Podcasts about mmhg

Take your veterinary dentistry expertise further — claim $100 off any online course with code START26! Start learning from top experts today: https://internationalveterinarydentistryinstitute.org/veterinary-dental-online-webinars-courses-discount/?utm_source=podcast&utm_medium=podcastlink&utm_campaign=start26  —------------------------------------------------------------------- Host: Dr. Brett Beckman, DVM, FAVD, DAVDC, DAAPM In this episode of The Vet Dental Show, Dr. Victoria Lukasik, DVM, DACVAA,  discusses the nuances of anesthesia monitoring, focusing on a case study involving a Siberian Husky with a fractured canine. They delve into recognizing and managing hypotension, troubleshooting capnogram waveforms, and addressing potential causes of hyperthermia during dental procedures. Learn practical strategies to ensure patient safety and optimize anesthetic outcomes. What You'll Learn:  ✅ Recognize dilutional patterns on capnograms and troubleshoot potential leaks.  ✅ Understand how to interpret systolic, diastolic, and mean blood pressure readings.  ✅ Master techniques for managing hypotension in anesthetized patients.  ✅ Differentiate between drug-induced fever and malignant hyperthermia.  ✅ Discover appropriate responses to hyperthermia based on potential causes. ✅ Simplify strategies for maintaining optimal body temperature during procedures. Key Takeaways:  ✅ The capnogram waveform should resemble "elephants following elephants," with a flat plateau indicating proper CO2 levels.  ✅ The diastolic blood pressure should be 30-40 mmHg below the systolic pressure; a wider difference may indicate diastolic hypotension.  ✅ Nordic breeds are physiologically adapted to generate and retain heat, making them prone to hyperthermia under anesthesia.  ✅ Drug-induced fevers can reset the thermal regulatory center in the brain, leading to elevated body temperatures.  ✅ Addressing airway issues, such as faulty endotracheal tube cuffs, is crucial for maintaining adequate ventilation and preventing complications. —------------------------------------------------------------------- Explore Dr. Beckman's complete library of veterinary dentistry courses and CE resources! Save $100 on any online course with code START26! https://internationalveterinarydentistryinstitute.org/veterinary-dental-online-webinars-courses-discount/?utm_source=podcast&utm_medium=podcastlink&utm_campaign=start26  —------------------------------------------------------------------- Questions? Leave a comment below with your thoughts, experiences, or cases related to veterinary dentistry! —------------------------------------------------------------------- KEYWORDS: Veterinary Dentistry, IVDI, Brett Beckman, Dog Dental Care, Cat Dental Care, VetTech Tips, Animal Health, Veterinary Education, Veterinary Dental Practitioner Program, Vet Dental Show, Anesthesia Monitoring, Hypotension, Hyperthermia, Capnography, Endotracheal Tube, Malignant Hyperthermia, Drug-Induced Fever

Contributor: Taylor Lynch, MD Educational Pearls: What is orbital compartment syndrome, and how is it assessed in the emergency room? Orbital compartment syndrome (OCS) is an emergent ophthalmic condition in which intraorbital pressure in the orbital compartment rises dramatically, compromising perfusion of the optic nerve and retina, leading to risk of irreversible vision loss. OCS occurs in the context of traumatic lesions with retrobulbar hemorrhage. Intraocular pressures (IOP) are measured via tonometry as a surrogate for intraorbital pressures, with emergent pathology being present when IOP exceeds 30-40 mmHg (normal being around 20 mmHg). What might be some physical exam findings beyond increased IOP for orbital compartment syndrome? Proptosis (physical outward protrusion of eye) with resistance to being pushed posterior. Afferent pupillary defect (when the non-impacted eye has light shown into it, the impacted eye will have pupillary constriction, and when light is removed it will begin to dilate, but when light is shown into the impacted eye, it will not constrict and continue to dilate). Generalized complaints of vision loss or an inability to move the eye. What is the treatment for orbital compartment syndrome? Lateral canthotomy must be performed immediately upon clinical suspicion as permanent vision loss can occur within minutes to hours.  Lateral canthotomy Step-by Step: Ideally have the patient sedated or highly cooperative. Numb and vasoconstrict the surrounding eye/orbital skin tissue with lidocaine and epinephrine. Take hemostats and clamp the interior and exterior eyelid at the lateral canthus at a 90º angle towards the orbital rim for 30-60 seconds to further devascularize the region. Take iris scissors and cut laterally to the orbital bone/rim to reveal the lateral lanthal tendon. Cut the inferior crus of the lateral lanthal tendon as this will provide the most significant reduction in IOP. Reassess IOP during each step of the procedure to measure procedure efficacy. If no pressure reduction is noted with inferior cantholysis, cutting the superior crus of the lateral canthal tendon may be required to further allow the eye to bulge out and reduce intraorbital pressure. Big takeaways? Ocular compartment syndrome is a rare but emergent vision threatening condition that requires immediate lateral canthotomy to reduce intraocular and intraorbital pressures. Lateral canthotomy done within 30-60 minutes of symptom development can save the patient from permanent vision loss. References: Mohammadi F, Rashan A, Psaltis A, et al. Intraocular Pressure Changes in Emergent Surgical Decompression of Orbital Compartment Syndrome. JAMA Otolaryngol Head Neck Surg. 2015;141(6):562-565. doi:10.1001/jamaoto.2015.0524 Haubner F, Jägle H, Nunes DP, et al. Orbital compartment: effects of emergent canthotomy and cantholysis. Eur Arch Otorhinolaryngol. 2015;272(2):479-483. doi:10.1007/s00405-014-3238-5 Bailey LA, van Brummen AJ, Ghergherehchi LM, Chuang AZ, Richani K, Phillips ME. Visual Outcomes of Patients With Retrobulbar Hemorrhage Undergoing Lateral Canthotomy and Cantholysis. Ophthalmic Plast Reconstr Surg. 2019;35(6):586-589. doi:10.1097/IOP.0000000000001401 Summarized by Dan Orbidan, OMS2 | Edited by Dan Orbidan and Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

🧭 REBEL Rundown 🗝️ Key Points ❌ Don’t chase perfect numbers: Adequate and safe is often better than “perfect but harmful.”💨 Oxygenation levers: Start with FiO₂ and PEEP, but remember MAP is the true driver.🫁 Ventilation levers: Adjust RR and TV, tailored to underlying physiology.🚫 Watch your obstructive patients: Sometimes less RR is more. Click here for Direct Download of the Podcast. 📝 Introduction Ventilator management can feel overwhelming—there are so many knobs to turn, numbers to watch, and changes to make. But before adjusting any settings, it’s crucial to understand why the patient is in distress in the first place, because the right strategy depends on the underlying cause. In this episode, we’ll walk through three different cases to see how the approach changes depending on the problem at hand. ️ The 4 Main Ventilator Settings Tidal Volume (Vt) 🌬️ Amount of air delivered with each breath Typically set based on ideal body weight (6–8 mL/kg for lung protection) Respiratory Rate (RR) ⏱️ Number of breaths delivered per minute Adjusted to control minute ventilation and manage CO₂ FiO₂ (Fraction of Inspired Oxygen) ⛽ Percentage of oxygen delivered Adjusted to maintain adequate oxygenation (goal SpO₂ 92–96%, PaO₂ 55–80 mmHg). PEEP (Positive End-Expiratory Pressure) 🎈 Pressure maintained in the lungs at the end of exhalation to prevent alveolar collapse and improve oxygenation 🧮 Modes of Ventilation AC/VC (Assist Control – Volume Control)How it Works: Delivers a set tidal volume with each breath (whether patient- or machine-triggered).When It’s Used / Pros: Most common initial mode; guarantees minute ventilation; good for patients with variable effort.Limitations / Cons: May cause patient–ventilator dyssynchrony if set volumes don’t match patient’s demand.AC/PC (Assist Control – Pressure Control)How it Works: Delivers a set inspiratory pressure for each breath; tidal volume varies depending on lung compliance/resistance.When It’s Used / Pros: Useful in ARDS (lung-protective strategy), limits peak airway pressures.Limitations / Cons: Tidal volume not guaranteed; must closely monitor volumes and minute ventilation.PRVC (Pressure-Regulated Volume Control)How it Works: Hybrid: set target tidal volume, ventilator adjusts inspiratory pressure breath-to-breath to achieve it (within limits).When It’s Used / Pros: Common default mode on newer vents; combines benefits of VC (guaranteed volume) + PC (pressure limitation).Limitations / Cons: Can increase pressures if compliance worsens.SIMV (Synchronized Intermittent Mandatory Ventilation)How it Works: Delivers set breaths, but allows spontaneous patient breaths in between (without guaranteed volume).When It’s Used / Pros: Used for weaning; allows patient effort.Limitations / Cons: Risk of increased work of breathing if spontaneous breaths are inadequate.PSV (Pressure Support Ventilation)How it Works: Every breath is patient-initiated; ventilator provides preset pressure support to overcome airway resistance.When It’s Used / Pros: Weaning trials; patients with intact drive who just need assistance.Limitations / Cons: Not a full-support mode; not for unstable patients without spontaneous drive. ♟️ Ventilation Strategies Airway ProtectionLow GCS, seizure, strokeLoss of gag/cough reflexHigh aspiration risk (vomiting, GI bleed, poor mental status)Hypoxemic Respiratory FailureSevere pneumoniaARDSPulmonary edemaInhalation injuryVentilatory (Hypercapnic) Failure / Increased Ventilation DemandSevere metabolic acidosis (DKA, sepsis, renal failure) → need high minute ventilationCOPD, asthma (if decompensating)Neuromuscular weakness (myasthenia, Guillain–Barré, spinal cord injury)Airway Obstruction / Anticipated Loss of AirwayTumor, anaphylaxis, angioedemaFacial or airway traumaPre-op / anticipated deterioration Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO) 👤 Show Notes Priyanka Ramesh, MD PGY 1 Internal Medicine Resident Cape Fear Valley Internal Medicine Residency Program Fayetteville NC Aspiring Pulmonary Critical Care Fellow 🔎 Your Deep-Dive Starts Here REBEL Core Cast – Pediatric Respiratory Emergencies: Beyond Viral Season Welcome to the Rebel Core Content Blog, where we delve ... Pediatrics Read More REBEL Core Cast 143.0–Ventilators Part 3: Oxygenation & Ventilation — Mastering the Balance on the Ventilator When you take the airway, you take the wheel and ... Thoracic and Respiratory Read More REBEL Core Cast 142.0–Ventilators Part 2: Simplifying Mechanical Ventilation – Most Common Ventilator Modes Mechanical ventilation can feel overwhelming, especially when faced with a ... Thoracic and Respiratory Read More REBEL Core Cast 141.0–Ventilators Part 1: Simplifying Mechanical Ventilation — Types of Breathes For many medical residents, the ICU can feel like stepping ... Thoracic and Respiratory Read More REBEL Core Cast 140.0: The Power and Limitations of Intraosseous Lines in Emergency Medicine The sicker the patient, the more likely an IO line ... Procedures and Skills Read More REBEL Core Cast 139.0: Pneumothorax Decompression On this episode of the Rebel Core Cast, Swami takes ... Procedures and Skills Read More The post REBEL Core Cast 146.0–Ventilators Part 4: Setting up the Ventilator appeared first on REBEL EM - Emergency Medicine Blog.

