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Title
Pub. Date
Duration
REBEL Core Cast 126.0 – Peds Hem Onc Emergencies
10 Jul 2024
00:24:51
Take Home Points
Early administration of antibiotics (within 60 min) in patients with fever and neutropenia is life saving.
Fever in sickle cell is an emergency and always requires cultures and antibiotics even if the child appears well.
Avoid sedation and lying supine and steroids in patients with mediastinal masses.
Red flags in patients with headaches that may suggest a brain tumor include signs of increased intracranial pressure, focal neurological signs, seizures or ataxia.
Note: Unlikely to have effect in patients taking beta-adrenoreceptor blocker medications
Sodium Bicarbonate (NaHCO3)
Evidence for the efficacy of NaHCO3 to lower serum potassium is scant and contradictory (Elliott 2010, Weisberg 2008)
Eliminate potassium from the body (see above)
Asymptomatic Patients with Minor EKG Changes
Minimal recommendations on managing this clinical entity
Eliminate potassium from the body (see above)
Consider calcium salt administration: patients can rapidly progress through EKG changes and calcium administration may prevent this from occurring. However, the effects of calcium are temporary and offer no long-term protection
Consider medications to shift potassium intracellularly while waiting for elimination
Take Home Points
Always obtain an EKG in patients with ESRD upon presentation
Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause
If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts
In patients who are anuric, early mobilization of dialysis resources is critical
References
Elliott MJ et al. Management of patients with acute hyperkalemia. CMAJ 2010; 182(15): 1631-5. PMID: 20855477
Wrenn K et al. The ability of physicians to predict hyperkalemia from the ECG. Ann Emerg Med 1991; 20(11): 1229-32. PMID: 1952310
Aslam S et al. Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in hemodialysis patients. Nephrol Dial Transplant 2002; 17: 1639-42. PMID: 12198216
Montague BT et al. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol 2008; 3:324–330. PMID: 18235147
Mattu A et al. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med 2000; 18: 721-9. PMID: 11043630
Allon M, Copkney C. Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients. Kidney Int 1990; 38:869–872. PMID: 2266671
Weisberg LS. Management of hyperkalemia. Crit Care Med 2008; 36: 3246-51. PMID: 18936701
Moussavi K et al. Reduced alternative insulin dosing in hyperkalemia: a meta-analysis of effects on hypoglycemia and potassium reduction. Pharmacotherapy 2021; 41(7): 598-607. PMID: 33993515
Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)
Management of severe beta-blocker and calcium-channel blocker toxicity should occur in a stepwise fashion: potential gastric decontamination, multiple lines of access, judicious fluids, calcium, glucagon, and vasopressors as needed.
Initiation of high dose insulin therapy requires a tremendous amount of logistical and cognitive resources as it requires cross-disciplinary collaboration and is prone to mismanagement.
If the patient doesn’t respond to maximum pharmacologic therapy, venous-arterial ECMO should be considered.
Shock secondary to beta-blocker (BB) or calcium-channel blocker (CCB) toxicity bears a tremendous degree of morbidity and mortality.
According to the 2022 Annual Report of the National Poison Data System from America’s Poison Center, CCBs and BBs account for the sixth and seventh largest number of fatalities from overdose.1
Recall that cardiac output is a function of both stroke volume and heart rate. The natural response to diminishing stroke volume is a compensatory rise in heart rate (tachycardia). Keep a low threshold to search a patient’s medication list for BB/CCBs, when a hypotension is seen with a “normal heart rate.”
Clinical Manifestations
Both BBs and CCBs ultimately cause reduced levels of intracellular calcium within myocytes. Depending on the degree of toxicity, subsequent effects include: decreased systemic vascular resistance, vasodilation, bradycardia, various conduction delays, and ultimately hypotension and cardiogenic shock.
In addition to abnormal vital signs, look for surrogates of poor clinical perfusion: acidemia, lactate, decreasing urinary output
Traditional Management
Consider GI decontamination to reduce systemic absorption: 1g/kg up to 50g of activated charcoal. Patient must be alert or the airway must be secured as to avoid aspiration.
Obtain multiple lines of intravenous access (3 PIVs or triple lumen CVC) and provide a judicious amount of fluids. (more on this below)
Pharmacotherapy
Calcium Gluconate: 1-3g intravenous
Glucagon: 3mg-5mg slow intravenous push. Rapid administration may induce nausea and emesis.
Vasopressors as a bridge to…
HIET
Mechanism of action is still not fully elucidated however several factors are implicated:
Insulin augments cardiac contractility by activating “reverse-mode” Na-Ca exchange and subsequently increasing calcium concentration in the sarcoplasmic reticulum. 2
At a resting physiologic state, the heart utilize free fatty acids as its primary energy course. Under stressed conditions, glucose is used instead. Insulin helps to facilitate glucose metabolism.
HIET Dosing: 1 unit/kg IV bolus. Then infusion starting at 1 unit/kg/hr infusion and titrate q30-60 minutes, keeping in mind that effects are not instant. Relative maximum is ~10 unit/kg/hr.
If glucose <250 mg/dL, administer a bolus of dextrose 25-50 g (or 0.5-1 g/kg) IV.
Ask pharmacy to concentrate insulin from 1 unit/mL to 10 units/ml.
Patients often succumb to volume overload given pre-existing cardiac disease and the volume of medical resuscitation through their hospital stay.
Once HIET is initiated, dextrose and potassium infusions should simultaneously be started to obviate hypoglycemia and hypokalemia
Dextrose: 0.5-1 g/kg/hr via D50/D20
Replete potassium to a minimum of 3.5mEq/L
A central venous catheter (often a triple lumen) is often needed to emergently replete potassium and provide D50/D20 safely (given its high osmolarity)
Serial monitoring of dextrose (q15-30 minutes) and potassium (q1 hour) is critical
HIET has been demonstrated to improve perfusion without necessarily increasing SVR/MAP – while MAPs may not markedly increase dramatically in the short term, obtain serial blood gases, lactate, and track urinary output to track perfusion. 3
Hyperinsulinemia Euglycemia Therapy (HIET) for BB/CCB Toxicity
Management of severe beta-blocker and calcium-channel blocker toxicity should occur in a stepwise fashion: potential gastric decontamination, multiple lines of access, judicious fluids, calcium, glucagon, and vasopressors as needed.
Initiation of high dose insulin therapy requires a tremendous amount of logistical and cognitive resources as it requires cross-disciplinary collaboration and is prone to mismanagement.
HIET Dosing: 1 unit/kg IV bolus. Then infusion starting at 1 unit/kg/hr infusion and titrate q30-60 minutes, keeping in mind that effects are not instant. Relative maximum is ~10 unit/kg/hr.
HIET therapy requires simultaneous dextrose and potassium infusions as insulin will induce hypoglycemia and shift potassium intracellularly.
If the patient doesn’t respond to maximum pharmacologic therapy, venous-arterial ECMO should be considered.
References
Gummin DD, Mowry JB, Beuhler MC, et al. 2022 Annual Report of the National Poison Data System® (NPDS) from America’s Poison Centers®: 40th Annual Report. Clin Toxicol (Phila). 2023;61(10):717-939. doi:10.1080/15563650.2023.226898
von Lewinski D, Bruns S, Walther S, Kögler H, Pieske B. Insulin causes [Ca2+]i-dependent and [Ca2+]i-independent positive inotropic effects in failing human myocardium. Circulation. 2005;111(20):2588-2595. doi:10.1161/CIRCULATIONAHA.104.497461
Holger JS, Engebretsen KM, Fritzlar SJ, Patten LC, Harris CR, Flottemesch TJ. Insulin versus vasopressin and epinephrine to treat beta-blocker toxicity. Clin Toxicol (Phila). 2007;45(4):396-401. doi:10.1080/15563650701285412
Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)
Typically will have heavy bleeding both anteriorly and posterior into the oropharynx. These patients have a tough time because they’re continually trying to spit out or swallow blood
Tachycardia is common and hypotension while not common isn’t unexpected. Very different from anterior epistaxis where VS usually unremarkable or maybe a bit of hypertension
Failure of anterior pressure or packing to stop bleeding: apply pressure but still see brisk posterior bleeding or even place b/l pack and see continued posterior bleeding
Start with the basics
IV, Supp O2, Monitor
Consider blood products if the patient appears to be losing a lot of blood or they report heavy blood loss. VS abnormalities can drive this as well
Strongly consider reversal of AC (this will typically come after control)
Stopping the Bleeding
PPE: these things bleed like stink. Anecdote. Gown, gloves and most importantly eye and face protection
Ideal: commercial posterior pack
Two balloons – one for anterior, one for posterior
Place the device (straight back parallel to the floor)
Inflate anterior balloon (10-15 cc) of air
If still bleeding, inflate posterior balloon (5-10 cc of air)
Foley: if no commercial device
Place foley catheter just as you would place a nasal tampon
When you see the tip of the foley in the posterior pharynx, inflate balloon (5-10 cc)
Need to pull back a bit and secure (can do this with tape on the nose)
Post Placement Care
Antibiotics: standard practice to give cephalexin or amox/clav. Literature doesn’t defend this approach but, the lit is pretty sparse. The idea behind abx is to prevent things like AOM and TSS but neither should be much of an issue with short term placement
ICU Admission?
Traditional teaching is that these patients are at risk for life-threatening bradydysrhythmias and should go to the ICU
Literature here is non-existent. Two oft-cited articles
Cassisi Laryngoscope 1971 – no mention of cardiac events in the article but widely cited
Zeyyan Laryngoscope 2010 – slightly lower HR in the packing group but no bradydysrhythmias
Before throwing ICU out
Hypoxia can occur – Cassisi found about a 20 mm Hg drop in PaO2 but all the patients in this publication were sedated so the packing may not have been the issue
look at Viducich 1995 Acad Emerg Med – showed that 18% of the 88 patients with posterior epistaxis required a surgical intervention. With that in mind, you want to consider placing patients into a setting where they can be frequently reassessed – perhaps SDU. This will be pretty location specific. If you treat a posterior bleed at a hospital without ENT, I would transfer as surgical intervention is pretty common
Cassisi NJ et al. Changes in arterial oxygen tension and pulmonary mechanics with the use of posterior packing in epistaxis: a preliminary report. Laryngoscope 1971; 81(8): 1261-6. PMID: 5569677
Zeyyan E et al. The effects on cardiac function and arterial blood gas of totally occluding nasal packs and nasal packs with airway. Laryngoscope 2010; 120: 2325-2330. PMID: 20938948
Loftus BC et al. Epistaxis, medical history and the nasopulmonary reflex: what is clinically relevant. Otolaryngol Head Neck Surg 1994; 110: 363-9. PMID: 8170679
Viducich RA et al. Posterior epistaxis: clinical features and acute complications. Acad Emerg Med 1995; 25(5): 592-6. PMID: 7741333
Corrales CE, Goode RL. Should patients with posterior nasal packing require ICU admission. Laryngoscope 2013; 123: 2928-9. PMID: 24114977
Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)
ANNEXA-1: Andexanet Alfa Associated with Harm in DOAC Reversal
23 May 2024
Background: In May of 2018, Andexanet alfa gained accelerated approval by the FDA for the reversal direct oral anticoagulants (DOACs) despite a lack of robust evidence for use. The 2022 AHA/ASA guidelines give the drug a level 2A recommendation and recommend it over the use of 4F-PCC (Greenberg 2022). FDA approval alongside guideline endorsement has led to the drug seeing a remarkable growth in use without a single high-quality study to support its use. The available data reports good hemostatic control: a subjective measure that is highly biased by unblinding and selection bias. More importantly, there are no studies comparing andexanet alfa to 4F-PCC or even placebo looking at important, patient-centered outcomes.
REBEL Cast WEE – ANNEXA-1 – Andexanet Alfa Associated with Harm in DOAC Reversal
Intervention: Andexanet alfa high-dose or low-dose bolus followed by infusion depending on time and dose from last DOAC use.
Control: Usual care
Design: Non-blinded, randomized controlled trial performed at 131 centers across 23 countries over 4 years.
Exclusions
GCS < 7 at the time of consent
NIHSS > 35
Surgery planned within 12 hours of enrollment
Thrombotic event within 2 weeks of enrollment
Time from symptom onset > 6 hours
Pregnancy
Results:
Primary results
581 patients were assessed for eligibility across 131 sites over 4 years
31 excluded prior to randomization
20 excluded after randomization due to consent issues
530 analyzed for the safety outcomes
263 patients assigned to andexanet alfa arm
267 patients assigned to usual care arm
452 patients were analyzed for the primary outcome
85.5% (195/228) patients in the usual care arm received 4F-PCC
78.1% (175/224) patients in the andexanet arm received the low-dose regimen
Critical Results
Andexanet alfa
Usual Care
Difference (95% CI)
P Value
Primary Outcome
Hemostatic Efficacy
67% (150/224)
53.1% (121/228)
13.4 (4.6 – 22.2)
0.003
NIHSS change < 7 points
87.9% (188/214)
83.0% (181/218)
4.6 (-2.0 – 11.2)
Secondary Outcome
Anti-Factor Xa % Change
-94.5% (-96.6 – 88.9)
-26.9% (-54.2 – -9.5)
Safety Outcome
Thrombotic Events
10.3%
5.6%
4.6 (0.1 – 9.2)
0.048
TIA
0
0
Ischemic Stroke
6.5%
1.5%
Myocardial Infarction
4.2%
1.5%
DVT
0.4%
0.7%
PE
0.4%
2.2%
Arterial Embolism
1.1%
0.7%
Death
27.8%
25.5%
0.51
Strengths:
This is the first randomized trial comparing andexanet alfa to standard care in this patient group.
Multicenter, multinational study increasing applicability of findings.
Outcome assessors were blinded to treatment arm.
Hematoma measurements were made with a standard protocol and central site adjudication.
12 hour NIHSS assessments were performed by health care professionals who were unaware of group assignments
Limitations:
Study funded, designed, and supervised by AstraZeneca Pharmaceuticals the maker of Andexanet alpha. Although, this does not refute the findings of this study, it should make readers skeptical.
Clinicians were not blinded to the treatment arm patients were randomized to. This may introduce bias particularly in terms of subsequent treatments (treatments outside of reversal are not detailed in the study).
Primary endpoint is not patient centered.
Convenience sample of patients which introduces bias.
There are some baseline differences between groups and it’s hard to say how this may have influenced the results.
Exclusion criteria are likely to be difficult for clinicians to assess real time leading to protocol violation (particularly items like planned surgery and recent thrombotic event).
Dose adjustment for time from ingestion likely to lead to protocol violation as this info difficult to assess.
Exclusion criteria: Removed the sickest patients.
Discussion:
The positive primary and secondary outcomes
Both the primary (hematoma expansion) and secondary (anti-factor Xa reduction) outcomes were better in the andexanet group.
Unfortunately, these are disease-oriented outcomes instead of patient centered outcomes: the patient doesn’t care if their hematoma expands by 20% or 25% or 30%. They care about clinically important outcomes like disability or death.
The authors note that in other studies, hematoma expansion has been associated with worse outcomes, but this was clearly not demonstrated in this study as 90d mRS and death were the same between groups.
Bottom line is that there wasn’t even a hint of improved clinical outcomes in the andexanet group.
Safety outcomes favored the usual care group
In general, larger studies or registries of patients are required to determine safety of a treatment.
In this study, however, there is a clear signal for harm even with a small group of patients under ideal circumstances (ie enrolled within a study).
Though death was not statistically different, the raw numbers favor usual care.
Thrombotic events were clearly increased in the andexanet group.
Across a larger group of patients outside of the pristine setting of a study, it is likely that we would see an increase in thrombotic events and death.
Only 85.5% of patients in the usual care group received 4F-PCC
Though there isn’t abundant evidence for the use of 4F-PCC in this setting, it does represent standard practice.
The authors do not report about the subgroup of patients who did not receive 4F-PCC and their outcomes.
If this data shows worse outcomes with no reversal treatment, it would suggest that usual care with 4F-PCC may be superior to andexanet alfa for clinical outcomes.
If this data shows improved outcomes with no reversal treatment, it would suggest that specific reversal agents aren’t necessary.
There were multiple protocol changes during the study. Typically, protocols should not be changed while the study is enrolling patients. This is often done to try to steer the data towards benefit.
Initial power calculation was for 900 patients to achieve a 90% power to detect and absolute difference of 10% points in terms of hemostatic efficacy but then made an addendum to the protocol to stop after 450 patients.
After this stop point, the safety and monitoring board recommended the trial be stopped.
Though the authors state they had no knowledge of the effect prior, there is no clear explanation given for this change and it raises the possibility that the trial was stopped prior to additional data showing harm was collected.
Drug cost
Andexanet alfa costs between $30 – 50,000/treatment. This only takes into account drug costs (ie not monitoring, nursing costs etc).
4F-PCC costs around $5-6,000/treatment.
Author Conclusion: “Among patients with intracerebral hemorrhage who were receiving factor Xa inhibitors, andexanet resulted in better control of hematoma expansion than usual care but was associated with thrombotic events, including ischemic stroke.”
Clinical Take Home Point: The authors conclusions are correct. However, they don’t properly stress the findings.
Treatment of patients with intracerebral hemorrhage on a DOAC with Anexanet alfa did not improve clinical outcomes when compared to usual care. Based on safety data, andexanet alfa resulted in increased harm to patients. Andexanet alfa should not be part of the standard treatment in this scenario based on the available evidence.
References:
Greenberg SM et al. 2022 Guidelines for the Management of Patients with Spontaneous Intracerebral Hemorrhage: A Guideline from the American Heart Association/American Stroke Association. Stroke 2022; 53(7). PMID: 35579034
Connolly SJ et al. Andexanet for Factor Xa Inhibitor-Associated Acute Intracerebral Hemorrhage (ANNEXA-1). NEJM 2024; 390(19): 1745-55. PMID: 38749032
Neutropenia: An absolute neutrophil count less than 500 cells/mm3 or less than 1000 cells/mm3 with a predicted decline to less than 500 cells/mm3
ANC = WBC x (neutrophil% + band%)
Mild: 1000 – 1500
Mod: 500 – 1000
Severe: 100 – 500
Profound: <100
Background
Neutrophils directly combat infection and are important to coordinating the body’s overall immune response.
The loss of these cells leads to immunosuppression as well as decreased responsiveness of the immune system as a whole
Patients with neutropenia will not only get very sick very quickly, but also will have blunted immune response and may not localize signs of infection well
Fever or malaise may be their only presenting symptoms.
Patients with hematologic malignancies are at highest risk for suffering profound and prolonged neutropenia. Particularly high risk are those undergoing induction chemotherapy or stem cell transplant. Allogeneic stem cell grafting is higher risk than autologous.
Neutropenic Fever: Fever (one reading of 38.3C or sustained 38.0C) + ANC < 500 cells/mm3 or expected to fall to < 500 cells/mm3 within the next 48 hours
Common problem during chemotherapy:
10-50% of patients with solid malignancy and >80% of patients with hematologic malignancy will experience at least one episode of neutropenia (IDSA 2010, Klastersky 2004)
Includes many drugs and drug regimens, all with the goal of killing rapidly dividing cells. Of note, this particularly affects:
Cancer cells – this is the reason chemotherapy works as treatment
Neutrophils – with a life cycle of only 1-6 days, their numbers are impacted dramatically by chemotherapy
Mucosa – destruction of dividing cells thins mucosal barriers, putting these patients at high risk for mucositis and bacterial invasion
This creates a dangerous situation where the body’s barriers against bacterial invasion are broken down and, thus, the ability to combat infection is severely blunted. Antibiotics are effectively the only thing standing between these patients and overwhelming sepsis.
The pathogens responsible for neutropenic fever have changed over time.
Initially, Gram (-) organisms translocated from the gut caused majority of cases of neutropenic fever
This changed in the 1990s. Gram(+) infections became more common due to more fluoroquinolone prophylaxis against Gram (-) organisms and due to more prevalent use of indwelling catheters for outpatient treatment
Over the past decade, there has been a resurgence of Gram (-) organisms due to increasing antibiotic resistance, particularly multidrug resistant E coli and klebsiella
Given the increasing rates of antibiotic resistance, antibiotic stewardship is becoming increasingly important
In the ED, we can contribute to antibiotic stewardship by checking old cultures and obtaining new ones prior to initiation of antibiotics
ED Evaluation and Management:
Resuscitate if necessary
Patients with neutropenic fever may rapidly progress to septic shock.
Give appropriate fluids, vasopressors, and antibiotics.
Antibiotics need to be given as quickly as possible if unstable
Perform a complete review of systems and physical exam looking for signs of focal infection
Basic Blood Work
CBC, BMP, LFTs, bilirubin levels
Blood cultures
If indwelling catheter present: 1 set from each line of indwelling catheter + 1 peripheral set
If no indwelling catheter present: 2x peripheral sets
Additional testing based on signs and symptoms:
Respiratory symptoms
CXR
Sputum cultures
Dysuria
Urinalysis
Urine culture
Abdominal pain
CT abdomen and pelvis
If diarrhea present, consider C difficile PCR (if available)
Isolation
Good hand hygiene is the most effective way to prevent these patients obtaining nosocomial infections
Use standard barrier precautions
Keep anyone with potentially communicable illness out of the patient’s room – visitors, other patients, or healthcare workers
No plants in the treatment room or nurse’s station
Any stem cell transplant patient should be in a private room. If they have an allogenic transplant, use a HEPA filter with >12 air exchanges per hour
Isolation is important for neutropenic patients, but do not let waiting on an isolation room delay obtaining cultures and initiating antibiotics
Specific Pathologies
Mucositis
Mucositis is a high risk feature indicative of bacterial invasion through thinned mucus membrane barriers.
Signs and Symptoms
oral pain, erythema, edema, or lesions
sinus pain or pressure
rectal pain or lesions, any swelling suggestive of perirectal abscess
abdominal pain
Inspect the rectum for swelling possibly indicative of perirectal abscess.
Digital rectal exam is generally discouraged due to concern of inducing bacteremia if mucus membranes are damaged in the process
Neutropenic Enterocolitis (Typhlitis):
A feared complication of neutropenic fever is direct bacterial invasion of the intestinal mucosa causing necrotizing infection
Most commonly at the ileocecal junction
It presents with classic triad of neutropenia, fever, and RLQ pain. Mortality approaches 50% when present (Gorschlüter 2005)
Surgery is avoided unless the bowel perforates, as these patients have poor wound healing and high surgical complication rates
Determine whether the patient is high or low risk:
The MASCC Score will identify more patients as low risk, but will have more treatment failures / bounce-backs than the CISNE score (Ahn 2017, Coyne 2016)
The CISNE score will identify fewer patients as low risk, but will result in fewer treatment failures/bounce-backs than the MASCC score (Ahn 2017, Coyne 2016).
Default to using whichever score your oncologist is more comfortable with.
Antibiotic Selection
Check old cultures for prior infections and sensitivities (if available).
Follow your hospital’s protocol (if available). This will have been formulated based on local resistance patterns and likely with input from your institution’s oncologists.
High Risk Patients will need hospitalization and IV antibiotics.
General approach for IV antibiotic therapy:
Begin with single broad spectrum agent which includes pseudomonas coverage such as cefepime, piperocillin-tazobactam, or a carbepenem
Penicillin allergies other than anaphylaxis are not considered a contraindication to the use of cephalosporins such as cefepime
If patient has anaphylactic reaction to penicillins, consider broad coverage with ciprofloxacin plus clindamycin or aztreonam plus vancomycin (IDSA 2010)
Do not routinely start vancomycin. Add vancomycin if there is clinical suspicion for Gram (+) infection
Signs of mucositis or cellulitis
Indwelling catheter present on arrival
Prior MRSA infection
Patient already on Gram (-) prophylaxis such as fluoroquinolone
Consider adding additional agents for unstable patients, or patients in which antibiotic resistant organisms are suspected (patient has known colonization or patient population has high endemic rates).
