Podcasts about verapamil

In this episode of the podcast Rob is solo as he interviews Dr. Anath Shalev, a diabetes researcher turned founder of startup Tiximed. Dr. Shalev discusses the discovery of TixnIP, a protein involved in oxidative stress in beta cells, and its potential for treating diabetes. The conversation covers the development of TIX 100, an oral medication targeting TixnIP, its implications for type 1 and type 2 diabetes, and the differences from existing diabetes treatments like SGLT2 inhibitors and GLP-1 agonists. Topics discussed: * Dr. Anas Shalev's background in diabetes research and founding of Tiximed * Discovery of TixnIP and its role in beta cell health * Potential of TIX 100 as a novel oral medication for diabetes treatment * Comparison of TIX 100 with existing diabetes treatments like SGLT2 inhibitors and GLP-1 agonists * Research process behind TixnIP inhibition and development of TIX 100 * Future of diabetes care, combination therapies, and impact on patients' lives * Information about Tiximed, clinical trials, and ways to support the research 00:18  Revolutionizing Diabetes Treatment: From Researcher to Founder 03:47  Revolutionizing Diabetes Treatment: Targeting Beta Cells and Glucagon Levels 13:47  Revolutionizing Diabetes Treatment: Targeting Beta Cells in Type 1 and Type 2 Diabetes 17:35  Revolutionizing Diabetes Treatment with Ticks 100: A Breakthrough in Addressing the Root Cause of the Disease 27:35  The Limitations and Advantages of Verapamil in Diabetes Care 29:47  Advancements in Diabetes Technology and Research: A Look into the Future 33:04  Exploring Diabetes Treatment Innovations with Dr. Shalev Topics discussed: 1. Mila's Personal Journey including leaving her job to focus on Hangry Woman full-time 2. Career Shift and Health Coaching: Transition from a marketer to a health coach 3. Bridging the gap between fear of eating and enjoying meals 4. Importance of Self-Care and Boundaries: Prioritizing self-care to avoid burnout 5. Support System in Content Creation: Managing overwhelm by acknowledging limitations 6. The role of support team members in providing feedback and managing projects 7. Navigating Changes in Diabetes Diagnosis: Transition from type 2 to type 1 diabetes diagnosis 8. Representing Diverse Voices in the Diabetes Community: Importance of diversity representation and transparency in collaborations 9. Kindness, Respect, and Accountability: Impact of chronic illness on behavior and comparison culture 10. Addressing misconceptions about online personas and supporting creators 11. Building a Supportive Diabetes App Key takeaways: * Embracing personal growth amidst challenges and life changes * Prioritizing self-care, setting boundaries, and recognizing emotional well-being * Navigating career shifts and advocating for representation in the diabetes community * Building a supportive community and offering personalized health support through technology * Upholding kindness, respect, and accountability in online interactions and content creation References: * The Hangry Woman * Glucose Guide App 00:00  Celebrating Diabetes Stories Worldwide 00:02  The Evolution of Mila Clarke: Navigating Life Changes and Diabetes Management 04:15  From Marketer to Health Coach: A Journey of Personal and Professional Growth 08:16  Learning to Set Boundaries and Prioritize Self-Care: A Journey of Self-Discovery and Growth 12:16  Navigating Burnout and Building a Support System in Content Creation 17:26  Navigating a Diabetes Diagnosis Change: Impact on Community, Relationships, and Advocacy 23:49  Navigating a New Diagnosis and its Impact on Personal Branding 28:04  Breaking Barriers and Building Bridges in the Diabetes Community 32:36  Debunking Myths and Realities of Being a Successful Black Woman Entrepreneur 42:36  Embracing Kindness and Abundance in a World of Competition 52:36  Navigating Social Media Etiquette and Misconceptions as a Creator 55:53  Navigating Online Criticism and Embracing the Journey to Success in Content Creation 01:02:49  Revolutionizing Diabetes Support with a Unique Pocket Guide App 01:06:10  Empowering Diabetes Management through Personalized Support and Community Connection 01:09:21  Building a Supportive Community Beyond Social Media Platforms 01:14:05  Empowering Health and Support Through a Unique Approach 01:17:12  The Value of Ads and Support in Providing Free Content and Services

La American Heart Association publicó un documento con recomendaciones específicas para el manejo del paciente en paro cardiaco por intoxicación. Este artículo repasará las principales recomendaciones. Este es el quinto episodio de una serie de episodios relacionados al manejo del paro cardiaco por envenenamientos. En este episodio discutimos el manejo de la intoxicación por digoxina. Índice terapéutico de la dioxina El índice terapéutico mide la seguridad de un medicamento. Un medicamento con un índice terapéutico reducido significa que es necesario mantener una concentración muy precisa en la sangre. De lo contrario, no es suficiente para ser efectiva, o se vuelve tóxica. Según la farmacocinética y farmacodinamia, para que un medicamento sea efectivo, el cuerpo tiene primero que absorberlo a la circulación. Una vez en la circulación, el cuerpo va a metabolizarlo hasta eliminarlo completamente. Luego de un tiempo determinado, la dosis que queda en el cuerpo ya deja de ser efectiva. Si es necesario mantener una concentración constante en la sangre, entonces es necesario seguir administrando otras dosis a intervalos definidos para asegurar que el cuerpo siga teniendo un suplido constante de la droga para reemplazar lo que se va eliminando. La digoxina tiene un índice terapéutico muy reducido. Quiere decir que es necesario administrar una cantidad precisa del medicamento y medir cuánto es el nivel en la sangre para evitar correr el riesgo de haber administrado demasiado. La digoxina se excreta a través de los riñones. Si un paciente desarrolla fallo renal agudo, pudiera tener un aumento clínicamente significativo de los niveles de digoxina. Medicamentos que alteran la fracción libre de la digoxina Disminución del efecto de la digoxina Carbamazepine, fosfenitoína y fenobarbital Rifampin Aumento del efecto de la digoxina Amiodarona, carvedilol, ranozaline, ticagrelol Verapamil, tacrolimus, cyclosporine Azitromicina, eritromicina y claritromicina Fungicidas azoles Signos y síntomas de la intoxicación por digoxina La intoxicación con digoxina puede producir una amplia gama de signos y síntomas gastrointestinales, neurológicos y cardiacos: Signos cardiacos Cambios en el segmento ST (La descripción clásica del EKG del paciente con intoxicación con digoxina es una depresión del segmento ST con una curva cóncava.) Cambios en el intervalo QTc Taquicardia atrial Taquicardia nodal Taquicardia ventricular (especialmente taquicardia ventricular bidireccional) Bradicardia y bloqueo AV (1er grado y 2ndo grado Tipo 1) Bigeminismo ventricular Fibrilación ventricular o asístole Signos gastrointestinales (intoxicación aguda) Anorexia Náusea Vómitos Diarrea Disturbios visuales (color amarillo o verde) Signos neurológicos (intoxicación crónica) Confusión Debilidad Síncope Convulsiones Hiperkalemia Nota: La hipokalemia (causada, por ejemplo, por el uso de diuréticos) puede causar toxicidad por digoxina. Si el paciente tiene hipokalemia, pudiera ser necesario suplementar con potasio si se va a usar anticuerpos antidigoxina porque estos van a bajar los niveles de potasio aún mas. Si el paciente toma digoxina, es posible que los signos y síntomas que ve sea por la digoxina. La hiperkalemia por digoxina La intoxicación por digoxina puede causar hiperkalemia, pero el mecanismo de la hiperkalemia inducida por digoxina es diferente al mecanismo de la hiperkalemia por otras causas. Por lo tanto, el manejo es diferente. Mecanismo de hiperkamia por digoxina Los glucósidos cardiacos inhiben la bomba de sodio y potasio en las células cardiacas. El movimiento de calcio hacia afuera de la célula depende del movimiento de sodio. Los glucósidos cardiacos inhiben la bomba de sodio y potasio, por lo tanto están inhibiendo el movimiento de sodio. La inhibición de la bomba de sodio y potasio produce que el potasio deje de entrar a la célula, acumulándose afuera (hiperkalemia). La bomba de sodio y potasio no produce un balance eléctrico perfecto, por lo que el cuerpo recurre al movimiento de sodio y calcio para completar la repolarización. Al dejar de funcionar la bomba de sodio y potasio, aumentan los niveles de calcio dentro de la célula. Normalmente, este aumento en la concentración de calcio produce un aumento en la fuerza de contractilidad del músculo cardiaco. En teoría, y una muy limitada evidencia, si se inyecta más calcio para tratar la hiperkalemia, se puede agravar los niveles ya elevados de calcio dentro de la célula y se puede producir una contracción continua (contracción tetánica) que lleva a paro cardiaco. Aunque esto es un riesgo teórico, no hay mucha data que apoye la teoría y tampoco hay mucha data de que el calcio apoye este tipo de hiperkalemia porque el mecanismo es diferente. Manejo de la hiperkalemia por digoxina El manejo de la hiperkalemia por inducida por digoxina consiste primariamente en la administración de anticuerpos antidigoxina. Consulte al Centro de Control de Envenenamientos En los Estados Unidos y Puerto Rico, 1-800-222-1222. Algunos pacientes con ingestas recientes (< 1 hr) pudieran beneficiarse del uso de carbón activado. Pero, en general, el manejo se centra alrededor del uso de los anticuerpos antidigoxina. Recomendaciones de la American Heart Association para paro cardiaco por intoxicación con digoxina Recomendamos la administración de anticuerpos antidigoxina para envenenamientos con digoxina o digitoxina. (Clase de recomendación: 1, Nivel de evidencia: B-NR) Es razonable administrar anticuerpos antidigoxina para envenenamiento por sapo bufo o adelfa amarilla. (Clase de recomendación: 2a, Nivel de evidencia: C-LD) Puede ser razonable administrar anticuerpos antidigoxina para tratar envenenamientos por glicósidos cardiacos que no sean digoxina, digitoxina, sapo bufo, o adelfa amarilla. (Clase de recomendación: 2b, Nivel de evidencia: C-LD) Puede ser razonable administrar atropina para bradidisritmias causadas por digoxina y otros envenenamientos por glicósidos cardiacos. (Clase de recomendación: 2b, Nivel de evidencia: C-LD) Puede ser razonable administrar un marcapasos eléctrico para tratar bradidisritmias debido a envenenamiento por digoxina y otros glicósidos cardiacos. (Clase de recomendación: 2b, Nivel de evidencia: C-LD) Puede ser razonable administrar lidocaína, fenitoína, o bretilio para tratar disritmias ventriculares causadas por digitálicos y otros glicósidos cardiacos hasta que se pueda obtener anticuerpos antidigitálicos. (Clase de recomendación: 2b, Nivel de evidencia: C-LD). No recomendamos el uso de hemodiálisis, hemofiltración, hemoperfusión, o plasmaféresis para tratar envenenamiento por digoxina. (Clase de recomendación: 3: no beneficio, Nivel de evidencia: B-NR) Referencias Lavonas EJ, Akpunonu PD, Arens AM, Babu KM, Cao D, Hoffman RS, Hoyte CO, Mazer-Amirshahi ME, Stolbach A, St-Onge M, Thompson TM, Wang GS, Hoover AV, Drennan IR; on behalf of the American Heart Association. 2023 American Heart Association focused update on the management of patients with cardiac arrest or life-threatening toxicity due to poisoning: an update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2023;148:e•••–e•••. doi: 10.1161/ CIR.0000000000001161 https://litfl.com/digoxin-toxicity-ecg-library/ https://litfl.com/digoxin-effect-ecg-library/ https://litfl.com/calcium-digoxin-toxicity-and-stone-heart-theory/#:~:text=This%20is%20based%20on%20the,by%20causing%20delayed%20after%2Ddepolarisations https://emcrit.org/ibcc/dig/#:~:text=mechanism%20of%20action%20of%20digoxin,in%20patients%20with%20digoxin%20overdose.

