• A Vieillard-Baron, Y Loubieres, J M Schmitt, B Page, O Dubourg, and F Jardin.
• Medical Intensive Care Unit, University Hospital Ambroise Paré, Assistance Publique Hôpitaux de Paris, 92104 Boulogne Cedex, France.
• J. Appl. Physiol. 1999 Nov 1;87(5):1644-50.

AbstractIn a context such as acute respiratory distress syndrome, where optimum tidal volume and airway pressure levels are debated, the present study was designed to differentiate the right ventricular (RV) consequences of increasing lung volume from those secondary to increasing airway pressure during tidal ventilation. The study was conducted by combined two-dimensional echocardiographic and Doppler studies in 10 patients requiring mechanical ventilation in the controlled mode because of acute respiratory failure. Continuous monitoring of airway pressure on echocardiographic and Doppler recordings provided accurate timing of each cardiac event during the respiratory cycle, with particular attention being paid to end-expiratory and end-inspiratory atrial diameters, RV dimensions, and pulmonary artery and tricuspid flow estimated by the velocity-time integral (PA(VTI) and T(VTI), respectively). At baseline, lung inflation during the inspiratory phase of mechanical ventilation produced a drop in PA(VTI) from 14.3 +/- 2.6 cm at end expiration to 11.3 +/- 2.1 cm at end inspiration. This drop occurred without reduction in right atrial diameter or in RV diastolic dimensions. It was not preceded but was followed by a decrease in T(VTI), thus confirming an increase in RV outflow impedance. Manipulation of tidal volume without changing airway pressure and manipulation of airway pressure without changing tidal volume demonstrated that tidal volume, but not airway pressure, was the main determinant factor of RV afterloading during mechanical ventilation.

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