Podcasts about metoprolol

See all the Healthcasts at https://www.biobalancehealth.com/healthcast-blog In my Anti-Aging-Longevity practice, one of the complaints my new patients tell me about is the fact that their hair is thinning, falling out or changing to a brittle texture, as well as the fact that their hair is turning grey. Hair DOES get thinner, coarser, and greyer as we age!  That is a fact, and one I can't fully explain to you, except that it happens to everyone!  My philosophy is that each of us should work with what we have, and optimize it, as well as treat any condition that makes hair loss work instead of wishing and wishing we had the hair we did when we were 25! Accepting the fact that your hair gets thinner after 40 and working with the hair you have takes knowledge to determine what is normal and what is not. Some of the things that everyone should know before looking for the best path forward to healthy hair. Aging and Slower Hair Growth Low Growth Hormone Lack of Estradiol and T in women and lack of T in men Aging causes Growth Hormone (GH) to decrease, which slows the growth of hair, fingernails, bone.  Your hair falls out at the same rate as it did when you were young, but the growth slows which results in losing more hair than you replace which thins your hair! If you started your young life with fine, thin hair, then this difference between growth and loss of hair can make your hair very thin.  To get to the root of the problem (I apologize) increasing GH will make your hair grow a bit faster. Testosterone replacement and Estradiol replacement both increase the growth of GH. Both hormone replacements increase hair thickness. Testosterone has a second benefit.  Testosterone makes your scalp oiler, which in turn increases the longevity of your hair. At menopause the lack of these two hormones causes a big change in hair thickness. Loss of hair in specific areas—Balding Genetics Scarring alopecia Androgenic alopecia Extensions Dread-locks Balding and alopecia both cause a person to lose hair follicles, not just slow the rate of hair growth.  Balding usually is genetically determined, so look at the older members of your family to determine what is in your future.  This type of hair loss is very difficult to treat. 50% of men have some balding by age 50, and 1/3 of women experience it sometime in their lives.  Until recently there was nothing to stop this process or grow more hair in those areas, however both men and women can resurrect their hair follicles (if they haven't been gone too long) and make them grow with the TED hair restoration painless ultrasound treatment by Alma. Other options are Hans Weiman hair transplants or weaves, both of which are extremely expensive, don't necessarily look natural (President Biden and his son) and must be redone every couple of years. Women can just cover over the problem with a wig, but even that answer has drawbacks—they are hot and itchy until you get used to it. Women can also get extensions to make their hair look thicker, but it ruins the quality of the hair you have which in the long run causes even more hair loss from scarring of the scalp. Women of color have traditionally used tight braids, cornrowing or dreadlocks to control their hair.  This cultural process causes them to break their hair off at the scalp and damage the hair follicle from tension, which results in hair no longer growing in multiple areas of the scalp. Change in Hair Texture and Dryness At menopause for women and when men's testosterone gets very low, we notice a change in texture of our hair. The cuticle area that covers the hair shaft becomes fragile and stops protecting the hair shaft, so the texture becomes frizzy, and hair breaks causing a dull look similar to what my mother used to call a “birds nest”. Our scalps become dry, and the oil glands dry up with age and loss of sex hormones, so hair is dry and frizzy, making us look like we just stuck our fingers in a light switch.  You can read about many “natural remedies” but beyond taking collagen, Biotin and B vitamins most supplements don't work in a dramatic way that would be noticeable. The remedies for hair loss include all the following and you will have to do most of them to improve your aging hair! Hormone replacement of Estradiol and Testosterone Conditioners (which only work a little) Hair color which covers the shaft with pigment and strengthens hair Brazilian treatment that drives straightener into the hair shaft and seals it with heat. Take supplements of Collagen every morning Take methyl B12 and Biotin daily Stop bleaching your hair Eat a diet with healthy fats and protein Wash your hair every 2-3 days Take the fat soluble vitamins A.E.K,D If you are anemic take iron supplements Avoid statins if possible   Other medical causes of frizzy, broken hair can be found in low thyroid hormones which slows hair growth, decreases oil production, and results in brittle hair all over the head. Replacing your thyroid hormones and supplementing your iodine can overcome this obstacle. All medicine changes should be managed by your doctor. Many drugs cause hair loss, and you can't change some of them: Metoprolol or any Beta blocker Blood pressure medication Prednisone and all steroids Cancer treatments Anything that inhibits your B vitamins like some autoimmune diseases What can you do to fix what you can fix! Nutrition: Hair is protein; however hair requires oil (fat) to grow and be beautiful—a diet rich in protein, and healthy fats give you the building blocks to make healthy hair and skin. Add Vitamins of A/E/K/D, vitamin C, Multi Methyl B vitamins with methyl folate and Biotin because our diets aren't perfect!   Hair care: Get hair products without sulfides.  They break hair and make it weak!  Wash your hair as little as possible. Decrease the use of hot hair tools like flat irons.  Color your hair and or Brazilian it to make it stronger. Medications not to take are listed above. But the medications to take to help your hair are your sex hormones, Estradiol, Testosterone, and make sure your DHT doesn't get too high which can cause hair loss in the male pattern. You may need Finasteride or Minoxidil if you have male pattern hair loss. Sun damage is important to maintain your hair in sunny areas.  Wear a hat or scarf when outside and comb some conditioner through your hair at the pool to “cover your hair from sun damage”.   Summary: Now that you know the possible causes and treatments for hair loss, you can do everything possible up to seeking medical care, and then medical care may be necessary. Hair thinning is often familial and also due to our estradiol and testosterone hormones decreasing after 35-40 years of age. You may need a scalp biopsy from a Dermatologist if your hair loss is in patches or severe over a short period of time, which implies an autoimmune disease. When you see a doctor be prepared with a list of your hair products, your diet, a list of medicines and a timeline for your hair loss.  This preparation will get you the best treatment per doctor visit, and your doctor will appreciate not having to ask you all those questions!

The JournalFeed podcast for the week of Feb 10-14, 2025.These are summaries from just 2 of the 5 articles we cover every week! For access to more, please visit JournalFeed.org for details about becoming a member.Monday Spoon Feed:Giving 1g IV tranexamic acid (TXA) prophylactically after delivering a baby in a high-risk patient prevented severe postpartum hemorrhage.Friday Spoon Feed:This systematic review of 13 studies found slightly higher rates of adverse events after administration of diltiazem versus metoprolol, when treating atrial fibrillation (a-fib) with RVR.

Should my stepson take a genetic test to evaluate his risk for pancreatic cancer?I had abdominal surgery last month. What can I do or take to minimize scarring?I have dry mouth. What treatments can I use to restore saliva?Could metoprolol be contributing to my restless legs syndrome?I've been diagnosed with a chemical imbalance and prescribed Zyprexa. What are your thoughts? 

En mamma misstänks för att ha låtit bli att matat sitt spädbarn, samt gett samma barn Metoprolol, en blodtryckssänkande medicin. Snart väcks misstankar om att detta rör sig om Münchhausen by proxy, eller barnmisshandel genom förfalskning av symptom. Idag hör ni förhören med mamman som misstänkts.Varning för våld mot barn i det här avsnittet.Av och med Tobias Henricsson/PRS Media.Mer om barnmisshandel genom förfalskning av symptom hittar du på www.bgfs.se.Glöm inte att sponsra oss på för att få fler och längre avsnitt! Gå in på patreon.com/krimmagasinet och donera en summa som podden får per månad.Du kan också swisha ett engångsbidrag till nummer 123 356 17 01 (betalningsmottagare: Tobias Henricsson).KONTAKT:E-post: krimmagasinet@prsmedia.seFacebook: www.facebook.com/prsmedia.seTänk om...? https://play.acast.com/s/tankom Get bonus content on Patreon Hosted on Acast. See acast.com/privacy for more information.

Welcome all to IS PHARMACOLOGY DIFFICULT Podcast! I am Dr Radhika VijayThis is the festive episode on the DIWALI day (2023) about Beta-1 Selective Antagonistic agents.Wishing everyone a Happy, Healthy, Wealthy Diwali '23 and great new year and season's greetings ahead!!In this episode, I will be describing the major features, Pharmacokinetics, Mechanisms, uses and side effects of Beta-1 Selective drugs like Metoprolol, Atenolol, Esmolol, Acebutolol, Bisoprolol and BetaxololThese would be the whole episode talk and it will be very useful to comprehend the various aspects and applications of these very important drugs.I will be wrapping up the episode with information and latest developments at my end like "Pharmacology Further" E-Newsletter and Podcast:The links for these are at all my websites and specifically:Link for E-Newsletter: https://pharmacologyfurther.substack.com/Link for the E-Newsletter Podcast: https://www.pharmacologyfurther.comFor all the updates and latest episodes of my podcast, please visit www.ispharmacologydifficult.com where you can also sign up for a free monthly newsletter of mine.It actually contains lot of updates about the medical sciences, drug information and my podcast updates also.You can follow me on different social media handles like twitter, insta, facebook and linkedin. They all are with same name "IS PHARMACOLOGY DIFFICULT". If you are listening for the first time, do follow me here, whatever platform you are consuming this episode, stay tuned, do rate and review on ITunes, Apple podcasts, stay safe, stay happy, stay enlightened, Thank you!!Please leave Review on Apple podcasts!My E-Newsletter sign up at Substack!Connect on Twitter & Instagram!My books on Amazon & Goodreads!

Welcome all to IS PHARMACOLOGY DIFFICULT Podcast! I am Dr Radhika VijayThis is the festive episode on the DIWALI day (2023) about Beta-1 Selective Antagonistic agents.Wishing everyone a Happy, Healthy, Wealthy Diwali '23 and great new year and season's greetings ahead!!In this episode, I will be describing the major features, Pharmacokinetics, Mechanisms, uses and side effects of Beta-1 Selective drugs like Metoprolol, Atenolol, Esmolol, Acebutolol, Bisoprolol and Betaxolol These would be the whole episode talk and it will be very useful to comprehend the various aspects and applications of these very important drugs.I will be wrapping up the episode with information and latest developments at my end like "Pharmacology Further" E-Newsletter and Podcast:The links for these are at all my websites and specifically:Link for E-Newsletter: https://pharmacologyfurther.substack.com/Link for the E-Newsletter Podcast: https://www.pharmacologyfurther.comFor all the updates and latest episodes of my podcast, please visit www.ispharmacologydifficult.com where you can also sign up for a free monthly newsletter of mine.It actually contains lot of updates about the medical sciences, drug information and my podcast updates also.You can follow me on different social media handles like twitter, insta, facebook and linkedin. They all are with same name "IS PHARMACOLOGY DIFFICULT". If you are listening for the first time, do follow me here, whatever platform you are consuming this episode, stay tuned, do rate and review on ITunes, Apple podcasts, stay safe, stay happy, stay enlightened, Thank you!! Please leave Review on Apple podcasts! My E-Newsletter sign up at Substack! Connect on Twitter & Instagram! My books on Amazon & Goodreads!

