Clinical management for patients admitted to a critical care unit with severe sepsis or septic shock

Cheung, William K.; Chau, Lai Sheung; Mak, Iun Ieng Laurinda; Wong, Mei Yi; Wong, Sai Leung; Tiwari, Agnes

doi:10.1016/j.iccn.2015.04.005

Cited by 5 publications

(5 citation statements)

References 28 publications

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“…Our model of sepsis had little effect on cardiac morphology and function. Sepsis has different influences on cardiac function according to the severity of the pathology: early sepsis increases the heart rate [6, 40] to fight against the systemic hypotension encountered in this situation [41]. With more severe sepsis, diastolic dysfunctions occur [8].…”

Section: Discussionmentioning

confidence: 99%

“…We observed that CLP tended to stimulate myocardial contractility ( p = 0.08) similarly in both groups (cross-interaction between the effect of the diet and that of CLP = 0.99). This indicates clearly that animals of both groups were in the initial hyperdynamic phase of sepsis [6].…”

Section: Methodsmentioning

confidence: 99%

“…Importantly, cardiac failure accounts for approximately 50% of deaths [5], the heart being one of the preferred targets of the infection. However, except for a stimulation of the heart rate occurring in the early phase of sepsis [6], changes in cardiac mechanical function are detected only in the sickest patients using the most recent techniques (echography, MRI): they are first characterized by an impaired diastolic function, which evolves toward a reduced systolic function in the most severe cases [7, 8].…”

Section: Introductionmentioning

confidence: 99%

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Antioxidant and Cardioprotective Effects of EPA on Early Low-Severity Sepsis through UCP3 and SIRT3 Upholding of the Mitochondrial Redox Potential

Leger

Azarnoush

Traoré³

et al. 2019

Oxidative Medicine and Cellular Longevity

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Sepsis still causes death, often through cardiac failure and mitochondrial dysfunction. Dietary ω3 polyunsaturated fatty acids are known to protect against cardiac dysfunction and sepsis lethality. This study set out to determine whether early low-severity sepsis alters the cardiac mitochondrial function in animals fed a Western-type diet and whether dietary eicosapentaenoic acid (EPA) administration protects the myocardium against the deleterious effects of sepsis and if so to seek possible mechanisms for its effects. Rats were divided into two groups fed either an ω3 PUFA-deficient diet (“Western diet,” DEF group) or an EPA-enriched diet (EPA group) for 5 weeks. Each group was subdivided into two subgroups: sham-operated rats and rats subjected to cecal ligation and puncture (CLP). In vivo cardiac mechanical function was examined, and mitochondria were harvested to determine their functional activity. Oxidative stress was evaluated together with several factors involved in the regulation of reactive oxygen species metabolism. Sepsis had little effect on cardiac mechanical function but strongly depressed mitochondrial function in the DEF group. Conversely, dietary EPA greatly protected the mitochondria through a decreased oxidative stress of the mitochondrial matrix. The latter was probably due to an increased uncoupling protein-3 expression, already seen in the sham-operated animals. CLP rats in the EPA group also displayed increased mitochondrial sirtuin-3 protein expression that could reinforce the upholding of oxidative phosphorylation. Dietary EPA preconditioned the heart against septic damage through several modifications that protect mitochondrial integrity. This preconditioning can explain the cardioprotective effect of dietary EPA during sepsis.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Antioxidant and Cardioprotective Effects of EPA on Early Low-Severity Sepsis through UCP3 and SIRT3 Upholding of the Mitochondrial Redox Potential

Leger

Azarnoush

Traoré³

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…The most evident abnormality of the cardiovascular function is a decrease in arterial pressure associated with an initial compensatory stimulation of the heart rate (Cheung et al. 2015). The activation of the cardiac pump has for a long period been made responsible for the exhaustion of cardiomyocytes and the cardiac failure associated with the septic shock.…”

