Oeckler, Richard A.

Body positioning exerts profound physiological effects in critically ill patients, influencing respiratory mechanics, ventilation-perfusion matching, hemodynamics, and overall clinical outcomes. Transitioning from an upright to a recumbent position alters thoracoabdominal pressure relationships, reduces ribcage contribution to tidal ventilation, and shifts ventilatory load to the diaphragm. These changes decrease functional residual capacity and promote airway closure in dependent lung regions, predisposing patients to atelectasis—an effect further amplified by intra-abdominal pathology or diaphragmatic weakness. Positioning also reshapes pulmonary perfusion and ventilation, which impact cardiopulmonary hemodynamics. These physiologic principles translate to important therapeutic applications across disease states. In ARDS, prone positioning improves oxygenation via a number of mechanisms, reduces ventilator-induced lung injury, and confers substantial mortality benefit. Prone position may also improve air flow distribution in COPD and enhance venous return in select cardiac physiologies. Conversely, conditions such as ascites, morbid obesity, and hepatopulmonary syndrome exemplify pathologic interactions between abdominal pressure, lung volumes, and posture, often requiring tailored positioning strategies to optimize respiratory performance. Overall, body positioning represents a potent, underutilized intervention in critical care. Understanding the mechanistic foundations of position-dependent changes in ventilation, perfusion, and pleural pressure can help clinicians strategically leverage positioning to improve patient outcomes across a spectrum of pulmonary and systemic illnesses.

Mechanical ventilation remains a cornerstone of acute respiratory failure management, but ventilator-induced lung injury persists despite lung-protective strategies focused on limiting tidal volume (V T ), plateau pressure, and driving pressure. Mechanical power has emerged as a comprehensive metric that quantifies the total energy delivered to the lungs per unit time by integrating V T , airway pressures, breathing frequency, flow, and PEEP into a single physiologic measure. Observational studies through 2025 show that elevated mechanical power is associated with worse outcomes, including increased mortality, fewer ventilator-free days, and longer ICU stays, with breathing frequency identified as a major contributor even when other settings remain within protective ranges. Although no universal injurious threshold exists because of patient variability, normalization strategies such as indexing mechanical power to predicted body weight or respiratory system compliance have shown promise in improving prognostic value, although consensus on the optimal method is lacking. Currently, mechanical power should be considered a complementary bedside tool that integrates multiple ventilator variables, helps identify key contributors to lung stress and strain, and may support individualized ventilator adjustments to reduce cumulative injury risk as further evidence and technology evolve.

