A simplified, non-invasive method for assessment of the performance of the right heart during supine leg exercise was described, which necessitated no more than a bicycle"ergometer"for leg exercise, a radiocardiograph for recording cardiac index (CI) and a"water"manometer for measuring cubital venous pressure (VP). Because the use of a cardiac catheter was omitted, right atrial pressure (RA), right ventricular diastolic pressure (RVd) or pulmonary arterial pressure (PA) were not measured. In 11 healthy subjects and 25 patients with primarily left-sided valvular disease and hypertension, the observed shift of CI-VP plot with exercise was similar to the published records of exercise-induced shift of CI-RA plot or CI-RVd plot in normal subjects and the same types of heart disease. With levels of load used in this study, a dividing line separating normal from abnormal elevation of VP during supine leg exercise (ΔVP) could be drawn at ΔVP=35 mm H2O and (2) in these types of heart disease, ΔVP in excess of 35 mm H2O was always associated with a"subnormal"increase in CI (ΔCI < 0.8 lit. min-1. M-2) with exercise, except in a few cases who appeared, clinically, to be in what may be termed"latent heart failure". Factors probably responsible for an impaired pumping ability of the right heart during exercise in left-sided heart disease were discussed, in relation to ΔVP.
When estimating the pulmonary extravascular water volume (PEWV) as the lung thermal volume (LTV), by the double indicator dilution technic using heat and indocyanine green (ICG), a part of the left ventricular wall comes to the thermal equilibrium, and this leads to an overestimation of PEWV, when the samplings are made in the aortic root. In a previous study from this laboratory, this overestimation was approximately 10% of the measured LTV in the aortic root. In the present study, we evaluated the extent to which the thermal equilibrium with the aortic wall would cause LTV to slightly overestimate PEWV. For this purpose, we injected a mixture of the indicators into the right atrium, and recorded the indicator dilution curves at the bifurcation of the aorta (AB). We then compared this LTV with the one calculated from the indicator dilution curves recorded simultaneously in the aortic root (Ao). We obtained the following results: Firstly, the values of cardiac output (CO) from the dye dilution curve and from the thermodilution curve at two sites, Ao and AB, were all in agreement. Secondly, LTV estimated in Ao (LTVAo) and LTV estimated in AB (LTVAB) were not the same, and their relationships were: LTVAB = 1.21 X LTVAo + 0.44 (ml/kg), n = 32, (r = 0.98, p less than 0.001) A close agreement of CO determined at two sites indicated that there was virtually no loss of heat between the two sampling sites, Ao and AB. An excess of LTVAB over LTVAo came to about 20%, and this excess appeared to be ascribable to the incorporation of the thermally equilibrated "volume" of the aortic wall. This finding appeared to be a challenge to the validity of estimating LTV when sampling the indicators in the distal abdominal aorta.
We measured mean circulatory pressure (MCP) in anesthetized, open-chest dogs before and after intravenous administration of Ca++-antagonists to estimate the effects on systemic capacitance vessels and on venous return (VR) curves both with and without continuous intravenous infusion of norepinephrine (NE). Diltiazem (300 micrograms/kg) decreased total peripheral resistance (TPR) and MCP significantly. Nifedipine (5 micrograms/kg), nicardipine (30 micrograms/kg) and verapamil (200 micrograms/kg) decreased TPR significantly without any change in MCP in the absence of NE, but with the exception of verapamil, they decreased MCP in the presence of NE. This indicates that diltiazem relaxed the systemic capacitance vessels, and nifedipine and nicardipine significantly decreased the tone of the systemic capacitance vessels that had been previously elevated by NE, but this action was very slight with verapamil. These Ca++-antagonists rotated VR curves clockwise, decreased resistance to VR (RVR) and increased VR both in the presence and absence of NE. It was suggested that the decrease in the RVR would be at least partially responsible for the increase in the VR.
