Biomedical subjects

M Ursino

Publications and source records attributed to M Ursino.

At least 37 records · Page 2Linked to original sources

PubMed2000

Evaluation of intradialytic solute and fluid kinetics. Setting Up a predictive mathematical model.

A mathematical model of solute kinetics for the improvement of hemodialysis treatment is presented. It includes a two-compartment description of the main solutes and a three-compartment model of body fluids (plasma, interstitial and intracellular). The main model parameters can be individually assigned a priori, on the basis of body weight and plasma concentration values measured before beginning the session. Model predictions are compared with clinical data obtained in vivo during 11 different hemodialysis sessions performed on 6 patients with a profiled sodium concentration in the dialysate and a profiled ultrafiltration rate. In all cases, the agreement between the time pattern of model solute concentrations in plasma and the in vivo data proves fairly good as to urea, sodium, chloride, potassium and bicarbonate kinetics. Only in two sessions was blood volume directly measured in the patient, and in both cases the agreement with model predictions was good. In conclusion, the model allows a priori computation of the amount of sodium removed during hemodialysis, and makes it possible to predict the plasma volume changes and plasma osmolarity changes induced by a given sodium concentration profile in the dialysate and by a given ultrafiltration profile. Hence, it can be used to improve clinical tolerance to the dialysis session taking the characteristics of individual patients into account, in order to minimize intradialytic hypotension.

Bicarbonates↗

PubMed2000

Modelling the interaction among several mechanisms in the short-term arterial pressure control.

A Mathematical model of the short-term arterial pressure control in humans is presented. It includes a six-compartment description of the vascular system, an elastance variable model of the pulsating heart, two groups of baroreceptors (high-pressure or sinoaortic baroreceptors and low-pressure or cardiopulmonary baroreceptors), the efferent activity in the sympathetic nerves and in the vagus, and the response of four distinct effectors (heart period, systemic peripheral resistance, systemic venous unstressed volume and heart contractility). Several experimental results reported in the physiological literature can be reproduced with the model quite well. The examples presented in this work include the effect of combined sympathetic and vagal stimulation on heart rate, the baroreflex response to mild and severe acute haemorrhages, and the baroreflex response to ventricular pacing at different rates performed during atrioventricular block. The results suggest that: i) The sympathetic nerves and the vagus interact linearly in regulating heart period. The apparent negative interaction observed experimentally can be ascribed merely to the hyperbolic relationship which links heart rate to heart period. ii) The cardiopulmonary baroafferents play a significant role in the control of systemic arterial pressure during mild haemorrhages (lower than 3-4% of the overall blood volume). In this range, they may allow arterial pressure to be maintained at its normal level without the intervention of the sinoaortic baroreceptors. In contrast, the sinoaortic baroreceptors become the major responsible of the observed cardiovascular adjustments during more severe haemorrhages, when the role of cardiopulmonary baroreceptors becomes progressively exhausted. iii) The stability margin of the closed-loop system is quite low. Increasing the static gain of the baroreceptors or reducing the rate-dependent component may result in self-sustained oscillations similar to Mayer waves.

Arteries↗

PubMed1999

Correlation between cerebral oxygen saturation measured by near-infrared spectroscopy and jugular oxygen saturation in patients with severe closed head injury.

UNLABELLED: Near-infrared spectroscopy has been used to monitor cerebral oxygen saturation during cerebral circulatory arrest and carotid clamping. However, its utility has not been demonstrated in more complex situations, such as in patients with head injuries. The authors tested this method during conditions that may alter the arteriovenous partition of cerebral blood in different ways. METHODS: The authors compared changes in measured cerebral oxygen saturation and other hemodynamic parameters, including jugular venous oxygen saturation, in nine patients with severe closed head injury during manipulation of arterial carbon dioxide partial pressure and after mean arterial pressure was altered by vasopressors. RESULTS: The Bland and Altman representation of cerebral oxygen saturation versus jugular oxygen saturation showed a uniform scatter. Values for changing arterial carbon dioxide partial pressure were: bias = 1.1%, 2 SD = +/-21%, absolute value; and those for alterations in mean arterial pressure: bias = 3.7%, 2 SD = +/-24%, absolute value. However, a Bland and Altman plot of changes in cerebral oxygen saturation versus changes in jugular oxygen saturation had a negative slope (alteration in arterial carbon dioxide partial pressure: bias = 2.4%, 2 SD = +/-17%, absolute value; alteration in mean arterial pressure: bias = -4.9%, 2 SD = +/-31%, absolute value). Regression analysis showed that changes in cerebral oxygen saturation were positively correlated with changes in jugular venous oxygen saturation during the carbon dioxide challenge, whereas correlation was negative during the arterial pressure challenge. CONCLUSIONS: Cerebral oxygen saturation assessed by near-infrared spectroscopy does not adequately reflect changes in jugular venous oxygen saturation in patients with severe head injury. Changes in arteriovenous partitioning, infrared-spectroscopy contamination by extracerebral signal, algorithm errors, and dissimilar tissue sampling may explain these findings.

