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1-20 of 889 results with category "Critical Care"

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Title: Tenecteplase Before Thrombectomy at 4.5 to 24 Hours for Basilar Artery Occlusion (ATTENTION LATE)

Category: Critical Care

Keywords: basilar artery occlusion, (PubMed Search)

Posted: 10/13/2026 by Quincy Tran, MD, PhD (Updated: 10/19/2026)

The BRIDGE-TNK trial in 2025 showed that Tenecteplase AND thrombectomy offered better functional outcome for patients with ischemic stroke from large vessel occlusion.

However, the ATTENTION LATE trial (published in September 2026) showed that for patients with basilar artery occlusion, routine administration of Tenecteplase before Thrombectomy did not improve functional outcome, when compared with thrombectomy alone, between 4.5-24 hour window, while rates of symptomatic intracranial hemorrhage were the same in both groups.

Show References

Li R, et al. JAMA. Published September 23, 2026. DOI: 10.1001/jama.2026.15496

Attachments

  • 2026_10_13 TNK for basilar occlusion-6ace89ba500f9.docx (18 Kb)


Title: Should we start home beta-blocker for patients with sepsis

Category: Critical Care

Keywords: beta-blocker, sepsis, mortality, hospital length of stay. (PubMed Search)

Posted: 10/6/2026 by Quincy Tran, MD, PhD (Updated: 10/19/2026)

In this retrospective study of 4635 patients, continuing oral beta blocker within 48 hours of presentation for patients with sepsis was associated with a reduced risk of all-cause mortality within 90 days of hospital admission (hazard ratio 0.77; 95% CI, 0.61–0.98; p = 0.03), and a shorter hospital stay (incidence rate ratio 0.39; 95% CI, 0.38–0.41; p < 0.001).

Therefore, it is reasonable to consider Beta-blocker if patients are adequately resuscitated.

Show References

Christian-Miller N, Lee KT, Pashun R, Ballut K, Prescott H, Cascino T, Taylor SP, Ansari S, Sjoding MW, Nagle M, Admon AJ. Continuing vs. Withholding Home Beta-Blockers at Admission for Suspected Infection: A Target Trial Emulation. Crit Care Med. 2026 Sep 1;54(9):2350-2360. doi: 10.1097/CCM.0000000000007229. Epub 2026 Jun 9. PMID: 42262489

Attachments

  • 2026_10_05 Christian-Miller oral beta blocker for sepsis-6ac4834dec2d9.docx (16 Kb)


Title: Atropine in Unstable Bradycardia

Category: Critical Care

Keywords: unstable bradycardia, AHA, ACLS, atropine (PubMed Search)

Posted: 9/29/2026 by Kami Windsor, MD

Background: The 2025 AHA guidelines changed their recommended initial IV atropine dose for unstable bradycardia from 0.5 mg to 1.0 mg, while the 2025 ERC guidelines continue to recommend an initial dose of 0.5 mg. A 2025 review found limited comparative studies and noted that using 0.5 mg as an initial dose seems “clinically reasonable" [1].

Now: One tertiary care center performed a retrospective propensity-score matched study [2] comparing the 2 groups of patients with unstable bradycardia who had received an initial dose of 0.5 mg versus 1 mg in their ED between 2020 and 2025.

  • Primary outcome = First-Dose Success (reaching a heart rate >50 bpm within 3 minutes without additional therapy). 
  • Notably excluded were patients with noncardiac secondary bradycardia (hyperkalemia, drowning, trauma, etc.) and those with pacemaker failure, amongst others.

Results in the propensity score-matched cohort:

  • First-dose success was significantly higher in the 1.0 mg vs the 0.5 mg group (45 vs 25%; p=0.007)
    • NNT of 6 (95% CI, 3-18)
  • The 1.0 mg group had lower rates of:
    • Additional atropine requirement (26 vs 48%, p=0.003)
    • Other rescue therapy requirement (51% vs 74%, p=0.002)
    • ICU admission (53% vs 74%, p=0.005).
  • No difference between groups in 30-day mortality or subsequent permanent pacemaker placement

Bottom Line: Acknowledging the small size & retrospective nature of the study, it appears that an initial dose of 1mg IV atropine helps us work smarter--not harder--in the stabilization of patients with unstable bradycardia.

Show References

  1. Yokose M, Sangawa M, Shiomi H, et al. Initial Dose of Intravenous Atropine for Patients With Symptomatic Bradycardia?- A Scoping Review. Circ Rep. 2025;7(11):1044-1050. Published 2025 Sep 27. doi:10.1253/circrep.CR-25-0169
  2. Kokulu K, Sert ET, Akar EH, Gül M. Initial atropine dose of 0.5 mg versus 1 mg in unstable bradycardia: A propensity score-matched retrospective cohort study. Am J Emerg Med. Published online August 2, 2026. doi:10.1016/j.ajem.2026.07.065


Title: "Everything in Excess is Opposed to Nature"

Category: Critical Care

Posted: 9/22/2026 by Caleb Chan, MD (Updated: 10/19/2026)

Question

The following is an actual case. 

An ED patient without any history of asthma or COPD is intubated to facilitate an emergent MRI. After the MRI is completed (and without abnormalities). The patient is breathing  synchronously and comfortably on minimal PS settings. Further sedation is weaned to facilitate extubation in the ED as the patient has no need for continued mechanical ventilation and no ICU requirements. All of a sudden, you are emergently called overhead to the patient's room because the patient is “blue” and hypoxic. 

These are the ventilator waveforms. 

The patient did not receive any contrast or bronchospastic medications. The ETT is clear and without obstruction.

What is going on?

Show Answer

There are a lot of issues that are apparent on this ventilator waveform. However, the focus for this pearl is the expiratory waveforms which show significant expiratory obstruction (compare to normal below). The patient is getting inspiratory volumes (VTi 553 mL in light blue bottom right corner), but limited expiratory waveforms (VTe 164 mL) . Given that the patient has no history of asthma, COPD, or reason for acute obstruction, the concern was that patient effort (as patient became more awake with decreased sedation) was actually causing expiratory obstruction. Sedation was increased and the obstruction resolved. 

