn. So as we know, undiagnosed atrial fibrillation is a potential hazard that can cause strokes. And if we can identify people who have undiagnosed atrial fibrillation early, we may be able to prevent strokes. In addition, undiagnosed atrial fibrillation may be associated with additional morbidity, which can be addressed through a number of different ways, if we can detect atrial fibrillation. Obviously, the challenge is to detect atrial fibrillation. We also know that people are increasingly wearing devices that have sensors on them, specifically using photoplethysmography technology, which can detect the pulse rate. Software algorithms can now be developed, that can assess that pulse rate for regularity or irregularity. But they really need to be assessed and validated, to minimize the potential for false positives, which can have obviously, downstream adverse consequences of their own, if atrial fibrillation is incorrectly identified or diagnosed as a result. As I was mentioning, we developed this novel software algorithm with frequent overlapping photoplethysmography, post tachogram sampling, which is unique. And then we tested the algorithm's positive predictive value for undiagnosed AFib in a large scale remote clinical trial, using a range of Fitbit wearable fitness trackers and smart watches. It was a remote trial, so participants were invited. These were people who already had a Fitbit account, they were invited to participate. And in span of just a few months, in the middle of the pandemic, over 455,000 people signed up to participate in the study. And so, big thank you to all of the participants in the study. Dr. Carolyn Lam: Wow, that is big. And what did you find? Dr. Steven Lubitz: So of the 455, over 455,000 participants that enrolled, over 4,000, had an irregular heart rhythm detection and received a notification. And after inviting those participants to attend a telehealth visit, and at that telehealth visit, the telehealth provider confirmed eligibility criteria, confirmed that they didn't have preexisting atrial fibrillation, for example, and a variety of other inclusion/exclusion criteria. They were mailed a one week ECG patch, that they applied themselves, and then returned that ECG patch. So in the end, after those exclusions, in participants that returned analyzable patches, 1057 participants were included in this ECG monitoring analytic cohort, of whom, 340 had atrial fibrillation during that ECG patch monitoring period. The primary endpoint of the study was the positive predictive value of irregular heart rhythm detection that occurred during the ECG patch monitoring period. So a participant had to have an irregular heart rhythm detection to get notified that they were eligible to meet with a telehealth provider and receive an ECG patch monitor. And then, they had to have another irregular heart rhythm detection during ECG patch monitor wear. So the primary outcome was the positive predictive value of the first irregular heart rhythm detection for concurrent atrial fibrillation that occurred during ECG patch monitoring. Dr. Carolyn Lam: Okay. Cool. So many questions here, but maybe you should tell us the results first. Dr. Steven Lubitz: Sure. So the primary endpoint, the positive predictive value of the IHRD during ECG patch monitoring was 98.2% in the overall cohort. And it was similar between men and women, and those aged 65 or older, or those aged less than 65. And I should mention that, in this study, about 13% of participants enrolled in this study overall, were above the age of 65. Dr. Carolyn Lam: And you included more women than in prior similar studies. Right, Steve? Dr. Steven Lubitz: Yeah. Dr. Carolyn Lam: I was going to congratulate you for that. Dr. Steven Lubitz: Yeah, that's right. That's right. We're very excited to see that. Dr. Carolyn Lam: Okay, so that's cool. Wow. A positive predictive value of 92%. So couple of things here with- Dr. Steven Lubitz: 98. Dr. Carolyn Lam: Sorry, 98%. That's right. Wow. Okay. Now with this AFib detection, it's always about duration. Right? And what do you call a positive alert? Could you maybe elaborate a bit about that here? Dr. Steven Lubitz: Sure. So I think this is an important point. A few points. One, the algorithm is designed. This particular algorithm requires at least 30 minutes of an irregular pulse to be detected, in order for a detection to occur. Which means that, this is unlikely to be detecting trivial amounts of atrial fibrillation. And indeed, that's what we observed. We observed that the median burden of atrial fibrillation was 7% among those who had AFib on the ECG patch monitor. We observed that the median longest episode of atrial fibrillation was seven hours. And just by way of comparison, in other studies in which ECG patch monitors have been distributed to people without this irregular pulse pre-screening, the burden is usually on the order of only a couple of percent, tops. So this, by nature, these types of algorithms, and this algorithm specifically, probably enriches for individuals who have a higher burden of atrial fibrillation. Meaning that, if these detections occur, then it's probably not detecting trivial amounts of atrial fibrillation. Dr. Carolyn