The objective of this study was to determine the constraining effect of the normal human pericardium. Accordingly, immediately after thoracotomy in nine patients undergoing elective cardiac surgery, we measured mean pericardial surface pressure over the lateral free wall of the left ventricle with a flat balloon as well as mean right atrial pressure while incrementally infusing up ALTHOUGH it is well recognized that the diseased pericardium may cause a significant impairment to ventricular filling, the effect of the normal pericardium on the diastolic properties of the ventricles remains controversial. Based on measurements obtained with fluid-filled catheters, there has been a general consensus that pericardial pressure is equal to intrathoracic pressure,. 2 and is thus of little hemodynamic significance. However, Holt et al. ,3 using a flat liquid-containing balloon, demonstrated that the magnitude of pericardial pressure was substantial and similar to right atrial pressure.To Patients and methods Nine patients (mean age 54 years) scheduled for elective cardiac surgery gave informed consent to participate in this investigation; the protocol was previously reviewed and approved by the institutional ethics committee on human research.

Despite the clinical prevalence of paradoxic interventricular septal (IVS) motion, its pathogenesis remains unclear. To assess the influence of the end-diastolic transseptal pressure tention to the large size of the RV compared with that of the left ventricle (LV) and postulated that the large RV stroke volume resulted in excessive systolic anterior movement of the entire heart.>' Subsequent studies with two-dimensional echocardiography have supported these conclusions and have also drawn attention to the abnormal diastolic shape of the septum,5 which is flattened toward the LV. Explanations for abnormal IVS motion in other conditions have been less satisfactory, ranging from an abnormal septal activation sequence in patients with left bundle branch block (LBBB)9' 11 to adhesions between the sternum and pericardium after cardiac surgery.'4None of these theories provide insight into the fundamental physiologic alteration that could account for the phenomenon being so common in clinical medicine. Since previous data6 suggest that the IVS behaves essentially as a membrane between two fluid-filled chambers, we postulated that its systolic motion pattern (in the absence of ischemic dysfunction) would be a function of the end-diastolic position between the CIRCULATION

The myocardium in patients with HCM is heterogeneously thickened and the fractional thickening and circumferential shortening of the abnormally thickened myocardium are reduced compared with healthy subjects. The decrease in fractional thickening and shortening is inversely related to the local thickness.

Volume loading is used to treat hemodynamically compromised patients with acute pulmonary embolism despite data to suggest that volume loading after embolism might cause a leftward shift of the ventricular septum with a subsequent decrease in left ventricular (LV) end-diastolic volume and stroke work. We studied 10 closed-chest, anesthetized, and ventilated dogs to assess the effects of volume loading after pulmonary embolism caused by autologous clot. LV, right ventricular, and right atrial pressures as well as LV anteroposterior, septum-to-right ventricular, and septum-to-LV free wall diameters (sonomicrometry) were measured. Pericardial pressure was measured with flat, liquid-containing balloons. The effects of volume loading were assessed before embolism, after one episode of embolization, and after repeated embolizations. The LV area index (as a reflection of LV volume) increased during volume loading before embolism (2,870 ±430 to 3,080±520 mm2; p<0.05), did not change significantly during infusion of fluid after one embolization (2,850+±470 to 2,860+±500 mm2; p=NS), and decreased significantly during volume expansion after repeated embolizations (2,760±440 to 2,660+420 mm2; p<0.01). An index of LV stroke work increased (188±+ 85 to 260±+-101 mm Hgxmm2; p

During mechanical ventilation, phasic changes in systemic venous return modulate right ventricular output but may also affect left ventricular function by direct ventricular interaction. In 13 anesthetized, closed-chest, normal dogs, we measured inferior vena cava flow and left and right ventricular dimensions and output during mechanical ventilation, during an inspiratory hold, and (during apnea) vena caval constriction and abdominal compression. During a single ventilation cycle preceded by apnea, positive pressure inspiration decreased caval flow and right ventricular dimension; the transseptal pressure gradient increased, the septum shifted rightward, reflecting an increased left ventricular volume (the anteroposterior diameter did not change); and stroke volume increased. The opposite occurred during expiration. Similarly, the maneuvers that decreased venous return shifted the septum rightward, and left ventricular volume and stroke volume increased. Increased venous return had opposite effects. Changes in left ventricular function caused by changes in venous return alone were similar to those during mechanical ventilation except for minor quantitative differences. We conclude that phasic changes in systemic venous return during mechanical ventilation modulate left ventricular function by direct ventricular interaction.

