动脉压力波形分析在麻醉诱导期的应用

为探索动脉波形分析方法的临床意义，使用波形分离法与储存压力波模型对采集到的25例进行全麻手术的高龄患者的动脉压力波形进行波形分析，在获得[Pf]、[Pb]以及[Pe]、[Pr]等波形形态参数后，将诱导前后的参数变化量与临床生命指标变化量进行相关性分析。在本文的研究群体中，波形分离法与储存压力波模型的参数均与诱导中的血压和心率变化量有相关性，其中△[Pe]与临床指标△PP相关系数最高（r=0.926）。从生理病理学的角度对波形参数的变化进行解读，旨在探索波形分析在诱导期对全麻患者麻醉水平的应用价值，可为动脉压力波形分析及其应用提供新的理论基础和技术方案。     

Magnetic sensor for arterial distension and blood pressure monitoring

A novel sensor for measuring arterial distension, pulse and pressure waveform is developed and evaluated. The system consists of a magnetic sensor which is applied and fixed to arterial vessels without any blood vessel constriction, hence avoiding stenosis. The measurement principle could be validated by in vitro experiments on silicone tubes, and by in vivo experiments in an animal model, thereby indicating the non-linear viscoelastic characteristics of real blood vessels. The sensor is capable to provide absolute measurements of the dynamically varying arterial diameter. By calibrating the sensor, a long-term monitoring system for continuously measuring blood pressure and other cardiovascular parameters could be developed based on the method described. This will improve diagnostics for high risk patients and enable a better, specific treatment.     

Non-invasive pulsatile arterial pressure and stroke volume changes from the human finger

In this paper we review recent developments in the methodology of non-invasive finger arterial pressure measurement and the information about arterial flow that can be obtained from it. Continuous measurement of finger pressure based on the volume-clamp method was introduced in the early 1980s both for research purposes and for clinical medicine. Finger pressure tracks intra-arterial pressure but the pressure waves may differ systematically both in shape and magnitude. Such bias can, at least partly, be circumvented by reconstruction of brachial pressure from finger pressure by using a general inverse anti-resonance model correcting for the difference in pressure waveforms and an individual forearm cuff calibration. The Modelflow method as implemented in the Finometer computes an aortic flow waveform from peripheral arterial pressure by simulating a non-linear three-element model of the aortic input impedance. The methodology tracks fast changes in stroke volume (SV) during various experimental protocols including postural stress and exercise. If absolute values are required, calibration against a gold standard is needed. Otherwise, Modelflow-measured SV is expressed as change from control with the same precision in tracking. Beat-to-beat information on arterial flow offers important and clinically relevant information on the circulation beyond what can be detected by arterial pressure.     

Blood pressure waveform analysis by means of wavelet transform

The assessment of cardiovascular function by means of arterial pulse wave analysis (PWA) is well established in clinical practice. PWA is applied to study risk stratification in hypertension, with emphasis on the measurement of the augmentation index as a measure of aortic pressure wave reflections. Despite the fact that the prognostic power of PWA, in its current form, still remains to be demonstrated in the general population, there is general agreement that analysis and interpretation of the waveform might provide a deeper insight in cardiovascular pathophysiology. We propose here the use of wavelet analysis (WA) as a tool to quantify arterial pressure waveform features, with a twofold aim. First, we discuss a specific use of wavelet transform in the study of pressure waveform morphology, and its potential role in ascertaining the dynamics of temporal properties of arterial pressure waveforms. Second, we apply WA to evaluate a database of carotid artery pressure waveforms of healthy middle-aged women and men. Wavelet analysis has the potential to extract specific features (wavelet details), related to wave reflection and aortic valve closure, from a measured waveform. Analysis showed that the fifth detail, one of the waveform features extracted applying the wavelet decomposition, appeared to be the most appropriate for the analysis of carotid artery pressure waveforms. What remains to be assessed is how the information embedded in this detail can be further processed and transformed into quantitative data, and how it can be rendered useful for automated waveform classification and arterial function parameters with potential clinical applications.     