Verapamil no DM1 --- Send in a voice message: https://podcasters.spotify.com/pod/show/endocrinopapers/message

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...

Check out “Heard on the Street” recorded during the ADA 2023 Conference. Hear from Dr. Guanlan Xu at University of Alabama as he shares his poster: Verapamil prevents decline of IGF-1 in subjects with T1D.

In this episode, hosts offer their reaction to topline data from the SURMOUNT-2 trial examining tirzepatide for weight management in T2D, the FDA's clearance of the Omnipod GO device, and results of the CLVer trial.

Editor's Summary by Kirsten Bibbins-Domingo, PhD, MD, MAS, Editor in Chief of JAMA, the Journal of the American Medical Association, for the March 28, 2023, issue. Related Content: March 28, 2023, Issue

In this segment, Dr. Mistry and Donna Lee talk about the causes of and treatments for Peyronie's disease. If you have developed a bend in your penis or if your erection stands at an unnatural angle, you may have Peyronie's disease. Whether it develops slowly from the accumulation of scar tissue caused by microtrauma, or suddenly from an acute traumatic event, there are many treatment options that can bend you right back into shape! Today, Dr. Mistry discusses penile stretching devices like the RestoreX and Andropenis and injections like Verapamil and Xiaflex. For patients who need surgical interventions, our partner Dr. Christopher Yang specializes in penile plastic surgeries such as penile plication, prostheses, and patch graft phalloplasty. Tune in to hear about the many treatment options for Peyronie's and how penile plastic surgery can straighten and lengthen your penis. To learn more, call or visit us online to schedule an appointment today! Voted top Men's Health Podcast, Sex Therapy Podcast, and Prostate Cancer Podcast by FeedSpotDr. Mistry is a board-certified urologist and has been treating patients in the Austin and Greater Williamson County area since he started his private practice in 2007.We enjoy hearing from you! Email us at armormenshealth@gmail.com and we'll answer your question in an upcoming episode.Phone: (512) 238-0762Email: Armormenshealth@gmail.comWebsite: Armormenshealth.comOur Locations:Round Rock Office970 Hester's Crossing Road Suite 101 Round Rock, TX 78681South Austin Office6501 South Congress Suite 1-103 Austin, TX 78745Lakeline Office12505 Hymeadow Drive Suite 2C Austin, TX 78750Dripping Springs Office170 Benney Lane Suite 202 Dripping Springs, TX 78620

In this podcast, Dr. Jon Cole - an emergency medicine physician with Hennepin Healthcare and medical director with Minnesota Poison Control Center and Samantha Lee, PharmD - managing director with Minnesota Poison Control Center discuss the poison control system - past and present; along with a disscusion around toxicology - the big, the bad, and the ugly. Enjoy the podcast. Objectives:Upon completion of this podcast, participants should be able to: Describe the purpose of the Minnesota Poison Control Center, and how it works. Name the most common call types coming into MN Poison Control Center. Summarize the management of toxicological exposures for APAP, bupropion and calcium channel blockers. CME credit is only offered to Ridgeview Providers & Allied Health staff for this podcast activity. After listening to the podcast, complete and submit the online evaluation form.  Upon successful completion of the evaluation, you will be e-mailed a certificate of completion within approximately 2 weeks. You may contact the accredited provider with questions regarding this program at Education@ridgeviewmedical.org. Click the link below, to complete the activity's evaluation. CME Evaluation (**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.)  DISCLOSURE ANNOUNCEMENT  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; and are property/rights of Ridgeview Medical Center & Clinics.  Any re-reproduction of any of the materials presented would be infringement of copyright laws.  It is Ridgeview's 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. Ridgeview's CME 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. Thank-you for listening to the podcast. SHOW NOTES:  *See the attachment for additional information.  HISTORY of MN POISON CONTROL CENTER TOXICOLOGYCalcium Channel Blockers - Diltiazem, Verapamil, Amlodipine - Causes bad distributive shock - Pulmonary edema is an issue - Norepinephrine infusion is recommended in setting of shock with high dose insulin simultaneously - "Red, white and blue" therapy for refractory Ca++ blocker overdose - Activated charcoal - not for all patients, give if patient not at risk of aspiration for potentially lethal ingestions Bupropion - Chemical structure similar to amphetamine and bath salts - Sympathomimetic effects (tachycardia, agitation, seizures, ultimately cardiogenic shock) - Treatment with benzodiazepines - usually high dose - may need intubation - Norepinephrine for cardiogenic shock - ECMO may be needed Sodium Nitrite - Salt used to cure meats - Internet suicide phenomenon - Effect: Life threatening methemoglobinemia (chocolate colored blood, pallor, low O2 sats) - Very rapid onset of symptoms - Methylene Blue use N-acetylcysteine (NAC) for acetaminophen poisoning - Transitioning from 3 bag Prescott regimen to a 2 bag regimen - Rumack-Matthew nomogram is the same Article Resources:Cole JB, Lee SC, Prekker ME, Kunzler NM, Considine KA, Driver BE, Puskarich MA, Olives TD. Vasodilation in patients with calcium channel blocker poisoning treated with high-dose insulin: a comparison of amlodipine versus non-dihydropyridines. Clin Toxicol (Phila). 2022 Nov;60(11):1205-1213. doi: 10.1080/15563650.2022.2131565. Epub 2022 Oct 25. PMID: 36282196.   Cole JB, Olives TD, Ulici A, Litell JM, Bangh SA, Arens AM, Puskarich MA, Prekker ME. Extracorporeal Membrane Oxygenation for Poisonings Reported to U.S. Poison Centers from 2000 to 2018: An Analysis of the National Poison Data System. Crit Care Med. 2020 Aug;48(8):1111-1119. doi: 10.1097/CCM.0000000000004401. PMID: 32697480. Coralic Z, Kapur J, Olson KR, Chamberlain JM, Overbeek D, Silbergleit R. Treatment of Toxin-Related Status Epilepticus With Levetiracetam, Fosphenytoin, or Valproate in Patients Enrolled in the Established Status Epilepticus Treatment Trial. Ann Emerg Med. 2022 Sep;80(3):194-202. doi: 10.1016/j.annemergmed.2022.04.020. Epub 2022 Jun 17. PMID: 35718575. Kline JA, Tomaszewski CA, Schroeder JD, Raymond RM. Insulin is a superior antidote for cardiovascular toxicity induced by verapamil in the anesthetized canine. J Pharmacol Exp Ther. 1993 Nov;267(2):744-50. PMID: 8246150.   Thanks to Dr. Jon Cole and Samantha Lee, PharmD for their knowledge and contribution to this podcast. Please check out the additional show notes for more information/resources.

Download the cheat: https://bit.ly/50-meds  View the lesson:     Generic Name verapamil Trade Name Isoptin Indication hypertension, angina, SVT, migraine Action prevents transport of calcium, leading to decreased contraction, decreases SA and AV node conduction Therapeutic Class antianginals, antiarrhythmic, antihypertensive, vascular headache suppressants Pharmacologic Class Ca Channel Blocker Nursing Considerations • don't use with 2nd and 3rd degree heartblock • don't use with systolic BP < 90 • may cause anxiety, confusion, cough, dyspnea, arrhythmias, CHF, bradycardia, hypotension, elevated liver enzymes, Steven's Johnson syndrome, hyperglycemia, gingival hyperplasia • grapefruit juice can increase effects • can increase levels of digoxin • monitor heart rhythm, intake and output, blood pressure • assess angina

Trade – IsoptinClass – Calcium Channel blockerMOA – Blocks calcium from moving into the heart muscle cell, which prolongs conduction of the electrical impulses through the AV node.Indications – AF, HTN, paroxysmal SVT, Paroxysmal SVT prohylaxisContraindications – 2nd or 3rd degree AV block, Hypotension, cardiogenic shock, Sick sinus syndrome, WPW.Side effects – Sinus bradycardia, 1st, 2nd, or 3rd degree AV blocks, CHF, reflex tachycardia, transient asystole, hypotension.Dosing Adult 2.5-10mg IV/IO over 2 minutes. May repeat at 5-10mg every 15-30 mins to a maximum dose of 30mgPedi 1-16 years old: 0.1mg/kg IV/IO max single dose 5mg over 2mins may repeat in 30 mins to a max dose of 10mg

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...

On this episode, I discuss verapamil pharmacology, adverse effects, and important drug interactions. There are numerous drug interactions to be aware of with verapamil as it inhibits the enzyme CYP3A4. Verapamil is a calcium channel blocker (non-dihydropyridine) that blocks calcium channels in the heart and vessels. In addition to hypotension and bradycardia, verapamil can cause constipation which may be more prominent in our geriatric patients.

