PATHOPHYSIOLOGY AND NATURAL HISTORY VENTRICULAR PERFORMANCE Septal geometry in the unloaded living human heart

Right ventricular loading leads to diastolic septal flattening in man without necessarily requiring right ventricular pressure to exceed left ventricular pressure. This observation suggested that the unstressed septal configuration is flat and that its normal concave shape is due to the left-to-right transseptal pressure gradient. To examine this hypothesis, we studied septal configuration by twodimensional echocardiography in nine patients with normal global and regional left ventricular function during surgery for coronary artery disease. The transseptal pressure gradient was obtained from pulmonary capillary wedge pressure minus right atrial pressure. Measurements were obtained at control (open chest, intact pericardium [C]), with the pericardium open (OP), on cardiopulmonary bypass (CPB), and after cardiac arrest (CA). There were no changes in any measurements between C and OP or between CPB and CA. Left ventricular end-diastolic cavity area decreased from 16.5 + 2.1 cm2 at C to 11.1 + 4.5 cm2 after CPB, and further decreased to 8.9 + 3.5 cm2 after CA (p < .001), yet the septum flattened, as shown by an increase in its radius of curvature from 1.7 0.5 cm during C to 2.5 0.7 cm after CPB, and to 2.9 + 1.0 cm after CA (p < .001), or from 0.4 0.1 to 0.8 0.4 to 1.1 0.5 U (p < .001) when normalized for cavity area. Diastolic transseptal pressure gradient was reduced from 4.1 ± 2.3 mm Hg during C to 1. 1 ± 1.8 mm Hg after CPB, and to 0.5 ± 1.4 mm Hg after CA (p < .01). Thus, in the unloaded human heart, the interventricular septum is more flat and occupies a neutral position between the left and right ventricle. Septal flattening due to a reduced but not reversed transseptal left-to-right gradient results from assumption of this unstressed shape as the right ventricular end-diastolic pressure approaches the left ventricular end-diastolic pressure. Circulation 74, No. 3, 463-468, 1986. OWING TO its anatomic position, the interventricular septum is postulated to be a mediator of ventricular interaction. 1-5 However, the mechanisms underlying the changes in septal position are still unclear. Previous work from our laboratory demonstrated leftward displacement of the interventricular septum with acute right ventricular loading during a Mueller maneuver in humans (a forced inspiration against a closed airway). 1 In an effort to determine whether these shifts occurred as a result of right ventricular diastolic pressure exceeding left ventricular diastolic pressures, we then measured the diastolic transseptal pressure gradient during the Mueller maneuver, and correlated these From the Cardiology Division, Department of Medicine, and the Department of Surgery, The Johns Hopkins Medical Institutions, Baltimore. Supported in part by U.S. Public Health Service grant (SCOR in Ischemic Heart Disease) No. 2P50-HL-17655 from the National Heart, Lung, and Blood Institute. Address for correspondence: James L. Weiss, M.D., 591 Carnegie Building, The Johns Hopkins Hospital, 600 N. Wolfe St., Baltimore, MD 21205. Received Feb. 4, 1986; revision accepted May 29, 1986. Vol. 74, No. 3, September 1986 changes with alterations in septal geometry. This study (again in humans) showed that the septal flattening that occurs with acute right ventricular loading is accompanied by a decrease in the diastolic left-to-right transseptal pressure gradient, without requiring a reversal of this gradient.2 This raised the possibility that the reason why the interventricular septum shifts leftward during acute right ventricular loading is that the normal septal configuration in the unloaded heart is flat, and that in the working heart it is held in its usual position concave to the left ventricular cavity by the normal and persistent left-to-right positive transseptal pressure gradient. The goal of the current study was to determine the position and configuration of the interventricular septum in the living human heart when the heart is arrested and the transseptal pressure approaches zero.