Jugular vein distensibility, a noninvasive parameter of fluid responsiveness?

Most critically ill patients in intensive care units (ICU) require fluid administration for volume expansion at some point during their hospital stay.(1) 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”.(2) Unfortunately, this basic principle is not frequently used in practice. A recent analysis of more than 2,000 fluid challenges showed that critically ill patients 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.(3) 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.(4,5) 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these measures, the respiratory change in arterial pulse pressure (ΔPp) is likely the most well-known method; its first historical reference was in 1669, when Lomer reported a pathological intensification of blood pressure changes in a case of pericarditis, defined by Kussmaul as pulsus paradoxus or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’.(6) 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.(7,8) Mechanical ventilation with positive pressure reverses the Glauco Adrieno Westphal1,2, Flávio Geraldo Rezende de Freitas3