PulmPEEPs

Today we’re kicking off another segment in our Guidelines Series, and doing a deep dive into the 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Over a series of episodes we’ll talk about the most recent updates to definitions around pulmonary hypertension, recognizing and diagnosing Group 1 – 5 pulmonary hypertension, risk stratification, and treatments. In this first episode, we will review the most recent definitions, including changes to the definitions that were new in 2022. We’ll then talk about recognizing and diagnosing pulmonary hypertension with tips and insights along the way.   Meet Our Co-Hosts Rupali Sood  grew up in Las Vegas, Nevada and made her way over to Baltimore for medical school at Johns Hopkins. She then completed her internal medicine residency training at Massachusetts General Hospital before returning back to Johns Hopkins, where she is currently a pulmonary and critical care medicine fellow alongside Tom. Rupali’s interests include interstitial lung disease, particularly as related to oncologic drugs. And she also loves bedside medical education. Tom Di Vitantonio  is originally from New Jersey and attended medical school at Rutgers, New Jersey Medical School in Newark. He then completed his internal medicine residency at Weill Cornell, where he also served as a chief resident. He currently is a pulmonary and critical care medicine fellow at Johns Hopkins, and he’s passionate about caring for critically ill patients, how we approach the management of pulmonary embolism, and also about medical education of trainees to help them be more confident and patient centered in the care they have going forward. Infographic Key Learning Points Why to have a high index of suspicion for pulmonary hypertension (PH) PH often presents subtly with slowly progressive dyspnea on exertion, fatigue, lightheadedness, exertional chest pain, or syncope. There’s often a delay of 1–2+ years from symptom onset to diagnosis, which is associated with worse mortality. Early recognition and treatment, especially for pulmonary arterial hypertension (PAH, WHO group 1), can significantly change outcomes.   When to suspect PH Think PH when: Dyspnea is out of proportion to: CT parenchymal findings (relatively normal lungs) Spirometry (normal FEV₁/FVC, volumes) There are subtle but progressive symptoms over months: Reduced exercise tolerance No obvious alternative explanation (e.g., no overt HF, CAD, big ILD, etc.) Physical exam may show (often late): Elevated JVP, V waves (TR) Peripheral edema, hepatomegaly, ascites Loud P2, RV heave In the case: a woman with systemic sclerosis + slowly progressive exertional dyspnea + relatively normal CT parenchyma and spirometry → high suspicion.   WHO classification: 5 PH groups (big picture + why it matters) Used for pathophysiology, prognosis, and treatment choices: Group 1 – PAH Idiopathic, heritable (e.g., BMPR2), drug-induced (e.g., dasatinib) Connective tissue disease (esp. systemic sclerosis) Portal hypertension (portopulmonary HTN) HIV, HHT, congenital heart disease/shunts Rare: PVOD, PCH Group 2 – PH due to left heart disease HFrEF, HFpEF, valvular disease Most common cause worldwide. Group 3 – PH due to lung disease/hypoxia COPD, ILD, combined pulmonary fibrosis–emphysema OSA/obesity hypoventilation, chronic hypoxemia Group 4 – CTEPH Chronic thromboembolic pulmonary hypertension Group 5 – Multifactorial/unclear Sarcoidosis, myeloproliferative disorders, CKD, sickle cell, etc. Patients can span multiple groups (e.g., systemic sclerosis: group 1 and/or group 3; sickle cell: many mechanisms).   