Lam: Right. And a lot of it seems to send a very clear message that this study, and perhaps even the algorithm, is designed to be specific. Right? So that duration, as well as what you used as the outcome. How much price do you pay in terms of sensitivity? Do you know what I mean? Since we optimized for specificity, am I right to say that? Dr. Steven Lubitz: Sure, that's a great point. The algorithm is really optimized for specificity, as you mentioned. And although we didn't specifically calculate the sensitivity of the algorithm, in a secondary analysis, we examined the sensitivity of an IHRD during that ECG patch monitoring period, to detect any AFib that was documented on the ECG patch monitor, and it was about 67%. So we know that we probably don't detect some atrial fibrillation. Largely, that's a function of this technology at the moment. It's very difficult to assess the pulse rate during periods of activity in motion. So a lot of these algorithms, and this algorithm in particular, doesn't operate during periods of motion. The accelerometers and the devices can tell the algorithm that motion is occurring, and then the algorithm won't operate on that information at that time. So a lot of this has to do with limitations of the technology at the moment. Dr. Carolyn Lam: Ah. So the detection probably occurs best at rest or at night. Dr. Steven Lubitz: That's exactly right. And we encourage participants to wear their devices at nighttime during the study. Dr. Carolyn Lam: Oh, cool. And then of course, I suppose a question you'd anticipate, I mean, we know about the Apple Heart Study, we know about the  watch study, and how does this compare? How is this technology different, and the results? Dr. Steven Lubitz: Essentially, one of the most remarkable things about these studies is that, it appears that this pulse rhythm pre-screening really enriches substantially for people who have atrial fibrillation. So for example, in the Fitbit Heart Study, we observed that about 32% of people who had an irregular heart rhythm detection and then returned an ECG patch monitor, had AFib on it. And by comparison, in the Apple Heart Study, that number was about exactly the same, just over 30% or so. So when we further compare this pre-screening type approach to confirming atrial fibrillation, using an ECG patch monitor, with other approaches in which say, elderly individuals were mailed ECG patch monitors to screen for atrial fibrillation, we usually only see detection in the order of four to 5% of people. So this irregular pulse based pre-screening markedly enriches for atrial fibrillation. And we also know, this is only a one week ECG patch monitor, and if we monitor people longer than one week, we're likely to detect more atrial fibrillation, since this is often paroxysmal atrial fibrillation that we're detecting. So there are a lot of similarities, and I think the point is that, these types of consumer electronic devices are going to be great tools for identifying undiagnosed atrial fibrillation in the community. I think we have a lot of challenges ahead of us, in terms of figuring out how to integrate that information into our routine healthcare workflow, and counseling consumers and users of these types of technology on exactly what they should be doing when they do get an alert. And then also, counseling providers on how to act on these findings, what they mean and how accurate the technology is. Dr. Carolyn Lam: Yeah. And I appreciated a sentence in your manuscript that talks of, what are our society guidelines going to say? If you could look into a crystal ball now, Steve, based on what you found, what would you advise both patients and clinicians, if you don't mind? Dr. Steven Lubitz: Well, I think that, in short, if a clinician is alerted by a patient, that they received in a regular heart rhythm detection on their device, in short, I would say, don't blow it off. Take it seriously. Because the odds are, that it does represent an abnormality, and the odds are that that abnormality is atrial fibrillation. And given the potential adverse consequences of undiagnosed atrial fibrillation, there's a real opportunity to intervene, and prevent morbidity in the patient. And then, if you're a consumer who happens to have one of these devices, and you've turned on this feature, and hopefully you have, if you do have an alert, don't blow it off. Contact a provider. Because it may very well mean that you have an irregular heart rhythm that merits attention, and could be addressed to prevent downstream consequences and morbidity for you. Dr. Carolyn Lam: Nice. And keep your Fitbit on at night. Dr. Steven Lubitz: Yes. And if you do want to maximize the utility of these algorithms that use photoplethysmography, probably wearing them at nighttime will maximize the sensitivity, or utility of the devices and algorithms. Dr. Carolyn Lam: Aw, that's just great. What nice take home messages. Thank you so much, Steve, for publishing this really unique and important study in Circulation. So audience, you heard it right here on Circulation on the Run. From me, Greg, and Peder, please do tune in again next week. Speaker 4: 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.

