134 research outputs found
sj-docx-1-jic-10.1177_08850666231173847 - Supplemental material for Effects of Etomidate on Postintubation Hypotension, Inflammatory Markers, and Mortality in Critically Ill Patients with COVID-19: An International, Multicenter, Retrospective Study
Supplemental material, sj-docx-1-jic-10.1177_08850666231173847 for Effects of Etomidate on Postintubation Hypotension, Inflammatory Markers, and Mortality in Critically Ill Patients with COVID-19: An International, Multicenter, Retrospective Study by Konstantinos Leou, Dianelys Mendez, George Horani, Nikolaos Papagiannakis, Roberto Jiménez Sánchez, Diana Mazzei, Isabel Mora, Rajapriya Manickam, Konstantinos Tourlakopoulos and
José Francisco Garrido Peñalver, David Jiménez Medina,
María Dolores Rodríguez Mulero, Konstantinos Annousis, Eleni Laou, Luis García de Guadiana-Romualdo, Ioannis Pantazopoulos, Kunwar Kaur, Athanasios Chalkias, in Journal of Intensive Care Medicine</p
sj-odt-2-jic-10.1177_08850666231173847 - Supplemental material for Effects of Etomidate on Postintubation Hypotension, Inflammatory Markers, and Mortality in Critically Ill Patients with COVID-19: An International, Multicenter, Retrospective Study
Supplemental material, sj-odt-2-jic-10.1177_08850666231173847 for Effects of Etomidate on Postintubation Hypotension, Inflammatory Markers, and Mortality in Critically Ill Patients with COVID-19: An International, Multicenter, Retrospective Study by Konstantinos Leou, Dianelys Mendez, George Horani, Nikolaos Papagiannakis, Roberto Jiménez Sánchez, Diana Mazzei, Isabel Mora, Rajapriya Manickam, Konstantinos Tourlakopoulos and
José Francisco Garrido Peñalver, David Jiménez Medina,
María Dolores Rodríguez Mulero, Konstantinos Annousis, Eleni Laou, Luis García de Guadiana-Romualdo, Ioannis Pantazopoulos, Kunwar Kaur, Athanasios Chalkias, in Journal of Intensive Care Medicine</p
sj-odt-3-jic-10.1177_08850666231173847 - Supplemental material for Effects of Etomidate on Postintubation Hypotension, Inflammatory Markers, and Mortality in Critically Ill Patients with COVID-19: An International, Multicenter, Retrospective Study
Supplemental material, sj-odt-3-jic-10.1177_08850666231173847 for Effects of Etomidate on Postintubation Hypotension, Inflammatory Markers, and Mortality in Critically Ill Patients with COVID-19: An International, Multicenter, Retrospective Study by Konstantinos Leou, Dianelys Mendez, George Horani, Nikolaos Papagiannakis, Roberto Jiménez Sánchez, Diana Mazzei, Isabel Mora, Rajapriya Manickam, Konstantinos Tourlakopoulos and
José Francisco Garrido Peñalver, David Jiménez Medina,
María Dolores Rodríguez Mulero, Konstantinos Annousis, Eleni Laou, Luis García de Guadiana-Romualdo, Ioannis Pantazopoulos, Kunwar Kaur, Athanasios Chalkias, in Journal of Intensive Care Medicine</p
Effects of Vasopressin Receptor Agonists during the Resuscitation of Hemorrhagic Shock: A Systematic Review and Meta-Analysis of Experimental and Clinical Studies
ackground: The clinical impact of vasopressin in hemorrhagic shock remains largely unknown. Objective: This systematic review and meta-analysis was designed to investigate the effects of vasopressin receptor agonists during the resuscitation of hemorrhagic shock. Methods: A systematic search of PubMed (MEDLINE), Scopus, and PubMed Central was conducted for relevant articles. Experimental (animal) and clinical studies were included. The primary objective was to investigate the correlation of vasopressin receptor agonist use with mortality and various hemodynamic parameters. Results: Data extraction was possible in thirteen animal studies and two clinical studies. Differences in risk of mortality between patients who received a vasopressin receptor agonist were not statistically significant when compared to those who were not treated with such agents [RR (95% CI): 1.17 (0.67, 2.08); p = 0.562; I2 = 50%]. The available data were insufficient to conduct a meta-analysis assessing the effect of vasopressin receptor agonists on hemodynamics. Drawing safe conclusions from animal studies was challenging, due to significant heterogeneity in terms of species and dosage of vasopressin receptor agonists among studies. Conclusions: Differences in risk of mortality between patients who received a vasopressin receptor agonist were not statistically significant when compared to those who were not treated with such agents after hemorrhagic shock. More data are needed to deduce certain conclusions
Current Challenges in the Management of Sepsis and Septic Shock: Personalized, Physiology-Guided Treatment
Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection affecting millions of people each year [...
