Michaelis G, Biscoping J, Sälzer A, Hempelmann G
Abteilung Anaesthesiologie und Operative Intensivmedizin Klinikum der Justus-Liebig-Universität Giessen.
Anasth Intensivther Notfallmed. 1988 Apr;23(2):102-8.
In two groups - eleven patients each - who underwent long lasting surgical procedures, arterial oxygen saturation was measured non-invasively (pulse oximeter) and invasively (CO-oximeter). In addition, total haemoglobin (THb), fractions of haemoglobin (metHb) and bloodgases were monitored. All patients of group I received an epidural anaesthesia via catheter with prilocaine combined with general anaesthesia. In group II a modified neurolept analgesia (balanced) was performed. As expepted we found a prilocaine-induced methaemoglobinaemia (metHb up to 11.6 Vol%) whereas in group II physiological values were not exceeded. Carboxyhaemoglobin up to 4 Vol% was found in the smokers of both groups, which decreased continuously - in contrast to metHb - during hyperoxic ventilation. Comparing the non-invasively and the invasively determined saturations no correlation (r = -0.002) was found in group I. However, a positive correlation (r = 0.652) was obtained in group II. After correction of SaO2 (pulse oximeter) using an adjusted formula a fair correlation (0.613) was found in group I, too. Using this equation for correction the correlation in group II increased to r = 0.824. Because of methodological facts (the pulse oximeter registers only desoxygenated haemoglobin) the arterial oxygen desaturation (O2Hb or fractional saturation) accompanying dyshaemoglobinaemia remains undetectable to the pulse oximeter. In the cases of known or expected dyshaemoglobinaemia pulse oximetry can yield only limited information; fractions of inactive haemoglobin should be measured by other means or accounted for by the given equation for correction (SaO2 corr. = SaO2 pulse oximeter - (COHb + metHb]. Pathophysiological effects of dyshaemoglobinaemia are discussed.
在两组各有11名患者接受长时间外科手术的过程中，采用无创（脉搏血氧仪）和有创（一氧化碳血氧仪）方式测量动脉血氧饱和度。此外，还监测了总血红蛋白（THb）、血红蛋白各组分（高铁血红蛋白（metHb））和血气。第一组所有患者通过导管接受含丙胺卡因的硬膜外麻醉并联合全身麻醉。第二组采用改良的神经安定镇痛（平衡麻醉）。正如预期的那样，我们发现丙胺卡因引起高铁血红蛋白血症（高铁血红蛋白高达11.6容积%），而第二组的生理值未被超过。两组吸烟者中均发现碳氧血红蛋白高达4容积%，与高铁血红蛋白不同，在高氧通气期间其含量持续下降。比较第一组无创和有创测定的饱和度，未发现相关性（r = -0.002）。然而，第二组获得了正相关（r = 0.652）。使用调整公式校正脉搏血氧仪测定的血氧饱和度（SaO2）后，第一组也发现了良好的相关性（0.613）。使用该方程进行校正后，第二组的相关性提高到r = 0.824。由于方法学原因（脉搏血氧仪仅记录脱氧血红蛋白），脉搏血氧仪无法检测到高铁血红蛋白血症伴随的动脉血氧饱和度降低（氧合血红蛋白（O2Hb）或分数饱和度）。在已知或预期有高铁血红蛋白血症的情况下，脉搏血氧测定只能提供有限的信息；应通过其他方法测量非活性血红蛋白组分，或用给定的校正方程计算（SaO2校正值 = 脉搏血氧仪测定的SaO2 - （碳氧血红蛋白 + 高铁血红蛋白））。文中讨论了高铁血红蛋白血症的病理生理效应。