The patient was subsequently diagnosed with excessive dynamic airway collapse, a condition where the posterior membrane of the tracheobronchial tree weakens and bulges anteriorly into the airways (this can sometimes be seen on expiratory CT chests). This movement is exaggerated during forced exhalation due to increased intrathoracic pressure and causes a more severe expiratory obstruction pattern compared to passive exhalation. Consequently, this can lead to a cycle of agitation, increased work of breathing, and breath-stacking/accumulation of intrinsic PEEP. 

Of note, EDAC often gets misidentified as “COPD” or “asthma,” and given its mechanism, does not respond to bronchodilators or steroids. The weakening of the posterior membrane is a chronic process and hence EDAC does not develop acutely, it simply becomes clinically apparent in an agitated intubated patient. Hence, the treatment for this patient was a sedative to calm the patient while preserving respiratory effort (i.e. dexmedetomidine) and extubating the patient to remove the exacerbating stimulus (being intubated). 

Extubating to NIPPV could be considered as a bridge granted it does not cause more agitation and increased work of breathing.

In summary, EDAC is a cause of expiratory obstruction that should  be considered in patients with evidence of obstruction and increased of work of breathing, particularly if they don’t have a history of COPD/asthma or reason for bronchospasm.



Title: SUSPECT Cardiogenic Shock: A Mnemonic to Help Make the Diagnosis

Category: Critical Care

Keywords: cardiogenic shock; cardiology; shock (PubMed Search)

Posted: 9/15/2026 by Shoshana Rudin, MD (Updated: 10/19/2026)

Cardiogenic Shock = a cardiac disorder that results in both clinical and biochemical evidence of sustained tissue hypoperfusion (1).

Cardiogenic shock has high mortality (approx 35-40% in many studies). Mortality worsens at higher stages of cardiogenic shock severity (2,3). Early recognition of cardiogenic shock is critical in order to initiate treatment and transfer patients to an appropriate level of care in a timely manner. 

As an ED physician, you need to SUSPECT cardiogenic shock so that you can ensure appropriate definitive management of your patient (4).

SUSPECT = Symptoms/Signs; Urine Output; Sustained Hypotension; Perfusion; EKG/Echo; Congestion; Triage

Take a look at the Additional Materials to break down this mnemonic in more detail and learn what might make you SUSPECT CS!

Show Additional Information

So what do you need to think about to SUSPECT CS?

Let's break down that mnemonic in a little bit more detail.

Symptoms/Signs:

  • Signs of Shock (Hypoperfusion): AMS, confusion, rapid pulse, cold and clammy extremities, delayed capillary refill
  • Signs of Congestion: Elevated JVP, crackles, rales, lower extremity edema, narrow pulse pressure (<25% of SBP)
  • Symptoms: Chest pain or pressure, chest pain equivalents, orthopnea, paroxysmal nocturnal dyspnea

Urine Output:

  • Oliguria or anuria
    • <0.5 mL/kg/h (roughly <30 mL/h in a 60 kg adult)
  • Place a foley (most accurate hourly UOP), or measure UOP into a urinal, bedpan, Purewick, or condom cath

Sustained Hypotension:

  • SBP <90, MAP <65 for >30 min
  • Or… relative hypotension! >30 mmHg decrease from baseline 
  • Or… anyone who needs pressors or mechanical support to maintain SBP >90
  • Not every patient with cardiogenic shock will have hypotension (yet)!

Perfusion:

  • Lactate: >2 
  • LFTs: ALT >200 U/L or >3x upper limit of normal 
  • Renal function: AKI, AKI on CKD, or Cr >2x upper limit of normal (very concerning)
  • Acidosis: pH <7.2 (very concerning), or metabolic acidosis without another clear etiology
  • You don't need all of the above to be concerned for cardiogenic shock

EKG/Echocardiogram:

  • EKG: STEMI? Arrhythmias? New conduction abnormalities (AV block, LBBB or RBBB)?
  • POCUS: Visually estimate EF, evaluate for LV and/or RV dilation and systolic dysfunction, look for regional wall motion abnormalities
  • More detailed echo: assess for valvular pathology, more accurate quantification of EF (LVOT-VTI, Simpson’s Biplane, etc)

Congestion:

  • Assess for presence or absence of congestion based on physical exam and hemodynamics
    • LV congestion: think about pulmonary edema
    • RV congestion: think about extremity edema, cardiac ascites, elevated JVP, hepatic dysfunction
    • Biventricular congestion: all of the above!

Triage:

  • ICU admission!
    • AMI-CS (Acute MI causing cardiogenic shock): activate cath lab
    • HF-CS (decompensated heart failure, either acute or chronic, causing cardiogenic shock): call heart failure team (if available at your hospital) to discuss advanced therapeutics
    • Choose cardiac ICU if available
  • Activate shock team (if available) to discuss advanced therapeutic options
    • No shock team? Call your ICU, call your on-call cardiologist, and talk through options!
  • Consider transfer to a higher level of care if: 
    • You don’t have access to a cath lab or advanced level of cardiology services
    • You don’t have a cardiac ICU or a MICU with capacity to do advanced hemodynamic monitoring 
    • Your patient might need mechanical circulatory support
    • Your patient might need evaluation for surgical treatment options (CABG, valve repair/replacement, etc)

Proposed Classification of Cardiogenic Shock Levels of Care (originally figure 3, Sinha et al)

Consider the resources that your hospital has available when deciding if/where to transfer a cardiogenic shock patient to a higher level of care.

Show References

1. Waksman R, Pahuja M, van Diepen S, et al. Standardized Definitions for Cardiogenic Shock Research and Mechanical Circulatory Support Devices: Scientific Expert Panel From the Shock Academic Research Consortium (SHARC). Circulation. 2023;148(14):1113-1126. doi:10.1161/CIRCULATIONAHA.123.064527

2. Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic shock: This document was endorsed by the American College of Cardiology (ACC), the American Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019. Catheter Cardiovasc Interv Off J Soc Card Angiogr Interv. 2019;94(1):29-37. doi:10.1002/ccd.28329

3. Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK Stage Classification Expert Consensus Update: A Review and Incorporation of Validation Studies. JACC. 2022;79(9):933-946. doi:10.1016/j.jacc.2022.01.018

4. Sinha SS, Morrow DA, Kapur NK, Kataria R, Roswell RO. 2025 Concise Clinical Guidance: An ACC Expert Consensus Statement on the Evaluation and Management of Cardiogenic Shock. JACC. 2025;85(16):1618-1641. doi:10.1016/j.jacc.2025.02.018



Title: What size blade should be used for intubation?

