A crucial part of cardiac arrest management is identification of the underlying rhythm, with key aspects of management diverging depending whether shockable (pulseless ventricular tachycardia/pVT or ventricular fibrillation/VF) or unshockable (pulseless electrical activity/PEA or asystole). 

A recent study prospectively evaluated adult atraumatic out-of-hospital-cardiac-arrests (OHCAs) presenting to the ED, to determine what percentage of cases had “Occult VF” –  VF found point-of-care echocardiogram but not by ECG. The researchers only included cases with simultaneous ECG and echo assessments for the initial 3 pulse checks. Echo and ECG determinations for the study were adjudicated by research team members.

They found that:

• 5.3% of patients had occult VF (43/811), with ECG reading PEA in 81.4%  (35/43) and asystole in 18.6% (8/43)
• Of the 202/811 patients with VF on ECG, only 23.3% had echo VF
• Interestingly, patients with ECG VF but no VF on echo had a lower rate of ROSC and successful defibrillation than those with Occult VF
• There was no statistically significant difference in survival to hospital discharge between the two
• A higher percentage of patients evaluated by TEE compared to TTE were found to have occult VF (12.5% vs 4.9%)

Major limitations: 

• Only have the cases with simultaneous ECG + echo for the first 3 pauses
• Only have the recorded echo clips, which are not the same as in-the-moment viewing during the arrests
• No comparison to how research team interpreted ECGs to how the treating team managed

Bottom Line: Point-of-care echocardiogram continues to have value in the management of cardiac arrest, potentially changing management and affecting post-ROSC decisions. Ensuring high-quality CPR, with appropriate defibrillation and anti-arrhythmic strategies, remains paramount in management of shockable OHCA.

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Settings: Secondary analysis of the Crystalloid Liberal or Vasopressors Early Resuscitation in Sepsis (CLOVERS) trial.

Participants:

1368 patients who survived on day 28 after enrollment, and were retrospectively assigned different subtypes:

1. Low risk, barriers to care. Younger patients with few comorbidities, less severe disease, 

2. Unhealthy baseline with severe illness: Previously healthy with severe illness and complex needs after discharge, barriers to care.

3. Multimorbidity. Older patients with more comorbidities and are frequently readmitted. 

4. Low functional status: Poor functional status. Older patients with high prevalence of frailty at discharge and high functional needs who are  often discharged to a facility.

5. Unhealthy baseline with severe illness: Existing poor health with severe illness and complex needs  after discharge. Older patients with severe comorbidities,  more severe illness, high functional needs, prolonged hospital stay, 

Outcome measurement: 

A) 90-day mortality, 

B) 6-month and 12-month EuroQol 5D five level score

Study Results:

A) 90-day mortality:

Unhealthy baseline  with severe illness (37.6%) >  low functional status (45.5%) > multimorbidity (17.4%) >  unhealthy baseline, severe illness (13.2%) > Low risk (5.1%).

B) 6-month EuroQol 5D-Five Level: lower score, lower functional outcomes)

Unhealthy baseline  with severe illness (0.53) >  unhealthy baseline, severe illness (0.68) > low functional status (0.69) > multimorbidity (0.78) >  Low risk (0.80).

Discussion:

a) The framework, readily available to clinicians provides good prognostic tools for mortality.

b) Although there was prediction of poor functional outcomes at 6-month and 12-month, the differences between subtypes in their EuroQoL 5D-5L did not seem to correspond to 90-day mortality. Low functional status group had 2nd-highest rate of mortality, but only 3rd in their EuroQoL 5D-3L score. Thus, there needs to be more studies in these nuances.

Conclusion: 

Sepsis survivor subtypes—assigned using only three routinely available discharge variables—are strongly associated with 3-month mortality and long-term disability and HRQOL up to 12 months

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Attachments

• 2026 Flick Figure 3-696f822c68572.jpg (137 Kb)

Recall that MAP = (cardiac output) x (systemic vascular resistance)

Consequently, a patient can be normotensive due to increased SVR despite a very low cardiac output and shock. In fact, normotensive shock may have worse outcomes compared to patients with isolated hypotension. 

