Although volume is commonly administered to patients with hemodynamic compromise during mechanical ventilation to improve cardiac output, excessive amounts may precipitate or aggravate pulmonary edema, especially in patients with predisposing pulmonary or cardiac conditions. The ability to predict the hemodynamic response to a volume challenge should facilitate patient management and might help to avoid harm in those who are unlikely to benefit from volume loading.Systolic arterial pressure variation (SPV) during mechanical ventilation is more pronounced in hypovolemic than in euvolemic patients [1][2][3]. Cyclical changes in left ventricular (LV) preload during mechanical ventilation and the resultant changes in stroke volume are related to complex cardiopulmonary interactions including changes in external constraint and LV afterload, as well as systemic and pulmonary venous return through series and direct ventricular interaction [4][5][6][7][8][9][10][11]. The magnitude of SPV has been shown to predict responsiveness to a volume challenge [1][2][3][12][13][14][15][16]. One might anticipate that as LV and right ventricular (RV) preload increase during volume loading, changes in intrathoracic pressure would affect ventricular filling (and output) less and thus, SPV would be less. Alternatively stated, at higher filling pressures, the ventricles are on a flatter part of the Starling curve (fiber length cannot be increased further by increasing the filling pressure further). Therefore, a given airway pressure is less likely to reduce fiber length at higher filling pressures than at lower pressures where the Starling curve is steeper.We therefore assessed the relations between LV preload, output and SPV in an oleic acid (OA) induced acute lung injury (ALI) model in which LV filling pressures and positive end-expiratory pressures (PEEP) were systematically varied. We also assessed the potential value of estimated transmural LV end-diastolic pressure [left atrial enddiastolic pressure (P LAED ) -RV end-diastolic pressure (P RVED )], which reflects LV preload, in predicting volume responsiveness in our model.
MethodsThis study was approved by the institutional animal care committee whose criteria are consistent with those of the American Physiological Society.
Animal preparationIn 8 mongrel dogs of either sex (20-30 kg, mean 24 kg), anesthesia was induced with thiopental sodium (25 mg/kg i.v.) and midazolam (5 mg/ml bolus) and was maintained with fentanyl citrate (0.04 mg/ml i.v., initially, followed by an infusion of 4 mg/h), which was adjusted
AbstractBackground: Systolic pressure variation (SPV) predicts responsiveness to volume loading during mechanical ventilation and may be related to changes in LV preload and the resultant changes in stroke volume (SV). We, therefore, tested the relations between LV preload, output and SPV in an acute lung injury (ALI) model during mechanical ventilation.