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.     

基于桡动脉脉搏波血流动力学检测的心输出量计算修正

目的心输出量是评估心血管功能的重要参数.长期以来,心输出量作为常规的心血管血流参数已被临床医生、药剂师和生理学家所接受.北京工业大学罗志昌等人通过多年研究,获得了心输出量的临床实用公式,但此公式中的一些近似是以正常健康人的生理条件为基准,在长期的实验中,发现由此得出的心输出量在一些情况下失真,因此有必要对这种失真进行修正.方法通过大量临床实验,用线性回归的方法,通过修正系数,对心输出量计算公式进行修正.结果修正系数与脉搏波特征参数K、年龄、血压和心率有关,修正后的公式计算的心输出量较为接近实际值.结论在没有经过心外科手术的无心瓣膜缺损、主动脉瘤、心衰、心率不齐等疾病的患者,以及健康的孕妇、运动员和普通的健康人中,通过脉搏波特征参数K、年龄、血压和心率计算心输出量是比较可靠的.     

Arterial haemodynamics on ventricular hypertrophy in rats with simulated aortic stiffness

Aortic stiffness (AS) exerts significant impact on the cardiovascular risks. We developed a new model to produce AS. The purposes were to evaluate the haemodynamic consequence and to correlate the haemodynamic parameters with the extent of ventricular hypertrophy (VH). We applied silicon gel for embedding of the abdominal and/or thoracic aorta. After 1–4 weeks of AS, the left ventricular weight (LVW), LVW to body weight (BW) ratio (LVW/BW), and the morphological changes in cardiomyotes were quantified for VH. We determined the aortic pressure (AP), stroke volume, cardiac output, total peripheral resistance (TPR), characteristic impedance (Zc), pulse wave reflection (P_b) and pulse wave velocity (PWV). Aortic embedding (AE) increased LVW, LVW/BW, systolic and pulse pressure (PP), Zc, P_b and PWV accompanied by decreases in diastolic pressure and arterial compliance. The magnitude of these haemodynamic and cardiac changes were in an order of combined, thoracic and abdominal AE. Correlation analysis revealed that the VH was well correlated with pulsatile haemodynamics such as Zc, PP, P_b and PWV, while less with steady components (Mean AP and TPR). Our results indicate that pulsatile haemodynamic parameters are significantly elevated after AS. The alterations in pulsatile haemodynamics are the major causes leading to VH.     

Non-invasive assessment of cardiac output during exercise in healthy young humans: comparison between Modelflow method and Doppler echocardiography method

AIMS: The Modelflow method can estimate cardiac output from arterial blood pressure waveforms using a three-element model of aortic input impedance (aortic characteristic impedance, arterial compliance, and systemic vascular resistance). We tested the reliability of a non-invasive cardiac output estimation during submaximal exercise using the Modelflow method from finger arterial pressure waveforms collected by Portapres in healthy young humans. METHODS: The Doppler echocardiography method was used as a reference method. Sixteen healthy young subjects (nine males and seven females) performed a multi-stage cycle ergometer exercise at an intensity corresponding to 70, 90, 110 and 130% of their individual ventilatory threshold for 2 min each. The simultaneous estimation of cardiac output (15 s averaged data) using the Modelflow and Doppler echocardiography methods was performed at rest and during exercise. RESULTS AND CONCLUSION: The Modelflow-estimated cardiac output correlated significantly with the simultaneous estimates by the Doppler method in all subjects (r = 0.87, P < 0.0001) and the SE of estimation was 1.93 L min-1. Correlation coefficients in each subject ranged from 0.91 to 0.98. Although the Modelflow method overestimated cardiac output, the errors between two estimates were not significantly different among the exercise levels. These results suggest that the Modelflow method using Portapres could provide a reliable estimation of the relative change in cardiac output non-invasively and continuously during submaximal exercise in healthy young humans, at least in terms of the relative changes in cardiac output.     

Non‐invasive assessment of cardiac output during exercise in healthy young humans: comparison between Modelflow method and Doppler echocardiography method

Aims: The Modelflow method can estimate cardiac output from arterial blood pressure waveforms using a three‐element model of aortic input impedance (aortic characteristic impedance, arterial compliance, and systemic vascular resistance). We tested the reliability of a non‐invasive cardiac output estimation during submaximal exercise using the Modelflow method from finger arterial pressure waveforms collected by Portapres in healthy young humans. Methods: The Doppler echocardiography method was used as a reference method. Sixteen healthy young subjects (nine males and seven females) performed a multi‐stage cycle ergometer exercise at an intensity corresponding to 70, 90, 110 and 130% of their individual ventilatory threshold for 2 min each. The simultaneous estimation of cardiac output (15 s averaged data) using the Modelflow and Doppler echocardiography methods was performed at rest and during exercise. Results and Conclusion: The Modelflow‐estimated cardiac output correlated significantly with the simultaneous estimates by the Doppler method in all subjects (r = 0.87, P < 0.0001) and the SE of estimation was 1.93 L min^?1. Correlation coefficients in each subject ranged from 0.91 to 0.98. Although the Modelflow method overestimated cardiac output, the errors between two estimates were not significantly different among the exercise levels. These results suggest that the Modelflow method using Portapres could provide a reliable estimation of the relative change in cardiac output non‐invasively and continuously during submaximal exercise in healthy young humans, at least in terms of the relative changes in cardiac output.     

