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Biomedical subjects

R Beyar

Publications and source records attributed to R Beyar.

At least 109 records · Page 6Linked to original sources
PubMed1990

Manipulation of external pressure as a method to assist the failing heart.

The development and state of the art in circulatory assistance using external pressure variations is reviewed. All of these techniques use the principle that by cyclic external pressure waves properly timed to the cardiac cycle, hemodynamic energy can be noninvasively transmitted to assist the circulation. Cyclic pressure waves to the lower body require that the high pressure phase occurs in diastole in order to augment cardiac output or coronary flow. In contrast, pressure waves to the chest would optimally augment cardiac output if they begin at the onset of ventricular systole. Manipulation of lung pressure by synchronized ventilation may be also utilized to augment cardiac output. The above methods are discussed in detail in the manuscript with special emphasis on the pathophysiology and mechanisms of cardiac assistance.

Animals↗
PubMed1990

Magnetic resonance imaging as a noninvasive standard for the quantitative evaluation of left ventricular mass, ischemia, and infarction.

Because magnetic resonance imaging (MRI) acquires data in a spatially unambiguous fashion and the three-dimensional interrelationships of one image plane to another are easily ascertained, there are far fewer technical restrictions imposed on this method than on other imaging techniques. Furthermore, the multiplanar nature of MRI image acquisition, in any plane desired, is a feature unique to this imaging technology. MRI is thus well suited to the highly accurate quantification of global and regional left ventricular (LV) size and function, and can be used as a standard for comparison to other techniques, once validated. Because the determination of LV mass by MRI requires no assumptions about ventricular shape, it should be well suited to the evaluation of both normal hearts and those distorted by infarction. We performed gated MRI on 15 dogs before and after myocardial infarction. LV mass was calculated with 5 short axis planes. The correlation was excellent between actual mass before infarction and after MI. Accuracy was similar for both end-diastole and end-systole. Thus, MRI accurately determines LV mass in both distorted and normal hearts. We have also developed a method for quantification and mapping of regional wall thickening throughout the LV as an index of regional ischemia by utilizing the 3D geometry to calculate the perpendicular wall thickness of a 3D volume element of tissue. This 3D volume element results in less variability of normal wall thickening and provides a better discriminator of ischemic from nonischemic zones in a canine model of acute ischemia, whereas there is considerably greater overlap between ischemic and normal zones with standard planar MRI techniques. The 3D method is more accurate than planar methods in avoiding biases resulting from the oblique course of an image plane through the LV wall, resulting in better distinction of ischemic from nonischemic tissue. Finally, the accurate assessment of regional LV function for the identification of ischemic or infarcted myocardium has been enhanced greatly by a new technique, myocardial tissue tagging, in which an electronic marker is applied to the myocardium which persists through ejection, enabling the accurate tracking of specific areas of the heart as they move and rotate through the cardiac cycle.

Cardiomegaly↗
PubMed1990

Three-dimensional mapping of acute ischemic regions using MRI: wall thickening versus motion analysis.

Three-dimensional (3D) endocardial wall motion and thickening were compared as quantitative methods for distinguishing ischemic from non-ischemic myocardium and for their potential to map regional left ventricular (LV) function. Data were obtained by gated magnetic resonance (MR) images in seven open-chest dogs with acute ischemia. The LVs were reconstructed in 3D at end diastole (ED) and end systole (ES) with a helical coordinate system that wraps the endocardium and epicardium. Thickness and percent wall thickening were calculated by a 3D volume element method. Wall motion was calculated by the 3D displacement of the endocardium perpendicular to the wall using both fixed and floating centroids. Monastral blue nonstaining identified the ischemic regions from five anatomical slices of the LV, which corresponded to the in vivo image planes. Thickening and motion were compared at the centers of the ischemic and the remote normal zones, in addition to comparing the functional maps of the entire LV to the postmortem anatomical maps. All methods distinguished between the center of the ischemic zone and the remote normal zone; however, thickening discriminated most strongly between zones. Comparison of the 3D in vivo maps with the 3D postmortem maps showed that the sensitivity, specificity, and overall accuracy of the thickening algorithm exceeded those obtained by the wall motion algorithms with fixed or floating centroids. Thus wall thickening utilizing the 3D volume element approach is superior to 3D wall motion algorithms in distinguishing ischemic from nonischemic zones and in mapping regional function in the entire LV.

