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Today we have another Pulm PEEPs Pearls episode about a core critical care topic. Furf and Monty will be giving a high level overview of the use of steroids in sepsis including a review of the relevant literature and recent guidelines, and pragmatic bedside points.

Contributors

This episode was prepared with research by Pulm PEEPs Associate Editor George Doumat.

Dustin Latimer, another Pulm PEEPs Associate Editor, assisted with audio and video editing.

Key Learning Points

Why Steroids in Sepsis?Steroids do not treat the infection — antimicrobials are always first and remain the cornerstone. The goal is addressing critical illness–related corticosteroid insufficiency (CIRCI), where cortisol production cannot keep up with the overwhelming inflammatory demand of septic shock.

Hydrocortisone helps in two main ways:

Blunts the dysregulated inflammatory response — tempers the excessive vasodilation and febrile response that drive harm beyond the infection itself.
Restores vascular sensitivity to catecholamines — sepsis downregulates adrenergic receptors; steroids turn that responsiveness back on.

Clinical takeaway: The first thing you notice is vasopressor weaning (or a bend in the escalation curve) — not a rapid improvement in fever or white count.

Caveat: These trials predate modern sepsis phenotyping. None distinguish hyperinflammatory vs. hypoinflammatory responders — they treat all comers.

The Evidence: Four Landmark TrialsEvery IM resident and critical care fellow will eventually journal-club these four. The most consistent signal across all of them is faster shock reversal and reduced vasopressor use; the mortality question remains unsettled.

Bottom line: Faster shock reversal is consistent. Mortality benefit appears in 2 of 4 trials (both used fludrocortisone) but not the others. A 2026 meta-analysis showed benefit for hydrocortisone + fludrocortisone vs. placebo, but

not for hydrocortisone + fludrocortisone vs. hydrocortisone alone — suggesting hydrocortisone drives the main effect.

Who Gets Steroids, and When? 2021 Surviving Sepsis: Consider steroids for norepinephrine or epinephrine ≥ 0.25 mcg/kg/min for ≥ 4 hours despite adequate resuscitation — a reasonable bedside trigger. * Early 2026 update: Moved away from a specific numeric trigger — consider steroids when a septic patient is not responding well to vasopressors or has escalating requirements. Make a clinical decision. (Quality of evidence: low to moderate.) * Go faster than the threshold when:* Known/suspected adrenal insufficiency or home steroids, or florid pressor-requiring shock on arrival.

A practical escalation sequence: escalating norepinephrine → add vasopressin (per VASST) → then add steroids if requirements keep climbing.

Do NOT wait for an ACTH stimulation test. It does not reliably predict who responds and only delays treatment. Sepsis is an elevated-cortisol state but can dissociate ACTH and cortisol, and cortisol-binding globulin is depleted — the test is too messy to guide care.

What to Give: The Regimen Standard dose: Hydrocortisone 200 mg/day, typically 50 mg IV Q6H. (Original trials often used continuous infusions, rarely used in the U.S.) Some start with a 100 mg bolus to gain control. * Higher dose: If chronically on steroids / adrenally insufficient, consider ~300 mg/day (e.g., 100 mg Q8H). * Fludrocortisone:* Unsettled. The two mortality-benefit trials added it (50 mcg PO/NG/OG daily), but hydrocortisone already has mineralocorticoid activity and meta-analyses don’t show added benefit over hydrocortisone alone. Most clinicians omit it — adding it is reasonable and safe, just be honest about the uncertainty.

Duration & Tapering Typical course: ~7 days is most common. Trial practices varied (ADRENAL ~7 days; VANISH used a taper after 6 days; some continue until pressors are off). * No taper needed.* You do not need to taper for adrenal insufficiency after a short course — just stop. If pressors dramatically rebound, you can restart, but most patients have gained the benefit they’ll get by day 7.

Pitfalls & Safety Hyperglycemia: Expected and must be managed (monitor closely; insulin drip if needed). No signal for major DKA / severe complications in the trials. * Superinfection / fungal infection: The most-quoted concern, but the overall literature does not show a convincing, statistically significant increase. Be disciplined about stopping on schedule. * Muscle weakness: Steroids can worsen critical illness myopathy; a short 7-day course likely has limited effect, but be aware. * Other:* GI bleeding (follow general PPI prophylaxis guidance) and sodium disturbances (watch for hyper-/hyponatremia).

Two things we know: (1) steroids shorten duration of vasopressor support, and (2) they are relatively safe in sepsis. Whether they improve mortality — and in whom — remains open.

The Five Pulm PEEPs Pearls1. Mechanism: Steroids restore catecholamine vascular sensitivity and blunt dysregulated inflammation. The clinical target is vasopressor weaning, not infection treatment. 2. Evidence: Faster shock reversal is the most consistent finding. Mortality benefit is seen in 2 of 4 trials but not the others — still controversial. Some patients likely benefit; we don’t yet know who. 3. Trigger: A practical 2021 threshold is levo/epi ≥ 0.25 mcg/kg/min for ≥ 4 hours. Newer guidance drops the strict number — make a clinical decision based on poor pressor response or escalation. 4. Dose: Hydrocortisone 200 mg/day (e.g., 50 mg Q6H). Adding fludrocortisone mirrors two trials, but meta-analyses find no benefit over hydrocortisone alone. 5. Safety: Steroids appear safe in sepsis. Monitor and treat hyperglycemia; no marked increase in superinfection.

References and Further Reading

Annane, Djillali et al. “Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock.” JAMA vol. 288,7 (2002): 862-71. doi:10.1001/jama.288.7.862

Sprung, Charles L et al. “Hydrocortisone therapy for patients with septic shock.” The New England journal of medicine vol. 358,2 (2008): 111-24. doi:10.1056/NEJMoa071366

Venkatesh, Balasubramanian et al. “Adjunctive Glucocorticoid Therapy in Patients with Septic Shock.” The New England journal of medicine vol. 378,9 (2018): 797-808. doi:10.1056/NEJMoa1705835

Annane, Djillali et al. “Hydrocortisone plus Fludrocortisone for Adults with Septic Shock.” The New England journal of medicine vol. 378,9 (2018): 809-818. doi:10.1056/NEJMoa1705716

Sun, Alin et al. “Correction: Hydrocortisone combined with fludrocortisone for treatment of adults with septic shock: an updated meta-analysis and systematic review.” Frontiers in medicine vol. 13 1811616. 2 Mar. 2026, doi:10.3389/fmed.2026.1811616

Prescott, Hallie C et al. “Executive Summary: Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2026.” Critical care medicine vol. 54,4 (2026): 715-724. doi:10.1097/CCM.0000000000007089

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Episode Transcript

Hey everyone, Dave Furfaro here from Pulm PEEPs. As you may have noticed in the last few weeks and months, we’ve had a little bit of a decrease in the content that we’ve been putting out, and I just wanted to share a couple things with you about why that is and the future of Pulm PEEPs coming up. In December of 2025, I was diagnosed with a large myxoid liposarcoma in my leg, and since then, I have been undergoing treatment for that.

Overall, treatment has been going well, but it’s certainly been a long road that, continues, and I hope that it continues to trend positively. Kristina has been an unbelievable support during this. We have continued to work on some content as a great way and distraction for me at times, but we haven’t been able to keep up the same pace of content that we usually put out. And given everything that is going on, I actually anticipate that will continue for a few months. Ee haven’t said anything so far yet because we were still figuring it out ourselves, but now we just wanted you all to know that, we, love doing Pulm PEEPs. We’re very committed to it. We wanna get back to doing it as consistently as we have been previously, and we plan on doing that, but it likely will be a little bit of time, and this is why.

I also may be sharing more about my journey through the medical system as a patient, in the future, but for now, I’m really just focusing on my treatment, my health, and my family. So the summer months will likely be, much slower, maybe even a break off together, and look forward to recovering and getting back to producing more regular Pulm PEEPs content in the Fall.

Hope everybody who’s listening is doing well. Thank you all, as always, for being supportive, for listening to the podcast, for reaching out to us on social media, for saying hi to us in person at conferences. It’s been, a true delight, and we can’t wait to get back to business as usual. Okay, everybody. Take good care of patients, be safe, be well, and we’ll see you soon.

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We’re excited today to launch our first episode in collaboration with the Irish Thoracic Society and their podcast series. The Irish Thoracic Society represents respiratory professionals throughout Ireland and is dedicated to championing excellence in the prevention, diagnosis, and clinical care of respiratory disease through its work in advocacy, education and research.

In today’s episode, we explore the complex and often overlooked world of refractory chronic cough — a condition that can significantly impact patients’ quality of life but is frequently misunderstood or underdiagnosed. With insights from leading respiratory specialists in Ireland and the United States, we discuss the latest thinking on diagnosis, management, and emerging treatments aimed at improving outcomes for patients and helping clinicians navigate this challenging area of respiratory medicine.

Joining us are renowned experts Professor Lorcan McGarvey and Professor Brendan Canning, both internationally recognised leaders in respiratory medicine and cough research. Together, they share their perspectives on the neurobiology of chronic cough, the considerable morbidity experienced by patients, and how clinicians can approach diagnostic investigations more effectively.

We also explore current treatment strategies and promising new therapies on the horizon as chronic cough increasingly gains recognition as a disease in its own right — rather than simply a symptom. Whether you’re a clinician, researcher, or simply interested in advances in respiratory medicine, this episode offers valuable insights into a condition that is finally receiving the attention it deserves.

Meet Our Co-Hosts

Marissa O’Callaghan is an Irish trained Respiratory fellow currently undertaking a post-doc fellow working in Erasmus MC Rotterdam in the Netherlands. She finished her Irish respiratory and Internal medicine training and Phd in 2025. Her areas of interest are interstitial and rare lung diseases. She enjoys clinical research, Med Ed, and dreaming up new medical innovations. Together with cohost Sandra Green, she founded the ITS podcast series in June 2024. Marissa O’Callaghan –LinkedIn

Sandra Green is an Irish-trained respiratory fellow with a strong track record in climate advocacy and multidisciplinary sustainable initiatives, as co-founder of Irish Doctors for the Environment. She has an MSc in Leadership and Innovation in Healthcare at the Royal College of Surgeons Ireland (2023–2025). With Marisssa, she co-founded the Irish Thoracic Society Podcast Productions, launching the platform in 2024 to share knowledge, insights, and innovations in respiratory care. Sandra Green – LinkedIn

Meet Our Guests

Lorcan McGarvey is a professor of respiratory medicine at the University of Belfast, with a focus on the neurobiology of cough. His research has significantly contributed to the understanding of cough hypersensitivity syndrome and the development of new therapeutic strategies. Lorcan is a respected voice in the field, known for his collaborative work and dedication to advancing respiratory health.

Brendan Canning is a distinguished researcher at Johns Hopkins University, specializing in the mechanisms of cough and airway diseases. His pioneering studies on neural pathways and receptor targets have paved the way for novel treatments in refractory chronic cough. Brendan’s expertise and innovative approach make him a key figure in the ongoing efforts to redefine chronic cough management.

In This Episode

The definitions and classifications of chronic cough, including unexplained, refractory, and unexplained refractory cough

The importance of a thorough clinical history and focused diagnostics over exhaustive testing

Common causes of chronic cough

The role of personalized, multidisciplinary management—combining pharmacologic, speech therapy, and psychological support—to improve quality of life for even the most challenging patients.

The concept of cough hypersensitivity syndrome and its role in refractory cases

Evidence-based approach to treatment, including pharmacologic and non-pharmacologic options

Emerging therapies on the horizon, including novel receptor modulators and neuromodulatory agents and ongoing clinical trials in this rapidly evolving field

The impact of chronic cough on mental health, social life, and overall quality of life

The importance of reframing chronic cough as a disease entity in its own right

References and Further Reading

Chung KF, Pavord ID. Prevalence, pathogenesis, and causes of chronic cough. Lancet. 2008;371(9621):1364-1374.

Gibson PG, Vertigan AE. Management of chronic refractory cough. BMJ. 2015;351:h5590.

Matsumoto H, Kanemitsu Y, Ohe M, Tanaka H, Terada K, Nishi K, et al. Real-world usage and response to gefapixant in refractory chronic cough. ERJ Open Res. 2025;11(4):01037-2024. doi:10.1183/23120541.01037-2024.

McGarvey LP, Birring SS. Cough hypersensitivity syndrome: a novel paradigm for understanding cough. Lancet Respir Med. 2014;2(8):647-656.

Morice AH, Millqvist E, Bieksiene K, Birring SS, Dicpinigaitis P, Ribas CD, et al. ERS guidelines on the diagnosis and treatment of chronic cough in adults and children. Eur Respir J. 2020;55(1):1901136.

Parker SM, Smith JA, Birring SS, Chamberlain-Mitchell S, Gruffydd-Jones K, Haines J, et al. British Thoracic Society clinical statement on chronic cough in adults. Thorax. 2023;78(Suppl 1):S3-S19.

Smith JA, Woodcock A. Chronic cough. N Engl J Med. 2006;354(2):136-144.

Song WJ, Dupont L, Birring SS, Chung KF, Dąbrowska M, Dicpinigaitis P, et al. Consensus goals and standards for specialist cough clinics: the NEUROCOUGH international Delphi study. ERJ Open Res. 2023;9(6):00618-2023. doi:10.1183/23120541.00618-2023.

Song WJ, McGarvey L, Cho PSP, Mazzone SB, Chung KF, editors. Chronic cough. Sheffield: European Respiratory Society; 2025.

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We are unbelievably excited this week to be reviewing the hot-off-the-presses 2026 Multi-Society (AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN) Pulmonary Embolism Guidelines with lead author Dr. Mark A. Creager. We will talk about key updates in these guidelines compared to prior practice, including the new risk classification model, and provide an overview from diagnosis to follow-up. Given the clinical importance and prevalence of pulmonary embolism, these guidelines are certainly going to shape practice going forward, so this episode is a can’t miss!

Watch the full video of this episode with graphics and helpful teaching visuals on our YouTube channel: https://www.youtube.com/@pulmpeeps

Meet Our Guest

Dr. Mark Creager is a Professor of Medicine at Dartmouth Hitchcock Medical Center where he specializes in Cardiovascular Medicine with an emphasis on venous thromboembolic disease. He served as the lead author of the 2026 Pulmonary Embolism Guidelines.

Article and Reference

Creager MA, Barnes GD, Giri J, Mukherjee D, Jones WS, Burnett AE, Carman T, Casanegra AI, Castellucci LA, Clark SM, Cushman M, de Wit K, Eaves JM, Fang MC, Goldberg JB, Henkin S, Johnston-Cox H, Kadavath S, Kadian-Dodov D, Keeling WB, Klein AJP, Li J, McDaniel MC, Moores LK, Piazza G, Prenger KS, Pugliese SC, Ranade M, Rosovsky RP, Russo F, Secemsky EA, Sista AK, Tefera L, Weinberg I, Westafer LM, Young MN. 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2026 Feb 19:S0735-1097(25)10161-7. doi: 10.1016/j.jacc.2025.11.005. Epub ahead of print. PMID: 41712898.

Key Learning Points

Why these guidelines matter:

This is the first joint AHA/ACC clinical practice guideline specifically on acute PE, bringing together a truly multidisciplinary writing committee (cardiology, pulmonology, hematology, emergency medicine, interventional radiology, surgery, and others). Prior guidelines existed from individual societies, but nothing this comprehensive had been updated in roughly five to six years.

New PE clinical categories (A through E):

One of the most impactful changes is replacing the old “massive/submassive” and “low/intermediate/high risk” labels with five categories that form a severity continuum. Category A is subclinical (incidental PE found on imaging in asymptomatic patients). Category B covers symptomatic but low-severity patients. Category C is where much of the clinical complexity lives — symptomatic, hemodynamically stable patients subdivided into C1, C2, and C3 based on RV function and biomarkers. Category D represents incipient cardiopulmonary failure (transient hypotension, normotensive shock with end-organ dysfunction). Category E is frank cardiopulmonary failure, with E2 being the sickest — refractory or recurrent cardiac arrest. Respiratory modifiers (hypoxia requiring supplemental oxygen) layer onto C, D, and E.

Diagnostic approach:

Clinical evaluation comes first — history, exam, and validated decision tools (Wells score, revised Geneva, PERC). If clinical probability is low and D-dimer is normal, imaging can be safely avoided. If either is concerning, imaging is warranted. CTPA remains the preferred imaging modality due to superior sensitivity, specificity, wide availability, and ability to assess clot burden and alternative diagnoses. VQ scanning is still appropriate when CTPA is contraindicated, and VQ SPECT offers better reproducibility and specificity than traditional planar VQ if available. Echocardiography is not a diagnostic test for PE but is important for risk stratification — RV size, TAPSE, and tissue Doppler measures all contribute prognostic information.

Anticoagulation updates:

Anticoagulation remains the cornerstone of treatment. For patients potentially needing advanced therapies (C3, D, E), parenteral anticoagulation is started first. A notable recommendation: low molecular weight heparin is generally preferred over unfractionated heparin, based on evidence showing more effective VTE risk reduction, more predictable pharmacokinetics, no need for routine monitoring, lower rates of heparin-induced thrombocytopenia, and no increase in major bleeding. The committee acknowledged this may create discomfort for clinicians accustomed to unfractionated heparin’s easy reversibility, but the difficulty of achieving and maintaining therapeutic levels with UFH was a significant concern.

Advanced therapies:

Catheter-based thrombolysis, mechanical thrombectomy, systemic thrombolysis, and surgical embolectomy all received mostly class 2B recommendations (“can consider”) for C3 and D categories, reflecting that current evidence shows improvement in short-term surrogate measures (RV/LV ratio, hemodynamics) but lacks definitive hard outcome data on mortality. For category E1 patients, recommendations are stronger (class 2A). Multiple trials are expected soon — HI-PEITHO, PEERLESS-2, PE-TRACT, PERSEVERE, TORPEDO, and PROG — that should substantially inform future updates.

PERT teams:

Pulmonary embolism response teams are encouraged, particularly for C3, D, and E patients. They’ve been shown to reduce length of stay. For institutions without PERT capability, establishing consultation networks with larger centers is recommended.

Post-PE follow-up:

Patients shouldn’t be “left in the wilderness” after discharge. The guidelines recommend communication within the first week to ensure understanding of diagnosis and treatment, an in-person visit at or before three months to assess for persistent symptoms and discuss anticoagulation duration, ongoing surveillance for chronic thromboembolic pulmonary disease, and periodic reassessment for those on extended anticoagulation.

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Furf and Monty are back with another Pulm PEEPs Pearls episode. The topic of today’s discussion is an often discussed, but often misunderstood, test; the methacholine challenge. They’ll review when to utilize this test, how it should be performed, and the appropriate interpretation.

Contributors

This episode was prepared with research by Pulm PEEPs Associate Editor George Doumat.

Dustin Latimer, another Pulm PEEPs Associate Editor, assisted with audio and video editing.

Key Learning Points

What the Test Measures

Methacholine challenge is a direct bronchial provocation test of airway hyperresponsiveness (AHR), a core physiologic feature of asthma.
Anyone will bronchoconstrict at high enough concentrations — the test looks for an abnormal threshold.
The key endpoint is the PC20: the methacholine concentration causing a 20% fall in FEV1.
- Abnormal in adults: PC20 ≤ 8–16 mg/mL

Test Performance

Meta-analyses: pooled sensitivity ~60%, specificity ~90%.
Real-world cohorts: sensitivity 55–62%, specificity 56–100% (varies by population, protocol, and threshold used).
Not a standalone yes/no test — best used as part of a broader diagnostic pathway.

Where It Fits in the Asthma Workup

The test belongs in a stepwise approach:

Step 1: Spirometry + bronchodilator response
Step 2: Add FeNO and/or peak flow variability (if available)
Step 3: If the picture is still unclear → methacholine challenge

It is most useful for symptomatic patients with normal spirometry and no bronchodilator reversibility. Given its cost, mild risk, and discomfort, it should not be a first-line test — most asthma diagnoses do not require it.

Technique and Medication Prep

Technique

ERS guidelines favor tidal breathing over deep inspiratory maneuvers.
Deep breaths can be bronchoprotective and blunt the response, reducing sensitivity — especially in mild or well-controlled asthma.

Medication Washout (to Avoid False Negatives)

Inhaled corticosteroids, leukotriene blockers, and antihistamines do not significantly affect the test acutely — continue these. Withdrawing ICS also carries its own risk for asthma patients.
Practical tip: Spell out exactly what to hold and when — for both the patient and the PFT lab — at the time the test is ordered.

Interpreting Results

Negative Test (PC20 > 16 mg/mL)

Very high negative predictive value in symptomatic adults.
Makes current asthma quite unlikely (assuming proper test conduct).
This is the test’s greatest strength: it is an excellent rule-out test.

Positive Test (PC20 ≤ 8–16 mg/mL)

More nuanced — airway hyperresponsiveness is not unique to asthma.
Can be positive in: chronic cough, allergic rhinitis, COPD, and even some healthy asymptomatic individuals.
A positive result raises probability but must be interpreted alongside the clinical story, variable respiratory symptoms, peak flow variability, FeNO, and ICS response.

Safety and Risks

Overall, the test is quite safe; significant adverse effects are rare.
Temporary breathing discomfort is expected (bronchoconstriction is being induced).
Severe bronchospasm is possible:
- A trained clinician should be available; SABA inhaler/nebulizer must be immediately on hand; a physician should be reachable in the facility.
Contraindications / cautions:
- Avoid if FEV1 < 70% predicted or < 1–1.5 L (baseline obstruction greatly increases risk).
- Avoid within 3 months of an acute cardiac event (rare risk of cardiac events with unstable cardiac disease).

Five Pearls — Quick Recap

What it tests: Methacholine challenge is a direct test of AHR with high specificity but variable sensitivity — it belongs inside a diagnostic pathway, not as a standalone asthma test.
When to use it: Most useful for symptomatic patients with normal spirometry and no bronchodilator response, after FeNO and peak flow variability have been considered.
Technique and meds matter: Use tidal breathing protocol; respect washout intervals — especially the 7-day LAMA washout and 24–48 hour LABA window — to avoid false negatives.
Safety: Generally safe, but can induce significant bronchoconstriction. Have a SABA available and avoid the test in patients with FEV1 < 70% predicted.
Interpretation: A negative test (PC20 > 16 mg/mL) strongly argues against current asthma. A positive test raises probability but is not specific — interpret alongside the full clinical picture.

References and Further Reading

Coates AL, Wanger J, Cockcroft DW, Culver BH; Bronchoprovocation Testing Task Force: Kai-Håkon Carlsen; Diamant Z, Gauvreau G, Hall GL, Hallstrand TS, Horvath I, de Jongh FHC, Joos G, Kaminsky DA, Laube BL, Leuppi JD, Sterk PJ. ERS technical standard on bronchial challenge testing: general considerations and performance of methacholine challenge tests. Eur Respir J. 2017 May 1;49(5):1601526. doi: 10.1183/13993003.01526-2016. PMID: 28461290.
Lee, J., & Song, J. U. (2021). Diagnostic comparison of methacholine and mannitol bronchial challenge tests for identifying bronchial hyperresponsiveness in asthma: a systematic review and meta-analysis. Journal of Asthma, 58(7), 883–891. https://doi.org/10.1080/02770903.2020.1739704
Davis BE, Blais CM, Cockcroft DW. Methacholine challenge testing: comparative pharmacology. J Asthma Allergy. 2018 May 14;11:89-99. doi: 10.2147/JAA.S160607. PMID: 29785128; PMCID: PMC5957064.

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This week’s Pulm PEEPs Pearls episode is all about spontaneous breathing trials (SBTs). SBTs are a standard part of the daily practice in the intensive care unit, but the exact methods vary across ICUs and institutions. Listen in to hear about the most common methods of SBTs, the physiology of each method, and what the evidence says.

Contributors

This episode was prepared with research by Pulm PEEPs Associate Editor George Doumat.