Catheter-manometer system damped blood pressures detected by neural nets

Degraded catheter-manometer systems cause distortion of blood pressure waveforms, often leading to erroneously resonant or damped waveforms, requiring waveform quality control. We have tried multilayer perceptron back-propagation trained neural nets of varying architecture to detect damping on sets of normal and artificially damped brachial arterial pressure waves. A second-order digital simulation of a catheter-manometer system is used to cause waveform distortion. Each beat in the waveforms is represented by an 11 parameter input vector. From a group of normotensive or (borderline) hypertensive subjects, pressure waves are used to statistically test and train the neural nets. For each patient and category 5–10 waves are available. The best neural nets correctly classify about 75–85% of the individual beats as either adequate or damped. Using a single majority vote classification per subject per damped or adequate situation, the best neural nets correctly classify at least 16 of the 18 situations in nine test subjects (bionomial P=0.001). More importantly, these neural nets can always detect damping before clinically relevant parameters such as systolic pressure and computed stroke volume are reduced by more than 2%. Neural nets seem remarkably well adapted to solving such subtle problems as detecting a slight damping of arterial pressure waves before it affects waveforms to a clinically relevant degree.     

用模型分析心肌血流与阻力的灌注压依赖性

合理考虑心肌内有代表性的血管网，选用实测主动脉压和左心室腔压作为输入数据，建立了一种适于研究左心室壁心肌血流动力学机制的模型，能够同时仿真冠脉系统的动、静脉及微循环血流。在预测心肌灌注时相分布接近现有结论的基础上，研究了心肌血流与血管床阻力的灌注压依赖性。结论有助于理解主动脉内气囊反搏和体外反搏的治疗机制。     

Noninvasive determination of elastic properties and diameter of human limb arteries

A method involving application of a standard cuff on human limbs has been developed making it possible by a single procedure to make a quantitative determination of blood pressure, elastic resistance of “uninfluenced” an mechanically relaxed arterial vessel walls, their bulk modulus and effective inner diameter. The method which is based on the “elasticity reservoir theory” involves recording arterial pressure recordings during periods of gradual compression and evaluation of the pulsatile blood volume increment under the cuff at the on step wise decompression. The reproducibility of the results and the errors involved were estimated by comparing the results with measurements made on a physical model and on human limbs. This paper presents some results of the application of the method to 113 healthy persons and shows the age dependence of the examined parameters in the upper arms and in the lower leg.     

A New Biomechanical Perfusion System for <Emphasis Type="Italic">ex vivo</Emphasis> Study of Small Biological Intact Vessels

The vascular endothelium transduces physical stimuli within the circulation into physiological responses, which influence vascular remodelling and tissue homeostasis. Therefore, a new computerized biomechanical ex vivo perfusion system was developed, in which small intact vessels can be perfused under well-defined biomechanical forces. The system enables monitoring and regulation of vessel lumen diameter, shear stress, mean pressure, variable pulsatile pressure and flow profile, and diastolic reversal flow. Vessel lumen measuring technique is based on detection of the amount of flourescein over a vessel segment. A combination of flow resistances, on/off switches, and capacitances creates a wide range of pulsatile pressures and flow profiles. Accuracy of the diameter measurement was evaluated. The diameters of umbilical arteries were measured and compared with direct ultrasonographic measurement of the vessel diameter. As part of the validation the pulsatile pressure waveform was altered, e.g., in terms of pulse pressure, frequency, diastolic shape, and diastolic reversal flow. In a series of simulation experiments, the hemodynamic homeostasis functions of the system were successfully challenged by generating a wide range of vascular diameters in artificial and intact human vessels. We conclude that the system presented may serve as a methodological and technical platform when performing advanced hemodynamic stimulation protocols. Niklas Bergh and Mikael Ekman, Both authors contributed equally to the work     

Total body vascular capacitance changes during high intracranial pressure in dogs

The active capacitance response to increased intracranial pressure (Pic) was studied in nine chloralose-anesthetized dogs. The vena cavae were cannulated and drained into a reservoir as blood was pumped at a constant flow (Q) into the right atrium. Central blood volume was determined as Q times the mean transit time of dye from the right atrium to the aortic root. Arterial compliance (Ca) was determined from the monoexponential decay of systemic arterial pressure (SAP) during vagal cardiac arrest to compute changes in arterial volume (delta SAP X Ca). Atropine was administered to prevent bradycardia and dangerous, constant cardiac output-induced increases in pulmonary arterial (PAP) and right and left atrial pressures. Blood volume shifts indicative of active venoconstriction, included changes in reservoir, central, and arterial volumes during Pic of 100-200 mmHg. Raised Pic, after atropine, induced a tachycardia, increased systemic and pulmonary resistances, and increased SAP and PAP. Venoconstriction caused marked blood shifts between 125 and 200 mmHg Pic. The extrapolated response threshold was about 112 mmHg. In the most sensitive range, venoconstriction amounted to 3.9 ml X kg-1 per 25-mmHg change in Pic. These results indicate that intense active capacitance vessel constriction is an important part of cardiovascular hemostasis during rapidly increased intracranial pressure.     