Initial workup & refining pre-test probability Once you suspect PH, you’re trying to answer: Does this patient likely have PH? If yes, what group(s) are most likely? Core non-invasive tests: NT-proBNP (preferred over BNP) Surrogate of RV strain and prognosis. Normal value makes significant RV failure less likely. Oxygenation & exercise Resting SpO₂ plus ambulatory sats; consider 6-minute walk test. Exertional desaturation is common and clinically meaningful. CXR & ECG Low yield but may show RV enlargement, right axis deviation, etc. Pulmonary function tests Full set: spirometry, volumes, DLCO. Clue: isolated or disproportionately low DLCO with relatively preserved FVC suggests pulmonary vascular disease. Imaging High-res CT chest – parenchymal disease (ILD, emphysema). V/Q scan – best screening test for CTEPH; better than CT angiography for chronic disease. Sleep testing / overnight oximetry When OSA/nocturnal hypoxemia suspected.   Echo: estimating PH probability (not diagnosis) TTE is the key screening tool but does not diagnose PH. Main elements: Peak tricuspid regurgitant (TR) velocity Used to estimate pulmonary artery systolic pressure (PASP). Categories: Low probability: TR velocity < 2.8 m/s, no other PH signs. Intermediate: 2.9–3.4 m/s ± other PH signs. High: > 3.4 m/s. The presence and severity of TR ≠ TR velocity. You can have severe TR without PH. “Other signs” of PH/RV dysfunction on echo: RV enlargement or systolic dysfunction (qualitative, TAPSE < ~1.7 cm, S′ ↓) RA enlargement Septal flattening (D-shaped LV; systolic = pressure overload, diastolic + systolic = volume + pressure) Dilated PA Pericardial effusion Interpretation pattern: Low pre-test probability + TR v < 2.8 + no other signs → PH unlikely. Intermediate TR v (2.9–3.4) + high pre-test probability and/or other PH signs → consider RHC. High TR v (>3.4) or clearly abnormal RV → strongly consider RHC if it would change management. Also: Echo is great to follow RV size/function and PASP over time once PH is diagnosed and treated. Case echo: TR velocity 3.1 m/s + mild RA enlargement + moderate RV enlargement + TAPSE 1.6 cm → intermediate probability, consistent with PH and RV involvement.   Right heart cath (RHC): gold standard & updated definitions You cannot definitively diagnose or classify PH without RHC. Key directly measured values: RA, RV, PA pressures Pulmonary capillary wedge pressure (PCWP/PAWP) ≈ LVEDP Oxygen saturations in chambers/vessels Cardiac output (thermodilution) Key derived values: Cardiac output (Fick) Pulmonary vascular resistance (PVR) Updated hemodynamic definitions: Pulmonary hypertension (PH) mPAP ≥ 20 mm Hg (lowered from ≥ 25). Pre-capillary PH (think PAH, group 1; also groups 3, 4, some 5): mPAP ≥ 20 PAWP ≤ 15 PVR > 2 Wood units (new lower threshold) Isolated post-capillary PH (IpcPH) (group 2) mPAP ≥ 20 PAWP > 15 PVR ≤ 2 Combined pre- and post-capillary PH (CpcPH) mPAP ≥ 20 PAWP > 15 PVR > 2 Rationale for the changes: Normal mPAP in healthy people is < ~19; 20 is about 2 SD above normal. Patients with mPAP 20–24 (esp. systemic sclerosis) already have worse outcomes than those < 20. Lowering PVR cutoff from 3 → 2 WU better aligns with these new thresholds and catches earlier precapillary disease. Practical interpretation: You use mPAP + PAWP + PVR to: Confirm PH. Distinguish pre- vs post-capillary. Identify mixed disease. Echo tells you probability; RHC tells you what type and how severe.   