Category: Critical Care

Keywords: airway, laryngoscopy, blade size, critical care (PubMed Search)

Posted: 9/1/2026 by Kristyn McLeod, MD

While many intubations in critically ill patients go smoothly, they are a high risk procedure that EM and ICU physicians seek to continuously improve upon. Blade size is one aspect of the procedure that has received attention over the past several years. We don’t have prospective trials addressing this question, but there are several retrospective analyses that have investigated it.

  • For Direct Laryngoscopy:
    • The 2022 MacSize-ICU study and a 2023 study by Landefeld and colleagues with the Pragmatic Critical Care Research Group suggested that when using Macintosh geometry blades for direct laryngoscopy there was improved first pass success with size 3 blade. Secondary outcomes for these studies point to a worse glottic view with a size 4 blade.
  • For Video Laryngoscopy:
    • This finding did not hold up in video laryngoscopy.  A 2023 study by Park et al. and now a 2026 retrospective study again by Landefeld et al. that looked at blade size for video laryngoscopy with Macintosh geometry blades found no difference in first pass success with size 3 vs size 4 blades.

Bottom Line: Continue to use your best clinical judgment when selecting a blade size, especially when performing video laryngoscopy. When performing direct laryngoscopy, if you are on the fence, consider using size 3 blade.

*These studies do not address intubation with hyperangulated designs

Show References

  • Godet, Thomas, et al. "Impact of Macintosh blade size on endotracheal intubation success in intensive care units: a retrospective multicenter observational MacSize-ICU study." Intensive Care Medicine 48.9 (2022): 1176-1184.
  • Landefeld, Kevin R., et al. "Effect of laryngoscope blade size on first pass success of tracheal intubation in critically ill adults." Critical Care Explorations 5.3 (2023): e0855.
  • Park, Jeongyong, et al. "Effect of blade size on the first-pass success rate of endotracheal intubation using the C-MAC video laryngoscope." Journal of Clinical Medicine 12.22 (2023): 7055.
  • Landefeld, Kevin R., et al. "Blade Size and Outcomes with Standard-Geometry Video Laryngoscopy in Emergency Tracheal Intubations: Secondary Analysis of Two Randomized Controlled Trials." CHEST Critical Care (2026): 100257.


Title: Linezolid: Crossing the Line for Severe CAP

Category: Critical Care

Posted: 8/25/2026 by Jon Hurst, MD

Severe Community Acquired Pneumonia (SCAP) is broadly defined as CAP that requires ICU admission. Although MRSA pneumonia is overall quite rare (1), it is associated with a high mortality rate. Therefore, empiric MRSA coverage is commonly used for patients with SCAP. Common empiric agents include vancomycin and linezolid. Linezolid has both pharmacologic and clinical data that suggest it may be a preferred option for many patients.

When approaching a patient with SCAP, a key consideration is whether empiric MRSA coverage is needed. Risk factors for MRSA pneumonia include prior MRSA infection or colonization, recurrent skin infections, post-influenza pneumonia, recent hospitalization or antibiotic use (1). 

If empiric MRSA coverage is determined to be needed, Linezolid offers several advantages for the treatment of SCAP. Highlights below:

  • Linezolid has 100% oral bioavailability which can be especially useful for those patients with difficult IV access
  • Linezolid has better lung epithelial lining penetration compared to vancomycin (6)
  • In direct comparison between linezolid and vancomycin for confirmed MRSA pneumonia, linezolid was shown to have improved microbiologic cure rates without an improvement in mortality (2, 7)
  • Linezolid was shown to have less nephrotoxicity than vancomycin (2, 7)

Side effects to consider with linezolid include:

  • Serotonin syndrome, although extremely rare (5). May consider discussion with your pharmacist if taking additional serotonergic agents.
  • Myelosuppression (typically thrombocytopenia), although usually with longer treatment courses. This study shows no significant difference in rates of thrombocytopenia compared to vancomycin (4).

If providing linezolid for treatment of SCAP:

  • Dose: Linezolid 600mg IV or PO q12 hours
  • Ideally should obtain blood cultures, sputum culture, MRSA nares prior to (or closely following) antibiotic administration

Show References

  1. Aliberti, Stefano, et al. "Global initiative for meticillin-resistant Staphylococcus aureus pneumonia (GLIMP): an international, observational cohort study." The Lancet Infectious Diseases 16.12 (2016): 1364-1376.
  2. Jiang, H., R-N. Tang, and J. Wang. "Linezolid versus vancomycin or teicoplanin for nosocomial pneumonia: meta-analysis of randomised controlled trials." European journal of clinical microbiology & infectious diseases 32.9 (2013): 1121-1128. 
  3. Nair, Girish B., and Michael S. Niederman. "Updates on community acquired pneumonia management in the ICU." Pharmacology & therapeutics 217 (2021): 107663.
  4. Nasraway, Stanley A., et al. "Linezolid does not increase the risk of thrombocytopenia in patients with nosocomial pneumonia: comparative analysis of linezolid and vancomycin use." Clinical infectious diseases 37.12 (2003): 1609-1616.
  5. McCreary, Erin K., et al. "Antibiotic myths for the infectious diseases clinician." Clinical Infectious Diseases 77.8 (2023): 1120-1125.
  6. Stein, Gary E., and Elizabeth M. Wells. "The importance of tissue penetration in achieving successful antimicrobial treatment of nosocomial pneumonia and complicated skin and soft-tissue infections caused by methicillin-resistant Staphylococcus aureus: vancomycin and linezolid." Current medical research and opinion 26.3 (2010): 571-588.
  7. Wunderink, Richard G., et al. "Linezolid in methicillin-resistant Staphylococcus aureus nosocomial pneumonia: a randomized, controlled study." Clinical Infectious Diseases 54.5 (2012): 621-629.


Title: Epidemiology, Ventilatory Patterns, and Outcomes in Acute Hypoxemic Respiratory Failure Among ICU Patients Requiring Respiratory Support

Category: Critical Care

Posted: 8/18/2026 by William Teeter, MD

Acute Hypoxemic Respiratory Failure (AHRF) is very common in the ED/ICU. In this multicenter cohort of 21,714 patients in a Canadian ICU registry (iCORE) receiving oxygen or respiratory support, 50% met criteria for acute hypoxemic respiratory failure within 24 hours of ICU admission, and 76% of those patients required invasive mechanical ventilation.

