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Cited by 620Sepsis Diagnosis and TreatmentHemodynamic Monitoring and TherapyElectrolyte and hormonal disorders

Physiology of Vasopressin Relevant to Management of Septic Shock

Holmes, Cheryl L., Patel, Bhavesh M., Russell, James A., Walley, Keith R.·2001·Chest
DOI 10.1378/chest.120.3.989
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Abstract

Vasopressin is emerging as a rational therapy for the hemodynamic support of septic shock and vasodilatory shock due to systemic inflammatory response syndrome. The goal of this review is to understand the physiology of vasopressin relevant to septic shock in order to maximize its safety and efficacy in clinical trials and in subsequent therapeutic use. Vasopressin is both a vasopressor and an antidiuretic hormone. It also has hemostatic, GI, and thermoregulatory effects, and is an adrenocorticotropic hormone secretagogue. Vasopressin is released from the axonal terminals of magnocellular neurons in the hypothalamus. Vasopressin mediates vasoconstriction via V1-receptor activation on vascular smooth muscle and mediates its antidiuretic effect via V2-receptor activation in the renal collecting duct system. In addition, vasopressin, at low plasma concentrations, mediates vasodilation in coronary, cerebral, and pulmonary arterial circulations. Septic shock causes first a transient early increase in blood vasopressin concentrations that decrease later in septic shock to very low levels compared to other causes of hypotension. Vasopressin infusion of 0.01 to 0.04 U/min in patients with septic shock increases plasma vasopressin levels to those observed in patients with hypotension from other causes, such as cardiogenic shock. Increased vasopressin levels are associated with a lesser need for other vasopressors. Urinary output may increase, and pulmonary vascular resistance may decrease. Infusions of > 0.04 U/min may lead to adverse, likely vasoconstriction-mediated events. Because clinical studies have been relatively small, focused on physiologic end points, and because of potential adverse effects of vasopressin, clinical use of vasopressin should await a randomized controlled trial of its effects on clinical outcomes such as organ failure and mortality.

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Crossref · 10.1378/chest.120.3.989

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  • Most studies on de-escalation were observational, and there are concerns that de-escalation is used primarily in patients who are getting better, so the reported improved short-term mortality should be interpreted with caution.

    “Most studies were observational, and there are concerns that de-escalation is used primarily in patients who are getting better, which is why the reported improved short-term mortality should be interpreted with caution (277,279).”

    From Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. (2021) · cites this paper as [277]

  • We identified direct evidence from 13 studies (1,968 patients), including one RCT, on antimicrobial de-escalation.

    “We identified direct evidence from 13 studies (1,968 patients) (277), including one RCT (278).”

    From Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. (2021) · cites this paper as [277]

  • Vasopressin concentration is elevated in early septic shock but decreases to normal range in most patients between 24 and 48 hours as shock continues.

    “Studies show that vasopressin concentration is elevated in early septic shock but decreases to normal range in the majority of patients between 24 and 48 h as shock continues [352, 353].”

    From Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021 (2021) · cites this paper as [352]

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Authors
Holmes, C. L., Patel, B. M., Russell, J. A., & Walley, K. R.
Affiliations
  • University of British Columbia (CA)
  • Mayo Clinic (US)
Corresponding author
Walley, Keith R.
ORCID
Venue
Chest
Publisher
Elsevier BV
Published
2001-09
Volume
120
Issue
3
Pages
989-1002
ISSN
0012-3692 (ISSN-L)
DOI
10.1378/chest.120.3.989
OpenAlex
W2156856199
Cited by
620
References
126
Citations by year
2026: 9 · 2025: 17 · 2024: 17 · 2023: 19 · 2022: 15 · 2021: 12 · 2020: 11 · 2019: 15 · 2018: 11 · 2017: 18 · 2016: 15 · 2015: 17 · 2014: 21 · 2013: 21 · 2012: 27
FWCI
6.10
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • CHEST Journal (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Sepsis Diagnosis and Treatment
  • Health Sciences › Medicine › Surgery › Hemodynamic Monitoring and Therapy
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Electrolyte and hormonal disorders
Keywords
vasopressin, septic shock, vasopressor therapy, V1 receptor, V2 receptor, systemic inflammatory response syndrome, vasodilatory shock, hypotension, plasma vasopressin levels, pulmonary vascular resistance, urine output, organ failure
MeSH terms
Animals, Humans, Kidney, Osmosis, Shock, Hemorrhagic, Shock, Septic, Vasoconstriction, Vasodilation, Vasopressins, Systemic Inflammatory Response Syndrome

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