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

Thanks for tuning in to the Armor Men's Health Hour Podcast today, where we bring you the latest and greatest in urology care and the best urology humor out there.In this segment, Dr. Mistry and Donna Lee talk about Peyronie's disease. This condition causes a bend to develop in the penis either suddenly or over time and can become quite painful and severe. Fortunately, there are many treatments for Peyronie's disease that address it's various causes and effects. There are different interventions depending on the degree of penile curvature and the severity of symptoms. Today, Dr. Mistry and Donna Lee describe the two phases of Peyronie's progression and explain what kinds of interventions are appropriate to each. While surgical interventions can be very effective, they're not recommended until the penile curvature has stabilized during the chronic phase, which can take some time. In the acute phase of Peyronie's disease, there is often pain associated with the development of plaques. This is an important time to ensure that erections during intercourse remain rigid to prevent any microtrauma, which can worsen (and/or cause) the effects of Peyronie's. For this reason, a daily dose of Tadalafil or Cialis are often used to improve erection rigidity. The other treatment offered for acute Peyronie's include shots of medications like Xiaflex and Verapamil, which can be very helpful in slowing disease progression. Only once these options have failed and the patient has entered the chronic phase of disease should surgery be considered. No matter your situation, getting an evaluation and proper measurement of your curvature by a urologist is essential in identifying the right treatment. If you enjoyed today's episode, don't forget to like, subscribe, and share us with a friend! As always, be well!Check our our award winning podcast!https://blog.feedspot.com/sex_therapy_podcasts/https://blog.feedspot.com/mens_health_podcasts/Dr. Mistry is a board-certified urologist and has been treating patients in the Austin and Greater Williamson County area since he started his private practice in 2007.We enjoy hearing from you! Email us at armormenshealth@gmail.com and we'll answer your question in an upcoming episode!Phone: (512) 238-0762Email: Armormenshealth@gmail.comWebsite: Armormenshealth.comOur Locations:Round Rock Office970 Hester's Crossing Road Suite 101 Round Rock, TX 78681South Austin Office6501 South Congress Suite 1-103 Austin, TX 78745Lakeline Office12505 Hymeadow Drive Suite 2C Austin, TX 78750Dripping Springs Office170 Benney Lane Suite 202 Dripping Springs, TX 78620

