Abstract
This report gives the following clinical evaluation on the hemodynamic study in regular dialysis treatment (RDT).1. Cardiac output was increased in chronic dialysis patients, due to anemia, increased venous return from subcutaneous A-V fistula and excess of body fluids. It was normalized by improved anemia, occlusion of A-V fistula and removal of fluid excess by hemodialysis (HD).2. There was no significant difference of cardiac output between the normotensive patients ana the hyper-and hypotensive patients. Peripheral vascular resistance (RVR) was increased in hypertensive patients than in normotensive patients, and was decreased in hypotensive patients than in normotensive patients. This suggested that the increase in PVR produced the high blood pressure and the decreased PVR did the reverse.3. The cardiac reserve in pulmonary congestion could be impaired, due to hypertensive cardiac changes (hypertrophy and/or dilatation) and myocardial injury, based on the following observations. The hemodynamic changes were studied before and after HD. Cardiac output in patients without pulmonary congestion was reduced significantly after HD, while in patients with pulmonary congestion cardiac output was usually increased after the correction of fluid excess by HD, showing no significant differences between them. Mean blood pressure of patients with pulmonary congestion in both pre-and post-dialytic readings was above that of patients without pulmonary congestion in pre-dialytic reading. Although the cardiothoracic ratio (CTR) was decreased significantly in the two groups, CTR of patients with pulmonary congestion remained above 50% even after HD, which was greater than the pre-dialytic value of patients without pulmonary congestion. This suggested the cardiac impairment including hypertrophy and dilatation might be the cause in patients with congestion.4. Cardiac function was studied analyzing the left ventricular conduction time, which disclosed the prolongation of Q-IIai and ICT in the two groups (with and without pulmonary congestion) compared with the controlled group. These abnormalities were not significant between the two groups, suggestive of the impaired myocardial function of them. Normalization of prolonged Q-IIai, shortening of ETi and increased PEP/ET ratio were noted after HD, suggesting that the myocardial function was suppressed in RDT.
