Numerical simulation of the hemodynamic response to hemodialysis-induced hypovolemia.
To provide a framework for analyzing cardiovascular response to hemodialysis-induced hypovolemia, we developed a computer model which simulates arterial pressure changes caused by loss of blood volume. The model includes arterial and venous systemic circulation, Starling's law and inotropic regulation of heart, arterial and cardiopulmonary baroreflex control of capacitance, and resistance vessels. The performance of this model was assessed by analyzing the hemodynamic responses recorded in 12 patients undergoing chronic hemodialysis, 6 classified as hypotension resistant (stable group) and 6 as hypotension prone (unstable group). Arterial pressure, heart rate, and blood volume were recorded during regular hemodialysis. Blood volume and heart rate were used as inputs to the simulator whereas the arterial pressure response obtained by simulation was fitted to the measured data by tuning simulator parameters relative to the capacitance and resistance controls. Although analyzed pressure responses exhibited a wide variety of time patterns, for each one it was possible to identify an optimal set of parameters allowing the recorded pressure data to be accurately reproduced by the model. Sensitivity analysis performed with the model indicated that pressure response strongly depends on the parameter Kv accounting for the capability to control vascular capacitance. According to these results, the parameter Kv in the stable group was 9 times that of the unstable group, thereby suggesting a possible cause of their different hemodynamic behavior.
Cavalcanti
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Biomedical Engineering Laboratory, Department of Electronics, Computer Science, and Systems, University of Bologna, Italy.
Di Marco
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D000704:Analysis of Variance; D017704:Baroreflex / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D001810:Blood Volume; D002302:Cardiac Output / Q000502:physiology; D003198:Computer Simulation; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D007022:Hypotension / Q000209:etiology / Q000503:physiopathology*; D020896:Hypovolemia / Q000209:etiology / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000628:therapy*; D011311:Pressoreceptors / Q000502:physiology; D006435:Renal Dialysis / Q000009:adverse effects*; D014655:Vascular Resistance / Q000502:physiology