JDRF began this year by funding more research projects than ever before, but after COVID changed everything, what does the future hold?  We caught up with CEO Aaron Kowalski to ask what their mission to "cure, prevent & treat" type 1 diabetes look like in a time when fund raising is down and the future is unclear. In Tell Me Something Good find out about two contests Stacey is running. One in our FB group (see link below) and the other over on Instagram. We're celebrating 1,000,000 downloads!! Get your free Ebook "Diabetes Connections Extras" full of expert advice for managing insulin-dependent diabetes. Terrific for newly diagnosed families or caregivers and friends who want to learn more. Get the Ebook here This podcast is not intended as medical advice. If you have those kinds of questions, please contact your health care provider. Check out Stacey's new book: The World's Worst Diabetes Mom! Join the Diabetes Connections Facebook Group! Sign up for our newsletter here ----- Use this link to get one free download and one free month of Audible, available to Diabetes Connections listeners! ----- Get the App and listen to Diabetes Connections wherever you go! Click here for iPhone      Click here for Android Episode Transcription (rough transcript - check back for edited version) Stacey Simms  0:00 Diabetes Connections is brought to you by One Drop created for people with diabetes by people who have diabetes by Gvoke Hypo Pen, the first premixed auto injector for very low blood sugar, and by Dexcom, take control of your diabetes and live life to the fullest with Dexcom.   Announcer  0:23 This is Diabetes Connections with Stacey Simms.   Stacey Simms  0:28 This week, catching up with JDRF’s CEO to talk about what this year has been like, and what it all means for their mission and research going forward. I also asked if he felt it was a good decision to keep those fundraising emails going during a pandemic.   Aaron Kowalski  0:44 But the decision to continue to ask people to support us was not to have people feel pressured that they were struggling, but for the folks who could who had the financial capabilities to lean in and help us preserve some of the incredible mission momentum we have.   Stacey Simms  1:00 Aaron Kowalski is the first CEO of JDRF to actually live with Type One Diabetes. We talked about a wide range of topics. Tell me something good a big milestone to share with you and of course, it is diabetes awareness month we've got contests to talk about. this podcast is not intended as medical advice. If you have those kinds of questions, please contact your health care provider. Welcome to another week of the show. I am so glad to have you here we aim to educate and inspire about type 1 diabetes by sharing stories of connection. I'm your host, Stacey Simms, and my son was diagnosed almost 14 years ago, his diversary is in early December. He's a sophomore in high school now he was diagnosed as a toddler, my husband lives with type two diabetes, I do not have diabetes. But I have a background in broadcasting local radio and television news. And that is how you get the podcast. It is of course diabetes Awareness Month, every year in the month of November. And we say that this is more for people outside the community, right, it's our chance to educate them about diabetes, because every day is diabetes Awareness Month once you have a type of diabetes, so I'm not going to do too many different things on the show for this month. But I have some efforts going to educate people outside of the usual suspects around here. I'm also going to be running two contests, I'm going to share all that information. After the interview one contest on Instagram one on Facebook, if you follow me, you will see them if you don't more information coming up. I also want to let you know that I have released an Ebook. This is something I've been working on for quite a while. It has selected transcripts from the podcast, but it is in a beautiful, easy to read form. And the theme of the book is a comprehensive look at some of the questions that we all get asked over and over again. So I'm going to put a link in the show notes. It is free. Yeah, yes, sign up for my newsletter. If you've already signed up for the newsletter, if you already get it every week, you can sign up again, I promise you won't get to. But you will get the free ebook. If you remember we've been doing these Diabetes Connections extra episodes, where I put out an excerpt and then the much longer episode a couple of days after. That's where these transcriptions come from. So it's all about CGM, all about insulin all about ketones all about blood sugar lows, basic stuff that I think is really good if you're newer diagnosed, if you're looking for a refresher, or if you want to share with a caregiver or a loved one who wants to learn more, but might learn better from an ebook, you know, on their Kindle than from a conversation with you. We all know people like that. So I hope you share it. I hope you like it. Again, it is free. You do have to sign up for the newsletter, more information in the Facebook group and in the show notes Just go to Diabetes connections.com and you will see it linked up right in this episode. Okay JDRF CEO coming up in just a moment, but first Diabetes Connections is brought to you by One Drop. And you know, when I spoke to people at One Drop, I was really impressed at how much they get diabetes. And it makes a lot of sense because their CEO Jeff was diagnosed with type one as an adult. One Drop is for people with diabetes by people with diabetes. The people at One Drop work relentlessly to remove all barriers between you and the care you need. Get 24 seven coaching support in your app and unlimited supplies delivered. No prescriptions or insurance required. Their beautiful sleek meter fits in perfectly with the rest of your life. They'll also send you test strips with a strip plan that actually makes sense for how much you actually check One Drop diabetes care delivered. learn more, go to Diabetes connections.com and click on the One Drop logo. My guest this week is Aaron Kowalski. He has been the CEO of JDRF since the spring of 2019. Of course this has been a challenging year for everybody to say the least. And when the crisis first started, I think we all knew that nonprofits were going to take a big hit. As you will hear in the interview. I sent to Aaron and email with my reservations look I'm a supporter of JDRF, financially, and I've been on the local board. And I felt that fundraising as usual would be a mistake. I advocated for a fund that would help people who we knew were going to lose their jobs and would need immediate help. But I am not inside JDRF. I haven't been on any board with them for about eight years, maybe maybe a little bit more. But I thought it would be helpful to have some background of my opinion, and where I stand at the start of this interview. But I also wanted to let Aaron give a research update at a sort of a state of the state. So there's a lot going on here. But I was really thrilled to he came on and was so upfront, really answered my questions and gave us a lot of information. Aaron, thanks so much for spending some time with me and my listeners. I appreciate it's good to talk to you again.   Aaron Kowalski5:46 Hey, Stacey, thanks for having me on.   Stacey Simms  5:48 I'm not exactly sure how to jump in. I feel like everything I say about this year has become a cliche, but I'll barrel through it in that this is a year like nothing we've seen before. Can you give us a little bit of a kind of a state of the state of JDRF as we sit here in November of 2020?   Aaron Kowalski6:06 Sure. I think like everybody, the the the last number of months have been very difficult. And certainly it's been for JDRF. I wish I could say a few things. One is pre COVID. I had a meeting and this goes back into early March with our board of directors and I, I told them that this was an unprecedented time for research progress, and amazing advancements happening on all fronts of diabetes research. And I'm sure we'll talk about those. And then of course, as we all know, COVID ahead, and fast forward to November. And I guess what I would say is just that I've had to make some changes, we reduced our staff somewhat significantly, we have a number of chapters we have from over 60 to 29. But the intention, the mission hasn't changed at all. And all of these changes, were focused upon making sure that we could continue to maintain the momentum we saw and research and development of life changing breakthroughs to help people to one day security one day preventing one day better treating one day, and that's what we're focused upon is maintaining research and mission momentum. We're not going to abandon any part of the United States. In fact, we hope to engage with more people. It's really just about how do we structure JDRF most efficiently in the face of not being able to get together for walks and galleries and the different fundraising events we do. So I'm an optimist by nature. So I'm optimistic that we have a lot of challenges in front of us with COVID. Still, but Gosh, when we do talk about research progress, you'll hear that there's so much excitement happening right now. And we we're doing everything we can to keep that going.   Stacey Simms  7:52 Well, let's just jump in and talk about it now tell us some of the research projects that are ongoing, that has not been affected by COVID. And in fundraising and things like that.   Aaron Kowalski8:02 Yeah, I think the good news is research has progressed, even in the face of COVID. We we've monitored this, we fund research in the United States, of course, but we also fund research in 20 other countries, and depending on the country, depending on the lab, the state, we are seeing research be done. It's not perfect. It's not 100%. It's not pre COVID levels, but it's still good. And you know the way our mission accelerating life changing breakthroughs, to cure prevent better to to end on each of these fronts, we're seeing incredible progress. Of course, many of you know that I worked on artificial pancreas for a long time. My brother and I are using a control IQ systems, we looped for a long time, you look at control IQ, which was amazing FDA approval, which spun out of research that we funded with the team at UVA, the 770 G, and I'm proud to have funded some of the work that went into the hybrid cluster, but Medtronic, the Insulet system that's coming down the pike is some of the work we funded at UC Santa Barbara and now at Harvard. So you know, the devices, these better treatment options. You and I have talked about this. I mean, it's a pretty life changing. And um, I literally almost took a picture of my blood sugar this morning, because I was like, gosh, I never could have done that before. Yeah, and here I am, you know, cruising at 100 for seven straight hours overnight. Yeah,   Stacey Simms  9:26 as I've mentioned, I have a teenage son who were supposed to be in the throes of the worst years of type one and instead he has the best time and range, the lowest agency and the least amount of work he's ever done. And it's it's just amazing to me.   Aaron Kowalski9:42 It's it's something I'm really really proud of and but some of your listeners might know that my brother has severe hypoglycemia problems. It was and started with diabetes when there was urine testing. And here we are now living a totally different life. And that is Yeah, of course, the JDRF was founded to cure to one date. And that's our number. That's our North Star. That's that's our number one goal. But in the meantime, I often said particularly back in the beginning of that project, when there was some controversy, if we should do it, we need to be healthy when there are cures. So the advancements that are happening on devices are awesome. And if we continue to push on that front, you may know that we have a big project with Tidepool bringing loop the DIY solution, through FDA in a Tidepool loop form, which will allow for a plug and play of sensors and algorithms and pumps, I'm really excited about that we have some projects and better infusion sets and faster insulin. So on the treatment side of the equation, JDRF is still focused there. What I would say though, is in the face of COVID, we realized that I don't want to say our work is through because we will continue to focus there. But there are a bunch of companies out there Medtronic Tandem Insulet, you name a title. So big foot, we realize that we can start to pass the baton, we have started to pass the baton on, on that work, and we're super excited is really on the work on preventing and curing to end to end cures. And we're gonna talk about why I pluralize that, because that's where the incredible action and it actually reminds me of the early days of the artificial pancreas project when people said, Oh, you've been hearing this forever. I've been hearing about an artificial pancreas for 35 years, you know, what's different now. And it was different. The science had moved the the the tech technologies had moved. And here we are now using hybrid closed loops. I see cell therapies and preventative therapies as being in a similar place. And I think the next coming years are going to be transformative on those fields.   Stacey Simms  11:52 All right, take us through a couple of those projects, if you could, because I'm with you. That sounds exciting.   Aaron Kowalski11:57 Yeah. Okay, so the first thing I'll start with cures, we always say we're gonna find a cure. And I think when I talk about this, there is a skepticism because people have been, you know, there's always I was promised five years or 10 years. And why was that? And so I get into often when I when I talk and you know, I'm sure your listeners will have similar questions is, when, if you step back in time, and think about the JDRF in the 90s, the decade of a cure is what they called it. Why did they say that? And the reason was, the people were being cured, and they were being cured through islet transplantation. So many of your listeners have heard of islet transplantation, somebody dies, they donate organs, one of the organs of pancreas, people can now harvest cells out of the pancreas and transplant them into people via an injection, and it actually restores normal blood sugars. You've probably heard of the Edmonton protocol, Dr. James Shapiro JDRF, worked for a whip and continues for decades. If you meet somebody who's had an islet transplantation, they will tell you they are cured. They're a one sees completely normalized. They don't take insulin, they don't test they can eat, you know, food and don't have high blood sugars. The downside is they take chronic immunosuppressants, and it requires an organ which is a supply demand issue. We know any organ donation is either always big lists. So you know that this idea of I was promised something that wasn't real is not exactly accurate. We could cure people and in fact, I was with Dr. Shapiro last year, he has people who have been off insulin for 20 years with an islet transplant. So that shows that it's possible.   Stacey Simms  13:52 Right back to Aaron. He'll finish that thought in just a moment. But first diabetes Connections is brought to you by Gvoke Hypo Pen and almost everybody who takes insulin has experienced a low blood sugar and that can be scary, but a very low blood sugar is really scary. And that's where Gvoke hypo pen comes in. gvoke is the first auto injector to treat very low blood sugar. Gvoke Hypo Pen  is pre mixed and ready to go with a new visible needle. That means it's easy to use. How easy is it you pull off the red cap, push the yellow end onto bare skin and hold it for five seconds. That's it. Find out more go to Diabetes connections.com and click on the Gvoke logo. Gvoke shouldn't be used in patients with pheochromocytoma or insulinoma visit Gvoke glucagon comm slash risk. Now back to Aaron Kowalski talking about pure research.   Aaron Kowalski14:43 And the reason I say cures is very similar to the you know the artificial pancreas work we did back in the day. I published a paper in I think 2008 and I said there is no single artificial pancreas. There are going to be a series of different solutions. Pump turns off insulin pump the proactively turns off insulin pump that lops off highs and lows, etc, and so forth and getting more and more sophisticated. And we call that the JDRF roadmap. Similarly, there's not going to be a single cure to type one, they're going to be multiple approaches. And that's where there's huge excitement because if you look at for example, there are multiple groups moving into human clinical trials of what I would call modern islet transplantation. Modern islet transplantation means enough cells for everybody, because now we're using stem cell derived eyelets, instead of what we would call calavera. Guy let somebody who passed away and donated their pancreas for so now via stem cell derived islets, you have an unlimited supply source. And it's not just one group that has an unlimited supply source. We have Harvard, Novo Nordisk University of British Columbia via sight, UCSF University of Sydney, there are multiple groups that can make stem cells into eyelids, that looks just like eyelids that came out of our person and can cure animals. So huge, huge advance. The other side of the equation is even a suppression. We have multiple approaches that are going to obviate the need for immunosuppressants. So this isn't getting real. I mean, this is violence and human clinical trials and seeing stem cell derived islet insulin production, these cells that are grown up in test tubes and petri dishes, transplanted into people now starting to make insulin. I was   Stacey Simms  16:33 just gonna ask those different groups that you mentioned, my first question was going to be what about human trials? So via sites in those are the other ones you mentioned moving in the next couple of years to human trials as well? Yeah.   Aaron Kowalski16:45 Oh, yeah. I very much anticipate other companies being in human trials in 2021. Wow. And that is awesome. Because, again, if you think about the process, and you know, why was I promised five years? Well, the process for a small group of selected people worked. But the process for a big group of people wasn't ready for primetime. And we needed different approaches, we needed stem cells, we needed immuno protectants. And now here we are in 2020. It's a, you know, there's been a lot of science since 2000. And we're going to see human trials now happening more and more.   Stacey Simms  17:23 We're going to talk about kind of today, and fundraising issues and some criticism in just a moment. But I also want to address I'd love for you to talk as well, and you already mentioned this prevention, because when I hear about to come up, and I'm very excited that I now know how to pronounce it. You know, that's one study that seems to be ongoing, doesn't even finished yet, is it?   Aaron Kowalski17:44 Well, there but you know, again, there are a number of these trials often happen in different stages and a patient population. So there, they've done some trials that have been very promising and they're ramping up and doing next gen trials.   Stacey Simms  17:57 Are there other prevention studies funded by JDRF, other than the one that I'm referring to, which is part of trial net, you know, Dennett USS,   Aaron Kowalski18:05 oh, yeah, we are working across the board. I mean, we have a number of different groups that are using different drugs that slow the progression of type 1 diabetes. You may have heard of Verapamil, which is actually a beta solid agent. ATG Novo Nordisk was a big program, the preventing to end and it's interesting when I talked to the community about this, sometimes, people bristle a little bit and they're like, well, what's prevention gonna do for me, preventing to end in caring to end are interlinked? No cell therapies are one way I mentioned cures. So there are there going to be multiple ways. Ultimately, what we want to do is get beta cell functioning, they are our own beta cells going again. And to do that, you have to restore immune balance. So what when you talk about sip lism AB, which is an immunotherapy JDRF, funded way back to the original Studies at the University of Chicago. Now legendary scientists, Dr. Jeff bluestone and Dr. Kevin Herold, that drug is now owned by a company called prevention. And they're going to for FDA approval in the current data delays type one for at least three years, and probably we'll see even longer in a number of people. So we're looking at Temple lism ab, we're looking at a variety of different approaches. And I just really want to convey to the listeners that one, even if you have full blown type 1 diabetes, like my brother, I mean, this these advancements are hugely important for future cures for TMD because he can't share to you one day, you know, aside from an immuno protected stem cell, but if you want to do it, quote unquote, true qR lights, you know, you restore your body to what it used to be, you need to restore immune balance, and that's what these drugs are aiming to do. The other part that I think is really important to remember is Type One Diabetes is a genetic disease. You know, most people don't Understand that, unfortunately, that the risk for my kids is 15 times the general population, the next generation of people in our families, we need to stop this disease. And that's, that's the reason. So it's curing to one day, it's preventing the actually going,   Stacey Simms  20:18 there are gonna be people listening who say a genetic disease. We never had any type one in my family until my child was diagnosed until I was diagnosed. But it is obviously a very strong component, right?   Aaron Kowalski20:28 Yes. So I the way I describe and answer that question, because it comes up, every single talk that I give, is just through math, the general population have about a four in 1000 chance of getting type 1 diabetes point 4% will get to end in the US, my kids have about a 5% chance of getting to five and 100 versus four and 1000. Now one of my good friends, Dr. Corey hood at Stanford, who's a psychologist, he says, Aaron, he's got to convey that the risk is that odds are 95% of its won't get it, even if you have a genetic risk, which is a glass half full, right and true. But just play that out from a Why didn't I have it in my family? So if five and 100, get it, you can say okay, insulin has been around for 100 years before that every single type one person died. So in your family, how many people are there in your first you know, your immediate family? And how many generations are there, you can just count, you know, so just say there are three kids and each generation, he may have like 12, nine to 12 kids. So if you see what I'm going here is the odds are even if you don't have the genetics, if you have the genetics, fortunately, most of the kids won't get it. But that's, you know, cold comfort to the ones who do like my brother, I was second. So I guess debate. And if you went back further, if we had through ability to look back in time and say, good kids die, pre 1921. In your family tree? The answer is almost certainly Yes. The kids died, because they didn't have the insulin to survive. So you know, five and 100, if you're a male with type one, three, and 100, if you're a female with type one for your kids, is, is elevated. And unfortunately, we're seeing the incidence of type one increasing for reasons we don't understand. So that's the simple kind of walking through the math that hopefully that makes sense. Because even if you don't have a family history, you probably do have a family history, you just don't know about it.   Stacey Simms  22:41 I'm gonna move on to some closing questions unless you want to focus anymore on research, or was there anything you wanted to mention?   Aaron Kowalski22:46 Yeah, I think the only other piece that we didn't talk about is I mentioned Cori hood, and psycho social, you know, and this is really wasn't related to COVID, before COVID. But we're certainly seeing more challenges with the emotional side have to end. And I think a lot of people don't appreciate that JDRF is now as part of our program focused on psychosocial aspects of diabetes. Now, this is kind of the unspoken part of the disease that affects everybody. And and I just want to put it out there that after years of not funding research in these important areas, and my very strong opinion, we are, and we're funding fellowship to train up a number of new psychologists who specialize in issues, their take on specific funding research programs for kids and people who are really, really struggling with significantly higher one season decays, depression. That's one area that people don't often talk about. But I think every family goes through low points and some very, very low points. And that, put it out there that we're working and see this is an area that needs more attention. I think   Stacey Simms  23:56 that's great. You mentioned COVID, which is actually why we've been talking this whole time about it. Can I ask you a couple of COVID questions that we get all the time, you know, at the beginning of this year? There were so many worries about type one, there wasn't a lot of information that separated from type two, there's been a little bit more as the year has gone on. Can you talk a little bit about what you've learned about COVID? and type 1 diabetes? Is there new research information to say what it seems to have said to me from what I've seen is people with type one are not any more likely to get COVID. But of course, any illness will mess with your blood sugars, but it doesn't seem to be as severe as people with type two.   Aaron Kowalski24:35 Yeah, that's the data. The challenge for us here in the us is we can't collect data as well as many other countries because many other countries can collect from every one of the citizens in the country and and then analyze it whereas our healthcare system doesn't work that way. So when we gather information, like you just described, it's often coming for example, that was there's a big study in England. Look at this. We've worked through a lot of the Scandinavian data. Australia. I think you're that what we're what I would say right now is we do think that people are type one have the same risk of getting COVID as anybody else, it's not increased. The big question, there's probably plenty that people with type one are probably at higher risk for worse outcomes. Type two people seem to be more and that may have to do with the increased weight and type two people. But again, the via more information, I think the big question on why would somebody with type one do worse and you brought up one of the potential issues is just blood sugar, we know that when when you're sick, your blood sugar is harder to manage. The treatments can exacerbate if you're on steroids, bad blood sugar, and that can contribute to infection problems. And particularly in COVID, I was literally on the phone with a person in the field yesterday, you know, one of the hypotheses is people would take one over time get vascular issues, we took on a higher degree of risk for heart attacks and strokes. And there's a fair amount of discussion about covid being you know, the impact on the back skillet. Sure. And that would then be exacerbated by P one d. So, you know, it's obviously for everybody. It's scary. It's scary. For me, it's scary for my brother and my family and my wife. And we urge people to be be extra cautious. You know, one of the things I heard in the beginning of the crisis is make sure you have a very tight plan. If God forbid, you have to go to the hospital, because one of the early readouts that I got in New York City, was the diabetes care was being delivered poorly to people because most if you're not an endocrinologist, most doctors don't see people with insulin frequently. And that can exacerbate, you know, again, blood sugar levels and side effects. So yeah, it's scary. We're learning a lot. I think we've seen improvements of treatments of people in the hospital. But I would urge caution for type one commodity, have a good plan, if you do get sick.   Stacey Simms  27:10 I'm sure in a few years, we'll have some very interesting research from the countries that do track more closely, like you said, and will know a lot more. Let me move into a different part of this interview. And I should, as you listen, just disclose that I was on the board have my local JDRF for six years. I am a financial supporter of JDRF. I think those are important things to know. But I am happy to pass along your questions. And I had some questions of my own. Aaron, I'm sure you were inundated with emails and suggestions earlier this year, and I sent you one and I know it wasn't alone in thinking this. My question was, and I'll eleska to you now, you know, I know how important JDRF research is, I really don't want it to stop. But you could see at the beginning of this year, the financial issue, the the unemployment issue, the economic problems that this country was going to experience. And it seemed to me like it might have been an opportunity for JDRF to pivot a little bit and give people who desperately need it some financial assistance, I assume that was discussed doing something with supplies, insulin, affordability, that sort of thing. But instead, you decided to continue to fund research. Can you tell us a little bit about that thought process and why obviously wasn't a viable option for JDRF?   Aaron Kowalski28:28 Sure. So of course, this year has been brutal. As we lead off, it's been so hard for everybody. And at the beginning of the crisis, we knew that this was going to have a big impact on JDRF. Because we raised most of our money through events, when you can't get together for a walk or bike ride or a gala that that was going to cause us to not be able to fund as much research as we want to be decision. I there are a couple of interesting kind of pieces to your question. One is I think, you know, the decision to ask people for money, which was something that we talked a lot about, and our feeling was our mission to cure to end, prevent, improve lives didn't go away. And I put type 1 diabetes, the COVID didn't type one, obviously, that people are still struggling. And I can tell you, we've had a couple of deaths through gay a neighbor of mine, her son was just diagnosed last month. And this problem, our mission is still critical. So that this isn't to continue to ask people to support us was not to have people feel pressured when they couldn't if they've lost their job if they were struggling. But for the folks who could who had the financial capabilities to lean in and help us preserve some of the incredible mission momentum we have and had going in March and in February and we were seeing across the board so that that was the logic on asking Money. It wasn't intended, again to pressure people it was intended for folks who could. And and I often said it wasn't mutually exclusive, supporting COVID. and supporting T one t are mutually exclusive. So the second part, and this, I think gets into some of our work in insulin access, and how much of our mission is focused on making sure people have access to care versus research. And the board and I have talked a lot about this, the JDRF mission is accelerating life changing breakthroughs to cure, prevent, and better treat TMD and its complications. So if you think about our work and insulin access, it's not our core mission. And people will criticize me or JDRF sometimes for that, but that's what it is. And when I look at other organizations like ADA, or for all or beyond type one, we have different missions. So we've talked to JDRF, about how much more Should we do. So for example, we have a we were doing a ton on policy on insulin access, we think it's critical. But if we were to shift and make that our mission, we would have to change everything we do, we would rearrange our staff, we would probably like a bunch of scientists, and we'd hire a bunch more policy people. So really, what what I think you're getting at is what is the mission of the organization. And our mission has been since 50 years ago, security one day, keep people healthy until we get there through the acceleration of life changing breakers. And that's my optic focus, we will continue to do some of the other critical work like insulin in Africa and developing nations or in the United States for people who can't afford it. I've testified on the hill three times as in front of the Senate and the House, my brother had to his wife had to switch jobs because he runs a small his own small company, and they had a like a $12,000 deductible. So I understand that said, are missing that, essentially outside the messenger apps. And while we do it, it's not the core mission.   Stacey Simms  32:12 If I could devil's advocate for a moment, though, you said earlier in this interview, that you got a lot of criticism and pushback for the artificial pancreas project. And your rationale for seeing it through was we need to keep people alive until there's a cure. When one in four people are rationing insulin in this country. I don't think you have to change your mission to focus more on insulin affordability. And I would even say, Is there no way and maybe Listen, I'm a bit of a pie eyed optimist, and I am not part of the inner workings of JDRF or these organizations. So you can tell me that this is silly. Is there no way to while you're fighting for affordability on the hill? And you're testifying? Is there no way for JDRF to do some kind of assistance program for those who most desperately need it?   Aaron Kowalski32:54 Yeah, no, I hear you, Stacy. And we have looked at this. In fact, I rallied our team to look at and explore essentially insulin exchanges that would allow volunteers to donate insulin. And the challenges that we've faced, it have been really around the legal ease of donating a prescription drug. Again, this isn't our core mission. But I can tell you are in terms of our policy, time and effort and work, I would say it's pretty much our number one thing that we're working on, right, and looking at different ways to make sure and I've said it a million times, nobody should make the decision of food or rent or car payment or insulin insane. So it is a priority of ours even as it's outside of our what I would call the center of our Bullseye of our mission. We're devoting countless hours and dollars to try and to rectify and reconcile the problem. Yeah. And it's very, very frustrating to me. I hate that we're even having the discussion for that drug that is required for us to live. It's absurd.   Stacey Simms  34:06 Yeah, it's so interesting, Aaron to talk to you because you are not a and I mean this as a compliment. So let me get through the whole thing. You're not really a CEO kind of guy. Right? You are. You are the first CEO of JDRF. To live with type 1 diabetes. You are a scientist. your background is not in corporate politics. It is in science. You were obviously chief mission officer for a long time. I know you know what you're doing. So I don't mean it in this way. But I can't think of a more challenging year for somebody who is not a business school kind of guy, if that makes sense. Are you looking at this position? Are you still trying to approach it from a scientific viewpoint? Are you using skills that you didn't think you would have to bring to the table? I mean, I hope the the spirit of my question makes   Aaron Kowalski34:52 sense. Yeah, no. And that was a big question when I applied when I started The board that I thought I could could be CEO is, well, you know, you're not a financial person or having run a big field organization, and what my response was, but I, I understand our community, I grew up in it, my brother and I and my brothers been doing it for 40 years, I haven't done it for 36 years or something, you know, work with the companies work with the community work with our partners. The beauty of, you know, JDRF is we are a volunteer driven organization. And I get to work with some of the smartest, most accomplished business people who volunteer their time, because their family's been impacted. So I've certainly benefited as a new CEO, from an I never a million years thought I'd be facing a pandemic, the first year, I took this job. But in terms of the areas that I wasn't as experienced in my team members of JDRF, who obviously have incredible capabilities. And then our volunteers, our board, we had a group on the board who helped us with the financials, the analyses, as we're going through the crisis, the people issues, the real estate issues. So just like you lean in and help, we're fortunate that we have so many volunteers who can help and I've taken a lot of those learnings and the experience they bring to the table to help I think Jeff become, I've always been proud of that we're a very efficient organization, and I think coming out of the Christmas will be even more efficient. My greatest strength, I think, is just my understanding of the disease, and the community, which I can bring to hopefully rally more people to support the mission.   Stacey Simms  36:43 This is airing during diabetes Awareness Month, which I personally think is a chance to educate people outside the community. I mean, we're all very much aware of diabetes all year round. So I'm curious, you know, what would your message be to people who are not in the diabetes community? What would you like them to know?   Aaron Kowalski36:59 That's a really good question. Because I think, diabetes, you know, as many of the listeners know, diabetes, type one and type two get lumped together. People don't understand them. They don't understand their genetic, they think it's weight driven. And so there's a couple things. One is diabetes. type one and type two are a huge problem in this country in the world. And we need more people leaning into support better solutions. I mean, just think of the advancement of CGM. Now go back in time, and there was a big fight over CGM, you know, was this a useful tool? No, was it too much information? And here we are now, where it's becoming the standard of care, but it's taken a long time. And even in type two, it's still a good question mark, we need to deploy more resources. My very strong personal belief is we need to unite as a type one and type two community, you know, people with type one tend to, I hate to say it, but I kind of look down on type two people. And type two is a genetic disease even more strongly genetic than type one. People don't over eat themselves. And so type two diabetes, it's a huge myth to people with type two, a lot of overweight people that don't have type two, it's a genetic disease. It's a disease. So and the other interesting point not to get too off topic here is, is probably not just type one and type two, it's probably more of a continuum. Oh, sure. So this whole idea of eat, we are an under resourced community, whether you break it into type one, or type two or lump sum us together, we need more effort. And that's where I've talked to Tracy, the brown at ADA, beyond type one, our alliance with the type one, the Helmsley trust, you know, uniting and fighting for better solutions for people with diabetes. Now, if you're not in this community, you're paying, because a third of the Medicare budget goes to treat people with diabetes complications. So we need this country and to appreciate the diabetes are diseases that are genetic that need more resources, because there are solutions on the horizon that will help people and help our economy.   Stacey Simms  39:16 Yeah, I completely believe we are much stronger together. And it's amazing to me how much diabetes is it's like a joke to so many people. It's a hashtag, you know, here's my desert, hashtag diabetes, they don't get it. And we as a community, need to work together to continue to educate and fight those stereotypes and not add to them and not throw people with type two under the bus. So I won't get on my soapbox. But Aaron, thank you so much. And thank you so much for joining me and spending so much time with me and my listeners. I always appreciate   Aaron Kowalski39:43 Oh, it's wonderful to speak with you and thanks, everybody. Hope to talk again soon.   Aaron Kowalski39:54 You're listening to Diabetes Connections with Stacey Simms.   Stacey Simms  40:00 We hit a lot of topics in that interview, I will be happy to link up more information about JDRF research and other things that Aaron mentioned, you can always go to the episode homepage where there is a transcription, just go to Diabetes connections.com. Or if you're listening in a podcast app, you know, every single one of them is a little different. So I hesitate to say open it up there. But if you can see the show notes, if you can see the links, that's an easy place to but it's all on the website. If you have any trouble on any apps. tell me something good coming up in just a moment. And I have some great news about the show to share with you. I'm so excited about this. But first diabetes Connections is brought to you by Dexcom. And we started with Dexcom back in the olden days before share. So trust me when I say using the share and follow apps makes a big difference. And Benny and I set parameters about when I'm going to call him track him down, you know how long to wait, that sort of thing. It really helps us talk and worry about diabetes less. And if he's at a sleep over or away on a trip, it really gives me peace of mind. It also helps if I need to troubleshoot with him, because we can see what's been happening over the last 24 hours. And not just at one moment. The alerts and alarms that we set also help us keep the highs from getting too high and jump on loads before they are a big issue. Internet connectivity is required to access separate Dexcom follow app. To learn more, go to Diabetes connections.com and click on the Dexcom logo. longtime listeners will know that this is a labor of love. I have been doing Diabetes Connections weekly since June of 2015. I have a wonderful editor. Of course, I mentioned john at the end of every episode. But other than that, it's just me producing and hosting and booking guests and, and pre editing before I send it to john which drives him crazy. He says stop cleaning for the cleaning lady. But I can't help myself after a career in audio. And I say all that to bring you the news that we have hit a really tremendous milestone, and that is 1 million downloads and views. I am stunned. This number really sort of came out of the blue for me, because I know this may sound silly, but I can I can tell you we're close here, no secrets, I look at my podcast statistics with my hosting service liberated syndication or libsyn. And every show, you know, we look at the episodes and we look at the geography where people are listening and all that kind of stuff. And it keeps track of all of the downloads and unique listeners. And they're just really a wonderful and very accurate hosting service. So we ticked over more than 900,000 listeners. So I was kind of tracking to see when we hit a million. But then I realized that we have our YouTube channel as well. And while I cannot conceive of listening to a podcast via YouTube, because most of the time, it's just a static image. We have so many listeners over there, especially in the last two years. And sure enough, I clicked over there and we've had more than 100,000, listens views. What do you call it on YouTube, I'm going to say views. And that's why together, I'll say 1 million downloads and views. I'm just so thrilled that I've been able to do this on a regular basis for so long with such terrific support from great listeners like you. And that number means a lot. That's a big one. So to celebrate, and this is great timing with diabetes Awareness Month because you deserve a reward for just living with diabetes or having somebody with diabetes in your family. We are going to be doing two different contests. Now these are going to start on the eighth. So that's a couple of days after this episode is released, you will get an email if you're on that newsletter. You will also see it in the Facebook group. Or if you follow me on Instagram, one contest on Instagram where I am Stacey Simms, and a different contest for people in the Facebook group. And the Facebook group is Diabetes Connections, the group so stay tuned for that, watch your email. If you are not already signed up for the newsletter. Like I said, click on the ebook link in this episode, or maybe you've seen the ads running in Facebook, or go to Diabetes connections.com the subscription thing should pop right up the newsletter subscription. But if it doesn't just scroll all the way to the bottom and it will have a little spot for you to sign up for the newsletter there. If you have any trouble just reach out to me Stacy at Diabetes connections.com. All right, here we go on to our second million downloads and listeners and views. Oh my goodness, I can't believe it. Thank you so much. Next week, we will have a special episode for Veterans Day talking to a veteran who was diagnosed while in the service was able to stay in the service. This is only the second person I know has been able to do this. And then what he did and has done after and the accomplishments that he's made in real the change that he did. It's really an interesting story. And I'm excited to bring it to you and that is next week. Okay, thanks to my editor John Bukenas  from audio editing solutions. And thank you so much for listening. I'm Stacey Simms. I'll see you back here next week. Until then, be kind to yourself.   Benny  45:02 Diabetes Connections is a production of Stacey Simms Media. All rights reserved. All wrongs avenged

