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    This best practice guideline has been designed for critical care units, however, it can be applied to other areas within your health service who use vasoactive infusions, such as anaesthetics, cardiology and emergency departments.

    Mechanism of action/pharmacology

    Endogenous vasopressin is a hormone secreted by the posterior pituitary gland that acts as a non-adrenergic vasopressor. Actions on vascular smooth muscle V1 receptors cause peripheral vasoconstriction and increase systemic vascular resistance and blood pressure. Less potent actions on V2 receptors in the kidneys cause an antidiuretic effect by promoting water reabsorption by the renal tubules.1 Vasopressin also increases adrenocorticotropic hormone (ACTH) and aldosterone levels.

    Vasopressin plays a minimal role in blood pressure regulation in normotensive states. During vasodilatory shock, administration may correct a relative endogenous vasopressin deficiency that develops when endogenous secretory stores become depleted.2

    Vasopressin augments the response to catecholamine therapy, reducing the required catecholamine dose,3,4 and may be a more effective vasopressor in patients with severe acidosis, when the efficacy of adrenergic agents is potentially reduced due to receptor down-regulation.5

    Onset of action: 1–2 minutes.6

    Duration of action: up to 20 minutes.6

    Half-life: 10–20 minutes.1


    To increase blood pressure in refractory vasodilatory shock when low systemic vascular resistance persists despite adequate fluid resuscitation and first-line vasopressor support with noradrenaline.7

    The optimal timing for initiating vasopressin therapy remains controversial. Under conventional management, the introduction of vasopressin is delayed until the patient’s noradrenaline requirement is greater than 20 to 30microg/min. Limited studies have investigated the role of vasopressin as a first-line agent in treating septic shock, and the benefits of this approach remain uncertain.8

    Vasopressin provides a component of physiological support in brain dead potential organ donors.9


    • Hypersensitivity to vasopressin or components – anaphylaxis has been reported1
    • Hypotension due to uncorrected hypovolaemia1
    • Conditions exacerbated by fluid overload or water intoxication including asthma, epilepsy and heart failure.1

    Medication presentation

    20 units/1 mL vial

    Medication storage

    Store vials below 25°C. Do not freeze.10

    Infusion solutions are only stable for 18 hours at room temperature1 or 24 hours at 2–8°C.10

    Stock not registered in Australia will require completion of a Special Access Scheme Category A form.



    Syringe driver


    20 units in 20 mL

    40 units in 40 mL

    Make up infusion in

    Glucose 5%*

    Glucose 5%*

    Volume to be drawn up into the syringe

    19 mL

    38 mL

    Drug dose to be added

    20 units (1 mL)

    40 units (2 mL)

    Final volume

    20 mL

    40 mL

    Final concentration

    1 unit/mL

    1 unit/mL

    1 mL/hr =

    1 unit/hr

    1 unit/hr

    *Glucose 5% is preferred for diluting all inotropes and vasopressors. However, Vasopressin is also compatible with sodium chloride 0.9%.10

    Administration - this guideline is intended for central access only

    Administer continuous intravenous infusion through a central access line.10

    Infusions should be administered via a syringe driver, preferably with medication error reduction software enabled.

    Avoid administration via lines where other drugs or fluids may be bolused or flushed.11


    Starting dose: 0.6 units/hr.

    Titrate in accordance with prescribed blood pressure parameters – for example, in increments of 0.6 units/hr.

    Usual dose range for vasodilatory shock: 0.6 to 2.4 units/hr.3,4,12

    Maximum dose: up to 3.6 units/hr has been used, but higher doses may increase the risk of ischaemic side effects.8

    As a general rule, consider commencing vasopressin wean when the patient’s noradrenaline requirement is below 20microg/min, and wean no more rapidly than in increments of 0.6 units/hr every 15 minutes.

    Usual dose range for physiological support for brain dead potential organ donors: 0.5 to 2.4 units/hr.9


    • Continuous blood pressure and cardiac monitoring for the duration of the infusion
    • Monitor fluid balance and electrolytes
    • Assess for organ ischaemia (including myocardium, kidneys, gastrointestinal tract and peripheral extremities) – see ‘Side effects’ for more information.

    Side effects

    • Decreased cardiac output, cardiac dysrhythmia and cardiac arrest6
    • Myocardial, mesenteric or peripheral (digital) ischaemia – can manifest as acute myocardial infarction, gastrointestinal infarction, decreased urine output/creatinine clearance or gangrene6
    • Hyponatraemia – due to water retention.6


    Consult the following references, which are available online through the Clinicians Health Channel:

    • Australian injectable drugs handbook
    • Trissel’s™ in IV compatibility (Micromedex) – from the site homepage, select the ‘IV Compatibility’ tab.

    Important drug interactions

    There are no known significant drug interactions.


    1. MIMS[online] (accessed 4 April 2017)
    2. Landry DW, Levin HR, Gallant EM, et al. Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation 1997; 95(5): 1122–1125
    3. Tsuneyoshi I, Yamada H, Kakihana Y, et al. Hemodynamic and metabolic effects of low-dose vasopressin infusions in vasodilatory septic shock. Critical Care Medicine 2001; 29(3): 487–493
    4. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock, 2012. Critical Care Medicine 2013; 41(2): 580–637
    5. Sharman A, Low J. Vasopressin and its role in critical care. Continuing Education in Anaesthesia Critical Care and Pain 2008; 8(4): 134–137
    6. Micromedex [online] (accessed 5 April 2017).
    7. Rhodes A, Evans LE, Alhazzani W, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock: 2016. Intensive Care Medicine 2017; 43(3): 304–377
    8. Gordon AC, Mason AJ, Thirunavukkarasu N, et al. Effect of early vasopressin vs norepinephrine on kidney failure in patients with septic shock: the VANISH randomized clinical trial. JAMA 2016; 316(5):509–518
    9. Australian and New Zealand Intensive Care Society. The ANZICS statement on death and organ donation (Edition 3.2). ANZICS, Melbourne, 2013.
    10. Australian injectable drugs handbook (AIDH) [online] (accessed 2 April 2016).
    11. University College London Hospitals (UCL). UCL hospitals injectable medicines administration guide: pharmacy department, 3rd edn. Wiley-Blackwell, Chichester, 2013.
    12. Russell JA, Walley KR, Singer J, et al. Vasopressin versus norepinephrine infusion in patients with septic shock. New England Journal of Medicine 2008; 358(9):877–887.

    Get in touch

    Centre of Clinical Excellence - Acute
    Safer Care Victoria


    We would like to thank the pharmacists involved in writing the guidelines: Melissa Ankravs, Melanie Kowalski, Rachel Fyfe, Robyn Ingram, Annalie Jones, Susan Trevillian, and Lucy Sharrock.

    Page last updated: 11 Nov 2020

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