Dustin Latimer, another Pulm PEEPs Associate Editor, assisted with audio and video editing.

Key Learning Points

What an SBT is really testing
An SBT is a stress test for post-extubation work of breathing, not just a ventilator check.
The goal is to balance sensitivity and specificity:
- Too hard → unnecessary failures and delayed extubation
- Too easy → false positives and higher risk of reintubation
Common SBT modalities and how they compare
T-piece
- No inspiratory support and no PEEP
- Highest work of breathing
- Most “physiologic” but often too strict
Pressure support (PS) + PEEP (e.g., 5/5 or 8/5)
- Offsets ETT resistance and provides modest assistance
- Easier to pass than T-piece
CPAP (0/5)
- No inspiratory help, but provides PEEP to counter ETT resistance
- Sits between PS and T-piece in difficulty
Evidence favors pressure-supported SBTs for most patients
Large meta-analysis (~6,000 patients, >40 RCTs):
- Pressure-supported SBTs increase successful extubation (~7% absolute benefit)
- No increase in reintubation rates
Trials (e.g., FAST trial):
- Patients pass SBTs earlier
- Leads to earlier extubation and fewer ventilator-associated risks
Bottom line: A 30-minute PS 5/5 SBT is evidence-based and appropriate for most stable ICU patients
When a T-piece still makes sense

T-piece SBTs are useful when:

Cost of reintubation is high
- Difficult airway
- Prior failed extubation
Pretest probability of success is low
- Prolonged or difficult weaning
- Tracheostomy vs extubation decisions
Need to mimic physiology without positive pressure
- In LV dysfunction or pulmonary edema even small amounts PEEP may significantly improve physiology
Some centers use a hybrid approach: PS SBT → short confirmatory T-piece before extubation
CPAP as a middle ground
Rationale:
- Allows full patient effort while compensating for ETT resistance
Evidence:
- Fewer and smaller trials
- Possible modest improvement in extubation success
- No clear mortality or LOS benefit
Reasonable option based on patient physiology, institutional protocols, and clinician comfort
No single “perfect” SBT mode
Across PS, T-piece, CPAP, and newer methods (e.g., high-flow via ETT) there are no consistent differences in mortality or length of stay
What matters most:
- Daily protocolized screening
- Thoughtful bedside clinical judgment
- Matching SBT difficulty to patient-specific risk
Institutional variation is normal—and acceptable
Examples:
- PS 10/5 in postoperative surgical ICU patients
- PS 5/0 as an intermediate difficulty option
Key question clinicians should ask: What does passing or failing this specific SBT tell me about this patient’s likelihood of post-extubation success?
Take-home pearls
SBTs are stress tests of post-extubation physiology.
PS 5/5 for 30 minutes is a strong default for most ICU patients.
T-piece trials are valuable when false positives are costly or physiology demands it.
CPAP is reasonable but supported by less robust data.
Consistency, daily screening, and judgment matter more than the exact mode.

References and Further Reading

Burns KEA, Khan J, Phoophiboon V, Trivedi V, Gomez-Builes JC, Giammarioli B, Lewis K, Chaudhuri D, Desai K, Friedrich JO. Spontaneous Breathing Trial Techniques for Extubating Adults and Children Who Are Critically Ill: A Systematic Review and Meta-Analysis. JAMA Netw Open. 2024 Feb 5;7(2):e2356794. doi: 10.1001/jamanetworkopen.2023.56794. PMID: 38393729; PMCID: PMC10891471.
Burns KEA, Sadeghirad B, Ghadimi M, Khan J, Phoophiboon V, Trivedi V, Gomez Builes C, Giammarioli B, Lewis K, Chaudhuri D, Desai K, Friedrich JO. Comparative effectiveness of alternative spontaneous breathing trial techniques: a systematic review and network meta-analysis of randomized trials. Crit Care. 2024 Jun 8;28(1):194. doi: 10.1186/s13054-024-04958-4. PMID: 38849936; PMCID: PMC11162018.
Subirà C, Hernández G, Vázquez A, Rodríguez-García R, González-Castro A, García C, Rubio O, Ventura L, López A, de la Torre MC, Keough E, Arauzo V, Hermosa C, Sánchez C, Tizón A, Tenza E, Laborda C, Cabañes S, Lacueva V, Del Mar Fernández M, Arnau A, Fernández R. Effect of Pressure Support vs T-Piece Ventilation Strategies During Spontaneous Breathing Trials on Successful Extubation Among Patients Receiving Mechanical Ventilation: A Randomized Clinical Trial. JAMA. 2019 Jun 11;321(22):2175-2182. doi: 10.1001/jama.2019.7234. Erratum in: JAMA. 2019 Aug 20;322(7):696. doi: 10.1001/jama.2019.11119. PMID: 31184740; PMCID: PMC6563557.
Burns KEA, Wong J, Rizvi L, Lafreniere-Roula M, Thorpe K, Devlin JW, Cook DJ, Seely A, Dodek PM, Tanios M, Piraino T, Gouskos A, Kiedrowski KC, Kay P, Mitchell S, Merner GW, Mayette M, D’Aragon F, Lamontagne F, Rochwerg B, Turgeon A, Sia YT, Charbonney E, Aslanian P, Criner GJ, Hyzy RC, Beitler JR, Kassis EB, Kutsogiannis DJ, Meade MO, Liebler J, Iyer-Kumar S, Tsang J, Cirone R, Shanholtz C, Hill NS; Canadian Critical Care Trials Group. Frequency of Screening and Spontaneous Breathing Trial Techniques: A Randomized Clinical Trial. JAMA. 2024 Dec 3;332(21):1808-1821. doi: 10.1001/jama.2024.20631. PMID: 39382222; PMCID: PMC11581551.
Mahul M, Jung B, Galia F, Molinari N, de Jong A, Coisel Y, Vaschetto R, Matecki S, Chanques G, Brochard L, Jaber S. Spontaneous breathing trial and post-extubation work of breathing in morbidly obese critically ill patients. Crit Care. 2016 Oct 27;20(1):346. doi: 10.1186/s13054-016-1457-4. PMID: 27784322; PMCID: PMC5081985.
Yi LJ, Tian X, Chen M, Lei JM, Xiao N, Jiménez-Herrera MF. Comparative Efficacy and Safety of Four Different Spontaneous Breathing Trials for Weaning From Mechanical Ventilation: A Systematic Review and Network Meta-Analysis. Front Med (Lausanne). 2021 Nov 22;8:731196. doi: 10.3389/fmed.2021.731196. PMID: 34881255; PMCID: PMC8647911.

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On this week’s episode, we’re continuing our Guidelines Series exploring the 2022 ESC/ERS Guidelines for the diagnosis and treatment of Pulmonary Hypertension. If you missed our first episode in the series, give it a listen to hear about the most recent recommendations regarding Pulmonary Hypertension definitions, screening, and diagnostics. Today, we’re talking about the next steps after diagnosis. Specifically, we’ll be discussing risk stratification, establishing treatment goals, and metrics for re-evaluation. We’ll additionally introduce the mainstays of pharmacologic therapy for Pulmonary Hypertension.

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. Rupali’s interests include interstitial lung disease, particularly as related to oncologic drugs, and 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.

Key Learning Points

1) Episode Roadmap

How to set treatment goals, assess symptom burden, and risk-stratify patients with suspected/confirmed pulmonary arterial hypertension (PAH).
What tools to use to re-evaluate patients on treatment
Intro to major PAH medication classes and how they map to pathways.

2) Case-based diagnostic reasoning

Patient: 37-year-old woman with exertional dyspnea, mild edema, abnormal echo, telangiectasias + epistaxis → raises suspicion for HHT (hereditary hemorrhagic telangiectasia) and/or early connective tissue disease.

Key reasoning move: start broad (Groups 2–5) and narrow using history/exam/testing.
In a young patient without obvious left heart or lung disease, think more about Group 1 PAH (idiopathic/heritable/associated).

HHT teaching point: HHT can cause PH in more than one way:

More common: high-output PH from AVMs (often hepatic/pulmonary)
Rare (1–2% mentioned): true PAH phenotype (vascular remodeling; associated with ALK1 in some patients), behaving like Group 1 PAH.

3) Functional class assessment

WHO Functional Class:

Class I: no symptoms with ordinary activity, only with exertion
Class II: symptoms with ordinary activity
Class III: symptoms with less-than-ordinary activity (can’t do usual chores/shopping without dyspnea)
Class IV: symptoms at rest

Practical bedside tip they give:

Ask if the patient can walk at their own pace or keep up with a similar-age peer/partner. If not, think Class II (or worse).

4) Risk stratification at diagnosis: why, how, and which tools

Big principle: treatment choices are driven by risk, and the goal is to move patients to low-risk quickly.

ESC/ERS approach at diagnosis (as described):

Use a 3-strata model predicting 1-year mortality:
- Low: <5%
- Intermediate: 5–20%
- High: >20%

ESC/ERS risk assessment variables (10 domains discussed):

Clinical progression, signs of right heart failure, syncope
WHO FC
Biomarkers (NT-proBNP)
Exercise capacity (6MWD)
Hemodynamics
Imaging (echo; sometimes cardiac MRI)
CPET (peak VO₂; VE/VCO₂ slope)

They note: even if you don’t have everything, the calculator can still be useful with ≥3 variables.

REVEAL 2.0:

Builds on similar core variables but adds further patient context (demographics, renal function, BP, DLCO, etc.)

Case result: both tools put her in intermediate risk (ESC/ERS ~1.6; REVEAL 2.0 score 8), underscoring that mild symptoms can still equal meaningful mortality risk.

5) Treatment goals and follow-up philosophy

What they explicitly prioritize:

Help patients feel better, live longer, and stay out of the hospital
Use risk tools to communicate prognosis and to track improvement
Reassess frequently (they mention ~every 3 months early on) until low risk is achieved
“Time-to-low-risk” is an important treatment goal

Also emphasized:

The diagnosis is psychologically heavy; patients need clear counseling, reassurance about the plan, and connection to support groups.

6) Medication classes for the treatment of PAH

Nitric oxide–cGMP pathway

PDE5 inhibitors: sildenafil, tadalafil
Soluble guanylate cyclase stimulator: riociguat
Important safety point: don’t combine PDE5 inhibitors with riociguat (risk of significant hypotension/hemodynamic effects)

Endothelin receptor antagonists (ERAs)

“-sentan” drugs: bosentan (less used due to side effects/interactions), ambrisentan, macitentan
Teratogenicity emphasized
Hepatotoxicity that requires LFT monitoring
Can cause fluid retention and peripheral edema

Prostacyclin pathway

Prostacyclin analogs/agonists:
- Epoprostenol (potent; short half-life; IV administration)
- Treprostinil (IV/SubQ/oral/inhaled options)
- Selexipag (oral prostacyclin receptor agonist)

7) Sotatercept (post-guidelines)

They note sotatercept wasn’t in 2022 ESC/ERS but is now “a game changer” in practice:

Mechanism: ligand trap affecting TGF-β signaling / remodeling biology
Positioned as potentially more disease-modifying than pure vasodilators
Still evolving: where to place it earlier vs later in regimens is an active question in the field

8) How risk category maps to initial treatment intensity

General approach they outline:

High risk at diagnosis: parenteral prostacyclin (IV/SubQ) strongly favored, often aggressive early
Intermediate risk: at least dual oral therapy (typically PDE5i + ERA); escalate if not achieving low risk
Low risk: at least one oral agent; many still use dual oral depending on etiology/trajectory

For the case: intermediate-risk → start dual oral therapy (they mention tadalafil + ambrisentan as a typical choice), reassess in ~3 months; add a third agent (e.g., selexipag/prostacyclin pathway) if not low risk.

References and Further Reading

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.

Hoeper MM, Badesch DB, Ghofrani HA, Gibbs JSR, Gomberg-Maitland M, McLaughlin VV, Preston IR, Souza R, Waxman AB, Grünig E, Kopeć G, Meyer G, Olsson KM, Rosenkranz S, Xu Y, Miller B, Fowler M, Butler J, Koglin J, de Oliveira Pena J, Humbert M; STELLAR Trial Investigators. Phase 3 Trial of Sotatercept for Treatment of Pulmonary Arterial Hypertension. N Engl J Med. 2023 Apr 20;388(16):1478-1490. doi: 10.1056/NEJMoa2213558. Epub 2023 Mar 6. PMID: 36877098.

Ruopp NF, Cockrill BA. Diagnosis and Treatment of Pulmonary Arterial Hypertension: A Review. JAMA. 2022 Apr 12;327(14):1379-1391. doi: 10.1001/jama.2022.4402. Erratum in: JAMA. 2022 Sep 6;328(9):892. doi: 10.1001/jama.2022.13696. PMID: 35412560.

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Luke Hedrick, Dave Furfaro, and recurrent RFJC guest Robert Wharton are joined again today by Nicole Ng to discuss the FIBRONEER-IPF trial investigating Nerandomilast in patients with IPF. This trial was published in NEJM in 2025 and looked at Neradomilast vs placebo for treating patients with IPF, on or off background anti-fibrotic therapy. This agents is now FDA approved for pulmonary fibrosis, and understanding the trial results is essential for any pulmonary physician treating patients with IPF or progressive pulmonary fibrosis.

Article and Reference

Today’s episode discusses the FIBRONEER-IPF trial published in NEJM in 2025.

Richeldi L, Azuma A, Cottin V, Kreuter M, Maher TM, Martinez FJ, Oldham JM, Valenzuela C, Clerisme-Beaty E, Gordat M, Wachtlin D, Liu Y, Schlecker C, Stowasser S, Zoz DF, Wijsenbeek MS; FIBRONEER-IPF Trial Investigators. Nerandomilast in Patients with Idiopathic Pulmonary Fibrosis. N Engl J Med. 2025 Jun 12;392(22):2193-2202. doi: 10.1056/NEJMoa2414108. Epub 2025 May 18. PMID: 40387033.

https://www.nejm.org/doi/abs/10.1056/NEJMoa2414108

Meet Our Guests

Luke Hedrick is an Associate Editor at Pulm PEEPs and runs the Rapid Fire Journal Club Series. He is a senior PCCM fellow at Emory, and will be starting as a pulmonary attending at Duke University next year.

Robert Wharton is a recurring guest on Pulm PEEPs as a part of our Rapid Fire Journal Club Series. He completed his internal medicine residency at Mt. Sinai in New York City, and is currently a pulmonary and critical care fellow at Johns Hopkins.

Dr. Nicole Ng is an Assistant Profess of Medicine at Mount Sinai Hospital, and is the Associate Director of the Interstitial Lung Disease Program for the Mount Sinai National Jewish Health Respiratory Institute.

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Key Learning Points

Why this trial mattered

IPF therapies remain limited: nintedanib and pirfenidone slow (but do not stop) decline and often cause GI side effects.
Nerandomilast is a newer agent (a preferential PDE4B inhibitor) with antifibrotic + immunomodulatory effects.
Phase 2 data (NEJM 2022) looked very promising (suggesting near-“halt” of FVC decline), so this phase 3 trial was a big test of that signal.

Trial design essentials

Industry-sponsored, randomized, double-blind, placebo-controlled, large multinational study (332 sites, 36 countries).
Population: IPF diagnosed via guideline-aligned criteria with central imaging review and multidisciplinary diagnostic confirmation.
Intervention: nerandomilast 18 mg BID, 9 mg BID, or placebo; stratified by background antifibrotic use.
Primary endpoint: change in FVC at 52 weeks, analyzed with a mixed model for repeated measures.
Key secondary endpoint: time to first acute exacerbation, respiratory hospitalization, or death (composite).

Who was enrolled

Typical IPF trial demographics: ~80% male, mean age ~70, many former smokers.
Many were already on background therapy (~45% nintedanib, ~30–33% pirfenidone).
Notable exclusions included significant liver disease, advanced CKD, recent major cardiovascular events, and psychiatric risk (suicidality/severe depression), reflecting class concerns seen with other PDE4 inhibitors.

Efficacy: what the primary endpoint showed

Nerandomilast produced a statistically significant but modest reduction in annual FVC decline vs placebo (roughly 60–70 mL difference).
Importantly, it did not halt FVC decline the way the phase 2 data suggested; patients still progressed.

Important nuance: interaction with pirfenidone

Patients on pirfenidone had ~50% lower nerandomilast trough levels.
Clinically: 9 mg BID looked ineffective with pirfenidone, so 18 mg BID is needed if used together.
In those not on background therapy or on nintedanib, 9 mg and 18 mg looked similar—suggesting the apparent “dose-response” might be partly driven by the pirfenidone drug interaction

Secondary and patient-centered outcomes were neutral

No demonstrated benefit in the composite outcome (exacerbation/resp hospitalization/death) or its components.
Quality of life measures were neutral and declined in all groups, emphasizing that slowing FVC alone may not translate into felt improvement without a disease-reversing therapy.
The discussants noted this may reflect limited power/duration for these outcomes and mentioned signals from other datasets/pooling that might suggest mortality benefit—but in this specific trial, the key secondary endpoint was not positive.

Safety and tolerability

Diarrhea was the main adverse event:
- Higher overall with the 18 mg dose, and highest when combined with nintedanib (up to ~62%).
- Mostly mild/manageable; discontinuation due to diarrhea was relatively uncommon (but higher in those on nintedanib).
Reassuringly, there was no signal for increased depression/suicidality/vasculitis despite psychiatric exclusions and theoretical class risk.

How to interpret “modest FVC benefit” clinically

The group framed nerandomilast as another tool that adds incremental slowing of progression.
They emphasized that comparing absolute FVC differences across trials (ASCEND/INPULSIS vs this trial) is tricky because populations and “natural history” in placebo arms have changed over time (earlier diagnosis, improved supportive care, etc.).
They highlighted channeling bias: patients already on antifibrotics may be sicker (longer disease duration, lower PFTs, more oxygen), complicating subgroup comparisons.

Practical takeaways for real-world use

All three antifibrotics are “fair game”; choice should be shared decision-making based on goals, tolerability, dosing preferences, and logistics.
Reasons they favored nerandomilast in practice:
- No routine lab monitoring (major convenience advantage vs traditional antifibrotics).
- Generally better GI tolerability than nintedanib.
- BID dosing (vs pirfenidone TID).
Approach to combination therapy:
- They generally favor add-on rather than immediate combination to reduce confusion about side effects—while acknowledging it may slow reaching “maximal therapy.”
Dosing guidance emphasized:
- Start 18 mg BID for IPF, especially if combined with pirfenidone (since dose reduction may make it ineffective).
- 9 mg BID may be considered if dose reduction is needed and the patient is not on pirfenidone (e.g., monotherapy or with nintedanib).

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This week’s Pulm PEEPs Pearls episode is a focused discussion between Furf and Monty about non-pharmacologic techniques for airway clearance in the non-Cystic Fibrosis bronchiectasis population. This is a focused, high-yield discussion of the key points about airway clearance, including practical tips and a discussion of the evidence.

This episode was prepared in conjunction with George Doumat MD. Goerge is an internal medicine resident at UT Southwestern and joined us for a Pulm PEEPs – BMJ Thorax journal club episode. He is now acting as a Pulm PEEPs Editor for the Pulm PEEPs Pearls series.

Key Learning Points

1) Why airway clearance matters in non-CF bronchiectasis

Non-CF bronchiectasis is defined by irreversible bronchial dilation with impaired mucociliary clearance, leading to mucus retention.
Retained sputum drives the classic vicious cycle: mucus → infection → neutrophilic inflammation → airway damage → worse clearance.
Airway clearance techniques (ACTs) are meant to interrupt this cycle, primarily by improving mucus mobilization and symptom control.

2) What ACTs are trying to achieve clinically

Main benefits are:
- More effective sputum clearance
- Reduced cough/dyspnea burden
- Improved activity tolerance and quality of life
Effects on spirometry are usually small.
Exacerbation reduction is possible, but evidence is mixed—some longer-term data suggest benefit for specific techniques.

3) The main ACT “families” and when to use them

Breathing-based techniques (device-free, flexible)

ACBT (Active Cycle of Breathing Technique): breath control → deep breaths with holds → huffing.
- Pros: portable, adaptable, good first-line option.
- Key requirement: teaching/coaching to get technique right.
Autogenic drainage: controlled breathing at different lung volumes to move mucus from peripheral → central airways.
- Pros: no device, can work well once learned.
- Cons: more technically demanding, needs training and practice.

PEP / Oscillatory PEP (stents airways + “vibrates” mucus loose)

PEP: back-pressure helps prevent small airway collapse during exhalation; often paired with huff/cough.
Oscillatory PEP (Flutter/Acapella/Aerobika): adds oscillation that many patients find easy and satisfying to use.
- Good fit for: people who benefit from airway stenting, want something portable, and prefer a device.

Mechanical/manual techniques (help when patient can’t self-clear well)

HFCWO (“the vest”): external chest wall oscillation; helpful for high sputum volumes, dexterity limits, or difficulty coordinating breathing maneuvers.
Postural drainage/percussion/vibration: caregiver/therapist-assisted options; still useful but consider:
- GERD/reflux risk with certain positions
- Hemoptysis risk with vigorous techniques

4) How to choose the “right” technique (the practical framework)

There is no one-size-fits-all. Match the tool to the patient:

Sputum burden (volume/viscosity)
Strength, coordination, cognition, dexterity
Comorbidities (GERD, hemoptysis history, severe obstruction/airway collapse)
Lifestyle + portability (what they’ll actually do)
Cost/access and availability of respiratory therapy/physio support

A key mindset from the script: this is not a lifetime contract—reassess and adjust over time with shared decision-making.

5) Evidence takeaways (what improves, what doesn’t)

ACTs reliably improve sputum expectoration and often symptoms/QoL.
QoL/cough scores (e.g., SGRQ, LCQ) tend to improve modestly, particularly with oscillatory PEP and some vest studies.
Lung function: typically minimal change; occasional short-term FEV₁ benefit is reported in some vest trials.
Exacerbations: mixed overall; the script highlights a longer-term RCT of ELTGOL showing fewer exacerbations at 12 months vs placebo exercises.
Safety: generally excellent; main cautions are hemoptysis and reflux (depending on technique/positioning).

6) Special population pearls

Hemoptysis / fragile airways: start with gentle breathing-based ACTs (ACBT, controlled huffing); avoid overly vigorous oscillatory/manual methods if concerned.
Severe obstruction or early airway collapse: PEP/oscillatory PEP can help by keeping small airways open on exhalation.
Mobility/coordination barriers: consider HFCWO vest or simple oscillatory PEP devices to enable daily adherence.
During exacerbations: keep it simple—1–2 reliable techniques, prioritize daily consistency, and re-check technique.

7) The “real” bottom line

Start with simple, self-manageable options (often ACBT ± PEP).
The “best” ACT is the one the patient will do consistently.
Reassess technique and fit over time; education and demonstration are part of the therapy.

References and Further Reading

Lee AL et al., “Airway clearance techniques for bronchiectasis,” Cochrane Database Syst Rev. 2015; PMC7175838. PMID: 26591003.

Athanazio RA et al., “Airway Clearance Techniques in Bronchiectasis,” Front Med (Lausanne). 2020; PMC7674976. PMID: 33251032.

Iacono R et al., “Mucociliary clearance techniques for treating non-cystic fibrosis bronchiectasis,” Eur Rev Med Pharmacol Sci. 2015; PMID: 26078380.

Polverino E et al., “European Respiratory Society statement on airway clearance techniques in bronchiectasis,” Eur Respir J. 2023; PMID: 37142337.

Doumat G, Aksamit TR, Kanj AN. Bronchiectasis: A clinical review of inflammation. Respir Med. 2025 Aug;244:108179. doi: 10.1016/j.rmed.2025.108179. Epub 2025 May 25. PMID: 40425105.

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Today, Dave Furfaro, Luke Hedrick, and Robert Wharton discuss the PREDMETH trial published in The New England Journal of Medicine in 2025. This was a non-inferiority trial comparing prednisone to methotrexate for upfront therapy in treatment-naive sarcoidosis patients. Listen in for a break down of the trial, analysis, and clinically applicable pearls.

