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J Cardiothorac Vasc Anesth. 2013 Dec;27(6):1101-7. doi: 10.1053/j.jvca.2013.03.030. Epub 2013 Sep 21.

Predicting fluid responsiveness during infrarenal aortic cross-clamping in pigs.

Author information

1
Emergency Department, University Hospital of Bordeaux, Bordeaux, France; Cardiovascular Adaptation to Ischemia, National Institute of Health and Medical Research, INSERM U1034, Pessac, France; Cardiovascular Adaptation to Ischemia, University of Bordeaux, Pessac, France. Electronic address: matthieu.biais@chu-bordeaux.fr.

Abstract

OBJECTIVE:

Infrarenal aortic cross-clamping (ACC) induces hemodynamic disturbances that may affect respiratory-induced variations in stroke volume and, therefore, affect the ability of dynamic parameters such as pulse-pressure variation (PPV) to predict fluid responsiveness. Since this issue has not been investigated yet to authors' knowledge, the hypothesis was tested that ACC may change PPV and impair its ability to predict fluid responsiveness.

DESIGN:

Prospective laboratory experiment.

SETTING:

A university research laboratory.

PARTICIPANTS:

Nineteen anesthetized and mechanically ventilated pigs.

INTERVENTIONS:

Two courses of volume expansion were performed using 500 mL of saline before and during ACC. Animals were monitored using a systemic arterial catheter, and a pulmonary arterial catheter (stroke volume, central venous pressure, pulmonary arterial occlusion pressure). Animals were defined as responders to volume expansion if stroke volume increased ≥ 15%.

RESULTS:

Before ACC, 13 animals were responders. Fluid responsiveness was predicted by a PPV ≥ 14% with a sensitivity of 77% (95% CI = 46%-95%) and a specificity of 83% (95% CI = 36%-97%). The area under the receiver operating characteristic curve was 0.90(95% CI = 0.67-0.99) and was higher than those generated for central venous pressure and pulmonary arterial occlusion pressure. ACC induced an increase in PPV (p<0.0005). During ACC, 8 animals were responders. An 18% PPV threshold discriminated between responders and non-responders to volume expansion, with a sensitivity of 87% (95% CI = 47%-98%) and a specificity of 54% (95% CI = 23%-83%). The area under the receiver operating characteristic curve was 0.72 (95% CI = 0.47-0.90) and was not different from those generated for central venous pressure and pulmonary arterial occlusion pressure.

CONCLUSIONS:

ACC induced a significant increase in PPV and reduced its ability to predict fluid responsiveness.

KEYWORDS:

IV; cardiac output; fluid responsiveness; fluids; monitoring; pulse pressure variation; vascular surgery

PMID:
24060469
DOI:
10.1053/j.jvca.2013.03.030
[Indexed for MEDLINE]

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