Take home points: 

• Shock does not equal hypotension
• In critically ill patients with reduced cardiac output, additionally use other markers for end-organ perfusion (mental status, renal function/urine output, LFTs, cap refill, lactate etc.) to assess for possible shock

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Yet another study (this time ED focused) has shown benefits to patients and hospital systems when implementing a Phenobarbital-based treatment algorithm. Shorter ED LOS, fewer admissions, and treatment with phenobarbital alone was independently associated with discharge when compared to mixed treatment regimens. Higher age and heart rate, as well as treatment with benzodiazepines alone were independently associated with hospitalization.

Cautions/contraindications include: pregnancy, cirrhosis with history of hepatic encephalopathy (consider dose reduction in hepatic dysfunction), acute intermittent porphyria, and prior chronic phenobarbital use.

Phenobarbital has a long half life (one of its benefits in AWS) and works synergistically with benzodiazepines, so should be used preferentially as monotherapy in patients where the diagnosis is relatively certain and who have not received high doses of benzos. Once the diagnosis is made, go with phenobarbital and stick with it. 

PulmCrit has an excellent in-depth article on this and also see Dr. Flint's pearl describing another centers experience in a hospital-wide rollout (links below).

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Perintubation hypotension is a major problem, and can precipitate hemodynamic collapse and cardiac arrest for a multitude of reasons.  To prevent this, many different strategies have been explored (some of which work and some of which don't), including empiric IV fluid boluses, additional resuscitation before intubation, switching or dose-reducing induction agents and much more.  But we know pressors  like norepinephrine raise blood pressure effectively, so should we just put everybody on a norepinephrine drip before we intubate them?

Probably not.  The EPITUBE trial included 210 patients at a single-institution undergoing cardiac surgery, and randomized them to empirically starting a norepinephrine infusion before induction vs just rescue ephedrine when needed (fairly standard anesthesia practice).  For the empiric norepinephrine group, they started at 0.06 ug/kg/min, and once the drip was up and running, they titrated for a MAP of 65-80 (which could include stopping the norepi if that the patient remained above 80 despite downtitration)

The incidence of severe hypotension (MAP < 55) did not differ between the groups, although fewer empiric norepinephrine patients had a MAP < 65 at any point (which was a secondary outcome).  Naturally, the differences between this practice setting (the cardiac surgery OR) and the emergency department should be noted and are not addressed by this study.

Bottom line: There isn't good evidence to support empirically starting all patients on a norepinephrine infusion prior to intubation as a method to prevent perintubation hypotension.  You should always have rapid access to vasopressors when intubating, and should continue to tailor your therapy to the individual patient, but probably don't start just putting everyone on norepinephrine before you intubate them.

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The emergency department serves many critically ill patients that require airway management and mechanical ventilation. Most of these patients go on to require ICU care. However, some patients require only brief intubation and should be appropriate candidates considered for emergency physician-driven extubation. Early extubation can minimize the risks associated with mechanical ventilation for patients such as ventilator associated pneumonia (VAP), ventilator induced lung injury (VILI), and others. Additionally, in setting of high levels of ED boarding and limited ICU resources, extubating appropriate candidates in the ED can reduce boarding times and improve patient flow.

Who?

1. Patients with temporary neurologic dysfunction (alcohol/drug intoxication)
2. Need for brief procedural sedation that cannot be accomplished without a definitive airway (endoscopy)
3. Patients transitioning to a palliative, comfort-focused approach to treatment

Screening Checklist

• Returned to baseline mental status, able to follow commands
• Appropriate vital signs on minimal ventilator support
• Breathing spontaneously with RR <30, FiO2 of 30-40%, PEEP 5-8 cmH2O, achieving TV > 6-8 cc/kg
• May be on low-dose vasopressor to manage sedation-related hypotension
• No history of difficulty intubation (in case emergent reintubation is required)

Testing

• Perform spontaneous breathing trial (SBT):
  • IPAP 10 cmH2O over EPAP of 5 cmH2O, also described as pressure support of 5 cmH2O over PEEP of 5 cmH2O
  • 30 minutes
  • Assess the RSBI (Rapid Shallow Breathing Index — available on MDCalc)
• Patient fails for EP-driven extubation if one or more of the following is present:
  • respiratory distress
  • severe anxiety
  • hypoxemia (SaO2 < 90%)
  • tachypnea (usually RR > 30)
  • somnolence
  • RSBI > 105 breaths/min/L

Prepare - depending on institution, may require consultation with the hospital intensivist