Article and Reference

Todays’ episode discusses the PREDMETH trial published in NEJM in 2025.

Kahlmann V, Janssen Bonás M, Moor CC, Grutters JC, Mostard RLM, van Rijswijk HNAJ, van der Maten J, Marges ER, Moonen LAA, Overbeek MJ, Koopman B, Loth DW, Nossent EJ, Wagenaar M, Kramer H, Wielders PLML, Bonta PI, Walen S, Bogaarts BAHA, Kerstens R, Overgaauw M, Veltkamp M, Wijsenbeek MS; PREDMETH Collaborators. First-Line Treatment of Pulmonary Sarcoidosis with Prednisone or Methotrexate. N Engl J Med. 2025 Jul 17;393(3):231-242. doi: 10.1056/NEJMoa2501443. Epub 2025 May 18. PMID: 40387020.

https://www.nejm.org/doi/full/10.1056/NEJMoa2501443

Meet Our Hosts

Robert Wharton is a recurring guest on Pulm PEEPs as a part of our Rapid Fire Journal Club Series. He completed his internal medicine residency at Mt. Sinai in New York City, and is currently a first year pulmonary and critical care fellow at Johns Hopkins.

Key Learning Points

Clinical context

Prednisone remains the traditional first-line treatment for pulmonary sarcoidosis when treatment is indicated, with evidence for short-term improvements in symptoms, radiographic findings, and pulmonary function—but with substantial, familiar steroid toxicities (weight gain, insomnia, HTN/DM, infection risk, etc.).
Despite widespread use, glucocorticoids haven’t been robustly tested head-to-head against many alternatives as initial therapy, and evidence for preventing long-term decline (especially in severe disease) is limited.
Immunosuppressants (like methotrexate) are often used as steroid-sparing agents, but guideline recommendations are generally conditional/low-quality evidence, and practice varies.

Why PREDMETH matters

It addresses a real-world question: Can methotrexate be an initial alternative to prednisone in pulmonary sarcoidosis, rather than being reserved only for steroid-sparing later?
It also probes a common clinical belief: MTX has slower onset than prednisone (often assumed, not well-proven).

Trial design (what to know)

Open-label, randomized, noninferiority trial across 17 hospitals in the Netherlands.
Included patients with pulmonary sarcoidosis who had a clear pulmonary indication to start systemic therapy (moderate/severe symptoms plus objective risk features like reduced FVC/DLCO or documented decline, plus parenchymal abnormalities).
Excluded: non–treatment-naïve patients and those whose primary indication was extrapulmonary disease.
Treat-to-tolerability with escalation: both drugs started low and were slowly increased; switch/add-on allowed for inadequate efficacy or unacceptable side effects.
Primary endpoint: change in FVC (with the usual caveat that FVC is “objective-ish,” but effort-dependent and not always patient-centered).
Noninferiority margin: 5% FVC, justified as within biologic/measurement variation and “not clinically relevant.”
Outcomes assessed at weeks 4, 16, 24; powered for ~110 patients to detect the NI margin.

Patient population (who this applies to)

Mostly middle-aged (~40s) with mild-to-moderate physiologic impairment on average (FVC ~77% predicted; DLCO ~70% predicted).
Netherlands-based cohort with limited Black representation (~7%), which matters for generalizability.
Would have been helpful to know more about comorbidities (e.g., diabetes), which can strongly influence prednisone risk.

Main findings (what happened)

Methotrexate was noninferior to prednisone at week 24 for FVC:
- Between-group difference in least-squares mean change at week 24: −1.17 percentage points (favoring prednisone) with CI −4.27 to +1.93, staying within the 5% NI margin.
Timing mattered:
- Prednisone showed earlier benefit (notably by week 4) in FVC and across quality-of-life measures.
- By week 24, those early differences largely washed out—possibly because MTX “catches up,” and/or because crossover increased over time.
- In their reporting, MTX didn’t meet noninferiority for FVC until week 24, supporting the practical message that prednisone works faster.

Crossover and analysis nuance (important for interpretation)

Crossover was fairly high, which complicates noninferiority interpretation:
- MTX arm: some switched to prednisone for adverse events and others had prednisone added for disease progression/persistent symptoms.
- Prednisone arm: some had MTX added.
In noninferiority trials, heavy crossover can bias intention-to-treat analyses toward finding “no difference” (making noninferiority easier to claim). Per-protocol analyses avoid some of that but introduce other biases. They reported both.

Safety signals (what to remember clinically)

Adverse events were very common in both arms (almost everyone), mostly mild.
Side-effect patterns fit expectations:
- Prednisone: more insomnia (and classic steroid issues).
- MTX: more headache/cough/rash, and notably liver enzyme elevations (about 1 in 4), with a small number discontinuing.
Serious adverse events were rare; numbers were too small to confidently separate “signal vs noise,” but overall known risk profiles apply.

Limitations (why you shouldn’t over-read it)

Open-label design, and FVC—while objective-ish—is still effort-dependent and can be influenced by expectation/behavior.
Small trial, limiting subgroup conclusions (e.g., severity strata, different phenotypes).
Generalizability issues (Netherlands demographics; US populations have higher rates of obesity/metabolic syndrome, which may tilt the steroid risk-benefit equation).
Crossover reduces precision and interpretability of between-group differences over time.

Practice implications (the “so what”)

For many patients with pulmonary sarcoidosis needing systemic therapy, MTX is a reasonable initial alternative to prednisone when thinking long-term tolerability and steroid avoidance.
Prednisone likely provides faster symptom/QoL relief in the first weeks—so it may be preferable when rapid improvement is important.
The trial strengthens the case for a patient-centered discussion: short-term relief vs side-effect tradeoffs, and the possibility of early combination therapy in more severe cases (suggested, not proven).

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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.

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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

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Furf and Monty are back today with another Pulm PEEPs Pearls episode, and discussing the use of methylene blue for patients with septic shock. They review the clinical scenarios when this comes up, the mechanism, some key data, and some take aways, all in 15 minutes! Let us know any other topics you’d like covered on the show and make sure to like, give us 5 stars, and subscribe wherever you’re listening to this podcast.

Key Learning Points

Clinical context: when does methylene blue even come up?
This is not a first-line sepsis drug.
It’s considered in catecholamine-refractory vasoplegic septic shock, typically when:
- Norepinephrine is at high dose
- Vasopressin is on board
- Often a 3rd or 4th vasopressor is being used (e.g., phenylephrine, angiotensin II)
The phenotype is strongly vasodilatory/vasoplegic (warm, distributive shock) rather than primarily cardiogenic.
Mechanism of action (why it might help)
Methylene blue:
- Inhibits inducible nitric oxide synthase and guanylate cyclase.
- Blunts excess nitric oxide and cyclic GMP–mediated vasodilation, which are key in vasoplegic sepsis.
Practical translation:
- It restores vascular tone and can make the vasculature more responsive to catecholamines.
It’s also used in post-CPB vasoplegia (e.g., after cardiac surgery, especially in patients on ACE inhibitors) and has migrated from that world into ICU sepsis practice.
Typical dosing strategy (as described in the episode)
Common approach:
- 1–3 mg/kg IV bolus, then
- Reassess hemodynamics (MAP, dynamic perfusion markers).
- If there’s a response, consider a continuous infusion or repeat bolus.
Key nuance: unlike other pressors that start as drips, methylene blue is often trialed as a bolus first to see if it’s doing anything.
What does the evidence suggest?

Most data are from small, single-center, heterogeneous studies, so evidence quality is low. Meta-analyses and systematic reviews (through ~2024–25) suggest:

Hemodynamics
- Can increase MAP (roughly 1–10 mmHg across studies).
- May shorten total vasopressor duration (one meta-analysis ~30 hours less, though this is not definitive).
Secondary physiologic effects
- Some small improvements in PaO₂/FiO₂ (P/F) ratio in certain studies.
Clinical outcomes
- Possible reduction in hospital length of stay (≈ up to 2 days in some pooled analyses).
- Some signal toward lower short-term mortality, but:
  - Studies are small
  - Heterogeneous
  - Evidence is very low certainty
Bottom line:
- There’s a repeatable signal that methylene blue:
  - Raises MAP
  - Helps reduce catecholamine requirements
- But hard clinical outcomes (mortality, LOS, ventilator days) remain uncertain.
Safety profile & important adverse effects

Things to watch for:

Methemoglobinemia
Serotonin syndrome
- Especially in patients on SSRIs, though in life-threatening refractory shock the hosts still lean toward using it with caution.
Pulse oximeter artifact
- Can distort SpO₂ readings.
Urine discoloration
- Blue/green urine—benign but striking.

Notably:

Methylene blue is both a treatment for and a potential cause of methemoglobinemia, depending on context and dosing.
Guidelines & where it fits in practice
Surviving Sepsis Campaign 2021:
- Does not recommend methylene blue for routine use in septic shock.
No major critical care society includes it in standard septic shock bundles or protocols.
The hosts frame methylene blue as:
- A rescue therapy, not guideline therapy.
- Something to consider only in refractory vasoplegic shock, ideally with:
  - Multidisciplinary discussion (intensivist, pharmacist, etc.).
  - Clear documentation that this is off-guideline, salvage use.
Practical bedside framing (“2 a.m. in the ICU”)

They emphasize three pillars of practice:

Physiology – mechanism makes sense (NO / cGMP / vasodilation).
Empiric evidence – small studies and meta-analyses show a signal but low-quality data.
Bedside reality – at 2 a.m., with a patient in multi-pressor, refractory vasoplegic shock, you sometimes reach for imperfect tools.

So, the practical take:

You should NOT:
- Use methylene blue early.
- Treat it as part of standard sepsis care.
You may consider it when:
- Shock is clearly vasoplegic and refractory.
- Norepi + vasopressin + at least one more vasopressor are maxed.
- Team agrees this is salvage therapy and understands the limited evidence and side effects.

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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.

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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 themes

Built 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 asthma- Obesity 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 therapy- Consider 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 biologics- Don’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):
1. 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 taper
Targets while stepping down: “normal” lung function when feasible, minimal/no day or night symptoms, full activity, no exacerbations.

When patients don’t respond to biologics- Re-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 pearls

Use 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.

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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.

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After a brief hiatus, we are excited to be back today with another Fellows’ Case Files! Today we’re virtually visiting the University of Kansas Medical Center (KUMC) to hear about a fascinating pulmonary presentation. There are some fantastic case images and key learning points. Take a listen and see if you can make the diagnosis along with us. As always, let us know your thoughts and definitely reach out if you have an interesting case you’d like to share.

Meet Our Guests

Dr. Vishwajit Hegde completed his internal medicine residency at University of Kansas Medical Center where he stayed for fellowship and is currently a second year Pulmonary and Critical Care medicine fellow.

Dr. Sahil Pandya is an Associate Professor of Medicine and Program Director of the PCCM Fellowship at KUMC.

Case Presentation

Imaging

Infographic

Key Learning Points

1) Initial frame & diagnostic mindset

Young (26), subacute → chronic dyspnea/cough with diffuse pulmonary nodules; avoid premature closure on TB.
Use a Bayesian approach: combine pre-test probability (epidemiology, exposures, tempo) with targeted tests to decide next steps.
Always confirm TB when possible (micro/path + resistance testing); empiric RIPE may be reasonable but shouldn’t replace tissue when stakes are high.

2) Imaging pearls—nodular pattern recognition

Ask three things: craniocaudal distribution, symmetry, central vs peripheral.
Centrilobular (spares pleura/fissures): airway-centered (e.g., NTM, bronchiolitis, tree-in-bud).
Perilymphatic (tracks fissures/pleura & septa): sarcoid, lymphangitic spread.
Random/diffuse (involves pleural surfaces): hematogenous spread → think miliary TB, disseminated fungal, septic emboli, metastatic disease.
Interval change matters: new cavitation and confluence can upweight infection or aggressive malignancy.

3) Neuro findings—ring-enhancing lesions

Differential: septic emboli/abscess, nocardia, fungal, TB, parasites, metastases, vasculitis, sarcoid.
Partner with neuroradiology for pattern nuances; treat seizures but keep searching for the unifying diagnosis.

4) Lab/serology strategy

Broad infectious workup (AFB × multiple, fungal serologies), HIV and basic immune screen.
Negative/indeterminate tests don’t end the search—revisit history (e.g., Ohio travel → histo/blasto risk).

5) “Tissue is the issue”—choosing the procedure

For diffuse nodules with mediastinal adenopathy and stable patient: EBUS-TBNA + BAL, consider transbronchial or cryobiopsy.
Cryobiopsy pros: larger, less crush artifact, better for molecular testing; cons: ↑ bleeding/pneumothorax vs forceps.
VATS still best for certain ILD questions or if less invasive routes are non-diagnostic—but weigh patient preference and stage/likelihood of yield.

6) ROSE (rapid on-site evaluation) in bronchoscopy

Confirms adequacy in real time, steers you away from necrotic zones, helps decide when you’ve got enough for molecular studies, and when to pivot sites—reduces anesthesia time and repeat procedures.

7) Final diagnosis & management

Path: TTF-1+, CK7+, napsin A → pulmonary adenocarcinoma with a fusion driver.
Therapy: Targeted TKI (crizotinib) → dramatic radiographic response of miliary lung disease and CNS lesions.
Teaching point: even “miliary TB-like” lungs + CNS lesions in a 20-something can be driver-positive lung cancer—don’t let age or pattern blind you.

References and Further Reading

Desai, S., Devaraj, A., Lynch, D., & Sverzellati, N. (2020). Webb, Müller and Naidich’s high-resolution CT of the lung (6th ed.). Lippincott Williams & Wilkins.
Rajeswaran, G., Becker, J. L., Michailidis, C., Pozniak, A. L., & Padley, S. P. G. (2006). The radiology of IRIS (immune reconstitution inflammatory syndrome) in patients with mycobacterial tuberculosis and HIV co-infection: appearances in 11 patients. Clinical radiology, 61(10), 833-843
Poletti, V., Ravaglia, C., & Tomassetti, S. (2016). Transbronchial cryobiopsy in diffuse parenchymal lung diseases. Current opinion in pulmonary medicine, 22(3), 289-296.
Norman, G. R., Monteiro, S. D., Sherbino, J., Ilgen, J. S., Schmidt, H. G., & Mamede, S. (2017). The causes of errors in clinical reasoning: cognitive biases, knowledge deficits, and dual process thinking. Academic Medicine, 92(1), 23-30.

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We are so excited to be launching a new series here at Pulm PEEPs! We’ll be talking about high yield topics in 15 minutes or less. In this series, Furf and Monty will tackle core points and provide an overview, key points, and further reading. We’re starting with a key point review of Immune Checkpoint Inhibitor Pneumonitis. Let us know if there are other topics you want to hear about!

Key Learning Points

Epidemiology & Pathophysiology
- Increasingly common as immunotherapy use grows in oncology.
- Caused by immune activation from PD-1, PD-L1, or CTLA-4 inhibitors.
- Mechanisms:
  1. Overactive T cells
  2. Autoantibody production
  3. Cytokine-mediated inflammation (e.g., ↑IL-1, ↑IL-6)
Clinical Suspicion & Diagnosis
- Any new respiratory symptoms in a patient currently or previously on ICI → consider ICI pneumonitis.
- CT findings are variable: can mimic organizing pneumonia, NSIP, ARDS, or diffuse ground glass opacities. Imaging pattern does not determine severity grade.
- Diagnosis is of exclusion — infection and malignancy progression must be ruled out first.
- Workup:
  - Broad infectious evaluation (cultures, viral panel, fungal markers).
  - Early bronchoscopy with BAL if feasible — typically lymphocyte-predominant in ICI pneumonitis.
  - Screen for TB and hepatitis early (in case infliximab is needed).
Severity Grading (Symptom- & O₂-based, not imaging-based)
- Grade 1: Asymptomatic → monitor, may hold ICI.
- Grade 2: Symptomatic but not hypoxic → prednisone 1 mg/kg/day PO.
- Grade 3–4: Hypoxemia or ICU-level care → methylprednisolone 1–2 mg/kg/day IV. Usually hold or permanently stop ICI.
Steroid Management
- Typical taper: over 6 weeks for grade ≥3. - Week 1: 1–2 mg/kg/day - Gradual step-down to 0.25 mg/kg/day by week 5, then stop week 6.
- Chronic/recurrent cases may need slower tapers over months.
- Add GI prophylaxis and PJP prophylaxis during prolonged steroid use.
If Steroids Fail (no improvement after 48–72 hrs)
- Consider adding: - IVIG (2 g/kg over 5 days) - Infliximab (TNF-α inhibitor — requires TB/hepatitis screening) - Mycophenolate mofetil (1–1.5 g/day BID or TID, start at effective dose quickly)
- IVIG may have lower mortality in some series but comes with risks (volume overload, thrombosis, infusion reactions).
Emerging Therapies
- JAK inhibitors are under investigation as possible future options.
Multidisciplinary Care
- ICU management is a team sport — coordinate with oncology, critical care, infectious disease, and pharmacy.

Infographic

References and Further Reading

Managing Immune Checkpoint Inhibitor Pneumonitis in the ICU. Montemayor, Kristina et al.CHEST Critical Care, Volume 3, Issue 1, 100126
Lavalle S, Masiello E, Valerio MR, Aliprandi A, Scandurra G, Gebbia V, Sambataro D. Immune checkpoint inhibitor therapy‑related pneumonitis: How, when and why to diagnose and manage (Review). Exp Ther Med. 2024 Jul 30;28(4):381. doi: 10.3892/etm.2024.12670. PMID: 39113908; PMCID: PMC11304171.
Delaunay M, Prévot G, Collot S, Guilleminault L, Didier A, Mazières J. Management of pulmonary toxicity associated with immune checkpoint inhibitors. Eur Respir Rev. 2019 Nov 6;28(154):190012. doi: 10.1183/16000617.0012-2019. PMID: 31694838; PMCID: PMC9488507.

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Today we’re talking about a topic that is relevant for all critical care physicians but under-examined: ICU Acquired Weakness. We are joined by two excellent guests to walk through a case and discuss the diagnosis, pathophysiology, prevention, and treatment of ICU Acquired Weakness. Check out our associated infographics and key learning points below.

Meet Our Guests

Jim Devanney is a Physiatrist who just completed a neurocritical care fellowship at BIDMC. He is transitioning to a clinical associate position at University Health Network – University of Toronto where he will be working as a PM&R consultant within the ICU.

Kalaila Pais is a third year internal medicine resident at BIDMC, interested in pulmonary and critical care and medical education and is returning for her third Pulm PEEPs episode.

Key Learning Points

Definition & Clinical Presentation

ICU-AW refers to new-onset, generalized muscle weakness that arises during critical illness, not explained by other causes.It typically presents as:
- Symmetric, proximal > distal weaknessRespiratory muscle involvementPreserved cranial nerve functionNo sensory deficits in myopathy (sensory loss points toward neuropathy) Differential Diagnosis Using Neuroanatomical ApproachAn anatomical approach (central → peripheral) helps localize the etiology weakness- CNS: trauma, stroke, encephalitis, seizuresAnterior horn cells: viral myelitis, motor neuron diseasePeripheral nerves: Guillain-Barré, vasculitis, critical illness polyneuropathy (CIP)Neuromuscular junction: myasthenia gravis, botulism, Lamber EatonMuscle: rhabdomyolysis, inflammatory or drug-induced myopathies, critical illness myopathy (CIM) Subtypes of ICU-AW- Critical Illness Myopathy (CIM):
- Muscle dysfunctionEarly onset (within 48 hrs)Sensation intactproximal > distal weakness
Critical Illness Polyneuropathy (CIP):
- Nerve involvementDistal > proximal weakness, sensory deficits
Critical Illness Polyneuromyopathy (CIPNM): Combination of both

Diagnosis

Medical Research Council Score (MRC-SS):
- Score < 48: ICU-AW
- Score < 36: severe ICU-AW
Handgrip dynamometry: <11 kg (men), <7 kg (women)
Electrophysiology: EMG/NCS to distinguish CIM vs CIP
Muscle ultrasound: bedside monitoring
MRI/CT/Muscle biopsy: rarely used due to practical limitation

Risk Factors

Modifiable:

Hyper/hypoglycemia
Electrolyte derangement
Parenteral nutrition
Immobility
Medications (steroids, NM blockers, sedatives, aminoglycosides)

Non-modifiable:

Age, female sex, comorbidities
Severity of illness, prolonged ventilation
Sepsis, multi-organ failure

Management & Prevention

Prevention is key:
- Early treatment of sepsis and inflammation
- Glycemic control
- Early enteral nutrition
- Minimize sedation (A-F bundle)
- Early mobilization and physical therapy
NMES (neuromuscular electrical stimulation): emerging therapy, needs more evidence

Outcomes

Short-term: increased LOS, ventilation duration, mortality
Long-term: decreased function, discharge to rehab, prolonged recovery

Final Takeaways

Prevention is crucial — start interventions early.
Systematic approach to ICU weakness helps rule out dangerous mimics.
ICU-AW is common but often under-recognized — awareness and early rehab can significantly impact recovery.

Infographics

References and Further Reading

Clinical Practice Guidelines for the Prevention and Management of Pain, Agitation/Sedation, Delirium, Immobility, and Sleep Disruption in Adult Patients in the ICU. Devlin JW, Skrobik Y, Gélinas C, et al. Critical Care Medicine. 2018;46(9):e825-e873. doi:10.1097/CCM.0000000000003299.

The ABCDEF Bundle: Science and Philosophy of How ICU Liberation Serves Patients and Families. Ely EW. Critical Care Medicine. 2017;45(2):321-330. doi:10.1097/CCM.0000000000002175.

Caring for Critically Ill Patients With the ABCDEF Bundle: Results of the ICU Liberation Collaborative in Over 15,000 Adults. Pun BT, Balas MC, Barnes-Daly MA, et al. Critical Care Medicine. 2019;47(1):3-14. doi:10.1097/CCM.0000000000003482.

Delirium in Critical Illness: Clinical Manifestations, Outcomes, and Management. Stollings JL, Kotfis K, Chanques G, et al. Intensive Care Medicine. 2021;47(10):1089-1103. doi:10.1007/s00134-021-06503-1.

ICU-acquired Weakness. Vanhorebeek I, Latronico N, Van den Berghe G. Intensive Care Medicine. 2020;46(4):637-653. doi:10.1007/s00134-020-05944-4.

Clinical Review: Intensive Care Unit Acquired Weakness. Hermans G, Van den Berghe G. Critical Care (London, England). 2015;19:274. doi:10.1186/s13054-015-0993-7.

Best Practices for Conducting Interprofessional Team Rounds to Facilitate Performance of the ICU Liberation (ABCDEF) Bundle. Stollings JL, Devlin JW, Lin JC, et al. Critical Care Medicine. 2020;48(4):562-570. doi:10.1097/CCM.0000000000004197.

ABCDE and ABCDEF Care Bundles: A Systematic Review of the Implementation Process in Intensive Care Units. Moraes FDS, Marengo LL, Moura MDG, et al. Medicine. 2022;101(25):e29499. doi:10.1097/MD.0000000000029499.

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Hi Pulm PEEPs! Today we have a special episode for you. Monty and Furf were invited on the Core IM Podcast to talk about the work up and management of pleural effusions. This is a great overview and we hope you enjoy listening as much as we did recording. If you want a deeper dive into pleural effusions check out our prior series:

Top Consults Series: Approach to Pleural Effusions

Top Consults: Approach to Parapneumonic Effusions

Top Consults: Malignant Pleural Effusions

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Today, we’re virtually visiting the University of Virginia for another Fellows’ Case Files. This is a fantastic case that covers ARDS, the infectious work up of an immunosuppressed patient, and the evaluation of undifferentiated shock. Please let us know what you think of the episode and always feel free to reach out with interesting cases!