Broadcast from KSQD, Santa Cruz on 12-04-2025: Dr. Dawn opens with an experimental vaccine that prevents severe allergic reactions by targeting IgE antibodies. The vaccine could eventually replace current monoclonal antibody treatments like omalizumab that require injections every two weeks. She explains how adjuvants work in vaccines as additives that irritate the immune system enough to notice the vaccine target. Aluminum hydroxide is s common adjuvant. Modern vaccines use small pathogen fragments rather than whole organisms, requiring adjuvants to trigger adequate immune response. Dr. Dawn expresses concern about the US Advisory Committee on Immunization Practices reviewing aluminum adjuvants this week. A Danish study of over one million children finding no connection between aluminum with autism and ADHA contradicts RFK,Jr's public claims.She worries that removing aluminum could devastate vaccine effectiveness and children's health, noting that whenever vaccination rates drop, diseases like measles return to native circulation. She recounts pertussis vaccine history—when Japan stopped vaccination due to rare adverse reactions (approximately one death per million doses), they lost about 5,000 children to whooping cough in the first year. The newer acellular vaccine using pathogen fragments plus adjuvants is safer but only lasts 4-5 years versus lifetime immunity from the older whole-cell version, necessitating "cocooning" strategies where everyone contacting newborns must be recently vaccinated. Dr. Dawn describes a vaccine to prevent fentanyl from reaching the brain now starting clinical trials in the Netherlands. It pairs a fentanyl-like molecule with a carrier protein large enough to trigger antibody production. Once primed, the immune system attacks any fentanyl entering the blood, preventing highs and overdoses—potentially helping people in addiction recovery and those accidentally exposed through contaminated drugs. She reports the first documented death from alpha-gal syndrome. Alpha-gal is a meat allergy triggered by Lone Star tick bites; the tick essentially vaccinates humans against the alpha-galactosidase protein found on beef and pork. Cases have increased since 2010 as climate change expands the tick's range northward, yet a 2023 survey found 42% of doctors had never heard of the condition. Dr. Dawn highlights research from Edith Cowan University showing that blood drawn after exercise suppresses cancer cell growth when added to tumor cultures. In breast cancer survivors, plasma from high-intensity interval training or weight lifting caused cancer cells to stop growing or die; blood drawn before exercise had no effect. The key mechanism involves myokines, particularly IL-6, released by contracting muscles. A Stanford study found colon cancer survivors who exercised were 37% less likely to experience recurrence. A caller asks about pig-to-human heart transplants and mask recommendations. Dr. Dawn clarifies that newer xenotransplant pigs have more genes edited to reduce rejection compared to the 2022 case. For masking, she recommends context-dependent use—especially in public restrooms where toilet flushing aerosolizes COVID-containing particles, transportation hubs, and hospitals, noting that COVID vaccination prevents death but not infection or long COVID. She advises the same caller about spacing vaccines because adjuvant loads stack. Most vaccines can be combined safely, but she recommends against pairing COVID and Shingrix vaccines due to their heavy adjuvant content—wait at least ten days between them. She suggests inducing a sweat the night of vaccination through hot baths, saunas, or exercise to reduce adjuvant-related discomfort without diminishing antibody response. Dr. Dawn discusses seasonal affective disorder. She recommends 5,000 units of vitamin D3 and morning light exposure. She suggests that sun avoidance advice may have gone too far. A UK study of 3.36 million people found 12-15% lower mortality with greater UV exposure even accounting for skin cancer risk. A Swedish study following 30,000 women for 20 years found sun-seekers had half the mortality risk. Benefits may involve nitric oxide production lowering blood pressure, with each 1,000 km from the equator correlating with 5 mmHg higher blood pressure. Lack of bright outdoor light also contributes to childhood myopia, with rates exceeding 80% in some Asian cities. Dr. Dawn concludes with Danish microbiologists at Copenhagen's Alchemist restaurant reviving an old Bulgarian practice of fermenting milk with live red wood ants. The resulting yogurt, cheese, and ice cream contain far more beneficial microbes than commercial products, with a complex lemony acidity. Only live ants work, and wild ants may carry parasites dangerous to humans.

Episode 207: Understanding Hypertension and Diabetes (Pidjin English)Written by Michael Ozoemena, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.HypertensionSegment 1: What Is Hypertension?HOST:Let's start with the basics. Blood pressure is the force of blood pushing against the walls of your arteries. Think of it like water running through a garden hose—if the pressure stays too high for too long, that hose starts to wear out.Hypertension, or high blood pressure, means this pressure is consistently elevated. It is measured using two numbers:Systolic: the pressure when the heart beatsDiastolic: the pressure when the heart relaxesNormally reading is around 120/80 mmHg. Hypertension is defined by the American College of Cardiology/American Heart Association (ACC/AHA) as 130/80 mmHg or higher.The American Academy of Family Physicians (AAFP) defines hypertension as persistent elevation of systolic and/or diastolic blood pressure, with the diagnostic threshold for office-based measurement set at 140/90 mm Hg or higher.Segment 2: Why Should We Care?HOST:Hypertension is known as “the silent killer” because most people have no symptoms. Even without symptoms, it steadily increases the risk of:Heart attackStrokeKidney diseaseThink of high blood pressure as a constant stress test on your blood vessels. The longer it goes uncontrolled, the higher the chance of complications.Segment 3: What Causes High Blood Pressure?HOST:Hypertension usually doesn't have a single cause. It often results from a combination of genetic factors, lifestyle, and underlying medical conditions.Modifiable FactorsHigh-salt diet and low potassium intakePhysical inactivityTobacco useExcessive alcohol intakeOverweight or obesityChronic stressPoor sleep or sleep apneaNon-Modifiable FactorsFamily history of hypertensionBlack race (higher prevalence and severity)Age over 65Hypertension may also be secondary to other conditions, such as kidney disease, thyroid disorders, adrenal conditions, or medications like NSAIDs or steroids.Segment 4: How Is It Diagnosed?HOST:Diagnosis requires multiple elevated blood pressure readings taken on different occasions. This includes office readings, home blood pressure monitoring, or ambulatory blood pressure monitoring.If you haven't had your blood pressure checked recently, this is your reminder. It's simple—and it could save your life.Segment 5: Treatment and ManagementHOST:Lifestyle changes are often the first line of treatment:Reduce salt intakeEat more fruits, vegetables, and whole grainsAim for 150 minutes of moderate exercise per weekManage stressMaintain a healthy weightGet enough sleepLimit alcoholQuit smokingIf these steps aren't enough, medications may be necessary. These include:Diuretics, ACE inhibitors, ARBs, Calcium channel blockers, Beta-blockersYour healthcare provider will choose the best medication based on your health profile.Segment 6: What You Can Do TodayHOST:Here are three simple, actionable steps you can take right now:Check your blood pressure—at a clinic, pharmacy, or at home.Pay attention to your salt intake—much of it is hidden in processed foods.Move more—even a 20-minute daily walk can help reduce blood pressure over time.Small steps can lead to big, lasting improvements.SummaryHypertension may be silent but understanding it gives you power. Early action can add healthy years to your life. Take charge of your blood pressure today.Diabetes1. Wetin Diabetes Be and Wetin E Go Do to Person Body?Q: Wetin diabetes mean?A: Diabetes na sickness wey make sugar (glucose) for person blood too high. E happen because the body no fit produce insulin well, or the insulin wey e get no dey work as e suppose.Q: Wetin go happen if diabetes no dey treated well?A: If diabetes no dey treated well, e fit damage the blood vessels, nerves, kidneys, eyes, and even the heart.2. Wetin Cause Diabetes and Why Black People Suffer Pass?Q: Wetin cause diabetes?A: E no be one thing wey cause diabetes. E dey happen because of mix of gene, lifestyle, environment, and society factors.Q: Why Black/African Americans get diabetes more?A: Black people for America get diabetes more because of long-standing inequality, stress, low access to healthcare, and the kind environment wey many of them dey live in. These things dey make Black people more at risk.3. Diabetes Rates for America and Black People?Q: How many people get diabetes for America?A: For America today, over 38 million people get diabetes, and the number dey rise every year.Q: Why Black people dey suffer diabetes more than White people?A: About 12% of Black adults get diabetes, compared to just 7% for White adults. Black people also dey get the sickness earlier and e dey more severe.4. Signs and Symptoms of Diabetes?Q: Wetin be the early signs of diabetes?A: The early signs no too strong, but when e show, e fit include:Too much urine (polyuria)Thirst (polydipsia)Hunger, tiredness, and blurred visionWounds no dey heal fastTingling for hand or legSometimes weight loss5. How Doctor Go Diagnose Diabetes?Q: How doctor fit confirm say person get diabetes?A: Doctor go do some lab tests to confirm:Fasting Plasma Glucose (FPG): 126 mg/dL (7.0 mmol/L) or higherHbA1c: 6.5% or higher2-hour Oral Glucose Tolerance Test (OGTT): 200 mg/dL (11.1 mmol/L) or higher after person drink glucose.Random Blood Glucose: 200 mg/dL (11.1 mmol/L) or higher plus classic symptoms like too much urination, thirst, or weight loss.Q: Wetin happen if HbA1c test no match the person?A: If HbA1c result no match person symptoms, doctor fit repeat test or try other tests like FPG or OGTT.6. Wetin Screening and Early Diagnosis Fit Do?Q: Why screening for diabetes dey important?A: Screening dey important because early detection fit prevent serious complications from diabetes.Q: How often person go do diabetes test?A: Adults wey get overweight or obesity, between 35–70 years, suppose do diabetes screening every three years. But because Black adults get higher risk, doctors dey start screening earlier and more often.7. How Person Fit Manage Diabetes?Q: Wetin be the best way to manage diabetes?A: The two main ways to manage diabetes be:Lifestyle changes: Eat better food (vegetables, fruits, whole grain, beans, fish, chicken) and exercise regularly.Medicine: If person sugar still high, doctor fit give drugs like metformin, SGLT-2 inhibitors, or GLP-1 receptor agonists.Q: Wetin be SGLT-2 inhibitors and GLP-1 drugs?A: SGLT-2 inhibitors dey help with kidney and heart problems, while GLP-1 drugs dey help with weight loss and prevent stroke.Q: Wetin be first-line treatment for diabetes?A: First-line treatment for diabetes be metformin, unless person no fit tolerate am.Q: How much exercise a person suppose do?A: Person suppose do at least 150 minutes of moderate exercise per week. This fit include things like brisk walking, swimming, or cycling. E also good to add muscle-strength training two or three times weekly to help control sugar.Q: When insulin therapy go be needed?A: Insulin therapy go be needed if person A1c is higher than 10%, or if person dey hospitalized and their glucose dey above the 140-180 range. This go help bring the blood sugar down quickly.8. Wetin Be the Complications of Diabetes?Q: Wetin fit happen if diabetes no dey well-managed?A: Complications fit include kidney disease, blindness, nerve damage, leg ulcers, heart attack, stroke, and emotional issues like depression.Q: Why Black adults get more complications?A: Black people get higher risk of these complications because of inequality, stress, and poor access to healthcare.9. Wetin Dey Affect Access to Diabetes Treatment?Q: Wetin make Black people struggle to get treatment for diabetes?A: Many Black people no dey get new effective treatments like GLP-1 and SGLT-2 inhibitors because of price, insurance issues, and lack of access. COVID-19 also worsen things.Q: Wetin government and doctors fit do?A: Policymakers dey work on improving access to drugs, better community programs, and screening for social issues wey fit affect diabetes care.10. ConclusionQ: Wetin be the solution to reduce diabetes impact?A: The solution go need medical treatment, early screening, lifestyle support, and policy changes. With proper treatment and community support, e possible to reduce the impact of diabetes, especially for Black communities.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References: Whelton PK, Carey RM. Overview of hypertension in adults. UpToDate. 2024.Carey RM, Moran AE. Evaluation of hypertension. UpToDate. 2024.Mann SJ, Forman JP. Lifestyle modification in the management of hypertension. UpToDate. 2024.Giles TD, Weber MA. Initial pharmacologic therapy of hypertension. UpToDate. 2024.American Heart Association. Understanding Blood Pressure Readings. Accessed 2025.American Heart Association. AHA Dietary and Lifestyle Recommendations. Accessed 2025.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Witam Państwa, nazywam się Jarosław Drożdż, pracuję w Centralnym Szpitalu Klinicznym Uniwersytetu Medycznego w Łodzi, skąd nagrywam podcast Kardio Know-How. W tym odcinku kontynuuję omawianie doniesień z tegorocznego kongresu ESC.Najnowsze wytyczne ESC 2025 dotyczące wad zastawkowych serca zastąpiły wersję sprzed 4 lat i wprowadzają 28 nowych oraz 50 zmodyfikowanych zaleceń. Podkreśla, że dokument jest kluczowy dla specjalistycznych ośrodków, gdzie decyzje terapeutyczne podejmuje zespół Heart Team. W stenozie aortalnej (AS) TAVI zaleca się od 70. r.ż. (wcześniej 75), a SAVR u pacjentów

Frequent standing breaks improve heart health. Research shows it reduced blood pressure by 2 to 3 millimeters of mercury (mmHg) in postmenopausal women within 12 weeks Prolonged sitting increases cancer risk significantly. Every additional two hours of daily sitting raises overall cancer risk by 6%, with longest sitters facing 56% higher cancer mortality Movement quality matters more than total sitting time. Breaking up sitting with frequent stands provides better health benefits than simply reducing total daily sitting hours Sedentary behavior triggers harmful biological changes. Sitting decreases muscle activity by 90%, slows metabolism to 1 calorie per minute, and promotes inflammation and insulin resistance Simple interventions can reduce health risks. Standing 10 minutes hourly, walking 30 minutes daily, and aiming for 10,000 steps significantly counteracts sedentary lifestyle dangers

