Podcasts about Digoxin

Lancet 1999;353:2001-07Background: Beta-blockers directly reduce cardiac contractility and myocardial oxygen demand. For decades, they were avoided in patients with acute and chronic heart failure over concerns they would facilitate decompensation of the condition. The therapeutic cornerstones of treatment, prior to the modern era of clinical trials, focused on managing symptoms and quality of life with diuretics and inotropic agents like digoxin; however, new paradigms were arising that focused on addressing neurohormonal mechanisms of chronic disease that were over-activated in the failing heart. The first major success came with inhibition of the renin angiotensin aldosterone system with angiotensin converting enzyme inhibitors whose effect on mortality for patients with mild and severe forms of chronic heart failure were demonstrated in the V-HEFT II, CONSENSUS, and SOLVD trials. Additional benefits were demonstrated with the mineralocorticoid receptor antagonist spironolactone in the RALES trial. These drug classes primarily work by reducing afterload and volume retention. Appreciating why they work for improving cardiac performance and managing symptoms in heart failure patients is straightforward when we consider the major factors that effect cardiac stroke volume - preload, afterload and contractility; however, it is also noteworthy the effects these agents have on sudden death. How beta-blockade benefits the failing heart is less obvious (outside prevention of sudden death). Mechanistic studies in patients with chronic heart failure have consistently shown that when beta blockers are used for more than 1 month, left ventricular function improves. Beta blocker therapy appears to restore the density of beta-adrenergic receptors after they have been downregulated by the chronic overactivity of the sympathetic nervous system. The first major placebo-controlled RCT to demonstrate a mortality benefit used the non-selective beta blocker carvedilol. The trial was small and not originally designed to test mortality and was stopped early without clearly predefined stopping rules. Furthermore, 8% of total patients selected for participation in the trial were excluded prior to randomization after a 2 week, open-label run-in phase with the study drug, which saw 2% of all patients experience worsening heart failure or death representing 24 patients (the difference in total deaths between groups was 9 when the trial was stopped). The Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF) was the first large scale trial designed to test the hypothesis that beta-blockade with metoprolol controlled/extended release (CR/XL) added to optimum medical therapy reduces mortality in patients with chronic systolic heart failure.Patients: Patients were recruited from 313 sites in 13 European countries and the United States. Eligible patients were men and women between the age of 40 to 80 years with symptomatic heart failure (NYHA class II-IV) for >/= 3 months before randomization. They had to be on a diuretic and ACE inhibitor for at least 2 weeks. Other drugs, including digoxin, could also be used. Patients also had to have an EF of /=68 beats per minute.Patients were excluded if: they had an MI or unstable angina within 28 days; had an indication or contraindication for treatment with beta-blocker; beta blockade within 6 weeks; heart failure due to systemic disease (i.e., amyloidosis) or alcohol abuse; scheduled or performed cardiac transplant; an ICD; procedures such as CABG or PCI planned or performed in the past 4 months; 2nd or 3rd degree AV block unless a pacemaker was present; unstable or decompensated heart failure defined by pulmonary edema or hypoperfusion or supine systolic BP 25% deviation of the number of observed versus expected consumed placebo tablets during the run-in period.Baseline characteristics: The mean age of patients was 64 years and approximately 78% were male. Slightly more than 30% of patients were above the age of 70. The average EF was 28%. The average SBP was 130 mmHg and heart rate was 82 bpm. Most patients had mild to moderate heart failure, with 41% in NYHA Class II, 56% in Class III, and only 3% in Class IV. Ischemic cardiomyopathy accounted for 65% of cases and nonischemic causes accounted for 35%. Most patients were on an ACE inhibitor or ARB (95%) and diuretic (90%). Digoxin was used in 63%. Trial procedures: Prior to randomization, the study was preceded by a single-blind, 2-week placebo run-in period. Patients meeting eligibility were then randomized to placebo or metoprolol CR/XL. The starting dose of placebo or metoprolol CR/XL was 12.5 mg daily for patients in NYHA class III or IV and 25 mg daily for patients in NYHA class II. The dose was doubled every 2 weeks until the target dose of 200 mg daily was reached. Patients were followed every 3 months.Endpoints: The primary outcome was all-cause mortality. It was estimated that 3,200 patients would need to be followed for 2.4 years to detect a 30% relative reduction in mortality based on annual mortality rate of 9.4% in the placebo group. This would achieve at least 80% power with a 2-sided alpha of 0.04. Patients were recruited faster then planned and so the final sample size of 3,991 patients increased the power of the study.The study was monitored by an independent safety committee and predefined stopping rules for efficacy were based on all-cause mortality, done when 25%, 50%, and 75% of expected deaths had occurred. Results: The trial was stopped early after the 2nd preplanned interim analysis when 50% of expected deaths had occurred. The mean duration of follow-up at the time of stopping was 1 year. The mean daily dose of metoprolol CR/XL was 159 mg once daily, with 87% receiving 100 mg or more and 64% receiving the target dose of 200 mg daily. In the placebo group, the corresponding values were 179 mg daily, 91% and 82%. The study drug was discontinued permanently in 14% of patients in the metoprolol group and 15% in the placebo group. Six months after randomization, heart rate decreased by 14 bpm in the metoprolol group compared to only 3 bpm in the placebo group. Systolic blood pressure decreased less in the metoprolol group (-2.1 vs 3.5 mmHg).Compared to placebo, metoprolol significantly reduced all-cause mortality (7.3% vs 10.8%; RR 0.66; 95% CI 0.53—0.81). Cardiovascular mortality accounted for 91% of all deaths; with sudden death accounting for 58% and death from worsening heart failure accounting for 24% of all deaths. All 3 of these causes of death were significantly reduced by metoprolol. The relative and absolute effects on death were greatest for patients with NYHA class III heart failure.Conclusions: In this trial of stable patients with mild to moderate chronic systolic heart failure, who were optimized on an ACEi or ARB and diuretic, metoprolol CR/XL significantly reduced all-cause mortality. Approximately 30 patients would need to be treated with metoprolol compared to placebo for 1 year to prevent 1 death. This trial represents a significant win for beta blockade in patients with chronic systolic heart failure. While the NNT in this trial is slightly higher than in SOLVD, it is important to appreciate that follow-up time in SOLVD was more than 3x longer. Limitations to external validity in this trial include the run-in period and stringent inclusion and exclusion criteria. Our enthusiasm is also tempered by early stopping, which has been found to be associated with false positive or exaggerated results but this concern is mitigated to some extent in this trial because the rules for early stopping were clearly defined in the protocol.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

In this episode, we review the high-yield topic Digoxin⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠from the Cardiovascular section at ⁠⁠⁠⁠⁠⁠Medbullets.com⁠⁠⁠⁠⁠⁠Follow⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Medbullets⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ on social media:Facebook: www.facebook.com/medbulletsInstagram: www.instagram.com/medbulletsofficialTwitter: www.twitter.com/medbulletsLinkedin: https://www.linkedin.com/company/medbullets

Digoxin is an essential medication every nurse needs to know about in a clinical setting and every nursing student needs to understand for the Next Generation NCLEX. This is why, in this week's episode of NCLEX Ready, I will be sharing with you everything you need to know about this important medication.Together, you and I will be learning about Digoxin's mechanism of action, its therapeutic use, its administration, the side effects it can cause, its toxicity, nursing monitoring, patient education, interactions with other substances, and more.Plus, we'll also be doing a quick Q&A together at the end of the episode, so make sure to listen till the last minute if you want to check your skills.Are you ready for the challenge?Let's dive in!Key Takeaways:  Introduction (00:00)What is Digoxin? (00:58)Let's go through some true or false statements (04:44)Time for a quick Q&A! (06:18)Additional Resources:

One of the oldest medications in our pharmacopeia is digoxin. It may be used for atrial fibrillation and heart failure, although not as a first-line agent. Despite this, digoxin use is on the rise. Join host, Geoff Wall, as he evaluates why more prescribers are using digoxin.The GameChangerNo new randomized controlled trials have been published to justify the increased use of digoxin. However, when used, providers should routinely monitor digoxin levels.  HostGeoff Wall, PharmD, BCPS, FCCP, BCGPProfessor of Pharmacy Practice, Drake UniversityInternal Medicine/Critical Care, UnityPoint Health ReferenceGazzaniga G, Menichelli D, Scaglione F, et al. Effect of digoxin on all-cause and cardiovascular mortality in patients with atrial fibrillation with and without heart failure: an umbrella review of systematic reviews and 12 meta-analyses. Eur J Clin Pharmacol. 2023 Apr;79(4):473-483. doi: 10.1007/s00228-023-03470-y. Epub 2023 Mar 6. PMID: 36872367; PMCID: PMC10039090.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10039090/ Pharmacist Members, REDEEM YOUR CPE HERE! Not a member? Get a Pharmacist Membership & earn CE for GameChangers Podcast episodes! (30 mins/episode)CPE Information Learning ObjectivesUpon successful completion of this knowledge-based activity, participants should be able to:1. Apply information on the potential uses and harms of digoxin 2. Apply a strategy for monitoring digoxin in heart failure patients 0.05 CEU/0.5 HrUAN: 0107-0000-23-400-H01-PInitial release date: 12/18/2023Expiration date: 12/18/2024Additional CPE details can be found here.Follow CEimpact on Social Media:LinkedInInstagram

Heute dreht sich alles um das Thema Magnesium: Dein Schlüssel zu Wohlbefinden und LeistungsfähigkeitHast du vielleicht manchmal Wadenkämpfe oder Krämpfe im Fuß? zuckt vielleicht manchmal dein Auge oder nimmst DU Magnesium kurz vor dem schlafen, da du sonst unter Schlafproblemen leidest?Oder hast du vielleicht gerade viel Stress, treibst viel Sport oder schwitzt auch als Frau in den Wechseljahren gerade mehr, wegen Hitzewallungen?Oder interessierst du dich vielleicht einfach für das Thema Magnesium, da dein Arzt dir empfohlen hat ein Magnesium Präperat einzunehmen und du weisst nun nicht, welches Du dir kaufen sollst?In der heutigen Episode klären wir unter anderem die Fragen:Für was ist Magnesium gut im Körper?Wie merkt man dass man Magnesiummangel hat?Sollte man jeden Tag Magnesium zu sich nehmen?Wo ist am meisten Magnesium drin? Brauchen wir eine Magnesium Präparat?Warum ist Magnesium Oxid nicht zu empfehlenWelches Magnesium solltest du zu Dir nehmen?Fakt ist: super viele Menschen leiden unter einem Magnesiummangel und wissen es gar nicht und ebenfalls super viele Menschen nehmen ausschliesslich ein Magnesium Oxid ein, was unser Körper aber gar nicht wirklich verwerten kann. Wenn du ein Magnesium aus dem Drogeriemarkt hast schau mal auf die Inhaltsstoffe!Magnesium spielt eine essentielle Rolle, von Muskelkontraktionen bis zu einem gesunden Herz-Kreislauf-System; auch unser Nervensystem ist auf Magnesium angewiesen. Es gilt aber auch einiges zu beachten, gerade wenn Erkrankungen eine Rolle spielen wie unter anderem Diabetes, Bluthochdruck und Nierenerkrankungen; oder falls bestimmte Medikamente eingenommen werden, wie unter anderem Cortison, Antibiotika, Protonenpumpenhemmer, Digoxin, Diuretika zur Entwässerung bei Bluthochdruck, Abführmittel  und Magenschutztabletten. Entdecke die besten Magnesium Quellen, erfahre, wie ein Magnesiummangel vermieden werden kann, und welches Magnesium wirklich helfen wird, das du endlich wieder schlafen kannst; denn nicht jedes Magnesium kann unser Körper gut aufnehmen und verwerten. Viel Spass beim Hören oder Nachlesen dieser wichtigen Podcast Episode,deine Mimi Lawrence*****Sponsor: No Coffee: Mimi15 Braineffect: MimiInstagram @mimilawrencefitnessYoutube: MIMI LAWRENCE FitnessWebseite: mimilawrence.comTik Tok @mimilawrencefitness

Show notes at pharmacyjoe.com/episode862. In this episode, I’ll discuss why hypokalemia can result from digoxin immune fab fragment administration. The post 862: Why hypokalemia can result from digoxin immune fab fragment administration appeared first on Pharmacy Joe.

Show notes at pharmacyjoe.com/episode862. In this episode, I’ll discuss why hypokalemia can result from digoxin immune fab fragment administration. The post 862: Why hypokalemia can result from digoxin immune fab fragment administration appeared first on Pharmacy Joe.

