This study surveyed 111 emergency medicine (EM) trainees to identify factors influencing their choice of critical care (CC) fellowship pathways, particularly surgical critical care (SCC). Respondents included 42 fellows and 69 residents, with most pursuing anesthesiology or medicine CC; only 15 intended SCC.
Key determinants of pathway selection were:
Limited exposure to EM-SCC during residency was noted—only 28% had access to such fellowships, and 42% interacted with surgical intensivists, despite 41% envisioning SCC practice.
Intellectual appeal ranked highest for entering CC, above job prospects or lifestyle.
Fellowship components most valued were:
While descriptive, the authors noted many respondents cited the "preliminary surgical year" as a reason that the Surgical Critical Care pathway is less attractive.
The authors conclude that respondents pursued a career in CC for "intellectual appeal and desire for additional expertise" and that improving EM-SCC matriculation requires targeted interventions.
Another month, another study of hemodynamic targets in sepsis… The age-old questions: is a MAP > 65 a good target for everybody, or should we individualize? Should we just give a bolus of fluids to everyone and then move to pressors, or should this strategy change patient to patient?
Huet et al have a preprint that'll appear in Intensive Care Medicine looking at this question in 517 patients. I can't reprint it here due to copyright (follow link below, go to full PDF and scroll to figures at bottom if curious), but basically their algorithm was 1) check if patient is fluid responsive via either echo or swan, 2) give fluid if yes, 3) do something else (pressors) if no.
Importantly the differences were not statistically significant, but they found a strong, nearly significant, trend towards benefit on SOFA score, ICU and hospital LOS in the “personalized therapy” group (also of note, these are dubious as patient oriented outcomes). The sickest patients (by SOFA) showed the most benefit.
Bottom Line: The “personalized hemodynamic therapy” literature continues to show a modest benefit of using tools like echo (e.g. LVOT VTI) to determine if the patient is fluid responsive (or fluid tolerant) and NOT give fluid (instead using pressors) if that is not the case, but for now there's relatively limited support for hyper-personalized approaches like varying MAP goals or otherwise mixing up your strategy. Some day we'll likely find a more nuanced approach, but for now I think a reasonable strategy in critically ill septic patients is to use ultrasound to determine if the patient needs fluid, if yes give fluid and reassess, and if not move to pressors, to maintain a MAP > 65.
A scoping review of literature involving norepinephrine use during cardiac arrest associated with a shockable rhythm found:
-evidence in animal and signal in human trials of improved myocardial and cerebral blood flow
-a suggestion of less re-arrest
There is not enough evidence comparing epinephrine to norepinephrine however this would be an excellent area of research with a theoretical advantage to norepinephrine.
Bottom line:
If a ventilated patient exhibits at least one of: persistent end expiratory flow, unequal inspiratory and expiratory flow-time areas, or ineffective breath triggers; autoPEEP must be evaluated by performing an end-expiratory hold.
If present, ventilator settings should be changed to maximize exhalation time.
In critically ill patients with obstructive lung disease, intubation and mechanical ventilation is often a last resort as it does not fix the underlying pathology of small airway disease. While many complications can arise, the most feared complication is autoPEEP.
What is autoPEEP?
AutoPEEP is excess air trapping in the lungs because the patient has insufficient time to fully exhale. Patients at highest risk include those with obstructive lung pathology due to their increased resistance (from bronchospasm) and sometimes increased compliance (such as in emphysema).
However, it is possible for any patient to develop autoPEEP depending on the amount of time they have to exhale. As respiratory rate increases, the expiratory time decreases proportionally if inspiratory time is kept constant. Ultimately, autoPEEP can lead to rapidly increasing intrathoracic pressures causing decreased preload leading to hemodynamic instability and potentially cardiac arrest. These elevated pressures also place the patient at significant risk of barotrauma/volutrauma.
How do I find it?
There are several signs on the ventilator waveforms for autoPEEP. Some patients may only exhibit one of the following signs of autoPEEP. They are demonstrated in the attached pictures in various ventilator modes.
Image A. Persistent end expiratory flow on the flow-time curve (middle curve) - demonstrated by the expiratory limb of the flow curve not returning to zero (remains negative)
Image B. Unequal inspiratory and expiratory volumes on the flow-time curve (area of flow curve inspiratory limb does not equal area of flow curve expiratory limb)
Image C. Ineffective triggering (seen on flow-time curve; patient has to perform more work to reach trigger threshold when autoPEEP is present; they are sometimes unable to trigger a breath)
If any of these are present, an end-expiratory hold maneuver should be performed.