Administration, Inhalation↗

PubMed1999

A mathematical model of the carotid baroregulation in pulsating conditions.

A mathematical model of short-term arterial pressure control by the carotid baroreceptors in vagotomized subjects is presented. It includes an elastance variable description of the left and right heart, the systemic and pulmonary circulations, the afferent carotid baroreceptor pathway, a central elaboration unit, and the action of five effector mechanisms. Simulation results suggest that the carotid baroreflex is able to significantly modulate the cardiac function curve, but this effect is masked in vivo by changes in arterial pressure and atrial pressure. During heart pacing, cardiac output increases with frequency at moderate levels of heart rate, then fails to increase further due to a reduction in stroke volume. Shifting from nonpulsatile to pulsatile perfusion of the carotid sinuses decreases the overall baroreflex gain. Finally, a sensitivity analysis suggests that venous unstressed volume control plays the major role in the early hemodynamic response to acute hemorrhage, whereas systemic resistance control is less important. In all cases, there has been satisfactory agreement between model and experimental results.

Baroreflex↗

PubMed1999

Mathematical modeling of solute kinetics and body fluid changes during profiled hemodialysis.

A mathematical model of solute kinetics oriented to improve hemodialysis treatment is presented. It includes a two-compartment description of the main solutes (K+, Na+, Cl-, urea, HCO3-, H+, CO2), acid-base equilibrium through two buffer systems (bicarbonate and non-carbonic buffers) and a three-compartment model of body fluids (plasma, interstitial and intracellular). The main model parameters can be individually assigned a priori, on the basis of body weight and plasma concentration values measured before beginning the session. Model predictions are compared with clinical data obtained during 11 different hemodialysis sessions performed on six patients with profiled sodium concentration in the dialysate and profiled ultrafiltration rate. In all cases, the agreement between the time pattern of model solute concentrations in plasma and clinical data turns out fairly good as to urea, sodium, chloride and potassium kinetics. Finally, the time patterns of plasma bicarbonate concentration and pH can be reproduced fairly well with the model, provided CO2 concentration remains constant. Only in two sessions, blood volume was directly measured in the patient, and in both cases the agreement with model predictions was good. In conclusion, the model allows a priori computation of the amount of sodium removed during hemodialysis, and may enable the prediction of plasma volume changes and plasma osmolarity changes induced by a given sodium concentration profile in the dialysate and by a given ultrafiltration profile. Hence, it can be used to improve the dialysis session taking the characteristics of individual patients into account, in order to minimize intradialytic imbalances (such as hypotension or disequilibrium syndrome).

Acid-Base Equilibrium↗

PubMed1999

CathSim: an intravascular catheterization simulator on a PC.

The development of a medical simulator that incorporates substantial training value and realism into an affordable product has been a huge challenge for the simulation community. A large hurdle to making an inexpensive simulator has been the high cost of the computers needed for adequate realism. We have met this challenge by developing CathSim, a low-cost medical simulator that integrates force feedback, multimedia, and 3D graphics simulation technology on an industry standard PC. This product is commercially available and is currently being used by numerous training institutions and hospitals. The CathSim system includes software and a force feedback interface device. The platform and device can be used to train health care providers to perform needle-stick medical procedures. Our first module teaches users the techniques of peripheral intravenous (i.v.) catheterization. Other training modules that will be added to the CathSim platform include central venous catheter (CVC) insertion and peripherally inserted central catheter (PICC) placement. This paper discusses the challenges of this project and the trade-offs and solutions that we developed to overcome them. We describe our process of analyzing and prioritizing the medical tasks necessary to correctly perform peripheral intravenous catheterization. This analysis and prioritization was used to decide which tasks would be included in the simulator and how the included tasks would be replicated. We discuss the method by which we obtained the needed realism in the 3D graphics rendering and in the tactile feedback of the input device. We illustrate how we blended together simulation and multimedia technology to ensure adequate immersion and training efficacy, while keeping the system cost to a minimum.