Elastic porous tube model of reactive hyperaemia

Reactive hyperaemia is the term given to the temporary increase in blood flow that follows release of an occlusion of the arterial supply. Measurement of reactive hyperaemia in the leg below the knee is useful in assessment of the vascular system, as resting flows remain unaffected even in the presence of quite severe occlusive arterial disease. An elastic porous tube representation of the vascular system is used to develop equations for the variation of the mean pressure, flow and vessel calibre in the vascular system. The tube represents the arteries and large arterioles, which respond passively to changes in pressure. Leakage through the tube walls represents flow into the small arterioles, which respond actively to the rise in pressure following release of the occlusion by constricting (the myogenic response). The capillaries are represented by rigid tubes, and the venous system is represented by a single compliant vessel. The model predicts variations in the flow, pressure and vessel calibre that are in agreement with experimental observations, and identifies that the pressure gradient is important in determining the initial transient increase in the flow following release of the occlusion. The subsequent development in the flow is governed by the small arteriolar flow, which is determined by the magnitude and duration of the myogenic response.     

Dermatan sulphate as an antithrombotic drug

Dermatan sulphate (DS) is a glycosaminoglycan which selectively catalyzes the inactivation of thrombin by Heparin Cofactor II without interacting with Antithrombin III. DS does not interact with other coagulation factors and, unlike heparin, is able to inactivate thrombin bound to fibrin or to the surface of an injured vessel. Efficacy and safety of DS have been validated in studies on thromboprophylaxis and on the anticoagulation for hemodialysis. Studies on thromboprophylaxis have been performed in "medical" patients as well as in general, orthopedic and oncological surgery. In this last setting, DS proved to be more efficacious than heparin, in the absence of excess bleeding. No statistically significant differences were observed between DS and heparin in hemodialysis. A low-molecular-weight DS,which shows a higher bioavailability after s.c. administration, has been tested in pilot studies on the treatment of venous thromboembolism with encouraging results. Two DS-containing compounds, sulodexide and, particularly, mesoglycan, have been clinically studied in a number of trials and found to be effective in the treatment of venous and arterial leg diseases.     

Cerebrovascular transmural pressure and autoregulation

The cerebral blood flow (CBF) response to changes in perfusion pressure mediated through decreases in arterial pressure, increases in cerebrospinal fluid (CSF) pressure and increases in jugular venous pressure was studied in anesthetized dogs. A preparation was developed in which each of the three relevant pressures could be controlled and manipulated independently of each other. In this preparation, the superior vena cava and femoral vein were cannulated and drained into a reservoir. Blood was pumped from the reservoir into the right atrium. With this system, mean arterial pressure and jugular venous pressure could be independently controlled. CSF pressure (measured in the lateral ventricle) could be manipulated via a cisternal puncture. Total and regional CBF responses to alterations in perfusion pressure were studied with the radiolabelled microsphere technique. Each hemisphere was sectioned into 13 regions: spinal cord, cerebellum, medulla, pons, midbrain, diencephalon, caudate, hippocampus, parahippocampal gyrus, and occipital, temporal, parietal and frontal lobes. Despite 30 mm Hg reductions in arterial pressure or increases in jugular venous pressure or CSF pressure, little change in CBF was observed provided the perfusion pressure (arterial pressure minus jugular venous pressure or CSF pressure depending on which pressure was of greater magnitude) was greater than the lower limit for cerebral autoregulation (approximately 60 mm Hg). However, when the perfusion pressure was reduced by any of the three different methods to levels less than 60 mm Hg (average of 48 mm Hg), a comparable reduction (25–35%) in both total and regional CBF was obtained. Thus comparable changes in the perfusion pressure gradient established by decreasing arterial pressure, increasing jugular venous pressure and increasing CSF pressure resulted in similar total and regional blood flow responses. Independent alterations of arterial and CSF pressures, and jugular venous pressure produce opposite changes in vascular transmural pressure yet result in similar CBF responses. These results show that cerebral autoregulation is a function of the perfusion pressure gradient and cannot be accounted for predominantly by myogenic mechanisms.     

Doppler flow velocity waveforms of human fetal ductus arteriosus and branch pulmonary artery.

Doppler waveforms of the human fetal ductus arteriosus and the branch pulmonary artery are distinct in their shape and might reflect fetal cardiovascular hemodynamics and vessel wall characteristics. The waveform of ductus arteriosus had two peaks, a higher one in systole and a lower one in diastole. Both peaks had slow acceleration and deceleration and looked like two narrow base isosceles triangles. This unique waveform might be due to vessel wall characteristics and an instantaneous pressure gradient between the main pulmonary artery and descending aorta. The waveform of the branch pulmonary artery showed very steep acceleration with the onset of ejection followed by steep decline, then low velocity flow during diastole. The characteristic shape of the branch pulmonary artery might be related to high vascular resistance, decreased capacitance and the earlier reflection wave of pulmonary vessels.     

