ブックタイトル第43回日本集中治療医学会学術集会プログラム・抄録集

概要

第43回日本集中治療医学会学術集会プログラム・抄録集

－166－organ failure and death. However, microcirculation alterations in muscle and skin blood flow already occur in these early stagesand measures of tissue cardiovascular reserve should be a sensitive early warning measure of impending cardiovascular collapse.Thus, a valid method to assess the microcirculatory status such the non-invasive measurement of tissue oxygen saturation（StO2）when coupled to a Functional Hemodynamic Monitoring test, such as the Vascular Occlusion Test（VOT）, may allow earlyidentification of compensated circulatory shock and thus guide initial resuscitation efforts.Non-invasive measurement of StO2 using near-infrared spectroscopy（NIRS）has been shown as a valid method to assess themicrocirculation status, especially in septic and trauma patients. The absolute StO2 value has a limited discriminating capacitybecause StO2 remains within the normal range until shock is quite advanced. But the addition of a dynamic ischemic challengesuch as the VOT, improves and expands the predictive ability of StO2 to identify tissue hypoperfusion［32］. The VOT measuresthe effect of total vascular occlusion-induced tissue ischemia and release on downstream StO2. StO2 is measured on the thenareminence and transient rapid vascular occlusion of the arm by sphygmomanometer inflation to 30 mm Hg above systolicpressure is performed either for a defined time interval, usually 3 min, or until StO2 declines to some threshold minimal value,usually 40%. The deoxygenation rate（DeO2）reflects the local metabolic rate and mitochondrial function, and the rate ofreoxygenation rate（ReO2）reflects local cardiovascular reserve and microcirculatory flow.Microcirculatory failure during shock is a major component of the end-organ dysfunction. Such microcirculatory dysfunction canbe characterized by oxygen shunting, vasoconstriction, thrombosis and tissue edema. The flow distribution within the tissue isimpaired［33］but improves rapidly in septic shock survivors whereas patients dying by organ failure have a lower percentageof perfused small vessels［34］.Creteur et al［35］showed that the alterations in VOT StO2 response are related to the outcome in patients with either severesepsis or septic shock. Furthermore, when comparing to hemodynamically stable patients without infection（controls）andhealthy volunteers, the difference in the septic patients were striking. Using NIRS VOT StO2 they assessed the slope of increasein StO2 release as well as by the difference between the maximum StO2 and the StO2 baseline（Δ）. Both, the slope of ReO2 andthe Δ were significantly lower in septic patients than in controls and healthy volunteers. In the sample of septic patients, theslopes were also significantly lower in the ones who had cardiovascular insufficiency. ReO2 slopes were higher in survivors thanin non-survivors and also tended to increase during resuscitation in survivors but not in non-survivors. Finally, the ReO2 slopewas found to be a good predictor of ICU death, with a cut-off value of 2.55%/sec（sensitivity 85%, specificity 73%）. These dataconfirm that the alterations in VOT StO2 ReO2 are related more to the sepsis process itself and its severity than to meanarterial pressure or vasopressor agent’s dose. Importantly, the magnitude of this ReO2 slope alteration is directly related to theseptic disease and their presence in the first 24 hours of septic process and their persistence of delayed ReO2 slope is related topatient´s outcome. Still, if the StO2 ReO2 does reflect inadequate tissue perfusion then it should also sensitive of an impendingcardiovascular insufficiency state（compensated shock）if matched with other static measures of tissue ischemia.To address this issue further, Mesquida et al.［36］followed the StO2 VOT in septic patients showing that impaired ReO2predicted organ failure. StO2 VOT-derived estimation of cardiovascular stress during a spontaneous breathing trials（increasedDeO2）also identified patients who subsequently failure that trial［37］. Furthermore, Guyette et al.［38］, measured both theVOT StO2 as baseline serum lactate, known to define existing cardiovascular insufficiency in trauma, in a cohort of traumapatients during the air transport to the Trauma Center. The aim of the study was to see if the StO2 measurement, including aVOT, was feasible in the prehospital environment and useful to predict in-hospital death and intensive care unit（ICU）admission. Not surprisingly, they did not find differences in baseline StO2 between survivors, non-survivors and patients admittedto the ICU, they showed significant differences in DeO2 and ReO2 slopes between survivors and non survivors, as well asbetween patients who need ICU admission and patients who did not. Furthermore, only one of the five patient deaths in theirsample had prehospital vitals signs that would have met the protocolized criteria for resuscitation（heart rate >120 bpm,systolic blood pressure < 90 mmHg）. Importantly, serum lactate alone was no better than lowest systolic pressure in predictingthose in need of Life Saving Interventions（LSI）or death, but if the baseline serum lactate was >1.7 mmol/dl the ReO2 was100% specific for the need of LSI. This study shows the usefulness of the microcirculation dynamic assessment in the earlystages of the trauma injury, when the cardiovascular insufficiency is not suspected with the macrocirculatory indexes, providingthe possibility to start early the appropriate treatment and decide the in-hospital disposition.References1. Pinsky MR, Payen D: Functional hemodynamic monitoring. Crit Care 2005, 9:566-572.2. Hadian M, Pinsky MR. Functional hemodynamic monitoring. Curr Opin Crit Care 2007, 13:318-323.3. Michard F, Boussat S, Chemla D, et al. Relation between respiratory changes in arterial pulse pressure and fluidresponsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med 2000, 162:134-138.4. Cannesson M, Ahioy M, Hofer CK, Rehman M. Pulse pressure variation: Where are we today? J Clin Monitor Comput 2011;25:45-56.