Critical care medicine:

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The unprimed right ventricle is exquisitely sensitive to acute elevations in afterload. High pulmonary vascular tone incurred with acute pulmonary embolism has the potential to induce obstructive shock and circulatory collapse. While emergent pulmonary reperfusion is essential in severe circumstances, an important subset of pulmonary embolism patients may exhibit a less extreme presentation posing a management dilemma. As intensive care therapies have the potential to both salvage and harm the failing right ventricle, a keen understanding of the pathophysiology is requisite in the care of the contemporary patient with hemodynamically significant pulmonary embolism. Here, we review right ventricular pathophysiology, an approach to risk stratification, and offer guidance on the medical and mechanical supportive and therapeutic strategies for the critically ill patient with acute pulmonary embolism.

The incidence of heat-related illnesses and heatstroke continues to rise amidst global warming. Hyperthermia triggers inflammation, coagulation, and progressive multiorgan dysfunction, and, at levels above 40 °C, can even lead to cell death. Blood cells, particularly granulocytes and platelets, are highly sensitive to heat, which promotes proinflammatory and procoagulant changes. Key factors in heatstroke pathophysiology involve mitochondrial thermal damage and excessive oxidative stress, which drive apoptosis and necrosis. While the kinetics of cellular damage from heat have been extensively studied, the mechanisms driving heat-induced organ damage and death are not yet fully understood. Converse to hyperthermia, hypothermia is generally protective, as seen in therapeutic hypothermia. However, accidental hypothermia presents another environmental threat due to arrhythmias, cardiac arrest, and coagulopathy. From a cellular physiology perspective, hypothermia generally supports mitochondrial homeostasis and enhances cell preservation, aiding whole-body recovery following resuscitation. This review summarizes recent findings on temperature-related cellular damage and preservation and suggests future research directions for understanding the tempo-physiologic axis.

CONCLUSIONS: The prevalence rates of post-intensive care cognitive impairment differed at different follow-up timepoints. The rates were highest within the first three months of follow-up, with a pooled prevalence of 49.8% at less than one month, 45.1% at one to three months, and 47.9% at three to six months. No significant differences in prevalence rates between studies that only included coronavirus disease 2019 survivors. These fundings highlight the need for further research to develop targeted interventions to prevent or manage cognitive impairment at short-term and long-term follow-ups.

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BACKGROUND: American College of Surgeons (ACS) trauma center verification has demonstrated improved outcomes at individual centers, but its impact on statewide Trauma Quality Improvement Program (TQIP) Collaboratives is unknown. A statewide TQIP Collaborative, founded in 2011, noted underperformance in six of eight patient cohorts identified in the TQIP Collaborative report. We hypothesized that requiring ACS verification for level I and II trauma centers would result in improved outcomes for the state collaborative.

CONCLUSIONS: Critical care clinicians ideally demonstrate functional knowledge of conditions that are directly related to, or are accompanied by, deranged lymphatic dynamics to direct timely diagnostic and therapeutic interventions during a patient's ICU care episode.

BACKGROUND: The association between bedside ventilatory parameters-specifically arterial carbon dioxide pressure (PaCO) and ventilatory ratio (VR)-and mortality in patients with acute respiratory distress syndrome (ARDS) remains a topic of debate. Additionally, the persistence of this association over time is unclear. This study aims to investigate the relationship between 28-day mortality in ARDS patients and their longitudinal exposure to ventilatory inefficiency, as reflected by serial measurements of PaCO and VR.

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The host and microbes play complex roles in balancing the pro- and anti-inflammatory pathways that cause sepsis. It is now increasingly recognized as a disorder of the mitochondrial system intrinsically or as a consequence of microcirculatory abnormalities leading to hypoperfusion/hypoxia ("microcirculatory and mitochondrial distress syndrome"). It is expected that improvements in endothelium or mitochondrial level therapy will lower sepsis-related morbidity and mortality. This article aimed to clarify the mitochondrial and microcirculation abnormalities in patients with sepsis and the futuristic research agenda for the management of sepsis.

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BACKGROUND: There is conflicting evidence regarding emergency medical service (EMS) provider level of training and outcomes in trauma. We hypothesized that advanced life support (ALS) provider transport is associated with lower mortality compared with basic life support transport.