title: Monitoring cardiovascular changes during hemodialysis in children.
abstract: Hemodialysis (HD) causes rapid volume shifts and circulatory changes. In chronic renal failure (CRF) Na+/K+ATP-ase is depressed, whereas endogenous digoxin-like factor (EDLF) is elevated. Our aim was to characterize HD-induced cardiovascular adaptation and its possible links to Na+/K+ATP-ase and EDLF. Eleven children with CRF on HD (aged 14.7 +/- 3.7 years) and 11 healthy children were investigated for basic circulatory parameters. Thoracic impedance (Zo) and circulatory parameters were monitored by impedance cardiography (ICG) during HD. Erythrocyte Na+/K+ATP-ase and EDLF were measured before and after HD. Up to the loss of 6% of total body weight, Zo rose linearly with fluid removal, above this no further increase occurred. Heart rate and mean arterial pressure (MAP) were inversely related (r = -0.97); MAP rose in the first and decreased in the second part of HD. Systemic vascular resistance paralleled MAP, whereas stroke volume rapidly decreased, but stabilized in the second part of HD. The ratio of preejection period/ventricular ejection time (PEP/VET) correlated positively with HD duration (r = 0.92), suggesting diminished cardiac filling. Cardiac index (CI) remained stable. EDLF was high in uremia accompanied by depressed Na+/K+ATP-ase (P < 0.05 and P < 0.01, respectively). Following HD Na+/K+ATP-ase normalized. Correlation between Na+/K+ATP-ase activity and MAP was linear (r = 0.85). In conclusion, ICG during HD provides detailed information concerning circulatory adaptation resulting in stable CI, suggesting that the dialysis-induced hypovolemia is compensated by the centralization of the blood volume. Changes of Na+/K+ATP-ase indicate that dialyzable blood pressure-regulating substance(s) inhibit(s) the pump. However, lack of further correlation between Na+/K+ATP-ase, EDLF, and cardiovascular parameters indicates the complexity of the regulatory processes.
authors.affiliation: 1st Department of Pediatrics, Semmelweis Medical University, Bókay u. 53, 1083 Budapest, Hungary.
authors.forename: G
authors.initials: G
authors.lastname: Miltényi
authors.forename: K
authors.initials: K
authors.lastname: Tory
authors.forename: G
authors.initials: G
authors.lastname: Stubnya
authors.forename: P
authors.initials: P
authors.lastname: Tóth-Heyn
authors.forename: B
authors.initials: B
authors.lastname: Vásárhelyi
authors.forename: P
authors.initials: P
authors.lastname: Sallay
authors.forename: A
authors.initials: A
authors.lastname: Szabó
authors.forename: T
authors.initials: T
authors.lastname: Tulassay
authors.forename: M
authors.initials: M
authors.lastname: Dobos
authors.forename: G S
authors.initials: GS
authors.lastname: Reusz
mesh_terms: D000293:Adolescent; D001794:Blood Pressure; D002298:Cardenolides; D002307:Cardiography, Impedance; D002648:Child; D004077:Digoxin; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000503:physiopathology / Q000628:therapy; D008297:Male; D006435:Renal Dialysis; D012503:Saponins / Q000097:blood; D000254:Sodium-Potassium-Exchanging ATPase / Q000097:blood; D014655:Vascular Resistance
chemical_list: D002298:Cardenolides; D012503:Saponins; C034504:digoxin-like factors; D004077:Digoxin; D000254:Sodium-Potassium-Exchanging ATPase