Cardiac function during mechanical ventilation in a canine model of oleic acid-induced acute lung injury

During mechanical ventilation with Positive End-Expiratory Pressure (PEEP), increased pulmonary vascular resistance (PVR) may adversely affect right ventricular (RV) function, and therefore, left ventricular (LV) function. Thus, increased resistance to RV output can result in decreased LV preload by series interaction, but importantly, also by direct ventricular interaction (leftward septal shift). Therefore, if the increase in PVR can be minimized, for example, by volume loading, the adverse effects of mechanical ventilation on cardiac function may be limited. In eight closed-chest dogs with oleic acid-induced acute lung injury, we measured LV and RV pressures, diameters and stroke volumes during mechanical ventilation with different levels of PEEP (0, 6, 12 and 18 cmH 2O) at different LV end-diastolic filling pressures (PLVED) (5, 12 and 18 mmHg). Increasing levels of PEEP increased PVR and decreased the size of the heart. At PLVED 5 mmHg, ventilation with PEEP increased PVR significantly compared to PLVED of 12 and 18 mmHg. Increased PVR decreased the transseptal pressure gradient (TSG) which suggests a leftward septal shift, thereby decreasing LV end-diastolic volume, transmural pressure, and stroke volume in addition to that caused by external constraint alone. Volume loading reduced PVR for a given level of PEEP. If the relation holds true, the reduction in PVR increased the TSG suggesting a rightward septal shift and increased LV end-diastolic volume and output. We conclude that volume loading reduced PVR which appeared to have a relation with improved LV performance by a rightward septal shift (direct ventricular interaction) and also decreased the effects of constraint on LV preload. Reduced PVR may be an important mechanism by which volume loading improves cardiac function in ventilated patients with acute lung injury.