title: Hemodynamic response during lower body negative pressure: role of volume status.
abstract: Sudden dialysis-related hypotension is characterized by paradoxical vasodilation, suggestive of sympathoinhibition. A similar hypotensive reaction can be evoked by lower body negative pressure (LBNP), which thus allows the study of the numerous factors involved in dialysis hypotension separately. This article examines the influence of changes in volume status on the hemodynamic response to LBNP (45 mmHg up to the iliac crest, maximum 60 min) in 12 healthy subjects. LBNP caused a decrease in cardiac index and pulse pressure, and an increase in heart rate and total peripheral resistance, most of which developed within the first 3 min of LBNP. Six subjects developed sudden hypotension characterized by vasodilation after 9 +/- 4 min of LBNP. After saline expansion (25 ml/kg), which increased blood volume by approximately 8%, five subjects endured LBNP for the full 60 min. However, after 60 min of LBNP, the circulatory parameters suggested a similar critical situation as that observed before presyncope in their first experiment. The other six subjects endured the full 60 min of LBNP. After furosemide-induced volume reduction associated with 1.6 +/- 0.2 kg weight loss and approximately 7% blood volume reduction, five of them developed vasodilatory presyncope after 17 +/- 5 min of LBNP. Comparison of presyncopal and nonpresyncopal experiments within subjects, as well as between subjects, showed that the early (3 min) response to LBNP was different: Despite similar decreases in cardiac index, the values for systolic pressure, pulse pressure, peripheral resistance, and stroke volume were lower, and the heart rate was higher in the experiments ending in presyncope. It is concluded that the volume status is a determinant of the tolerance to LBNP, probably by affecting the vasoconstrictive response. By inference, this study suggests that the vasoconstrictive response to the hemodynamic stress of hemodialysis is also influenced by the volume status.
authors.affiliation: Department of Nephrology and Hypertension, University Hospital Utrecht, The Netherlands.
authors.forename: G
authors.initials: G
authors.lastname: Ligtenberg
authors.forename: P J
authors.initials: PJ
authors.lastname: Blankestijn
authors.forename: H A
authors.initials: HA
authors.lastname: Koomans
mesh_terms: D000328:Adult; D001810:Blood Volume / Q000187:drug effects / Q000502:physiology*; D004198:Disease Susceptibility; D004232:Diuretics / Q000494:pharmacology; D005260:Female; D005665:Furosemide / Q000494:pharmacology; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D007022:Hypotension / Q000503:physiopathology; D008150:Lower Body Negative Pressure; D008297:Male; D012965:Sodium Chloride / Q000494:pharmacology
chemical_list: D004232:Diuretics; D012965:Sodium Chloride; D005665:Furosemide