Abstract Rationale Lung-protective ventilation protocols use predicted body weight (PBW) to set tidal volumes. However, biases exist in these formulas, with overestimation of lung capacity in older, shorter, female, and non-White patients—groups that experience higher mortality rates during invasive mechanical ventilation (IMV). This study investigated associations between pre-admission forced vital capacity (FVC), driving pressure, and patient outcomes. Methods This multicenter retrospective study included adults (18-95 years old) with pre-admission spirometry who required IMV between 01/01/2016 and 05/31/2025 across the Mayo Clinic, spanning 11 ICUs within 5 hospitals in 4 states. Patients were stratified by FVC/PBW ratio quartiles. The primary outcome was 28-day mortality. Trends were assessed using linear or logistic regression, with FVC/PBW as a continuous variable. Mediation analysis examined pathways between FVC/PBW and mortality, with driving pressure (cm H2O, standardized) as the mediator, and adjusted for covariates including age, sex, SOFA score, and BMI. Absolute risk differences and number needed to harm (NNH) were estimated for key thresholds (e.g. FVC/PBW ≥45 mL/kg, PFTs within 2 years). Results Among 4,839 patients (38.7% female, mean (±SD) age 64.5±13.5 years), FVC/PBW ratio demonstrated substantial individual variation, with a mean of 48.3 ± 13.4 mL/kg. There was systematic variation by demographics (Figure): females had significantly lower ratios than males (45.4 versus 50.2 mL/kg, P < 0.001), and ratios were lower with older age from 52.5 mL/kg in patients <65 to 43.2 mL/kg in those ≥85 years (P < 0.001 for trend). Patients in the lowest FVC/PBW quartile had higher 28-day mortality compared to the highest quartile (26.0% versus 17.0%, P < 0.001) and higher driving pressures (14.0 versus 10.0 cm H2O, P < 0.001; Figure). In mediation analysis (n = 4,147), driving pressure mediated the relationship between FVC and mortality. Each 1-SD increase in FVC/PBW was associated with 0.364-SD lower driving pressure (P < 0.001) and 2.4% lower mortality. The adjusted indirect effect through driving pressure was significant (ACME -0.024, 95% CI: -0.029 to -0.019), accounting for the mortality effect. Sensitivity analyses across binary thresholds, age quartiles, outlier exclusion, and obstructive pathology confirmed robust mediation. Patients with FVC/PBW <45 mL/kg (N = 1,644; 39.6%) had 28-day mortality of 17.8% versus 13.5% for ≥45 mL/kg (risk difference 4.3%, 95% CI 1.8-6.8%; NNH: 23 patients). Conclusions Pre-admission lung function was strongly associated with mortality in adults receiving IMV through driving pressure-mediated pathways. Driving pressure is a modifiable target, especially in patients with smaller lung capacities at highest risk for ventilator-induced lung injury. Further prospective investigation is needed to confirm these findings. This abstract is funded by: National Heart, Lung, and Blood Institute (NHLBI) of the National Institute of Health (NIH) Grant Number K23HL151671

Abstract Rationale Hyperchloremia, characterized by elevated chloride levels (>110 mEq/L) in the blood, frequently occurs in critically ill patients following aggressive fluid resuscitation with chloride-rich solutions. It is associated with metabolic acidosis, leading to negative clinical outcomes such as higher morbidity and mortality. However, the impact of hyperchloremia on the duration of mechanical ventilation remains unclear. This study evaluates the correlation between hyperchloremia and the duration of mechanical ventilation in critically ill patients. Methods A retrospective analysis was conducted on intensive care unit patients admitted between 2018 and 2023 who required mechanical ventilation. Patients were categorized into hyperchloremic (serum chloride >110 mEq/L) and non-hyperchloremic groups. The hyperchloremic group was further subdivided into those with metabolic acidosis (pH <7.35) and those without acidosis (pH >7.35). The primary outcome measured was the duration of mechanical ventilation across these groups. Results The study included 7,333 patients, 408 in the hyperchloremic group and 6,926 in the non-hyperchloremic group. Patients with hyperchloremia experienced significantly longer ventilation durations, with an average of 5.9 days compared to 2.6 days in the non-hyperchloremic group (p < 0.01). Among the hyperchloremic subgroups, those with metabolic acidosis had a mean ventilation duration of 4.9 days compared to 6.2 days in those without acidosis (p = 0.7), suggesting no apparent significant influence of acid-base status on ventilation duration. Discussion The study found that hyperchloremia correlates with longer ventilation duration (4.9-6.2 days vs. 2.6 days), independent of pH. While metabolic acidosis might impair respiratory function and increase ventilatory needs, evidence is mixed. Hyperchloremic metabolic acidosis can alter respiratory regulation, causing issues like tachypnea, ventilator dyssynchrony, and the need for sedation, complicating weaning from ventilation. However, hyperchloremia does not always impair respiratory muscle function. The study is limited by its retrospective nature, making causal conclusions difficult. However, the study suggests that better electrolyte management may reduce ventilation duration and improve patient outcomes. Conclusion This study demonstrates a significant association between hyperchloremia and prolonged mechanical ventilation, independent of pH status. The findings suggest that hyperchloremia may either be a marker of severe illness or aggressive resuscitation and directly contribute to prolonged ventilatory support. These findings offer hope for improved patient outcomes, as they suggest that chloride management strategies, including chloride-sparing resuscitation, could potentially reduce mechanical ventilation duration in critically ill patients.