Carbapenemase producing organisms (such as klebsiella): polymixin-colistin or tigecycline
If there is clinical suspicion for influenza (or positive PCR testing), treatment with oseltamivir is recommended
Other antiviral and antifungal agents should NOT be started routinely.
Only start antiviral or antifungal therapies if the patient has a known viral or fungal infection (ex: patient spikes a fever while already on antifungal treatment) or if they have a clinical picture strongly suggestive of viral or fungal etiology
Antifungals are generally not initiated until a patient has had >4 days of fever unresponsive to antibiotic treatment with no clear source identified
Low risk
If the patient has no high risk features, is found to be low risk on MASCC or CISNE scoring, and has good oncology follow-up, it may be preferable to discharge them home with 24hr oncology follow-up
Send patients home ONLY after discussion with the patient’s oncologist and only if there are no high risk features present
Outpatient antibiotic choice:
Ciprofloxacin plus amoxicillin-clavulanate is recommended by IDSA guidelines for oral empiric therapy (IDSA 2010)
Levofloxacin or ciprofloxacin monotherapy, or ciprofloxacin plus clindamycin are less well studied but are commonly used
Avoid fluoroquinolones if the patient is already on fluoroquinolone prophylaxis
Take Home Points:
There are many causes of neutropenia, chemotherapy being by far the most dangerous.
Febrile neutropenia is a condition conveying high mortality. Early administration of antibiotics is the only factor known to reduce this mortality.
For a patient with neutropenic fever, remember that the body’s own flora is the greatest danger. Isolate, but do not wait to initiate treatment.
Check old blood cultures and obtain new cultures prior to starting treatment.
Identify low risk patients and send them home with PO antibiotics and close oncology follow-up in conjunction with your oncologist.
Ahn S, Rice TW, Yeung SJ, Cooksley T. Comparison of the MASCC and CISNE scores for identifying low-risk neutropenic fever patients: analysis of data from three emergency departments of cancer centers in three continents. Support Care Cancer. 2018 May;26(5):1465-1470. doi: 10.1007/s00520-017-3985-0. Epub 2017 Nov 22.
Clarke, R. T., Warnick, J., Stretton, K., Littlewood, T. J., Improving the immediate management of neutropenic sepsis in the UK: Lessons from a national audit. British Journal of Haematology. 2011 Jun;153(6):773-9. doi: 10.1111/j.1365-2141.2011.08693.x. Epub 2011 Apr 22
Coyne CJ, Le V, Brennan JJ, Castillo EM, Shatsky RA, Ferran K, Brodine S, Vilke GM. Application of the MASCC and CISNE Risk-Stratification Scores to Identify Low-Risk Febrile Neutropenic Patients in the Emergency Department. Ann Emerg Med. 2017 Jun;69(6):755-764. doi: 10.1016/j.annemergmed.2016.11.007. Epub 2016 Dec 29.
Ellis M. Febrile Neutropenia. Annals of New York Academy of Sciences. 2008 Sep;1138:329-50. doi: 10.1196/annals.1414.035.
Freifeld, A. G., Bow, E. J., Sepkowitz, K. A., Boeckh, M. J., Ito, J. I., Mullen, C. A., Raad, II, et al., Clinical practice guideline for the use of antimicrobial agents in neutropenic patients with cancer: 2010 update by the infectious diseases society of america, Clinical Infectious Diseases, 2011, 52(4):e56-93.
Gibson C, Berliner N. How we evaluate and treat neutropenia in adults. Blood. 2014 Aug 21;124(8):1251-8; quiz 1378. doi: 10.1182/blood-2014-02-482612. Epub 2014 May 28.
Gorschlüter M, Mey U, Strehl J, et al. Neutropenic enterocolitis in adults: systematic analysis of evidence quality. Eur J Haematol 2005; 75:1.
Gudiol C, Bodro M, Simonetti A, et al. Changing aetiology, clinical features, antimicrobial resistance, and outcomes of bloodstream infection in neutropenic cancer patients. Clin Microbiol Infect 2013; 19:474
Klastersky J. The changing face of febrile neutropenia-from monotherapy to moulds to mucositis. Why empirical therapy? J Antimicrob Chemother. 2009;14(Suppl 1):i14–i15
Klastersky J. Management of fever in neutropenic patients with different risks of complications. Clin Infect Dis. 2004;39(Suppl. 1):S32–S37
Kuderer NM, Dale DC, Crawford J, Cosler LE, Lyman GH. Mortality, morbidity, and cost associated with febrile neutropenia in adult cancer patients. Cancer. 2006 May 15;106(10):2258-66.
Marín M, Gudiol C, Ardanuy C, Garcia-Vidal C. Jimenez L, Domingo-Domenech E, Pérez FJ, Carratalà J. Factors influencing mortality in neutropenic patients with haematologic malignancies or solid tumours with bloodstream infection. Clinical Microbiology and Infection. Volume 21, Issue 6, June 2015, Pages 583-590
Perron T, Emara M, Ahmed S. Time to antibiotics and outcomes in cancer patients with febrile neutropenia. BMC Health Services Research. 2014;14:162. doi:10.1186/1472-6963-14-162.Radiologypics, P. B. (2014, November 10). Neutropenic Colitis (Typhlitis). Retrieved from https://radiologypics.com/2014/11/10/neutropenic-colitis-typhlitis/Rosa RG, and
Goldani LZ. Cohort Study of the Impact of Time to Antibiotic Administration on Mortality in Patients with Febrile Neutropenia. Antimicrob Agents Chemother. 2014 Jul; 58(7): 3799–3803. doi: 10.1128/AAC.02561-1
Stiff, PJ. Coding for Mucositis. From presentation at ICD-9-CM Coordination and Maintenance Committee Meeting. Loyola University Medical Center. Centers for Disease Control. September 30, 2005. Retreived from https://www.cdc.gov/nchs/ppt/icd9/att_mucositis_sep05.ppt
Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)
REBEL Cast Ep126: Should We Not Be Recommending Small Adult BVMs in OHCA?
13 May 2024
00:12:48
Background: The holy grail of outcomes in OHCA is survival with good neurologic outcome. The only interventions proven to increase this outcome are high quality CPR and defibrillation in shockable rhythms. Ventilation is also an important component of resuscitation in OHCA. Excess minute ventilation can adversely affect hemodynamics due to increased intrathoracic pressure (i.e. decreased venous return). Additionally, low CO2 levels from hyperventilation can lead to cerebral vasoconstriction which could lead to worsened secondary brain injury.
Most organizations recommend adults to be ventilated with tidal volumes of 500 to 600mL/breath during ongoing CPR. Large adult BVMs can have maximum tidal volumes of ≈1500mL and deliver about 750mL per one handed ventilation. Simulation studies have shown that health care professionals often provide minute ventilation well above these recommended ranges.
One of the recommendations from many experts to mitigate the perceived risk of large adult BVMs is using smaller adult BVMs. This change would result in decreasing the maximum volume from 1500 to 1000mL and an expected delivered tidal volume from 750 to 450mL/breath (much more inline with recommended ranges). However, evidence that this approach makes is difference is lacking.
REBEL Cast 126: Should We Not Be Recommending Small Adult BVMs in OHCA?
Paper: Snyder BD et al. Association of Small Adult Ventilation Bags with Return of Spontaneous Circulation in Out of Hospital Cardiac Arrest. Resuscitation 2023. PMID: 37805062
Clinical Question: Is large adult BVM or small adult BVM associated with more ROSC in adult patients treated with advanced airway placement for nontraumatic OHCA?
What They Did:
Retrospective, observational cohort analysis of prospectively obtained data from a single urban EMS system
Evaluating adults treated with advanced airway placement for nontraumatic OHCA
Jan 2015 to Dec 2021
Changed from large adult BVMs to small adult BVMs in summer of 2017 (3 month crossover period was allowed and excluded from analysis)
Used a Mercury medical CPR-2 small ventilation bag
Compared rates of ROSC, ventilation rate, and mean end tidal carbon dioxide (ETCO2) by minute before and after small adult BVM implementation
Outcomes:
Primary: ROSC at the end of EMS care (i.e. Arrival to ED or terminated efforts in the field)
Secondary:
Ventilation rate
Mean end-tidal CO2 (ETCO2) during CPR
Inclusion:
Adult patients with nontraumatic OHCA
Treated with an advanced airway (i.e. Endotracheal intubation or iGel)
Exclusion:
Age <18 years
Received basic life support only
Termination of resuscitation due to advanced directives
ALS interventions prior to EMS arrival
Insufficient capnography data
Cricothyrotomy
Advanced airway placed while patient had spontaneous circulation
Airway was managed with BVM only
Did not receive CPR while under EMS ALS care
Results:
1994 Patients included in analysis
1331 (67%) treated with small adult BVM
663 (33%) treated with large adult BVM
21% had an initial shockable rhythm
ROSC
Small Adult BVM: 33%
Large Adult BVM: 40%
uOR 0.74; 95% CI 0.61 to 0.90; P = 0.003
After adjustment for age, sex, witnessed arrest, bystander CPR, and initial rhythm this finding remained statistically significant (aOR 0.74; 95% CI 0.61 to 0.91)
Ventilation rates did not differ between cohorts (≈12BPM)
ETCO2
Small Adult BVM: 36.9 +/- 19.2mmHg
Large Adult BVM: 33.2 +/- 17.2mmHg
P <0.01
Strengths:
Written records are compared to cardiac monitor files and audio recordings to adjudicate differences before integrating information into the registry
Intubations confirmed with ETCO2
Took into account the COVID-19 pandemic time period
Also took into account the potential for trends over time by visualizing the incidence of ROSC by month over a seven year period and found no significant change in the slope before and after the implementation of the small adult BVM
Limitations:
Only included patients that were intubated with an endotracheal tube or iGel (these results may not apply in patients without these devices)
There were some confounding baseline differences (explained more in discussion)
Unclear what other interventions were performed in terms of ACLS medications or what the specific causes of the cardiac arrest were from
This was a before and after study not allowing for a control group. Before and after studies can introduce numerous biases particularly if other pieces of care changed between the two time periods. (Can also go in the discussion)
The actual tidal volume delivered was not measured in this trial and therefore the delivered minute ventilation is unknown
As this is a retrospective study, we can only show association, BUT NOT causation of the size of the adult BVM affecting ROSC outcomes
Discussion:
There are some key BASELINE DIFFERENCES that could account for the results of this trial (i.e. confounders):
More patients in the small adult BVM cohort received bystander CPR (64% vs 59%). This would favor more ROSC in the small adult BVM cohort
Unwitnessed arrest was slightly greater in the large adult BVM cohort (58% vs 53%)…This would favor more ROSC in the small adult BVM cohort
Fewer patients in the small adult BVM cohort arrested in public (22% vs 27%…Unclear how this would impact ROSC
The interval from 911 call to start of CPR (10 vs 9min) and advanced airway placement (20 vs 18min) were longer in the small adult BVM cohort…Not sure 1 to 2min of difference would result in more ROSC in the large adult BVM cohort
Adherence to guideline recommended ventilation rates of 10 BPM was more common in the small adult BVM cohort (28.4% vs 31.2%)…This would favor more ROSC in the small adult BVM cohort
It would appear most things at baseline favored the small adult BVM cohort (Although the authors did account for most of these in adjusted analyses)
The end of this trial took place during the COVID-19 PANDEMIC:
Anyone who took care of cardiac arrest patients during the COVID-19 pandemic knows that there were significant delays in care
According to the authors any cases of OHCA that occurred after the start of the pandemic (Feb 2020) were censored from the analysis and the results were evaluated again
When looking at cases of OHCA that occurred prior to Feb 2020 the small adult BVM cohort had a similarly lower odds of ROSC (OR 0.75; 95% CI 0.60 to 0.93; p = 0.008) as the entire time period this intervention was implemented
This remained the case even after adjusting for initial rhythm, age, sex, witnessed arrest and bystander CPR (aOR 0.76; 95% CI 0.61 to 0.95; p = 0.018)
While I would imagine during a code most people are bagging faster than 10BPM, in this study 6 to 18 BPM were delivered in 82.5% of the measured ventilations. Is this a result of Hawthorne effect or the implementation of a metronome to guide chest compression and ventilation rates (implemented June of 2015) or simply a well trained EMS system? This addition would seem to favor the small adult BVM group
This EMS organization appears to be very high functioning with lots of training and education which may not be the standard at other agencies. The fact that the medics are providing a good RR and good TV throughout a 7-year period would suggest this and in doing so a simple change from a large adult BVM to a small adult BVM may have resulted in the association of lower ROSC whereas an agency that does not get as much training or high functioning may actually still be causing harm with the large adult BVM
Finally, there was a higher ETCO2 in the small adult BVM cohort compared to the large adult BVM cohort. As ventilatory rate was essentially similar between groups, this most likely means a smaller tidal volume was delivered with each breath. This smaller tidal volume could have lead to physiologic changes that are potentially harmful:
Hypoventilation
Increased dead space fraction
Alveolar decruitment
Atelectasis causing shunt physiology
Author Conclusion: “Use of small adult bag during OHCA was associated with lower odds of ROSC at the end of EMS care. The effects on acid base status, hemodynamics, and delivered minute ventilation remain unclear and warrant additional study.”
Clinical Take Home Point: This is a really messy trial, with lots of methodological and confounding issues that make it difficult to interpret. It does show that when experts recommend an intervention it is important to study it. Until better evidence shows us differently it is probably best to stick with a large adult BVM but use one hand for bagging and maintain a rate of 10BPM.
References:
Snyder BD et al. Association of Small Adult Ventilation Bags with Return of Spontaneous Circulation in Out of Hospital Cardiac Arrest. Resuscitation 2023. PMID: 37805062
Post Peer Reviewed By: Anand Swaminathan, MD (Twitter/X: @EMSwami)
ARS with a bacterial etiology without clinical evidence of extension outside the paranasal sinuses and nasal cavity
Bacterial superinfection: 0.5-2% of all ARS
●Complicated acute bacterial rhinosinusitis
ARS with bacterial etiology with clinical evidence of extension outside the paranasal sinuses and nasal cavity
Sinusitis: Viral vs. Bacterial:
Color change in sputum does not determine whether infection is viral or bacterial
Viral infections
Tend to begin resolution by 7-10 days
Rarely have associated fevers
If fever present, usually only in the first 48 hours.
Guidelines for diagnosing ABRS are
Presence of URI/cold symptoms that
Don’t improve after 10 days
Worsen after 5-7 days of improvement
Severe symptoms including high fever, purulent discharge or facial pain for 3-4 days
The Data Behind Antibiotic Use
Clinically diagnosed acute sinusitis
Multiple studies show the same cure rate at 7 days, but improved cure rate at 7-14 days for those who use antibiotics (Lemiengre 2012, Berg 1986, Gwaltney 1996)
IDSA Recommendations for Antibiotic Treatment (Chow 2012)
Patients that should be treated
Persistent symptoms w/o improvement (> 10 days)
Severe symptoms (> 3-4 days)
Worsening (“double-sickening”) (> 3-4 days)
Antimicrobials
1st Line
Amoxicillin 875 mg PO BID X 5-7 days
Doxycycline 100 mg PO BID X 5-7 days
2nd Line
Amoxicillin/Calvulanate 875/125 mg PO BID X 5-7 days
Levofloxacin 500 mg PO Q24 X 5 days
Bottom Line: Given the risk for adverse events associated with antibiotic use, the growing specter of resistance and the lack of significant differences in outcomes with antibiotic use, it is better to avoid antibiotics in most patients with ARS. Antibiotics should be considered in those with severe disease and in immunocompromised patients
Take Home Points
Acute rhinosinusitis is a clinical diagnosis
The vast majority of acute rhinosinusitis cases are viral in nature and do not require antibiotics
Consider the use of antibiotics in select groups with severe disease or worsening symptoms after initial improvement.
References
Anon JB et al. Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. Otolaryngol Head Neck Surg 2004; 130(Suppl 1): 1-45. PMID: 14726904
Lemiengre MB et al. Antibiotics for Clinically Diagnosed Acute Rhinosinusitis in Adults. Cochrane Database Syst Rev 2012. PMID: 23076918
Berg O et al. Occurence of asymptomatic sinusitis in common cold and other acute ENT-infections. Rhinology 1986; 24(3): 223-5. PMID: 3775189
Ahovuo-Saloranta A et al. Antibiotics for acute maxillary sinusitis. Cochrane Database Syst Rev 2008. PMID: 18425861
Chow AW et al. IDSA Clinical practice guideline for acute bacterial rhino sinusitis in children and adults. Clin Infect Dis 2012; 54(8): e72-e112. PMID: 22438350
Resa E Lewiss MD is a Professor of Emergency Medicine at the University of Alabama at Birmingham. A TEDMED speaker and TimesUp Healthcare founder, she’s an internationally renowned point-of-care ultrasound educator and champion for diverse, equitable, and inclusive workplaces. She attended college at Brown, medical school at Penn, Emergency Medicine residency at Harvard, and fellowship at Mount Sinai St. Luke’s Roosevelt. She led point-of-care ultrasound sections at St. Luke’s Roosevelt, the University of Colorado, and Thomas Jefferson. A physician healthcare design consultant for Perkins&Will, her design focus has been ultrasound hardware and workflows. She’s helped to redesign the built environment of a Harvard ICU and an infectious diseases unit in Malawi. As host and founder of the Visible Voices Podcast, she’s interviewed dozens of subject matter experts in healthcare, equity, and current trends. Her writings are published in the popular press and scientific journals, such as Harvard Business Review, Slate, Nature, and Fast Company. Her new book, MicroSkills : Small Actions, Big Impact is forthcoming from HarperCollins in 2024.
Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)
Toxic alcohols generally refer to methanol and ethylene glycol as these substances pose significant metabolic derangement and end-organ damage.
Patient who present shortly after ingestion will simply look inebriated – no different than ethanol intoxication. At this point, patients will have an elevated osmolar gap and little to no anion gap.
Patient who presents in a delayed fashion after ingestion may have a normal osmolar gap however will manifest the signs of end-organ damage: anion gap metabolic acidosis, visual impairment, or renal dysfunction.
The osmolar gap is poorly sensitive, specific surrogate measure that is used to detect the presence of toxic alcohols. A normal osm gap does not rule out a toxic alcohol ingestion.
Management includes fomepizole, hemodialysis, and vitamin supplementation.
Reference: Wiener SW. Chapter 106. Toxic Alcohols. In: Nelson LS, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS, , Flomenbaum NE. eds. Goldfrank’s Toxicologic Emergencies, 11e New York, NY: McGraw-Hill; 2019. Accessed October 2, 2024.
Anticipate anatomically challenging airways and consider early intubation prior to loss of airway anatomy.
Skip the zones of the neck and focus on hard signs of vascular (Shock w/o another source, Pulsatile bleeding, Expanding hematoma, Audible bruit, Signs of stroke) or aerodigestive (Airway compromise, Bubbling wound, Extensive SubQ air, Stridor, Significant hemoptysis/hematemesis). The presence of hard signs indicates the need to go to the OR or for angiographic intervention.
Control hemorrhage with a single finger and direct pressure.
Orogastric lavage may still play an important role in treatment of the overdose patient. Do not perform lavage if the ingestion has limited toxicity at any dose or the ingested dose is unlikely to cause significant toxicity.
Strongly consider orogastric lavage in a patient who has taken an overdose of drugs that are particularly toxic, suspected extreme doses associated with high morbidity/mortality and do not have easily available and effective antidotes.
Secure the airway prior to placing the lavage tube to minimize aspiration risk.
Early diagnosis: erythema and warmth of the skin surrounding the umbilicus isn’t normal. Get labs, start abx and get the patient admitted
Consult peds surgery on all of these patients as progression to nec fast, while uncommon, is devastating
If the patient appears toxic or has systemic symptoms, the simply omphalitis has progressed and aggressive treatment including surgery is likely indicated
Always suspect an open joint if there is a laceration, regardless of size, the lies over joint
CT scan of the affected joint is widely considered to be the standard approach to evaluation but the saline load test may be useful in certain circumstances.
Obtain emergency orthopedics consultation for all open joints and administer antibiotics and update tetanus in all patients
Study limited by small numbers, inclusion bias + inadequate gold standard
May be considered the standard evaluation modality in many settings.
Saline load test
Has mainly been supplanted by CT scan due to ease in obtaining, reported performance characteristics, consultant recommendation and difficulty in interpreting test.
Useful if physical examination equivocal or plain radiographs non-diagnostic
Obtain early orthopedic evaluation for joint exploration, and washout to be performed within 6-24 hours
Tetanus prophylaxis
Prophylactic antibiotics (best if given within 6 hours)
Staph/strep coverage: 1st generation cephalosporin (i.e. cefazolin or cefuroxime)
If risk factors for MRSA present, use agent with activity against MRSA (i.e. vancomycin)
If significant soft tissue injury, add gram negative coverage like late generation cephalosporin, extended-spectrum penicillin, or aminoglycoside (i.e. gentamycin)
If concern for fecal or clostridial infection, add high dose penicillin (i.e. zosyn)
If seawater contamination and concern for vibrio vulnificus, add doxycycline
Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)
REBEL Core Cast – DKA: Beyond the Basics Part 2 – SCOPE DKA-Trial
21 Oct 2025
00:15:47
🧭 REBEL Rundown
🔑Key Points
💧 Fluid Choice Matters: Plasma-Lyte, a balanced crystalloid, corrected acidosis faster than normal saline in severe DKA patients, with no increase in adverse events.
🧪 Chloride Load Concerns: Normal saline’s high chloride content can worsen acidosis, potentially slowing bicarb recovery even after the anion gap closes.
🔬 Study Design Strengths: The SCOPE-DKA trial was a cluster crossover, open-label RCT, protocolizing all variables except fluid type, enhancing the reliability of its findings.
🧮 Base Excess & Strong Ion Difference: Base excess/deficit and strong ion difference are valuable but underutilized tools for assessing acid-base status—don’t rely solely on pH or bicarb.
⚠️ Limitations & Next Steps: The study did not include lactated Ringer’s, and fluid rates were left to clinical discretion. More research, including three-arm trials, is needed for definitive guidance.
Managing diabetic ketoacidosis (DKA) requires careful consideration of fluid therapy, especially in severe cases. In part two of our REBEL Cast DKA series, we shifted from insulin strategies to fluid choice in severe DKA, diving into the SCOPE-DKA trial—a cluster, crossover, open-label RCT from Australia. While normal saline (NS) is commonly used, concerns about its high chloride content and impact on acidosis have sparked growing interest in balanced solutions like Plasma-Lyte.
Clinical Question
Does the fluid you choose affect how quickly acidosis resolves in DKA?
IV Fluid Composition
🚨 Clinical Bottom Line
Plasma-Lyte showed a modest but meaningful benefit over normal saline in resolving metabolic acidosis in patients with severe DKA. Though safety profiles were similar, the more balanced electrolyte composition of Plasma-Lyte helped normalize acid-base status slightly faster—without worsening ketosis. While this won’t revolutionize care overnight, it’s one more step toward physiologic resuscitation in DKA. Understanding fluid composition and its impact on acid-base balance is crucial for optimal patient care.
Post Peer Reviewed By: Marco Propersi (Twitter/X: @Marco_propersi), and Kim Bambach, MD
Show Notes By: Mark Ramzy, DO
Authors
Mark Ramzy, DO
Co-Editor-in-Chief
RWJBH / Rutgers Health, Newark, NJ
Frank Lodeserto
Associate Editor
Cape Fear Valley Medical Center,
Fayetteville NC
🔎 Your Deep-Dive Starts Here
It seems we can't find what you're looking for.
