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Abstract Background Optimal oxygen targets in patients resuscitated after cardiac arrest are uncertain. The primary aim of this study was to describe the values of partial pressure of oxygen values (PaO2) and the episodes of hypoxemia and hyperoxemia occurring within the first 72 h of mechanical ventilation in out of hospital cardiac arrest (OHCA) patients. The secondary aim was to evaluate the association of PaO2 with patients’ outcome. Methods Preplanned secondary analysis of the targeted hypothermia versus targeted normothermia after OHCA (TTM2) trial. Arterial blood gases values were collected from randomization every 4 h for the first 32 h, and then, every 8 h until day 3. Hypoxemia was defined as PaO2 300 mmHg. Mortality and poor neurological outcome (defined according to modified Rankin scale) were collected at 6 months. Results 1418 patients were included in the analysis. The mean age was 64 ± 14 years, and 292 patients (20.6%) were female. 24.9% of patients had at least one episode of hypoxemia, and 7.6% of patients had at least one episode of severe hyperoxemia. Both hypoxemia and hyperoxemia were independently associated with 6-month mortality, but not with poor neurological outcome. The best cutoff point associated with 6-month mortality for hypoxemia was 69 mmHg (Risk Ratio, RR = 1.009, 95% CI 0.93–1.09), and for hyperoxemia was 195 mmHg (RR = 1.006, 95% CI 0.95–1.06). The time exposure, i.e., the area under the curve (PaO2-AUC), for hyperoxemia was significantly associated with mortality (p = 0.003). Conclusions In OHCA patients, both hypoxemia and hyperoxemia are associated with 6-months mortality, with an effect mediated by the timing exposure to high values of oxygen. Precise titration of oxygen levels should be considered in this group of patients. Trial registration: clinicaltrials.gov NCT02908308 , Registered September 20, 2016.

Introduction Mechanical ventilation is a fundamental component in the management of patients post cardiac arrest. However, the ventilator settings and the gas-exchange targets used after cardiac arrest may not be optimal to minimise post-anoxic secondary brain injury. Therefore, questions remain regarding the best ventilator management in such patients.Methods and analysis This is a preplanned analysis of the international randomised controlled trial, targeted hypothermia versus targeted normothermia after out-of-hospital cardiac arrest (OHCA)–target temperature management 2 (TTM2). The primary objective is to describe ventilatory settings and gas exchange in patients who required invasive mechanical ventilation and included in the TTM2 trial. Secondary objectives include evaluating the association of ventilator settings and gas-exchange values with 6 months mortality and neurological outcome. Adult patients after an OHCA who were included in the TTM2 trial and who received invasive mechanical ventilation will be eligible for this analysis. Data collected in the TTM2 trial that will be analysed include patients’ prehospital characteristics, clinical examination, ventilator settings and arterial blood gases recorded at hospital and intensive care unit (ICU) admission and daily during ICU stay.Ethics and dissemination The TTM2 study has been approved by the regional ethics committee at Lund University and by all relevant ethics boards in participating countries. No further ethical committee approval is required for this secondary analysis. Data will be disseminated to the scientific community by abstracts and by original articles submitted to peer-reviewed journals.Trial registration number NCT02908308.

Background: Long‐term recovery following critical COVID‐19 has not been sufficiently studied. Objective: The primary objective was to describe changes in functional outcome and Health‐Related Quality of Life (HRQoL) between 3 and 12 months in critically ill COVID‐19 survivors. The secondary objective was to investigate factors associated with good functional outcome and HRQoL at 12 months. Methods: Prospective multicentre cohort study including critically ill COVID‐19 patients admitted to six intensive care units in Sweden between May 2020 and May 2021. Surviving patients were invited to face‐to‐face follow‐ups at 3 and 12 months. Functional outcome was assessed using the Glasgow Outcome Scale Extended (GOSE), ranging from 1 to 8. Physical and mental HRQoL was assessed by the physical component summary (PCS) and mental component summary (MCS) scores of the Short form health survey version 2 (SF‐36v2®). Multivariable logistic regression models were used to identify factors associated with good functional outcome (GOSE ≥7) and good physical and mental HRQoL (PCS and MCS ≥45) at 12 months. Results: The percentage of participants with a good functional outcome increased from 35% to 64% between 3 and 12 months (p <.001). Mean PCS improved from 40 to 44 between 3 and 12 months (p <.001), while the mean MCS was within the normal range at 3 months, with no change at 12 months (46 vs. 48, p =.05). Increasing age was associated with a good functional outcome. Lower clinical frailty and absence of diabetes mellitus were associated with a good PCS. A shorter duration of mechanical ventilation was associated with a good outcome for all three outcome measures. Conclusion: Survivors of critical COVID‐19 showed improved functional outcome and physical HRQoL from 3 to 12 months post‐ICU. A shorter duration of mechanical ventilation is associated with good functional outcome and good HRQoL, while older age is associated with good functional outcome. Younger patients and those with comorbidities or higher frailty may require targeted follow‐up and rehabilitation. Study registration ClinicalTrials.gov Identifier: NCT04974775, registered April 28, 2020. [ABSTRACT FROM AUTHOR]

