title: Myocardial contractile function and intradialytic hypotension.
abstract: Dialysis-induced hypotension remains a significant problem in hemodialysis (HD) patients. Numerous factors result in dysregulation of blood pressure control and impaired myocardial reserve in response to HD-induced cardiovascular stress. Episodic intradialytic hypotension may be involved in the pathogenesis of evolving myocardial injury. We performed an initial pilot investigation of cardiovascular functional response to pharmacological cardiovascular stress in hypotension-resistant (HR) and hypotension-prone (HP) HD patients. We studied 10 matched chronic HD patients (5 HP, 5 HR). Dobutamine-atropine stress (DAS) was performed on a nondialysis short interval day, with noninvasive pulse-wave analysis using the Finometer to continuously measure hemodynamic variables. Baroreflex sensitivity was assessed at rest and during DAS. Baseline hemodynamic variables were not significantly different. The groups had differing hemodynamic responses to DAS. The Mean arterial pressure was unchanged in the HR group but decreased in HP patients (-13.6 +/- 3.5 mmHg; P<0.001). This was associated with failure to significantly increase cardiac output in the HP group (cf. increase in cardiac output in the HR group of +33.4 +/- 6%; P<0.05), and a reduced response in total peripheral resistance (HP -10.3 +/- 6.8%, HR -22.7 +/- 2.9%, P=NS). Baroreflex sensitivity was not significantly different between groups at baseline or within groups with increasing levels of DAS; however, the mean baroreflex sensitivity was higher in HR cf. HP subjects throughout pharmacological stress (P<0.05). Hypotension-prone patients appear to have an impaired cardiovascular response to DAS. The most significant abnormality is an impaired myocardial contractile reserve. Early identification of these patients would allow utilization of therapeutic strategies to improve intradialytic tolerability, potentially abrogating aggravation of myocardial injury.
authors.affiliation: Department of Renal Medicine, Derby City General Hospital, Derby, United Kingdom.
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Owen
authors.forename: William S
authors.initials: WS
authors.lastname: Priestman
authors.forename: Mhairi K
authors.initials: MK
authors.lastname: Sigrist
authors.forename: Stewart H
authors.initials: SH
authors.lastname: Lambie
authors.forename: Stephen G
authors.initials: SG
authors.lastname: John
authors.forename: Lindsay J
authors.initials: LJ
authors.lastname: Chesterton
authors.forename: Christopher W
authors.initials: CW
authors.lastname: McIntyre
mesh_terms: D000328:Adult; D000368:Aged; D001285:Atropine; D001794:Blood Pressure / Q000187:drug effects; D004280:Dobutamine; D004562:Electrocardiography / Q000379:methods; D005260:Female; D006801:Humans; D007022:Hypotension / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D006435:Renal Dialysis / Q000009:adverse effects*
chemical_list: D004280:Dobutamine; D001285:Atropine