Welcome back to Analyze Scripts, where a psychiatrist and a therapist analyze what Hollywood gets right and wrong about mental health. Today, we are analyzing the 2007 film "Awake." This movie stars Hayden Christensen, Jessica Alba and Terrence Howard. There is a nefarious plot to kill Clay who finds out during surgery. According to our guest, Dr. Gonzalez from the Yale Anesthesia Department, Clay experiences intraoperative awareness AKA "awareness" during surgery. The movie is filled with plot holes and some pretty inaccurate medical information. We learn so much from Dr. Gonzalez about anesthesia and patient pain. PTSD, medical factiods and financial stressors are topics in this episode. We hope you enjoy! Dr. Gonzalez Podcast Episode on Interoperative Awareness Website TikTok Instagram Dr. Katrina Furey, MD: Hi, I'm Dr. Katrina Fieri, a psychiatrist. And I'm Portia Pendleton, a licensed clinical social worker. And this is Analyze Scripts, a podcast where two shrinks analyze the depiction of mental health in movies and TV shows. Our hope is that you learn some legit info about mental health while feeling. Portia Pendleton, LCSW: Like you're chatting with your girlfriends. Dr. Katrina Furey, MD: There is so much misinformation out there, and it drives us nuts. And if someday we pay off our. Portia Pendleton, LCSW: Student loans or land a sponsorship, like. Dr. Katrina Furey, MD: With a lay flat airline or a major beauty brand, even better. So sit back, relax, grab some popcorn and your DSM Five, and enjoy. Welcome back for another very exciting episode of Analyze Scripts. As part of our Halloween month today, we are covering the 2007 thriller mystery movie called Awake with our wonderful guest, Dr. Antonio Gonzalez. And I cannot think of anything scarier than being awake during a surgery, so this is perfect for our Halloween month. But just as a quick bio, dr. Gonzalez is an associate professor of anesthesiology and the director of the Obstetrics anesthesia Fellowship at Yale New Haven Hospital. He completed his residency program at Rutgers in New Jersey and decided to pursue a fellowship in obstetric anesthesia at Columbia University in New York. And I will actually be joining one of his podcasts in the near future to talk about eternal mental health and anesthesia, which I'm really excited about. But thank you so much, Dr. Gonzalez, for joining us. Dr. Antonio Gonzalez, MD: Thank you so much for the invitation. I'm really happy to be here with you today. Dr. Katrina Furey, MD: So, Portia, where do we even get started with this movie? Have you seen it before? Portia Pendleton, LCSW: I have not seen the movie ever. I think that something like this would probably have been a little scary to watch. Yeah, I think a lot of people who are not in medicine and maybe people who are in medicine, I think it's a common fear to wake up during surgery. I think a lot of people going in get really calmed down once talking to the anesthesiologist or telling them that this is their process or this is. Dr. Katrina Furey, MD: How it's going to be. Portia Pendleton, LCSW: And all of the machines and monitors that they now have, you were saying a little bit before we got started today. So I think this is just like a pretty common fear that people have going into surgery. Dr. Katrina Furey, MD: What do you think, Dr. Gonzalez? Dr. Antonio Gonzalez, MD: Yes, I think that definitely introvertive awareness. It's definitely a fear of our patients. And unfortunately, this movie actually may have hyped that fear. But fortunately, the reality is that introvertive awareness is relatively rare, particularly these days. We have way better medications, way better monitors that help us to prevent intraperative awareness. The incidence has been documented to be somewhere around 0.1% to 0.2% in the United States. Dr. Katrina Furey, MD: So what is that, like, one to two out of 1000 cases? Something like that? Dr. Antonio Gonzalez, MD: That is correct, yeah. Because there are so many surgeries in the united States, that's about 20,000 to 40,000 cases a year, which still a lot. Right. The consequences of interoperative awareness can go from just having fear of future surgeries, even withholding surgeries for some of their relatives, particularly their kids, because they are so scared of what happened to them, they may actually be very fearful of letting their relatives go through surgery. Yeah. So that is one of the consequences. But, again, it's relatively rare these days. Dr. Katrina Furey, MD: Okay. Dr. Gonzalez. Portia Pendleton, LCSW: Is there anything in common. Dr. Katrina Furey, MD: That the people who this happens to. Portia Pendleton, LCSW: With each other, or is it just kind of like yeah. Dr. Katrina Furey, MD: Is there, like, a way to predict it that it could? Dr. Antonio Gonzalez, MD: So we don't have particularly great ways of predicting who will have operative awareness. We do know that there is a certain patient population or certain surgeries. So there are surgeries like trauma, cardiac surgery, and Obstetric. Anesthesia. Obstetric cases seem to be and when I mean Obstetric cases, Caesarean deliveries, particularly. These are cases that are very well known to have an increased risk of intraperative awareness. The reason behind it is because trauma patient and cardiac patients have a very delicate hemodynamics, meaning their blood pressure, it's low, tends to be on the lower side. They have a high risk of coronary vascular disease. So having their blood pressure too high or too low, it's at extreme risk. So in order to maintain that balance between the anesthesia that it's provided and the hemodynamics, those patients tend to be at a higher risk. And that implies for both trauma patients and cardiac patients. Now, the Obstetric patient population is at increased risk because of the risk that the anesthesiologist may perceive from the drugs transferring to the baby. So all the medications we give to mom will go to baby, and that increase in medications has been thought to be pretty dangerous to the baby. So anesthesiologists at some point, we're very scared of giving extra medications to mom nowadays. Again, I think that because our monitoring and the drugs that we have available and the awareness that introvertive awareness in this particular patient population, it's higher, we have improved the techniques that we have for providing general anesthesia. Now, that being said, we do a lot of our anesthesia under regional, and having pain during a surgery, even with epidural or a spinal, can be equally as scary, if not even more scary than having introvertive awareness while asleep. Dr. Katrina Furey, MD: I was wondering that. So, before we get into this a little further, I just want to give a quick recap of the plot of this movie. So, in the movie Awake, we see Hayden Christensen playing the main character, Clay Bearsford Jr. Who is, like a fancy pants financial person, super uber rich. He does something with stocks, probably, that I don't understand. And you see this interesting relationship with his mom early on, who's played her name's Lilith, and she's played by Lena Olin. And then we see Jessica Alba. This is one of her big roles, playing Sam Lockwood, who's his fiance. They get married very quickly because he is waiting for a cardiac transplant due to history of cardiomyopathy, which is something that happens. That seemed pretty accurate. And then we see Terrence Howard playing his friend and surgeon, Dr. Jack Harper. And spoiler alert, turns out all of the medical professionals on the team, including his fiance, were in on this plot to murder him during the transplant in order to inherit all his money and pay off some malpractice debt. Luckily, I think it was the anesthesiologist. The original one backed out. So this other guy was there, and somehow he figured out the plot, and he alerted authorities. And eventually, I think Dr. Harper injected the heart with adriamycin. I believe the Clay did, I guess, technically die on the table. When they delivered that news to his family, the mother committed suicide. I can't remember what she overdosed on. I'm assuming maybe Digoxin, which was in his bag. And then they wheeled the mom in and gave him her heart. And so he survived, and all the people got arrested. The end. That's basically the plot. Really quick. So getting back to what you were saying, Dr. Gonzalez, about the intraoperative awareness. So when you were saying that with these certain cases, trauma, cardiac, and OB with regional anesthesia, I'm thinking like an epidural, like for a C section or something like that. Like, if they give the epidural and it fails either in a C section or a regular delivery, vaginal delivery, would that be considered interoperative awareness? Dr. Antonio Gonzalez, MD: Well, if the patient is experiencing pain, yes, that can be as traumatic as experiencing intraperative awareness, because the patient mentally is completely there, but the patient is completely feeling the experience of the pain. And the definition of pain, actually, it's not only physical, but there is an emotional component to pain. Right. So what you describe as pain, you can only be the person that knows what pain is for you. So what we've learned through the years is that we are not the best judge of what pain is. The patient is the best judge of what pain is because pain is what the patient tells you pain is. Portia Pendleton, LCSW: I'm so glad you said that. Dr. Katrina Furey, MD: I think that's really important and to keep in mind the emotional side of it. Portia Pendleton, LCSW: I like that also, just as I don't know a similarity right. In mental health, like pain mental pain, emotional pain is, like, what the patient is describing versus my definition in the DSM. But I really like that. Or just validating their experience. Well, this is what they experienced. Maybe someone else's was different. Dr. Katrina Furey, MD: Right. Portia Pendleton, LCSW: I really like that. Dr. Antonio Gonzalez, MD: Yeah. I think that it's a great opportunity, because, as you mentioned, sometimes if, as physicians, we try to give an explanation to pain, right. We may actually minimize the patients. And at the end of the day, what ends up happening is that the patients feels that their feelings, they're being gaslighted. So the patient is telling you, this is what I feel, and you say, well, it's not that big of a deal. Right. But it is to the patient, it is. So pain is, again, what the patient tells you pain is. Dr. Katrina Furey, MD: No, I think that's great. And in my line of work, in private practice, I do end up seeing well, I see primarily women around pregnancy and postpartum. So I've heard many cases where the epidural failed, or it only took on half the side, or someone had a history of back surgery, so they met with the anesthesiologist ahead of time to talk about pain management options. And it is a super important aspect of prenatal care, especially delivery, and I'm sure that extends to other surgeries as well. So, Dr. Gonzalez, what are your thoughts about the way anesthesia was depicted in this movie? What they get right, what they get wrong? Dr. Antonio Gonzalez, MD: Well, there are so many things that they well, the one thing that they got right was to select the patient that was having a cardiac surgery. As we mentioned, patients with cardiac surgery have an increased risk of having introvertive awareness. So they got that one part right. Then the other thing is that it seems like they have a substitute anesthesiologist that's coming from another institution. It doesn't quite happen that way. You need to have privileges at that place. It's a little credentialed. Yeah. Unless he's a traveler. Sometimes we have anesthesiologists that are considered what is the term? Locums. That's correct, yes. So locums might have been a locums that they call in to substitute, but it's actually quite hard to find locums for very specific cardiac surgery. So I think that the other thing that I think was very wrongfully depicted was how easy he may look. The induction. The induction was basically he took this three CC syringe or four CC syringe. He gave it to the patient. He said, count back to ten. Cardiac inductions are very complicated. It requires a balance of many medications. Again, because there is this hemodynamic balance that you want to maintain. You don't want the patient's blood pressure to go too high. Do you want the patient's blood pressure to go too low? So that also it seems like it was completely off. And there is a point where the surgeons are discussing, like, well, we won't need you for a little bit, so go get a drink. We never leave the operating room. Dr. Katrina Furey, MD: Right. Dr. Antonio Gonzalez, MD: I know there is always somebody from anesthesia in the room that be like the anesthesiologist or anesthetist, but we just don't leave the patient in the or. Just because the surgeon tells us that they're not going to need us for a bit. So that was totally wrong. Dr. Katrina Furey, MD: Right. In my experience in medical school, rotating through that's exactly right. Even these long cases like cardiothoracic surgery, the anesthesiologist, maybe a resident, maybe the nurse, anesthetist. These words are hard to say. Someone's always there watching the monitor. They might be doing something else at the same time. I remember one time there was a resident practicing his golf swing, and I was like, this seems pretty unprofessional. But they're always watching the monitors. And I would imagine like this, especially watching the blood pressure, the heart rate, things like that. And they're always checking. They kept checking, at least in the cases I would be in, they would do things to check. The patient was still under enough. Not too far under. Not coming out of it either. Dr. Antonio Gonzalez, MD: Yes. And as you mentioned, sometimes the anesthesiologist, a lot of what we do, we may not be actually looking at the monitors, but because we're actually trained for so it's a three year program. By the sound of the machines, you actually know what is wrong. Like the pulse oximeter has a very typical sound. When the saturation drops, the alarms on the monitors are set off to go at X levels. Right. So you can set up your alarms. So even if we're like, let's say, fixing our medication drips or we're working on something that it's not necessarily looking at the monitor, just hearing the monitor, we are aware of what actually the vital signs are, and of course, the alarms are ever present. So we're always very aware of these alarms and everything that surrounds. We use pretty much all our senses when caring for patients. Dr. Katrina Furey, MD: That makes a lot of sense. Portia Pendleton, LCSW: It's interesting. I think there was an episode on Grey's Anatomy years ago about the anesthesiologist at the hospital was like, has a substance use disorder. And he was, like, falling asleep next to the patient. And of course, it's a drama, so the young resident had to do something and didn't want to get in trouble by the attending or something. But I feel like I've seen not a lot of medical dramas. I mean, that's not like my jam. But the couple that I have there seems to always be the anesthesiologist is like sometimes a villain. I don't know. Dr. Katrina Furey, MD: Is that a stereotype? Yeah. Is that a stereotype? Portia Pendleton, LCSW: Or like, maybe just in TV, the. Dr. Katrina Furey, MD: Psychopath is often the villain too, so we can empathize. Portia Pendleton, LCSW: Yeah, it seems like it's a lot of risk with that job. Dr. Antonio Gonzalez, MD: I think that psychiatrists, dentists, and anesthesiologist seems to be the highest the physicians with the highest incidence of substance use. Dr. Katrina Furey, MD: Disorder, I believe that's right, yeah. Dr. Antonio Gonzalez, MD: And suicide as well, I think. Yeah. Maybe media has picked up on that. Maybe. Dr. Katrina Furey, MD: Interesting. I think in my training, I was taught that in those specialties, you have the easiest access to controlled substances in terms of the risk of substance use disorders. So that's one reason the rates are higher. And then suicide. I didn't know anesthesiologists also had a high rate of suicide. Dr. Antonio Gonzalez, MD: Yeah. I haven't reviewed the statistics on this, but I think that it used to be that way. I think actually, dentists might be number one. For some strange reason, anesthesiologists are high up in there. Dr. Katrina Furey, MD: One big issue I had with this movie was the plot, because I feel like they went to great lengths to pay off a prior malpractice lawsuit. And I feel like they'd all have malpractice insurance, right? Even if I know there's certain specialties. Like, I think OB, for example, has a really high rate of malpractice insurance. Wouldn't they have malpractice to cover any claims? Dr. Antonio Gonzalez, MD: Yes, they would. Dr. Katrina Furey, MD: Think. And Portia, I think you were reading some criticisms of the movie. I think the general public also caught on to that, like, wow, this is like a really intricate plot to go through to pay off prior lawsuits. Portia Pendleton, LCSW: I don't know. Murdering someone, you have to be so backed into the corner hopeless, like no other options. And it's like, I mean, A, yeah, like, you're right about the malpractice. You should have an insurance through the hospital. You're not even in private practice paying for your own, and that maybe you cut corners with that. It just seems OD that they taking going to these lengths of murdering a patient that Dr. Jack Harper was, like, friend. And it's like, at what point did the friendship turn into this? Was it fake? The whole, like, I think that's know, I watched the movie, you know, taking. Dr. Katrina Furey, MD: Notes because we're professionals. Portia Pendleton, LCSW: We're professionals at watching TV here, and I was just lost with a lot of the line, so I'm glad to hear it know, I guess just me, but pretty gaping holes in some of it. Dr. Katrina Furey, MD: Yeah. And what did you think about that relationship of the friendship between Dr. Harper and Know? Because at least in psychiatry, we are big and not just psychiatry, but mental health in general, we are big boundary people. We really talk about boundaries and how to maintain them, especially in professional settings. I think in some other fields of medicine, I'm thinking more like primary care pediatrics in the old school days when you'd have the family doctor who took care of everyone in the town, I think the boundaries would have been a little different. But I always thought, especially when it came to things like surgery, it was really important not to operate or doing a seizure on people you're close to. Is that still the case? Dr. Antonio Gonzalez, MD: Well, I think it's probably the right thing to do because your feelings for your significant other or friend may actually interfere with your judgment. But again, I think it's more of a judgment call than a set rule. I do think that there are certain surgeries and certain procedures that we probably shouldn't be doing for our family members or for close friends, because, again, our judgment may be cloud by our feelings for that person. You may not necessarily take the best decision when you're put in that place. Dr. Katrina Furey, MD: Yeah, I think suturing up a superficial wound like your child cuts their knee. Oh, I can suture that up real quick. Feels very different to me than doing cardiac anesthesia or surgery on your buddy that you go fishing with. Yeah, right. Yeah, I would agree. Portia Pendleton, LCSW: I could see I was thinking just, like, what would I be comfortable with a friend doing? But maybe I don't know. I mean, I'm thinking of specialties, like, ortho I could see a friend doing but not OB. It's, like, all private, and then definitely not psychiatry, but I don't know. Cardiac surgery? I don't think cardiac no, it's like your heart opening my chest. I don't want you I think it's. Dr. Katrina Furey, MD: Important you feel like you trust the surgeon and the anesthesiology team, but to have it be like your buddy, that's risky. And what an ultimate betrayal. Portia Pendleton, LCSW: I mean, he trusted this person. He chose to have this procedure done by, I guess, at least rating wise, like a doctor with a lower success rate than right. The mom brought in this specialist who was operating on presidents and had all. Dr. Katrina Furey, MD: This prestige play picked Dr. Harper. Portia Pendleton, LCSW: And then right. To have this nefarious plot going on was just I was really shocked. I was also really shocked that Sam was in on it, his fiance, because at first, I think the movie kind of sets you up to not, like the mom. Right. Like, Lilith seems, you know, like, she doesn't have his best interests at heart. Dr. Katrina Furey, MD: It's controlling. Maybe they're enshring and not letting him. Portia Pendleton, LCSW: Live or be independent. Right. But then know, I was like, wow, really weaseled her way in. So I don't but she was a nurse, I think, so she had some info about his medications, which the mom, Lilith, was first, really surprised and pleased. Like, wow, like, you really have been taking care of him. I see all the medications in your bag. But then that's also ultimately how she found out that Sam was in on it. Right. Dr. Katrina Furey, MD: She saw, like, I think Sam left her purse behind, and the medications fell out. And when she went to go put everything back in the purse, she saw some mail where the name didn't match up, and then somehow she put it. Portia Pendleton, LCSW: Together, but that wasn't clear. Dr. Katrina Furey, MD: But again, also like, okay, so the names don't match up. That wouldn't automatically make me think, like. Portia Pendleton, LCSW: Oh, no, you're in on it to. Dr. Katrina Furey, MD: Murder my son while he's in this heart transplant. The plot was a little far fetched, but I did think it was entertaining, and I did know with Clay on the table, often the anesthesiologist is, like, the first person you meet when you're coming in for surgery that day and. Portia Pendleton, LCSW: The first person you see when you wake up. Dr. Katrina Furey, MD: So I think that's very important, as well, to your whole experience of surgery. And can you tell us a little bit, Dr. Gonzalez, about in your role, what that entails and how you sort of take care of the patient in broad strokes. And if this movie we've already talked about how the induction was totally off, but what the movie sort of got right and wrong. Dr. Antonio Gonzalez, MD: Yeah. So I think that the role of the anesthesiologist is very important. And I think that as anesthesiologist, we realize that, as you mentioned, unfortunately, the way our system is, we usually meet our patients just the day of surgery, right? So what that entails is that we actually need to create rapport with our patients very quickly. We know that the patients are coming in for a very stressful moment in their life. Sometimes it's very big surgery, sometimes it's very minor surgeries, right? But independently of what type of surgery the patients are coming for, we need to create that rapport and we need to bring the confidence to the patient. And as anesthesiologist, I think that we try to do that the moment we're talking to the patient. The first time we talk to the patients, it's all about creating rapport and creating a team experience in which you let me know what are your goals and we can try to meet those goals and expectations. What are your fears? Some patients tell you that their major fear is pain. Some patients tell you their major fear is throwing up because all the nausea, they've experienced so much nausea after. So then you can reassure the patient, okay, so this is our plan. This is going to be our plan to address the pain. This is going to be our plan to address the nausea. And again, we do this for all types of surgery. And I think that's very important as anesthesiologist to try to create that rapport and always be, when talking to the patient, basically addressing what are your major fears and how this is our plan to address those. Portia Pendleton, LCSW: That's such an important question. I think such an important part of the team. I think other people are just kind of part of the team, which makes sense. Like, okay, this is a surgery. They ask you a million questions like why are you here? What's your name? What's your birthday? Over and over again. So they're doing the right thing. But then for someone to ask, right, what are you scared of? Dr. Katrina Furey, MD: Right? Portia Pendleton, LCSW: What are you scared of today? How can we help you? Do you have any questions? Is really helpful. And I think just lets see the patient feel like they're a part of the team, like they're being validated, listened to, important, which of course they are. But I think in the system when you have maybe two to five, maybe surgeries that day, it's just like it becomes for everybody that's working, there just procedure. So I think those questions just stand out as really helpful and nice, good patient care. Dr. Katrina Furey, MD: And the anesthesiologist is the person who you really meet at the beginning, who asks you all these questions, checks on your allergies, looks in your mouth to see like, okay, how big are those tonsils? How are we going to sort of intubate? You most comfortably asks you what you're worried about, and then they walk with you in most of the time, and they're with you, getting you on the table, getting you positioned, making sure you're comfortable, saying, okay, it's going to be cold in here, let's put a blanket on. They do a lot of that caretaking right away. I think when people are really scared, even if it's a minor surgery, I don't know who's not scared when they're going into a surgery. And of course, the surgeon comes in and they're really focused on the surgery, and of course, they want to make the experience good, too. But you're usually, like with the anesthesiologist, I think, the longest as you're consciously awake and then coming out of the surgery, that's who's also waking you up and making sure you're okay. That's who's checking on you in post op and things like that. So it is interesting that such an important member of the team and you're right, you really meet them that day and then you don't see them again, right? Like at the follow up for the surgery and stuff, you never get to see them. Is that a part of the job? Do you mind that, or do you wish that you could check on these people again? Dr. Antonio Gonzalez, MD: Well, it's actually very interesting that you ask because one of the things that actually inspired me to become an obstetric anesthesiologist, particularly, was I sometimes felt that I was in these very long surgeries, and when I went to see the patients post op, they would not remember me. And there wasn't really a problem with the patient not remembering me. It wasn't really an ego thing. It was more like, I don't feel like he thinks I'm part of this team taking care of him. I didn't feel like I was part of the team again. But on the other hand, I just happened to see a patient in a hallway and he's like, oh, you did my epidural for labor. And I'm like, oh, I did. And that was like, oh, these patients do remember me. Do appreciate what we're doing. And although, again, it's not an ego thing, but it's just that feeling of being part of something more, like, you know, that you help somebody and they actually remember that you were part of that, alleviating the pain, and it just feels good. It makes you feel like you're really part of a team that addresses the patient's pain and all this. And that's what really brought me into obstetric anesthesia. Going back to what we were talking about, the patients, the pre op part. Again, because of my obstetric anesthesia background, most of the literature that I've reviewed is on that field. And there is a very interesting article that has changed the way I practice that basically addressed what we were just discussing, which was basically, you ask the patients would you rather have better analgesia or more side effects, depending on the dose? And the interesting thing it's a very interesting study, but the outcome of the study was that patients actually knew exactly what they wanted. The patients that were overly concerned about pain ended up consuming more pain medication. And the patients that were overly concerned with the side effects did not consume as many medications. So the patients always know. And that's why always asking your patients, what are your weigh the risk and benefits, or what are your main outcomes? What do you want to experience here? More pain, slightly less pain, slightly more side effects of the medications, or you're okay with pain knowing that your side effects are going to be less? Dr. Katrina Furey, MD: The patients know that's actually really interesting and really important to keep sort of their autonomy and their preferences. So, Dr. Gonzalez, I know you're not like a transplant surgeon, but I thought it was pretty unlikely that the mother would just be, like, wheeled in, especially after having overdosed on something and her heart would be given right to her son. Dr. Antonio Gonzalez, MD: Yeah, absolutely. Dr. Katrina Furey, MD: What do you think about that? Dr. Antonio Gonzalez, MD: Yeah, absolutely. I think you're absolutely right. And at some point, I was hoping to bring that up. First of all, as you mentioned, there is a battery of tests that the donor needs to go through before they can be a donor. Portia Pendleton, LCSW: That's number one blood type, right? Dr. Katrina Furey, MD: It's not just like, oh, it's a blood type match. There's like, so many more things they have to check. Dr. Antonio Gonzalez, MD: There's so many more tests. And it seems from the movie that the mom have actually taken the purse from Sam, right? So presumably she took medications that could have actually make her heart stop. Right, which means that the period of ischemia of the heart may not have make her a good donor for her heart. She might have been able to donate her cornea and other things that actually don't have a very specific ischemia time. But there are organs that have a very limited ischemia time, meaning that the time that the organ is without perfusion or without oxygenation, without blood flow. And that is very important. The heart is one of the organs that needs perfusion for very crucial timing. It's a very small window of ischemia for the heart yes. Dr. Katrina Furey, MD: That she'd take, again, cardiac medication that likely stopped her heart. It does seem like she called her surgeon of choice ahead of time and was like, get here now. We only have so much time. But still, it's just completely unlikely that that would have happened. It was kind of a beautiful, I guess, part of the story that they could both, in this other realm, connect with each other and she could talk to him and they got to say this goodbye. That was pretty beautiful. But in terms of accuracy, there's no way that would have happened. And so getting. Back to the title of the movie Awake, and the whole premise that he's awake in surgery and aware of everything that's going on. I think a fascinating question that comes to my mind is like, how do we define awake? Is it consciousness? Is it memory? Is it feeling? And then how do you assess it during and after something like a major surgery? Dr. Antonio Gonzalez, MD: Yeah, that's a very interesting question. And I was thinking myself the same thing throughout the movie. And at the end, I'm still not even clear that either he was awake. We probably will never know the answer, according to the movie. But interoperative awareness, it's basically the incidence of a failure to suppress arousal, experience and episodic memory. So for you to have recall, in order for you to have introoperative awareness, there has to be recall. There are some incidents of patients actually hearing things, but they may not have necessarily distress about it because hearing and depth of sedation, the depth of sedation goes anywhere from hearing to actually not even being able to have recall. So you're going to see the worst cases of interoperative awareness when there is recall, and the patient can actually tell you how stressed they were about the experience. So they've come up with some classification. It's called the Michigan Awareness Classification, and it goes from zero, class zero, which is basically no awareness, to class one, which is auditory perceptions, class two, which is tactile perception. So they feel the surgical manipulation, they feel the endotracheal tube. And then there is class three, which is they actually feel pain. Class four, they actually have paralysis. And this is what seems to actually be happening here. He's experiencing paralysis because he said, just move something, right? He's trying to move something. He can't move anything. So he probably is there at a class four. Later on, we know that he's definitely at class five, where he's probably experiencing pain and paralysis. And then you can actually assign a D if the patient tells you that it was very stressful. They have the fear, they had fear, they had anxiety, a sense of suffocation or doom. So basically all these classifications, you can actually add a D to them. And the higher they are, and especially if they have a D next to them, the more likely these patients will have sequela. As in your profession, you can probably talk about what happens to these patients that have interpreted awareness. Right? And you were talking about moms that have pain during surgery. So that could lead to post traumatic stress disorder. But I'm not the expert there. Dr. Katrina Furey, MD: I would imagine it would. Right. I would imagine when we think about post traumatic stress disorder, I like to think of that as a disorder of Stuckness. And I always tell my patients, like, it's normal after you've lived through something traumatic, to have the symptoms of PTSD, the hyperarousal, the hyper, vigilance, intrusive thoughts, altered avoidance, altered mood, altered line of thinking and things like that initially, because who wouldn't? We sort of call that an acute stress response. But then once it persists, usually after, like, a month or continues beyond that, then we start to think of it as something called PTSD or post traumatic stress disorder. And there's some really great treatments out there for that, including things like cognitive processing therapy or CPT, EMDR, different types of psychotherapies and medications, and patients can really get a lot better. I love treating PTSD for that reason. But I would imagine the first criterion to meet diagnostic criteria for PTSD is to have a life threatening situation happen to you or to be vicariously exposed to it, which I think is really important as a new addition to the DSM criteria. I think this will qualify. Portia Pendleton, LCSW: Yeah, I'm just even imagining a patient coming in and describing this. I would expect a person to develop PTSD from it, and then it's like. Dr. Katrina Furey, MD: Is that a disorder, or is that, like, a normal human response to being consciously awake but paralyzed during cardiac surgery? Right. Portia Pendleton, LCSW: That's where you're like, well, like, trouble sleeping following. I would imagine maybe some nightmares. Might be afraid to fall asleep 100%. Or obviously, like you were saying before, Dr. Gonzalez, afraid of returning for future medical care or surgeries or telling loved ones to not do it, or their experience. So it feels really serious. And obviously, many traumas can be, but also unique. I haven't worked with someone that this has occurred to, obviously, because it is rare, but I'm just imagining, like, poor Clay when he wakes up, and if he does recall at one of those levels that you described, then what? And also write the murder plot. I mean, that was like taking the cake, let alone feeling pain. Dr. Katrina Furey, MD: I know. Like, such intense pain, right. And being so paralyzed and helpless. I almost can't imagine anything worse. Portia Pendleton, LCSW: He's standing up. We talked a little bit about the dissociation. That being an interesting way to show it. So sometimes when somebody's experiencing a trauma, they might dissociate and kind of see. Dr. Katrina Furey, MD: Themselves from up above. And they did show that when he sort of zoomed out, then it took a turn where he's then solving the. Portia Pendleton, LCSW: Plot, like, walking around, figuring it out. Dr. Katrina Furey, MD: Like, I don't think yeah, that's not quite dissociation, but up until that point. Portia Pendleton, LCSW: It was a great depiction of. Dr. Antonio Gonzalez, MD: It. Portia Pendleton, LCSW: Just it was wild. Dr. Katrina Furey, MD: It was wild. What a wild movie. Dr. Gonzalez, as we wrap up, is there anything else you'd like to add or anything we haven't touched on that you think is important? Dr. Antonio Gonzalez, MD: What it's really important here is for the patients to really voice out their experience. Right. One of the things that we see as physicians, we're not necessarily, particularly not psychiatrists or psychologists, we are not necessarily very well versed in how to deal with the consequences of what happens interoperatively. And it's important for the patients to say, hey, this is what I felt. But equally as important is for physicians to actually avoid minimizing what the patient felt and actually acknowledge that something happened and say, hey, I'm really sorry that you went through this. Let's try to figure out what resources we have to help you to get better, to get through these. It's actually something that I've always wondered is when is the best time to reach out for the patients? When, for example, in our case, we do C sections, right? And the patients are telling us that they're feeling pain, so they actually quickly voice out their experience so we can quickly do something about it. And even then, it's hard to figure out if you should approach the patient, shouldn't approach the patient, because not every patient won't consider a short time of discomfort or pain as traumatic. So it's a thin line in which basically we rely on the patient telling us, this is what I felt, this is how I feel now, so that we can actually look for help again, because as anesthesiologist or, surgeons may not be the best person to deal with it, but we can look for the resources. Dr. Katrina Furey, MD: And I do think, actually, at least in my clinical experience, given what I do, it has been I can tell you without a shadow of a doubt, it has been so validating and healing for my patients who have experienced trauma within previous childbirth deliveries or IVF procedures or other things like that, who felt minimized by the team at the time when they go in for the next thing and their anesthesiologist is the one who asks them just the questions you're mentioning. Now, I'm wondering if it was you. Portia Pendleton, LCSW: Or if you've just trained, like, some. Dr. Katrina Furey, MD: Really good team members. But when they ask them about these things and they share their prior traumatic experience, which is very hard for them, right, like, to even share, period, but then, especially if they've felt minimized or invalidated in the past, when they share it this time, and it's met with compassion and validation, it goes so far in their healing. And so I think you're spot on, and I hope this can serve and your continuing education can serve to just keep reinforcing that to the anesthesiology team that that is really important and such a crucial time to give that validation to patients who might really need it. And I think that would go for any patient, but especially any patient with a history of PTSD prior to that. And that's a hard thing to ask about. Portia Pendleton, LCSW: Yeah, I could definitely see it in pregnancy traumas. I think it's a pretty common experience with just, like, whether or not it's their perspective of something happening. Everything moves fast sometimes, as both of you know, I'm sure if it's supposed to be a regular delivery and all of a sudden it's not like that can be scary. And sometimes you have to prioritize saving a patient so things aren't explained slowly. It's the after of, like, okay, I know. That was really scary. Dr. Katrina Furey, MD: Kind of debriefing. Portia Pendleton, LCSW: Yeah, the debrief I would imagine being really helpful. Dr. Katrina Furey, MD: And we always I think in mental health, we always assume our patients have a trauma history rather than assume they don't. And I don't think that's because there's like I mean, maybe there is a higher incidence given the patients we're seeing. But I think then if you can just sort of approach it in more of like a trauma informed framework and just assume, like, okay, let's just assume this person has had some experience in their life where they felt helpless or stuck or not heard. How do we approach them here so that they don't feel that you don't even have to ask, do you have a trauma history? You could just assume. And then I think that just goes a really far away. So I'm so glad, Dr. Gonzalez, to hear that you're just doing know that makes this psychiatrist very happy. Dr. Antonio Gonzalez, MD: Yeah, well, I think that a lot of it has to do with the fact that some time ago, we actually read this very nice article that came out that was titled Failure of Communication, and it was actually written by a patient who experienced interoperative pain. I actually had the pleasure to have a podcast with Susanna Stanford, who is a patient who experienced introvertive pain, and she shared with us through that paper that was a couple of years ago, her experience. And from the time I read that paper, I started realizing how important that communication part is and not minimizing their pain and actually trying to address the situation in the moment and offering alternatives. Right. The most important thing, as you mentioned, is the patient needs to feel that first of all, they're being heard and that their concerns will be addressed. The worst we can do is tell them that it's not that big of a deal. Baby is okay. That's usually what we hear. Oh, the baby's okay. So it's going to be fine. The means doesn't justify the end. Dr. Katrina Furey, MD: Well, that's wonderful. Thank you so much, Dr. Gonzalez, for joining us today. I think we will try to link to that paper in our show Notes. If anyone is interested in reading that. Portia Pendleton, LCSW: Further and maybe also your podcast, if you want to tell us, give us. Dr. Katrina Furey, MD: A little shout out yeah. Portia Pendleton, LCSW: Where they can find your podcast. Dr. Antonio Gonzalez, MD: Yes, the podcast is Yale Anesthesiology, and I will share the link as well. Dr. Katrina Furey, MD: Thank you. And we want to thank all of our listeners for joining us today. You can find us at Analyze Scripts podcast on Instagram and TikTok. We recently updated our Instagram handle, so now it's Analyze Scripts podcast across the board, and we hope that you will join us next week as we cover the Nightmare Before Christmas on our Halloween month. Portia Pendleton, LCSW: Yes. Dr. Katrina Furey, MD: So we'll see you next Monday. Portia Pendleton, LCSW: Thank you so much for joining us. Dr. Katrina Furey, MD: Bye. Dr. Antonio Gonzalez, MD: All right. Thank you so much for having me. This was great. Thank you. Dr. Katrina Furey, MD: This podcast and its contents are a copyright of analyzed scripts, all rights reserved. Any redistribution or reproduction of part or all of the contents in any form is prohibited. Unless you want to share it with your friends and rate review and subscribe, that's fine. All stories and characters discussed are fictional in nature. No identification with actual persons, living or deceased places, buildings, or products is intended or should be inferred. This podcast is for entertainment purposes only. The podcast and its contents do not constitute professional mental health or medical advice. Listeners might consider consulting a mental health provider if they need assistance with any mental health problems or concerns. As always, please call 911 or go directly to your nearest emergency room for any psychiatric emergencies. Thanks for listening and see you next time. Dr. Katrina Furey, MD: Our don't.

