Podcasts about mmhg

Live Long and Well with Dr. Bobby

Play Episode Listen Later Mar 24, 2026

We discuss the diagnosis and treatment of one of EM's paradoxes: High-Output Heart Failure. Hosts: Nicolas Gonzalez, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/HOHF.mp3 Download Leave a Comment Tags: Cardiology Show Notes Core EM Modular CME Course Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. Course Highlights: Credit: 12.5 AMA PRA Category 1 Credits™ Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics. Cost: Free for NYU Learners $250 for Non-NYU Learners Click Here to Register and Begin Module 1 1. Core Definition & Hemodynamic Profile Clinical Paradox: Congestive symptoms (pulmonary edema, JVD, peripheral edema) in the setting of a hyperdynamic, supranormal cardiac function. Hemodynamic Criteria: Cardiac Index (CI): >4.0 L/min/m2. Cardiac Output (CO): >8 L/min. Systemic Vascular Resistance (SVR): Pathologically low (vasodilated or shunted state). The “Warm” Phenotype: Unlike standard HFrEF/HFpEF (often “Cold and Wet”), HOHF presents as “Warm and Wet” due to low SVR and bounding pulses. 2. Pathophysiology: The Hemodynamic Paradox Primary Insult: Decreased SVR (either via peripheral vasodilation or arteriovenous shunting). Effective Arterial Blood Volume: Paradoxically low despite high total CO. Neurohormonal Cascade: Activation of Renin-Angiotensin-Aldosterone System (RAAS). Increased Sympathetic Nervous System tone. Increased Antidiuretic Hormone (ADH) secretion. Resultant State: Avid renal salt and water retention leading to massive plasma volume expansion. Cardiac Response: Chronic volume overload → eccentric remodeling → chamber dilation → eventual secondary myocardial failure/dilated cardiomyopathy. 3. Differential Diagnosis: Etiological “Buckets” Category A: Increased Metabolic Demand (Systemic) Hyperthyroidism/Thyrotoxicosis: Direct T3 effects: increased chronotropy/inotropy. Indirect effects: metabolic byproduct accumulation causing peripheral vasodilation. Myeloproliferative Disorders: High cell turnover and increased oxygen consumption drive compensatory CO increase. Sepsis (Hyperdynamic Phase): Cytokine-mediated global vasodilation. Note: Often transient; may transition to sepsis-induced myocardial depression. Category B: Peripheral Vascular Effects (Shunting/Vasodilation) Arteriovenous Fistulas (AVF) / Malformations (AVM): Most Common Cause: Iatrogenic AVF for Hemodialysis (ESRD population). Bypasses high-resistance capillary beds, dumping arterial blood directly into venous circulation. Chronic Liver Disease (Cirrhosis): Formation of “spider angiomata” and internal AV shunts. Impaired clearance of endogenous vasodilators (e.g., Nitric Oxide). Thiamine Deficiency (Wet Beriberi): Accumulation of pyruvate/lactate → systemic vasodilation. Histopathology: Vacuolation, myofiber hypertrophy, and interstitial edema. Chronic Lung Disease: Hypoxia/Hypercapnia-driven systemic vasodilation. Concomitant pulmonary HTN (RV remodeling) but preserved/high LV output. Others: Paget's disease of bone (extensive micro-shunting), Carcinoid syndrome, Mitochondrial diseases, Acromegaly, Erythroderma. 4. Special Focus: Hemodialysis Access-Induced HOHF Physiologic Phases of AVF Creation: Acute Phase: Immediate ↓ SVR. ↑ Stroke volume and Heart Rate (SNS-mediated). Endothelial shear stress → Nitric Oxide release → further arterial dilation. Subacute Phase (Days to 2 Weeks): RAAS-driven volume expansion. ↑ Right Atrial, Pulmonary Artery, and LV End-Diastolic Pressures (LVEDP). Natriuretic peptide surge (BNP/ANP) peaks around Day 10. Chronic Phase (Weeks to Months): Adaptive hypertrophy. Decompensation occurs when dilation exceeds contractility limits. 5. Point-of-Care Physical Exam & Maneuvers Nicoladoni-Branham Sign (Pathognomonic for Shunt-driven HOHF): Maneuver: Manually compress the AVF (or inflate cuff to >50 mmHg above SBP) for 30 seconds. Positive Result: Reflexive bradycardia or a transient rise in systemic BP. Significance: Confirms the shunt is a major contributor to the cardiac workload. Peripheral Pulse Assessment: Water Hammer Pulses: Rapid upstroke and collapse. Quincke's Pulse: Visible capillary pulsations in the nail beds. Traube's Sign: “Pistol-shot” sounds auscultated over the femoral arteries. Volume Status: Rales, S3 gallop, peripheral edema (standard HF signs). 6. Diagnostic Workup (Technical Targets) POCUS / Echocardiography: Left Ventricle: Hyperdynamic function; EF typically >60%. Left Atrium: Significant dilation (Left Atrial Volume Index >34 mL/m2; Case study noted 72 mL/m2). IVC: Plethoric with minimal respiratory variation. Doppler: High flow velocities across the AV access if applicable. Laboratory Evaluation: BNP/NT-proBNP: Often markedly elevated (e.g., >70,000 in severe cases), though mean values in literature hover around 700–800 pg/mL. Hematology: CBC to evaluate for severe anemia (trigger for HOHF if Hgb7–8 g/dL to reduce demand. Beriberi: High-dose IV Thiamine (100–500 mg). Thyrotoxicosis: Beta-blockers (Propranolol) + Antithyroid meds (PTU/Methimazole). Phase 3: Surgical/Interventional Salvage (Refractory AVF Cases) Closure of Accessory Sites: If multiple fistulas exist, close the non-dominant/unused sites. Flow Reduction (Banding): Surgical narrowing of the fistula to target flow