  • AHRF severity was categorized using the same Pao2/Fio2 thresholds as the Berlin definition for ARDS: mild (201–300), moderate (101–200), and severe (<100). 
  • When Pao2/Fio2 ratios were unavailable, severity was assigned using Spo2/Fio2 thresholds: mild (236–315), moderate (149–235), and severe (< 148). One-third of patients were actually classified this way.

PaO2/FiO2 remains the conventional standard and is important for ARDS severity/prognosis, but SpO2/FiO2 is noninvasive, continuous, inexpensive, and showed good agreement with PaO2/FiO2-based severity classification. According to these authors, SpO2/FiO2 can be a practical substitute for PaO2/FiO2 when an ABG is unavailable. 

  • Important limitations are the reduced accuracy of SpO2 at high saturations and potential pulse-oximetry bias, including overestimation of oxygenation in patients with darker skin tones.

Worsened hypoxemia strongly tracked with worse outcomes. ICU mortality increased from 17% in mild AHRF to 26% in moderate and 44% in severe AHRF; severe disease was also associated with fewer ventilator-free days and a lower probability of ICU discharge.

  • AHRF patients were often treated using ARDS-style lung-protective ventilation. Median tidal volume was about 6.5 mL/kg predicted body weight, and most measured plateau/driving pressures were within protective ranges. However, plateau pressure was infrequently documented. 
  • Among patients with severe AHRF, 26% received neuromuscular blockade, 13% received prone positioning, 12% received iNO, and 12% received ECLS within the first 30 days of ICU admission..

Show References

https://journals.lww.com/ccmjournal/fulltext/10.1097/ccm.0000000000007284

https://jamanetwork.com/journals/jama/article-abstract/1160659



Title: Autonomous Oxygen Titration

Category: Critical Care

Posted: 8/11/2026 by Mark Sutherland, MD

Rarely do more than a few months go by without us posting yet another pearl about the dangers of hypoxemia or hyperoxemia.  The data in general is strong that patients with significant exposure to either very high or very low oxygen levels do worse than patients with normoxia.  But if the first step intervention is simple – if the SpO2/PaO2 is high, turn the oxygen support down, and if the SpO2/PaO2 is low, turn the oxygen support up - then in this day and age can we improve this with a closed-loop system?  Click the Additional Information to find out!

Show Additional Information

Douin et al recently published the SAVE-O2 AI trial.  It used the O2matic PRO100 (of note, it is approved in Europe and Australia/New Zealand, but NOT currently FDA approved in the US), which autotitrates the oxygen flow rate to maintain a goal SpO2 (usually of 90-96%).  This study was not powered to look at patient outcomes, but they did find statistically significant greater time in goal SpO2 range for the autonomous system vs standard care.  Their primary outcome was time under an SpO2 of 87%, but I was even more interested in time above 96%, which dropped from 29% in the standard care group to 9% in the autonomous device group, because we know often times we are not good about turning the oxygen DOWN when the saturation is high.  

Bottom Line: Autonomous closed-loop oxygen titration devices likely increase time in goal SpO2 range.  Whether they impact the outcomes of hospitalized patients remains unknown.



Title: How much oxygen after cardiac arrest: LOGICAL trial

Category: Critical Care

Keywords: cardiac arrest, ischemic encephalopathy, ROSC, post arrest care (PubMed Search)

Posted: 8/8/2026 by Zach Wynne, MD

Bottom Line

This trial showed that the percentage of mechanically ventilated patient post arrest who received conservative oxygen therapy (SaO2 90-95%) with favorable neurological outcomes was not significantly different compared to the percentage of patients who received liberal oxygen therapy (minimum FiO2 of 0.3, SaO2 > 90%). While avoiding hypoxemia along with hypercapnia remains a hallmark of post arrest care, exact oxygenation goals above SaO2 of 90% remain unclear.

Show Additional Information

LOGICAL trial - NEJM Aug 2026

Background:

Patients who are status post cardiac arrest remain some of the sickest patients in medicine, requiring optimization of physiologic markers to promote the best neurological outcome. One of the most important parameters is oxygenation. However, exact oxygenation goals have been unclear with some trials showing benefit to using more conservative (lower) oxygenation targets in hopes of preventing neuronal death from relative hyperoxia and reperfusion injury. Thus, the Low Oxygen Intervention for Cardiac Arrest Injury Limitation (LOGICAL) trial was conducted.

Patients: > 18 years old mechanically ventilated with suspected ischemic encephalopathy from 53 ICU's in Australia, New Zealand, and Ireland. Exclusions included previous enrollment or inappropriate to enroll (such as imminent death)

Intervention: Conservative oxygen therapy defined as SaO2 goal of 90-95% with alarms for outside these parameters; FiO2 could be increased if SaO2 at goal but PaO2 < 60 mmHg

Control: Liberal oxygen therapy defined as Sa02 goal > 90% with alarms for below this parameter; FiO2 was at 0.3 minimum for mechanical ventilation

Outcome: Extended Glasgow Outcome Scale (GOS-E) score of 5-8 at 180 days reflecting lower moderate disability to upper good recovery ("favorable neurological outcome"); other outcomes include all cause and specific mortality, duration of mechanical ventilation/ICU stay/hospital stay, and discharge to home

Results:

1840 patients enrolled with 1821 analyzed by intention to treat. There were similar baseline characteristics between groups. Less than 1% of patients in each group did not receive assigned conservative/liberal treatment. 26.3% of patients in the conservative oxygen group failed to have FiO2 weaned and 8.4% of liberal oxygen group had an FiO2 less than 0.3. 

A favorable GOS-E (5-8) was observed in 38.2% of the conservative oxygen therapy group vs. 39.7% in the liberal oxygen therapy group (RR of 0.97, p = 0.65). Secondary outcomes showed no statistically significant difference.

Discussion:

Overall, the trial did not find a statistically significant difference in favorable neurological outcome or other outcomes in conservative vs. liberal oxygen therapy. The protocol deviations, noted above, likely lessened between-group difference in oxygen exposure. Additionally, time from ROSC to randomization was longer than previous studies which likely did not have a large effect. The trial adds to the literature that conservative oxygen therapy does not lead to improved neurological outcomes compared to liberal oxygen therapy. 

