Cyclic changes in arterial pulse during respiratory support.
- 1 August 1983
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation
- Vol. 68 (2), 266-274
- https://doi.org/10.1161/01.cir.68.2.266
Abstract
In 13 patients on respiratory support 2-dimensional echocardiography was combined 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 3 distinct consecutive phases of the controlled respiratory cycle: exhalation (phase I), preinspiratory pause (phase II) 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 ventilation along with beat-to-beat 2-dimensional echocardiographic left ventricular end-systolic and end-diastolic 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 step fall (31.7 .+-. 12.4 ml/m2) at this time. An oposite variation was also observed during exhalation, during which a fall in left ventricular stroke output (31.9 .+-. 11.2 ml/m2) 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). Such an inspiratory increase in left ventricular stroke output during lung inflation was no doubt largely due to a transient improvement in left ventricular preload and this is supported by the finding of a concomitant increase in left ventricular filling pressure and end-diastolic dimensions during the inspiratory phase.This publication has 13 references indexed in Scilit:
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