Here's a few clinical pearls from a cardiologist on beta blockers and how to use them correctly. Metoprolol and carvedilol and labetalol and propranolol and nebivolol are not interchangeable. https://dralo.net/links

The following question refers to Sections 6.1 and 7.3 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. The question is asked by Keck School of Medicine USC medical student & former CardioNerds Intern Hirsh Elhence, answered first by Greater Baltimore Medical Center medicine resident and CardioNerds Academy Fellow Dr. Alaa Diab, and then by expert faculty Dr. Mark Drazner. Dr. Drazner is an advanced heart failure and transplant cardiologist, Professor of Medicine, and Clinical Chief of Cardiology at UT Southwestern. He is the past President of the Heart Failure Society of America.  The Decipher the Guidelines: 2022 AHA / ACC / HFSA Guideline for The Management of Heart Failure series was developed by the CardioNerds and created in collaboration with the American Heart Association and the Heart Failure Society of America. It was created by 30 trainees spanning college through advanced fellowship under the leadership of CardioNerds Cofounders Dr. Amit Goyal and Dr. Dan Ambinder, with mentorship from Dr. Anu Lala, Dr. Robert Mentz, and Dr. Nancy Sweitzer. We thank Dr. Judy Bezanson and Dr. Elliott Antman for tremendous guidance. Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values. Question #25 A 50-year-old man with a history of type 2 diabetes mellitus, persistent atrial fibrillation, coronary artery disease with prior remote percutaneous coronary intervention, and ischemic cardiomyopathy with HFrEF (LVEF 38%) presents to your outpatient clinic. He denies dyspnea on exertion, orthopnea, bendopnea, paroxysmal nocturnal dyspnea, or peripheral edema. His heart rate is irregularly irregular at 112 beats per minute and blood pressure is 112/67 mmHg. Routine laboratory studies reveal a hemoglobin A1c of 7.7%. Which of the following medications should not be used to control this patient's comorbidities? A Metoprolol succinate B Verapamil C Dapagliflozin D Pioglitizone E Both B and D Answer #25 Explanation The correct answer is E – both verapamil and pioglitazone should be avoided here. Both verapamil and pioglitizone are associated with harm in patients with LVEF < 50% (Class 3: Harm). Verapamil and diltiazem are non-dihydropyridine calcium channel blockers. These medications can cause negative inotropic effects through inhibition of calcium influx and may be harmful in this patient population. Pioglitizone belongs to a class of diabetic medications known as the thiazolidinediones. This class of medications may increase the risk of fluid retention, heart failure, and hospitalization in patients with LVEF of less than 50%. Metoprolol succinate, and other evidence-based beta blockers, have a Class 1 recommendation for patients with reduced ejection fraction ≤ 40% to prevent symptomatic heart failure and reduce mortality. It may additionally help with rate control in this patient with atrial fibrillation and rapid ventricular response. SGLT2 inhibitors including dapagliflozin have a Class I recommendation for patients with symptomatic chronic HFrEF to reduce hospitalization for HF and cardiovascular mortality, irrespective of the presence of type 2 diabetes (Class 1, LOE A). They also have a Class I recommendation in patients with type 2 diabetes and either established CVD or at high cardiovascular risk to prevent hospitalization for HF (Class 1, LOE A). Our patient has asymptomatic, or pre-HF (Stage B) heart failure with poorly controlled diabetes, and so use of an SGLT2 inhibitor would be appropriate. Main Takeaway Non-dihydropyridine calcium channel blockers and thiozolidinediones both have Class 3 recommendations for harm in patients with reduced LV systolic dysfunction. Guideline Loc. Section 6.1 and 7.3   Decipher the Guidelines: 2022 Heart Failure Guidelines PageCardioNerds Episode PageCardioNerds Academ...

Have you been prescribed metoprolol tartrate or metoprolol succinate for a heart condition and want to know more about them? Would you like to save money on your medication costs? CareCard has all the answers and discounts you're looking for!Visit https://carecard.com/blog/metoprolol-tartrate-vs-metoprolol-succinate CareCard 6 St Johns Ln., New York, NY 10013, United States Website https://www.carecard.com Email prc.pressagency@gmail.com

The management of atrial fibrillation with rapid ventricular response is often complicated by the presence of heart failure with reduced ejection fraction. The presence of HFrEF limits pharmacologic options for rate control. This podcast will cover a retrospective study looking at the use of metoprolol vs diltiazem in patients with A fib with RVR and concomitant heart failure

In this month's episode, Assistant Editor and Amy Ho, MD, MPH, FACEP, chats with Ken Milne, MD, about his clinical column. Then, Dr. Ho speaks with Ron Stewart, MD, about his experiences within the emergency department as a patient. Registration is open for ACEP's Leadership & Advocacy Conference. ACEP Nowcast listeners can save $100 on registration with promo code POWERUP. Read more on ACEPNow.com Revisit ACEP Nowcast podcast episodes.  Catch up on all of ACEP Now in past issues.

Generic Name metoprolol Trade Name Lopressor, Toprol XL Indication tachyarrhythmias, HTN, angina, prevention of MI, heart failure management, may be used for migraine prophylaxis Action blocks the stimulation of beta1 receptors in the SNS, does not usually effect on beta2 receptors (cardioselective) Therapeutic Class antianginal, antihypertensive Pharmacologic Class beta blocker Nursing Considerations • monitor hemodynamics • may lead to bradycardia, pulmonary edema • use caution with MAOIs • assess I&Os and monitor for signs of CHF

To get a hold of my books, you can find Memorizing Pharmacology Second Edition HERE or Memorizing Pharmacology Mnemonics HERE In this episode, I go over how you can use PRO BAM CARLAB to remember the beta blocker generations and what that means for pharmacology indications and adverse effects.  

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat coming to you from Children's Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania from Cleveland Clinic Children's Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let's get into our episode: Welcome to our Episode: A Somnolent Toddler. Here's the case: A 2 yo M presents to the PICU after being found increasingly sleepy throughout the day. The toddler is otherwise previously healthy and was noted to be in his normal state of health prior to today. The mother dropped the toddler off at his Grandmother's home early this morning. Grandmother states that he was playing throughout the day, and she noticed around lunchtime the toddler stumbles around and acts more sleepy. She states that this was around his nap time so she did not feel it was too out of the ordinary. The toddler 1 hr later was still very sleepy, and the grandmother noticed that the toddler had some shallow breathing. She called mother very concerned as she also found her purse open where she typically keeps her pills. The grandmother has a history of MI and afib as well as hypertension. She is prescribed a multitude of medications. Given the child's increased lethargy, the grandmother presents the patient to the ED. In the ED, the child is noted to be afebrile with HR 55 & RR of 18. His blood pressure is 78/40. On exam he has minimal reactivity to his pupils, he has shallow breathing and laying still on the bed. A POC glucose is 68 mg/dL. Acute resuscitation is begun and the patient presents to the PICU. To summarize key elements from this case, this patient has: Drowsiness Bradycardia Normotension This is in the setting of being at grandma's home and having access to many medications Given the hemodynamic findings and CNS obtundation, this patient's presentation brings up concern for a clonidine or beta-blocker ingestion. This episode will be organized: Beta-Blocker poisoning We will also examine other medications that potentially can be toxic to a toddler (one pill can kill) present in Grandma's purse which include: TCA, CCB, Opioids, oral anti-diabetic agents, digoxin, etc. The presence of a grandparent is a risk factor for unintentional pediatric exposure to pharmaceuticals commonly referred to as the Granny Syndrome. Grandparents' medications account for 10% to 20% of unintentional pediatric intoxications in the United States. To kids, all pills look like candy. Let's start with a multiple choice. An overdose of which of the following medications may mimic the presentation of Metoprolol overdose? A. Verapamil toxicity B. Ketamine toxicity C. Valium toxicity D. Lithium toxicity The correct answer is A, verapamil toxicity. Verapamil is a non DHP CCB. It acts at the level of the SA and AV node similar to Metoprolol, a beta-1-specific antagonist. Both cause bradycardia and AV node block. Valium though a CNS depressant, can cause CV depression as well, however, would have fewer changes on the conduction system compared to a non-DHP CCB.  What is the mechanism of toxicity with beta-blockers? Beta-blockers are competitive inhibitors at beta-adrenergic binding sites, which results in decreased production of intracellular cyclic adenosine monophosphate (cAMP) with a resultant blunting of multiple metabolic and cardiovascular effects of circulating catecholamines. They attenuate the effect of adrenergic catecholamines on the heart Decrease inotropic and chronotropic response. Some drugs like Propranolol can act as Na channel blockers (myocyte membrane stabilizing activity) at high doses resulting in arrhythmias and seizures. Toxic doses of drugs like Sotalol can result in K channel blockade giving rise to prolonged QT and risk for...

Today, we're talking about metoprolol, which is a beta-blocker.  Examples of other beta blockers are atenolol, labetalol, and propranolol.   I picked metoprolol because it has three different pronunciations.  This is the only drug name I have encountered [so far] in the USP Dictionary Online that has more than one pronunciation.   Thank you for listening to episode 177 of The Pharmacist's Voice ® Podcast! To read the full show notes, visit https://www.thepharmacistsvoice.com.  Click on the podcast tab, and search for episode 177.  