Computer Simulation↗

PubMed1998

Vasomotion and blood flow regulation in hamster skeletal muscle microcirculation: A theoretical and experimental study.

A mathematical model of a microvasculature was used to study the effects of myogenic and flow-dependent stimuli on the characteristics of vasomotion and microvascular perfusion regulation. The model includes three branching orders of arterioles derived from in vivo observations and incorporates a mechanism for terminal arteriolar closure during vasomotion. Simulations were performed to evaluate the effect of vasodilation and vasoconstriction on vasomotion pattern, and the changes in arteriolar effective diameter and flow in response to arterial blood pressure variations triggering the regulatory mechanisms. Vasomotion patterns were studied in the hamster cutaneous muscle, visualized by fluorescent microscopy, in control conditions and after injection of acetylcholine (Ach) or NG-monomethyl-L-arginine (L-NMMA). We have found that vasomotion may be caused by different combinations of feedback mechanisms, including a strong rate-dependent myogenic response or a strong flow-dependent mechanism with no rate-dependent response. Decreasing the rate-dependent component of the myogenic mechanism and increasing the time constant of the flow-dependent mechanism causes vessel stabilization and disappearance of vasomotion. In hamster microcirculation, Ach decreased vasomotion frequency and increased vasomotion amplitude and arteriolar effective diameter, whereas L-NMMA caused a slight increase in vasomotion frequency and decrease in effective diameter. Model simulations, under dilatory and constrictory stimuli, confirmed these results. Moreover, the model predicted that mean blood flow is maintained closer to normal despite arterial pressure changes (+/-15% flow changes versus +/-50% pressure variations) when the vessels were in nonoscillatory than when they are in oscillatory state. In conclusion, a large variety of vasomotion patterns affect arteriolar resistance and microvessel perfusion in skeletal muscle. Furthermore, in the presence of vasomotion the network exhibits a poorer aptitude for regulating blood flow during arterial pressure changes (i.e., worse autoregulation) than the nonoscillatory network.

Animals↗

PubMed1998

Estimation of the main factors affecting ICP dynamics by mathematical analysis of PVI tests.

A simplified model of intracranial dynamics is used to reproduce the intracranial pressure (ICP) time pattern in 20 patients with severe brain damage during PVI tests. A comparison of model responses and clinical tracings was achieved by minimizing a least square criterion function and adjusting just 5 parameters. These are: the CSF outflow resistance, the intracranial elastance coefficient, the autoregulation gain and time constant, and the basal values of arteriolar compliance. Based on the value of the autoregulation gain, the patients were classified into two groups: those with damaged autoregulation (8 out of 12) and those with preserved autoregulation (12 out of 20). Finally, analysis of the correlation between parameter estimates provided suggestions on the combination of a parameter changes which may have the greater impact on ICP in the individual cases. Once these parameters have been identified, they may become possible targets for therapeutic interventions.

Blood Flow Velocity↗

PubMed1998

Clinical use of profiled hemodialysis.