Observational studies, another defense of digoxin, CTO-PCI, BP measurement, and a possible revolution in cardiovascular protection are the topics John Mandrola, MD, discusses in this week's podcast. This podcast is intended for healthcare professionals only. To read a partial transcript or to comment, visit: https://www.medscape.com/twic I. Observational Research Yeh; Credibility in Observational  Research https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.123.064645 Hernan; Causal Language in Observational Research  https://ajph.aphapublications.org/doi/full/10.2105/AJPH.2018.304337 Wang; RCT Duplicate Initiative https://jamanetwork.com/journals/jama/fullarticle/2804067 II. Defense of Digoxin Brophy; Beta Blockers, Digoxin, or Both https://doi.org/10.1016/j.cjca.2023.06.009 Dorian editorial https://doi.org/10.1016/j.cjca.2023.07.013 Ziff Digoxin Meta-analysis https://www.bmj.com/content/351/bmj.h4451.long DIG trial  https://www.nejm.org/doi/full/10.1056/nejm199702203360801 Davila Analysis of DIG Trial https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6801940/ Kotecha Meta-analysis of Beta Blockers https://pubmed.ncbi.nlm.nih.gov/25193873/ RATE-AF https://jamanetwork.com/journals/jama/fullarticle/2774407 III. CTO-PCI PCI of Chronic Total Occlusions Improves Angina, Quality of Life in Trials https://www.medscape.com/viewarticle/994739 JAMA Network Open Meta-analysis IV. BP Measurement One Size Doesn't Fit All in Blood Pressure Measurement https://www.medscape.com/viewarticle/995216 Ishigami Blood Pressure Measurement Comparison https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2807853 V. GLP-1 SELECT Trial Semaglutide Cuts Cardiovascular Events in Landmark Trial https://www.medscape.com/viewarticle/995270 SELECT Protocol Paper You may also like: Medscape editor-in-chief Eric Topol, MD, and master storyteller and clinician Abraham Verghese, MD, on Medicine and the Machine https://www.medscape.com/features/public/machine The Bob Harrington Show with Stanford University Chair of Medicine, Robert A. Harrington, MD. https://www.medscape.com/author/bob-harrington Questions or feedback, please contact news@medscape.net

Visit: https://nursing.com/140meds to request your free copy of "140 Must Know Meds" Generic Name Digoxin Trade Name Lanoxin Indication CHF, AFib, A-flutter Action Positive inotropic effect (increases force of myocardial contraction), prolongs refractory period, ↓ conduction through SA and AV nodes. Essentially digoxin is given to increase cardiac output and slow the rate. Therapeutic Class Antiarrhythmic, inotropics Pharmacologic Class Digitalis glycosides Nursing Considerations • Excreted by kidneys • Assess patient for hypersensitivity • Contraindicated with uncontrolled ventricular arrhythmias • Hypokalemia increase risk for toxicity • Hypercalcemia ↑ risk for toxicity • Use caution with diuretic use as they may cause electrolyte abnormalities that can lead to toxicity • Assess patient for cardiac arrhythmias including bradycardia • Signs of toxicity include vision changes (blurred vision, yellow, green vision disturbances) • Monitor pulse rate for 1 full minute prior to dosing patient (hold for pulse

In this week's episode we delve into the evidence for digoxin reducing mortality in the interstage period following Norwood palliation for HLHS. We speak with Assistant Professor of Pediatrics at the University of Pennsylvania, Dr. Michael O'Byrne about a recent analysis of the PHIS database using the relatively novel “preference based instrumental variable” approach to analysis of an observational data set. How does this approach allow for possible proof of causation of effect of a variable? Why might digoxin reduce mortality in the HLHS patient following stage I palliation? Are there patients in which the impact of this agent might be greater than others? These are amongst the many questions reviewed this week with Dr. O'Byrne.https://doi.org/10.1016/j.ahj.2023.05.005

A while back, we did a mini-series on peptides and sexual wellness. We covered PT-141 (bremelanotide), a peptide therapy used to help women and men with low sex drive. And Kisspeptin-10, a peptide that helps with increased arousal and may help with infertility. But we really didn't focus on what causes a low sex drive. So today, we'll touch on the possible mental and physical causes that may affect your sex drive, but we'll focus on medications that may lead to a decreased interest in sex. It's important to know that a low sex drive can affect both men and women. Medical conditions like depression, hypothyroidism, diabetes, and high blood pressure, may all cause a low sex drive. Even hormonal changes (e.g., during pregnancy, after childbirth, or while breastfeeding) can decrease interest in sex. And some people who use alcohol, have relationship issues, or certain infections (e.g., vaginal yeast infections, urinary tract infections) have a low sex drive. Certain medications may cause low sex drive as a side effect. But remember that not everyone taking certain medications will have the same issues.  Some antidepressants and antipsychotics are more likely to cause a low sex drive than others. For example, selective serotonin reuptake inhibitors (SSRIs) like Paxil, Zoloft, and Proac are more likely to cause a low sex drive than Wellbutrin or Remeron. While older antipsychotics like Haldol, used to treat schizophrenia and bipolar disorder, are more likely to cause a low sex drive than Risperdal.  Benzodiazepines like Xanax, Ativan, and Valium, used to treat anxiety and seizure disorder, can lower your sex drive. Many people with heart failure report having a low sex drive. This is because people with heart failure need different medications to reduce how fast or hard their heart has to work and medications that get rid of extra fluid. Unfortunately, some heart failure medications like Digoxin, Spironolactone, beta-blockers, and other water pills like hydrochlorothiazide can lower their sex drive. Acid reflux or "heartburn" happens when stomach acid travels back into the esophagus. And people who take medications for "heartburn" (e.g., Pepcid and Zantac) have reported a lower sex drive. Even medications that affect sex hormones (e.g., estrogen, testosterone, and progesterone) can decrease libido. Examples of these medications include birth control and Lupron (used to treat prostate cancer). And lastly, people who use opioids like Norco and Ultram to treat pain can also have a lower sexual desire. How to improve sex drive caused by medications? Always talk to your healthcare provider first. They can determine if your low sex drive is due to your medications or if there's another cause, like an infection or hormonal changes. If your medication is causing a low sex drive, your healthcare provider may have you stop the medication if it's not needed. Or they may switch you to an alternate medication that doesn't cause a low sex drive. But don't stop your medication without speaking to your healthcare provider first. Your healthcare provider may suggest other medications or peptides like PT-141 or Kisspeptin-10.  What is PT-141? PT-141 (bremelanotide) is a melanocortin receptor agonist peptide. Melanocortin is a natural hormone in your body that works on receptors in your brain and nervous system to cause sexual arousal and influence sexual behavior. However, we don't know exactly how it works to improve sex drive. It can also work on receptors in cells that produce skin color (melanocytes). You may know PT-141 as Vyleesi. This medication was originally FDA-approved in 2019 to help low sex drive in women who haven't gone through menopause yet. While it's not approved for low sex drive in men, some may use it off-label.  In these cases, men also use PT-141 to help improve erections, libido, sex drive, and performance. What is Kisspeptin-10? Kisspeptin-10 is a neuropeptide involved in reproduction, sexual behavior, and sexual attraction. It helps increase activity in the brain associated with sexual attraction and arousal.  Kisspeptin-10 also stimulates the hypothalamus to release gonadotropin-releasing hormone (GnRH), which in turn signals the pituitary gland to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH). These hormones play a role in the production of both testosterone and estradiol.  Thanks again for listening to The Peptide Podcast. You can find more information at pepties.com. We love having you as part of our community. If you love this podcast, please share it with your friends and family on social media. Have a happy, healthy week! Pro Tips We're huge advocates of using daily collagen peptide supplements in your routine to help with skin, nail, bone, and joint health. But what do you know about peptides for health and wellness? Giving yourself a peptide injection can be scary or confusing. But we've got you covered. Check out 6 tips to make peptide injections easier. And, make sure you have the supplies you'll need. This may include syringes, needles, alcohol pads, and a sharps container. They work to kill bacteria (bactericidal) by preventing them from making their own protective coating in your body.

Medicine's made from plants have been used throughout human history. Today, over 100 pharmaceutical drugs and medicines trace their "roots" to chemical compounds found in plants.  For example the medication Taxol which is a powerful chemotherapeutic medication to treat breast cancer is extracted from the Pacif Yew plant and the medication Digoxin used for irregular heart beats is extracted from the Foxglove plant. Listen to this episode of The Medical Truth Podcast as host James Egidio interviews medicinal herbalist and aromatherapist  Dr. Amber Robinson. For current and previous podcast episodes and show transcripts go to www.MedicalTruthPodcast.comFor Current and Previous Podcast Episodes, Show Notes, and Videos go to www.MedicalTruthPodcast.comYou can also find the Medical Truth Podcast on Facebook, Twitter, YouTube, Rumble, and Substack, as well as all the major podcast platforms such as Apple Podcast, Spotify, Google Podcast, Amazon Music, iHeart, and Podchaser

Toxicologist Dr. Caitlin Wolfe is back to talk about how to manage digoxin toxicity. When to use the antidote and how to dose it, how to manage dysrhythmias and that pesky hyperkalemia. For more FOAM resus related content, head to www.theresuscourse.com

Folge 120: Cotrimoxazol aus UK, Insekten im Essen und Digoxin-Ersatz

In this episode we'll be discussing digoxin and how it works in the heart. Then, we'll look at how it becomes toxic, what you'll need to look for, and how to fix it. reach out: instagram: @coffeebreakhems facebook: Austin Kiser email: kisercpr@gmail.com Check out our reference guides and vent management book: www.kisercpr.com/shop

Multiple Sclerosis News Today's multimedia associate, Price Wooldridge, reads a news article about how people with MS have significantly higher and potentially damaging blood levels of zinc. He also reads “MS News That Caught My Eye Last Week: Vitamin D, Brain Health, Digoxin, Natalizumab” by Ed Tobias, from his column “The MS Wire”. =================================== Are you interested in learning more about multiple sclerosis? If so, please visit: https://multiplesclerosisnewstoday.com/ ===================================== To join in on conversations regarding multiple sclerosis, please visit: https://multiplesclerosisnewstoday.com/forums/

Qual a relação de uma planta com o James Bond? Digoxina é remédio ou veneno? Ainda tem espaço para essa medicação na cardiologia? Como prescrever? Quais os cuidados? Como é e como tratar a intoxicação? Cada vez menos prescrevemos essa droga e seu uso está ficando escasso e, por isso, as dúvidas e angústias surgem. Nesse episódio, Rapha Rossi e Mateus Prata debatem todos esses tópicos sobre a digoxina, de maneira bem descontraída.

Multiple Sclerosis News Today's multimedia associate, Price Wooldridge, reads the news article about an approved heart med that could promote myelin repair in MS. He also reads “MS News That Caught My Eye Last Week: Intermittent Fasting, Roe v. Wade, IRLs” by Ed Tobias, from his column "The MS Wire". =================================== Are you interested in learning more about multiple sclerosis? If so, please visit: https://multiplesclerosisnewstoday.com/ ===================================== To join in on conversations regarding multiple sclerosis, please visit: https://multiplesclerosisnewstoday.com/forums/

In this episode, we review the high-yield topic of Digoxin from the Cardiovascular section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets

Download the cheat: https://bit.ly/50-meds  View the lesson: https://bit.ly/DigoxinLanoxinNursingConsiderations    Generic Name Digoxin Trade Name Lanoxin Indication CHF, AFib, A-flutter Action Positive inotropic effect (increases force of myocardial contraction), prolongs refractory period, ↓ conduction through SA and AV nodes. Essentially digoxin is given to increase cardiac output and slow the rate. Therapeutic Class Antiarrhythmic, inotropics Pharmacologic Class Digitalis glycosides Nursing Considerations • Excreted by kidneys • Assess patient for hypersensitivity • Contraindicated with uncontrolled ventricular arrhythmias • Hypokalemia increase risk for toxicity • Hypercalcemia ↑ risk for toxicity • Use caution with diuretic use as they may cause electrolyte abnormalities that can lead to toxicity • Assess patient for cardiac arrhythmias including bradycardia • Signs of toxicity include vision changes (blurred vision, yellow, green vision disturbances) • Monitor pulse rate for 1 full minute prior to dosing patient (hold for pulse

Today is a Kass-tastic episode, where we let her screech out something cool she learned about! She chose to help us unwind by giving us the origin tale of Digoxin, AKA foxglove. Ever wandered where grandma got her heart medicine? This might be the answer. So grab yourself a coconut margarita like we did, sit back, and fill your earholes with some new knowledge.

Contributor: Chris Holmes, MD Educational Pearls: Foxglove plant contains the cardiac glycoside digoxin   Foxglove leaf potions were once used to treat Dropsy; a historic term for symptoms of heart failure  Digoxin, previously used for treating heart failure, works by increases heart contraction strength and slows heart rate Of note, the EKG of patient on digitalis may have a ‘Dali Mustache' appearance Digoxin toxicity can lead to a variety of dysrhythmias as well as neurological, GI, and metabolic effects Treatment of digoxin toxicity is digoxin-immune fab, which is an antibody that binds digoxin References David MNV, Shetty M. Digoxin. [Updated 2021 Dec 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556025/ Cummings ED, Swoboda HD. Digoxin Toxicity. [Updated 2021 Jul 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470568/?report=classic Summarized by Kirsten Hughes, MS4 | Edited by John Spartz MS4 & Erik Verzemnieks, MD   The Emergency Medical Minute is excited to announce that we are now offering AMA PRA Category 1 credits™ via online course modules. To access these and for more information, visit our website at https://emergencymedicalminute.org/cme-courses/ and create an account.  Donate to EMM today!

This episode will provide information about Heart Failure or Congestive Heart Failure and the causes with a brief outline and reference to treatments explained in previous episodes. It will explain, in understandable language, what is Heart Failure how it effects us, possible causes and preventions, and where medications work.  It will talk about the medication Digoxin, what are it's common side effects and cautions to be aware of. All links to references used in the episode will be made available in the show notes  

In this episode, we review the high-yield topic of Cardiac Glycosides (Digoxin) from the Cardiovascular section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbulletsIn this episode --- Send in a voice message: https://anchor.fm/medbulletsstep1/message

Podcast put out by the faculty at WCU LA for students with an aim at sharing NCLEX tips, testing tips, topic explanation, and any questions WCU grads and current students may have! To contact Joan Wheeler about ATI/VATI/Board Vital resources or to do your weekly check-in, email her at jwheeler@westcoatuniversity.edu To request particular topics to be discussed in our podcasts email me at dreid@westcoastuniversity.edu or message me on Remind --- Send in a voice message: https://anchor.fm/wculaoperationpassnclex/message

The 11 Worst Medications Causing Atrial Fibrillation Could one of your medications actually be causing your AFib? Over the years I've seen a number of patients either significantly decrease their AFib episodes or even put their AFib into remission for a few years just by getting off an AFib causing medication. For those who needed a particular medication, catheter ablation was very helpful in eliminating the AFib so that they could continue to take their necessary medication. Below are my 11 worst medications causing atrial fibrillation. 1. Diuretics With the exception of spironolactone (Aldactone) and triamterene, diuretics can be problematic for atrial fibrillation patients. The reason is that most diuretics are well-known to cause mineral depletion in the body. Depletion of those key minerals, especially potassium and magnesium, is often enough to trigger atrial fibrillation. 2. NSAIDs Non-steroid anti-inflammatory drugs, or NSAIDs, can also induce AFib. NSAIDs are relatively common drugs like ibuprofen and naproxen that are often used to fight pain. NSAIDs are particularly troublesome for AFib patients because they also increase the risk of heart and kidney failure. For those who are also on a blood thinner, NSAIDs increase the risk of an emergency room visit for a life-threatening gastrointestinal bleed. 3. Proton Pump Inhibitors Proton pump inhibitors, which suppress stomach acid, can also atrial fibrillation by blocking magnesium absorption or possibly by changing a person's gut microbiome. These drugs include omeprazole, lansoprazole and pantoprazole, which are often sold under the brand names Prilosec, Prevacid, and Nexium, respectively. 4. Steroids Steroids, like prednisone and Solu-medrol, can cause atrial fibrillation, too, by raising blood glucose levels to very high levels and increasing blood pressure through fluid retention and weight gain. Over my career, I've even seen many cases of steroid injections triggering AFib. 5. Any Stimulant Cardiac stimulant medications, like albuterol inhalers or theophylline for asthma, have long been associated with AFib. Even over-the-counter decongestants such as pseudoephedrine, which is sold as Sudafed, or medications for attention deficit hyperactivity disorder can trigger an AFib attack. The bottom line is that anything that revs up the cardiovascular system has a risk of causing AFib. 6. Digoxin, Diltiazem, Verapamil, and Beta-Blockers Perhaps a bit counterintuitively, some if the classic drugs used to treat abnormal heart rhythms such as digoxin, calcium-channel blockers such as verapamil and diltiazem, and beta-blockers have all been associated with an increased risk of AFib. While the exact mechanisms whereby these drugs may increase the AFib risk aren't entirely clear, plenty of cases have been documented in the medical literature. We've even seen beta-blockers, which are often used to treat AFib, linked to AFib episodes due to associated weight gain, particularly with women. 7. Fish Oil As many readers know, there is prescription-strength fish oil, like Lovaza, as well as the over-the-counter fish oil. Prescription-strength fish oil is used to treat high triglycerides whereas the over-the-counter version is used to treat a myriad of complaints. Regardless of which form it is, fish oil has now been implicated as a potential cause of AFib. If fish oil has been particularly helpful for you, try keeping the dose under 1 gram per day to minimize the risk of AFib. Or, alternatively, you can do what I've done and go back to eating wild-caught fish high in omega 3s instead of taking a supplement. Interestingly, since stopping fish oil for myself, I've noticed a lot fewer palpitations. 8. Antiarrhythmics like Amiodarone, Flecainide, and Propafenone Another surprise to many readers is that the antiarrhythmic drugs, the ones that are supposed to prevent AFib, have been linked to AFib. For example, amiodarone is well-known to cause hyperthyroidism which ca...

In this episode we discuss 3 fellowship vivas - management of morbidly obese patients in cardiac arrest, patients admitted with digoxin toxicity and management of post-traumatic hepatic injury. 

Want to experience the greatest in board studying? Check out our interactive question bank podcast- the FIRST of its kind here: emrapidbombs.supercast.com Ever get the feeling we live on a yellow submarine? When we're trapped in the ED with wait times >8 hours, we feel it… Let's talk digoxin toxicity, perhaps the most classic toxidrome ever told.

Digoxin also goes by the brand names Digox, Digitalis, and Lanoxicaps. Digoxin comes as tablets, a solution, and an injection. In both Adults and Pediatrics, when calculating doses it is important to use the patient's lean body weight (LBW) with dose adjustments based on levels. It is important to also remember that concentrations of >2 ng/mL lead to digoxin toxicity and can also be identified with signs and symptoms such as anorexia, nausea, vomiting, and visual changes. The most common indications are for treating Heart Failure with reduced Ejection Fraction (HFrEF) and Atrial Fibrillation (AFib). Digoxin is poorly protein bound with a long duration of action between 3-4 days. THe most common side effects are dizziness, headache, bradycardia, weakness, and confusion. FREE Drug Card Sheet is available for this episode at DrugCardsDaily.com along with ALL past FREE drug card sheets! Please SUBSCRIBE, FOLLOW, and RATE on Spotify, Apple Podcasts, or wherever your favorite place to listen to podcasts are. I'd really appreciate hearing from you! Leave a voice message at anchor.fm/drugcardsdaily or find me on most all socials @drugcardsdaily or send an email to contact.drugcardsdaily@gmail.com to leave feedback, request a drug, or say hello! --- Send in a voice message: https://anchor.fm/drugcardsdaily/message

The Blame Game This week, Alex and Mary discuss the harmful effects of patient blaming, when a medical professional, friends, family, or self-help authors infer, suggest, or outright say something akin to, “If you had a better attitude, you could beat cancer” or “Maybe if you had lost weight, you wouldn't have gotten diabetes” or “You should have gone to the doctor sooner, before you got cancer.” Their discussion was inspired by Kate Bowler's journey through colon cancer, after having been diagnosed at the age of 35. Why does patient blaming exist and what can we do about it? Listen on our website, www.downthereaware.com/podcast, or wherever you get your podcasts. Episode Highlights Welcome back! [0:40] Please subscribe, rate, review, and follow us! [1:10] Patient Blaming [2:28] Kate Bowler [2:54] The Today Show [3:10] Self-help books that blame [4:30] Toxic positivity [7:30] It's ok not to be ok [8:18] A doctor's genuine apology [9:05] TX Heart Institute Journal [10:55] Peabody's Corner [11:10] Francis Weld Peabody [11:15] Patient Care [11:25] Cardiac Consult [13:23] Digoxin [14:03] Placebo effect [16:02] Emphasis is on disease rather than patient [18:09] Obesity [18:58] Lung cancer bias [19:55] Shame and blame [20:22] Character defect [21:55] Non-compliant [22:16] Physician bias ]22:50] Where do you draw the line? [23:26] Disparity in funding [24:08] Relationship between behavior and disease [25:02] Medical malpractice and patient blame [26:08] Grey's Anatomy [28:20] Importance of healthy lifestyle [29:10] Patients should get best care [30:35] Valuable lessons to be learned [31:45] Update on Kate Bowler [32:45] Thanks for listening! [33:15] Stay Connected Email Us: downthereaware@gmail.com Instagram:@downthereaware Facebook: Down There Aware Twitter: @downthereaware Pinterest: Down There Aware TikTok: Down There Aware Links Mentioned in the Episode When All Else Fails, Blaming the Patient Often Comes Next (Published 2008) Blaming the Patient: A Common Defense Tactic Today Show - Kate Bowler Perspective | What happens when the doctor blames you for your own cancer? Flying Blind: Why Do We Keep Blaming The Victims Of Medical Errors? "Everything happens for a reason" -- and other lies I've loved | Kate Bowler - TED Talk https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3233310/pdf/20111200s00004p620.pdf https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3233310/pdf/20111200s00004p620.pdf

The tale of Mary Bateman, aka the Yorkshire witch: a woman who was chronically incapable of going to the store. She also never met a scam she did like or a sheet she couldn't steal.  Sources: Catherine Curzon on Mental Floss. Extraordinary Life and Character of Mary Bateman, the Yorkshire Witch From the Earliest Thefts of her Infancy, Through a Most Awful Course of Crimes and Murders, Till Her Execution at the New Drop, Near the Castle of York, On Monday the 20th of March 1809 (12th Edition) Vision of Britain Through Time Ellen Castelow on Historic UK Kelly Buchanan on LOC. Wikipedia. Digoxin. National Library of Scotland.      Hull Packet via Gale Primary Sources Murderpedia The Lineup On Yorkshire Magazine Newspapers.com: Lancaster Gazette/Leeds Mercury Morning Chronicle   Music: Evil Plan by Kevin MacLeod Link: https://incompetech.filmmusic.io/song/3725-evil-plan License: http://creativecommons.org/licenses/by/4.0/ Tavern Loop One by Alexander Nakarada Link: https://filmmusic.io/song/6282-tavern-loop-one License: https://filmmusic.io/standard-license Listen to Kristy and Chris over on Short Story, Short Podcast.  Come on up and see us sometime:  Patreon  Facebook  Instagram Twitter MERCH  Amazon Wishlist Email    

Charles Cullen, AKA The Angel of Death, was responsible for 30-40 murders throughout his 16 year nursing career. Authorities believe the death toll is much higher. Cullen was able to slip through the cracks and worked for a staggering 10 different hospitals during his reign of terror.Sources:https://www.youtube.com/watch?v=KRiPXMMu-JEGraeber, Charles (2013). The good nurse : a true story of medicine, madness, and murder (First ed.). https://www.amazon.com/Good-Nurse-Medicine-Madness-Murder/dp/1455574139Pérez-Peña, Richard; Kocieniewski, David; George, Jason (February 29, 2004). "DEATH ON THE NIGHT SHIFT: 16 Years, Dozens of Bodies; Through Gaps in System, Nurse Left Trail of Grief".http://nl.newsbank.com/nl-search/we/Archives?p_product=PI&s_site=philly&p_multi=PI&p_theme=realcities&p_action=search&p_maxdocs=200&p_topdoc=1&p_text_direct-0=10675BFF5AB3F791&p_field_direct-0=document_id&p_perpage=10&p_sort=YMD_date:D&s_trackval=GooglePMhttps://www.newspapers.com/clip/79547917/https://www.newspapers.com/clip/79548043/https://www.newspapers.com/clip/79548267/https://www.newspapers.com/clip/79548681/https://www.newspapers.com/clip/79548822/https://www.newspapers.com/clip/79548746/

As we finish up we focus on the contemporary management of systolic heart failure or so called heart failure with reduced ejection fraction. Our focus in this episode is on RAAS blockade which includes the aldosterone antagonists along with a new kid on the block, Entresto. How does Entresto compare and where does it fit in to our contemporary management of systolic heart failure? We'll discuss that, along with the reason why we dont see much Digoxin anymore. When we're done, we'll have a very complete contemporary approach to how best to use pharmacotherapy in our patients with heart failure.

Emergency Physician and Toxicology Fellow John Rague joins us to discuss the presentation and management of digoxin toxicity in addition to other cardiac glycosides. Digoxin is not as commonly prescribed anymore thus our teaching on this topic has become less common. But digoxin and other cardiac glycosides are still available and used today so it's still important to understand the recognition and treatment of this toxicity. 

