Arginine-vasopressin (AVP) is a non-catecholaminergic hormone produced in the hypothalamus and released into the circulation via the neurohypophysis. It has different actions depending on the receptors through which it acts: V1 (vasoconstriction, platelet aggregation, efferent arteriole constriction of the renal glomerulus, glycogenolysis); V2 (water reabsorption, release of von Willebrand factor and factor VIII); V3 (increased cortisol and insulin).
Septic shock is the most common cause of vasoplegic shock and its management includes control of the focus, early antibiotic therapy, volume resuscitation, vasopressor therapy, support of various organ dysfunctions, as well as monitoring and follow-up.
The Surviving Sepsis Campaign (a global initiative to improve sepsis management) recommends noradrenaline as the first line of vasopressor therapy and early addition of AVP as a second line rather than further up-titration of noradrenaline when signs of hypoperfusion persist, through its action primarily on V1.
The rationale for its use in septic shock would be:
* endogenous vasopressin deficiency present in septic shock; * as a catecholamine-sparing strategy, reducing the side effects of catecholamines; * its potential nephroprotective effect; * its use should be early.
The uncertainties surrounding the use of AVP in septic shock and other types of shock are many, hence the need for this registry.
Any patient over 18 years of age who is in shock and requires the administration of vasoconstrictors, to whom vasopressin is administered in the operating theatre and/or critical care unit, according to best clinical practice.
Non-consent by patient/legal representatives
Patients in shock receiving vasopressin
Other
Prospective
Vasopressin
DrugPatients treated with vasopressin
Characterise the clinical practice of vasopressin use in the context of shock in a multicentre observational study.
Describing the time sequence of vasopressin and/or noradrenaline use (what is initiated first) during shock
Assess what prompted the decision to initiate AVP
Assess what prompted the decision to initiate AVP: type of shock (vasoplegic, hypovolemic,...), perfusion parameters (as lactate) or noradrenaline dose (microgram/kg/minute)
Define the impact of starting AVP on noradrenaline dose
Define the impact of starting AVP on noradrenaline dose (microgram/kg/minute)
Define the impact of starting AVP on lactate level
Define the impact of starting AVP on lactate level (mmol/L)
Observe when AVP is discontinued and how
Describe number of participants what AVP is discontinued first and how (abruptly or progressively)
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