title: Epoprostenol-induced pulmonary vasodilatation in patients with pulmonary hypertension measured by electrical impedance tomography.
abstract: Electrical impedance tomography (EIT) has been proposed as a method to monitor dynamic changes in the pulmonary vascular bed. In this study we examined the validity of EIT in the measurement of pulmonary vasodilatation in eight patients with primary and secondary pulmonary hypertension when given the vasodilating agent epoprostenol (Flolan). Therefore, catheterization of the pulmonary artery was performed in the ICU and the cardiac output was measured by means of the Fick method. The pulmonary vascular resistance (PVR) and mean pulmonary arterial pressure (mPAP) were determined. Epoprostenol was given in increasing doses to test reversibility of pulmonary hypertension. The maximum test dose was 12 ng kg(-1) min(-1). During each step simultaneous EIT (DAS-01 P Portable Data Acquisition System, Sheffield, England) measurements were performed with the 16 electrodes equidistantly positioned in the third intercostal space. The maximal systolic impedance change, relative to end-diastole, deltaZperf, was chosen as a measure of pulmonary perfusion. The impedance change between baseline and highest tolerable epoprostenol concentration was compared with the change in PVR. The mean PVR (dyn s/cm5) decreased from 636 (+/-399) to 366 (+/-242); p < 0.01. DeltaZperf (in arbitrary units) for the whole patient group increased from 901 (+/-295) x 10(-3) to 1082 (+/-472) x 10(-3) (p<0.05). Only one patient showed a reduction in pulmonary artery pressure >20%, which is defined as significant vasodilatation. A strong relationship was found between the impedance changes and the change in PVR and mPAP in the patient with a significant vasodilatation on epoprostenol. From these results we conclude that EIT is a reliable method to measure blood volume changes due to pharmacologically induced vasodilatation in the pulmonary bed.
authors.affiliation: Department of Pulmonary Medicine, Vrije Universiteit Medical Center, Amsterdam, The Netherlands. HJ.Smit@VUmc.nl
authors.forename: H J
authors.initials: HJ
authors.lastname: Smit
authors.forename: A
authors.initials: A
authors.lastname: Vonk Noordegraaf
authors.forename: R J
authors.initials: RJ
authors.lastname: Roeleveld
authors.forename: J G F
authors.initials: JG
authors.lastname: Bronzwaer
authors.forename: P E
authors.initials: PE
authors.lastname: Postmus
authors.forename: P M J M
authors.initials: PM
authors.lastname: de Vries
authors.forename: A
authors.initials: A
authors.lastname: Boonstra
mesh_terms: D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D017097:Electric Impedance; D011464:Epoprostenol / Q000627:therapeutic use*; D005260:Female; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D011651:Pulmonary Artery / Q000187:drug effects / Q000502:physiology; D011652:Pulmonary Circulation / Q000187:drug effects*; D011669:Pulmonary Wedge Pressure / Q000187:drug effects / Q000502:physiology; D014054:Tomography / Q000379:methods*; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D000959:Antihypertensive Agents; D011464:Epoprostenol