Cited by 990Sepsis Diagnosis and TreatmentElectrolyte and hormonal disordersHemodynamic Monitoring and Therapy

Vasopressin Deficiency Contributes to the Vasodilation of Septic Shock

Landry, Donald W., Levin, Howard R., Gallant, Ellen M., Ashton, Robert C., Seo, Susan, D'Alessandro, David, Oz, Mehmet C., Oliver, Juan A.·1997·Circulation

Abstract

Background The hypotension of septic shock is due to systemic vasodilation. On the basis of a clinical observation, we investigated the possibility that a deficiency in vasopressin contributes to the vasodilation of septic shock. Methods and Results In 19 patients with vasodilatory septic shock (systolic arterial pressure [SAP] of 92±2 mm Hg [mean±SE], cardiac output [CO] of 6.8±0.7 L/min) who were receiving catecholamines, plasma vasopressin averaged 3.1±1.0 pg/mL. In 12 patients with cardiogenic shock (SAP, 99±7 mm Hg; CO, 3.5±0.9 L/min) who were also receiving catecholamines, it averaged 22.7±2.2 pg/mL ( P <.001). A constant infusion of exogenous vasopressin to 2 patients with septic shock resulted in the expected plasma concentration, indicating that catabolism of vasopressin is not increased in this condition. Although vasopressin is a weak pressor in normal subjects, its administration at 0.04 U/min to 10 patients with septic shock who were receiving catecholamines increased arterial pressure (systolic/diastolic) from 92/52 to 146/66 mm Hg ( P <.001/ P <.05) due to peripheral vasoconstriction (systemic vascular resistance increased from 644 to 1187 dyne·s/cm 5 ; P <.001). Furthermore, in 6 patients with septic shock who were receiving vasopressin as the sole pressor, vasopressin withdrawal resulted in hypotension (SAP, 83±3 mm Hg), and vasopressin administration at 0.01 U/min, which resulted in a plasma concentration (≈30 pg/mL) expected for the level of hypotension, increased SAP from 83 to 115 mm Hg ( P <.01). Conclusions Vasopressin plasma levels are inappropriately low in vasodilatory shock, most likely because of impaired baroreflex-mediated secretion. The deficiency in vasopressin contributes to the hypotension of vasodilatory septic shock.

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Crossref · 10.1161/01.cir.95.5.1122

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Authors
Landry, D. W., Levin, H. R., Gallant, E. M., Ashton, R. C., Seo, S., D'Alessandro, D., Oz, M. C., & Oliver, J. A.
Affiliations
  • Allegheny General Hospital (US)
  • the Departments of Medicine (D.W.L., H.R.L., E.M.G., S.S., J.A.O.) and Surgery (D.D., M.C.O.), Columbia University, College of Physicians &amp; Surgeons, New York, NY, and the Department of Surgery (R.C.A.), Allegheny General Hospital, Pittsburgh, Pa.
Venue
Circulation
Published
1997-03-04
Volume
95
Issue
5
Pages
1122-1125
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
OpenAlex
W2062054105
Cited by
990
References
26
Citations by year
2026: 28 · 2025: 29 · 2024: 31 · 2023: 27 · 2022: 22 · 2021: 22 · 2020: 30 · 2019: 26 · 2018: 34 · 2017: 29 · 2016: 25 · 2015: 21 · 2014: 22 · 2013: 32 · 2012: 33
FWCI
11.24
Type
journal article
Language
en
Open access
closed
Locations
  • Circulation (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Sepsis Diagnosis and Treatment
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Electrolyte and hormonal disorders
  • Health Sciences › Medicine › Surgery › Hemodynamic Monitoring and Therapy
Keywords
vasopressin deficiency, septic shock, vasodilation, hypotension, baroreflex, vasopressin infusion, systemic vascular resistance, catecholamines, cardiogenic shock
MeSH terms
Adult, Blood Pressure, Cardiac Output, Dopamine, Epinephrine, Heart Rate, Hemodynamics, Humans, Norepinephrine, Shock, Cardiogenic, Shock, Septic, Sodium, Vascular Resistance, Vasodilation, Vasopressins

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