It's another session of CardioNerds Rounds! In these rounds, Dr. Stephanie Fuentes (EP FIT at Houston Methodist) joins Dr. Hugh Calkins (Professor of Medicine and Director of the Electrophysiology Laboratory and Arrhythmia Service at Johns Hopkins Hospital) to discuss the nuances of atrial fibrillation (AF) management through challenging cases. As an author of several guideline and expert consensus statements in the management of AF and renowned clinician, educator, and researcher, Dr. Calkins gives us many pearls on the management of AF, so don't miss these #CardsRounds!  This episode is supported with unrestricted funding from Zoll LifeVest. A special thank you to Mitzy Applegate and Ivan Chevere for their production skills that help make CardioNerds Rounds such an amazing success. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. Case details are altered to protect patient health information. CardioNerds Rounds is co-chaired by Dr. Karan Desai and Dr. Natalie Stokes.  Speaker disclosures: None Challenging Cases - Atrial Fibrillation with Dr. Hugh Calkins CardioNerds Rounds PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Show notes - Challenging Cases - Atrial Fibrillation with Dr. Hugh Calkins Case #1 Synopsis: A woman in her mid-60s presents with symptomatic paroxysmal atrial fibrillation (AF). An echocardiogram has demonstrated that she has a structurally normal heart. Her primary care doctor had started Metoprolol 50 mg twice a day but she has remained symptomatic. In office, an EKG confirms AF, but she converts to sinus while there. She is seeking advice to prevent further episodes and in general wants to avoid additional medications Case #2 Takeaways We discussed several potential options for treatment. Amongst the first things we discussed was amiodarone. In a patient of this nature without structural heart disease and under the age of 70, Dr. Calkins discussed that he would probably consider amiodarone as a 2nd line option. While amiodarone may be effective in maintaining sinus rhythm in comparison to other antiarrhythmic medications like sotalol, flecainide, and propafenone, it does have significant toxicity.If antiarrhythmic drugs (AAD) were to be considered, we also discussed the options of dofetilide versus sotalol. Dofetilide typically requires inpatient initiation due to the risk of QT prolongation and Torsades. Since women tend to have longer corrected QT (QTc) intervals, high dose dofetilide may be more proarrhythmogenic in women. Though, Dr. Calkins noted that many patients don't tolerate sotalol due to fatigue and generally dofetilide is well tolerated.When it comes to the “pill in the pocket” approach, Dr. Calkins noted that its utility is more so in patients with persistent AF that is known to not stop on its own. For instance, an individual who has AF a few times a year that is persistent may benefit from flecainide or propafenone (“in the pocket”) instead of being brought in for an electrical cardioversion. In this scenario, the first time one of these agents is used, the patient ought to be closely monitored. For our patient, her episodes were too frequent and self-terminating for a “pill in the pocket” approach to be effective.Current guideline recommendations for catheter ablation include a Class IA recommendation for patients with paroxysmal AF refractory to AADs, and a Class IIA recommendation as first-line therapy for patients with paroxysmal AF.In the 2020 ESC Atrial Fibrillation Guidelines, catheter ablation is given a Class IA recommendation to improve symptoms of AF recurrences in patients who have failed or are intolerant of one Class I or III AADs. For patients who have failed or have been intolerant of beta blocker alone for rhythm control,

Trade– Lopressor, Toprol XLClass– Beta Blocker ( Class II antiarrhythmic) MOA– Inhibits the strength of the hearts contraction as well as the heart rateIndication– ACS, HTN, SVT, atrial flutter, Afib, thyrotoxicosis Contraindications– Cardiogenic Shock, AV Block, BradycardiaSide effects – Tiredness, dizziness, diarrhea, heart block, bradycardia, bronchospasm, drop in blood pressure.Dosing Adult: 5mg slow IV/IO over 2 minute period, Repeat at 5 minute intervals as necessary up to 15mgPediatric: Not Recommended 

Commentary by Dr. Valentin Fuster

Want to hear key medical literature facts to help become that awesome doctor, whilst also being able to tell if people like beer by their facial expressions?Your ears are in the right place.Dr LJ Smith, Dr Camille Hirons, Dr Jonathan Hudson and Dr Barnaby Hirons scour and digest the latest and greatest medical literature out there... and some other fun stuff too: Why pulse oximeters miss deadly hypoxia in people of colour. How paracetamol and sodium can kill. Are sweeteners a safe alternative to sugar? Empagliflozin in acute heart failure - EPULSE trial. Should we be banning tanning salons? Metoprolol vs Diltiazem in AF with RVR? How much exercise to save lives? Drug induced liver injury causes.Facial expressions drinking beer!Tell us what you think! Twitter @JournalSpotting, journalspotting@gmail.com, www.journalspotting.com.Rate us on apple podcasts or spotify.Share us everywhere.Want a free JS mug for your doctors' mess? Just get in touch.

It's the JournalFeed Podcast for the week of February 28 - March 4, 2022. We cover molnupiravir for COVID, bacterial meningitis, diltiazem vs metoprolol for a-fib with RVR, PLUS RCT on balanced fluids, and pad placement for a-fib cardioversion.

It's our last episode in 2021! This episode we have Dr. Libo Wang and Dr. Jon Harrison on to talk about their new paper in the Annals of Internal Medicine about ultrasound JVP for estimating CVP, validated with right heart catheterization. We also ask them their thoughts on a new meta-analysis looking at metoprolol vs diltiazem for atrial fibrillation with RVR. We also look at a new large retrospective study of apixaban vs rivaroxaban for stroke prevention, a study looking at reducing sleep interruptions in the hospital, and two new outpatient therapies for COVID-19 infection. Happy New Year! Ultrasound JVP for estimating CVPIV Diltiazem vs Metoprolol for A fib with RVRMajor Ischemic and Hemorrhagic Events in Apixaban vs Rivaroxaban for AFReducing Sleep Interruptions in Hospitalized Patients Early Remdesivir for Outpatient COVID-19Molnupiravir for Outpatient COVID-19Music from Uppbeat (free for Creators!):https://uppbeat.io/t/soundroll/dopeLicense code: NP8HLP5WKGKXFW2R

Commentary by Dr. Valentin Fuster

Welcome back to our weekend Cabral HouseCall shows! This is where we answer our community's wellness, weight loss, and anti-aging questions to help people get back on track! Check out today's questions:  Ryan: I know you're not a big fan of artificial sweeteners, but from what I've been able to find in the research, there seems to be many meta-analyses and RCTs, in humans, showing that there is no negative effect on bodyweight, glycemic variability or the microbiome, or that there is actually beneficial effects on bodyweight. Studies that show otherwise either seem to be in animals, or providing extremely large doses that would not be realistic for everyday life, or both. Is this a case of the science not being caught up to clinical practice and current times? Or is there definitive research showing the negative effects of artificial sweeteners in humans, in realistic doses? Would love if to hear your valued opinion on this. Thanks for all that you do! Marianne: Hi Dr. Cabral, I love your show. My husband was diagnosed with PVC or Pulmonary Ventricular Contraction. He is on the medication Metoprolol to regulate his heartbeat. He's trying to reduce his stress at work and reduce his alcohol consumption. He drinks about 2 cups of coffee per day. Is there anything else he can do or take to help regulate the heartbeat without medication? Anonymous: Huge fan of the podcast, I listen everyday! One topic I've never heard discussed is the use of anti-viral medications. I've heard a lot about antibiotics and the bad effects they can have on our guts, but I've never heard about anti-virals. The reason I ask, my 3 yr old has been taking low dose acyclovir daily for the past year to prevent frequently recurring cold sores. We think they picked this up from an extended family member or daycare, since nobody else in our family has ever had a cold sore. A year ago they were getting them about every other week. When one would show up, we'd immediately start acyclovir to knock it out quickly, but when we'd stop, another one would pop up a week or so later. We've also tried low arginine high lysine diet, which didn't seem to make much of a difference. I asked our pediatrician about taking a lysine supplement, but they didn't feel comfortable with that b/c of age. The low dose daily has worked really well for us, but now I'm concerned it may be causing other problems. Since early July, I've noticed hives about every other day on my child. They're mostly on the legs and torso, not huge, and they don't seem too bothersome, but I'm wondering if long term use of acyclovir could've caused this, thoughts? And any thoughts on daily lysine use? Tony: Hi Dr C, I can't find anything on your podcasts about amino acid BPC-157. Have asked your support team they said to ask here. Carpenter since a young boy, now in my 60s, used a lot of pressure on my knees for my job property developing, floor tiling etc, at one point (in my 50s) it was so bad I couldn't get up off the floor; lucky enough found a fantastic acupuncturist which made it a lot better. Unfortunately can't find him anymore. Job slowed down but knee pain got a lot worse, struggled to walk on my right knee, even considered knee replacement, prefer to avoid GPs, hospitals etc and go down an alternative route. My daughter had me on a decent turmeric/curcumin, MSM, Proteolytic Enzymes and arnica oil, until she found BPC-157. After a few days of this I could walk. The only thing that bothers her is that it is synthetic. So we gave it a couple of weeks then stopped. Knee has been overall good since apart from an odd day here and there but to go from barely walking to what feels normal is more than expected. My mood has also improved maybe because I can walk! Previously felt as though the bones or ligaments in my knee were rubbing together and there was no fluid. Normal weight, 5'9 don't do any strenuous exercise, other than my job and walking. Thank you Elizabeth: Hi Dr Cabral, My dad has had a dark spot (almost black and the size of a small mole) on the very right corner edge of his lower lip for the past year or so which has not changed. He has no desire to go to GP (had a few wrongful family experiences of being told something awful by a GP and it turning out to be wrong, so don't want to be looped into any fear mongering or pharmaceuticals). He is fine otherwise, in 60s, generally in good health apart from some stressful phases, eats a balanced diet, does love wine but never smoked/taken meds. I'm thinking maybe Angiokeratoma / vitamin deficiency or possibly hormone related. I've looked at the natural topical remedies that may help but wondered what may be best and whether topical iodine could be a solution? P.s. are you familiar with Indiumease? Thank you for all you do and this community Thank you for tuning into today's Cabral HouseCall and be sure to check back tomorrow where we answer more of our community's questions!  - - - Show Notes & Resources: http://StephenCabral.com/2122 - - - Get Your Question Answered: http://StephenCabral.com/askcabral   - - - Dr. Cabral's New Book, The Rain Barrel Effect https://amzn.to/2H0W7Ge - - - Join the Community & Get Your Questions Answered: http://CabralSupportGroup.com - - -  Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Stress, Sleep & Hormones Test (Run your adrenal & hormone levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - > View all Functional Medicine lab tests (View all Functional Medicine lab tests you can do right at home for you and your family)

