title: Hemodynamic and metabolic effects of low-dose vasopressin infusions in vasodilatory septic shock.
abstract: OBJECTIVE
  To investigate the physiologic effects of exogenous vasopressin as a potential alternative to traditional high-dose catecholamine therapy for septic patients with vascular hyporeactivity to catecholamines.
  
  
  METHODS
  Prospective, case-controlled study.
  
  
  METHODS
  Intensive care unit of a university hospital.
  
  
  METHODS
  Vasopressin was infused in 16 critically ill septic patients who remained persistently hypotensive despite infusions of pharmacologic doses of catecholamines.
  
  
  METHODS
  Continuous intravenous infusion of vasopressin at 0.04 units/min for 16 hrs, in place of escalating the amount of catecholamines being infused.
  
  
  RESULTS
  After administration of vasopressin, systemic vascular resistance and mean arterial pressure were immediately and significantly increased in comparison with the values obtained just before vasopressin. When the vasopressin infusions were discontinued, mean arterial pressure decreased immediately and dramatically. We did not detect any obvious adverse cardiac effects during the vasopressin infusions. Vasopressin had no effect on other hemodynamic parameters or any of the metabolic parameters studied, including measures of oxygenation, plasma glucose, or electrolytes. Urine output increased significantly during the administration of vasopressin, although this effect may be nonspecific. Lactate concentrations decreased, particularly in the survival group, but the decreases were not significant. Overall survival was 56%.
  
  
  CONCLUSIONS
  Low-dose vasopressin infusions increased mean arterial pressure, systemic vascular resistance, and urine output in patients with vasodilatory septic shock and hyporesponsiveness to catecholamines. The data indicate that low-dose vasopressin infusions may be useful in treating hypotension in these patients.
authors.affiliation: Division of Intensive Care Medicine, Kagoshima University Hospital, Kagoshima, Japan. tsuneyo@morpheus.wustl.edu
authors.forename: I
authors.initials: I
authors.lastname: Tsuneyoshi
authors.forename: H
authors.initials: H
authors.lastname: Yamada
authors.forename: Y
authors.initials: Y
authors.lastname: Kakihana
authors.forename: M
authors.initials: M
authors.lastname: Nakamura
authors.forename: Y
authors.initials: Y
authors.lastname: Nakano
authors.forename: W A
authors.initials: WA
authors.lastname: Boyle
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood / Q000187:drug effects; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000187:drug effects; D001784:Blood Gas Analysis; D001786:Blood Glucose / Q000032:analysis / Q000187:drug effects; D016638:Critical Illness; D016903:Drug Monitoring; D004573:Electrolytes / Q000097:blood; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007262:Infusions, Intravenous; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012083:Renin / Q000097:blood / Q000187:drug effects; D012772:Shock, Septic / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D016019:Survival Analysis; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000627:therapeutic use*; D014667:Vasopressins / Q000627:therapeutic use*
chemical_list: D001786:Blood Glucose; D004573:Electrolytes; D014662:Vasoconstrictor Agents; D014667:Vasopressins; D000804:Angiotensin II; D019344:Lactic Acid; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012083:Renin