Mathematical modeling of arterial pressure response to hemodialysis-induced hypovolemia.

A computer model of pressure response to hemodialysis-induced hypovolemia is reported. Heart rate and hematocrit, measured in the course of hemodialysis, are imposed as computer model inputs and the model computes the arterial pressure response after tuning model parameters representative of patient's cardiovascular reactivity. Computer model reproduced with good accuracy experimental data (arterial pressure, cardiac output and total peripherical resistance). Parameter identification over successive sessions of the same patients revealed satisfactory reliability, providing a physiological interpretative key to patient's hemodynamic behavior during hemodialysis.

Role of short-term regulatory mechanisms on pressure response to hemodialysis-induced hypovolemia.

BACKGROUND: A large inter-subject variability exists in the arterial pressure response to hemodialysis-induced blood volume (BV) withdrawal. We investigated the hypothesis that this variability is due to the inter-subject differences in the short-term reflex capacity to compensate for hypovolemia. METHODS: Mean arterial pressure (MAP), heart rate (HR) and the percentage reduction in BV (%R-BV) were recorded in 32 subjects during their regular hemodialysis sessions. On the basis of absolute MAP changes between the beginning and the end of the session with respect to %R-BV at the end of the session, three distinct pressure responses were identified: (1) hypotension-prone response; (2) unstable response with delayed hypotension; and (3) hypotension-resistant response. For each kind of response, one patient was selected and a computer model of the cardiovascular system including the main short-term reflex compensatory mechanisms was used to analyze data collected over five consecutive sessions. The %R-BV and HR were used as model inputs, while simulated arterial pressure was fitted to the measured MAP by the tuning model parameters representing the efficiency in the control of venous capacity, microvascular resistance and heart inotropism. RESULTS: The model-based analysis related the hypotension-prone response to a lack of efficacy in capacity and resistance regulation. In the unstable response with delayed hypotension, the control of venous capacity was not effective and resistance control alone kept the pressure stable only for a limited %R-BV reduction (<5%). In the hypotension-resistant response, an efficient compensation of capacitance vessels was evidenced, and the slightly increasing arterial pressure was referred to a prevalence of cardiopulmonary pathway in the compensatory process. CONCLUSIONS: The model ascribes differences in pressure response to differences in the effectiveness of reflex compensatory mechanisms.