Sempre cheque pessoalmente o ECG dos seus pacientes by Cardiopapers

In a follow-up preview, Jörn Schattenberg, Louise Campbell, Mazen Noureddin, Ian Rowe and patient advocate Jeff McIntyre join Roger Green to discuss key presentations and posters of interest at the 73rd Annual Meeting of the American Association for the Study of Liver Diseases (AASLD). On November 4th-8th in Washington DC, as many as 10,000 attendees will convene in an effort to advance and disseminate the science and practice of hepatology, and to promote liver health and quality patient care. Continuing from the previous conversation, Roger starts by questioning what the right long-term commercial model for remote patient wellness management companies might be. He recalls the early successes of Jenny Craig or Nutrisystem, achieved from selling food and Weight Watchers by branding other companies' white-or black-labled food products. Is there the potential for these companies to marry strong coaching to services offering high-quality, pre-cooked foods for an integrated offering? Jeff agrees and refers to his own experience working with groups on medically-tailored meals. He briefly notes the push he sees to get these meals paid for by Medicare or private insurers. Louise mentions that the kinds of programs described exist at Safari parks as part of a full-wellness program for the animals. From a different perspective, she notes the importance of patient volition in program success and that volitional assessments are not included in trial design. The app Tawazun Health recently launched adds a volitional element. Roger returns to a comment made in the first preview episode.  He had talked about finding improved primary care screening tools that might serve a dual purpose by also educating front-line providers how NAFLD often sits at the core of the galaxy of metabolic diseases. Two abstracts for posters are described that address this issue. The first of which is a meta-analysis of 121,975 patients. This study looked at significance of the odds and hazard ratios of the TyG index, computed based on triglyceride and glucose levels. It also investigated the ability over time for that ratio to predict disease. All results were highly significant and clinically meaningful. The second poster  is titled Performance of Artificial Intelligence Enabled Electrocardiogram and the Prediction of Fatty Liver Disease. This paper showed that an AI analysis of ECG results based on a convolutional neural network produced an area under the curve far superior to FIB-4. It also showed to be superior or equal to BMI and simple metabolic parameters. Roger's general point: using these metrics can improve on FIB-4 while, at the same time, focusing on the links between NAFLD and other metabolic diseases. As the conversation winds down, Mazen and Jörn agree with a few additional comments.