Simple and accurate way for estimating total and segmental arterial compliance: The pulse pressure method

We derived and tested a new, simple, and accurate method to estimate the compliance of the entire arterial tree and parts thereof. The method requires the measurements of pressure and flow and is based on fitting the pulse pressure (systolic minus diastolic pressure) predicted by the two-element windkessel model to the measured pulse pressure. We show that the two-element windkessel model accurately describes the modulus of the input impedance at low harmonics (0–4th) of the heart rate so that the gross features of the arterial pressure wave, including pulse pressure, are accounted for. The method was tested using a distributed nonlinear model of the human systemic arterial tree. Pressure and flow were calculated in the ascending aorta, thoracic aorta, common carotid, and iliac artery. In a linear version of the systemic model the estimated compliance was within 1% of the compliance at the first three locations. In the iliac artery an error of 7% was found. In a nonlinear version, we compared the estimates of compliance with the average compliance over the cardiac cycle and the compliance at the mean working pressure. At the first three locations we found the estimated and “actual” compliance to be within 12% of each other. In the iliac artery the error was larger. We also investigated an increase and decrease in heart rate, a decrease in wall elasticity and exercise conditions. In all cases the estimated total arterial compliance was within 10% of mean compliance. Thus, the errors result mainly from the nonlinearity of the arterial system. Segmental compliance can be obtained by subtraction of compliance determined at two locations.     

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。     

Effects of carotid hypotension on aortic hemodynamics in the unanesthetized dog.

The effects of occlusion of the brachiocephalic artery on aortic hemodynamics were assessed in 12 chronically instrumented dogs in the unanesthetized state. Continuous measurements of ascending aorta pressure and flow were made. In the steady state following occlusion, heart rate increased by 36% and mean arterial pressure by 45%, while cardiac output was unchanged from preocclusion levels. Hydraulic power delivery to the systemic circulation by the left ventricle was increased during occlusion, while the fraction of total power associated with pulsations decreased. Values of peripheral resistance and ascending aorta input impedance were both increased during occlusion. Graded occlusions of the brachiocephalic artery produced graded, monotonic increases in the entire aortic impedance spectrum between 2 and 20 Hz with more sensitive responses occurring with the smaller, submaximal responses. Considered with results of previous studies, these results suggest that activation of smooth muscle in large conduit arteries is also associated with the pressor response which accompanies carotid hypotension and that such activation has a hemodynamically significant effect.     

Improved method for cardiac output determination in man using ultrasound Doppler technique

An existing ultrasound Doppler method for measuring cardiac output has been improved and refined, partly by locating the sampling volume higher up in the aorta while still using the aortic ring size as the effective transverse flow area. The basis for using this technique is the approximately rectangular systolic velocity profile in the aortic orifice in physiologically and anatomically normal subjects, and the fact that this profile velocity is conserved as the maximum velocity in the ascending aorta for some 3 to 4 cm above the valves. This higher location of the sampling volume improves Doppler signal quality, and does not reduce the accuracy of the method, as can be confirmed in each experimental subject. Together with automatic computer-based online signal analysis, the technique employed enables us to make continuous long-term beat-to-beat measurements of cardiac output in subjects without aortic valve disease or grossly deforming disease of the aortic root.     

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.     

A system for providing an on-line analogue display of beat-by-beat cardiac output

A system for an on-line analogue display of beat-by-beat cardiac output and other cardiovascular functions is described. The phasic aortic blood flow signal, derived from an electromagnetic flowmeter with the flow probe implanted around the ascending aorta, drives a multi-channel recorder with a combination of associated signal conditioning input couplers and peripheral electronic circuitry, to provide a continuous analogue display of beat-by-beat phasic stroke volume, integrated stroke volume, heart rate, and cardiac output. These cardiovascular functions, which permit instantaneous on-line feedback of these parameters, were all derived from the single aortic flow measurement.     

