High volume hemofiltration improves right ventricular function in endotoxin-induced shock in the pig

This study assessed the influence of continuous high volume hemofiltration on right ventricular function of pigs with endotoxin induced shock. Eighteen anesthetized and ventilated pigs were studied for 240 min after the start of infusion of 0.5 mg/kg endotoxin over 30 min. Right ventricular ejection...

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Bibliographic Details
Published in:Intensive care medicine 1992-04, Vol.18 (4), p.235-240
Main Authors: GROOTENDORST, A. F, VAN BOMMEL, E. F. H, VAN DER HOVEN, B, VAN LEENGOED, L. A. M. G, VAN OSTA, A. L. M
Format: Article
Language:English
Subjects:
Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Animals
Binding Sites
Biological and medical sciences
Cardiac Output
Disease Models, Animal
Emergency and intensive care: infection, septic shock
Endotoxins
Evaluation Studies as Topic
Hemofiltration - instrumentation
Hemofiltration - methods
Hemofiltration - standards
Intensive care medicine
Medical sciences
Shock, Septic - physiopathology
Shock, Septic - therapy
Stroke Volume
Swine
Thermodilution
Vascular Resistance
Ventricular Function, Right
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Summary:This study assessed the influence of continuous high volume hemofiltration on right ventricular function of pigs with endotoxin induced shock. Eighteen anesthetized and ventilated pigs were studied for 240 min after the start of infusion of 0.5 mg/kg endotoxin over 30 min. Right ventricular ejection fraction (RVEF) was measured by rapid response thermodilution technique. After endotoxin infusion, the pigs were randomly divided into 3 groups: group 1 as a control group, receiving endotoxin only, group 2 to observe the effects of zero balance high volume veno-venous hemofiltration with removal of ultrafiltrate at a rate of 6000 ml/h, and group 3 to evaluate the effect of the extracorporeal circuit itself on RVEF. The decline of RVEF in group 2 was less than in group 1 (0.04 +/- 0.02 vs 0.21 +/- 0.03 (mean +/- SEM); p less than 0.001). The decline of RVEF in group 3 (0.24 +/- 0.02) was more pronounced than that in group 1 (p less than 0.05). The differences in the course of RVEF between group 1 and group 2 could not be explained by differences in heart rate, preload or afterload. Cardiac output and mean arterial pressure were significantly higher in group 2 than in group 1 (p less than 0.01). It is concluded that in this model, high volume hemofiltration improves RVEF and cardiac performance by removal of vasoactive mediators, responsible for myocardial depression.
ISSN:0342-4642
1432-1238
DOI:10.1007/BF01709839