No abstract

Although left ventricular dysfunction is common during ventilatory support with positive end-expiratory pressure (PEEP), the mechanism of this disorder remains unclear. In 10 patients with the adult respiratory-distress syndrome we studied the effects of a stepwise increase in PEEP from 0.to 30 cm H2O on left ventricular output, intracardiac transmural pressures, and two-dimensional echocardiographic measurements of left ventricular cross-sectional area at end-systole and at end-diastole. Increasing PEEP was associated with progressive declines in cardiac output, mean blood pressure, and left ventricular dimensions and with equalization of right and left ventricular filling pressures. The radius of septal curvature decreased at both end-diastole and end-systole, implying a leftward shift of the interventricular septum. At the highest PEEP, blood-volume expansion did not restore cardiac output, although left ventricular transmural filling pressures had returned to base-line values. We conclude that decreased cardiac output during PEEP is mediated by a leftward displacement of the interventricular septum, which restricts left ventricular filling.

In patients with MFS, local PP, estimated from carotid PP, was a major determinant of ascending aorta diameter, whereas brachial PP was not. Increased arterial stiffness was confined to the aorta.

In 13 patients on respiratory support we combined two-dimensional echocardiography with hemodynamic monitoring to determine the mechanism of cyclic changes in arterial pulse, defined as an inspiratory rise in radial artery pulse pressure. Beat-to-beat evaluation of cardiac performance was obtained during the following three distinct consecutive phases of the controlled respiratory cycle: exhalation (phase I), preinspiratory pause (phase LI), and lung inflation (phase III). Airway pressure, left ventricular filling pressure (i.e., pulmonary capillary wedge minus esophageal pressure), and pulmonary artery and radial artery pressures were simultaneously recorded during mechanical ventila-'tion along with beat-to-beat two-dimensional echocardiographic left ventricular end-systolic and enddiastolic dimensions. From a reference value for pulmonary artery and radial artery pulse contour obtained during a brief period of imposed apnea, beat-to-beat measurements of left and right ventricular stroke output were also performed during the controlled respiratory cycle with the pulse contour method. Cyclic changes in arterial pulse appeared to result directly from a transitory increase in left ventricular stroke output during lung inflation (41.4 + 14.6 ml/m2), whereas right ventricular stroke output exhibited a steep fall (31.7 ± 12.4 ml/m2) at this time. An opposite variation was also observed during exhalation, during which a fall in left ventricular stroke output (31.9 ± 11.2 mI/i2) was accompanied by a rise in right ventricular stroke output (38.6 11.9 ml/m2). Both stroke outputs reached an identical level during preinspiratory pause (37.4 + 14. 1 ml/m2 for left ventricle and 39.1 ±-13.8 ml/m2 for right ventricle