Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Background : Mortality in cardiogenic shock (CS) is up to 40%, and although risk scores have been proposed to stratify and assess mortality in CS, they have been shown to have inconsistent performance. The purpose was to compare CS prognostic scores and describe their performance in a real-world Latin American country. Methods : We included 872 patients with CS. ⋯ In non-AMI-CS, SCAI was the best (0.642). Conclusions : Clinical scores show a time-sensitive AUC, suggesting that performance could be influenced by time and the type of CS. Understanding the temporal influence on the scores could provide a better prediction and be a valuable tool in CS.
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Introduction : COVID-19-induced coagulopathy (CIC) can increase the risk of thromboembolism without underlying clotting disorders, even when compared with other respiratory viruses. Trauma has a known association with hypercoagulability. Trauma patients with concurrent COVID-19 infection potentially have an even greater risk of thrombotic events. ⋯ Positive patients had longer median ICU LOS ( P = 0.0012) and total LOS ( P < 0.001). Conclusion : There were no increased rates of VTE complications between COVID-19-positive and -negative trauma patients, despite a longer time to initiation of chemoprophylaxis in the COVID-19-positive group. COVID-19-positive patients had increased ICU LOS, total LOS, and mortality, which are likely due to multifactorial causes but primarily related to their underlying COVID-19 infection.
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Background: Sepsis is a life-threatening medical emergency, frequently complicated with intensive care unit-acquired weakness syndrome (ICU-AW). ICU-AW patients display flaccid weakness of the limbs, especially in the proximal limb muscles. However, little is known regarding its pathogenesis. ⋯ Muscle strength of septic mice was improved upon metformin treatment. Metformin intervention is therefore proposed as a potential therapeutic strategy for ICU-AW. Conclusion: Taken together, we revealed a previously unappreciated linkage between cellular senescence and sepsis-induced muscle weakness and propose metformin as a potential therapeutic drug for the treatment of ICU-AW.
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Background: The assessment of cardiac output (CO) is a major challenge during shock. The criterion standard for CO evaluation is transpulmonary thermodilution, which is an invasive technique. Speckle tracking is an automatized method of analyzing tissue motion using echography. ⋯ The correlation coefficient between fADV and SV was 0.71 (95% confidence interval [CI], 0.62 to 0.78; P < 0.01). The correlation coefficient between SV and abdominal aorta ADV, subclavian ADV, and carotid ADV was 0.30 (95% CI, 0.13 to 0.46; P < 0.01), 0.56 (95% CI, 0.45 to 0.66, P < 0.01), and 0.15 (95% CI, -0.01 to 0.30, P = 0.06), respectively. Conclusions : In this hemorrhagic shock model using piglets, fADV was strongly correlated with SV.
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Studies in animal models of sepsis have elucidated an intricate network of signaling pathways that lead to the dysregulation of myocardial Ca 2+ handling and subsequently to a decrease in cardiac contractile force, in a sex- and model-dependent manner. After challenge with a lethal dose of LPS, male animals show a decrease in cellular Ca 2+ transients (ΔCa i ), with intact myofilament function, whereas female animals show myofilament dysfunction, with intact ΔCa i. Male mice challenged with a low, nonlethal dose of LPS also develop myofilament desensitization, with intact ΔCa i. ⋯ Myofilament dysfunction is due to hyperphosphorylation of troponin I, troponin T cleavage by caspase-3, and overproduction of cGMP by NO-activated soluble guanylate cyclase. Depleted, dysfunctional, or uncoupled mitochondria likely synthesize less ATP in both sexes, but the role of energy deficit is not clear. NO produced by NO synthase (NOS)-3 and mitochondrial NOSs, protein kinases and phosphatases, the processes of autophagy and sarco/endoplasmic reticulum stress, and β-adrenergic insensitivity may also play currently uncertain roles.