The new population on dialysis today consists mainly of high risk patients (the elderly, diabetics, etc.) with high cardiovascular scores, and such vascular pathology is the most important predisposing factor for the occurrence of a frequent intradialytic clinical complication, vascular instability syndrome, which covers a range of clinical problems. Recently a new dialysis technique, profiled hemodialysis (PHD), has been set up and proposed for routine use. PHD consists of the clinical use of preestablished individual dialysis profiles aimed at antagonizing the changes in intradialytic plasma osmolarity by continuous modulation of dialysate sodium concentration throughout the whole extracorporeal session. In particular, PHD aims at reducing the fall of plasma osmolarity in the first half of the session (when it is higher) by reducing the sodium removal rate through increasing its dialysate concentration while taking into account the desired individual sodium balance to be reached at the end of the session. In this work, we report clinical experience with PHD compared to standard hemodialysis with constant sodium dialysate (SHD) in terms of its efficacy to maintain a more stable intradialytic blood volume (BV) and more stable hemodynamics. The PHD used in this work has been implemented by a mathematical model for computing the individual dialysate sodium profile which we have recently validated (Ursino M, Coli L, La Manna G, Grilli Cicilioni M, Dalmastri V, Guidicissi A, Masotti P, Avanzolini G, Stefani S, Bonomini V. A simple mathematical model of intradialytic sodium kinetics: "in vivo" validation during hemodialysis with constant or variable sodium. Int J Artif Organs 1996;19:393-403.). Eleven uremic patients affected by hypotension at the beginning of dialysis treatment were studied. Each patient first underwent an SHD treatment and 1 week later a PHD treatment. The 2 extracorporeal sessions (one on SHD and the other on PHD) were performed in each individual patient under identical operative conditions including the sodium mass removal by the end of the session and the ultrafiltration rate. The crit line and Doppler echocardiography were used to determine BV, cardiac output (CO), and stroke volume (SV) throughout the sessions. The mean blood pressure (MBP) and heart rate (HR) were simultaneously monitored. PHD was associated with a more stable intradialytic BV and more stable hemodynamics compared to SHD. The higher stability of BV and cardiac function (in terms of SV and CO maintenance) which was obtained above all in the first half of the PHD session was associated with a higher stability of the MBP and the HR. This resulted in an enhancement in cardiovascular tolerance to ultrafiltration throughout the session in all tested patients. In contrast, SHD in the same patients was characterized by early significant changes in BV and cardiovascular parameters resulting in a significant decrease of the MBP and a significant increase of the HR throughout the session and also 1 h after the end of dialysis. Our results indicate that PHD may represent an efficient approach for the treatment of patients suffering from intradialytic vascular instability. If long-term clinical practice confirms the efficacy of PHD in controlling dialysis intolerance symptoms, it will have great scope as a routine procedure.

Aged↗

PubMed1998

Interaction among autoregulation, CO2 reactivity, and intracranial pressure: a mathematical model.

The relationships among cerebral blood flow, cerebral blood volume, intracranial pressure (ICP), and the action of cerebrovascular regulatory mechanisms (autoregulation and CO2 reactivity) were investigated by means of a mathematical model. The model incorporates the cerebrospinal fluid (CSF) circulation, the intracranial pressure-volume relationship, and cerebral hemodynamics. The latter is based on the following main assumptions: the middle cerebral arteries behave passively following transmural pressure changes; the pial arterial circulation includes two segments (large and small pial arteries) subject to different autoregulation mechanisms; and the venous cerebrovascular bed behaves as a Starling resistor. A new aspect of the model exists in the description of CO2 reactivity in the pial arterial circulation and in the analysis of its nonlinear interaction with autoregulation. Simulation results, obtained at constant ICP using various combinations of mean arterial pressure and CO2 pressure, substantially support data on cerebral blood flow and velocity reported in the physiological literature concerning both the separate effects of CO2 and autoregulation and their nonlinear interaction. Simulations performed in dynamic conditions with varying ICP underline the existence of a significant correlation between ICP dynamics and cerebral hemodynamics in response to CO2 changes. This correlation may significantly increase in pathological subjects with poor intracranial compliance and reduced CSF outflow. In perspective, the model can be used to study ICP and blood velocity time patterns in neurosurgical patients in order to gain a deeper insight into the pathophysiological mechanisms leading to intracranial hypertension and secondary brain damage.

Animals↗

PubMed1998

Modeling cerebral autoregulation and CO2 reactivity in patients with severe head injury.