What are the effects of digoxin on mortality in patients with A. Fib? Answers from Drs. William Baker and Rob DiDomenico. Full manuscript available at: https://accpjournals.onlinelibrary.wiley.com/doi/10.1002/phar.2510

“The Brady Bunch” – Beta-Blockers, Calcium Channel Blockers, Digoxin, Clonidine Treatment of Beta Blocker OD Activated Charcoal – Only if ingestion time was

Show notes at pharmacyjoe.com/episode582. In this episode, I’ll discuss why hypokalemia can result from digoxin immune fab fragment administration. The post 582: Why hypokalemia can result from digoxin immune fab fragment administration appeared first on Pharmacy Joe.

Theme: Toxicology. Participants: Dr Satish Mitter, Pramod Chandru, Samoda Wilegoda Mudalige, Kit Rowe, Rachel Ng, Shreyas Iyer, and Caroline Tyers.Discussion 1:“Clinical outcomes from early use of digoxin specific antibodies versus observation in chronic digoxin poisoning (ATOM-4)”Betty S. Chan, Geoffrey K. Isbister, Colin B. Page, Katherine Z. Isoardi, Angela L. Chiew, Katharine A. Kirby & Nicholas A. Buckleyhttps://doi.org/10.1080/15563650.2018.1546010.Take-Home Points: The results from this study suggest no benefit from routine use of DigiFab for chronic digoxin toxicity.  Clinical indications for DigiFab use include - cardiac arrest, ventricular arrhythmias or runs of ventricular ectopic complexes and bradyarrhythmias associated with hypotension.  Digoxin levels should only be performed under specific circumstances (not routinely for all patients on digoxin but rather in the context of an AKI or when there is a clinical suspicion of potential toxicity).  When managing chronic digoxin toxicity, correcting any precipitating factors such as volume depletion and electrolyte abnormalities is critically important. Identifying patients at risk of digoxin toxicity (the typical patient is the elderly patient with multiple comorbidities) and drugs that impair digoxin toxicity (NSAIDs and diuretics) is also vital to your overall assessment.  Discussion 2:Case of malathion (organophosphate) poisoning.  55-year-old male found unconscious surrounded by chemicals at home.  Developed clear cholinergic toxidrome, tachycardia, and hypotension in ICU. Received atropine on a doubling regimen every 5 minutes: reaching 16mg (and then a continuous infusion) with improvement in his symptoms (including this tachycardia). Infusion weaned after 24 hours with recurrence of hemodynamic instability requiring inotropic support and recommencement of atropine on day 3. Required atropine for 31 days in total.   Take-Home Points: The standard, routinely taught presentations for cases do not always apply: this patient was tachycardic rather than bradycardic with his organophosphate toxicity (and this tachycardia responded to atropine).  Atropine for organophosphate toxicity is vital.  Oximes (such as pralidoxime) are occasionally used in the treatment of organophosphate toxicity but should be discussed with toxicology specialists prior to use.  Discussion 3:“Use of antipsychotics and risk of myocardial infarction: a systematic review and meta‐analysis”Zheng-he Yu, Hai-yin Jiang, Li Shao, Yuan-yue Zhou, Hai-yan Shi and Bing Ruan                            https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5338104/.Take-Home Points: This study suggests an association between antipsychotic use and an increased risk of MI (OR 1.88).  This risk appeared to be greater within the first 30 days of use (when taking daily doses); with the risk decreasing over time.  There was however significant heterogeneity in the data studied.  The recent commencement of an antipsychotic may be worth considering as an added risk factor for ischaemic heart disease in a patient presenting with chest pain. Credits:The discussions were mediated by ED consultant and toxicologist Dr Satish Mitter and ED consultant Dr Pramod Chandru.This episode was produced by the ­­­­Emergency Medicine Training Network 5 with the assistance of Dr Kavita Varshney, Deepa Dasgupta, Cynthia De Macedo Franco, and Paul Scott.Sound Effects Sound effects from https://www.free-stock-music.com. Machinery 909 by Glitch | https://soundcloud.com/glitch, Music promoted by https://www.free-stock-music.com, Creative Commons Attribution 3.0 Unported License, https://creativecommons.org/licenses/by/3.0/deed.en_US. Sax by MBB | https://soundcloud.com/mbbofficial, Music promoted by https://www.free-stock-music.com, Creative Commons Attribution-ShareAlike 3.0 Unported, https://creativecommons.org/licenses/by-sa/3.0/deed.en_US. 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What does Digoxin, Lidocaine, and a household pesticide have in common? Find out by listening to our review of the movie Run, released November 2020. Oh, and by the way, spoiler alert is on! This is NOT your physician's podcast. Hosts Shane Garrettson and Cal Vandergrift dive into the pharmacy world with fun, interesting, and downright weird topics! Tune in for NEW episodes, available on Spotify, Apple, Anchor, and more! Check out our Facebook, Twitter, and Instagram pages at Let's Pharmonize to view videos and images relevant to every episode! If you have any questions, comments, or even corrections, e-mail us at pharmonization@gmail.com. PLEASE READ: Shane and Cal are NOT medical professionals. DO NOT USE the information presented in this podcast to aid in your own personal health or medicinal benefit. This is a light-hearted podcast that should not be taken with the same seriousness as your own personal health, A special thanks to Kelly Kerr for creating the music used in the intro and outro. All Rights Reserved --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/calvin-vandergrift8/support

CardioNerds (Amit Goyal & Karan Desai) join University of Illinois at Chicago cardiology fellows (Brody Slostad, Kavin Arasar, and Mary Rodriguez-Ziccardi) for a cup of tea from atop Hancock Tower! They discuss an illuminating case of altered mental status & electrical instability due to digitalis poisoning. Program director Dr. Alex Auseon and APD Dr. Mayank Kansal provide the E-CPR and a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Tommy Das with mentorship from University of Maryland cardiology fellow Karan Desai.   Jump to: Patient summary - Case media - Case teaching - References Episode graphic by Dr. Carine Hamo CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor RollSubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Check out CardioNerds SWAG! Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A woman in her late 80s with history of systemic arterial hypertension and dementia presented with 2 weeks of nausea, vomiting, confusion, and yellow-tinted vision. When she presented to the hospital, initial history was limited as her caregiver was unaware of her medications and medical history. An initial ECG showed isorhythmic A-V dissociation and scooping ST segments laterally. Given her clinical history, this raised the suspicion for Digoxin toxicity, and a serum digoxin level was significantly elevated. However, this was not a home medication for the patient, nor did she have access to it! Listen to the episode now as the UIC Cardionerds masterfully take us through this case that would surely stump Dr. House!   Case Media through the Differential ABCDEFClick to Enlarge A. Initial ECGB. CXR- Patchy opacities of the left lower lobe consistent with pulmonary edema and/or aspiration​ pneumonia.C. Repeat ECG: AF with AV block, persistent scooped T waves​D. Post arrest ECG: Flutter/fib with AV block, VERY LONG PAUSES up to 6 secondsE. ECG post TVP: A flutter, slow V response (pacing picking up), intrinsic ventricular rate 20-40, PM set to 50 bpmF. Most recent ECG: Normal sinus rhythm TTE Episode Schematics & Teaching The CardioNerds 5! – 5 major takeaways from the #CNCR case 1) This episode featured a challenging case of digitalis toxicity. Cardionerds, what is the mechanism of action of cardiac glycosides?   Cardiac Glycosides (such as digoxin, digitalis, and oubain), inhibit the myocardial Na/K ATPase pump. This leads to an increased concentration of intracellular sodium, which then drives the influx of calcium into cardiac myocytes via the Na/Ca exchanger. This increase in intracellular calcium leads to further calcium release from the sarcoplasmic reticulum making even more calcium available to bind to troponin, increasing contractility. In addition to their effect on inotropy, cardiac glycosides increase vagal tone, reducing SA node activity and slowing conduction through the AV node by increasing the refractory period  2) The first published account of digitalis to treat heart failure dates back to the 18th century, when botanist and physician William Withering published "An account of the Foxglove and some of its medical uses with practical remarks on dropsy, and other diseases". A lot has changed over the years; what are some of the uses of digoxin in the modern day?   The DIG trial (1997) demonstrated a reduction in hospitalizations in patients with HFrEF treated with digoxin. However, no impact on mortality was shown. A major limitation from randomized trials of digoxin is the lack of contemporary background HF treatment (e.g., ARNI, SGLT2i, MRA, Device Therapy). Thus, its role in modern HFrEF management is typically limited to reducing hospitalizations in patients with persistent NYHA Class III or IV symptoms despite maximally tolerated guideline-directed medical therapy Digoxi...

Editor's Summary by Howard Bauchner, MD, Editor in Chief of JAMA, the Journal of the American Medical Association, for the December 22/29, 2020 issue

Kathryn Solie shares about engaging energetically with poisonous plants for healing. You’ll also hear about: Attuning to the language of the plants  Therapy as magic  What is poison and how to engage with poison plants  ♥♥♥ Join The Earth Speak Collective Membership! Join like-hearted folks in a sacred container and community where you'll: Connect deeply to yourself, others, nature & spirit Learn to trust your intuition Activate your Earth magic Expand your healing & divination skills Put your intuition into practice in everyday life Stop feeling lonely on your spiritual path Embody & express your creative power & truths Experience safe space without agenda or judgement When you join the Collective, you get access to all of our past workshops, any live workshops happening while you're a member, live weekly energetic reset calls, monthly community rituals, all the secret episodes, member-run meetups to explore magical topics, and a lively members only forum (that's not on FB!). ▶▶▶ Learn more and sign up for the Collective membership here: https://www.earthspeak.love/collective ***** Kathryn Solie is an herbalist specializing in ‘poisonous’ plants & plant consciousness, a tarot reader, and a meditation enthusiast. She works to create community where people can reconnect with the ancient human lineage of plant spirit communication. She gives voice to the almost forgotten medicine of ‘poisonous’ plants through her courses and other offerings. We are thrilled to share that on the 29th of December, Kathryn is hosting a workshop with Earth Speak, all about Poison Plant Speak! In this workshop, you’ll be introduced to working with poisonous plants through plant spirit communication as they guide you to your whole, true self. This is a skill that everybody can develop! You do not need any prior experience with spiritual work, witchcraft, or herbalism - all levels of experience are welcome. In this episode, we talk about: Working with the plants of our lineage  What is poison and what does it mean to take the poison path  Communicating with plant consciousness Why the dose makes the poison The story of Persephone and the Underworld  The current collective Tower moment  Kathryn's experience with body-centered psychotherapy  Making healing modalities more accessible The space is the medicine We are nature  Cycles of the Underworld and shadow self Being disconnected from the cyclical nature of being Why the poisonous plants are the plants of the Underworld  Coffee as plant medicine Learning the language of the body and your intuition Engaging with poison plants for healing How the plants show up when you need them most Journeying with poisonous plants Perception as healing  Why shouldn’t ingest poisonous plants The poison, the medicine, and the folklore of foxglove Kathryn's upcoming workshop with Earth Speak - Poison Plant Speak And so much more! Bonus Secret Episode! Secret episode with Kathryn Solie coming soon at https://www.earthspeak.love/secret. Links: Join the Earth Speak Collective Membership at https://www.earthspeak.love/collective Learn more about Kathryn’s offerings at www.kathrynsolie.com/ Connect with Kathryn on Instagram @persephonespath Connect with Kathryn on Facebook @persephonespath0 Support Kathryn on Patreon @kathrynsolie Sign up for the Poison Plant Speak Workshop  Get the secret episodes at https://www.earthspeak.love/secret References: Henbane https://en.wikipedia.org/wiki/Hyoscyamus_niger  Rainbow Bridge to Asgard https://en.wikipedia.org/wiki/Bifr%C3%B6st  Mandrake https://en.wikipedia.org/wiki/Mandrake  Amanita muscaria https://en.wikipedia.org/wiki/Amanita_muscaria  Paracelsus https://en.wikipedia.org/wiki/Paracelsus   Monkshood https://en.wikipedia.org/wiki/Aconitum   Persephone https://en.wikipedia.org/wiki/Persephone  The Tower https://en.wikipedia.org/wiki/The_Tower_(Tarot_card)  Rider-Waite https://en.wikipedia.org/wiki/Rider-Waite_tarot_deck  Hakomi https://en.wikipedia.org/wiki/Hakomi  Somatic Experiencing https://en.wikipedia.org/wiki/Somatic_experiencing  Ayahuasca https://en.wikipedia.org/wiki/Ayahuasca  Holotropic Breathwork https://en.wikipedia.org/wiki/Breathwork  Datura https://en.wikipedia.org/wiki/Datura   Shakti https://en.wikipedia.org/wiki/Shakti  Shiva https://en.wikipedia.org/wiki/Shiva  Three of Swords https://en.wikipedia.org/wiki/Three_of_Swords  Ten of Swords https://en.wikipedia.org/wiki/Ten_of_Swords  Clairvoyance https://en.wikipedia.org/wiki/Clairvoyance  Kathryn’s 6 week Poison Plant course https://www.kathrynsolie.com/poisonous-plant-medicine-course   Duck Duck Go https://duckduckgo.com/about  Belladonna https://en.wikipedia.org/wiki/Atropa_belladonna  Yew Tree https://en.wikipedia.org/wiki/Taxus_baccata  Hellebore https://en.wikipedia.org/wiki/Hellebore  Foxglove https://en.wikipedia.org/wiki/Digitalis   Saturn Return https://en.wikipedia.org/wiki/Saturn_return  Lisa Frank https://shop.lisafrank.com/  Witches Confluence https://witchesconfluence.org/  Nightshade Family https://en.wikipedia.org/wiki/Solanaceae  Brugmansia https://en.wikipedia.org/wiki/Brugmansia  Tropane alkaloid https://en.wikipedia.org/wiki/Tropane_alkaloid  William Withering https://www.britannica.com/biography/William-Withering  Digoxin https://en.wikipedia.org/wiki/Digoxin  ► Leave us a written review on iTunes, and get shouted out on the show! Theme music is “It’s Easier” by Scarlet Crow http://www.scarletcrow.org/ and “Meeting Again” by Emily Sprague  https://mlesprg.info/ ► Join the Earth Speak Collective Membership at https://www.earthspeak.love/collective Follow Earth Speak on Instagram and tag us when you share @earthspeak https://www.instagram.com/earthspeak

Kathryn Solie shares about engaging energetically with poisonous plants for healing. You’ll also hear about: Attuning to the language of the plants  Therapy as magic  What is poison and how to engage with poison plants  ♥♥♥ Join The Earth Speak Collective Membership! Join like-hearted folks in a sacred container and community where you'll: Connect deeply to yourself, others, nature & spirit Learn to trust your intuition Activate your Earth magic Expand your healing & divination skills Put your intuition into practice in everyday life Stop feeling lonely on your spiritual path Embody & express your creative power & truths Experience safe space without agenda or judgement When you join the Collective, you get access to all of our past workshops, any live workshops happening while you're a member, live weekly energetic reset calls, monthly community rituals, all the secret episodes, member-run meetups to explore magical topics, and a lively members only forum (that's not on FB!). ▶▶▶ Learn more and sign up for the Collective membership here: https://www.earthspeak.love/collective ***** Kathryn Solie is an herbalist specializing in ‘poisonous’ plants & plant consciousness, a tarot reader, and a meditation enthusiast. She works to create community where people can reconnect with the ancient human lineage of plant spirit communication. She gives voice to the almost forgotten medicine of ‘poisonous’ plants through her courses and other offerings. We are thrilled to share that on the 29th of December, Kathryn is hosting a workshop with Earth Speak, all about Poison Plant Speak! In this workshop, you’ll be introduced to working with poisonous plants through plant spirit communication as they guide you to your whole, true self. This is a skill that everybody can develop! You do not need any prior experience with spiritual work, witchcraft, or herbalism - all levels of experience are welcome. In this episode, we talk about: Working with the plants of our lineage  What is poison and what does it mean to take the poison path  Communicating with plant consciousness Why the dose makes the poison The story of Persephone and the Underworld  The current collective Tower moment  Kathryn's experience with body-centered psychotherapy  Making healing modalities more accessible The space is the medicine We are nature  Cycles of the Underworld and shadow self Being disconnected from the cyclical nature of being Why the poisonous plants are the plants of the Underworld  Coffee as plant medicine Learning the language of the body and your intuition Engaging with poison plants for healing How the plants show up when you need them most Journeying with poisonous plants Perception as healing  Why shouldn’t ingest poisonous plants The poison, the medicine, and the folklore of foxglove Kathryn's upcoming workshop with Earth Speak - Poison Plant Speak And so much more! Bonus Secret Episode! Secret episode with Kathryn Solie coming soon at https://www.earthspeak.love/secret. Links: Join the Earth Speak Collective Membership at https://www.earthspeak.love/collective Learn more about Kathryn’s offerings at www.kathrynsolie.com/ Connect with Kathryn on Instagram @persephonespath Connect with Kathryn on Facebook @persephonespath0 Support Kathryn on Patreon @kathrynsolie Sign up for the Poison Plant Speak Workshop  Get the secret episodes at https://www.earthspeak.love/secret References: Henbane https://en.wikipedia.org/wiki/Hyoscyamus_niger  Rainbow Bridge to Asgard https://en.wikipedia.org/wiki/Bifr%C3%B6st  Mandrake https://en.wikipedia.org/wiki/Mandrake  Amanita muscaria https://en.wikipedia.org/wiki/Amanita_muscaria  Paracelsus https://en.wikipedia.org/wiki/Paracelsus   Monkshood https://en.wikipedia.org/wiki/Aconitum   Persephone https://en.wikipedia.org/wiki/Persephone  The Tower https://en.wikipedia.org/wiki/The_Tower_(Tarot_card)  Rider-Waite https://en.wikipedia.org/wiki/Rider-Waite_tarot_deck  Hakomi https://en.wikipedia.org/wiki/Hakomi  Somatic Experiencing https://en.wikipedia.org/wiki/Somatic_experiencing  Ayahuasca https://en.wikipedia.org/wiki/Ayahuasca  Holotropic Breathwork https://en.wikipedia.org/wiki/Breathwork  Datura https://en.wikipedia.org/wiki/Datura   Shakti https://en.wikipedia.org/wiki/Shakti  Shiva https://en.wikipedia.org/wiki/Shiva  Three of Swords https://en.wikipedia.org/wiki/Three_of_Swords  Ten of Swords https://en.wikipedia.org/wiki/Ten_of_Swords  Clairvoyance https://en.wikipedia.org/wiki/Clairvoyance  Kathryn’s 6 week Poison Plant course https://www.kathrynsolie.com/poisonous-plant-medicine-course   Duck Duck Go https://duckduckgo.com/about  Belladonna https://en.wikipedia.org/wiki/Atropa_belladonna  Yew Tree https://en.wikipedia.org/wiki/Taxus_baccata  Hellebore https://en.wikipedia.org/wiki/Hellebore  Foxglove https://en.wikipedia.org/wiki/Digitalis   Saturn Return https://en.wikipedia.org/wiki/Saturn_return  Lisa Frank https://shop.lisafrank.com/  Witches Confluence https://witchesconfluence.org/  Nightshade Family https://en.wikipedia.org/wiki/Solanaceae  Brugmansia https://en.wikipedia.org/wiki/Brugmansia  Tropane alkaloid https://en.wikipedia.org/wiki/Tropane_alkaloid  William Withering https://www.britannica.com/biography/William-Withering  Digoxin https://en.wikipedia.org/wiki/Digoxin  ► Leave us a written review on iTunes, and get shouted out on the show! Theme music is “It’s Easier” by Scarlet Crow http://www.scarletcrow.org/ and “Meeting Again” by Emily Sprague  https://mlesprg.info/ ► Join the Earth Speak Collective Membership at https://www.earthspeak.love/collective Follow Earth Speak on Instagram and tag us when you share @earthspeak https://www.instagram.com/earthspeak

In the first episode in the mini-series on narrow therapeutic index drugs, we're starting with warfarin and digoxin. I speak about INR, indications of warfarin and digoxin, counselling points and what to watch out for in practice.

CardioNerds (Amit Goyal & Daniel Ambinder) join Stanford cardiology fellows (Pablo Sanchez, Natalie Tapaskar, Jimmy Tooley) for tacos while enjoying the sunshine on the Stanford Oval! They recount the story of a man with adult congenital heart disease (ACHD): L-TGA (levo-transposed great arteries) with double inlet LV post-Fontan complicated by VF arrest. Dr. Christiane Haeffele provides the E-CPR and program director Dr. Joshua Knowles provides a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Evelyn Song with mentorship from University of Maryland cardiology fellow Karan Desai and Cleveland clinic cardiology fellow Josh Saef. Jump to: Patient summary - Case media - Case teaching - References The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus. We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director. CardioNerds Case Reports PageCardioNerds Episode PageCardioNerds AcademySubscribe to our newsletter- The HeartbeatSupport our educational mission by becoming a Patron!Cardiology Programs Twitter Group created by Dr. Nosheen Reza Patient Summary A man in his mid-30s with past medical history notable for L-TGA (levo-transposed great arteries) with double inlet LV s/p Fontan palliation was playing golf when he suddenly collapsed.  EMS arrived after three minutes of bystander CPR. An AED indicated the patient had suffered a VF arrest. ROSC was achieved after 1 round of Epi and 1 shock delivered. He was intubated and started on targeted temperature management protocol. Home medications were  notable for digoxin 0.25mg daily, sotalol 120mg BID, and warfarin 5mg daily. Initial labs were notable for Na 127, K 5.4, Cr 1.0 (unknown baseline), INR 4.5, Lactate 4.6, Troponin-I 0.532, VBG 7.06/61, and random Digoxin level 2.7.  EKG showed AV sequential pacing at a rate of 70 bpm. QTc prolonged at 571ms. No ischemic ST changes. Device interrogation showed sustained VT for 5 minutes prior to external shock. No internal shock was delivered. He was initially stabilized and his acidosis and hyperkalemia were corrected. Course was complicated by hemoptysis due to alveolar hemorrhagic and he was given concentrated prothrombin complex to reverse his coagulopathy. He eventually stabilized, and a formal TTE was obtained which showed a hypoplastic RV, single dilated LV with an akinetic posterior wall and hypokinetic lateral wall, all similar to his prior TTE in 2019. No obstruction noted at the IVC/Fontan anastomotic site. Coronary angiogram performed after his kidney function improved also did not show any significant obstructions or coronary anomalies. After multidisciplinary discussion, his VF arrest was attributed to a combination of prior ventricular fibrosis/scar, suspected digoxin toxicity, sotalol, dehydration, and renal failure. He had a subcutaneous ICD lead placed and was ultimately discharged home.  Case Media ABClick to Enlarge A. CXRB. ECG Episode Schematics & Teaching Coming soon! Click to enlarge! The CardioNerds 5! – 5 major takeaways from the #CNCR case

Written By: Caleb Dusdal Peer Review: Thomsen D'hont https://thegenerehlist.ca/2020/11/01/episode-two-acls-part-i/www.thegenerehlist.ca 1. Keep up to date with ACLS recommendations 2. Know how to recognize and defibrillate a patient with Ventricular Fibrillation, or ventricular tachycardia that is either pulseless or symptomatic. 3. Be able to diagnose worrysome arrhythmias such as: a. Ventricular tachycardia b. Ventricular fibrillation c. Supraventricular tachycardia d. Atrial fibrillation e. Second and third-degree heart block 4. Know when to suspect a few specific causes of arrhythmias, even before confirmatory testing. a. Hyperkalemia b. Digoxin toxicity c. Cocaine intoxication 5. Know how and when to ensure adequate ventilation and secure the airway in a timely manner 6. In patients who do require resuscitation, you want to be able to assess the context to help decide when stopping resuscitation is the most appropriate decision. 7. Patients who arrest or are at risk of arresting, with serious medical problems or end stage disease, you need to know how and when to discuss code status and making end-of-life decisions 8. Ensure you attend to the family members as well, both during and after resuscitation the patient. Eg. Counselling availability, whether or not they are present in the code, etc. 9. In paediatric resuscitation, know what resources you can use to determine the correct drug dosing and tube sizes. As well as how to use these.  