REBEL Cast
is the blogs audio version. The podcast typically starts by setting a clinical stage with a pertinent clinical question, followed by a discussion of the paper with pertinent results, strengths, limitations, and further discussion. Finally, we end every podcast with clinical take home points from the papers being reviewed. If there are papers you think we should evaluate, email them to srrezaie@gmail.com.
REBEL EM stands for Rational Evidence Based Evaluation of Literature in Emergency Medicine. We cover a myriad of topics, primarily focusing on evidence-based clinical topics.
At its core, evidence-based medicine (EBM) incorporates clinical judgment, relevant scientific evidence, and patient values/preferences. Research and scientific evidence help inform care but should not dictate care of patients.
With the constant influx of new published research, it makes it difficult to stay current with the latest and greatest. REBEL EM was created October 2013 in an effort to cut down knowledge translation of research to clinical application (Bench to Bedside), using a structured critical appraisal method of evaluation.
Managing diabetic ketoacidosis (DKA) requires careful consideration of fluid therapy, especially in severe cases. In part two of our REBEL Cast DKA series, we shifted from insulin strategies to fluid choice in severe DKA, diving into the SCOPE-DKA trial—a cluster, crossover, open-label RCT from Australia. While normal saline (NS) is commonly used, concerns about its high chloride content and impact on acidosis have sparked growing interest in balanced solutions like Plasma-Lyte.
REBEL Core Cast – DKA: Beyond the Basics Part 1 – The SQuID Protocol
17 Oct 2025
00:15:29
🧭 REBEL Rundown
🗝️ Key Points
🛏️ Fewer ICU Admissions Only 5 patients in the SQuID group required ICU care vs 99 in the traditional insulin drip group.
⏱️ Shorter ED Stays ED length of stay dropped by ~3 hours in the SQuID group—an operational win in crowded departments.
💉 No Drop in Nursing Workload Despite using subQ insulin, nurses still performed hourly glucose checks and frequent injections.
🧪 Focus on the Anion Gap DKA resolution = closing the anion gap, not just normalizing blood sugar—critical concept for trainees and nurses alike.
👶 Peds Has the Edge Pediatric ICUs routinely use a 2-bag system (D10 + electrolytes vs electrolytes alone) to safely continue insulin while managing glucose—adult medicine should take note.
In this episode of REBEL Cast, we dive into part one of our Diabetic Ketoacidosis (DKA) series with a twist—subcutaneous insulin instead of the traditional IV drip. We explore the SQuID Protocol (Subcutaneous Insulin in DKA), which could potentially shift how we manage mild to moderate DKA—from the ICU to the general floor.
With ICU bed shortages, ED boarding, and nursing resource challenges, it’s time to ask: Do all DKA patients really need a drip and an ICU bed?
We reviewed a quasi-experimental study comparing traditional insulin drips versus subcutaneous insulin (lispro q4h + glargine at time zero) in a busy urban ED. The results? Promising—but not without caveats.
🦑 SQuID Protocol
🚨 Clinical Bottom Line
The SQuID Protocol appears safe and effective for carefully selected patients with mild to moderate DKA. It may reduce ICU admissions and shorten ED stays. But implementation requires thoughtful coordination, nursing comfort, and institutional buy-in. This isn’t ready for prime time everywhere—but it’s worth knowing and considering when ICU resources are tight.
Post Peer Reviewed By: Marco Propersi (Twitter/X: @Marco_propersi), and Kim Bambach, MD
Show Notes By: Mark Ramzy, DO
Authors
Mark Ramzy, DO
Co-Editor-in-Chief
RWJBH / Rutgers Health, Newark, NJ
Frank Lodeserto
Associate Editor
Cape Fear Valley Medical Center,
Fayetteville NC
🔎 Your Deep-Dive Starts Here
In this episode, we focus on the bedside evaluation of the tachypneic patient. Tachypnea (increased respiratory rate) can be an early indicator of serious illness, but not every tachypneic patient is on the verge of arrest. The key is honing your bedside assessment to recognize who is at risk for rapid deterioration and why. We break down a practical approach you can use immediately at the bedside.
🔑 Key Concepts
First Priorities at the Bedside
Chest Rise:
Short, shallow respirations with poor chest rise are a major red flag.
Patients with minimal tidal volumes are often approaching respiratory failure.
Diaphoresis and Tachycardia:
Diaphoresis + tachycardic patients with shallow breathing demand urgent attention as this is a sign of high catecholamine surge and impending respiratory collapse.
Immediate Action:
Use your eyes (chest rise), your ears (stethoscope), and brain (putting together all of the pieces together)
Short, Shallow Breathing: Think Three Major Buckets
A careful, simple bedside assessment can rapidly identify which tachypneic patients need immediate intervention—and help you avoid missing those headed toward respiratory collapse. Stay sharp, stay systematic!
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
In this episode, we break down a practical bedside approach to hypoxemia. We clarify the difference between hypoxemia (low oxygen in the blood) and hypoxia (low oxygen at the tissue level), and walk through the major causes of hypoxemia that you need to recognize quickly at the bedside.
🔑 Key Concepts
Hypoxemia vs. Hypoxia: Know the Difference
Hypoxemia = Low oxygen in the blood.
Measured indirectly by SpO₂ (pulse oximeter) or directly by PaO₂ (arterial oxygen tension) or SaO₂ (oxygen saturation).
Hypoxia = Low oxygen at the tissue level.
Can happen with or without hypoxemia.
Four Types of Hypoxia
Hypoxemic Hypoxia: Blood oxygen is low, so tissues get less oxygen. (e.g., severe pneumonia)
Anemic Hypoxia: Low hemoglobin levels mean less oxygen-carrying capacity, even if oxygen levels are normal. (e.g., hemorrhage, hemolysis)
Ischemic Hypoxia: Blood flow to tissues is blocked or reduced. (e.g., MI, stroke, severe shock)
Histotoxic Hypoxia: Oxygen delivery is normal, but tissues can’t use it. (e.g., carbon monoxide or cyanide poisoning)
Five Major Causes of Hypoxemia
Hypopnea/Apnea (Decreased Respiratory Drive)
Inadequate breaths (or no breaths) means lower oxygen intake.
Seen in cardiac arrest, drug overdose, severe brain injury.
Easy to recognize as patients are encephalopathic or apneic.
High Altitude
Lower barometric pressure = less available oxygen, despite 21% FiO₂.
Rarely relevant inside hospitals, but important to know.
Diffusion Defect
Impaired oxygen transfer across alveoli, often due to chronic lung disease.
Key Move: High FiO₂ (non-rebreather mask) → if still hypoxemic, they need positive pressure (NIV or intubation).
🛌 Practical Bedside Approach
Give as much FiO₂ as possible (non-rebreather mask).
Watch SpO₂ response:
If it improves → V/Q mismatch or dead space more likely.
If it doesn’t improve → think shunt physiology.
If refractory hypoxemia persists → Start positive pressure ventilation (HFNC, CPAP, BiPAP, or intubation depending on the situation).
🚨 Clinical Bottom Line
Mastering the basics of hypoxemia helps you recognize dangerous physiology early — before your patient crashes. Keep in mind the four types of hypoxia and the five major causes of hypoxemia.
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
👤 Guest Contributor
Eric Acker MD
Internal Medicine Resident,
Rising Chief Resident,
Cape Fear Valley Medical Center,
Fayetteville NC
Acetaminophen (APAP) overdose remains one of the most common causes of acute liver failure in the United States. While its therapeutic use is widespread and generally safe, unintentional overdoses and delayed presentations can lead to devastating outcomes. In this episode of REBEL Cast, we break down the pathophysiology, clinical course, diagnostic approach, and evidence-based management of APAP toxicity—including when to initiate NAC, how to apply the Rumack-Matthew nomogram, and the evolving role of adjunctive therapies like fomepizole. Whether you’re in the ED or elsewhere , this is core content every clinician should know.
After ingestion of a therapeutic dose, immediate release APAP is absorbed with a time to peak concentration anywhere between 30-45 minutes. In the context of extended-release, formulations, full absorption is typically reached by 4 hours post-ingestion.1
In therapeutic dosing, the vast majority of APAP undergoes hepatic conjugation with glucuronide or sulfate to form benign metabolites that ultimately get excreted in the urine. The remaining ~5% is oxidized by CYP2E1 to form N-acetyl-p-benzoquinoeimine (NAPQI). NAPQI is hepatotoxic. Glutathione combines with NAPQI to generate non-toxic metabolites that are also eliminated in the urine.
In overdose, the amount of NAPQI that is generated is increased as the typical metabolic pathways become saturated. The NAPQI that remains leads to hepatocellular death in Zone 3 of the liver (or the centrilobular location) which is the area with the largest degree of oxidative metabolism.
Clinical Manifestations and Diagnostic Evaluation
The clinical course of acute APAP toxicity is classically broken into four different stages.
Stage1: this is generally within 24 hours. Patients are either asymptomatic or have non-specific GI symptoms (nausea, vomiting, malaise). At this point, hepatic function testing is normal.
Stage2: ~24-72 hours. The onset of hepatic injury marks this stage. Aspartate aminotransferase (AST) is the most sensitive marker to detect hepatic dysfunction; AST elevated is nearly universal by 36 hours post-ingestion.
Stage3: defined as peak hepatotoxicity; generally between 72-96 hours post-ingestion. Patients may manifest hepatic encephalopathy or coma. AST and/or ALT might rise above 10,000 IU/L. Other lab abnormalities include: INR/PT, glucose, lactate, pH, and creatinine. Death from fulminant hepatic failure usually occurs anywhere between 3-5 days after an acute ingestion. Mortality is often secondary to multiorgan failure, ARDS, sepsis, or cerebral edema.
Stage4: often called the “recovery phase.” Patient who survive demonstrate complete hepatic generation without any evidence of hepatic dysfunction.
The following labs should be obtained for severe APAP ingestions:
APAP Concentration, hepatic panel, pH, coagulation panel, renal function, lactate and phosphate. These labs will ultimately dictate disposition (see King’s College Criteria below)
Management
Consider GI decontamination with activated charcoal as this can reduce systemic absorption and limit subsequent clinical sequalae.
Ingestions should be classified as acute or repeated supratherapeutic (“chronic” ingestions)
Single Acute Ingestion
If feasible, obtain a 4 hour post-ingestion APAP concentration. Any concentration earlier than 4 hours is uninterpretable as subsequent concentrations may increase or decrease depending on the clinical scenario.
Concentrations between 4-8 hour post-ingestion can be plotted on the Rumack-Matthew nomogram to determine when NAC should be initiated.
If the APAP concentration is above the plotted line, NAC should be started.
NAC is nearly 100% effective if started within 8 hours post-ingestion.2
If an APAP concentration is unable to be drawn before 8 hours or if LFTs are already elevated, NAC should be empirically started if the pre-test probability is high enough for clinical concern.
Repeated Supratherapeutic/Chronic Ingestions
Cannot apply the Rumack-Matthew Nomogram
If LFTs are elevated or if there is a positive APAP concentration, NAC should generally be started however consultation with a toxicologist or Poison Control Center is advised as these cases are often complicated.
N-Acetyl-Cysteine (NAC) Dosing
“3 Bag Protocol” – 21 hour regimen
150mg/kg over 1 hour loading dose
50mg/kg over 4 hours = 12.5 mg/kg/hr
100mg/kg over 16 hours = 6.25 mg/kg/hr
Risk: anaphylactoid reaction
Reaction is rate related and typically occurs during the loading dose
Symptoms: flushing, urticaria.
NAC should be continued until all of the following criteria are met:
Negative APAP concentration
“Significant Decreased in AST”: defined as either <1000 IU/L or a 25-50% drop from the peak.
No evidence of hepatic failure
If criteria are not met, the third bag should be extended indefinitely.
The King’s College Criteria should be used as this set of lab work is used to determine which patients should be referred for possible liver transplant evaluation.3, 4
Arterial pH < 7.30
INR > 6.5 (PT >100 sec)
Creatinine > 3.4
Grade III or IV hepatic encephalopathy
Hyperlactatemia
Hyperphosphatemia
Fomepizole (traditionally used for the treatment of toxic alcohols) has been used as an adjunctive treatment for massive acetaminophen toxicity as it has demonstrated efficacy in mitigating serum transaminase elevation, hepatic necrosis, and oxidative stress in both mouse and human models.5-8
As large scale human studies have yet to be published, fomepizole should NOT be routinely administered for APAP toxicity.
Take Home Points
Acetaminophen (APAP), most commonly referred to as “Tylenol” in the United States, is in a variety of pharmaceuticals. Medications like Excedrin, Fioricet, Percocet, Vicodin, and Day/Nyquil all contain acetaminophen.
Given the lack of a toxidrome, there should be a low threshold to obtain a screening acetaminophen concentration in the undifferentiated poisoned patient.
In overdose, acetaminophen leads to generation of NAPQI which is hepatotoxic. N-Acetylcysteine (NAC) is the antidote of choice and ideally should be administered within 8 hours of an acute ingestion.
To determine which patients should be treated with antidotal therapy, the Rumack-Matthew Nomogram should be utilized. Of note, this nomogram was validated for a single concentration obtained at or greater than 4 hours after a single, acute ingestion. (i.e. patients with repeated ingestions cannot be applied to the nomogram).
In patients with a high pre-test probability of APAP poisoning, the King’s College Criteria should be considered; this is a set of lab markers that help determine when patients should be immediately referred for liver transplant.
While physiologic plausibility exists for the use of fomepizole to treat severe APAP toxicity, no large scale human studies exist at this time to suggest that it should be routinely given for toxicity. As with all cases of toxicity, please call your local poison control center for assistance.
References
Hendrickson RG, McKeown NJ. Chapter 33. Acetaminophen. In: Nelson LS, et al., editors. Goldfrank’s Toxicologic Emergencies. 11th ed. New York: McGraw-Hill; 2019.
Smilkstein MJ, Knapp GL, Kulig KW, Rumack BH. Efficacy of oral N-acetylcysteine in the treatment of acetaminophen overdose: Analysis of the National Multicenter Study (1976 to 1985). N Engl J Med. 1988;319(24):1557-1562. PMID: 3059186
O’Grady JG, Alexander GJ, Hayllar KM, Williams R. Early indicators of prognosis in fulminant hepatic failure. Gastroenterology. 1989;97(2):439-445. PMID: 2490426
Akakpo JY, Ramachandran A, Duan L, et al. Delayed treatment with 4-methylpyrazole protects against acetaminophen hepatotoxicity in mice by inhibition of c-jun N-terminal kinase. Toxicol Sci. 2019;170(1):57-68. PMID: 30903181
Akakpo JY, Ramachandran A, Kandel SE, et al. 4-Methylpyrazole protects against acetaminophen hepatotoxicity in mice and in primary human hepatocytes. Hum Exp Toxicol. 2018;37(12):1310-1322. PMID: 29739258
Shah KR, Beuhler MC. Fomepizole as an adjunctive treatment in severe acetaminophen toxicity. Am J Emerg Med.2020;38(2):410.e5-410.e6. PMID: 31785979
Kang AM, Padilla-Jones A, Fisher ES, et al. The effect of 4-methylpyrazole on oxidative metabolism of acetaminophen in human volunteers. J Med Toxicol. 2020;16(2):169-176. PMID: 31768936
Street Medicine: Compassionate Care for the Unhoused
02 Apr 2025
00:55:01
Introduction: In this episode of Rebel Cast, host Marco Propersi, along with co-hosts Steve Hochman and Kim Baldino, delve into the practice and importance of street medicine—the direct delivery of healthcare to homeless and unsheltered individuals. Special guests Dr. Jim O’Connell, a pioneer of street medicine, and Dr. Ed Egan, a recent street medicine fellowship graduate, share their experiences and insights on serving this vulnerable population. They discuss the origins, scope, and challenges of street medicine, the ethical dilemmas faced, and the profound impact of building trust and community with patients. The conversation underscores the necessity of integrating street medicine with mainstream healthcare systems and emphasizes that small acts of kindness and persistence can significantly improve the lives of those experiencing homelessness.
REBEL Cast – Street Medicine: Compassionate Care for the Unhoused
A Winning Hand in Cardiology: Queen of Hearts AI Model Enhances OMI Detection
22 Jul 2024
00:44:56
Background: Cath lab activation based on ST-elevation myocardial infarction (STEMI) criteria is founded on aging data and requires evolution. In the “Occlusive Myocardial Infarction (OMI) Manifesto,” emergency physicians Dr. Steve Smith, Dr. Pendell Meyers, and Dr. Scott Weingart introduced a new paradigm —OMI vs. non-occlusive myocardial infarction (NOMI).
The OMI/NOMI paradigm focuses on the presence of coronary occlusion, while STEMI/NSTEMI categorizes myocardial infarctions based on electrocardiogram (ECG) findings. Patients with OMI exhibit higher mortality and worse left ventricular function compared to those with NOMI.1, 2, 3 Detecting OMI is more difficult and necessitates scrutiny of the ECG, which is challenging in a busy emergency department where ED clinicians are interrupted more than ten times per hour.4, 5 Some OMI ECG signs include ST elevation in only one lead, subtle ST elevation with minimal reciprocal changes, isolated ST depressions, and hyperacute T waves.
To meet this challenge, Dr. Steve Smith, Dr. Pendell Meyers (Dr. Smith’s ECG Blog), and their team developed The Queen of Hearts, a machine-learning AI model that has the potential to aid in the early detection of subtle OMI ECG changes. Accurately identifying OMI changes in ECG that STEMI criteria might otherwise miss would allow for more timely intervention, potentially salvaging more myocardium. An AI model that is highly sensitive in detecting OMI while maintaining a high degree of specificity would be an ideal tool to support emergency physicians’ clinical decision-making. The performance of this tool is unknown.
Paper: Herman R, Meyers HP, Smith SW, et al. International evaluation of an artificial intelligence-powered electrocardiogram model detecting acute coronary occlusion myocardial infarction. Eur Heart J Digit Health. 2023;5(2):123-133. Published 2023 Nov 28. PMID: 38505483
Clinical question: “Can an AI model detect an OMI lesion using a single 12-lead ECG?”
What They Did:
Investigators performed a retrospective derivation study followed by validation on an internal data set from the same Acute Coronary Syndrome (ACS) database.
Cases eligible for inclusion were randomly assigned to a model development training set (derivation set) and testing set (validation set).
The training set included ECG feature extraction and classification
Feature extraction used 60,000 parameters
The classification component combined all extracted features and used an additional 150,000 parameters.
The validation data set was used for hyperparameter tuning and threshold selection.
Investigators then tested the AI model on two data sets
An internal European data set (internal validation set)
A separate US data set (external validation set) from the DOMI ARIGATO database.
They compared the AI model with the existing criteria for detecting OMI on 12-lead ECGs and analyzed the AI model in various subgroups.
Population:
Derivation Set: Random selection of ACS patients from the Cardiovascular Centre Aalst in Belgium and ACS patients from an international image database patient.
EU Internal Test Set: Random Selection of ACS patients from the Cardiovascular Centre Aalst in Belgium and ACS patients from an international image database patient.
US External Test Set: Patients from the DOMI ARIGATO database.
Exclusion:
ECGs >24 h before CAG and post-CAG
ECGs with poor signal quality
ECGs with missing Expert Annotation, undigitizable ECGs, Baseline ECGs (additionally excluded from the US External Database)
Intervention:
AI-powered ECG model implemented on ECGs from the internal EU and external US datasets.
Comparator:
Blinded physician annotations of the standard ‘STEMI criteria’ on ECG
Blinded subjective ECG expert annotations of OMI
Angiographic clinical outcome data
Outcomes:
Primary Outcome: AI model’s ability to identify patients with angiographically confirmed OMI using only the 12-lead ECG.
Secondary Outcomes:
OMI AI model performance across demographic and ECG subgroups
A comparison of the AI model performance against the existing STEMI criteria for detecting acute coronary occlusion from 12-lead ECGs
A sensitivity analysis of AI model performance using various angiographic and laboratory cut-offs of OMI
An evaluation of misclassified cases
Results:
The derivation set used in the AI model development included 18,616 ECGs from 10,543 patients with clinically validated outcomes.
The overall test set included 3254 ECGs from 2222 patients
The internal EU testing cohort 2016 ECGs from 1630 patients
The US testing cohort 1238 ECGs from 633 patients
The prevalence of OMI differed between the internal EU and the external US test sets, 16% compared with 36.2%, respectively ( < 0.001).
The patients in the US test set were younger, had more ECGs recorded before catheterization, and were more likely to present with a STEMI-positive ECG.
AI Model Performance:
Achieved an Area Under the ROC Curve (AUC) of 0.938 [95% CI: 0.924–0.951].
Accuracy of ECG experts was 90.8% [95% CI: 89.5–91.9].
Sensitivity: 73.0% [95% CI: 68.7–77.0].
Specificity: 95.7% [95% CI: 94.7–96.6].
OMI AI Model vs. STEMI Criteria:
The OMI AI model performs significantly better than the STEMI criteria in sensitivity, Negative Predictive Value (NPV), Matthews correlation coefficient (MCC), and AUC.
However, it has lower specificity and Positive Predictive Value (PPV) compared to the STEMI criteria.
OMI AI Model vs. ECG Experts:
The OMI AI model has higher sensitivity and NPV than ECG experts.
It shows equal performance in AUC and is adjudicated as equal overall to ECG experts.
Specificity and PPV are lower than ECG experts, and MCC is neutral.
ECG Experts vs. STEMI Criteria:
ECG experts have higher sensitivity, NPV, MCC, and AUC than STEMI criteria.
They perform the same in specificity and PPV compared to STEMI criteria, leading to significantly better adjudication.
Strengths:
Rigorous Methodological Approach: The study follows a comprehensive methodological approach, encompassing stages of development, validation, and comparison.
Large and Diverse Dataset: The model was trained and tested on a substantial dataset of 18,616 ECGs from 10,543 patients with ACS across multiple international cohorts. This diversity enhances the model’s generalizability and robustness.
Expert Interpretation and Validation: All cases in the derivation set included expert ECG interpretations alongside clinically validated angiographic outcome data, ensuring high accuracy in the model’s training process.
High Agreement Among Experts: Two authors, serving as ECG experts, annotated all tracings for the presence of OMI while being blinded to all clinical data. They achieved a 94% agreement (kappa = 0.849), demonstrating the reliability of the expert annotations.
Independent Review: Blinded independent clinical reviewers adjudicated all angiographic data in the EU internal testing set, adding an extra layer of objectivity and reliability to the validation process.
Comprehensive Performance Comparison: The study compares the AI model’s performance with existing STEMI criteria and expert ECG interpretations. This sets a quantifiable humanistic standard, highlighting the AI model’s enhanced performance.
Limitations:
Applicability Limited to ACS Patients: The AI model was developed using patients and ECGs exclusively from ACS databases, restricting its applicability to only those with ACS.
Disease-Oriented Outcomes: The outcomes in this study are disease-oriented. While facilitating the diagnosis of OMI may lead to improved patient-oriented outcomes, this was not directly studied.
Limited Generalizability to Asymptomatic Patients: The study is not generalizable to a broader population of asymptomatic patients and was not designed to quantify other relevant clinical endpoints such as mortality, in-hospital complications, or major adverse cardiovascular events (MACE).
Lack of Prospective Validation: The validation set was analyzed retrospectively, lacking prospective validation to confirm the model’s effectiveness in real-world clinical settings.
Randomization Process Not Mentioned: The randomization process used to allocate cases to the derivation or validation set is not mentioned, which may impact the robustness of the findings.
Comparison Limited to 12-Lead ECG: The AI model was compared to the 12-lead ECG alone. Some patients undergo emergency angiography without clear STEMI criteria based on the full clinical picture. Therefore, the interpretation of the overall gain is limited without a pragmatic comparison to real-world clinical practices and patient-oriented outcomes.
