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      The impact of inspiratory pressure on stroke volume variation and the evaluation of indexing stroke volume variation to inspiratory pressure under various preload conditions in experimental animals

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          Stroke volume variation (SVV) measures fluid responsiveness, enabling optimal fluid management under positive pressure ventilation. We aimed to investigate the effect of peak inspiratory pressure (PIP) on SVV under various preload conditions in experimental animals and to ascertain whether SVV indexed to PIP decreases the effect.


          Mild and moderate hemorrhage models were created in nine anesthetized, mechanically ventilated beagle dogs by sequentially removing 10 and then an additional 10 ml/kg of blood, respectively. In all the animals, PIP was incrementally increased by 4 cmH 2O, from 5 to 21 cmH 2O. SVV was measured by arterial pulse contour analysis. Stroke volume was derived using a thermodilution method, and central venous pressure and mean arterial pressure were also measured.


          SVV increased according to PIP with significant correlation at baseline, with mild hemorrhage and moderate hemorrhage. PIP regression coefficients at baseline and in the mild and moderate hemorrhage models were 0.59, 0.86, and 1.4, respectively. Two-way repeated-measures analysis of variance showed that PIP and the degree of hemorrhage had a significant interaction effect on SVV ( p = 0.0016). SVV indexed to PIP reflected the hemorrhage status regardless of PIP changes ≥9 cmH 2O.


          PIP is significantly correlated with SVV, even under hypovolemia, and the effect is enhanced with decreasing preload volumes. Compared with SVV, the indexed SVV was less susceptible to higher inspiratory pressures.

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          Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome.

          In patients with the acute respiratory distress syndrome, massive alveolar collapse and cyclic lung reopening and overdistention during mechanical ventilation may perpetuate alveolar injury. We determined whether a ventilatory strategy designed to minimize such lung injuries could reduce not only pulmonary complications but also mortality at 28 days in patients with the acute respiratory distress syndrome. We randomly assigned 53 patients with early acute respiratory distress syndrome (including 28 described previously), all of whom were receiving identical hemodynamic and general support, to conventional or protective mechanical ventilation. Conventional ventilation was based on the strategy of maintaining the lowest positive end-expiratory pressure (PEEP) for acceptable oxygenation, with a tidal volume of 12 ml per kilogram of body weight and normal arterial carbon dioxide levels (35 to 38 mm Hg). Protective ventilation involved end-expiratory pressures above the lower inflection point on the static pressure-volume curve, a tidal volume of less than 6 ml per kilogram, driving pressures of less than 20 cm of water above the PEEP value, permissive hypercapnia, and preferential use of pressure-limited ventilatory modes. After 28 days, 11 of 29 patients (38 percent) in the protective-ventilation group had died, as compared with 17 of 24 (71 percent) in the conventional-ventilation group (P<0.001). The rates of weaning from mechanical ventilation were 66 percent in the protective-ventilation group and 29 percent in the conventional-ventilation group (P=0.005): the rates of clinical barotrauma were 7 percent and 42 percent, respectively (P=0.02), despite the use of higher PEEP and mean airway pressures in the protective-ventilation group. The difference in survival to hospital discharge was not significant; 13 of 29 patients (45 percent) in the protective-ventilation group died in the hospital, as compared with 17 of 24 in the conventional-ventilation group (71 percent, P=0.37). As compared with conventional ventilation, the protective strategy was associated with improved survival at 28 days, a higher rate of weaning from mechanical ventilation, and a lower rate of barotrauma in patients with the acute respiratory distress syndrome. Protective ventilation was not associated with a higher rate of survival to hospital discharge.
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            Changes in arterial pressure during mechanical ventilation.

            Mechanical ventilation induces cyclic changes in vena cava blood flow, pulmonary artery blood flow, and aortic blood flow. At the bedside, respiratory changes in aortic blood flow are reflected by "swings" in blood pressure whose magnitude is highly dependent on volume status. During the past few years, many studies have demonstrated that arterial pressure variation is neither an indicator of blood volume nor a marker of cardiac preload but a predictor of fluid responsiveness. That is, these studies have demonstrated the value of this physical sign in answering one of the most common clinical questions, Can we use fluid to improve hemodynamics?, while static indicators of cardiac preload (cardiac filling pressures but also cardiac dimensions) are frequently unable to correctly answer this crucial question. The reliable analysis of respiratory changes in arterial pressure is possible in most patients undergoing surgery and in critically ill patients who are sedated and mechanically ventilated with conventional tidal volumes.
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              Ventilator-induced injury: from barotrauma to biotrauma.

              Mechanical ventilation is an indispensable tool in the management of respiratory and ventilatory failure. However, ventilation per se may also initiate or exacerbate lung injury, contributing to patient morbidity and mortality. In this review, we examine the current mechanisms of ventilator-induced injury including those that primarily involve physical disruption of the lung, as well as those more recently described that involve cell- and inflammatory-mediator-induced injury. The latter have received attention of late because of the possible systemic sequelae such as multiple system organ failure, the primary cause of death of patients with acute respiratory distress syndrome. Although much remains to be elucidated about the mechanisms of ventilator-induced injury, it is hoped that novel approaches addressing both the physiologic as well as molecular effects of ventilation will lead to innovative therapeutic approaches that improve patient outcome.

                Author and article information

                +81-73-441-0603 ,
                J Anesth
                J Anesth
                Journal of Anesthesia
                Springer Japan (Tokyo )
                15 March 2015
                15 March 2015
                : 29
                : 4
                : 515-521
                [ ]Department of Emergency and Critical Care Medicine, Wakayama Medical University, 811-1, Kimiidera, Wakayama, 641-8510 Japan
                [ ]Department of Advance Clinical Medicine, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, 1-58, Rinku Ohrai Kita, Izumisano, Osaka 598-8531 Japan
                © The Author(s) 2015

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.

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                © Japanese Society of Anesthesiologists 2015


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