Meet Our Guests

John Popovich completed his residency training and chief year at UVA and has stayed on there for his pulmonary and critical care fellowship.

Tim Scialla is an associate professor of medicine at UVA. He completed his residency and fellowship at Johns Hopkins Hospital where he was also an ACS. His clinical and research focuses are advanced airways disease. He is also the program director of the PCCM fellowship.

Matt Freedman completed his residency training at Virginia Commonwealth University and is currently a second year fellow at University of Virginia.

Case Presentation

Patient: 52-year-old male with psoriasis, HIV/AIDS (CD4 count: 71), presenting with progressive shortness of breath, fever, non-productive cough, and weight loss.

Vital signs: Febrile (103°F), tachycardic (HR 110), hypoxemic on 6L O₂ (SpO₂ 90–92%).

Exam: Diffuse crackles, ill-appearing.

Imaging: CXR and CT showed bilateral upper lobe infiltrates, ground-glass opacities, septal thickening, and peripheral cystic changes.

Infographics

POCUS algorithms for investigating shockShock physiology:

Key Learning Points

Diagnostic Reasoning in Immunocompromised Hosts

Framework: Anchor the differential based on type of immunosuppression.
- HIV/AIDS → T-cell dysfunction, affecting susceptibility to PCP, TB, CMV, fungi (e.g. histo/blasto), and common CAP organisms.
PCP considerations:
- PCP can occur despite prophylaxis (e.g. Bactrim), especially if adherence or resistance issues exist.
- Classic symptoms in AIDS: acute, febrile, hypoxemic respiratory failure.

Use of Serum Markers and Imaging

LDH: Elevated in PCP, but non-specific. High negative predictive value when normal.
1,3-β-D-glucan: Elevated in PCP and other fungal infections. Very sensitive for PCP (up to 95%).
Imaging: Ground-glass opacities with cystic changes support PCP diagnosis.

Role of Bronchoscopy and Diagnostic Yield

BAL studies to obtain:
- DFA for PCP (rapid, high specificity, lower sensitivity)
- PCR for PCP (higher sensitivity, slower turnaround)
- Cultures: bacterial, fungal, mycobacterial
- Cytology, galactomannan, histo/blasto urine antigens
Bronch Risk-Benefit:
- Can change management in 40–60% of cases.
- Complication rate: ~10–15%, most often hypoxemia.
- Heuristic for pre-bronch ABG on non-rebreather:
  - PaO₂ >150 → likely safe
  - 100–150 → ~25% risk of intubation
  - <100 → high risk of decompensation

Steroids in PCP and Severe CAP

Steroids indicated in PCP with significant hypoxemia (PaO₂ <70 mmHg).
With new CAP guidelines (Cape Cod trial), steroids may also be considered in severe bacterial CAP.

Shock Evaluation in ICU

Framework: Simplify into likely causes — distributive most common, but rule out cardiogenic, obstructive, hypovolemic.
Physical exam + POCUS essential early.
- POCUS: cardiac views, IVC, lung US, abdominal free fluid.
- Low EF doesn’t exclude distributive shock.
PA catheter (Swan) utility:
- Useful when physiology unclear or when tracking response to therapy is critical.
- Swan data in this patient: low CVP and wedge, high SVR → distributive shock, not cardiogenic despite low EF.

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Today is our third episode in our collaborative series with BMJ Thorax. 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. This week’s episode covers four articles related to obstructive sleep apnea therapies, and the use of non-invasive ventilation and high flow nasal cannula for intubation and COPD exacerbations.

Meet Our Guests

Natalie McLeod is a resident in respiratory medicine and is currently doing a clinical fellowship in sleep and ventilation at Oxford University Hospitals.

Journal Club Papers

Journal club article from Thorax
Effect of CPAP therapy on blood pressure in patients with obstructive sleep apnoea: a worldwide individual patient data meta-analysis
Hypoglossal nerve stimulation for obstructive sleep apnea in adults: An updated systematic review and meta-analysis
Noninvasive Ventilation for Preoxygenation during Emergency Intubation
Nasal high flow or noninvasive ventilation? navigating hypercapnic COPD exacerbation treatment: A randomized noninferiority clinical trial

To submit a journal club article of your own to Thorax, you can contact Chris directly – christopher.turnbull@ouh.nhs.uk

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We’re back with another Rapid Fire Journal Club. Luke Hedrick and Dave Furfaro discuss the NAVIGATOR trial published in NEJM in 2021 evaluating tezepelumab for adults with asthma.

Article and Reference

We are talking today about the NAVIGATOR trial evaluating the use of tezepelumab in adults with asthma.

Menzies-Gow A, Corren J, Bourdin A, Chupp G, Israel E, Wechsler ME, Brightling CE, Griffiths JM, Hellqvist Å, Bowen K, Kaur P, Almqvist G, Ponnarambil S, Colice G. Tezepelumab in Adults and Adolescents with Severe, Uncontrolled Asthma. N Engl J Med. 2021 May 13;384(19):1800-1809. doi: 10.1056/NEJMoa2034975. PMID: 33979488.

https://www.nejm.org/doi/full/10.1056/NEJMoa2034975

Key Learning Points

Background & Rationale

Asthma biologics already exist, targeting IgE and type 2 cytokines (IL-4, IL-5, IL-13), but there’s an unmet need for patients with non-allergic or non-eosinophilic phenotypes.
Tezepelumab is a monoclonal antibody targeting TSLP (thymic stromal lymphopoietin), an upstream mediator of both T2 and non-T2 inflammation, offering a potentially broader therapeutic effect.

Study Design (Navigator Trial)

Phase 3, double-blind, placebo-controlled RCT
Conducted in 18 countries from 2017-2020
N = 1,061 patients, aged 12-80 with moderate to severe asthma
All were on medium/high-dose ICS + controller med
Required ≥2 exacerbations in prior year

Outcomes

Primary Outcome: Annualized rate of asthma exacerbations (events per patient-year)
Secondary Outcomes:
- Change in pre-bronchodilator FEV₁
- Symptoms & quality of life (with predefined MCIDs)
- Subgroup analyses by eosinophil count, FeNO, and perennial allergen sensitivity

Key Inclusion/Exclusion

Inclusion: 12-80 years, guideline-based therapy, ≥2 exacerbations
Exclusion: recent biologic use, mild/asymptomatic asthma, no reversibility on spirometry

Patient Population (Table 1 Summary)

Middle-aged, predominantly white, female
Poorly controlled severe asthma despite high-intensity therapy
~75% on high-dose ICS, ~10% on oral steroids
~40% had normal FeNO
~60% had eosinophils <300
Median IgE ~195

Results

Efficacy:

Annualized exacerbation rate:
- 0.93 (tezepelumab) vs. 2.1 (placebo)
- Rate ratio: 0.44, p<0.001 (very positive)
In eosinophils <300 group: rate ratio 0.59, still effective
FEV₁ improved by ~+0.25 L (vs. +0.09 L placebo), significant & sustained from week 2 onward
Quality of life: statistically improved but did not meet MCID, so unclear clinical impact
Severity of exacerbations reduced: fewer hospitalizations & ED visits in the treatment arm
~40% of treated patients still had some exacerbations → not a cure, but improves severity

Safety:

Very well tolerated
77% reported adverse events (more common in placebo)
No anaphylaxis, no GBS, no cancer signal
Most common AEs: URTI, headache, nasopharyngitis
Injection site reactions: 3.6%
Serious AEs were lower in drug arm than placebo

Overall Takeaway

Tezepelumab significantly reduces asthma exacerbations (including in patients with low eosinophils), improves lung function, and is safe and well tolerated.
Provides a broad-acting biologic option even for patients who may not be eligible for existing T2-high biologics.
Now widely used as part of the asthma biologic armamentarium for poorly controlled asthma despite maximal inhaled therapy.

Infographic:

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We are podcasting today directly from ATS 2025 in San Francisco! Every year, in collaboration with the ATS Critical Care Assembly, we highlight some of the scientific symposium programming from the conference. Today, Furf and Monty sit down with the three chairs of the scientific symposium entitled: Mechanical Ventilation of the Future: New Foundations For Ventilator Strategies.

Meet Our Guests

Juliana Ferreira is an Associate Professor at the University of Sao Paulo, Brazil where she is also co-director of the pulmonary and critical care fellowship program. She is an MD, PhD, and a physician scientist with specific interests in mechanical ventilation and medical education. Finally, she serves ATS as the ATS MECOR Latin America Director.

Bhakti Patel is an Assistant Professor Medicine at the University of Chicago. She is a dedicated researcher and educator. Her research focuses on non-invasive ventilator support.

Akram Khan is an Associate Professor of Medicine at Oregon Health and Science University. Akram is a pulmonary, critical care, and sleep provider with specific clinical interests in critical illness, pulmonary vascular disease and sleep apnea. Additionally, he is an accomplished translational science researcher.

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We’re back with another edition of Fellows’ Case Files! Today, we’re virtually visiting Rutgers University, Robert Wood Johnson Medical School to work through a fascinating pulmonary case. Enjoy, and let us know your thoughts.

Meet Our Guests

Khalil El Gharib completed his residency training at Northwell at Staten Island University Hospital Program and is currently a first year fellow at Rutgers Robert Wood Johnson Medical School.

Sabiha Hussain completed her residency training at Robert Wood Johnson Medical School and her fellowship training at Columbia Presbyterian Medical Center in New York. She is currently a Professor of Medicine and the fellowship Program Director.

Case Presentation

Patient: 28-year-old male with Asperger’s syndrome and IgA nephropathy.
Symptoms: 3-month history of progressive dry cough and dyspnea on exertion; later developed mild hemoptysis.
Notable exposure: Questionable black mold in the patient’s apartment.

Initial Workup and Diagnostic Reasoning

Vital signs: Hypoxemia (SpO₂ 91% on room air).
Exam: Inspiratory crackles.
ABG findings: Elevated A–a gradient (~50), indicating a gas exchange problem.
Chest X-ray: Bilateral, patchy infiltrates without specific lobar preference.
Initial management: Discharged with empiric antibiotics for presumed multifocal pneumonia.

Re-Presentation and Further Testing

Symptoms worsened; now with blood-tinged sputum.
Chest CT: Showed diffuse ground-glass opacities (GGOs) without fibrosis, consolidation, or lymphadenopathy.

Imaging and Pathology

Pathology images a courtesy to Dr Isago Jerrett, pathology resident at RWJMS

Key Learning Points

Diagnostic Framework for Hypersensitivity Pneumonitis (HP)

New classification: Based on fibrotic vs. non-fibrotic phenotype (not acute/chronic).
CT features of HP:
- GGOs with lobular air trapping.
- “Three-density sign” (normal lung, low-density air-trapping, and ground-glass opacities).
BAL: Typically shows lymphocytic predominance in chronic HP, neutrophilic in early stages.
Serum IgG testing: Helps identify antigen exposure but doesn’t confirm disease alone.
Lung biopsy (VATS): Revealed poorly formed granulomas and airway-centered inflammation—consistent with HP.

Differential Diagnosis of Granulomatous Disease

Infectious: TB, fungal (must rule out with stains/cultures).
Non-infectious: Sarcoidosis, HP, granulomatosis with polyangiitis.
Key pathology clues for HP: Loosely formed granulomas, airway inflammation, giant cells.

Management and Outcome

Primary treatment: Antigen avoidance (patient moved out of mold-exposed apartment).
Adjunct therapy: Oral prednisone with a slow taper.
Outcome: Symptomatic and radiographic improvement over six months.

Teaching Pearls

Always take a detailed environmental and occupational exposure history.
Hypoxemia with an elevated A–a gradient in a young adult should trigger concern for interstitial/parenchymal lung disease.
CT and history are often enough to diagnose HP—biopsy is reserved for uncertain cases.
Remember evolving terminology: think fibrotic vs. non-fibrotic HP, not acute/chronic.

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Today, we continue our review of the Global Initiative for Asthma (GINA) guidelines on asthma. We’ve covered asthma diagnosis and phenotyping, and the initial approach to therapy. On today’s episode we’re talking about biologic therapies for asthma and will cover … Continue reading →

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In this episode, we add another article to our Rapid Fire Journal Club. Luke Hedrick and Dave Furfaro discuss the MIST 2 trial published in NEJM in 2011 evaluating enzymatic therapy for complex parapneumonic effusions and empyemas. Article and … Continue reading →

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We’re back with our second episode in our guideline initiative, and continuing our review of the Global Initiative for Asthma (GINA) guidelines on asthma. In our first episode of this series, we talked about making the diagnosis of asthma, the … Continue reading →

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Today we have a mini-episode / clinical pearl. We previously discussed the PROSEVA trial and the evidence for prone positioning in ARDS. In that trial, patients with elevated intracranial pressure (ICP) were excluded. We are joined now by Dr. Jon … Continue reading →

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On February 7, 2025 it was announced that the National Institutes of Health (NIH) would be capping indirect cost payments for research grants at 15%. This is a massive reduction from the current standard, and will have widespread impacts on … Continue reading →

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Today we are launching a new Pulm PEEPs initiative! We are going to be reviewing some of the major guidelines that are available in pulmonary and critical care. We are starting by diving into the Global Initiative for Asthma (GINA) … Continue reading →

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Today is our second episode in our collaborative series with BMJ Thorax. 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. … Continue reading →

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This week we’re talking about a case as a lens for discussing Tylenol toxicity and Acute Liver Failure. These relatively common critical care presentations are essential knowledge for anyone practicing in the ICU. Listen in for some key discussion both … Continue reading →

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We are excited to be back with a Rapid Fire Journal Club. Today’s episode is hosted by PulmPEEPs Associate Editor, Luke Hedrick, and will delve into the ANDROMEDA-SHOCK trial published in JAMA in 2019. Meet our Guests Jose Meade Aguilar … Continue reading →

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Our episode today is diving into a broader initiative to discuss the management of interstitial lung disease. In this episode we will be talking about the treatment of Idiopathic Pulmonary Fibrosis through the lens of a journal club discussion of … Continue reading →

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We are joined today by two amazing educators from NYU for our latest Fellows’ Case Files Episode. Listen today as we go through a great case with some fantastic teaching points highlighted throughout the episode. Meet Our Guests Dr. Jeremy … Continue reading →

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Here at Pulm PEEPs we have always loved the CHEST Annual Meetings. We have enjoyed learning at them, reuniting with and meeting colleagues, and having conference specific episodes the past two years. This year, we had the opportunity to podcast … Continue reading →

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We are excited to be back with our colleagues from CHEST to be previewing the CHEST 2024 Annual Meeting. CHEST his year is in Boston, MA from October 5th to October 9th. Listen in to hear about some great new features at CHEST this year, some old favorites, and to learn how to optimize your conference experience. See you all in two weeks!

Meet Our Guests

Sandhya Khurana is a Professor of medicine at University of Rochester school of medicine and Director of the Mary Parkes Asthma Center. Her clinical and research interest is in asthma. She is the Vice-Program Chair for CHEST 2024 and will be the program Chair for CHEST 2025 next year in Chicago.

Gabe Bosslet is the Program Chair for CHEST this year. In addition he is a Professor of Clinical Medicine at Indiana University School of Medicine. He is also an Assistant Dean at IU, and the Director of Mentoring and Faculty Development for the Division Pulmonary, Critical Care, Allergy and Occupational Medicine.

Huzaifah Salat is a clinician educator who is currently working as a consultant pulmonologist and intensivist at Advocate Aurora Health in Wisconsin. He completed his Pulmonary and Critical Care Fellowship at the University of Oklahoma Health Sciences Center

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We are extremely excited today to announce a new collaboration with BMJ Thorax. 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. We hope you enjoy!

Meet Our Guests

Imran Howell is an Asthma Fellow at the Nuffield Department of Medicine, University of Oxford

Journal Club Papers

Journal club article from Thorax
Blood eosinophil-guided oral prednisolone for COPD exacerbations in primary care in the UK (STARR2): a non-inferiority, multicentre, double-blind, placebo-controlled, randomised controlled trial
Nutritional supplementation to prevent tuberculosis incidence in household contacts of patients with pulmonary tuberculosis in India (RATIONS): a field-based, open-label, cluster-randomised, controlled trial
The airway microbiome mediates the interaction between environmental exposure and respiratory health in humans
Respiratory syncytial virus infection during infancy and asthma during childhood in the USA (INSPIRE): a population-based, prospective birth cohort study

To submit a journal club article of your own to Thorax, you can contact Chris directly – christopher.turnbull@ouh.nhs.uk

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In this podcast episode, we continue our summer series reviewing landmark ARDS studies. Today, Dave and Luke discuss the Driving Pressure trial (published in NEJM in 2015) which evaluated the impact of driving pressure on survival in patients with ARDS.

Article and Reference

We are talking about the Driving Pressure trial today which evaluated the impact of driving pressure, as an independent variable, on survival in patients with ARDS.

Amato MB, Meade MO, Slutsky AS, Brochard L, Costa EL, Schoenfeld DA, Stewart TE, Briel M, Talmor D, Mercat A, Richard JC, Carvalho CR, Brower RG. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med. 2015 Feb 19;372(8):747-55. doi: 10.1056/NEJMsa1410639. PMID: 25693014.

Infographic

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In the penultimate episode in our ARDS Rapid Fire Journal Club Summer Series we are talking about the DEXA-ARDS trial (published in Lancet Respiratory Medicine in 2020). This trial evaluated the impact of dexamethasone in the treatment of ARDS.

Article and Reference

Today we’re discussing the DEXA-ARDS trial published in Lancet Respiratory Medicine in 2020. This trial evaluated the impact of dexamethasone on mortality and duration of mechanical ventilation for patients with ARDS.

Villar J, Ferrando C, Martínez D, Ambrós A, Muñoz T, Soler JA, Aguilar G, Alba F, González-Higueras E, Conesa LA, Martín-Rodríguez C, Díaz-Domínguez FJ, Serna-Grande P, Rivas R, Ferreres J, Belda J, Capilla L, Tallet A, Añón JM, Fernández RL, González-Martín JM; dexamethasone in ARDS network. Dexamethasone treatment for the acute respiratory distress syndrome: a multicentre, randomised controlled trial. Lancet Respir Med. 2020 Mar;8(3):267-276. doi: 10.1016/S2213-2600(19)30417-5. Epub 2020 Feb 7. PMID: 32043986.

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Article Notes

DEXA-ARDS; Lancet Respiratory Medicine, 2020
- DOI:10.1016/S2213-2600(19)30417-5
- Link: https://doi.org/10.1016/s2213-2600(19)30417-5
- Background: ARDS is an intense inflammatory process without proven, specific pharmacotherapies. Previous work and a recent meta-analysis demonstrated improvements in inflammation, gas exchange, and ventilator and ICU liberation but did not adequately address mortality.
- Study Design (design, primary outcome, participants, etc)
  - Design: investigator-initiated, multicenter, unblinded, randomized controlled trial in 17 academic ICUs in Spain, conducted from 3/2013 to 12/2018
  - Primary Outcome
    - VFD at 28d
    - Secondary:
      - 60d mortality
      - Actual duration of ventilation in ICU survivors
      - ICU acquired infections
  - Participants
    - Inclusion ARDS with P/F < 200 for < 24hr on LTVV
    - Exclusion:
      - Already receiving steroids or immunosuppression
      - CHF
      - Severe COPD
      - DNR
    - Summary: Middle aged, mostly male patients with < 24hr of moderate to severe ARDS receiving LPV without chronic heart or lung disease
      - Like many ARDS trials, just over 3/4 of patients’ ARDS was caused by PNA or sepsis. Mean P/F was ~140
- Intervention/Limitations
  - N = 277, stratified by center and then randomized
  - Intervention: dexamethasone 20mg qd for 5d followed by 10mg qd for 5d
    - Stopped early for extubation before day 10
    - First dose given no more than 30 hours after P/F < 200
  - Control: no placebo, just SOC
  - All patients received LTVV
- Outcomes/Safety
  - Power: with N = 314 (actual N = 277), 80% power to detect 2 additional VFD and 15% mortality reduction
    - As an aside, this seems to be a theme in ICU trials: massively ambitious proposed benefits during power calculations and then under-enrolling for that power calculation ultimately resulting with a point estimate that favors the intervention but is not statistically significant.
  - Efficacy:
    - 60d mortality: 21% vs 36%, P = 0.0047
      - NNT of just < 7!
    - VFD at 28d: 12.3 vs 7.5, P < 0.0001
    - Actual duration of ventilation in ICU survivors: 14.2d vs 19.5d (P = 0.0009)
  - Safety:
    - Hyperglycemia: 76% vs 70%, P = 0.33
      - Always interesting in steroid trials when no change in glucose control is seen. This isn’t the most EBM thing I’ll ever say, but frankly I disregard this and assume steroids will cause hyperglycemia regardless of the trial results.
    - ICU acquired infections: 24% vs 25%, P = 0.75
- Takeaway
  - In a narrowly selected population of patients without chronic heart or severe lung disease and with early, moderate ARDS (mostly from sepsis or pneumonia), dexamethasone reduced mortality and duration of mechanical ventilation.
    - If time, insert soap-box about etiology of ARDS being very important (EG, flu, fungal, parasitic, mycobacterial infections)

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We have another great case in our Fellows’ Case Files coming today from UMass Chan. Listen in for a great discussion about a fascinating case with interesting physical exam and radiographic findings.

Meet Our Guests

Dr. Jen Kodela completed her residency training at UMass Memorial Medical Center and is currently a third year PCCM fellow at UMass Chan.

Dr. Ariel McKenna completed her residency training at Maine Medical Center and is also currently a third year PCCM fellow at UMass Chan.

Dr. Will Wong is an Assistant Professor of Medicine and is the Program Director of the PCCM fellowship at UMass Chan

Case Presentation

A 75 y/o F presenting with acute on chronic SOB, cough, L sided chest pain and rash. She has had ~7 months of progressive dyspnea, now a/w 2 months of productive cough, and several weeks of L sided chest pain and rash. She has been seen multiple times in the past two months for these sxs. During that time she received multiple antibiotic courses (urgent care, outpatient providers), including augmentin, azithromycin and levaquin, and asthma directed therapy (no steroids). Imaging throughout that time (CXRs, CTPE) show progression from a LLL infiltrate to bibasilar infiltrates. Despite these interventions, sxs continue to worsen. One month prior she was admitted to an OSH w/ continued worsening, vitals stable, exam nonfocal, mild leukocytosis but infectious w/u bland. Received broad spectrum abx. Bronch w/ BAL offers negative cultures, cytology, cell count w/ 66% neutrophils, 14% eosinophils. Discharged w/ dx of PNA on a 10 day course of levaquin and new exertional oxygen requirement of 2L. She then presents to Umass ~1 month later w/ continued progression of sxs

Key Learning Points

Formulate a differential diagnosis for non-resolving pneumonia
Evaluate the utility of transbronchial biopsy in the workup of undifferentiated ILD
Describe the clinical manifestations of antisynthetase syndrome and identify the differences in presentation associated with PL-12 positivity

References and Further Reading

Kuru T, Lynch JP 3rd. Nonresolving or slowly resolving pneumonia. Clin Chest Med. 1999 Sep;20(3):623-51. doi: 10.1016/s0272-5231(05)70241-0. PMID: 10516909.
Troy LK, Grainge C, Corte TJ, Williamson JP, Vallely MP, Cooper WA, Mahar A, Myers JL, Lai S, Mulyadi E, Torzillo PJ, Phillips MJ, Jo HE, Webster SE, Lin QT, Rhodes JE, Salamonsen M, Wrobel JP, Harris B, Don G, Wu PJC, Ng BJ, Oldmeadow C, Raghu G, Lau EMT; Cryobiopsy versus Open Lung biopsy in the Diagnosis of Interstitial lung disease alliance (COLDICE) Investigators. Diagnostic accuracy of transbronchial lung cryobiopsy for interstitial lung disease diagnosis (COLDICE): a prospective, comparative study. Lancet Respir Med. 2020 Feb;8(2):171-181. doi: 10.1016/S2213-2600(19)30342-X. Epub 2019 Sep 29. PMID: 31578168.
Hallowell RW, Danoff SK. Diagnosis and Management of Myositis-Associated Lung Disease. Chest. 2023 Jun;163(6):1476-1491. doi: 10.1016/j.chest.2023.01.031. Epub 2023 Feb 9. PMID: 36764512.
Hallowell RW, Paik JJ. Myositis-associated interstitial lung disease: a comprehensive approach to diagnosis and management. Clin Exp Rheumatol. 2022 Feb;40(2):373-383. doi: 10.55563/clinexprheumatol/brvl1v. Epub 2021 Mar 25. PMID: 33769263; PMCID: PMC8855729.
Marie I, Josse S, Decaux O, Dominique S, Diot E, Landron C, Roblot P, Jouneau S, Hatron PY, Tiev KP, Vittecoq O, Noel D, Mouthon L, Menard JF, Jouen F. Comparison of long-term outcome between anti-Jo1- and anti-PL7/PL12 positive patients with antisynthetase syndrome. Autoimmun Rev. 2012 Aug;11(10):739-45. doi: 10.1016/j.autrev.2012.01.006. Epub 2012 Feb 3. PMID: 22326685.