Limited Generalizability to Younger Population and Women: Approximately 10% of ECGs were from patients ≤45 years of age, and three-quarters of the cases were from males, limiting the generalizability to younger populations and women.
Inappropriate Use of P-Values: The inclusion of p-values in Tables 1 and 2 is puzzling, as this is not a randomized controlled trial (RCT). Demographic differences between validation sets are expected and desired for external validity.
Variability in Care Standards: Significant differences in clinical presentation and management between patients in Europe and the USA (e.g., the USA had younger patients and more ECGs before catheterization) could affect the model’s performance across different healthcare systems.
Subjective Outcome Verification: The detection of OMI relied on visual verification of TIMI flow on angiograms, which may be subjective.
Conflict of Interest: The lead author disclosed a conflict of interest as the co-founder and Chief Medical Officer of Powerful Medical. Other authors have disclosed employee or shareholder status in Powerful Medical.
Discussion:
Inside the Numbers: The data for this AI model is impressive, showcasing a remarkable capability in early and accurate detection of OMI on ECGs, demonstrating a sensitivity of 80.6% (76.8–84.0) and specificity of 93.7% (92.6–94.8). The AI model not only surpassed the standard STEMI ECG criteria [sensitivity 32.5% (28.4–36.6) and specificity 97.7% (97.0–98.3)] but also matched the performance of Dr. Steve Smith and Dr. Pendell Meyers, two well known ECG experts [sensitivity 73.0% (68.7–77.0) and specificity 95.7% (94.7–96.6)]. Additionally, when considering the existing evidence, the AI model would likely outperform ED physicians’ and cardiologists’ ability to detect ischemia on ECG, who achieved sensitivities of approximately 65% and specificities ranging from 65–79% in multiple studies.7, 8, 9 This high accuracy demonstrates AI’s potential to improve diagnostic processes and patient outcomes in emergency settings.
The AI model’s PPV in this study was 0.780 (0.742–0.816), and the NPV was 0.946 (0.935–0.957) for the primary outcome. PPV and NPV are heavily influenced by disease prevalence, and a high prevalence increases the PPV, indicating that a positive test result is more likely to be a true positive. The 16% and 36.2% prevalence of OMI in the internal and external validation sets are likely much higher than expected from a random group of patients assessed for ACS in the ED on any given day. Consequently, the PPV is likely lower in a less risky population with a lower prevalence for ACS.
The AI model’s AUC for detecting OMI was 0.938 (0.924–0.951), with an optimal threshold of 0.1106. The optimal threshold refers to the chosen point that maximizes the AI model’s accuracy. The point is a probability that ranges from 0–1. However, investigators must choose the value (optimal threshold) at which the model determines whether the ECG is positive or negative. Therefore, the optimal threshold converts a continuous variable (probability) into a binary decision, such as distinguishing between the presence or absence of OMI on ECG. If the threshold is set too low, it might result in high sensitivity but low specificity, leading to many false positives. The ROC curve is a graphical plot that illustrates the diagnostic ability of a binary classifier as its discrimination threshold is varied. In this instance, a ROC curve with an AUC of 0.938 is outstanding and highlights the potential of the AI model to optimize clinical decision-making processes.
Critical Biases and Considerations: The primary flaw in this paper is selection bias. All patients included in the derivation and validation sets were selected from ACS databases. As mentioned, the prevalence of OMI in the internal and external validation sets is very high. Physicians should exercise caution when applying this data more broadly (i.e., all patients with an ECG in the ED).
The AI model detected OMI in 979 cases total, 267 of which also met the STEMI criteria on ECG. Therefore, 27% of the OMIs detected by the AI model might have been more obvious and less noteworthy to an emergency physician aiming to improve their diagnostic capabilities. However, the remaining 73% of AI-detected OMIs are particularly interesting because they require meticulous ECG scrutiny for accurate diagnosis. While not all these AI-detected OMI cases met the primary outcome criteria, technology can fill a void in identifying patients who may benefit from emergent intervention despite the lack of STEMI-specific criteria on ECG.
“Time is myocardium,” and the primary goal in ACS treatment is to detect OMI on ECG as early as possible to prevent myocardial necrosis. Utilization of STEMI criteria missed 330 OMI patients —false negatives. Among these, 133 had a median revascularization time of 9.3 hours but were correctly identified by the AI model on the first ECG. Early detection can potentially improve patient outcomes, especially in cases with real-world median angiography time of 9 hours. While this data is compelling, it highlights the need for prospective evaluation of the AI model compared to the performance of the average emergency physician to fully assess its clinical effectiveness.
The Future and Transformative Potential of AI: This AI model’s development and validation process mirrors that of a clinical decision instrument, beginning with retrospective derivation followed by internal and external validation. Before widespread implementation, prospective validation in various clinical settings with diverse populations is necessary. Additionally, utilization studies should confirm that the AI model achieves its intended goals, such as earlier detection of OMI and improved patient-oriented outcomes.
While the idea of AI taking over the world might be an exaggeration, its transformative impact cannot be overstated. The continuous advancement and integration of AI technologies can lead to more efficient, accurate, and personalized solutions. Moreover, AI’s continuous refinement through machine learning suggests its performance will only improve over time. As the AI model is exposed to more data and varied cases, it can refine its algorithms, enhance its accuracy, and adapt to new patterns, making it an invaluable tool in the medical field. And, unlike human counterparts, AI will not fatigue and will maintain high accuracy levels, even after the 12th hour on duty and dozens of ECG interpretations. The possibilities for AI applications in healthcare are virtually limitless.
Author’s conclusion: “AI model outperformed gold-standard STEMI criteria in the diagnosis of OMI, but further prospective clinical studies are needed to define the role of the OMI AI model in guiding ACS triage and the timely referral of patients benefiting from immediate revascularization.”
Clinical Bottom Line:
The Queen of Hearts AI model demonstrates impressive accuracy, surpassing STEMI criteria and matching expert interpretation for detecting OMI on ECG. However, the high prevalence of OMI in the study’s datasets may overestimate AI’s ability to detect OMI in a general ED population with a lower disease prevalence. Ultimately, the model requires prospective validation in diverse clinical settings before widespread adoption— but this could be a winning hand.
References:
Wang TY, Zhang M, Fu Y, et al. Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non-ST-elevation acute coronary syndromes undergoing diagnostic angiography. Am Heart J. 2009;157(4):716-723. PMID: 19332201
Pride YB, Tung P, Mohanavelu S, et al. Angiographic and clinical outcomes among patients with acute coronary syndromes presenting with isolated anterior ST-segment depression: a TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis In Myocardial Infarction 38) substudy. JACC Cardiovasc Interv. PMID: 20723851
Khan AR, Golwala H, Tripathi A, et al. Impact of total occlusion of culprit artery in acute non-ST elevation myocardial infarction: a systematic review and meta-analysis. Eur Heart J. 2017;38(41):3082-3089. PMID: 29020244
Ratwani RM, Fong A, Puthumana JS, Hettinger AZ. Emergency Physician Use of Cognitive Strategies to Manage Interruptions. Ann Emerg Med. 2017;70(5):683-687. PMID: 28601266
Chisholm CD, Dornfeld AM, Nelson DR, Cordell WH. Work interrupted: a comparison of workplace interruptions in emergency departments and primary care offices. Ann Emerg Med. 2001;38(2):146-151. PMID: 11468609
Herman R, Meyers HP, Smith SW, et al. International evaluation of an artificial intelligence-powered electrocardiogram model detecting acute coronary occlusion myocardial infarction. Eur Heart J Digit Health. 2023;5(2):123-133. Published 2023 Nov 28. PMID: 38505483
Veronese G, Germini F, Ingrassia S, et al. Emergency physician accuracy in interpreting electrocardiograms with potential ST-segment elevation myocardial infarction: Is it enough?. Acute Card Care. 2016;18(1):7-10. PMID: 27759433
McCabe JM, Armstrong EJ, Ku I, et al. Physician accuracy in interpreting potential ST-segment elevation myocardial infarction electrocardiograms. J Am Heart Assoc. 2013;2(5):e000268. Published 2013 Oct 4. PMID: 24096575
Paez Perez Y, Rimm S, Bove J, et al. Does the Electrocardiogram Machine Interpretation Affect the Ability to Accurately Diagnose ST-Elevation Myocardial Infarction by Emergency Physicians?. Crit Pathw Cardiol. 2023;22(1):8-12. PMID: 36812338
Guest Post By:
Marco Propersi, DO FAAEM
Vice-Chair, Emergency Medicine
Assistant Emergency Medicine Residency Program Director
Vassar Brothers Hospital, Poughkeepsie, New York
Twitter/X: @marco_propersi
Joseph Bove, DO FAAEM
Associate Director Emergency Medicine
Co-Director of the EM Residency Clerkship
St. Joseph’s University Medical Center
Email: bovej@sjhmc.org
Post Peer Reviewed By: Anand Swaminathan, MD (Twitter/X: @EMSwami)
When you take the airway, you take the wheel and you now control the patient’s oxygenation and ventilation. In this REBEL Crit episode, Dr. Lodeserto and Dr. Acker walk through the physiology, ventilator strategies, and clinical curveballs that separate calm control from chaos at the bedside.
️ The Two Pillars of Vent Management
1. Oxygenation — Getting O₂ In
Primary levers: FiO₂ (fraction of inspired oxygen) and PEEP (positive end-expiratory pressure).
Real driver: Mean Airway Pressure (MAP) : the average pressure applied to the lungs across the entire respiratory cycle.
Key physiology:
Oxygen enters blood by diffusion down a concentration gradient.
Adequate alveolar surface area is critical → PEEP keeps alveoli open, prevents collapse/reopen injury, and ensures FiO₂ delivery actually translates into effective oxygenation.
MAP analogy: Just as mean arterial pressure drives perfusion, mean airway pressure drives oxygenation. Prolonged inspiratory time or sustained pressure (e.g., APRV, inverse I:E) can raise MAP.
Risks: Excessive pressure/volume can cause barotrauma or volutrauma.
2. Ventilation — Getting CO₂ Out
Primary levers: Tidal Volume (TV) and Respiratory Rate (RR).
Minute Ventilation = RR × TV.
Mechanism: Ventilation removes CO₂ through bulk convection (movement of air in and out).
Disease-specific strategies:
Obstructive Disease (COPD / Asthma)
RR ↓ to allow more time for exhalation.
Ensure expiratory flow = inspiratory flow → prevents air trapping.
If not equal → auto-PEEP → increased intrathoracic pressure → ↓ preload, risk of hypotension, cardiac arrest, or pneumothorax.
Metabolic Acidosis
RR ↑ to blow off CO₂ and buffer acidosis.
ARDS
Tidal volume limited to 4–6 mL/kg IBW to minimize ventilator-induced lung injury.
RR becomes the main adjustment knob.
Exception: in obstructive lung disease, patients need extra time to exhale (I:E may be 1:4–1:6).
💡 Why This Matters
Ventilator management is part science, part art. Understanding the physiology and knowing when to bend or break the rules helps protect patients from ventilator-induced injury and improves outcomes.
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
Show Notes By: Rubén Tapia-Bucheli, M.D.
👤 Guest Contributors
Rubén Tapia-Bucheli, M.D.
3rd Year Internal Medicine Resident
Cape Fear Valley Internal Medicine Residency Program
Fayetteville NC
Aspiring Pulmonary Critical Care Fellow
🔎 Your Deep-Dive Starts Here
REBEL Core Cast 142.0–Ventilators Part 2: Simplifying Mechanical Ventilation – Most Common Ventilator Modes
22 Sep 2025
00:20:28
🧭 REBEL Rundown
🗝️ Key Points
💨 Start with Breath Types: Controlled, assisted, and supported breaths are the foundation of all modes.
🛌 Comfort Over “Best Mode”: No mode improves mortality — focus on patient synchrony and comfort.
Know the Big 5 Modes: AC: All controlled or assisted (volume or pressure). PS: Fully spontaneous, great for SBTs. PRVC: Pressure-delivered, volume-targeted hybrid. SIMV: Mixed mode, less favored in adults. VS: Spontaneous mode with adaptive pressure.
⚠️ Watch for Pitfalls: PRVC may under-ventilate in agitation. SIMV often causes dyssynchrony.
🎯 Bottom Line: Master mode mechanics and match the vent to the patient — not the other way around.
Mechanical ventilation can feel overwhelming, especially when faced with a sea of ventilator modes and unfamiliar terminology. In Part 2 of the series, we go beyond breath types and delivery mechanics to explore the most used modes in the ICU. We will break down each one; explaining how it works, when to use it, and why the goal isn’t the “best mode” but the most comfortable one for the patient.
️ Ventilator Modes Explained
Assist Control (AC)
Commonly mislabeled as “volume control” or “pressure control.”
Two main types:
AC Volume: Delivers a preset tidal volume with each breath, whether machine-initiated (controlled) or patient-initiated (assisted).
AC Pressure: Delivers a preset pressure; tidal volume varies based on compliance.
All breaths are either controlled or assisted.
Pressure Support (PS)
All breaths are spontaneous initiated by the patient.
The ventilator provides a preset level of pressure support, like a resistance band during a pull-up.
No set rate, but a backup mode (often AC) activates during apnea.
Commonly used for spontaneous breathing trials (SBTs) to assess extubation readiness.
Typical goal: Patient breathing comfortably with PS ~5 cmH₂O and reasonable rate.
Pressure Regulated Volume Control (PRVC)
Also called autoflow or adaptive pressure ventilation.
A hybrid mode: Pressure-delivered, volume-targeted.
Delivers breaths with a decelerating flow waveform, mimicking physiologic breathing.
Adjusts pressure breath-to-breath to meet a target tidal volume with minimal required pressure.
Safety feature: Pressure limit (e.g., 30–35 cm H₂O). If exceeded, volume delivery stops early.
Pitfall: In agitated patients, rapid breathing may trick the ventilator into reducing pressure, causing under-ventilation.
Less common in adult ICU but still commonly used in pediatrics.
Delivers a set number of mandatory (controlled or assisted) breaths.
Allows spontaneous, pressure-supported breaths between mandatory ones.
Example: SIMV 10 = 10 guaranteed AC breaths; additional breaths are spontaneous + supported.
Why it’s less popular: Found to be less effective than daily SBTs for weaning and frequent dyssynchrony from not giving enough PS (PS should target at least 2/3 of the AC breath volumes) .
Volume Support (VS)
A newer, fully spontaneous mode (like PS + PRVC).
Patient initiates all breaths.
The ventilator automatically adjusts pressure support to achieve a target tidal volume.
Think of it as the spontaneous cousin of PRVC—adaptive and volume-driven.
🚨 Clinical Bottom Line
Understanding ventilator modes starts with knowing breath types, delivery mechanics, and clinical goals. When it comes to choosing the right mode:
Focus less on the “best” mode and more on patient comfort and synchrony.
Recognize the strengths, limitations, and pitfalls of each mode.
Stay tuned for future episodes that dive into ventilator troubleshooting and advanced respiratory strategies.
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
Show Notes By: Nicole Ebalo, DO
👤 Guest Contributors
Eric Acker, MD
Internal Medicine, Chief Resident,
Cape Fear Valley Medical Center,
Fayetteville NC
Nicole Ebalo, DO
Internal Medicine, Chief Resident,
Cape Fear Valley Medical Center,
Fayetteville NC
🔎 Your Deep-Dive Starts Here
00:10 Highlighting the Incrementum Conference 2026
00:34 Meet the Founders of Incrementum
01:21 The Journey to Incrementum
04:27 The Recognition of Emergency Medicine in Spain
06:04 What is Incrementum?
08:14 Bringing Together Top Emergency Medicine Experts
11:38 Exciting Sessions to Look Forward To
15:54 Conclusion and Invitation to Incrementum 2026
📝 Introduction
In this special episode of Rebel Cast, we spotlight the Incrementum Conference in Spain, a significant event in emergency medicine. Hosts welcome Dr. Francisco ‘Paco’ Campillo Palma and Dr. Carmen Maria Cano, founders of Incrementum, to discuss the recognition of emergency medicine as a specialty in Spain. They share their journey of creating the conference, emphasizing the importance of education, collaboration, and growth. The discussion also touches on this year’s conference highlights, including sessions on mental health and evidence-based medicine, and the exceptional lineup of speakers. Listeners are encouraged to attend the conference in April 2026 for an enriching experience.
📌 Bottom Line
Join us in Spain this April for the Increment Conference!
For many medical residents, the ICU can feel like stepping into a pressure cooker. At the heart of that stress often lies one intimidating machine: the ventilator. Rather than diving headfirst into complex ventilator modes, this episode lays a critical foundation by breaking down the basic building blocks of mechanical ventilation, something every clinician should master before moving on to more advanced concepts. Once you know the 3 types of breaths and how those breaths are delivered, you can more easily understand most of the mechanical ventilator modes.
🧮 The 3 Types of Breaths
To simplify things, we use a pull-up analogy to explain the types of ventilator breaths:
🫁 The 3 Types of Breaths…It's Like
😮💨 Breath Delivery: Volume vs. Pressure
Once you know the type of breath, the next key concept is how it’s delivered:
1. Volume-Targeted Delivery
The ventilator delivers a fixed tidal volume (e.g., 400 mL) with each control or assist breath.
What to monitor: Pressure. As lung compliance worsens, pressure increases.
Risk: Barotrauma if the pressure becomes too high.
2. Pressure-Targeted Delivery
The ventilator delivers air to a preset pressure (e.g., 15 cm H₂O).
What to monitor: Tidal volume. As compliance drops, so does delivered volume.
Adjustment: Modify pressure to maintain appropriate ventilation.
🧱 Putting It All Together: Lung Compliance
The relationship between pressure and volume is described by compliance:
📐 Compliance = Δ Volume / Δ Pressure
In volume mode:
Rising pressure to achieve the same volume = decreased compliance (stiff)
Decreasing pressure to achieve the same volume = increased compliance (loose)
In pressure mode:
Dropping tidal volume at a constant pressure = decreased compliance (stiff)
Rising tidal volume at a constant pressure = increased compliance (loose)
🚨 Clinical Bottom Line
Before tackling advanced ventilator modes, master these foundational concepts:
The three breath types
The two delivery methods
The role of lung compliance
Once you’ve got these down, the rest of mechanical ventilation becomes far easier to understand.
Stay tuned for Part 2, where we’ll build on this foundation and unpack the most commonly used ventilator modes.
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
Show Notes By: Nicole Ebalo, DO
👤 Guest Contributors
Eric Acker, MD
Internal Medicine, Chief Resident,
Cape Fear Valley Medical Center,
Fayetteville NC
Nicole Ebalo, DO
Internal Medicine, Chief Resident,
Cape Fear Valley Medical Center,
Fayetteville NC
🔎 Your Deep-Dive Starts Here
REBEL Core Cast 140.0: The Power and Limitations of Intraosseous Lines in Emergency Medicine
01 Sep 2025
🧭 REBEL Rundown
📌 Key Points
💉 IO Lines Are Life-Saving in Extremis: IO access is fast, reliable, and can deliver nearly any resuscitative medication or fluid during cardiac arrest or hemorrhagic shock.
🧭 Location Matters for Flow. Sternal IO: 💨 Fastest (up to 500cc/5 min). Humerus IO: ⚡ Faster than tibia (300cc/5 min). Tibial IO: 🐢 Slower (200cc/5 min) but easier to place during CPR
⚠️ Watch for Contraindications: Avoid IO placement in bones with fractures, prior IO attempts, or compromised circulation proximal to the site.
🩸 Labs From IO = ❌: Labs drawn from IO lines are generally unreliable. Once stabilized, obtain bloodwork through IV access.
🎯 Stabilize or Lose It: IO dislodgement is common—always use a stabilizer or secure with gauze and tape if none is provided.
🧠 Don’t Forget Non-Trauma Uses: IO isn’t just for trauma—think about it in medical arrests, shocked pediatric patients, and patients with difficult IV access.
Welcome to the Rebel Core Content blog, your go-to source for core medical concepts applicable to practitioners anywhere, anytime. Today, we delve into the world of Intraosseous (IO) lines—a crucial tool in emergency medicine. Swami shares insights into the effectiveness and limitations of IO usage in diverse clinical scenarios.
🧠 Background
The sicker the patient, the more likely an IO line is the right choice. In emergencies such as cardiac arrest or hemorrhagic shock, the speed and reliability of IO access outshine traditional intravenous (IV) or central line placements. There’s virtually no resuscitation medication or blood product that cannot be administered through an IO, making it indispensable in life-threatening situations.
🧭 Location
While proximal humerus site portents faster infusion rates than proximal tibia site, the main limitation of the proximal humerus site is that the arm must be held in internal rotation to avoid dislodgement of the IO
Proximal tibia may be easier to landmark than proximal humerus
Other sites include distal tibia, distal femur and sternum but are uncommonly employed in EDs
🚰 Flow Rates
Proximal Humerus IO
~300cc over 5 minutes
Faster than tibia
May be harder to access in some trauma or positioning scenarios
Tibial IO
~200cc over 5 minutes
Slower flow compared to humerus
Easier to access, especially during CPR or transport
Sternal IO
Up to 500cc over 5 minutes
Highest flow rate
Best for rapid volume resuscitation
Risk of dislodgement or interfering with CPR compressions
⚠️ Limitations
Placing an IO in a bone with a proximal fracture, a previous IO placement attempt or any circulatory compromise proximal to the site is contraindicated
Blood work drawn from an IO are generally not accurate, so once the patient has been resuscitated with the IO, intravenous blood draws are recommended
Dislodgement is common; it is best to use the stabilizer that comes with the IO kit; if the kit does not have a stabilizer, stack lots of gauze on both sides of the IO needle and tape it down
🚨 Clinical Bottom Line
Intraosseous lines are a powerful tool, particularly in acute resuscitation scenarios involving cardiac arrest or severe trauma. While they offer quick and effective access, Clinicians must remain vigilant about their limitations and be prepared to switch to more stable options as patients stabilize.
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
🧠 Think Beyond Trauma: Don’t forget to suspect tension pneumothorax in ventilated patients who suddenly crash or after a central line placement! 🫁⚠️
🔍 Confirm with Ultrasound: If the patient is stable enough, grab the probe! 🖐️📟Ultrasound can rapidly confirm tension PTX and avoid unnecessary delays.
💉🚫 Needles Are Out: Needle decompression? Meh. Finger thoracostomy is faster, more reliable, and more definitive. 🖐️🫁
On this episode of the Rebel Core Cast, Swami takes a deep dive into pneumothorax decompression, focusing on the need for improvements beyond the classic teachings. Covering scenarios where immediate decompression is critical, particularly in tension pneumothorax, Swami discusses the limitations of needle decompression, especially in the second intercostal space at the midclavicular line. He highlights the importance of using POCUS for diagnosis and recommends skipping needle decompression in favor of finger thoracostomy for a more reliable and effective treatment. Key takeaways emphasize recognizing tension pneumothorax in various clinical situations and the advantages of finger thoracostomy over traditional techniques.
⏰ Highlights
00:00 Introduction to Pneumothorax Decompression
00:17 Recognizing Tension Pneumothorax
01:00 Common Scenarios for Pneumothorax
01:34 Confirming Diagnosis with POCUS
01:50 Issues with Needle Decompression
03:21 Advantages of Finger Thoracostomy
04:11 Key Takeaways and Conclusion
📚 References
Ferrie EP et al. The right place in the right space? Awareness of site for needle thoracentesis. Emerg Med J 2005; 22: 788-9 PMID: 16244336
Laan DV et al. Chest wall thickness and decompression failure: a systematic review and meta-analysis comparing anatomic locations in needle thoracostomy. Injury; 2016; 47(4): 797-804 PMID: 26724173
Terboven T et al. Chest wall thickness and depth to vital structures in paediatric patients – implications for prehospital needle decompression of tension pneumothorax. Scan J Trauma Resusc Emerg Med 2109; 27(1). PMID: 30992028
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
REBEL Core Cast 138.0: A Simple Bedside Approach to Shock
04 Aug 2025
🧭 REBEL Rundown
📌 Key Points
🧠 Shock is a Clinical Diagnosis — Not Just a Number Patients can be in compensated shock with normal BP. Look for signs like AMS, cool extremities, ↓ UOP, and ↑ HR/RR.