Background: Acute kidney injury (AKI) is a common and severe complication in patients treated at an Intensive Care Unit (ICU). The pathogenesis of AKI has been reported to involve hypoperfusion, diminished oxygenation, systemic inflammation, and damage by increased intracellular iron concentration. Hepcidin, a regulator of iron metabolism, has been shown to be associated with sepsis and septic shock, conditions that can result in AKI. Heparin binding protein (HBP) has been reported to be associated with sepsis and AKI. The aim of the present study was to compare serum hepcidin and heparin binding protein (HBP) levels in relation to AKI in patients admitted to the ICU. Methods: One hundred and forty patients with community acquired illness admitted to the ICU within 24 hours after first arrival to the hospital were included in the study. Eighty five of these patients were diagnosed with sepsis and 55 with other severe non-septic conditions. Logistic and linear regression models were created to evaluate possible correlations between circulating hepcidin and heparin-binding protein (HBP), stage 2–3 AKI, peak serum creatinine levels, and the need for renal replacement therapy (RRT). Results: During the 7-day study period, 52% of the 85 sepsis and 33% of the 55 non-sepsis patients had been diagnosed with AKI stage 2–3 already at inclusion. The need for RRT was 20% and 15%, respectively, in the groups. Hepcidin levels at admission were significantly higher in the sepsis group compared to the non-sepsis group but these levels did not significantly correlate to the development of stage 2–3 AKI in the sepsis group (p = 0.189) nor in the non-sepsis group (p = 0.910). No significant correlation between hepcidin and peak creatinine levels, nor with the need for RRT was observed. Stage 2–3 AKI correlated, as expected, significantly with HBP levels at admission in both groups (Odds Ratio 1.008 (CI 1.003–1.014, p = 0.005), the need for RRT, as well as with peak creatinine in septic patients. Conclusion: Initial serum hepcidin, and HBP levels in patients admitted to the ICU are biomarkers for septic shock but in contrast to HBP, hepcidin does not portend progression of disease into AKI or a later need for RRT. Since hepcidin is a key regulator of iron metabolism our present data do not support a decisive role of initial iron levels in the progression of septic shock into AKI. [ABSTRACT FROM AUTHOR]

Purpose We hypothesized that a targeted temperature of 33 °C as compared to that of 36 °C would increase survival and reduce the severity of circulatory shock in patients with shock on admission after out-of-hospital cardiac arrest (OHCA). Methods The recently published Target Temperature Management trial (TTM-trial) randomized 939 OHCA patients with no difference in outcome between groups and no difference in mortality at the end of the trial in a predefined subgroup of patients with shock at admission. Shock was defined as a systolic blood pressure of 30 min or the need of supportive measures to maintain a blood pressure [greater than or equal to]90 mmHg and/or clinical signs of end-organ hypoperfusion. In this post hoc analysis reported here, we further analyzed the 139 patients with shock at admission; all had been randomized to receive intervention at 33 °C (TTM33; n = 71) or 36 °C (TTM36; n = 68). Primary outcome was 180-day mortality. Secondary outcomes were intensive care unit (ICU) and 30-day mortality, severity of circulatory shock assessed by mean arterial pressure, serum lactate, fluid balance and the extended Sequential Organ Failure assessment (SOFA) score. Results There was no significance difference between targeted temperature management at 33 °C or 36 °C on 180-day mortality [log-rank test, p = 0.17, hazard ratio 1.33, 95 % confidence interval (CI) 0.88-1.98] or ICU mortality (61 vs. 44 %, p = 0.06; relative risk 1.37, 95 % CI 0.99-1.91). Serum lactate and the extended cardiovascular SOFA score were higher in the TTM33 group (p < 0.01). Conclusions We found no benefit in survival or severity of circulatory shock with targeted temperature management at 33 °C as compared to 36 °C in patients with shock on admission after OHCA., Author(s): Martin Annborn [sup.1] [sup.2], John Bro-Jeppesen [sup.3], Niklas Nielsen [sup.2] [sup.4], Susann Ullén [sup.5], Jesper Kjaergaard [sup.3], Christian Hassager [sup.3], Michael Wanscher [sup.6], Jan Hovdenes [sup.7], Tommaso Pellis [sup.8], [...]

Patients admitted to intensive care after cardiac arrest are at risk of circulatory shock and early mortality due to cardiovascular failure. The aim of this study was to evaluate the ability of the veno‐arterial pCO2 difference (∆pCO2; central venous CO2 – arterial CO2) and lactate to predict early mortality in postcardiac arrest patients. This was a pre‐planned prospective observational sub‐study of the target temperature management 2 trial. The sub‐study patients were included at five Swedish sites. Repeated measurements of ∆pCO2 and lactate were conducted at 4, 8, 12, 16, 24, 48, and 72 h after randomization. We assessed the association between each marker and 96‐h mortality and their prognostic value for 96‐h mortality. One hundred sixty‐three patients were included in the analysis. Mortality at 96 h was 17%. During the initial 24 h, there was no difference in ∆pCO2 levels between 96‐h survivors and non‐survivors. ∆pCO2 measured at 4 h was associated with an increased risk of death within 96 h (adjusted odds ratio: 1.15; 95% confidence interval [CI]: 1.02–1.29; p =.018). Lactate levels were associated with poor outcome over multiple measurements. The area under the receiving operating curve to predict death within 96 h was 0.59 (95% CI: 0.48–0.74) and 0.82 (95% CI: 0.72–0.92) for ∆pCO2 and lactate, respectively. Our results do not support the use of ∆pCO2 to identify patients with early mortality in the postresuscitation phase. In contrast, non‐survivors demonstrated higher lactate levels in the initial phase and lactate identified patients with early mortality with moderate accuracy. [ABSTRACT FROM AUTHOR]