The influence of a nonlinear resistance element upon in vitro aortic pressure tracings and aortic valve motions

In vitro testing of biological heart valves requires pressure and flow waveforms closely simulating natural conditions, which are mainly influenced by the characteristics of the vascular system. Simulation of the arterial function in artificial circulations was mostly performed by the useful Windkessel model but sometimes failed by generating inadequate systolic pressures. The integration of a novel nonlinear resistance element may improve the Windkessel function. Native porcine aortic valves were studied in a mock circulation with a novel nonlinear resistance element combined with the Windkessel compared with an aperture plate resistance. Pressure and flow measurements were performed at varying heart rates and stroke volumes and analyzed in the time and frequency domain. Aortic valve motions were evaluated using high speed video recording. With the classical afterload configuration including an aperture plate resistance, the pressure tracings showed a nonphysiologic decrease of pressure during systole after early peak pressure. By integration of the novel nonlinear resistance, peak systolic pressure occured later, peak pressure was higher, and the pressure waveform was more physiologically shaped. Leaflet motions of the aortic valves were less oscillatory and compared well with in vivo characteristics. In conclusion, a novel nonlinear resistance element in a mock circulation has the potential to provide more physiologic aortic pressure waveforms as influencing aortic valve dynamics and thus may be a helpful tool for investigation of biological heart valves.     

Role of total arterial compliance and peripheral resistance in the determination of systolic and diastolic aortic pressure.

The goal of the study was to define the major arterial parameters that determine aortic systolic (Ps) and diastolic (Pd) pressure in the dog. Measured aortic flows were used as input to the two-element windkessel model of the arterial system, with peripheral resistance calculated as mean pressure over mean flow and total arterial compliance calculated from the decay time in diastole. The windkessel model yielded an aortic pressure wave from which we obtained the predicted systolic (Ps, wk) and diastolic (Pd, wk) pressure. These predicted pressures were compared with the measured systolic and diastolic pressures. The measurements and calculations were carried out in 7 dogs in control conditions, during aortic occlusion at four locations (the trifurcation, between trifurcation and diaphragm, the diaphragm and the proximal descending thoracic aorta) and during occlusion of both carotid arteries. Under all conditions studied the predicted systolic and diastolic pressure matched the experimental ones very well: Ps, wk = (1.000 +/- 0.0055) Ps with r = 0.958 and Pd, wk = (1.024 +/- 0.0035) Pd with r = 0.995. Linear regression for pulse pressure gave PPwk = (0.99 +/- 0.016) PP (r = 0.911). We found the accuracy of prediction equally good under control conditions and in presence of aortic or carotid artery occlusions. Multiple regression between pulse pressure and arterial resistance and total arterial compliance yielded a poor regression constant (r2 = 0.19) suggesting that the two arterial parameters alone cannot explain pulse pressure and that flow is an important determinant as well. We conclude that, for a given ejection pattern (aortic flow), two arterial parameters, total arterial resistance and total arterial compliance are sufficient to accurately describe systolic and diastolic aortic pressure.     

Arterial windkessel parameter estimation: A new time-domain method

We developed and validated a new, more accurate, and easily applied method for calculating the parameters of the three-element Windkessel to quantitate arterial properties and to investigate ventriculoarterial coupling. This method is based on integrating the governing differential equation of the three-element Windkessel and solving for arterial compliance. It accounts for the interaction between characteristic impedance and compliance, an important phenomenon that has been ignored by previously implemented methods. The new integral method was compared with four previously published methods as well as a new independent linear least-squares analysis, using ascending aortic micromanometric and volumetric flow measurements from eight dogs. The parameters calculated by the new integral method were found to be significantly different from those obtained by the previous methods but did not differ significantly from maximum likelihood estimators obtained by a linear leastsquares approach. To assess the accuracy of parameter estimation, pressure and flow waveforms were reconstructed in the time domain by numerically solving the governing differential equation of the three-element Windkessel model. Standard deviations of reconstructed waveforms from the experimental ensemble-averaged waveforms, which solely reflect the relative accuracy of the Windkessel parameters given by the various methods, were calculated. The new integral method invariably yielded the smallest error. These results demonstrate the improved accuracy of our new integral method in estimating arterial parameters of the three-element Windkessel.     