Acute Disease↗
PubMed1990

Quantification and validation of left ventricular wall thickening by a three-dimensional volume element magnetic resonance imaging approach.

We have developed a method to quantify and map regional wall thickening throughout the left ventricle (LV) with magnetic resonance imaging. In contrast to methods that measure planar wall thickness and thickening, this method uses the three-dimensional (3D) geometry of the left ventricle to calculate the perpendicular thickness of the wall. We tested this method at three levels of increasing complexity using 1) phantom studies, 2) in vivo experiments in dogs with normal cardiac function, and 3) in vivo studies in dogs during acute ischemia. Experiments were conducted in 15 open-chest dogs imaged by a 0.38 T iron core magnet. Five short-axis images at end diastole and end systole were obtained with the spin echo technique by use of the QRS as a trigger for end diastole and the second heart sound, S2, to time end systole. After acquisition of preischemic images, acute ischemia was induced by either coronary artery ligation (n = 5) or intracoronary dental rubber injection (n = 5), which produced severe transmural ischemia. By use of computer-aided contouring of the endocardial and epicardial borders, each image was divided into 16 segments with radial lines originating from the midwall centroid. A 3D volume element was defined as that generated by connecting two matched planar segments in two adjacent image planes. This defined 64 volume elements comprising the entire left ventricle. Thickness and thickening before and during ischemia were then calculated by using the planar segments and the 3D volume elements. In phantom studies, the 3D method was accurate, independent of the angle of inclination of the image plane to the phantom wall, whereas the planar method showed considerable overestimation of thickness when the image plane was oblique to the phantom wall. In the dogs before induction of ischemia, the 3D method demonstrated the well-established normal taper in end-diastolic wall thickness from 1.10 +/- 0.02 cm at the base to 1.05 +/- 0.11 cm at the apex (p less than 0.01). By contrast, the planar method did not detect the decrease in thickness toward the apex (1.13 +/- 0.07 cm at the base vs. 1.16 +/- 0.14 cm at the apex, p = NS). During acute ischemia, thickening was calculated by both methods at the center of the ischemic zone defined by Monastral blue nonstaining and compared with the preischemic values.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗
PubMed1990

Noninvasive quantification of left ventricular rotational deformation in normal humans using magnetic resonance imaging myocardial tagging.

It has been postulated that rotation of the left ventricular apex with respect to the base is a component of normal systolic function in humans, but it has been difficult to measure it noninvasively. Tagging is a new magnetic resonance imaging technique that labels specific areas of myocardium by selective radio-frequency excitation of narrow planes orthogonal to the imaging plane before acquiring an image. Tags appear as black lines and persist in myocardium for 400-500 msec and, if applied at end diastole, will move with the myocardium through systole. Tagging was used to noninvasively quantify left ventricular torsion and circumferential-longitudinal shear (shearCL) in humans. Eight normal volunteers, aged 24-38 years, were imaged in a 0.38-T iron-core resistive magnet. Five short-axis left ventricular images, positioned to encompass the entire left ventricle (LV), were obtained separately at end systole. Four equiangular radial tags had been applied at end diastole, intersecting the myocardium at eight locations. We calculated the difference in angular displacement of each epicardial and endocardial tag point (a tag point being where the tag crossed the epicardium or endocardium) at end systole from the systolic position of the corresponding tag point on the basal plane. This value was called the torsion angle. From this, shearCL, the angle inscribed on the epicardial or endocardial surface between the systolic tag position, the corresponding basal tag position, and its projection onto the slice of interest could be calculated at 32 points in the left ventricular wall.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Aortic diameter and pressure-flow sequence identify mechanism of blood flow during external chest compression in dogs.

Aortic flow and pressure relations and aortic diameter were examined during sinus rhythm, internal cardiac massage, vest cardiopulmonary resuscitation, conventional manual cardiopulmonary resuscitation and high impulse manual cardiopulmonary resuscitation in 14 anesthetized large dogs. During sinus rhythm and during internal cardiac massage, ascending aortic flow and pressure increased simultaneously and the rise in ascending aorta pressure preceded the rise in descending aortic pressure by (mean +/- SEM) 28 +/- 4 and 30 +/- 1 ms, respectively. In contrast, during vest, conventional and high impulse cardiopulmonary resuscitation, ascending aortic flow lagged behind the initial rise in aortic pressure by 40 +/- 4 to 46 +/- 4 ms and ascending and descending aortic pressure increased simultaneously (p less than 0.001 for each external compression mode versus sinus rhythm and internal massage). The ratio of pulse pressure to stroke volume increased by an order of magnitude during all modes of external chest compression (p less than 0.001 versus sinus rhythm and internal massage) and aortic diameter decreased during vest and high impulse cardiopulmonary resuscitation (p less than 0.05 versus sinus rhythm and internal massage). The hemodynamics of external chest compression depart from the normal physiologic sequence of stroke volume-induced increase in aortic pressure and diameter. The rise in aortic pressure precedes flow into the aorta, stroke volume does not fully account for pulse pressure, and aortic diameter decreases during chest compression. These data support the hypothesis that blood flow is due to fluctuations in intrathoracic pressure for high impulse as well as vest and conventional cardiopulmonary resuscitation.