Vasoreactivity testing (acute vasodilator testing) Only indicated in: Idiopathic (IPAH) Heritable PAH Drug-induced PAH→ Not routine for all PH patients. Performed in the cath lab with short-acting vasodilator (e.g., inhaled NO). Positive test: ↓ mPAP ≥ 10 mm Hg To an absolute mPAP ≤ 40 mm Hg No fall in cardiac output Why it matters: Identifies a small subset who can be treated with high-dose calcium channel blockers long-term and often have better prognosis. Does not predict response to other PAH therapies (ERA, PDE5i, prostacyclin, etc.).   Screening high-risk populations Some groups warrant systematic screening because of high PAH risk. a) Systemic sclerosis / systemic sclerosis spectrum Annual screening if: Disease duration ≥ 3 years FVC ≥ 40% predicted DLCO < 60% predicted DETECT algorithm (2-step): Step 1: uses labs and simple tests (FVC/DLCO ratio, NT-proBNP, autoantibodies, right axis deviation on ECG, telangiectasias). If positive → Step 2: adds echo (TR velocity, RA size). If high risk after Step 2 → RHC. Goal: catch early PAH before symptoms are severe. b) Other high-risk groups Annual screening (usually with echo ± NT-proBNP, PFTs) for: Known heritable PAH mutations (e.g., BMPR2) Portal hypertension (esp. considering liver transplant or TIPS) HIV Always layer this on top of clinical symptoms and progression.   Big practical takeaways (what to apply on Monday) Don’t label “pulmonary hypertension” off CT or echo alone. Enlarged PA on CT or elevated PASP on echo ≠ diagnosis. RHC is required. Think PH early when: Dyspnea is out of proportion to imaging and spirometry. There is a relevant risk factor (systemic sclerosis, portal HTN, HIV, prior PE, congenital heart disease, etc.). Use the WHO groups to structure your differential and workup: Group 1 vs 2 vs 3 vs 4 vs 5 → drives what tests you order and what treatments you eventually consider. Echo = probability. RHC = truth. Echo gives you low / intermediate / high PH probability. RHC gives you pre- vs post-capillary, PVR, and hemodynamics needed for therapy. Know the new numbers: mPAP ≥ 20 = PH PAWP cutoff = 15 PVR > 2 WU = precapillary component Don’t forget NT-proBNP, DLCO, V/Q scan, and high-risk screening (especially in systemic sclerosis and BMPR2 carriers).   References Humbert M, Kovacs G, Hoeper MM, Badagliacca R, Berger RMF, Brida M, Carlsen J, Coats AJS, Escribano-Subias P, Ferrari P, Ferreira DS, Ghofrani HA, Giannakoulas G, Kiely DG, Mayer E, Meszaros G, Nagavci B, Olsson KM, Pepke-Zaba J, Quint JK, Rådegran G, Simonneau G, Sitbon O, Tonia T, Toshner M, Vachiery JL, Vonk Noordegraaf A, Delcroix M, Rosenkranz S; ESC/ERS Scientific Document Group. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart J. 2022 Oct 11;43(38):3618-3731. doi: 10.1093/eurheartj/ehac237. Erratum in: Eur Heart J. 2023 Apr 17;44(15):1312. doi: 10.1093/eurheartj/ehad005. PMID: 36017548. Condon DF, Nickel NP, Anderson R, Mirza S, de Jesus Perez VA. The 6th World Symposium on Pulmonary Hypertension: what’s old is new. F1000Res. 2019 Jun 19;8:F1000 Faculty Rev-888. doi: 10.12688/f1000research.18811.1. PMID: 31249672; PMCID: PMC6584967. Maron BA. Revised Definition of Pulmonary Hypertension and Approach to Management: A Clinical Primer. J Am Heart Assoc. 2023 Apr 18;12(8):e029024. doi: 10.1161/JAHA.122.029024. Epub 2023 Apr 7. PMID: 37026538; PMCID: PMC10227272.

Dive into the intriguing world of methylene blue and its potential role in managing septic shock. The hosts unravel its mechanism, showing how it inhibits nitric oxide synthase to restore vascular tone. Discover the specific clinical scenarios where it shines, especially in vasodilatory shock. They discuss the evidence from meta-analyses, showing improved MAP and shorter vasopressor duration, though the mortality benefit remains murky. Plus, learn about practical dosing strategies and important safety considerations. It's a concise yet enlightening discussion!

