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

－170－IL5Department of Pulmonary and Critical care medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul,KoreaYounsuck KohAcute respiratory distress syndrome（ARDS）is a permeability pulmonary edema characterized by refractory hypoxemiatogether with severely decreased respiratory system compliance. The revised ARDS definition presents a severity-orientedmethod for respiratory management of ARDS. Right diagnosis is the first step for better outcome by initiating requiredtreatments in earlier stage of ARDS, because most ARDS patients die of multi-organ failure rather than irreversible respiratoryfailure. Management of modifiable risk factors of ARDS development and the avoidance of aggravating factors its severityprogression, such as nonprotective mechanical ventilation, multiple blood product transfusions, positive fluid balance, ventilatorassociatedpneumonia, and gastric aspiration, should be carefully addressed. Up to now, the efficacy of low dose corticosteroidsfor the alleviation of inflammation, to reduce organ dysfunction, and to improve survival, especially in sepsis associated ARDS,has not been fully elucidated. A 48 h of paralysis by using a neuromuscular blockade in early stage of severe ARDS improvedthe outcome in terms of 90-day survival and total ventilation time. Appropriate less sedation approach in mechanically ventilatedpatients is highly recommended to improve outcome. The ventilator strategies should be different depending on the patient’sseverity and pathologic phase. High driving pressure to attain a desire tidal volume is frequently required because of decreasedrespiratory-system compliance in ARDS. The stress to injured alveloli is exaggerated in nonhomogenous alveoli such as ARDS.Limiting strain and stress through low tidal volume（6 mL per Kg of predicted body weight）and limitation of plateau pressureunder optimal PEEP（less than 28 cm H2O of peak airway pressure）has been a current guideline to set ventilator support inARDS. In a refractory hypoxemic patient in exudative phase of ARDS, decremental PEEP trial after ARM or prone ventilationcan be considered. Other adjunctive measures to reduce level of stress and alveolar strain include high frequency oscillation andveno-venous extracorporeal membrane oxygenation（ECMO）. The ECMO applied in the experienced centers seems to improvesurvival of severe ARDS patients.招聘講演 5 2月13日（土）　14：40～15：30　第4会場What we should concern in ARDS treatmentIL6Critical Care Medicine, Bioengineering, Cardiovascular Disease, Clinical & Translational Disease and Anesthesiology,Department of Critical Care Medicine, University of Pittsburgh And Department of Anesthesiology, University of California,San Diego, USAMichael R. PinskyThe goals of hemodynamic monitoring are multiple, including identification of cardiovascular deterioration, diagnosis and monitorresponse to therapy. Within the context of guiding resuscitation therapies, static hemodynamic variables are singularly notuseful for decision making. The combined clinical literature to date support the concept that traditional static measures of leftventricular（LV）preload, such as right atrial pressure（Pra）, pulmonary artery occlusion pressure（Ppao）, right ventricular（RV）end-diastolic volume（EDV）or LV end-diastolic area（EDA）do not predict well volume responsiveness across any group ofcritically ill patients（1）. Furthermore, neither Pra nor Ppao reflect well their respective ventricle’s EDV, nor do changes ineither pressure reflect changes in either EDV or stroke volume. Static measures of Pra and Ppao do not take into accountpericardial pressure to calculate a true transmural pressure（2）. However, if during fluid resuscitation, Pra increases rapidly（>2mmHg）fluid infusion should be stopped and RV function reassessed, as this is a marker of impending cor pulmonale（3）.Measures of RV EDV are inaccurate if tricuspid regurgitation is present, and LV EDA often does not reflect LV EDV. Still,even if RV or LV EDV were accurately known, these estimates would still be poor predictors of preload responsiveness.Clearly, patients with heart failure with preserved ejection fraction（diastolic dysfunction）, the most common form of heartfailure, have small ventricles but are not responsive to fluid loading whereas patients with large ventricles can be volumeresponsiveness. Still, if fluid resuscitation does increase EDV, then by the Starling mechanism stroke volume does increase involume responsive patients. The reasons for this apparent paradox is that Starling mechanisms work on a beat-to-beat basis,whereas steady state changes in stroke volume over minutes reflects changes in intrinsic contractility（4）. Thus, preload cannotbe equated with preload-responsiveness. The probable reason why all these estimates of LV preload are such poor predictors offluid responsiveness is that they are poor estimates of the wrong parameter. Functional hemodynamic monitoring accepts thisreality and uses small reversible volume loading challenges to see if cardiac output will change. If it does not change, then thatsubject is not preload responsiveness, even if filling pressures and ventricular volumes are decreased. And if it does changethen that subject is preload responsive even if filling pressure and ventricular volumes are increased. Once a subject has beenidentified as either preload responsive or no-responsive, then specific therapies can be used with confidence that rely on these招聘講演 6 2月13日（土）　14：40～15：30　第5会場Using hemodynamic monitoring to diagnose and treat critical illness