Lit Matters #2: Out-of-Hospital Rapid Sequence Intubation with Ketamine

Ketamine does not appear to cause clinically important post-intubation hypotension during rapid sequence intubation when induction dosing is appropriate. In out-of-hospital RSI for traumatic brain injury, the more credible question is not ketamine versus another agent, but fixed dosing versus hemodynamically tailored induction.

Ketamine RSI and Hypotension

• Dosing over drug choice: Post-intubation hypotension after RSI is framed here as a dosing problem more than an agent problem, especially when one pathway allows blood-pressure adjustment and the ketamine pathway uses a fixed 1.5 mg/kg dose.
• Observational signal limits: The prehospital TBI study found a 5% step-up in hypotension after ketamine rollout, but the interrupted time-series design cannot tell whether the signal came from ketamine itself or from who got it.
• Granular confounding concern: Paramedics could down-titrate midazolam and fentanyl based on systolic pressure, while ketamine was protocolized at a fixed dose, creating a built-in hemodynamic mismatch that matters more than the label on the syringe.
• Best comparative evidence: A stronger randomized trial comparing ketamine 2 mg/kg with etomidate 0.3 mg/kg found no meaningful difference in blood pressure or 28-day mortality after RSI. We get into why that trial should outweigh this newer paper in the episode.
• Prehospital airway context: Overall intubation success was 97.5% in the cohort, but the practical takeaway is not that ketamine is dangerous; it is that induction strategy in field RSI has to match the patient's shock risk.

References:

1.) Jabre P et al. Etomidate Versus Ketamine for Rapid Sequence Intubation in Acutely Ill Patients: A Multicentre Randomised Controlled Trial. Lancet 2009. PMID: 19573904