EBB 244: Evidence on Artificial Rupture of Membranes, Assisted Vaginal Delivery, and Internal Monitoring.   We are so excited to announce the upcoming release of a new Evidence Based Birth(R) Pocket Guide, all about Interventions! To give you a sneak peek to the Invention Pocket Guide,  we are diving into the research and evidence on artificial rupture of membranes, assisted vaginal delivery an internal monitoring.   Content note: Discussion of the benefits and risks of these interventions, including forceps and vacuum-assisted deliveries, which can be associated with birthing trauma for birthing people and babies, as well as the risk of mortality. Resources: Make sure you're on the Pocket Guide wait list by going here  Amniotomy References: Kawakita, T., Huang, C-C, and Landy, H. J. (2018). Risk Factors for Umbilical Cord Prolapse at the Time of Artificial Rupture of Membranes. AJP Rep 8(2): e89-e94. https://pubmed.ncbi.nlm.nih.gov/29755833/ Simpson, K. R. (2020). Cervical Ripening and Labor Induction and Augmentation, 5th Edition. AWHONN Practice Monograph 24(4): PS1-S41. https://bmcpregnancychildbirth.biomedcentral.com/articles/10.1186/s12884-019-2491-4 Smyth, R. M., Markham, C. & Dowswell, T. (2013). Amniotomy for shortening spontaneous labour. Cochrane Database Syst Rev 6:CD006167. https://pubmed.ncbi.nlm.nih.gov/23780653/ Alfirevic, Z., Keeney, E., Dowswell, T., et al. (2016). Methods to induce labour: a systematic review, network meta-analysis and cost-effectiveness analysis. BJOG 123(9):  1462-1470. https://pubmed.ncbi.nlm.nih.gov/27001034/  de Vaan, M. D. T., ten Eikelder, M. L. G., Jozwiak, M., et al. (2019). Mechanical methods for induction of labour. Cochrane Database of Systematic Reviews 10: CD001233. https://www.cochrane.org/CD001233/PREG_mechanical-methods-induction-labour Simpson, K. R. (2020). Cervical Ripening and Labor Induction and Augmentation, 5th Edition. AWHONN Practice Monograph, 24(4), PS1-S41. https://nwhjournal.org/article/S1751-4851(20)30079-9/abstract   Assisted Vaginal Delivery References: NHS article on forceps or vacuum delivery https://www.nhs.uk/pregnancy/labour-and-birth/what-happens/forceps-or-vacuum-delivery/ Bailey, P. E., van Roosmalen, J., Mola, G., et al. (2017). Assisted vaginal delivery in low and middle income countries: an overview. BJOG 124(9): 1335-1344. https://pubmed.ncbi.nlm.nih.gov/28139878/ CDC Wonder Database Feeley, C., Crossland, N., Betran, A. P., et al. (2021). Training and expertise in undertaking assisted vaginal delivery (AVD): a mixed methods systematic review of practitioners views and experiences. Reprod Health 18(1): 92. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8097768/ Crossland, N., Kingdon, C., Balaam, M. C. (2020). Women's, partners' and health care providers' views and experiences of assisted vaginal birth: a systematic mixed methods review. Reprod Health 17:83. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7268509/ Hook, C. D., Damos, J. R. (2008). Vacuum-Assisted Vaginal Delivery. Am Fam Physician 78(8): 953-960. https://www.aafp.org/afp/2008/1015/p953.html Tsakiridis, I., Giouleka, S., Mamopoulos, A., et al. (2020). Operative vaginal delivery: a review of four national guidelines. J Perinat Med 48(3): 189-198. https://pubmed.ncbi.nlm.nih.gov/31926101/ Verma, G. L., Spalding, J. J., Wilkinson, M. D., et al. (2021). Instruments for assisted vaginal birth. Cochrane Database Syst Rev. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD005455.pub3/full   Internal Monitoring References: Euliano, T. Y., Darmanjian, S., Nguyen, M. T., et al. (2017). Monitoring fetal heart rate during labor: A comparison of three methods. J Pregnancy 2017: 8529816. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5368359/ Neilson, J. P. (2015). Fetal electrocardiogram (ECG) for fetal monitoring during labor. Cochrane Database Syst Rev 12: CD000116. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD000116.pub5/full Harper, L. M., Shanks, A. L., Tuuli, M. G., et al. (2013). The risks and benefits of internal monitors in laboring patients. Am J Obstet Gynecol 209(1): 38.e1-38.e6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3760973/ Bakker, J. J. H., Verhoeven, C. J. M., Janssen, P. F., et al. (2010). Outcomes after internal versus external tocodynamometry for monitoring labor. N Engl J Med 362(4): 306-13. https://www.nejm.org/doi/10.1056/NEJMoa0902748?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200www.ncbi.nlm.nih.gov Frolova, A. I., Stout, M. J., Carter, E. B., et al. (2021). Internal fetal and uterine monitoring in obese patients and maternal obstetrical outcomes. Am J Obstet Gynecol MFM 3(1): 100282. https://pubmed.ncbi.nlm.nih.gov/33451595/ Bakker, J. J. H., Janssen, P. F., van Halem, K. (2013). Internal versus external tocodynamometry during induced or augmented labor. Cochrane Database Syst Rev 8: CD006947. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD006947.pub3/full van Halem, K., Bakker, J. J. H., VerHoeven, C. J., et al. (2011). Does use of an intrauterine catheter during labor increase risk of infection? J Maternal Fetal Neonatal Med 25(4): 415-418. https://www.tandfonline.com/doi/abs/10.3109/14767058.2011.582905 For more information and news about Evidence Based Birth®, visit www.ebbirth.com. Find us on:  TikTok Instagram  Pinterest   Ready to get involved?  Check out our Professional membership (including scholarship options) here  Find an EBB Instructor here  Click here to learn more about the Evidence Based Birth® Childbirth Class.