Image D - End-expiratory hold maneuver (done if patient is passive on the ventilator) - the pressure-time curve will begin at ventilator set PEEP and reach total PEEP at the end of the maneuver. The difference between total PEEP and set PEEP is autoPEEP.
If autoPEEP is present, ventilator changes to allow for more exhalation time should be made. The most effective change is by decreasing the respiratory rate though small improvements can be made by changing the inspiratory time and tidal volume. Appropriate bronchodilator therapy, sedation, and treatment of underlying pathology is also critical in these patients.
For more information on autoPEEP, check out this post by Dr. John Greenwood discussing autoPEEP on MarylandCCProject with video demonstrations!
Check for Elevated ICP in the Post-ROSC Patient
Delirium is common among critically ill patients. Some of the common Acetylcholinesterase inhibitors (AChEI), rivastigmine, donepezil, have been used to prevent delirium in ICU patients. However, their efficacy was just recently re-examined in a meta-analysis of only Randomized Control Trials.
Ten studies and 731 patients were included- 365 in the treatment (AChEI) group and 366 in the control group.
AChEI was associated with lower occurrence of delirium (RR 0.68, 95% CI 0.47-0.98, p=0.039. However, there was no significant difference in the delirium duration (mean difference -0.16 day, 95% CI -0.95 to 0.62 day, p=0.23). There was no difference in delirium severity nor length of hospital stay.
Among the medication, interestingly, rivastigmine 4.5 mg/day significantly reduced delirium occurrence (RR = 0.61 [0.39– 0.97]) and severity (SMD = –0.33 [–0.58 to –0.08]), as well as length of hospital stay (MD = –1.29 [–1.87 to –0.72]).
Discussion:
This meta-analysis was well-conducted.
The cholinergic dysregulation—especially elevated acetylcholinesterase activity—can lead to the imbalance between attention and cognition, contributing to delirium in ICU patients. Thus, the use of AChEI and reduction of occurrence of delirium proves that acetylcholine deficiency may be associated with delirium among ICU patients.
Subgroup analysis showed that prophylactic use of AChEI was associated with significant reduction of delirium duration. Thus, further studies are needed to define which populations will benefit from AChEI.
Conclusion:
AChEIs are effective in reducing occurrence of delirium, but they did not affect delirium duration, severity or hospital LOS.
Q: Can you use high flow nasal cannula (HFNC) to manage acute hypercapnic respiratory failure?
A: It probably depends.
Background: While we now frequently utilize HFNC as an initial therapy for most acute hypoxic respiratory failure, its appropriateness in managing acute respiratory failure with hypercarbia has historically been opposed. With more recent data indicating that HFNC may be as good as noninvasive ventilation (NIV) for management of hypercapnia as well, this seemed like a good time to point out a few things:
The RENOVATE trial was a larger multicenter randomized noninferiority trial looking at HFNC vs NIV in all-comer acute respiratory failure, summarizing that HFNC was noninferior in the primary composite outcome of death + intubation at 7 days.
BUT this conclusion is not clearly supported in the smaller COPD (or acute cardiogenic pulmonary edema) subgroup:
What does seem to be clear across studies that HFNC has the capacity to clear some CO2 and is by and large better tolerated than facemask NIV.
Bottom Line: For mild-moderate acute COPD exacerbations with patient intolerance or exclusion criteria for NIV therapy, trialing HFNC is a reasonable option. For patients with severe acute or acute on chronic hypercapnia, as indicated by a [pseudo-arbitrary] pH < 7.25 and PaCO2 >70-80, noninvasive ventilation should be your go-to… or be ready to promptly intubate if/when the high flow fails.
Settings: multinational, randomized, double- blind, placebo-controlled clinical trial conducted in 17 centers in Italy, Russia, and Kazakhstan
Participants: A total of 307 ICU patients with sepsis or septic shock. Patients who were likely to die (APACHE II > 65 points) were excluded.
Treatment group: 80 mg bolus of omeprazole at randomization, at 12 hours and infusion of 12 mg/hour for 72 hours. Total dose of 1024 mg.
Outcome measurement: primary outcome of the study was organ dysfunction measured as the mean daily SOFA score during the first 10 days. Secondary outcomes were antibiotics-free days at 28 days; all-cause mortality at 28 days
Study Results:
Discussion:
Conclusion:
In sepsis patients, Esomeprazole did not re- duce organ dysfunction, despite demonstrating in vivo immunomodulatory effects
This review article reminds us that abdominal hypertension and compartment syndrome need to remain on our differential diagnosis for critically ill and injured patients. Pressure is measured with an intra-bladder catheter. Normal pressure is 5-7 mm HG. Sustained over 12 mm Hg is hypertension and sustained over 20 mm Hg is compartment syndrome.
