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Biomedical subjects

R Beyar

Publications and source records attributed to R Beyar.

At least 127 records · Page 7Linked to original sources
PubMed1987

Time-dependent coronary blood flow distribution in left ventricular wall.

A mathematical model of the coronary circulation in the left ventricular (LV) wall, which describes the time-dependent local blood perfusion throughout the myocardium and the coronary flow in the epicardial vessels, is presented. The myocardial perfusion is essentially controlled by the intramyocardial resistance and the coronary pressure driving force, whereas the epicardial arterial flow is dominated by the epicardial and intramyocardial arterial capacitance and the local transmural pressure on the vessels. The temporal and spatial intramural pressure [P im(y,t)], calculated based on a nested-shell spheroidal model of the LV, is used to evaluate the local intramural resistance to flow and the corresponding zero flow pressure. The calculation of the instantaneous flow in each layer is based on a local, time-dependent modification of the back-pressure concept. A function representing the local tonus of the small blood vessels [T wf(y)] is used to adjust the average coronary flow rate to the metabolic demand of each layer. The calculated results are compared with experimental data, and the assumptions of the model are examined against a variety of experimental conditions. The model provides a qualitative tool for comprehending the distributed flow phenomenon within the myocardium and its relation to cardiac mechanics and autoregulation.

Blood Pressure↗
PubMed1987

Atrioventricular interactions: a theoretical simulation study.

A quantitative model that describes the complex atrioventricular interactions, based on the structure and myocardial properties of the left atrium (LA) and left ventricle (LV), is presented. The description of the LV follows our earlier study that assumes a nested-shell spheroidal structure with fanlike fiber angle distribution, transmural electrical activation velocity, and the muscle fiber dynamics with the classical passive and active features of the sarcomeres. The LV model is extended here to include an exponential load-dependent relaxation and viscous (strain rate-dependent) features of the LV passive myocardium. The proposed LA model is based on a thin-wall spherical geometry with a random fibrous structure. The atrial muscle features differ from the ventricular muscle by being much stiffer in the passive state and weaker but faster in the active state. The LV and LA compartments are connected to a preload and afterload scheme and interconnected by the mitral flow with its inertial properties. The complex interactions between the LA and the LV are thoroughly studied here, and the calculated results are consistent with well-established experimental data.

Atrial Function↗
PubMed1987

Interaction between cardiac chambers and thoracic pressure in intact circulation.

A comprehensive model that describes the interaction between the cardiovascular system (CVS) and the intrathoracic pressure (ITP) based on a lumped parameter vascular representation and a time-varying elastance concept for the four cardiac chambers is presented. Special attention is given to two possible mechanisms of interventricular interaction; the constraining effects of the pericardium and direct interventricular interaction that results from the fact that the two ventricles share a common interventricular septum. The response of the CVS to positive and negative perturbations in the ITP and to injection of fluid into the pericardium was simulated and compared with experimental literature data. The results show that 1) the total heart volume is relatively constant throughout the cycle both for ITP of 0 and +15 mmHg, which is consistent with experimental data in dogs, thus suggesting that intrinsic properties of the cardiac chambers rather than a restricting pericardium is the mechanism for that observation. 2) The pericardium has a major role in modifying the transient and steady-state response to a step decrease in the ITP with a transient decrease in left ventricle (LV) end-diastolic volume followed by gradual increase afterwards. 3) The response to sudden injection of fluid into the pericardial space is a larger transient decrease in right ventricle than LV volume, which is consistent with experimental data. 4) Transmission across the septum has a relatively minor role in modifying the response of the CVS to negative pressure. Thus the model reasonably predicts the effects of intrathoracic and pericardial pressures on the circulation in a reflex-blocked animal and provides a means for placing multiple potential mechanisms in proper hierarchial order with regard to contributions to LV and overall CVS function.

Cardiovascular Physiological Phenomena↗
PubMed1986

Spatial energy balance within a structural model of the left ventricle.

