Fluid administration is one of the first-line therapies for most patients with acute
circulatory failure. And it was supposed to increase cardiac preload and thus output
significantly. However, it only has this effect if cardiac output is dependent on cardiac
preload, that is if both ventricles work on the ascending part of the Frank-Starling curve.
Our group had already shown that, in half of the critically ill patients admitted in ICU,
fluid administration is likely to exert only deleterious effects without any hemodynamic
benefit. To predict whether it will exert beneficial effects or not before administering the
fluid therapy, a "dynamic approach" has been developed. It consists of observing the effects
of changes of preload induced by various tests on cardiac output. 1) Pulse pressure
variation: mechanical ventilation induces cyclical changes in cyclical changes in cardiac
preload and right ventricular afterload due to cardiopulmonary interactions. If both
ventricles are in a preload-dependent state, these variations will induce a cyclical
variation in stroke volume. The latter being physiologically related to the pulsed arterial
pressure (systolic - diastolic), the respiratory variation of the pulsed arterial pressure
(PPV) indicates the existence of a preload-dependence of the two ventricles. 2) The
End-expiratory occlusion test (EEOT): this is another method that takes advantage of
heart-lung interactions to predict fluid responsiveness in ventilated patients. During
mechanical ventilation, each insufflation increases intrathoracic pressure, which hinders
systemic venous return. Thus, interrupting the respiratory cycle at the end of expiration
inhibits this cyclic hindrance to venous return, increases cardiac preload and cardiac output
if both ventricles are preload dependent. The duration of the EEOT must be at least 15
seconds. 3): Passive leg raising (PLR): when a patient is in a recumbent position, the
elevation of the lower extremities and the horizontalization of the trunk passively transfers
a significant volume of blood from the lower part of the body to the heart chambers and
mimics volume expansion.
Numerous studies have reported that the increased cardiac output induced by PLR predicts
fluid responsiveness. There is always the question of the prevalence of cases in which the
different predictive indices of fluid responsiveness are not applicable and data on this
issue are scarce, incomplete, and unsatisfactory.
Few studies have systematically investigated the number of patients in whom PPV cannot be
used in the ICU settings. Some studies have reported a very low prevalence of cases where PPV
was usable but they included the entire ICU population on a given day, including many
patients who did not have an acute circulatory failure, which had no sense since PPV is only
used in patients in whom the question of fluid therapy arises. Other studies have reported a
higher prevalence of cases where PPV is usable, but they have only looked at the first 24
hours of hospitalization or have focused on patients with an unstable hemodynamic event.
Finally, no study has ever studied the prevalence of cases where the respiratory variation of
the PLR, or the EEOT are not applicable.