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Hemodynamic assessment is of primary importance in guiding volume therapy and vasoactive drug administration to optimize organ perfusion and to avoid fluid overload with lung edema in critically ill patients [1, 2]. Clinical examination has been shown to be of minimal value in detecting inadequate cardiac preload [3]. Several methods for preload determination, such as central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP), have been widely used [4]. Cardiac filling pressures are not always accurate indicators of ventricular preload because of erroneous readings of pressure tracings, discrepancy between measured and transmural pressures, and changes in ventricular compliance [5]. In recent years, right ventricular end-diastolic volume (RVEDV) evaluated by fast response pulmonary artery catheters (PACs), left ventricular end-diastolic area (LVEDA) measured by echocardiography, and the intrathoracic blood volume (ITBV) evaluated by the transpulmonary indicator dilution technique, have been proposed to assess cardiac preload at the bedside [6–8]. [ABSTRACT FROM AUTHOR]

Optimization of volume status to improve cardiac performance in critically ill and in high risk patients requires adequate preload monitoring. The pulmonary artery catheter (PAC) has been a milestone in the management of the hemodynamically unstable patient in the intensive care unit (ICU) for the last 30 years. Recently, the therapeutic utility of the PAC has been challenged based on studies (whose primary objective was ‘presumed' to be patient outcome) suggesting an unfavorable balance of risk and benefits [1, 2]. Kern and Shoemaker in a meta-analysis reviewed 21 randomized controlled trials with various approaches to treatment and revealed statistically significant mortality reductions with hemodynamic optimization when patients with acute critical illness were treated early to achieve optimal goals before the development of organ failure, when there were control group mortalities of more than 20%, and when therapy produced differences in oxygen delivery between the control and protocol group [3]. However, that paper stressed the timing of treatment and not the technique used for monitoring. Squara and colleagues performed a study to look at the variability of treatment with the PAC and concluded that the problem lies in the users [4]. Kumar and colleagues in a prospective, nonrandomized, non blinded interventional study demonstrated that neither central venous pressure (CVP) nor pulmonary artery occlusion pressure (PAOP) appeared to be useful predictors of ventricular preload with respect to optimizing cardiac performance 5. [ABSTRACT FROM AUTHOR]