A model describing the local instantaneous energetic needs within the left ventricle (LV) myocardium is presented. The model, which combines the myocardial oxygen consumption (MVO2) with the mechanical activity of the cardiac muscle, is based on the theory of cross bridge kinetics between the actin and myosin fibers within the sarcomere. The microscale relationship between the stress, stress development, strain rate and basal metabolism demand is incorporated into the LV model which describes the mechanical activities of different layers within the myocardium. The model shows a significant increase in the oxygen consumption in the endocardial layers as compared with the epicardial layers. Integrating the spatial and temporal oxygen consumption distribution within the myocardium yields the total myocardial oxygen consumption. The quantitative relationships between the heat rate, stress, contractility and external work and the MVO2 are in agreement with known data. The model thus offers a tool to assess the local instantaneous as well as the time averaged overall energy consumption, over a wide range of loading conditions of the LV.

Actins↗
PubMed1986

The dynamic twisting of the left ventricle: a computer study.

A mathematical analysis which relates the dynamic twisting motion of the heart around its longitudinal axis to the mechanical function of the left ventricle (LV) is presented. The study thus extends our earlier model which relates the micro-scale sarcomere dynamics, the fibrous structure of the myocardium, and the electrical transmural activation wave to the global LV function. The analysis demonstrates that although the angular twisting motion of the heart moderates the sarcomere length (SL) and the strain rate distributions throughout the myocardium, the global characteristics of the LV function are almost independent of the twisting phenomenon. The endocardial sarcomeres are nevertheless subjected to higher strains and higher (negative) strain rates than the corresponding (positive) epicardial sarcomeres. Utilizing the sarcomere stress length area to predict oxygen demand, it is shown that the twisting motion of the heart produces the metabolic gradient across the LV wall. In spite of the moderating effect of the twist, a larger than normal gradient in oxygen demand is predicted for cases of concentric hypertrophy.

Aortic Valve Stenosis↗
PubMed1986

Source parameters of the left ventricle related to the physiological characteristics of the cardiac muscle.

An attempt is made here to correlate the physiological muscle parameters with the dynamic source parameters of the left ventricle (LV), i.e. the source (isovolumic) pressure Po and the source (internal) resistance, Rs. The internal resistance is described here as a time-dependent parameter, corresponding to the pressure drop (from the theoretical instantaneous isovolumic pressure) associated with the instantaneous ejection flow rate. The source pressure, which relates to the muscle stress and the ventricular volume, is represented by the time-varying elastance concept and a spheroidal model relating the average wall stress to LV pressure. Linear and exponential force-velocity relationships (FVR), expressed in stress-strain rate terms, are compared. Two possible characteristics of the dynamic FVR in the partially active state, based on either a parallel or a fanlike shift of the stress-strain rate curve, are studied by utilizing simple analytical models as well as a computer simulation model. Comparing the calculated results with experimental data indicates that the dynamic FVR shift occurs in a fanlike pattern in which the maximum strain rate remains constant throughout the cycle. This pattern of the FVR shift is consistent with experimental data that show that the internal resistance is linearly related to the instantaneous isovolumic pressure. The analysis also indicates that the difference between the hyperbolic and linear FVR is rather minor, and in spite of some effects on the ejection pattern and the value of Rs, the functional shape has no effect on the global LV characteristics, such as the ejection fraction and stroke volume.

Animals↗
PubMed1986

Augmentation of cardiac output and carotid blood flow by chest and abdomen phased compression cardiopulmonary resuscitation.