Simulation of systolic and diastolic left ventricular dysfunction in a mock circulation: the effect of arterial compliance

Arterial compliance (AC) is expected to play a major role on cardiac efficacy by acute or long-term mechanisms. The aim of this study was to investigate the purely mechanical effect of AC on left ventricular (LV) performance, for different conditions of LV dysfunction (systolic versus diastolic). A hydraulic, Windkessel model of systemic circulation was used. LV function and aortic flow were simulated using a left ventricular assist device (LVAD). Two cases of LV dysfunction were simulated: Case A, systolic and Case B, diastolic dysfunction. In Case A, AC increased from 1.14 to 2.85 ml mm Hg(-1) leading to an increase in LVAD stroke volume up to 6%, while no significant effect was observed in Case B. LVAD systolic work was decreased by 4% in systolic and by 11% in diastolic LVAD dysfunction. The purely mechanical effect of AC changes on LVAD function was different between systolic and diastolic dysfunction. It might be expected that even an acute reduction in arterial stiffness could enhance LV performance by different means in systolic compared to diastolic dysfunction.     

Simulation of systolic and diastolic left ventricular dysfunction in a mock circulation: the effect of arterial compliance

Arterial compliance (AC) is expected to play a major role on cardiac efficacy by acute or long-term mechanisms. The aim of this study was to investigate the purely mechanical effect of AC on left ventricular (LV) performance, for different conditions of LV dysfunction (systolic versus diastolic). A hydraulic, Windkessel model of systemic circulation was used. LV function and aortic flow were simulated using a left ventricular assist device (LVAD). Two cases of LV dysfunction were simulated: Case A, systolic and Case B, diastolic dysfunction. In Case A, AC increased from 1.14 to 2.85 ml mm Hg &#109 1 leading to an increase in LVAD stroke volume up to 6%, while no significant effect was observed in Case B. LVAD systolic work was decreased by 4% in systolic and by 11% in diastolic LVAD dysfunction. The purely mechanical effect of AC changes on LVAD function was different between systolic and diastolic dysfunction. It might be expected that even an acute reduction in arterial stiffness could enhance LV performance by different means in systolic compared to diastolic dysfunction.     

Quantification of aortic regurgitation by Doppler echocardiography: a new method evaluated in pigs

We have developed a method to quantify aortic regurgitant orifice and volume, based on measurements of the velocity of the regurgitant jet, aortic systolic flow, the systolic and diastolic arterial pressures, a Windkessel arterial model, and a parameter estimation technique. In six pigs we produced aortic regurgitant flows between 2·1 and 17·8 ml per beat, i.e. regurgitant fractions from 0·06 to 0·58. Pulmonary and aortic flows were measured with electromagnetic flow probes, aortic pressure was measured invasively, and the regurgitant jet velocity was obtained with continuous-wave Doppler. The parameter estimation procedure was based on the Kalman filter principle, resulting primarily in an estimate of the regurgitant orifice area. The area was multiplied by the velocity integral of the regurgitant jet to estimate regurgitant volume. A strong correlation was found between the regurgitant volumes obtained by parameter estimation and the electromagnetic flow measurement. These results from our study in pigs suggest that it may be possible to quantify regurgitant orifice and volume in patients completely noninvasively from Doppler and blood pressure measurements.     

