Article

Passive leg raising does not produce a significant or sustained autotransfusion effect.

University of Texas at Dallas, Richardson, Texas, United States
The Journal of trauma (Impact Factor: 2.96). 04/1982; 22(3):190-3. DOI: 10.1097/00005373-198203000-00003
Source: PubMed

ABSTRACT Passive leg raising is widely used to treat hypotension associated with hypovolemia. Presumably gravity causes a central translocation of leg venous blood and an increase in filling pressure, cardiac output, and arterial pressure. Ten healthy volunteers, 25 to 35 years old, had measurements of heart rate, blood pressure, and cardiac output in the supine position after 20 sec and 7 min of 60 degrees passive leg elevation. The protocol was performed 3 and 45 min after the subjects changed from an ambulatory upright to a supine position. Stroke volume and cardiac output increased transiently (8-10%) when the legs were raised after 3 min rest in the supine position. By 7 min of leg elevation, these beneficial effects disappeared. After 45 min supine, leg raising had no effect on stroke volume or cardiac output but increased blood pressure (4 mm Hg) by increasing peripheral resistance (15%). Thus, leg raising, like application of the MAST trousers, fails to produce any sustained increase in cardiac output or stroke volume. Small venous leg volumes and time-dependent changes in the distribution of venous volume and compliance may explain the absence of any sustained 'autotransfusion' effect.

4 Followers
 · 
181 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Pendant de nombreuses années, la gestion du remplissage vasculaire en réanimation a reposé essentiellement sur le concept de fluid challenge (1). Il s’agit d’une évaluation a posteriori de la réponse au remplissage, basée sur un monitorage invasif du débit cardiaque et des pressions intracardiaques (1). Une expansion volémique est jugée efficace lorsqu’elle entraîne une augmentation significative du débit cardiaque associée à une faible augmentation des pressions de remplissage, le coeur fonctionnant alors sur la portion raide de la courbe de Starling (2); elle est jugée inefficace lorsqu’elle n’entraîne qu’une augmentation modeste voire nulle du débit cardiaque mais importante des pressions de remplissage, le coeur fonctionnant alors sur la portion plate de la courbe de Starling (2). Cette attitude a été rendue nécessaire par l’absence de paramètres hémodynamiques permettant de prédire fidèlement l’efficacité du remplissage. Historiquement, les paramètres évaluant la précharge cardiaque (droite ou gauche) avaient été préconisés pour guider le remplissage vasculaire. La pression veineuse centrale (PVC), comme la pression artérielle pulmonaire d’occlusion, ont été montrées insuffisamment fiables pour prédire le bénéfice hémodynamique du remplissage vasculaire (3, 4). Les dimensions ventriculaires ne le sont pas davantage (5, 6). Si l’efficacité de l’expansion volémique reste vraisemblable pour les valeurs très basses de précharge parfois rencontrées chez les patients non encore réanimés (7), l’attitude basée sur l’analyse des marqueurs statiques de précharge cardiaque est peu recommandable, une fois passées les toutes premières heures de la réanimation hémodynamique.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: A difference in warfarin binding by liver tissue of Sprague-Dawley and warfarin-resistant rats has been localized in the membranous portion of the endoplasmic reticulum. In the presence of deoxycholate, the warfarin binding proteins co-sedimented through 2 M sucrose with the polysomal fraction. By using differences in warfarin binding as a criterion of purity, these binding proteins were isolated by chromatography on DEAE-cellulose of KCl extracts of polysomes derived from the two strains of rats. The warfarin binding protein isolated from Sprague-Dawley rats was half-saturated at 8 μM warfarin and bound 0.7 mol of warfarin/mol of protein at saturation. The corresponding protein from warfarin-resistant rats did not saturate at levels of 30 μM warfarin and bound only 0.1 mol of warfarin/mol of protein. The molecular weight of the binding protein from normal and warfarin resistant rats was each 32,000 by sodium dodecyl sulfate-gel electrophoresis. Maximum warfarin binding by the protein from normal rats occurred at 37° at pH 7.3 in the presence of 200 mM KCl. [14C]Warfarin binding was inhibited by unlabeled warfarin, phylloquinone, and tryptic digestion. The (S)-enantiomer of warfarin was the preferred ligand. On the basis of these data it is likely that this protein is the warfarin receptor protein which mediates the effect of the drug on prothrombin synthesis. The yield of the receptor protein was 1.9 mg/kg of liver from both strains of rat.
    Journal of Biological Chemistry 10/1977; 252(18):6260-7. · 4.60 Impact Factor