Non-invasive detection of hypovolemia or fluid responsiveness in spontaneously breathing subjects

Éva Zöllei,Péter Csábi,László Rudas,József Kaszaki,Andrea Németh,Viktória Bertalan,Ildikó László

doi:10.1186/1471-2253-13-40

Éva Zöllei, Péter Csábi + Show 5 more

Open Access

https://doi.org/10.1186/1471-2253-13-40

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Journal: BMC Anesthesiology	Publication Date: Nov 5, 2013
Citations: 54	License type: CC BY 2.0

Affiliation: University of Szeged

Abstract

BackgroundIn the assessment of hypovolemia the value of functional hemodynamic monitoring during spontaneous breathing is debated. The aim of our study was to investigate in spontaneously breathing subjects the changes in hemodynamic parameters during graded central hypovolemia and to test whether slow patterned breathing improved the discriminative value of stroke volume (SV), pulse pressure (PP), and their variations (SVV, PPV). In addition, we tested the alterations in labial microcirculation.Methods20 healthy volunteers participated in our study. Central hypovolemia was induced by lower body negative pressure (LBNP). Continuous signals of ECG, non-invasive blood pressure and central venous pressure were recorded. During baseline and each stage of LBNP the labial microcirculation was investigated by orthogonal polarization spectral imaging, 3 minute periods of patterned breathing at 6 and 15/min respiratory rate were performed, and central venous blood gas analysis was done. Data from baseline and those of different LBNP levels were compared by analysis of variance and those of different breathing rates by t-test. Finally, we performed ROC analysis to assess the discriminative values of SV, PP, SVV and PPV.ResultsModerate central hypovolemia induced by LBNP caused significant, clinically relevant falls in PP (p < 0.05) and SV and central venous oxygen saturation (ScvO2) (p < 0.001). The proportion of perfused vessels (p < 0.001) and microvascular flow index decreased (p < 0.05). PPV increased (p < 0.001), however the magnitude of fluctuations was greater during slow patterned breathing (p < 0.001). SVV increased only during slow patterned breathing (p < 0.001). ROC analysis confirmed the best predictive value for SV (at 56 ml cut-off AUC 0.97, sensitivity 94%, specificity 95%). Slow patterned breathing improved the discriminative value of SVV (p = 0.0023).ConclusionsFunctional hemodynamic monitoring with slow patterned breathing to control spontaneous respiration may be worthy for further study in different populations for the assessment of hypovolemia and the prediction of volume responsiveness.

Highlights

In the assessment of hypovolemia the value of functional hemodynamic monitoring during spontaneous breathing is debated
The typical recording of one subject is shown in Figure 2. at different lower body negative pressure (LBNP) levels and at 6/min and 15/min patterned breathing, which demonstrates the enhanced fluctuations at moderate hypovolemia and slow patterned breathing in heart rate, arterial blood pressure and central venous pressure
Central venous blood gas analysis showed that pH and Hb significantly increased, pCO2, pO2 and Central venous oxygen saturation (ScvO2) significantly deceased at −40 mmHg LBNP, and this change was even significant between baseline and −20 mmHg in Hb, pO2 and ScvO2, and between −20 mmHg and −40 mmHg in Hb (Table 1)

Summary

Introduction

In the assessment of hypovolemia the value of functional hemodynamic monitoring during spontaneous breathing is debated. This is especially important in severe civil or military mass trauma situations where a parameter or a combination of parameters would be very useful to help to triage patients who are still “stable” but are approaching cardiovascular collapse due Clinical signs and laboratory or blood gas data often help to establish the diagnosis of hypovolemia Hemodynamic parameters such as cardiac filling pressures (central venous pressure, CVP, and pulmonary artery occlusion pressure, Paop) and static volumetric preload parameters (global end-diastolic volume index, GEDVI; intrathoracic blood volume index, ITBVI) have been used to approximate cardiac preload and to guide fluid therapy. The so-called dynamic hemodynamic parameters have been found to be more accurate in the diagnosis of hypovolemia and fluid responsiveness [3,4,5] For calculating these parameters we use preload alterations (most often induced by respiration) and the resulting changes in either right atrial pressure, blood pressure, pulse pressure, stroke volume or cardiac output. Significant arrhythmias, pulmonary hypertension, increased intraabdominal pressure, right and left heart failure and the use of catecholamines influence their predictive value [19,27,28,29]

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