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In this podcast episode, we continue our summer series reviewing landmark ARDS studies. Today, Dave and Luke discuss the PROSEVA trial (published in NEJM in 2013) which evaluated the impact of early, prolonged proning in patients with severe ARDS.

Article and Reference

We are talking about the PROSEVA trial today which evaluated the patients with severe ARDS (P/F < 150) to undergo prone-positioning sessions of at least 16 hours or to be left in the supine position.

Guérin C, Reignier J, Richard JC, Beuret P, Gacouin A, Boulain T, Mercier E, Badet M, Mercat A, Baudin O, Clavel M, Chatellier D, Jaber S, Rosselli S, Mancebo J, Sirodot M, Hilbert G, Bengler C, Richecoeur J, Gainnier M, Bayle F, Bourdin G, Leray V, Girard R, Baboi L, Ayzac L; PROSEVA Study Group. Prone positioning in severe acute respiratory distress syndrome. N Engl J Med. 2013 Jun 6;368(23):2159-68. doi: 10.1056/NEJMoa1214103. Epub 2013 May 20. PMID: 23688302.

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In this podcast episode, we continue our summer series reviewing landmark ARDS studies. Today, Dave and Luke discuss the ROSE trial (published in NEJM in 2019) which investigated use of continuous neuromuscular blockade in moderate to severe ARDS.

Article and Reference

We are talking about the ROSE trial today which was a comparison of early continuous neuromuscular blockade in patients with ARDS who were receiving mechanical ventilation.

Reference: National Heart, Lung, and Blood Institute PETAL Clinical Trials Network; Moss M, Huang DT, Brower RG, Ferguson ND, Ginde AA, Gong MN, Grissom CK, Gundel S, Hayden D, Hite RD, Hou PC, Hough CL, Iwashyna TJ, Khan A, Liu KD, Talmor D, Thompson BT, Ulysse CA, Yealy DM, Angus DC. Early Neuromuscular Blockade in the Acute Respiratory Distress Syndrome. N Engl J Med. 2019 May 23;380(21):1997-2008. doi: 10.1056/NEJMoa1901686. Epub 2019 May 19. PMID: 31112383; PMCID: PMC6741345.

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In this podcast episode, we continue our summer series reviewing landmark ARDS studies. Today, Dave and Luke discuss the FACTT trial, which investigated fluid management strategies in ARDS. This was published in the NEJM in 2006.

Article and Reference

We’re talking about the FACTT trial today which was a “Comparison of Two Fluid-Management Strategies in Acute Lung Injury”

Reference: National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network; Wiedemann HP, Wheeler AP, Bernard GR, Thompson BT, Hayden D, deBoisblanc B, Connors AF Jr, Hite RD, Harabin AL. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. 2006 Jun 15;354(24):2564-75. doi: 10.1056/NEJMoa062200. Epub 2006 May 21. PMID: 16714767.

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Summary of discussion:

Background: The FACT trial aimed to address fluid balance in ARDS, given the complexity of managing pulmonary edema and systemic organ failure. The challenge has been finding the right balance between managing fluid to optimize cardiac function and avoiding exacerbation of pulmonary edema.

Study Design:

Randomized Controlled Trial: Conducted at 20 North American medical centers from 2000 to 2005.
Participants: Included intubated ARDS patients who required or were planned to receive a central venous catheter. Excluded patients with chronic diseases, recent MI, or irreversible conditions. Shock was not an exclusion criterion.
Interventions: Patients were randomly assigned to either a liberal or conservative fluid management strategy, and also received either a PA catheter or a central line.

Fluid Management Protocol:

Liberal Strategy: Aimed for higher filling pressures (CVP of 10-14 or wedge pressure of 14-18).
Conservative Strategy: Aimed for lower filling pressures (CVP less than 4 or wedge pressure under 14).
Fluid Balance: The liberal group had a net positive fluid balance of around 7 liters, while the conservative group had a net negative balance of about 130 cc.

Results:

Mortality: No statistically significant difference in 60-day mortality between the liberal and conservative groups (25.5% vs. 28.4%, respectively).
Ventilator and ICU-Free Days: The conservative strategy resulted in more ventilator-free and ICU-free days.
Shock and Dialysis: There was no difference in shock rates, but the conservative group had a trend toward fewer dialysis requirements (10% vs. 14%, p=0.06).

Conclusion: The trial indicated that a conservative fluid management strategy in ARDS patients can reduce ventilator dependence and ICU length of stay without worsening shock or end-organ function. It underscores the benefit of managing fluid conservatively to protect lung function, even though it didn’t significantly reduce mortality.

Overall, the FACT trial supports the practice of conservative fluid management in ARDS, advocating that “dry lungs are happy lungs” for improving patient outcomes.

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Today, we’re going to be talking about pre-oxygenation methods for endotracheal intubation and the PREOXI Trial which is hot off the presses in the New England Journal of Medicine in June of 2024. This trial has potentially widespread, practice changing results and we’re lucky enough to be joined by two of the authors to discuss.

Meet Our Guests

Dr. Kevin Gibbs is an Associate Professor of Medicine at Wake Forest University School of Medicine. He obtained his MD at George Washington University School of Medicine, and completed his residency and fellowship training at Johns Hopkins. He is an active researcher in critical care, ARDS, mechanical ventilation, and pragmatic trial design.

Dr. Jon Casey is an Assistant Professor of Medicine for the Division of Allergy, Pulmonary, and Critical Care Medicine at Vanderbilt University Medical Center. He obtained his MD from the University of Louisville School of Medicine, and completed his residency training at Brigham and Women’s Hospital before going to Vanderbilt for fellowship training. He is a physician scientist and also has his Masters of Science in Clinical Investigation. His research is focused on comparative effectiveness of ICU treatments and he also has a focus on pragmatic trials. He is supported with NIH funding and is active in the American Thoracic Society Critical Care Assembly.

Summarized Key Points

Significance of the Problem: Tracheal intubation in emergency and ICU settings is common, with significant risks such as hypoxemia (10-20% incidence) and cardiac arrest (2% incidence) associated with the procedure. This makes effective pre-oxygenation crucial.
Methods of Pre-oxygenation: Common methods include face mask oxygen (e.g., non-rebreather, bag-mask devices) and more advanced techniques like non-invasive ventilation (used in about 15% of cases globally). Each method has pros (e.g., simplicity, no risk of aspiration for face masks; 100% oxygen delivery, positive pressure for non-invasive ventilation) and cons (e.g., potential for gastric insufflation with non-invasive ventilation).
Study Design: The study discussed in the podcast is a pragmatic trial aiming to optimize pre-oxygenation strategies to prevent peri-intubation hypoxemia. Eligibility criteria were broad, encompassing most patients undergoing tracheal intubation in the ED or ICU, with exclusions mainly for safety reasons.
Primary Outcome: The primary outcome of the trial was hypoxemia, defined as oxygen saturation < 85%. This threshold was chosen because it signifies a critical point on the oxygen dissociation curve, where patients are at higher risk of further desaturation and adverse outcomes.
Secondary Outcomes: Secondary exploratory outcomes included more severe levels of hypoxemia (oxygen saturation < 80% and < 70%), aiming to capture varying degrees of oxygenation failure during intubation. Rates of cardiac arrest during intubation were an additional outcome.
Intervention Comparison:
- The trial compared two methods of pre-oxygenation: non-invasive ventilation (NIV) and oxygen mask (face mask)
- Both methods aimed to provide at least three minutes of pre-oxygenation before intubation.
- NIV group specifics: Expiratory pressure of 5 cm H2O, Inspiratory pressure of 10 cm H2O, respiratory rate of 10 breaths per minute, and 100% oxygen delivery
- Oxygen mask group specifics: Non-rebreather or bag mask device with at least 15 liters per minute oxygen flow.
- Nasal cannulas and HFNC could be used in both groups.
Logistics and Equipment Use:
- The trial allowed flexibility in using available equipment (invasive ventilator capable of NIPPV vs. dedicated BiPAP machine).
- Sites were encouraged to use the same ventilator for both pre-oxygenation and subsequent ventilation to streamline workflow and reduce logistical challenges.
Primary and Secondary Outcomes:
- Results showed a significant reduction in hypoxemia incidents in the NIV group compared to the oxygen mask group.
- There was also a reduction in severe hypoxemia and a notable decrease in cardiac arrest incidents in the NIV group.
Aspiration Safety:
- There was no statistical difference in aspiration-related outcomes between the NIV and oxygen mask groups, indicating that NIV did not increase the risk of aspiration.
Conclusions:
- The trial concluded that NIV for pre-oxygenation significantly reduced the incidence of hypoxemia and possibly cardiac arrest during tracheal intubation.
- It also dispelled concerns about increased aspiration risk with NIPPV as pre-oxygenation, suggesting it can be safely used in clinical practice.

Reference

Gibbs KW, Semler MW, Driver BE, Seitz KP, Stempek SB, Taylor C, Resnick-Ault D, White HD, Gandotra S, Doerschug KC, Mohamed A, Prekker ME, Khan A, Gaillard JP, Andrea L, Aggarwal NR, Brainard JC, Barnett LH, Halliday SJ, Blinder V, Dagan A, Whitson MR, Schauer SG, Walker JE Jr, Barker AB, Palakshappa JA, Muhs A, Wozniak JM, Kramer PJ, Withers C, Ghamande SA, Russell DW, Schwartz A, Moskowitz A, Hansen SJ, Allada G, Goranson JK, Fein DG, Sottile PD, Kelly N, Alwood SM, Long MT, Malhotra R, Shapiro NI, Page DB, Long BJ, Thomas CB, Trent SA, Janz DR, Rice TW, Self WH, Bebarta VS, Lloyd BD, Rhoads J, Womack K, Imhoff B, Ginde AA, Casey JD; PREOXI Investigators and the Pragmatic Critical Care Research Group. Noninvasive Ventilation for Preoxygenation during Emergency Intubation. N Engl J Med. 2024 Jun 20;390(23):2165-2177. doi: 10.1056/NEJMoa2313680. Epub 2024 Jun 13. PMID: 38869091.

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This episode is launching our 2024 Rapid Fire Journal Club summer series on ARDS! This summer we will be talking about landmark ARDS trials that have defined the literature and shaped patient care. Journal clubs often focus on new trials, and so learners may have a less thorough understanding of the baseline literature that defines many of our ICU practices. The goal of this series is to provide a quick, but in-depth look at these papers so that learners understand the modern landscape of ARDS.

Today, we’re kicking this initiative off by looking at the ARMA or ARDSNet Trial published in the NEJM in 2000. Enjoy!

Article and Reference

We’re talking about the ARMA trial today which examined “Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome.”

Reference: Acute Respiratory Distress Syndrome Network; Brower RG, Matthay MA, Morris A, Schoenfeld D, Thompson BT, Wheeler A. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000 May 4;342(18):1301-8. doi: 10.1056/NEJM200005043421801. PMID: 10793162.

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Today we’re back with another stop on our Fellows’ Case Files journey and making our way to the University of Rochester. Tune in to hear about this fascinating case and learn some key teaching points along the way.

Meet Our Guests

Dr. Shiv Patel completed his IM residency and a Chief year at the California Pacific Medical Center- Van Ness Campus and is currently a second-year PCCM fellow at the University of Rochester.

Dr. Mary Anne Morgan is an Associate Professor of Medicine and the Fellowship Program Director for the PCCM Fellowship at the University of Rochester. Her clinical interests range from the care of critically ill patients in the ICU to the diagnosis and management of rare lung disease in her role as Director of the University of Rochester LAM Clinic. She loves unwrapping clinical reasoning with trainees, exploring issues around communication and teamwork in the ICU, and is excited about curriculum revitalization in the growing URMC PCCM fellowship program.

Case Presentation

A 75 y.o. female with a history of Hypertension, Hyperlipidemia, and Type 2 Diabetes presented for evaluation of hypoglycemia and generalized fatigue. She had felt poorly for about a week with symptoms of back pain, generalized weakness, and dyspnea, all of which acutely worsened on the day of presentation.

She was found to be hypoglycemic with a blood glucose level in the to 40’s. Initial vital signs included a heart rate of 56, blood pressure of 70/40, respiratory rate of 30, and temperature of 28.5 degrees Celsius.

Key Learning Points

Lactic Acidosis: Type A, Type B and Type D

Type A: Typically secondary to conditions that impair oxygen delivery (respiratory failure, PE) to tissues or decrease tissue perfusion (severe anemia, shock). Patients typically present with hypotension, tachycardia, tachypnea, altered mental status, and signs of organ dysfunction.

Type B: Typically secondary to conditions that directly affect cellular metabolism or lactate clearance and characterized by the presence of hyperlactatemia without evidence of tissue hypoperfusion or hypoxia. Conditions associated include liver dysfunction (e.g., liver failure, cirrhosis), malignancies (especially hematological malignancies), medications/toxins (e.g., metformin, cyanide poisoning), inborn errors of metabolism, and mitochondrial disorders.

Type D: Less common presentation and can be seen in patients with short gut syndrome.

References

1.Blough B, Moreland A, Mora A Jr. Metformin-induced lactic acidosis with emphasis on the anion gap. Proc (Bayl Univ Med Cent). 2015 Jan;28(1):31-3. doi: 10.1080/08998280.2015.11929178. PMID: 25552792; PMCID: PMC4264704.

2.Callelo et al. Extracorporeal Treatment for Metformin Poisoning: Systematic Review and Recommendations From the Extracorporeal Treatments in Poisoning Workgroup. DOI: 10.1097/CCM.0000000000001002

3.Friesecke, S., Abel, P., Roser, M. et al. Outcome of severe lactic acidosis associated with metformin accumulation. Crit Care 14, R226 (2010). https://doi.org/10.1186/cc9376

4.Madias NE. Lactic acidosis. Kidney Int. 1986 Mar;29(3):752-74. doi: 10.1038/ki.1986.62. PMID: 3702227.

Stiller RH, Luks AM, Çoruh B. All That Raises Lactate Is Not Sepsis. ATS Sch. 2023 Jun 12;4(3):385-386. doi: 10.34197/ats-scholar.2023-0032OT.

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We’re back with our Rapid Fire Journal Club, and talking about the NEJM 2023 STELLAR Trial of Sotatercept in Pulmonary Arterial Hypertension. This is a landmark trial that is actively changing the face of PAH treatment today. Listen to hear the details of the trial and how its findings can be utilized to help patients.

Article and Reference

We’re looking at the STELLAR Trial today which is a Phase 3 trial of Sotatercept in Pulmonary Arterial Hypertension.

Reference: Hoeper MM, Badesch DB, Ghofrani HA, Gibbs JSR, Gomberg-Maitland M, McLaughlin VV, Preston IR, Souza R, Waxman AB, Grünig E, Kopeć G, Meyer G, Olsson KM, Rosenkranz S, Xu Y, Miller B, Fowler M, Butler J, Koglin J, de Oliveira Pena J, Humbert M; STELLAR Trial Investigators. Phase 3 Trial of Sotatercept for Treatment of Pulmonary Arterial Hypertension. N Engl J Med. 2023 Apr 20;388(16):1478-1490. doi: 10.1056/NEJMoa2213558. Epub 2023 Mar 6. PMID: 36877098.

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We have had a number of episodes on Acute Respiratory Distress Syndrome or ARDS. These episodes have ranged from how to titrate PEEP, subphenotypes in ARDS, and the future of ARDS research. Today, we are talking about how we all think about and define ARDS, and work that has highlighted a newer global definition of ARDS.

Meet our GuestsDr. Elisabeth Riviello is an Assistant Professor of Medicine at Harvard Medical School, and a PCCM physician at Beth Israeal Deconess Medical Center. She is also an Affiliate of the HMS Department of Global Health and Social Medicine and an honorary Associate Professor of Emergency Medicine and Critical Care at the University of Rwanda. She is passionate about improving critical care delivery in resource limited settings and has served on Committees for the World Health Organization. She is the Principal Investigator of BREATHE or the (Building Respiratory Support in East Africa Through High flow versus standard flow oxygen Evaluation); a RCT looking at HFNC in five sites in Kenya, Malawi, and Rwanda.

Dr. Theogen Twagirumugabe is an Anesthesiologist and Intensivist at the College of Medicine and Health Sciences, and a Professor at the University of Rwanda. In addition to clinical work, he has his PhD in Medical Sciences. He is a widely succesful researcher with over 70 publications in critical care and anesthesia delivery and is also a lead investigator in the BREATHE initiative.

References

Matthay MA, Arabi Y, Arroliga AC, Bernard G, Bersten AD, Brochard LJ, Calfee CS, Combes A, Daniel BM, Ferguson ND, Gong MN, Gotts JE, Herridge MS, Laffey JG, Liu KD, Machado FR, Martin TR, McAuley DF, Mercat A, Moss M, Mularski RA, Pesenti A, Qiu H, Ramakrishnan N, Ranieri VM, Riviello ED, Rubin E, Slutsky AS, Thompson BT, Twagirumugabe T, Ware LB, Wick KD. A New Global Definition of Acute Respiratory Distress Syndrome. Am J Respir Crit Care Med. 2024 Jan 1;209(1):37-47. doi: 10.1164/rccm.202303-0558WS. PMID: 37487152; PMCID: PMC10870872.

Riviello ED, Buregeya E, Twagirumugabe T. Diagnosing acute respiratory distress syndrome in resource limited settings: the Kigali modification of the Berlin definition. Curr Opin Crit Care. 2017 Feb;23(1):18-23. doi: 10.1097/MCC.0000000000000372. PMID: 27875408.

ARDS Definition Task Force; Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, Fan E, Camporota L, Slutsky AS. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012 Jun 20;307(23):2526-33. doi: 10.1001/jama.2012.5669. PMID: 22797452.

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Welcome to our second episode of ATS 2024 highlighting content featured through the ATS Critical Care Assembly. Today we are going to be talking about one of the Critical Care Assembly Symposiums entitled: “Care of Dying in the ICU: End of Life Care in 2024 and Beyond”

Meet our GuestsDr. Theodore “Jack: Iwashyna is a Bloomberg Distinguished Professor at Johns Hopkins School of Medicine and the Johns Hopkins Bloomberg School of Public Health. Jack is a critical care physician and has a broad focus on research that understands the broader context of critical illness, and the long term impact on patients’ lives. He is an enormously productive and successful researcher with numerous publications in the field of critical care, and is a pioneer in the field of ICU survivorship. He is a devoted mentor and has received accolades from numerous societies

Dr. Molly Hayes is an Associate Professor of Medicine at Beth Israel Deaconess Medical Center and Harvard Medical School, the Director of the MICU at BIDMC, and the Director of External Education at the Carl J Shapiro Institute for Education and Research. She additionally is a co-founder of the BIDMC Center for Humanizing the ICU. Molly has been extensively involved with ATS with leadership roles in the Critical Care Assembly, and the newly minted Steering Committee on the Advancement of Learning.

Meet our CollaboratorsThe American Thoracic Society Critical Care Assembly is the largest Assembly in the American Thoracic Society. Their members include a diverse group of intensivists and care providers for both adult and pediatric critically ill patients. The primary goal of the Critical Care Assembly is to “improve the care of the critically ill through education, research, and professional development.”

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Welcome to our first episode of ATS 2024 highlighting content featured through the ATS Critical Care Assembly. Today we are going to be talking about one of the Critical Care Assembly Symposiums entitled: “A New Reality for Critical Care after Dobbs.”

Meet our GuestsDr. Katie Hauschildt is a Faculty Research Associate at The Johns Hopkins University School of Medicine where she conducts research on equity in healthcare and critical illness recovery. She has her PhD in Sociology from the University of Michigan and an Advanced Fellowship in Health Services Research from the VA Ann Arbor Healthcare System, and is a board certified patient advocate.

Dr. Kathleen Akgün is an Associate Profess or Medicine at the Yale School of Medicine. She is the Association Section Chief for the VA section of Pulmonary, the Co-Director of the Network of Dedicated Enrollment Sites Program, the director of the MICU at the VA Connecticut health care system, and a member of the DEI Working Group at Yale.

References and Further ReadingGood Trouble Indiana: https://www.goodtroubleindiana.org/

McHugh K, Bosslet GT, Rouse C, Wilkinson T. Doctors think “advocate” is a dirty word. But it’s our ethical responsibility. STAT News. https://www.statnews.com/2023/06/01/caitlin-bernard-indiana-abortion-10-year-old-advocacy/. Published June 1, 2023.

MacDonald A, Gershengorn HB, Ashana DC. The Challenge of Emergency Abortion Care Following the Dobbs Ruling. JAMA. 2022;328(17):1691-1692. doi:10.1001/jama.2022.17197

Ashana DC, Chen C, Hauschildt K, et al. The Epidemiology of Maternal Critical Illness Between 2008-2021. Ann Am Thorac Soc. Published online June 14, 2023. doi:10.1513/AnnalsATS.202301-071RL

Sonntag E, Akgun KM, Bag R, et al. Access to Medically Necessary Reproductive Care for Individuals with Pulmonary Hypertension. Am J Respir Crit Care Med. Published online June 13, 2023. doi:10.1164/rccm.202302-0230VP

Griffin KM, Oxford-Horrey C, Bourjeily G. Obstetric Disorders and Critical Illness. Clin Chest Med. 2022;43(3):471-488. doi:10.1016/j.ccm.2022.04.008

Her Body, Our Laws: https://bookshop.org/p/books/her-body-our-laws-on-the-front-lines-of-the-abortion-war-from-el-salvador-to-oklahoma-michelle-oberman/9007091?ean=9780807089071

Watson K, Oberman M. Abortion Counseling, Liability, and the First Amendment. N Engl J Med 2023;389(7):663–7.

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Today we’re visiting the University of New Mexico for another interesting entry in our Fellows’ Case Files.

Meet Our Guests

Neel Vahil is a second-year internal medicine resident at the University of New Mexico. He completed medical school at New York Medical College and is planning on applying to pulmonary critical care fellowship programs.

Ishan Patel is a third year PCCM fellow at the University of New Mexico and will be pursuing a second fellowship in clinical informatics this year. He completed medical school and residency in Internal Medicine at Oregon Health & Science University. His fellowship research has focused on clinical outcomes of intensivist-led ECMO programs.

Dr. Lucie Griffin completed her internal medicine residency and PCCM fellowship at the University of New Mexico and is currently the Director of the Albuquerque VA medical intensive care unit.

