title: Exploring haemodynamics of haemodialysis using extrema points analysis model.
abstract: BACKGROUND
  Haemodialysis is a form of renal replacement therapy used to treat patients with end stage renal failure. It is becoming more appreciated that haemodialysis patients exhibit higher rates of multiple end organ damage compared to the general population. There is also a strong emerging evidence that haemodialysis itself causes circulatory stress. We aimed at examining haemodynamic patterns during haemodialysis using a new model and test that model against a normal control.
  
  
  METHODS
  We hypothesised that blood pressures generated by each heart beat constantly vary between local peaks and troughs (local extrema), the frequency and amplitude of which is regulated to maintain optimal organ perfusion. We also hypothesised that such model could reveal multiple haemodynamic aberrations during HD. Using a non-invasive cardiac output monitoring device (Finometer®) we compared various haemodynamic parameters using the above model between a haemodialysis patient during a dialysis session and an exercised normal control after comparison at rest.
  
  
  RESULTS
  Measurements yielded 29,751 data points for each haemodynamic parameter. Extrema points frequency of mean arterial blood pressure was higher in the HD subject compared to the normal control (0.761Hz IQR 0.5-0.818 vs 0.468Hz IQR 0.223-0.872, P < 0.0001). Similarly, extrema points frequency of systolic blood pressure was significantly higher in haemodialysis compared to normal. In contrary, the frequency of extrema points for TPR was higher in the normal control compared to HD (0.947 IQR 0.520-1.512 vs 0.845 IQR 0.730-1.569, P < 0.0001) with significantly higher amplitudes.
  
  
  CONCLUSIONS
  Haemodialysis patients potentially exhibit an aberrant haemodynamic behaviour characterised by higher extrema frequencies of mean arterial blood pressure and lower extrema frequencies of total peripheral resistance. This, in theory, could lead to higher variation in organ perfusion and may be detrimental to vulnerable vascular beds.
authors.affiliation: Division of Vascular Medicine, Faculty of Medicine and Health Sciences, School of Graduate Entry Medicine and Health, The University of Nottingham, Nottingham, UK. tarek.eldehni@nhs.net
authors.forename: Mohamed Tarek
authors.initials: MT
authors.lastname: Eldehni
authors.forename: Aghogho
authors.initials: A
authors.lastname: Odudu
authors.forename: Christopher William
authors.initials: CW
authors.lastname: McIntyre
mesh_terms: D000368:Aged; D001794:Blood Pressure; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008962:Models, Theoretical; D009200:Myocardial Contraction