Tag Archives: Critical Care

Critical Care

117. Pulm PEEPs Pearls: Spontaneous Breathing Trials

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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

  1. 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
  1. 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
  1. 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
  1. 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
  1. 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
  1. 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
  1. 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?
  1. Take-home pearls
  1. SBTs are stress tests of post-extubation physiology.
  2. PS 5/5 for 30 minutes is a strong default for most ICU patients.
  3. T-piece trials are valuable when false positives are costly or physiology demands it.
  4. CPAP is reasonable but supported by less robust data.
  5. 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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111. Pulm PEEPs Pearls: Methylene Blue

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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.

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. 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.
  1. 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.
  1. 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.
  1. 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.
  1. 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.
  1. 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.
  1. Practical bedside framing (“2 a.m. in the ICU”)

They emphasize three pillars of practice:

  1. Physiology – mechanism makes sense (NO / cGMP / vasodilation).
  2. Empiric evidence – small studies and meta-analyses show a signal but low-quality data.
  3. 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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106. Pulm PEEPs Pearls: ICI Pneumonitis

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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

  1. 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)
  1. 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).
  1. 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.
  1. 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.
  1. 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).
  1. Emerging Therapies
    • JAK inhibitors are under investigation as possible future options.
  1. Multidisciplinary Care
    • ICU management is a team sport — coordinate with oncology, critical care, infectious disease, and pharmacy.

 

Infographic

 

References and Further Reading

  1. Managing Immune Checkpoint Inhibitor Pneumonitis in the ICU. Montemayor, Kristina et al.CHEST Critical Care, Volume 3, Issue 1, 100126
  2. 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.
  3. 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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105. ICU Acquired Weakness

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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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    103. Fellows’ Case Files: University of Virginia

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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 shock

    Shock 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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    102. Journal Club with BMJ Thorax – Sleep and Non-Invasive Ventilation

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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

    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.

    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

    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.

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    100. ATS 2025 Critical Care Assembly: The Future of Mechanical Ventilation

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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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    99. Fellows’ Case Files: Rutgers – Robert Wood Johnson Medical School

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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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    91. Tylenol Toxicity and Acute Liver Failure

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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 about toxicology and the diagnosis and management of acute livery injury and failure.

     

    Meet Our Guests

    Kalaila Pais received her MD from Howard University College of Medicine and is currently a second year internal medicine resident at BIDMC. She is interested in pulmonary and critical care, as well as medical education. She also had the idea for this episode and was essential in its writing and production.

    Hima Veeramachaneni received her MD from University of Missouri-Kansas City School of Medicine, and her residency at Emory where she was also a Chief Resident at Grady Memorial Hospital. She is a gastroenterologist and completed her GI and transplant hepatology training at Emory. She is also now doing a critical care medicine fellowship year.

     

    Case Presentation

    Presentation: Patient found down, surrounded by liquor bottles, with coffee-ground emesis, hemodynamic instability, scleral icterus, and metabolic derangements.

    Key Lab Findings:

    • Severe transaminitis (AST >10,000, ALT ~3,000).
    • Elevated bilirubin (5.8), lactate (16), and INR (>2).
    • Metabolic acidosis with a pH of 7.04.
    • Tylenol level: 41 (slightly elevated but inconclusive without ingestion timing).

     

    Key Learning Points

    Infographic:

    Acute Liver Injury vs. Acute Liver Failure

    • Acute Liver Injury (ALI): Elevated liver enzymes without encephalopathy or significant synthetic dysfunction.
    • Acute Liver Failure (ALF): Defined by:
      • Presence of encephalopathy.
      • Coagulopathy (elevated INR).
      • Rapid onset (<26 weeks) in patients without pre-existing liver disease.
    • ALF often leads to complications such as cerebral edema, which necessitates aggressive management.

    Tylenol Toxicity and Interpretation

    • Pathophysiology:
      • Tylenol overdose overwhelms liver glutathione, leading to accumulation of NAPQI, which causes hepatocyte necrosis.
    • Interpretation of Tylenol Levels:
      • Timing of ingestion is critical to interpreting levels.
      • The Rumack-Matthew Nomogram is used for acute ingestions but requires a known ingestion time.
    • Management:
      • N-acetylcysteine (NAC): Standard of care; acts as a glutathione precursor and mitigates liver damage.
      • Early use is recommended in suspected cases of Tylenol toxicity, even if ingestion timing is unclear.

    Critical Management Principles

    • Stabilization: Focus on airway, hemodynamics, and perfusion.
      • Monitor for signs of cerebral edema (e.g., pupillary changes, seizures).
      • In select patients, use hypertonic saline to maintain sodium levels (145–150 mmol/L) to mitigate cerebral edema risks.
    • CRRT and Plasma Exchange:
      • Continuous renal replacement therapy (CRRT) for hyperammonemia and acidosis.
      • Plasma exchange (PLEX) may stabilize cytokine storms and improve survival.
    • Organ-Specific Considerations:
      • Renal failure: Common due to hepatorenal syndrome; requires CRRT.
      • Coagulopathy: Managed with blood products as needed but indicates worsening liver synthetic dysfunction.

