Evidence
A claim is only as strong as its study design.
AIRCHILL follows a conservative evidence hierarchy. Exploratory mechanism data can justify the next study. It cannot substitute for airway safety, technical performance or outcome evidence.
Clinical context
TTM2 reached target temperature about five hours in. It cannot answer the early question.
TTM2 randomised patients a median of 136 minutes after return of circulation and then needed a median of three more hours to reach 34 °C. What it compared was late temperature control against fever control, and it found no mortality benefit while reporting more arrhythmias with haemodynamic compromise. No arm of that trial cooled within the first minutes on scene. A neutral result for a late intervention is not a result for an early one — the early question was never in the design.
136 minutes, then three hours
Median time from return of circulation to randomisation 136 minutes; median time from randomisation to 34 °C three hours, interquartile range two to four. Target temperature therefore around five hours after the event.
Late cooling is answered
Routine cooling to 33 °C begun hours after the event does not improve outcomes. We state that plainly and we do not build anything on it.
Early cooling is untested there
TTM2 says nothing about a temperature effect produced in the first minutes, because it never produced one. Using it either for or against ultra-early cooling is a misreading of the trial.
This is the counterweight, and we state it before anyone else does. PRINCESS cooled transnasally during resuscitation in 677 patients across 11 EMS systems in seven countries and missed its primary endpoint. Taccone et al., Crit Care 2024;28:335 filtered the HACA-like shockable subgroup out of TTM2 (n = 600) and found no advantage there either — which hits our own target-group logic directly. So ultra-early selective cooling is an open question, not a promising one. We treat it as a hypothesis with a defined test, not as a thesis to defend.
Dankiewicz J, Cronberg T, Lilja G et al. Hypothermia versus Normothermia after Out-of-Hospital Cardiac Arrest. N Engl J Med 2021;384:2283–2294 (TTM2, n = 1,861; median time to randomisation 136 minutes in the hypothermia arm and 133 in the normothermia arm, measured from sustained return of circulation; median three hours from randomisation to 34 °C, IQR 2–4) · Nordberg P, Taccone FS, Truhlář A et al. JAMA 2019;321:1677–1685 (PRINCESS) · Taccone FS, Cariou A, Zorzi S et al. Crit Care 2024;28:335 · ERC-ESICM Post-Resuscitation Care Guidelines 2025.
Our own data
Peer-reviewed mechanism data — and the limits we found ourselves.
Carried out at the Department of Diagnostic and Interventional Neuroradiology, University Medical Center Hamburg-Eppendorf, under BMBF Go-Bio grant 031A530. Fabian Temme is a co-author on the publication and on the award-winning poster.
MR thermogram of the porcine brain with cooling off and on. Five anaesthetised pigs, 3 T proton-resonance-frequency thermometry. Whole brain −0.33 ± 0.30 °C after five minutes; anterior brain −0.83 ± 0.51 °C, significant in every experiment. 73 ± 14 % of the maximum effect was reached within three minutes.
Sedlacik J et al., Therapeutic Hypothermia and Temperature Management, doi 10.1089/ther.2017.0031.
Anatomy, before, during and after cooling in a healthy volunteer. Two volunteers, three experiments, hollow mask over mouth and nose. −0.33 °C in the inferior frontal gyrus, p < 0.05 in all three experiments; the three other brain regions showed no significant change.
ISMRM 2016, Singapore, Magna cum laude poster award. Conference abstract, not a patient study.
Porcine lung after six hours of ventilation with air at −20 °C through an endotracheal tube. All entities histomorphologically intact: bronchiole, cartilage, blood vessels, alveoli. No pathological findings in lung or brain.
Final report, BMBF grant 031A530, 28 March 2017.
Contrast-enhanced 2D lung perfusion before and after cooled ventilation. No relevant change. MR perfusion gave the same result, and intraprocedural CT showed no evidence of pulmonary oedema. The animals remained cardiorespiratorily stable throughout.
Final report, BMBF grant 031A530, 28 March 2017.
Eleven volunteers
Eleven healthy volunteers tolerated cold air down to −20 °C for up to ten minutes, subjectively well. This is a different cohort from the two-person MRI thermometry group — tolerability and measured cooling must not be conflated.
73 % within three minutes
Averaged over eight experiments the anterior brain reached 73 ± 14 % of its minimum temperature after three minutes. Time to first measurable effect is the property that matters prehospital.
Stroke model
The report notes that infarct development may be limited by immediately initiated cold air therapy. This is an uncontrolled indication, not an efficacy study.
Sedlacik J, Kjørstad Å, Nagy Z, Buhk JH, Behem CR, Trepte CJ, Fiehler J, Temme F. Feasibility Study of a Novel High-Flow Cold Air Cooling Protocol of the Porcine Brain Using MRI Temperature Mapping. Therapeutic Hypothermia and Temperature Management, doi 10.1089/ther.2017.0031 · Final report “Airchill – Gekühlte Beatmung”, BMBF grant 031A530, Department of Diagnostic and Interventional Neuroradiology, University Medical Center Hamburg-Eppendorf, 28 March 2017 · Kjørstad Å, Temme F, Fiehler J, Sedlacik J, ISMRM 24th Annual Meeting, Singapore 2016.
What we did not achieve
A strong effect through the lower airway.
“Eine Kühlung des gesamten Hirns ist mit der evaluierten Methode nicht erreichbar.”
Cooling through the tracheal route was tolerated but thermally weak — dead-space ventilation limits the transferable energy, and our own report recommends the endonasal route instead. The endonasal route is thermodynamically what RhinoChill does, and RhinoChill missed its primary endpoint in PRINCESS. The effect we measured is local: our authors attribute it to direct airway exposure rather than cooling of carotid blood, so whole-brain cooling is not established and a comparison with whole-body trials such as TTM2 is not admissible.
We publish this for two reasons. It is the honest reading of our own data, and it defines the engineering problem precisely. Dead-space ventilation is a design constraint, not a law of physics: flow, temperature, timing and circuit geometry were not optimised in 2017. Whether it can be overcome is an open development question — and the reason our evidence plan starts at mechanism rather than outcomes.
An early market entry is planned around a narrow performance and safety claim, not a neurological outcome claim. The latter requires a separate and substantially larger evidence pathway. Sample sizes and claim strategy will be updated after the intended-purpose decision, Notified Body feedback and the gate results.
Claim register
Every claim, and exactly how strong it is.
This is the internal release list that governs our investor, policy and media communication. No statement anywhere in our materials may be stronger than its level here.
Levels taken from the project’s single source of truth, 8 August 2026. “Withdrawn” marks two statements from an older poster of our own that carry no source and no derivation; they are blocked and are not used in any document. External evidence: Kim F et al., JAMA 2014 · Dankiewicz J et al., N Engl J Med 2021 · Nordberg P et al., JAMA 2019 · Taccone FS et al., Crit Care 2021 and Crit Care 2024;28:335 · ERC-ESICM Guidelines 2025 · § 137e SGB V and BT-Drs. 21/6808.
Claim policy
What this website does not claim.
No claim of established clinical efficacy. No claim of proven patient safety. No claim of improved survival or neurological outcome. No implication that preliminary or small-sample findings are equivalent to a pivotal trial.
Read the study material yourself.
The publication, the final report and the poster are available on request, together with our assessment of what they do and do not support.