What was it like to be born in 1965 with a severe congenital heart defect in Venezuela? What kind of care was available there? What was a parent to do?Tune in to this week's episode of "Heart to Heart with Anna" to hear Belen Blanton talk with Anna about her heart journey, how she made it to the USA, and why she has started a nonprofit organization to help children with congenital heart defects in her native country - Venezuela.Here is the foundation Belen has started for children with CHDs in Venezuela on Facebook:@Fundacion Estrellita de Belenand on the Internet: www.fundacionestrellitadebelen.orgFind Belen on Instagram:@youdonthavetolooksickLinks to 'Heart to Heart with Anna' Social Media and Podcast Pages:Apple Podcasts (https://itunes.apple.com/us/podcast/heart-to-heart-with-anna/id1132261435?mt=2)Facebook (https://www.facebook.com/HearttoHeartwithAnna/)YouTube (https://www.youtube.com/channel/UCGPKwIU5M_YOxvtWepFR5Zw)Instagram (https://www.instagram.com/hugpodcastnetwork/)If you enjoy this program and would like to be a Patron, please check out our Patreon page (https://www.patreon.com/HeartToHeart)Support the show (https://www.patreon.com/HearttoHeart)

Kimberly was a member of the Dr. Joanna Burdette lab and worked on projects related to the origins of ovarian cancer. She also discusses the learning curve of being a new member of a research lab. Kimberly's citations: Ren, Y., Ribas, H. T., Heath, K., Wu, S., Ren, J., Shriwas, P., & Kinghorn, A. D. (2020). Na+/K+-ATPase-Targeted Cytotoxicity of (+)-Digoxin and Several Semisynthetic Derivatives. Journal of Natural Products, 83(3), 638-648. [link] Hardy, L. R., Pergande, M. R., Esparza, K., Heath, K. N., Önyüksel, H., Cologna, S. M., & Burdette, J. E. (2019). Proteomic analysis reveals a role for PAX8 in peritoneal colonization of high grade serous ovarian cancer that can be targeted with micelle encapsulated thiostrepton. Oncogene, 38(32), 6003-6016. [link] Ren, Y., Tan, Q., Heath, K., Wu, S., Wilson, J. R., Ren, J., ... & Chen, X. (2020). Cytotoxic and non-cytotoxic cardiac glycosides isolated from the combined flowers, leaves, and twigs of Streblus asper. Bioorganic & Medicinal Chemistry, 115301. [link]

Digitalis, digoxin toxicity, dig toxic, apical pulse, Lanoxin, lanoxicaps, Digitek, Digitaline Nativelle, Digox, Lanoxicaps Lanoxin Lanoxin Pediatric Atrial Fibrillation, Cardiac Pharmacology, heart failure pharmacology, HF drugs, CHF drugs, Cardiac glycoside, Chronotropic, inotropic, Dromotropics Free quiz & full course at https://Simplenursing.com/nursing-school  Pharmacology Master Class - 100 videos not on YouTube - Try it for Free!    Pharmacology Master Class - Try it for Free: https://Simplenursing.com/nursing-school  100 videos not on YouTube    FREE Access to new app + 1,000 videos not on youtube!  https://Simplenursing.com/nursing-school   NCLEX FREE TRIAL:  https://simplenursing.com/NCLEX   STAY IN TOUCH

Episode 9 of Dose Makes the Poison: The Toxcast. Let's talk about Digitalis (digoxin, digitoxin) and Convallaria (convallatoxin) - what are these plants? What are these poisons? How do they work in the body? Have they been used for murder? Poisonings? Have they been referenced in pop culture? All audio clips are taken from Kevin Shanks' music and movie archives in which he personally purchased. He does not own any licenses to any of the sounds or music, but used them for discussion and educational purposes. If you have an issue with their use in this podcast episode, please contact dosemakesthepoisonpodcast@gmail.com. Intro and Outro music is Psychedelic Mushrooms by T Morri. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app

Dr Greg Hundley: Welcome listeners. This is Dr Greg Hundley from the VCU Pauley Heart Center in Richmond, who is in the second of his two-week stint without his dear friend, Dr Carolyn Lam who will be returning in a week or two. Our feature article this week is from Dr Mikhail Kosiborod from Saint Luke's Mid America Heart Institute and the Georgia Institute for Global Health, and University of New South Wales. And we'll review the effects of dapagliflozin on quality of life and other metrics in patients with heart failure and reduced ejection fraction. But first, let's have a look at the other articles in this issue and just like last week we've got four other original manuscripts. The first two are sort of clinically related and that very first article comes from Dr Ben Levine from University of Texas Southwestern and he serves as the corresponding author and he's examining future predictors of the development of heart failure and preserved ejection fraction or HFpEF. His team tested the hypothesis as to whether patients with LVH and elevated cardiac biomarkers would demonstrate elevated LV myocardial stiffness when compared to healthy controls as a key marker for future HFpEF. The team recruited 46 patients with LVH. The LV septum was greater than 11 millimeters and elevated cardiac biomarkers, so the NTproBNP was greater than 40 or the cardiac troponin T was greater than 0.6. And they were recruited along with 61 age and sex-matched cohort of healthy controls. To define LV pressure volume relationships, right heart catheterization and 3D echocardiography were performed while preload was manipulated using lower body negative pressure and rapid saline infusion. They found that the left ventricle was less distensible in the LVH patients relative to the controls, that is they had a smaller volume for the same filling pressure. When preload was expressed as transmural filling pressure or wedge pressure minus right atrial pressure left ventricular myocardial stiffness was nearly 30% greater in the LVH group compared to the controls. The author's note that although LV myocardial stiffness of LVH patients was greater than that of the healthy controls at this relatively early stage, further studies are required to clarify whether interventions such as exercise training to improve LV compliance may prevent the full manifestation of the HFpEF syndrome in these high-risk individuals. Well, the second paper comes from Professor John McMurry of the British Heart Foundation Cardiovascular Research Center at the University of Glasgow in the United Kingdom. And the paper is somewhat similar to our feature article because it emanates from the DAPA Heart Failure dataset that we will hear about later. So in this paper, the authors examined the effects of Dapagliflozin according to age, given potential concerns about the efficacy and safety of therapies in the elderly in the prior trial. A clinical trial that as we know, demonstrated that a reduced risk of mortality and heart failure hospitalizations occurred in patients with HFrEF. So in this current study, a total of 4,744 patients that were 22 to 94 years of age were randomized. 636 were less than 55 years of age, 1,242 we're 55 to 64 years of age 1,717 were 65 to 74, and finally 1,149 were greater than 75 years of age. Consistent benefits were observed for the components of the primary outcome of all-cause mortality and symptoms across all the age groups. Although the adverse events and the study drug discontinuation increased with age, neither was significantly more common with Dapagliflozin across any of the age groups. There was no significant imbalance and tolerability or safety events between Dapagliflozin and placebo, even in the very old population group. So we'll have more to discuss later in the feature discussion with a second paper that really looks also at the DAPA-HF study. The next original article comes from our world of Basic Science and it reports that the deficiency of circulating monocytes ameliorates the progression of myxomatous valve degeneration in the Marfan syndrome. And this paper comes from Dr Katherine Yutzey from Cincinnati Children's Medical Center. Well, first is some background, leukocytes comprised primarily of macrophages have recently been detected in myxomatous valves, but the timing of the presence and the contributions of these cells in myxomatous mitral valve degeneration is not known. So the authors found in this study that Marfan syndrome mice recapitulated the histopathologic features of myxomatous valve disease by two months of age, including mitral valve thickening, increased leaflet cellularity and extracellular matrix abnormalities characterized by proteoglycan accumulation and collagen fragmentation. Concurrently, disease mitral valves of the Marfan syndrome mice exhibited a marked increase of infiltrating and resident macrophages along with increased chemokine activity and inflammatory extracellular matrix modification. Likewise, mitral valve specimens obtained from gene-edited Marfan syndrome pigs as well as human subjects exhibited increased monocytes and macrophages detected by immunofluorescence. So remarkably deficiency of monocytes was protected against mitral valve disease progression resulting in a significant reduction of macrophages, had minimal leaflet thickening and preserved mitral valve integrity. So the authors identify for the first time in this interesting study from the world of basic science that monocytes are a viable candidate for targeted therapy in myxomatous valve degeneration. The second basic science original article in this issue is entitled "Genetic IL-6 Signaling Deficiency Attenuates Cardiovascular Risk in Clonal Hematopoiesis" and the corresponding there is Pradeep Natarajan from the Mass. General is background clonal hematopoiesis of indeterminate potential or CHIP is a term that refers to clonal expansion of hematopoietic STEM cells due to acquired leukemic mutations in genes such as DNMT3A or TET2. In humans, CHIP associates with prevalent myocardial infarction. In mice CHIP accelerates atherosclerosis and increases IL-6 and IL-1 beta expression raising the hypothesis that IL-6 pathway antagonism in CHIP carriers would decrease cardiovascular disease risk. So in this study, the authors observed some really exciting results. They analyzed over 34,000 samples from the UK Biobank and identified 1,079 individuals with CHIP, including 432 with large clones an LV fraction greater than 10%. During a 6.9-year median follow-up CHIP presence was associated with increased incidents, cardiovascular disease event risk with greater risk from large CHIP clones. IL6R attenuated cardiovascular event risk among participants with large CHIP clones but not in individuals without CHIP. This really exciting research results suggest that CHIP is associated with increased risk of incident cardiovascular disease. And among carriers of large CHIP clones, genetically reduced IL-6 signaling abdicated this risk. Really exciting results in an emerging area of science. So what else is in the issue? Well, in our in depth review feature, Professor Stephan Rosencrantz from the University of Cologne Heart Center reviews the systemic consequences of pulmonary hypertension with right side heart failure. And then an On My Mind piece, our own associate editor, Dr Vlad Zaha coupled with doctors Walter Myers and Javid Moslehi from Vanderbilt discuss the impact of evolving immunotherapies for cancer and their impact on the cardiovascular system. In our mailbag, Dr Xiayan Shen from the Medical Classification Center of the Singapore Armed Forces discusses in a research letter the prevalence of Brugada Syndrome in a large Singaporean young male population. In letters to the editor, Dr Muddassir Mehmood from University of Tennessee Medical Center in one letter and Dr Goodarz Danaei from Boston in a response letter discuss the importance of diet relative to the development of HFpEF and how heart failure may be coded in by the World Health Organization when assessing global cardiovascular outcomes. Bridget Kuhn in our cardiology news feature reports on preliminary results from the International Childhood Cardiovascular Cohort or i3C Consortium that was presented at the 2019 European Society of cardiology Congress. The i3C Consortium used data on 40,000 patients who participated in seven major longitudinal cohort studies that evaluated childhood cardiovascular risk factors from repeated measures during childhood and adolescence. And finally, our own Molly Klemarczyk at Circulation gathered and combined a very nice serial update that highlights important articles from our circulation family of journals, including electrophysiology, imaging, heart failure, and others. Well, listeners, that's a summary of what's in the journal. But let's now proceed to our feature discussion to learn more about the rapidly emerging field of SGLT2 inhibition. Well listeners, we are very excited for this feature discussion we have today, Dr Mikhail Kosiborod from Saint Luke's Mid America heart Institute and our own associate editor, Dr Justin Ezekowitz from Alberta, Canada. And we're going to be discussing the paper related to the effects of Dapagliflozin on symptoms, function and quality of life in patients with heart failure and reduced ejection fraction. They're going to be presenting results from the DAPA Heart Failure trial. Well Mikhail, I was wondering could you orient us a little bit to the DAPA heart failure trial. And then what was the hypothesis that you were trying to address in the current study? Dr Mikhail Kosiborod: DAPA-HF was the first heart failure outcome trial trying to answer two critical questions about the effects of SGLT2 inhibitors in patients with heart failure and reduced ejection fraction. We knew from prior trials, outcome trials in patients with diabetes SGLT2 agents can effectively prevent heart failure inpatients, overwhelming majority of which did not have heart failure and baseline. But what we didn't know was whether these agents can also be used as therapies for patients with established heart failure, and specifically heart failure with reduced ejection fraction. And they reduce death or worsening heart failure in the patient population. And the second question was whether that effect, if in fact this medications can significantly improve outcomes in patients with heart failure reduced ejection fraction. Can they do that even in patients who do not have type 2 diabetes? Because, in a diabetes trial it appears that that heart failure protective effect may be completely independent on the hemoglobin AONC. And so DAPA-HF was specifically designed to test those two hypotheses. It enrolled about 4,800 patients with heart failure and reduced ejection fraction about 45% of which had types 2 diabetes. And there's a majority of us, 55% did not. And the main trial results that were published prior to risk analysis showed that in fact dapagliflozin significantly reduced the risk of the composite endpoint of cardiovascular death and worsening heart failure. It was a 26% relative risk reduction and the effects were identical in patients with or without type two diabetes. So both of those hypothesis were proven to be correct. It was effective therapies for established heart failure and reduced ejection fraction, and it was equally effective regardless of diabetes status. Now what we did in this study is really trying to understand the effects not just on cardiovascular deaths and hospitalization for heart failure, but on health status, which is symptoms, physical limitations, and quality of life. He knows that heart failure is a debilitating disease, causes high burden of symptoms, and physical limitations, has adverse impact on quality of lives. We know that two key goals of managing heart failure are to; one, reduce deaths and hospitalizations for heart failure and two to reduce the burden of symptoms and physical limitations and improve the quality of life. So, that was really the focus of this specific analysis that we're talking about today. Dr Greg Hundley: Excellent. So I understand you use the KCCQ-12, maybe help us understand what that test is and then tell us a little bit about your methods and your study population. Did you use the whole study population? Dr Mikhail Kosiborod: KCCQ stands for Kansas City Cardiomyopathy Questionnaire and we actually in the study we use KCCQ-23 which is the full Kansas City Cardiomyopathy Questionnaire, consists of 23 items. And it a disease-specific tools for evaluating health status and heart failure. So it essentially assesses four key domains, which are the symptom burden, physical implementations, quality of life, and social limitations. In this particular study is a primary endpoint as a primary part of the KCCQ as KCCQ total symptom score, which is a domain that focuses on symptoms. And the idea behind KCCQ is that you have a debilitating disease, which is heart failure. That disease has impact on the patient by causing symptoms, the symptoms then translate to physical limitations. And the combination of the symptom burden physical limitations has an impact on quality of life and social limitation. So that's why are this four different domains assessing these four components of the adverse effects of the heart failure compared to health status. And just very briefly, to mention that KCCQ has been proven to be responsive to clinical change. It's highly for data predictive of death and hospitalizations from heart failure. It has been extensively validated both of them hearts failure was reduced enters and the ejection fraction. And so we essentially focused, or the primary focus of the paper was really to evaluate the effect of dapagliflozin versus placebo on a Kansas City Cardiomyopathy Questionnaire or KCCQ level symptom score. But we also looked at other domains as well. We looked at the clinical summary score, which includes both symptoms and physical limitations and we looked at the overall summary score, which includes all of the four domains that I mentioned before. Dr Greg Hundley: What did you find? Dr Mikhail Kosiborod: The patients treated with dapagliflozin had a greater improvement in health status as assessed by a KCCQ total symptom score or for that matter KCCQ clinical summary overall summary score as compared to patients treated with placebo. So if you look at the mean effect, there is some improvement in the patients taking placebo. That's what we call a placebo effect. And it's very commonly seen in clinical trials. We assessed health status, but there was a greater improvement with dapagliflozin as compared with the placebo, it was statistically significant even in four months. But as the effects were further amplified to eight months and this differences were, I would say favorable when you kind of compare the effect of Dapagliflozin versus other established heart failure therapies when you look at the effects on health status. What I think was even more important than analysis from a clinician standpoint, and then they think it's actually much more meaningful clinically is what we call a responder analysis. And that's where we look as the proportion of patients that have a clinically meaningful improvement with one type of therapy versus other in this case Dapagliflozin versus placebo. So it's been previously established that at five-point difference or a five-point change rising KCCQ is what's considered to be clinically meaningful or minimal clinically meaningful difference. So a 5.2 grade deterioration KCCQ means it's a clinically important deterioration. And a five-point or greater improvement is a clinically important improvement. And then we also looked at the proportion of patients with moderate and large improvements in health status as well defined as STEM point of grade of two, or two point a great improvement. And essentially what we found was that significantly fewer patients treated with dapagliflozin and as compared with placebo had a clinical importance deterioration. And significantly greater proportion of patients treated with dapagliflozin has small, moderate, large improvements in health status. And the numbers needed to treat to see those differences, as the small moderate large improvements was very favorable ranging typically between 12 and 18 and over eight-months-treatment period. Dr Greg Hundley: Outstanding. So both clinically relevant as well as statistically significant findings. Now we're going to bring in Justin, our associate editor. Justin, help us put these results into the just our perspective in looking at SGLT2 inhibitors, particularly for treatment for heart failure. Dr Justin Ezekowitz: This is an exciting class of medications and we're eagerly awaiting these results because we saw the DAPA-HF Overall results. The majority of us treat patients with a pretty symptomatic disease and as such this quality of life is quite an important change. There's ongoing trials we're eagerly awaiting which are also going to be using other medications in the same class, but I think one question that remained was, are these simply improving symptoms by one meaning, so the total symptom score? Or the overall quality of life? And I think you nicely, elegantly portrayed that in the figures and you have. The one other part maybe Mikhail, you could expand upon, which is when you think about DAPA-HF, and the quality of life gains and across all the three different ways of looking at quality of life, where do you see this in terms of its relationship to other things that we know improve quality of life? Where we send patients, for example, CRT or put them on an RNE. Where does this fit on top of those types of changes? Dr Mikhail Kosiborod: Thanks Justin. I think it's a really important question because it says think critical from a clinical standpoint to put it in the context of other therapies that had been previously shown to improve health status, which means again, reduced symptoms, improve physical and patient quality of life. And there are a number of perhaps the types of therapies on heart failure and LVCF that have been evaluated particularly on side this one there also have been studies with exercise training in heart failure or and the ones that you brought up, which is cardiac resynchronization therapy in patients with heart failure reduced ejection fraction and left bundle branch block. And as that perhaps, if you kind of think about it. What are some of the most effective treatments to improve the health status? That is ones that we typically would consider as such, which is CRT in patients with half RAF and a left bundle branch block. And in fact, if you look at the mean effects dapagliflozin compares very favorably even with highly effective therapies such as TRT. Relatively few studies have previously reported to this responder in analysis. But if you look at Digoxin comparing those to dapagliflozin, one of the recent ones that I can think of is [inaudible 00:20:23], again dapagliflozin compares very favorably when you look at this types of responder analysis where again you look at proportion of patients, it was a clinically meaningful change. So I think the beautiful thing about putting the study in the context of further studies looking at health status and also in the original main results that were published from a DAPA-HF early this year is that it's really kind of a full house if you will. So as the agent reduced deaths, reduced hospitalizations and made patients feel better and all of that, with very favorable safety profile. So, if you kind of think about risk benefit analysis and you look at numbers need to treat both for clinical outcomes such as CVS and hospitalizations for heart failure for example, where health status, it looks really impactful from a clinical standpoint. Dr Greg Hundley: So relevance to other therapeutic interventions for heart failure is what this whole class of agents seems to be showing? So briefly, what do you see is the next important study in the field? Dr Mikhail Kosiborod: I will waffle on this question a little bit and say there was more than one, but my views are there kind of two key components to this. One is that there are additional trials going on and heart failure with reduced ejection fraction with other agents. And so seeing what happens with those other agents in the class in a similar patient population and whether is this a class effect or not? Now the diabetes trials would suggest that these may well be class effects but I think it's nice to have validation of that. I would say that is one real important questions that hopefully we will have additional answers to in the coming year or so. And the second and perhaps I would argue even more important question is whether these agents can also be effective in improving outcomes in patients with heart failure and preserved ejection fraction. That's a patient population that has also very high debilitating burden of symptoms that has poor prognosis and for which unlike them, half rubs, there are very few, if any medications that have been proven to be disease-modifying and actually have shown outcomes and benefit. So I would say those in my mind, are the two critical developments that we'll be seeing. And the good news is, there are the trials going on with more than one agent in a class and half to half as well. Great. Dr Greg Hundley: And Justin? Dr Justin Ezekowitz: Yeah, I think that there's been an explosion of therapies and Mikhail is bang on with this is the one class where we're excited about. I think the other groups of medications include Omecamtiv Mecarbil we'll know in a year or two. We'll hear more details in the spring and then there's a few other medications that Mikhail mentioned. I think this is a real good message though, that both HFrEF and HFpEF, it's the rise of medications again. Because we were on a device track for a while, but I think the medications have such more potent effect on the underlying structure and function that it's great to see that there's been such a development and explosion of medications that may obviate the need for implanted devices or advanced therapies, so we're very excited about that. Dr Greg Hundley: Outstanding. Well, listeners, we've had the opportunity to hear from Mikhail Kosiborod from Saint Luke's Mid America Heart Institute and our own associate editor, Dr Justin Ezekowitz from Alberta, Canada, and learn more about SGLT2 inhibition and its importance in improving clinically symptomatology both in those with diabetes and heart failure, but also those with heart failure alone. On behalf of Carolyn and myself, we wish you a great week and we look forward to running and having a coffee chat next week. Take care of. This program is copyright the American Heart Association, 2020  

Terkadang kita suka banget nemuin apa apa kalau Heart failure main kasih digoxin aja. Udah bener belom sih pemakaiannya? Yuk simak penjelasan nya!

Digoxin Mechanism of Action --- Support this podcast: https://anchor.fm/kamesa-anota/support

Celecoxib is easy to remember as its mechanism of action is "COX"-2 Inhibition. This can result in result in reduced prostaglandin formation and help with pain and inflammation. Kidney function is important to monitor in our patient on celecoxib. It is especially important in patients taking ACE inhibitors, ARBs, and/or diuretics. While GI bleed may be less likely with celecoxib compared to traditional NSAIDs like indomethacin and ibuprofen, it still needs to be monitored for. Digoxin concentrations may be increased with the use of celecoxib. Celecoxib is generally dosed twice per day as the half-life of the drug is in the ballpark of 10-12 hours.

Digoxin, acupuncture and angina, heart failure with preserved ejection fraction, bariatric surgery, and cardiac device complications are the topics John Mandrola covers in this week's podcast.

Commentary by Dr. Valentin Fuster

Podcast summary of articles from the October 2018 edition of Journal of Emergency Medicine from the American Academy of Emergency Medicine.  Topics include intranasal vasoconstrictors, pre-oxygenation with NIPPV and nasal cannula, cardiac glycoside toxicity, age adjusted D-dimer for pulmonary embolism, antibiotic use after abscess drainage, and board review on immune checkpoint inhibitor toxicities.  Guest speaker is Dr. Matthew Addis.

In this episode of the eLife Podcast, signs that trees exchange genes over hundreds of kilometres, how our gut bacteria protect us from plant toxins, and new insights into the placebo effect... Get the references and the transcripts for this programme from the Naked Scientists website

Tiffany Proffitt's Digoxin Overdose Review by Jesse Kellar, MD

Dr. Leonard Ganz discusses pharmacologic rate control of atrial fibrillation (AF) and findings of a recent study published in the Journal of the American College of Cardiology regarding the use of digoxin and mortality in patients with AF. Dr. Nancy Sokol hosts. Dr. Ganz is a clinical cardiologist and Director of Cardiac Electrophysiology at the Heritage Valley Health System, in Western Pennsylvania, and Section Editor of the cardiac arrhythmias section in UpToDate. Reference: Lopes RD, Rordorf R, De Ferrari GM, et al. Digoxin and Mortality in Patients With Atrial Fibrillation. J Am Coll Cardiol 2018; 71:1063. Contributor Disclosure: Speaker’s Bureau: Amgen [Heart failure (Ivabradine)]; Pfizer, BMS [Anticoagulation (Apixaban)]; St. Jude Medical, Biotronik [Cardiac rhythm (Pacemaker/ICD)]; Lundbeck [Orthostatic hypotension (Northera)]. Consultant/Advisory Boards: Unequal Technologies [Commotio cordis (Protective equipment)]. Equity Ownership/Stock Options: Unequal Technologies [Commotio cordis (Protective equipment/apparel)].