Estimation of aortic compliance using magnetic resonance pulse wave velocity measurement

A method for compliance estimation employing magnetic resonance pulse wave velocity measurement is presented. Time-resolved flow waves are recorded at several positions along the vessel using a phase contrast sequence, and pulse wave velocity is calculated from the delay of the wave onsets. Using retrospective cardiac gating in combination with an optically decoupled electrocardiogram acquisition, a high temporal resolution of 3 ms can be achieved. A phantom set-up for the simulation of pulsatile flow in a compliant vessel is described. In the phantom, relative errors of pulse wave velocity estimation were found to be about 15%, whereas in a volunteer, larger errors were found that might be caused by vessel branches. Results of pulse wave velocity estimation agree with direct aortic distension measurements which rely on a peripheral estimate of aortic pressure and are therefore less accurate. Studies in 12 volunteers show values of pulse wave velocity consistent with the literature; in particular the well-known increase in pulse wave velocity with age was observed. Preliminary results show that the method can be applied to aortic aneurysms.     

Afferent aortic nerve fibers with their pathways in cardiac sympathetic nerves.

The effect of mechanical and chemical stimulation on activity of afferent aortic nerve fibers with pathways in the cardiac sympathetic nerves has been examined. Action potentials were derived from the second or third thoracic communicating ramus of the left side of anesthetized dogs. Thirty myelinated and 19 unmyelinated fibers responded to tapping the ascending aorta, aortic arch, and descending aorta. Both groups of fibers also responded to a rise as well as to a fall in aortic pressure. Spontaneous discharge of myelinated fibers was related to aortic pressure pulse whereas that of unmyelinated fibers was related to respiration. Asphyxia caused excitation of unmyelinated fibers but not of myelinated fibers. Both groups of fibers responded to topical application of lactic acid. Mechanical and chemical stimulation of the aorta after vagotomy caused a rise in systemic blood pressure and extension of the limbs. The results indicate the existence of afferent aortic fibers in the cardiac sympathetic nerves that cause circulatory and somatic responses.     

Sensitivity and afterload independence of zero-load aortic flow

The computed zero-load flow is the expected aortic flow when the aortic pressure is zero, thus eliminating the effect of afterload on ventricular ejection. Zero-load flow was computed in 15 anesthetized dogs (sodium pentobarbital 25 mg/kg, iv) by studying the response of left-ventricular pressure or aortic pressure, and aortic flow to the change in aortic input impedance induced by partial snare occlusion of the aorta. The waveform and peak value of zero-load flow were computed from a theoretical model of the left ventricle and verified by measurements of aortic flow in the first beat after transection of the aorta. To study the sensitivity, changes of zero-load flow were computed under the enhanced inotropic state produced by isoproterenol (0.1 μg/kg/min), and under the depressed contractile state induced by propranolol (0.15 mg/kg). Administration of isoproterenol resulted in an increase in the peak zero-load flow by 143.9% (p<0.001), compared with a 50.6% increase (p<0.05) in peakdp/dt. The difference of the variations was statistically significant in a pairedt test. After injection of propranolol, peak zero-load flow decreased by 32.0% (p<0.005). Afterload independence of zero-load flow was studied by computing zero-load flow before and after increasing arterial pressure by partial aortic occlusion or injection of 5 mg methoxamine. After injection of methoxamine in denervated dogs, the peak zero-load flow increased by 11.2% (N.S.), while input resistance increased by 153% (p<0.025). The peak zero-load flow decreased by 8% (N.S.) after partial aortic occlusion, while cardiac output decreased by 26.7% (p<0.001). These results may suggest that the computed peak zero-load flow is an afterload independent index of the pumping capability of the left ventricle in the intact heart.     

Pulse pressure waveform estimation using distension profiling with contactless optical probe

The pulse pressure waveform has, for long, been known as a fundamental biomedical signal and its analysis is recognized as a non-invasive, simple, and resourceful technique for the assessment of arterial vessels condition observed in several diseases. In the current paper, waveforms from non-invasive optical probe that measures carotid artery distension profiles are compared with the waveforms of the pulse pressure acquired by intra-arterial catheter invasive measurement in the ascending aorta. Measurements were performed in a study population of 16 patients who had undergone cardiac catheterization. The hemodynamic parameters: area under the curve (AUC), the area during systole (AS) and the area during diastole (AD), their ratio (AD/AS) and the ejection time index (ETI), from invasive and non-invasive measurements were compared. The results show that the pressure waveforms obtained by the two methods are similar, with 13% of mean value of the root mean square error (RMSE). Moreover, the correlation coefficient demonstrates the strong correlation. The comparison between the AUCs allows the assessment of the differences between the phases of the cardiac cycle. In the systolic period the waveforms are almost equal, evidencing greatest clinical relevance during this period. Slight differences are found in diastole, probably due to the structural arterial differences. The optical probe has lower variability than the invasive system (13% vs 16%). This study validates the capability of acquiring the arterial pulse waveform with a non-invasive method, using a non-contact optical probe at the carotid site with residual differences from the aortic invasive measurements.     