Although magnesium can be used in the treatment of other medical conditions such as eclampsia, asthma, & digitalis toxicity; for ACLS, magnesium is primarily used to treat Torsades de Pointes. Identification of torsades on the ECG. Administration of a magnesium infusion for stable patients vs slow IV push for patients in cardiac arrest. Procainamide use for stable patients with a monomorphic wide-complex tachycardia. Procainamide dosing and when to stop the infusion. Tip for determining whether magnesium or Procainamide should be used when treating stable patients with V-Tach. For more information on antiarrhythmics, check out the Pod Resource Page at passacls.com. The podcast episodes from Ninja Nerd and Coffee Break HEMS are great. Connect with me: Website:  https://passacls.com (https://passacls.com) https://twitter.com/PassACLS (@PassACLS) on Twitter https://www.linkedin.com/company/pass-acls-podcast/ (@Pass-ACLS-Podcast) on LinkedIn Good luck with your ACLS class!

Artificial Intelligence in Automated ECG Analysis Guest: Peter Macfarlane, Ph.D., D.Sc. Hosts: Anthony H. Kashou, M.D. (@anthonykashoumd) Joining us today to discuss artificial intelligence in automated ECG analysis is Peter Macfarlane, Ph.D., D.Sc. He is a University of Glasgow emeritus professor and honorary senior research fellow who in 2014 was awarded Commander of the British Empire for his services to health care. Tune in to hear what the role of computer interpretation looks like today and where do artificial intelligence-based models fit in with the future of the field. Specific topics discussed: Can you share a little bit about your background and how you got into computerized electrocardiography? How do you see the role of computerized ECG in clinical practice today, and has that evolved over the years? What are your thoughts on this growing field applying artificial intelligence to the electrocardiogram? Where do you see the potential benefits and limitations with this technology? And will this technology eventually become commonplace and adopted into medical practice? Connect with Mayo Clinic's Cardiovascular Continuing Medical Education online at https://cveducation.mayo.edu or on Twitter @MayoClinicCV and @MayoCVservices. Facebook: MayoCVservices LinkedIn: Mayo Clinic Cardiovascular Services NEW Cardiovascular Education App: The Mayo Clinic Cardiovascular CME App is an innovative educational platform that features cardiology-focused continuing medical education wherever and whenever you need it. Use this app to access other free content and browse upcoming courses. Download it for free in Apple or Google stores today! No CME credit offered for this episode. Podcast episode transcript found here.

#997-Esse é o principal motivo dos médicos não dominarem ECG by Cardiopapers

In atrial fibrillation (A-Fib) and atrial flutter (A-Flutter) the electrical impulse for cardiac contraction is in the atria but isn't the normal pacemaker of the heart, the SA node. The ECG characteristics of A-Fib and A-Flutter. Recognition and treatment of unstable patients in A-Fib/Flutter with rapid ventricular response (RVR). Team safety when cardioverting an unstable patient in A-FIB. Adenosine's role for stable SVT patients with atrial rhythms. Treatment of stable patients in A-Fib/Flutter with RVR. **American Cancer Society (ACS) Fundraiser This is the fourth year that I'm participating in Real Men Wear Pink to increase breast cancer awareness and raise money for the American Cancer Society's life-saving mission. I hope you'll consider contributing. Every donation makes a difference in the fight against breast cancer! http://main.acsevents.org/goto/paultaylor (Paul Taylor's ACS Fundraiser) THANK YOU! Connect with me: Website:  https://passacls.com (https://passacls.com) https://twitter.com/PassACLS (@PassACLS) on Twitter https://www.linkedin.com/company/pass-acls-podcast/ (@Pass-ACLS-Podcast) on LinkedIn Good luck with your ACLS class!

The American College of Cardiology released a new consensus statement endorsing several signs on the electrocardiogram (ECG) as "STEMI Equivalents." In this podcast, we review these signs. Show notes / graphics / references: FOAMcast.org Thanks for listening! Lauren Westafer

Following the "Made by Google" launch event last week, we talk through how the Pixel Watch, Pixel 7, Pixel 7 Pro, and Pixel Tablet compare to Apple's devices on the latest episode of The MacRumors Show podcast. The Pixel Watch features a striking round design with a 41mm stainless steel casing, and offers an always-on display, 24-hour battery life, and Fitbit sleep tracking, for a price of $349. With Apple Watch features like blood oxygen monitoring, ECG, Fall Detection, Emergency SOS, 32GB of memory, and more, we talk through how the Pixel Watch compares to Apple's long-reigning smart watch. The Pixel 7 and Pixel 7 Pro offer many features that will be familiar to iPhone users such as 2x crop mode to simulate a telephoto lens, Cinematic Blur for video, Active Stabilization mode, and Face Unlock, but adds faster Night Sight, Photo Unblur, 8GB of memory, and the custom-silicon Tensor G2 chip. The devices look to directly compete with Apple's latest iPhone 14 and iPhone 14 Pro models. Google also offered an early look at the Pixel Tablet that is set to launch next year. The tablet comes alongside a speaker dock that charges the device and turns it into a home-focused device to glance at information, display photos, and control smart home accessories. You can follow us on Twitter @danbarbera and @HartleyCharlton. Be sure to visit macrumors.com for all of the latest Apple news and rumors.See omnystudio.com/listener for privacy information.

