Vasoactive Agent Use in Septic Shock: Beyond First‐Line Recommendations

Sacha, Gretchen L.; Bauer, Seth R.; Lat, Ishaq

doi:10.1002/phar.2220

Cited by 24 publications

(14 citation statements)

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“…ANG II also enhances the release of NE from sympathetic nerve endings (6). The exogenous application of ANG II improves the sensitivity of blood vessels to catecholamines, constricts the glomerular efferent arteries, increases the glomerular perfusion pressure, and elevates the glomerular filtration rate (20)(21)(22).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II-mediated improvement of renal mitochondrial function via the AMPK/PGC-1α/NRF-2 pathway is superior to norepinephrine in a rat model of septic shock associated with acute renal injury

Chen

et al. 2021

Ann Transl Med

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Background: This study sought to compare the therapeutic effects of angiotensin II (ANG II) and norepinephrine (NE) on cecal ligation and puncture (CLP)-induced septic acute kidney injury (AKI) in rats.Methods: Sepsis shock was induced in anesthesia Sprague-Dawley male rats by CLP model for 24 hours.A total of 40 rats were divided into five groups, including control group, sham group, CLP group, CLP + ANG II group, and CLP + NE group. CLP + ANG II and CLP + NE group were administration of ANG II or NE after sepsis shock respectively, maintaining the MAP at 75-85 mmHg. CLP group was administration of saline for contrast. At 0, 18, 24 hours measured the renal blood grades and resistant index (RI) by ultrasound equipment. At 6, 12, 18 and 24 hours collected 0.5 mL blood sample for creatinine and lactic acid examination. Rats were observed for 24 hours after CLP procedure and then sacrificed for subsequent examination, rat serum were used to determine the levels of inflammatory response factors, kidney tissues were used to examine the oxidative stress factors and mitochondrial related proteins." We added the sentence as following: "The AMPK, PGC-1α and NRF-2 expression in renal cortex was significantly increased in the CLP + ANG Ⅱ group.Results: Compared to the vehicle treatment, both ANG II and NE administration restored the decrease in the mean arterial pressure (MAP) and alleviated mitochondrial impairments in CLP rats. However, only ANG II alleviated CLP-induced abnormalities in serum creatinine and lactic acid concentrations, renal blood flow, the renal resistant index, renal histopathology, the production of proinflammatory cytokines, and oxidative stress markers in rats. ANG II was also found to be superior to NE in reversing the CLP-induced suppression of mitochondrial biogenesis-related protein expression in the kidneys of rats.Conclusions: ANG II was better than NE in alleviating CLP-induced septic AKI in rats.

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Section: Discussionmentioning

confidence: 99%

Angiotensin II-mediated improvement of renal mitochondrial function via the AMPK/PGC-1α/NRF-2 pathway is superior to norepinephrine in a rat model of septic shock associated with acute renal injury

Chen

et al. 2021

Ann Transl Med

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“…Several recent articles have described the detrimental effects of catecholamines and optimal use of alternative vasopressors such as vasopressin and angiotensin II. [19][20][21][22][23] However, despite their appeal, studies have not demonstrated conclusive benefits of alternative vasopressors over adrenergic agents. 5,19 Although retrospective studies have suggested a benefit of early vasopressin initiation, [24][25][26] a large interventional study did not find a benefit in kidney failure-free days or mortality with this approach.…”

Section: Discussionmentioning

confidence: 99%

Mortality, Morbidity, and Costs After Implementation of a Vasopressin Guideline in Medical Intensive Care Patients With Septic Shock: An Interrupted Time Series Analysis

2019

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Background: Vasopressin decreases vasopressor requirements in patients with septic shock. However, the optimal norepinephrine dose for initiation or cessation of vasopressin is unclear. Objective: Analyze monthly intensive care unit (ICU) mortality rates 1 year preimplementation and postimplementation of a guideline suggesting a norepinephrine dose of 50 µg/min or more for initiation of vasopressin and early cessation of vasopressin. Methods: This retrospective quasi-experimental study included adult patients with septic shock admitted to the medical ICU of a tertiary care medical center over 2 years. Time periods were evaluated with interrupted time series analysis. Results: A total of 1148 patients were included: 573 patients preguideline and 575 patients postguideline. Group characteristics were well balanced at baseline, except patients postguideline had higher sequential organ failure assessment scores. Postguideline, fewer patients were initiated on vasopressin (305 [53.2%] vs 217 [37.7%], absolute difference −15.5% [95% CI −21.2% to −9.8%]), and the norepinephrine dose at vasopressin initiation was higher (median 25 [interquartile range 18, 40] µg/min vs 40 [22, 52] µg/min; median difference 15 [95% CI 11 to 19] µg/min; P < 0.01). After guideline implementation, there was no evidence for a difference in ICU mortality rate slope (slope change 0.07% [95% CI −0.8% to 1.0%] per month; P 0.87), but the vasoactive cost level decreased by US$183 (95% CI −US$327 to −US$39) per patient immediately after implementation. Conclusion and Relevance: Implementation of a guideline suggesting a high norepinephrine dose threshold for vasopressin initiation and early vasopressin cessation in patients with septic shock appears to be safe and may decrease vasoactive costs.

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“…Vasopressin reduces the dose of catecholamine vasopressors, but does not appear to affect patient mortality [2]. It is often used as a replacement dose after initiation of norepinephrine [29].…”

Section: Management/treatmentmentioning

confidence: 99%

Sepsis and Septic Shock

Mehta¹,

Ali²,

Swaroop³

2020

Clinical Management of Shock - The Science and Art of Physiological Restoration

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Sepsis and septic shock are life-threatening conditions that remain an enormous burden of morbidity and mortality to millions of patients globally and cause organ dysfunction, leading to death in as many as one in four patients, often even more. Early management and appropriate treatment are essential to improve outcomes and reduce morbidity and mortality. In 2016, the Third International Consensus Definition for Sepsis and Septic Shock (Sepsis-3) defined sepsis as life-threatening organ dysfunction resulting from dysregulated host responses to infection, and defined septic shock as a subset of sepsis in which underlying circulatory, cellular, and metabolic abnormalities are profound enough to substantially increase the risk of mortality. That same year the group also implemented the application of the sequential organ failure assessment (SOFA) score over the systemic inflammatory response syndrome (SIRS) score. Sepsis in pregnancy remains a leading cause of maternal morbidity and mortality worldwide, with no current standard definition for severe sepsis for the pregnant or peripartum woman. The prevalence of pediatric septic shock is on the rise and brings with it the consequences of long-term morbidity and also death. Since the advent of programs for early recognition and treatment, mortality has decreased. Even so, globally, many children succumb to septic shock despite evidence-based care and years of research.

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Vasoactive Agent Use in Septic Shock: Beyond First‐Line Recommendations

Cited by 24 publications

References 100 publications

Angiotensin II-mediated improvement of renal mitochondrial function via the AMPK/PGC-1α/NRF-2 pathway is superior to norepinephrine in a rat model of septic shock associated with acute renal injury

Angiotensin II-mediated improvement of renal mitochondrial function via the AMPK/PGC-1α/NRF-2 pathway is superior to norepinephrine in a rat model of septic shock associated with acute renal injury

Mortality, Morbidity, and Costs After Implementation of a Vasopressin Guideline in Medical Intensive Care Patients With Septic Shock: An Interrupted Time Series Analysis

Sepsis and Septic Shock

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