In my practice of patient including post arrest patients, I continue to aim for an SaO2 of mid 90's for most of my patients, avoiding hypoxemia (SaO2 < 90% generally) or the persistent SaO2 of 100.

Show References

  • LOGICAL Investigators and the Australian and New Zealand Intensive Care Society Clinical Trials Group; Hodgson CL et al. Conservative Oxygen for Unresponsive Patients after Cardiac Arrest. N Engl J Med. 2026 Aug 6;395(6):571-581. doi: 10.1056/NEJMoa2513814. Epub 2026 Jun 10. PMID: 42267831.


Title: Therapeutic AC May Shorten Time to Resolution of Acute Chest Syndrome in Adults

Category: Critical Care

Keywords: acute chest syndrome, microthrombi, pulmonary vasoocclusion, sickle cell disease, anticoagulation (PubMed Search)

Posted: 7/21/2026 by Jessica Downing, MD (Updated: 10/19/2026)

A multicenter double-blind RCT published in 2025 found that adult patients hospitalized with acute chest syndrome (ACS) who received 7 days of prophylactic therapeutic anticoagulation had a shorter time to ACS resolution (by approx 1 day) and reduced opioid consumption when compared to those receiving standard VTE prophylaxis.

Show Additional Information

Acute Chest Syndrome (ACS) is known to be associated with severe pulmonary vascular dysfunction. Prior studies have identified local vaso-occlusion leading to pulmonary infarct as the underlying etiology of up to 16% of ACS episodes, and have demonstrated relatively high rates of PE and pulmonary microthrombi. 

The TASC (Therapeutic Anticoagulation for Acute Chest Syndrome in Sickle Cell Disease) trial randomly assigned adult patients hospitalized for acute chest syndrome with no PE on CTA to prophylactic or therapeutic low-molecular weight heparin for 7 days or until hospital discharged. 172 patients were randomized - 84 in the prophylactic-dose group and 88 in the therapeutic-dose group. Patients in the therapeutic-dose group had a shorter time to ACS resolution (4.8?±?0.4 days vs. 6.1?±?0.5 days, HR 0.71; 95% CI 0.51–0.99; P?=?0.044 ). There were no major bleeding events in either group. The therapeutic dose group used an almost 45% lower cumulative dose of parenteral opioids (124 vs 219 morphine equivalent units, difference ?96; 95% CI ?202 to ?46; P?=?0.02).

Details:

  • ACS was defined by: new pulmonary infiltrate on CXR or CT AND respiratory symptom (s) OR abnormality on pulmonary auscultation
  • ACS resolution was defined by “joint improvement of four criteria, including fever, chest pain, dyspnea, and hypoxemia.” The hypoxemia component was excluded in the 62% of patients who were not hypoxemic at baseline. 
  • Study setting: across 12 health centers in France from 2016-2021.
  • Key exclusion criteria: 
    • Age < 18
    • ACS diagnosed >48h prior
    • Body weight <40kg or >100kg
    • CrCl <60 ml/min (if enrolled, treatment was discontinued if a patient developed severe AKI with CrCl <30 ml/min)
    • RBC transfusion “deemed highly risky”
    • Interestingly, the presence or absence of active COVID infection was not discussed
  • The anticoagulation used here was tinzaparin (a type of  low-molecular-weight heparin that is FDA approved but has been discontinued in the US; it has a higher molecular weight and greater anti-thrombin activity than enoxaparin). Prophylactic dosing was 4500 IU/24h and therapeutic dosing was 175 IU/kg/24h (both standard dosing for their indications).

Show References

Mekontso Dessap A, Habibi A, Arlet JB, Fartoukh M, Guerin L, Guillaud C, Roux D, Oziel J, Ngo S, Carpentier B, Lopez-Sublet M, Affo L, Melica G, Etienne-Julan M, Delacroix I, Lionnet F, Loko G, Da Silva D, Michel M, Razazi K, Charles-Nelson A, Bartolucci P, Gendreau S, Katsahian S, Maitre B. Comparison of Prophylactic and Therapeutic Doses of Anticoagulation for Acute Chest Syndrome in Sickle Cell Disease: The TASC Double-Blind Controlled Randomized Clinical Trial. Am J Respir Crit Care Med. 2025 May;211(5):832-841. doi: 10.1164/rccm.202409-1727OC. PMID: 40209087.



Title: What factors mean badness for patients with necrotizing fasciitis

Category: Critical Care

Posted: 7/7/2026 by Quincy Tran, MD, PhD (Updated: 10/19/2026)

University of Maryland Medical Center is a referral center for patients with necrotizing fasciitis in the region, as we have a major hyperbaric chamber, and a specialized Soft Tissue Surgery team. Therefore, patients with soft tissue infection make up a group with frequent transferring to UMMC.

Some of the factors, from recent meta-analysis, suggest higher rate of mortality among this particular group of patients. When they display these factors, which are also consistent with our clinical observations,  we should be more aggressive with their treatment:

Acute kidney injury   OR   3.23 (2.76–5.04)

Bacteremia                    OR  3.89 (1.39–10.85)

Hypotension                 OR  1.97 (1.26–3.10)

Coagulopathy              OR    2.81 (1.23–6.40)

Show References

Kruger N, Durr K, Fernando SM, Rochwerg B, Inaba K, Kim D, Yadav K, Kubelik D, Engels PT, Glen P, Tran A. Prognostic Factors Associated With Mortality Among Patients With Necrotizing Soft-Tissue Infection: A Systematic Review and Meta-Analysis. Crit Care Med. 2026 Jul 1;54(7):1779-1787. doi: 10.1097/CCM.0000000000007147. Epub 2026 May 15. PMID: 42138515.



Title: Airway Management in Critically Ill Patients with Obesity

Category: Critical Care

Posted: 6/30/2026 by Caleb Chan, MD (Updated: 10/19/2026)

FRC is key in obesity.

Show Additional Information

Functional residual capacity (FRC) is the volume left in the lungs at the end of a tidal volume breath. One way to think about FRC is as a reservoir of oxygen that continues to supply gas exchange even after a patient stops breathing (i.e. after RSI). The rate of oxygen consumption (VO2) determines how quickly this reservoir gets depleted (safe apnea time). FRC is significantly decreased in obesity. VO2 is also higher in obese patients. Both of these factors decrease the length of safe apnea time in obese patients. 

