UMEM Educational Pearls - Critical Care

Check for Elevated ICP in the Post-ROSC Patient

• More than 600,000 people experience out-of-hospital cardiac arrest (OHCA) in North America each year.
• Unfortunately, only 10% of patients with OHCA survive to hospital discharge.
• A key component of the ED management of the post-cardiac arrest patient centers on minimizing secondary cerebral injury.
• In addition to monitoring for seizure activity in the comatose post-arrest patient, it is also recommended to assess the post-ROSC patient for elevated intracranial pressure (ICP).
• This can be accomplished with neuroimaging (CT head) to look for cerebral edema, physical exam (pupillary asymmetry) and with POCUS measurements of the optic nerve sheath diameter.
• In post-ROSC patients with signs of elevated ICP, raise the head of the bed, provide adequate sedation/analgesia, consider hypertonic saline, and optimize the mean arterial blood pressure.

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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.

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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:

• Most of the existing studies are small, with a notable amount of heterogeneity
• These studies look at mild to moderate hypercapnia, not severe
• There are various amounts of crossover from HFNC to NIV as rescue
• Most acute hypercapnic studies involve COPD, not other etiologies such as obesity hypoventilation, etc.

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:

• The median pH / PaCO2 for HFNC was 7.32 / 55 mmHg and for NIV was 7.3 / 64
• 13% of the HFNC group were on NIV prior to randomization
• 23% crossed over to NIV use
• Posthoc analysis indicated possible harm with HFNC in the COPD group

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.

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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:

• At 10 days, there was no difference in the median mean daily SOFA score: 5 (IQR, 3–10) in the mega- dose esomeprazole and 5 (IQR, 3–9) in the placebo groups (risk difference [RD], 0.1; 95% CI, –0.8 to 1.0; p > 0.99).
• At day 28, the median antibiotic-free days were 15 (IQR, 0–21) in the mega-dose esomeprazole group vs. 13 (IQR, 0–21) in the placebo group (p = 0.62).
• All-cause mortality at 28 days was 25% in the mega- dose esomeprazole group and 20% in the placebo group (RD, 4.9; 95% CI, –4.5 to 14.2; p = 0.31).

Discussion:

• The authors also did in vitro assays and they detected reduced levels of anti-inflammatory cytokines among patients receiving megadose of omeprazole. However, these in vitro results did not translate into clinical benefits in these patients with sepsis.
• Apparently, this study is another example that animal studies may not translate into clinical benefits in human studies, especially sepsis , as this condition is highly heterogeneous.

Conclusion: 

In sepsis patients, Esomeprazole did not re- duce organ dysfunction, despite demonstrating in vivo immunomodulatory effects

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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. 

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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.

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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:

• Conservative and usual therapy groups were randomized 1:1 and had similar characteristics
• 90 day all-cause mortality - 35.4% in conservative group vs. 34.9% in usual care group (p=0.28)
• Time at 88-92% SaO2 -  62.6 hrs in conservative group vs. 27.2 hrs in usual care group (did not look at oxygen exposure peri-intubation) 
• No difference in secondary outcomes - duration of ICU stay, days alive and free of organ support, duration of acute hospital stay, and others

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).

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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.

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Predicting NIV Failure

• Noninvasive ventilation (NIV) is often used in the resuscitation of critically ill patients with acute hypoxemic or hypercapnic respiratory failure.
• Given the frequency of its use in both EDs and ICUs, it is important to recognize NIV failure and when patients should undergo intubation and initiation of mechanical ventilation.
• Patients should be re-evaluated within approximately 60 minutes of initiation of NIV.
• The HACOR score is a risk scoring tool comprised of heart rate, acidosis, consciousness, oxygenation, and respiratory rate and can be used to detect NIV failure in the hypoxemic patient.
• Consider intubation in a patient with a HACOR score > 5 at 1-2 hours after NIV initiation.