Commentary by Dr. Valentin Fuster

Dr. Ian Stiell'in izniyle aslına sadık kalarak Türkçe'ye çevrilerek yayınlanmıştır.​1​ Bu Yazıda: A. Değerlendirme ve risk sınıflandırmasıB. Hız ve ritim kontrolüC. İnmenin ÖnlenmesiD. Taburculuk ve TakipKısaltmalar 2021 CAEP Akut Atriyal Fibrilasyon/Flutter En İyi Uygulamalar Kontrol Listesi A. Değerlendirme ve risk sınıflandırması Hızlı ventriküler yanıtlı AF/AFL, primer bir aritmi mi yoksa başka tıbbi nedenlere sekonder mi?Tıbbi nedenlere sekonder kalp hızı hızlanması (genellikle önceden var olan/kalıcı AF'si olan hastalarda), örneğin sepsis, kanama, PTE, KY, AKS, vb.:Altta yatan nedenleri agresif bir şekilde araştırın ve tedavi edinKardiyoversiyon zararlı olabilirAgresif hız kontrolünden kaçınınPrimer aritmi, örneğin ani başlangıçlı AF/AFL İPUCU: Tıbbi bir sebebe sekonder kalp hızı hızlanması düşündüren durumlar: Ani başlangıçlı değil, çarpıntı yokBilinen kalıcı AF hastası, OAK kullanıyor, eski EKG'sinde AF varAcil serviste KV özgeçmişi yokKalp hızı < 150 vuru/dkAteş, dispne, ağrı Hasta anstabil mi?Akut primer AF/AFL'ye bağlı instabilite, hızlı ventriküler yanıtlı preeksitasyon (WPW) ile AF'nin beraber olduğu durum dışında yaygın değildir:Hipotansiyon: SKB  2 mm)Pulmoner ödem: belirgin dispne, raller ve hipoksiAnstabil hastayı tedavi edin:Başlangıç  48 saat ise önce hız kontrolünü deneyin Bu primer AF/AFL hastasında KV yapmak güvenli mi?Güvenli ise, genellikle ritim kontrolü hız kontrolüne tercih edilir: Yaşam kalitesi, daha kısa kalış süresi, daha az hastane kaynağıAşağıdaki durumlarda KV yapmak güvenlidir:Hasta en az 3 hafta süreyle yeterince antikoagüle edilmiş ise, VEYAHasta 3 haftadan uzun süredir yeterince antikoagüle edilmemiş, inme veya GİA öyküsü yok, kalp kapak hastalığı yok VE:Başlangıç 

Hoy revisamos el grupo de medicamentos conocidos como beta bloqueadores o antagonistas beta adrenérgicos, revisamos cómo se pueden usar en enfermedades como la insuficiencia cardiaca, el infarto al corazón, la angina de pecho y en particular la hipertensión, también revisamos su uso en ansiedad y en migraña.Revisamos también los posibles eventos adversos asociados a estos fármacos como la bradicardia, los bloqueos cardiacos, la hipotensión y algunos que no son del sistema cardiovascular como la hipoglucemia o la dislipidemia y la precauciones en cuanto a combinación de medicamentos.Visita nuestra tienda en línea para comprar nuestros libros y material educativo:https://bit.ly/3i6eAnGCheca el video aquí: https://youtu.be/e5hU54wrsPkSi necesitas una consulta aquí nos puedes encontrar:http://bit.ly/3aUSt12Unete al equipo de Mecenas en YouTube desde 1 dolar al mes: http://bit.ly/2O1AtsXSupport the show (https://www.paypal.com/donate?hosted_button_id=2ENWQ7V289PBE)