El índice de perfusión periférica (PPI) es una medida no invasiva que refleja la relación entre el flujo sanguíneo pulsátil y el flujo sanguíneo no pulsátil en los tejidos periféricos. En términos simples, permite valorar la calidad de la perfusión sanguínea en áreas distales, como los dedos de las manos. Su medición es rápida y sencilla, ya que se obtiene a través de sensores de oxímetro de pulso avanzados que calculan esta relación y ofrecen un valor numérico. En el contexto del shock séptico, donde la perfusión tisular se ve comprometida a pesar de que los parámetros macro-hemodinámicos (como la presión sanguínea) puedan estar dentro de rangos aceptables, el PPI se convierte en una herramienta innovadora. Permite evaluar directamente el estado microcirculatorio, clave en la supervivencia del paciente crítico. El artículo publicado en The American Journal of Emergency Medicine (Yılmaz et al., 2025) ofrece evidencia de que usar el índice de perfusión periférica para guiar la resucitación del paciente en shock séptico mejora la supervivencia y acelera la depuración del lactato, en comparación con las estrategias tradicionales basadas únicamente en la presión arterial media (MAP). Tabla de Contenido Resumen del Estudio: PPI vs. Manejo Estándar Resultados clave: Implicaciones Clínicas: Cambiando el Paradigma en Sepsis Relación con la Formación Profesional: Cursos Clave en ECCtrainings a) Critical Care Transport b) Emergency Nursing c) Critical Care Nursing Casos Clínicos: Aplicación del PPI en la Práctica Beneficios de Integrar el PPI en Protocolos El Riesgo de No Adoptar el PPI Transformación Profesional: Del Conocimiento a la Acción Conclusión Referencia (APA) Resumen del Estudio: PPI vs. Manejo Estándar El estudio, diseñado como un ensayo clínico prospectivo y controlado, incluyó 200 pacientes divididos en dos grupos: manejo estándar vs. manejo guiado por PPI. Grupo control: manejo basado en guías tradicionales (SSC), con objetivo de mantener la MAP ≥ 65 mmHg. Grupo experimental: manejo basado en el índice de perfusión periférica para guiar la resucitación del paciente en shock séptico. Los pacientes con PPI

We review the diagnosis, risk stratification, & management of acute pulmonary embolism in the ED. Hosts: Vivian Chiu, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acute_Pulmonary_Embolism.mp3 Download Leave a Comment Tags: Pulmonary Show Notes Core Concepts and Initial Approach Definition: Obstruction of pulmonary arteries, usually from a DVT in the proximal lower extremity veins (iliac/femoral), but may be tumor, air, or fat emboli. Incidence & Mortality: 300,000–370,000 cases/year in the USA, with 60,000–100,000 deaths annually. Mantra: “Don't anchor on the obvious. Always risk stratify and resuscitate with precision.” Risk Factors: Broad, including older age, inherited thrombophilias, malignancy, recent surgery/trauma, travel, smoking, hormonal use, and pregnancy. Clinical Presentation and Risk Stratification Presentation: Highly variable, showing up as anything from subtle shortness of breath to collapse. Acute/Subacute: Dyspnea (most common), pleuritic chest pain, cough, hemoptysis, and syncope. Patients are likely tachycardic, tachypneic, hypoxemic on room air, and may have a low-grade fever. Chronic: Can mimic acute symptoms or be totally asymptomatic. Pulmonary Infarction Signs: Pleuritic pain, hemoptysis, and an effusion. High-Risk Red Flags: Signs of hypotension (systolic blood pressure < 90 mmHg for over 15 minutes),

En este episodio del ECCpodcast, exploramos el SCAPE, o “Sympathetic Crashing Acute Pulmonary Edema”. Este síndrome representa una forma dramática de edema agudo de pulmón mediado por un colapso súbito de la función cardiopulmonar, con un componente simpático dominante que desencadena una cascada crítica de deterioro. A lo largo del episodio, desglosamos la fisiopatología, el diagnóstico diferencial, el manejo clínico y las estrategias avanzadas de intervención para SCAPE. Este artículo resume y amplía los puntos clave discutidos, con la intención de ofrecerte un recurso educativo robusto, ya seas médico, paramédico, enfermero o profesional de atención crítica. ¿Qué es SCAPE? SCAPE (Sympathetic Crashing Acute Pulmonary Edema) se refiere a una forma de edema pulmonar agudo con características distintivas: Inicio súbito: El paciente suele estar previamente normotenso o hipertenso, sin antecedentes inmediatos de insuficiencia cardiaca congestiva descompensada. Activación simpática intensa: Elevaciones abruptas en la presión arterial y frecuencia cardíaca desencadenan un círculo vicioso de congestión pulmonar y deterioro ventilatorio. Hipoxia severa y ansiedad extrema: El paciente se presenta en franca angustia respiratoria, luchando por aire y con sensación inminente de muerte. Esta condición es potencialmente reversible con un tratamiento rápido y apropiado, lo cual contrasta con otras causas de edema pulmonar en pacientes con falla sistólica crónica. Fisiopatología de SCAPE: Una tormenta simpática SCAPE no es simplemente edema pulmonar. Es el resultado de una descarga adrenérgica descontrolada, en muchos casos precipitada por un evento hipertensivo agudo o crisis de ansiedad. Hipertensión severa repentina → aumento de la poscarga → disfunción ventricular izquierda transitoria. Esto causa congestión pulmonar aguda, en minutos, con extravasación de líquido en los alvéolos. El resultado: edema pulmonar con dificultad respiratoria extrema, hipoxia, y ansiedad severa. En lugar de una descompensación progresiva de insuficiencia cardíaca, aquí vemos una crisis hemodinámica inducida por una tormenta simpática, en pacientes que usualmente tienen una fracción de eyección normal. Presentación clínica: El paciente que “se estrella” frente a ti El paciente con SCAPE puede presentarse con: Disnea súbita y severa Sibilancias generalizadas (puede confundirse con un cuadro asmático) Presión arterial muy elevada, típicamente ≥180 mmHg sistólica Frecuencia respiratoria y cardíaca elevadas Sudoración profusa, ansiedad extrema Rales bilaterales hasta vértices Uso de músculos accesorios Saturación de O₂ marcadamente reducida Estos signos deben diferenciarse de otras causas de disnea aguda como EPOC, asma, TEP, síndrome ansioso o neumonía. Diagnóstico diferencial: ¿Es SCAPE o no? El diagnóstico de SCAPE es principalmente clínico. Algunos elementos clave para distinguirlo incluyen: Diagnóstico diferencial Diferenciador clave Asma No hay historia asmática, no hay respuesta a broncodilatadores EPOC No hay hipersecreción crónica ni patrón obstructivo previo TEP No suele haber hipertensión severa ni edema pulmonar radiológico Neumonía Inicio más insidioso, fiebre, consolidación localizada Ansiedad No explica rales ni saturación baja sostenida El hallazgo de rales bilaterales, taquicardia, hipertensión severa, y signos de hipoxia crítica, especialmente en ausencia de historia de ICC, apunta fuertemente a SCAPE. Tratamiento inmediato: Qué hacer en los primeros 5 minutos En SCAPE, cada minuto cuenta. El manejo temprano es vital para revertir el curso clínico. El tratamiento se enfoca en tres pilares fundamentales: 1. Ventilación no invasiva (VNI) inmediata Iniciar CPAP o BiPAP en cuanto se identifica el cuadro. CPAP de inicio: 10 cmH₂O Mejora la oxigenación, recluta alvéolos colapsados, y reduce la precarga. Reduce la necesidad de intubación orotraqueal. 2. Nitroglicerina en bolos y goteo No es una hipertensión “de fondo” — se trata de una crisis aguda. Bolos de nitroglicerina IV de 400-800 mcg cada 2-3 minutos son preferibles al goteo lento. Luego se inicia goteo continuo a dosis altas (100-200 mcg/min). Objetivo: reducir rápidamente la poscarga. 3. Evitar intubación temprana La intubación agrava el cuadro si no se ha optimizado primero la poscarga. El uso agresivo de VNI y vasodilatadores puede evitar la necesidad de intubación en la mayoría de los casos. ¿Y los diuréticos? Un error común es administrar furosemida o torasemida como primer paso. En SCAPE: El paciente no tiene sobrecarga de volumen, sino redistribución aguda de fluidos por hipertensión. El diurético puede empeorar la hipotensión posterior. Puede considerarse después de estabilizar la presión y la oxigenación, no antes. Rol del ultrasonido en SCAPE El ultrasonido pulmonar y cardíaco a pie de cama puede ser útil: Pulmonar: líneas B difusas bilaterales, indicativas de edema intersticial. Cardíaco: disfunción ventricular izquierda, cavidades no dilatadas (útil para diferenciar de ICC crónica). El uso del ecógrafo puede reforzar el diagnóstico clínico y guiar intervenciones tempranas. Perlas prácticas del ECCpodcast Durante el episodio, se destacan múltiples “perlas clínicas” útiles para el manejo operativo de SCAPE: La mayoría de los pacientes con SCAPE tienen FEVI normal: no son pacientes con ICC descompensada. La sibilancia no siempre es asma: los rales y sibilancias en SCAPE vienen de edema, no de broncoespasmo. La nitroglicerina en bolo es tu mejor aliada: no temas usar dosis elevadas bajo monitoreo. No pierdas tiempo con diuréticos ni con salbutamol en estos casos. Usa CPAP agresivamente desde el inicio. No intubes a menos que hayas fallado en revertir el cuadro con VNI + nitro. Contexto prehospitalario: ¿Qué puede hacer el paramédico? Desde la perspectiva de atención prehospitalaria: Iniciar CPAP tan pronto como se identifique el cuadro. Administrar nitroglicerina sublingual en dosis repetidas, si no se cuenta con acceso IV. Monitorear la presión constantemente. SCAPE requiere agresividad controlada, no intervención ciega. Notificar al hospital del cuadro clínico temprano para que se preparen con VNI e intervenciones avanzadas. Conclusiones del episodio SCAPE representa una emergencia hipertensiva de alta mortalidad si no se trata de forma rápida y dirigida. El abordaje debe ser: Rápido Guiado por la fisiopatología Alejado de viejos esquemas de manejo de ICC Centrado en VNI + nitroglicerina Recursos adicionales Algoritmo de manejo de SCAPE en formato PDF Infografía resumen de SCAPE para descargas clínicas Referencias a estudios y guías clínicas mencionadas

In this episode, we review the newly published 2025 ACC/AHA hypertension guidelines. Key Concepts Instead of the Pooled Cohort Equations (PCE) from 2013, the 2025 hypertension guidelines recommend a new risk equation called PREVENT, which incorporates new risk factors and does not include race as part of the risk calculation. The guidelines recommend starting two antihypertensive medications for initial therapy in stage II hypertension and one antihypertensive medication for stage I hypertension. The guidelines no longer recommend specific first-line therapies for black patients. Instead, all patients without compelling indications should be initiated on a thiazide, ACE inhibitor, ARB, or dihydropyridine calcium channel blocker regardless of race/ethnicity. All patients should have a blood pressure goal of < 130/80 mmHg. Some patients may consider a more stringent goal of < 120/80 if they have diabetes or are at a higher risk of future ASCVD events. References Jones DW, Ferdinand KC, Taler SJ, Johnson HM, Shimbo D, Abdalla M, Altieri MM, Bansal N, Bello NA, Bress AP, Carter J, Cohen JB, Collins KJ, Commodore-Mensah Y, Davis LL, Egan B, Khan SS, Lloyd-Jones DM, Melnyk BM, Mistry EA, Ogunniyi MO, Schott SL, Smith SC Jr, Talbot AW, Vongpatanasin W, Watson KE, Whelton PK, Williamson JD. 2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM Guideline for the Prevention, Detection, Evaluation and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2025 Aug 14. doi: 10.1161/CIR.0000000000001356. Epub ahead of print. PMID: 40811497.