For today’s podcast we have a special episode. We were extremely grateful to be invited to present live at CHEST 2025 this year. Kristina Montemayor, and Pulm PEEPs Associate Editors Luke Hedrick, Tom Di Vitantonio, and Rupali Sood hosted a session entitled “Widened Airways and Narrowed Differentials”. It is a great session around bronchiectasis. Enjoy!   Meet Our Guests Dr. Doreen Addrizzo-Harris is  a Professor of Medicine at NYU where she is also Associate Director of Clinical and Academic Affairs for the pulmonary and critical care division. In addition to that, she’s the director of the bronchiectasis and NTM program and also serves as a program director for the pulmonary and critical care fellowship. Case Snapshot 60-year-old with CLL (in remission) → recurrent “pneumonias,” diffuse (not single-lobe), later dx’d with CVID; serial CTs: upper-lobe–predominant bronchiectasis, tree-in-bud, mucus impaction; multiple AFB+ cultures (MAC, later M. abscessus); recurrent bacterial flares (MSSA/MRSA).   CT Images   Key Learning Points Imaging pearls Tree-in-bud = small airways (bronchiolar) impaction/inflammation, not a diagnosis. Differential guided by distribution + chronicity: Acute/diffuse → bacterial/viral/NTM infection Dependent/basal → aspiration Persistent + nodular + bronchiectasis → NTM common Bronchiectasis CT signs (think: “ring, taper, edge”): Broncho-arterial ratio >1 (signet-ring) Lack of normal tapering Visible bronchi within 1 cm of pleura Location matters: Upper lobes → CF, sarcoid, prior TB/radiation Middle lobe/lingula → NTM classic; consider ABPA if central Lower lobes → aspiration, PCD, CTD, immunodeficiency NTM: diagnosis & when to treat Use all three (2020 guideline frame): clinical symptoms, compatible CT, microbiology (≥2 sputum cultures or 1 bronch +, etc.). Not every positive culture = disease needing drugs. If you defer pharmacologic therapy, follow closely (symptoms, sputum, PFTs, interval CT if change). Bug matters: MAC, M. abscessus, kansasii etc. “Low-virulence” species (e.g., M. gordonae) can still flag underlying airway disease. Regimens (MAC, macrolide-susceptible): azithro + ethambutol + rifampin (intermittent for nodular-bronchiectatic; daily ± IV amikacin for fibro-cavitary/advanced). Macrolide is the backbone; the others protect against resistance. M. abscessus: check for inducible macrolide resistance (prolonged in-vitro testing). Monitoring: sputum q1–3 mo; labs (CBC/CMP), vision (ethambutol), hearing (aminoglycosides). Treat ~12 months beyond culture conversion. Anti-inflammatory macrolide for bronchiectasis is contraindicated if macrolide-susceptible NTM is present—risk of resistance. Bronchiectasis management essentials It’s a syndrome: symptoms/exacerbations plus CT changes. Airway clearance is foundational (exercise + devices ± hypertonic saline/DNase when indicated). Expect CT and symptom gains with adherence. Exacerbations often need ~14 days of pathogen-directed antibiotics (short courses may fail). Take the “easy win” when a conventional pathogen explains the flare. Workup framework (start with a core bundle, then target) Core “every patient” bundle CBC with diff (look for eosinophilia/hematologic clues) Quantitative IgG/IgA/IgM (primary/secondary immunodeficiency) ABPA screen: total IgE + Aspergillus-specific IgE/IgG Sputum cultures: routine bacteria + AFB + fungal (if producing) Baseline PFTs Targeted tests (guided by history, distribution, microbes) CF evaluation: sweat chloride and/or CFTR genotyping (especially with upper-lobe disease, chronic sinusitis/nasal polyps, pancreatitis/malabsorption, infertility/CAVD). PCD: nasal NO, genetics, specialized ciliary studies (adult cases may be mild and missed by genetics alone). Alpha-1 antitrypsin (never-smoker emphysema, liver hx) CTD serologies (RA, Sjögren’s, etc.), if suggestive Aspiration/upper-GI assessment when basal-predominant or reflux symptoms For suspected/known CVID: vaccine response assessment if not on replacement (this patient was already on IVIG). Practical diagnostic habits Re-read the CT yourself—radiology may under-call mild bronchiectasis in ED/PE-protocol scans. Use a diagnostic time-out when the course isn’t fitting: name your working dx, list fits/mismatches, consider common diseases with atypical presentations, multi-morbidity, and can’t-miss alternatives; ask for help early; communicate uncertainty. Teach-to-remember pearls from the case Recurrent, geographically scattered pneumonias → think systemic causes (immunodeficiency, CF/PCD), not just focal anatomic problems. Upper-lobe bronchiectasis + CAVD is a CF red flag—even in the 60s. Adult-onset CF is real and actionable. In CF today, MSSA can be more common than Pseudomonas on culture; don’t let absence of Pseudomonas dissuade you. Airway clearance adherence can change CTs; instruct patients to ramp up before surveillance scans for a fair assessment. If symptoms abate with targeted therapy to a conventional pathogen, you may avoid immediate NTM re-treatment—but keep a tight follow-up loop.  