    Prognosis and Transplant Considerations

    • King’s College Criteria: Guides transplant listing for ALF patients.
      • Factors: Encephalopathy severity, INR, lactate, bilirubin trends.
    • Ethical considerations for liver transplant in patients with substance use or overdose:
      • Emphasis on assessing social support and addressing psychiatric needs.
      • Efforts are made to ensure equitable access to transplant when warranted.

    Takeaways for Clinical Practice

    1. Broad Differential Diagnosis: Keep a wide perspective for acute liver presentations, considering toxins, infections, and systemic conditions.
    2. Early Use of NAC: Err on the side of initiating NAC when Tylenol toxicity is suspected.
    3. CNS Focus in ALF: Monitor and manage cerebral edema aggressively.
    4. CRRT & PLEX: Advanced liver support techniques are critical in select cases.
    5. Interdisciplinary Collaboration: Psychiatrists, neurocritical care, and hepatologists play pivotal roles in management.

     

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    90. Rapid Fire Journal Club: ANDROMEDA-SHOCK

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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 is a second year Internal Medicine resident at Boston University Medical Campus (BUMC).

    Article and Reference

    Today the discussion highlights the ANDROMEDA-SHOCK trial (JAMA, 2019) which evaluated whether resuscitation guided by capillary refill time (CRT) is superior to lactate-guided resuscitation in reducing mortality in patients with septic shock.

    Hernández G, Ospina-Tascón GA, Damiani LP, Estenssoro E, Dubin A, Hurtado J, Friedman G, Castro R, Alegría L, Teboul JL, Cecconi M, Ferri G, Jibaja M, Pairumani R, Fernández P, Barahona D, Granda-Luna V, Cavalcanti AB, Bakker J; The ANDROMEDA SHOCK Investigators and the Latin America Intensive Care Network (LIVEN); Hernández G, Ospina-Tascón G, Petri Damiani L, Estenssoro E, Dubin A, Hurtado J, Friedman G, Castro R, Alegría L, Teboul JL, Cecconi M, Cecconi M, Ferri G, Jibaja M, Pairumani R, Fernández P, Barahona D, Cavalcanti AB, Bakker J, Hernández G, Alegría L, Ferri G, Rodriguez N, Holger P, Soto N, Pozo M, Bakker J, Cook D, Vincent JL, Rhodes A, Kavanagh BP, Dellinger P, Rietdijk W, Carpio D, Pavéz N, Henriquez E, Bravo S, Valenzuela ED, Vera M, Dreyse J, Oviedo V, Cid MA, Larroulet M, Petruska E, Sarabia C, Gallardo D, Sanchez JE, González H, Arancibia JM, Muñoz A, Ramirez G, Aravena F, Aquevedo A, Zambrano F, Bozinovic M, Valle F, Ramirez M, Rossel V, Muñoz P, Ceballos C, Esveile C, Carmona C, Candia E, Mendoza D, Sanchez A, Ponce D, Ponce D, Lastra J, Nahuelpán B, Fasce F, Luengo C, Medel N, Cortés C, Campassi L, Rubatto P, Horna N, Furche M, Pendino JC, Bettini L, Lovesio C, González MC, Rodruguez J, Canales H, Caminos F, Galletti C, Minoldo E, Aramburu MJ, Olmos D, Nin N, Tenzi J, Quiroga C, Lacuesta P, Gaudín A, Pais R, Silvestre A, Olivera G, Rieppi G, Berrutti D, Ochoa M, Cobos P, Vintimilla F, Ramirez V, Tobar M, García F, Picoita F, Remache N, Granda V, Paredes F, Barzallo E, Garcés P, Guerrero F, Salazar S, Torres G, Tana C, Calahorrano J, Solis F, Torres P, Herrera L, Ornes A, Peréz V, Delgado G, López A, Espinosa E, Moreira J, Salcedo B, Villacres I, Suing J, Lopez M, Gomez L, Toctaquiza G, Cadena Zapata M, Orazabal MA, Pardo Espejo R, Jimenez J, Calderón A, Paredes G, Barberán JL, Moya T, Atehortua H, Sabogal R, Ortiz G, Lara A, Sanchez F, Hernán Portilla A, Dávila H, Mora JA, Calderón LE, Alvarez I, Escobar E, Bejarano A, Bustamante LA, Aldana JL. Effect of a Resuscitation Strategy Targeting Peripheral Perfusion Status vs Serum Lactate Levels on 28-Day Mortality Among Patients With Septic Shock: The ANDROMEDA-SHOCK Randomized Clinical Trial. JAMA. 2019 Feb 19;321(7):654-664. doi: 10.1001/jama.2019.0071. PMID: 30772908; PMCID: PMC6439620.

    Infographic

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