Et si une simple infusion pouvait rivaliser avec certains médicaments contre l'hypertension ? Ce n'est pas une promesse farfelue, mais une réalité scientifique : l'hibiscus, cette fleur tropicale aux couleurs vives, s'est révélée aussi efficace que certains traitements hypotenseurs légers. Une solution naturelle qui intrigue de plus en plus les chercheurs et les professionnels de santé.L'hypertension artérielle touche plus d'un milliard de personnes dans le monde et augmente considérablement les risques de maladies cardiovasculaires. Le traitement repose généralement sur des médicaments appelés hypotenseurs, mais certains patients cherchent des alternatives naturelles ou complémentaires. C'est là que l'hibiscus, et plus précisément l'Hibiscus sabdariffa, entre en jeu.En 2008, une étude rigoureuse menée par le Tufts University Medical Center à Boston a comparé l'effet de l'infusion d'hibiscus à celui d'un médicament bien connu : le captopril, un inhibiteur de l'enzyme de conversion de l'angiotensine (IECA). Publiée dans la revue Journal of Nutrition, l'étude a suivi pendant six semaines un groupe de 65 adultes souffrant d'hypertension modérée. Résultat : les participants qui ont bu 3 tasses d'infusion d'hibiscus par jour ont vu leur pression artérielle systolique baisser en moyenne de 7 mmHg, un effet comparable à celui de certains traitements de première intention.Mais comment agit l'hibiscus ? Ses effets hypotenseurs seraient liés à plusieurs mécanismes : une action diurétique, une dilatation des vaisseaux sanguins, et une réduction de l'inflammation. L'hibiscus est également riche en antioxydants, notamment les anthocyanes, qui protègent les parois vasculaires.Attention toutefois : si cette plante est prometteuse, elle n'est pas adaptée à tous. Elle peut interagir avec certains médicaments, notamment les diurétiques ou les traitements pour la tension. Elle est également déconseillée chez les femmes enceintes ou allaitantes, faute d'études suffisantes. Par ailleurs, l'automédication n'est jamais recommandée : toute démarche de substitution ou d'ajout de traitement naturel doit être discutée avec un professionnel de santé.En résumé, l'hibiscus n'est pas un remède miracle, mais elle peut être un allié efficace et naturel contre l'hypertension, surtout en complément d'une bonne hygiène de vie. Une tasse d'hibiscus, ce n'est pas seulement agréable au goût : c'est peut-être aussi un pas de plus vers un cœur en meilleure santé. Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

No episódio de hoje do Check-up Semanal, o Dr. Ronaldo Gismondi, diretor médico da Afya e editor-chefe médico do Portal Afya e do Whitebook, apresenta os principais destaques do mês na área de Terapia Intensiva, com foco em evidências clínicas e diretrizes atualizadas.O que você vai ouvir neste episódio:- Vasopressina precoce no choque sépticoEstudo observacional (OVISS) mostra que iniciar vasopressina mais cedo e com menor dose de norepinefrina reduz mortalidade hospitalar e necessidade de diálise.- Traqueostomia precoce em pacientes críticosRevisão de ensaios clínicos sugere que realizar a TQT entre o 7º e 10º dia diminui a incidência de pneumonia associada à ventilação (PAV), ainda que não reduza mortalidade.- Extubação em vias aéreas difíceisEstratégias para reduzir risco de reintubação, com uso do escore REVERSE e cuff leak test para avaliação pré-extubação.- Hemorragia intracerebral (HIC): tempo é cérebroProtocolo Code-ICH propõe metas de tempo e controle rigoroso de pressão arterial, glicemia e temperatura para limitar expansão do hematoma.- Estudo OPTPRESS: alvo pressórico ideal em idosos sépticosPAM mais elevada (80–85 mmHg) aumenta mortalidade e eventos adversos em comparação com o alvo tradicional de 65–70 mmHg, mesmo em pacientes hipertensos.Aperte o play e mantenha-se atualizado com as principais evidências que impactam a prática em terapia intensiva!#TerapiaIntensiva #CheckupSemanal #ChoqueSéptico #Vasopressina #Traqueostomia #HemorragiaIntracraniana #UTI #PortalAfya #AtualizaçãoMédica

Welcome back to our weekend Cabral HouseCall shows! This is where we answer our community's wellness, weight loss, and anti-aging questions to help people get back on track! Check out today's questions:    Trish: Hi Dr. Cabral - I'm a 55-year-old female working on lowering overall inflammation in my body. My CRP levels are (4.1), ApoB (118 nmol/L and Lipoprotein (A) (281 nmol/L) as you can see are high. Total Cholesterol 221 and Triglycerides are 70. I have a lot of stiffness with joint discomfort. I started taking 2 Proteolytic Enzymes upon waking. Then your DNS, D3/k2, Cell Boost, Inflamma Soothe, Collagen with GLP Tone System and some of your other products (eye and hair). I follow your Med diet. My pain and stiffness have improved ALOT in a matter of days. I'm going to retest my CRP and chol levels in 4 months. My question is how long can I take Proteolytic Enzymes and in your opinion am I taking the proper protocol for these issues? I'm retesting in 4 mos. Thank you in advance          Sheena: Hi Dr Cabral! Hope you and all of your health family are well. I'm a surgical Processor and on my feet all day. I've tried all kinds of compression socks but by the end of the day, after taking it off, my leg are soo itchy! I scratch it sometimes so bad it starts to bleed. I'm only wearing the average 15-20 mmHG so its not too tight. I'm curious if you have a recommendation for compression socks that wont causes itching but is effective? Thanks in advance for answering!      Christina: Stephen, I have listened on one of your podcasts about Rheumatoid Arthritis and detoxing. My mother is in her early 70s and her fingers are twisting. I am 48 and recently the base of my thumbs have started bothering me. My question is, what detox protocol should my mother start with to prevent further twisting of her fingers and what detox protocol should I do to prevent this from happening to me? I would love to do the heavy metals and organic acid tests, but unfortunately I live in NY. Would my functional medicine doctor be able to order them for me? I have had HELLP, HUS, DIC, Guillian Barre, and Pulminary Edema in my pregnancy at 21. My son was delivered with no issues! At this time, we learned that I have ITTP. I have had IBS issues. Thank you, Christina                      Ryan: Hi dr cabral, Im a 29 year old male who has addisons disease, chronic post nasal drip, food intolerance's and teeth grinding a stool test confirmed klebsiella pneumonie overgrowth and blastocystis hominis as well as some yeast and fungus with no Bifidobacteria and Lactobacillus detected, I recently started the cbo protocol with citricidal drops im 7 days in untill i came across one of your videos where you mentioned you should go for the parasite first should i stop the cbo protocol and start the para support protocol and then continue the cbo after or just continue the cbo protocol Thank you for your time wishing you all the best ryan.                                                                                                                                     Kay: Hi Dr. Cabral, I I love your podcasts and look forward to them every week. Anyway, I was wondering if you could please explain how a traumatic event could spur the onset of a "dis-ease" such as asthma. My daughter's asthma began shortly after her father and I were separated and he moved out of state. According to her pediatrician at the time, she was "more prone to having asthma because she also had eczema." This was 2 decades ago, and now she's 31 and we know more about autoimmune issues. Although she continues to carry an inhaler with her, she hardly needs to use it anymore. What would you recommend for a more root cause approach to someone with her condition? Thank you.                                  Thank you for tuning into today's Cabral HouseCall and be sure to check back tomorrow where we answer more of our community's questions!    - - - Show Notes and Resources: StephenCabral.com/3466 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!  

Kelly is referred to physical therapy six days after coronary artery bypass graft (CABG) surgery. She reports mild fatigue but denies chest pain or shortness of breath. Her resting heart rate is 85 bpm, and her blood pressure is 125/80 mmHg. The therapist plans to begin light aerobic exercise as part of her cardiac rehabilitation. Which of the following is the MOST appropriate guideline to follow during this session?A) Monitor for a target heart rate of 70–80% of her age-predicted maximumB) Avoid upper extremity exercises to minimize sternal stressC) Limit aerobic exercise to a maximum of 1–2 METs during this phaseD) Emphasize light aerobic exercise with an intensity below 13 on the Borg RPE scaleTEXT OUR TEAM:(727) 732-4573

What's the ideal blood pressure target for older adults with hypertension? Should we aim for a systolic BP of 120 mmHg in all older adults, as suggested by the SPRINT trial? Or should we be more flexible—especially for those who are frail or among the oldest old? This week on the GeriPal Podcast, we explore the nuances of managing blood pressure in older adults with our guests Dr. Mark Supiano, Dr. Mitra Jamshidian, and Dr. Simon Ascher.  Now, some of our astute GeriPal listeners may say, “wait, didn't you already talk about this with Mark Supiano in a 2017 podcast titled How Low Should We Go with Blood Pressure in Older Adults?”  Yes, we sure did, but we decided to revisit this topic as Mitra Jamshidian and Simon Ascher published a new JAGS research study focused on developing a framework to individualize the net benefit of intensive blood pressure control based on the results of the SPRINT trial.  Their key finding: most community-dwelling older adults in the SPRINT trial experienced greater benefits than harms from more aggressive blood pressure targets—even those who were older, frail, or on multiple medications. Join us for an in-depth discussion on balancing risks, benefits, and patient preferences in hypertension management for older adults. Plus, we might just sneak in a little Frank Sinatra for good measure.

Bailey presents with a history of osteoarthritis and hypertension and is referred to physical therapy for knee pain management. She reports taking over-the-counter medication daily for pain relief. During the session, she mentions experiencing mild stomach discomfort and occasional dizziness. Her blood pressure is 138/86 mmHg. Which medication is MOST likely contributing to the patient's symptoms?A) AcetaminophenB) IbuprofenC) Calcium-channel blockerD) Glucosamine supplementDOWNLOAD THIS EPISODE'S CHEATSHEET:www.nptecheatsheet.com/common-med

Pouria presents with secondary lymphedema following breast cancer treatment. The patient reports heaviness in the arm and mild discomfort but denies significant pain. The affected arm shows a circumference 3 cm greater than the contralateral arm. She has no open wounds or signs of infection. Which compression and therapy strategy is MOST appropriate to manage this patient's lymphedema?A) High-stretch bandages to provide consistent pressure during rest and activityB) Intermittent pneumatic compression at 60 mmHg pressure, followed by elastic sleeve applicationC) Short-stretch bandages with manual lymphatic drainage techniquesD) Compression garments with 40-50 mmHg pressure for daily useTEXT OUR TEAM: (727) 732-4573

Today's Case A 44-year-old female presents to the emergency department with acute onset epigastric pain for the past 2 days, constant, with radiation to the back. Her eyes and skin “turned yellow” 1 day ago. She denies any fevers. The patient drinks one or two beers per week, does not smoke, denies nonsteroidal antiinflammatory drug (NSAID), use and is not on glucocorticoids. She denies any heartburn or acid reflux symptoms. She had right upper quadrant (RUQ ) abdominal pain that was colicky and worsened with food intake 1 week before, which resolved spontaneously after 1 day and she therefore did not seek medical attention. Her blood pressure is 118/55 mmHg, pulse rate is 105/min, respiration rate is 20/min, oxygen saturation is 97% on room air, and body mass index is 38. Her skin is noted to be jaundiced and scleral icterus is present. Murphy's sign is negative. Today's Reader Jared Fehlman is an Internal Medicine Resident at Huntington Health Hospital in Pasadena, California. About Dr. Raj Dr Raj is a quadruple board certified physician and associate professor at the University of Southern California. He was a co-host on the TNT series Chasing the Cure with Ann Curry, a regular on the TV Show The Doctors for the past 7 seasons and has a weekly medical segment on ABC news Los Angeles. More from Dr. Raj The Dr. Raj Podcast Dr. Raj on Twitter Dr. Raj on Instagram Want more board review content? USMLE Step 1 Ad-Free Bundle Crush Step 1 Step 2 Secrets Beyond the Pearls The Dr. Raj Podcast Beyond the Pearls Premium USMLE Step 3 Review MedPrepTGo Step 1 Questions MedPrepTGo Step 2 Questions Learn more about your ad choices. Visit megaphone.fm/adchoices

The Lancet Volume 353, Issue 9146 p9-13 January 02, 1999Background: Accumulating data at the time suggested functional benefits of antagonism of beta-adrenoreceptors in patients with heart failure. Multiple specific beta-blockers were being tested in trials. The CIBIS 1 trial found a trend towards 20% lower mortality in the bisoprolol (a highly cardio-selective beta-blocker) group and 30% fewer admissions to hospital for worsening heart failure. The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II) trial was designed to test this evidence further.Patients Eligible patients had New York Heart Association Class III-IV symptoms with LVEF ≤ 35% and were stable on diuretics and ACE-inhibitors. Exclusion criteria included recent MI or coronary intervention, AV block or resting heart rate less 60 bpm and systolic BP < 100 mmHg. Patients already on beta-blockers or with planned therapy with beta-blockers were also not enrolled.Cardiology Trial's remains independent, free of industry ads, due to reader generosity. Please consider becoming a free or paid subscriber.Baseline Characteristics The mean age of patients was 61 years, 81% male, and 83% Class III. The mean LVEF was 28%. About half the patients had ischemic heart disease, 12% primary dilated cardiomyopathy and nearly 40% had a mixture of valvular heart disease, hypertensive heart disease or unproven ischemic disease.The mean SBP on enrollment was 130 mmHg and resting HR was 80 bpm. The mean duration of heart failure before enrollment was 3.5 years. About 20% had AF at baseline. Nearly all patients were on ACE-I and half were on digoxin.Trial Procedures There was no run-in period. CIBIS II was double blinded. Slightly more than 2,600 patients were randomized 1:1 to bisoprolol or placebo in 274 hospitals across 18 countries.Patients in the bisoprolol group were started at 1.25 mg daily and titrated up weekly to as high as 10 mg daily. The goal was to attempt the highest tolerated dose. Patients were seen every 3 months.Endpoints The primary endpoint was all-cause mortality. Secondary endpoints included all-cause hospital admissions, cardiovascular mortality, combined CV death and CV hospital admissions, and premature treatment withdrawals.The authors estimated a 11.2% mortality in the placebo group and powered the trial to find a 25% reduction in death in the bisoprolol arm over 2 years.Results The trial was sopped early (mean follow-up 1.3 years) after the planned second interim analysis for benefit. The primary outcome of all-cause death occurred in 11.8% in the bisoprolol group vs 17.3% in the placebo arm (HR 0.66 (95% CI 0.54-0.81, p < 0.0001)).Bisoprolol reduced sudden death (3.6% vs 6.3%), all-cause hospitalization (33% vs 39%), CV death (9% vs 12%). Permanent treatment withdrawal occurred in 15% of both arms.The subgroup analysis showed no substantial treatment heterogeneity. The most common dose was 10 mg daily reached in 43% of patients.Conclusion The 34% reduction in death was clinically meaningful and statistically robust. Our confidence in such a large effect size stems from a) previous data on beta-blockers, which found similar effects, b) the 42% reduction in sudden death in the bisoprolol arm and c) the large reductions in all-cause hospitalization. In addition, the trial conduct appeared strong with almost no lost-to-follow up. The lack of run-in period strengthens the external validity of CIBIS II.The same caveats seen in the US carvedilol trial also apply to CIBIS II, namely that patients were ambulatory, outpatients, mostly with Class III symptoms. Patients enrolled in the trial had a mean SBP of 130 mmHg and a resting heart rate of 80. Nearly all patients were tolerating ACE-I and half were taking digoxin. In addition, patients were started on low-dose and gradually titrated higher. The majority of patients were on higher than 5 mg daily.The authors warned against applying these results to non-ambulatory patients with Class IV symptoms, especially if there was recent instability. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

