This Week in Critical Care — Oct 7, 2026

This AudioScholar briefing is generated by artificial intelligence for healthcare professionals and trainees. It is not medical advice.

Welcome to This Week in Critical Care. This week we're covering 10 notable papers spanning blood pressure management in shock and hypertensive emergencies, rhythm and drug decisions in cardiac arrest, anti-inflammatory therapy in lung injury, and how care processes such as weaning and transfusion are organised. Let's dive in.

We start with vasopressors and blood pressure targets, where two trials question long-standing habits in septic shock. In Critical Care, Kalamar and colleagues report TRICYCLE, a phase two randomised trial of 79 patients with septic shock already on at least 0.15 micrograms per kilogram per minute of norepinephrine [1]. One group received angiotensin II, vasopressin and norepinephrine together early; the other followed the classic stepwise escalation. The primary outcome was a biomarker, the rate of fall in plasma renin, and renin did fall faster with the multimodal approach, as did lactate. Organ failure scores improved by about three points at 72 hours in the intervention group versus no change in controls, and tachyarrhythmias were far less common, affecting roughly one in six patients versus about two in three. Mortality was numerically lower but not statistically different, and the trial was explicitly not powered for survival. The authors frame this as a rationale for a larger trial, not as proof of benefit, so it supports the physiological case for combination vasopressors without settling whether patients do better. A complementary angle comes from Annals of Intensive Care, where Shimazui and colleagues revisited the OPTPRESS trial of 489 patients aged 65 or over, which had already found worse outcomes with a mean arterial pressure target of 80 to 85 millimetres of mercury [2]. Under the standard target of 65 to 70, mortality fell as body mass index rose, the familiar obesity paradox. Under the high target that pattern disappeared, and patients with higher body mass index had roughly seventy percent higher mortality than normal-weight patients. This is a post hoc analysis, so it is hypothesis-generating, but it adds texture to the existing argument against high pressure targets in older patients, possibly through differences in fluid and vasopressor exposure. Also in Annals of Intensive Care, Demiselle and colleagues offer a narrative review of hypertensive crisis in the critically ill [3]. They emphasise that emergencies are defined by pressure of at least 180 over 110 with acute organ damage, that the speed of the rise matters more than the absolute number, and that drug choice and target should be tailored to the specific organ injured. It is a useful synthesis rather than new evidence.

Our second theme is cardiac arrest, and specifically what happens when the rhythm changes during resuscitation. In Resuscitation, Knapp and colleagues used the German Resuscitation Registry to study out-of-hospital arrests that began in a non-shockable rhythm and later converted to a shockable one, a group current guidelines do not specifically address for amiodarone [4]. Among more than five thousand patients, propensity matching produced about eighteen hundred pairs. Amiodarone was associated with more patients admitted with a pulse, better 24-hour survival, and survival to discharge rising from about four percent to six and a half percent. Favourable neurological outcome was not significantly different. As a retrospective registry analysis, it cannot exclude confounding, and the authors call for controlled studies to define timing. Also in Resuscitation, Marabotti and colleagues pooled ten observational studies covering more than five thousand extracorporeal resuscitation recipients [5]. Conversion from a non-shockable to a shockable rhythm roughly tripled the chance of a good neurological outcome, while decay from a shockable rhythm cut it by more than half. Decay to asystole was the strongest signal, reducing good neurological recovery by about four fifths, whereas decay to pulseless electrical activity was not statistically significant. Certainty ranged from low to moderate. Read together, these two papers suggest the rhythm trajectory during resuscitation carries prognostic and perhaps therapeutic weight, with the meta-analysis authors proposing that decay to asystole should prompt reconsideration of extracorporeal support. Both rest on observational data.

The third theme is anti-inflammatory therapy in lung injury, and this week's results are largely sobering. In the American Journal of Respiratory and Critical Care Medicine, Kim and colleagues report SAFER, a multicentre open-label randomised trial in eight South Korean hospitals comparing pulse methylprednisolone at 10 milligrams per kilogram for three days against 1 milligram per kilogram for seven days in 100 adults with acute exacerbation of idiopathic pulmonary fibrosis [6]. Pulse dosing did not lower mortality at 28 or 90 days, and secondary outcomes including intensive care admission and ventilation were not different. The trial is small and the intervals are wide, so modest benefit or harm cannot be excluded, but it removes the assumption that higher doses are better for a widely used practice. In Chest, Huang and colleagues tested TISA-818, a montelukast-peptide conjugate, in a phase two trial of 58 patients with infection-related ARDS, notably using the 2023 global definition that includes non-intubated patients [7]. The primary endpoint, safety, was acceptable, but treatment-related adverse events were more common on active drug, and day-28 mortality was numerically higher in the once-daily arm, about a quarter of patients versus one in twenty on placebo, though that gap did not persist at day 60. Signals favouring the twice-daily dose in non-intubated patients came from just nine patients per arm. This is early-phase work and supports only further trials. Finally, in Critical Care, Boyle and colleagues examined whether ferritin or suPAR identify COVID-19 patients who benefit from anakinra within REMAP-CAP [8]. Ferritin did not identify responders. Among 145 patients with suPAR measured, the probability of benefit was about 95 percent in those with low suPAR and under 40 percent in those with high suPAR, the opposite of what trials in non-critically ill patients suggested. The authors call this hypothesis-generating, and it highlights how biomarker-guided immunomodulation remains unsettled in critical illness.

Our last theme is how care is organised. In Critical Care, Trudzinski and colleagues report PRiVENT, a non-randomised multicentre study of a specialist-led interprofessional weaning programme for high-risk ventilated patients, compared against controls drawn from insurance claims [9]. Successful weaning was about 58 percent with the programme versus about 52 percent in controls, but the prespecified adjusted primary analysis narrowly missed statistical significance. A matched analysis was positive, and overall ventilation duration was longer in the intervention group, partly because some patients were transferred to weaning centres. The design limits causal conclusions, so this is a feasibility signal rather than proof. In the Journal of Critical Care, Le Marec and colleagues describe 975 platelet transfusions given to 310 patients across several French units [10]. Overall, 42 percent of transfusions did not align with guidelines, and prophylactic transfusions in thrombocytopenic patients were the least adherent, with a predicted non-adherence of about three quarters. This observational data points to a clear target for stewardship, though it does not tell us whether the non-adherent transfusions caused harm.

If you only have time for one paper this week, make it the SAFER trial in the American Journal of Respiratory and Critical Care Medicine [6]. It is the first randomised test of pulse-dose steroids in acute exacerbation of pulmonary fibrosis, a practice used widely on almost no evidence, and it found no survival advantage over a lower-dose regimen.

Here is what this week's evidence adds up to in Critical Care. First, early combination vasopressor therapy improves physiological markers and reduces arrhythmias in a small phase two trial, but survival benefit is unproven and awaits a larger trial. Second, the case against high blood pressure targets in older patients with septic shock gains a further post hoc layer, suggesting the harm may concentrate in patients with higher body mass index. Third, rhythm trajectory during resuscitation appears prognostically meaningful, and registry data associate amiodarone with better survival after conversion to a shockable rhythm, though neither finding comes from randomised evidence. Fourth, higher-dose steroids in fibrotic lung exacerbations showed no benefit in a modest trial, and biomarker-guided immunomodulation in critical illness remains exploratory. Finally, structured weaning programmes and platelet transfusion stewardship both show room for improvement, but the supporting evidence is observational.

That's your roundup for This Week in Critical Care. The full transcript and references are available on the episode page in your AudioScholar library. This is an AI-curated summary — for clinical decisions, always consult primary sources and current guidelines. See you next week.

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