First join author Marc Dweck and Associate Editor Victoria Delgado as they discuss the article "Effect of Denosumab or Alendronic Acid on the Progression of Aortic Stenosis: A Double-Blind Randomized Controlled Trial." Then, join authors Torbjørn Omland and Geeta Gulati as they discuss the article "Prevention of Cardiac Dysfunction During Adjuvant Breast Cancer Therapy (PRADA) Extended Follow-Up of a 2×2 Factorial, Randomized, Placebo-Controlled, Double-Blind Clinical Trial of Candesartan and Metoprolol." Dr. Carolyn Lam: Welcome to Circulation On The Run. Your weekly podcast summary and backstage pass to the journal and its editors. We're your co-hosts. I'm Dr. Carolyn Lam Associate Editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: I'm Dr. Greg Hundley, Associate Editor, Director of the Pauley Heart Center, VCU Health in Richmond, Virginia. Dr. Carolyn Lam: Hooray, it's another double feature week! And guess what, these two papers are two randomized control trials. One looking at progression of aortic stenosis and the other, looking at a prevention of cardiac dysfunction following adjuvant breast cancer therapies. Dr. Carolyn Lam: So, very interesting two papers coming right up. But Greg, why don't you start by highlighting some of your favorite papers from today's issue. Dr. Greg Hundley: You bet Carolyn. Dr. Greg Hundley: So my first study was conducted by Dr. Gabriela Trifan and colleagues from University of Illinois who performed a meta analysis of major studies that compare the efficacy and safety of dual anti-platelet therapy versus monotherapy for secondary prevention of recurrent stroke or transient ischemic attack in those previously experiencing minor non cardioembolic stroke. And their primary outcomes were stroke and the composite of stroke, TIA, acute coronary syndrome and death of all cause. And the safety outcome was major hemorrhage. Dr. Carolyn Lam: Oh, okay. Very important study. What did they find? Dr. Greg Hundley: Right Carolyn. So the analysis included 27,358 patients. And compared with monotherapy, dual anti-platelet therapy reduced the risk of recurrent stroke and the composite outcome, but increased the risk of major bleeding. And in subgroup analysis at less than or equal to 30 days, dual anti-platelet therapy increased the risk of hemorrhage relative to monotherapy. In sensitivity analyses, the risk for hemorrhage with less than or equal to 30 days of dual anti-platelet therapy, after excluding the combination of aspirin plus Ticagrelor, was comparable to monotherapy. However, the risk of stroke recurrence and composite outcomes in the subgroup and sensitivity analyses remained decreased compared to monotherapy. Dr. Greg Hundley: And so Carolyn, the take-home message from this paper is that dual anti-platelet therapy decreases the risk of recurrent stroke and composite events compared with monotherapy. But, dual anti-platelet therapy increases the risk of major hemorrhage, except if the treatment is limited to 30 days and does not include the combination of aspirin plus Ticagrelor. Dr. Carolyn Lam: Ah, thanks for that last take home message. Thank you. Dr. Carolyn Lam: Well, the paper I'm going to tell you about is the first to examine the role of epicardial fat derived extracellular vesicles in the pathogenesis of atrial fibrillation. And this comes from Dr. Leor from Sheba Medical Center, Tel Aviv University in Israel and his colleagues who collected epicardial fat specimens from patients with and without atrial fibrillation during elective heart surgery. Dr. Carolyn Lam: Epicardial fat samples were grown as organ cultures and the culture medium was collected every two days. And the authors then isolated and purify these epicardial fat extracellular vesicles from the culture medium. Dr. Carolyn Lam: They found that epicardial fat extracellular vesicles of patients with atrial fibrillation had unique pro-inflammatory, profibrotic and proarrhythmic properties. Epicardial fat extracellular vesicles could in fact induce cellular, molecular and electrophysiological remodeling that could result in atrial fibrosis, myopathy and the development of atrial fibrillation. Dr. Greg Hundley: Wow Carolyn, so what are the clinical implications of epicardial fat extracellular vesicles? Dr. Carolyn Lam: Hmm, good question. Well, understanding their role in the pathogenesis of atrial fibrillation may for one lead to the discovery of new diagnostic markers or new targets for the prevention and treatment of atrial fibrillation. And that combined pro-inflammatory profibrotic and proarrhythmic effects of these epicardial fat and extracellular vesicles may in fact be relevant to the pathogenesis of other cardiovascular diseases associated with obesity and abnormal adipose tissue deposition. Dr. Greg Hundley: Very nice Carolyn. Dr. Greg Hundley: My next paper comes again to us from the world of preclinical science and these authors led by Dr. Masanori Aikawa from Harvard Medical School applied a systems approach in mouse experiments to discovering therapeutic targets for vein graft failure. They use global proteomics and high dimensional clustering on multiple vein graft tissues to identify potential pathogenic mechanisms. And experiments were conducted in both in vivo mouse models and in vitro human macrophages. Dr. Carolyn Lam: Oh wow. So what did they find? Dr. Greg Hundley: So Carolyn, peroxisomes proliferator activated receptors or PPAR alpha agonism by pemafibrate retarded the development and inflammation of vein graft lesions in mice, while gene silencing worsened plaque formation. Pemafibrate also suppressed arteriovenous fistula lesion development. Dr. Greg Hundley: Now, metabolomics, lipidomics, functional metabolic assays and single cell analysis of cultured human macrophages revealed that PPAR alpha modulates macrophage glycolosis, citrate metabolism, mitochondrial membrane sphingolipid metabolism and heterogeneity. Dr. Carolyn Lam: Okay. So what is the take home message Greg? Dr. Greg Hundley: Right Carolyn, thought you would ask me that. Dr. Greg Hundley: So PPAR alpha activation suppresses the development of vein graft and arterial venous fistula lesions. And PPAR alpha reduces macrophage activation by influencing macrophage heterogeneity, mitochondrial integrity, and the metabolome. So Carolyn, given that peripheral arterial disease and chronic kidney disease prevalences are increasing, warranting needs for more vein grafts and arterial venous fistulas, this target discovery platform is applicable to investigating therapies for these diseases. Dr. Greg Hundley: And a really nice accompanying editorial is provided by doctors Reilly and Bornfeldt. Dr. Greg Hundley: Well Carolyn, how about we turn to look at what is in the mailbag this week? Dr. Carolyn Lam: Well let me tell you about it Greg. We've got a cardiovascular case series by Dr. Borlaug on things are not always as they seem, multimodality exercise assessment and evaluation of dyspnea. In cardiology news by Kuhn there's a discussion of Evinecumab approval adds a new option for homozygous familial hypercholesterolemia with a hefty price tag. A perspective piece by Dr. Watkins on time to think differently about sarcomere negative hypertrophic cardiomyopathy. And finally a research letter by Dr. Ahn on reduction in Kawasaki disease after non-pharmaceutical interventions in the COVID-19 era, a nationwide observational study in Korea. Dr. Carolyn Lam: Wow. That wraps it up for the summaries. Let's go on to the feature discussions shall we, Greg? Dr. Greg Hundley: You bet. Dr. Carolyn Lam: We are about to talk about the extended follow-up results of the PRADA trial. Oh, so interesting. So happy to have with us today, doctors Geeta Gulati and Dr. Torbjørn Omland, both from the Akershus University hospital in Norway, and you would probably recognize that Dr. Torbjørn Omland is also one of our associate editors, but both here are the co-corresponding authors of this beautiful paper. Dr. Carolyn Lam: Thank you so much for coming here today. Torbjørn, maybe you could start with what is the PRADA trial? Why did you decide to do an extended follow-up? Dr. Torbjørn Omland: Yeah so PRADA was a two times two factorial randomized double blind clinical trial that sought to evaluate the effects of intervention with receptor blocker Candesartan. And a beta blocker Metoprolol in patients with early breast cancer who received anthracycline therapy as part of their chemotherapy. And then we wanted to assess the effect of this sort of preventative therapy, left ventricular function and injury. Dr. Torbjørn Omland: So we reported the primary results of the trial a few years ago and showed that intervention with Candesartan most associated with a significant elevation of the reduction in left ventricular ejection fraction that these patients may experience, and also that treatment with the beta blocker Metoprolol was associated with an intimation of the increase in cardio proponents suggesting a beneficial effect on myocardial injury. However, whether these results were or these effects were sustained after termination of the study drugs was unknown. And that was what we really wanted to address with extended follow-up study. Dr. Carolyn Lam: Yeah, makes a lot of sense, especially because these injuries I suppose could still continue. And just to be very clear, the medications though were only taken during the adjuvant chemotherapy and therefore could be a variable duration from what I understand. Right? Great. Dr. Carolyn Lam: So Geeta then, could you tell us what did the extended analysis show? Dr. Geeta Gulati: The extended follow-up was interesting and it was something we really wanted to figure out because there are not many studies who have been done on the extended follow-up and you're not giving these study medications afterwards. Dr. Geeta Gulati: So very interestingly we saw that the decline in the ejection fraction was still there in the whole group. But this time there was no difference in the group who received Candesartan do those who didn't. And we show that there was a different in the primary results, but now in the extended follow-up there was no difference. And then also in the Metoprolol group that had previously shown that there was lesser rise in the troponins. Again, there was no difference in the groups now on the extended follow-up. Dr. Geeta Gulati: So this is very interesting because this shows that there is a small, modest decline in a left ventricular ejection fraction during and after the breast cancer therapy. But what does this really mean? It's a small decline and it's within the normal range and the cardioprotection is not working. So, are we perhaps looking at the wrong group? Perhaps we should look at patients who have the higher cardiovascular risk factors. Perhaps even we should look at more novel heart failure or cardiac drugs that may have a stronger effect on the ejection fraction. Dr. Carolyn Lam: Right. So Geeta though, can we unpack that a little bit? You see, the patients were not on the medication anymore at the time of follow-up. So you're saying that even though they were given adjuvant chemotherapy and covered with the drug, that even not having any more chemotherapy, their ejection fraction still fell. And if I'm not wrong, this was an MRI analysis. And so it was only by an ejection fraction of two percent on mean fall, right? How do we think about that clinically? Dr. Geeta Gulati: And that's the important question, isn't it? Because a decline in the ejection fraction of less than two percent within the normal range, what does it really mean? Well initially we thought that if there was a different in those who had cardioprotective medication compared to those that didn't, it may prevent development of further decline in the cardiac function and then heart failure in the future. But now, there is really no difference between the groups. So perhaps the clinical implication of giving cardio protection to all cancer patients is not really that useful. Perhaps they should look at those who are at higher risk because they would have a greater fall in ejection fraction and then more cardioprotective effect of these drugs. Dr. Carolyn Lam: Yeah, totally. And perhaps the metrics that we're used to seeing in the past with greater falls of ejection fraction, maybe it just doesn't apply currently or perhaps with the specific chemotherapeutic regimens perhaps that you're using now. Because with a very small fall, and I believe you only had one heart failure event, right? If I'm not wrong in this extended follow-up. So, just to let the audience know, it was very small fall, little number of events. It's hard to really tease apart what that clinically means. Now, could I ask though, does it mean we need actually a more sensitive marker? Because there was some interesting stuff about global longitudinal strain. Could you- Dr. Geeta Gulati: I would throw that question back to Torbjørn I think. Dr. Torbjørn Omland: Yes. So that's a very interesting question Carolyn. So we did observe what seemed to be a beneficial, but a sort of minor effect on global longitudinal strain. So we know that that is the more sensitive index of systolic function than left ventricular ejection fraction, that was the pre defined primary outcome. So that's raises of course questions whether a future trial should more focus on these more sensitive indices of cardiac function. Dr. Carolyn Lam: Yeah. Geeta, could I then really put it back to you? And the tough question I always get, how do we apply these results clinically then? I mean, you see these patients right? Now what? Do you give or do you don't give? And which one do you give? And how do you identify high risk patients? I don't know. Dr. Geeta Gulati: Again, I think all the patients are unique aren't they? So that's where we have to start. So in my clinic, if I have a high risk patient with hypertension, diabetes, hypercholesterolemia, yeah perhaps they even have had a cardiovascular disease before something like this. Then I will take more care of these patients and be more careful with the echo measurements I'm doing and if I find that they have a decline in their cardiac function, I may be more eager to start them on cardioprotective medication. Dr. Geeta Gulati: But then in R-Regen we follow all the HER two positive breast cancers with echo. If I don't have echoparamaties that clearly tells me that they have a decline in the cardiac function, then I may wait to start cardio protection because none of the studies has really so far show that all patients should have these cardioprotective medication or prevention. Dr. Carolyn Lam: Nice. Thank you. That was a tough one to get at. And I suppose Torbjørn I have to give you another tough one then. Because how to address the remaining unanswered questions, right? Because one of them on my mind too, is how to identify the high risk, do biomarkers play a role? And then the other is if we then start the preventive therapies like ERBs and beta blockers, should we actually continue it forever? And so on. But anyway Torbjørn please, please, what does the future hold? Dr. Torbjørn Omland: I think it's worthy of a recap or underscoring that these are really good news for many breast cancer patients that actually the risk of an important decline in ventricular function is lower than we thought. So that may be because of several things. I think in general, those whose used these cardiotoxic drugs are lower. And we also, I think that there's increased collaboration between oncologists and cardiologists. Also meaning that we are better to pick up the high-risk patients at an early stage. Dr. Torbjørn Omland: But of course, it's very important questions that you asked regarding how to identify the high risk patients. And I think that's where really future research should focus. So there we know that traditional risk factors are important. We are looking into whether biomarkers can be used, if there's more sensitive imaging in this can be used. But so far we haven't really succeeded in getting the risk model that really identifies it on the patient level. So that's work that remains to be done. Dr. Torbjørn Omland: And then we are also looking for new types of intervention, good exercise, good other drugs. We are doing now a PRADA two study where we look at the effects of Sacubitril Valsartan in this setting. And those are also very exciting, I think, and we look very much forward to present that in the future. Dr. Carolyn Lam: Oh wow thank you so much Torbjørn and Geeta. The PRADA two trial. I've got to ask you, why do you then call it the Chanel trial? But I think I'll save that for another day. So thank you. Thank you once again, this is fabulous and congratulations to you both. Dr. Torbjørn Omland: Thank you. Dr. Geeta Gulati: Thank you. Dr. Greg Hundley: Well listeners, welcome to our second feature discussion today. And we have with us Dr. Marc Dweck from University of Edinburgh in Scotland and our own associate editor, Victoria Delgado from Leiden in the Netherlands. Welcome to both of you. Dr. Greg Hundley: Marc, we're going to get started with you. Could you tell us a little bit about the background for your study and what was the hypothesis that you wanted to test? Dr. Marc Dweck: Thanks very much Greg for the invitation. So I guess aortic stenosis is perhaps the last major cardiovascular condition where we don't have a medical therapy. We're unable to treat these patients. We're unable to prevent progression. We're only left with a valve replacement. And so we, like a lot of groups around the world, want to develop a treatment for aortic stenosis. Our group did the first SALTIRE trial, where we looked at statins seeing if we could slow aortic stenosis progression. And that, like similar trials, was neutral. No effect on the valve progression. Dr. Marc Dweck: And so actually I've spent the last 10 years looking at some of the factors associated with aortic stenosis progression in particular. The answers that we've had from those trials have kind of come back telling us that really it's a process of calcification. If you look at what triggers progressive valve narrowness is this calcific process, that seems to be a self perpetuating disease. Dr. Marc Dweck: So the question is, how do you target this calcification process? How can you interrupt it? And how can you do that without compromising bone health in these elderly patients? So in trying to come up with a solution to that we thought about using osteopetrosis agents, which we hypothesized would maintain both bone health and reduce vascular calcification on the basis of observational data and also animal data suggesting that. And that was really where we came from in the design of the SALTIRE two trial. Dr. Marc Dweck: And doing a big trial with clinical endpoints wasn't felt to be feasible and instead we decided to look at imaging end points and see whether we could slow disease progression using these agents. Dr. Greg Hundley: Very nice Marc. And so you're really leading us into, tell us a little bit more about your study population and your study design. Dr. Marc Dweck: Yeah so we wanted to take patients from our outpatient clinic with mild, moderate and even early severe disease, asymptomatic patients crucially, patients that aren't scheduled for aortic valve replacement and see the effects of these drugs on disease progression. Dr. Marc Dweck: So we did a randomized control trial. There was three arms. Patients were randomized to Alendronate, Denosumab, these are the two osteopetrosis agents, or placebo. We then did a series of baseline imaging tests. So the primary end point was based on CT calcium scoring. So they had a baseline CT calcium score. They also had a baseline echocardiogram and they had a baseline fluoride PET scan. So this measures calcification activity in the valve. And then we essentially repeated those tests after a period of time on the drugs, or on placebo. We repeated the calcium score and the echo after two years and repeated the PET scan after one year. Dr. Greg Hundley: Very nice, and so before you tell us your results, a little bit, how many patients? And maybe their average age and the rough distribution of men versus women. Dr. Marc Dweck: Yeah so study recruited roughly 50 patients in each arm. The average age was 72 and there was 21% females in the study. So, like a lot of studies in aortic stenosis, a low female prevalence. Despite our best efforts, that's something we need to attend to in the future, but otherwise, a representative age group and patients with this disease. Dr. Greg Hundley: And what did you find? Dr. Marc Dweck: Well we found that the drugs didn't have an effect on any of these imaging assessments. So, there was no effect on the progression for CT calcium score at two years, no effects on any of the echocardiographic assessments of hemodynamic severity, and no effect on calcification activity as measured with the fluoride. Dr. Marc Dweck: So a very consistent result using multiple different imaging modalities, which I think gives us confidence that there isn't at least a dramatic effect of these drugs on disease activity or disease progression, in aortic stenosis. Dr. Greg Hundley: Very good. Well listeners, we're now going to turn to one of our associate editors, Dr. Victoria Delgado, and she is really a valvular heart disease expert member of our team. Dr. Greg Hundley: Victoria, I know you see a lot of papers that kind of come across your desk. What attracted you to this manuscript? And then how do you put the results in the context of other research that's going on to halt the progression of aortic stenosis. Dr. Victoria Delgado: Thank you Greg. So first the first thing that attracted my attention for this article is the question. We know that we don't have any medical therapy for halting the progression of aortic stenosis. And even if the previous studies have been negative or neutral, still there is the interest of trying to find a less invasive therapy for these patients, or even prevent that they arrive to surgical or transcatheter aortic valve replacement. Dr. Victoria Delgado: And the second is that these are very strong analysis because it's a randomized clinical trial and using as end points imaging. So that trial also in a way answers the question of which imaging technique we need to use in order to see the effects of specific therapies. Previous studies have used mainly echocardiography, but that only gave us information on the modynamic effects of the aortic stenosis. While in this study, we have the combination of CT and a combination of a PET that he give us also information on how the calcification is happening. So that makes the study very comprehensive and give us more insights into this pathophysiology, to this pathology particularly. Dr. Greg Hundley: Very nice. So it sounds like looking at aortic stenosis from multiple different angles, whether it be echocardiography or perhaps imaging processes that look at the progression of calcification. Dr. Greg Hundley: Well, Marc, I want to come back to you. What do you think is the next, sounds like you've been working in this area for an extended period of time. What do you see as the next research study that you and your group may undertake in this area? Dr. Marc Dweck: I Think we've got the study design about right. I think if in the future studies we want to do, I think we would adopt a similar design using these imaging end points. Dr. Marc Dweck: I have to say I'm very influenced by the recovery trial that has been conducted in the UK with COVID. I mean, here's a disease where we wanted to get a treatment as quickly as we can. And in doing that, developing a platform type trial where you potentially test multiple different promising agents simultaneously across multiple centers across the world or the UK, I think that would be the quickest way to developing a treatment. And so I'm encouraged that there are five or six very good targets where we could, for a new therapy in aortic stenosis. And I think a platform type design where we engage multiple groups using imaging as that initial end point. And then, the drugs that appear to have an effect on these imaging end points we can start to recruit more patients at those sites, into those centers, looking for clinical end points. Dr. Marc Dweck: I think that kind of discussion is happening around the world now between groups that are interested because we want to crack this problem quickly. We don't want to wait and do these different studies sequentially. We want to try and do them simultaneously. And I'm excited about that. I think if we do that, we've got a real shot at developing a treatment over the next five to 10 years say. Dr. Greg Hundley: Fantastic. Dr. Greg Hundley: And Victoria, I know you have interest in this particular area. Do you have anything you'd like to add? Dr. Victoria Delgado: Yeah. I think that those studies that Mark said are really welcome and I hope that they are positive. And give us a little bit of more to treat these patients. My main fear is that these patients are not as frequent, for example, as heart failure patients. Where we have several therapies where we have possibility to enroll patients in trials for new drugs, that we know that probably are going to be effective. But for valvular heart disease it has been always the end point to reach surgery or to reach an aortic valve replacement or indication of the mitral valve and mitral valve repair. So in early phase of the disease, my main concern is that maybe the patient is not going to be well-trained to understand what are the consequences. I want to always wait until maybe when is needed for the surgical or transcatheter procedure. Dr. Victoria Delgado: But I think that increasing the awareness of the prevalence of valvular heart disease and the consequences may help people to understand, to put more attention for an early diagnosis and develop new drugs that can help, like in this case, aortic stenosis one of the most frequent valvular heart disease, to prevent the proliferation and to prevent the replacement of the valve. Dr. Greg Hundley: Very nice. Well listeners, this has been a wonderful discussion and we greatly appreciate the input that we've been able to gather today from Dr. Marc Dweck from Edinburgh in Scotland and our own associate editor, Dr. Victoria Delgado. Bringing this information from a randomized trial, evaluating osteoporosis drugs, and really indicating they did not disrupt the progression of calcification in patients with aortic stenosis. Dr. Greg Hundley: Well, on behalf of Carolyn and myself, we want to wish you a great rest of your week and we will catch you next week on The Run. Dr. Greg Hundley: This program is copyright of the American Heart Association, 2021. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, visit ahajournals.org.  