Animals↗
PubMed1989

Dependence of left ventricular twist-radial shortening relations on cardiac cycle phase.

Cardiac models have proposed tight coupling between the systolic twisting motion of the left ventricle about its longitudinal axis and muscle shortening. Whether a similar relationship holds during diastole is unknown. The present study determined the dynamic twist-radial shortening relationship throughout the cardiac cycle in six in situ canine left ventricles. Radiopaque markers (15-26) were implanted throughout the myocardial midwall in six canine left ventricles. Three-dimensional marker location was determined by computer analysis of biplane cineradiograms (60 frames/s), and the results were transformed to cardiac cylindrical coordinates. Mean chamber twist was defined as the gradient along the long axis of circumferential rotation relative to end diastole. Changes in chamber dimension were indexed by average radial shortening, normalized to span from 0 at end diastole to 1.0 at end systole. During systole, ventricular twist and radial shortening were linearly related with an average slope of -0.058 radians (r = 0.99). However, during early diastolic relaxation there was substantial untwist (48 +/- 20% of total) despite only an approximately 15% increase in mean radial dimension resulting in a much steeper twist-percent shortening relationship (-0.24 radians, r = 0.96). During most of the remainder of diastolic filling, the twist-shortening relation was shallower (-0.02, r = 0.91) than the corresponding systolic relation (P less than 0.05). Thus the twist-radial shortening relation depends on the phase of the cardiac cycle. These data suggest that models of chamber mechanics that incorporate twisting motion need to account for the matrix surrounding the muscles in addition to the shortening and lengthening of the muscle fibers.

Animals↗
PubMed1989

Influence of contractile state on curvilinearity of in situ end-systolic pressure-volume relations.

Although in situ end-systolic pressure-volume relations (ESPVRs) are approximately linear throughout a limited load range, they often yield seemingly "negative" volume axis intercepts (V0) and V0 shifts with inotropic interventions. We tested whether or not these findings could stem from in situ ESPVR nonlinearity, and we examined the physiologic meaning and limitations of linearized ESPVR variables frequently used for assessing contractile state. Continuous left ventricular pressures and volumes were obtained by micromanometer and conductance (volume) catheters in six open-chest dogs. Left ventricular loading was varied throughout a wide range by rapid left atrial hemorrhage into a reservoir. Propranolol and verapamil were administered to reduce inotropic state, with heart rate maintained by atrioventricular sequential pacing. ESPVRs were fit to nonlinear [Pes = a(Ves-V'0)2 + b(Ves-V'0)] and linear (Pes = Ees (Ves-V0)] models. Contractile state was assessed by the slope of the ESPVR at V'0 (b, of nonlinear model) and by two other ESPVR model-independent measures: the slope of the dP/dtmax and end-diastolic volume relation, and the slope of the stroke work and end-diastolic volume relation. ESPVR was frequently curvilinear, and a significant correlation existed between the extent of nonlinearity (a) and contractile state. Volume intercepts derived from linear fits to the high load ESPVR range were mostly negative and were dependent on changes in Ees. V0 estimates derived from the low load portion were positive and relatively insensitive to Ees. Thus, in situ ESPVR displays contractility-dependent curvilinearity. The contractility range throughout which ESPVRs are essentially linear is typical for isolated hearts, but the range represents low values for in situ ventricles. Despite curvilinearity, Ees determined in situ throughout limited load ranges can accurately assess inotropic state; however, comparisons between ESPVRs should consider potential nonlinearity, and if possible, they should be made within similar end-systolic pressure ranges.

Animals↗
PubMed1989

Determination of left ventricular mass by magnetic resonance imaging in hearts deformed by acute infarction.