On this episode I explain digoxin pharmacology and also run through some scenarios where I've seen digoxin toxicity actually happen. I also discuss the relationship of low potassium and how digoxin can have an exacerbated effect in this setting.  Hope you enjoy the episode and please feel free to reach out and give me some feedback! All subscribers to the website/podcast will get access to a FREE Top 200 Drug Study Guide where I highlight the 3 most highly testable pearls from each medication (this is a 31 page PDF!)  In addition, you'll get a free 100 question pharmacology test.  Both resources are free, simply for following the podcast!  What are you waiting for? Click Here to Subscribe Eric Christianson, PharmD, BCGP, BCPS

Dr. Paul Wang:           Welcome to the monthly podcast On the Beat for Circulation Arrhythmia and Electrophysiology. I'm Dr Paul Wang, editor-in-chief, with some of the key highlights for this month's issue. We'll also hear from Dr. Suraj Kapa reporting on new research from the latest journal articles in the field.                                                 In our first article, Barry Maron associates report on the long term clinical course of hypertrophic cardiomyopathy patients following ICD therapy for ventricular arrhythmias. They studied a cohort of 486 high-risk hypertrophic cardiomyopathy patients with ICDs from eight international centers. Of these 486 patients over 6.4 years, 94 patients or 19% experienced appropriate ICD interventions, terminating VT or VF. Of the 94 patients receiving appropriate ICD therapy, 87 were asymptomatic or only mildly symptomatic at the time of appropriate ICD interventions. Of these 87 patients, 74 or 85% remained in classes one or two without significant change in clinical status of the subsequent 5.9 years up to 22 years. Among the 94 patients, there was one sudden death in three patients who died from non arrhythmic hypertrophic cardiomyopathy related processes. Post ICD intervention, freedom from hypertrophic cardiomyopathy, mortality was 100% at one year, 97% at five years, and 92% at 10 years, distinctly lower than the risk of ischemic or non ischemic cardiomyopathy in ICD trials.                                                 Hypertrophic cardiomyopathy patients with ICDs interventions reported the heightened anxiety and expectation of future shocks. However, they did not affect general psychological well-being or quality of life. The authors concluded that in hypertrophic cardiomyopathy, unlike ischemic heart disease, prevention of sudden death with ICD therapies unassociated with a significant increase in cardiovascular morbidity and mortality, nor transformation into heart failure deterioration, ICD therapy does not substantially impair overall psychological and physical well-being. In our next article, Abdulla Damluji and associates examined the cost of hospitalizations for cardiac arrest using the US nationwide inpatient sample from 2003 to 2012. Using the log transformation of inflation adjusted costs the authors examined 1,387,396 patients who were hospitalized after cardiac arrest. They had a mean age of 66 years. Inpatient procedures included coronary angiography in 15%, PCI in 7%, intra-aortic balloon pump in 4.4%, therapeutic hypothermia in 1.1%, and mechanical circulatory support in 0.1% of patients.                                                 Notably the rates of therapeutic hypothermia increased from 0 in 2003 to 2.7 in 2012, p less than 0.001. Both hospital charges inflation adjusted costs linear increased over time. In a multi-variant analysis predictors of inflation adjusted costs included large hospitals size, urban teaching hospital, and length of stay. Among co-morbidities, atrial fibrillation or fluid and electrolytes imbalance were the most common associated with cost. The authors found that during the period between 2003 and 2012 post cardiac arrest, hospitalizations had a steady rise and associated healthcare costs likely related to increase length of stay, medical procedures and systems of care.                                                 In our next paper, Peter Huntjens and associates examined intrinsic interventricular dyssynchrony as a predictor of human dynamic response to cardiac resynchronization. The authors use a cardiovascular computational model CircAdapt to characterize the isolated effect of intrinsic interventricular or intraventricular activation on resynchronization therapy response that is the change in LV dP/dt max. The simulated change in LV dP to dt max had a range of 1.3 to 26.5% increased considerably with increasing inter ventricular dyssynchrony. In contrast, the isolated effect of intra ventricular dyssynchrony was limited with the change in the LV dP/dt max range and the left ventricle from 12.3 to 18.3% in the right ventricle from 14 to 15.7%.                                                 Secondly, electrocardiographic imaging derived activation characteristics of 51 CRT candidates were used to create individual models of ventricular activation in CircAdapt. The model predicted change in LV dP/dt max was close to the actual value in left bundle branch block patients with 2.7% difference between measured and simulated when only intrinsic interventricular dyssynchrony was personalized. Among non left bundle branch block patients a change in LV dP/dt max was systematically over predicted by CircAdapt with a 9.2% difference between measured and simulated. Adding intra ventricular activation to the model did not improve the accuracy of response prediction. The authors found that computer revealed intrinsic interventricular dyssynchrony is the dominant component of the electrical substrate driving the response to CRT.                                                 In the next paper Kenji Kuroki and associates examined the use of voltage limit adjustment of substrate mapping and fast Fourier transform analysis of local ventricular bipolar electrograms during sinus rhythm to predict VT isthmuses. They performed these studies and nine post infarction patients who underwent catheter ablation for total of 13 monomorphic ventricular tachycardias. Relatively higher voltage areas on electroanatomical map or defined as high voltage channels, which were further classified as full or partial if the entire or more than 30% of the high voltage channel was detectable. 12 full high voltage channels were identified in seven of nine patients. Relatively higher fast Fourier transform areas were defined as high frequency channels, which were located on seven of 12 full high voltage channels. Five VT isthmuses or 71% were included in the seven full high voltage channels positive in high frequency channel positive sites.                                                 While no VT isthmuses were found in five full high voltage channel positive but high frequency channel negative sites, high frequency channels were identical to 9 out of 16 partial high voltage channels. Eight VT isthmuses or 89% were included in nine partial high voltage channel positive in high frequency channel positive sites, whereas no VTs isthmuses were found in the seven partial high voltage channel positive and high frequency channel negative sites.                                                 All high voltage channel positive in high-frequency channel positive sites predicted VT isthmus with a sensitivity of 100% and specificity of 80%. The authors concluded that based on this small series that combined use of voltage, limited adjustment and fast Fourier transform analysis may be useful method to detect VT isthmuses.                                                 In the next study, John Whitaker and associates examined the use of lesion index, LSI index, a proprietary algorithm combining contact force, radio-frequency application duration, and RF current. Cardiac CT was used to assess atrial tissue thickness. Ablation lines two to three per animal were created in the right atrium in seven mini pigs with point lesions using 25 watts of energy. Two weeks after the ablation, serial sections of targeted atrial tissue or examine histologically to identify gaps and transmural ablation. LSI guidelines had a lower incidence of histological gaps. Four gaps in the 69 catheter moved or 5.8% compared to ablation using LSI plus two millimeter lines in which there is seven gaps in 33 catheter moves or 21.2% and using LSI plus four millimeter lines in which there are 15 gaps in 23 moves or 65.2% p less than 0.0. The change in LSI was calculated retrospectively is a distance between two adjacent lesions above the mean LSI of the two lesions. Changing LSI values of 1.5 or less were associated with no gaps in transmural ablation.                                                 The authors concluded that in this mod of chronic atrial ablation delivery of uninterrupted transmural linear lesions may be facilitated using LSI to guide catheter movement. When change in LSI between adjacent legions is 1.5 millimeters or lower, no gaps in atrial linear lesions should be expected.                                                 In our next paper, Matthew Bennett and associate examined whether their response to antitachycardia pacing in patients with ICD could further discriminate ventricular from super ventricular arrhythmias in patients receiving ATP in the RAFT trial. The RAFT trial randomized 1,798 patients with New York Heart Association class two or three heart failure, left ventricular ejection fraction less than or equal to 30%, in QRS duration 120 millisecond or greater, to an ICD plus or a minus cardiac resynchronization. Beginning with 10,916 ATP attempts for 8,150 tachycardia episodes in 924 patients, the author's excluded tachycardias where ATP terminated the episode or were the specific etiology tachycardia was uncertain. In this study, they analyzed 3,676 ATP attempts delivered to 2,046 tachycardia episodes in 541 patients. The authors found that a shorter difference between the post pacing interval is PPI minus TCL, was more likely to be associated with VT than SVT, mean of 138.1 milliseconds for VT and 277.4 milliseconds for SVT p, less than 0.001. A PPI minus TCL value of less than or equal to 300 milliseconds had a sensitivity in 97.4% and a specificity of 28.3% for VT.                                                 The authors concluded that specifically the PPI minus TCL following antitachycardia pacing may help distinguish ventricular from supraventricular arrhythmias.                                                 In the next study, Shailee Shah and Amr Barakat and associates examined the outcomes after repeat AF ablation. The authors examined 137 patients out of a total of 10,378 patients undergoing Afib ablation who had had initial long-term success defined from recurrent arrhythmias for greater than 36 months off anti-arrhythmic drugs in subsequent underwent repeat ablation for recurrent atrial fibrillation. The median arrhythmia free period that define long-term success was 52 months. In redo-ablations reconnection of at least one of the pulmonary veins was found in 111 or 81% of patients. Additional non PV ablations were performed in 127 or 92.7% of patients. After a mean follow-up of 17 months, 103 patients or 75% were arrhythmia-free, 79 off anti-arrhythmics, and 24 on arrhythmics. The authors found that repeat ablations with re-isolation to the point of veins and modifying the atrial substrate had a good success rate.                                                 In the next article Qiongling Wang and associates hypothesized that genetic inhibition of CaMKII oxidation in a mouse model of Duchenne muscular dystrophy can alleviate abnormal calcium homeostasis thus preventing ventricular arrhythmias. The authors tested whether the selective loss of oxidation of the CaMKII effects ventricular arrhythmias in the mouse model of Duchenne muscular dystrophy. Genetic inhibition of ox-CaM kinase II by knocking replacement of the regulatory domain methionines with valines, which we'll call MMVV, prevented ventricular tachycardia in the mdx mice. Confocal calcium imaging of ventricular myocytes, isolated from the mdx MMVV mice revealed normalization of intra-calcium release events compared to myocytes from the mdx mice. Abnormal action potentials as assessed by optical mapping mdx were also alleviated by genetic inhibition of ox-CaMK II. Knockout of the NADPH oxidase regulatory sub-unit P 47 Fox normalized elevated ox-CaMK II, repaired intracellular calcium hemostasis and rescued inducible ventricular arrhythmias in the mdx mice. The authors concluded that inhibition of ROS or ox-CaMK II protects against pro-arrhythmic intracellular calcium handling, preventing ventricular arrhythmias in a mouse model of Duchenne muscular dystrophy.                                                 In the next article, Kyohei Marume and Teruo Noguchi and associates examined whether the combination of QRS duration of 120 milliseconds or greater in late gadolinium enhancement is a precise prognostic indicator for the primary endpoint of all cause death and a composite of sudden cardiac death or aborted sudden cardiac death in 531 patients with dilated cardiomyopathy. They also analyzed the association between the combination of late gadolinium enhancement and increased QRS duration in these end points among patients with a class one indication for implantable defibrillator. The author's divided study patients in three groups according to late gadolinium enhancement in QRS duration. Two negative indices that is late gadolinium enhancement negative and narrow QRS, one positive index with either late gadolinium enhancement positive or wide QRS or two positive indices late gadolinium positive and wide QRS and followed them for 3.8 years. Multiple variable Cox regression analysis identified to positive indices as significant predictors of all cause death. A hazard ratio of 4.29 p equals 0.026. Among the 317 patients with a class one indication for ICD, the five year event rate of sudden cardiac death or aborted sudden cardiac death was lowest in the two negative indices groups, 1.4%. With propensity score matching cohorts the two negative indices group had a significant lower event rate of sudden cardiac death or aborted sudden cardiac death than to two other groups hazard ratio 0.2, p equals 0.046.                                                 The authors concluded that the combination of late gadolinium enhancement in wide QRS provides additional prognostic stratification compared to late gadolinium enhancement status alone.                                                 In the next study, Matthew Sulkin and associates examined whether a novel local impedance measurement on an ablation catheter identifies catheter tissue coupling and is predictive of lesion formation. The author's first studied explanted hearts, 10 swine, and then in vivo 10 swine, using an investigational electro anatomical mapping system that measures impedance from an ablation catheter with mini electrodes incorporated into the distal electrode. Rhythmia and Intellanav, Boston Scientific.                                                 Explanted tissue was placed in a warmed 37 degree celsius saline bath mounted on a scale, and the local impedance was measured 15 millimeters away from the tissue to five millimeters of catheter tissue compression at multiple catheter angles. Lesions were created for 31 and 50 watts from 5 to 45 seconds for an N of 70. During in vivo valuation of the local impedance measurements of the myocardium 90 and blood pool 30 were guided by intracardiac ultrasound while operators were blinded to the local impedance data. Lesions were created with 31 and 50 watts for 45 seconds in the ventricle with an n of 72. The local impedance of myocardium, which was 119.7 ohms, was significantly greater than in blood pool 67.6 ohms the p of less than 0.01. Models that incorporate local impedance drop to predict lesion size had better performance that models incorporate force time integral r squared of 0.75 versus r squared of 0.54 and generator impedance drop r squared of 0.2 versus r squared of 0.58. Steam pops displayed a significantly higher starting local impedance and a larger change in local impedance compared to successful RF applications, p less than 0.01.                                                 The authors concluded that local impedance recorded for miniature electrodes provides a valuable measure of catheter tissue coupling and the change in local impedance is predictive of lesion formation during RF ablation.                                                 In the next paper, Boaz Avitall and associates found that the rising impedance recorded from a ring electrode placed two millimeters from the cryoballoon signifies ice formation covering the balloon surface and indicates ice expansion. The authors studied 12 canines in a total of 57 pulmonary veins, which were targeted for isolation. Two cryoapplications were delivered per vein with a minimum of 90 and a maximum 180 second duration. Cryoapplications was terminated upon reaching a 500 ohm change from baseline. Animals recovered 38 plus or minus six days post procedure, and the veins were assessed electrically for isolation. Heart tissue was histological examined. Extra cardiac structures were examined for damage. Pulmonary vein isolation was achieved in 100% of veins if the impedance reached 500 ohms in 90 to 180 seconds. When the final impedance was between 200 and 500 ohms within 180 seconds of freeze time, pulmonary vein isolation was achieved in 86.8%. For impedance of less than 200 ohms pulmonary vein isolation was achieved in 14%. No extra cardiac damage was recorded. The authors found that impedance rise of 500 ohms at less than 90 seconds with a freeze time of 90 seconds resulted in 100% pulmonary vein isolation.                                                 In our final papers Sally-Ann Clur and associates examined left ventricular isovolumetric relaxation time as the potential diagnostic marker for fetal Long QT Syndrome. Left ventricular isovolumetric contraction time, ejection time, left ventricular isovolumetric relaxation time, cycle length, and fetal heart rate were measured using pulse doppler wave forms in fetuses. Time intervals were expressed as percentage of cycle length, and the left ventricular myocardium performance index was calculated. Single measurements were stratified and compared between Long QT Syndrome fetuses and controls. Receiver operator curves were reformed for fetal heart rate in normalized left ventricular isovolumetric relaxation time. A linear mixed effect model including multiple measurements was used to analyze fetal heart rate, the left ventricular iso volume metric relaxation time, and the left ventricular myocardial performance index. There were 33 Long QT fetuses in 469 controls. In Long QT fetuses the left ventricular isovolumetric relaxation time was prolonged in all groups, p less than 0.001, as was the left ventricular isovolumetric relaxation time.                                                 The best cutoff to diagnose Long QT syndrome was the normalized left ventricular isovolumetric relaxation time greater than equal to 11.3 at less than or equal to 20 weeks, giving a sensitivity in 92% and a specificity of 70%. Simultaneous analysis of the normalized left ventricular isovolumetric relaxation time and fetal heart rate improved the sensitivity and specificity of Long QT Syndrome, AUC of 0.96. The normalized left ventricular isovolumetric relaxation time, the left ventricular myocardial performance index, and fetal heart rate trends differed significantly between Long QT Syndrome fetuses and controls throughout gestation.                                                 The authors concluded that left ventricular volumetric relaxation time is Prolonged QT fetuses. Findings of a prolonged normalize left ventricular isovolumetric relaxation time, and sinus bradycardia can improve the prenatal detection of fetal Long QT Syndrome.                                                 That's it for this month, but keep listening. Suraj Kapa will be surveying all journals for the latest topics of interest in our field. Remember to download the podcasts On the Beat. Take it away Suraj. Suraj Kapa:                          Thank you, Paul and welcome back to On the Beat were we will be summarizing hard-hitting articles across the entire electrophysiologic literature. Today we'll be starting within the realm of atrial fibrillation where we're review an article within the realm of anticoagulation and stroke prevention. Quon et al. published in last month's issue of JACC cardiac electrophysiology on anticoagulant use and risk of ischemic stroke and bleeding in patients with secondary atrial fibrillation. It is well known that use of anticoagulation in atrial fibrillation can reduce overall thromboembolic outcomes. However, its role in secondary atrial fibrillation is unclear. Thus, the authors sought to evaluate the effects anticoagulant use on stroke and bleeding risk. Amongst those where atrial fibrillation occurred in the setting of acute coronary syndrome, pulmonary disease, or sepsis. Amongst around 2300 patients evaluated retrospectively there was no evidence of a lower incidence of ischemic stroke among those treated with anticoagulants compared to those who are not.                                                 However, anticoagulation was associated with a higher risk of bleeding in those with new onset AF associated with acute pulmonary disease. The authors suggest as a result that there is unclear overall benefit for long-term anticoagulation in patients with presumed secondary atrial fibrillation. The difficulty in assessing this is how to define secondary atrial fibrillation. However, in many studies patients who developed in the setting of acute illness still had a high risk of developing quote unquote clinically significant AF in long-term follow-up. However, this was not necessarily absolute as many patients not necessarily develop AF that could be considered clinically significant. Thus, the clinical question that arises is: how long should we treat a patient with anticoagulation when they have presumed secondary atrial fibrillation. These data seem to suggest that there may be no net overall benefits. In other words, all-comers with secondary atrial fibrillation should not necessarily be forever treated with anti-coagulation. However, this slightly requires clinical trials to evaluate further.                                                 Next we delve into the realm of cardiac mapping and ablation where we view an article by Gaita et al. entitled 'Very long-term outcome following transcatheter ablation of atrial fibrillation. Are results maintained after 10 years of follow-up?', published in Europace last month. While pulmonary vein isolation is a widely accepted approach for treatment of atrial fibrillation, most reported studies review outcomes in terms of freedom of AF over a relatively short time period, generally two to five years. However longer term follow up is inconsistently reported. Gaita et al. sought to review 10 year outcomes amongst 255 patients undergoing ablation in a single center. They noted 52% remainder arrhythmia-free amongst a mixed cohort of both paroxysmal and persistent patients while 10% progressed to permanent atrial fiBrillation. They found that absence of increases in blood pressure, BMI, and fasting glucose was protective against an arrhythmia recurrence.                                                 These findings suggest that in a relatively small cohort of patients limited to a single center that even long-term outcomes after pulmonary vein isolation are generally quite good, exceeding 50%. However, future freedom from atrial fibrillation is heavily tied to control of other risk factors. In other words, if a patient is going to have poor control of diabetes, blood pressure, or gain weight, the benefit of their pulmonary vein isolation over long-term follow-up is likely less. These data thus highlight both the potential long-term benefit of PVI, but also the importance of counseling patients regarding the need for continued management and control of future and existing risk factors.                                                 Staying within the realm of atrial fibrillation we next review an article by Weng et al. entitled 'Genetic Predisposition, Clinical Risk Factor Burden, and Lifetime Risk of Atrial Fibrillation' published in last month's issue of circulation. The probability of detecting atrial fibrillation in patients based on clinical factors and genetic risk is unknown. Weng et al. sought to clarify whether a combination of clinical and polygenic risk scores could be used to predict risk of developing atrial fibrillation over long-term followup in the Framingham Heart Study. Amongst 4,600 individuals, 580 developed incident atrial fibrillation and had an overall lifetime risk of developing atrial fibrillation of 37%. Those are the lowest risk tertile based on clinical risk factor burden and genetic predisposition had a lifetime risk of 22% versus 48% in the highest. Furthermore, a lower clinical risk factor burden was associated with delayed atrial fibrillation onset. In order to identify patients with atrial fibrillation, before negative sequelae such as stroke occur, patient and physician understanding of risk and monitoring needs is necessary. The fact is that it will be great to identify every single patient who has atrial fibrillation before they have a negative sequela of that atrial fibrillation such as ischemic stroke.                                                 However, performing continuous monitoring of all patients with potential negative sequelae of atrial fibrillation is extraordinarily difficult. The reason is it's excessively costly. We cannot monitor the entire population irrespective of whatever the risk factors are. However, if we're able to identify the highest risk cohorts early on before the atrial fibrillation onsets, this may offer opportunities for use of newer cheaper monitors. The work by Weng et al. suggests one such possible approach combines clinical and polygenic risk scores. Actionability of these data, however, remains to be seen and further validation other cohorts is necessary to clarify generalized ability.                                                 The next article we review is published in last month's issue of the Journal of American College of Cardiology by Lopes at al. entitled 'Digoxin and Mortality in Patients With Atrial Fibrillation. Lopes et al. sought to evaluate the impact of the Digoxin on mortality in patients with atrial fibrillation and the association with the Digoxin serum concentration and heart failure status. They value this association in over 17,000 patients. At baseline 32% were receiving Digoxin. Baseline Digoxin use did not associate with risk of death, but even in these patients a serum concentration of greater than 1.2 nanograms per milliliter was associated with a 56% increase in mortality risk. For each .5 nanogram per milliliter increase in oxygen concentration the hazard ratio increased by 19% for overall mortality. This was irrespective of heart failure status. Furthermore, in patients who are newly started in Digoxin over the follow-up period, the risk and death and sudden death was higher. These data suggests a significant risk associated with Digoxin use for management of atrial fibrillation irrespective of heart failure status. Furthermore, serum valleys above 1.2 require close consideration of dose de-escalation. Whether there is any optimal dose, however, from the study is unclear. These data amongst a host of prior data strongly suggest again strategic use of Digoxin  principally for the management of atrial fibrillation.                                                 Moving on within the realm of atrial fibrillation, we review an article published in last month's issue of Circulation Research by Yan et al. entitled Stress Signaling JNK2 Crosstalk with CaMKII Underlies Enhanced Atrial Arrhythmogenesis. In this more acellular based study the mechanism underlying atrial arrhythmogenesis associated with aging was evaluated. Yan et al. sought to figure out whether the stress response JNK in calcium mediated arrhythmias might contribute to atrial arrhythmogenesis in aged transgenic mouse models. They demonstrated significant increased activity of JNK2 and aging atria, those furthermore associated with rhythmic remodeling. This association was mediated through CaMKII and ryanodine receptor channel function, with activation of the former leading to increased calcium leak mediated by the ladder. This in turn related to increase atrial fibrillation likelihood. Identifying novel targets for atrial fibrillation therapy is critical. Given atrial fibrillation is a complex disease process related to a multitude of risk factors it can be assumed that the contribution of any single factor may be mediated through distinct mechanisms.                                                 Aging in particular as well regarded, but considered to be non-modifiable risk factor for atrial fibrillation. Identifying genes or pathways, the immediate aging associated fibrillation, may take the risk of aging as no longer a non-modifiable thing. The finding of the significance of JNK2 and associate downstream effects with AF risks and aging hearts may hold potential in offering unique therapeutic targets.                                                 Finally, within the realm of atrial fibrillation, we're viewing article by Chen et al. in last month's issue of the Journal of the American Heart Association entitled Association of Atrial Fibrillation With Cognitive Decline and Dementia Over 20 Years: The ARIC-NCS Study. Multiple studies have suggested a significant association between atrial fibrillation risk of dementia. However, these studies have limited time follow-up and were often done and predominantly white patients. Thus, the authors sought to use the data from ARIC, the Atherosclerosis Risk in Communities Neurocognitive Study, to assess the risk of cognitive decline associated with atrial fibrillation. Amongst over 12,000 participants, a quarter of whom are black and half of whom are white, they noted 2100 patients developed atrial fibrillation and 1,150 develop dementia over a 20 year follow up period.                                                 There was a significantly greater risk of cognitive decline amongst those who developed atrial fibrillation. In turn incident atrial fibrillation for the follow-up period was associated with a higher risk of dementia even after adjusting for other clinical and cardiovascular risk factors such as incidents that ischemic stroke. These data further strengthened prior evidence of a direct link between atrial fibrillation and risk of cognitive decline and dementia. Understanding this long-term risk raises the need to additionally identify approaches to prevent this occurrence, which in turn is dependent on understanding the underlying mechanisms. The finding that the risk of cognitive decline dementias independent of ischemic stroke events raises concern that either subclinical micro-embolic events or other factors may be playing a role in this risk and in turn raises question as to how best to prevent them. Until better understood, however, the question of whether the association is causal remains to be seen.                                                 