Vasoplegia treatments: the past, the present, and the future

Lévy, Bruno; Fritz, Caroline; Tahon, Elsa; Jacquot, Audrey; Auchet, Thomas; Kimmoun, Antoine

doi:10.1186/s13054-018-1967-3

Cited by 162 publications

(193 citation statements)

References 79 publications

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“…Increased levels of intracellular calcium cause a cascade of events starting with myosin phosphorylation leading to myosin-actin filament crosslinking and vasoconstriction. The influx of cytoplasmic calcium is generated by agonism of Gprotein coupled receptors via catecholamines (alpha-1 adrenergic receptor), arginine vasopressin (vasopressin-1 receptor), and angiotensin II (angiotensin type-1 receptor) [11]. This mechanism is dysregulated during CPB, as the exposure of blood to foreign surfaces inside of the CPB circuit stimulates the release of inflammatory mediators, such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF).…”

Section: Pathophysiologymentioning

confidence: 99%

Vasoplegic syndrome following cardiothoracic surgery—review of pathophysiology and update of treatment options

2020

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Vasoplegic syndrome is a common occurrence following cardiothoracic surgery and is characterized as a highoutput shock state with poor systemic vascular resistance. The pathophysiology is complex and includes dysregulation of vasodilatory and vasoconstrictive properties of smooth vascular muscle cells. Specific bypass machine and patient factors play key roles in occurrence. Research into treatment of this syndrome is limited and extrapolated primarily from that pertaining to septic shock, but is evolving with the expanded use of catecholamine-sparing agents. Recent reports demonstrate potential benefit in novel treatment options, but large clinical trials are needed to confirm.

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Section: Pathophysiologymentioning

confidence: 99%

Vasoplegic syndrome following cardiothoracic surgery—review of pathophysiology and update of treatment options

2020

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“…Septic shock is characterized by micro-and macrocirculatory disturbances with a decrease in peripheral vascular resistance, maldistribution of cardiac output to organs, and impairment of oxygen extraction. Several mechanisms contribute to sepsis-related vasodilatation, and vasodilatation occurs despite high endogenous catecholamines levels and activation of the renin-angiotensinaldosterone system [11,12].…”

Section: Physiopathological Mechanisms Involved In Septic Shockmentioning

confidence: 99%

“…In addition to the deficiency of circulating vasopressin, Landry et al also highlighted the hypersensitivity of patients with septic shock to exogenous vasopressin administration: while arterial hypotension was corrected [13,17] in patients with septic shock, similar infusion rates had no effect on blood pressure in healthy subjects. All these observations together with the fact that exogenous vasopressin offers an alternative mechanism of action independent of adrenergic receptor activation prompted the interest for this hormone in the management of patients with septic shock [12].…”

Section: Physiopathological Mechanisms Involved In Septic Shockmentioning

confidence: 99%

Vasopressin and its analogues in shock states: a review

Demiselle

Fage

Radermacher

et al. 2020

Ann. Intensive Care

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Activation of arginine-vasopressin is one of the hormonal responses to face vasodilation-related hypotension. Released from the post-pituitary gland, vasopressin induces vasoconstriction through the activation of V1a receptors located on vascular smooth muscle cells. Due to its non-selective receptor affinity arginine-vasopressin also activates V2 (located on renal tubular cells of collecting ducts) and V1b (located in the anterior pituitary and in the pancreas) receptors, thereby potentially promoting undesired side effects such as anti-diuresis, procoagulant properties due to release of the von Willebrand's factor and platelet activation. Finally, it also cross-activates oxytocin receptors. During septic shock, vasopressin plasma levels were reported to be lower than expected, and a hypersensitivity to its vasopressor effect is reported in such situation. Terlipressin and selepressin are synthetic vasopressin analogues with a higher affinity for the V1 receptor, and, hence, potentially less side effects. In this narrative review, we present the current knowledge of the rationale, benefits and risks of vasopressin use in the setting of septic shock and vasoplegic shock following cardiac surgery. Clearly, vasopressin administration allows reducing norepinephrine requirements, but so far, no improvement of survival was reported and side effects are frequent, particularly ischaemic events. Finally, we will discuss the current indications for vasopressin and its agonists in the setting of septic shock, and the remaining unresolved questions.