14th ACC 2025: SBP < 130 mmHg Linked to Reduced CV Mortality in Adults +80 Y

La hipertensión arterial es una enfermedad silenciosa que puede provocar infartos, accidentes cerebrovasculares y daño renal si no se trata a tiempo. Es importante acudir al cardiólogo si tus cifras superan 140/90 mmHg, tienes antecedentes familiares, diabetes, obesidad, o si presentas síntomas como mareos, palpitaciones o dolores de cabeza frecuentes. Un diagnóstico y tratamiento temprano son clave para proteger tu salud cardiovascular y evitar complicaciones graves. Cuidar tu corazón es invertir en tu salud a largo plazo.El Dr. David Arturo Castán Flores invita a escuchar el #podcast para conocer más del tema. ¡No te pierdas sus recomendaciones! ¡Disfruta del episodio 265 y continúa escuchando cada uno de nuestros #PodcastsMédicos  preparados especialmente para ti!➡️ ENLACES DE INTERÉSOtros episodios de Actitud Saludable | Hipertensión arterial

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

N Engl J Med 1996;334:1349-1355Background Before 1990, the prevailing idea held that the negative inotropy of beta-blockers would harm patients with impaired systolic function. Yet part of the progression of systolic heart failure involved over stimulation of the sympathetic nervous system. Norepinephrine can exert adverse effects on the circulation, both directly and indirectly. Smaller trials of beta-blockers in systolic heart failure found trends for benefit with beta-blockers, however, a mortality benefit had not yet been proven. The U.S. Carvedilol Heart Failure Study aimed to study mortality in patients with heart failure with a reduced ejection fraction.Cardiology Trial's Substack remains free of industry ads because of your support. Thank you. Please consider becoming a free or paid subscriber.Patients The study enrolled 1094 patients with chronic heart failure symptoms for at least 3 months, LVEF ≤ 0.35%, at least 2 months of treatment with diuretics and an angiotensin-converting enzyme (ACE) inhibitor (if tolerated). Treatment with digoxin, hydralazine, or nitrates was permitted but not required.Exclusion criteria were extensive and important to understand. These included any recent major cardiac events or surgery within the previous 3 months, uncorrected valvular disease, active myocarditis, sustained VT or higher degrees of AV block not controlled by pacing, systolic blood pressure of more than 160 or less than 85 mm Hg or diastolic blood pressure of more than 100 mm Hg, clinically significant kidney or liver disease or use of calcium-channel blockers, adrenergic agonists/antagonists, or class IC/III antiarrhythmic agents. Patients receiving β-adrenergic agonists or antagonists (presumably for another indication) were not enrolled.Baseline Characteristics The results of this and other beta-blocker trials in heart failure will be clear. One of the most important points for translating this evidence to patients will be the baseline characteristics. It is vital to understand who these patients were.The mean age was 58 years and approximately 76% were male. Most patients had mild to moderate heart failure, with 53% in NYHA Class II, 44% in Class III, and only 3% in Class IV. The etiology of heart failure was nearly evenly split between coronary artery disease (47%) and nonischemic cardiomyopathy (53%). Patients had significantly impaired cardiac function with a mean LVEF of 0.23. The mean six-minute walk distance ranged from 386 to 390 meters. Hemodynamic parameters were relatively stable, with mean systolic blood pressure of 116 mmHg, and mean heart rate of 83-84 beats per minute. Most patients were receiving standard heart failure therapy at baseline, including digitalis (90-91%), loop diuretics (95%), and ACE inhibitors (95%), while approximately one-third (32%) were on direct-acting vasodilators.Trial Procedures Patients were assessed for eligibility during a 3-week screening period during which exercise capacity was assessed with a 6-minute walk test. Notable was that these were outpatients able to complete a 6-minute walk test. Enrollment was stratified to one of four treatment protocols on the basis of the patients' performance on the exercise test: patients able to walk between 426 and 550 m when tested were assigned to the mild-heart-failure protocol; those able to walk between 150 and 425 m were assigned either to the moderate-heart-failure protocol or to a dose-ranging protocol, depending on the location of the study center; and those able to walk only less than 150 m were assigned to the severe-heart-failure protocol.After this base-line testing, all patients received 6.25mg of carvedilol twice daily for two weeks in an open-label run-in period. Those who tolerated this initial dose were then randomized to receive either placebo (n=398) or carvedilol (n=696) on a double-blind basis, in addition to their usual medications.The allocation ratio (carvedilol:placebo) was 2:1 in the mild and severe heart failure protocols and 1:1 in the moderate heart failure protocol. The dose was gradually increased to target levels of 25-50mg twice daily over 2-10 weeks, followed by maintenance therapy for an additional 6 months (12 months for mild heart failure).Endpoints At the time of trial planning, the original intent was safety. That is, to show that carvedilol did not increase mortality. The original intent was to enroll 1100 patients. As smaller trials on beta-blockers were published, the statistical plan included the possibility of beta-blocker benefit. The trialists therefore planned two sided statistical analysis.Cumulative survival curves were constructed as time-to-first-event plots by Kaplan–Meier survivorship methods and differences between the curves were tested for significance by the log-rank statistic with use of a Cox proportional-hazards regression model (which included the protocol as a covariate).Results Median follow-up was only 6.5 months due to early termination for benefit. The patients mean total daily dose of carvedilol was 45±27 mg. Overall mortality was 7.8% in the placebo group vs. 3.2% in carvedilol group. The relative risk reduction from carvedilol vs placebo was 65% (95% CI, 39-80%; p

N Engl J Med 1987; 314:1429-35Background Prior to the publication of this study, digoxin and diuretics were the mainstay of chronic heart failure management. No therapy had yet been shown to reduce mortality or improve heart failure outcomes in patients with severe disease. The results of the V-HEFT trial had been published in the prior year, which demonstrated that the vasodilator combination of hydralazine and isosorbide reduced death in patients with chronic, stable heart failure. CONSENSUS was the first study to test whether vasodilator therapy in general, and angiotensin converting enzyme inhibitors in particular could modify heart failure disease trajectory for those with severe disease when used as part of chronic disease management. The CONSENSUS trial was designed to test the hypothesis that Enalapril compared to placebo reduced mortality in patients with severe (NYHA IV) congestive heart failure.Patients Men and women with severe (NYHA IV) congestive heart failure and cardiomegaly based on heart size >600 ml/m2 in men or >550 ml/m2 in women were recruited from 35 centers in Finland, Norway and Sweden. Measurement of LV function was not required. Patients were excluded if they had 1) acute pulmonary edema, 2) hemodynamically important aortic or mitral valve stenosis, 3) MI within the previous 2 months, 4) unstable angina, 5) planned cardiac surgery, 6) right heart failure due to pulmonary disease, or 7) serum creatinine >3.4 mg/dL.It is not specified whether patients could be recruited from the inpatient or outpatient setting or both but prior to randomization, a 14-day period was allowed to stabilize patients on digoxin and diuretics. If during this period, their condition improved to NYHA class III or less they were not randomized.Baseline characteristics The majority of participants were male (70%) and their average age was 70. The average heart rate and blood pressure were 80 bpm and 120/75 mmHg and the average serum creatinine was about 1.5 mg/dL. Coronary artery disease was present in over 70% of participants and nearly 50% had suffered a previous heart attack. Hypertension and diabetes were present in over 20% and atrial fibrillation in 50%. The use of medications at baseline was evenly distributed between groups with nearly all patients being on digoxin and furosemide. About 50% of participants were also taking spironolactone as well as other vasodilator drugs. About 50% of patients had heart failure for more than 4 years.Procedures Treatment with enalapril or an identical placebo was initially started in the hospital with a dose of 5 mg twice a day. After 1 week it was increased to 10 mg twice a day if the patient did not have symptoms of hypotension or other side effects. According to the clinical response, a further increase in dosage could occur up to a maximum dose of 20 mg twice a day.Patients were evaluated after 1, 2, 3, 6, and 16 weeks, 6, 9, and 12 months and at the end of the study. In patients with worsening symptoms, additional vasodilator therapy with isosorbide dinitrate, hydralazine, or prazosin, in that sequence was recommended.Early in the trial the occurrence of symptomatic hypotension led to revision of the protocol after 67 patients had been randomized. No patient's treatment was unblinded but in patients with 1) serum sodium

N Engl J Med 1986; 314:1547-52Background Into the mid-1980's, digoxin and diuretics were the mainstay of chronic disease management for congestive heart failure. Vasodilator agents were also commonly used based on limited data of their favorable hemodynamic effects. No sufficiently powered trials in this space had been performed to assess whether administration of vasodilators or any other agents improved long-term morbidity or mortality for heart failure patients. The V-HEFT trial was undertaken to test the hypotheses that 2 widely used vasodilator regimens (prazosin or a combination of hydralazine and isosorbide dinitrate) were superior for reducing death versus placebo. The trial was sponsored by the Veterans Administration and only enrolled men.Patients Men between the ages of 18 and 75 were recruited from 11 participating Veterans Administration hospitals and had to have chronic congestive heart failure based on either evidence of cardiac dilatation or left ventricular dysfunction (EF 0.7 ng/mL and euvolemic volume status. Clinical evaluations and exercise-tolerance tests on 2 consecutive visits, two weeks apart, had to reveal clinical and exercise stability before randomization could occur. Following randomization, patients continued to receive the optimal dose of digoxin and diuretic along with 1 of 3 study regimens. The placebo group was given placebo tablets and placebo capsules and instructed to take them 4 times a day. The prazosin group took 2.5 mg prazosin capsules and placebo tablets 4 times a day. The hydralazine-isosorbide dinitrate group took 37.5 mg hydralazine capsules and 20 mg isosorbide dinitrate tablets 4 times a day.In all groups, therapy began with 1 capsule and 1 tablet to be taken 4 times a day. In the absence of side effects, this was increased to 2 capsules and 2 tablets 4 times a day for a total of 20 mg of prazosin or 300-160 mg of hydralazine-isosorbide dinitrate. If drug-related side effects occurred, the dose could be reduced to half a tablet 4 times per day or to one capsule 2 times per day. If the dose was reduced, an attempt was made later to reinstitute the full dose.In order to limit dropouts, rigorous criteria were established for “treatment failures.” Physicians were advised to hospitalize patients with worsening symptoms, and, if appropriate, to use temporary intravenous vasodilator or inotropic interventions for stabilization. Physicians were encouraged to resume study medications upon discharge. At least 2 such hospitalizations were required, along with objective evidence of deterioration, before the study medications were discontinued and replaced with known therapy.Endpoints The primary endpoint was all-cause mortality.Results 642 patients were enrolled (273 in placebo group, 183 in prazosin group and 186 in the hydralazine-isosorbide dinitrate group). Excluding discontinuations that took place within 1 month before death, 47 patients (17%) discontinued one or both types of placebos, 43 patients (23%) discontinued prazosin, and 60 patients (32%) discontinued either one or both drugs in the hydralazine-isosorbide group. Six months after randomization, the average prescribed doses were 18.6 mg per day of prazosin, 270 mg per day of hydralazine, and 136 mg per day of isosorbide dinitrate. More than 85% of the prescribed drugs were taken in each treatment group.The mean follow-up was 2.3 years (range 6 months to 5.7 years). Only 4 patients were lost to follow up (2 in placebo group, 1 in prazosin group, and 1 in hydralazine-dinitrate group). There were 120 deaths in placebo group (44%; 19 per 100 patient years), 91 in the prazosin group (50%; 22 per 100 patient years), 72 in the hydralazine-dinitrate group (39%; 17 per 100 patient years). A reduction in mortality over the entire follow-up period was observed in the hydralazine-nitrate group compared with placebo (p = 0.093 on the log-rank test and p = 0.046 on the generalized Wilcoxon test, which gives more weight to treatment differences occurring in the earlier part of the mortality curves and less weight to the latter part, where the numbers are smaller). The absolute difference in mortality between these groups increased during three years and then began to diminish. The absolute difference in mortality between the placebo group and hydralazine-isosorbide groups at years 1 through 4 was 7%, 9%, 11% and 4%, respectively.Prespecified subgroup analysis in CAD vs no CAD stratification showed no significant treatment effect heterogeneity for hydralazine-nitrate among those with CAD although the absolute difference in mortality between groups was numerically higher for patients with CAD.At 8 weeks and 1 year, SBP (-4.1 and -4.6 mmHg) and DBP (-3.2 and -2.7 mmHg) decreased the most in the prazosin group compared to placebo. Hydralazine-nitrate was not associated with a statistically significant nor clinically significant difference in BP with exception of DBP at 8 weeks. The EF rose significantly at 8 weeks and 1 year in the hydralazine-nitrate group (+2.9 and +4.2) compared to placebo but not in the prazosin group.Side effects were reported in 4.0% of placebo patients, 11% of prazosin patients and 19% of hydralazine-nitrate patients, respectively. The most common side effects were headache and dizziness. Headache was reported in 12% of hydralazine-nitrate patients.Conclusions This study compared the combination of hydralazine-isosorbide dinitrate or prazosin to placebo in patients with chronic congestive heart failure who were optimized on digoxin and diuretic therapy. In what appears to be a young (58 years) and highly selected population of clinically stable, male veterans with dilated cardiomyopathies and low symptom burdens, the combination of hydralazine-isosorbide reduced death by 2 per 100 patient years, increased EF by 4% at 1 year and did not significantly alter BP compared to placebo. Side effects were reported in approximately 1 out of 5 patients with the most common being headache and approximately 1 out of 3 discontinued 1 or both study drugs. Prasozin did not reduce death or increase EF but did reduce BP compared to placebo. The internal validity of the study is high with only a few minor imbalances in baseline characteristics, which do not appear clinically relevant nor to consistently favor any one group. Less than 1% of patients were lost to follow up with no significant imbalances between groups. The external validity is limited by the fact that this is a population of male veterans and the etiologic distribution of cardiomyopathy and heart failure is likely different from a general heart failure population; etiologic causes of death are also likely to be different. Furthermore, the population is highly selected and its unclear how many patients from the general heart failure population would meet study criteria.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