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#65: Can I Eat All the Salt That I Want?

Play Episode Listen Later Mar 10, 2026 30:28 Transcription Available

Send a textYou read everywhere that you “should” cut salt—especially if your blood pressure is up. But salt also makes food enjoyable. In this episode, I walk through the human evidence (not animal studies) and frame salt as a risk–benefit tradeoff: when does sodium meaningfully matter, for whom, and how can you test your sensitivity?Big questions we answerIf you have high blood pressure: does lowering salt always help?If your BP is normal but you have heart/kidney risk: does salt matter?If you're basically healthy: how worried should you be?Key takeawaysSodium is essential (nerves, muscles, fluid balance)—the issue is dose and individual response.Most sodium comes from packaged/restaurant foods (not your salt shaker).Salt restriction lowers BP, but the average effect is modest compared with typical BP meds (context matters).Salt sensitivity varies: roughly ~30% of healthy people and ~40–50% of people with hypertension may be “salt-sensitive” (with higher rates in older adults, women, and some ancestry groups).If you're salt-sensitive—especially with hypertension—being mindful of sodium is likely worth it. If you're not, the “must be low-salt for everyone” story is less clear.Practical: Do an N-of-1 salt sensitivity testMeasure home BP daily (or a few times/day) for a weekGo lower-sodium for 1–2+ weeks (at least within guidelines, possibly lower)Track BP changeAdd salt back and watch what happensOptional: repeat the low-salt phase for confirmation If BP shifts meaningfully (often ~3–5 mmHg+), you may be salt-sensitive.Food reality check (why sodium adds up fast)~10% of a 2,300 mg/day sodium “budget”: 2 slices bread, 1 Tbsp ketchup, or a pinch of salt~1/3: 1 cup canned soup, 1 slice pizza, or a Big Mac~1/2: frozen lasagna, a few deli slices, or a 6” cold-cut sub Cooking mostly from whole foods makes staying lower-sodium much easier.Studies & resources mentioned (links embedded)CDC hypertension awareness/treatment/control stats: https://www.cdc.gov/nchs/products/databriefs/db511.htmHypertension outcomes review (risk of events/death): https://pmc.ncbi.nlm.nih.gov/articles/PMC8292050/Population sodium/BP overview (JACC): https://www.jacc.org/doi/10.1016/j.jacc.2019.11.055DASH-Sodium trial (NEJM): https://www.nejm.org/doi/full/10.1056/NEJM200101043440101Sodium restriction meta-analysis (BP/outcomes): https://pmc.ncbi.nlm.nih.gov/articles/PMC12624901/Salt sensitivity overview (AHA/Hypertension): https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.123.17959Heart failure trials/meta (salt restriction): https://www.ahajournals.org/doi/10.1161/CIRCHEARTFAILURE.122.009879Salt substitute trial (NEJM): https://www.nejm.org/doi/full/10.1056/NEJMoa2105675Call to action Are you going to run your own N-of-1 salt test? If you do, I'd love to hear what you learn.Reminder: I'm an educational resource, no