Measurement of left ventricular (LV) mass by magnetic resonance imaging (MRI) is accurate in normal hearts. Because determination of mass by MRI does not require assumptions about ventricular shape, this method may be well suited for evaluating hearts distorted by infarction. To test this hypothesis, gated MRI was performed in 15 dogs before and after acute myocardial infarction. The LV mass of each dog was calculated from five short-axis images acquired at end systole, when shape distortion is greatest, at end diastole, and also from slices at varying phases of the cycle with a multiphase mode that required only one acquisition. Correlation was excellent between actual mass and end-systolic mass before infarction (p less than 0.001, r = 0.98, and SEE = 5.1 g) and after infarction (p less than 0.001, r = 0.97, and SEE = 6.6 g). Likewise, values correlated closely at end diastole before (p less than 0.001, r = 0.96, and SEE = 6.7 g) and after infarction (p less than 0.001, r = 0.94, and SEE = 8.7 g). Surprisingly, measurements of mass by a multiphase mode were also very accurate before (p less than 0.001, r = 0.98, and SEE = 5.1 g) and after (p less than 0.001, r = 0.95, and SEE = 6.49 g) infarction. Therefore, at the same phase and at multiphases of the cardiac cycle, MRI permits accurate determination of LV mass in distorted hearts.

Animals↗
PubMed1989

Circulatory assistance by intrathoracic pressure variations: optimization and mechanisms studied by a mathematical model in relation to experimental data.

The hemodynamic effects of phasic variations in intrathoracic pressure (ITP) timed to the cardiac cycle were predicted by a mathematical model and were compared with data from canine experimental studies. The model was used to predict the hemodynamic effects of changing the onset of the ITP rise relative to the start of cardiac systole, as well as the hemodynamic effects of changes in the duration and amplitude of the ITP rise. The predictions of the model were compared with hemodynamic data from seven anesthetized dogs. Cardiac function was depressed with large doses of verapamil and propranolol, and the hearts were atrioventricular sequentially paced at a rate of 72 beats/min. Phasic ITP variations were generated by a perithoracic vest and were electronically timed to the cardiac cycle. The model predicted, and the experimental data confirmed, that phasic intrathoracic pressure variations generated by vest inflation, timed to the cardiac cycle, can augment both peak and mean aortic flow. The following predictions of the model were also confirmed by the experimental data: 1) Maximum flow augmentation occurs when the onset of the ITP rise is simultaneous with the onset of left ventricular isovolumic contraction, and the ITP rise has a duration of 400 msec. 2) The magnitude of the flow augmentation is a function of the amplitude of the ITP rise. The experimental data showed that there was little further flow augmentation when the ITP rise was greater than 30-40 mm Hg. 3) The magnitude of flow augmentation was inversely proportional to the peak left ventricular elastance (Emax). The best fit between the measured and predicted flow augmentations was obtained for an assumed Emax of 0.5 mm Hg/ml, while Emax measurements in three dogs, using a volume conductance catheter and transient vena caval occlusion, yielded values of 0.4-1.6 mm Hg/ml. Thus, both the mathematical model and canine experiments showed that relatively low-amplitude ITP variations, rising synchronously with the onset of cardiac systole and having an optimal duration, assist the failing heart by augmentation of aortic flow. The degree of cardiac assistance decreases if the ITP variations do not rise synchronously with the onset of systole, or if their duration is not optimal. Thus, properly applied ITP variations may be used as an efficient, noninvasive method to temporarily assist the failing heart.

Animals↗
PubMed1989

Intermittent coronary sinus occlusion after coronary arterial ligation results in venous retroperfusion.

Coronary sinus occlusion retards necrosis of ischemic myocardium. To test the hypothesis that coronary sinus occlusion induces retrograde venoarterial flow, the coronary arteriovenous pressure gradient and the coronary arterial oxygen saturation were measured distal to a left anterior descending coronary artery ligature in dogs. In parallel, we constructed a mathematical model of known coronary physiology to characterize pressure and flow patterns during coronary sinus occlusion. In dogs, coronary sinus occlusion produced a systolic pressure gradient between the coronary artery and the coronary sinus of -20 +/- 9 mm Hg (higher venous pressure, p less than 0.0001) and a positive diastolic gradient of 3 +/- 5 mm Hg (lower venous pressure p less than 0.01). An average reduction in the oxygen saturation in the ligated coronary artery of 20 +/- 13% was also observed (p less than 0.005) consequent to admixture of venous (desaturated) blood. By graded inflation of the coronary sinus balloon, it was demonstrated that desaturation of arterial blood typically occurs above a coronary sinus systolic pressure of 40-50 mm Hg. The mathematical model indicates the possibility of venoarterial pressure gradients and reversal of flow at the microcirculatory level during coronary sinus occlusion. These studies provide evidence that retrograde flow into the ischemic zone occurs in association with intermittent coronary sinus occlusion. Thus, alternating flow over the ischemic territory may be the mechanism of myocardial salvage during intermittent coronary sinus occlusion.