Story at-a-glance Breastfeeding for at least six months increases gut microbiome diversity in infants, reducing inflammation and supporting immune function, which contributes to lower blood pressure in early childhood A one-unit increase in gut microbiome diversity at one month of age correlates with a 1.86 mmHg decrease in systolic blood pressure by age 6, lowering long-term cardiovascular risk Formula-fed infants have a less diverse gut microbiome with more inflammatory bacteria, increasing the likelihood of gut imbalance, immune dysfunction, and higher blood pressure later in life Human milk oligosaccharides (HMOs) in breastmilk selectively feed beneficial bacteria, enhancing digestion, immune support, and disease protection, advantages formula cannot replicate Secretory immunoglobulin A (SIgA) in breastmilk strengthens gut lining integrity, prevents infections, and trains the immune system to differentiate between harmful and harmless substances

N Engl J Med 2017;377:2419-2432Background: A small fraction of patients with acute myocardial infarction (5-10%) have cardiogenic shock. These patients have a high baseline mortality. Early revascularization had been established as better than initial stabilization with medical therapy. Many patients with cardiogenic shock due to acute myocardial infarction (AMI) have multivessel disease. The question arises about whether to do culprit-only percutaneous coronary intervention (PCI) or more complete PCI at the time of the initial intervention.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.The Culprit Lesion Only PCI versus Multivessel PCI in Cardiogenic Shock (CULPRIT-SHOCK) trial was designed to test the hypothesis that PCI of the culprit lesion only, with the option of staged revascularization of nonculprit lesions, would result in better clinical outcomes than immediate multivessel PCI among patients who have multivessel coronary artery disease and acute myocardial infarction with cardiogenic shock.Patients: The trial enrolled 706 patients with acute myocardial infarction (ST-segment elevation or non-ST-segment elevation) complicated by cardiogenic shock who had multivessel coronary artery disease. Cardiogenic shock was defined as SBP < 90 mmHg for more than 30 minutes or requiring pressors, clinical signs of pulmonary congestion, and signs of organ hypoperfusion (altered mental status, cold/clammy skin, oliguria, or lactate > 2 mmol/L).Exclusion criteria were extensive and designed to exclude patients with extremely poor prognosis: prolonged resuscitation, no intrinsic heart action, fixed dilated pupils, an indication for urgent CABG, a mechanical cause of shock, age > 90 years, massive pulmonary embolism, or severe renal insufficiency at baseline.Baseline Characteristics: The median age was 70 years, and approximately 75% were male. About 63% of patients had three-vessel disease. More than half the patients had ST-segment elevation myocardial infarction (about 62%), and anterior ST-segment elevation MI accounted for approximately 54% of these cases. About 53% of patients required resuscitation before randomization. The median left ventricular ejection fraction was between 30-33%.Procedures: In the culprit-lesion-only PCI group, only the culprit lesion was treated during the initial procedure, with staged revascularization encouraged based on residual ischemic lesions. In the multivessel PCI group, PCI of all major coronary arteries with >70% stenosis was performed, including attempts to recanalize chronic total occlusions. Crossover from the culprit-lesion-only PCI group to the multivessel PCI group occurred in 12.5% of patients, while crossover in the opposite direction happened in 9.4% of patients. The overall dose of contrast material was significantly higher and the duration of fluoroscopy significantly longer in the multivessel PCI group. Other interventional therapeutic measures were allowed, independent of the assigned treatment strategy.Endpoints: The primary endpoint was a composite of death from any cause or severe renal failure leading to renal-replacement therapy within 30 days after randomization. Secondary endpoints included the individual components of the primary endpoint, recurrent myocardial infarction, rehospitalization for heart failure, repeat revascularization, time to hemodynamic stabilization, catecholamine therapy duration, ICU stay duration, and measurements of renal and myocardial injury. Safety end points included bleeding, which was defined as type 2, 3, or 5 on the Bleeding Academic Research Consortium (BARC) scale.Trialists estimated an event rate of the composite primary endpoint of 38% in the culprit-only group vs 50% in the complete group. Using a global type I error level of 0.05, the authors calculated that a sample of 684 patients would give the trial 80% power to rule out the null hypothesis of no difference between the two treatment groups in the event rate for the primary end point.Results: At 30 days, the composite primary endpoint occurred in 45.9% of patients in the culprit-lesion-only PCI group versus 55.4% in the multivessel PCI group (relative risk, 0.83; 95% CI, 0.71 to 0.96; P=0.01). Death occurred in 43.3% of the culprit-lesion-only PCI group versus 51.6% of the multivessel PCI group (relative risk, 0.84; 95% CI, 0.72 to 0.98; P=0.03). The rate of renal-replacement therapy was 11.6% in the culprit-lesion-only PCI group and 16.4% in the multivessel PCI group (relative risk, 0.71; 95% CI, 0.49 to 1.03; P=0.07).Rates of recurrent myocardial infarction, rehospitalization for heart failure, bleeding, and stroke did not differ significantly between groups. Subgroup analyses showed consistent results across all prespecified subgroups. The time to hemodynamic stabilization, the use of catecholamine therapy and the duration of such therapy, the duration of the ICU stay, and the use of mechanical ventilation and the duration of such therapy also did not differ significantly between the two groups.Conclusion: In patients with myocardial infarction and cardiogenic shock, culprit-only PCI was superior to multivessel PCI. Both components of the primary endpoint, death and severe renal failure were lower in the culprit-only arm. The authors and editorialists speculate why these findings contrast with trials in hemodynamically stable myocardial infarction patients, where early multivessel PCI showed benefit over culprit-only PCI.If you accept the thesis that multi-vessel PCI was superior to culprit-only PCI in stable AMI patients, the likely reason for the disparate results are that patients with cardiogenic shock differ substantially from stable patients. The sicker patients with cardiogenic shock benefit from a less-is-more approach where culprit-only PCI reduces treatment harm relative to multivessel PCI.We at CardiologyTrials, however, find the evidence for complete revascularization in stable AMI patients less than clear. The COMPLETE trial found benefit from multivessel PCI over culprit-only, but both composite endpoints were driven largely by non-fatal MI. CV death was not substantially different. The difference in MI could have been related to excluding procedure-related MI.What's more, the FULL-REVASC trial, which also compared culprit-only and multivessel PCI, failed to replicate the COMPLETE trial results. In FULL-REVASC the rates of the composite primary outcome of death, MI or unplanned revascularization were not significantly different. Sadly, FULL-REVASC was stopped early when COMPLETE results were published, which led to a possible loss of power.It's possible, likely even, that the null results of CULPRIT-SHOCK are not really that disparate from prior trials in patients with more stable AMI.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

Jamie is a 62-year-old female who is referred to outpatient cardiac rehabilitation 3 weeks after a myocardial infarction. She reports feeling fatigued with moderate exertion but denies chest pain. Her resting vitals are HR 80 bpm, BP 128/82 mmHg, and SpO₂ 98%. She completed Phase I rehabilitation without complications and is eager to begin exercising to improve her endurance. Which activity is MOST appropriate to initiate during Phase II of cardiac rehabilitation?A) Jogging on a treadmill at 70% maximum heart ratB) Cycling on a stationary bike at 3-5 METsC) Strength training at 50% of 1-rep maxD) Stretching and light walking onlyDOWNLOAD THIS EPISODES CHEATSHEET:www.nptecheatsheet.com/cardiac-rehab1

In this video on research published in JACC and presented at ACC.25, Yuan Lu, ScD, JACC: Executive Associate Editor, discusses her study on optimal blood pressure management for adults aged 80 and above. Her study found that systolic blood pressure below 130 mmHg is associated with lower cardiovascular risk, while levels above 145 mmHg increase heart-related mortality. The study supports intensive blood pressure management but emphasizes the need for personalized treatment and further research on long-term effects and potential risks.#jacc #jaccjournals #acc25

