Abstract
SummaryCardiac performance during hemodialysis is dependent on preexisting conditions (i.e., coronary artery disease, myocardial hypertrophy, LV compliance, anemia, hypertension, etc.) and the hemodynamic alterations caused by the dialysis procedure itself (osmotic shifts, ionized calcium changes, etc.). Clinical hemodynamic investigations of cardiac performance during uremia have been hampered by the difficulty in isolating individual parameters of ventricular function. Myocardial reserve in dialysis patients is often reduced because of antecedent ischemic disease, hypertension, and the presence of autonomic dysfunction in many patients. Rapid volume losses or gains are likely to be less well tolerated with resultant hypotensive syndromes or pulmonary edema as the result. The controlled volume loss achievable with newer dialysis machines, the use of higher dialysate sodium concentrations, and the wider availability of erythropoietin may improve the tolerance to the procedure for many patients.
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