title: Portopulmonary hypertension and liver transplantation: hemodynamic consequences at reperfusion.
abstract: BACKGROUND
  The absence of portopulmonary hypertension (PH) upon preoperative evaluation for liver transplantation (OLT) does not exclude the occasional occurrence of an acquired PH while awaiting a graft. We sought to estimate hemodynamic changes and right ventriculoarterial coupling during reperfusion.
  
  
  METHODS
  We studied 11 cirrhotic patients diagnosed with mild PH, according to the current classification: mean pulmonary artery pressure (MPAP)-25 to 34 mm Hg. These patients underwent OLT, using the piggyback technique (group PH). None of them had exhibited criteria for PH on preoperative echocardiography. This cohort was compared with 20 consecutive cirrhotic patients with normal MPAP at OLT. We performed a complete hemodynamic profile using a pulmonary artery catheter (RVEF, Baxter-Edwards, Calif, USA) before and 5 minutes after reperfusion. The variables were MPAP and right ventricular (RV) end-diastolic volume index (RVEDVI). Using standard formulas we calculated RV stroke work index (RVSWI), RV end-systolic elastance (Ees), pulmonary effective elastance (Ea), and RV-arterial coupling efficiency as the Ees/Ea ratio. Systolic ventricular function was expressed as RVSWI versus RVEDVI.
  
  
  RESULTS
  During the anhepatic phase, MPAP, Ees, Ea, and RVSWI were higher in the PH group; but RVEDVI was lower. After reperfusion the pressure (MPAP), contractility (RVSWI) and preload (RVEDVI) increased in both groups. However, afterload (Ea) decreased in the non-PH group; accordingly, Es/Ea increased only in these patients.
  
  
  CONCLUSIONS
  At reperfusion, the expansion in preload and cardiac output, without a similar afterload decrease, is responsible for the steady increase in pressure. Our results have shown that in the PH patient group, systolic ventricular function improves during reperfusion by a Frank-Starling mechanism; however, ventricular-arterial uncoupling is maintained (Ees/Ea < 1) because ventricular contractility is not appropriately balanced by simultaneous declines in afterload.
authors.affiliation: Liver Transplantation Unit, University Hospital V, Arrixaca, Murcia, Spain. franciscoj.acosta@carm.es
authors.forename: F
authors.initials: F
authors.lastname: Acosta
authors.forename: T
authors.initials: T
authors.lastname: Sansano
authors.forename: C G
authors.initials: CG
authors.lastname: Palenciano
authors.forename: P
authors.initials: P
authors.lastname: Domenech
authors.forename: L
authors.initials: L
authors.lastname: Falcon
authors.forename: R
authors.initials: R
authors.lastname: Robles
authors.forename: F S
authors.initials: FS
authors.lastname: Bueno
authors.forename: P
authors.initials: P
authors.lastname: Ramirez
authors.forename: P
authors.initials: P
authors.lastname: Parrilla
mesh_terms: D006439:Hemodynamics; D020065:Hepatopulmonary Syndrome / Q000503:physiopathology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000503:physiopathology*; D016031:Liver Transplantation / Q000379:methods / Q000502:physiology*; D015424:Reperfusion; D016278:Ventricular Function, Right