Ich und hoher Blutdruck? Kann gar nicht sein! Doch, kann es. Selbst wenn die Werte immer ganz niedrig oder sogar unangenehm niedrig waren. Denn sie steigen in der Lebensmitte an. Noch dazu ist es total von gestern, den Blutdruck erst ab 140 zu 90 mmHg so richtig zu beachten. Denn für die Gesundheit ist 120 zu 70 am besten. Diana im Gespräch mit der Kardiologin Dr. Christa Bongarth über den Einfluss der Menopause auf den Blutdruck, den enormen Nutzen von Blutdrucksenkern und warum sie sie trotzdem auch bei erhöhten Werten nicht immer verordnet.INFOS ZUR FOLGE:Dr. Christa Bongarth im Internet: https://hoehenried.de/home/abteilungen/kardiologie/... und in einem Text der Deutschen Herzstiftung über Frauen und Blutdruck: https://herzstiftung.de/ihre-herzgesundheit/gesund-bleiben/bluthochdruck/frauen-bluthochdruck (Darin steht auch ein bisschen was zur Hormonersatztherapie, das Thema machen wir in einer weiteren Folge zum weiblichen Blutdruck auf.)Hier kommt Ihr zu einem Text der Deutschen Hochdruckliga über die neuen Leitlinien vom August 2024: https://www.hochdruckliga.de/pressemitteilung/deutsche-hochdruckliga-begruesst-esc-empfehlung-zur-fruehzeitigen-medikamentoesen-intervention-bei-erhoehten-blutdruckwerten Hier geht es zum Positionspapier der Deutschen Gesellschaft für Kardiologie: https://leitlinien.dgk.org/2024/geschlechterspezifische-aspekte-kardiovaskulaerer-erkrankungenHier geht es zum Newsletter "Saisonwechsel" von der BRIGITTE: https://brigitte.guj-medien.de/newsletter-anmeldung-saisonwechselHier zum neuen meno_brigitte-Insta-Account: https://www.instagram.com/meno_brigitte/Diana auf Instagram: https://www.instagram.com/apothekerin_ihres_vertrauens/Julia auf Instagram: https://www.instagram.com/julia_jortzig/In unserer Eigenwerbung geht es um die BRIGITTE Masterclass Finanzen Premium: https://academy.brigitte.de/masterclass?utm_source=menoanmich&utm_medium=podcast&utm_campaign=mcf-premium-kh10Es gibt auch einen MENO AN MICH-Rabattcode, MENO15 (gilt für viele BRIGITTE-Angebote).WEITERE ANGEBOTE aus der BRIGITTE Redaktion:Masterclass Finanzen Basic: https://academy.brigitte.de/course/masterclass-finanzen-basic?utm_source=menoanmich&utm_medium=podcast&utm_campaign=mcf-basicKostenloses Webinar Rentenlücke berechnen: https://academy.brigitte.de/webinar-aufzeichnung-rentenluecke-berechnenETF Kurs: https://academy.brigitte.de/course/etf-kurs?utm_source=menoanmich&utm_medium=podcast&utm_campaign=etf-kurs-mOn Demand Video-Kurs "Wechseljahre: Wissen, was hiilft": https://academy.brigitte.de/course/wechseljahre?utm_source=podcast&utm_medium=meno&utm_campaign=wechseljahreDossier "Wechseljahre": https://produkte.brigitte.de/products/brigitte-dossier-wechseljahre?utm_campaign=briwebsite&utm_medium=link&utm_source=podcastmenoanmichDossier "Stoffwechsel anregen": https://produkte.brigitte.de/products/stoffwechsel-anregen?utm_source=podcast&utm_medium=menoanmich&utm_campaign=stoffwechselDossier "Gehen oder blieben?": https://produkte.brigitte.de/products/gehen-oder-bleiben?utm_source=podcast&utm_medium=menoanmich&utm_campaign=gobIhr habt Anregungen, wollt uns Eure Geschichte erzählen oder selbst bei uns zu Gast im Podcast sein? Dann schreibt uns beiden persönlich, worüber Ihr gern mehr wissen würdet, was Euch bewegt, rührt, entsetzt und Freude macht an podcast@brigitte.de. Wir freuen uns auf Euch! Und bewertet und abonniert unseren Podcast gerne auch auf Spotify, iTunes, Amazon Music oder Audio Now. Noch mehr spannende Beiträge findet Ihr zudem auf Brigitte.de sowie dem Instagram- oder Facebook-Account von BRIGITTE –schaut vorbei! +++ Weitere Infos zu unseren Werbepartnern finden Sie hier: https://linktr.ee/menoanmich ++++++Unsere allgemeinen Datenschutzrichtlinien finden Sie unter https://datenschutz.ad-alliance.de/podcast.html +++Wir verarbeiten im Zusammenhang mit dem Angebot unserer Podcasts Daten. Wenn Sie der automatischen Übermittlung der Daten widersprechen wollen, klicken Sie hier: https://datenschutz.ad-alliance.de/podcast.htmlUnsere allgemeinen Datenschutzrichtlinien finden Sie unter https://art19.com/privacy. Die Datenschutzrichtlinien für Kalifornien sind unter https://art19.com/privacy#do-not-sell-my-info abrufbar.

Teniah was admitted to the acute care hospital with community-acquired pneumonia. She reports shortness of breath and fatigue. Auscultation reveals decreased breath sounds in the right lower lobe, and SpO₂ drops from 95% to 88% with exertion. Resting vital signs: HR 92 bpm, BP 142/86 mmHg, RR 22 breaths per minute. Which finding requires the MOST immediate communication with the medical team?A) Decreased breath sounds in the right lower lobeB) Blood pressure of 142/86 mmHgC) Resting respiratory rate of 22 breaths per minuteD) Oxygen desaturation to 88% with exertionJoin the FREE Facebook Group: www.nptegroup.com

Join CardioNerds EP Council Chair Dr. Naima Maqsood and Episode Lead Dr. Jeanne De Lavallaz as they discuss the results of the ARREST-AF Trial with expert faculty Dr. Prashanthan Sanders and Dr. Mehak Dhande. The ARREST-AF trial enrolled 122 patients with a BMI of 27 kg/m2 or greater and at least one cardiovascular risk factor with either paroxysmal or persistent AF and were scheduled to undergo de novo AF ablation. They were randomized to an intensive risk factor management (RFM) program versus usual care. The RFM program addressed obesity, sleep apnea, HTN, HLD, tobacco, and alcohol abuse, whereas the usual care arm had a discussion of risk factors but without an extensive risk factor modification or follow-up program. The study population had a mean age of 60 years, a mean BMI of 33 kg/m2, and 56-60% of patients with persistent AF. A third of the study population was female. The trial showed a significant improvement in the primary endpoint of the percentage of patients free from atrial fibrillation after ablation in those receiving the intensive lifestyle RFM program. At the end of the 12.3-month follow-up period, 66% percent of patients in the RFM group were free from AF compared to 42% in the usual care group (HR 0.53, p = 0.03). The RFM group also showed significant improvement in AF symptom severity, decline in body weight, systolic blood pressure, glycemic control, and exercise capacity. On average, patients in the RFM arm lost 9 kg of weight compared to 1 kg in the control group. Similarly, systolic blood pressure decreased by 13.1 mmHg in the RFM group but increased by four mmHg in the control group. This episode was planned in collaboration with Heart Rhythm TV with mentorship from Dr. Daniel Alyesh and Dr. Mehak Dhande. CardioNerds Journal Club PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! References - The SUMMIT Trial Pathak, Rajeev K., et al. "Aggressive Risk Factor Reduction Study for Atrial Fibrillation and Implications for the Outcome of Ablation: The ARREST-AF Cohort Study." Journal of the American College of Cardiology, vol. 64, no. 21, 2014, pp. 2222–2231.

Caso real Controlar el colesterol alto sin recurrir a medicamentosHoy os traigo un caso real que creo que puede resonar con muchos de vosotros, porque se trata de una condición muy común: el colesterol alto.Anamnesis del pacienteSe trata de un paciente de 45 años, con un diagnóstico reciente de hipercolesterolemia y riesgo cardiovascular alto debido a un síndrome metabólico.Este diagnóstico incluía obesidad abdominal, hipertensión arterial y triglicéridos elevados.Cuando llegó a consulta, el paciente mostró preocupación por su colesterol alto y su riesgo cardiovascular. Quería evitar el tratamiento farmacológico, ya que prefería controlar su salud mediante cambios en su estilo de vida.Valores iniciales de colesterol y perfil lipídico:Colesterol total: 260 mg/dLLDL (colesterol malo): 180 mg/dLHDL (colesterol bueno): 35 mg/dLTriglicéridos: 220 mg/dLAdemás, tenía obesidad abdominal con un perímetro de cintura de 110 cm y presión arterial elevada (140/90 mmHg).Cambios iniciales mal enfocadosAntes de venir a consulta, el paciente ya había intentado hacer algunos cambios en su alimentación. Sin embargo, aunque bienintencionados, estos no eran efectivos. Por ejemplo:Había sustituido la leche de vaca por bebidas vegetales, pero las que estaba tomando eran azucaradas.Cambió los yogures naturales por yogures edulcorados pensando que eran más sanos.Redujo el consumo de carnes grasas, pero lo sustituyó por embutidos magros como pavo o jamón cocido.Consumía galletas "digestive" pensando que eran una buena fuente de fibra.Optaba por aceite de girasol en lugar de aceite de oliva por el precio.A pesar de estos esfuerzos, sus análisis seguían mostrando niveles altos de colesterol y triglicéridos, y no entendía por qué.Intervención en consultaTras analizar su dieta y su estilo de vida, diseñamos un plan personalizado enfocado en:Ajustes en la dieta:Reemplazar las bebidas vegetales azucaradas por opciones sin azúcar añadido o volver a la leche desnatada.Cambiar los yogures edulcorados por yogures naturales sin azúcar, añadiendo fruta fresca para endulzarlos.Sustituir los embutidos magros por fuentes de proteínas saludables, como pescado azul, huevo o legumbres.Eliminar las galletas "digestive" y optar por avena, pan integral 100% o frutas enteras como fuente de fibra.Incorporar grasas saludables, como aceite de oliva virgen extra, frutos secos y aguacate.Educación alimentaria:Le enseñamos a leer etiquetas nutricionales para identificar azúcares ocultos, grasas saturadas y elegir productos más saludables.Incorporación de actividad física:Empezó con caminatas de 30 minutos 4 días a la semana. A medida que se sintiera más cómodo, añadiría sesiones de fuerza moderada.Gestión del estrés:Introdujimos técnicas de relajación como respiración profunda y pausas activas durante su jornada laboral.Resultados tras cuatro mesesAl cabo de tres meses, el paciente mostró una mejora significativa en su perfil lipídico:Colesterol total: Reducido a 200 mg/dLLDL (colesterol malo): Reducido a 130 mg/dLHDL (colesterol bueno): Aumentado a 45 mg/dLTriglicéridos: Reducidos a 150 mg/dLAdemás, su perímetro de cintura disminuyó a 102 cm, su presión arterial bajó a 125/80 mmHg, y comenzó a sentirse con más energía y motivado para seguir cuidándose.ConclusiónEste caso nos demuestra que, aunque los cambios iniciales no siempre sean efectivos, con la guía adecuada y un plan bien estructurado, se pueden lograr grandes avances. Lo más importante es no desanimarse y buscar apoyo profesional.Recordad, pequeños pasos bien dirigidos pueden transformar vuestra salud.Conviértete en un seguidor de este podcast: https://www.spreaker.com/podcast/comiendo-con-maria-nutricion--2497272/support.

A cardiologist reveals his natural method for lowering blood pressure and treating hypertension.   Dr. Steve Lome joins Chuck Carroll on The Exam Room Podcast.   Key points discussed include:   Hypertension epidemic: The rising rates of hypertension are highlighted, with an emphasis on the fact that individuals have more control over their blood pressure than they may realize.   Blood pressure guidelines: Dr. Lome explains the American Heart Association's guidelines for normal blood pressure, which is defined as less than 120/80 mmHg, and discusses the implications of readings above this threshold.   Lifestyle vs. genetics: The conversation emphasizes that while genetics can play a role in hypertension, lifestyle choices, particularly diet, have a far more significant impact. Dr. Lome shares his personal journey of weight loss and how dietary changes can reverse hypertension.   Dietary recommendations: The discussion includes the importance of a whole food plant-based diet, the dangers of ultra-processed foods, and the high sodium content in common foods like chicken. Dr. Lome stresses the need to eliminate animal-based foods and processed foods to improve blood pressure.   Individual variability: The interview touches on the concept of individual variability in health outcomes, noting that while some may tolerate unhealthy foods, this does not mean they are beneficial for overall health.   — — SHOW LINKS — — Dr. Steve Lome YouTube: https://www.youtube.com/@DrStevenLome IG: https://www.instagram.com/stevenlome Web: https://www.PBNM.org — — EVENTS — — Dr. Bulsiewicz and Chuck in Miami Where: Dr. Barnard's Bon Voyage Bash Date: March 7, 2025 https://www.pcrm.org/events/bon-voyage-party-2025 — — — Free Athlete Nutrition E-Book https://www.pcrm.org/athlete — — BECOME AN EXAM ROOM VIP — — https://www.pcrm.org/examroomvip — — THIS IS US — — The Exam Room Podcast Instagram: https://www.instagram.com/theexamroompodcast — — — Chuck Carroll Instagram: https://www.instagram.com/ChuckCarrollWLC Facebook: http://wghtloss.cc/ChuckFacebook X: https://www.twitter.com/ChuckCarrollWLC — — — Physicians Committee Instagram: https://www.instagram.com/physicianscommittee Facebook: https://www.facebook.com/PCRM.org X: https://www.twitter.com/pcrm YouTube: https://www.youtube.com/user/PCRM Jobs: https://www.pcrm.org/careers — — SUBSCRIBE & SHARE — — 5-Star Success: Share Your Story Apple: https://apple.co/2JXBkpy​​ Spotify: https://spoti.fi/2pMLoY3 Please subscribe and give the show a 5-star rating on Apple Podcasts, Spotify, or many other podcast providers. Don't forget to share it with a friend for inspiration!