Animals↗
PubMed1989

Air trapping in the lungs during cardiopulmonary resuscitation in dogs. A mechanism for generating changes in intrathoracic pressure.

To test the hypothesis that during cardiopulmonary resuscitation, chest compression with an unobstructed trachea raises and maintains intrathoracic pressure by collapsing airways and trapping air in the lung, we studied 11 dogs (20-32 kg). An inflatable vest compressed the thorax after induction of ventricular fibrillation. First, tracheal airflow was measured by a pneumotachometer during vest inflation and deflation in nine of the dogs. As expected, during the initial phase of vest inflation of cycles after ventilation, air moved out of the lungs, but then airflow stopped. After vest deflation, however, more air moved out of the lungs in eight of the nine dogs; this occurrence indicated that a portion of the inspired tidal volume was trapped during vest inflation. During cycles without prior ventilation, the amount of air expired by chest compression decreased, paradoxically, at higher peak vest pressure (p less than 0.002); this occurrence indicated that air was trapped at the higher vest pressures. The change in right atrial pressure was higher on cycles after ventilation than on cycles without prior ventilation (79 +/- 12 vs. 67 +/- 12 mm Hg [mean +/- SEM], p less than 0.005), and lung volume was higher on cycles after ventilation (p less than 0.001). Next, a 5-Fr micromanometer was advanced down the airway in eight of the dogs. With the tip of the micromanometer 5-8 cm distal to the carina, a zone of high pressure was noted in seven dogs; this high pressure suggested a zone of airway collapse distal to the carina.(ABSTRACT TRUNCATED AT 250 WORDS)

Air↗
PubMed1989

Radionuclide ventriculography and central aorta pressure change in noninvasive assessment of myocardial performance.

Systolic pressure-volume diagrams were obtained noninvasively by measuring the systolic central aortic pressure with a new device and by combining the pressure measurements, thus obtained, with absolute volume measurements obtained by radionuclide ventriculography during ejection. By dividing the peak power by the time elapsed from the beginning of ejection to the peak power point, the ejection rate of change of power (ERCP) was calculated. The ability of this index to assess left ventricular function at rest and exercise was evaluated in ten healthy subjects. ERCP proved to be more sensitive than global left ventricular ejection fraction increasing fivefold from rest to exercise compared with only 20% increase in global ejection fraction. ERCP increased dramatically postexercise from 3411 +/- 2173 to 18,162 +/- 14,633 gm/sec2, median 12,750, 95% confidence interval 9700-29,600, in healthy, while in patients it increased twofold from 2637 +/- 824 to 5062 +/- 1897 gm/sec2, median 4070, 95% confidence interval 2800-7030, p less than 0.001. ERCP had an excellent discriminative power in differentiating healthy subjects from patients, having 100% sensitivity, 90% specificity, 95% accuracy, 95% positive predictive value, and 90% negative predictive value. Thus, this noninvasive index seems to have a more comprehensive ability to evaluate changes in left ventricular function and shows a promising potential for clinical applications.

Adult↗
PubMed1989

Quantitative characterization and sorting of three-dimensional geometries: application to left ventricles in vivo.

A procedure for automatic sorting of three-dimensional (3-D) shapes is proposed. The procedure is applied to sort into normal and abnormal categories, human left ventricles (LV) using in vivo data from 19 subjects (ten normal and nine abnormal LV's) studied by ultrafast tomography (Cine-CT). The procedure starts by utilizing a vector in a helical coordinate system to describe the spatial geometry of each individual LV cavity. This individual vector is then anatomically aligned and normalized to eliminate effects due to size, yielding a dimensionless vector, denoted as "geometrical cardiogram" (GCG). The GCG characterizes the instantaneous 3-D geometrical information of the individual LV. For the group of healthy subjects, the Karhunen-Loeve Transform (KLT) is then applied to compress the geometric information contained in their individuals' GCG vectors, at end diastole (ED) and end systole (ES), and yield a unique set of basis vectors. The "normal shape domain" is next defined as a truncated set of the KLT basis vectors from which a normal GCG can be reconstructed with a mean squared error (MSE) smaller than a defined threshold. The calculated MSE of any individual GCG reconstructed in this domain is then used as a criterion for sorting the 3-D shapes. Hearts which yield MSE greater than the threshold are considered abnormal. When applied to the study group of 19 subjects a significant difference (p less than 0.0001) between the MSE values obtained for the normal LV's, and those obtained for the abnormal LV's was detected, thus leading to a successful sorting of all the studied LV's. Finally, the KLT is applied to yield a compact representation of the 3-D geometry of any LV (normal or abnormal).