Geniş Kompleks Taşikardi Geniş kompleks taşikardi, QRS süresi 0.12 saniye veya daha fazla olan hızlı bir ritim (genellikle bir aritmiye atfedilebildiğinde 150 atım / dakika veya daha fazla) olarak tanımlanır. Aberran iletili supraventriküler taşikardi, atriyoventriküler reentry'nin neden olduğu paroksismal SVT, aberran iletili atriyal fibrilasyon, atriyal flutter veya ektopik atriyal taşikardi dahil olmak üzere anormal şekilde geçirilen herhangi bir supraventriküler taşikardiyi temsil edebilir. Geniş kompleks taşikardinin ilk tedavisi, hastanın hemodinamik stabilitesinin hızlı bir şekilde değerlendirilmesini gerektirir. Stabil olmayan hastalar acil elektriksel kardiyoversiyon gerektirir. Hemodinamik stabil olan hastalara ise taşikardi özelliklerini değerlendirmek için 12 derivasyonlu bir EKG çekilmelidir. Hemodinamik olarak stabil ritimler değerlendirme ve farmakolojik tedavi için bir fırsat sağlarken, unstabil hastalarda ise acil kardiyoversiyon uygulanmalıdır. Düzenli geniş kompleks taşikardinin paroksismal SVT olduğundan şüpheleniliyorsa, farmakolojik tedavilere başlamadan önce vagal manevralar düşünülebilir. Geniş kompleks taşikardisi olan stabil hastalarda, özellikle VT olduğundan şüpheleniliyorsa veya adenozin başarısızlığı varsa IV antiaritmik ilaçlar düşünülebilir. Daha uzun etki süreleri nedeniyle, antiaritmik ajanlar, geniş kompleks taşikardinin nüksetmesini önlemek için de yararlı olabilir. Lidokain, farklılaşmamış geniş kompleks taşikardi için bir tedavi seçeneği olarak dahil edilmemiştir çünkü SVT için etkisiz olan nispeten dar spektrumlu bir ilaçtır. Amiodaron, prokainamid ve sotalol, lidokaine göre "daha geniş spektrumlu" antiaritmiklerdir ve hem SVT'yi hem de VT'yi tedavi edebilir, ancak hipotansiyona neden olabilirler. Verapamil, aupraventriküler kökenli olduğu ve aksesuar yol iletimini içermediği bilinen geniş kompleks bir taşikardinin tedavisinde etkili olsa da negatif inotropik ve hipotansif etkileri VT'yi dengesizleştirebilir ve önceden uyarılmış atriyal fibrilasyonu ve flutter'ı hızlandırabilir. Hemodinamik Olarak Stabil Geniş Kompleks Taşikardide Elektrikli Tedavi Yönetimi ÖnerisiHemodinamik olarak stabil geniş kompleks taşikardinin tedavisinde farmakolojik tedavi başarısız olursa, kardiyoversiyon veya acil uzman konsültasyonu istemek mantıklıdır (2a) Torsades de Pointes Polimorfik VT, QRS kompleksinin atımdan atıma farklı konfigürasyonları ile geniş kompleksli ventriküler kaynaklı taşikardiyi ifade eder Polimorfik VT'nin Elektriksel Tedavi ÖnerisiSürekli, hemodinamik olarak kararsız polimorfik VT için acil defibrilasyon önerilir (1) Altta yatan QT aralığı ne olursa olsun, tüm polimorfik VT formları hemodinamik ve elektriksel olarak unstabil olma eğilimindedir. Tekrarlayabilir, kendiliğinden hafifleyebilir, sürekli hale gelebilir veya elektriksel şok gerekebilecek VF'ye dönüşebilirler. Polimorfik VT, her QRS kompleksinin farklı özellikleri nedeniyle güvenilir bir şekilde senkronize edilemez ve yüksek enerjili senkronize edilmemiş defibrilasyon gerektirir. Uzun QT Aralığı (Torsades De Pointes) ile İlişkili Polimorfik VT'nin Farmakolojik Tedavisi ÖnerisiUzun bir QT aralığı (torsades de pointes) ile ilişkili polimorfik VT'nin tedavisi için magnezyum düşünülebilir (2b) Torsades, QT aralığını uzatabilen ve aritmiyi artırabilen antiaritmik ilaçlarla tedavi edilemez. Magnezyumun, torsades'te görülen VT salvolarını tetikleyebilen miyokardiyal aksiyon potansiyelindeki dalgalanmalar olan erken depolarizasyonları baskıladığına inanılıyor. Bunun yanında herhangi bir elektrolit anormalliğinin, özellikle hipokaleminin düzeltilmesi de tavsiye edilir. Uzun QT Aralığı ile İlişkili Olmayan Polimorfik VT'nin Farmakolojik Tedavisi İçin ÖnerilerIV lidokain, amiodaron ve miyokardiyal iskemiyi tedavi etmeye yönelik önlemler, uzun QT aralığı yokluğunda polimorfik VT'yi tedavi etmek için düşünülebilir (2b)Normal bir QT aralığı ile polimorfik VT tedavisinde rutin magnezyum ...

