Liberal and overaggressive use of vasopressors during the initial period of shock resuscitation may compromise organ perfusion and worsen outcome. When transiently applying the concept of permissive hypotension, it would be helpful to know at which arterial blood pressure terminal cardiovascular collapse occurs. In this retrospective cohort study, we aimed to identify the arterial blood pressure associated with terminal cardiovascular collapse in 140 patients who died in the intensive care unit while being invasively monitored. Demographic data, co-morbid conditions and clinical data at admission and during the 24 hours before and at the time of terminal cardiovascular collapse were collected. The systolic, mean and diastolic arterial blood pressures immediately before terminal cardiovascular collapse were documented. Terminal cardiovascular collapse was defined as an abrupt (50% compared to preceding values) followed by cardiac arrest. The mean ± standard deviation (SD) values of the systolic, mean and diastolic arterial blood pressures associated with terminal cardiovascular collapse were 47 ± 12 mmHg, 35 ± 11 mmHg and 29 ± 9 mmHg, respectively. Patients with congestive heart failure (39 ± 13 mmHg versus 34 ± 10 mmHg; P = 0.04), left main stem stenosis (39 ± 11 mmHg versus 34 ± 11 mmHg; P = 0.03) or acute right heart failure (39 ± 13 mmHg versus 34 ± 10 mmHg; P = 0.03) had higher arterial blood pressures than patients without these risk factors. Patients with severe valvular aortic stenosis had the highest arterial blood pressures associated with terminal cardiovascular collapse (systolic, 60 ± 20 mmHg; mean, 46 ± 12 mmHg; diastolic, 36 ± 10 mmHg), but this difference was not significant. Patients with sepsis and patients exposed to sedatives or opioids during the terminal phase exhibited lower arterial blood pressures than patients without sepsis or administration of such drugs. The arterial blood pressure associated with terminal cardiovascular collapse in critically ill patients was very low and varied with individual co-morbid conditions (for example, congestive heart failure, left main stem stenosis, severe valvular aortic stenosis, acute right heart failure), drug exposure (for example, sedatives or opioids) and the type of acute illness (for example, sepsis).

Individuals ascending rapidly to altitudes >2500 m may develop symptoms of acute mountain sickness (AMS) within a few hours of arrival and/or high-altitude pulmonary edema (HAPE), which occurs typically during the first three days after reaching altitudes above 3000–3500 m. Both diseases have distinct pathologies, but both present with a pronounced decrease in oxygen saturation of hemoglobin in arterial blood (SO₂). This raises the question of mechanisms impairing the diffusion of oxygen (O₂) across the alveolar wall and whether the higher degree of hypoxemia is in causal relationship with developing the respective symptoms. In an attempt to answer these questions this article will review factors affecting alveolar gas diffusion, such as alveolar ventilation, the alveolar-to-arterial O₂-gradient, and balance between filtration of fluid into the alveolar space and its clearance, and relate them to the respective disease. The resultant analysis reveals that in both AMS and HAPE the main pathophysiologic mechanisms are activated before aggravated decrease in SO₂ occurs, indicating that impaired alveolar epithelial function and the resultant diffusion limitation for oxygen may rather be a consequence, not the primary cause, of these altitude-related illnesses.

In critically ill children, in-line microfilters may reduce the incidence of the systemic inflammatory response syndrome (SIRS), the overall complication and organ dysfunction rate. No data on the use of in-line microfilters exist in critically ill adults. In this prospective, randomized, controlled open-label study, we evaluated the influence of in-line microfilters on systemic immune activation in 504 critically ill adults with a central venous catheter in place and an expected length of stay in the intensive care unit >24 h. Patients were randomized to have in-line microfilters placed into all intravenous lines (intervention group) or usual care (control group). The primary endpoint was the number of intensive care unit days with SIRS. Secondary endpoints were the incidence of SIRS, SIRS criteria per day, duration of invasive mechanical ventilation, intensive care unit length of stay, the incidence of acute lung injury, maximum C-reactive protein, maximum white blood cell count, incidence of new candida and/or central-line-associated bloodstream infections, incidence of new thromboembolic complications, cumulative insulin requirements and presence of hyper- or hypoglycemia. The study groups did not differ in any baseline variable. There was no difference in the number of days in the intensive care unit with SIRS between microfilter and control patients [2 (0.8–4.7) vs. 1.8 (0.7–4.4), p = 0.62]. Except for a higher incidence of SIRS in microfilter patients (99.6 vs. 96.8 %, p = 0.04), no difference between the groups was observed in any secondary outcome parameter. Results did not change when only patients with an intensive care unit length of stay of greater than 7 days were included in the analysis. The rate of adverse events was comparable between microfilter and control patients. In two patients allocated to the microfilter group, the study intervention was discontinued for technical reasons. Use of in-line microfilters was associated with additional costs. The use of in-line microfilters failed to modulate systemic inflammation and clinical outcome parameters in critically ill adults. Trial registration: Clinical Trials NCT01534390