Consequently, pre-oxygenation with NIPPV and/or BVM with PEEP is key to increasing FRC and as a result, the safe apnea time while intubating obese patients.

Show References

Russotto V, Casey JD, Myatra SN, et al. Airway management in critically ill patients with obesity. Intensive Care Med. 2026;52(6):1256-1268. doi:10.1007/s00134-026-08454-x



Title: Calcium supplementation following Trauma

Category: Critical Care

Posted: 6/23/2026 by William Teeter, MD

Taking a slight detour into the trauma critical care realm today…

BLUF: Favor aggressive calcium supplementation following trauma, especially when patient requires transfusion. Recent evidence is pointing towards a signal for improved outcomes.

Hypocalcemia in trauma is common. Roughly half to two-thirds of trauma patients are hypocalcemic on arrival, driven by both shock physiology and citrate chelation from blood products. Some authors advocate for hypocalcemia to be added as the fourth element of a "lethal diamond" alongside coagulopathy, acidosis, and hypothermia. See reference 1&2 for good discussions of this physiology.

Time for a grain of salt: A recent article in JTACS advocates for favoring calcium chloride during whole-blood or massive transfusion and was associated with improved early survival. Calcium chloride at a threshold of at least 1 g per 2 units of low-titer O whole blood was independently associated with an 84% (!) reduction in 24-hour mortality, with the benefit strongest at this 1:2 ratio and weaker at less aggressive thresholds. (LOTS of caveats with this finding, but interesting nonetheless).

Current major civilian guidelines say only that hypocalcemia should be prevented, with limited specificity on timing or dose, and the Joint Trauma System recommends 1 g calcium after the first unit and after every fourth unit thereafter. The current CAVALIER trial is evaluating prehospital calcium specifically. Those results and other recent literature could push major trauma organizations to update their recommendations in the near future.

Show References

https://pubmed.ncbi.nlm.nih.gov/41995161/

https://pmc.ncbi.nlm.nih.gov/articles/PMC13082262/

https://clinicaltrials.gov/study/NCT05958342



Title: Corticosteroids in Cardiogenic Shock

Category: Critical Care

Keywords: shock, cardiogenic shock, corticosteroids (PubMed Search)

Posted: 6/16/2026 by Mark Sutherland, MD (Updated: 10/19/2026)

There were a handful of big name critical care studies published the last few weeks (LOGICAL, ARISE FLUIDS, SODa-BIC to name a few) but many of you probably already saw those so we're gonna stick with something a little more off the beaten path.

A retrospective observation trial was published recently by Gastanadui et al in Journal of Intensive Care looking at the mortality impact of corticosteroids in cardiogenic shock.  They looked at 167,721 patients from the Vizient database admitted with cardiogenic shock (excluded patients with other indications for steroids).  The unadjusted mortality was a whopping 48.8% in the steroid group and 29.6% in the non-steroid group.  They did Inverse Probability Treatment Weighting (IPTW), which attempts (imperfectly, but best as you can retrospectively) to control for treatment selection bias, and still found a roughly 3% mortality increase in the steroid group.

Bottom Line: Corticosteroids were already controversial (at best) in cardiogenic shock, but this further adds to the reasons to avoid them in this condition.  Of note, this trial excluded patients with classic hard-indications (e.g. adrenal insufficiency, COPD exacerbation, etc) and steroids should still be given to those groups, but in my opinion if you feel cardiogenic is the primary driver of the patient's shock and they do not have another indication, I would consider avoiding steroids solely for the shock.

Show Additional Information

Show References

Gastanadui MG, Murphy HR, Shahu A, Safiriyu I, Heck C, Hysolli M, Callegari S, Garimella S, Ali T, Jentzer JC, Gage A, Jacobs M, Katz JN, Miller PE. Early Corticosteroid use and Clinical Outcomes in Patients with Mixed and Cardiogenic Shock. J Intensive Care Med. 2026 Jun 1:8850666261437767. doi: 10.1177/08850666261437767. Epub ahead of print. PMID: 42223374.



Title: Can Lactate Lie?: Common Pitfalls with Lactate Interpretation

Category: Critical Care

Keywords: lactate, fluids, resuscitation, sepsis, septic shock (PubMed Search)

Posted: 6/12/2026 by Zach Wynne, MD

Bottom Line: Lactate is a useful but imperfect marker of critical illness. Below are some key points to consider when interpreting lactate.

  1. Lactated ringers should generally not significantly increase your measured lactate unless there is poor clearance (liver injury).
  2. Many medications can cause an elevation in lactate through multiple mechanisms that do not improve with fluid resuscitation.
  3. Lactate should be interpreted within the company it keeps (history, exam, vitals, urine output, hemodynamics).

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Lactate is one of the most commonly used lab markers used in the emergency department to identify critically ill patients. However, the lactate is often used in isolation which leads to potentially excessive fluid administration (previously identified by cited physicians as the “Lacto-Bolo reflex”). Some studies have demonstrated signal towards harm in excessive fluid resuscitation. Additionally, an elevated lactate can sometimes be representative of an etiology that requires alternative treatment to fluids (mesenteric or limb ischemia, severe anemia, and others). Therefore, it is important to use the lactate in context with other clinical data (vitals, urine output, hemodynamics, etc) to determine need for fluid resuscitation.

Below are some common pitfalls with lactate management to consider on your next shift:

“I can't give Lactated Ringer's solution if I'm measuring lactates!?”

The human body makes 20 mmol/kg/day of lactate under normal conditions. A liter of lactated ringers contains 28 mmol/liter of lactate. This means three liters of lactated ringer's would be only about 5% of normal lactate in a 70 kg person. With normal clearance this is unlikely to have a clinically significant effect unless there is issue with clearance (liver injury). This was demonstrated in a study by Zitek et al that showed lactated ringer's and normal saline boluses had similar effects on lactate concentration.

"Medications rarely cause lactate elevation"

While lactate elevations are often ascribed to anaerobic metabolism (leading to pyruvate being metabolized into lactate), there are other mechanisms through which lactate elevation occurs including (with a few associated medications):

  • Increased sympathetic stimulation (leads to excess pyruvate, causing lactate elevation) - albuterol, epinephrine, sympathomimetics
  • Increased NADH/NAD ratio - ethanol, toxic alcohols
  • Blockage of electron transport chain in mitochondria (prevents aerobic metabolism) - metformin, propofol (esp with propofol related infusion syndrome)

While lactate is a useful screening marker, it is not helpful in isolation alone and requires trending as well as clinical context. So next time you see an elevated lactate, think BEFORE you bolus.