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Resistant Hypertension. Target Aldosterone. Transform Care

Play Episode Listen Later Mar 7, 2026 3:35

Resistant hypertension remains one of the most stubborn challenges in cardiovascular medicine. The Bax24 phase 3 trial, published in The Lancet (2026), evaluated baxdrostat, a selective aldosterone synthase inhibitor, in patients already receiving multiple antihypertensive agents. Key findings: • −16.6 mmHg reduction in 24-hour ambulatory SBP • −14.0 mmHg placebo-corrected difference (p

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Episode 220: Post-ROSC Care

Play Episode Listen Later Mar 3, 2026

We explore how to refine and optimize care in the vital minutes following ROSC. Hosts: Jonathan Elmer, MD, MS Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Post-ROSC_care.mp3 Download Leave a Comment Show Notes Core EM Modular CME Course Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. Course Highlights: Credit: 12.5 AMA PRA Category 1 Credits™ Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics. Cost: Free for NYU Learners $250 for Non-NYU Learners Click Here to Register and Begin Module 1 I. Phase 1: Stabilization (Minutes 0–10) The “Rearrest” Window & Pathophysiology High-Risk Period: Rearrest rates reach 30% within the first minutes post-ROSC. Shock Incidence: Two-thirds of patients develop profound hypotension/shock as initial resuscitative efforts subside. Catecholamine Washout: Super-physiologic “code-dose” epinephrine (1mg IV) typically wears off within ~3 minutes post-ROSC, leading to predictable hemodynamic collapse. Secondary Injuries: Evaluate for “CPR-induced trauma” (blunt thoracic trauma, rib fractures, pneumothorax, liver/splenic lacerations). Immediate Resuscitative Actions Vascular Access: Transition rapidly from IO to reliable IV access within 1–2 minutes. Prioritize Intraosseous (IO) placement within 5 minutes if IV attempts fail; intra-arrest data suggests no significant difference in early outcomes. Vasoactive “Bridge”: Maintain a “bolus-dose” pressor at the bedside for immediate push-dose titration. Options: Phenylephrine, dilute Epinephrine, or dilute Norepinephrine (titrated to effect rather than rigid dosing). Physician-Specific Task: Arterial Line: Goal: Placement within 5 minutes of ROSC. Preferred Site: Femoral (by landmarks/blind if necessary) for speed; should be a 80 mmHg. The BOX Trial Nuance: While the BOX trial showed no difference between MAP 63 vs. 77, its cohort (Denmark) had exceptionally high survival rates (70% back to work) and short response times, which may not generalize to North American populations with lower shockable rhythm incidence. Permissive Hypertension: If the patient is “self-driving” to higher pressures, do not aggressively lower them, as this may be a physiologic demand for cerebral blood flow. Ventilation and Oxygenation PaCO2 Management: Target: High-normal to slightly hypercarbic (45–55 mmHg). Rationale: Avoid accidental hyperventilation (PaCO2

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Episode 218: Sympathetic Crashing Acute Pulmonary Edema (SCAPE)

