Hemofiltration and left ventricular function in sepsis: mechanisms and clinical implications.

Over the last decade, it became clear that left ventricular (LV) dysfunction is typical of animal and human septic shock [1]. Circulating myocardial depressant substances [2] and local release of mediators [3], rather than global myocardial hypoperfusion [4,5], seem responsible for this phenomenon. Indeed, a series of reports [3] by Parrillo et al. in the 1980s were able to conclusively link left ventricular systolic dysfunction in septic patients to the effects of a myocardial depressant substance in the patient's own serum. Moreover, immunoabsorption of both tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta from the sera of patients with septic shock completely eliminated its cardiac myocyte depressant activity, suggesting that TNF-alpha and IL-1 beta contribute to septic myocardial depression [2]. Removing various proinflammatory substances by hemofiltration became consequently very attractive, especially as several studies showed that the left ventricular systolic function of septic animals was improved by hemofiltration and confirmed the presence of a depressive substance in the plasma and ultrafiltrate of septic animals [6,7].