Episode Details

Date: January 17, 2026 Reference:  Casey et al. RSI Investigators and the Pragmatic Critical Care Research Group. Ketamine or Etomidate for Tracheal Intubation of Critically Ill Adults. NEJM. 2025 Dec Guest Skeptic: Dr. Scott Weingart is an ED Intensivist from New York. He did fellowships in Trauma, Surgical Critical Care, and ECMO. Scott is best known for talking to himself about Resuscitation and Critical Care on the podcast EMCrit, which has been downloaded more than 50 million times. Scott and I will both be presenting at Incrementum 2026 in Spain.  Case:  You’re working an evening shift in a busy tertiary-care emergency department (ED). Emergency Medical Services (EMS) rolls in a 62-year-old woman with a history of hypertension and type 2 diabetes. She’s febrile at 39.2°C, tachycardic at 125 beats/min, hypotensive at 86/52 mm Hg despite 2 L of crystalloid and breathing 32/min on a non-rebreather with oxygen saturation of 88%. Chest X-ray shows a right‑lower‑lobe infiltrate; lactate is 5.6 mmol/L. She’s now on a norepinephrine infusion at 0.15 µg/kg/min and still looks exhausted and altered. You decide she needs emergent rapid sequence intubation (RSI) for worsening work of breathing and impending respiratory failure. The respiratory therapist is at the bedside, the pharmacist has arrived with the RSI box, and your resident says: “For induction, should we go with ketamine because she’s septic and hypotensive, or etomidate because we’re worried about pushing her over the edge?” Background: Intubating critically ill patients can be one of those high-stakes, high-adrenaline things we do often in emergency medicine (EM), but the physiology is stacked against us. These patients are often hypoxic, hypotensive, acidotic and catecholamine-depleted before we even reach for the laryngoscope. Emergency airway registries and multicentre cohorts consistently report serious peri-intubation complications (profound hypotension, hypoxemia, cardiac arrest, failed or difficult intubation) in roughly 10% to 20% of critically ill adult intubations in the ED and ICU [1].  Even a single episode of severe hypotension or hypoxemia during intubation is associated with increased mortality and organ failure in the ICU population [2].  So, the choice of induction agent seems to matter. Etomidate became the darling of emergency RSI because it has a rapid onset, short duration, and relatively preserved hemodynamics compared with agents like thiopental or high‑dose propofol [3].  The flip side is adrenal suppression: a single dose transiently inhibits 11‑β hydroxylase and measurably blunts cortisol production for 24–72 hours. Observational studies and post‑hoc analyses in septic shock raised alarms that etomidate might increase mortality by worsening relative adrenal insufficiency, leading some guidelines and regulators to discourage or even remove etomidate in sepsis [4]. But those were mostly non-randomized data, and prior RCTs comparing etomidate with other agents were small and gave conflicting signals about mortality. Ketamine, by contrast, is a dissociative NMDA antagonist with a very different vibe. It provides profound amnesia and analgesia, maintains airway reflexes to some degree, and has sympathomimetic properties that can increase heart rate and blood pressure by catecholamine release [5]. Those properties have made ketamine attractive in shocked patients where we’re worried that propofol or midazolam will “tank the pressure”. However, in catecholamine-depleted septic shock, ketamine’s direct myocardial depressant effects may become more apparent, and registry data suggest its hemodynamic advantage over etomidate is not as clear as many of us were taught on shift.  Old concerns that ketamine raises intracranial pressure have largely been debunked in modern neurocritical care literature, further widening its appeal.  Other agents are still in the mix. Propofol remains widely used in operating theatre practice and some EDs because of its fami