Cardiac Pharmacology, Antihypertensive drugs, blood pressure medications, heart failure pharmacology, HF drugs, CHF drugs, hypertensive drugs, high blood pressure drugs, amlodipine (Norvasc),  diltiazem (Cardizem LA, Tiazac),  felodipine (Plendil),  isradipine (Dynacirc),  nifedipine (Adalat, Procardia),  nicardipine (Cardene),  nimodipine (Nimotop),  nisoldipine (Sular), and  verapamil (Covera-HS, Verelan PM, Calan).  Verapamil, diltiazem, nicardipine, Chronotropic, inotropic, Dromotropics Free quiz & full course at https://Simplenursing.com/nursing-school  Pharmacology Master Class - 100 videos not on YouTube - Try it for Free!    Pharmacology Master Class - Try it for Free: https://Simplenursing.com/nursing-school  100 videos not on YouTube    FREE Access to new app + 1,000 videos not on youtube!  https://Simplenursing.com/nursing-school   NCLEX FREE TRIAL:  https://simplenursing.com/NCLEX   STAY IN TOUCH

Ray's healthy tidbit about transdermal verapamil, Peyroine's disease, and AK

Unsere neue Folge ist da ! Wir haben natürlich wieder unseren Journal-Club, Akutes Management von LVAD-Notfällen, Verapamil als Medikament des Monats, als Kochrezept den BEFAST-Score und das Management akut lebensbedrohlicher Herzrhythmusstörungen. Dazu ein kleines Gewinnspiel ! Hört rein ! Kommentare https://whereisscihub.now.sh/ Vermischtes Alexander, Elizabeth, et al. „Oral lefamulin vs moxifloxacin for early clinical response among adults with community-acquired bacterial pneumonia: […] Der Beitrag Podcast Dezember 2019 – Folge 11 erschien zuerst auf pin-up-docs - don't panic.

The post Verapamil (Isoptin) Nursing Pharmacology Considerations appeared first on NURSING.com.

If you get cluster headaches, you should be aware of these drugs!

