Key PointsQuestionIn patients with witnessed refractory out-of-hospital cardiac arrest, does early intra-arrest transport, extracorporeal cardiopulmonary resuscitation, and invasive assessment and treatment improve outcomes compared with standard resuscitation?FindingsIn this randomized clinical trial that included 256 patients, survival with neurologically favorable outcome (Cerebral Performance Category 1-2) at 180 days occurred in 31.5% in the invasive strategy group and 22.0% in the standard resuscitation group, a difference that was not statistically significant.MeaningAmong patients with refractory out-of-hospital cardiac arrest, the bundle of early intra-arrest transport, extracorporeal cardiopulmonary resuscitation, and invasive assessment and treatment did not significantly improve survival with neurologically favorable outcome at 180 days compared with standard resuscitation, although the trial was possibly underpowered to detect a clinically relevant difference.

Recently diagnosed immunodeficiency is associated with a much better prognosis in ECMO-treated severe ARDS. However, low 6-month survival of our large cohort of immunocompromised patients supports restricting ECMO to patients with realistic oncological/therapeutic prognoses, acceptable functional status and few pre-ECMO mortality-risk factors.

Severity of metabolic acidosis, state of consciousness, and serum ethanol on admission were the only significant parameters associated with mortality. The type of dialysis or antidote did not appear to affect mortality. Recommendations that were issued for hospital triage of fomepizole administration allowed conservation of valuable antidote in this massive poisoning outbreak for those patients most in need.

Aims Ventricular septal rupture (VSR) became a rare mechanical complication of myocardial infarction in the era of percutaneous coronary interventions but is associated with extreme mortality in patients who present with cardiogenic shock (CS). Promising outcomes have been reported with the use of circulatory support allowing haemodynamic stabilization, followed by delayed repair. Therefore, we analysed our experience with an early use of Veno‐Arterial Extracorporeal Membrane Oxygenation (V‐A ECMO) for postinfarction VSR. Methods and results We conducted a retrospective search of institutional database for patients presenting with postinfarction VSR from January 2007 to June 2016. Data from 31 consecutive patients (mean age 69.5 ± 9.1 years) who were admitted to hospital were analysed. Seven out of 31 patients with VSR who were in refractory CS received V‐A ECMO support preoperatively. ECMO improved end‐organ perfusion with decreased lactate levels 24 hours after implantation (7.9 mmol/L vs. 1.6 mmol/L, p = 0.01), normalized arterial pH (7.25 vs. 7.40, p < 0.04), improved mean arterial pressure (64 mmHg vs. 83 mmHg, p < 0.01) and lowered heart rate (115/min vs. 68/min, p < 0.01). Mean duration of ECMO support was 12 days, 5 out of 7 patients underwent surgical repair, 4 were weaned from ECMO, 3 survived 30 days and 2 survived more than 1 year. The most frequent complication (5 patients) and the cause of death (3 patients) was bleeding. Conclusions Our experience suggests that early V‐A ECMO in patients with VSR and refractory CS might prevent irreversible multiorgan failure by improved end‐organ perfusion. Bleeding complications remain an important limitation of this approach.

Saving the heart 30 beats/min did not demonstrate adverse impact on global haemodynamics in rates above 110/min. Using well titratable betablocker seems to be safe and cardioprotective in septic shock patients with high cardiac output.

Perioperative initiation of intensive insulin therapy during cardiac surgery reduces postoperative morbidity in nondiabetic patients while having a minimal effect in diabetic subjects.

Purpose:The optimal ventilatory settings in patients after cardiac arrest and their association with outcome remain unclear. The aim of this study was to describe the ventilatory settings applied in the first 72 h of mechanical ventilation in patients after out-of-hospital cardiac arrest and their association with 6-month outcomes.Methods: Preplanned sub-analysis of the Target Temperature Management-2 trial. Clinical outcomes were mortality and functional status (assessed by the Modified Rankin Scale) 6 months after randomization.Results: A total of 1848 patients were included (mean age 64 [Standard Deviation, SD = 14] years). At 6 months, 950 (51%) patients were alive and 898 (49%) were dead. Median tidal volume (V T ) was 7 (Interquartile range, IQR = 6.2-8.5) mL per Predicted Body Weight (PBW), positive end expiratory pressure (PEEP) was 7 (IQR = 5-9) cmH 2 0, plateau pressure was 20 cmH 2 0 (IQR = 17-23), driving pressure was 12 cmH 2 0 (IQR = 10-15), mechanical power 16.2 J/min (IQR = 12.1-21.8), ventilatory ratio was 1.27 (IQR = 1.04-1.6), and respiratory rate was 17 breaths/minute (IQR = 14-20). Median partial pressure of oxygen was 87 mmHg (IQR = 75-105), and partial pressure of carbon dioxide was

Context: Acidemia is a marker of prognosis in methanol poisoning, as well as compounding formateinduced cytotoxicity. Prompt correction of acidemia is a key treatment of methanol toxicity and methods to optimize this are poorly defined. Objective: We studied the efficiency of acidemia correction by intermittent hemodialysis (IHD) and continuous renal replacement therapy (CRRT) in a mass outbreak of methanol poisoning. Methods: The study was designed as observational cohort study. The mean time for an increase of 1 mmol/L HCO 3 -, 0.01 unit arterial blood pH, and the total time for correction of HCO 3 -were determined in IHD-and CRRT-treated patients. Results: Data were obtained from 18 patients treated with IHD and 13 patients treated with CRRT. At baseline, CRRT group was more acidemic than IHD group (mean arterial pH 6.79 ± 0.10 versus 7.05 ± 0.10; p ¼ 0.001). No association was found between the rate of acidemia correction and age, weight, serum methanol, lactate, formate, and glucose on admission. The time to HCO 3 -correction correlated with arterial blood pH (r¼ À0.511; p ¼ 0.003) and creatinine (r ¼ 0.415; p ¼ 0.020). There was association between the time to HCO 3 -correction and dialysate/effluent and blood flow rates (r¼ À0.738; p < 0.001 and r¼ À0.602; p < 0.001, correspondingly). The mean time for HCO 3 -to increase by 1 mmol/L was 12 ± 2 min for IHD versus 34 ± 8 min for CRRT (p < 0.001), and the mean time for arterial blood pH to increase 0.01 was 7 ± 1 mins for IHD versus 11 ± 4 min for CRRT (p ¼ 0.024). The mean increase in HCO 3 -was 5.67 ± 0.90 mmol/L/h for IHD versus 2.17 ± 0.74 mmol/L/h for CRRT (p < 0.001). Conclusions: Our study supports the superiority of IHD over CRRT in terms of the rate of acidemia correction. ARTICLE HISTORY