title: Inspiratory resistance maintains arterial pressure during central hypovolemia: implications for treatment of patients with severe hemorrhage.
abstract: OBJECTIVE
  To test the hypothesis that an impedance threshold device would increase systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure and delay the onset of symptoms and cardiovascular collapse associated with severe central hypovolemia.
  
  
  METHODS
  Prospective, randomized, blinded trial design.
  
  
  METHODS
  Human physiology laboratory.
  
  
  METHODS
  Nine healthy nonsmoking normotensive subjects (five males, four females).
  
  
  METHODS
  Central hypovolemia and impending cardiovascular collapse were induced in human volunteers by applying progressive lower body negative pressure (under two experimental conditions: a) while breathing with an impedance threshold device set to open at -7 cm H2O pressure (active impedance threshold device); and b) breathing through a sham impedance threshold device (control).
  
  
  RESULTS
  Systolic blood pressure (79 +/- 5 mm Hg), diastolic blood pressure (57 +/- 3 mm Hg), and mean arterial pressure (65 +/- 4 mm Hg) were lower (p < .02) when subjects (n = 9) breathed through the sham impedance threshold device than when they breathed through the active impedance threshold device at the same time of cardiovascular collapse during sham breathing (102 +/- 3, 77 +/- 3, 87 +/- 3 mm Hg, respectively). Elevated blood pressure was associated with 23% greater lower body negative pressure tolerance using an active impedance threshold device (1639 +/- 220 mm Hg-min) compared with a sham impedance threshold device (1328 +/- 144 mm Hg-min) (p = .02).
  
  
  CONCLUSIONS
  Use of an impedance threshold device increased systemic blood pressure and delayed the onset of cardiovascular collapse during severe hypovolemic hypotension in spontaneously breathing human volunteers. This device may provide rapid noninvasive hemodynamic support in patients with hypovolemic hypotension once the blood loss has been controlled but before other definitive therapies are available.
authors.affiliation: U.S. Army Institute of Surgical Research, Fort Sam Houston, TX, USA. victor.convertino@amedd.army.mil
authors.forename: Victor A
authors.initials: VA
authors.lastname: Convertino
authors.forename: Kathy L
authors.initials: KL
authors.lastname: Ryan
authors.forename: Caroline A
authors.initials: CA
authors.lastname: Rickards
authors.forename: William H
authors.initials: WH
authors.lastname: Cooke
authors.forename: Ahamed H
authors.initials: AH
authors.lastname: Idris
authors.forename: Anja
authors.initials: A
authors.lastname: Metzger
authors.forename: John B
authors.initials: JB
authors.lastname: Holcomb
authors.forename: Bruce D
authors.initials: BD
authors.lastname: Adams
authors.forename: Keith G
authors.initials: KG
authors.lastname: Lurie
mesh_terms: D000328:Adult; D000403:Airway Resistance; D001794:Blood Pressure; D005260:Female; D006801:Humans; D020896:Hypovolemia / Q000150:complications* / Q000503:physiopathology; D008297:Male; D011446:Prospective Studies; D012771:Shock, Hemorrhagic / Q000209:etiology* / Q000503:physiopathology* / Q000517:prevention & control