We've got supine positioning and prone positioning... what about something in-between? Ye et al studied 2,159 patients coming out of anesthesia in a PACU after extubation. As sedation wore off, they placed one group in lateral decubitus, and left the other group supine. The lateral decubitus group had less hypoxia, a higher lowest SpO2, and required fewer airway rescue maneuvers.
Of note, the investigators didn't compare lateral or supine to prone positioning, which is often felt to be the best position for oxygenation (depending on patient characteristics and pathophysiology). And of course, this study represents a very specific scenario quite different from the ED (PACU patients post-extubation), so it's not clear how broadly extrapolatable this is. But this does add to the argument that supine is a poor position for oxygenating patients.
Bottom Line: If your supine patient is oxygenating marginally and you want a small bump without going all the way to prone positioning, consider lateral positioning. May make the most sense for procedural sedation and post-extubation patients in terms of similarity to this particular study.
What is the ideal oxygen saturation goal for a mechanically ventilated patient? Literature over the past decade has led away from the perfect 100% oxygen saturation due to its association with worse patient outcomes across many disease states. It is theorized that excess oxygen leads to free radical production causing a lung injury pattern. However, there is no clear guidance for the ideal range of oxygen saturation goals, particularly in the mechanically ventilated patient, despite a meta-analysis and several recent trials.
UK-ROX Trial - JAMA - June 2025
Question: Does an oxygen saturation goal of 88-92% lead to a lower 90-day mortality compared to usual care?
Population: 16,500 mechanically ventilated adult patients in 97 ICU’s across the UK, excluded patients on ECMO
Intervention: Goal oxygen saturation of 88-92%, using the lowest possible FiO2
Control: Usual care, defined as oxygen supplementation at the discretion of the treating physician (no limits set to FiO2 or SaO2)
Outcomes:
Bottom Line:
Ideal oxygenation targets remain elusive. UK-ROX adds to the growing literature of oxygenation targets in mechanically ventilated patients but does not clearly show that lower oxygen saturation targets lead to improved ICU outcomes. In your emergency department ICU boarder, avoid a 100% oxygen saturation to prevent oxygen toxicity associated lung injury and consider an oxygen saturation goal of 90-96% (88-92% if history of COPD).
You've encountered it at ABEM General Hospital, but now a SCUBA diver actually comes into your ED and you're concerned for DCS. What next?
Evaluation:
Symptom nature and timing are key in detailed history. Transient neurocognitive symptoms at depth suggest nitrogen narcosis or oxygen toxicity. Neurological symptoms within 10 minutes of surfacing suggest AGE. Widely variable symptoms within 24 hours of surfacing suggest DCS. Symptom onset greater than 24 hours suggests alternative diagnosis (still discuss with Hyperbaric Medicine or DAN).
Thorough physical exam. DCS may manifest only as localized pain. Look for marine envenomation or trauma to the area.
Neurological exam including detailed sensation and ataxia/balance - get the patient on their feet!
Unbiased differential. E.g. DCS may cause chest pain or SOB, but divers still have heart attacks. SCUBA setting may raise alert for AGE, but divers still have strokes. People go to the tropics to dive, but they also eat local fish (Scombroid and Ciguatera for a future pearl).
Management:
Early consult to Hyperbaric Medicine. In settings with no such team available, a good resource is the Divers Alert Network (DAN) Emergency Hotline at 1-919-684-9111
100% O2 via NRB or highest available delivery. You're not titrating to spO2, you're creating a diffusion gradient for tissue inert gas washout.
IV access and isotonic Fluids. PO if tolerable and unable to obtain IV access.
NSAIDs unless otherwise contraindicated. No special regimen. Standard dosing Ibuprofen or Naproxen are fine. Toradol is ok if limitations to PO.
Horizontal positioning in bed for AGE. Trendelenburg is not recommended.
Manage end organ effects as applicable. E.g. Spinal DCS may yield bladder retention requiring foley
Give consideration to activity specific considerations: hypothermia, restrictive clothing, etc
IV lidocaine has mixed evidence for neuroprotection in AGE. Discuss with Hyperbaricist before starting.
Pre-hospital considerations:
Transport should occur via ground or pressurized air transit capable of 1.0 ATA (sea level) cabin pressure. If non-pressurized aircraft transport is absolutely necessary, maintain continuous oxygen supplementation and altitude less than 2000 feet. This also applies to the inter-hospital setting.
O2 delivery by best means available to include SCUBA regulator mouthpiece or even a rebreather apparatus if present.
PO fluids if tolerable and no IV available.