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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:

• Timing: 4h after diagnosis of shock (vs. 5h)
• NE dose: 0.2 mcg/kg/min (vs. 0.37mcg/kg/min)
• Serum lactate: 2.5 mmol/L (vs. 3.6 mmol/L)
• SOFA score: 7 (vs. 9)

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)

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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.

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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.

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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.

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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.

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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.

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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:

• No significant difference in time to extubation between dexmedetomidine vs. propofol (HR of 1.09, p=0.2) OR clonidine vs. propofol (HR of 1.05, p=0.34)
• Higher rates of agitation in the dexmedetomidine group (HR of 1.54, CI 1.21-1.97) and clonidine group (HR of 1.55, CI 1.22-1.97) compared to propofol group
• Mortality at 180 days similar between all groups
• Severe bradycardia seen more frequently in dexmedetomidine and clonidine groups compared to propofol group although unclear if ongoing propofol administration had any effect on these groups
• Subgroup analysis showed a weak interaction with age as a continuous variable showing reduced benefit on time to extubation with dexmedetomidine vs. propofol at later decades of life (i.e. dexmedetomidine showing potential benefit at younger ages)

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.

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When To Initiate RRT in the Critically Ill Patient

• Acute kidney injury (AKI) occurs in more than half of critically ill patients admitted to the ICU.
• When and how to initiate renal replacement therapy (RRT) in the critically ill patient remains debated.
• While a strategy of deferred RRT is preferable in many, indications for immediate RRT in patients with AKI include the following:
  • Potassium > 6.5 that is refractory to medical therapy
  • pH < 7.15 that is not responsive to bicarbonate administration
  • Fluid overload (worsening pulmonary edema, P/F ratio < 200 mm Hg) that is refractory to diuretics

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Patient-ventilator dyssynchrony is a sign of a disagreement between the patient's breathing and the ventilator's settings. Recognizing and fixing it is a critical skill to prevent lung injury and improve comfort. Ineffective triggering and double-trigger are two common types of dyssynchrony.

Ineffective Triggering

The patient tries to take a breath, but they are too weak to trigger the ventilator. This is the most common type of dyssynchrony. It causes increased work of breathing and discomfort.

Look for a small dip in the pressure waveform and a simultaneous scoop out of the expiratory flow waveform that is not followed by a delivered breath.

Troubleshooting options:

• Try making the trigger more sensitive (e.g., decrease flow trigger from 3 L/min to 1 L/min).
• Try increasing the respiratory support based on the mode of ventilation. The patient may need higher pressure or volume to support the breaths they are able to trigger.
• Check for and treat auto-PEEP, which makes it harder for the patient to trigger the next breath. This is especially critical for patients with COPD or asthma!
• Try a different mode of ventilation

Double-Triggering ("Breath Stacking")

The patient's own breath outlasts the ventilator's set inspiratory time (Ti), causing one patient effort to trigger two stacked breaths. This results in delivery of large tidal volumes, risking lung injury (volutrauma).

Look for two consecutive breaths on the ventilator screen without a full exhalation in between.

Troubleshooting options:

• Increase the set tidal volume Vt or the inspiratory time Ti to better match patient demand.
• Address underlying causes of high respiratory drive (e.g., pain, anxiety, acidosis).
• Increase sedation if appropriate.
• Try a different mode of ventilation, such as pressure support, where the patient has more control over inspiratory time.

Bottom Line

Dyssynchrony means the ventilator settings do not match the patient's needs. Watch the waveforms to diagnose the mismatch, then either adjust the ventilator or treat the underlying problem.

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Acute respiratory distress syndrome (ARDS) is an acute, inflammatory lung injury that effects the lung diffusely and can be triggered by various insults.  Aside from the Kigali modification, the most recent updated definition of ARDS was the Berlin definition in 2012.  There have been many advances and changes in the understanding and clinical practice for managing patients with ARDS since then.  In 2024, Matthay, et al. proposed the new global definition to build upon the Berlin criteria [1].  They addressed several important issues with the Berlin definition to improve the diagnostic criteria and improve ability for diagnosis in resource-limited settings.

