Peripheral vascular effects on auscultatory blood pressure measurement.

Experiments were conducted to examine the accuracy of the conventional auscultatory method of blood pressure measurement. The influence of the physiologic state of the vascular system in the forearm distal to the site of Korotkoff sound recording and its impact on the precision of the measured blood pressure is discussed. The peripheral resistance in the arm distal to the cuff was changed noninvasively by heating and cooling effects and by induction of reactive hyperemia. All interventions were preceded by an investigation of their effect on central blood pressure to distinguish local effects from changes in central blood pressure. These interventions were sufficiently moderate to make their effect on central blood pressure, recorded in the other arm, statistically insignificant (i.e., changes in systolic [p < 0.3] and diastolic [p < 0.02]). Nevertheless, such alterations were found to modify the amplitude of the Korotkoff sound, which can manifest itself as an apparent change in arterial blood pressure that is readily discerned by the human ear. The increase in diastolic pressure for the cooling experiments was statistically significant (p < 0.001). Moreover, both measured systolic (p < 0.004) and diastolic (p < 0.001) pressure decreases during the reactive hyperemia experiments were statistically significant. The findings demonstrate that alteration in vascular state generates perplexing changes in blood pressure, hence confirming experimental observations by earlier investigators as well as predictions by our model studies.

Cardiac adaptation of sarcomere dynamics to arterial load: a model of hypertrophy.

In the past, the dynamics of the left ventricle were studied by its response to altered venous and arterial load for a given heart. This led researchers to propose the concept of an arterioventricular match or optimal point of function. The model of this paper reverses that idea by fixing preload and afterload while computing cardiac function due to altered left ventricular size or shape, resulting from modification of the number of parallel and series sarcounits. A mathematical model of physiological hypertrophy is introduced. Series and parallel arrangements of sarcounits constitute a cylindrical model of the left ventricle. Filling occurs from a venous reservoir with constant pressure through a valve, while ejection takes place into a three-element model of the systemic arterial system through another valve. It is found that the dynamics of the myofibrils can be matched to those of the left ventricle by choosing a ventricular shape that results in a minimum in myocardial O2 consumption (MVO2) for any constant ventricular load. A unique solution for the size of the ventricle results if the rate of MVO2 is specified. The model is able to predict correctly hypertrophy due to hypoxia and due to pressure (concentric) and volume (eccentric) overloads.

Diastolic mechanics and the origin of the third heart sound.

The third heart sound (S3) is observed for various hemodynamic conditions in both the normal and diseased heart. A theory is proposed in which myocardial viscoelasticity is primarily responsible for S3. A mathematical model is developed based on the mechanical aspects of diastolic function: nonlinear elasticity, viscoelasticity, and pressure generation. The model is provided as an electrical analogy of the left ventricle and circulatory system. S3 is predicted for the normal heart and the heart with dilated cardiomyopathy. An elevation of S3 intensity is indicated for cardiomyopathy, as is often observed in the clinic. S3 is produced experimentally by volume loading of the open-chest canine preparation and mathematically by imposing the conditions of volume loading on the model. Consistency of theory and experiment imply that it is valid to attribute S3 to myocardial viscoelasticity. The animal whose heart possessed the largest constant of viscoelasticity produced the greatest level of S3, in both cases. Nonlinear ventricular compliance is not found to be an essential requirement for sound generation, although increased compliance led to an increase in sound. S3 is predicted to change in response to venous return, ventricular stiffness, contractility, heart rate, and duration of contraction, as observed by others. In general, the coupling of these quantities to S3 is explained in terms of an excitation of viscous properties of the ventricle.

A nonlinear model of the arterial system incorporating a pressure-dependent compliance.

The three-element modified Windkessel model has been widely used to study the characteristics of the systemic arterial system. This model provides most of the features of the systemic input impedance, but does not describe the nonlinear effect of the pressure dependence of arterial compliance. The current investigation examines the hemodynamic consequences of such an inclusion. Simultaneous aortic pressure and flow during control and brief descending aortic occlusion were measured in open chest anesthetized experimental dogs. A numerical procedure was implemented to compute constant compliance linear and nonlinear compliance model-predicted pressure waveforms with flow as the input. Results show that the nonlinear compliance model in general can more accurately predict the measured pressure waveforms during control and during acute pressure loading. The difference between the predicted waveforms is more pronounced when blood pressure is high and when the pulse pressure is large.