Show References

  1. Spiegel R, Gordon D, Marik PE. The origins of the Lacto-Bolo reflex: the mythology of lactate in sepsis. J Thorac Dis. 2020 Feb;12(Suppl 1):S48-S53.
  2. Wardi G, Brice J, Correia M, Liu D, Self M, Tainter C. Demystifying Lactate in the Emergency Department. Ann Emerg Med. 2020 Feb;75(2):287-298. doi: 10.1016/j.annemergmed.2019.06.027. Epub 2019 Aug 29. Erratum in: Ann Emerg Med. 2020 Apr;75(4):557.
  3. Garcia-Alvarez M, Marik P, Bellomo R. Sepsis-associated hyperlactatemia. Crit Care. 2014 Sep 9;18(5):503.
  4. Zitek T, Skaggs ZD, Rahbar A, Patel J, Khan M. Does Intravenous Lactated Ringer's Solution Raise Serum Lactate? J Emerg Med. 2018 Sep;55(3):313-318.


Title: Bicarbonate for metabolic acidosis

Category: Critical Care

Keywords: Bicarbonate, metabolic acidosis (PubMed Search)

Posted: 5/26/2026 by Quincy Tran, MD, PhD

Sodium bicarbonate significantly reduced the need of renal replacement therapy (risk ratio [RR] 0.69; 95% CI, 0.61–0.78) but not mortality (RR, 0.84; 95% CI, 0.55–1.30). However, there was not enough sample size to support the outcome of mortality.

There was still significant heterogeneity between studies as the sources of metabolic acidosis were different between different studies in this meta-analysis study of randomized control trial. One study recruited patients with septic shock only, while other studies enrolled patients with different disease states.
There was also heterogeneity in the threshold for pH to enter the study.

Show References

Sodium Bicarbonate for Acute Metabolic Acidosis in Critically Ill Adults: A Meta-Analysis of Randomized Clinical Trials. Chen, Jia-Jin MD; Lee, Tao-Han MD; Chang, Chih-Hsiang MD, PhD, Lai, Pei-Chun MD, PhD; Tu, Yu-Kang PhD; Huang, Yen-Ta MD, MSc, PhD. Critical Care Medicine ():10.1097/CCM.0000000000007179, May 22, 2026. | DOI: 10.1097/CCM.0000000000007179



Title: The 2026 Acute PE Guidelines

Category: Critical Care

Keywords: Pulmonary embolism, massive PE, submassive PE, RV failure, cardiogenic shock, guidelines (PubMed Search)

Posted: 5/19/2026 by Kami Windsor, MD

Not all patients with an acute PE will be crashing and critically ill, but it seemed worthwhile to remind everyone that there are new guidelines and recommendations from AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN/XYZLMNOP about the management of patients with acute pulmonary embolism in the 2026 AHA/ACC Joint Committee statement.  A few key takeaways, with highlights for the sicker PE patients: 

  1. New Classifications A through E for acute PE (see images below)
    • Get familiar with the clinical scores! Hestia, PE Severity Index (PESI), simplified PESI (sPESI)
    • ED discharge recommended for Category A and supported for Category B
  2. LMWH recommended over unfractionated heparin when parenteral AC is needed, unless contraindicated
  3. DOACs recommended over warfarin unless contraindicated

Highlights for the sicker PE patients, i.e. Categories C+:

  • Get a look at the RV! (POCUS, CT, formal echo)
    • Further stratify Category C patients/identify Category D earlier
    • Find out how close to decompensation the patient might be
    • Inform your management if the patient decompensates
      • For PE patients with e/o RV strain (C2+ per this document; for me, particularly those C3+ with respiratory complaints as a marker of poor pulmonary perfusion, or Category D+), consider use of inhaled vasodilators
  • Be careful with any sedation even if normotensive – decreasing preload / blunting the body's compensatory adrenergic response can be disastrous, have hemodynamic support available
  • If you have to intubate, choose induction meds wisely and have hemodynamic support ready
  • For patients with Category D-E acute PE:
    1. Norepinephrine = initial vasopressor of choice for hypotension due to modest inotropic effects; max at 15mcg/min due to effects on pulmonary vascular resistance at higher doses, if second vasopressor needed, reach for vasopressin
    2. Dobutamine as additional inotropic support OR for normotensive shock 
    3. Avoid fluid boluses unless patient is also hypovolemic, and then give small boluses (250mL) only
  • Consider advanced therapies for Category D and particularly E
  • PE Response Team (PERT) Consultation recommended – and depending on where you practice, can help get the patient transferred if advanced therapies are an option

For a great breakdown and further discussion of the new guidelines, I recommend checking out the Life in the Fast Lane blogpost here.

Show References

Creager MA et al. 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. Circulation. 2026 Mar 24;153(12):e977-e1051.



Title: Can Abx at Intubation Prevent VAP?

Category: Critical Care

Keywords: ventilator associated pneumonia, intubation, stroke, brain injury, antibiotics (PubMed Search)

Posted: 5/12/2026 by Jessica Downing, MD

Should we give a dose of antibiotics after intubating to reduce risk of VAP down the line? A multicenter RCT conducted in 2024 - the PROPHY-VAP Trial - found that a single dose of 2g ceftriaxone administered within 12 hours of intubation reduced VAP within the first week of hospitalization for patients intubated for airway protection due to TBI, stroke or SAH, with a VAP rate of 14% in the CTX group vs 32% in the VAP group (HR 0.60; 95% CI 0.38-0.95).