ARDS Berlin Definition

• Acute onset of respiratory failure or worsening respiratory failure that occurs within one week of a risk factor/insult
• Pulmonary edema is NOT solely due to cardiogenic pulmonary edema or fluid overload.
• Hypoxemia is NOT solely due to atelectasis
• Bilateral opacities on chest imaging (x-ray or CT) that isn’t due to pleural effusion, atelectasis or masses
• PaO2:FiO2 of </= 300 mm Hg with categories of mild (>200 and </=300 mm Hg), moderate (>100 and </= 200 mm Hg) and severe ( </=100 mm Hg) with PEEP or CPAP of 5 cm H20

Important updates for the Global definition of ARDS

• Ultrasound can be utilized to diagnose bilateral infiltrates
• SpO2:FiO2 can be used to diagnose and assess severity.  SpO2 should be < 97%
• Modified ARDS definition to not require PaO2:FiO2 cutoff (can use S:F ratio instead) or PEEP requirement
• Non-intubated patients who otherwise meet criteria for ARDS and are managed with high-flow nasal cannula (HFNC) with at least 30 L/min of flow would meet the diagnostic criteria

Diagnostic Criteria for the New Global Definition of ARDS from Matthay et al.

The Global Definition of ARDS expands upon the Berlin definition.  It was shown that this new definition improves diagnosis in resource-limited settings, allows for earlier detection, and better classification [2].  A retrospective study evaluating this new global definition found that there was a significant number of patients identified using this new definition who would have been missed using the Berlin definition [3].  These patients may benefit from ARDS directed therapies and further prospective studies will be needed to assess how this new definition effects clinical management of these patients using the new definition.

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Pulse Checks in Cardiac Arrest: Your Fingers Are Not Reliable.

Summary:  Whenever possible, use an ultrasound or an arterial line for pulse checks.  Our fingers are not reliable. 

Key points:

1. It is very difficult to obtain a palpable pulse in a hypotensive patient, even in the best of conditions.  In cardiac arrest patients specifically, manual pulse checks are not a reliable method to detect return of spontaneous circulation (ROSC).  
2. Yet manual pulse checks remain the standard of care in ACLS algorithms.  
3. Better options to determine ROSC include ultrasound and arterial lines.  
4. End title CO2 is a useful adjunct, but should not replace ultrasound and arterial lines to determine ROSC.
5. There is a lack of evidence to determine a measured arterial pressure in which it is safe to stop chest compressions, but in the absence of an evidence based, established standard, a MAP > 50 or SBP > 60 can be used as a tentative guide.

Multiple studies have demonstrated that manual pulse checks are not a reliable method to determine ROSC.  Arterial lines and ultrasound are far more reliable methods.  However, using more accurate measures of circulation lead to an additional dilemma: at what MAP, SBP, or ultrasound measured flow should we stop chest compressions?  There is no agreed upon number, and as with most dilemmas in clinical medicine, the best answer is, “it depends”.  However, a MAP > 50 or SBP > 60 for most patients is a reasonable choice to stop chest compressions.  MAP < 50 or  SBP < 60 are unlikely to provide adequate perfusion to the brain, and chest compressions should be resumed.  

References:

1. https://pubmed.ncbi.nlm.nih.gov/35131404/
2. https://pmc.ncbi.nlm.nih.gov/articles/PMC6042301/
3. https://pubmed.ncbi.nlm.nih.gov/30902687/
4. https://pubmed.ncbi.nlm.nih.gov/36646373/
5. https://pubmed.ncbi.nlm.nih.gov/35792305/
6. https://emcrit.org/emcrit/further-disambiguating-pea/
7. https://emcrit.org/emcrit/pea-is-stupid/