Time domain analysis of the arterial pulse in clinical medicine

The arterial pulse at any site is created by an impulse generated by the left ventricle as it ejects blood into the aorta, together with multiple impulses travelling in the opposite direction from reflecting sites in the peripheral circulation. The compound wave at any site depends on the pattern of ventricular ejection, the properties of large arteries, particularly their stiffness (which determines rate of propagation) and the distance to and impedance mismatch at reflecting sites. Physicians are familiar with waveform analysis in the time domain, as in the electrocardiogram (ECG) where the principal features are explicable on the basis of atrial depolarisation followed by ventricular depolarisation, then repolarisation. Effects of cardiac functional and structural disease can be inferred from the ECG. It is more difficult to make similar interpretations from the pulse waveform and clinicians usually use this only to count heart rate, extremes of the pressure pulse to express systolic and diastolic pressure, and (sometimes) time from wave foot to incisural notch to measure time of systole and diastole. More information can be gleaned from the shape of the arterial pressure wave through consideration of the factors which create it—on stiffening of large arteries with age, effects of drugs on smallest arteries, and changes in such arterial properties on left ventricular load and function. Such is a major challenge to future physicians. It is aided by better and more accurate methods for measuring flow and diameter as well as pressure waveforms, and by appropriate use of other analytic techniques such as analysis of the pulse in the frequency domain. Michael F. O’Rourke is a founding director of AtCor Medical, manufacturer of systems for analysing the arterial pulse.     

Tuning Multidomain Hemodynamic Simulations to Match Physiological Measurements

In recent years, considerable progress has been made in creating more realistic models of the cardiovascular system, often based on patient-specific anatomic data, whereas comparatively little progress has been made on incorporating measured physiological data. We have developed a method to systematically adjust the parameters of three-element windkessel outlet boundary conditions of three-dimensional blood flow models such that desired features of pressure and flow waveforms are achieved. This tuning method was formulated as the solution of a nonlinear system of equations and employed a quasi-Newton method that was informed by a reduced-order model. The three-dimensional hemodynamic models were solved using a stabilized finite-element method incorporating deformable vessel walls. The tuning method was applied to an idealized common carotid artery, an idealized iliac arterial bifurcation, and a patient-specific abdominal aorta. The objectives for the abdominal aortic model were values of the maximum and minimum of the pressure waveform, an indicator of the pressure waveform’s shape, and the mean, amplitude, and diastolic mean of the flow waveform for an infrarenal measurement plane. The hemodynamic models were automatically generated and tuned by custom software with minimal user input. This approach enables efficient development of cardiovascular models for applications including detailed evaluation of cardiovascular mechanics, simulation-based design of medical devices, and patient-specific treatment planning.     

动脉中的发展流动与其锥度角的关系

本文推导了动脉血管流动的速度分布和压力分布公式，并从数学上论证出动脉血管中之所以总是发展流动的主要原因是动脉血管存在着锥度角，此外，还讨论了锥度角对动脉血液流动的速度分布的影响问题。     

Systems analysis of arterial pressure regulation and hypertension

In this paper we have presented briefly three different aspects of arterial pressure regulation and of the hypertension problem: (1) the basic principles of arterial pressure control, progressing from simple, individual regulatory mechanisms to complex interactions between these mechanisms; (2) several systems analyses of arterial pressure regulation and of hypertension, also progressing from simple to complex; and (3) animal and human verification of both the logical principles and the systems analyses. Both the systems analyses and the experiments on which they are based show that different feedback control mechanisms are responsible for acute versus long-term control of arterial pressure. Furthermore, some of the concepts of pressure control based on acute experiments and then extrapolated to the problem of hypertension have proved to be wrong, such as the widely heralded concept that chronic hypertension is “caused by” increased total peripheral resistance. Though, on the surface, this concept has long appeared to be a logical one, the systems analysis approach has made it possible to differentiate between the primary causes of hypertension and dependent variables of the system. The basic causes of chronic hypertension predicted by the analyses are: (1) abnormally low renal output of water and electrolytes (mainly salt) at each arterial pressure level, and (2) excess net intake of water and electrolytes. Other causes of chronic hypertension must operate by affecting one of these two basic effects. Total peripheral resistance is one of the dependent variables of the pressure control system, as is also cardiac output, but is never a primary determinant of the long-term level of arterial pressure. This work supported by NIH Grants HL 11678 and HL 08375. This paper is based on the ALZA lecture given by Arthur C. Guyton before the Annual Meeting of the Biomedical Engineering Society in Baltimore, Marylan, April 7, 1972.     