In this episode, we’re concluding our review of the Global Initiative for Asthma (GINA) guidelines on asthma today with a cased based episode on special considerations in asthma care. We’ve covered asthma diagnosis and phenotyping, the approach to therapy inhaler and oral medical therapy, and biologic therapy. On today’s episode we’re talking about complex cases that are at the edges of the guidelines, or may be in future guidelines. To help us with this exciting topic we’re joined by an expert in the field. Enjoy!  Meet Our Guest Dr. Meredith McCormack is a Professor of Medicine at Johns Hopkins, where she leads multiple NIH funded endeavors at understanding lung health and disease. She is the Division Director for Pulmonary and Critical Care Medicine, while also directing the Asthma Precision Medicine Center of Excellence, and the BREATHE Center, which focuses on understanding the effects of the environment on lung health and disease through research and community engagement.  She is an internationally recognized expert in asthma management and is a dedicated member of the faculty who is committed to the trainees. Meet Our Co-Hosts Rupali Sood  grew up in Las Vegas, Nevada and made her way over to Baltimore for medical school at Johns Hopkins. She then completed her internal medicine residency training at Massachusetts General Hospital before returning back to Johns Hopkins, where she is currently a second year pulmonary and critical care medicine fellow alongside Tom. Rupali’s interests include interstitial lung disease, particularly as related to oncologic drugs. And she also loves bedside medical education. Tom Di Vitantonio  is originally from New Jersey and attended medical school at Rutgers, New Jersey Medical School in Newark. He then completed his internal medicine residency at Weill Cornell, where he also served as a chief resident. He currently is a second year pulmonary and critical care medicine fellow at Johns Hopkins, and he’s passionate about caring for critically ill patients, how we approach the management of pulmonary embolism, and also about medical education of trainees to help them be more confident and patient centered in the care they have going forward. Key Learning Points Episode themesBuilt on GINA 2024: final capstone focusing on evolving topics + case-based application.Three focal areas: (1) obesity/metabolic health (GLP-1s, metformin), (2) dual biologics vs switching, (3) de-escalating inhalers while on biologics.Emphasis throughout on personalized care, shared decision-making, and multidisciplinary collaboration.Obesity & metabolic health in asthmaObesity affects mechanics, inflammation, and treatment response; tackling metabolic dysfunction can improve asthma control.GLP-1 receptor agonists may provide additive benefit beyond weight loss for some patients (early clinical signals; trials ongoing).Metformin is being studied as a potential adjunct targeting metabolic-inflammatory pathways.Practical approach: screen/counsel on weight, activity, and metabolic disease; partner with primary care/endocrine/sleep clinics; consider GLP-1/other agents when indicated for comorbidities, with potential asthma “bonus.”Biologics: switching vs dual therapyConsider switching/adding when control is not achieved or sustained on a biologic despite adherence.Upstream vs downstream targets:Upstream: anti-TSLP (e.g., tezepelumab) may help when multiple pathways/biomarkers (e.g., high IgE + eos) suggest broader blockade.Downstream: IL-5/IL-4/13/IgE agents selected to match phenotype/endotypes.Comorbidities can drive choice:Nasal polyps or upper airway syndromes: there are biologic options that improve upper airway symptoms in addition to asthmaAtopic dermatitis: agents with dual indications can be life-changing.Logistics matter: injection burden/needle phobia and dosing cadence (e.g., every 2 vs 4–8 weeks) can determine real-world success.De-escalating inhalers on biologicsDon’t step down immediately. Ask patients to maintain their full regimen for ~3 months after starting a biologic to gauge true benefit.Set expectations early and share a step-down plan to prevent unsupervised discontinuation.Typical order (individualize):Remove non-essential add-ons first (e.g., antihistamines, leukotriene modifiers).Reduce ICS dose gradually (high → medium → low).Keep ICS/LABA combination among the last therapies to taperTargets while stepping down: “normal” lung function when feasible, minimal/no day or night symptoms, full activity, no exacerbations.When patients don’t respond to biologicsRe-check the fundamentals:Adherence/technique for inhalers and biologic.Biomarkers behaving as expected (e.g., eosinophils falling on anti-IL-5).Revisit the diagnosis and contributors/mimics (e.g., vocal cord dysfunction, upper-airway disease). Consider moving upstream (e.g., to TSLP) if a downstream agent underperforms.Communication & practical pearlsUse visual aids to verify what patients actually take and how (e.g., Asthma & Allergy Network inhaler pictogram).Needle issues are common; home vs clinic administration and family support can make or break adherence.Biologics are transformative for the right patient—consider them early in steroid-dependent or poorly controlled severe asthma.Think longitudinally: plan for monitoring, comorbidity management, and timely adjustments. 