Play Episode Listen Later Jan 17, 2026 12:45

We discuss the diagnosis and management of SCAPE in the ED. Hosts: Naz Sarpoulaki, MD, MPH Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/SCAPEv2.mp3 Download Leave a Comment Tags: Acute Pulmonary Edema, Critical Care Show Notes Core EM Modular CME Course Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. Course Highlights: Credit: 12.5 AMA PRA Category 1 Credits™ Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics. Cost: Free for NYU Learners $250 for Non-NYU Learners Click Here to Register and Begin Module 1 The Clinical Case Presentation: 60-year-old male with a history of HTN and asthma. EMS Findings: Severe respiratory distress, SpO₂ in the 60s on NRB, HR 120, BP 230/180. Exam: Diaphoretic, diffuse crackles, warm extremities, pitting edema, and significant fatigue/work of breathing. Pre-hospital meds: NRB, Duonebs, Dexamethasone, and IM Epinephrine (under the assumption of severe asthma/anaphylaxis). Differential Diagnosis for the Hypoxic/Tachypneic Patient Pulmonary: Asthma/COPD, Pneumonia, ARDS, PE, Pneumothorax, Pulmonary Edema, ILD, Anaphylaxis. Cardiac: CHF, ACS, Tamponade. Systemic: Anemia, Acidosis. Neuro: Neuromuscular weakness. What is SCAPE? Sympathetic Crashing Acute Pulmonary Edema (SCAPE) is characterized by a sudden, massive sympathetic surge leading to intense vasoconstriction and a precipitous rise in afterload. Pathophysiology: Unlike HFrEF, these patients are often euvolemic or even hypovolemic. The primary issue is fluid maldistribution (fluid shifting from the vasculature into the lungs) due to extreme afterload. Bedside Diagnosis: POCUS vs. CXR POCUS is the gold standard for rapid bedside diagnosis. Lung Ultrasound: Look for diffuse B-lines (≥3 in ≥2 bilateral zones). Cardiac: Assess LV function and check for pericardial effusion. Why not CXR? A meta-analysis shows LUS has a sensitivity of ~88% and specificity of ~90%, whereas CXR sensitivity is only ~73%. Importantly, up to 20% of patients with decompensated HF will have a normal CXR. Management Strategy 1. NIPPV (CPAP or BiPAP) Start NIPPV immediately to reduce preload/afterload and recruit alveoli. Settings: CPAP 5–8 cm H₂O or BiPAP 10/5 cm H₂O. Escalate EPAP quickly but keep pressures to avoid gastric insufflation. Evidence: NIPPV reduces mortality (NNT 17) and intubation rates (NNT 13). 2. High-Dose Nitroglycerin The goal is to drop SBP to < 140–160 mmHg within minutes. No IV Access: 3–5 SL tabs (0.4 mg each) simultaneously. IV Bolus: 500–1000 mcg over 2 minutes. IV Infusion: Start at 100–200 mcg/min; titrate up rapidly (doses > 800 mcg/min may be required). Safety: ACEP policy supports high-dose NTG as both safe and effective for hypertensive HF. Use a dedicated line/short tubing to prevent adsorption issues. 3. Refractory Hypertension If SBP remains > 160 mmHg despite NIPPV and aggressive NTG, add a second vasodilator: Clevidipine: Ultra-short-acting calcium channel blocker (titratable and rapid). Nicardipine: Effective alternative for rapid BP control. Enalaprilat: Consider if the above are unavailable. Troubleshooting & Pitfalls The “Mask Intolerant” Patient Hypoxia is the primary driver of agitation. NIPPV is the best sedative. * Pharmacology: If needed, use small doses of benzodiazepines (Midazolam 0.5–1 mg IV). AVOID Morphine: Data suggests higher rates of adverse events, invasive ventilation, and mortality. A 2022 RCT was halted early due to harm in the morphine arm (43% adverse events vs. 18% with midazolam). The Role of Diuretics In SCAPE, diuretics are not first-line. The problem is redistribution, not volume excess. Diuretics will not help in the first 15–30 minutes and may worsen kidney function in a (relatively) hypovolemic patient. Delay Diuretics until the patient is stabilized and clear systemic volume overload (edema, weight gain) is confirmed. Disposition Admission: Typically requires CCU/ICU for ongoing NIPPV and titration of vasoactive infusions. Weaning: As BP normalizes and work of breathing improves, infusions and NIPPV can be gradually tapered. Take-Home Points Recognize SCAPE: Hyperacute dyspnea + severe HTN. Trust your POCUS (B-lines) over a “clear” CXR. NIPPV Immediately: Don’t wait. It saves lives and prevents tubes. High-Dose NTG: Use boluses to “catch up” to the sympathetic surge. Don’t fear the dose. Avoid Morphine: Use small doses of benzos if the patient is struggling with the mask. Lasix Later: Prioritize afterload reduction over diuresis in the hyperacute phase. Read More