Predicting NIV Failure
Norepinephrine (NE) is widely accepted as the first-line vasopressor for the management of septic shock, supported by the Surviving Sepsis Guidelines (1). The use of vasopressin as a second-line agent is also supported by the Surviving Sepsis Campaign, although the appropriate “triggers” for its addition remain vague. The SSG recommend adding vasopressin when NE infusion rates reach 0.25-0.6 mcg/kg/min, citing a catecholamine-sparing effect and potentially improved mortality (1, 2, 3).
What’s New?
The OVISS study (“Optimal vasopressin initiation in septic shock. The OVISS reinforcement learning study”) used machine learning to derive and internally validate a set of rules guiding the addition of vasopressin to NE for patients with septic shock using multiple databases of patient encounters across multiple institutions (4).
The machine learning model suggested initiation of vasopressin in more patients (87% vs 31%), earlier, and in less sick patients than was seen to be common practice:
Practice consistent with the above triggers was associated with decreased odds of in-hospital mortality (AOR 0.81, 95% CI 0.73-0.91).
Limitations
This was not a prospective study or RCT and was only internally validated. Using databases may limit the number of clinical variables available for analysis, and clinical judgment (how the patient looks) is not reflected.
Bottom Line
Consider adding vasopressin for patients with vasodilatory shock with low MAP despite NE >0.2mcg/kg/min and adequate fluid resuscitation, though more evidence is needed for a strong recommendation. As dual-pressor therapy may be riskier via peripheral IV and vasopressin does not have a direct antidote for extravasation, consider central line placement when adding vasopressin (5,6)
Whether you agree or disagree that “roc rocks and succ sucks,” evidence shows that approximately 3-4% of intubated patients experience awareness while paralyzed [1,2], and more of these patients are in the rocuronium subgroup [2,3,4]. Rocuronium acts in a dose-dependent fashion; the relatively standard 1-1.2 mg/kg in emergency department rapid sequence intubation (RSI) can result in a duration of paralysis can of up to 60-90 minutes. Commonly used sedatives in RSI, however, such as etomidate and ketamine, wear off quickly, before before rocuronium's paralytic effects have abated.
A recent single-center study showed that the majority of patients (60%) receiving rocuronium for paralysis during rapid sequence intubation (RSI) received no additional sedation until more than 15 minutes after induction, whether in the ED or ICU [5].
Patients experiencing awareness during paralysis with post-traumatic stress disorder [1,2] including distress from being restrained, feeling procedures, and feeling of impending death.
Bottom line: Start appropriate dose sedation promptly after RSI, especially with rocuronium, to avoid short- and long-term distress to patients.
Have you ever wondered what happened to your mechanically ventilated patients who developed diarrhea. Apparently, a multicenter study involving 2650 patients from 44 ICUs in the US, Canada and Saudi Arabia investigated the prevalence of diarrhea among these patients.
This study was the Editor’s choice for June 2025.
Results:
The mean age for the population was 59.8 (16.5) years, with APACHE II Score of 22.0 (7.8). Up to 61% of the patients received vasopressors or inotropes on day 1, which mean these patients are relatively ill.
Up to 60% of patients had diarrhea during their ICU stay, with 15% had diarrhea on day 1 or 2.
Initiating laxatives and antibiotics (who in the ICU would not receive vitamin V and Vitamin Z?) were associated with increased risk of diarrhea: HR for laxatives 1.28 (1.13–1.44), p<0.001; HR for antibiotics 1.41 (1.20–1.67), P< 0.001.
Furthermore, enteral feeding with high/moderate protein concentration was also associated with diarrhea (HR 1.13, 1.00-1.28, P=0.045.
Not surprisingly, diarrhea was associated with higher number of C. Diff testing.
Although patients with diarrhea were associated with longer ICU stay (15 [10-23] days) vs. those without diarrhea (8 [6-12] days), it was not associated with higher mortality (HR 0.70, 95% CI 0.57-0.86, P<0.001)
Discussion:
1. The authors did not report the rates of positive C. Diff. infection in these patients during ICU stay, although they did report that for another study in this population, the rate of positive C. Diff. infection during ICU stay was 2.2%. If only 2.2% had C. Diff. infection while up to 60% had diarrhea. Consequently, for every 30 patients with diarrhea, only one patient had C. Diff. infection. Therefore, do we have to check C. Diff. in those ICU patients with diarrhea every time?
2. The authors hypothesized that patients with diarrhea had longer ICU stay and lower mortality because they survived long enough to develop diarrhea. Thus, diarrhea is bad for clinicians, but may not be too bad for patients?