The mathematical model presented in a previous work is used to simulate the time pattern of intracranial pressure (ICP) and of blood velocity in the middle cerebral artery (VMCA) in response to maneuvers simultaneously affecting mean systemic arterial pressure (SAP) and end-tidal CO2 pressure. In the first stage of this study, a sensitivity analysis was performed to clarify the role of some important model parameters [cerebrospinal fluid (CSF) outflow resistance, intracranial elastance coefficient, autoregulation gain, and the position of the regulation curve] during CO2 alteration maneuvers performed at different SAP levels. The results suggest that the dynamic "ICP-VMCA" relationship obtained during changes in CO2 pressure may contain important information on the main factors affecting intracranial dynamics. In the second stage, the model was applied to the reproduction of real ICP and velocity tracings in neurosurgical patients. Ten distinct tracings, taken from six patients during CO2 changes at different mean SAP levels, were reproduced. Best fitting between model and clinical curves was achieved by minimizing a least-squares criterion function and adjusting certain parameters that characterize CSF circulation, intracranial compliance, and the strength of the regulation mechanisms. A satisfactory reproduction was achieved in all cases, with parameter numerical values in the ranges reported in clinical literature. It is concluded that the model may be used to give reliable estimations of the main factors affecting intracranial dynamics in individual patients, starting from routine measurements performed in neurosurgical intensive care units.

Blood Flow Velocity↗

PubMed1998

Interaction between carotid baroregulation and the pulsating heart: a mathematical model.

A mathematical model of short-term arterial pressure control by the carotid baroreceptors in pulsatile conditions is presented. The model includes an elastance variable description of the left and right heart, the systemic (splanchnic and extrasplanchnic) and pulmonary circulations, the afferent carotid baroreceptor pathway, the sympathetic and vagal efferent activities, and the action of several effector mechanisms. The latter mechanisms work, in response to sympathetic and vagal action, by modifying systemic peripheral resistances, systemic venous unstressed volumes, heart period, and end-systolic elastances. The model is used to simulate the interaction among the carotid baroreflex, the pulsating heart, and the effector responses in different experiments. In all cases, there has been satisfactory agreement between model and experimental results. Experimental data on heart rate control can be explained fairly well by assuming that the sympathetic-parasympathetic systems interact linearly on the heart period. The carotid baroreflex can significantly modulate the cardiac function curve. However, this effect is masked in vivo by changes in arterial and atrial pressures. During heart pacing, cardiac output increases with frequency at moderate levels of heart rate and then fails to increase further because of a reduction in stroke volume. Shifting from nonpulsatile to pulsatile perfusion of the carotid sinuses decreases the overall baroreflex gain and significantly modifies operation of the carotid baroreflex. Finally, a sensitivity analysis suggests that venous unstressed volume control plays the major role in the early hemodynamic response to acute hemorrhage, whereas systemic resistance and heart rate controls are a little less important.

Animals↗

PubMed1998

Relationships among cerebral perfusion pressure, autoregulation, and transcranial Doppler waveform: a modeling study.

OBJECT: The aim of this study was to analyze how the main values extrapolated from the transcranial Doppler (TCD) waveform (systolic, mean, and diastolic velocity; velocity peak-to-peak amplitude; and pulsatility index [PI]) are affected by changes in intracranial pressure (ICP), systemic arterial pressure (SAP), autoregulation, and intracranial compliance. METHODS: The analysis was performed using a mathematical model of the intracranial dynamics. This model includes a passive middle cerebral artery, the biomechanics of large and small pial arteries subjected to autoregulatory mechanisms, a collapsing venous cerebrovascular bed, the cerebrospinal fluid circulation, and the ICP-volume relationship. The results indicate that there are approximately three distinct zones characterized by different relationships between cerebral perfusion pressure (CPP) and velocity parameters in patients with preserved autoregulation. In the central autoregulatory zone (CPP > 70 mm Hg) the mean velocity does not change with decreasing CPP, whereas the PI and velocity peak-to-peak amplitude increase moderately. In a second zone (CPP between 4045 and 70 mm Hg), in which vasodilation of small pial arteries becomes maximal, the mean velocity starts to decrease, whereas the PI and velocity amplitude continue to increase. In the third zone, in which autoregulation is completely exhausted (CPP < 40 mm Hg), arterioles behave passively, mean velocity and velocity amplitude decline abruptly, and the PI exhibits a disproportionate rise. Moreover, this rise is quite independent of whether CPP is reduced by increasing ICP or reducing mean SAP. In contrast, in patients with defective autoregulation, the mean velocity and velocity amplitude decrease linearly with decreasing CPP, but the PI still increases in a way similar to that observed in patients with preserved autoregulation. CONCLUSIONS: The information contained in the TCD waveform is affected by many factors, including ICP, SAP, autoregulation. and intracranial compliance. Model results indicate that only a comparative analysis of the concomitant changes in ultrasonographic quantities during multimodality monitoring may permit the assessment of several aspects of intracranial dynamics (cerebral blood flow changes, vascular pulsatility, ICP changes, intracranial compliance, CPP, and autoregulation).