🖐️ Start with the 4 L’s Lucid (mental status), Limbs (warm/cold), Leak (urine output), and Lactate give you rapid bedside insight into perfusion status.
💡 Pulse Pressure Helps Pinpoint the Type
➡️ Narrow PP = Cardiogenic, Hypovolemic, or Obstructive shock
In this episode, we will dive into a simple yet effective bedside approach to a patient in shock. By using quick physical exam findings and bedside vitals (particularly pulse pressure), you can form a quick assessment of the likely underlying etiology of a critically ill patient.
🔑 Key Concepts
What is Shock?
Supply vs. Demand mismatch:
Inadequate perfusion relative to metabolic demands
Leading to tissue hypoxia and cell death
DO2 = CO x (Hb x Sat + (0.003 x paO2))
CO = Heart Rate x Stroke Volume
Determinants of Stroke Volume: Preload, Contractility, and Afterload
4 L’s of Hypotension
Lucid: What’s their mental status?
Limbs: Are they cold vs. warm? What is the cap refill?
Leak: Are they taking a “leak”? What is the urine output?
Lactate
Remember:
Shock DOES NOT equal hypotension
A patient in shock can still have normotensive pressures in “Compensated Shock”
A brief but thorough bedside exam remembering the 4 “L’s”, a quick history, and examining the pulse pressure can help a clinician form a quick differential into the underlying etiology for a critically ill patient in shock. Stay sharp, stay systematic!
💡 Shock is a clinical diagnosis based on bedside findings — not just blood pressure readings.
You don’t always need invasive monitoring to identify shock. Look at HR, RR, UOP, and mentation.
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
👤 Guest Contributors
Eric Acker, MD
Internal Medicine Resident, Rising Chief Resident,
Cape Fear Valley Medical Center,
Fayetteville NC
Micheal Bass DO
Internal Medicine Resident, Rising Chief Resident
Cape Fear Valley Medical Center,
Fayetteville NC
Frank J. Lodeserto MD
Associate Professor and Internal Medicine Residency Program Director
Adult & Pediatric Critical Care Medicine, Cape Fear Valley Medical Center, Fayetteville, NC
🔎 Your Deep-Dive Starts Here
https://rebelem.com/rebel-core-cast-128-0-toxic-alcohols/REBEL Core Cast 128.0 – Toxic Alcohols
Take Home Points Toxic alcohols generally refer to methanol and ...
Sinus tachycardia is the most prevalent cardiac dysrhythmia in critically ill patients, yet it often receives less attention than it warrants. While the rhythm itself is not inherently dangerous, it serves as a crucial indicator of underlying physiological disturbances that require prompt evaluation and management.
🔑 Key Concepts
Sinus Tachycardia as a Clinical Sign: Rather than focusing solely on the elevated heart rate, clinicians should interpret sinus tachycardia as a symptom pointing toward an underlying cause that needs to be identified and addressed.
Oxygen Delivery Equation: Understanding the components of oxygen delivery—hemoglobin concentration, oxygen saturation, and cardiac output—is essential. An increase in heart rate may be a compensatory mechanism to maintain adequate oxygen delivery when other components are compromised.
8 Causes of Sinus Tachycardia
Airway/Hypoxia: Ensure the airway is patent and assess for hypoxemia.
Breathing: Evaluate for respiratory distress or pulmonary pathology.
Circulation: Consider shock states, including hypovolemia, hemorrhage, or distributive shock.
Drugs: Review medications and substances that may cause tachycardia, including stimulants and withdrawal states.
Erythrocytes (Anemia): Assess for low hemoglobin levels that may impair oxygen delivery.
Fever: Recognize that fever increases metabolic demand, leading to tachycardia.
Glucose: Identify hypoglycemia or hyperglycemia as potential contributors.
Holy Cow That Hurts: (Pain/Anxiety): Acknowledge that pain and emotional distress can elevate heart rate.
🛌 Practical Bedside Approach
Holistic Assessment: Always interpret sinus tachycardia within the broader clinical context.
Avoid Reflexive Treatment: Refrain from immediately administering rate-controlling medications without identifying and managing the underlying cause.
Continuous Monitoring: Regularly reassess the patient’s status, as the underlying cause of tachycardia may evolve over time.
🚨 Clinical Bottom Line
Sinus tachycardia is a vital clinical sign that necessitates a thorough and systematic evaluation to uncover and treat the root cause. By adopting this structured approach, clinicians can improve patient outcomes and avoid the pitfalls of symptomatic treatment without addressing underlying issues.
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
👤 Guest Contributors
Eric Acker, MD
Internal Medicine Resident, Rising Chief Resident,
Cape Fear Valley Medical Center,
Fayetteville NC
Thirumala “Keerthi” Kammaripalle, MD
Internal Medicine Resident, Rising Chief Resident
Cape Fear Valley Medical Center,
Fayetteville NC
🔎 Your Deep-Dive Starts Here
REBEL CAST – IncrEMentuM26 Speaker Spotlight : Drs. Tarlan Hedayati, Jess Mason and Simon Carley
20 Nov 2025
00:20:17
🧭 REBEL Rundown
📝Introduction
Welcome to this special edition of the REBEL Cast, where we unravel key highlights and educational insights from the IncrEMentuM Conference in Spain. This event is a cornerstone for advancing emergency medicine education, drawing esteemed speakers and participants from around the globe. As emergency medicine gains traction in Spain, this conference has become an essential platform for knowledge exchange and professional growth. Today, host Dr. Mark Ramzy shines a spotlight on three distinguished speakers: Dr. Jess Mason, Dr. Tarlan Hedayati, and Dr. Simon Carley, who shared their expertise and experiences at this transformative gathering last spring.
A new conference and a pivotal gathering for emergency medicine professionals worldwide, has become an essential platform for education, collaboration, and advocacy, especially in light of emergency medicine’s recent recognition as a specialty in Spain. The conference is praised for its outstanding production quality, engaging speakers, and its capacity to foster a global community of emergency care professionals.
🦪Pearls from Their IncrEMentuM 2025 Lectures
Think about alternative diagnoses that could be driving the patient’s atrial fibrillation
Maybe the atrial fibrillation is an adaptive response and slowing them down (whether chemically or electrically) may cause more harm than good
Get in the mental space before having to perform a High Acuity Low Occurrence (HALO) procedure and walk through each of the parts step by step
Like many things in critical care, a patient with a severe head injury requires you to do many little things very well (ie. reducing ICP increases by taking off the C-collar if able, positioning the patient appropriately, knowing when to use certain medications)
The QT interval is a vital part of ECG interpretation, reflecting the heart’s electrical recovery after each beat. When prolonged, it can set the stage for torsades de pointes. Understanding how to measure and correct the QT interval, identify high-risk medications, and act quickly when TdP occurs is essential for every clinician. This guide walks you through the physiology, interpretation, common causes, and emergency management of QTc prolongation to keep your patients safe.
🤔 Definition and Physiology
QT evaluation is a fundamental component of EKG analysis. The QT interval reflects the time from ventricular depolarization and contraction through ventricular repolarization and relaxation.
Clinically, QT prolongation increases the risk of torsades de pointes (TdP) – a form of polymorphic ventricular tachycardia (a non-perfusing rhythm) that is classically described as a pattern of “twisting points” or alternating amplitudes. This occurs when a premature ventricular contraction leads to an R on T phenomenon during the repolarization period.
The differential for QT prolongation is long and varied: congenital long QT, electrolyte disturbances (hypoK, hypoMg, hypoCa), hypothermia, myocardial ischemia, and increased intracranial pressure. Moreover, a whole host of xenobiotics can prolong the QT interval: methadone, anti-microbials, anti-emetics, anti-psychotics, and anti-dysrhythmics.
🧮 ECG Interpretation
The QT interval must be interpreted in conjunction with the patient’s heart rate. The QT interval with shorten in the context tachycardia and length in the context of bradycardia. In other words, tachycardia is protective when evaluating the patient with prolonged QT.
With that in mind, many EKG machines will calculate a corrected QT interval or QTc. The QTc is a standardized way to account for variations in heart rate so clinicians are able to compared QT intervals at different heart rates over time and thus calculate risk.
Generally, a QTc is considered prolonged if greater than 440ms in males or 460ms in females. Once the QTc > 500msec, the risk of TdP increases 2-3 fold.1
A variety of different correction formulas exist: Bazett, Fridericia, Hodges, Framingham, Rautaharju.
Manually, the QT interval should be measured from the beginning of the QRS complex to the end of the T wave – and thus should be measured in leads where all portions can be visualized, most frequently lead II or V5/V6. Ideally, the QT interval should be average over 3 or more beats.2 To determine the end of the T wave, a tangent line should be drawn through the maximum slope of the T wave – the point at which this line crosses the isoelectric line is the end of the T wave.3
💊 Commonly Used QTc Prolonging Medications
Methadone: particularly concerning because not only does it inherently prolong QT but also induces a bradycardia
Assess electrolytes (Mg, Ca, K) and replete as needed
Telemetry Monitoring
If patient happens to fall into TdP, initiate ACLS with immediate defibrillation and magnesium.
Withdrawal of offending agents.
📚 References
Drew BJ, Ackerman MJ, Funk M, Gibler WB, Kligfield P, Menon V, Philippides GJ, Roden DM, Zareba W. Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation. Circulation. 2010 Mar;121(8):1047-1060.
Postema PG and Wilde AAM. The measurement of the QT interval. Curr Cardiol Rev. 2014 Aug;10(3): 287-294.
https://litfl.com/qt-interval-ecg-library/
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
🩸 Tourniquets save lives and limbs: Apply immediately when you’ve got arterial bleeding.
📍 Placement matters: Position the tourniquet 5–6 cm proximal to the arterial bleed, or if you can’t identify the exact source, place it as high up on the limb as possible.
🔧 Windlass technique: The windlass provides only a small amount of extra pressure. Tighten the velcro first, then twist the windlass 1–2 turns to complete compression.
In this episode of the Rebel Core Content podcast, Swami provides crucial tips on using tourniquets. Highlighting the significance of these life and limb-saving devices, the discussion focuses on the optimal placement of tourniquets, emphasizing placing them 2-3 inches (5-6 cm) above the bleeding source and avoiding joints. Swami also advises on the correct way to tighten the tourniquet using the Velcro strap first, followed by minimal use of the windless. The importance of noting the application time to avoid prolonged arterial flow interruption is also discussed. The episode concludes with a reminder to visit the podcast’s website for more valuable content.
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
REBEL CAST – IncrEMentuM26 Speaker Spotlight : George Willis and Mark Ramzy
23 Oct 2025
00:17:53
🧭 REBEL Rundown
📝Introduction
In this exciting episode of REBEL Cast, host Dr. Mark Ramzy joins forces with renowned educator and speaker, Dr. George Willis. Broadcasting straight from the ACEP 25 in Salt Lake City, the duo talk about bringing together the international emergency medicine community, as they reflect on their experiences at the Increment Conference in Murcia, Spain, and preview the upcoming event this spring.
A new conference and a pivotal gathering for emergency medicine professionals worldwide, has become an essential platform for education, collaboration, and advocacy, especially in light of emergency medicine’s recent recognition as a specialty in Spain. The conference is praised for its outstanding production quality, engaging speakers, and its capacity to foster a global community of emergency care professionals.
🦪Pearls from George's IncrEMentuM 2025 Lectures:
Sodium Bicarbonate Use:
Appropriate Use: Focus on specific instances like metabolic acidosis with renal failure or severe metabolic cases with tox patients (e.g., salicylate or TCA overdose).
Emphasis on Patient-Centric Care: Treat the patient, not the number; avoid harmful overreliance on bicarb based solely on lab results
Diabetic Ketoacidosis (DKA):
Balanced Solutions: Preferenced over normal saline to prevent hyperchloremic acidosis.
Potassium Management: Oral potassium is effective and should be utilized, challenging the myth of impaired gastric absorption in DKA.
Squid Protocol: Usage of ultra-rapid insulin subcutaneously as an alternative to insulin drips in mild to moderate DKA cases.
We covered this topic before on REBEL EM. Check out the post here and the podcast here
Crashing Aortic Dissection:
Hypotension Insights: Do not attribute sudden hypotension solely to medication; prioritize ruling out tamponade or cardiogenic shock.
Ultrasound Utilization: Essential tool for detecting complications like tamponade or low EF due to myocardial infarction or aortic valve regurgitation.
Controlled Pericardial Drainage: Crucial technique to stabilize hemodynamics without increasing mortality, avoiding extensive fluid removal.
Here’s a helpful algorithmic infographic to reference for aortic dissection patients:
Not every patient needs calcium. Dont just give it prophylatically, only those with EKG changes should get it and get enough of it.
Give an appropriate dose of your other medications. That includes giving 10 units of insulin and 2 amps of dextrose 50. One when they get the 10 units of insulin and the other 30 minutes later
Patients may be dehydrated, dont give them furosemide or diuretics. Those patients need fluid to help perfuse their kidneys and eliminate potassium
Here’s the Algorithm George mentioned in the episode
Here’s a REBEL REVIEW breaking down the different electrolytes in each of the types of fluids:
🫣Teasers from George's IncrEMentuM 2026 Lectures:
Severe Thyroid Storm:
Diagnosis Reminder: Consider thyroid storm in febrile patients with altered mental status; order TSH tests.
Beta Blocker Administration: Use ultrasound to assess heart function before administering propranolol to prevent low output heart failure.
Medication Timing: Administer iodine after antithyroid drugs.
Refractory Hypoglycemia:
Early Use of Octreotide: Beneficial in sulfonylurea-induced cases; initiate treatment promptly for better efficacy.
Broadened Perspective: Consider other endocrine disorders as potential causes beyond typical measures.
Modern Management of SCAPE:
Bolus Dose Nitroglycerin: A recommended practice for quick patient stabilization and improved outcomes in SCAPE scenarios.
We covered this topic before on REBEL EM, see Dr. Marco Propersi’s post here
Ventilator management can feel overwhelming—there are so many knobs to turn, numbers to watch, and changes to make. But before adjusting any settings, it’s crucial to understand why the patient is in distress in the first place, because the right strategy depends on the underlying cause. In this episode, we’ll walk through three different cases to see how the approach changes depending on the problem at hand.
️ The 4 Main Ventilator Settings
Tidal Volume (Vt) 🌬️
Amount of air delivered with each breath
Typically set based on ideal body weight (6–8 mL/kg for lung protection)
Respiratory Rate (RR) ⏱️
Number of breaths delivered per minute
Adjusted to control minute ventilation and manage CO₂
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
👤 Show Notes
Priyanka Ramesh, MD
PGY 1 Internal Medicine Resident
Cape Fear Valley Internal Medicine Residency Program
Fayetteville NC
Aspiring Pulmonary Critical Care Fellow
🔎 Your Deep-Dive Starts Here
REBEL Core Cast – Pediatric Respiratory Emergencies: Beyond Viral Season
04 Dec 2025
🧭 REBEL Rundown
📝 Introduction
Welcome to the Rebel Core Content Blog, where we delve into crucial knowledge for emergency medicine. Today, we share insightful tips from PEM specialist Dr. Elise Perelman, shedding light on respiratory challenges in infants, toddlers, and young children during the viral season. Understanding that most cases involve typical viruses, we aim to equip you with diagnostic pearls to identify more serious pathologies.
Begin exams from the doorway. Observing patterns such as accessory muscle usage can reveal a patient’s respiratory effort. Specify whether the work of breathing occurs during inspiration, expiration, or both. Inspiratory work indicates difficulty getting air in, while expiratory work suggests trouble pushing air out. Silent tachypnea may point to other issues, like acidemia or pneumothorax.
🩺 Localizing Sounds for Accurate Diagnosis
Pearl #2: Localize the Sound
Breathing noises signal varied respiratory issues. Stridor, often heard on inspiration, results from obstructions above the thoracic inlet. Conversely, wheezing, generally linked to exhalation, indicates obstructions in the lower airways. Watch for signs like ‘silent chest’—a dangerous, severe obstruction, and distinguish grunting as a bodily mechanism to prevent alveolar collapse. Correctly identifying the sound assists in determining the appropriate intervention.
💉 Tailoring Treatment for Effective Results
Once a sound is localized, treatments vary. We explore Soder from nasal congestion, typically needing supportive care and suctioning. Stridor from conditions like croup is eased with interventions to reduce airway swelling, such as steroids or inhaled epinephrine. Conversely, wheezing in infants is often due to bronchiolitis—not bronchospasms—and over-treatment is to be avoided. Supportive measures including suction, hydration, and oxygen are preferred unless improvement warrants bronchodilators.
🌬️ Intervening with Severe Asthma
In severe cases of asthma or bronchiolitis, where standard at-home treatments fail, immediate adjunct therapies like intramuscular epinephrine become essential. Administering this quickly can alleviate obstruction when inhalants aren’t effective due to low air movement.
🦓 Navigating the Zebras of Respiratory Cases
When recognizing Zebras—uncommon cases overshadowed by routine diagnoses—remain vigilant for histories or presentations that don’t conform. Conditions like pneumonia, bacterial tracheitis, and even myocarditis may mimic more common issues.
📌 Conclusion
As attending physicians, our role extends beyond conventional treatment—it’s about discerning the atypical from the typical. Dr. Perelman urges continual reassessment, emphasizing reliance on observational skills as much as technological aid. Keeping keen on respiratory nuances ensures we catch those outlier cases, paving the way for adept medical care despite the overwhelming prevalence of viral infections.
Stay tuned for more pearls and insights in our future posts, as Dr. Perelman shares further strategies for effective pediatric emergency care. For more resources, continue exploring our faculty’s valuable contributions on our site. Until then, stay safe and perceptive in your practice.
Post Peer Reviewed By: Mark Ramzy, DO (X: @MRamzyDO), and Marco Propersi, DO (X: @Marco_Propersi)
👤 Guest
Elise Perlman MD
Pediatric Emergency Medicine
Assistant Professor, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell
Non-invasive ventilation (NIV) refers to respiratory support provided without endotracheal intubation. The most common modalities include continuous positive airway pressure (CPAP), bilevel positive airway pressure (BiPAP), and high-flow nasal cannula (HFNC). These therapies aim to improve oxygenation, reduce the work of breathing, and potentially prevent invasive mechanical ventilation.
💨 CPAP and BiPAP
CPAP delivers a single, continuous pressure during inspiration and expiration. This pressure (commonly 5–10 cm H₂O) helps recruit atelectatic alveoli, reduce shunt, and improve oxygenation. It is commonly used for conditions like pulmonary edema, obstructive sleep apnea, or mild hypoxemia without significant ventilatory failure.
Expiratory positive airway pressure (EPAP), maintains alveolar recruitment and improves oxygenation. The differential between IPAP and EPAP is critical for reducing hypercapnia in patients with COPD exacerbations or acute hypercapnic respiratory failure.
Indications
CPAP: hypoxemia without major ventilatory failure (e.g., cardiogenic pulmonary edema, atelectasis, OSA).
BiPAP: hypercapnia with increased work of breathing (e.g., COPD exacerbation, neuromuscular weakness, obesity hypoventilation).
A helpful way to conceptualize CPAP and BiPAP is through the hairdryer analogy. Imagine placing a hairdryer in your mouth:
🩺 Clinical Considerations
Masks can be uncomfortable, impair secretion clearance, and limit oral intake.
Some patients require sedation to tolerate NIV, but this carries risks in patients with unprotected airways.
NIV is thus a high-stakes intervention requiring close monitoring.
Common starting dose to understand titration, but start at the level appropriate for your patient: IPAP 10 cm H₂O / EPAP 5 cm H₂O (“10/5”) and are titrated:
Increase IPAP to improve tidal volume and CO₂ clearance.
Increase EPAP to recruit alveoli and improve oxygenation.
Both may be raised simultaneously if the patient is both hypoxemic and hypercapnic.
🚀 High-Flow Nasal Cannula (HFNC)
H: Heated & humidified – improves mucociliary clearance, prevents airway drying, and enhances tolerance. I: Inspiratory flow – high flow meets or exceeds patient demand, reducing respiratory rate and effort.
L: Lighter – generally more comfortable and less restrictive than mask-based NIV.
O: Oxygen dilution – minimizes entrainment of room air, delivering higher and more predictable FiO₂.
W: Washout – flushes anatomical dead space, reducing CO₂ rebreathing.
HFNC delivers heated, humidified oxygen at high flow rates (30–60 L/min) through wide-bore nasal prongs. A mnemonic, H-I-F-L-O-W, helps summarize its mechanisms:
Indications: Traditionally used for acute hypoxemic respiratory failure (e.g., pneumonia), HFNC is increasingly studied for hypercapnic failure as well, with trials suggesting non-inferiority to BiPAP in select populations.
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
Welcome to REBEL MIND—Mastering Internal Negativity during Difficulty. In this series, we turn the same critical lens REBEL EM uses for literature inward—into mindset, leadership, and psychological safety—so we can deliver better care outward to patients and teams.
In this episode and blog post, hosts Mark Ramzy and Kim Bambach (Assistant Professor of Emergency Medicine, The Ohio State University) explore a deceptively simple question: How accurately can we assess our own performance? The answer hinges on a classic cognitive bias that touches all of us in emergency medicine.
🧾 Paper
Kruger J, Dunning D. Unskilled and unaware of it: how difficulties in recognizing one’s own incompetence lead to inflated self-assessments. J Pers Soc Psychol. 1999 Dec;7 PMID: 10626367
Cognitive Question
How accurately can we assess our own performance?
💭 What is the Dunning-Kruger Effect?
The Dunning–Kruger Effect is a cognitive bias where:
Lower-skill individuals tend to overestimate their competence, and
Higher-skill individuals often underestimate theirs.
Translation for the busy clinician: early on the learning curve, confidence spikes (“Mount Stupid”) because we don’t yet see the complexity. As experience accrues, confidence dips (“Valley of Despair”) with growing awareness, then rises again—grounded in nuance and humility. Key insight: True expertise ≠ louder certainty; it’s often quieter, more curious, and more collaborative.
How It Applies to the Emergency Department
Procedures (e.g., central lines, TVP): Watching a 5-minute video creates “I got this” energy—until the wire won’t pass, the patient thrashes, or you hit carotid. Competence includes troubleshooting in context.
Skill Decay is Inevitable: If you haven’t done a chest tube or a TVP in months, you’re not as sharp as last time. Without deliberate refreshers, you drift below the safe-performance line.
Everyone’s a Novice Somewhere: New disease entities, evolving algorithms, new tools (POCUS, decision support) mean even attendings routinely re-enter novice zones.
Feedback Blind Spots: Lower performers can both overestimate their skills and resist feedback—while many high performers (particularly women, per discussed literature) undervalue their abilities.
Culture is Clinical: The ED demands decisive action amid uncertainty. Psychological safety + confident humility lets teams surface alternative diagnoses, challenge momentum, and correct course fast.
⏩Immediate Action Steps for Your Next Shift
Run a 60-second debrief on two cases What went well? What would I do differently next time? Write one improvement you’ll test today.
Play “What if the opposite were true?” Anchored on “lumbosacral strain”, Ask, What if fever/incontinence appears? How does that change my path?
Solicit 360° micro-feedback Ask a nurse, resident, and peer: “One thing I did well; one thing to improve.” Say “thank you,” not “but.”
Schedule a HALO refresher this week Pick one high-acuity, low-occurrence procedure (TVP, cric, thoracotomy). Do a 10-minute mental model + equipment walk-through; book sim time if available.
