title: Does a positive end-expiratory pressure-induced reduction in stroke volume indicate preload responsiveness? An experimental study.
abstract: BACKGROUND
  Increases in positive end-expiratory pressure (PEEP) are often associated with cardiovascular depression, responding to fluid loading. Therefore, we hypothesized that if stroke volume (SV) is reduced by an increase in PEEP this reduction is an indicator of hypovolemia or preload responsiveness, i.e. that SV would increase by fluid administration at zero end-expiratory pressure (ZEEP). The relationship between the cardiovascular response to different PEEP levels and fluid load as well as the relation between change in SV as a result of change in preload (Frank-Starling relationship) were evaluated in a porcine model. In addition, other measures of fluid status were assessed.
  
  
  METHODS
  Eight, 20-22 kg, anesthetized, mechanically ventilated pigs were subjected to 0, 10, and 20 cm H(2)O PEEP at 10% (of estimated blood volume) hypovolemia, normo- and 10% hypervolemia, and to ZEEP at 20% hypervolemia. SV, cardiac output, intrathoracic blood volume and airway, esophageal, vascular pressures, stroke volume variations, left ventricular end-diastolic and end-systolic areas and respiratory variations in the diameter of the inferior vena cava were obtained.
  
  
  RESULTS
  At hypovolemia and normovolemia, 10 cm H(2)O PEEP induced a significant decrease in SV, while no change occurred at 10% hypervolemia. SV measured at ZEEP increased from hypovolemia to normovolemia and 10% hypervolemia, while no change was found between 10% and 20% hypervolemia. The sensitivity and specificity decrease in SV by PEEP indicating an increase in SV by fluids was 60-88% and 67%, respectively, depending on the volemic (preload) levels.
  
  
  CONCLUSIONS
  Although the overall results suggest that a change in SV by PEEP might predict preload responsiveness, the individual response of SV by 10 cm H(2)O PEEP and of the successive fluid administration seemed to be dependent on where on the Frank-Starling curve the heart function was located.
authors: Department of Anesthesia and Intensive Care Medicine, Center for Cardiovascular Research, Aalborg Hospital, Arhus University Hospitals, Aalborg, Denmark.
authors: P
authors: P
authors: Lambert
authors: E
authors: E
authors: Sloth
authors: B
authors: B
authors: Smith
authors: L K
authors: LK
authors: Hansen
authors: J
authors: J
authors: Koefoed-Nielsen
authors: E
authors: E
authors: Tønnesen
authors: A
authors: A
authors: Larsson
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D002302:Cardiac Output; D002496:Central Venous Pressure; D004195:Disease Models, Animal; D004452:Echocardiography / Q000379:methods; D004947:Esophagus / Q000503:physiopathology; D005440:Fluid Therapy / Q000379:methods; D006352:Heart Ventricles; D020896:Hypovolemia / Q000503:physiopathology*; D011175:Positive-Pressure Respiration / Q000379:methods*; D011669:Pulmonary Wedge Pressure; D012121:Respiration, Artificial / Q000379:methods; D013318:Stroke Volume; D013552:Swine; D013997:Time Factors; D014132:Trachea / Q000503:physiopathology