Arteries↗

PubMed1998

A simple mathematical model applied to selection of the sodium profile during profiled haemodialysis.

BACKGROUND: Among dialysis patients in the last 10 years the incidence of intradialytic dysequilibrium syndrome and symptomatic hypotension has increased significantly. Profiled haemodialysis (PHD), a new dialysis technique based on intradialytic modulation of the dialysate sodium concentration according to pre-elaborated individual profiles, has been set up to reduce intradialytic imbalances and the incidence of dysequilibrium syndrome and symptomatic hypotension. The present paper illustrates a new mathematical model for solute kinetics, single-compartment for sodium and two-compartment for urea, aimed at improving the use of PHD. The model allows the sodium profile to be elaborated a priori, before each dialysis session, according to the patient's clinical needs and respecting the individual sodium mass removal and weight gain. METHOD: The mathematical model was first derived and then applied to determining a rational dialysate sodium profile. A procedure which allows the method to be tuned to individual clinical needs on the basis of routine measurements performed before each session is also presented. The proposed method was validated in vivo during seven dialysis sessions, each performed on a different patient. RESULTS: The comparison between data predicted by the model and those obtained in vivo shows a good correspondence in particular concerning the time pattern of blood urea and sodium. The comparison between the model prediction and in vivo determined sodium and urea plasma curves showed standard deviations (2.25 mEq/l for sodium and 0.87 mmol/l for urea) only slightly higher than those attributable to laboratory measurement errors. Moreover, in vivo implementation of PHD by our model enables one to remove an amount of sodium mass comparable with the a priori quantity predicted by the model.

Aged↗

PubMed1998

Evidence of profiled hemodialysis efficacy in the treatment of intradialytic hypotension.

In the last 10 years the percentage of dialysis patients suffering from clinical intradialytic intolerance has greatly increased. Profiled hemodialysis (PHD) is a new technical approach, alternative to standard hemodialysis (SHD) for the treatment of intradialytic symptomatic hypotension. It is based on intradialytic modulation of the dialysate sodium concentration, using a dialysate sodium concentration profile elaborated by a new mathematical kinetic model. The aim of PHD is to reduce the intradialytic blood volume decrease, thanks to a dialysate sodium profile, which allows a reduction in the plasma osmolarity decrease, thereby boosting intravascular fluid refilling. This work aims at clinically validating the PHD technique, by testing its ability against SHD, to maintain a more stable intradialytic blood volume; this evaluation was supported by monitoring some hemodynamic parameters. Twelve dialysis patients on SHD treatment were selected because of their intradialytic symptomatic hypotension. Twelve SHD (one per patient) and 12 PHD sessions (one per patient) were performed to achieve the same sodium mass removal and body weight decrease on both PHD and SHD. During these sessions we monitored the blood volume variation % by the crit-line (a non invasive blood volume monitoring device), the mean blood pressure and heart rate directly and, finally, the stroke volume and cardiac output indirectly by bidimensional doppler-echocardiography. Comparison of the results obtained with the two techniques shows PHD to achieve a significantly more stable blood volume, blood pressure and cardiovascular function than SHD, in particular during the second and the third hour of the dialysis session.

Aged↗

PubMed1997

Modeling arterial hypotension during hemodialysis.