Adopt a pre-procedure pause If X goes wrong, I’ll do Y. Name two likely failure modes (e.g., “wire won’t advance,” “delirium/agitation”) and your first corrective step.
Language shift on shift Swap “I’m sure” → “I’m reasonably confident, here’s my plan B.” Invite input: “What am I missing?”
Conclusion
The Dunning–Kruger Effect isn’t a moral failing; it’s a predictable human pattern that every clinician rides—often multiple times per day in the ED. The antidote is metacognition: routine reflection, explicit debiasing, deliberate practice, and feedback within a psychologically safe culture.
🚨 Clinical Bottom Line
Competence is quiet and curious. The more we know, the more we recognize what we don’t—and the better we become at caring for patients and each other.
Further Reading
Dunning D, Kruger J. Unskilled and Unaware of It (1999). Classic paper introducing the effect.
Croskerry P. Cognitive forcing strategies in clinical decision-making.
Kahneman D. Thinking, Fast and Slow. Heuristics & biases in high-stakes decisions.
Ericsson KA. Peak: Secrets from the New Science of Expertise. Deliberate practice & skill acquisition.
Edmondson AC. The Fearless Organization. Psychological safety and learning culture in teams.
Meet the Authors
Mark Ramzy, DO
Co-Editor-in-Chief
Cardiothoracic Intensivist and EM Attending
RWJBH / Rutgers Health, Newark, NJ
Kim Bambach, MD
Podcasting Manager
Assistant Professor of Emergency Medicine
Ohio State University
REBEL Core Cast 147.0–Ventilators Part 5: Key Mechanical Ventilator Pressures & Definitions Made Simple
22 Dec 2025
00:14:20
🧭 REBEL Rundown
🗝️ Key Points
💨 Peak vs. Plateau Pressures: PIP reflects total airway resistance and compliance, while Pplat isolates alveolar compliance—elevations in both suggest decreased lung compliance (e.g., ARDS, pulmonary edema, pneumothorax).
🧱 PEEP Protects Alveoli: Maintains alveolar recruitment and prevents collapse; typical range 5–8 cmH₂O, but higher levels may benefit moderate–severe ARDS.
️ Driving Pressure (ΔP = Pplat − PEEP): Lower ΔP reduces atelectrauma and improves outcomes; optimize by adjusting PEEP thoughtfully.
💥 Prevent VILI: Keep Pplat < 30 cmH₂O, use low tidal volumes (6 mL/kg IBW), and monitor for barotrauma, volutrauma, atelectrauma, and biotrauma.
📚 Evidence-Based Practice: ARDSNet and subsequent trials confirm that lung-protective ventilation—low Vt, limited pressures, and individualized PEEP—improves survival in ARDS.
Ideal Body Weight: Based on height and sex, not actual weight.
Typical patient: Tidal Volume: 6–8 mL/kg IBW
ARDS: Tidal Volume: 4–6 mL/kg IBW
Atelectrauma:
Mechanism: Repeated opening/collapse of unstable alveoli.
Prevention: Optimize PEEP to keep alveoli open and reduce driving pressure.
Biotrauma:
Mechanism: Inflammatory cascade (↑ IL-6, TNF-α) from mechanical injury.
Effect: Can trigger systemic inflammation & multiorgan dysfunction.
Prevention: Minimize all other forms of VILI.
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
👤 Show Notes
Joel Rios Rodriguez, MD
PGY 3 Internal Medicine Resident
Cape Fear Valley Internal Medicine Residency Program
Fayetteville NC
Aspiring Pulmonary Critical Care Fellow
🔎 Your Deep-Dive Starts Here
REBEL MIND: The Power of Performance Coaching in Medicine
28 Jan 2026
00:30:35
🧭 REBEL Rundown
📌 Key Points
💪 Building Resilience: Rebel MIND, in partnership with Arena Labs, introduces a science-based performance coaching platform specifically tailored for healthcare professionals, focusing on stress management and burnout prevention. 🤝 Personal Insights: Jackie Penn shares her journey from exercise science to digital coaching, highlighting the importance of tailored coaching in high-pressure environments like healthcare. 🎯 Clinician-Centric Approach: Understanding unique challenges faced by ER doctors, the program provides practical tools for stress and transition management, improving both professional and personal life balance. 💻 Revolutionary Wearables: Utilizing wearables, the program offers objective feedback on recovery and health metrics, allowing personalization of strategies to enhance clinician well-being.
Welcome back to REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. In this episode, we’re excited to continue collaboration with Arena Labs, where host Dr. Marco Propersi interviews Jackie Pen, Heading of Performance Coaching at Arena Labs. Arena Labs is helping us measure healthcare performance through innovative programs designed to combat burnout and enhance personal wellness using data-driven strategies.
How do specific performance coaching strategies and tools assist healthcare professionals, particularly those in emergency medicine, in managing stress and preventing burnout effectively?
💭 Why This is Important
Burnout among healthcare workers is a growing concern, especially in such high-pressure environments as emergency and intensive care units. The collaboration with Arena Labs brings forth a vital focus on using data and coaching to build resilience among medical professionals.
🏥How This Applies to the Emergency Department or ICU?
In the chaotic and high-stakes environment of the ED/ICU, healthcare professionals are often required to make split-second decisions under pressure while managing emotional stress. This necessitates not just clinical acumen but also strong emotional resilience and stress management skills. Performance coaching provides the tools and frameworks to enhance these skills, offering strategies like the de-stress breath and transition protocols to help clinicians navigate between high-pressure situations efficiently. These tools are designed to not only improve their professional performance but also ensure they are emotionally present for their personal lives, ensuring a healthier work-life balance.
⏩ Things You Can Do on Your Next Shift
Practice the De-stress Breath: Before moving from one critical case to another, take a moment to take two inhales through the nose followed by an extended exhale, helping to reset your nervous system by activating your parasympathetic nervous system.
Implement a Transition Protocol: Choose a point in your journey home to mentally switch from clinician to family member, helping you to be more present outside of work.
Optimize Your Nutrition and Rest: Even small changes during your shift, like meals that promote easy digestion or quick physical activities, can make a significant difference in your energy levels.
Engage with Wearables: If possible, use wearables to monitor your physiological responses, helping tailor personalized strategies for your shifts
👀 Where to Learn More
Intrigued by the possibilities this partnership offers? You can explore more by visiting Arena Labs’ website here. Also, check out the comprehensive coaching program available, designed specifically for healthcare providers looking to enhance their well-being and performance.
🚨 Clinical Bottom Line
In an era where burnout is pervasive, our collaboration with Arena Labs offers a beacon of hope for healthcare workers. By leveraging cutting-edge data insights and practical coaching, this partnership aims to redefine healthcare wellness, fostering a sustainable, resilient workforce that’s equipped to navigate the pressures of modern medicine.
Join us in this journey towards enhanced well-being and workforce empowerment, ensuring that those who care for us are also cared for.
Meet the Authors
Marco Propersi
Co-Editor-in-Chief
Vassar Brothers Medical Center, Poughkeepsie, NY
Jackie Pen
Head of Performance Coaching
Arena Labs
Welcome back to REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. In this episode, hosted by Drs. Mark Ramzy and Marco Propersi, we’re excited to introduce a collaboration with Arena Labs. Arena Labs is helping us measure healthcare performance through innovative programs designed to combat burnout and enhance personal wellness using data-driven strategies.
Cognitive Question
What would it look like in emergency medicine and critical care to be set up with the same tools as elite teams and professional athletes when it comes to measuring performance and recovery? How would our patients benefit?
💭 Why This is Important
Burnout among healthcare workers is a growing concern, especially in such high-pressure environments as emergency and intensive care units. The collaboration with Arena Labs brings forth a vital focus on using data and coaching to build resilience among medical professionals.
🌟Be Brilliant at the Basics
Ask yourself — “What is it on your time off that gives you a deep sense of fulfillment?”
On your time off are you doing things that fill your bucket and add to your recovery?
What is Allostasis and Allostatic Load
Allostasis: Our body’s ability to adapt over time to stress. It’s relevant to the phase you are in during this particular season in your life.
Ex. You are a first year medical student freaking out about your very first exam. Over time as you do more exams, they are still stressful, but by now you have developed modified study habits to succeed and get used to the frequent exams
In the context of emergency medicine, you may be nervous or stressed about your first shift at a new hospital but overtime you learn the staff, the location of equipment, the acuity of that particular site, the patient population so over time you get used to the stress of a shift at that new hospital
Allostatic Load: The wear and tear on the body from chronic stress due to maladaptation or poor recovery methods.
This refers to the cumulative burden of chronic stress and life events. It involves the interaction of different physiological systems at varying degrees of activity.
Ex. You are an emergency medicine physician at a very busy, high acuity center and have never prioritized taking care of yourself on/during a shift. As a result, external factors add to not being able to fully recover when you get home or are off shift (ie. Admin work, teaching obligations, family/friends) and so you never fully recover before you have to go back on shift to the same stressors you just exposed yourself to. So the cycle continues
🏥How This Applies to the Emergency Department or ICU?
Healthcare workers in emergency departments (ED) and intensive care units (ICU) are often under enormous stress due to the nature of their work. Arena Labs’ program offers tailored solutions, helping ED and ICU staff manage their unique challenges through effective recovery techniques and performance tools. This approach caters specifically to the demanding schedules and the unpredictability inherent in these environments.
👀 Where to Learn More
Intrigued by the possibilities this partnership offers? You can explore more by visiting Arena Labs’ website here. Also, check out the comprehensive coaching program available, designed specifically for healthcare providers looking to enhance their well-being and performance.
🚨 Clinical Bottom Line
In an era where burnout is pervasive, our collaboration with Arena Labs offers a beacon of hope for healthcare workers. By leveraging cutting-edge data insights and practical coaching, this partnership aims to redefine healthcare wellness, fostering a sustainable, resilient workforce that’s equipped to navigate the pressures of modern medicine.
Join us in this journey towards enhanced well-being and workforce empowerment, ensuring that those who care for us are also cared for.
📚References
Guidi J, et al. Allostatic Load and Its Impact on Health: A Systematic Review. Psychother Psychosom. 2021; Epub 2020 Aug 14. PMID: 32799204
Frueh BC, et al. “Operator syndrome”: A unique constellation of medical and behavioral health-care needs of military special operation forces. Int J Psychiatry Med. Epub 2020 Feb 13. PMID: 32052666
Meet the Authors
Mark Ramzy, DO
Co-Editor-in-Chief
Cardiothoracic Intensivist and EM Attending
RWJBH / Rutgers Health, Newark, NJ
Marco Propersi
Co-Editor-in-Chief
Chair of Emergency Medicine at Vassar Brothers Medical Center, Poughkeepsie, NY
REBEL CAST – IncrEMentuM26 Speaker Spotlight : Drs. Sara Crager and Ryan Ernst
29 Jan 2026
00:36:38
🧭 REBEL Rundown
📝Introduction
Welcome to this special edition of the REBEL Cast, where we unravel key highlights and educational insights from the IncrEMentuM Conference in Spain. This event is a cornerstone for advancing emergency medicine education, drawing esteemed speakers and participants from around the globe. As emergency medicine gains traction in Spain, this conference has become an essential platform for knowledge exchange and professional growth. Today, host Dr. Mark Ramzy shines a spotlight on two phenomenal educators: Drs. Sara Crager and Ryan Ernst who shared their expertise and experiences at this transformative gathering last spring.
A new conference and a pivotal gathering for emergency medicine professionals worldwide, has become an essential platform for education, collaboration, and advocacy, especially in light of emergency medicine’s recent recognition as a specialty in Spain. The conference is praised for its outstanding production quality, engaging speakers, and its capacity to foster a global community of emergency care professionals.
️What's an Essential Question?
Essential questions are open-ended, thought-provoking, and intellectually engaging inquiries that inspire deeper exploration into topics. In the context of medical education, they challenge practitioners to think critically and reflect on their practice deeply. By focusing on essential questions, medical educators aim to inculcate a culture of continuous learning and curiosity, ensuring that medical professionals stay adaptable and insightful in their approach to patient care.
🎮Rapid Sequence (no not the intubating style...)
The Rapid Sequence game is an innovative tool that Sara and Ryan designed to enhance the learning experience for emergency medicine clinicians. It mimics real-life scenarios requiring rapid decision-making in high-pressure situations, such as those faced in emergency medical settings. This clinical case-based game aims to improve cognitive and procedural skills, allowing participants to hone their ability to respond effectively under pressure, thereby enhancing their real-world clinical performance.
An arboretum is a space that cultivates a wide variety of diverse, unique, and symbiotic growth. Arboretum provides a creative space to decrease barriers, open opportunities, and support the development of extraordinary teachers. The Arboretum Teaching Collective is a non-profit organization dedicated to supporting emergency medicine education in countries where it is a new or evolving specialty. Their aim to facilitate the development of expert teachers by reducing barriers, providing opportunities, and curating talent. Their goal is to create a community of educators around the globe who share a vision of bringing excellent, innovative emergency medicine teaching to where it is most needed. Their approach is driven by curiosity, humility, and sustainability.
🌱 Growth mindset transforms learning – Residents and students who believe skills can be developed are more open to feedback, more resilient after failure, and more engaged in practice.
🧠 Language matters in feedback – Simple reframes such as “You’re developing procedural skills” instead of “You’re not strong at procedures” encourage persistence and normalize the learning curve.
🤝 Mindset shapes team culture – Growth mindset leaders foster psychological safety, invite input, and create collaborative teams. Fixed mindset hierarchies, on the other hand, silence voices and can compromise patient care.
🔥 Growth mindset protects against burnout – By reframing mistakes as part of the process, clinicians reduce perfectionism and shame, bolstering resilience and wellness.
🔍 Practical steps start with self-talk – Add the word “yet” to limiting beliefs (“I’m not good at X…yet”) and shift feedback questions toward improvement (“What’s one thing I can do better next time?”).
🛠️ Embracing mistakes with a growth mindset – Leads to more effective feedback loops and improvement do this by building a culture of psychological safety is crucial for growth and reducing medical errors.
Welcome to this episode of REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine.
Mindset shapes everything we do in medicine—from how we teach and learn to how we show up for patients at the bedside. Drawing from Carol Dweck’s influential book Mindset, this episode of REBEL MIND explores the critical difference between a fixed mindset (believing abilities are innate and static) and a growth mindset (seeing skills as things that can be developed through effort and feedback).
We sat down with Dr. Kim Bambach, an emergency medicine physician and medical educator, and Dr. Frank Lodeserto, a dual-trained intensivist and internal medicine program director, to unpack how mindset influences medical education, bedside performance, and physician wellness. In this episode, we delve into how the mindset of clinicians can profoundly influence their performance, professional growth, and ultimately patient care
Cognitive Question
How does adopting a growth versus a fixed mindset influence clinical performance, medical education and patient outcomes?
🌱What is Growth vs Fixed Mindset?
In Carol Dweck’s research, two primary mindsets are highlighted:
Fixed mindset: Which sees intelligence and skills as static
In the medical field, adopting a fixed mindset might lead a clinician to avoid complex cases due to fear of failure.
Growth mindset: Which views abilities as improvable through dedication and effort.
In contrast, a growth mindset encourages embracing challenges as opportunities for learning and development.
🏥How This Applies to the Emergency Department or ICU?
In high-stakes environments like the ICU or the ED, the mindset adopted by healthcare providers can distinctly shape patient care and team dynamics.
A fixed mindset might lead to defensive behaviors and a reluctance to engage in challenging cases, potentially stunting personal and professional growth.
Conversely, a growth mindset not only fosters resilience and adaptability but also enhances team collaboration and patient outcomes by encouraging open communication, continuous learning, and acceptance of constructive feedback.
⏩Immediate Action Steps for Your Next Shift
**Monitor Self-Talk**: Notice your internal narrative when faced with challenges. Replace negative, fixed-mindset thoughts with growth-oriented ones like “Not yet” or “What can I learn from this?”
**Promote a Culture of Inquiry**: Challenge yourself and your team to engage in constructive questioning and explore alternative diagnoses or treatment plans to encourage a growth-centered environment.
**Model Vulnerability**: Share personal learning experiences and mistakes with colleagues to normalize the growth process and reduce the stigma of imperfection.
**Reframe Feedback**: Instead of broadly asking, “How did I do?” inquire, “What’s one thing I can improve on next time?” This shift helps maintain focus on growth rather than performance validation
Feedback is a whole another topic that we plan to have dedicated episodes and blog posts. This is an area where sometimes faculty struggle and often learners are asking for more/improved feedback.
💬Conclusion
Cultivating a growth mindset in medicine isn’t merely about staying positive; it’s about embracing continuous learning in the face of challenges. It involves creating supportive environments that encourage vulnerability, experimentation, and resilience. By adopting these practices, clinicians can improve not just personal competencies but also enhance patient care quality and safety.
🚨 Clinical Bottom Line
Clinicians who embrace a growth mindset not only enhance their skills but also contribute to a more dynamic, adaptive, and error-resilient healthcare environment. Remember, the best clinicians are those who never stop learning, not the ones who never make mistakes.
Episode Audio Edited By: Kim Bambach, MD and Mark Ramzy, DO (Twitter/X/IG: @MRamzyDO) Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_Propersi)
Further Reading and References
Claro S, Paunesku D, Dweck CS. Growth mindset tempers the effects of poverty on academic achievement. Proc Natl Acad Sci U S A. 2016 Aug 2. Epub 2016 Jul 18. PMID:27432947
Blackwell LS, et al. Implicit theories of intelligence predict achievement across an adolescent transition: a longitudinal study and an intervention. Child Dev. 2007 Feb; PMID: 17328703
Hopkins SR, et al. Trainee growth vs. fixed mindset in clinical learning environments: enhancing, hindering and goldilocks factors. BMC Med Educ. 2024 Oct 23 PMID: 39443909
Memari M, Gavinski K, Norman MK. Beware False Growth Mindset: Building Growth Mindset in Medical Education Is Essential but Complicated. Acad Med. 2024 Mar 1. Epub 2023 Aug 30. PMID: 37643577
Meet the Authors
Mark Ramzy, DO
Co-Editor-in-Chief
Cardiothoracic Intensivist and EM Attending
RWJBH / Rutgers Health, Newark, NJ
Kimberly Bambach, MD
Assistant Professor of Emergency Medicine
The Ohio State University Wexner Medical Center, Columbus, OH
Frank Lodeserto, MD
Internal Medicine Residency Program Director
Cape Fear Valley Medical Center, Fayetteville, NC
REBEL MIND – How to Sleep When the World Says You Can’t
04 Mar 2026
00:27:30
🧭 REBEL Rundown
🔑Key Points
Try the coffee nap! Where you combine caffeine and a 30-minute nap to then have that boost energy and alertness by the time it kicks in.
💤 Sleep isn’t optional—it’s crucial for memory, mood regulation, and physical recovery. It is fundamentally different from rest
❌ Replacing sleep with caffeine isn’t effective and can have negative health impacts. Make getting enough sleep a priority
🌞 Sunlight exposure is important for maintaining circadian rhythms and sleep quality. This applies even if you work as a nocturnist
💡 Creating a personalized sleep system enhances quality and consistency. It gives you back control of a schedule that you may feel like is out of your hands.
🧩 If you’ve tried these strategies and you’re still struggling, consider true sleep pathology (insomnia, shift work disorder, sleep apnea) and get help—this is not a “be tougher” problem.
🩺 Better sleep isn’t just about feeling good; it’s directly tied to error reduction, patient safety, and longevity in EM/ICU careers.
Welcome to this episode of REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine.
Today we are exploring the imperative topic of rest and why it’s not just about sleeping. The second of a two part series, hosted by Dr. Mark Ramzy with guests Dr. Maureen Aiad and Dr. Amil Badoolah, continue our discussion but this time on the multifaceted nature of sleep, how it serves as medicine and how we can use our tools deliberately to get more of it!
Cognitive Question
How would your clinical performance, patience with families, and long-term career sustainability change if you treated sleep as a non-negotiable clinical intervention rather than a flexible “nice-to-have”?
💤How is Sleep Different From Rest?
1. Rest reduces load; sleep repairs systems
We previously talked about the 7 types of rest and you can check that out here
Examples of physical rest include: pausing tasks, stepping away from the monitor, taking a walk, stretching, breathing, journaling, connecting with a colleague. This lightens your cognitive/emotional burden.
Sleep is fundamentally different in that it’s an active biologic process that helps:
Consolidates memory and learning (yes, including the tough cases from last night).
Regulates mood, impulse control, and emotional reactivity.
Supports immunity, metabolic health, and cardiovascular function.
Repairs tissue, replenishes neurotransmitters, and fine-tunes neural networks.
You can have “rested but underslept” days (you took breaks but got 4 hours in bed), and “slept but unrested” days (you got hours, but all junk sleep). Both matter, but they are not interchangeable.
2. Sleep architecture vs. “knocking out”
True restorative sleep cycles through NREM and REM in predictable patterns.
Alcohol, late caffeine, and fragmented nights may help you fall asleep faster but:
Suppress REM.
Shorten deep sleep.
Increase awakenings and light sleep.
The result: you technically slept, but your brain didn’t get the “software updates” it needed.
Biology isn’t built for your schedule
Circadian rhythms were designed for light-day / dark-night cycles, not:
10 pm–7 am ED shifts.
24-hour calls.
6 nights in a row followed by days.
Your body can adapt partially, but not instantly and not perfectly. That’s why:
You can feel “jet-lagged” even when you haven’t traveled.
Sleep before and after nights feels odd and fragile.
Recognizing that “this is biologically unnatural” is key: you’re not weak; you’re fighting physiology.
🏥How This Applies to the Emergency Department or ICU?
Performance & safety
Sleep deprivation:
Slows reaction time and increases error rate.
Impairs risk assessment and complex decision-making.
Drops your frustration tolerance with consultants, families, and staff.
In both emergency medicine and critical care, that translates into:
Anchoring on the wrong diagnosis.
Missing subtle clinical changes.
Snapping at a tech, nurse or resident and damaging team culture.
Chronic health for chronic shift work Long-term sleep disruption is associated with:
Hypertension, diabetes, obesity.
Depression, anxiety, burnout.
Arrhythmias (e.g., AFib) and increased stroke risk.
Possibly increased all-cause mortality.
You’re already in a high-stress, high-exposure specialty. Chronically poor sleep amplifies that risk profile and can end a career early—or make you miserable while you’re still in it.
Culture of “heroics” vs. health
Skipping sleep to pick up extra shifts, late meetings, or “just one more note” is often praised.
We rarely celebrate:
The attending who says “no” to a 2 pm meeting post-nights.
The resident who defends their blackout-curtains-and-earplugs routine.
🛏️Different Ways to Improve Your Sleep
Clarify your “sleep non-negotiables”
Decide how many hours you realistically need to function (e.g., 7–9 on off days, realistic blocks on nights).
Treat those hours as you would a procedure time—blocked, protected, and respected.
Use caffeine like a drug, not a reflex
Aim for ≤ 2 cups equivalent on most days.
Avoid caffeine within 4–6 hours of your planned sleep time (remember: it can hang around up to 12 hours).
Consider scheduling caffeine for:
Early in the shift for alertness.
Strategic “coffee naps” (see below), not late-night chugging.
Respect alcohol’s impact on sleep
Recognize that even small to moderate doses degrade sleep architecture.
Avoid using alcohol as a “sleep aid”—you’ll fall asleep faster but sleep worse.
If you do drink, separate it from bedtime and keep it modest.
Optimize food and fluid timing
Hydrate consistently on shift, but taper fluids ~4 hours before bed to reduce nocturnal bathroom trips.
Avoid heavy, spicy, or large meals within 2–3 hours of sleep to decrease reflux and discomfort.