Angiotensin II in the treatment of distributive shock: a systematic-review and meta-analysis.
BACKGROUND
While non-norepinephrine vasopressors are increasingly used as a rescue therapy in cases of norepinephrine-refractory shock, data on their efficacy are limited. This systematic review and meta-analysis aims to synthesize existing literature on the efficacy of Angiotensin II (ATII) in distributive shock.
METHODS
We pre-registered our meta-analysis with PROSPERO (CRD42023456136). We searched PubMed, Scopus, and gray literature for studies presenting outcomes on ATII use in distributive shock. The primary outcome of the meta-analysis was all-cause mortality. We used a random effects model to calculate pooled risk ratio (RR) and 95% confidence intervals (CI).
RESULTS
By incorporating data from 1555 patients included in 10 studies, we found that however all-cause mortality was similar among patients receiving ATII and controls (RR 1.02, 95% CI 0.89 to 1.16, p = 0.81), the reduction in norepinephrine or norepinephrine-equivalent dose at 3 h after treatment initiation was greater among patients receiving ATII (MD -0.06, 95% CI -0.11 to -0.02, p = 0.008), while there were no higher rates of adverse events reported among ATII patients.
CONCLUSIONS
While ATII did not reduce mortality among distributive shock patients, it allowed for significant adjunctive vasopressor reduction at 3 h without an increase in reported adverse events, deeming it a viable alternative for the increasingly adopted multimodal vasopressor for minimizing catecholamine exposure and its adverse events
Airway pressure and outcome of out-of-hospital cardiac arrest: A prospective observational study
Aim To assess the usefulness of airway pressure as predictor of return of spontaneous circulation (ROSC), as well as to investigate the optimized ventilation compression strategy during cardiopulmonary resuscitation (CPR). Methods In this prospective observational study, 300 out-of-hospital cardiac arrest victims were intubated and resuscitated with the use of a ventilator. Mean airway pressure (mPaw) was measured at pre-defined phases of CPR. Results A significant difference in mPaw was observed between survivors and non-survivors after the onset of the third minute of CPR. An mPaw value of 42.5 mbar during CPR had specificity and sensitivity of 0.788 and 0.804, respectively, for ROSC (AUC = 0.668, p = 0.047). During CPR, we found statistically significant differences in mPaw at phases zero (F = 4.526, p = 0.002), two (F = 4.506, p = 0.002), four (F = 8.187, p < 0.0001), five (F = 2.871, p = 0.024), and six (F = 5.364, p < 0.0001). Conclusion Mean airway pressure was higher in survivors. A value of 42.5 mbar was associated with ROSC
Increasing stress volume vs. increasing tissue perfusion in septic patients
[No abstract available
Shear Stress and Endothelial Mechanotransduction in Trauma Patients with Hemorrhagic Shock: Hidden Coagulopathy Pathways and Novel Therapeutic Strategies
Massive trauma remains a leading cause of death and a global public health burden. Post-traumatic coagulopathy may be present even before the onset of resuscitation, and correlates with severity of trauma. Several mechanisms have been proposed to explain the development of abnormal coagulation processes, but the heterogeneity in injuries and patient profiles makes it difficult to define a dominant mechanism. Regardless of the pattern of death, a significant role in the pathophysiology and pathogenesis of coagulopathy may be attributed to the exposure of endothelial cells to abnormal physical forces and mechanical stimuli in their local environment. In these conditions, the cellular responses are translated into biochemical signals that induce/aggravate oxidative stress, inflammation, and coagulopathy. Microvascular shear stress-induced alterations could be treated or prevented by the development and use of innovative pharmacologic strategies that effectively target shear-mediated endothelial dysfunction, including shear-responsive drug delivery systems and novel antioxidants, and by targeting the venous side of the circulation to exploit the beneficial antithrombogenic profile of venous endothelial cells
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