• Notify the respiratory therapist (extubation ideally performed by the RT, if available)
• Have standard AND difficult airway equipment at bedside
• These specifically selected patients can usually be extubated to temporary standard nasal cannula
  • Optimal respiratory support post-extubation for palliative patients depends on patient-specific care plan
• For patients with respiratory distress with plan for compassionate extubation, we advise palliative opiate and anxiolytic administration closely titrated to patient comfort, adjusted as ventilator support is weaned down to a pressure support of 0 over PEEP of 0-5. This ensures the patient remains comfortable with minimal distress and air hunger when ventilator support is removed. Other palliative patients with no tachypnea or distress do not necessarily require this measure.
• Some of these patients may be anxious when transitioning off mechanical ventilation; consider use of dexmedetomidine in the peri-extubation period to facilitate patient comfort while maintaining respiratory drive

Perform - see this video courtesy of Respiratory Skills - LSC on performing extubation

• Make sure to monitor for post-extubation hypoxemia and post-extubation stridor
• Always be prepared for the potential need for re-intubation

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Pitfalls in Lactate Interpretation

• Lactate is one of the most common biomarkers used in critical care.
• While an elevated lactate level is often attributed to impaired tissue oxygenation, an important pitfall in lactate interpretation in the critically ill is the failure to consider non-hypoxic causes of increased levels.  These include:
  • Enhanced glycolysis (B2-agonist administration, increased metabolic activity)
  • Reduced clearance (hepatic failure, renal dysfunction, muscular dysfunction)
  • Impaired tissue metabolism (mitochondrial dysfunction due to drug intoxication)
• Additional pitfalls in lactate use in the critically ill include:
  • Use of an isolated value rather than assessing longitudinal trends
  • Failure to correlate elevated lactate levels with other markers of perfusion (i.e., capillary refill time)
  • Use of rigid normalization targets rather than targeting therapeutic interventions to the full clinical picture

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Last month, Mark Sutherland posted an overview of a new article investigating the use of personalized MAP targets in resuscitation for septic shock (1). Now, the authors of ANDROMEDA-SHOCK-2 (2) suggest a new multimodal approach to personalize resuscitation in septic shock that largely operates outside of the traditional focus on MAP and lactate.

In 2019, the ANDROMEDA-SHOCK Trial (3) suggested that capillary refill time (CRT) may be a better resuscitation in septic shock than lactate. Now, the same group is suggesting that a stepwise algorithm to guide resuscitation may provide more optimal and “personalized” results when compared to usual care for patients with abnormal CRT:

Tier 1: If CRT is abnormal, assess pulse pressure (PP) and DBP: 

• PP (<40mmHg) OR DBP (>50mmHg)?  Assess for fluid responsiveness and challenge with up to 1L IVF if fluid responsive.
• PP (>40mmHg) AND DBP (<50mmHg)? Increase norepinephrine (NE) for DBP >50mmHg, followed by assessment for fluid responsiveness and possible fluid challenge if CRT remains abnormal.

Tier 2: If CRT remains abnormal despite the above, use POCUS to assess for cardiac dysfunction.

• LV dysfunction? Trial dobutamine @ 5-75 mcg/kg/min (stop for HR > 120 or tachyarrhythmia, or if it doesnt help CRT)
• RV dysfunction? The authors recommend avoiding fluids, increasing pressors if needed, as well as decreasing PEEP, limiting plateau pressures, and/or proning the patient if they have ARDS
• If there is no cardiac dysfunction, assess for fluid responsiveness and fluid challenge if fluid responsive. Continue this cycle until CRT normalizes or there is evidence of harm (evidence of pulmonary edema, worsening oxygenation/ventilation, or high central venous pressure).
  • If the patient is not fluid responsive, investigate for a history of HTN
    • If they have a history of HTN, push MAP to 80-85 for 1h and see if it improves CRT (if not, revert back)
    • If they do not, trial dobutamine @ 5 for 1h and see if it improves CRT (if not, DC dobutamine)
• If CRT remains abnormal after all of this, move on to “rescue therapies” (high dose steroids, hemofiltration, ECMO).

The authors found that at 6 hours, following the protocol resulted in increased use of dobutamine, lower fluid balance, and similar CVP and MAP with lower lactate levels and CRT. They reported an improvement in their composite hierarchical outcome at 28 days, primarily driven by a shorter duration of organ support (vasoactives, mechanical ventilation, renal replacement therapy) and among sicker patients. No difference in mortality was observed between groups.

