Quantitative two-dimensional echocardiography in massive pulmonary embolism: Emphasis on ventricular interdependence and leftward septal displacement

In 14 patients requiring aggressive therapy for circulatory failure resulting from massive pulmonary embolism, hemodynamic and two-dimensional echocardiography data were obtained at bedside (acute phase) and again after circulatory improvement (intermediate phase) and during recovery. The acute stage was characterized by a low cardiac output state despite inotropic support (cardiac index 1.9 ± 0.6 liters/min per m2) associated with increased right atrial pressure (12.4 ± 4.2 mm Hg), increased right ventricular end-systolic and end-diastolic area (12.4 ± 3.4 and 15.4 ±4.1 cm2/m2, respectively) and reduced right ventricular fractional area contraction (20.1 ± 8.6%). Two-dimensional echocardiography also revealed interventricular septal flattening at both end-systole and end-diastole and markedly decreased left ventricular end-diastolic dimensions. Left ventricular fractional area contraction remained normal. Hemodynamic improvement occurred during the intermediate phase as shown by restoration of cardiac index (3.3 ± 0.6 liters/min per nr), decrease in right atrial pressure (8.3 ± 4.8 mm Hg), reduction in right ven- tricular end-systolic area (9.0 ± 3.6 cm2/m2at the intermediate stage and 6.1 ± 1.8 cm2/m2at recovery) and end-diastolic area (10.5 ± 3.6 cm2/m2at the intermediate stage and 8.9 ± 2.9 cm2/m2at recovery) and improvement in right ventricular fractional area contraction (31.5 ± 16.4%). The interventricular septum progressively returned to a more normal configuration at both endsystole and end-diastole, and left ventricular diastolic dimension steadily increased. It is concluded that circulatory failure secondary to massive pulmonary embolism was mediated through a profound decrease in left ventricular preload, resulting from both pulmonary outflow obstruction and reduced left ventricular diastolic compliance. Acute dilation of the right ventricle with the concomitant restraining action of the pericardium accounted for the leftward shift of the interventricular septum and reduced left ventricular compliance. Left ventricular systolic function was unaltered.