A mathematical model of the hemodynamic response to hemodialysis is presented. This model includes the dynamics of sodium, urea, and potassium in the intracellular and extracellular pools; fluid balance equations for the intracellular, interstitial, and plasma volumes; systemic and pulmonary hemodynamics; and the action of several short-term arterial pressure control mechanisms. The control mechanisms are triggered by information coming from both arterial and cardiopulmonary pressoreceptors, and they work on systemic arterial resistance, heart rate, and systemic venous unstressed volume. Moreover, the model hypothesizes that decreasing left atrial pressure below a given threshold causes a paradoxical withdrawal of the sympathetic drive and a consequent vasodepressor syncope. The model is used to simulate the pattern of the main hemodynamic quantities (systemic arterial pressure, heart rate, total systemic resistance, and cardiac output) during hemodialysis in several groups of patients (both hypotension resistant and hypotension prone) whose data were drawn from the clinical literature. The simulation results point out that the model is able to reproduce a variety of different conditions, including no hypotension, moderate hypotension, and severe hypotension with ultimate vasodepressor syncope, by adjusting a few parameters with clear physiological meanings. Hypotension is principally imputed to a loss of the sympathetic mechanisms working on systemic resistance and to an impairment of vascular refilling at the capillary wall. The results suggest that hypotension during hemodialysis is a complex phenomenon that depends on the superimposition of several concomitant factors working together that can lead to a variety of distinct individual patterns.

Baroreflex↗

PubMed1997

Mathematical investigation of some physiological factors involved in hemodialysis hypotension.

A previously developed mathematical model is used to investigate the role of some hemodynamic, regulatory, and osmotic factors in the development of symptomatic hypotension during hemodialysis. Sensitivity analysis of the model parameters suggests that a decrease in atrial pressure, with a consequent fall in cardiac output (Frank-Starling mechanism), is the primary hemodynamic perturbation induced by ultrafiltration. Also, during the first hours of a hemodialysis session, the sympathetic mechanism working on systemic resistance is the main factor responsible for arterial pressure maintenance, and the physiological response is probably characterized by a prevalence of the cardiopulmonary over the arterial baroreflex control. During this period, a decrease in plasma osmolarity, caused mainly by urea removal, may contribute to the reduction of vascular refilling. During the last hours of the session, the arterial pressure level is also significantly affected by other factors that influence vascular refilling and mean circulatory filling pressure (systemic compliance; action of feedback mechanisms working on venous unstressed volume; plasma oncotic pressure; and, especially, capillary wall permeability and interstitial space elastance). Simulation of hemodialysis with different modalities emphasizes the importance of avoiding high ultrafiltration rates and of maintaining the sodium concentration in the dialysate close to the sodium concentration of the extracellular fluid to limit the risk of symptomatic hypotension. Higher values of sodium in the dialysate are, however, associated with poor sodium removal from the extracellular pool with risks of interdialytic morbidity. In the future, the model may be used to optimize the ultrafiltration rate and sodium profile in the dialysate according to individual patient prescriptions.

Baroreflex↗

PubMed1997

A simple mathematical model of the interaction between intracranial pressure and cerebral hemodynamics.

A simple mathematical model of intracranial pressure (ICP) dynamics oriented to clinical practice is presented. It includes the hemodynamics of the arterial-arteriolar cerebrovascular bed, cerebrospinal fluid (CSF) production and reabsorption processes, the nonlinear pressure-volume relationship of the craniospinal compartment, and a Starling resistor mechanism for the cerebral veins. Moreover, arterioles are controlled by cerebral autoregulation mechanisms, which are simulated by means of a time constant and a sigmoidal static characteristic. The model is used to simulate interactions between ICP, cerebral blood volume, and autoregulation. Three different related phenomena are analyzed: the generation of plateau waves, the effect of acute arterial hypotension on ICP, and the role of cerebral hemodynamics during pressure-volume index (PVI) tests. Simulation results suggest the following: 1) ICP dynamics may become unstable in patients with elevated CSF outflow resistance and decreased intracranial compliance, provided cerebral autoregulation is efficient. Instability manifests itself with the occurrence of self-sustained plateau waves. 2) Moderate acute arterial hypotension may have completely different effects on ICP, depending on the value of model parameters. If physiological compensatory mechanisms (CSF circulation and intracranial storage capacity) are efficient, acute hypotension has only negligible effects on ICP and cerebral blood flow (CBF). If these compensatory mechanisms are poor, even modest hypotension may induce a large transient increase in ICP and a significant transient reduction in CBF, with risks of secondary brain damage. 3) The ICP response to a bolus injection (PVI test) is sharply affected, via cerebral blood volume changes, by cerebral hemodynamics and autoregulation. We suggest that PVI tests may be used to extract information not only on intracranial compliance and CSF circulation, but also on the status of mechanisms controlling CBF.

Biomechanical Phenomena↗