It’s the JournalFeed Podcast for the week of Feb 1-5, 2021. We cover the accuracy of history, exam, labs, and POCUS for diagnosing giant cell arteritis; diltiazem vs. metoprolol for atrial fibrillation with rapid ventricular response; and IV ketorolac dosing for renal colic.

Der Klinisch Relevant Podcast liefert Ärztinnen und Ärzten, sowie Angehörigen der Pflegeberufe kostenlose und unabhängige medizinische Fortbildungsinhalte, die Du jederzeit und überall anhören kannst.

Metoprolol is an anti-anginal, anti-hypertensive agent that works by selectively inhibiting the beta1 adrenergic receptor. Some of the brand names are Lopressor, Toprol XL, and Kapspargo Sprinkle. Dosing may vary based on if the formulation is the IR or ER form and by indication. For Angina in adults the IR tartrate form starts at 50 mg po bid with weekly increases to a max of 400 mg/day. There is a black box warning for Ischemic Heart Disease warning that abrupt cessation of therapy may harm patients and if therapy is to be discontinued, the patient should be titrated down over 1-2 weeks. The most common side effect is orthostatic hypotension. Go to DrugCardsDaily.com for episode show notes which consist of the drug summary, quiz, and link to the drug card for FREE! Please SUBSCRIBE, FOLLOW, and RATE on Spotify, Apple Podcasts, or wherever your favorite place to listen to podcasts are. The main goal is to go over the Top 200 Drugs with the occasional drug of interest. Also, if you'd like to say hello, suggest a drug, or leave some feedback I'd really appreciate hearing from you! Leave a voice message at anchor.fm/drugcardsdaily or find me on twitter @drugcardsdaily --- Send in a voice message: https://anchor.fm/drugcardsdaily/message

In this week's LIVE Q&A Show, Dr. Rogers answers YOUR questions! This week's questions: 1. I have read that taking the high blood pressure medicine, Valsartan, helps with Covid. What is your opinion on this? Also, what do you think about taking Metoprolol? 2. Would Phentermine be okay to take if you have restless leg syndrome? 3. Is Botox safe? I feel weird about injecting something foreign in my face. 4. How do you treat Adrenal Fatigue? How do you know you have adrenal fatigue? 5. When is the best time to start BHRT for a woman? What did you think of this episode of the podcast? Let us know by leaving a review! Connect with Performance Medicine! Sign up for our weekly newsletter: https://performancemedicine.net/doctors-note-sign-up/ Facebook: @PMedicine Instagram: @PerformancemedicineTN YouTube: Performance Medicine Audio

Você sabe qual é a diferença entre o tartarato e o succinato de metoprolol? E quais os critérios para a correta dispensação de medicamentos contendo estas diferentes formas moleculares? Neste vídeo, o Prof. Lincoln Cardoso esclarece estas e outras dúvidas. Quer saber? #SaberFarmácia

