Most critically illpatients in intensive care units (ICU) require fluid administration for
volume expansion at some point during their hospital stay.( In most cases, initial volume expansion does not require
more sophisticated or invasive measures. Clinical history data and clinical signs of low
flow may suggest the likelihood of a response to the initial fluid infusion. As suggested
by Vincent and Weil, “the concept of volemic expansion parallels that of feeding a crying
baby who may be thirsty or hungry. The baby’s response to feeding is rapidly apparent as a
need is satisfied”.(Unfortunately, this basic principle is not frequently used in practice. A recent analysis
of more than 2,000 fluid challenges showed that critically illpatients tend to be treated
in the same manner, regardless of the initial response to volume expansion. Half of the
patients who were responsive to the initial fluid challenge did not receive additional
fluid and were subjected to hypoperfusion, and half of the non-responsive patients received
fluid and were subjected to fluid overload. In addition, the initial clinical evaluation of
the cardiovascular response of approximately 1/3 of the patients was uncertain. Even in
these cases, additional fluid tended to be administered to more than half of the patients
without a more thorough evaluation.(
These findings suggest that the fluid challenge frequently depends on a “proof of faith”,
which is more strongly based on the belief of the possibility of a clinical response to a
fluid challenge than on objective parameters.It is essential to use monitoring methods capable of quickly and precisely identifying
volume deficits to minimize tissue damage related to hypovolemia and avoid iatrogenic fluid
overload.(Several invasive and noninvasive methods, known as dynamic parameters for the evaluation of
the cardiovascular responsiveness to volume, have been suggested to improve volume
replacement. Among these measures, the respiratory change in arterial pulse pressure (∆Pp)
is likely the most well-known method; its first historical reference was in 1669, when
Lomer reported a pathological intensification of blood pressure changes in a case of
pericarditis, defined by Kussmaul as pulsus paradoxus or ‘paradoxical
pulse’.( In 1899, Otto Frank
developed an experimental model consisting of air chambers that simulated the heart-vessel
interaction, which helped to define the relationship between arterial tone, stroke volume,
and arterial pulse pressure.( Mechanical ventilation with positive
pressure reverses the intrathoracic pressure and increases arterial pressure during
inspiration, which was defined as reversed pulsus paradoxus in
1973.( In 1978, researchers began
to evaluate the relationship between the volemic state and systolic arterial pressure
variation,( until 2000, when Michard et al.( demonstrated the high accuracy of the clinical use of ∆Pp
in the evaluation of fluid responsiveness in septic patients. The pressure changes observed
in the arterial bed match those found in the venous bed. Thoracic pressurization acts on
the right heart and vena cava, influencing blood return to the heart resulting in changes
of the central venous pressure during ventilatory movements.(In an individual’s responsive to volume, the pressure around the intrathoracic veins
(mechanical inspiration) exceeds the internal vessel pressure, and the vascular structure
tends to collapse.( This constriction
generated in the intrathoracic portion of the venous bed during mechanical inspiration
functions as a flow resistor, engorging and distending the extrathoracic portions of the
great venous vessels, such as the intradiaphragmatic portion of the inferior vena cava
(IVC) and the jugular veins. Therefore, responsive patients tend to present with an
increase in the inspiratory collapse index of the superior vena cava (SVC) and in the
distensibility indices of the inferior vena cava (IVC) and the internal jugular veins
during mechanical ventilation.(In this issue of RBTI, Broilo et al.(
reinforce the idea that the respiratory variation in the internal jugular vein diameter
(ΔDRIJ) is correlated with the respiratory variation in the inferior vena cava
diameter (ΔDIVC), suggesting that the internal jugular distensibility may be an
easy, noninvasive alternative to evaluate fluid responsiveness in mechanically ventilated
patients. IVC imaging can be difficult in obesepatients and patients with abdominal
distension and ascites, and SVC imaging requires transesophageal echocardiography, which
limits its application.( Because
internal jugular vein imaging does not require transesophageal echocardiography and is
technically more simple than visualizing the IVC, this technique seems to be a simple and
promising bedside method for the evaluation of fluid responsiveness. However, the
limitations of the study should be considered when interpreting the results. Broilo et
al.( evaluated the correlation
between ΔDRIJ and ΔDIVC without testing the capacity of ΔDRIJ to
predict fluid responsiveness to volemic expansion based on the cardiac output behavior. In
addition, recent studies have questioned the accuracy of ΔDRIJ in predicting the
response to volume infusion.( Thus, as the authors themselves forewarn,
the results should be interpreted with caution until new studies are published. We also
highlight that the method is applicable for sedated and mechanically ventilated patients.
Additionally, data on patients with conditions that lead to an increase in venous pressure
(cor pulmonale or ventricular insufficiency) as well as to jugular vein engorgement due to
the inadequate position of the head of the bed should be interpreted with
caution.(
Authors: Glauco A Westphal; Eliezer Silva; Milton Caldeira Filho; Anderson R Roman Gonçalves; Luiz F Poli-de-Figueiredo Journal: Shock Date: 2006-08 Impact factor: 3.454
Authors: Fabio Guarracino; Baldassarre Ferro; Francesco Forfori; Pietro Bertini; Luana Magliacano; Michael R Pinsky Journal: Crit Care Date: 2014-12-05 Impact factor: 9.097