title: Impact of epinephrine and norepinephrine on two dynamic indices in a porcine hemorrhagic shock model.
abstract: BACKGROUND
  Pulse pressure variations (PPVs) and stroke volume variations (SVVs) are dynamic indices for predicting fluid responsiveness in intensive care unit patients. These hemodynamic markers underscore Frank-Starling law by which volume expansion increases cardiac output (CO). The aim of the present study was to evaluate the impact of the administration of catecholamines on PPV, SVV, and inferior vena cava flow (IVCF).
  
  
  METHODS
  In this prospective, physiologic, animal study, hemodynamic parameters were measured in deeply sedated and mechanically ventilated pigs. Systemic hemodynamic and pressure-volume loops obtained by inferior vena cava occlusion were recorded. Measurements were collected during two conditions, that is, normovolemia and hypovolemia, generated by blood removal to obtain a mean arterial pressure value lower than 60 mm Hg. At each condition, CO, IVCF, SVV, and PPV were assessed by catheters and flow meters. Data were compared between the conditions normovolemia and hypovolemia before and after intravenous administrations of norepinephrine and epinephrine using a nonparametric Wilcoxon test.
  
  
  RESULTS
  Eight pigs were anesthetized, mechanically ventilated, and equipped. Both norepinephrine and epinephrine significantly increased IVCF and decreased PPV and SVV, regardless of volemic conditions (p < 0.05). However, epinephrine was also able to significantly increase CO regardless of volemic conditions.
  
  
  CONCLUSIONS
  The present study demonstrates that intravenous administrations of norepinephrine and epinephrine increase IVCF, whatever the volemic conditions are. The concomitant decreases in PPV and SVV corroborate the fact that catecholamine administration recruits unstressed blood volume. In this regard, understanding a decrease in PPV and SVV values, after catecholamine administration, as an obvious indication of a restored volemia could be an outright misinterpretation.
authors.affiliation: From the Intensive Care Unit (R.G., N.S., D.A., K.B.), Geneva University Hospitals; Geneva Medical Faculty (R.G., N.S., K.B.), University of Geneva; and Geneva Hemodynamic Research Group (R.G., N.S., K.B.), Geneva, Switzerland.
authors.forename: Raphaël
authors.initials: R
authors.lastname: Giraud
authors.forename: Nils
authors.initials: N
authors.lastname: Siegenthaler
authors.forename: Diego
authors.initials: D
authors.lastname: Arroyo
authors.forename: Karim
authors.initials: K
authors.lastname: Bendjelid
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D004195:Disease Models, Animal; D004837:Epinephrine / Q000494:pharmacology*; D006439:Hemodynamics / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology*; D011446:Prospective Studies; D013318:Stroke Volume / Q000187:drug effects; D013552:Swine; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D014662:Vasoconstrictor Agents; D009638:Norepinephrine; D004837:Epinephrine