The slope of the stroke work (SW)-pulmonary capillary wedge pressure (PCWP) relation may be negative in congestive heart failure (CHF), implying decreased contractility based on the premise that PCWP is simply related to left ventricular (LV) end-diastolic volume. We hypothesized that the negative slope is explained by decreased transmural LV end-diastolic pressure (LVEDP), despite the increased LVEDP, and that contractility remains unchanged. Rapid pacing produced CHF in six dogs. Hemodynamic and dimension changes were then measured under anesthesia during volume manipulation. Volume loading increased pericardial pressure and LVEDP but decreased transmural LVEDP and SW. Right ventricular diameter increased and septum-to-LV free wall diameter decreased. Although the slopes of the SW-LVEDP relations were negative, the SW-transmural LVEDP relations remained positive, indicating unchanged contractility. Similarly, the SW-segment length relations suggested unchanged contractility. Pressure surrounding the LV must be subtracted from LVEDP to calculate transmural LVEDP accurately. When this was done in this model, the apparent decrease in contractility was no longer evident. Despite the increased LVEDP during volume loading, transmural LVEDP and therefore SW decreased and contractility remained unchanged.

Diastolic ventricular interaction is associated with septal shift and deformation, the consequences of which have not been fully assessed. A model was therefore developed to describe the mechanisms involved in interaction between the ventricles under different loading conditions. We assumed a circular cardiac minor-axis geometry surrounded by a pericardial membrane with the left ventricle (LV) and septum described by three layers. To define the equilibrium condition, we required the net force-balance at the right ventricular (RV)-LV intersection points to equal zero. The model was tested with and without consideration of bending forces associated with a change of curvature of a thick-walled structure. Model results were compared with data from animal experiments subjected to aortic and pulmonary constriction. LV and RV end-diastolic pressures as well as pericardial pressure were measured. In six dogs, septal segment length was measured using sonomicrometry, and in seven dogs, endocardial curvature was measured using echocardiography. Model and experimental results show that 1) with severe RV loading, septal inversion occurs at a negative transseptal gradient, and 2) the end-diastolic septal segment length continues to shorten after septal inversion during pulmonary constriction. Model simulation suggests that bending moments account for the septal curvature at zero transseptal pressure. In addition, the model predicts the shift in the pressure-area relationship of each ventricle by a change in loading of the opposite ventricle and predicts that large transmural gradients in stress and strain are associated with septal inversion. Thus the model and the experimental data agree and describe the important factors that modulate diastolic septal mechanics during acute differential ventricular loading.

Although stroke volume may decrease markedly after acute pulmonary embolism, left ventricular end-diastolic pressure (LVEDP) usually changes very little, which suggests that compliance or contractility or both are reduced. To test the hypothesis that the altered LV function during pulmonary embolism is primarily due to reduced preload mediated by increased pericardial constraint, hemodynamics and chamber dimensions (measured by sonomicrometry) were assessed in seven anesthetized dogs during control volume loading, after pulmonary embolism (with autologous blood clot), and after repeated pulmonary embolism in the volume-loaded state. The correlation between LVEDP and an index of LVED volume (LVED area index) throughout a wide range of LVEDP before and after embolism was poor (mean r= 0.42; range, 0-0.82). However, the correlation between transmural LVEDP (LVEDP -directly measured pericardial pressure) and LVED area index (mean r = 0.78; range, 0.61-0.94) was significantly higher (p=0.03). Similarly, an index of stroke work (LV area stroke work) correlated less well (p<0.01) with LVEDP (mean r=0.43; range, 0.07-0.77) than with transmural LVEDP (mean r=0.82; range, 0.68-0.92). LV area stroke work also correlated well with the LV area index (mean r = 0.84; range, 0.70-0.95). These data indicate that neither compliance nor contractility is substantially altered during acute pulmonary embolism. The altered LV performance is due to reduced LV preload as reflected by a decrease in transmural LVEDP. This study also demonstrates that LVEDP is a poor index of LV preload during pulmonary embolism, whereas transmural LVEDP accurately reflects LVED dimensions. (Circulation 1988;78:761-768) H emodynamic effects of acute pulmonary embolism include increased pulmonary artery and right ventricular (RV) pressures, and when embolism is severe, the effects include decreased cardiac output, systemic hypotension, and death.1-9 The reduction in stroke volume has been attributed to reduced left ventricular end-diastolic (LVED) volume.910 However, LV filling pressure is usually altered only slightly and may even increase,34,7 which suggests that pulmonary embolism may result in decreased LV compliance or contractility or both.Based on earlier studies from our laboratory1ll12and from other laboratories,10,13-2' we hypothesized