Biomedical subjects

G S Tyson

Publications and source records attributed to G S Tyson.

24 records · Page 2Linked to original sources

PubMed1984

Pericardial influences on ventricular filling in the conscious dog. An analysis based on pericardial pressure.

Twenty-five dogs were chronically instrumented to investigate the effects of the normal pericardium on cardiac function. Pulse-transit ultrasonic transducers were implanted to measure multiple ventricular dimensions. The pericardium was incised transversely at the base of the heart and precisely reapproximated, so as to disturb its characteristics minimally. One week later, the dogs were studied in the conscious state, and left ventricular, right ventricular, pericardial, and pleural pressures were measured with matched micromanometers. Data were recorded before and after blood volume expansion. Absolute end-diastolic pericardial pressure varied directly with pleural pressure during the respiratory cycle. Transpericardial pressure (pericardial-pleural pressure) varied little with respiration and was related directly to ventricular diameter during the cardiac cycle with peak transpericardial pressure uniformly occurring at end-diastole. With volume infusion, normalized end-diastolic minor axis diameter and left ventricular transmural pressure (left ventricular-pleural pressure) increased significantly from 0.14 +/- 0.01 and 9.5 mm Hg +/- 1.0 mm Hg, respectively, in the control state to 0.20 +/- 0.01 and 19.3 mm Hg +/- 1.2 mm Hg after volume loading. End-diastolic transpericardial pressure also increased significantly from 2.3 +/- 0.5 mm Hg to 4.1 +/- 0.3 mm Hg, and represented approximately 21% of transmural left ventricular pressure. When measurements were obtained sequentially after implantation, transpericardial pressure was initially high but decreased with time, presumably due to pericardial creep. After volume loading, right ventricular end-diastolic transmural pressure averaged 9.6 mm Hg, and pericardial pressure constituted 42% of right ventricular pressure. Thus, pericardial restraining effects may predominantly influence right ventricular filling and affect the left ventricle through series interaction. In the normal conscious dog, transpericardial pressure remains low over the entire physiological range, and the direct influence of the normal pericardium on diastolic filling of the left ventricle appears to be minimal.

Animals↗

PubMed1983

Dynamic ventricular interaction in the conscious dog.

In nine conscious, chronically instrumented dogs, ultrasonic dimension transducers measured left ventricular anterior-posterior and septal-free wall minor axis and major axis diameters. Matched micromanometers measured right and left ventricular transmural and transeptal pressures. Ventricular pressures and volumes were varied by inflation of implanted vena caval and pulmonary artery occluders, and the functional significance of the two types of ventricular interaction, i.e., direct and series, was determined. The left ventricle was represented by a modified ellipsoidal geometry. Left ventricular stroke volume calculated from the dimension data correlated well with that measured directly from ascending aortic electromagnetic flow probes during all interventions (r greater than or equal to 0.96). Partial pulmonary artery occlusion significantly increased right ventricular diastolic and systolic pressures as compared to values obtained during control and venal caval occlusion. During pulmonary artery occlusion, latitudinal septal eccentricity was increased throughout the cardiac cycle compared to control and vena caval occlusion (P less than 0.05), indicating leftward interventricular septal shifting and significant alteration of left ventricular shape. The normalized diastolic pressure-volume curve was shifted to the left with pulmonary artery occlusion compared to control and indicated a decrease in left ventricular chamber compliance. However, when selected cardiac cycles with similar end-diastolic volumes from vena caval and pulmonary artery occlusions were compared, parameters of left ventricular systolic function (stroke volume, percent systolic shortening, peak aortic blood flow, peak left ventricular pressure, and its first derivative) remained relatively constant. These data suggest that mean myocardial fiber length is the major preload determinant of left ventricular systolic function independent of chamber pressure and shape, and that direct ventricular interaction mediated by interventricular septal shifting has minimal effects on systolic myocardial performance in this model. Thus, series ventricular interaction during acute imbalances in biventricular loading, where the output of the right ventricle determines the input of the left, seems to be far more important than direct interaction to the regulation of overall cardiac function.

Animals↗

PubMed1983

Experimental mitral regurgitation. Physiological effects of correction on left ventricular dynamics.