Design and control of the atrio-aortic left ventricular assist device based on O2 consumption.

The left ventricular assist device (LVAD) is used in parallel with the left ventricle to temporarily assist patients with diminished cardiac function for the purpose of minimizing heart workload and to maintain systemic arterial perfusion. The proper adjustment and timing of the pneumatic LVAD is important such that this goal is achieved. Previous investigations into the left ventricular assist device are inconclusive regarding the optimal utilization of this device. This paper documents a protocol for optimal timing of the LVAD. Timing is studied using a closed-loop analog model of the heart, vascular system, and the LVAD. The model is tested for basic representation of the physiological system. The LVAD is incorporated into the model to discover its interaction with cardiac preload and afterload. Heart workload is computed via the pressure-volume-area method. The normal and impaired heart are modeled, in each case the pump control variables are adjusted. A protocol for adjustment of the LVAD is proposed based on reduced heart oxygen consumption. It was found that the pump should begin ejection immediately after the close of the aortic valve and that the pump filling pressure should be set to a value which produces maximum filling of the pump. Although aortic pressure and flow could be improved at pump rates above the heart rate, oxygen utilization of the heart could only be minimized for synchronous pumping. The adjustment of the pump ejection pressure is a tradeoff between d/dt (LVO2) and stroke volume and mean arterial pressure. The LVAD should be designed to minimize inflow and outflow resistance and to maximize pump compliance. The process of weaning the patient from the LVAD is considered. The overall results provide quantitative guidance for the use of the AA-LVAD.

Physiological basis for mechanical time-variance in the heart: special consideration of non-linear function.

A relationship between ventricular pressure and volume is developed starting from basic cardiac muscle mechanics. The known and measurable properties of myocardium, such as the Hill law, the periodic excitation-contraction mechanism, and non-linear elasticity of the surrounding elastin and collagen structure, are formulated into a myofibril unit. A cylindrical geometry is chosen to represent the structure of the ventricle, using the myofibril unit as the basic building block. Pressure-volume isochrones computed from this model illustrate non-linear function in the heart which arises from both geometric effects and muscle effects. The above theory and model is linearized to provide a special study case. The behavior that resulted is that of a time-varying elastance, E(t), and, hence, can help in the interpretation of its meaning. It is found that the minimum in E(t) is the consequence of the stiffness of the myocardial fibrous network, adjusted by a geometric factor. In addition, the magnitude of E(t) is governed by myocardial contractility, a geometric factor, and the excitation-contraction mechanism, where time-dependency is imparted by periodic excitation. Since the elastic fibers are the only true elastic elements, the quantity of elastance is determined by controlled volume feedback. A circuit model is provided to illustrate this concept. The non-linear active and passive heart function curves are specified independently. These curves are required to intersect below the resting volume and result in a negative pressure at the intersection. This is found to explain the phenomenon of ventricular suction. In addition, they lead to a time-varying dead volume by virtue of time-dependent isochronal slope. Non-linear function is introduced to the model and is found to explain the variation in curvature of the ventricular isochrones.

The Korotkoff sound.

As the auscultatory method of blood pressure measurement relies fundamentally on the generation of the Korotkoff sound, identification of the responsible mechanisms has been of interest ever since the introduction of the method, around the turn of the century. In this article, a theory is proposed that identifies the cause of sound generation with the nonlinear properties of the pressure-flow relationship in, and of the volume compliance of the collapsible segment of brachial artery under the cuff. The rising portion of a normal incoming brachial pressure pulse is distorted due to these characteristics, and energy contained in the normal pulse is shifted to the audible range. The pressure transient produced is transmitted to the skin surface and stethoscope through deflection of the arterial wall. A mathematical model is formulated to represent the structures involved and to compute the Korotkoff sound. The model is able to predict quantitatively a range of features of the Korotkoff sound reported in the literature. Several earlier theories are summarized and evaluated.

Arterial tonometry: review and analysis.

A review is presented of the field of arterial tonometry and of the problems involved with its application. A second generation model is developed which interprets most of the difficulties encountered in previous experimental work. The model also identifies barriers that must be overcome to allow tonometry to become a practical technique for obtaining measurement of continuous, absolute blood pressure. Problems addressed include those of calibration, positioning sensitivity, design standardization, material properties and vascular loading characteristics. Theoretical and experimental studies provide support for the application of basic biomechanical concepts for solution of these problems and suggest required design features.