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Reversing "Incurable" Cancer with Nature's Most Powerful Molecule | Samuel Shepherd

The Longevity Formula

Play Episode Listen Later Jan 16, 2026 64:47 Transcription Available

Send us a textDr. Brandon Crawford is joined by Samuel Shepherd, a former Department of Defense biochemical engineer who used his expertise in weapons development to reverse-engineer a cure for his own "incurable" bone cancer. They deep-dive into the science of oxidative stress, the hierarchy of antioxidants, and the specific molecule that allows animals like naked mole rats and sharks to resist cancer and aging.Samuel recounts his 2003 diagnosis of polycythemia vera, where his blood pressure reached levels that "pegged" medical monitors at 300 mmHg. After years of grueling phlebotomies, Sam used a screening algorithm to find a commonality among cancer-resistant species. That common thread was Astaxanthin. However, he didn't just find a supplement; he discovered a way to modify the molecule into a glucosidic form that bypasses the body's digestive barriers to target disease at the atomic level.Key TakeawaysThe Root of All Evil: 92% of inflammatory disease deaths are driven by the hydroxyl free radical. By neutralizing this specific ROS, you address the cause of disease (the trunk) rather than just the symptoms.Molecular Saponification: By using a glucosidic "Trojan Horse" delivery, astaxanthin enters cancer cells and converts acidic free radicals into alkaline ions, dissolving the cancer cell membrane in seconds.The Antioxidant Cliff: Natural cellular protection (Glutathione, SOD) fails significantly after age 42 W or 50 M, making external supplementation essential for longevity.Beyond Brain Barriers: Unlike many antioxidants, this specialized form of astaxanthin crosses the blood-brain barrier, allowing it to neutralize neurotoxins linked to Parkinson's and Alzheimer's.ResourcesUse code CRAWFORD at checkout on Valasta.net for a discount on your order.Valasta.net (testimonials, NIH research papers, dosing information)NIH Research Database (search: "NIH + astaxanthin + [disease]")ProQuest Government Research DatabaseLife Extension (publishes astaxanthin research papers)Dr. Fred Bisci (mentioned as colleague)HSCRP (high-sensitivity C-reactive protein) testing for inflammation markersHematococcus Pluvialis (algae source of astaxanthin)Products 528 Innovations Lasers NeuroSolution Full Spectrum CBD NeuroSolution Broad Spectrum CBD NeuroSolution Stimpod STEMREGEN® Learn MoreFor more information, resources, and podcast episodes, visit https://tinyurl.com/3ppwdfpm

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Glaucoma risk, dry eye breakthroughs & Creatine for weight loss

Ask The Doctor Podcast

Play Episode Listen Later Jan 10, 2026 49:58

Today’s episode of Ask the Dr was hosted by Dr. Michael Lange and Dr. Susan Summerton, delivering an information-packed program focused on eye health, wellness, longevity, and disease prevention.

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My blood pressure is 120/80 mmHg

Tyus Mcafee podcast

Play Episode Listen Later Jan 5, 2026 19:14 Transcription Available

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Episode 202 - Real-Time Veterinary Anesthesia Monitoring for Better Outcomes

The Vet Dental Show

Play Episode Listen Later Dec 10, 2025 21:36

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

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Episode 986: Lateral Canthotomy in Emergency Settings

Emergency Medical Minute

Play Episode Listen Later Dec 8, 2025 4:38

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/

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REBEL Core Cast 146.0–Ventilators Part 4: Setting up the Ventilator

REBEL Cast

Play Episode Listen Later Dec 8, 2025 19:06

🧭 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.

