title: Arginine vasopressin as a supplementary vasopressor in refractory hypertensive, hypervolemic, hemodilutional therapy in subarachnoid hemorrhage.
abstract: BACKGROUND
  Hypertensive, hypervolemic, and hemodilutional (HHH) therapy for vasospasm in subarachnoid hemorrhage (SAH) refractory to phenylephrine requires high doses of catecholamines, leading to adverse adrenergic effects. Arginine vasopressin (AVP) has been shown to stabilize advanced shock states while facilitating reduction of catecholamine doses, but its use has never been reported in SAH. In this retrospective study, we investigated the hemodynamic effects and feasibility of supplementary AVP in refractory HHH therapy in SAH.
  
  
  METHODS
  Hemodynamic response (mean arterial pressure [MAP], heart rate, central venous pressure, cardiac index, systemic vascular resistance index, and end diastolic volume index) to a supplementary AVP infusion (0.01-0.04 IU/minute) was recorded within the first 24 hours in 22 patients. Secondary endpoints (serum sodium concentration, incidence of vasospasm, and intracranial pressure [ICP]) were compared to controls on HHH therapy with phenylephrine alone.
  
  
  RESULTS
  After initiation of AVP, MAP increased significantly compared to baseline. Phenylephrine doses decreased significantly, whereas other hemodynamic parameters remained stable. Serum sodium concentrations decreased similarly in both groups (-5 +/- 7 mmol/L versus -6 +/- 4 mmol/L; p = 0.25). No detrimental effects on vasospasm incidence or ICP and cerebral perfusion pressure were noted.
  
  
  CONCLUSIONS
  AVP may be considered as an alternative supplementary vasopressor in refractory HHH therapy with phenylephrine in SAH. Although we did not observe any deleterious effect of AVP on cerebral circulation, close observation for development of cerebral vasospasm should be undertaken, until it is clearly demonstrated that AVP has no adverse effects on regional cerebral blood flow and symptomatic cerebral vasospasm. Our limited data suggest that low-dose AVP does not cause brain edema, but further study is merited.
authors.affiliation: Division of Vascular Neurology and Neurocritical Care, Department of Neurology, Massachusetts General Hospital/Brigham Women's Hospital, Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA. smuehlschlegel@partners.org
authors.forename: Susanne
authors.initials: S
authors.lastname: Muehlschlegel
authors.forename: Martin W
authors.initials: MW
authors.lastname: Dunser
authors.forename: Andrea
authors.initials: A
authors.lastname: Gabrielli
authors.forename: Volker
authors.initials: V
authors.lastname: Wenzel
authors.forename: A Joseph
authors.initials: AJ
authors.lastname: Layon
mesh_terms: D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001127:Arginine Vasopressin / Q000008:administration & dosage / Q000627:therapeutic use*; D001810:Blood Volume / Q000187:drug effects / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D005260:Female; D006438:Hemodilution / Q000379:methods; D006801:Humans; D007262:Infusions, Intravenous; D002532:Intracranial Aneurysm / Q000188:drug therapy; D007427:Intracranial Pressure / Q000187:drug effects / Q000502:physiology; D008297:Male; D008875:Middle Aged; D013345:Subarachnoid Hemorrhage / Q000188:drug therapy*; D014662:Vasoconstrictor Agents / Q000008:administration & dosage / Q000627:therapeutic use*
chemical_list: D000959:Antihypertensive Agents; D014662:Vasoconstrictor Agents; D001127:Arginine Vasopressin