It has been suggested that mitral valve replacement for mitral regurgitation can precipitate acute myocardial failure by increasing left ventricular afterload. However, most studies of this problem have involved anesthesia, acute surgical trauma, or ischemic cardioplegia, each of which can influence myocardial function. The pure hemodynamic consequences of mitral valve replacement were investigated by surgically instrumenting eight dogs with ultrasonic transducers to measure left ventricular diameter, electromagnetic flow probes to measure ascending aortic blood flow, and micromanometers to measure left ventricular and pleural pressures. At the time of implantation, an 8 mm stainless steel shunt was inserted through the left ventricular myocardium at the base of the anterior wall and sutured to the left atrial appendage, producing simulated mitral regurgitation of 20% to 40% of total ventricular output. Balloon occluders were placed around the left atrial shunt and both venae cavae. One to 7 days after implantation, each dog was studied in the conscious state, and data were recorded during acute occlusion of the shunt. After shunt occlusion, left ventricular mean ejection pressure increased significantly in all studies. Systolic wall tension also increased by an average of 8%, diameter shortening decreased by 21%, and forward cardiac output increased by 17%. Thus the higher afterload associated with elimination of mitral regurgitation produced an acute fall in stroke shortening and total left ventricular output. However, forward cardiac output increased in all studies, implying improved pump efficiency and overall cardiac performance. Thus the improvement in pump efficiency associated with restoration of mitral valve competence uniformly increases forward cardiac output despite an increased ventricular afterload and a decreased total stroke volume. Although there may be differences between this relatively acute model and chronic forms of mitral regurgitation encountered clinically, these data suggest that forward cardiac output should increase with correction of mitral regurgitation and that the associated augmentation in afterload is probably not a major factor causing low cardiac output after correction.

Animals↗

PubMed1982

Cardiovascular effects of ventilation with positive expiratory airway pressure.

The broad clinical application of positive and expiratory pressure (PEEP) in the treatment of a variety of respiratory disorders has led to the observation that positive airway pressure can result in cardiac dysfunction. Recent attempts to integrate and extend the results of past research have led to diverse explanations of the overall cardiopulmonary effects of PEEP. This review summarizes previous work in the field and attempts to explain the basis of the divergent conclusions of previous investigators. Data are presented from several experimental models, as well as studies in postoperative patients to formulate an overall analysis of the influence of airway pressure on the central circulation. It appears that the effects of PEEP are primarily mechanical and are mediated through a combination of right ventricular preload limitation and outflow obstruction. Both effects are additive in limiting left ventricular preload and can be ameliorated by volume loading in the absence of significant right ventricular or pulmonary vascular disease. Neural, humoral and ventricular interactive forces appear to be insignificant under most circumstances. The clinical implications of these advances in the current understanding of PEEP are reviewed.

Animals↗

PubMed1982

The effects of airway pressure on cardiac function in intact dogs and man.

Ventilation with positive end-expiratory pressure (PEEP) is associated with reduced cardiac output, but the mechanisms involved are controversial. Possible explanations include increased intrathoracic pressure, reflex changes in myocardial inotropism, pulmonary vascular obstruction and abnormal ventricular interaction. Three types of conscious canine preparations were developed to examine simultaneously each of these factors during ventilation with PEEP. In addition, similar measurements were obtained in patients after cardiac surgical procedures and compared with the results of animal experiments. The primary cause of reduced cardiac output during PEEP appeared to be a diminished end-diastolic volume of the left ventricle, and this appeared to be the result of elevated intrathoracic pressure and increased impedance to blood flow through the lungs. Abnormal interventricular septal shifting and reflex autonomic alterations did not appear to be significant in the normal cardiovascular system. These data provide insight into the cardiac effects of PEEP and emphasize the importance of simultaneous quantification of biventricular performance when assessing cardiopulmonary function.

Animals↗

PubMed1982

Dimensional characteristics of left ventricular function after coronary artery bypass grafting.

During coronary artery bypass grafting, 20 patients underwent epicardial placement of miniature ultrasonic dimension transducers across the minor-axis diameter of the left ventricle to monitor cardiac function postoperatively. Left atrial or left ventricular pressure was measured in all patients, and thermodilution cardiac outputs were obtained routinely. Data from 1, 6, 12 and 20 hours postoperatively were analyzed. Directional changes in systolic shortening of the left ventricular diameter correlated well with stroke volume measured by thermodilution techniques and could be used as an on-line index of cardiac output. In five patients who had preoperative abnormalities in wall motion, systolic bulging of the minor-axis diameter was seen initially after revascularization and then gradually resolved over the next 12 hours. Systolic bulging that did not resolve was the earliest indication of a perioperative myocardial infarction in another patient. The end-diastolic diameter increased progressively in all patients in the first 12 hours postoperatively and was associated with stabilization of cardiac function. This improvement in diastolic left ventricular filling was not reflected (p greater than 0.2) by changes in mean left atrial pressure. Therefore, ultrasonic assessment of left ventricular diameter is a simple, precise and safe method of monitoring systolic and diastolic ventricular function postoperatively.

Adult↗