Hypertension is a silent killer; check it before it's too late. Synopsis: Every first Wednesday of the month, The Straits Times helps you make sense of health matters that affect you. Do you know if you have high blood pressure or what's also known as hypertension? According to the National Population Health Survey 2022, about one in three Singaporeans aged 18 to 74 has hypertension. This condition puts them at risk of heart disease and stroke. However, a significant proportion remains unaware because the symptoms become obvious only when the condition is severe.  Hypertension is present when a person's blood pressure is at 140/90 mmHg or higher. But a slightly lower reading doesn't reduce the risk. In August 2024, the European Society of Cardiology, an influential society among cardiologists, introduced a new high blood pressure or BP category of 120-139. This implies that even readings in this range are not 'normal' as doctors once thought. In this episode, ST senior health correspondent Joyce Teo talks to Assoc Prof Chin Chee Tang, a cardiologist from the National Heart Centre Singapore, about the new category and what to make of it. They also discuss renal denervation, a procedure that the same society said may be considered for some patients with uncontrolled, drug-resistant high blood pressure. Highlights (click/tap above): 2:19 Should I be worried about a new category of hypertension?  5:30 How do I manage my blood pressure? 11:39 Monitoring the impact of salt reduction on your blood pressure 13:32 Can high blood pressure be lowered to normal levels?  19:39 Is renal denervation the right procedure for resistant hypertension? Check out ST's new series, No health without mental health: https://str.sg/mentalhealthmatters Read Joyce Teo's stories: https://str.sg/JbxN Host: Joyce Teo (joyceteo@sph.com.sg) Produced and edited by: Amirul Karim Executive producers: Ernest Luis and Lynda Hong Follow Health Check Podcast here and get notified for new episode drops: Channel: https://str.sg/JWaN Apple Podcasts: https://str.sg/JWRX Spotify: https://str.sg/JWaQ Feedback to: podcast@sph.com.sg --- Follow more ST podcast channels: All-in-one ST Podcasts channel: https://str.sg/wvz7 ST Podcast website: http://str.sg/stpodcasts ST Podcasts YouTube: https://str.sg/4Vwsa --- Get The Straits Times' app, which has a dedicated podcast player section: The App Store: https://str.sg/icyB Google Play: https://str.sg/icyX --- #healthcheckSee omnystudio.com/listener for privacy information.

JACC Associate Editor Theresa McDonagh, MBBCH  speaks with author Akshay S. Desai, MD, FACC about this paper on pulse pressure published in JACC and presented at AHA. In a pooled analysis of 16,950 patients with chronic HFmrEF or HFpEF enrolled from 4 global randomized clinical trials, a J-shaped relationship was observed between SBP and the risk of adverse CV events, with the lowest risk occurring at SBP values between 120 and 130 mmHg. A similar pattern was seen with PP, with the lowest risk found between 50 and 60 mmHg. Both higher SBP and higher PP independently predicted adverse CV events. Notably, PP remained a strong predictor of CV risk, independent of baseline SBP.

The following question refers to Sections 7.4 and 7.5 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by the Director of the CardioNerds Internship Dr. Akiva Rosenzveig, answered first by Vanderbilt AHFT cardiology fellow Dr. Jenna Skowronski, and then by expert faculty Dr. Randall Starling.Dr. Starling is Professor of Medicine and an advanced heart failure and transplant cardiologist at the Cleveland Clinic where he was formerly the Section Head of Heart Failure, Vice Chairman of Cardiovascular Medicine, and member of the Cleveland Clinic Board of Governors. Dr. Starling is also Past President of the Heart Failure Society of America in 2018-2019. Dr. Staring was among the earliest CardioNerds faculty guests and has since been a valuable source of mentorship and inspiration. Dr. Starling's sponsorship and support was instrumental in the origins of the CardioNerds Clinical Trials Program.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. American Heart Association's Scientific Sessions 2024As heard in this episode, the American Heart Association's Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It's a special year you won't want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you're among the first 20 to sign up, you'll receive a free 1-year AHA Professional Membership! Question #38 Mrs. M is a 65-year-old woman with non-ischemic dilated cardiomyopathy (LVEF 40%) and moderate to severe mitral regurgitation (MR) presenting for outpatient follow-up. Despite improvement overall, she continues to experience dyspnea on exertion with two flights of stairs and occasional PND. She reports adherence with her medication regimen of sacubitril-valsartan 97-103mg twice daily, metoprolol succinate 200mg daily, spironolactone 25mg daily, empagliflozin 10mg daily, and furosemide 80mg daily. A transthoracic echocardiogram today shows an LVEF of 35%, an LVESD of 60 mm, severe MR with a regurgitant fraction of 60%, and an estimated right ventricular systolic pressure of 40 mmHg. Her EKG shows normal sinus rhythm at 65 bpm and a QRS complex width of 100 ms. What is the most appropriate recommendation for management of her heart failure?AContinue maximally tolerated GDMT; no other changesBRefer for cardiac resynchronization therapy (CRT)CRefer for transcatheter mitral valve intervention Answer #38 ExplanationChoice C is correct. The 2020 ACC/AHA Guidelines for the management of patients with valvular heart disease outline specific recommendations.In patients with chronic severe secondary MR related to LV systolic dysfunction (LVEF

The following question refers to Sections 2.1 and 4.2 of the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.The question is asked by CardioNerds Academy Intern Dr. Adriana Mares, answered first by CardioNerds FIT Trialist Dr. Christabel Nyange, and then by expert faculty Dr. Shelley Zieroth. Dr. Zieroth is an advanced heart failure and transplant cardiologist, Head of the Medical Heart Failure Program, the Winnipeg Regional Health Authority Cardiac Sciences Program, and an Associate Professor in the Section of Cardiology at the University of Manitoba. Dr. Zieroth is a past president of the Canadian Heart Failure Society. She has been a PI Mentor for the CardioNerds Clinical Trials Program. 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. American Heart Association's Scientific Sessions 2024As heard in this episode, the American Heart Association's Scientific Sessions 2024 is coming up November 16-18 in Chicago, Illinois at McCormick Place Convention Center. Come a day early for Pre-Sessions Symposia, Early Career content, QCOR programming and the International Symposium on November 15. It's a special year you won't want to miss for the premier event for advancements in cardiovascular science and medicine as AHA celebrates its 100th birthday. Registration is now open, secure your spot here!When registering, use code NERDS and if you're among the first 20 to sign up, you'll receive a free 1-year AHA Professional Membership! Question #36 A 50-year-old woman presents to establish care. Her medical history includes COPD, prediabetes, and hypertension. She is being treated with chlorthalidone, amlodipine, lisinopril, and a tiotropium inhaler. She denies chest pain, dyspnea on exertion, or lower extremity edema. On physical exam, blood pressure is 154/88 mmHg, heart rate is 90 beats/min, and respiration rate is 22 breaths/min with an oxygen saturation of 94% breathing ambient room air. BMI is 36 kg/m2. Jugular venous pulsations are difficult to assess due to her body habitus. Breath sounds are distant, with occasional end-expiratory wheezing. Heart sounds are distant, and extra sounds or murmurs are not detected. Extremities are warm and without peripheral edema. B-type natriuretic peptide level is 28 pg/mL (28 ng/L). A chest radiograph shows increased radiolucency of the lungs, flattened diaphragms, and a narrow heart shadow consistent with COPD. An electrocardiogram shows evidence of left ventricular hypertrophy. The echocardiogram showed normal LV and RV function with no significant valvular abnormalities. In which stage of HF would this patient be classified?AStage A: At Risk for HFBStage B: Pre-HFCStage C: Symptomatic HFDStage D: Advanced HF  Answer #36 Explanation The correct answer is A – Stage A or at risk for HF. This asymptomatic patient with no evidence of structural heart disease or positive cardiac biomarkers for stretch or injury would be classified as Stage A or “at risk” for HF. The ACC/AHA stages of HF emphasize the development and progression of disease with specific therapeutic interventions at each stage. Advanced stages and disease progression are associated with reduced survival. The stages were revised in this edition of guidelines to emphasize new terminologies of “at risk” for Stage A and “pre...

Vidcast:  https://www.instagram.com/p/DBKC_95vO1b/ Where your arm rests while taking your blood pressure could deliver inaccurate measures of both your peak or systolic pressure and your baseline or diastolic pressure.  Inaccurate pressure measurements with your arm at your side or in your lap can adversely affect blood pressure medication dosing. Reporting their work in JAMA Internal Medicine, Johns Hopkins researchers tested 133 adults comparing pressure measurement with the cuffed arm hanging down or resting in the lap with the proper positioning resting on a surface at the heart's level.  A hanging arm overestimated the systolic pressure by 6.5 mmHg and the diastolic pressure by 4.4 mmHg.  An arm in the lap yielded overestimates of about 4 mmHg for both measurements. Everyone should be measuring their blood pressures regularly at home with relatively cheap automatic pressure cuffs.  Maintaining a normal blood pressure is critical for preventing a devastating stroke and avoiding heartbreaking dementia. https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2824754 #bloodpressure #armposition #overestimates #stroke #dementia 

Hola !!En el podcast de hoy os explico todo lo relacionado con el síndrome metabólicoOs dejo un breve resumen:Para diagnosticarlo hay que cumplir 3 o mas de los siguientes puntos: - Exceso de grasa abdominal: perímetro de la cintura > 80 cm en las mujeres y 94 cm en los hombres  - Glucosa en ayunas mayor o igual a 100 mg/dL ( o en tratamiento especifico para ella)Triglicéridos mayor de 150mg/dL ( o en tratamiento especifico) Colesterol HDL < 50 mg/dL en mujeres o < 40 mg/dL en hombres - Tension arterial mayor igual a 130 mmHg de “maxima” o mayor o igual de 85 mmHg de “minima” ( o en tratamiento para la tension) Sobre uno de los componentes del síndrome metabólico: la resistencia a la insulina, se calcula con la formula siguiente:Indice HOMA DE RESISTENCIA A LA INSULINA= [Glucosa en ayunas (mg/dL) x insulina en ayunas ] / 405 Si ese valor HOMA es > 2-2,5 nos indica que tus células son resistentes a la insulina Los tips para mejorar y prevenir el síndrome metabólico: Crear masa muscular con ejercicioAumentar el consumo de fibraSuplementos que mejoren todos los componentes del síndrome metabólico.Mi suple  MetabolicMax que esta en mi web https://ivbwellness.com  contiene los compuestos claves para optimizar los componentes del sindrome metabólico. Pero si por X motivo no lo queréis, en el podcast os digo cuales buscar ☝

Contributor: Aaron Lessen, MD Educational Pearls: How does an automated blood pressure cuff work? Automated blood pressure cuffs work differently than taking a manual blood pressure. While taking a manual blood pressure, one typically listens for Korotkoff sounds (turbulent flow) while slowly deflating the cuff. An automatic blood pressure cuff only senses the pressure in the cuff itself and specifically pays attention to oscillations in the pressure caused by when the pressure of the cuff is between the systolic (heart squeezing) and diastolic (heart relaxed) pressures. These oscillations are at a maximum when the pressure in the cuff matches the mean arterial pressure (MAP) and therefore the machines are most accurate at reporting the MAP. The machines then use the MAP and other information about the oscillations to estimate the systolic and diastolic pressures, which are less accurate. What should you do if you need more accurate systolic and diastolic blood pressures? Take a manual blood pressure. Get an arterial-line (a-line), which provides continuous data for the blood pressure at the end of a catheter. What happens if the cuff is too big or too small for the patient? If the cuff is too small it will overestimate the pressure. If the cuff is too large it will underestimate the pressure. What should you do if the cuff cycles a bunch of times before reporting a blood pressure? It probably isn't very accurate so consider another method. Bonus fact! The MAP is not directly in the middle of the systolic and diastolic pressures but is weighted towards the diastolic pressure. The MAP can be calculated by adding two-thirds of the diastolic pressure to one third of the systolic pressure. For example if the BP is 120/90 the MAP is 100 mmHg. References Benmira, A., Perez-Martin, A., Schuster, I., Aichoun, I., Coudray, S., Bereksi-Reguig, F., & Dauzat, M. (2016). From Korotkoff and Marey to automatic non-invasive oscillometric blood pressure measurement: does easiness come with reliability?. Expert review of medical devices, 13(2), 179–189. https://doi.org/10.1586/17434440.2016.1128821 Liu, J., Li, Y., Li, J., Zheng, D., & Liu, C. (2022). Sources of automatic office blood pressure measurement error: a systematic review. Physiological measurement, 43(9), 10.1088/1361-6579/ac890e. https://doi.org/10.1088/1361-6579/ac890e Vilaplana J. M. (2006). Blood pressure measurement. Journal of renal care, 32(4), 210–213. https://doi.org/10.1111/j.1755-6686.2006.tb00025.x Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3  

The McCullough Report with Dr. Peter McCullough – Hypertension is diagnosed if, when it is measured on two different days, the systolic blood pressure readings on both days is ≥140 mmHg and/or the diastolic blood pressure readings on both days is ≥90 mmHg. Modifiable risk factors include unhealthy diets, physical inactivity, consumption of tobacco and alcohol, and being overweight or obese...

The McCullough Report with Dr. Peter McCullough – Hypertension is diagnosed if, when it is measured on two different days, the systolic blood pressure readings on both days is ≥140 mmHg and/or the diastolic blood pressure readings on both days is ≥90 mmHg. Modifiable risk factors include unhealthy diets, physical inactivity, consumption of tobacco and alcohol, and being overweight or obese...