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- Jul 28, 202614 min
123. Critical Care Medicine for Non-Intensivists
Today we're joined by Dr. Molly Hayes and talking about an upcoming CME course: Principles of Critical Care Medicine for Non-Intensive Care Specialists. This is a wonderful education course covering a wide array of topics in critical care in a case-based, systematic, and peer-reviewed fashion. The course is interactive and all resources will be available for attendees afterwards for their review. You can sign up at https://learn.hms.harvard.edu/criticalmed and save using the discount code "PulmPEEPS50"!
- Jun 16, 202621 min
122. Pulm PEEPs Pearls: Steroids in Sepsis
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 Trials Every 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. Trial (Year)NRegimenKey FindingAnnane (2002)~300Hydrocortisone + fludrocortisoneMortality benefit in ACTH non-responders; criticized methodology and messy cortisol-response testing; not cleanly replicated.CORTICUS (2008)~500Hydrocortisone aloneFaster shock reversal but no mortality benefit, regardless of cortisol responsiveness. Raised (later allayed) superinfection concern. Cornerstone for abandoning routine cort-stim testing.ADRENAL (2018)~3,800Hydrocortisone aloneFaster vasopressor weaning; no 90-day mortality benefit.APROCCHSS (2018)~1,200Hydrocortisone + fludrocortisoneMortality benefit at 90 days. 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 day
- Jun 9, 20262 min
121. My Diagnosis
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.
- Apr 7, 202655 min
120. Pulm PEEPs & Irish Thoracic Society: Understanding Refractory Chronic Cough
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—combini
- Mar 24, 202647 min
119. Guideline Series: Pulmonary Embolism
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 pharmaco
- Feb 24, 202617 min
118. Pulm PEEPs Pearls: Methacholine Challenge
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) Medication ClassWashout PeriodShort-acting beta-agonists (SABA)≥ 6 hoursLong-acting beta-agonists (LABA)~24 hoursUltra-long-acting beta-agonists~48 hoursShort-acting anticholinergics (e.g., ipratropium)~12 hoursLong-acting muscarinic antagonists (LAMA, e.g., tiotropium)7 days 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 diagno
- Feb 10, 202617 min
117. Pulm PEEPs Pearls: Spontaneous Breathing Trials
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
- Jan 27, 202644 min
116. Guidelines Series: Pulmonary Hypertension – Risk Stratification and Treatment Goals
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.
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