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Clinical Investigations in Critical Care |

Changes in BP Induced by Passive Leg Raising Predict Response to Fluid Loading in Critically Ill Patients*

Thierry Boulain, MD; Jean-Michel Achard, MD; Jean-Louis Teboul, MD; Christian Richard, MD; Dominique Perrotin, MD; Guy Ginies, MD
Author and Funding Information

*From the Service de Réanimation Médicale (Drs. Boulain, Achard, Teboul, and Richard), Hôpital de Bicêtre, Faculté de Médecine Paris-Sud, Paris, France; and Service de Réanimation Médicale (Drs. Perrotin and Ginies), Centre Hospitalier Universitaire de Tours, Tours, France.

Correspondence to: Thierry Boulain, MD, Service de Réanimation, Centre Hospitalier Régional d’Orléans-La Source, BP 6709, 45067 Orleans, France; e-mail: boulain@hotmail.com



Chest. 2002;121(4):1245-1252. doi:10.1378/chest.121.4.1245
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Objective: To test the hypothesis that passive leg raising (PLR) induces changes in arterial pulse pressure that can help to predict the response to rapid fluid loading (RFL) in patients with acute circulatory failure who are receiving mechanical ventilation.

Design: Prospective clinical study.

Setting: Two medical ICUs in university hospitals.

Patients: Thirty-nine patients with acute circulatory failure who were receiving mechanical ventilation and had a pulmonary artery catheter in place.

Interventions: PLR for > 4 min and a subsequent 300-mL RFL for > 20 min.

Measurements and main results: Radial artery pulse pressure (PPrad), heart rate, right atrial pressure, pulmonary artery occlusion pressure (PAOP), and cardiac output were measured invasively in a population of 15 patients at each phase of the study procedure (ie, before and during PLR, and then before and after RFL). PPrad, PAOP, and stroke volume (SV) significantly increased in patients performing PLR. These changes were rapidly reversible when the patients’ legs were lowered. Changes in PPrad during PLR were significantly correlated with changes in SV during PLR (r = 0.77; p < 0.001). Changes in SV induced by PLR and by RFL were significantly correlated (r = 0.89; p < 0.001). Finally, PLR-induced changes in PPrad were significantly correlated to RFL-induced changes in SV (r = 0.84; p < 0.001). In a second population of 24 patients, we found the same relationship between PLR-induced changes in PPrad and RFL-induced changes in SV (r = 0.73; p < 0.001).

Conclusion: The response to RFL could be predicted noninvasively by a simple observation of changes in pulse pressure during PLR in patients with acute circulatory failure who were receiving mechanical ventilation.

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