Influence of central and peripheral changes on the hydraulic input impedance of the systemic arterial tree

The input impedance of the systemic arterial tree of the dog has been computed by Fourier analysis. It was shown that a distance between pressure and flow transducers of less than 2 cm results in appreciable errors which manifest themselves mainly in the phase of the input impedance. The input impedance for controls, occlusions at various locations in the aorta, and an increase and decrease of peripheral resistance were studied. For the same experiments, the total arterial compliance was calculated from the peripheral resistance of the diastolic aortic-pressure curve. The characterstic impedance of the ascending aorta was also estimated. The impedance in the control situation may be modelled by means of a 3-element Windkessel consisting of a peripheral resistance and (total) arterial compliance, together with a resistance equal to the characteristic impedance of the aorta. The occlusions of the aorta show that blockage at (and beyond) the trifurcation do not result in a detectable change in input impedance, except for a slight increase of the peripheral resistance. The more proximal an aortic occlusion, the more effect it has on the pattern of the input impedance. When the aorta is occluded at the diphragm, or higher, the single (uniform) tube appears to be a much better model than the Windkessel. Occlusion of one or both carotid arteries increases the mean pressure; consequently not only the peripheral resistance increases but also the total arterial compliance decreases. The Windkessel with increased peripheral resitance and decreased compliance is again a good model. After a sudden release of occlusion of the aorta, the arterial system has a low peripheral resistance and may also be modelled by the Windkessel.     

Precise quantification of pressure flow waveforms of a pulsatile ventricular assist device

Unreliable quantification of flow pulsatility has hampered many efforts to assess the importance of pulsatile perfusion. Generation of pulsatile flow depends upon an energy gradient. It is necessary to quantify pressure flow waveforms in terms of hemodynamic energy levels to make a valid comparison between perfusion modes during chronic support. The objective of this study was to quantify pressure flow waveforms in terms of energy equivalent pressure (EEP) and surplus hemodynamic energy (SHE) levels in an adult mock loop using a pulsatile ventricle assist system (VAD). A 70 cc Pierce-Donachy pneumatic pulsatile VAD was used with a Penn State adult mock loop. The pump flow rate was kept constant at 5 L/min with pump rates of 70 and 80 bpm and mean aortic pressures (MAP) of 80, 90, and 100 mm Hg, respectively. Pump flows were adjusted by varying the systolic pressure, systolic duration, and the diastolic vacuum of the pneumatic drive unit. The aortic pressure was adjusted by varying the systemic resistance of the mock loop EEP (mm Hg) = (integral of fpdf)/(integral of fdt) SHE (ergs/cm3) = 1,332 [((integral of fpdt)/(integral of fdt))--MAP] were calculated at each experimental stage. The difference between the EEP and the MAP is the extra energy generated by this device. This difference is approximately 10% in a normal human heart. The EEP levels were 88.3 +/- 0.9 mm Hg, 98.1 +/- 1.3 mm Hg, and 107.4 +/- 1.0 mm Hg with a pump rate of 70 bpm and an aortic pressure of 80 mm Hg, 90 mm Hg, and 100 mm Hg, respectively. Surplus hemodynamic energy in terms of ergs/cm3 was 11,039 +/- 1,236 ergs/cm3, 10,839 +/- 1,659 ergs/cm3, and 9,857 +/- 1,289 ergs/cm3, respectively. The percentage change from the mean aortic pressure to EEP was 10.4 +/- 1.2%, 9.0 +/- 1.4%, and 7.4 +/- 1.0% at the same experimental stages. Similar results were obtained when the pump rate was changed from 70 bpm to 80 bpm. The EEP and SHE formulas are adequate to quantify different levels of pulsatility for direct and meaningful comparisons. This particular pulsatile VAD system produces near physiologic hemodynamic energy levels at each experimental stage.     