Dr Paul Wang:                   Welcome to the monthly podcast On The Beat, where Circulation: Arrhythmia and Electrophysiology. I'm Doctor Paul Wang, editor in chief, with some of the key highlights from this month's issue.                                                 In our first paper, Parikshit Sharma and associates reported on the use of permanent his bundle pacing to improve hemodynamics in 39 patients with right bundle branch block. His bundle pacing was successfully performed in 37, or 95 percent of the patients, and resulted in narrowing of the QRS complex from 158 milliseconds to 127 milliseconds. P = 0.0001. An increase in left ventricular ejection fraction from 31 percent to 39 percent. P = 0.004, an improvement in the New York Heart Association functional class from 2.8 to 2.0 P = 0.0001. This work suggests that his bundle pacing maybe helpful in right bundle branch block patients with left ventricular dysfunction.                                                 In our next paper, Philippe Debruyne and associates added to our understanding of using catheter ablation to modulate the autonomic nervous system in patients with neurally mediated syncope, signs of no dysfunction and functional AV block. Prior reports of autonomic modulation using catheter ablation have required extensive ablation in both atria. In this article, the authors report a significant 95% reduction in syncope at six months as a result of targeted ablation in the right atrium alone, focusing on partial ablation of the interior right ganglionated plexus. Ablation is quite limited, taking a mean of seven minutes and creating a mean surface area of 11 millimeters squared. This technique has promise as a possible treatment for avoiding a need of pacemaker implantation in some patients.                                                 In our next paper, Shankar Baskar and associates examined the characteristics and outcomes of pediatric patients receiving implantable cardioverter defibrillators and compared them to their adult counterparts. They examined ICD recipients in the NCDRICD registry from 2010 to 2016. There were 562,209 total ICD implants, including 3461 pediatric patients. Of the pediatric patients, 60 percent of implants were for primary prevention with non-ischemic cardiomyopathy being present in 60 percent of the patients, the most common underlying disease. Over time, there is an increasing trend of both primary and secondary prevention ICD implantations, P less than 0.05. Compared to adults, pediatric patients were likely to have structural heart disease, hypertrophic cardiomyopathy, ion channelopathy, and to receive a single chamber device. All P less than 0.001. There is no difference in in-hospital complications between the adult and the pediatric cohorts, 2.4 percent versus 2.6 percent. However, among pediatric patients, lower weight, Ebstein's anomaly, worse New York Heart Association class dual chamber and resynchronization defibrillator were associated with greater risk of complications. Although, re-intervention for generator replacement or upgrade was more common in adults, the time to re-intervention was shorter in the pediatric cohort.                                                 In our next paper, Ahmed Hussein and associates examine the effect of using ablation index guiding ablation in 40 patients with persistent HO fibrillation on the rate of pulmonary vein reconnection. Pulmonary vein reconnection was seen as a mandatory repeat electro-physiologic study in 22 percent of patients, effecting seven percent of pulmonary veins. Ablation on the intravenous cryna was required in 44 percent of patients to achieve durable pulmonary vein isolation. Atrial tachyarrhythmia occurrence was documented in eight to 20 percent of patients, only one of whom had pulmonary vein reconnection at repeat study. At 12 months, 30 out of 40, or 95 percent of patients, were in sinus rhythm, with four or 10 percent of patients having starting antiarrhythmic drugs. Higher body mass index and excessive alcohol consumption were the only significant factors associated with atrial tachyarrhythmia occurrence.                                                 In our next paper, Atsushi Hirayama and associates examined whether acute exasperation of chronic obstructive pulmonary disease increases the risk of repeated atrial fibrillation related health care utilization. They examine 944 patients who are hospitalized for acute exasperation of chronic obstructive pulmonary disease and had emergency department visit or hospitalization for atrial fibrillation during a 450 day period. Compared to the reference period, the rate of atrial fibrillation related emergency department visits or hospitalizations significantly increased in the first 90 days after acute exasperation of chronic obstructive pulmonary disease. 7.3 versus 14.1 per one hundred person months, resulting in a risk ratio of 1.93.                                                 In our next paper, Namsik Yoon and associates examined the mechanisms underlying the electrocardiographic and arrhythmic manifestation of experimental models of early repolarization syndrome and the ameliorative effects of radio-frequency ablation. The authors recorded axis potentials, bi-polar electrograms, and transmural pseudo electrocardiograms for coronary perfused canine left ventricular wedge preparations in 11 animals.                                                 The ITO agonist, NS5806, the calcium channel blocker Verapamil and acetylcholine were used to pharmacologically mimic the effects of genetic defects associated with early repolarization syndrome. The provocative agents induce prominent j waves in the ECG secondary to the accentuation of the action potential notch in the epicardium but not the endocardium. Bipolar recordings displayed low voltage fractionated potential in the epicardium due to temporal and spatial variability and appearance of the action potential dome conceal the phase two reentry develop when the axon potential dome was lost at some epicardial sites but not others. Appearing in the bipolar electrogram, is discrete high frequency spikes. Successful propagation of the concealed phase two reentered beat precipitated ventricular tachycardia or ventricular fibrillation. Radiofrequency ablation of epicardium destroyed the cell displaying abnormal repolarization and thus suppressed the j waves and the development of ventricular tachycardia and ventricular fibrillation in six out of six preparations.                                                 Stavros Stavrakis and associates described ten patients out of 843 patients, or 1.2 percent with AV nodal reentry tachycardia who required ablation of the basal inferolateral left atria, during stable antegrade slow, retrograde fast, AV nodal reentry tachycardia, a single late atrial extra stimulus was delivered at the inferolateral left atria, near the mitral annulus. All patients had failed ablation in the inferior triangle of Koch, and or roof of the coronary sinus. In all ten patients, a late atrial extra stimulus advanced the his bundle potential by at least ten milliseconds and reset the tachycardia. Ablation at that site, eliminates slow pathway conduction and terminated the tachycardia. Ablation was successful at the site of the latest atrial extra stimulus delivered 49 milliseconds after the onset of this his bundle potential. In their series, no recurrent tachycardia was noted at one year follow up.                                                 In our final paper, Justine Bhar-Amato and Malcolm Finlay and associates examine the hypothesis that increased cholinergic tone exerts its pro-rhythmic effects in Brugada Syndrome through increasing dispersion of transmural repolarization in patients with spontaneous and drug induced Brugada Syndrome. Using a recording array in the right ventricular outflow tract and a micro-catheter in the great cardiac vein to record intracardial and epicardial signals, the authors constructed S1S2 restitution curves from the right ventricular apex at baseline and after edrophonium challenge.                                                 The authors studied eight Brugada Syndrome patients and compared them to eight control patients with super ventricular tachycardia. Electrophysiological studies in controls demonstrated shorter endocardial than epicardial right ventricular activation times, mean difference 26 milliseconds. In contrast, Brugada Syndrome patients showed longer endocardial than epicardial activation times, mean difference -15 milliseconds. Brugada Syndrome patients significantly larger transmural gradient in their activation recovery intervals, mean intervals 20.5 versus 3.5 milliseconds, with longer endocardial than epicardial activation recovery intervals. Edrophonium challenge increased the gradients in both controls to a mean of 16 milliseconds. In Brugada Syndrome, to 29.7 milliseconds. However, these changes were attributed to epicardial activation recovery, interval prolongation in control patients. In endocardial activation recovery interval prolongation in Brugada Syndrome patients. Dynamic changes in repolarization gradients were also observed across the right ventricular wall in Brugada Syndrome patients.                                                 That's it for this month. We hope that you'll find the journal to be the go to place for everyone interest in the field. See you next time.  