Click the link below for details and additional discussion

Show Additional Information

Details:

  • The PROPHY-VAP trial included 345 patients across 9 university-affiliated ICUs in France.
  • Inclusion:
    • Intubation for airway protection in the setting of neurologic injury, defined as TBI, ischemic or hemorrhagic stroke, or SAH
    • Intubation <12h and hospitalized <48h at the time of randomization
    • Expected mechanical ventilation >48h
    • No pre-existing infection or antibiotic therapy
  • Exclusion:
    • Hospitalization within 30d
    • Beta lactam allergy
  • Patients: Well-matched between groups, mostly hemorrhagic insults (hemorrhagic stroke, SAH, TBI), all with GCS <12 and majority GCS 4-8. 
  • Intervention: Single dose of CTX 2g IV. Mean time from intubation to antibiotics was 7h.
  • Primary Outcome: Early VAP (2-7d after intubation) was less common in the CTX group (14% vs. 32%; HR 0.60; 95% CI 0.38-0.95, p = 0.03).
  • Secondary Outcomes: The CTX group had more antibiotic-free and ventilator-free days, lower mortality, and lower incidence of VAP at 28d.
  • Safety Outcomes: C diff and MDR organism infection were not more common in the CTX group

Background: prior studies have investigated different antibiotic regimens in different groups. In 2023, the AMIKIHAL trial suggested that a 3d course of inhaled amikacin would reduce 28d risk of VAP among patients ventilated for >3d (not just neuro patients). In 2022, the SuDDICU trial suggested that “selective decontamination of the digestive tract” with a combination of IV abx, oral suspension of antibiotics, and topical abx to the oropharynx and buccal mucosa suggested a lower risk of in-hospital mortality in Baysian meta-analysis (though not in the primary study statistics). In 2005, the ANTHARTIC trial suggested a lower rate of VAP with a 2 days course of amoxicillin-clavulanate among patients admitted after OHCA.

Closing Thoughts: Together, these studies suggest that there may be a role for an early and short course of antibiotics for preventing VAP in a few patient populations. A single dose of CTX is easier and more benign than prior suggested regimens, and based on the available data, seems to offer benefit with minimal risk.

Show References

Dahyot-Fizelier C, Lasocki S, Kerforne T et al. Ceftriaxone to prevent early ventilator-associated pneumonia in patients with acute brain injury: a multicentre, randomised, double-blind, placebo-controlled, assessor-masked superiority trial. The Lancet Respiratory Medicine, 2024; 12, 375-385

Additional References

  1. Ehrmann S, Barbier F, Demiselle J, Quenot JP, Herbrecht JE, Roux D, Lacherade JC, Landais M, Seguin P, Schnell D, Veinstein A, Gouin P, Lasocki S, Lu Q, Beduneau G, Ferrandiere M, Plantefève G, Dahyot-Fizelier C, Chebib N, Mercier E, Heuzé-Vourc'h N, Respaud R, Gregoire N, Garot D, Nay MA, Meziani F, Andreu P, Clere-Jehl R, Zucman N, Azaïs MA, Saint-Martin M, Gandonnière CS, Benzekri D, Merdji H, Tavernier E; Reva and CRICS-TRIGGERSEP F-CRIN Research Networks. Inhaled Amikacin to Prevent Ventilator-Associated Pneumonia. N Engl J Med. 2023 Nov 30;389(22):2052-2062. 
  2. The SuDDICU Investigators for the Australian and New Zealand Intensive Care Society Clinical Trials Group. Effect of Selective Decontamination of the Digestive Tract on Hospital Mortality in Critically Ill Patients Receiving Mechanical Ventilation: A Randomized Clinical Trial. JAMA. 2022;328(19):1911–1921. doi:10.1001/jama.2022.17927
  3. Acquarolo A, Urli T, Perone G, Giannotti C, Candiani A, Latronico N. Antibiotic prophylaxis of early onset pneumonia in critically ill comatose patients. A randomized study. Intensive Care Med. 2005 Apr;31(4):510-6. doi: 10.1007/s00134-005-2585-5. Epub 2005 Mar 8. PMID: 15754197.


Title: P:F vs S:F Ratio

Category: Critical Care

Keywords: Oxygenation, ARDS, P:F Ratio, S:F Ratio, Hypoxia, Mechanical Ventilation (PubMed Search)

Posted: 4/21/2026 by Mark Sutherland, MD (Updated: 10/19/2026)

PaO2 to FiO2 (P:F) ratios, are often considered the gold standard in critical care for assessing the degree of oxygen-refractory hypoxia in various pathologies, particularly ARDS.  P:F does have some limitations, including not accounting for the PEEP, but probably the most limiting is that it requires collecting an ABG, which is invasive and not always feasible or a top priority when resuscitating a critically ill hypoxic patient.  On the other hand, SpO2 (pulse ox saturation) is routinely available, and of course the FiO2 should be known, so many have suggested perhaps using an SpO2 to FiO2 (S:F) ratio instead.  But how S:F maps to P:F and how well they correlate is not fully known.  Chaudhuri et al recently conducted a meta-analysis, published in Critical Care Medicine this month, which reviewed the literature on this. 

Bottom Line: Yes, S:F ratios correlate well with P:F ratios, especially when the SpO2 is less than 97%, but you can't just substitute the S:F for P:F, you have to use one of the accepted formulas.  See additional info on the website for the actual formula to apply and how a given S:F translates to P:F.

Show Additional Information

The authors identified 4 particularly high performing formulas from well-done studies.  One was logarithmic, and two were non-linear, making the math hard, so the best is probably the linear one (correlation coefficient was 0.89, which is quite good).  It is:

SF = 64 + 0.84 x PF

Usually you have the SF and want to figure out the PF, so rearranging to solve for PF (to save you all the trouble):

PF = (SF - 64) / 0.84

Since we usually care about P:F < 300 (mild ARDS), < 200 (moderate ARDS), and < 100 (severe ARDS), here are the S:F mappings for those P:Fs to make things super simple:

If P:F is 300 then S:F is 315

If P:F is 200 then S:F is 235

If P:F is 100 then S:F is148

And 150 is another P:F that is important since we often consider proning and/or paralysis under this level.  That would equate to an S:F of 190 using this formula.

Don't forget!  The SpO2 is expressed as a percentage, and FiO2 as a decimal.  So for example, for a patient with a sat of 97% on RA (21% FiO2):

97 / 0.21 = 461 would be their S:F.

Show References

Chaudhuri D, Lazarte J, Shah K, Pitre T, Pekkarinen PT, Sendagire C, Martin GS, Jung C, Laffey JG, Rochwerg B; Sequential Organ Failure Assessment (SOFA)-2 study group. Approaches to Converting Sp o2 /F io2 Ratio to Pa o2 /F io2 Ratio for Assessment of Respiratory Failure in Critically Ill Patients: A Systematic Review. Crit Care Med. 2026 Apr 1;54(4):950-959. doi: 10.1097/CCM.0000000000007018. Epub 2026 Jan 2. PMID: 41493393.



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