Evidence on sex-related mortality differences in critically ill older adults is inconsistent, and frailty is rarely incorporated despite its major prognostic relevance in geriatric intensive care. We performed a pooled analysis of acute ICU admissions from three prospective multinational cohorts within the Very Old Intensive Care Patients project: VIP1 and VIP2, which enrolled patients aged 80 years or older, and COVIP, which enrolled patients aged 70 years or older with COVID-19. Frailty was assessed before the acute illness using the Clinical Frailty Scale. The primary endpoint was 30-day mortality. Associations between sex and mortality were examined using robust Poisson regression adjusted for age, frailty, Sequential Organ Failure Assessment score, organ support, and treatment limitations, with Bayesian models used to estimate posterior probabilities of clinically relevant effect sizes. Among 10,363 acute ICU admissions, 43% were women. Women were older and more often frail, whereas men more frequently received invasive mechanical ventilation, vasopressors, and renal replacement therapy. Crude 30-day mortality was higher in men than in women (44%vs. 40%). Frailty was a strong independent predictor of mortality, with each 1-point increase in the Clinical Frailty Scale associated with an 8% increase in adjusted mortality risk (incidence-rate ratio 1.08, 95% CI 1.06-1.10). After multivariable adjustment for frailty and clinical covariates, male sex remained associated with a small residual increase in 30-day mortality (incidence-rate ratio 1.08; 95% CI 1.01-1.15). This association was attenuated with greater illness severity and more intensive organ support. Bayesian analyses yielded adjusted posterior median incidence-rate ratios of 1.04 to 1.06, and the probability of at least 10% excess mortality in men was low after adjustment (2% to 13%). In older critically ill adults, pre-admission frailty is a major driver of mortality. After explicit adjustment for frailty and illness severity, male sex was associated with only a small residual increase in 30-day mortality. Bayesian analyses suggest that large clinically meaningful sex-based mortality differences are unlikely after accounting for case mix and treatment intensity.

Objectives: EuroSCORE II is widely used to predict perioperative and 30-day mortality in cardiac surgery, yet data on its ability to predict long-term outcomes remain limited. This study investigates whether EuroSCORE II is associated with one-year and long-term mortality in a heterogeneous population undergoing major cardiac surgery with cardiopulmonary bypass. Methods: A retrospective cohort study was conducted including 2179 patients who underwent elective or urgent cardiac surgery with cardiopulmonary bypass between 2017 and 2021 at the University Hospital Salzburg. Data were extracted from the Salzburg Intensive Care database (SICdb) and supplemented with mortality information from Statistik Austria. EuroSCORE II values were compared between survivors and non-survivors. Kaplan–Meier analyses, Cox regression and logistic regression with ROC analysis were performed to evaluate the predictive association of EuroSCORE II with mortality. Results: EuroSCORE II was significantly higher in patients who died within one year and in those who died during a mean follow-up period of 1152.67 ± 521.39 days. Patients who survived at least one year had a median EuroSCORE II of 2.2, whereas those who died within one year had a median of 7.0. Cox regression demonstrated a hazard ratio of 1.062 for one-year mortality and 1.058 for long-term mortality. Kaplan–Meier curves showed significantly reduced survival with increasing EuroSCORE II quartiles. Logistic regression for one-year mortality yielded an AUC of 0.773, indicating good discriminative ability. Conclusions: EuroSCORE II is significantly associated with long-term mortality after major cardiac surgery, demonstrating good discriminatory performance. These findings support its potential utility not only as a short-term but also as a long-term prognostic indicator in cardiac surgery populations.