In this Live Friday CME Series recap, Dr. Todd Holcomb, an Internist and hospitalist with Lakeview Clinic and Ridgeview Medical Center, presents an interesting Internal Medicine case that is sure to scratch some heads, and remind us of the need to go back to the beginning, if it's not making sense after several attempts. Dr. Holcomb is accompanied by cardiologist Dr. Joshua Buckler, with Minneapolis Heart Institute, Dr. Jonathan Larson, family physician at Lakeview Clinic, Dr. Carl Dean, nephrologist with Kidney Specialists of Minnesota, and Dr. David Gross, radiologist with Consulting Radiologists.  So put on your thinking caps, listen closely and ask yourself what you would do as Dr. Holcomb guides us through this interesting case. Enjoy the podcast! OBJECTIVES:    Upon completion of this podcast, participants should be able to: Identify secondary causes of hypertension. Identify when further testing is warranted. Discuss newer treatments available for cholesterol related conditions. CME credit is only offered to Ridgeview Providers for this podcast activity. Complete and submit the online evaluation form, after viewing the activity.  Upon successful completion of the evaluation, you will be e-mailed a certificate of completion within 2 weeks.  You may contact the accredited provider with questions regarding this program at  rmccredentialing@ridgeviewmedical.org.   CLICK ON THE FOLLOWING LINK FOR YOUR CME CREDIT: CME Evaluation: "2019 Internal Medicine Case Conference" (**If you are listening to the podcasts through iTunes on your laptop or desktop, it is not possible to link directly with the CME Evaluation for unclear reasons. We are trying to remedy this. You can, however, link to the survey through the Podcasts app on your Apple and other smart devices, as well as through Spotify, Stitcher and other podcast directory apps and on your computer browser at these websites. We apologize for the inconvenience.)  The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition.   FACULTY DISCLOSURE ANNOUNCEMENT  It is our intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker’s outside interest may reflect a possible bias, either the exposition or the conclusions presented. Planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event. SHOW NOTES: PART 1: Alright, let's break down the first portion of this case discussion. This is a 60 yo male with chest pain for over a year. Intermittent aching and burning in right anterior chest, worse with activity and lately has worsened overall with a stressful job and strong family hx of heart disease. General exam ins unremarkable. ECG normal. HDL is 60 and LDL slightly up at 137. PFTs and CXR are normal.  Stress echo is normal.  Cardiology referral results in a low Ca++ score but some plaque in the LAD. Dr. Buckler, the cardiologist, feels this is ischemic heart disease until proven otherwise. Therefore, a coronary angiogram is necessary. Imaging has its limitations, as do stress tests. When the history still doesn't point in another explicable direction, we must follow the logic and most likely etiology, which is till coronary artery disease and ACS. One of the problems with stress tests in general, is there are limitations inherent. It's hard to miss the big stuff, but the more minor findings can be missed. With a high pretest probability, he could have perhaps gone straight to angio. In this case, though, he was started on a statin and aspirin. Per Dr. Buckler, Imdur could also have been given. Two year later, he comes in with headaches in the same area of the head since his wife recently passed away. He takes Advil for this. BP has been elevated at home. Dr. Jonathan Larson, family physician, questions the type of headache, it's location and possible etiologies. Is the Advil causing rebound headaches or contributing to the headaches? The elevated home blood pressures also need further investigation. His kidney function is temporarily normal. NSAIDs are d/c'd and Lisinopril is started. A month later, the headaches have improved. BP improved, but not tremendously. In addition, his chest pain has gone away. A new antihypertensive, a combo HCTZ/Lisinopril regimen is started. Although Amlodipine would have been a reasonable choice. A year later, he returns with the same chest pain on exertion. Normal ECG. Normal renal function too. He now goes back to a CT angiogram showing multi-vessel disease. Per Dr. Buckler, one of the reasons he has worsened on a statin is that we may have limited understanding of his pathology, or potentially the CTA was not accurate the first time. Virtual FFT now can show the flow and how significant the lesion is, which is an advancement in this technology. Unfortunately, despite aggressive lipid therapy, sometimes people progress. A few days after the CTA, his Creatinine goes up a bit and GFR goes to 43. This is also after years of Lisinopril. Dr. Carl Dean comments on this alteration in renal function. He feels this is not entirely unexpected, but the data doesn't really reflect CIN (contrast induced nephropathy). Yet intuitively and experientially, we sometimes see this. The amount of contrast used is significantly more on a CTA than on an invasive angio. At this point, the ACE inhibitor is held and Amlodipine is started. Renal function now has improved. The angiogram demonstrates significant 3 vessel disease, with good downstream targets. The SYNTAX surgical risk score directs the cardiologist toward CABG instead of PCI. Post angio, he develops some lower extremity edema, and he is discontinues on Amlodipine, resumed on the HCTZ, Lisinopril. The creatinine is now 2.4. Did he receive enough fluids for the angiogram? Or was the few hundred cc's he obtained during the angio okay? Again, hindsight is 20/20, but the data doesn't support a causality for AKI due to CIN, nor is there a true preventable measure, including n-acetylcysteine or bicarbonate. Perhaps, in this case, CIN as a possibility in the past as discussed, that many would not argue with overhydrating. Ultimately it was felt the ACE and contrast contributed to his creatinine elevation. The ACE combo is now stopped and he is started on Hydralazine and Metoprolol. Creatinine improves, and he goes into CABG surgery. He is discharged and he continues on aspirin and Plavix for 3 months, and Carvedilol and Hydralazine. Atorvastatin is increased to 80 mg daily, a more aggressive dose. EF is normal on echo.  Do statins affect kidney function positively or negatively? According to Dr. Dean, there is no trial that supports either. His BP starts to increase, and Lisinopril is once again added, along with an increase of creatinine, and the ACE is again d/c'd. HCTZ was added. Then spironolactone for ongoing HTN. He's still running high though. Labetalol is replacing carvedilol now. And the pressure is still running high. What is happening here? What to do next? Do we try Lisinopril again? It is attempted, and he once again fails the creatinine test. It goes up again. PART 2: What we do now for this patient? It seems he can only improve on Lisinopril for blood pressure, but his creatinine continues to go up. According to Dr. Dean, in this patient, Lisinopril may not be a great option going forward, not only due to creatinine increase, but it will not help him in terms of mortality outcome. renal artery stenosis is a concern in this case. Dr. Tara McMichael interjects the question, could a loop diuretic have been tried? With a creatinine of 2.3, a loop diuretic could have been an option, since volume and sodium retention could be contributing to the hypertension. Isosorbide with hydralazine is also an option if more meds were to be added. Per Dr. Buckler, however, a four drug regimen that is poorly controlling blood pressure doesn't necessarily indicate adding a fifth drug. We need to know if there is a secondary cause of HTN. Sometimes, even in the setting of renal artery stenosis, patients still require significant anti-HTN drug regimens. Also, per Dr. Dean, the pretest probability in this type of patient for renal artery disease is high. And will an intervention be desirable if it is found? The ASTRAL trial demonstrated no improvement in outcomes. The CORAL trial was also done and considered to be a negative trial. One of the trial criticisms though was that it didn't include patients with severe enough disease. According to Dr. Dean, refractory hypertension should cause screening for this and an intervention should be done if it is seen.  Our patient has a renal u/s that shows bilateral RAS. Dr. David Gross, radiologist discussed the results of the MRA. The aorta, SMA and celiac trunk show atherosclerosis. The renal arteries are paired bilaterally. They have moderate to high grade narrowing of the arteries. Dr. Buckler asks the question of the safety of gadolinium in renal disease. In the setting of low GFR, in other words, less than 30, the risk for nephrogenic systemic fibrosis exists, although very rare. This is usually fatal, though. Basically, he has 4 out of 4 arteries occluded. Dr. Dean feels referral to a center of excellence for this unique issue is best for the patient. He undergoes transaortic endarterectomy, as his creatinine is rapidly going up. A significant plaque is resected from the aorta which was extending into the renal arteries. Post-procedure, he is placed on metoprolol, requiring nothing further. Rosuvastatin, Zetia and baby aspirin is started. Basically, unclogging the pipes resulted in a cure. And a while later, he's no longer on any antihypertensives. Blood pressures are great now. LDL now 57 on the new cholesterol meds. Zetia has limited data, but the PcsK9 inhibitor and his LDL is now 1. Dr. Buckler states there is a lot of unknowns about the LDL levels and whether there is a point of diminishing returns, but the science is not there yet. In this case, Dr. Buckler feels that stopping the Zetia and continuing the pcksk9 inhibitor makes sense. PART 3: Renovascular HTN is more commonly found in the setting of acute, severe, refractory, very high blood pressure. Work-up is needed when there is a strong possibility of secondary cause, and in the absence of another secondary cause, like pheochromocytoma or hyperaldosteronism. Also in an acute rise in BP, a young age, elevated Cr after starting an ace inhibitor, etc. Renal asymmetry on imaging and flash pulmonary edema are other clues. If Cr and BP are stable in the setting of stenosis, no intervention is indicated. Testing can potentially worsen function, as can the interventions performed to treat the disease. Who benefits most? People with short term hx of HTN, people who fail optimal medical therapy, not tolerating medical therapy and progressive renal failure. Ultrasound and CTA or MRA are the options for work-up. US is cheaper, but time consuming and operator dependent, with modest sensitivity/specificity. CTA is accurate for atherosclerosis. Highly sensitive and better if GFR below 30. MRA is highly sens/spec. Gadolinium complications can ensue in low GFR situations. Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9) will lower LDL up to 60%. 50% decease in stroke and MI risk. The PCSK9 enzyme binds to liver LDL receptors and thereby increases plasma LDL levels. so inhibiting this enzyme leads to a lower LDL level. These inhibitors also can decrease triglycerides, increase HDL somewhat and decrease the volume of atheroma. Low adverse effects are noted with the med as well. Regarding renovascular HTN, Dr. Dean also reminds us that someone who is significantly older with chronic renal ischemia in the setting of this disease, may not have improvement in renal function even after intervention. Therefore, some of these patients who suddenly reperfuse a chronically ischemic kidney may actually worsen. Renal artery stenosis is also not an absolute contraindication for ACE. Such as in low EF heart failure. If the creatinine markedly rises, it can be discontinued again. Fibromuscular dysplasia patients, unlike atherosclerosis patients, should all receive an intervention. This is more commonly found in younger patients. Dr. Buckler addresses the ease of use and cost of the PCSK9 inhibitors. It turns out the cost is high at this point, up to $14k/year. But coverage has shown promise in FH and refractory high LDL. As it was alluded to by Dr. Holcomb, the patient really doesn't exercise and has a very stressful job, as it turns out. His dies wasn't discussed. Was he managing his risk factors very well? What does that mean nowadays? We have potent medications and skillful intervention options for reacting to this sort of pathology nowadays, but where are we at with prevention? Hopefully a conversation for another day.

Metoprolol is a beta-blocker commonly used in the management of hypertension, heart failure, and atrial fibrillation. There is an extended release dosage form and immediate release dosage form with metoprolol. The advantage of the extended release product is that it doesn't require as frequent dosing. Metoprolol is selective for beta-1 receptors. It is less likely to interact with asthma medications. CYP2D6 plays an important role in breaking down metoprolol. Alterations in this enzyme's activity can alter concentrations of the drug.

Dr. Rupp is back! Today we talk about whether it's safe to give group 2 gadolinium based contrast agents to patients with CKD stage 4 and 5 and whether metoprolol can be used to prevent COPD exacerbations. We also shine some more sunlight on the sunshine vitamin's inability to change any meaningful outcomes, and discuss some interesting data from the Intern Health Study. Risk of Nephrogenic Systemic Fibrosis in Patients with Stage 4 or 5 CKD Receiving Group II Gadolinium Based Contrast AgentMetoprolol for the Prevent of Acute Exacerbations of COPDEarly High-Dose Vitamin D3 for Critically Ill, Vitamin D-Deficient PatientsPolitical events and mood among young physiciansMusic from https://filmmusic.io"Sneaky Snitch" by Kevin MacLeod (https://incompetech.com)License: CC BY (http://creativecommons.org/licenses/by/4.0/)

Betablokker sa du? En blokk med beta; da eller noe som stopper beta? Hva ER dette her for noe?