Food for Thought:

• CRT is a subjective assessment, and all participating clinicians in this study underwent mandatory training. Other, more objective measures that can be used to assess organ perfusion (lactate clearance, urine output, MAP) were excluded from this protocol.
• Fluid responsiveness was assessed using the “preferred technique by each center.” Suggested techniques included pulse pressure/stroke volume variation, change in VTI with passive leg raise, IVC variability, or change in CO with end expiratory pause.
• There was no standardization regarding the integration of vasopressin, and steroids were reserved as “rescue therapies” and considered at the same point as mechanical hemodynamic support. 
• The effect of other inotropic agents (like low dose epinephrine) was not discussed.

Study Details:

• Setting: multicenter randomized control trial conducted in 86 ICUs across 19 countries
• Patients:
  • >1450 adults from the ED, ICU, OR, or floor with septic shock based on Sepsis-3 criteria - suspected/confirmed infection + lactate >2 + pressor requirement to maintain MAP> 65 despite 1L+ IVF bolus.
  • Patients with Child B or C cirrhosis, acute hematologic malignancy, severe ARDS, or anticipated surgery or HD within 8h of being diagnosed with septic shock, or who could not be enrolled within 4h of diagnosis were excluded. Pregnant patients were also excluded.
  • Almost half had an abdominal source of infection, followed by respiratory and urinary.
  • The median time to enrollment was 2h from meeting sepsis criteria
• Outcome: a hierarchical composite outcome using all-cause mortality, duration of vital support (vasoactives, invasive mechanical ventilation, or renal replacement therapy), and hospital LOS at 28d.
  • The primary outcome was assessed in a hierarchical fashion using “wins” and “losses.” The intervention group “won” in 48.9% of cases, while the usual care group “won” in 42.1%, for a Stratified Win Ration of 1.16 (95% CI 1.02-1.33).

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We have all been there – an ED patient with circulatory shock requiring vasoactive medications and, therefore, an arterial line for accurate and close monitoring of the MAP and appropriate titration of the infusions. But does it save lives?

The recently published NEJM article by Muller et al. takes a look at noninvasive BP monitoring (NIBP) by cuff versus early arterial catheterization in patients with hypotension and evidence of tissue hypoperfusion: 

• Open-label, pragmatic, parallel-group, noninferiority, multicenter RCT across 9 ICUs in France
• Adult patients enrolled within 24h of ICU admission, randomized to NIBP (n=506) or arterial line placement within 4h of enrollment (n=504)
  • 15% of NIBP group received art line during study period as deemed necessary by predefined safety criteria (unable to get NIBP or SpO2, for ex)
  • 50% septic shock, >90% medical patients, 90% on pressors at randomization
• Notable exclusions: BMI >40, high-dose vasopressors (total norepi tartrate* + epi infusion rate >2.5 mcg/kg/min) 
• Findings: 
  • No difference in primary outcome of 28-day mortality (34.3% NIBP vs. 36.9% art line)
  • No difference in 90 day mortality, 28-day ventilator, vasopressor, or RRT-free days
  • More arterial puncture attempts in the NIBP group (742 vs. 269 per 1000 ICU days)
  • No increase in arterial line-associated infections or ischemia
  • More (8 vs 1%) hematoma or hemorrhage at art line site in arterial line group
  • More patients in NIBP group reported serious pain/discomfort related to device (13 vs 9%)

Bottom Line: This trial indicates that in appropriately-selected patients with shock, such as those not on high doses of vasopressors, with BMI < 40 and an ability to consistently obtain NIBP measurements, early arterial line placement in the ED for vasopressor titration is unlikely to improve outcomes. It is important to note other potential indications for arterial line placement (severe hypoxia, inability to obtain reliable SpO2 with need for ABG monitoring, cardiac arrest, pain related to NIBP cuff monitoring, intracranial hemorrhage, etcetera) may still make arterial line placement in the ED prudent and better for overall patient care.

*France refers to norepi by the tartrate formulation dose, US refers to the base norepi dose (ratio is 2:1 tartrate: base).

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Settings: this is a meta-analysis of 17 observational studies about boarding of critically ill patients in US Emergency Departments. All studies were from urban, academic centers.

Participants:

• There was a total of 407,178 patients, 194,814 (485) were boarding vs. 212,364 (52%) non-boarding patients.
• 355,86 (87%) patients were at centers with the presence of a resuscitation service.
• Ther was a mixture of critical illnesses: trauma (29.4 %), medical conditions (29.4 %) and mixed critical illness (41.2 %).