We’re back with our 4th episode in our collaborative series with BMJ Thorax. This week’s episode covers four articles related to bronchiectasis and covers a range of topics in this domain including novel therapeutics, registry data to understand risk, and health related quality of life. Our mission at Pulm PEEPs is to disseminate and promote pulmonary and critical care education, and we highly value the importance of peer reviewed journals in this endeavor. Each month in BMJ Thorax, a journal club is published looking at high yield and impactful publications in pulmonary medicine. We will be putting out quarterly episodes in association with Thorax to discuss a journal club publication and synthesize four valuable papers. Meet Our Guests Chris Turnbull is an Associate Editor for Education at Thorax. He is an Honorary Researcher and Respiratory Medicine Consultant at Oxford University Hospitals. In addition to his role as Associate Editor for Education at BMJ Thorax, he is also a prominent researcher in sleep-related breathing disorders. Dr. George Doumat completed his medical school at the American University of Beirut and now is an internal medicine resident at UT south western in his second year of training. Prior to starting residency he was a research fellow at MGH studying chronic lung disease. Journal Club Papers Journal club paper from BMJ Thorax Phase 3 Trial of the DPP-1 Inhibitor Brensocatib in Bronchiectasis Cathepsin C (dipeptidyl peptidase 1) inhibition in adults with bronchiectasis: AIRLEAF, a phase II randomised, double-blind, placebo-controlled, dose-finding study Five-Year Outcomes among U.S. Bronchiectasis and NTM Research Registry Patients Anxiety, depression, physical disease parameters and health-related quality of life in the BronchUK national bronchiectasis cohort To submit a journal club article of your own to Thorax, you can contact Chris directly – christopher.turnbull@ouh.nhs.uk To engage with Thorax, please use the social media channels (Twitter – @ThoraxBMJ; Facebook – Thorax.BMJ) and subscribe on your preferred platform, to get the latest episodes directly on your device each month. Key Learning Points Four recent papers (2 RCTs, 2 large cohorts) chosen to show both new therapeutics and real-world comorbidities/outcomes, pushing toward precision medicine. 1) ASPEN trial – brensocatib (DPP-1 inhibitor) Design: Phase 3, ~1,700 pts, 35 countries, 52 weeks; stratified randomization by region. Results: ↓ annualized exacerbation rate (~1.0 vs 1.3/yr; RR≈0.8), longer time to first exacerbation, ~10% absolute ↑ in “exacerbation-free” patients at 1 year, QoL improved, modest FEV1 decline difference (~40 mL/yr). Take: First targeted therapy with consistent benefit; effect on lung function small but directionally supportive. Gaps: Need long-term durability, adolescent data, and comparisons/positioning in pts with asthma/COPD overlap. 2) AIRLEAF (BI 1291583) – reversible cathepsin C inhibitor Design: Phase 2, 4 arms (3 doses + placebo), model-based dose–response analysis to optimize dose selection. Results: Overall dose–response signal; individual low-dose arms trended to fewer exacerbations but not statistically significant; skin events more common at higher doses. Take: Promising class targeting neutrophil pathway, but needs Phase 3 before clinical use. 3) U.S. Bronchiectasis & NTM Registry – 5-year outcomes Cohort: >2,600 CT-confirmed; ~59% with baseline NTM identified. Results: 5-yr mortality ~12%; no mortality difference with vs without NTM; predictors = lower baseline FEV1, older age, male sex, prior hospitalization. FEV1 decline ~38 mL/yr. Baseline NTM group had fewer exacerbations (counterintuitive). Interpretation cautions: Likely mix of colonization vs active disease; referral/management effects in specialized centers; registry strengths (size, real-world, longitudinal) vs pitfalls (confounding, data quality, causality). 