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

－164－IL2Critical 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. PinskyFunctional Hemodynamic Monitoring is the assessment of the dynamic interactions of hemodynamic variables in response to adefined perturbation［1］. Such dynamic responses result in emergent parameters of these commonly reported variables, suchas arterial pulse pressure and stroke volume variation during positive pressure breathing or transient increases in cardiacoutput in response to passive leg raising or interruption of positive pressure breathing［2］,Predicting volume responsivenessA primary question asked in the management of a patient in shock is whether or not the patient will increase their cardiacoutput in response to intravascular volume infusion. Volume responsiveness has been arbitrarily defined as a ? 15% in cardiacoutput in response to a 500 ml bolus fluid challenge［3］. Michard et al. documented that the dynamic variations in arterial pulsepressure during positive-pressure breathing（8 ml/kg）when averaged over at least 3 breaths, referred to as pulse pressurevariation（PPV）, accurately predicts which patients would be volume responsive［3］. For a detailed review of the evolution ofPPV as a monitoring tool over this 14 year interval the reader is referred to a recent review on this topic［4］. The physiologicbasis for this phenomena is the positive-pressure ventilation induced cyclic changes in right atrial pressure（Pra）as it ispassively increased by the increasing intrathoracic pressure（ITP）, owing to lung distention. Importantly, all the differentmeasures including not only PPV, but also LV stroke volume variation（SVV）, changes in inferior and superior vena cavaediameters, systolic pressure variation and pulse oximeter pleth density variation are based on fundamental physiologicalprinciples underlying heart-lung interactions. And all have been documented to be robust predictors of volume responsiveness［5］.The physiologic basis for these parameters follows. During the inspiratory phase of positive pressure ventilation, intrathoracicpressure increases passively increasing right atrial pressure causing venous return to decrease, decreasing right ventricular（RV）output, and after two or three heart beats, LV output, if both RV and LV are volume responsive［3］. Thus, in preloaddependent patients cyclic changes in LV stroke volume and its coupled arterial pulse pressure are seen and the magnitude ofthe changes is proportional to volume responsiveness. The actual calculation of PPV and SVV from the commercially availableminimally-invasive monitoring devices quantified these two parameters in various ways（e.g. PiCCO, LiDCO, FloTrac）. Ingeneral both PPV and SVV are defined as the ratio of the maximal minus the minimal values to the mean values, usuallyaveraged over 3 or more breaths. We showed that increasing the sampling window to include at least 5 breaths minimizingsampling error in estimating both PPV and SVV［6］. Since all commercially-available devices reporting PPV and SVV use asampling window of 15-20 second, they all incorporate this into their measure. Numerous studies have documented that a SVV>10% or a PPV> 13-15% on a tidal volume of 8 ml/kg or greater is highly predictive of volume responsiveness［3,7,8］. Clearly,changes in tidal volume, chest wall compliance and contractility will all affect these measures［9］. When ventilation includesspontaneous breathing or irregular heartbeats, PPV and SVV become inaccurate. Still, one study in septic shock patients showedthat if the threshold values for PPV were increase to >15% the test still predicted volume responsiveness in spontaneouslybreathing patients［10］. Also, PPV remains predictive in elderly patients with varying degrees of diastolic heart failure［11］.Still, caution needs to be used wen interpreting these parameters when spontaneous breathing efforts are exaggerated. Onedebate that has arisen comes from the interpretation of PPV or SVV values in the “grey zone’ of 10-15%. Since many patientsare ventilated with low tidal volumes and may also be vasodilated due to general anesthesia, such values often exist. Lakhal etal.［12］underscored that reality in their study of intraoperative patients with presumed hypovolemia. They found thatincreasing the threshold values to >23% markedly increased the positive predictive value of these test to identify volumeresponders. Under these conditions either a volume challenge or a passive leg raising（PLR）maneuver to assess dynamicincreases in cardiac output can be done［13］. Thus, the bedside clinician has the option to examine real-time PPV or SVVduring positive-pressure breathing or the dynamic changes in cardiac output in response to a PLR maneuver in assessing fluidresponsiveness without the need to give a fluid bolus. A clear example of using PLR to guide fluid therapy in a difficult patientwas recently presented as a case conference［14］Since the perturbation causing these cyclic changes in flow is dependent of the cyclic changes in intrathoracic pressure, tidalvolume, a major determinant of changes in intrathoracic pressure, needs to be great enough to alter central venous pressure.Thus, tidal volumes of ? 6 ml/kg decrease the sensitivity but not specificity of this parameter［9,15］. Similarly, in the presenceof intra-abdominal hypertension, chest wall compliance is markedly decreased. This must alter venous return and blood flowdistribution. Still, PPV and SVV remain sensitive and specific if tidal volume is maintained［16,17］. However, intra-abdominalhypertension does reduce the sensitivity of the passive leg raising（PLR）test to identify volume responsiveness［18］,presumably because intra-abdominal hypertension increases during the PLR maneuver altering unstressed blood volume［18］.Although PPV can be computed at the bedside by direct analysis of the arterial pressure waveform signal［3］and by personalsoftware analysis of such signals［19］most clinicians use commercially-available minimally-invasive monitoring devices that招聘講演 2 2月12日（金）　10：00～10：50　第5会場Physiological basis for functional hemodynamic monitoring