title: Pulmonary hypertension attenuates the dynamic preload indicators increase during experimental hypovolemia.
abstract: Pulse pressure (PPV) and stroke volume (SVV) variations may not be reliable in the setting of pulmonary hypertension and/or right ventricular (RV) failure. We hypothesized that RV afterload increase attenuates SVV and PPV during hypovolemia in a rabbit model of pulmonary embolism (PE) secondary to RV dysfunction.
  
  
  
  Seven anesthetized and mechanically ventilated rabbits were studied during four experimental conditions: normovolemia, blood withdrawal, pulmonary embolism and fluid loading of a colloidal solution. Central venous, RV and left ventricular (LV) pressures, and infra-diaphragmatic aortic blood flow (AoF) and pressure were measured. SV was estimated by the integral of systolic AoF. We analyzed RV and LV function through stroke work output curves. PPV and SVV were obtained by the variation of beat-to-beat PP and SV, respectively. We assessed RV and LV diastolic and systolic function by the time rate of relaxation (tau) and the ratio of the first derivative of ventricular pressure and the highest isovolumic developed pressure (dP/dt/DP), respectively. The vasomotor tone was estimated by the dynamic arterial elastance (Eadyn= PPV/SVV).
  
  
  
  PPV and SVV increased significantly during hemorrhage and returned to baseline values after PE which was associated to biventricular right-downward of the stroke work curves and a decrease of AoF and SV (P < 0.05). RV systo-diastolic function and LV systolic function were impaired. All the animals were nonresponders after volume expansion. Eadyndid not show any significant change during the different experimental conditions.
  
  
  
  The dynamic preload indicators (SVV and PPV) were significantly reduced after a normotensive PE in hypovolemic animals, mainly by the systo-diastolic dysfunction of the RV associated with LV systolic impairment, which makes the animals nonresponsive to volume loading. This normalization of dynamic preload indices may prevent the detrimental consequence of fluid loading.
authors.affiliation: Department of Anesthesia, School of Medicine, Hospital de Clínicas, Universidad de la República, Montevideo, Uruguay.
authors.forename: Juan P
authors.initials: JP
authors.lastname: Bouchacourt
authors.affiliation: Department of Anesthesia, School of Medicine, Hospital de Clínicas, Universidad de la República, Montevideo, Uruguay.
authors.forename: Juan
authors.initials: J
authors.lastname: Riva
authors.affiliation: Department of Pathophysiology, School of Medicine, Hospital de Clínicas, Universidad de la República, Avda Italia 2870, PC 11600, Montevideo, Uruguay. jgrig@fmed.edu.uy.
authors.forename: Juan C
authors.initials: JC
authors.lastname: Grignola
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D005260:Female; D005440:Fluid Therapy; D006439:Hemodynamics / Q000502:physiology; D006976:Hypertension, Pulmonary / Q000150:complications / Q000503:physiopathology*; D020896:Hypovolemia / Q000503:physiopathology*; D011655:Pulmonary Embolism / Q000150:complications / Q000503:physiopathology*; D011817:Rabbits; D013318:Stroke Volume / Q000502:physiology; D018497:Ventricular Dysfunction, Right / Q000503:physiopathology; D016278:Ventricular Function, Right / Q000502:physiology
keywords: Preload dynamic indices; Pulmonary hypertension; Pulse pressure variation; Right ventricular dysfunction; Stroke volume variation