The arterial Windkessel

Frank’s Windkessel model described the hemodynamics of the arterial system in terms of resistance and compliance. It explained aortic pressure decay in diastole, but fell short in systole. Therefore characteristic impedance was introduced as a third element of the Windkessel model. Characteristic impedance links the lumped Windkessel to transmission phenomena (e.g., wave travel). Windkessels are used as hydraulic load for isolated hearts and in studies of the entire circulation. Furthermore, they are used to estimate total arterial compliance from pressure and flow; several of these methods are reviewed. Windkessels describe the general features of the input impedance, with physiologically interpretable parameters. Since it is a lumped model it is not suitable for the assessment of spatially distributed phenomena and aspects of wave travel, but it is a simple and fairly accurate approximation of ventricular afterload. J.-W. Lankhaar is supported by a grant from the Netherlands Heart Foundation, the Hague, the Netherlands (NHS2003B274).     

Use of a model for simulating individual aortic dynamics in man

A simulation model is suggested for the analysis of aortic dynamics in man. The aortic model consists of six segments and is part of a larger model of the closed-loop human circulation. The model is simulated on a special-purpose analogue computer. Three parameters are employed to characterise the arterial system; peripheral resistance, aortic compliance and peripheral damping. Using a method for adapting the model to the individual patient, measurements of aortic pressure, cardiac output and pulse transmission time from 29 patients were used to test the validity of this approach. The model is able to simulate the pressure course along the aorta satisfactorily. The compliance calculated from the transmission properties of the aorta was compared with the complicance calculated from the stroke volume and pressure pulse. An adequate correlation (r=0.98) was found between these two independent methods. The mean compliance of the total aorta was 0.6 ml/mm Hg at a mean pressure of 104 mm Hg. The compliance showed large individual variations and decreasing values with increasing age of the patient. It is concluded that the model enables simulation of the individual aorta.     

硝普钠对动物血管力学参数的影响

有研究表明硝普钠具有增加动脉顺应性的趋势和降低外周阻力的作用,但是硝普钠对血管中血流惯性的影响却不统一。本文以Coldwyn等建立的动脉系改良风箱力学模型为主要研究方法对动物动脉血管顺应性(包括中央和外周顺应性),血流惯性和外周阻力等进行了研究,并建立了动脉系总阻抗的公式。然后评价硝普钠对总阻抗的影响以及总阻抗做为一种血管力学参数的灵敏性。实验结果表明:硝普钠具有统计学意义地增加外周血管的顺应性(P<0.05);有增加中央动脉顺应性和血流惯性的趋性;并能降低外周阻力和动脉系总阻抗(P<0.05)。结果还表明动脉系总阻抗是一种灵敏度高的血管力学参数。因此,硝普钠能影响血管参数,对外周血管顺应性和血管总阻抗的作用尤其明显。     

Elevated arterial blood pressure in cardiac tamponade.

BACKGROUND. In cardiac tamponade cardiac output falls, but peripheral vascular resistance increases, so that systemic blood pressure may be maintained at normal or near-normal levels. We recently observed a patient with cardiac tamponade whose blood pressure was markedly elevated. METHODS. To determine the frequency of elevated blood pressure in patients with cardiac tamponade and their hemodynamic characteristics, we studied 18 consecutive patients with cardiac tamponade from a variety of causes using right heart catheterization. RESULTS. Six of the 18 patients had systolic arterial blood pressures ranging from 150 to 210 mm Hg (mean [+/- SD], 176 +/- 26) and diastolic pressures ranging from 100 to 130 mm Hg (mean, 113 +/- 14). All six had previously been hypertensive. After pericardiocentesis there was a significant decrease in blood pressure (to 139 +/- 13 mm Hg systolic, P less than 0.05; and 83 +/- 6 mm Hg diastolic, P less than 0.01) and peripheral vascular resistance (from 2150 +/- 588 to 1207 +/- 345 dyn.sec.cm-5, P less than 0.01). Cardiac output increased in all six. The other 12 patients, 3 of whom had a history of hypertension, had significant increases in cardiac output and systolic blood pressure (from 119 +/- 13 to 127 +/- 7 mm Hg, P less than 0.05) after pericardiocentesis, whereas peripheral vascular resistance decreased. Both groups had similar degrees of cardiac tamponade, as indicated by measurements of cardiac output and intrapericardial, right atrial, and pulmonary-artery wedge pressures. CONCLUSIONS. Elevated blood pressure may occur in some patients with cardiac tamponade who have preexisting hypertension. Moreover, blood pressure may fall after pericardiocentesis in patients who have elevated blood pressure associated with tamponade.     