Dr Paul Wang:                   Welcome to the monthly podcast, On the Beat for Circulation: Arrhythmia and Electrophysiology. I'm Dr Paul Wang, Editor-in-Chief, with some of the key highlights from this month's issue. In our first paper this month, Shaan Khurshid and associates determine the frequency of rhythm abnormalities in 502,627 adults in the UK Biobank, a national prospective cohort. They found that 2.35% had a baseline rhythm abnormality. The prevalence increased with age, with 4.84% of individuals aged 65 to 73 years having rhythm abnormalities. During over three million person- years of follow up, nearly 16,000 new rhythm abnormalities were detected. Atrial fibrillation was the most frequent with three per thousand person-years. Bradyarrhythmia with almost one per thousand person-years. Conduction system disease is about one per one thousand years. Supraventricular and ventricular arrhythmias, each about one half per one thousand person-years. Older age was associated with a hazard ratio of 2.35 for each 10 year increase. Male sex, hypertension, chronic kidney disease and heart failure were all associated with new rhythm abnormalities. In our next paper, Fabien Squara and associates evaluated a method of determining the septal or free wall positioning of pacemaker or ICD leads during fluoroscopy. They compared in 50 patients a classical approach using posterior anterior, right anterior oblique 30 degrees, and left anterior oblique 40 degrees fluoroscopic imaging’s to 50 patients undergoing an individualized left anterior oblique or LAO approach. This individualized LAO approach view provided a true view of the interventricular septum. This angle was defined by the degree of LAO that allowed the perfect superimposition of the RV apex, using the tip of the right ventricular lead, temporarily placed at the apex, and one of the superior vena cava, inferior vena cava access using a guide wire. Transthoracic echo was used to confirm position of the right ventricular lead. Septal, or free wall, right ventricular lead positioning was correctly identified in 96% of patients in the individualized group, versus 76% in the classical group. P equals 0.004. For septal lead positioning fluoroscopy had 100% sensitivity, and an 89.5 specificity in an individualized group, versus 91.4% sensitivity, and a 40% specificity in the classical group. In our next paper, Elsayed Soliman and associates examined the lifetime risk of atrial fibrillation based on race and socioeconomic status. In the atherosclerosis risk in communities, ARIC, cohort, of 15,343 participants without atrial fibrillation, patients were recruited in 1987 to 1989, when they were 45 to 64 years of age, and followed through 2014. The authors identify 2,760 atrial fibrillation cases during a mean follow up of 21 years. The authors found that the lifetime risk of atrial fibrillation in the ARIC cohort was approximately one in three among whites, and one in five among African Americans. And, the socioeconomic status was inversely associated with cumulative incidents of atrial fibrillation before the last decades of life. In our next paper, Jonathan Steinberg and associates sought to determine the impact of atrial fibrillation episode duration threshold on atrial fibrillation incidents and burden in pacemaker patients in a prospective registry. In 615 pacemaker patients was device detected atrial fibrillation over a mean follow up of 3.7 years, 599 had one or more atrial fibrillation episodes of 30 seconds duration, with a mean number of 22 episodes. At 12 months, freedom from atrial fibrillation ranged from 25.5% to 73.1%, based on a duration threshold from 30 seconds up to 24 hours. Of patients with a first episode of 30 seconds to two minutes, 35.8% were free from subsequent episodes greater than two minutes at 180 days. The mean atrial fibrillation burden of 0.2% for patients with first episodes between 30 seconds and 3.8 hours, was significantly less than the 9.5% burden for those with greater than 3.8 hours. The authors concluded that small differences in atrial fibrillation episode duration definition can significantly affect the perceived incidents of atrial fibrillation impact reported outcomes, including atrial fibrillation success. An initial atrial fibrillation episode of 30 seconds does not predict clinically meaningful atrial fibrillation burden. In the next paper, Hongwu Chen and Linsheng Shi and associates examined the distinct electrophysiologic features of bundle branch reentrant ventricular tachycardia in patients without structural heart disease. They described nine patients, mean age 29.6 years, with normal left ventricular function and bundle branch reentrant ventricular tachycardia, with a right bundle branch block pattern in one patient, and left bundle branch block patterns in nine patients. In all left bundle branch block pattern ventricular tachycardia, the mean ventricular tachycardia cycling was 329.3 milliseconds, and the median HV interval during tachycardia was longer than that of baseline, 78 versus 71 milliseconds. The H to right bundle interval during ventricular tachycardia was slightly shorter, however, the right bundle to ventricular interval was markedly longer than that during sinus rhythm, 50 versus 30 milliseconds. In six patients with three dimensional mapping of the left ventricle, a slow anterograde, or retrograde conduction over the left His-Purkinje system with normal myocardial voltage was identified. In addition, Purkinje related ventricular tachycardias were also induced in five patients. Ablation was applied to the distal left bundle branch block in patients with baseline left bundle branch block, and in one narrow QRS patient with sustained Purkinje related ventricular tachycardia, while right bundle branch was targeted in other patients. During a mean follow up at 31.4 months, frequent premature ventricular contractions occurred in one patient, and new ventricular tachycardia developed in the other patient. In the next paper, Michel Haissaguerre and associates examined detailed mapping in 24 patients who survived idiopathic ventricular fibrillation. They used multi-electrode body surface recordings to identify the drivers maintaining ventricular fibrillation, and analyze electrograms in the driver regions, using endocardial and epicardial catheter mapping during sinus rhythm. Ventricular fibrillation occurred spontaneous in three patients, and was induced in 16, while VF was non-inducible in five. Ventricular fibrillation mapping demonstrated reentrant and focal activities, 87% and 13% respectively. The activities were dominant in one ventricle in nine patients, while they were biventricular in the others. During sinus rhythm, areas of abnormal electrograms were identified in 15 out of 24 patients, or 62.5%, revealing localized structural alterations, in the right ventricle in 11, the left ventricle in one, in both in three. They covered a limited surface, 13 centimeters squared, representing 5% of the total surface, and recorded predominantly on the epicardium. 76% of these areas were co-located with ventricular fibrillation drivers. In nine patients without structural alterations, the authors observed a high incidence of Purkinje triggers, seven out of nine, versus four out of 15. Catheter ablation resulted in arrhythmia-free outcomes in 15 out of 18 patients at a 17 month follow up. In our next paper, David Spar and associates describe the effectiveness, safety, and compliance of the wearable cardioverter defibrillator in the identification and treatment of life-threatening ventricular arrhythmias in all US pediatric patients who wore a wearable defibrillator from 2009 to 2016, ages less than 18 years. The 455 patients had a median age of 15 years, median duration of wearable cardioverter defibrillator use of 33 days, and median patient wear time of 20.6 hours per day. The study population was divided into two groups, 63 patients with an ICD problem, or 392 patients without an ICD problem. The wear time was greater than 20 hours in both groups. There were seven deaths, or 1.5%. All patients were not wearing the wearable cardioverter defibrillator at the time of death. Eight patients, 1.8%, received at least one wearable cardioverter defibrillator shock treatment. Of the six patients who had appropriate therapy, there were seven episodes of either polymorphic ventricular tachycardia, or ventricular fibrillation, with a total of 13 treatments delivered. All episodes were successfully converted, and the patient survived. In our next paper, Marc Lemoine and associates used human-induced pluripotential stem cell-derived cardiomyocytes to examine differences in repolarization reserve. The authors compared the contribution of IKs and IKr on action potential durations in human left ventricular tissue, and the human induced pluripotential stem cell derived cardiomyocytes, or IPS-derived engineered heart tissue. They found that the IPS-derived heart tissue showed spontaneous diastolic depolarization in action potential duration, which were sensitive to low concentrations of Ivabradine. IKr block by E-4031 prolonged action potential duration 90 with similar EC50 in both the IPS-derived heart tissue and the human left ventricular tissue. But a larger effect size in the IPS-derived heart tissue, 281 milliseconds versus 110 milliseconds, in the human left ventricular tissue. While IKr block alone evoked early after depolarizations, it triggered activity in 50% of the IPS-derived heart tissue. Slow pacing reduced extracellular potassium blocking of IKr, IKs and IK1 were necessary to induce early after depolarizations in human left ventricular tissue. In accordance with their clinical safety, Moxifloxacin and Verapamil did not induce EADs in IPS-derived heart tissue. In both IPS-derived heart tissue and human left ventricular tissue, IKs block by HMR 1556 prolonged action potential duration 90 slightly in the combined presence of E-4031 and isoprenaline. In our next paper, Elizabeth Saarel and associates sought to obtain contemporary digital ECG measurements in healthy children from North America to evaluate the effects of sex and race, and to compare the results to commonly published data sets, using 2400 digital ECGs, collected for children less than 18 years of age with normal electrocardiograms at 19 centers in the pediatric heart network. The authors found that the QTc in lead II was greater for females compared to males for age groups three years or older, for whites compared to African Americans, for ages 12 years or older. The R wave amplitude in V6 was greater for males compared to females for age groups 12 years and greater; for African Americans compared to white or other race categories for age groups three years or greater; and greater compared to commonly used public data set groups for ages 12 years and greater. In our next paper, Pyotr Platonov and associates examined T-wave morphology as a possible predictor of cardiac events in patients with type 2 long QT syndrome mutation carriers with normal QTc intervals. The authors compared 154 LQT2 mutation carriers with QTc less than 360 milliseconds in men, and less than 470 milliseconds in women, with 1007 unaffected family members. Flat, notched, or negative T-waves in leads II or V5 on baseline ECG were considered abnormal. Using Cox regression analysis, the associations between T-wave morphology, the presence in mutations in the poor region of KCNH2, and the risk of cardiac events defined that syncope aborted cardiac arrest, defibrillator therapy, or sudden cardiac arrests were assessed. The authors found that LQT2 female carriers with abnormal T-wave morphology had a threefold increased risk of cardiac events compared to LQT2 female carriers with normal T-waves, while this association was not seen in males. LQT2 males with poor location of mutations had a six-fold increased risk of cardiac events than non-poor location males, while no such association was found in females. In our last paper, Yaniv Bar-Cohen and associates describe a percutaneous pacemaker entirely implanted in the pericardium, using a sheath for sub-xiphoid access to the pericardial space, and a miniaturized camera with fiber optic illumination, the micro-pacemakers were successfully implanted in six pigs. All animals were studied during follow up, survived without symptoms. That's it for this month. We hope that you'll find the Journal to be the go-to place for everyone interested in the field. See you next time!  

On this podcast we review some background on AVNRT and focus on Emergency Department management. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_20_0_Final.m4a Download 2 Comments Tags: AVNRT, PSVT, REVERT Trial, Tachydysrhythmias Show Notes AVNRT with Aberrancy vs. VT REBEL EM: SVT with Aberrancy Versus VT Amal Mattu's ECG Case of the Week: August 26th, 2013 Valsalva Maneuver ALiEM: Tricks of the Trade: Valsalva Maneuver By Using a 10cc Syringe St. Emlyn's: JC The REVERT Trial Adenosine in AVNRT Larry Mellick: Treating SVT with Adensoine ALiEM: Trick of the Trade: Combining Adenosine with the Flush Verapamil in AVNRT RAGE Podcast:

On this podcast we review some background on AVNRT and focus on Emergency Department management. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_20_0_Final.m4a Download 2 Comments Tags: AVNRT, PSVT, REVERT Trial, Tachydysrhythmias Show Notes AVNRT with Aberrancy vs. VT REBEL EM: SVT with Aberrancy Versus VT Amal Mattu’s ECG Case of the Week: August 26th, 2013 Valsalva Maneuver ALiEM: Tricks of the Trade: Valsalva Maneuver By Using a 10cc Syringe St. Emlyn’s: JC The REVERT Trial Adenosine in AVNRT Larry Mellick: Treating SVT with Adensoine ALiEM: Trick of the Trade: Combining Adenosine with the Flush Verapamil in AVNRT RAGE Podcast:

On this podcast we review some background on AVNRT and focus on Emergency Department management. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_20_0_Final.m4a Download 2 Comments Tags: AVNRT, PSVT, REVERT Trial, Tachydysrhythmias Show Notes AVNRT with Aberrancy vs. VT REBEL EM: SVT with Aberrancy Versus VT Amal Mattu's ECG Case of the Week: August 26th, 2013 Valsalva Maneuver ALiEM: Tricks of the Trade: Valsalva Maneuver By Using a 10cc Syringe St. Emlyn's: JC The REVERT Trial Adenosine in AVNRT Larry Mellick: Treating SVT with Adensoine ALiEM: Trick of the Trade: Combining Adenosine with the Flush Verapamil in AVNRT RAGE Podcast:

Thu, 10 Jul 2014 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/17849/ https://edoc.ub.uni-muenchen.de/17849/1/Zhao_Lu.pdf Zhao, Lu

The discussion of verapamil as an option for the treatment of supraventricular tachycardia (SVT) in RAGE Session Two went off like a fire cracker in the FOAM world. In this RAGEback, Minh Le Cong from the PHARM podcast explains why the RAGE discussion is not going to change his practice, which is to use adenosine as a first line agent. This is followed by a response by RAGErs Karel and Cliff. You — the listener — are left to make up your own mind about which patients (if any) you'll consider verapamil as an option.

Hypertrofická kardiomyopatie je nejčastější dědičné kardiovaskulární onemocnění a nejčastější příčina náhlé smrti u mladých sportovců. Když ji nepoznáte - lidé budou umírat...

In der vorgestellten Studie wurde die Effektivität von peroral verabreichtem Magnesium, welches in seiner Wirkung durch Kalium verstärkt werden sollte, bei der Dauertherapie von Patienten mit chronischem, tachykarden Vorhofflimmern überprüft. Wir wählten dazu ein prospektives, multizentrisches, randomisiertes, doppel-blindes Studiendesign. Da die Akutwirkung von intravenös angewendetem Magnesium zur Frequenzsenkung von tachykardem Vorhofflimmern durch experimentelle und klinische Studien bereits bestätigt wurde, verzichteten wir auf einen Placeboarm und verglichen Magnesium-Kaliumhydrogenaspartat im Rahmen eines parallel-Gruppen kontrollierten „non-inferiority-trials„ mit Verapamil. Eine Gleichwertigkeit von Magnesium-/Kaliumhydrogenaspartat und Verapamil bei der Behandlung des tachykarden chronischen Vorhofflimmerns konnte nicht gezeigt werden. Während der Wachperiode kam es zu einem Anstieg der mittleren Herzfrequenz unter Magnesium um 0,2 Schläge pro Minute, während unter Verapamil eine Reduktion um 13,4 Schläge pro Minute zu verzeichnen war. Die mittlere Herzfrequenzsenkung analysiert in 6-Stunden-Segmenten ergab - ebenso wie alle anderen Effektivitätsparameter - korrespondierende Ergebnisse, die durch einen zusätzlichen definierten Belastungstest bestätigt werden konnten. Mit der vorliegenden Arbeit konnte in statistisch und klinisch zuverlässiger Weise, gezeigt werden konnte, dass die Gabe von Magnesium-/ Kaliumhydrogenaspartat in der von uns verwendeten Dosis bei der Frequenzsenkung des tachykarden, chronischen Vorhofflimmern der Gabe von Verapamil unterlegen und wahrscheinlch gänzlich ohne klinisch relevante Wirkung ist.