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“…Patients with sepsis and acidaemia often require increased concentrations of exogenous (and endogenous) catecholamines to produce the same increase in arterial pressure when compared with patients without sepsis, a phenomenon known as vascular hyporesponsiveness. 25 Vascular hyporesponsiveness describes a decreased doseeresponse relationship, and its aetiology is multifactorial. In patients with sepsis it includes downregulation of catecholamine receptors, increased nitric oxide and prostacyclin production, generation of oxygen free radicals and peroxynitrite, and the activation of ATP-sensitive potassium channels caused by acidaemia and increased circulating lactate; this leads to hyperpolarisation of cell membranes and vasodilatation.…”

Section: Vasoactive Agentsmentioning

confidence: 99%

Pharmacokinetics in sepsis

Charlton

Thompson

2019

BJA Education

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By reading this article you should be able to:Describe the effects of sepsis on drug absorption, distribution, metabolism, and elimination. Detail the potential effects of sepsis-associated organ dysfunction on pharmacokinetics. Explain the practical implications of sepsis on the pharmacokinetics of drugs used commonly in anaesthesia and critical care.Sepsis is a heterogeneous syndrome caused by a dysregulated host response to systemic infection whereby uncontrolled pro-and anti-inflammatory processes lead to tissue injury, immune suppression, and organ dysfunction. 1 The response to sepsis has profound effects on many physiological processes and body systems. These can have significant effects on absorption, distribution, metabolism, and elimination of drugs, with potential implications for treatment regimens and the incidence of adverse effects. Furthermore, these adverse effects may be increased or decreased by our therapeutic interventions. In addition to requiring treatment in critical care, many patients with sepsis undergo anaesthesia and surgery.This article reviews the pathophysiology of sepsis in relation to its effects on the pharmacokinetics of the drugs commonly used in anaesthesia and critical care. This is needed to predict pharmacodynamic effects, ensure correct dosing, and avoid harm. Altered pharmacokinetics in sepsis also has implications for drugedrug interactions, but this is outside the scope of this article. Effects of sepsis on pharmacokineticsdgeneral principlesSepsis is characterised by the widespread release of cytokines, proteases, and reactive oxygen species, which lead to both direct and indirect cellular damage. 2 Vasodilatation and capillary leak ensue, resulting in relative and absolute intravascular hypovolaemia in the first instance, followed by the potential for considerable increase in total body fluid after resuscitation. 3 Microcirculatory blood flow is impaired leading to heterogeneous organ perfusion, mitochondrial dysfunction, cellular hypoxia, and subsequently organ dysfunction and failure. 2 The extent to which these changes occur depends on the complex interplay between infectious factors (causative organisms and microbial load), patient factors (age, physiological status/ fitness, comorbidities, genetic characteristics, and treatment interventions) and treatment factors (volume of fluid resuscitation, use of vasoactive agents). 1,2 Because these processes are both dynamic and interacting, pharmacokinetics may be altered to a variable extent that can be difficult to predict. Matthew Charlton FRCA FFICM is a specialty trainee and clinical lecturer in anaesthesia and critical care at the University of Leicester and University Hospitals of Leicester NHS Trust. Jonathan Thompson BSc (Hons), MD, FRCA, FFICM is honorary professor of anaesthesia and critical care at the University of Leicester and a consultant at Leicester Royal Infirmary. He is a former editor of the British Journal of Anaesthesia, current editorial board member of the BJA and Perioperative Medicine, and cur...

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Vasoplegia treatments: the past, the present, and the future

Cited by 162 publications

References 79 publications

Vasoplegic syndrome following cardiothoracic surgery—review of pathophysiology and update of treatment options

Vasoplegic syndrome following cardiothoracic surgery—review of pathophysiology and update of treatment options

Vasopressin and its analogues in shock states: a review

Pharmacokinetics in sepsis

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