Implication of the systolic hump in systemic arterial pressure waves

The systolic hump in the aortic blood pressure wave is defined as the aorticresistance component proportional to the aortic blood flow superimposed on the windkessel component. An electrical analogue comprising a series resistance (aortic resistance) plus a resistance (peripheral resistance) and capacitance (aortic compliance) in parallel (i.e. windkessel component) is used for analysis. Curve fitting using the leastsquares method is performed on calculated and measured blood pressure waves from dogs under haemodynamical conditions induced by infusion of three drugs (noradrenaline, isoproterenol and acetylcholine). The curve fitting RMS (root mean square) errors are <3% for blood pressure waves and <30% for blood flow waves, with good agreement between measured and calculated blood flow waveforms. Infusion of noradrenaline and acetylcholine is found to induce a significant decrease and increase in the aortic resistance, respectively. Although only a small fraction of the blood pressure wave, the systolic hump has a marked effect on the systolic pressure waveform.     

Experimental analysis of the hemodynamics in punctured vascular access grafts

The hemodynamics in the vascular access graft are influenced by the flow aspirated and injected through the two needles during hemodialysis. For the first time, the impact of needle flow on vascular access performance, measured in an in vitro set up, is reported. A vascular access model, consisting of a loop polytetrafluoroethylene graft sewn to a compliant artery and vein, simulated the patient. The extracorporeal circuit was connected to the model. Three mean access flow rates (QG; 500, 1,000, and 1,500 ml/min) and five roller pump flow rates (Q(R); 0, 200, 300, 400, and 500 ml/min) were studied. Mean, systolic, and diastolic pressure and according pressure drops were derived at 14 loci. Systolic, diastolic, and mean pressures drop along the graft decreased with increasing Q(R) and decreasing Q(G). At Q(R) = 500 ml/min and Q(G) = 500 ml/min, the mean pressure drop over the graft was negative (-10 mm Hg), indicating a reversed pressure profile, originating at the puncture site of the venous needle. Mean pressure in the venous outlet segment was about 100 mm Hg compared with only 75 mm Hg without needle flow. The combination of a low Q(G) (500 ml/min) and high Q(R) (> 300 ml/min) must be avoided because venous pressures can rise to 100 mm Hg and load the venous system. The results of this in vitro setup indicate that high Q(R) (> 400 ml/min) should be avoided at Q(G) up to 1,000 ml/min; however, in vivo tests have to be performed to prove this thesis. This study demonstrates the need for a well-functioning vascular access (Q(G) > 600 ml/ min) to perform adequate dialysis and to avoid venous system loading.     

Interference resistance in automated oscillometric sphygmomanometers

Conclusions 1. Parameters of valid signal in oscillometric methods of measurement of arterial blood pressure depend on values of diastolic and pulse arterial blood pressure, heart rate, type of elasticity and collapse of the humeral artery, volume of the artery, volume of the blood pressure cuff, and the ratio of the duration of arterial pressure oscillations to valid signal period. The peak amplitude of the valid signal varies over a range from 0.31 to 7.34 mm Hg, and heart rate varies from 0.66 to 3.33 Hz. The characteristic point for determining systolic arterial blood pressure is the maximum of the envelope of the “negative” part of oscillometric signals, and for diastolic arterial blood pressure is the maximum rate of the decrease of the envelope of the “positive” part of oscillometric signals. The correlation coefficient between experimental signal and theoretical calculations was found to be 0.84. 2. Two types of interferences, related to breathing and movement of patient, have the largest affect on the results of arterial blood pressure measurements by the oscillometric method. 3. An interference-rejecting algorithm was developed for measuring systolic and diastolic arterial blood pressure. The algorithm was implemented in prototype models of the SA-02 and SA-03 automated sphygmomanometers. Clinical trial of the SA-02 automated sphygmomanometer revealed overall error in determination of systolic and diastolic arterial blood pressure in a sample of 144 patients to beS=6.6 mm Hg for systolic arterial blood pressure andS=6.4 mm Hg for diastolic arterial blood pressure. The results of the trial meet the requirements of the United States standard. Scientific Research Institute for Medical Instrument Engineering, Moscow. Translated from Meditsinskaya Tekhnika, No. 3, pp. 19–28, May–June, 1993.     