Changing gears yet again, we now delve into the realm of ICDs, pacemakers and CRT. Published in last month, issue of Heart Rhythm Tarakji et al. published a paper entitled 'Unrecognized venous injuries after cardiac implantable electronic device transvenous lead extraction.' Overall risk of transvenous lead extraction includes that of potentially fatal venous laceration. The authors sought to evaluate the incidence of venous injury that may be unrecognized based on microscopic study of extracted leads. Amongst 861 leads obtained from 461 patients they noted 80 leads or almost 9%. Amongst 15% of patients showed segments vein on the lead body, most of which were transmural including the tissue layer. However, in terms of clinical significance, only 1% had need for emergent surgical intervention for clinically significant venous laceration. Risk factors for having the entire vein on the lead included age of lead, ICD leads, and the use of the laser sheath.                                                 These findings suggest that there may be a high incidence of subclinical venous injury after lead extraction though rarely resulting clinically apparent sequelae. As would be expected, venous injury, including transmural removal of portions of the vein traversed by the lead, was more common amongst older leads, which generally more often require laser sheets and ICD leads. The question is however, whether this carries any direct clinical implications. One they may be considered is the potential additive risk of an advancing new lead through the same venous channel, particularly in the setting of potential transmural venous injury that already exists.                                                 Next in last month's issue of Heart Rhythm we review an article by Sharma at al. entitled 'Permanent His-bundle pacing as an alternative to biventricular pacing for cardiac resynchronization therapy: A multicenter experience.' The use of resynchronization therapy for treatment of patients with heart failure and wide QRS has been shown to offer morbidity and mortality benefits. However, many patients maybe non-responders, and recent studies on His bundle pacing of suggested potential clinical benefits. His bundle pacing essentially only requires one pacing catheter attached within the region of the His bundle Sharma et al. sought to evaluate the safety and success rates of His bundle pacing for patients who have either failed standard resynchronization therapy or in whom most tried as a primary intervention. They noted His bundle pacing was successful in 90% of patients with reasonable myocardial and His bundle capture thresholds. Patients in both groups exhibits significant narrowing of QRS morphology and improvement in left ventricular ejection fraction from a mean of 30 to 43%. However, a total of seven patients had lead related complications.                                                 These database on a retrospective analysis of two types of patients, those failing standard biventricular therapy, and those on whom his bundle pacing was attempted as a primary modality suggest overall safety and efficacy in a handful of experienced centers. The promise of His bundle pacing is that a may allow for more effective resynchronization than standard approaches. The high rate of success suggests that His bundle pacing maybe both safe and reasonable to pursue. However randomized trials across more centers are needed to fully prove its benefit, particularly as a primary modality of treatments.                                                 Next we review ICDs and chronic kidney disease. In last month's issue of JAMA cardiology by Bansal at al. entitled 'Long-term Outcomes Associated With Implantable Cardioverter Defibrillator in Adults With Chronic Kidney Disease.' While the benefit of ICDs in patients with low EF is widely recognized, modifying factors that may increase risk of death are not as well defined. These include things like advanced age and chronic kidney disease. Bansal et al. sought to evaluate long-term outcomes and ICD therapy in patients with chronic kidney disease. In retrospective study of almost 5,900 ambulatory patients amongst whom 1550 had an ICD, they found no difference in all cause mortality. However, ICD placement was associated with an increased risk of subsequent hospitalization due to heart failure or any cause hospitalization.                                                 In light of recent studies such as DANISH the robust sense of ICD benefit is being questioned. One of the thoughts for the absence of similar benefit to prior studies lies in the improving care of ambulatory heart failure patients. In patients with chronic kidney disease several questions rises to the risk with ICD, including infectious risk in dialysis patients and the concomitant mortality risk with renal dysfunction. The author suggested in retrospective study, no incremental benefit of ICDs in patients with chronic kidney disease and perhaps some element of added risk is related to hospitalization. However, this study has several limitations. It is retrospective and many patients received ICDs may have been perceived to be sicker in some way. Thus care must be taken in interpretation, but consideration of randomized studies to adjudicate benefit are likely necessary.                                                 Finally, within the realm of devices, we reviewed an article by Tayal et al. entitled "Cardiac Resynchronization Therapy in Patients With Heart Failure and Narrow QRS Complexes.' publishing the Journal of American College of Cardiology last month. Several parameters have been stressed to identify benefit of resynchronization therapy in patients with wide QRS include cross correlation analysis with tissue doppler imaging. However, many patients may have evidence in mechanical dyssynchrony even in the absence of an apparent wide QRS thus Tayal et al. sought to evaluate the benefit of resynchronization therapy amongst 807 patients with heart failure and a narrow QRS mean criteria in a randomized study. Of the 807 46% had delayed mechanical activation. Those without delay mechanical activation had underwent we standardization therapy and were associated with worse overall outcomes likely due to new delayed mechanical activation potentially related to CRT pacing. These data support the absence of a role for resynchronization therapy in patients with a narrow QRS. This is expected as resynchronization therapy likely offers the most benefit in patients with mechanical dyssynchrony that results from electrical dyssynchrony.                                                 Since by its very nature resynchronization therapy relies on non physiologic cardiac pacing thus compared to normal cardiac activation the nature of resynchronization pacing is desynchronization. These data support the absence of a role for resynchronization therapy in patients with heart failure and narrow QRS complexes.                                                 Moving on to cellular electrophysiology we review an article by Kozasa et al. published in last month's issue of Journal of Physiology entitled 'HCN4 pacemaker channels attenuate the parasympathetic response and stabilize the spontaneous firing of the sinoatrial node.' Heart rate is controlled by an interplay between sympathetic and parasympathetic components. In turn HCN4 abnormalities have been implicated in congenital sick sinus syndrome. The authors sought to clarify the contribution of HCN4 to sinus node autonomic regulation. They created a novel gain-of-function mouse where the HCN4 activity could be modulating from zero to three times normal. They then evaluated ambulatory heart-rate variability and responsive heart rate to vagus nerve stimulation. They found HCN4 over-expression did not increase heart rate, but attenuated heart-rate variability. It also attenuated bradycardic response to vagus nerve stimulation. Knockdown of HCN4 in turn lead to sinus arrhythmia and enhanced parasympathetic response. These data suggest HCN4 attenuates sinus node response to vagal stimuli thus stabilizing spontaneous firing of the node. The clinical application of this remain to be seen but are maybe important in that they highlight a mechanism for a heretofore poorly understood mechanism for how exactly HCN4 abnormalities may lead to sick sinus syndrome.                                                 Within the realm of ventricular arrhythmias we highlighted a number of articles published this past month. The first article we review was published in last month's issue of JACC clinical electrophysiology, entitled characterization of the electrode atomic substrate and cardiac sarcoidosis: correlation with imaging findings of scarring inflammation published by [inaudible 00:41:40] et al. In patients with cardiac sarcoidosis one of the questions is how to define the electronic atomic substrate, particularly before we entered the electrophysiology laboratory. Both active inflammation and replacement fibrosis maybe be seen in patients. The authors evaluated in 42 patients with cardiac sarcoidosis, the association between an abnormal electrograms and cardiac imaging findings including PET and Computed Tomography, as well as Cardiac MRI. They noted that amongst these 40 patients, a total of 21,000 electrograms were obtained, and a total of 19% of these were classified as abnormal. Most of the abnormalities occurred in the basal paravalvular segments and intraventricular septum. They further noted that many of these abnormalities in terms of electrograms were located outside the low voltage areas, particularly as it relates to fractionation. In about 90% of patients they notice late gadolinium enhancements and they noted abnormal FDG uptakes suggesting active inflammation in about 48%.                                                 However, it should be noted that only 29 of the 42 patients underwent cardiac imaging. Segments with abnormal electrograms tended to have more late gadolinium enhancement evidence scar transmurality, and also they noted that the association of abnormal PET scan did not necessarily occur with abnormal electrograms. Thus, they concluded that in patients with cardiac sarcoidosis and ventricular tachycardia pre-procedural imaging with cardiac MRI could be useful in detecting electroanatomic map abnormalities that may in turn be potential targets for substrate ablation. However, they were more likely associated with more scar transmurality and lower degrees of inflammation on PET scanning. These data are important in that they highlight potential non-invasive means by which to understand where substrate might occur in patients with the cardiac sarcoidosis. It is well recognized that cardiac sarcoidosis is associated with increased risk of ventricular arrhythmias. These risks have increased ventricular arrhythmias, might be targetable with ablation. Newer therapies might even offer non invasive means by which to perform ablation in patients best. Thus if we could identify non based on mechanisms of identifying the substrate, this will be even more critical.                                                 The critical findings of this particular paper lie in noting that most of the abnormalities still is in intra ventricular sePtum in basal segments, and also that it is MRI in late gadolinium enhancement and associates more with the abnormal electrograms. Interestingly, the absence of inflammation correlating with the presence of more abnormal electrograms suggests that it is not so much the act of inflammation as being reflected in the endocardial map, but the existence of scar.                                                 Next, again within JACC clinical electrophysiology we review an article by Porta-Sánchez et al. entitled 'Multicenter Study of Ischemic Ventricular Tachycardia Ablation With Decrement Evoked Potential Mapping With Extra Stimulus.' The authors sought to conduct a multicenter study of decrement evoked potential base functional tech ventricular tachycardia substrate modification to see if such mechanistic and physiologic strategies could result in reduction in VT burden. It is noted that really only a fraction of the myocardium in what we presume to be substrate based on the presence of low voltage areas are actually involved in the initiation and perpetuation of VT. Thus if we can identify the critical areas within the presumed substrate for ablation, this would be even a better way of potentially honing in on our targets. They included 20 consecutive patients with ischemic cardiomyopathy. During substrate mapping fractionated late potentials were targeted and an extra stimulus was provided to determine which display decrements. All patients underwent DEEP focus ablation with elimination being correlated with VT non-inducibility after radio-frequency ablation. Patients were predominantly male, and they noted that the specificity of these decrement evoked potentials to detect the cardiac isthmus for VT was better than that of using late potentials alone. They noted 15 of 20 patients were free of any VT after ablation of these targets over six months of follow-up, and there was a strong reduction in VT burden compared to six months pre ablation.                                                 They concluded that detriment evoked potential based strategies towards ablation for ventricular tachycardia might identify the functional substrate and those areas most critical to ablation. They in turn regarded that by its physiologic nature it offers greater access to folks to ablation therapies.                                                 This publication is important in that it highlights another means by which we can better hone in on the most critical regions for substrate evaluation in patients with ventricular tachycardia. The fact is more extensive ablation is not necessarily better and might result in increased risk of harm if we think about the potential effects of longer ablations or more ablation lesions. Thus if we could identify ways of only targeting those areas that are most critical to the VT circuits, we could perhaps short and ablation procedural time, allow for novel ways of approaching targeted ablation with limited amounts of ablation performed, or perhaps even improve overall VT outcomes by knowing the areas that are most critical to ensure adequate ablation therapy provided. However, we need to understand that this is still a limited number of patients evaluated in a non randomized manner. Thus whether or not more extensive ablation performed might have been better is as of yet unclear                                                 Staying within the realm of ventricular tachycardia we review an article published in last month's issue of Heart Rhythm by Winterfield et al. entitled the 'Impact of ventricular tachycardia ablation on healthcare utilization.' Catheter ablation of atrial tachycardia has been well accepted to reduce recurrent shocks in patients with ICDs. However, this is a potentially costly procedure, and thus effect on overall long-term health care utilization remains to be seen. The authors sought to evaluate in a large scale real world retrospective study the effect of VT ablation on overall medical expenditures in healthcare utilization. A total 523 patients met study inclusion criteria from the market scan database. After VT ablation median annual cardiac rhythm related medical expenditures actually decreased by over $5,000. Moreover the percentage of patients with at least one cardiac rhythm related hospitalization an ER visit decreased from 53 and 41% before ablation respectively, to 28 and 26% after ablation. Similar changes we're seeing in number of all cause hospitalizations and ER visits. During the year before VT ablation interestingly there was an increasing rate of healthcare resource utilization, but a drastic slowing after ablation.                                                 These data suggests that catheter ablation may lead to reduced hospitalization in overall healthcare utilization. The importance of these findings lies in understanding why we do the things we do. We can provide a number of therapies to patients, but we seek two different effects. One is the individual effect of improving their particular health. The second thing is trying to avoid increasing healthcare expenditures on a population level and making sure resources are utilized. If we can reduce recurrent hospitalizations and overall healthcare expenditure in patients by providing a therapy in addition to provide individual benefit, this is the optimal situation. These data suggests that VT ablation might provide such a benefits, that in fact it reduces overall healthcare utilization while improving overall outcomes.                                                 Next and finally within the realm of ventricular arrhythmias, we review more on the basic side the role of Titin cardiomyopathy leads to altered mitochondrial energetics, increased fibrosis and long-term life-threatening arrhythmias, published by Verdonschot et al. in last month's issue of European Heart Journal. It is known now that truncating Titin variants might be the most prevalent genetic cause of dilated cardiomyopathy. Thus, the authors sought to study clinical parameters and long term outcomes related to Titin abnormalities in dilated cardiomyopathy. They reviewed 303 consecutive and extensively phenotype dilated cardiomyopathy patients who underwent cardiac imaging, Holter monitoring, and endomyocardial biopsy and in turn also underwent DNA sequencing of 47 cardiomyopathy associated genes. 13% of these patients had Titin abnormalities. Over long-term followup they noted that these patients had increased ventricular arrhythmias compared to other types of dilated cardiomyopathy, but interestingly, they had similar survival rates. Arrhythmias in those Titin abnormal patients were most prominent in those who were subjected to an additional environmental trigger, including viral infection, cardiac inflammation, other systemic disease or toxic exposure. They also noted the cardiac mass was relatively reduced in titan admirable patients.                                                 They felt that all components of the mitochondrial electron transport chain we're simply up-regulated in Titin abnormal patients during RNA sequencing and interstitial fibrosis was also augmented. As a result, they concluded that Titin variant associated dilated cardiomyopathy was associated with an increased risk of ventricular arrhythmias, and also with more interstitial fibrosis. For a long time we have reviewed all non ischemic cardiomyopathy as essentially equal. However, more recent data has suggested that we can actually hone in on the cause. In turn, if we hone in on the cause, we might be able to understand the effects of specific therapies for ventricular arrhythmias based on that underlying cause. Patchy fibrosis might not be as amenable, for example, to ablation as discreet substrate that we might see in infarct related VT. Understanding the relative benefit in very specific types of myopathies might hold benefit in understanding how to, one, risk stratify these patients, and two, understand what type of therapy, whether pharmacologic or ablative, might result in greatest benefit to the patients.                                                 Changing gears entirely now to the role of genetics, we review multiple articles in various genetic syndromes published this past month. First, we reviewed an article by Providência et al. published in the last month's issue of heart entitled 'Impact of QTc formulae in the prevalence of short corrected QT interval and impact on probability and diagnosis of short QT syndrome.' The authors sought to assess the overall prevalence of short corrected QT intervals and the impact on diagnosis of short QT syndrome using different methods for correcting the QT interval. In this observational study they reviewed the sudden cardiac death screening of risk factors cohorts. They then applied multiple different correction formulae to the ECGs. They noted that the prevalence of individuals with the QTc less than 330 and 320 was extremely low, namely less than .07 and .02% respectively. They were also more frequently identified using the Framingham correction. The different QTc correction formulae could lead to a shift of anywhere from 5 to 10% of individuals in the cohort overall.                                                 They further noted, that based on consensus criteria, instead of 12 individuals diagnosed with short gut syndrome using the Bazett equation, a different number of individuals would have met diagnostic criteria with other formulae, 11 using Fridericia, 9 with Hodges, and 16 using the Framingham equation. Thus, they noted that overall the prevalence of short QT syndrome exceedingly low and an apparently healthy adult population. However, reclassification as meeting criteria might be heavily dependent on which QT correction formula is used. The importance of these findings is that not all QTs are created equal.                                                 Depending on how you compute the QT interval in which formula to use may affect how you actually risk characterize a patient. Unfortunately, these data do not necessarily tell us which is the right formula, but this highlights that it might be relevant to in the future evaluate the role of different formulae and identifying which is the most necessary to classify a patient.                                                 Moving on to an article published in last month's issue of the journal of clinical investigation by Chai et al. we review an article entitled 'Physiological genomics identifies genetic modifiers of Long QT Syndrome type 2 severity.' Congenital Long QT Syndrome is a very well recognized, inherited channelopathy associated life-threatening arrhythmias. LQTS type 2 is specifically caused by mutations in casein to encoding the potassium channel hERG. However, even with the mutation not all patients exhibit the same phenotype. Namely some patients are more at risk of life threatening arrhythmias in spite of having the same mutation as others who do not exhibit the same severity phenotype. The authors sought to evaluate whether specific modifiable factors within the remaining genetic code might be modifying the existing mutation. Thus, they sought to identify contributors to variable expressivity in an LQT 2 family by using induced pluripotent stem cell derived cardiomyocytes and whole exome sequencing in a synergistic manner.                                                 They found that patients with severely effected LQT 2 displayed prolonged action potentials compare to sales from mildly effected first-degree relatives. Furthermore, stem cells derived from patients were different in terms of how much L-type calcium current they exhibited. They noted that whole exome sequencing identified variants of KCNK17 and the GTP-binding protein REM2 in those patients with more severe phenotypes in whom greater L-type calcium current was seen. This suggests that abnormalities or even polymorphisms in other genes might be modifying the risk attributed to by mutations in the primary gene. This showcases the power of combining complimentary physiological and genomic analysis to identify genetic modifiers and potential therapeutic targets of a monogenic disorder. This is extraordinarily critical as we understand on one level that when we sequence a monogenic disorder that there might exist variants of uncertain significance, namely they have not been classified as disease causing, but could be. In turn, we also recognize that mutations in a family might effect different relatives differently. However, why this is has been relatively unclear.                                                 If we can understand and identify those patients who are most at risk of dangerous abnormal rhythms, this will be useful in how much to follow them, and what type of therapy to use in them. The fact that other genes might modify the risk even in the absence of specific mutations, suggests that novel approaches to characterizing the risk might help for the risk modified patients classification in general. Clinical use, however, remains to be seen.                                                 Moving on from long QT, we evaluate 'The Diagnostic Yield of Brugada Syndrome After Sudden Death With Normal Autopsy' noted in last month's issue of the Journal of American College of Cardiology and published by Papadakis et al. It is well known, the negative autopsies are not uncommon in patients, however, families might be wondering how at risk they are. Thus, the authors sought to assess the impact of systematic ajmaline provocation testing using high right precordial leads on the diagnostic yield Brugada syndrome in a large cohort of Sudden Arrhythmic Death syndrome families. Amongst 303 families affected by Sudden Arrhythmic Death Syndrome evaluation was done to determine whether or not there was a genetic inherited channelopathy cause. An inherited cardiac disease was diagnosed in 42% of the families and 22% of relatives Brugada syndrome was the most prevalent diagnosis overall amongst 28% of families. Ajmaline testing was required, however, to unmask the Brugada Syndrome in 97% of diagnosed individuals. Furthermore, they use of high right precordial leads showed a 16% incremental diagnostic yield of ajmaline testing for diagnosing Brugada syndrome.                                                 They further noted that a spontaneous type 1 regard or pattern or a clinically significant rhythmic event developed in 17% of these concealed regardless syndrome patients. The authors concluded the systematic use of ajmaline testing with high right precordial leads increases the yield of Brugada Syndrome testing in Sudden Arrhythmic Death Syndrome families. Furthermore, they noted that assessments should be performed in expert centers or patients could also be counseled appropriately. These findings are important and one of the big questions always becomes how aggressively to test family members of patients or of deceased individuals who experienced sudden arrhythmic death. Many of these patients have negative autopsies, and genetic autopsy might not be possible due to lack of tissue or blood products that can be adequately tested.                                                 The data here suggest that amongst a group of 303 sudden arrhythmic death, families that Brugada Syndrome is by far the most frequent diagnosis. If an inherited cardiac disease was identified. In turn, it is not ECG alone or echo alone that helps identify them, but requires drug provocation testing in addition to different electrode placements. Whether or not this will consistently offer benefit in patients in general or my result in overcalling remains to be seen next within the realm of genetic predisposition.                                                 We view an area where we don't know if there's a genetic predisposition in article published by Tester et al. entitled Cardiac Genetic Predisposition in Sudden Infant Death Syndrome in last month's issue of the journal of american college of cardiology. Sudden Infant Death Syndrome is the leading cause of post-neonatal mortality and genetic heart diseases might underlie some cases of SIDS. Thus the authors sought to determine the spectrum and prevalence of genetic heart disease associated mutations as a potential monogenic basis for Sudden Infant Death Syndrome. They study the largest cohort to date of unrelated SIDS cases, including a total of 419 individuals who underwent whole exome sequencing and targeted analysis for 90 genetic heart disease susceptibility genes. Overall, 12.6% of these cases had at least one potentially informative genetic heart disease associated variants. The yield was higher in those mixed European ancestry than those of European ancestry.                                                 Infants older than four months were more likely to host a potentially informative gene. Furthermore, they noted that only 18 of the 419 SIDS cases hold a [inaudible 01:01:26] or likely pathogenic variant. So in other words, only 4% of cases really had a variant that they could say was distinctly pathogenic or likely pathogenic. Thus, overall, the minority of SIDS cases have potentially informative variant in genetic heart disease susceptibility gene, and these individuals were mostly in the 4 to 12 month age group. Also, only 4% of cases had immediately clinically actionable variance, namely a variant, which is well recognized as pathogenic and where we could actually say that a specific therapy might have had some effect. These findings can have major implications for how best to investigate SIDS cases in families. It might suggest that SIDS cases where the individual was older, nearly 4 to 12 months of age might have a greater yield in terms of identifying variance.                                                 While this might not affect the deceased in fit, it might affect, families are planning on having another child in whom a variant can be identified.                                                 Finally, within the realm of genetics, we review an article published in last month's issue of Science Advances by Huang. et al. entitled 'Mechanisms of KCNQ1 Channel Dysfunction in Long QT Syndrome Involving Voltage Sensor Domain Mutations'. Mutations that induce loss of function of human KCNQ1 underlie the Long QT Syndrome type 1. While hundreds of mutations have been identified the molecular mechanism by which they result in impaired function are not as well understood. The authors sought to investigate impact of 51 specific variants located within the voltage sensor domain and emphasized effect on cell surface expression, protein folding, and structure. For each variant efficiency of trafficking of the plasma membrane, impact of proteasome inhibition, and protein stability were evaluated. They noted that more than half of the loss of function mutations were seen to destabilized structure of the voltage sensor domain, generally accompanied by mistrafficking and degradation by the proteasome.                                                 They also noted that five of the folding defective Long QT Syndrome mutant sites were located in the S0 helix, where they tend to interact with a number of other loss of function mutation sites in other segments of the voltage sensor domain. They suggested these observations reveal a critical role for the S0 helix as a central scaffold to help organize and stabilized KCNQ1 overall. They also note the importance of these findings is that mutation-induced destabilization of membrane proteins may be a more common cause of disease functioning in humans. The importance of these findings lies in better understanding why specific mutations lead to appa

