[Cardiac preload and central venous pressure]

The force of cardiac contraction is strongly influenced by myocardial fibre length at the beginning of systole. Because the length of cardiac sarcomers and muscle fibres primarily depends on the end-diastolic ventricular volume, filling pressures a priori can only act as indirect parameters of cardiac preload. Central venous pressure (CVP) gives information on right ventricular end-diastolic pressure, which parallels changes in left ventricular end-diastolic pressure as long as ventricular function is not impaired. Since the pressure-volume relationship of cardiac ventricles is not linear and shows great variability, filling of the ventricles cannot be directly derived from end-diastolic pressure. Further limitations of CVP as a surrogate variable of preload are caused by the influence of intrathoracic and intra-abdominal pressures. A valid parameter of preload should describe the relationship between preload and stroke volume as given by the Frank-Starling law. Furthermore, estimates of cardiac preload should enable prediction of fluid responsiveness. Many studies have demonstrated that under clinical conditions CVP cannot meet these demands and thus does not appear to be a useful predictor of cardiac preload. Variables which more directly represent end-diastolic ventricular volume (e.g. intrathoracic blood volume or end-diastolic ventricular area) offer a higher validity as estimates of cardiac preload. Furthermore, dynamic parameters of ventricular preload, such as pulse pressure variation or stroke volume variation, seem to be more predictive of volume responsiveness in ventilated patients than CVP. These limitations, however, do not impair the importance of CVP as the downstream pressure of the systemic venous system.