Observations on coronary collateral communications and the control of flow in the coronary circulation of the dog

1. Pressure was measured in the small arterial anastomosing branches of the coronary vascular network. The mean value was 30 mm Hg not significantly different from the mean value of 33 mm Hg for peripheral coronary pressure measured distal to a ligature on the anterior descending branch of the left coronary artery. Evidence was adduced to show that either the anterior descending or the circumflex artery had the capacity to maintain network pressure at levels adequate for tissue perfusion.2. The network has both capacity and compliance. Filling of the network compliance during systole probably accounts for the systolic phase of coronary flow. Flow through the microcirculation is probably entirely diastolic, the combined compliance of the aorta and large vessels together with the network provides the necessary reservoir, the potential energy indicated by diastolic pressure provides the perfusion pressure head.3. Resistance of vessels between the aorta and network cannula (pre-net) was approximately double that of the microcirculation (post-net). The smaller pre-network vessels are of the order 70 mum in diameter. Both pre- and post-network vessels are vaso-active and respond similarly to adrenaline and haemorrhage.     

Role of vascular bed compliance in vasomotor control in human skeletal muscle

The current view of neurogenic vasomotor control in skeletal muscle is based largely on changes in vascular bed resistance. The purpose of this study was to determine to what extent vascular bed compliance may also play a role in this regulation. For this purpose, pressure waveforms (Millar and Finometer) and flow waveforms (Doppler ultrasound) were measured simultaneously in the brachial artery of seven healthy individuals during physiological manoeuvres which were expected to produce non-neurogenic changes in resistance (wrist-cuff occlusion; n = 5) or compliance (arm elevation; n = 6) of the forearm vascular bed. Vascular resistance (R) was calculated from the average flow and pressure values. A lumped Windkessel model was used to obtain vascular bed compliance (C) from these concurrently measured waveforms. Compared with baseline (3.81 +/- 1.59 ml min(-1) mmHg(-1)), wrist occlusion increased R (65 +/- 75%; P < 0.05) with minimal change in C (-15 +/- 16%; n.s.). Compared with the arm in neutral position (0.0075 +/- 0.003 ml mmHg(-1)), elevation of the arm above heart level produced a 86 +/- 41% increase in C (P < 0.05) with little change in R (-5 +/- 11%). In addition, neurogenic changes were assessed during lower body negative pressure (LBNP) and a cold pressor test (CPT; n = 7). Lower body negative pressure induced a 29 +/- 24% increase in R and a 26 +/- 12% decrease in C (both P < 0.05). The CPT induced no consistent change in R but a 22 +/- 7% reduction in C (P < 0.05). It was concluded that vascular bed compliance is an independent variable which should be considered along with vascular bed resistance in the mechanics of vasomotor regulation in skeletal muscle.     

