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

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

In this model of acute RV hypertension, aortic constriction improves cardiac function, at least in part, by altering ventricular interaction independent of changes in RCA flow. Changes in RCA flow do not appear to have a significant impact on cardiac function in this model in which coronary artery pressure was maintained at normal or increased levels.

BACKGROUND To determine the transmural pressure-dimension relations of the right atrium (RA) and right ventricle (RV) before and after pericardiectomy, six open-chest dogs were instrumented with pericardial balloons placed over the RA and RV free walls. METHODS AND RESULTS PA appendage dimensions and RV free-wall segment lengths were measured using sonomicrometry. Intact-pericardium RA and RV transmural pressures were calculated by subtracting the pericardial pressures (measured using balloons) from the cavitary pressures. Pooled data from six animals with pericardium intact indicate that at RA and RV cavitary pressures of 5, 10, and 15 mm Hg, RV pericardial pressure was 4.3 +/- 0.3, 8.6 +/- 1.0, and 13.3 +/- 1.5 mm Hg, respectively, and RA pericardial pressure was 4.8 +/- 0.3, 9.6 +/- 0.6, and 14.6 +/- 0.6 mm Hg, respectively (mean +/- SD). With calculated unstressed dimensions, the cavity dimension data were normalized to strain (in percent). We determined that in the dog, RV strain would increase by 14% and RA by 68% to maintain cavitary pressure at 10 mm Hg on pericardiectomy. To compare these results with clinical data, RV (n = 7) and RA (n = 6) transmural pressures were measured using balloons in patients (age, 19 to 76 years) undergoing cardiac surgery. RA transmural pressure of six patients was 1.0 +/- 1.5 mm Hg when central venous pressures (CVPs) ranged from 3 to 16 mm Hg. RV transmural pressure equaled 1.2 +/- 1.9, 2.3 +/- 1.9, and 3.4 +/- 2.0 mm Hg when CVP was 5, 10, and 15 mm Hg, respectively. CONCLUSIONS Pericardial constraint (as evaluated by the ratio of pericardial to intracavitary pressures when CVP is 10 mm Hg) accounted for 96% of RA cavitary pressure in the dog and 89% in humans and at least 86% of RV cavitary pressure in the dog and 77% in humans.

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