title: Effects of continuous vasopressin infusion in patients with septic shock.
abstract: BACKGROUND
  Small studies have reported that vasopressin improves hemodynamic instability in patients with septic shock.
  
  
  OBJECTIVE
  To determine whether vasopressin infusion increases blood pressure, decreases catecholamine vasopressor use, and improves renal function in a large patient population with septic shock when used in a clinical setting.
  
  
  METHODS
  A retrospective chart audit was conducted of critically ill patients who received vasopressin infusion for septic shock from January 2000 through September 2002. Demographic, hemodynamic, laboratory, vasopressor, and adverse event data were collected. Statistical methods included ANOVA with Tukey's test for post hoc analysis.
  
  
  RESULTS
  A total of 102 of 353 patients met study criteria. The mean +/- SD vasopressin dosage regimen was 0.11 +/- 0.17 units/min for 53.8 +/- 71.5 hours. Compared with baseline, vasopressin infusion improved mean arterial pressure (MAP) by 15% within one hour (p < 0.05), reduced heart rate by 9% within 4 hours (p < 0.05), and reduced hourly dopamine dosage by 25% within 8 hours (p < 0.05). These effects persisted through 96 hours. Other hemodynamic variables and catecholamine vasopressor usage parameters were not statistically different from baseline. Urine output, serum creatinine, and serum sodium concentrations were not statistically changed from baseline. Adverse events possibly associated with vasopressin infusion included ischemic digits/extremities, myocardial infarction, and hyponatremia.
  
  
  CONCLUSIONS
  Vasopressin infusion was effective in increasing MAP and reducing heart rate while decreasing the dopamine dosage in patients with septic shock. Comparative studies with catecholamine vasopressors are needed to define the optimal role of vasopressin in septic shock therapy. In the meantime, vasopressin infusion at <or=0.03 units/min should be considered only if response to 1 or 2 catecholamine vasopressors is inadequate or as a method to reduce the dose of these therapies.
authors.affiliation: University of Colorado Hospital, Denver, CO 80262, USA.
authors.forename: Marilee D
authors.initials: MD
authors.lastname: Obritsch
authors.forename: Rose
authors.initials: R
authors.lastname: Jung
authors.forename: Douglas N
authors.initials: DN
authors.lastname: Fish
authors.forename: Robert
authors.initials: R
authors.lastname: MacLaren
mesh_terms: D001794:Blood Pressure / Q000187:drug effects; D004359:Drug Therapy, Combination; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012772:Shock, Septic / Q000188:drug therapy*; D014556:Urine; D014662:Vasoconstrictor Agents / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*; D014667:Vasopressins / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*
chemical_list: D014662:Vasoconstrictor Agents; D014667:Vasopressins