Case Presentation

A 69 year old male veteran who presents with 6 weeks of weight loss, cough, and malaise. He has ongoing tobacco use, and history of rheumatoid arthritis on HCQ and weekly MTX with etanercept, which he had stopped taking in the three prior months. Vitals: Afebrile, mildly tachycardic to 101, BP of 93/59, saturating appropriately on room air without any signs of respiratory distress

Key Learning Points

Rheumatoid effusions can be a pulmonary manifestation of uncontrolled, active rheumatoid arthritis
The pleural fluid characteristics of rheumatoid effusions can be similar to that of malignancy, active bacterial infection, or tuberculosis including a high ADA level, low glucose, and a low pH
The presence of Rheumatoid factor with concomitant negative evaluation for active infection or malignancy can help narrow the differential diagnosis to rheumatoid effusion
Complications are mostly related to long-standing residual inflammatory fluid and can be a fibrothorax with the presence of pneumothorax ex vacuo, which can be managed by observation unless severe

See infographic belowReferences and Further Reading

Komarla A, Yu GH, Shahane A. Pleural effusion, pneumothorax, and lung entrapment in rheumatoid arthritis. J Clin Rheumatol. 2015;21(4):211-215.

Boddington MM, Spriggs AI, Morton JA, Mowat AG. Cytodiagnosis of rheumatoid pleural effusions. J Clin Pathol. 1971;24(2):95-106.

Balbir-Gurman A, Yigla M, Nahir AM, Braun-Moscovici Y. Rheumatoid pleural effusion. Semin Arthritis Rheum. 2006;35(6):368-378

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We’re super excited to have a joint episode this week with Dr. Cyrus Askin and Dr. Nick Mark from Critical Care Time! We discuss all the ways that bronchoscopy can be your best friend in the ICU and how to be prepared for the unexpected scary situations that arise in the ICU. This ranges from airway bleeds, difficult intubations, lobar collapse, and trach emergencies. Don’t miss this great discussion!

Key Learning Points

Utility of bronchoscopy in people with critical illness

Bronchoscopy can be both diagnostic and therapeutic; both are potentially lifesaving.
General situations where bronchoscopy is useful in the ICU:
- Placing (or confirming placement of) an endotracheal tube or tracheostomy tube
- Removing a foreign body or mucous plugs from the lungs
- Localizing the source of pulmonary hemorrhage or performing interventions to stop/contain the bleed
- Diagnosing certain rare conditions, particularly those where the diagnosis can substantially change management (e.g. DAH, AEP, rare infections, etc).
Proficiency with bronchoscopy is important to realize the benefits. Simply “having the equipment” is insufficient, regular practice/simulation is essential
- Anesthesiologists, emergency physicians, and other specialists may have limited experience with bronchoscopy in training. Even experienced pulmonologists, who may be good at diagnostic bronchoscopy often have limited experience deploying bronchial blockers, using retrieval baskets, etc.
- Remember: “People don’t rise to the occasion, they sink to the level of their training.”
- If you haven’t regularly practiced with a bronchoscope, you are not going to be able to use it effectively under stress when performing high acuity low occurrence (HALO) procedures such as in emergent airways, deploying bronchial blockers, retrieving foreign bodies, etc.

Practice practice practice: High fidelity bronchoscopy simulators are available. Low cost bronchoscopy simulators (e.g. 3D printed DIY) are available.

Difficult Airways

Two broad situations where a bronchoscope is generally used:
- Awake intubation in the anticipated difficult airway (e.g. someone with abnormal anatomy, airway tumor, etc)
- Rescue method in the unanticipated difficult airway (e.g. very anterior cords, difficulty with Bougie, etc)
Nasal vs Oral approach:
- Oral approach is usually used in an unanticipated difficult airway
- Nasal approach: More common if performing an awake intubation. Nasal is often better tolerated however epistaxis can make a difficult airway almost impossible.
Sedation strategy:
- Full topicalization: lidocaine vs cocaine (equally effective and lidocaine is normally preferred, however the vasoconstriction action of cocaine may be helpful in preventing epistaxis).
  - Which types of topicalization work best?
    - Spray as you go w/ or w/o and atomizer
    - Nebulization (maybe better? maybe)
    - Gurgling (Nick: from personal experience lidocaine is super gross)
  - Remember total dose of lidocaine: < 8 mg/kg
- Ketamine
  - Ideal because it’s dissociative and analgesic, maintains respiratory drive and (maybe) airway reflexes
  - Consider scopolamine patch to reduce oral secretions
- Dexmedetomidine
  - Great adjunct
One vs two operator
- Especially in unanticipated difficult airways; the second operator can use VL/DL to facilitate visualization of the vocal cords.
- Second operator can also be preparing for a surgical airway.
Equipment considerations:
- Preload the endotracheal tube onto the bronchoscope. Use the bronchoscope as a bougie to guide the ETT through the vocal cords.
- Suction! You want two – one connected to the bronch and one connected to a yankuer.
- Disposable vs “good” scope
- Remember to load the tube first!
- Also remember to lube the tube!

Tracheostomy troubleshooting

Similarly to intubation, bronchoscopy can be very useful to confirm placement
Mechanics are similar to above
Goal is to avoid inadvertent placement of the tracheostomy tube into the soft tissues of the neck and to avoid putting air into those tissues (false lumen).
Advanced trick for exchanging tubes: You can use a disposable bronchoscope to exchange tubes: you can get it in, confirm placement, then cut it with trauma shears! Now you can slide the old tube out and put a new one in. (Don’t try this on a $40,000 fiberoptic bronchoscope!)
Ideally you should load the ETT onto the bronchoscope in advance (red arrow). If necessary however, you can cut the ETT and turn the disposable bronchoscope into a improvised exchange catheter. This technique is very useful for exchanging tracheostomy tubes.

Foreign Body Removal from airways

Bronchoscopy is invaluable for both diagnosis and treatment of foreign body aspirations.
Most commonly these aspirations are food (nuts, seeds, etc), teeth, pills, etc
Great overview of the procedure.
Intubated vs awake
- Intubated is harder in many cases: no cough to help, hard to get foreign body out of the ETT.
Flexible vs rigid
- Most objects can be retrieved using flexible bronchoscope; however 15-20% require rigid bronchoscopy
- Flexible can reach smaller foreign bodies that are lodged more distally.
- Rigid bronchoscopy is usually done if flexible bronchoscopy fails; an interventional pulmonologist wielding a rigid is superior but more invasive (requires GA)
Many different retrieval devices; technique depends on what equipment is available.
- Forceps
  - Many types: shark tooth, rat tooth, alligator are most common
- Basket
- Grasper
- Snare
- Net (GI device repurposed)
- Cryoprobe can be especially useful for frangible materials (e.g. food)

Mucous Plugs & Lobar collapse

Presentation can be subtle or dramatic.
Bronchoscopy can remove mucous plugs and help re-expand collapsed lung areas, which is potentially life saving.
Additionally, bronchoscopy can permit diagnosis of tracheal bronchus (bronchus sui)
- Pig bronchus – 1-3% of people – have a RUL bronchus that comes off the trachea.
- Often presents with RUL collapse in an intubated person.
Suction considerations and bronchoscope size
- Remember that suctioning force is highly dependent (i.e. radius raised to the fourth power!) upon the working channel size. Use the largest size bronchoscopy possible when suctioning.
Remember that other interventions: regular inline suctioning, chest PT, adequate hydration, mucolytics are also important to prevent recurrent mucous plugging.

Localization & Isolation of Pulmonary Hemorrhage

Pre-bronch interventions
- Stabilization
- Nebulized TXA
- Bad side down → counter-intuitive because shifting blood flow, but also the goal is to protect the non-bleeding lung.
- etc
Bronch can localize the bleeding site. Bronch can also perform interventions such as:
- Cold saline
- Epinephrine 1:100,000
- Bronchial blockers – comparison of types
  - CRE balloon
  - Fogarty
- Cryo probe – great for removing clots
- Delivering ETT to contralateral side → single lung ventilation

Making “bronchoscopy only” diagnoses

Diffuse Alveolar Hemorrhage (DAH)
- Finding: Increasingly bloody returns on serial lavages
Infections not covered by empiric therapies:
- Invasive fungal infection (e.g. mucor), azole resistant fungi (C glabrata)
- Rare/unusual infections (PJP, histoplasmosis, etc)
Infection mimics:
- Acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP)
  - Finding: eosinophils > 20%
- E-Cigarette Vaping Associated Lung Injury (EVALI)
  - Foamy lymphocytes
- Organizing Pneumonia
- Others
Remember to always send a cell count on a BAL! And cytology!
How often does bronchoscopy change management? Surprisingly often!
- A study of how often bronchoscopy changes management in an oncology population. 500+ patients with AML or high grade myeloid neoplasms who underwent bronchoscopy at one center over 5+ years.
- 1) an unexpected diagnosis was made and followed by a management change (as the most rigorous estimate of utility)
  - 13% of the time a diagnosis was only made because of bronchoscopy which changed management
- 2) the post-bronchoscopy diagnosis was discordant from the leading diagnosis considered before this procedure and was followed by a management change
  - 48% of the time pre and post procedure leading diagnoses were different
  - 26% of the time the change in leading diagnosis led to a change in therapy
- 3) a change in management was made following bronchoscopy regardless of whether the diagnosis was expected or considered.
  - 32% escalation of antibiotics
  - 30% de-escalation of antibiotics
  - 9% addition of steroids
  - 2% mold → surgery
Remember that in critically ill patients whose symptoms are unexplained or failing to resolve with therapy, diagnostic flexible bronchscopy can provide useful insights.

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Today on Rapid Fire Journal Club we’re reviewing a new article type and discussing a meta-analysis of Single Maintenance and Reliever Therapy (SMART) for asthma.

Article and Reference

Today we’re taking a deeper diver into SMART treatment for asthma to continue our discussion of inhalers.

Reference: Sobieraj DM, Weeda ER, Nguyen E, Coleman CI, White CM, Lazarus SC, Blake KV, Lang JE, Baker WL. Association of Inhaled Corticosteroids and Long-Acting β-Agonists as Controller and Quick Relief Therapy With Exacerbations and Symptom Control in Persistent Asthma: A Systematic Review and Meta-analysis. JAMA. 2018 Apr 10;319(14):1485-1496. doi: 10.1001/jama.2018.2769. PMID: 29554195; PMCID: PMC5876810.

Infographic

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We’re back with another Case Files episode from Mt. Sinai Morningside. Listen in to hear another great case and some key learning points along the way.

Meet Our Guests

Dr. Sara Luby is a third-year Internal Medicine resident and rising chief resident at Mt. Sinai Morningside/West and planning on applying to Pulmonary and Critical Care fellowship this upcoming year.

Dr. Javier Zulueta is the Chief of the Division of Pulmonary, Critical Care, and Sleep Medicine at Mount Sinai Morningside. He completed residency training at St. Luke’s Medical Center/Case Western in Cleveland and fellowship in Pulmonary/Critical Care at Tufts Medical Center in Boston. His research focuses on lung cancer screening and incidental lung findings.

Dr. Mirna Mohanraj is the Associate Program Director for the Pulmonary and Critical Care Fellowship at Mt. Sinai Morningside / Beth Israel and an associate professor of medicine and medical education at the Icahn School of Medicine at Mount Sinai. She completed residency training at University of Chicago and fellowship training at Mt. Sinai Hospital.

Case Presentation

A 51 year old male presents with two days of acute on chronic chest pain and shortness of breath, worsening over the last month. His initial vitals: 143/ 100, pulse 85, temperature 36.5 °C (97.87°F), RR 16, SpO2 97 % on room air, BMI 29.8

Pre and Post Treatment Imaging

References and Further Reading

Shroff N, Choi W, Villanueva-Meyer J, Palacio DM, Bhargava P. Pulmonary vein occlusion: A delayed complication following radiofrequency ablation for atrial fibrillation. Radiol Case Rep. 2021;16(12):3666-3671. doi:10.1016/j.radcr.2021.09.015

Fender EA, Widmer RJ, Hodge DO, et al. Assessment and Management of Pulmonary Vein Occlusion After Atrial Fibrillation Ablation. JACC: Cardiovascular Interventions. Vol 11(16); 2018. doi:10.1016/j.jcin.2018.05.020

López-Reyes R, García-Ortega A, Torrents A, et al. Pulmonary venous thrombosis secondary to radiofrequency ablation of the pulmonary veins. Respir Med Case Rep. 2018;23:46-48. doi:10.1016/j.rmcr.2017.11.008

Mizuno A, Mauler-Wittwer S, Muller H, Noble S. Recurrent pneumonia post atrial fibrillation ablation: do not forget to look for pulmonary vein stenosis. BMJ Case Rep. 2022;15(12):e250896. doi:10.1136/bcr-2022-250896

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Listen in today to another stop on our Fellows’ Case Files journey. We’re at Northwestern University for another great case presentation. Tune in, check out our associated infographic, and let us know what you think!

Meet Our Guests

Jamie Rowell is a first-year clinical fellow in the Northwestern PCCM program. She completed medical school at the Medical University of South Carolina and her internal medicine residency and Chief Residency at the University of Vermont Medical Center.

Cathy Gao is an Instructor of Medicine at Northwestern and completed her PCCM fellowship there last year. Her research focuses on using machine learning applied to ICU EHR data to characterize patient trajectories and identify potential interventions to improve outcomes.

Clara Schroedl is an Associate Professor of Medicine in Pulmonary and Critical Care and Medical Education. She is the program director of the Northwestern PCCM fellowship program, with an interest in medical education and simulation.

Case Presentation

A 25-year-old previously healthy woman presents with recurrent episodes of right chest pain and cough. In October she was treated with antibiotics and felt somewhat better but in December, she presented again with chest pain, and again was treated with antibiotics. The pain improved but she still felt breathless. In February, again she had intense chest pain interfering with life, and was given NSAIDs and took high dose TID without clear benefit.

One month later, she coughed up some bloody mucus, so now she is presenting for evaluation. The chest pain is worse with deep breaths and improves in between these episodes. She only notes it on her right side. At this point, she does sometimes feel short of breath; she used to run 5 miles but is now struggling to run two miles. She denies any unusual exposures. She went to school in central rural Ohio for a while. She has no history of pulmonary infections, no exposure to mold or animals, and no history of vaping.

Key Learning Points

1.Making the diagnosis of Fibrosing Mediastinitis :

–Etiologies: histoplasmosis, sarcoidosis, tuberculosis, IgG4, Behcet, ANCA vasculitis

–Imaging modalities: CT chest, perfusion studies, pulmonary angiogram

–Imaging characteristics: infiltrative, heterogeneous, fibrotic process that crosses fat planes and encroaches on nearby structures causing airway or vascular stenoses

Management strategies:

–No curative therapies. Goal to relieve symptom burden

–Airway stents

–Vascular stents

–Rituximab

–Antifungals, steroids generally not considered effective

References and Further Reading

Kern et al. Bronchoscopic Management of Airway Compression due to Fibrosing Mediastinitis. Annals of the American Thoracic Society 2017. 14: 1235-1359

Welby JP, Fender EA, Peikert T, Holmes DR Jr, Bjarnason H, Knavel-Koepsel EM. Evaluation of Outcomes Following Pulmonary Artery Stenting in Fibrosing Mediastinitis. Cardiovasc Intervent Radiol. 2021 Mar;44(3):384-391. doi: 10.1007/s00270-020-02714-z. Epub 2020 Nov 17. PMID: 33205295.

Westerly, BD Targeting B Lymphocytes in Progressive Fibrosing Mediastinitis. Am J Respir Crit Care Med. 2014 Nov 1; 190(9): 1069–1071.

https://rarediseases.org/rare-diseases/fibrosing-mediastinitis/#complete-report

https://pubmed.ncbi.nlm.nih.gov/21422386/

https://academic.oup.com/cid/article/30/4/688/421789

https://pubmed.ncbi.nlm.nih.gov/22033450/

https://www.sciencedirect.com/science/article/pii/S2352906715300087

https://www.atsjournals.org/doi/pdf/10.1513/AnnalsATS.201610-782RL

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We are excited to bring an a dedicated episode all about inhalers. We know there are many type of inhalers, formulations and techniques that are needed for successful use and we cover them all. Take a listen today!

Meet our Guests

Amber Lanae Martirosov is an Associate Clinical Professor at Wayne State University and is an Ambulatory Care Pharmacy Specialist in Pulmonary at Henry Ford Health in Detroit, Michigan. Amber’s specific interests include appropriate inhaler use, medication access, ILD and advocating for pharmacy collaborations.

Nick Ghionni is a first year attending at the MedStar Baltimore Hospital System. He is fresh out of PCCM fellowship at MedStar Washington Hospital Center. He completed his Internal Medicine residency at Mercy Catholic Medical Center and his specific interests include mechanical ventilation, POCUS, and medical education. Nick is our newest member of the PulmPEEPs team and serves as an Associate Editor.

Device Overview

Metered dose inhaler (MDI): delivers a dose of medication when you press on the canister. 2. Dry powder inhaler (DPI): delivers powered medication with each inhalation. 3. Soft mist inhaler (SMI): which sprays a dose of medication when pressed

Inhaler Charts

We partnered with Pyrls to show common inhaler devices, formulations and dosing. You can create a free Pyrls account at pyrls.com or our app they can download an additional bundle/more awesome charts just like these totally free!

Additional Resources

COPD Foundation

References and Further Reading

Brand P, Hederer B, Austen G, Dewberry H, Meyer T. Higher lung deposition with Respimat Soft Mist inhaler than HFA-MDI in COPD patients with poor technique. Int J Chron Obstruct Pulmon Dis. 2008;3(4):763-70. PMID: 19281091; PMCID: PMC2650591.

Levy ML, Carroll W, Izquierdo Alonso JL, Keller C, Lavorini F, Lehtimäki L. Understanding Dry Powder Inhalers: Key Technical and Patient Preference Attributes. Adv Ther. 2019 Oct;36(10):2547-2557. doi: 10.1007/s12325-019-01066-6. Epub 2019 Sep 2. PMID: 31478131; PMCID: PMC6822825.

Jindal S K, Pandey K K, Bose P P. Dry powder inhalers: Particle size and patient-satisfaction. Indian J Respir Care 2021;10:14-8

Spitzer WO, Suissa S, Ernst P, Horwitz RI, Habbick B, Cockcroft D, Boivin JF, McNutt M, Buist AS, Rebuck AS. The use of beta-agonists and the risk of death and near death from asthma. N Engl J Med. 1992 Feb 20;326(8):501-6. doi: 10.1056/NEJM199202203260801. PMID: 1346340.

Chang, YL., Ko, HK., Lu, MS. et al. Independent risk factors for death in patients admitted for asthma exacerbation in Taiwan. npj Prim. Care Respir. Med. 30, 7 (2020). https://doi.org/10.1038/s41533-020-0164-4

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Today we’re continuing our Rapid Fire Journal Club series. We’ve mainly been discussing landmark trials, but today we’re delving into a new study with interesting findings that are applicable to a common presentation in pulmonary medicine: treatment naive sarcoidosis. We’re discussing the SARCORT trial published in the European Respiratory Journal in 2023. This study evaluated a high vs low dose steroid trial in patients with sarcoidosis. Pulm PEEPs Associate Editor Luke Hedrick walks us through the study.

Article and Reference

Today we’re discussing the 2023 SARCORT Trial published in the European Respiratory Journal.

Reference: Dhooria S, Sehgal IS, Agarwal R, Muthu V, Prasad KT, Dogra P, Debi U, Garg M, Bal A, Gupta N, Aggarwal AN. High-dose (40 mg) versus low-dose (20 mg) prednisolone for treating sarcoidosis: a randomised trial (SARCORT trial). Eur Respir J. 2023 Sep 9;62(3):2300198. doi: 10.1183/13993003.00198-2023. PMID: 37690784.

Infographic

This can be downloaded on our website and will be shared on Twitter and Instagram.

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Hi everyone, we’re here with another Fellows’ Case Files. Today, we’re going virtually to Emory University School of Medicine. We’re joined by Associated Editor Luke Hedrick to dive into a critical care case. Listen in and let us know if you have any additional thoughts or questions!

Meet Our Guests

Luke Hedrick is a first-year pulmonary and critical care fellow at Emory University. He did his internal medicine residency at BIDMC in Boston. He is also one of our amazing Associate Editors here at Pulm PEEPs

Shirine Allam is an Associate Professor of Medicine at the Emory University School of Medicine where she is the Program Director of both the Pulmonary and Critical Care Medicine fellowship as well as the Critical Care Medicine fellowship. She completed her PCCM training at the Mayo Clinic in Rochester, followed by a Sleep Medicine fellowship at Stanford. She has received multiple teaching awards throughout her career

Case Presentation

A 32-year-old male is brought in by his coworkers unresponsive. He is a construction worker and was his usual self in the morning at the start of the day, but when they broke for lunch they noticed he was acting different—his arms were drooping, and while he initially was able to answer yes/no, he soon started babbling, then grunting, then vomited and became unresponsive. They laid him flat, threw cold water on him because it was 110 degrees and humid outside that day, and brought him to the ED.

When they arrive in the ED, he is unresponsive and warm to the touch. His vitals are notable for an oral temperature of 105, HR in the 160s, BP 76/34, a RR in the high 30s, and an SpO2 100% RA. His exam is relatively unremarkable other than for significant diaphoresis and both bowel and bladder incontinence.

Key Learning Points

Definition and recognition of heat stroke: Heat stroke is characterized by hyperthermia (>104°F or 40°C) accompanied by CNS dysfunction, primarily caused by exertion or exposure. Encephalitis without significant heat load does not constitute heat stroke.
Management priorities: Rapid cooling is paramount to minimize long-term complications and organ failure. Cooling should be initiated as soon as possible, even before transportation to a hospital, particularly in cases of exertional heat stroke.
Cooling methods: Surface cooling, such as immersion in ice water, is the most effective way to cool heat-stroke patients. Alternative methods include the TACO method and evaporative cooling, although they are less efficient. Refrigerated IV fluids can be used as an adjunct, but they do not replace the need for surface cooling.
Monitoring and goals: Shivering during cooling should be monitored to prevent excessive heat generation. The goal is to reach a normal core body temperature (~38°C or 100.4°F). Traditional antipyretics like aspirin and acetaminophen should be avoided due to ineffectiveness and potential toxicity.
Approach to endotracheal tube (ETT) exchange: ETT exchange requires preparation for potential complications. This includes ensuring the availability of airway equipment, sedation of the patient, and having additional personnel for assistance. Direct visualization using a video laryngoscope is recommended, along with measuring and marking the exchange catheter for proper insertion depth.

The following infographic can be downloaded from our website:

References and Further Reading

1.Epstein Y, Yanovich R. Heatstroke. New England Journal of Medicine. 2019;380(25):2449-2459. doi:10.1056/NEJMra1810762

Sorensen C, Hess J. Treatment and Prevention of Heat-Related Illness. New England Journal of Medicine. 2022;387(15):1404-1413. doi:10.1056/NEJMcp2210623

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Today on our Rapid Fire Journal Club series, we’re discussing the Novel START study published in the NEJM in 2019. This study evaluated multiple strategies for the management of mild asthma with exacerbations, and it guides our current therapeutic approach. Pulm PEEPs Associate Editor Luke Hedrick walks us through the study. If you take care of asthma patients, be it in a primary care clinic, pulmonary clinic, or the hospital, make sure to listen in!

Article and Reference

Today we’re discussing the 2019 Novel START Study published in NEJM

Reference: Beasley R, Holliday M, Reddel HK, Braithwaite I, Ebmeier S, Hancox RJ, Harrison T, Houghton C, Oldfield K, Papi A, Pavord ID, Williams M, Weatherall M; Novel START Study Team. Controlled Trial of Budesonide-Formoterol as Needed for Mild Asthma. N Engl J Med. 2019 May 23;380(21):2020-2030. doi: 10.1056/NEJMoa1901963. Epub 2019 May 19. PMID: 31112386.

Infographic

This can be downloaded on our website and will be shared on Twitter and Instagram.

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We’re starting off 2024 with a bang!! Today we’re hosting another expert Roundtable discussion and we’re joined by internationally recognized experts in the field. We’ll tackle everything from teaching about sepsis, to how to incorporate guidelines into education and practice, to future research directions in the field. This is a can’t-miss discussion. Let us know what you think and other sepsis questions you have!