4) Bronch-UK cohort – anxiety & depression Cohort: 1,340 adults; HADS screening. Prevalence: Anxiety ~33%, depression ~20%; many undiagnosed (≈26%/16%). Impact: Worse QoL, more severe disease; depression ~1.8× higher hospitalization risk and shorter time to severe exacerbation. Caveat: Association ≠ causation; sicker patients may have more mental health burden. Practical takeaways for clinic Consider brensocatib for appropriate non-CF bronchiectasis patients once accessible; frame benefits around fewer exacerbations and QoL, not big lung function gains. Do not introduce cathepsin C inhibitors outside trials yet; discuss as pipeline only. Risk stratify using FEV1, age, sex, and prior hospitalizations; expect ~40 mL/yr average FEV1 decline. Screen mental health routinely (HADS, PHQ-9, GAD-7). Build multidisciplinary pathways; consider brief CBT-style supports embedded in bronchiectasis clinics, with targeted referrals. Registry data ≠ RCTs: Use for counseling and service design, but avoid causal claims. Research/implementation gaps highlighted Long-term safety/efficacy and subgroup effects for brensocatib (adolescents, asthma/COPD overlap). Phase 3 confirmation for cathepsin C inhibition and dose selection. Granular NTM phenotyping (colonization vs disease) to reconcile paradoxical exacerbation signals. Scalable mental-health interventions integrated into respiratory clinics; trials to test impact on exacerbations/hospitalizations. Pro tip from the episode When appraising trials, check the CONSORT diagram for generalizability and look for stratification methods in multinational RCTs; in phase 2 programs, expect model-based dose–response designs that trade breadth for power.

Dr. Vishwajit Hegde, a second-year Pulmonary and Critical Care fellow, shares a captivating case of a 26-year-old with chronic cough and pulmonary nodules. Dr. Sahil Pandya, an Associate Professor and program director, dives into diagnostic strategies, emphasizing a Bayesian approach to avoid premature conclusions. They discuss interpreting intricate imaging patterns and the decision-making process for bronchoscopic tissue sampling. The big reveal? A diagnosis of miliary lung adenocarcinoma leading to a targeted therapy breakthrough. Insights into KU's fellowship culture shine as both guests emphasize mentorship and trainee education.

Dive into the complexities of Immune Checkpoint Inhibitor Pneumonitis, a growing concern in oncology due to increased immunotherapy usage. Discover essential diagnostic strategies, including how to identify respiratory symptoms in patients on immunotherapy. Learn about the varying CT findings and the importance of ruling out infections. The hosts break down treatment protocols for different severity levels and explore alternative options when steroids aren't enough. This engaging discussion sheds light on emerging therapies and the need for teamwork in managing these cases.

Join Jim Devanney, a physiatrist transitioning to a role at the University Health Network, and Kalilah Pais, a third-year internal medicine resident passionate about critical care. They dive into the often-overlooked issue of ICU Acquired Weakness, detailing its clinical presentation and potential causes. A compelling case study reveals the significant challenges faced by a sepsis patient experiencing muscle weakness. The duo emphasizes the importance of systematic diagnosis and early intervention strategies to improve recovery in critical care settings.

Chris Kapp, an interventional pulmonologist at Northwestern, shares invaluable insights on managing pleural effusions. He discusses the importance of thoracentesis and pleural fluid analysis, emphasizing accurate diagnosis with the LIGHTS criteria. Kapp clarifies the distinctions between transudative and exudative effusions and explains the role of pleural pH and cell counts in clinical assessment. He also delves into diagnostic challenges like eosinophilic effusions and the significance of adenosine deaminase in identifying tuberculosis pleuritis.

In this fascinating discussion, Matt Freedman, a pulmonary fellow at UVA, presents the complex case of an immunocompromised patient suffering from respiratory failure. Joining him are fellow doctors John Popovich, who discusses diagnostic strategies, and Tim Scialla, who offers insights on bronchoscopy and shock assessment. They delve into challenges of diagnosing ARDS in immunosuppressed patients, weighing the risks of steroids against potential infections, and the intricacies of shock evaluation using POCUS. Their expert commentary reveals the nuances of critical care management.