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Vol. 6, No. 7
July 2001


CHANGES IN PEAK AORTIC VELOCITY PREDICT RESPONSE TOVOLUME EXPANSION

PARIS—Because it may improve hemodynamics, volume expansion has been proposed as a first-line therapy for septic shock. It is not always effective in this capacity, though, and may lead to interstitial fluid buildup that worsens gas exchange, decreases myocardial compliance, and limits oxygen diffusion to the tissues.

Intensivists have therefore been seeking a reliable bedside measurement that would predict a positive hemodynamic response to volume expansion in septic shock patients. French researchers believe that they have found one—the respiratory changes in peak velocity (VPEAK) of aortic blood flow.[1]

“A positive response to volume expansion was very likely when we observed a more than 12% variation in [peak velocity] over one respiratory cycle,” reported Frédéric Michard, MD, one of the researchers, in an interview with PULMONARY REVIEWS. “In contrast, a positive response was very unlikely if the variation was 12% or less,” said Dr. Michard, an assistant physician in the medical intensive care unit (ICU) of Bicêtre Hospital in Paris.

NONINVASIVE BEDSIDE MEASUREMENTS

The researchers produced their findings noninvasively with transesophageal echocardiography. Their subjects were 19 mechanically ventilated patients in the medical ICUs of two French hospitals. The patients all had septic shock. To standardize the study protocol and ensure the best conditions for echocardiography, only sedated patients were included.

The protocol included duplicate beat-to-beat echocardiographic measurements of the VPEAK of aortic blood flow before and immediately after volume expansion with 8 mL/kg of 6% hydroxyethyl starch. On each measurement, the investigators determined maximum and minimum VPEAK values over one respiratory cycle.

The respiratory changes in VPEAK were calculated by dividing the difference between the maximum and minimum VPEAK by the mean of those two values. The result was expressed as a percentage.

The researchers also evaluated the cardiac index at the end of the expiratory period. Patients who had a 15% or greater rise in the cardiac index were classified as responders to volume expansion, while those who had a less than 15% increase in cardiac index were considered nonresponders.

THIRD PARAMETER ASSESSED

The ability of a third measurement—the indexed left ventricular end-diastolic area (EDAI)—to predict the response to volume expansion was also assessed. To obtain the EDAI, the researchers measured the left ventricular short-axis, end-diastolic, cross-sectional area on echocardiographic images and divided the measurement by the surface body area.

PEAK VELOCITY PROVED AN ACCURATE PREDICTOR

The respiratory changes in VPEAK before fluid administration were significantly greater among the 10 responders to volume expansion than among the nine nonresponders (20% vs 10%). The change in VPEAK exceeded 12% in all of the responders and was 12% or lower in eight nonresponders.

The 12% threshold distinguished responders with 100% sensitivity and 89% specificity and had a positive predictive value of 91%.

Furthermore, the respiratory changes in VPEAK before volume expansion correlated closely with the post-infusion changes in cardiac index.

The EDAI, however, was not significantly different between groups and showed no correlation with the volume expansion–related changes in the cardiac index.

VPEAK LOOKS PROMISING; WARRANTS MORE STUDY

The researchers’ conclusion: The respiratory changes in the VPEAK accurately predict fluid responsiveness in sedated, mechanically ventilated septic shock patients with preserved left ventricular systolic function, but the EDAI does not. Therefore, the former measurement could facilitate the hemodynamic management of these patients.

More studies are necessary to determine if these findings apply to nonsedated septic shock patients, Dr. Michard told PULMONARY REVIEWS. Because a fractional area of contraction of less than 30% was cause for exclusion from the study, its results also cannot be extrapolated to septic shock patients with left ventricular systolic dysfunction, he pointed out.

—Timothy Begany

Reference
1. Feissel M, Michard F, Mangin I, et al. Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated patients with septic shock. Chest. 2001;119:867-873.

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