Meet Our Guests

Dr. Derek Angus is a Professor at the University of Pittsburgh where he holds the Mitchell P. Fink Endowed Chair in Critical Care Medicine and is the Chair of the Department of Critical Care Medicine. He is a world-renowned researcher in a range of critical care topics including sepsis, has hundreds of publications, and has led numerous NIH-funded studies.

Dr. Hallie Prescott is an Associate Professor in Pulmonary and Critical Care Medicine at the University of Michigan. She is the Co-Chair of the Surviving Sepsis Campaign Guidelines and is also an internationally recognized expert due to her research in improving sepsis outcomes. She has been recognized by both medical journals and professional societies for her outstanding contributions to the field.

Summary of Episode Discussion Topics

1. Sepsis Guidelines and Education

Surviving Sepsis Guidelines: Stressed as essential reading for professionals in pulmonary and critical care. They provide a structured approach to sepsis management.
Teaching Approaches: Transition from during-rounds teaching to focused, separate teaching sessions for trainees. Emphasizes the need to go beyond guidelines to include discussions on seminal articles, management strategies, and areas lacking robust data.

2. Clinical Skills and Decision Making in Sepsis Care

Early Recognition and Polypharmacy: Highlighted the need for timely sepsis identification and caution against excessive polypharmacy.
Mental Models in Care: Encourages building comprehensive mental models for understanding sepsis, stressing the importance of not just treating symptoms but understanding underlying causes.

3. Implementation of Sepsis Guidelines

Guideline Application in Bedside Care: Discusses the challenge of applying guidelines while considering patient-specific factors.
Fluid Resuscitation Practices: Identifies fluid resuscitation as a key area for improvement, with a shift towards more conservative approaches.
Overcoming Institutional Barriers: Addresses the fear of causing harm as a significant barrier to guideline implementation and emphasizes the need for balanced decision-making.

4. Advances in Sepsis Care and Prevention

Pre-Hospital Sepsis Management: Explores the role of early intervention in community settings and the potential of wearables for early detection.
Paramedic Role in Early Antibiotic Administration: Underlines the importance of starting antibiotics in the ambulance for suspected sepsis cases.

5. Recovery and Post-Discharge Care

Post-Discharge Initiatives: Focuses on improving handoffs from ICU to ward and from hospital to home. Highlights the importance of medication reconciliation and clear communication with primary care.
Challenges in Continuity of Care: Discusses the need for clear documentation and communication during patient transitions to ensure continuity of care.

6. Future Directions in Sepsis Treatment and Research

Phenotyping for Targeted Treatment: The potential of identifying patient subgroups through phenotyping for more effective, tailored treatments.
Adaptive Trial Designs: Advocates for large-scale adaptive platform trials that can test multiple interventions across diverse patient populations.

7. Personal Involvements and Perspectives

Experts’ Current Work: The panelists share their ongoing projects and research in sepsis care, reflecting a commitment to advancing the field through comprehensive and adaptive approaches.

References and Further Reading

Evans L, Rhodes A, Alhazzani W, Antonelli M, Coopersmith CM, French C, Machado FR, Mcintyre L, Ostermann M, Prescott HC, Schorr C, Simpson S, Wiersinga WJ, Alshamsi F, Angus DC, Arabi Y, Azevedo L, Beale R, Beilman G, Belley-Cote E, Burry L, Cecconi M, Centofanti J, Coz Yataco A, De Waele J, Dellinger RP, Doi K, Du B, Estenssoro E, Ferrer R, Gomersall C, Hodgson C, Hylander Møller M, Iwashyna T, Jacob S, Kleinpell R, Klompas M, Koh Y, Kumar A, Kwizera A, Lobo S, Masur H, McGloughlin S, Mehta S, Mehta Y, Mer M, Nunnally M, Oczkowski S, Osborn T, Papathanassoglou E, Perner A, Puskarich M, Roberts J, Schweickert W, Seckel M, Sevransky J, Sprung CL, Welte T, Zimmerman J, Levy M. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021 Nov 1;49(11):e1063-e1143. doi: 10.1097/CCM.0000000000005337. PMID: 34605781.
Rudd KE, Kissoon N, Limmathurotsakul D, Bory S, Mutahunga B, Seymour CW, Angus DC, West TE. The global burden of sepsis: barriers and potential solutions. Crit Care. 2018 Sep 23;22(1):232. doi: 10.1186/s13054-018-2157-z. PMID: 30243300; PMCID: PMC6151187.
Talisa VB, Yende S, Seymour CW, Angus DC. Arguing for Adaptive Clinical Trials in Sepsis. Front Immunol. 2018 Jun 28;9:1502. doi: 10.3389/fimmu.2018.01502. PMID: 30002660; PMCID: PMC6031704.
Prescott HC, Angus DC. Enhancing Recovery From Sepsis: A Review. JAMA. 2018 Jan 2;319(1):62-75. doi: 10.1001/jama.2017.17687. PMID: 29297082; PMCID: PMC5839473.
https://mi-hms.org/quality-initiatives/sepsis-initiative
Kowalkowski M, Chou SH, McWilliams A, Lashley C, Murphy S, Rossman W, Papali A, Heffner A, Russo M, Burke L, Gibbs M, Taylor SP; Atrium Health ACORN Investigators. Structured, proactive care coordination versus usual care for Improving Morbidity during Post-Acute Care Transitions for Sepsis (IMPACTS): a pragmatic, randomized controlled trial. Trials. 2019 Nov 29;20(1):660. doi: 10.1186/s13063-019-3792-7. PMID: 31783900; PMCID: PMC6884908.
Schmidt K, Worrack S, Von Korff M, Davydow D, Brunkhorst F, Ehlert U, Pausch C, Mehlhorn J, Schneider N, Scherag A, Freytag A, Reinhart K, Wensing M, Gensichen J; SMOOTH Study Group. Effect of a Primary Care Management Intervention on Mental Health-Related Quality of Life Among Survivors of Sepsis: A Randomized Clinical Trial. JAMA. 2016 Jun 28;315(24):2703-11. doi: 10.1001/jama.2016.7207. PMID: 27367877; PMCID: PMC5122319.

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This week we are excited to bring you our podcast cross-over event as we are joined by Eddie Qian and Todd Rice, the co-founders of the ICU Ed and Todd-Cast. Listen today as we discuss the recent ACORN trial evaluating the use of Cefepime versus Pipercillin-Tazobactam in adults hospitalized with acute infection.

References: Qian ET, Casey JD, Wright A, Wang L, Shotwell MS, Siemann JK, Dear ML, Stollings JL, Lloyd BD, Marvi TK, Seitz KP, Nelson GE, Wright PW, Siew ED, Dennis BM, Wrenn JO, Andereck JW, Han JH, Self WH, Semler MW, Rice TW; Vanderbilt Center for Learning Healthcare and the Pragmatic Critical Care Research Group. Cefepime vs Piperacillin-Tazobactam in Adults Hospitalized With Acute Infection: The ACORN Randomized Clinical Trial. JAMA. 2023 Oct 24;330(16):1557-1567.

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This week for our Rapid Fire Journal Club we’re talking about The Lung Health Study published in 1994 in JAMA. This study evaluates the impact of smoking cessation and short-acting bronchodilators on the decline of lung health. Pulm PEEPs Associate … Continue reading →

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We’re back with our Top Consults series to talk about Lung Transplant! This is a topic that every pulmonologist should have background knowledge about since it impacts the care of patients with end-stage lung disease of any cause. We will … Continue reading →

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We are excited to bring you a fantastic episode today where we are joined by two guest experts to discuss the recent JAMA Surgery manuscript, “Clinical Implications of Removing Race-Corrected Pulmonary Function Tests for African American Patients Requiring Surgery for … Continue reading →

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Rapid Fire Journal Club returns with a deep dive into the 2020 ETHOS Trial published in The New England Journal of Medicine examining triple therapy for moderate to severe COPD. Pulm PEEPs Associate Editor Luke Hedrick takes us through this … Continue reading →

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This week on Pulm PEEPs, we are excited to be cross-posting an episode that Dave Furfaro did on the ATS Breathe Easy Podcast. Listen to hear a discussion about the best way to create a positive learning environment in the … Continue reading →

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We are excited to bring you a special episode where we are joined by author Dr. Hanna Wunsch and will discuss her book, “The Autumn Ghost: How the Battle Against a Polio Epidemic Revolutionized Modern Medical Care. Meet our Guests … Continue reading →

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We are thrilled to be back with another episode in our Top Consults series. We are talking about Solitary Pulmonary Nodules, which is something every pulmonologist will encounter in the clinic and on in-patient consults. We go through a number … Continue reading →

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We are thrilled today to be previewing CHEST 2023! The Annual Meeting is taking place October 8th – 11th in Honolulu, Hawaii, and we are joined today by CHEST enthusiasts and the past, present, and future conference chairs. Listen now … Continue reading →

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We’re excited to be back with another Fellows’ Case Files. Today, we’re visiting the University of Pittsburgh to meet a fantastic fellow and a dedicated educator, and to hear about a fascinating case. Let us know if you’ve ever had … Continue reading →

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Welcome to our final episode highlighting content featured through the ATS Critical Care Assembly from ATS 2023. Today we are going to be talking about one of the Critical Care Assembly symposiums entitled: Fail Smarter and Learn Faster: Moving Beyond … Continue reading →

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We’re back with our second episode of our Rapid Fire Journal Club. As a reminder, we will be reviewing articles in 10 minutes or less and sharing them with an infographic describing the findings of the trial. We are focusing … Continue reading →

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We’re diving back into some pleural fluid today (okay that is kind of gross to think about and we apologize). If you haven’t listened to our prior pleural effusion episodes and want to start from the top, then check out … Continue reading →

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Today we’re back with another stop on our Fellows’ Case Files journey. We’re at Boston University and Boston Medical Center with an outstanding fellow, the program director, and an expert guest to dive into a new case. Tune in to … Continue reading →

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We are introducing a new feature today on Pulm PEEPs! In our Rapid Fire Journal Club series, we will be reviewing landmark trials in pulmonary and critical care medicine in 10 minutes or less, and sharing a high-yield summary graphic. … Continue reading →

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We are thrilled to spend time with Dr. Jessica Zitter who is an expert in critical care and palliative care medicine, author, speaker, and documentary filmmaker. We are honored to have her join the show today to discuss her work … Continue reading →

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We are so excited to be joined today by the Glaucomfleckens. Listen today as we meet Kristin Flannary or Lady Glaucomflecken as well as Will Flanary better known as Dr. Glaucomflecken. Learn about the history behind the Glaucomflecken name, the … Continue reading →

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We are extremely excited to be hosting this episode in collaboration with CardioNerds! We have known Amit and Dan for many years, and they have been huge supporters of Pulm PEEPs, so it is an honor to address a topic … Continue reading →

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We’re podcasting again today from #ATS2023! Yesterday, we heard all about the conference in general, with some great recaps and previews of the remaining sessions. Today, we are coming to you in collaboration with the Critical Care Assembly to preview one of the symposiums they are hosting. This session is about Cardiac Arrest: New Science and Changing Guidelines and is happening today (the day of podcast release, 5/23/23)! If you’re interested in hearing more after the episode then please plan to attend at 2:15 PM in Room 150 A-B.

For those of you who aren’t at the conference, or couldn’t make this session, we’ll talk about some of the key points and discussion topics. We will additionally be talking to the chairs of other symposiums over the next coming months so stay tuned for some more highlights from ATS 2023.

Meet Our Guest

Ari Moskowitz is an Assistant Professor of Medicine at Montefiore Medical Center / Albert Einstein College of Medicine. He is additionally the MICU Director at Montefiore Einstein and Director of Critical Care Quality Improvement. He is an NIH-funded researcher and has conducted research in cardiac arrest care, sepsis, and ARDS.

Meet our Collaborators

The American Thoracic Society Critical Care Assembly is the largest Assembly in the American Thoracic Society. Their members include a diverse group of intensivists and care providers for both adult and pediatric critically ill patients. The primary goal of the Critical Care Assembly is to “improve the care of the critically ill through education, research, and professional development.”

References and Further Reading

Nielsen N, Wetterslev J, Cronberg T, Erlinge D, Gasche Y, Hassager C, Horn J, Hovdenes J, Kjaergaard J, Kuiper M, Pellis T, Stammet P, Wanscher M, Wise MP, Åneman A, Al-Subaie N, Boesgaard S, Bro-Jeppesen J, Brunetti I, Bugge JF, Hingston CD, Juffermans NP, Koopmans M, Køber L, Langørgen J, Lilja G, Møller JE, Rundgren M, Rylander C, Smid O, Werer C, Winkel P, Friberg H; TTM Trial Investigators. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013 Dec 5;369(23):2197-206. doi: 10.1056/NEJMoa1310519. Epub 2013 Nov 17. PMID: 24237006.
Dankiewicz J, Cronberg T, Lilja G, Jakobsen JC, Levin H, Ullén S, Rylander C, Wise MP, Oddo M, Cariou A, Bělohlávek J, Hovdenes J, Saxena M, Kirkegaard H, Young PJ, Pelosi P, Storm C, Taccone FS, Joannidis M, Callaway C, Eastwood GM, Morgan MPG, Nordberg P, Erlinge D, Nichol AD, Chew MS, Hollenberg J, Thomas M, Bewley J, Sweet K, Grejs AM, Christensen S, Haenggi M, Levis A, Lundin A, Düring J, Schmidbauer S, Keeble TR, Karamasis GV, Schrag C, Faessler E, Smid O, Otáhal M, Maggiorini M, Wendel Garcia PD, Jaubert P, Cole JM, Solar M, Borgquist O, Leithner C, Abed-Maillard S, Navarra L, Annborn M, Undén J, Brunetti I, Awad A, McGuigan P, Bjørkholt Olsen R, Cassina T, Vignon P, Langeland H, Lange T, Friberg H, Nielsen N; TTM2 Trial Investigators. Hypothermia versus Normothermia after Out-of-Hospital Cardiac Arrest. N Engl J Med. 2021 Jun 17;384(24):2283-2294. doi: 10.1056/NEJMoa2100591. PMID: 34133859.
Vallentin MF, Granfeldt A, Meilandt C, Povlsen AL, Sindberg B, Holmberg MJ, Iversen BN, Mærkedahl R, Mortensen LR, Nyboe R, Vandborg MP, Tarpgaard M, Runge C, Christiansen CF, Dissing TH, Terkelsen CJ, Christensen S, Kirkegaard H, Andersen LW. Effect of Intravenous or Intraosseous Calcium vs Saline on Return of Spontaneous Circulation in Adults With Out-of-Hospital Cardiac Arrest: A Randomized Clinical Trial. JAMA. 2021 Dec 14;326(22):2268-2276. doi: 10.1001/jama.2021.20929. PMID: 34847226; PMCID: PMC8634154.
Yannopoulos D, Bartos J, Raveendran G, Walser E, Connett J, Murray TA, Collins G, Zhang L, Kalra R, Kosmopoulos M, John R, Shaffer A, Frascone RJ, Wesley K, Conterato M, Biros M, Tolar J, Aufderheide TP. Advanced reperfusion strategies for patients with out-of-hospital cardiac arrest and refractory ventricular fibrillation (ARREST): a phase 2, single centre, open-label, randomised controlled trial. Lancet. 2020 Dec 5;396(10265):1807-1816. doi: 10.1016/S0140-6736(20)32338-2. Epub 2020 Nov 13. PMID: 33197396; PMCID: PMC7856571.
Suverein MM, Delnoij TSR, Lorusso R, Brandon Bravo Bruinsma GJ, Otterspoor L, Elzo Kraemer CV, Vlaar APJ, van der Heijden JJ, Scholten E, den Uil C, Jansen T, van den Bogaard B, Kuijpers M, Lam KY, Montero Cabezas JM, Driessen AHG, Rittersma SZH, Heijnen BG, Dos Reis Miranda D, Bleeker G, de Metz J, Hermanides RS, Lopez Matta J, Eberl S, Donker DW, van Thiel RJ, Akin S, van Meer O, Henriques J, Bokhoven KC, Mandigers L, Bunge JJH, Bol ME, Winkens B, Essers B, Weerwind PW, Maessen JG, van de Poll MCG. Early Extracorporeal CPR for Refractory Out-of-Hospital Cardiac Arrest. N Engl J Med. 2023 Jan 26;388(4):299-309. doi: 10.1056/NEJMoa2204511. PMID: 36720132.

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We are thrilled today here at Pulm PEEPs to be coming to you live from the American Thoracic Society 2023 Annual Meeting. We are joined by three fantastic speakers, and ATS leaders to discuss the highlights and events of the conference, and to share some great learning points along the way. The episode is being released immediately after recording today, Monday 5/22/23, so if you’re at the conference now make sure to listen for some extremely timely recommendations. If you’re not here in DC, we’ve highlighted some learning points that you can take away and some wisdom on how to maximize your conference experience!

We will be coming out with another episode tomorrow highlighting one of the ATS sessions, and we will continue to review symposiums from the conference throughout the year with ATS members and organizers.

Meet The Guests

Debra Boyer is a Pediatric Pulmonologist at Nationwide Children’s Hospital and has devoted much of her career to her patients and numerous trainees. Debra has been extensively involved with ATS as a prior chair of the Education Committee, and the Assembly on Pediatrics Planning Committee, and is currently on the Board of Directors and current Co-Chair of the ATS International Conference Committee.

Molly Hayes is an Assistant Professor of Medicine at Beth Israel Deaconess Medical Center and Harvard Medical School, the Director of the MICU at BIDMC, and the Director of External Education at the Carl J Shapiro Institute for Education and Research. She is also a course director for a yearly CME course on principles of critical care medicine run by BIDMC and HMS. Molly has been extensively involved with ATS as well and has served on the Education Committee, currently as a vice chair, chairs the Core Curriculum for the conference, is the chair for the Subcommittee on Education in Critical Care for the Critical Care Assembly’s Programming Committee, and has been very involved in the Section of Medical Education for the last several years.

Julianna Ferreria is an Associate Professor of Pulmonary and Critical Care Medicine at the University of Sao Paulo Medical School in Brazil, and her work focuses on mechanical ventilation. She has made a significant impact on global health initiatives and serves as the Co-Director of the MECOR program in Latin America for ATS. Julianna has also been extremely involved with ATS Critical Care Assembly Program Committee and was just awarded the Inaugural Philip Hopewell Prize for her commitment to research in low and middle-income countries.

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This week we are joined by one of our Associate Editors, Tess Litchman, as well as two guest experts to discuss two disease states that involve both the liver and the lung. Join us as we go through how to differentiate portopulmonary hypertension and hepatopulmonary syndrome.

Meet the Guests

Tess Litchman is a senior resident at Beth Israel Deaconess Medical Center and is one of the Associate Editors for PulmPEEPs. Tess will be continuing her training as a Pulmonary and Critical Care Medicine fellow at Brigham and Women’s Hospital next year.

Tyler Peck is an Instructor in Medicine at Beth Israel Deaconess Medical Center in the Division of Pulmonary and Critical Care Medicine. Tyler’s clinical and research interests are in pulmonary vascular disease and pulmonary hypertension.

Michael Curry is an Associate Professor of Medicine at Beth Israel Deaconess Medical Center and Section Chief of the Hepatology Department at BIDMC.

Further Readings and References

Rodríguez-Roisin R, Krowka MJ. Hepatopulmonary syndrome–a liver-induced lung vascular disorder. N Engl J Med. 2008 May 29;358(22):2378-87. doi: 10.1056/NEJMra0707185. PMID: 18509123

Krowka MJ, Fallon MB, Kawut SM, et al. International Liver Transplant Society Practice Guidelines: Diagnosis and Management of Hepatopulmonary Syndrome and Portopulmonary Hypertension. Transplantation 2016; 100:1440.

Peppas, S., Nagraj, S., Koutsias, G., Kladas, M., Archontakis-Barakakis, P., Schizas, D., Giannakoulas, G., Palaiodimos, L., & Kokkinidis, D. G. (2022). Portopulmonary Hypertension: A Review of the Current Literature. Heart, lung & circulation, 31(9), 1191–1202. https://doi.org/10.1016/j.hlc.2022.04.056

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This week on Pulm PEEPs we are thrilled to share a collaboration with the American Thoracic Society Assembly on Respiratory Cell & Molecular Biology. We are joined by two expert members of the ATS RCMB Assembly who have done basic and translational research in respiratory biology and lung disease. We explore the topic of Short Telomeres and their role in lung disease. With the annual ATS Conference just around the corner, this is a great intro episode for everyone from aspiring researchers and clinical pulmonologists.

Meet The Guests

Mark Snyder is an Assistant Professor of Medicine at the University of Pittsburgh Medical Center, and a member of the Graduate Program in Microbiology and Immunology there. He does research on the role of the adaptive immune system’s role in chronic rejection after lung transplantation and has received both a Parker B Francis Foundation award and an NIH K23 grant for this work.

Jonathan Alder is an Assistant Professor of Medicine at the University of Pittsburgh. His research focuses on telomeres and their role in human health and disease. He is an accomplished researcher, was a Parker B Francis fellow, and now has an NIH RO1 studying Telomere-mediated Lung disease.

Further Reading and References

Alder JK, Armanios M. Telomere-mediated lung disease. Physiol Rev. 2022 Oct 1;102(4):1703-1720. doi: 10.1152/physrev.00046.2021. Epub 2022 May 9. PMID: 35532056; PMCID: PMC9306791.

Alder JK, Chen JJ, Lancaster L, Danoff S, Su SC, Cogan JD, Vulto I, Xie M, Qi X, Tuder RM, Phillips JA 3rd, Lansdorp PM, Loyd JE, Armanios MY. Short telomeres are a risk factor for idiopathic pulmonary fibrosis. Proc Natl Acad Sci U S A. 2008 Sep 2;105(35):13051-6. doi: 10.1073/pnas.0804280105. Epub 2008 Aug 27. PMID: 18753630; PMCID: PMC2529100.

Armanios MY, Chen JJ, Cogan JD, Alder JK, Ingersoll RG, Markin C, Lawson WE, Xie M, Vulto I, Phillips JA 3rd, Lansdorp PM, Greider CW, Loyd JE. Telomerase mutations in families with idiopathic pulmonary fibrosis. N Engl J Med. 2007 Mar 29;356(13):1317-26. doi: 10.1056/NEJMoa066157. PMID: 17392301.

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Join us as we head to Indiana University! Listen in as we discuss another great case and hear teaching points from our amazing guests.

Meet our Guests

Parth Savsani is currently an internal medicine resident at Indiana University School of Medicine. He received his undergraduate degree from the University of Wisconsin-Madison and his medical degree from the University of Illinois College of Medicine. He enjoys medical education and was selected to be the VA chief resident next year.

Maria Srour is a Pulmonary and Critical Care Fellow at Indiana University School of Medicine. She completed her internal medicine residency at Saint Louis University where she was also a chief resident, and received her medical degree from IU. She works in global health to improve care for sepsis patients in low resources settings, and is currently pursuing her MPH.

Laura Hinkle is a Indiana University die hard and has been there from her since medical school through residency and fellowship, and is now an Assistant Professor of Clinical Medicine and the Associate Program Director for the Pulmonary and Critical Care Medicine Fellowship. She will be taking over as the Program Director July 1, 2023. She is a dedicated educator and is the Key Clinical Educator for Pulmonary and Critical Care, and the Director of the Clinical Transitions Curriculum. Additionally, she is working on a Master’s Degree in Education through the University of Cincinnati.

Case Presentation

A male in her early 60s is transferred from a neighboring facility with a 1 week history of fatigue and lethargy. Three days prior to presentation he developed dyspnea and increased weakness with a near fall at home. HIs family also reported recent fevers, chills, dyspnea, and diarrhea. On his way to seek evaluation, he developed slurred speech without any other focal abnormalities.