Phased compression cardiopulmonary resuscitation, whereby the chest and abdomen are compressed sequentially, is a new approach to the classical cardiopulmonary resuscitation technique, which is based on the compression of the chest alone. Six dogs with cardiac arrest were treated by external chest and abdominal compression using a rigid plexiglas suit lined with flexible perithoracic and periabdominal bladders. Fast inflation and deflation of the two independent bladders, together with forced ventilation of the lung, generated phased pressure pulses. The physiological variables monitored throughout the experiment included central venous, left ventricular, and central arterial pressures, carotid blood flow, cardiac output, and acid base balance. The phased compression technique was performed with phased time lags of 0, 150, 300, 400, 600, 700, and 850 ms between the abdominal and thoracic pressure pulses. A random sequence of the different phased compression modes, each lasting for 3-10 minutes, was applied during the prolonged resuscitation procedure that lasted for up to 70 minutes. By starting the abdominal compression 300-400 ms before the thoracic compression the carotid flow index improved by 77% (from 13% with simultaneous compression to 23% with phased compression) and the cardiac output index increased by 65% (from 7.8% with simultaneous compression to 12.5%). The results provide insight into the chest pump concept and the role of intrathoracic and intra-abdominal pressures in generating improved blood circulation during cardiopulmonary resuscitation, and show the advantages of phased compression over chest compression alone and simultaneous chest and abdominal compression.

Animals↗
PubMed1986

Relating left ventricular dimension to maximum elastance by fiber mechanics.

The dependence of the pressure-volume slope, which defines the maximum elastance (Emax) and the zero pressure-volume intercept (Vd) on the size and dimensions of the left ventricle (LV), is theoretically studied, and a normalizing parameter for Emax is suggested for normal and hypertrophied hearts. The study is based on our earlier model of the mechanics of the LV contraction, which assumes a nested-shell spheroidal shape, Streeter's fiber angle distribution, given stress-length and stress-strain rate functions of the sarcomeres, a radial propagation of the electrical activation front, and a windkessel arterial model. The study shows that Emax is linearly related to the maximum force that the optimal length sarcomeres can develop (sigma o), which is a characteristic measure of the contractility. Emax decreases and Vd increases with an increase in ventricular size, at a constant end-diastolic ratio (h/b)ed, where h is the wall thickness, and b is the semiminor axis of the prolate spheroidal LV. When the reference unstressed volume (V0) is held constant and the wall thickness increases, as in pure concentric hypertrophy, Emax decreases slightly and shifts to the left to a lower Vd value. In pure eccentric hypertrophy, wherein chamber size increases while the wall thickness remains constant, Emax decreases and Vd increases. A good index for myocardial function at constant configuration ratio (h/b)ed is obtained by multiplying Emax with the LV muscle volume (Vm). (h/b)ed is constant (= 0.45) for the normal heart but increases for concentric hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Biomechanical Phenomena↗
PubMed1986

Left ventricular mechanics related to the local distribution of oxygen demand throughout the wall.

The complex interactions between left ventricular mechanics and the oxygen demand is studied by relating the left ventricular transmural oxygen demand to the myocardial structural and dynamic characteristics. The study utilizes a recent model of left ventricular contraction, which is based on a nested shell spheroidal geometry, a fan-like fibrous structure, the twisting motion of the left ventricle over its long axis, a transmural electrical activation propagation and the basic laws of sarcomere dynamics. The local "axial" stress (in the direction of the fibers) and the instantaneous sarcomere length are used to calculate the spatial distribution of the intramural oxygen demand per beat Vo2(y), where y is the distance from the endocardium. The normalized local sarcomere stress-length area SLAn(y) is related linearly to Vo2(y) by: Vo2(y) = K1 X SLAn(y) + K2, where K1 and K2 are constants. The calculations show a transmural metabolic gradient which is characterized by higher values of Vo2(y) in the endocardial layers than in the epicardial layers. Shorter endocardial sarcomeres and the twisting motion of the left ventricle around the long axis decrease the metabolic gradient across the wall, while a slow transmural electrical propagation wave as well as a wider angle of distribution of the fan-like fiber architecture increases the transmural metabolic gradient. Integration of the local oxygen demand across the left ventricular wall yields global values in agreement with those based on Suga's pressure-volume area approach. The model thus provides a qualitative and quantitative tool to assess the relation of the local and global oxygen demand to the complex left ventricular structure, fiber mechanics, and the dynamics of contraction.

Computers↗
PubMed1986

The "jaundiced heart": a possible explanation for postoperative shock in obstructive jaundice.