Measurement of pulse wave "augmentation index (AI) "and its clinical application

Hypertension, hyperlipidemia, diabetes mellitus and obesity, all of these life-style related diseases advance arteriosclerosis and cause a cardiovascular event. It is said that the event can be greatly reduced by improvement of lifestyle or medication. The device is recently developed that enables us easily to measure AI i.e. augmentation index, and the studies applying the device have been clarifying the clinical usefulness of the index. The reflected wave from the peripheral artery is superimposed on the ejection wave generated by cardiac contraction, although the blood pressure waveform is observed as the synthesized one of those two. AI is defined as the proportion of the amplitude of the reflected wave to that of the ejection wave, and it does not only express a cardiac load, but also arterial stiffness. The vessel with arteriosclerosis generates a large reflected wave, and it reaches the left ventricle at high speed. Thereby the heart receives large mechanical stress which may cause cardiac hypertrophy, and as a result, the sustained stress may cause a serious accident. Thus, it is the management for both situations of the heart and the artery that matters, and AI can be regarded as a new marker of cardiovascular disease for suitable clinical management on both heart and artery.     

In vitro evaluation of left ventricular assistance by cannulation of both femoral arteries

The possibility of achieving effective mechanical ventricular assistance without the need for thoracotomy provides great clinical advantages. Two in vitro systems were used to assess left ventricular unloading by means of a small-diameter cannula inserted retrograde into the left ventricle by cannulation of the femoral artery. This cannula is connected to the inlet of a centrifugal blood pump (CP) that delivers the blood into the contralateral femoral artery. Steady-flow test circulation was used to pump fluid in a closed loop from a reservoir through the test cannula back into the reservoir. Pressure drops over cannulae with inner diameters of 4, 5, 6, 7, and 8 mm at flows of 2, 2.5, 3 L/min, against a pressure of 60, 80, 100, and 120 mmHg were calculated. A stationary pressure drop of 120 mmHg was measured at a flow of 3 L/min through a 100 cm cannula with an inner diameter of 6 mm. The second system was a pulsatile mock circulation composed of an atrial and an arterial reservoir linked by a pneumatic prosthetic ventricle. This system was coupled with a 100 cm cannula, 6.1 mm inner diameter, which was passed across the outflow valve of the pulsatile prosthetic ventricle and connected to a CP. Fluid was withdrawn from the ventricle and pumped back into the arterial reservoir. Pulsatile pressure drop over the cannula was measured at different CP flows for increasing systolic ventricular pressure; heart unloading was quantified as a function of CP flow under baseline and failing conditions of the prosthetic left ventricle model. At a constant CP flow the pressure drop over the cannula increased with the pulsatility inside the ventricle. The work of the prosthetic ventricle was reduced by more than 50% when the CP pump was set to 3 L/min; at the same flow setting, when the situation of a failing left ventricle was simulated, the CP was able to take over all the work of the prosthetic ventricle, establishing a stationary flow and a 25% higher mean aortic pressure. This approach to left ventricular assistance may have significant clinical relevance.     

The influence of plaque composition on underlying arterial wall stress during stent expansion: The case for lesion-specific stents

Intracoronary stent implantation is a mechanical procedure, the success of which depends to a large degree on the mechanical properties of each vessel component involved and the pressure applied to the balloon. Little is known about the influence of plaque composition on arterial overstretching and the subsequent injury to the vessel wall following stenting. An idealised finite element model was developed to investigate the influence of both plaque types (hypercellular, hypocellular and calcified) and stent inflation pressures (9, 12 and 15 atm) on vessel and plaque stresses during the implantation of a balloon expandable coronary stent into an idealised stenosed artery. The plaque type was found to have a significant influence on the stresses induced within the artery during stenting. Higher stresses were predicted in the artery wall for cellular plaques, while the stiffer calcified plaque appeared to play a protective role by reducing the levels of stress within the arterial tissue for a given inflation pressure. Higher pressures can be applied to calcified plaques with a lower risk of arterial vascular injury which may reduce the stimulus for in-stent restenosis. Results also suggest that the risk of plaque rupture, and any subsequent thrombosis due to platelet deposition at the fissure, is greater for calcified plaques with low fracture stresses.