CVP is traditionally assessed as an estimate of cardiac preload since true preload, which is defined as end-diastolic myocardial fiber tension, cannot be measured at the bedside.
It is known that measurement of the intrathoracic blood volume (ITBV) is a more accurate estimate of cardiac preload than pressure measurements using central venous or pulmonary artery occlusion pressures.
Can the results obtained by Rivers and cowokers [ 1] be replicated even when less invasive forms of monitoring (e.g. esophageal Doppler-based estimates of cardiac output and preload responsiveness) are substituted for measurements of ScvO2?
Evidence accumulated over the past 40 years shows that CVP, as a reflection of right ventricular preload, is a poor estimate of left ventricular preload in critically ill patients, and particularly in sepsis [ 10].
Although it is not a pure measure of preload, Doppler-based estimates of stroke volume and FTc have been used successfully to guide volume resuscitation in high-risk surgical patients undergoing major operations [ 53].
The introduction of the PAC (which could measure pulmonary artery wedge pressure as a more accurate estimate of left ventricular preload) has allowed for better definition of the cardiovascular dysfunction in septic shock and has improved volume resuscitation.
In the assessment of preload dependency, a slight majority of intensivists reported to use mainly dynamic indices (PPV), volumetric indices estimated with the TPTD technique (GEDV), or echocardiography, although a strong consensus was lacking.
To better understand the relevance of preload in this analysis, we secondarily fit separate regression models (controlling for vasopressor infusion rate and APACHE II) for patients with low preload, intermediate preload, or high preload.
The CVP is a good marker of preload (not preload responsiveness) and a key determinant of cardiac function.