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.     

Control of blood pressure during sleep in lambs

We investigated the effect of sleep on blood pressure control in seven lambs aged 10-14 days. Each lamb had previously been anesthetized and instrumented for measurements of electrocorticogram, electron-oculogram, nuchal and diaphragm electromyograms, pulmonary blood flow (electromagnetic flow transducer), and aortic and pulmonic blood pressure. The lambs were allowed to recover from surgery at least 3 days before they were studied. Measurements were made at the highest and lowest mean aortic pressure during quiet wakefulness, quiet sleep, and active sleep. The lowest values of mean aortic pressure progressively decreased as the animals went from quiet wakefulness to quiet sleep to active sleep. Mean aortic pressure was most variable during active sleep. During active sleep, transient hypertensive episodes were superimposed upon a tonic hypotensive phase. During the transient hypertensive episodes in active sleep, changes in mean aortic pressure were primarily caused by an increase in systemic vascular resistance rather than by changes in cardiac output. Heart rate was always lower during active sleep than during quiet wakefulness or quiet sleep. These results provide evidence that sleep state has a marked influence on blood pressure control in lambs.     

Continuous Left Ventricular Ejection Fraction Monitoring by Aortic Pressure Waveform Analysis

We developed a technique to monitor left ventricular ejection fraction (EF) by model-based analysis of the aortic pressure waveform. First, the aortic pressure waveform is represented with a lumped parameter circulatory model. Then, the model is fitted to each beat of the waveform to estimate its lumped parameters to within a constant scale factor equal to the arterial compliance (C _a). Finally, the proportional parameter estimates are utilized to compute beat-to-beat absolute EF by cancelation of the C _a scale factor. In this way, in contrast to conventional imaging, EF may be continuously monitored without any ventricular geometry assumptions. Moreover, with the proportional parameter estimates, relative changes in beat-to-beat left ventricular end-diastolic volume (EDV), cardiac output (CO), and maximum left ventricular elastance (E _max) may also be monitored. To evaluate the technique, we measured aortic pressure waveforms, reference EF and EDV via standard echocardiography, and other cardiovascular variables from six dogs during various pharmacological influences and total intravascular volume changes. Our results showed overall EF and calibrated EDV root-mean-squared-errors of 5.6% and 4.1 mL, and reliable estimation of relative E _max and beat-to-beat CO changes. These results demonstrate, perhaps for the first time, the feasibility of estimating EF from only a blood pressure waveform.     

Comparison of electrical field plethysmography with electrical impedance plethysmography

As a means for assessing cardiac function, electrical field plethysmography (EFP) has been shown to have some features quite different from electrical impedance plethysmography (EIP). Here the two techniques are compared by using the two systems simultaneously on a subject and also with independent use in different electrode configurations. The results conform with the view that EIP is related primarily to volumetric changes of the aorta, whereas EFP is affected predominantly by changes in cardiac dimensions and orientation. Because of this difference, the standard time differential formula used for EIP is not applicable for the computation of cardiac output from the EFP waveforms. An alternative method of computation based on the amplitude of the EFP waveform is suggested.     

The effect of an increase in aortic pressure upon the inotropic state of eat and dog left ventricles

1. The effect of increased aortic pressure on the inotropic state of the left ventricle was studied in isolated cat hearts, perfused with bovine red cells in Tyrode solution, ejecting into a hydraulic model with the same input impedance as that of the cat aorta.2. Inotropic state was assessed at a controlled left ventricular end-diastolic pressure by interpolating single isovolumic beats by means of an occluder in the aortic cannula.3. When such isovolumic beats during periods of raised aortic pressure were compared with those during control periods, the difference in peak isovolumic pressure ranged from -0.3 to +0.5 kPa indicating differences in inotropic state which were small and inconsistent in direction.4. The maximum rate of rise of left ventricular pressure (dP/dt(max).) of ejecting beats was little affected by a rise of aortic pressure and the direction of changes was inconsistent.5. The effect of increased aortic pressure was studied in intact dogs after cardiac denervation; left ventricular end-diastolic pressure was uncontrolled and therefore rose to a higher steady level.6. No consistent change of dP/dt(max). was found during the period of increased aortic pressure.7. All flow and pressure variables remained steady during the period of increased aortic pressure after the higher level of left ventricular end-diastolic pressure had been established.8. These results demonstrate that neither the positive inotropic effect nor the negative inotropic effect of increased load dominates in these preparations. This may be the result of a balance between the two effects, or they may be of unimportant magnitude under physiological conditions.