Hallo und herzlich Willkommen zurück. Zum Schlüsselsatz:“ Medikamente haben keine Ziele.“ Wenn Du zu einem weit Verwandten oder Bekannten fahren willst, Du hast aber absolut kein Plan wie Du da hinkommst. Dann gibt es die Lösung: Navi. Du tippst die Daten ein und weißt Dein Navi führt Dich genau zu Deinem Ziel. Bei einem Medikament ist das nicht so. Stell Dir vor Du hast richtig doofe Kopfschmerzen.Die Schmerzen sind so stark, das Du sagst: Ich halte es nicht mehr aus, ich zieh mir jetzt eine Tablette rein. Die Kopfschmerzen direkt im oberen Stirnbereich. Die Tablette die Du geschluckt hast, wird jetzt nicht direkt zu Deinem Kopf wandern und Deine Stirnbehandeln. Sondern wirkt in Deinem ganzen Körper. Und das sind meist die sogenannten Nebenwirkungen. Tabletten haben keine Ziele. Du glaubst vielleicht das die Kopfschmerztablette nur Deinen Schmerz besiegt hat, das stimmt aber nicht. Das tut die Tablette nur nebenbei. Ein Beispiel: Die Paracetamoltablette: sehr bekannt, rezeptfrei erhältlich und bis zu 50 Millionen mal im Jahr verschrieben.Sie macht zwar die Schmerzen weg, aber gleichzeitig wirkt sie überall im Körper, besonders auf die Leber. Mehr als 4 Gramm täglich führt kürzer oder später zu Leberschaden oder Leberversagen. Kaum ein Mensch guckt sich den Beipackzettel an. Ca. 500 Menschensterben jährlich in den Vereinigten Staaten an Paracetamolvergiftung. Das ist jetzt nur ein Beispiel von vielen.Ich habe dir unter dem Video Links verlinkt. Da geht es darum einmal, zu verstehen, was Medikamente mit dem Körper machen. Das Medikamente nicht nur Deine kranke Stelle behandeln, sondern im gesamten Körper wirkt. Peter Götzsche bekanntester Pharmakritiker, Professor für klinische Studien in Kopenhagen. Er sagt sogar das Medikamente die 3 häufigste Todesursache ist. Kommen wir zu Kern. Wie ist das bei Bluthochdruck. Es gibt zig Tabletten. Bisolisch, Ramipril, Amlodipin usw. Mir geht’s heute um die Betablocker, weil es die meist verschriebenen Medikamente sind z.B. Metoprolol, Bisoprolol, Cardeviol. Diese haben alle den gleichen Wirkstoff. Wie der Name Betablocker schon sagt. Sie blockieren. Hier ist Dein Herz. An Deinem Herzen hast Du Knöpfe. Wenn das Hormon Adrenalin kommt und den Knopf betätigen und auf diesem Knopf bleibt. Dann wird der Puls schneller, Gefäße werden eng und der Blutdruck steigt. Du kennst es selber. Das erste mal....freier Fall ...z.B. Heidepark oder Moviepark. Das Karussell fährt immer höher und höher. Du willst am liebsten aus diesem Sitz raus. Du hast Angst.Was passiert Dein Blutdruck und Puls steigen. Warum? Weil das Stresshormon Adrenalin Deine Knöpfe im Herzen betätigt.Weil Dein Körper zu dem Zeitpunkt unter Stress steht. Du willst am liebsten fliehen, kannst aber nicht mehr aus deinem Sitz raus, weil das Karussell auf den Weg nach oben ist. Bei Bluthochdruck sind die Adrenalinknöpfe an Deinem Herzen immer an. Immer besetzt. Warum? Dein Körper steht unter Dauerstress. Du sitzt jetzt vielleicht gemütlich am Tisch, hast absolut kein Bedürfnis zu Fliehen oder zu Kämpfen. Aber Dein Körper steht unter Adrenalin.Was machen Betablocker. Sie blockieren das Adrenalin. Es kann nicht am Herzen andocken. Und so wird der Blutdruck nicht erhöht. Sondern runtergefahren. Jetzt denkst Du vielleicht. Ja Super. Ist doch top. Adrenalin kann nicht mehr ans Herz, somit kein erhöhter Druck. Das Problem ist: Medikamente haben keine Ziele. d.h. Du hast diese Betarezeptoren nicht nur am Herzen, sondern in der Niere Lunge, Leber z.B. die Lunge: die kleinen Atemwege der Lunge werden eng. Folge: Luftnot. Die Nieren scheiden weniger Natrium und Wasser aus. Folge: Zu viel Wasser im Körper. Die Leber gibt zu wenig Zucker ab. Folge Unterzuckerung. Und das schlimmste die Blutfettwerte können sich erhöhen, was zu einer Ablagerung in den Gefäßen führt. Du kannst Durch die Betablocker Ablagerungen bekommen. Betablocker blockieren, aber behandeln nie die Ursache. Betablocker behandeln keine Gefäßablagerung, Betablocker reduzieren künstlich den Stress, der auch anders zu beseitigen ist.Betablocker machen Nebenwirkungen und schaden langfristig. In diesem Video hast Du gelernt, das Betablocker blockieren und die Herztriebkraft runter fährt. Das Medikamente im gesamten Körper wirken und nicht nur an einer Stelle. Deshalb die Message an Dich: Wenn Du Betablocker nimmst, dann setzte sie nicht abrupt ab, sondern langsam. Dein Körper muss wieder die eigene Funktion übernehmen.Das haben bis jetzt nämlich die Betablocker übernommen. Lerne die Ursachen im Kurs kennen, und werde Medikamentenfrei. Bis gleich im nächsten Video zum Schlüsselsatz: Sauer macht krank.

January Quick Summary January Podcast Articles Pediatric ApOx, Metoprolol vs Dilt for Afib in HF patients, Premedication for Adults with Ketamine sedation, Early IV fluids by EMS and sepsis mortality, Prehospital Sepsis Alerts, C-spine clearance with distracting injuries, Pediatric FAST for solid organ injury, Financial conflicts with stroke guidelines, and the HOUR rule for opioid overdoses.

In addition to the three main classes of anti-hypertensives we already discussed, ACE Inhibitors like Lisinopril and Captopril, Beta Blockers like Metoprolol and Propranolol, and Calcium Channel Blockers like Nicardipine and Diltiazem, there are a number of other classes of… The post Cardiac Labs and Meds for Nurses appeared first on NURSING.com.

Commentary by Dr. Valentin Fuster

The post Metoprolol (Lopressor) Nursing Pharmacology Considerations appeared first on NURSING.com.

Commentary by Dr. Valentin Fuster

This week we discuss an age-old debate: Calcium Channel Blockers or Beta Blockers for rate control in atrial fibrillation. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_64_0_Final_Cut.m4a Download Leave a Comment Tags: Atrial Fibrillation, Beta Blocker, Calcium Channel Blocker, Cardiology, Rate Control Show Notes CoreEM: Recent Onset Atrial Fibrillation ALiEM: Atrial Fibrillation Rate Control in the ED: Calcium Channel Blockers or Beta Blockers? ALiEM: Beta Blockers vs Calcium Channel Blockers for Atrial Fibrillation Rate Control: Thinking Beyond the ED Fromm C, et al. Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department. J Emerg Med. 2015 Apr 22. PMID 25913166

This week we discuss an age-old debate: Calcium Channel Blockers or Beta Blockers for rate control in atrial fibrillation. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_64_0_Final_Cut.m4a Download Leave a Comment Tags: Atrial Fibrillation, Beta Blocker, Calcium Channel Blocker, Cardiology, Rate Control Show Notes CoreEM: Recent Onset Atrial Fibrillation ALiEM: Atrial Fibrillation Rate Control in the ED: Calcium Channel Blockers or Beta Blockers? ALiEM: Beta Blockers vs Calcium Channel Blockers for Atrial Fibrillation Rate Control: Thinking Beyond the ED Fromm C, et al. Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department. J Emerg Med. 2015 Apr 22. PMID 25913166

This week we discuss an age-old debate: Calcium Channel Blockers or Beta Blockers for rate control in atrial fibrillation. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_64_0_Final_Cut.m4a Download Leave a Comment Tags: Atrial Fibrillation, Beta Blocker, Calcium Channel Blocker, Cardiology, Rate Control Show Notes CoreEM: Recent Onset Atrial Fibrillation ALiEM: Atrial Fibrillation Rate Control in the ED: Calcium Channel Blockers or Beta Blockers? ALiEM: Beta Blockers vs Calcium Channel Blockers for Atrial Fibrillation Rate Control: Thinking Beyond the ED Fromm C, et al. Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department. J Emerg Med. 2015 Apr 22. PMID 25913166

Commentary by Dr. Valentin Fuster

In this episode of the Heart Podcast, Heart associate editor Dr James Rudd is joined by Dr Kaspar Broch of the Oslo University Hospital, Norway to discuss his recent paper in Heart entitled: "Controlled release metoprolol for aortic regurgitation: A randomised clinical trial" They discuss the rationale for beta-blockers in aortic regurgitation and the results of this first clinical trial of these agents. Full paper >> heart.bmj.com/content/102/3/191.…-a075-27b877e18613

This week we discuss the management of hyperkalemia + a journal update on beta blockers vs Ca channel blockers in AF https://media.blubrry.com/coreem/content.blubrry.com/coreem/Core_EM_Podcast_7_Final.m4a Download Leave a Comment Tags: Atrial Fibrillation, Hyperkalemia Show Notes Core EM: Hyperkalemia REBEL EM: Is Kayexalate Useful in the Treatment of Hyperkalemia in the Emergency Department? Core EM: Diltiazem vs. Metoprolol for Rate Control in Atrial Fibrillation Read More

This week we discuss the management of hyperkalemia + a journal update on beta blockers vs Ca channel blockers in AF https://media.blubrry.com/coreem/content.blubrry.com/coreem/Core_EM_Podcast_7_Final.m4a Download Leave a Comment Tags: Atrial Fibrillation, Hyperkalemia Show Notes Core EM: Hyperkalemia REBEL EM: Is Kayexalate Useful in the Treatment of Hyperkalemia in the Emergency Department? Core EM: Diltiazem vs. Metoprolol for Rate Control in Atrial Fibrillation Read More

This week we discuss the management of hyperkalemia + a journal update on beta blockers vs Ca channel blockers in AF https://media.blubrry.com/coreem/content.blubrry.com/coreem/Core_EM_Podcast_7_Final.m4a Download Leave a Comment Tags: Atrial Fibrillation, Hyperkalemia Show Notes Core EM: Hyperkalemia REBEL EM: Is Kayexalate Useful in the Treatment of Hyperkalemia in the Emergency Department? Core EM: Diltiazem vs. Metoprolol for Rate Control in Atrial Fibrillation Read More