Adolescent↗
PubMed1988

Combining transmural left ventricular mechanics and energetics to predict oxygen demand.

This study relates to our earlier study which predicts the transmural distribution as well as the global left ventricular (LV) function and oxygen demand, based on the LV structure, geometry and sarcomere function. Here, we test the predicted global oxygen demand against experimental data in anesthetized, open chest dogs under changing working conditions. The experimental oxygen demand was calculated from the arterio-venous difference in oxygen content times the measured coronary flow. LV load was manipulated by a combination of a pressurized chamber connected to the femoral artery, phenylephrine infusion and an adjustable arteriovenous shunt. The heart was paced in two present heart rates. The study demonstrates that the global predictions, based on the local distributed oxygen demand model, are comparable to those obtained by other methods of global metabolic predictions. However, unlike other global methods, the distributed model gives spatial information and predicts an endo/epi ratio of oxygen demand ranging between 1.05 to 1.14, depending on the loading conditions, which is comparable to available experimental data. For the experimental conditions studied here (stroke volume, heart rate, aortic pressure), the theoretical analysis shows that only the end diastolic volume is significantly correlated to the endo/epi ratio of the transmural oxygen demand.

Animals↗
PubMed1987

Model studies of the effects of the thoracic pressure on the circulation.

Two models of the cardiovascular system subjected to changes in intrathoracic pressure (ITP) are used to simulate the response to normal and positive pressure ventilation and the Mueller maneuver. The first model, based on our earlier model for cardiopulmonary resuscitation and cardiac assist by ITP variations, is based on lumped parameter representation of the cardiovascular system with two ventricles which function based on the time-varying elastance concept using their transmural pressures as the load. The ITP is assumed to be equally distributed in the thoracic cavity and equally affecting all cardiovascular structures within the chest. The model shows that a decrease in ITP is associated with an initial decrease in aortic pressure and flow and an increase in left ventricular end-diastolic and end-systolic volumes. A transient decrease in left ventricular volume which was suggested to occur by a few studies cannot be predicted based on this model. Such a decrease in left ventricular volume can be only predicted when a pericardial constraint is included, as done in the second model. Positive pressure interventions are associated with decreased heart volumes and cardiac output which is primarily a "preload" effect. In general the model reasonably predicts the hemodynamics as a function of the ITP changes and may be used as a tool to investigate the response of the cardiovascular system to various ITP interventions.

Blood Circulation↗
PubMed1987

Intrathoracic pressure fluctuations move blood during CPR: comparison of hemodynamic data with predictions from a mathematical model.

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. We developed a mathematical model that predicts that blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, the model predicts that flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. The model was validated for direct cardiac compression by studying the hemodynamics of cyclic cardiac deformation following thoracotomy in four anesthetized, 21-32-kg dogs. As predicted by the model, there was no change in myocardial or cerebral perfusion pressures when the duration of compression was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. The model was validated for intrathoracic pressure changes by studying the hemodynamics produced by a thoracic vest (vest CPR) in eight dogs. The vest contained a bladder that was inflated and deflated. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. As predicted by the model and opposite to direct cardiac compression, there was no change in perfusion pressures when the rate was increased from 60 to 150/min at a constant duration of 45% of the cycle. Manual CPR was then studied in eight dogs. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres and behaved as predicted from the model of intrathoracic pressure, not direct cardiac compression. At nearly constant peak sternal force (378-426 N), flow was significantly increased when the duration of compression was increased from short (13%-19% of the cycle) to long (40%-47%), at a rate of 60/min. Flow was unchanged, however, for an increase in rate from 60 to 150/min at constant compression duration. In addition, myocardial and cerebral flow correlated with their respective perfusion pressures.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