Plan a light, balanced “pre-sleep” snack if going to bed hungry keeps you awake.
Move your body (but not right before bed)
Regular exercise improves sleep depth and latency.
Try to avoid intense workouts within 2 hours of bedtime.
On shift: micro-movement (stairs, brisk walks between pods, quick stretch sessions) can help alertness without wrecking sleep later.
Control light exposure
Maximize sunlight or bright light after waking (even if that’s 3–4 pm after a night).
Minimize bright light and screens before sleep:
Dim lights.
Use night mode/blue-light filters if you must scroll.
For daytime sleep:
Use blackout curtains, tinfoil, cardboard, or sleep masks.
Yes seriously use tinfoil if you have to, we talk about it on the podcast episode!
Aim for “I might be blind” darkness—so dark you can’t see your hand in front of your face.
Dial in your sleep environment
Cool room temperature (fan or AC if possible).
White noise or sound machine to mask household/traffic noise.
Earplugs and eye masks as needed.
Bed used primarily for sleep (and sex)—not for charting, doom scrolling, or email.
Strategic power naps
Keep naps ≤ 20–30 minutes to avoid sleep inertia.
Prefer early-afternoon or pre-night-shift naps.
Coffee nap strategy:
Drink a small coffee.
Immediately lie down for a 20–30 min nap.
Wake up as the caffeine kicks in, combining nap benefit + stimulant.
Thoughtful melatonin use
Remember melatonin is a hormone, not a vitamin gummy.
Lower doses often work as well as (or better than) large OTC doses.
Use it intentionally and intermittently, not as a crutch every night.
Over-reliance may reduce your own natural production and its effectiveness over time.
Build pre-sleep rituals
Repeated, calming habits signal your body it’s time to downshift:
Warm shower, gentle stretching, or yoga.
Guided breathing or body scan.
Brief journaling or “brain dump” of tasks to get them out of your head and onto paper.
Protect from pathologic patterns
If despite consistent effort you:
Snore heavily, stop breathing, or gasp in sleep.
Feel excessively sleepy driving home or at work.
Cannot fall asleep or stay asleep for weeks to months.
Consider evaluation for sleep apnea, insomnia, or shift-work sleep disorder with your physician or sleep specialist.
⏩Immediate Action Steps for Before/During/After Your Next Shift
1. **Before the Shift**:
Plan a 20–90 minute nap before your first night shift (many clinicians find 3–5 hours earlier in the day is ideal).
I treat ED and ICU shifts very differently. I always sleep 3-5 hours before my night shifts aiming for the full 5 (sometimes 6 or more) hours for my ED shifts because you always have to be “on”. Depending on the ICU I’m working in, I may have a bit more downtime so 3 to 5 hours is plenty.
Set a caffeine plan: decide in advance when your last dose will be (e.g., none after 2–3 am if sleeping at 8–9 am).
Tell your household, “This is my sleep block” and agree on a plan for kids, pets, deliveries, etc.
On my calendar, I completely block off time called “Pre-call sleep” so no meetings can be scheduled and then put my phone in airplane mode
2. **During the Shift**
Hydrate early; taper fluids in the last 3–4 hours of your shift
Eat something light but adequate; avoid “last-minute” heavy meals right before sign-out.
Build in micro-breaks and movement: one or two short walks, a few stretches, even a quick stair run if safe.
Get outside or near a window for a few minutes of light exposure if possible.
3. **After the Shift**
On the way home:
Use sunglasses to reduce bright morning light if you’re aiming for sleep soon.
Avoid “just checking” email or messages; shift into wind-down mode.
At home:
Do a brief, calming decompression (shower, light snack, 10–15 minutes of low-stimulation TV or reading).
Make your room cold, quiet, and dark (blackout curtains, tinfoil/cardboard, white noise, fan).
Put your phone on Do Not Disturb and physically place it away from the bed.
On my calendar, I completely block off time called “Post-call sleep” so again no meetings can be scheduled and then I personally don’t just put my phone on Do Not Disturb but rather in airplane mode and WIFI OFF
If you can’t sleep after ~20–30 minutes:
Get out of bed, do something calming in dim light (breathing, gentle stretching, journaling).
Return to bed when sleepy—this trains your brain to associate bed with sleep, not frustration.
Conclusion
Rest and sleep are both critical—but they’re not interchangeable. Rest helps you step out of the constant “on” of our jobs, while sleep is the biological intervention that restores your ability to show up safely and sustainably. Rest ≠ sleep. Rest reduces load; sleep repairs your brain and body. You need both, on purpose.
As EM and ICU clinicians, we’re trying to perform formula-one-level medicine with engines that often only see half their maintenance. You won’t fix shift work. You can build a sleep system that respects your biology, your schedule, and your life at home.
That system starts with valuing sleep, then prioritizing it, personalizing it, trusting the process when it’s imperfect, and actively protecting both your routine and your mindset.
🚨 Clinical Bottom Line
Sleep is medicine. Shift work is biologically unnatural. Struggling does not mean you’re weak; it means you’re human fighting physiology. Use your tools deliberately. Caffeine, naps, light, food, movement, melatonin, and environment can be leveraged—or can quietly sabotage you. Build and defend a personalized sleep routine. Communicate it, normalize it, and protect it from casual encroachment. You can’t control every trauma, code, or admission—but you can control how seriously you take your own recovery. Your patients, your team, and your future self all benefit when you do.
Further Reading
Espie CA. The ‘5 principles’ of good sleep health. J Sleep Res. 2022 Jun; PMID: 34676592
Solodar, J
“Sleep hygiene: Simple practices for better rest.” Harvard Health, 31 January 2025 Link is Here
Suni, E.
“Mastering Sleep Hygiene: Your Path to Quality Sleep.” Sleep Foundation, 7 July 2025, Link is Here
Meet the Authors
Mark Ramzy, DO
Co-Editor-in-Chief
Cardiothoracic Intensivist and EM Attending
RWJBH / Rutgers Health, Newark, NJ
Maureen Aiad, DO
Assistant Professor of Emergency Medicine
NYU Grossman Long Island School of Medicine, New York
Amil Badoolah, DO
Assistant Professor of Emergency Medicine
NYU Grossman Long Island School of Medicine, New York
The RSI Trial: Ketamine vs Etomidate in Rapid Sequence Intubation
08 Jan 2026
🧭 REBEL Rundown
📌 Key Points
💀 Mortality: No statistically significant difference in 28-day mortality between ketamine vs etomidate for intubation in critically ill patients, though there was a ~1% absolute difference favoring ketamine. 📉
🫀⚠️ Hemodynamics: Ketamine induction was associated with more cardiovascular collapse, mainly driven by new/increased vasopressor use (dose escalation or addition of a vasoactive agent). 💉⬆️
Etomidate or ketamine? The debate over the ideal agent for emergency rapid sequence intubation (RSI) has raged for years with no clear winner. Etomidate has been touted in the past for its rapid onset and minimal intrinsic effects on hemodynamics. However, the drug is well known as a transient adrenal suppressant though the impact of this suppression isn’t clear. Ketamine has risen in recent years as an alternative, due to its perceived hemodynamic stability, analgesic properties and absence of adrenal suppression. Additionally, recent data points towards improved mortality when ketamine was selected over etomidate (Kotani 2023). High quality randomized controlled trials are needed to further elucidate which agent should be selected in critically ill patients.
🧾 Paper
Casey JD et al. Ketamine or etomidate for tracheal intubation of critically ill adults. NEJM 2025. PMID: 41369227
Composite secondary outcome with non-equivalent endpoints (e.g., cardiac arrest vs vasopressor titration)
Ketamine dosing by actual body weight (vs ideal) → may have increased dose/exposure in some patients
🗣️ Discussion
The increase in cardiovascular collapse seen with ketamine was driven by the “new or increased vasopressor use” piece of the composite outcome not by the more clinically relevant severe hypotension (SBP < 65 mm Hg) or cardiac arrest.
The increase in CV collapse is a secondary outcome and hypothesis generating only
Care beyond induction agent isn’t clearly delineated and may have varied between groups
Reasons why there was more CV collapse in the ketamine group:
Patients in the etomidate group weremore likely to be on pressors or have pressor increases prior to induction agent administration
Ketamine has analgesic properties which may affect hemodynamics (etomidate does not have analgesic effects)
The standard ketamine dose of 2 mg/kg is higher than the induction dose used by most (1-1.5 mg/kg)
Ketamine dosing was based on actual body weight though ideal body weight dosing is more accepted. This may have resulted in unnecessarily large ketamine doses that may have had a greater effect on hemodynamics.
This is a study of patients with clinical equipoise
Patients who the clinician determined would clearly benefit from one agent or the other or in whom one agent or the other was contraindicated were excluded from the study.
This may add a selection bias to the results.
Clinicians were not blinded to the induction agent administered
The absence of blinding can introduce bias.
For instance, knowledge of the agent the patient was randomized to may result in different resuscitative treatment prior to intubation.
An induction agent nomorgram was provided to allow clinicians to choose their induction dose depending on patient stability.
A 5% difference in mortality may be overly ambitious. As Josh Farkas points out in his post on this article, PCI for STEMI only has a 3% absolute difference in mortality versus standard care.
The 1% absolute difference in mortality while not statistically significant would be clinically significant if it was real.
The study would have to be much larger to show a statistically significant 1% difference.
About 2% of patients in each group received additional medications during induction (propofol, benzodiazepines, opiates). It is unclear why these agents were selected in specific cases and how they may have affected the outcomes in question.
📘 Author's Conclusion
“Among critically ill adults undergoing tracheal intubation, the use of ketamine to induce anesthesia did not result in a significantly lower incidence of in-hospital death by day 28 than etomidate.“
💬 Our Conclusion
In this well done RCT, induction with ketamine did not result in a lower 28-day mortality when compared to induction with etomidate in critically ill adults. The secondary outcome of an increase in cardiovascular collapse is interesting and should be studied more in the future.
🚨 Clinical Bottom Line
This data should not drive clinicians to abandon the use of ketamine in RSI. To the contrary, the study leaves open the possibility of a clinically meaningful difference in mortality favoring ketamine that may be borne out in a larger study. However, etomidate can be considered as a first-line option for RSI and may be the superior drug in patients at high-risk for cardiovascular decompensation.
Post Peer Reviewed By: Post Peer Reviewed By: Mark Ramzy, DO (X: @MRamzyDO) and Marco Propersi, DO
📚 References
Kotani Y et al. Etomidate as an induction agent for endotracheal intubation in critically ill patients: a meta-analysis of randomized trials J Crit Care 2023;77:154317. PMID: 37127020
REBEL MIND: Applying Performance Science In and Out of the Emergency Department
18 Feb 2026
00:34:03
🧭 REBEL Rundown
📌 Key Points
🔍 Understanding the Why: The significance of understanding underlying causes, beyond initial diagnoses, in both sports and emergency medicine is explored. ⏱️ Recovery Focus: Emphasizing the importance of recovery time and small daily choices in optimizing performance for both athletes and emergency physicians. 📊 Data-Driven Insights: The Arena Labs approach uses personalized data, leveraging wearable technology and expert coaching to tackle burnout and enhance well-being. 🤝 Personalization and Partnership: Arena Labs’ collaboration with emergency clinicians sheds light on personalized performance solutions rooted in scientific evidence.
Welcome back to REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. In this episode, we’re excited to continue collaboration with Arena Labs, where host Dr. Mark Ramzy interviews Allyn Abadie, Arena Labs’ Principal Scientist on how we can apply performance science in and out of the emergency department. Arena Labs is helping us measure healthcare performance through innovative programs designed to combat burnout and enhance personal wellness using data-driven strategies.
How can emergency department clinicians utilize techniques inspired by athletic performance to better manage stress, prevent burnout, and optimize recovery?
💭 Why This is Important
Burnout among healthcare workers is a growing concern, especially in such high-pressure environments as emergency and intensive care units. The collaboration with Arena Labs brings forth a vital focus on using data and coaching to build resilience among medical professionals.
🏥How This Applies to the Emergency Department or ICU?
Emergency medicine, akin to high-performance sports, demands intense energy and quick decision-making under pressure, often leading to stress and burnout. By applying principles from athletic recovery and personalized data tracking, clinicians can moderate their performance intensity, enhance their recovery even in short breaks, and prevent long-term burnout. This approach allows emergency physicians to maintain endurance and clarity, improving patient care and team dynamics.
⏩ Things You Can Do on Your Next Shift
Measure and Reflect: Start tracking your vital health metrics like heart rate with wearable sensors. Reflect on how daily activities impact these measurements to identify stress patterns.
Implement Quick Recovery Techniques: Use short, actionable exercises such as deep breathing or the de-stress breath method between patient encounters to moderate stress levels.
Invest in Self-Care: Dedicate brief time slots for essential self-care activities like hydration or quick reflection journaling, aiming to enhance mental resilience throughout your shift.
Utilize Coaching Tools: Engage with personalized coaching apps or resources that offer science-backed recovery strategies tailored to your personal and professional needs.
👀 Where to Learn More
Intrigued by the possibilities this partnership offers? You can explore more by visiting Arena Labs’ website here. Also, check out the comprehensive coaching program available, designed specifically for healthcare providers looking to enhance their well-being and performance.
🚨 Clinical Bottom Line
In an era where burnout is pervasive, our collaboration with Arena Labs offers a beacon of hope for healthcare workers. By leveraging cutting-edge data insights and practical coaching, this partnership aims to redefine healthcare wellness, fostering a sustainable, resilient workforce that’s equipped to navigate the pressures of modern medicine.
Join us in this journey towards enhanced well-being and workforce empowerment, ensuring that those who care for us are also cared for.
Meet the Authors
Mark Ramzy, DO
Co-Editor-in-Chief
RWJBH / Rutgers Health, Newark NJ
Today we’re tackling one of the most important (and most under-taught) skills in emergency medicine: how to call a consult in the ED and what to do when a consultant pushes back.
To call a consult in the ED, start with a brief introduction, lead with the outcome you need (“the ask”), give a focused decision-relevant summary, and close the loop with timeline and next steps. If the consultant resists, clarify the “why,” restate the ask, offer alternatives, and escalate when patient safety or disposition is at risk.
After two decades in emergency medicine and countless consult calls, here’s a simple framework—plus copy/paste scripts—to make your consults faster, clearer, and easier to say “yes” to.
🤔 Why Consult Skills Matter in Emergency Medicine
Consults aren’t a formality—they’re a patient-care intervention. Strong consult communication:
Reduces delays in time-sensitive care
Improves ED throughput and disposition
Decreases conflict and miscommunication
Clarifies ownership and next steps
Protects the patient (and the team) when plans are unclear
🪜 The 4-Step ED Consult Framework (Introduction → Ask → Summary → Close the Loop)
Most consult friction comes from one of two problems: unclear expectations or excessive noise. This four-step structure solves both.
1) Introduce yourself and your role
A simple intro sets a professional tone and removes ambiguity.
Script:
“Hey, this is Swami, one of the ED attendings. I’m calling for an ortho consult.”
2) Lead with the outcome (the ask)
Don’t bury the lede. The consultant wants to know what you need—immediately.
Script:
“I’m calling about a patient with a suspected septic knee. I need you to evaluate for operative management.”
3) Give a focused, decision-relevant summary
Your summary should answer:
Why this is your service’s problem
What’s already been done
What I’m worried about / what decision is needed now
Script:
“43-year-old man with no major PMH, 3 days of knee pain and swelling. XR negative. Febrile. Aspiration yielded purulent fluid—cultures sent. We started antibiotics after the tap. He’s hemodynamically stable.”
High-yield pearl: Add quick “stability anchors” when relevant:
“Airway stable, pain controlled.”
“Neurovascularly intact.”
“No signs of compartment syndrome.”
“No hypotension or escalating oxygen requirement.”
4) Close the loop (timeline + next steps)
This prevents the consult from floating in limbo and protects patient flow.
Script:
“When do you expect to see the patient, and do you want anything done before you arrive—NPO, repeat labs, additional imaging?”
📝 ED Consult Script
General ED Consult Script
“Hi, this is Dr. ___ in the ED. I’m calling for a ___ consult. The reason is ___. Briefly: ___ year-old with ___. We’ve done ___ and started ___. I’m concerned about ___. Can you see them today, and what’s your preferred next step?”
Septic joint / Ortho Example
“Hi, this is Swami in the ED. I need an ortho consult for suspected septic arthritis. 43-year-old with 3 days of atraumatic knee swelling and fever. XR negative. Tap produced purulent fluid—cultures sent. Antibiotics started after aspiration. Can you evaluate for operative management, and when can you see the patient?”
Neurology example (time-sensitive)
“Hi, this is Dr. ___ in the ED. I need neurology for suspected acute stroke. Last known well ___. NIHSS ___. CT/CTA completed (or pending). I’m calling to discuss candidacy for thrombolysis/thrombectomy and next steps. When can you evaluate and what additional workup do you want now?”
⛓️💥 Common ED Consult Mistakes (and Fixes)
Mistake: Long story before the ask
Fix: Lead with the outcome in the first sentence
Mistake: Unfiltered data dump
Fix: Provide only decision-relevant details
Mistake: No timeline
Fix: Ask explicitly when they’ll see the patient and what they need first
Mistake: Implicit “ownership”
Fix: Clarify who is admitting, who is following, and what happens if the patient worsens
✋ What to Do When a Consultant Pushes Back
Even a perfect consult can meet resistance. Your job is to stay calm, keep it professional, and protect the patient.
1) Ask “why?”
Don’t argue first—diagnose the refusal.
Script:
“Help me understand your concern about seeing this patient.”
Many refusals are based on misunderstanding: wrong service, missing key detail, or incorrect assumption about stability.
2) Restate the consult in one sentence, then offer options
If the conversation starts spiraling, reset it.
Script:
“To be clear, I’m concerned this is septic arthritis and needs ortho evaluation. If you don’t feel you’re the right service, who should be—rheum, medicine, or another surgical team?”
This keeps you collaborative while preventing dead ends.
3) Humanize the decision (use sparingly)
This is a “high-voltage” tool. Use it when stakes are high and you’ve already clarified the medical facts.
Script:
“I’m worried we’re missing something time-sensitive. If this were your family member, what would you want us to do next?”
Use it to re-anchor to patient risk—not as a guilt tactic.
⚡️When and How to Escalate a Consult
Escalation isn’t personal—it’s a safety mechanism when there’s an impasse that threatens timely care.
When to escalate
Time-sensitive condition is delayed (e.g., septic joint, cord compression, testicular torsion, GI bleed with instability)
No clear disposition plan despite reasonable ED evaluation
Patient safety or deterioration risk is increasing in the ED
How to escalate (lowest to highest intensity)
Ask for the consultant’s attending (if speaking to a resident)
Call the on-call attending directly
Involve ED leadership/medical director
Escalate to service chief/department chair (rare, but real)
Hospital supervisor/admin escalation for immediate operational impasse
Script:
“We’re at an impasse and the patient needs a decision. I’m escalating to clarify ownership and ensure timely care.”
️ Documentation Tips for Consult Refusals
Documentation should be factual and patient-centered, not punitive.
Include:
Your clinical concern and why the consult is needed
Who you spoke with (name/role)
Their stated reason for refusal or delay
Alternatives discussed
Escalation steps taken and final plan
👉 FAQ: Emergency Medicine Consults
What is the best way to call a consult in the ED?
Introduce yourself, lead with the specific ask, summarize only decision-relevant details, and close the loop with a clear plan and timeline.
What should I say when a consultant refuses to see a patient?
Ask why, clarify misunderstandings, restate your concern and the ask, and request an alternative plan or appropriate service.
When should I escalate a consult?
Escalate when an impasse delays time-sensitive care, threatens patient safety, or prevents appropriate disposition.
How do I document a refused consult?
Document the clinical concern, who you spoke with, their stated reason, alternatives discussed, and escalation steps taken.
🏁 Conclusion
Mastering emergency medicine consults makes you faster, safer, and easier to work with. The goal isn’t to “win” a consult call—it’s to get the patient the right care, with clear ownership and a shared plan.
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)
REBEL CAST – RENOVATE Trial: HFNC vs BPAP in Acute Respiratory Failure
05 Feb 2026
00:19:11
🧭 REBEL Rundown
📌 Key Points
💨 HFNC met criteria for non-inferiority to BPAP for preventing intubation or death within 7 days in four of the five ARF subgroups.
🧪 Bayesian dynamic borrowing increased power across subgroups but created variable certainty, especially in smaller groups such as COPD.
🫁 The immunocompromised hypoxemia subgroup did not meet non-inferiority, leading to early trial stopping for futility.
️ Rescue BPAP use, subgroup-specific exclusion criteria, and non-standardized BPAP delivery are important contextual factors that influence how subgroup results should be interpreted.
Bilevel Positive Airway Pressure (BPAP) has long been a foundational modality in the management of acute respiratory failure (ARF), particularly in COPD exacerbations and cardiogenic pulmonary edema, where it can rapidly reduce work of breathing and improve gas exchange. It remains a core tool in our respiratory support arsenal.
High-flow nasal cannula (HFNC), however, has expanded what we can offer patients by delivering many of the same physiologic benefits through a far more comfortable interface. With high flows, modest PEEP, and effective dead-space washout, HFNC can improve oxygenation and decrease work of breathing while preserving the ability to talk, cough, eat, and interact with staff and family. This combination of physiologic support and tolerability makes HFNC especially attractive in patients where comfort, anxiety, or cardiovascular stability are key considerations, and in settings where prolonged noninvasive support may be needed. Rather than competing with BPAP, HFNC broadens our options in ARF and allows us to better match the modality to the patient and their underlying disease process.
The RENOVATE trial set out to answer a high-impact question across five distinct etiologic groups: Is HFNC non-inferior to BPAP (NIV) for preventing intubation or death in acute respiratory failure?
🧾 Paper
Azoulay É, et al. High-Flow Nasal Oxygen vs Noninvasive Ventilation in Patients With Acute Respiratory Failure: The RENOVATE Randomized Clinical Trial. JAMA. 2025 PMID: 39657981
Is HFNC non-inferior to BPAP for rate of endotracheal intubation or death at 7 days in patients with acute respiratory failure due to a variety of causes?
STUDY DESIGN
Multicenter, randomized non-inferiority trial
33 Brazilian hospitals
Nov 2019 – Nov 2023
Adaptive Bayesian hierarchical modeling with dynamic borrowing
Hypercapnic ARF due to neuromuscular/chest wall disease
Palliative care or DNI
Chronic pulmonary disease other than COPD
6 hours BPAP prior to randomization (hypoxemic non-immunocompromised, immunocompromised, and COPD groups)
Prior BPAP use in ACPE
INTERVENTION & COMPARATOR
Intervention (HFNC Group):
Flow:
COPD: Start 30 L/min
All others: Start 45 L/min
Titrated up to 60 L/min or highest tolerated
FiO₂:
Start at 50% and titrate to maintain target SpO₂
SpO₂ Targets:
COPD: 88–92%
Others: 92–98%
Rescue Therapy (COPD & ACPE only):
If failing maximal HFNC → 1 hour of rescue BPAP
If failing BPAP → immediate intubation
Weaning
Begin ≥24 hrs once RR <25 and no distress
Gradual reductions in FiO₂/flow
Considered weaned at:
FiO₂ <30% and Flow <25–30 L/min
Comparator (BPAP Group):
Via ICU ventilator or BiLevel device
Initial Settings:
COPD: IPAP 12–16 / EPAP 4
Others: IPAP 12–14 / EPAP 8
Max settings: IPAP 20 / EPAP 12
SpO₂ Targets:
COPD: 88–92%
Others: 92–98%
Titration: Not standardized
Sedation: Not standardized
Weaning:
After 24 hrs
At clinician discretion
Considered weaned at FiO₂ 30% and EPAP/PS <6
OUTCOMES
Primary Outcome:
Endotracheal intubation or death within 7 days.