Vaccine Science: Anaphylaxis Prevention, Adjuvant Controversies, Fentanyl Immunization, Exercise Fighting Cancer, and Sunlight's Hidden Benefits

Ask Doctor Dawn

Play Episode Listen Later Dec 6, 2025 50:01

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)

Rio Bravo qWeek

Play Episode Listen Later Nov 28, 2025 40:19

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/.

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Play Episode Listen Later Oct 11, 2025 5:12

Standing More Often Helps Protect Heart Health

Dr. Joseph Mercola - Take Control of Your Health

Play Episode Listen Later Oct 10, 2025 7:28

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

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Índice de Perfusión Periférica para Guiar la Resucitación del Paciente en Shock Séptico: Innovación y Formación en Emergencias Críticas

ECCPodcast: Emergencias y Cuidado Crítico

Play Episode Listen Later Oct 8, 2025 17:42

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

Episode 214: Acute Pulmonary Embolism

ECCPodcast: Emergencias y Cuidado Crítico

Play Episode Listen Later Oct 2, 2025

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),

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SCAPE - Sympathetic Crashing Acute Pulmonary Edema

Play Episode Listen Later Sep 30, 2025 19:33

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

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193 - Elevate Your Guideline Knowledge, Not Your BP: The New 2025 Hypertension Guidelines

HelixTalk - Rosalind Franklin University's College of Pharmacy Podcast

Play Episode Listen Later Sep 19, 2025 35:07

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.

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Quelle plante est aussi efficace que les hypotenseurs ?

Choses à Savoir SANTE

Play Episode Listen Later Sep 11, 2025 2:09

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.

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Play Episode Listen Later Aug 29, 2025 4:44

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Renal Nerves

PEBMED - Notícias médicas

Play Episode Listen Later Aug 20, 2025 6:44

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Check-up Semanal #Terapia Intensiva: vasopressina precoce, traqueostomia, hemorragia intracraniana e mais!

Play Episode Listen Later Aug 13, 2025 12:20

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

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3466: Proteolytic Enzymes & Inflammation, Itchy Compression Socks, Rheumatoid Arthritis & Twisting Fingers, Para Support Protocol or CBO Protocol, Trauma & Dis-ease

The Cabral Concept

Play Episode Listen Later Aug 2, 2025 20:22

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!

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Hypertension: Treat Early, Treat All, Save More

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Play Episode Listen Later Jul 27, 2025 4:37

CABG / Post-Op PT Guidelines

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Play Episode Listen Later Jul 23, 2025 12:18

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

Individualizing Blood Pressure Goals in Older Adults: A Podcast with Mitra Jamshidian, Simon Ascher and Mark Supiano

GeriPal - A Geriatrics and Palliative Care Podcast

Play Episode Listen Later Jul 10, 2025 46:41

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.

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Play Episode Listen Later Jul 5, 2025 3:45

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Pharmacology for PTs

Play Episode Listen Later Jul 2, 2025 8:39

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

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Lymphedema Management - Compression & Therapy

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Play Episode Listen Later Jun 25, 2025 11:39

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

Review of the CIBIS II Trial

Cardiology Trials

Play Episode Listen Later Jun 17, 2025 5:17

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

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Review of the MERIT-HF trial

Cardiology Trials

Play Episode Listen Later May 22, 2025 10:36

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

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Review of the U.S. Carvedilol Heart Failure Study

Cardiology Trials

Play Episode Listen Later May 14, 2025 8:45

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

study patients treatments substack av smaller notable enrollment cox vt exclusion heart failure hg cumulative new england journal of medicine norepinephrine mmhg hemodynamics class iii class iv kaplan meier lvef results median

Why Breastfeeding Matters for Your Child's Future - AI Podcast

Dr. Joseph Mercola - Take Control of Your Health

Play Episode Listen Later Apr 22, 2025 10:51

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

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Cardiac Rehab Phases

Play Episode Listen Later Apr 2, 2025 9:45

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

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