Outcome measurement: all cause mortality, as reported by the authors of the original studies.

Study Results:

• Overall, boarding patients were not associated with higher mortality, than non-boarding patients (Odd ratios 1.06, 95 % CI 0.94–1.19 p=0.383).
• Boarding patients were not associated with longer hospital length of stay (mean difference 0.38 days, 95%CI 0.94-1.50, P=0.51).
• However, among subgroup analyses, boarding patient population with mixed critical illnesses was associated with higher odds for mortality (OR 1.2, CI 1.04–1.4, p = 0.02 ) and longer HLOS (difference = 1.9, 95 % CI 0.81–3.1, I2 = 0 %, p = 0.001).

Discussion:

• All studies were observational so there was risk of bias and there was a presence of a small publication bias. This means that there were a few unpublished studies out there that showed that Boarding patients might have better outcomes.
• The findings that patient population with mixed illnesses were associated with higher odds for mortality, compared with Trauma-only or medical-only patients, might suggest that ED are not well equipped to take care of a wide spectrum of disease states. We seem to do better with populations with protocols such as sepsis, stroke, trauma.
• There was no clear consensus about how researchers approach this topic. A few studies did not even report their patient populations’ age (I cannot understand how these got published). Researchers used different thresholds for boarding, likely reflecting their institutional variabilities. There was quite a significant heterogeneity about patients’ acuity: some studies used SOFA, others used mSOFA.
• All of the studies were from urban academic centers so their results may not be applicable to non-academic centers which may not have many boarding issues

Conclusion: 

Critically ill patients boarding in the U.S. Emergency Departments were associated with a non-statistically signi?cant increase in odds of mortality and hospital length of stay compared to non-boarded patients

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The role of sodium bicarbonate in the treatment of severe acidemia has been controversial, with some studies suggesting no benefit, and others indicating that it may help reduce need for renal replacement therapy (RRT) and even improve mortality. The BICARICU-2 Trial was an open-label multicenter RCT conducted in France that evaluated the impact of a bicarb infusion among patients with metabolic acidosis and moderate to severe AKI. 

There was no difference in 90 day mortality, but patients in the bicarb group were less likely to be started on RRT (38% vs 47% in the control group) using pre-defined criteria for RRT initiation, and had a 50% lower rate of bloodstream infections. Patients in the bicarb group who were started on RRT met criteria for RRT later than those in the control group (median 31h vs 15.5h).

Study Details:

Patient Population: 

• SOFA score >4 OR arterial lactate > 2mmol/L within 48h of ICU admission
• Metabolic acidosis, defined by pH < 7.2, HCO3- < 20mEq/L, and PaCO2  < 45mmHg
• Moderate to severe AKI, defined as Cr >2.0 x baseline or UOP < 0.5 mL/kg/h for >12h. 
• Patients with severe baseline CKD, ketoacidosis, intoxication with exogenous acids (metformin, salicylate, methanol, ethylene glycol), or ongoing bicarb losses via GI or urinary tracts were excluded.
• The presumed etiology of acidemia was septic shock in over half of included patients, and over 75% were on vasopressors.

Intervention: 

• 4.2% bicarb infusion administered in 125-250 aliquots with a target pH >7.3, though not to exceed 1L/500mEq within 24h. 
• The intervention continued for a maximum of 28d or until ICU DC. 
• Patients in the intervention group received a median of 750mL in the first 48h.

RRT Triggers:

• Immediate: K > 6.5mEq/L with EKG changes or cardiogenic pulmonary edema with no UOP and hypoxia
• 24h after enrollment: UOP <0.3 Ml/kg/h over 24h, pH <7.2 despite resuscitation, K > 6.5 MEq/L.

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Question

This is an actual patient case:

65 y/o pt intubated for hemoptysis and started on nebulized transexamic acid. Overnight, the pt is found to have severe breath stacking/auto-PEEPing and consequently is started on neuromuscular blockade. The pt has no history of asthma or COPD and the ETT is clear without obstruction. 

Ventilator waveforms are as shown. What is the issue?

Show Answer

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:

•  exposure to specialty units
• geographic considerations
• multidisciplinary team experience.

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:

• CC knowledge
• Institutional support for EM/CC
• ECMO exposure

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.

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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.

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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.

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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!

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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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