title: Low-dose vasopressin in the treatment of vasodilatory septic shock.
abstract: BACKGROUND
  Despite appropriate therapy, refractory hypotension often occurs in septic shock. A double-blinded placebo controlled clinical trial was performed to assess the role of low-dose vasopressin (VP) as a pressor agent in septic shock.
  
  
  METHODS
  Patients admitted to a trauma intensive care unit with vasodilatory septic shock were randomized to receive either VP at 0.04 U/min (n = 5) or placebo (n = 5). Vasodilatory septic shock was defined as a need for catecholamine agents to maintain a mean arterial pressure more than or equal to 70 mm Hg, despite a cardiac index more than 2.5 L/min and a minimal pulmonary artery wedge pressure more than 12 mm Hg. After 1 hour of initiation of the study drug, attempts to discontinue norepinephrine, phenylephrine, and/or dopamine, in respective order, were undertaken provided that the mean arterial pressure remained more than or equal to 70 mm Hg.
  
  
  RESULTS
  A vasopressin infusion increased systolic arterial pressure (98 +/- 5 to 125 +/- 8 mm Hg, p < 0.008) because of peripheral vasoconstriction (systemic vascular resistance increased from 878 +/- 218 to 1,190 +/- 213 dynes/s per cm(-5) p < 0.05). Arterial pressure and systemic vascular resistance were statistically unaffected in the placebo group. Before study termination, measured at 24 hours after drug initiation, two patients in the placebo group died of refractory hypotension. However, all patients receiving VP survived the 24-hour study period and had all other catecholamine pressors withdrawn and blood pressure maintained solely with a low-dose VP infusion.
  
  
  CONCLUSIONS
  A VP infusion improved arterial pressure and permitted the withdrawal of catecholamine vasopressors. VP is a useful agent in the treatment of refractory septic shock.
authors.affiliation: Allegheny General Hospital, Division of General Surgery, Pittsburgh, Pennsylvania 15212, USA.
authors.forename: M B
authors.initials: MB
authors.lastname: Malay
authors.forename: R C
authors.initials: RC
authors.lastname: Ashton
authors.forename: D W
authors.initials: DW
authors.lastname: Landry
authors.forename: R N
authors.initials: RN
authors.lastname: Townsend
mesh_terms: D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D002316:Cardiotonic Agents / Q000627:therapeutic use; D004298:Dopamine / Q000627:therapeutic use; D004311:Double-Blind Method; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000627:therapeutic use; D010656:Phenylephrine / Q000627:therapeutic use; D011669:Pulmonary Wedge Pressure / Q000187:drug effects; D012772:Shock, Septic / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology; D016019:Survival Analysis; D014655:Vascular Resistance / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology / Q000627:therapeutic use*; D014667:Vasopressins / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D002316:Cardiotonic Agents; D014662:Vasoconstrictor Agents; D014667:Vasopressins; D010656:Phenylephrine; D004298:Dopamine; D009638:Norepinephrine