Patients with obstructive jaundice are susceptible to postoperative shock and kidney failure. The cause of these potentially fatal complications has not been fully clarified. The present study was designed to assess the role of myocardial dysfunction in the hemodynamic disturbance of obstructive jaundice. We studied the effect of isolated cholemia on left ventricular performance in five conscious dogs before and 2 weeks after choledochocaval anastomosis by using measurements of systolic time intervals (STIs) and maximal dp/dt. Mean left ventricular ejection tiem (LVET) decreased after cholemia from 159 +/- 2.8 msec to 139 +/- 2.6 msec (p less than 0.005), while mean preejection period (PEP) and mean PEP/LVET were increased from 41 +/- 8.5 msec to 87 +/- 14 msec (p less than 0.05) and from 0.39 +/- 0.06 to 0.62 +/- 0.1 (p less than 0.01), respectively. During cholemia, STIs were unchanged after intravenous administration of ouabain, whereas in the control period, there was shortening of mean PEP from 71 +/- 8.8 msec to 58 +/- 7.6 msec (p less than 0.05) and of Q-S2 from 257 +/- 12 msec to 235 +/- 14 msec (p less than 0.005) in response to ouabain. Maximal dp/dt decreased after choledochocaval anastomosis from 4543 +/- 593 mm Hg/sec to 3666 +/- 648 mm Hg/sec (p less than 0.025). We conclude that cholemia in the dog is clearly associated with impaired left ventricular performance. The present data also support a previously published in vitro study from our laboratory showing that cholemia blunts the myocardial contractile response to sympathomimetic agents. The cardiodepressor effect of cholemia may explain the increased tendency of patients with obstructive jaundice to postoperative shock and renal failure.

Animals↗
PubMed1985

Computer simulation of cardiopulmonary resuscitation.

Based on recent experiments attributing blood flow in cardiopulmonary resuscitation (CPR) to intra-thoracic pressure variations a computer study of the complete cardiovascular system with an arrested heart is presented. The model is based on a lumped parametric description of the vascular elements subjected to external pressure variations. The blood flow, which is generated in the system, is found to be within the reported experimental findings in similar conditions, and is highly sensitive to valving mechanisms within the heart and the large veins. Optimal conditions for CPR were searched mathematically and found to be consistent with known experimental data. Mechanisms of blood flow in CPR are discussed. The above model thus offers a tool to understand the various mechanisms involved in CPR and the relative importance of different physiological parameters, and may help in the design of an optimal CPR mode.

Animals↗
PubMed1985

Intrathoracic and abdominal pressure variations as an efficient method for cardiopulmonary resuscitation: studies in dogs compared with computer model results.

Intrathoracic pressure variations are currently proposed as the main flow-generation mechanisms in standard and modified cardiopulmonary resuscitation (CPR) techniques. A method of changing pressure within the thorax and abdomen without any degree of heart compression was developed and tested in dogs. Intrathoracic and abdominal pressure waves were induced by cyclic inflation and deflation of the lungs and of perithoracic and periabdominal balloons. Various modes of CPR, depending on the rate of cycling, the use of a periabdominal balloon inflation, and a delay between the abdominal and thoracic pressure waves, were studied during ventricular fibrillation. During artificial systole (high intrathoracic pressure phase), the pressure which developed in the right ventricle (96.7 +/- 20.5 mmHg) was higher than the pressure in the aorta (89.3 +/- 20.5 mmHg, p less than 0.001). In artificial diastole (low intrathoracic pressure phase), the right ventricular pressure (11.7 +/- 2.6 mmHg) was lower than the aortic pressure (17.5 +/- 3.3 mmHg, p less than 0.001). The average flow in the carotid artery was 21.7 +/- 7.8 ml . min-1, which was 18 +/- 6% of the baseline carotid flow before CPR. Three different factors were found to improve the efficiency of CPR: periabdominal balloon inflation simultaneous with the intrathoracic pressure waves; increased frequency of the pressure waves from 60 to 100 cycles per minute; and inflation of the periabdominal balloon 50 to 100 ms before the thoracic balloon. Blood-gas and acid-base balance analysis during CPR revealed well-oxygenated arterial blood with a marked respiratory alkalosis and a slowly developing metabolic acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