title: Insights into the mechanism of the nitroprusside-induced increase in cardiac output in failing hearts: an attempt at its prediction with Doppler echocardiography.
abstract: Increased left ventricular (LV) diastolic pressure is consistently decreased by the administration of nitroprusside; however, nitroprusside-induced changes in cardiac output (CO) vary among patients with failing hearts. Although the variation has been considered to be related to interindividual inhomogeneity of LV diastolic performance, nitroprusside-induced changes in CO are not predictable before drug administration in individual subjects. We attempted to clarify whether nitroprusside-induced changes in CO may be predicted by analysis of the mitral flow velocity pattern in failing hearts. LV diastolic pressure was increased by the combination of the decrease in LV function and the volume expansion, and 15 conditions with LV end-diastolic pressure (EDP) > or =15 mm Hg were obtained in 8 dogs. In each condition, pulsed Doppler mitral flow velocity patterns were recorded simultaneously with hemodynamic variables before and during intravenous nitroprusside infusion. After nitroprusside administration, LV systolic pressure and LVEDP decreased in all dogs, and CO increased in eight conditions but decreased in seven conditions. CO was more likely to increase with administration of nitroprusside, and its change was greater in the conditions in which deceleration time of the early diastolic filling wave before nitroprusside infusion was longer (r = 0.56, p<0.05, n = 15). Better correlation was obtained with multiple-regression analysis, using the deceleration time and peak filling velocity at atrial contraction (r = 0.67, p<0.05, n = 15). The deceleration time correlated with LV dynamic compliance (r = 0.66, p<0.01, n = 30). Analysis of mitral flow velocity patterns may be useful in predicting nitroprusside-induced changes in CO in failing hearts.
authors.affiliation: First Department of Medicine, Osaka University School of Medicine, Suita, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Nagano
authors.forename: T
authors.initials: T
authors.lastname: Masuyama
authors.forename: K
authors.initials: K
authors.lastname: Yamamoto
authors.forename: J
authors.initials: J
authors.lastname: Naito
authors.forename: T
authors.initials: T
authors.lastname: Mano
authors.forename: M
authors.initials: M
authors.lastname: Inoue
authors.forename: M
authors.initials: M
authors.lastname: Hori
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects*; D004285:Dogs; D018619:Echocardiography, Doppler, Pulsed; D006333:Heart Failure / Q000503:physiopathology*; D009599:Nitroprusside / Q000494:pharmacology*; D012044:Regression Analysis; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
chemical_list: D009599:Nitroprusside