Heart failure — sometimes known as congestive heart failure — occurs when the heart muscle doesn't pump blood as well as it should. When this happens, blood often backs up and fluid can build up in the lungs, causing shortness of breath."The most recognized, the most common symptom of heart failure is breathlessness," says Dr. Gosia Wamil, a cardiologist at Mayo Clinic Healthcare in London. "And the type of breathlessness that patients would describe most often is the inability to lie flat, waking up in the middle of the night or gasping for air."Heart failure is often thought to be a disease of advanced age, but it can actually develop at any time in life. In many cases, heart failure can be prevented or treated if people are aware of the risk factors and warning signs. Coronary artery disease is the main cause of heart failure. Stiffening of the heart muscle is mostly a result of poorly controlled hypertensionor diabetes. Proper treatment can improve the signs and symptoms of heart failure and may help some people live longer. Lifestyle changes — such as losing weight, exercising, reducing salt (sodium) in your diet and managing stress — can improve your quality of life. "All the risks of developing heart attack, if we reduce those risks, we improve their lifestyle," explains Dr. Wamil. "If we reduce the risk of diabetes, hypertension, stop smoking, this will reduce the risk of heart attacks, but at the same time, will reduce the risk of heart failure."Dr. Wamil's research efforts include studies aimed at understanding the connection between diabetes and heart disease and using novel medical imaging techniques to identify heart failure early on. Other research underway at Mayo Clinic includes the use of artificial intelligence and machine learning tools to detect heart failure early."An area of research interest at Mayo Clinic is the use of large databases, such as randomized controlled trials, electronic health care records, and applying not only statistical methods but also AI, machine learning models and algorithms to try to identify how we can detect early signs of heart failure risks," explains Dr. Wamil. On the Mayo Clinic Q&A podcast, Dr. Wamil, discusses warning signs of heart failure and advances in early detection of heart disease.Related posts: "Mayo Clinic London Healthcare expert shares heart failure signs, symptoms people may not be aware of." "Mayo Clinic Q&A podcast: Understanding the connection between diabetes and heart disease." "AI-guided screening uses ECG data to detect a hidden risk factor for stroke." "Mayo researchers use AI to detect weak heart pump via patients' Apple Watch ECGs."

Mikah Sargent and Rosemary Orchard are wearing their new Apple Watches (Series 8 & Ultra!) and are ready to take you through very helpful HealthKit apps for better sleep, temperature, teeth and more! Withings Health Mate Withings Sleep Analyzer Withings Thermo Smart Temporal Thermometer Beautyrest Sleeptracker Monitor KardiaMobile 6L by Alivecor Oral-B 7000 SmartSeries Apple Watch Blood Oxygen Measurements Apple Watch ECG News iOS 16.0.2 released to fix iPhone 14 Pro camera shake issue Mark Gurman thinks October Apple products could be announced via press releases instead of an actual event Shortcuts Corner Chris wants to feed his fish at lunchtime every "other" day, which prompts Rosemary to do some mathematical functions! Feedback & Questions Doug's iPhone 14 Pro Max is rebooting when charging, and he's not alone! Also featuring Linux & Chewie! Michael wants to use the Family Sharing feature but NOT share payment cards. How can he disable that? App Caps Rosemary's App Cap: Sticker Drop Mikah's pick: AirPods Pro 2nd Gen Hosts: Mikah Sargent and Rosemary Orchard Download or subscribe to this show at https://twit.tv/shows/ios-today. Get episodes ad-free with Club TWiT at https://twit.tv/clubtwit You can contribute to iOS Today by leaving us a voicemail at 757-504-iPad (757-504-4723) or sending an email to iOSToday@TWiT.tv. Sponsor: itpro.tv/twit promo code TWIT30