Secondary Outcomes:
28-day mortality
90-day mortality
Mechanical ventilation free days at 28 days
ICU-free days at 28 days
Tertiary Outcomes:
Hospital and ICU length of stay within 90 days
Vasopressor-free days within 28 days
New DNI orders within 7 days
Patient comfort
📈 Results:
💥 Critical Results
MOR: Median Odds Ratio MHR: Median Hazard Ratio
💪 Strengths
Broad, multicenter design: Large multicenter randomized trial comparing HFNC vs BPAP across several etiologies of acute respiratory failure in ED and ICU settings.
Etiology-based and COVID-specific subgroups: Patients were stratified into prespecified clinical subgroups (COPD with acidosis, ACPE, immunocompromised hypoxemia, non-immunocompromised hypoxemia), and COVID-19 was later added and analyzed as a separate subgroup rather than being combined with the original ARF categories.
Bayesian hierarchical model with dynamic borrowing: The primary analysis used a Bayesian hierarchical framework that allowed information to be borrowed across subgroups when treatment effects were similar and reduced borrowing when subgroups differed.
Prespecified non-inferiority and futility rules: Each subgroup had predefined non-inferiority and futility boundaries, and enrollment in the immunocompromised subgroup was stopped early after crossing a futility threshold.
Standardized BPAP delivery system: BPAP was delivered using a single BPAP system/interface across participating centers.
Single healthcare system and population: All sites were within one national healthcare system, with broadly similar clinician training, practice patterns, and patient populations for that country.
Current practice relevance: The trial addresses a post-COVID era question in which HFNC is widely used, providing comparative HFNC vs BPAP data across multiple ARF etiologies in a pragmatic ED/ICU population.
⚠️ Limitations
Small subgroup sizes: The COPD (35 vs 42) and immunocompromised (28 vs 22) subgroups included relatively few patients compared with the other etiologic groups.
Dependence on borrowing for COPD estimates: COPD treatment-effect estimates in the primary model were heavily influenced by borrowing from other subgroups, and no-borrowing sensitivity analyses showed wider intervals.
Pre-randomization BPAP and exclusion criteria: COPD patients could receive up to 6 hours of BPAP before randomization, and ACPE patients judged to require immediate BPAP were excluded from enrollment.
Rescue BPAP in the HFNC arm: Patients assigned to HFNC could receive rescue BPAP; BPAP settings were not standardized, and detailed reporting of rescue BPAP management and outcomes (including number of episodes) was limited.
Non-standardized weaning strategies: Weaning protocols for HFNC and BPAP were not tightly protocolized or aligned, and HFNC weaning permitted flows down to 25–30 L/min.
Single-country setting: All participating centers were located in one country.
🛣️Side Tangent on Bayesian Adaptive Model
Prior to our deep dive into the discussion, lets first explain the importance of the statistical method used in the RENOVATE trial, the Bayesian Adaptive Model.
A Bayesian Adaptive Model is a trial design that keeps updating its understanding of which treatment works better as new data are collected, and it allows the trial to change course in real time based on those results.
Now imagine you’re comparing two pairs of running shoes. Your goal is to see which one helps runners finish faster, so you measure their race times. Runners try Shoe A or Shoe B, and as the results come in, you analyze the times.
If runners wearing Shoe A and Shoe B are finishing within a few seconds of each other, you would conclude the shoes perform similarly, meaning they are non-inferior.
If runners wearing one shoe are consistently finishing much faster, you can say that shoe is superior, and the trial may stop early because you’ve clearly found the better option.
If one shoe repeatedly produces slower times compared to the standard, you may stop the trial for inferiority, because continuing would not benefit runners.
This approach allows the study to learn as it goes and make decisions based on accumulating evidence rather than waiting until the very end.
The Bayesian adaptive model also utilizes a statistical tool known as dynamic borrowing. Dynamic borrowing is a statistical method that allows data from related groups to be shared or pooled when their outcomes appear similar, but automatically reduces or stops that sharing when the groups differ, ensuring accuracy and preventing misleading conclusions.
For example, if Shoes A and B are producing similar race times (non-inferior), the coach can combine or “borrow” data from both groups and average their times, which increases statistical precision.
However, if one shoe becomes clearly superior or clearly inferior, dynamic borrowing stops, because the race times are no longer comparable and averaging them would distort the results.
In this running-shoe analogy, the RENOVATE trial was essentially comparing Shoe A (BPAP) and Shoe B (HFNC) to see which helped patients “run faster,” or achieve better clinical outcomes in 5 different pathologies.
In this running-shoe analogy, the RENOVATE trial was essentially comparing Shoe A (BPAP) and Shoe B (HFNC) to see which helped patients “run faster,” or achieve better clinical outcomes across five different respiratory pathologies. As results accumulated, the Bayesian adaptive model used dynamic borrowing and could combine results when both devices performed similarly, but stopped pooling data if one clearly helped patients more or less.
🗣️ Discussion
What RENOVATE asked and what it found: The RENOVATE trial is the first multicenter randomized study to directly evaluate whether HFNC is non-inferior to BPAP for preventing intubation or death across multiple etiologies of acute respiratory failure. Overall, HFNC met non-inferiority criteria in four of the five predefined subgroups, with much of the statistical strength coming from the Bayesian borrowing structure. However, several design and analytic choices limit how confident we can be in these findings across all groups.
Bayesian model, borrowing, and small numbers: The Bayesian hierarchical model improves precision by “sharing” information between subgroups when outcomes look similar, but this does not fully fix the problem of small sample sizes. In subgroups with low numbers, the model still has less power and more uncertainty, and the apparent stability of the estimates is heavily influenced by the borrowing framework rather than large, subgroup-specific datasets.
COPD and ACPE – who actually got randomized: In both COPD and ACPE, enrollment decisions likely removed many of the sickest patients from randomization. COPD patients could be stabilized for up to six hours on BPAP before being randomized, and ACPE patients who clearly required immediate BPAP were excluded altogether. Because the trial never reported how many patients were treated or excluded in the ACPE group, we do not have a clear picture of how sick the randomized patients really were.
Rescue BPAP in the HFNC arm: Rescue therapy adds another layer of ambiguity. Nearly a quarter of COPD patients in the HFNC arm required rescue BPAP, yet the study did not describe the BPAP pressure settings used, how many times rescue could be repeated, or whether these patients ultimately improved, failed, or required intubation. This is particularly important because the primary endpoint is intubation within seven days, and we do not know how much non-standardized BPAP rescue influenced that outcome in patients initially assigned to HFNC.
Different weaning strategies between HFNC and BPAP: Weaning practices also differed meaningfully between HFNC and BPAP. HFNC patients could be considered “weaned” while still receiving flows that are well above physiologic baseline (25–30 L/min), whereas BPAP weaning was left largely to clinician judgment without tightly aligned criteria. This lack of standardized weaning makes it difficult to directly compare the two modalities in terms of duration of support and when a treatment should be considered to have “failed.”
Value of multiple etiologic subgroups: Rather than asking a single global question of whether HFNC works for all causes of acute respiratory failure, the trial was designed with multiple etiologic subgroups. This allows us to compare HFNC and BPAP within distinct pathologies commonly seen in the ED and ICU. In practice, this design helps us look across each subgroup and think about which modality—HFNC or BPAP—may be most appropriate for a given underlying diagnosis.
Immunocompromised subgroup had early futility and inadequate support: In immunocompromised patients, HFNC clearly underperformed BPAP on early outcomes. Intubation rates were higher with HFNC (50.0% vs 31.8%), and early deaths were also higher (17.9% vs 13.6%), leading this subgroup to cross a prespecified futility boundary and stopping further enrollment. By 28 and 90 days, mortality was similar between HFNC and BPAP in this cohort, suggesting that HFNC alone did not provide enough up-front respiratory support for this high-risk group rather than causing a lasting difference in long-term outcomes.
Why COVID was separated from the original ARF subgroups: Early in the COVID-19 pandemic, clinicians were making treatment decisions in real time without established guidelines or a solid understanding of disease trajectory. Many COVID patients behaved clinically like an immunocompromised or atypical ARF cohort. If COVID patients had been left inside the original ARF subgroups, they could have distorted those results and biased the trial toward an apparent signal of HFNC futility. By separating COVID into its own subgroup, the investigators preserved the integrity of the non-COVID etiologic groups while still including COVID patients in the overall study population. This approach allowed for cleaner estimates within each subgroup and more appropriate borrowing across groups without letting a large, atypical population dominate the model.
Standardized BPAP delivery as a control: Using one BPAP delivery method for all patients created a built-in control on the BPAP side of the trial. The interface and mode were standardized, so the main difference between patients was their underlying disease and assignment to HFNC vs BPAP. This consistency across BPAP subgroups reduces “noise” in how BPAP was delivered and makes it easier to attribute differences in outcomes to the disease process and modality choice rather than variation in the BPAP setup itself.
Single-country setting and external validity: Running the entire study in one country means clinicians share similar training, practice patterns, and system-level resources, which helps keep management more consistent across subgroups and centers. The trade-off is external validity: what is considered “standard” care in this health system may look very different in other countries, particularly in resource-limited settings, so these findings may not translate perfectly to other practice environments.
📘 Author's Conclusion
“HFNC met criteria for noninferiority to NIV for the primary outcome in 4 of the 5 patient groups. Small sample sizes and sensitivity to the analysis model suggest further study is needed in COPD, immunocompromised patients, and ACPE.”
💬 Our Conclusion
HFNC appears to perform comparably to BPAP in non-immunocompromised hypoxemic and COVID-positive patients. However, the data in COPD, ACPE, and immunocompromised patients are limited and statistically fragile—heavily influenced by small numbers and modeling assumptions—so BPAP should remain the preferred modality when ventilatory support is clearly required and may offer more reliable benefit in these groups.
🚨 Clinical Bottom Line
HFNC is a great option for many patients with acute respiratory failure, but some patients clearly need BPAP up front. In patients with obvious BPAP-responsive physiology—such as COPD with acidosis, ACPE with increased work of breathing, or frank hypercapnia—or in those who are crashing at the door, BPAP remains the first-line choice. In more stable patients, especially those without a strong indication for BPAP, with limited hypercapnia, or where comfort and longer-term tolerance matter, HFNC is a reasonable first-line option for extra respiratory support while you closely watch their trajectory and stay ready to escalate.
📚 References
RENOVATE Investigators and BRICNet Authors. High-flow nasal oxygen vs noninvasive ventilation in patients with acute respiratory failure: The RENOVATE randomized clinical trial. JAMA. 2025;333(10):875–890. PMID: 39657981
Tempo G, Grieco DL. Article review: The RENOVATE randomised clinical trial. European Society of Intensive Care Medicine (ESICM) Article Review. 2025. Available here
Roca O, Messika J, Caralt B, et al. Predicting success of high-flow nasal cannula in pneumonia patients with hypoxemic respiratory failure: The utility of the ROX index. J Crit Care. 2016;35:200–205. PMID: 27481760
Rochwerg B, Brochard L, Elliott MW, et al. Official ERS/ATS clinical practice guidelines: Noninvasive ventilation for acute respiratory failure. Eur Respir J. 2017;50(2):1602426. PMID: 28860265
Post Peer Reviewed By: Post Peer Reviewed By: Mark Ramzy, DO (X: @MRamzyDO), Frank Lodeserto, MD and Anand Swaminathan, MD (X: @EMSwami)
👤 Guest Contributor
Jonathan Bradshaw, DO Emergency Medicine Resident (PGY-3) Cape Fear Valley Medical Center Fayetteville, NC
Welcome to this episode of REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine.
Today we are exploring the imperative topic of rest and why it’s not just about sleeping. The first of a two part series, hosted by Dr. Mark Ramzy with guests Dr. Maureen Aiad and Dr. Amil Badoolah, our discussion sheds light on the multifaceted nature of rest, especially in the demanding field of emergency medicine. If you’re a clinician striving to perform at your best under pressure, this episode offers valuable insights into achieving the rest you deserve.
Cognitive Question
How do healthcare professionals in high-stress environments distinguish between rest and sleep, and how can they effectively incorporate various types of rest into their routines to manage stress and improve performance?
💤How is Rest Different From Sleep?
Sleep is biological. It’s essential—but it’s only one form of recovery.
Rest, on the other hand, is intentional, multifaceted, and active.
You can sleep for 8 hours and still feel depleted—because what you needed wasn’t sleep, it was rest—in a different dimension.
🏥How This Applies to the Emergency Department or ICU?
In the fast-paced, high-pressure world of the ED or ICU, medical professionals often overlook the importance of rest, perceiving it as unproductive.
Yet, rest is crucial for maintaining cognitive function and emotional resilience. The unique concept of rest outlined in the ‘seven types of rest’ can be particularly beneficial.
Understanding and implementing these can help practitioners handle the rigors of patient care and decision-making more effectively.
7️⃣The Seven Types of Rest
1️⃣Physical Rest: Passive (like sleep) and active (like stretching, massage, gentle movement).
2️⃣Mental Rest: Reducing decision fatigue. Tools like brain dumping, meditation, or taking real breaks during work.
3️⃣Sensory Rest: This involves reducing the input from your senses, such as limiting screen time, turning off the lights, or enjoying quiet time.
4️⃣Creative Rest: Reconnecting with awe. Nature, art, music—things that refill your inspiration tank
5️⃣Emotional Rest: Being around people you don’t have to perform for. Saying “I’m not okay.” spaces and people where you can be your authentic self and be at peace
6️⃣Social Rest: Taking space from draining interactions; spending time with life-giving people.
7️⃣Spiritual Rest: Connection to a greater purpose—faith, community, reflection, meditation
⏩Immediate Action Steps for Your Next Shift
**Identify Your Rest Needs**: Reflect on what kind of fatigue you’re experiencing and tailor rest activities accordingly, whether it’s sensory detox or emotional unwinding.
**Practice Sensory Rest**: Take brief moments to close your eyes, or step outside for fresh air to manage overstimulation during shifts.
**Plan Intentional Breaks**: Schedule specific times for rest that focus on particular dimensions you identify as lacking.
**Engage in Active Rest**: Incorporate activities like stretching or meditation during your breaks to enhance mental clarity and reduce physical exhaustion.
**Connect with Supportive Colleagues**: Seek interactions with peers who offer emotional and social support, promoting a healthy work-life balance.
🛌🏽The Many Aspects of What Makes Up Rest
Rest is multifaceted – it comes in more than one form
Rest is productive – it improves performance, decision-making, empathy
Rest is intentional – it requires thoughtful engagement, not autopilot. Make a real plan
Rest is layered – especially sensory, which uses all 5 senses
Rest is about input and detox – what you consume, and what you remove. Social rest is a good example
Rest is personal – one person’s recharge is another’s stressor
Rest is deserved, not earned – full stop.
Conclusion
Rest is a pivotal, multi-dimensional tool that extends beyond mere sleep. For healthcare professionals navigating the strenuous environment of an emergency setting, recognizing and implementing varied forms of rest can enhance overall well-being, decision-making, and patient care. Make rest a deliberate part of your routine, understand its different forms, and remember that it’s a necessity you deserve.
🚨 Clinical Bottom Line
Incorporating rest into your lifestyle aligns with the demands of your professional roles and personal health needs. By understanding and employing various types of rest, you not only support your individual wellness but also enhance your ability to care for patients effectively. Rest is vital; it is not a privilege earned but an essential right you deserve every day.
Further Reading
Dalton-Smith, S. Sacred Rest: Recover Your Life, Renew Your Energy, Restore Your Sanity. Hachette Nashville, 2017.
Dalton-Smith, S. The 7 Types of Rest: Seven Ways to Live a More Energized Life. Hachette Book Group, 2022
Abramson, A “Seven types of rest to help restore your body’s energy.” American Psychological Association, 6 May 2025, Link is Here
Meet the Authors
Mark Ramzy, DO
Co-Editor-in-Chief
Cardiothoracic Intensivist and EM Attending
RWJBH / Rutgers Health, Newark, NJ
Maureen Aiad, DO
Assistant Professor of Emergency Medicine
NYU Grossman Long Island School of Medicine, New York
Amil Badoolah, DO
Assistant Professor of Emergency Medicine
NYU Grossman Long Island School of Medicine, New York
REBEL Core Cast 149: Review of Corticosteroids in Community-Acquired Pneumonia
02 Feb 2026
00:14:20
🧭 REBEL Rundown
🗝️ Key Points
💉 Hydrocortisone Saves Lives: The 2023 Cape Cod Trial (NEJM) showed a clear mortality benefit and reduced need for intubation in severe CAP patients treated with hydrocortisone.
📊 Guidelines Are Catching Up: The SCCM (2024) and ERS now recommend steroids for severe CAP, while ATS/IDSA updates are still pending.
🔥 Redefining “Severe”: Patients requiring high FiO₂ (>50%), noninvasive or mechanical ventilation, or PSI >130 meet criteria for steroid therapy — even outside the ICU.
🍬 Main Risk = Hyperglycemia: Elevated glucose was the most consistent adverse effect, but rates of GI bleed and secondary infection were not increased.
🧭 Early, Targeted Use Matters: Start hydrocortisone within 24 hours of identifying severity — especially in patients with high CRP (>150) or strong inflammatory response.
Corticosteroids have long sparked debate in the treatment of bacterial pneumonia — once viewed with skepticism, now increasingly supported by high-quality evidence. In this episode, Dr. Alex Chapa joins the REBEL Core Cast team to explore how the 2023 Cape Cod Trial (NEJM) reshaped practice and guideline recommendations for severe community-acquired pneumonia (CAP).
📖 Historical Context & Long-Standing Skepticism
For decades, the use of steroids in pneumonia was controversial.
Early Use: Steroids entered practice in the 1940s and 50s for autoimmune inflammation, but there was immediate hesitation regarding secondary superinfections.
Mixed Data: From the 1980s to the 2000s, small studies emerged on severe pneumonia and ARDS, but the data was inconsistent. Different trials used varying definitions of “severe” pneumonia and different C-reactive protein (CRP) cutoffs, making the data “spread” and easy to “cherry pick” to support or deny a benefit.
Past Guidelines: This uncertainty was reflected in official guidelines:
2007 (ATS/IDSA): The American Thoracic Society and the Infectious Diseases Society of America did not address the topic due to insufficient data.
2019 (ATS/IDSA): Pre-COVID, the guidelines recommended against using corticosteroids in severe CAP. They acknowledged no benefit for non-severe pneumonia, but the data for severe pneumonia was considered too weak to endorse.
Pre-Trial Consensus: Prior to 2023, the consensus was to avoid steroids in non-severe pneumonia, while severe pneumonia remained a “gray area” with no treatment showing a clear mortality difference.
📜 The Landmark Cape Cod Trial (NEJM 2023)
The Cape Cod trial, published in the New England Journal of Medicine in 2023, reignited the discussion by providing robust, positive data.
Intervention: 800 patients randomized to two groups, Hydrocortisone as a continuous infusion (200mg/day) versus a placebo infusion.
Taper: On day 4, clinicians would decide whether to continue the infusion or begin a taper based on clinical response.
Population: Patients with severe CAP, defined by meeting at least one of the following criteria:
Pneumonia Severity Index (PSI) > 130.
O2 by FiO2 ratio < 300.
Need for mechanical or non-invasive ventilation (with PEEP ≥ 5).
Need for high FiO2 (>50%) via non-rebreather or heated high flow.
Primary Outcomes: Death for any cause 6.2% (hydrocortisone) vs 11.9% (placebo)
Secondary outcomes:
Death from any cause at 90 days 9.3% (hydrocortisone) vs 14.7% (placebo)
Endotracheal intubation 18% (hydrocortisone) vs 29% (placebo)
Hospital-acquired infections 9.8% (hydrocortisone) vs 11.1% (placebo)
Gastrointestinal bleeding 2.3% (hydrocortisone) vs 3.3% (placebo)
Vasopressor initiation by day 28 15.3% (hydrocortisone) vs 25.0% (placebo)
Key Findings: The trial demonstrated superiority for hydrocortisone
📋 Updated Guidelines & Current Practice
The Cape Cod trial, along with subsequent meta-analyses, has begun to change official recommendations.
Society of Critical Care Medicine (SCCM): In 2024, an SCCM expert panel, reviewing the Cape Cod trial and 18 others, strongly recommended corticosteroids for severe CAP. They concluded that steroids reduce mortality and the need for mechanical ventilation.
Meta-Analysis (Smit et al.): A 2024 meta-analysis in Lancet Respiratory confirmed the 30-day mortality benefit.
European Respiratory Society (ERS): The ERS has issued a recommendation to use steroids for severe pneumonia but still urges caution regarding side effects.
ATS/IDSA: As of the podcast recording, the ATS/IDSA had not yet updated their 2019 guidelines.
🛠️ Practical Application for Clinicians
Defining “Severe” CAP: The key is to identify patients who qualify as “severe”. This can be done using:
Scoring Tools: The PSI is the best validated tool for mortality but is cumbersome. Simpler tools like CURB-65 or SMART-COP are practical and acceptable for defining severity. 2023 meta-analysis from by Zaki et al showed both work well, but CURB-65 has better mortality prediction early on.
Cape Cod Criteria: Any patient meeting the trial’s inclusion criteria (e.g., high-flow O2, non-invasive ventilation) qualifies, regardless of location (ED, floor, or ICU).
Biomarkers: While not required, a CRP level was used in many studies. A CRP > 150 (Cape Cod) or > 204 (Smit meta-analysis) strongly indicates severe inflammation that would benefit from steroids.
Clinical Judgment: A patient who looks “sick,” has “soft” blood pressure, or has dense infiltrates and high oxygen needs (e.g., >50% FiO2 on high flow) is a candidate.
Adverse Effects:
Hyperglycemia: This was the most significant risk identified, with rates between 6-12%. This is a primary concern, especially in patient populations with high BMI.
GI Bleed & Secondary Infection: Fears of these side effects, which contributed to historical skepticism, were not borne out in the Cape Cod trial. The data does not support being overly concerned.
Other Side Effects: Mood changes, delirium, insomnia, and agitation in the elderly are known side effects of steroids that were not specifically addressed in the trial but remain clinical concerns.
🔄 Clinical Pathway for Steroids in Severe CAP
Unanswered Questions & Future Research
Possible remaining questions:
Biomarkers: Can we find a more precise CRP level to distinguish moderate from severe disease? Could other markers like ferritin or IL-6 be used?
Dosing & Tapering: How much immunomodulation is needed, and when is it truly safe to taper?
Gender Differences: Early data suggests females may respond better to steroids and experience fewer side effects. The question of female patients with severe CAP require less corticosteroids needs further exploration.
👉 Clinical Bottom Line
The current literature, spearheaded by the Cape Cod trial, now supports the use of corticosteroids in severe community-acquired pneumonia. The best evidence currently points to hydrocortisone, started early (within 24 hours) after severity is identified using a validated tool. While hyperglycemia is a risk, the previous fears of GI bleeding and secondary infections were not substantiated in recent, rigorous trials.
📚 References
Chapa-Rodriguez A, Abou-Elmagd T, O’Rear C, Narechania S. Do patients with severe community-acquired bacterial pneumonia benefit from systemic corticosteroids?. Cleve Clin J Med. 2025;92(10):600-604. PMID: 41033846
Dequin PF, Meziani F, Quenot JP, et al. Hydrocortisone in Severe Community-Acquired Pneumonia. N Engl J Med. 2023;388(21):1931-1941. PMID: 36942789
Chaudhuri D, Nei AM, Rochwerg B, et al. 2024 Focused Update: Guidelines on Use of Corticosteroids in Sepsis, Acute Respiratory Distress Syndrome, and Community-Acquired Pneumonia. Crit Care Med. 2024;52(5):e219-e233. PMID: 38240492
Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)