Additional information is summarized as below:

Follow along our episode to hear the final diagnosis and key teaching points from the case!

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Join us as we head to the Texas Medical Center and are joined by Dr. Bitar and Dr. Gotur from Houston Methodist Pulmonary and Critical Care Medicine.

Meet our Guests

Dr. Mohamad Bitar is a Pulmonary and Critical Care Fellow at the Houston Methodist Pulmonary and Critical Care Program in Houston, Texas. Dr. Bitar completed his medical school at Misr University for Science and Technology and his Internal Medicine residency at Good Samaritan Hospital.

Dr. Deepa Gotur is an Associate Professor of Clinical Medicine at Weill Cornell Medical College and an Adjunct Associate professor at Texas A&M. She is also the Pulmonary and Critical Care Program Director at Houston Methodist. She is a sepsis and ARDS researcher, as well as a dedicated educator.

Case Presentation

A 40s-year-old male presents with 3 months of progressive shortness of breath. He was diagnosed with COVID and given treatment with steroids, and antibiotics with no response.

He presented to the hospital 3 months later after not being able to carry out daily activities and was found to have low oxygen saturation

Admitted, initial CT Chest – showed “Non-specific patchy ground-glass bilateral pulmonary infiltrates with Coarsened interstitial markings that could be related to COVID-19/atypical infection”

References and further reading

Silva, C. Isabela S. MD, PhD; Müller, Nestor L. MD, PhD. Idiopathic Interstitial Pneumonias. Journal of Thoracic Imaging 24(4):p 260-273, November 2009.

2.Gruden JF, Naidich DP, Machnicki SC, Cohen SL, Girvin F, Raoof S. An Algorithmic Approach to the Interpretation of Diffuse Lung Disease on Chest CT Imaging: A Theory of Almost Everything. Chest. 2020 Mar;157(3):612-635.

Ryu JH, Daniels CE, Hartman TE, Yi ES. Diagnosis of interstitial lung diseases. Mayo Clin Proc. 2007 Aug;82(8):976-86.

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We continue our Top Consult Series on Pleural Disease and bring you a dedicated episode on Parapneumonic effusions. We are joined by two guest experts, Dr. David Feller-Kopman and Dr. Mihir Parikh. Listen in as we discuss the spectrum of parapneumonic effusions, including simple parapneumonic effusions, complicated parapneumonic effusions, and empyema. You will hear what to look for on imaging, what tests to send with pleural drainage as well as discuss the need for surgical consultation.

Meet our Guests

Dr. Mihir Parikh is currently an Assistant Professor of Medicine and academic interventional pulmonologist at Beth Israel Deaconess Medical Center. He is a highly esteemed educator and has worked to incorporate simulation training to improve procedural training for trainees and is a master of pleural disease.

Dr. David Feller-Kopman is a Professor of Medicine and the Section Chief of Pulmonary and Critical Care Medicine at Darmouth whose clinical and research expertise span the field of interventional pulmonology. Dr. Feller-Kopman is a true master of pleural disease, and has authored more than 225 peer-reviewed manuscripts and has been a leader for both ATS and CHEST committees.

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Today the PulmPEEPs are joined by two amazing educators as we start off our Top Consult series on Pleural Disease. Join us today as we go through cases to learn a systematic approach for evaluation and management of pleural effusions.

Meet our Guests

Dr. Mira John received her medical degree from Tulane University School of Medicine in New Orleans and completed internal medicine residency at Icahn School of Medicine at Mount Sinai. She is currently a second-year pulmonary and critical fellow at the University of Washington.

Dr. Ylinne Lynch completed her fellowship training at the University of Washington and is currently a Clinical Instructor at the UW. She is a great medical educator and spends her clinical time on the pulmonary consult service as well as in the ICU.

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We are extremely excited for another PulmPEEPs Roundtable table discussion today. We have spent multiple episodes talking about different aspects of ARDS and respiratory failure. Today, multiple expert guests return, as well as a new guest to the show, to discuss the future of ARDS research. This is a can’t miss discussion that is so jam-packed with pearls you’ll have to listen twice!

Meet Our Guests

Carolyn Calfee is a Professor of Medicine and Anesthesia at the University of California, San Francisco. She is a world-renowned ARDS researcher and has authored multiple landmark studies in the field. She previously joined us for a discussion on ARDS precision medicine and phenotypes.

Ewan Goligher is an Assistant Professor at the University of Toronto and University Health Network. He has published many practice-changing papers in ARDS. These have included prospective studies and some fantastic retrospective analyses that have fundamentally shaped our interpretation of trial results. He previously came on the show discussing lung and diaphragm protection.

Sarina Sahetya is an Assistant Professor of Medicine at Johns Hopkins. She is a funded researcher in ARDS and respiratory physiology and has published multiple studies on lung protection and ARDS. She last helped us understand how to titrate PEEP in ARDS.

Matthew Semler is an Assistant Professor of Medicine and Biomedical Informatics at Vanderbilt University Medical Center, where he is also the Associate MICU Director and the co-director of the Inpatient Division of the Learning Healthcare System at Vanderbilt. Through his role as Chair of the Steering Committee for the Pragmatic Critical Care Research Group, he has helped lead more than two dozen randomized trials leading to multiple high-impact publications.

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Welcome back to Pulm PEEPs Fellows’ Case Files series. We are traveling to the midwest to visit The Ohio State University College of Medicine and hear about another great pulmonary case.

Meet Our Guests

Kashi Goyal is a second-year Pulmonary and Critical Care Fellow at The Ohio State University Wexner Medical Center. She obtained her MD at OSU, and then completed her Internal Medicine residency at Beth Israel Deaconess Medical Center. She worked as a hospitalist and educator before going back to fellowship and remains passionate about medical education.

Lynn Fussner is an Associate Professor of Internal Medicine at OSU and has been there since completing her fellowship and Post-doctorate at Mayo Clinic. In addition to her clinical work in the multidisciplinary vasculitis clinic, she is a translational researcher with a focus on inflammatory pulmonary disorders and vasculitis.

Avi Cooper is an Assistant Professor of Medicine at Ohio State University College of Medicine and the Program Director of the Pulmonary and Critical Care Fellowship. He is an Associate Editor at the Journal of Graduate Medical Education. Last but not least, he co-hosts the Curious Clinician Podcast, one of the most popular medical education podcasts.

Patient Presentation

Key Learning Points

*Spoilers Ahead* If you want to think through the case on your own we advise listening to the episode first before looking at these points.

The three most common causes of cough in adults in the USA are cough variant asthma, GERD, and post-nasal drip
A post-viral cough can last for 8-12 weeks and still be within normal
Sinus symptoms in a chronic cough can just be sinusitis and post-nasal drip, but should consider eosinophilic granulomatosis with polyangiitis (EGPA), aspirin exacerbated respiratory disease (AERD), cystic fibrosis, or ciliary dyskinesia.
Examination of a wheeze
- Fixed sound vs variable
- Pitch: larger central airways vs lower peripheral airways
- Is it throughout the cycle or at a certain phase?
- Ask the patient to cough before listening and ask them to breathe out through their mouth
Approach to eosinophilia in a patient with cough and dyspnea
- Multi-system involvement vs lungs
  - Multi-system involvement
    - Vasculitis
    - Parasitic infection
    - Hematologic malignancy
    - Medication side effect
    - Primary hypereosinophilic syndromes
  - Within the lungs:
    - Parenchymal disease
      - Loeffler’s syndrome
      - Eosinophilic pneumonia
    - Airway disease
      - Asthma
      - ABPA
If you have a high suspicion for airways disease, PFTs should be requested with bronchodilator testing regardless of the degree of obstruction on baseline spirometry
Asthma alone should not cause ground glass opacities, so if see these in a patient with asthma we think about:
- Infection, especially atypical infections
- EGPA
- Vasculitis with DAH
- ABPA
- Hypogammaglobulinemia or other immunodeficiency
EGPA diagnosis
- ANCA testing is only positive in 60% of patients with EGPA so a negative test doesn’t rule it out by any means
- It is easiest to make a diagnosis when there is a clear small vessel manifestation
  - Alveolar hemorrhage
  - Mononeuritis multiplex
  - Glomerulonephritis
- Many patients with asthma, nasal polyposis, and high peripheral eosinophilia have EGPA but don’t have a clear small vessel feature of vasculitis or a positive ANCA
  - These patients typically have eosiniophilia a lot higher than when thinking about allergic phenotype asthma alone. As a rule of thumb, at least an absolute eosinophil count > 1000

*References and Further Reading*

Carr TF, Zeki AA, Kraft M. Eosinophilic and Noneosinophilic Asthma. Am J Respir Crit Care Med. 2018;197(1):22-37. doi:10.1164/rccm.201611-2232PP
Cottin V. Eosinophilic Lung Diseases. Clin Chest Med. 2016;37(3):535-556. doi:10.1016/j.ccm.2016.04.015
Grayson PC, Ponte C, Suppiah R, et al. 2022 American College of Rheumatology/European Alliance of Associations for Rheumatology Classification Criteria for Eosinophilic Granulomatosis with Polyangiitis. Ann Rheum Dis. 2022;81(3):309-314. doi:10.1136/annrheumdis-2021-221794
Wechsler ME, Akuthota P, Jayne D, et al. Mepolizumab or Placebo for Eosinophilic Granulomatosis with Polyangiitis. New England Journal of Medicine. 2017;376(20):1921-1932. doi:10.1056/NEJMoa1702079

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Today the PulmPEEPs are discussing Lung and Diaphragm Protective Ventilation with two experts in the field. We are joined by Dr. Jose Dianti and Dr. Ewan Goligher.

Meet Our Guests

Dr. Jose Dianti is a clinical and research fellow at the University of Toronto and University Health Network. He completed his residency in Critical Care and worked as a critical care attending previously at the Hospital Italiano in Buenos Aires, Argentina. He is particularly interested in ventilator induced lung injury and personalized ventilation strategies. Dr. Ewan Goligher is an Assistant Professor at the University of Toronto and University Health Network, and is a world renowned researcher in the mechanisms of ventilator induced lung and diaphragm injury.

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For the first Pulm PEEPs episode of 2023, we are starting off with a bang and a Roundtable discussion about venovenous extracorporeal membrane oxygenation (VV-ECMO). VV-ECMO has been increasing in use in the intensive care unit for patients with severe respiratory failure, especially during the COVID-19 pandemic. We are joined by experts in the field, Cara Agerstrand, Eddy Fan, and Nida Qadir, to discuss the basics of how ECMO works, physiologic goals, when to use ECMO for patients with ARDS, and much more. Let us know your thoughts and stay tuned for more great content in 2023.

Meet Our Guests

Cara Agerstrand is an Associate Professor of Medicine at Columbia University Irving Medical Center / NewYork-Presbyterian Hospital, where she is also the Director of the Medical ECMO Program. She is an international renown ECMO expert and is the current Conference Chair for the Extracorporeal Life Support Organization (or ELSO). Finally, she is a lauded educator and has received the American College of Chest Physicians Distinguished Educator Award.

Eddy Fan is an Associate Professor at the University of Toronto, and the University Health Network / Mount Sinai Hospital. He is also the Director of Critical Research and the Medical Director of the Extracorporeal Life Support Program. He has literally 100s of publications about ARDS, ECMO, and critical care, chairs the ELSO Research Committee, and spearheads multiple international collaborative studies.

Nida Qadir is an Associate Professor at the University of California Los Angeles and is an Associate Director of the MICU, as well as the co-director of the Post-ICU Recovery Clinic. Nida is also on the Critical Care Editorial Board for CHEST and is a highly regarded pulmonary and critical care educator.

Key Learning Points

VV- ECMO Basic Components and Core Physiology

Oxygenation Delivery on VV-ECMO

ECMO Flow / Total CO = 0.5ECMO Flow / Total CO = 0.7 Carbon Dioxide Removal on VV-ECMO

Flows and Line Pressures on VV-ECMO

ECMO for ARDS

Should be considered after conventional therapies have failed (including ventilator optimization and proning)
Allows for ultra-lung protective ventilation
Lung rest means settings that minimize ventilator-induced lung injury
EOLIA Trial (see below) shows that ECMO can be delivered safely, and likely has a benefit in severe ARDS, although the magnitude of that benefit remains uncertain. A Bayesian re-analysis showed a high likelihood of benefit even if skeptical of ECMO

ECMO For Bridge to Lung Transplant

Allows for patients to maintain gas exchange while awaiting transplant
Ideally done with patient extubated
Can allow for patients to maintain nutrition and mobility while awaiting transplant

References and Further Reading

Brodie D, Bacchetta M. Extracorporeal Membrane Oxygenation for ARDS in Adults. N Engl J Med. 2011;365(20):1905-1914. doi:10.1056/NEJMct1103720
Munshi L, Brodie D, Fan E. Extracorporeal Support for Acute Respiratory Distress Syndrome in Adults. NEJM Evidence. 2022;1(10):EVIDra2200128. doi:10.1056/EVIDra2200128
Combes A, Hajage D, Capellier G, et al. Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome. New England Journal of Medicine. 2018;378(21):1965-1975. doi:10.1056/NEJMoa1800385
Goligher EC, Tomlinson G, Hajage D, et al. Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome and Posterior Probability of Mortality Benefit in a Post Hoc Bayesian Analysis of a Randomized Clinical Trial. JAMA. 2018;320(21):2251-2259. doi:10.1001/jama.2018.14276
Erdeneochir E, Strunina S. Analysis of blood flow in extracorporeal membrane oxygenation circuit. Published online 2017.
Schmidt M, Pham T, Arcadipane A, et al. Mechanical Ventilation Management during Extracorporeal Membrane Oxygenation for Acute Respiratory Distress Syndrome. An International Multicenter Prospective Cohort. Am J Respir Crit Care Med. 2019;200(8):1002-1012. doi:10.1164/rccm.201806-1094OC
Tonna JE, Abrams D, Brodie D, et al. Management of Adult Patients Supported with Venovenous Extracorporeal Membrane Oxygenation (VV ECMO): Guideline from the Extracorporeal Life Support Organization (ELSO). ASAIO Journal. 2021;67(6):601-610. doi:10.1097/MAT.0000000000001432
Hayanga JWA, Hayanga HK, Holmes SD, et al. Mechanical ventilation and extracorporeal membrane oxygenation as a bridge to lung transplantation: Closing the gap. J Heart Lung Transplant. 2019;38(10):1104-1111. doi:10.1016/j.healun.2019.06.026

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Today we have a Pulm PEEPs special episode! Dave and Kristina chat post-call about their respective nights in the ICU. Hear about clinical reasoning on the fly, some crucial learning points, insights on procedural troubleshooting, and about the value of end-of-life discussions. The post-call brain fog and jokes only add to the learning fun!

*References and Further Reading*

Stein PD, Yaekoub AY, Matta F, Kleerekoper M. Fat embolism syndrome. Am J Med Sci. 2008 Dec;336(6):472-7. doi: 10.1097/MAJ.0b013e318172f5d2. PMID: 19092320.

Kainoh T, Iriyama H, Komori A, Saitoh D, Naito T, Abe T. Risk Factors of Fat Embolism Syndrome After Trauma: A Nested Case-Control Study With the Use of a Nationwide Trauma Registry in Japan. Chest. 2021 Mar;159(3):1064-1071. doi: 10.1016/j.chest.2020.09.268. Epub 2020 Oct 13. PMID: 33058815.

Lara AR, Schwarz MI. Diffuse alveolar hemorrhage. Chest. 2010 May;137(5):1164-71. doi: 10.1378/chest.08-2084. PMID: 20442117.

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We’re excited to be back with another episode in our Pulm PEEPs Fellows’ Case Files series! This is a particularly exciting case since it is our first episode where some intrepid fellows reached out to us with an interesting case they had encountered. If you have a great case, please let us know and you can follow in their footsteps! Pack your bags, and let’s head to Mississippi to learn about another great pulmonary and critical care case.

Meet our Guests

Meredith Sloan is a pulmonary and critical care fellow at the University of Mississippi. She completed her medical school at the Medical University of South Carolina College of Medicine, and her residency at the University of Mississippi.

Kevin Kinloch is a senior fellow at the University of Mississippi Medical Center where he also completed his internal medicine residency. He completed medical school at Meharry Medical College.

Jessie Harvey is an Associate professor of Medicine at the University of Mississippi and is the Pulmonary and Critical Care Program Director. She is also the Director of the MICU, and has been at MMC since medical school. She is a dedicated educator and leads the POCUS curriculum for IM residents and PCCM fellows

Patient Presentation

A 65-year-old man presented to the ED with worsening hemoptysis over the last several days after a recent lung biopsy. The patient is an active smoker with at least a 50-pack-year history, and he had been having a cough with small-volume hemoptysis. He ultimately had a chest CT that revealed a large LUL mass (10.3 x 6.4 cm). Given this suspicious mass, three days prior to his ED presentation, he was taken for bronchoscopy with BAL, transbronchial biopsies, endobronchial biopsy, EBUS guided TBNA of 11L, along with TBNA, brushing and radial EBUS TBNA of his left upper lobe mass.

Key Learning Points

*Spoilers Ahead* If you want to think through the case on your own we advise listening to the episode first before looking at these points.

Staging procedures for masses

Enough tissue so we can make a diagnosis and do molecular testing
Highest staging when getting your biopsy

POCUS for respiratory failure

Absence of lung slidings
- Especially post procedure
The presence of a new pleural effusion after a procedure could indicate hemothorax
- Hematocrit sign – an echogenic layering of material in an effusion
New B-lines, especially if prior there were only A-lines
- Cardiogenic or non-cardiogenic pulmonary edema, alveolar hemorrhage, or infection
Diaphragmatic function
- Excursion
- Diaphragm thickness

*References and Further Reading*

1.Scorsetti M, Leo F, Trama A, D’Angelillo R, Serpico D, Maerelli M, Zucali P, Gatta G, Garassino MC. Thymoma and thymic carcinomas. Critical Reviews in Oncology/Hematology. 2016; 99:332-350.

Singh TD, Wijdicks EFM. Neuromuscular respiratory failure. Neurol Clin 2021; 39:333-353.

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This week on Pulm PEEPs, Dave and Kristina are joined by Jason Maley and Ann Parker, two pulmonary and critical care physicians who are leaders in treating patients with Long COVID, or Post-Acute Sequelae of SARS-CoV-2. Both of them help run the Long COVID clinics at their respective institutions and are part of broader consortiums dedicated to patient care. They also both participate in research to improve outcomes for patients with Long COVID and Post-Intensive Care Syndrome. In this conversation, we cover the diagnosis of Long COVID, common symptoms, abnormal test findings, possible mechanisms of disease, the impacts of variants and vaccines, treatments, and the natural history of this condition. We hope this will be helpful for providers, patients, and family members.

Meet Our Guests

Jason Maley is an Assistant Professor of Medicine at Beth Israel Deaconess Medical Center and Harvard Medical School. He is the Director of the BIDMC Critical Illness and COVID-19 Survivorship Program, and the Co-Chair of the American Academy of Physical Medicine and Rehabilitation Postacute Sequeleae of SARS-CoV-2 infection (PASC) initiative. He is NIH funded to study post-COVID patients.

Ann Parker is an Assistant Professor of Medicine at Johns Hopkins and is the Co-Director of the Johns Hopkins Post-Acute COVID-19 team. She is NIH funded with her research focusing on survivors of respiratory failure and critical illness.

Key Learning Points

Long COVID or Post-Acute Sequelae of SARS-CoV-2 or Post-COVID condition

Long COVID was first described this way by patients so this is the common nomenclature that is used. It is also referred to as Post-Acute Sequelae of SARS-CoV-2 or Post-COVID condition
Defined by patients that have not returned to their baseline health 3 months after their acute episode of COVID-19
Major organizations in describing this disease and doing research are:
- World Health Organization
- Multiple patient-led organizations
- CDC – INSPIRE
- NIH – RECOVER

Post-COVID Clinic

Seeing patients across the spectrum of illness. Not all patients had to be critically ill or hospitalized
- The standard patient has changed over time and now the vast majority had a mild initial illness, but afterward had unusual and persistent symptoms
Patients are generally referred by their PCP or self-referred
The criteria for being seen in clinic are very loose to make sure patients are not excluded
- Many patients do not have a confirmed case of COVID since patients early in the pandemic often did not have a positive test available, and now many people are testing positive at home
Initial records review to make sure that can help patients
Standardized questionnaires
- Screening for physical impairment, mental health impairment, and cognitive impairment
Rehabilitation and multi-disciplinary based approach
It is extremely important to be aware of the bias in patient populations in Post-COVID clinics
- The population that can make it to clinic may not, and does not, represent all patients who have had COVID or have Long COVID. Patients may be limited in their ability to get to clinic based on their physical condition, financial resources, location, support, and language barriers.

Overlap of Long COVID and PICS

These conditions are very similar and certainly have a lot of overlap
For patients coming out of the ICU, screening should start with looking for known PICS symptoms.
- These domains are mental health, physical impairment, and cognitive function
There may be some unique aspects, such as:
- Severe persistent fatigue
- Extreme changes in taste and smell

Common symptoms

Many symptoms are complex and multifactorial
Neuropsycholgoicl impairment – termed “brain fog”
- Difficulty with concentration, and cognition
Anxiety
Depression
Persistent shortness of breath
- Dyspnea can be reported even with just talking for long periods of time
- “Deep breaths are just not satisfying”
Cough
Chest pain
Dysautonomia
- Palpitations, dizziness, orthostasis
Fatigue
Post-exertional malaise
Cognitive blunting or “brain fog”
Changes in sleep
Headaches

Common findings on testing in patients with Long COVID

Shortness of breath
- Some may have impaired diffusion (low DLCO) on PFTs
- However, often patients have normal or near-normal PFTs
- 10 – 20 % have air trapping on inspiratory/expiratory chest CTs that could indicate bronchiolitis
- One study showed that CPETs showed impaired oxygen extraction
  - Preserved cardiac output to exercise and no evidence of deconditioning
  - This study indicated an issue at the peripheral level (ex: vascular, mitochondrial) with oxygen extraction.

Variants

It is very difficult to say if variants differ in rates of Long COVID given that often patients do not get sequencing to know the variant and because there is overlap in the timing of variants
Further testing will continue on this going forward

Vaccines

Reduced risk of Long COVID with vaccination
- Boosting further decreases the risk compared to just the initial vaccination
There is a variable response to getting vaccinated if a patient has Long COVID
- Most patients tolerate it well and some patients have relief of symptoms
- There are some patients who can develop worsened Long COVID symptoms

References and further reading

Chippa V, Aleem A, Anjum F. Post Acute Coronavirus (COVID-19) Syndrome. In: StatPearls. StatPearls Publishing; 2022. Accessed November 14, 2022. http://www.ncbi.nlm.nih.gov/books/NBK570608/
Crook H, Raza S, Nowell J, Young M, Edison P. Long covid—mechanisms, risk factors, and management. BMJ. 2021;374:n1648. doi:10.1136/bmj.n1648
Durstenfeld MS, Sun K, Tahir P, et al. Use of Cardiopulmonary Exercise Testing to Evaluate Long COVID-19 Symptoms in Adults: A Systematic Review and Meta-analysis. JAMA Network Open. 2022;5(10):e2236057. doi:10.1001/jamanetworkopen.2022.36057
Nalbandian A, Sehgal K, Gupta A, et al. Post-acute COVID-19 syndrome. Nat Med. 2021;27(4):601-615. doi:10.1038/s41591-021-01283-z
Soriano JB, Murthy S, Marshall JC, Relan P, Diaz JV. A clinical case definition of post-COVID-19 condition by a Delphi consensus. Lancet Infect Dis. 2022;22(4):e102-e107. doi:10.1016/S1473-3099(21)00703-9
Sudre CH, Murray B, Varsavsky T, et al. Attributes and predictors of long COVID. Nat Med. 2021;27(4):626-631. doi:10.1038/s41591-021-01292-y

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