Section: Introductionmentioning

confidence: 99%

Early sepsis does not stimulate reactive oxygen species production and does not reduce cardiac function despite an increased inflammation status

et al. 2017

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If it is sustained for several days, sepsis can trigger severe abnormalities of cardiac function which leads to death in 50% of cases. This probably occurs through activation of toll‐like receptor‐9 by bacterial lipopolysaccharides and overproduction of proinflammatory cytokines such as TNF‐α and IL‐1β. In contrast, early sepsis is characterized by the development of tachycardia. This study aimed at determining the early changes in the cardiac function during sepsis and at finding the mechanism responsible for the observed changes. Sixty male Wistar rats were randomly assigned to two groups, the first one being made septic by cecal ligation and puncture (sepsis group) and the second one being subjected to the same surgery without cecal ligation and puncture (sham‐operated group). The cardiac function was assessed in vivo and ex vivo in standard conditions. Several parameters involved in the oxidative stress and inflammation were determined in the plasma and heart. As evidenced by the plasma level of TNF‐α and gene expression of IL‐1β and TNF‐α in the heart, inflammation was developed in the sepsis group. The cardiac function was also slightly stimulated by sepsis in the in vivo and ex vivo situations. This was associated with unchanged levels of oxidative stress, but several parameters indicated a lower cardiac production of reactive oxygen species in the septic group. In conclusion, despite the development of inflammation, early sepsis did not increase reactive oxygen species production and did not reduce myocardial function. The depressant effect of TNF‐α and IL‐1β on the cardiac function is known to occur at very high concentrations. The influence of low‐ to moderate‐grade inflammation on the myocardial mechanical behavior must thus be revisited.

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“…[3] Septic shock treatment protocols are well established around the world, and it is briefly composed of a triad that includes hemodynamic resuscitation with crystalloid, infusion of vasopressors and administration of antimicrobials within the first hour of diagnosis. [4] Although this triad has been shown to reduce mortality, [5][6][7] mortality rates from septic shock are still above 40%, which is a major health problem affecting millions of people around the world each year despite all the technological and scientific advancement. [8] In this context, new therapeutic improvements are needed and are under study.…”

Section: Introductionmentioning

confidence: 99%

Effect of methylene blue on hemodynamic and metabolic response in septic shock patients

et al. 2022

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Introduction: Septic shock is a lethal disease responsible for a large proportion of deaths in the Intensive Care Unit (ICU), even with therapy centered on fluid resuscitation, use of vasopressors and empirical antibiotic therapy applied within the first hour of diagnosis. Considering the multifactorial pathophysiology of septic shock and the mechanism of action of vasopressors, some patients may not respond adequately, which can lead to the maintenance of vasodilatation, hypotension and increased morbidity, and mortality. This protocol aims to verify whether the use of methylene blue in septic patients with an early diagnosis can contribute to an earlier resolution of a shock compared to standard treatment.Methods and analysis: This is a study protocol for a single-center randomized clinical trial design in an ICU of a tertiary university hospital. In this study, we intend to include 64 patients aged between 18 and 80 years with a diagnosis of septic shock, of any etiology, with up to 72 hours of evolution after volume restoration, using norepinephrine at a dose ≥0.2 mg/kg/min and vasopressin at a dose of 0.04 IU/min. After the initial approach, we will randomize patients into two groups, standard care, and standard care plus methylene blue. The sample size was calculated in order to show 30% differences in septic shock resolution between groups. The Research Ethics Committee approved the study, and all patients included will sign an informed consent form (Clinical registration: RBR-96584w4). Abbreviations: ARDS = acute respiratory distress syndrome, CI = cardiac index, cNOS = constitutive nitric oxide synthase, CO = Cardiac Output, EFG = global ejection fraction, HR = heart rate, IAPF = pulmonary extravascular water index, ICU = Intensive Care Unit, IDFG = global end-diastolic volume index, iNOS = induced nitric oxide synth, IPVP = pulmonary vascular permeability index, IRVSi = systemic vascular resistance index, IVSi = systolic volume index, MAP = mean arterial pressure, PVC = central venous pressure, SAPS-3 = Simplified Acute Physiology Score, SVV = systolic volume variation.

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Clinical management for patients admitted to a critical care unit with severe sepsis or septic shock

Cited by 5 publications

References 28 publications

Antioxidant and Cardioprotective Effects of EPA on Early Low-Severity Sepsis through UCP3 and SIRT3 Upholding of the Mitochondrial Redox Potential

Antioxidant and Cardioprotective Effects of EPA on Early Low-Severity Sepsis through UCP3 and SIRT3 Upholding of the Mitochondrial Redox Potential

Early sepsis does not stimulate reactive oxygen species production and does not reduce cardiac function despite an increased inflammation status

Effect of methylene blue on hemodynamic and metabolic response in septic shock patients

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