A Fib is the most common arrhythmia that is encountered in the ED. Knowing how to manage it when it is causing problems is important! Join the EM GuideWire Team as they discuss a-fib with RVR management with esteemed Cardiologist (and friend of us in the ED), Dr. Laszlo Littmann.

Commentary by Dr. Valentin Fuster

Update your management of heart failure (HF) with expert tips from Cardiologist Dr. Eric Adler, Associate Professor of Medicine and Director of Cardiac Transplant and Mechanical Circulatory Support at UC San Diego. We cover how to use BNP, a simple way to examine jugular venous distention, medical therapy for heart failure, the PARADIGM-HF trial, and how to use sacubitril/valsartan (Entresto). Full show notes available at http://thecurbsiders.com/podcast Join our newsletter mailing list. Rate us on iTunes, recommend a guest or topic and give feedback at thecurbsiders@gmail.com. Time Stamps 00:00 Intro 04:25 Rapid fire questions 06:00 Palliative care and heart failure 08:40 Book recommendation 10:20 Advice for teachers and learners 12:27 Clinical case of HF 13:38 Classification and staging of HF 17:07 Discussion of BNP 19:35 How to perform neck vein exam for JVD 21:20 BNP for prognosis 23:00 BNP at hospital discharge 26:36 Factors that affect BNP 27:25 Initial patient counseling 32:35 Exercise in HF 34:00 Additional testing at time of diagnosis 36:28 Initial medical therapy 38:30 Discussion of diuretics and dosing 42:50 Aldosterone antagonists 44:30 PARADIGM-HF and entresto 51:27 Medications to avoid in HF 54:14 Digoxin 57:30 Dr. Adler’s take home points 59:11 Stuart questions dosing conventions 60:48 Outro Tags: arni, assistant, care, diuretics, doctor, education, failure, family, foam, foamed, health, heart, hospitalist, hospital, internal, internist, neprilysin, nurse, management, medicine, medical, physician, practitioner, primary, resident, sacubitril, student

Eye Conditions in (not) ABC Order If something happens to your eyes that makes you want to ask the pharmacist if you should go to the doctor, the answer will most likely be "yes, go see a doctor."  Even at emergency rooms, they will treat you and make you comfortable but always tell you to follow up with your eye doctor. Photopsias This is seeing things that aren't really there, the visual cortex translates other sensations as "sight". Floaters: "shadows" that float around in your field of vision.  They *can* be a sign of a detaching retina, but that is usually not the case.  They are normal for most people. Inside your eyeball is a gel, called vitreous gel.  Throughout your life, that gel begins to liquify.  As it turns to liquid, it may have other bits of gel still floating in that liquid.  And you see "shadows" because they block light from reaching your retina.  Floaters may worsen with dehydration or exhaustion.  If you try to focus on them, they "float" away. Flashes: "seeing stars" - when the vitreous gel/liquid combo gets shook up and sloshed around (i.e. head trauma).  You can also get "flashes" with Digitalis toxicity (Digoxin is a medication derived from the Foxglove plant and developed for arrhythmias.)  This is a medication that the doctor will test your levels for to make sure toxicity doesn't happen. Waves: looks like radiating heat; caused by spasms of the blood vessels in your eyes.  This may be one explanation of the "aura" that comes before a migraine.  If it happens and no headache follows, it's caused an "ocular migraine". Glaucoma It is the 2nd leading cause of blindness in the US and around the world.  Glaucoma is known for increased pressure in your eyes.  The fluid around the eyes typically have adequate drainage so nutrients can flow in and waste can flow out.  If that drainage becomes inadequate, the pressure builds up and it can put pressure on the optic nerve (the nerve that connects from the retina to the brain).  It starts with decreasing peripheral vision, and can become "tunnel vision" where a person can only see right in the middle of their field of vision. Medications are eye drops that control pressure and help open up drainage pathways as much as possible.  It doesn't hurt, and it takes a while for the decreased peripheral vision to be noticeable.  It's not reversible, but it can be slowed with medication.  Eye doctors have a way to check the pressure in your eyes each time you get your eyes checked. (Macular Degeneration is the #1 cause of blindness in the US, Cataract is the #1 cause of blindness worldwide).   Nystagmus Pronounced nigh-stag-mus.  It is the involuntary rapid eye movement side to side.  Caused by a neurological issue, either related to the eye muscles and nerves or the inner ear (one cause a vertigo).  The shaking seems to be worse when a person looks straight at something or someone.  For someone dealing with nystagmus, they usually discover they can tilt or turn their head to make their eyes slightly off center where the shaking wills stop - this is called a "null point".  Strengthening eye muscles can help the shaking, but it still worsens with exhaustion or stress. This can be a result of a stroke, multiple sclerosis (autoimmune).  Dilantin is a medication for seizures, and is another medication that has to be regularly measured because too much can cause temporary nystagmus. Connect with me Support us on Patreon *NEW* Join the Pharmacist Answers Podcast Community on Facebook Subscribe: iTunes, Stitcher, GooglePlay, TuneIn Radio Like the Facebook page Music Credits:  “Radio Martini” Kevin MacLeod (incompetech.com)  Licensed under Creative Commons: By Attribution 3.0  http://creativecommons.org/licenses/by/3.0/

Dr. Renato Lopes and Dr. C. Michael Gibson Discuss

Everything you need to know about digoxin - it's not as complicated as you think. Make sure and get our FREE pharmacology sheet sheets: https://physicianassistantboards.com/pharm-cheat-sheets/

Today, we're going to be answering a readers question regarding digoxin's mechanism of action when used for atrial fibrillation. We'll also touch on some other important aspects of the drug - if you have a question email: andrew@physicianassistantboards.com   Subscribe to youtube.com/paboards Website: http://physicianassistantboards.com Personal IG: https://www.instagram.com/and_reid PABoards IG: https://www.instagram.com/paboards FB: https://www.facebook.com/paboards1

  Carolyn: Welcome to Circulation On The Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr. Carolyn Lam, Associate Editor from the National Heart Center and Duke National University of Singapore. Today we will be diving deep into issues of resistant hypertension, adherence to anti-hypertensive medication, and renal denervation. All this by looking closely at new data from the Renal Denervation for Hypertension trial. First, here are your summaries of this week's journal.     The first paper sought to answer these questions: How can we better re-stratify patients with long QT syndrome type 3? You will remember that as the type caused by a gain of function mutation in the SCN5A sodium channel, and the type that has a more lethal course than types 1 and 2. Another question is, are we sure that beta blockers are effective in type 3 long QT syndrome? Well the current study is by co-first-authors, Dr. Wilde of Academic Medical Center, Amsterdam, and Dr. Moss from University of Rochester School of Medicine and Dentistry, which is the largest multi-center long QT type 3 syndrome cohort described to date.     This study was designed to identify the risk and therapeutic factors associated with cardiac events in patients. The risk factors evaluated included clinical features such as age, gender, ECG measurements, the mutation type, and the therapeutic effects of beta blockers, other medications, and ICD. In almost four hundred patients with type 3 long QT syndrome, 30% experienced at least one cardiac event; that is syncope, aborted cardiac arrest, or sudden death. The risk of a first cardiac event was directly related to the degree of QT prolongation. Each 10 millisecond increase in QTC up to 500 milliseconds was associated with a 19% increase in cardiac events. Prior syncope doubled the risk of life threatening events. Beta blocker therapy was associated with an 83% percent reduction in cardiac events in females, however the efficacy in males could not be conclusively determined due to low number of events. The take-home message is, in your patients with long QT syndrome type 3, recognize the very high risk sub-population with prolonged QTC and a history of syncope.     The next paper is a basic science paper that reveals a novel way in which mitochondrial dysfunction may be targeted in heart failure. This paper is from first author Dr. Li, corresponding author Dr. Tian, and colleagues from the Mitochondria and Metabolism Center at University of Washington. These authors previously found that elevation in the NADH to NAD ratio induces mitochondrial protein hyperacetylation, and renders hearts highly susceptible to stresses, and they showed this in a mouse model of primary mitochondrial dysfunction caused by genetic defects. In the current study they defined the molecular intermediaries linking specific NAD sensitive hyperacetylation targets to the development of heart failure, and further demonstrated the relevance of these mechanisms in human heart failure. Specifically, they identified that hyperacetylation of the regulators of mitochondrial permeability transition poor and malate-aspartate shuttle, mediates the increased susceptibility to cardiac stresses. Further, expanding the cardiac NAD pool via pharmacological or genetic approaches normalized the NADH to NAD ratio, and thereby normalized protein acetylation in hypertrophied and failing hearts. Importantly, these measures improved cardiac function and reduced pathological hypertrophy in mice. Thus, the clinical implication is that restoring the NADH to NAD ratio may be an effective and translatable strategy to treat mitochondrial dysfunction in heart failure.     The next study broadens our considerations of the benefits versus risks of intensive anti-platelet therapy in patients with a prior myocardial infarction, and really suggests that more intensive anti-platelet therapy should be considered, not only to reduce the risks of coronary events, but also to reduce the risk of stroke. This is a paper from Dr. Bonaca and colleagues of the TIMI study group from Brigham and Women's Hospital in Boston, Massachusetts, who investigated the efficacy of ticagrelor, 60 milligrams twice a day, for reducing stroke in patients with a prior myocardial infarction from the Pegasus-TIMI 54 trial.     You will remember that in the Pegasus-TIMI 54 trial, ticagrelor was already shown to reduce the risk of major adverse cardiovascular events when added to low-dose aspirin in stable patients with prior MI. Of more than 14,000 patients randomized to placebo or Ticagrelor, 213 experienced a stroke, 85% of which were ischemic. 18% of strokes were fatal, and another 15% led to either moderate or severe disability at 30 days. Ticagrelor significantly reduced the risk of stroke, with a hazards ratio of 0.75, and this was driven by a reduction in ischemic stroke. Hemorrhagic stroke occurred in nine patients on placebo and eight patients on ticagrelor. Furthermore, a meta-analysis of four placebo-controlled trials of more intensive antiplatelet therapy in more than 44,800 patients with coronary disease confirmed a marked reduction in ischemic stroke, with a combined hazards ratio of 0.66. Thus this study really broadens our considerations of benefits versus risks of intensive antiplatelet regimens for the long-term secondary prevention in patients with patients with prior myocardial infarction. It really highlights the broader benefits in reducing ischemic stroke, and not just coronary events. In summary, overall, for 1,000 patients initiated on ticagrelor 60 milligrams twice daily for three years, 13 primary endpoint events would be prevented, including approximately five ischemic strokes. This benefit would come at a cost of nine TIMI major bleeds, but no hemorrhagic strokes or fatal bleeds.     That wraps it up for our summaries! Now for our feature paper. Our feature paper today discusses a really important issue that we face everywhere around the world, and that is the management of resistant hypertension. We're taking a very interesting look at the Renal Denervation for Hypertension trial, because we're actually looking at the adherence to anti-hypertensive therapy, and what we've learned in this trial. I'm so excited because I am sitting right here with first and corresponding author Dr. Michel Azizi, from Georges Pompidou hospital in Paris, France. Hello Michel, thank you!   Michel: Hello, Carolyn. Thank you also for the invitation to discuss about the paper.   Carolyn: We're also so lucky to have the associate editor who handled the paper, Dr. Wanpen Vongpatanasin, associate editor from UT Southwestern. Welcome, Wanpen.   Wanpen: Hi, Carolyn.   Michel: Hi, Wanpen.   Carolyn: This whole issue of resistant hypertension, I'll tell you, to me that means someone who's adequately treated, and despite all the treatment that we can throw at them, they still have a blood pressure that is above a certain level, right?   Michel: Yes.   Carolyn: But your study seems to tell us that that assumption, that everyone's receiving treatment and still having high blood pressure, may need to be questioned, so please tell us a little bit more about what you found.   Michel: This is a clinical trial where we compared the effect of renal denervation to medical treatment, optimal medical treatment. We standardized the anti-hypertensive treatment in the cohort of patients with resistant hypertension, and then we followed them on a monthly basis with home blood pressure monitoring. We also increased the intensity of the treatment every month after randomization between renal denervation against nothing, because this is a probe trial, it is not a double blind trial. We gave them the same treatment in both arms. At the end of the many study we demonstrated that there was 6 millimeter of difference, in terms of ABPM, in favor of renal denervation, against the same medical treatment alone.     However, because this trial was an open trial, it was open to a Hawthorne effect, and the possibility that patients or doctors behave differently in each arm of the study. Those having renal denervation may be more adherent to the treatment, and those not being given the new therapy, not being really adherent to treatment. This was an issue, so we specified analysis. We also measured drug levels in urine after six months of followup, and also assessed the exposure to each individual using a peptide in urine, which is N-acetyl-serylaspartyl-lysyl-proline (AcSDKP)/creatinine.     What we found after six months of followup in patients who really participated to this trial, they were willing to participate to the study, they signed an informed consent where it was written that, indeed, we will monitor drug levels. They knew that we would do this. They also knew that we will follow them very carefully every month, et cetera, that we'll provide them home blood pressure monitor for free. They had access to the same doctor, same nurse, same everything. They could arrive at the time they wanted in the morning for being investigated. After six months of followup we found that more than half of these patients did not take correctly their treatment, and even 15% of them, in reality, took zero medication over seven medications. This was a major, major surprise for us in this trial.   Carolyn: I think that's one of the most significant findings, even in a trial setting, that is such a lot of non-adherents, anti-habitants, of therapy. It really makes us question when we say someone has resistant hypertension, is it really that, or do we have just a very non-compliant patient?   Michel: Yes.   Carolyn: Because it can only be worse in the real-world setting, isn't it? Congratulations, that was a very striking message to me as well. What was the other main finding that you wanted to ... ?   Michel: The other finding was that the rate of non-adherence was similar in both arms. That there was absolutely no influence of being randomized to the renal denervation group or the medical treatment group only. This means that the patients were not influenced, and other physicians behaved similarly in both arms. Because at the end you have exactly the same rate of non-adherence to treatment. This is also very important.   Carolyn: Yes, indeed. Wanpen, I was wondering what your thoughts were, and take-home messages from this paper. We definitely thought it was significant in the editorial board because you even commissioned a wonderful editorial by Dr. David Calhoun on this. What are your thoughts?   Wanpen: In the United States, using the same technique, we found as much non-adherence. I think there is a lot that we need to do and to understand what caused non-adherence. The patient should not be the only party that's to blame. I think that the doctor's as much of a culprit here to try to tease out what's the barrier to the treatment. Also, as pointed out by Dr. Calhoun, is that although the trials show improvement in blood pressure in both groups, at the end number of medications of patients in resistant hypertension, they require to take four to five drugs to get the blood pressure under control. I think this is going to be a lifelong continuing medication treatment that the physicians have to face, and to deal with the adherence problem as well. Just lastly, I think that although people believe that doing drug levels is only for research purpose, but many people don't realize that actually many drug levels for anti-hypertensive drugs actually is clinical available and can be ordered. It takes a little bit more effort to order it, but it can be done, and actually our center has been doing that already anyway.   Carolyn: Wow. I cannot say that my center has been doing that in Asia, but I really have to admit that this paper made me think about it. Especially the editorial when he highlights it, the very unique information that is provided by actually measuring the blood levels. Michel, you were nodding your head vigorously when Wanpen was saying that we should not just blame the patient. Tell me, what are your thoughts, and how does this affect your clinical practice?   Michel: I fully agree with Wanpen. We have to now integrate the fact that it's accessible, you can measure drug levels through technology, with mass spectrometry, et cetera. This is very important to integrate and to change our paradigm that we have to put in our brain. We have to monitor drug levels. Using this technology we have to establish a partnership with the patient.     I think the truth, also, is somewhere, as Wanpen said, we are also culprits. If patients do not take their treatment, okay, there may be some benefit and e have to look why they are not taking pill treatment, but also we are culprits because we don't listen to them, we don't take enough time, et cetera, et cetera. But I think patients should not be only blamed, so it opens a new possibility to discuss with the patient about the fact that we didn't find the drug in levels in their urine, et cetera.     However, taking into account that there will be this toothbrush effect, that is, "Patient, brush your teeth when you go to see the dentist," you'll take the pills when you go to see the doctor so you can be treated. This is one of the difficulties. However I think it's a new possibility to discuss with the patient of his or her difficulties in taking the pills. It gives us the opportunity to discuss, to take time with our patients.   Carolyn: It's really fascinating, you're talking from a system based in Europe. You're based in Paris.   Michel: Yes.   Carolyn: Wanpen just said that she's doing it, and she's based in the US. Do you now routinely, maybe, monitor these medication levels?   Michel: Yes, yes, yes.   Carolyn: Wow.   Michel: In the hospital we have these mass spectrometer platforms, so we have access to this, and we are working with the house authority to have the reimbursement. Because I think it's important, because if it's not reimbursed there is also a problem.   Carolyn: Of course.   Michel: We are working to see how it could be reimbursed for labs doing these measurements.   Carolyn: But this is for maybe selected resistant hypertensive patients that are difficult to ... ?   Michel: Yes, absolutely. Those very difficult to manage. I think, as a rule of thumb, that after four or five drugs given to the patient, if the patient-   Carolyn: Yeah, we should start questioning, are they taking it.   Michel: If the patients do not have secondary hypertension, we should really start questioning ourself whether they are taking or not the treatment, even if they are looking right in your eyes and telling you, "Yes, doctor, I'm taking all the pills."   Carolyn: Wanpen, how about the reimbursement issues and things like that in the United States? How are you getting it done in your institution?   Wanpen: Actually the coding for doing drug levels, it's actually generic. It's the same coding for Digoxin or Cyclosporine. They actually don't care about what the name of the drug. Strangely, they're coded by the technique, so that's how we go with it, but we have to put in miscellaneous "other" for, we wanted to test for this. That's how we get around it.   Carolyn: Do you do that again routinely, or in selected patients that are difficult to manage hypertensive?   Wanpen: Obviously we have to be selective, so we select from people who we would suspect are non-adherent, but they say they're taking it. But if they already came in and made that they're not taking the drug, there's no point doing that for the clinical purpose. We're doing it for people who we suspect it, and we use it the way ... Actually we shall describe very well, not only just to find what drug they're not taking, because when they're not taking, only about 30% are not taking everything, about 20% not taking one or two drugs. When we drill down to that drug they say, "I have side effects to beta blocker and I don't want to tell my physician that I have problems taking it, but I just not take it." I think that's what led us to pinpoint the problem a little bit better with this technique.   Carolyn: What a lot of practical advice, and congratulations once again for very, very meaningful findings. I learned a lot this time. I don't do this, and so I'm definitely going to think about this much more because of your work. Thank you very much Wanpen, Michel.     And thank you, listeners, for tuning in this time. Remember, you're listening to circulation on the run. Listen in again next week. Thanks.    

You'll see renewed focus on appropriate med use in patients 65 and older...due to new Beers Criteria from the American Geriatrics Society. Continue to think of these guidelines as a "warning light" to be cautious with certain meds...NOT a "stop sign" to always avoid them. PPIs are new to the list. Discourage using PPIs for over 8 weeks without a good reason, such as chronic oral steroid use. Explain PPIs are linked to a higher risk of C. difficile, fractures, pneumonia, etc. Help patients taper off a PPI if needed. Advise lowering the dose, then taking it every OTHER day for a week or more before stopping. "Z drugs" (zolpidem, zaleplon, eszopiclone) are a concern now when used for ANY duration...not just over 90 days. Potential harms...such as delirium, falls, and fractures...seem to outweigh any benefit. Keep in mind not to turn to benzos...they're still on the list and aren't safer for sleep. Instead, emphasize nondrug strategies. Or consider suggesting low doses of trazodone or doxepin...or ramelteon. Nitrofurantoin used to be discouraged for UTIs if CrCl < 60 mL/min. But now feel comfortable suggesting it short-term if CrCl ≥ 30 mL/min...since new evidence supports its safety and efficacy in these patients. Digoxin should now be saved for atrial fib or heart failure patients only when other options aren't enough...since it may increase mortality. If digoxin must be used, recommend a max of 0.125 mg/day. Warfarin with amiodarone, anticholinergic combos, and other interactions can be riskier in seniors. Suggest avoiding if possible. Direct oral anticoagulants (dabigatran, etc), famotidine, gabapentin, and others may cause more side effects in renal impairment. Advise reducing the med's dose or avoiding it...based on renal function. Expect the Star Ratings high-risk med list to catch up eventually.

The post Digoxin (Lanoxin) appeared first on NURSING.com.

May Yen, toxicologist, talks about Digoxin and CCB toxicity in older adults. For the full description and to leave comments, please go to: http://gempodcast.com/2016/02/11/geriatric-toxicology-part-3-digoxin-and-ccbs/ Connect on twitter: @gempodcast Digoxin and Calcium Channel Blockers are both medications that can cause unstable bradycardias. Patients who overdose on them can present extremely ill-appearing, and require rapid intervention and stabilization. In this final geri-tox episode, Dr. May Yen talks about identifying and managing patients, particularly older adults, with these overdoses. Who needs digibind? How much insulin is used in high-dose insulin euglycemic therapy? What are some last ditch efforts for severe calcium channel blocker overdoses? We also drop some board review pearls. For example, those halos classically associated with cardiac glycosides such as digoxin seem to be much more prevalent on board exams than in real life. Image credit: en.wikipedia.org/wiki/File:Van_Go…_Art_Project.jpg Sound credits: sounds from freesound.org by Jobro and HerbertBoland

Tox-Dogmalysis is a talk about evidence in Toxicology. It’s been said that 50% of what we learn is incorrect; we just don’t know which 50%. As the complexity of medicine increases, it is of the utmost importance for clinicians to be skeptical of old data and new data alike. Many in the FOAM community have made huge strides in busting myths that have persisted over time. However, sometimes we may declare myths busted too prematurely based on incomplete or misunderstood data. This talk will explore three topics in toxicology for which the perceived myths may actually be true, or at least not completely busted.

Fahad and Amol want you to recognize that: 1. Idarucizumab as an agent that specifically reverses the hemostatic effects of dabigatran.  2. A post-hoc analysis of the ROCKET-AF study showed that digoxin is associated with increased mortality in patients with atrial fibrillation. The papers Idaracizumab for Dabigatran reversal. Digoxin use and mortality in ROCKET-AF. Good stuff http://www.smacc.net.au/about-us/welcome/ http://emupdates.com/wp-content/uploads/2015/06/Strayer-Opioid-Misuse-SMACC-Slideset.pdf ...The post Season Finale: Dabigatran Reversal and Digoxin Mortality appeared first on Healthy Debate.

Fahad and Amol want you to recognize that: 1. Idarucizumab as an agent that specifically reverses the hemostatic effects of dabigatran.  2. A post-hoc analysis of the ROCKET-AF study showed that digoxin is associated with increased mortality in patients with atrial fibrillation. The papers Idaracizumab for Dabigatran reversal. Digoxin use and mortality in ROCKET-AF. Good stuff http://www.smacc.net.au/about-us/welcome/ http://emupdates.com/wp-content/uploads/2015/06/Strayer-Opioid-Misuse-SMACC-Slideset.pdf ... The post Season Finale: Dabigatran Reversal and Digoxin Mortality appeared first on Healthy Debate.

Commentary by Dr. Valentin Fuster

Commentary by Dr. Valentin Fuster

PhysicianAssistantBoards.com - Lets go over everything you need to know about digoxin.  I made digoxin out to be this evil mythelogical drug that couldn't be understood while in school.  In reality, its very easy to understand.  After this podcast, you will know everything about digoxin!

Tina discusses the following rate control medications for atrial fibrillation: Beta blockers Bisoprolol Metoprolol Atenolol Calcium channel blockers (non-dihydropyridines) verapamil diltiazem Digoxin   References: CCS Guideline www.onlinecjc.ca/article/S0828-282X(12)00046-3/fulltext UptoDate uptodate.com  e-CPS www.e-therapeutics.ca/ RXFiles www.rxfiles.ca Lexicomp www.lexi.com The post A Fib 3: Rate Control Medications appeared first on Family Pharm Podcast.

This episode: Bacteria in the gut can affect dosaging of medications! Download Episode (7.1 MB, 7.75 minutes)Show notes:News item 1/News item 2/Journal Paper Post questions or comments here or email to bacteriofiles at gmail dot com. Thanks for listening! Subscribe at iTunes, check out the show at Twitter or Facebook

Emma Stoye on digoxin, a toxic product of foxgloves, and the birth of modern pharmacology

Mark & Associates, P.C. is currently representing victims of Digitek/digoxin overdose or toxicity due to pills containing twice the normal dose of active ingredient. Digitek is prescribed to treat heart failure and irregular heartbeat (arrhythmia). Tablets were sold with double the thickness as typical tablets, and it is suspected that these pills contained double the active ingredient. The double strength pills may lead to digitalis toxicity in patients experiencing renal failure or in those patients with decreased tolerance to the drug. If you or a loved one received these defective Digitek pills and suffered an adverse side effect, please contact us today for a free legal consultation about your case. We can be reached day or night by calling 1-866-50-RIGHTS (1-866-507-4448) or by visiting our websites: http://www.youhaverights.com and http://www.digitekdigoxinlawsuit.com

Mark & Associates, P.C. is currently representing victims of Digitek/digoxin overdose or toxicity due to pills containing twice the normal dose of active ingredient. Digitek is prescribed to treat heart failure and irregular heartbeat (arrhythmia). Tablets were sold with double the thickness as typical tablets, and it is suspected that these pills contained double the active ingredient. The double strength pills may lead to digitalis toxicity in patients experiencing renal failure or in those patients with decreased tolerance to the drug. If you or a loved one received these defective Digitek pills and suffered an adverse side effect, please contact us today for a free legal consultation about your case. We can be reached day or night by calling 1-866-50-RIGHTS (1-866-507-4448) or by visiting our websites: http://www.youhaverights.com and http://www.digitekdigoxinlawsuit.com

Mon, 1 Jan 1990 12:00:00 +0100 http://epub.ub.uni-muenchen.de/3551/ http://epub.ub.uni-muenchen.de/3551/1/3551.pdf Garry, F. B.; Klee, Wolfgang Garry, F. B. und Klee, Wolfgang (1990): Untersuchungen zur biologischen Halbwertszeit und Toxizität von Digoxin bei Kälbern. In: Tierärztliche Umschau, Vol. 45, Nr. 10: pp. 750-754.