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* From the Service de Réanimation et de Maladies Infectieuses (Drs. Feissel, Mangin, Ruyer, and Faller), Centre Hospitalier, Belfort, France; and the Service de Réanimation Médicale (Drs. Michard and Teboul), CHU de Bicêtre, AP-HP, Université Paris XI, Le Kremlin Bicêtre, France.
Correspondence to: Frédéric Michard, MD, Service de Réanimation Médicale, CHU de Bicêtre, 78 Rue du Général Leclerc, 94275 Le Kremlin-Bicêtre Cedex, France; e-mail: f.michard{at}wanadoo.fr
Study objective: To investigate whether the respiratory changes in peak velocity (Vpeak) of aortic blood flow could be related to the effects of volume expansion on cardiac index.
Design: Prospective clinical study.
Setting: Medical ICUs of a university hospital (20 beds) and of a nonuniversity hospital (15 beds).
Patients: Nineteen sedated septic shock patients who were receiving mechanical ventilation and who had preserved left ventricular (LV) systolic function.
Intervention: Volume expansion.
Measurements and results: Analysis of aortic blood flow by
transesophageal echocardiography allowed beat-to-beat measurement of
Vpeak before and after volume expansion. Maximum values of Vpeak
(Vpeakmax) and minimum values of Vpeak (Vpeakmin) were determined over
one respiratory cycle. The respiratory changes in Vpeak (
Vpeak) were
calculated as the difference between Vpeakmax and Vpeakmin divided by
the mean of the two values and were expressed as a percentage. The
indexed LV end-diastolic area (EDAI) and cardiac index were obtained at
the end of the expiratory period. The volume expansion-induced increase
in cardiac index was
15% in 10 patients (responders) and < 15%
in 9 patients (nonresponders). Before volume expansion,
Vpeak was
higher in responders than in nonresponders (20 ± 6% vs 10 ± 3%;
p < 0.01), while EDAI was not significantly different between the
two groups (9.7 ± 3.7 vs 9.7 ± 2.4
cm2/m2). Before volume expansion, a
Vpeak
threshold value of 12% allowed discrimination between responders and
nonresponders with a sensitivity of 100% and a specificity of 89%.
Volume expansion-induced changes in cardiac index closely correlated
with the
Vpeak before volume expansion
(r2 = 0.83; p < 0.001).
Conclusion: Analysis of respiratory changes in aortic blood velocity is an accurate method for predicting the hemodynamic effects of volume expansion in septic shock patients receiving mechanical ventilation who have preserved LV systolic function.
Key Words: aortic blood velocity cardiac output fluid responsiveness left ventricular end-diastolic area mechanical ventilation septic shock transesophageal echocardiography volume expansion
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