Systolic Hypertension Mechanisms: Effect of Global and Local Proximal Aorta Stiffening on Pulse Pressure

Decrease in arterial compliance leads to an increased pulse pressure, as explained by the Windkessel effect. Pressure waveform is the sum of a forward running and a backward running or reflected pressure wave. When the arterial system stiffens, as a result of aging or disease, both the forward and reflected waves are altered and contribute to a greater or lesser degree to the increase in aortic pulse pressure. Two mechanisms have been proposed in the literature to explain systolic hypertension upon arterial stiffening. The most popular one is based on the augmentation and earlier arrival of reflected waves. The second mechanism is based on the augmentation of the forward wave, as a result of an increase of the characteristic impedance of the proximal aorta. The aim of this study is to analyze the two aforementioned mechanisms using a 1-D model of the entire systemic arterial tree. A validated 1-D model of the systemic circulation, representative of a young healthy adult was used to simulate arterial pressure and flow under control conditions and in presence of arterial stiffening. To help elucidate the differences in the two mechanisms contributing to systolic hypertension, the arterial tree was stiffened either locally with compliance being reduced only in the region of the aortic arch, or globally, with a uniform decrease in compliance in all arterial segments. The pulse pressure increased by 58% when proximal aorta was stiffened and the compliance decreased by 43%. Same pulse pressure increase was achieved when compliance of the globally stiffened arterial tree decreased by 47%. In presence of local stiffening in the aortic arch, characteristic impedance increased to 0.10 mmHg s/mL vs. 0.034 mmHg s/mL in control and this led to a substantial increase (91%) in the amplitude of the forward wave, which attained 42 mmHg vs. 22 mmHg in control. Under global stiffening, the pulse pressure of the forward wave increased by 41% and the amplitude of the reflected wave by 83%. Reflected waves arrived earlier in systole, enhancing their contribution to systolic pressure. The effects of local vs. global loss of compliance of the arterial tree have been studied with the use of a 1-D model. Local stiffening in the proximal aorta increases systolic pressure mainly through the augmentation of the forward pressure wave, whereas global stiffening augments systolic pressure principally though the increase in wave reflections. The relative contribution of the two mechanisms depends on the topology of arterial stiffening and geometrical alterations taking place in aging or in disease.     

A physical model of the human systemic arterial tree

A physical model of the human arterial tree has been developed to be used in a computer controlled mock circulatory system (MCS). Its aim is to represent systemic arterial tree properties and extend the capacity of the MCS to intraortic balloon pump (IABP) testing. The main problem was to model the aorta simply and to accurately reproduce aortic impedance and related flow and pressure waveforms at different sections. The model is composed of eight segments; lumped parameter models are used for its peripheral loads. After the numerical simulation, the physical model was reproduced as a silicon rubber tapered tube. This rubber was chosen for its stability over time and the acceptable behaviour of its Young's modulus (Ey = 22.23 gf x mm(-2)) with different loads and in comparison with data from the literature (Ey approximately 20.4 gf x mm(-2)). The properties of each segment of the aorta were defined in terms of compliance, resistance and inertance as a function of length, radius and thickness. The variable thickness was obtained using positive and negative molds. Total static compliance of the aorta model is about 1.125 x 10(-3) g(-1) x cm4 x sec2 (1.5 cm3 x mmHg(-1)). Measurements were performed both on numerical and physical models (in open and closed loop configuration). Data reported show pressure and flow waveforms along with input impedance modulus and phase. The results are in good agreement with data from the literature.     

Relationships between short-term blood-pressure fluctuations and heart-rate variability in resting subjects II: a simple model

A simple model of the beat-to-beat properties of the cardiovascular system is used to interpret the results of spectral analysis of blood-pressure and interval data. The model consists of two equations, one representing the fast regulation of interval by the systolic pressure (baroreflex), the other one representing a Windkessel approximation of the systemic arterial system. The model, when applied to interval and blood-pressure data from resting subjects, explains the lack of respiratory variability in the diastolic pressure values. The baroreflex equation seems to describe the data only in the region of respiratory frequencies. The shape of the phase spectrum of systolic pressures against intervals is modelled by difference equations, but no physiological interpretation of these equations is given.