Conclusion:
Diarrhea is common among invasively ventilated patients. Patients who received laxatives, antibiotics, enteral feeding with high protein amount are at higher risk for diarrhea.
PEEP is often titrated up along with FiO2 to increase oxygen saturation. Although the potential negative hemodynamic effect of high PEEP is often recognized, it is important to also note that high PEEP can also paradoxically worsen oxygen saturation.
The primary physiologic explanation for this phenomenon in a patient with pulmonary disease is due to the varying impact of PEEP on the intra- vs. extra-alveolar blood vessels. PEEP preferentially distends more normal/compliant lung which causes compression of intra-alveolar vessel at excessively high levels of PEEP. This causes pulmonary blood to be diverted to areas of lower vascular resistance (e.g. consolidated lung which is less distended due to its worsened compliance) and lower VQ matching. Essentially, blood flow to normal/healthy lung is decreased and is instead increased to diseased lung, worsening hypoxemia.
Bottom line:
High PEEP can potentially worsen hypoxemia and should be considered as an etiology for worsening oxygen saturation, particularly when the hypoxemia is out of proportion to the patient’s radiographic findings.
Secondary analysis of a multicenter, prospective, observational study ICE-CRASH study in Japan including adult patients admitted with moderate-to-severe accidental hypothermia between 2019 and 2022.
Some structural generalizability (median age 81 years!) issues with this study but well done overall.
Authors undertook some rather complex modeling to predict outcomes related to rapid rewarming, showing that “the rewarming rate and predicted probability of each outcome increased significantly up to 3°C/hr, but when the rewarming rate exceeded 3°C/hr, the predicted probability of each outcome was almost constant.”
Suggests that for those with severe hypothermia that an initially rapid rate of up to 3C/hr is a good target for a ceiling, but above this may be associated with less favorable risk:benefit ratio. Benefit in moderate hypothermia was not as clear.
Conclusion: The mode of rewarming in severe hypothermia should still be based on local protocols and capabilities (e.g. external, intravascular, extracorporeal rewarming) but the rate of rewarming up to 3C/hr is associated with better outcomes.
Following up Dr. Flint's pearl from the other day, the largest study to date looking at a lower Mean Arterial Pressure (MAP) target in elderly ICU patients is the “65” Trial, published in JAMA in 2020. This trial compared a MAP target of 60-65 to the usual goal of >65, in critically ill patients age 65 and older. It included 2,455 patients in 65 ICUs in the UK, and found no difference between the groups.
Bottom Line: Although most intensivists still target a MAP > 65 regardless of patient age, you do have some evidence to support you if you want to target 60-65 in patients over age sixty-five. However, there are some important limitations (well outlined in the PulmCrit article linked below), and therapy should always be optimized to the patient and markers of end organ perfusion.
The presence of an endotracheal tube by itself does not mandate sedation and many patients require no sedatives while intubated in the ICU. However, patients intubated in the emergency department usually require initial sedation while still paralyzed from RSI. Sedation can also help facilitate procedures and imaging in critically ill patients during initial management.
Current literature has found increased mortality and length of ventilator requirement in oversedated ED patients. The target sedation level for the general population remains a goal RASS (Richmond Agitation-Sedation Scale) of 0 to -1. Society of Critical Care Medicine guidelines from early 2025 recommend dexmedetomidine over propofol as the preferred sedative for light sedation and reducing delirium risk in intubated critically ill patients. A recent trial re-examined other clinical outcomes between these two common sedative agents.
A2B Randomized Clinical Trial - JAMA 2025
Clinical Question: Does alpha 2 adrenergic receptor agonist sedation (dexmedetomidine or clonidine) reduce duration of mechanical ventilation in mechanically ventilated patients compared to a propofol based regimen (usual care)?
Where: 41 UK ICU’s from December 2018 to October 2023
Who: 1438 adults receiving mechanical ventilation for less than 48 hours, receiving propofol and opioid for sedation/analgesia, expected to require mechanical ventilation for greater than 48 hours
Intervention: protocol driven sedation to reach a RASS score of -2 to +1 (either dexmedetomidine, clonidine, or propofol). Of note, propofol could be added to achieve deeper sedation goal if deemed necessary by care team.
Outcomes:
Bottom Line:
While either dexmedetomidine or propofol, with appropriate use of opiates for pain management, are appropriate agents in non-paralyzed mechanically-ventilated patients, propofol may be a more appropriate choice in patients with greater agitation while boarding in the emergency department. However, close attention is needed to avoid the overly deep analgosedation associated with increased mortality. Maintain a goal RASS of 0 to -1 with frequent re-evaluation of your ICU boarders.
