Whyte M K, Hughes J M, Peters A M, Ussov W, Patel S, Burroughs A K
Department of Medicine, Imperial College School of Medicine, Hammersmith Hospital, London, UK.
J Hepatol. 1998 Jul;29(1):85-93. doi: 10.1016/s0168-8278(98)80182-7.
BACKGROUND/AIMS: Severe hypoxaemia in patients with chronic liver disease in the absence of intrinsic lung disease, the hepatopulmonary syndrome, is associated with pulmonary vascular dilatation and may be an indication for liver transplantation. Divergence between two methods of measuring right to left shunt (radiolabelled albumin macroaggregates and 100% oxygen breathing) has been described, but the mechanism and reason for the inter-patient variability for this shunt difference are not well understood.
Eight hepatopulmonary syndrome patients were studied, with characteristic pulmonary diffusion abnormalities (carbon monoxide transfer factor 41+/-5 (mean+/-SE)% predicted) and significant decreases in arterial oxygen saturation (%) on standing vs. supine (-10%+/-3) and on exercise vs. rest (-15%+/-2). All had hypoxaemia at rest (arterial oxygen tension 8.2+/-0.6 kPa), partially corrected by breathing 100% oxygen (48.2+/-8.8 kPa). Pulmonary angiography was performed and right to left shunt measured by two independent methods: (a) 100% oxygen breathing and (b) i.v. injection of radiolabelled microspheres.
Measurement of right to left shunt with 99mTc-labelled albumin macroaggregates confirmed significant intrapulmonary microvascular dilatation, i.e. an "anatomical" shunt equalling 32+/-4% of cardiac output. Shunt measurements made simultaneously by the classical 100% oxygen technique were significantly smaller (19+/-3%, p=0.01). For individuals, the difference between the 99mTc-albumin macroaggregate shunt and the 100% oxygen shunt ranged from 2% to 30% absolute, convergence suggesting larger shunt channels (pure anatomical shunt) and divergence representing a combination of anatomical shunt and alveolar-capillary diffusion limitation (smaller microvascular channels).
Hypoxaemia in the hepatopulmonary syndrome may be due functionally either to right to left shunting or to diffusion limitation, depending upon the degree of dilatation of the pulmonary microvessels.
背景/目的：慢性肝病患者在无内在肺部疾病（即肝肺综合征）时出现的严重低氧血症与肺血管扩张有关，可能是肝移植的指征。已有研究描述了两种测量右向左分流的方法（放射性标记白蛋白大聚合体和吸入100%氧气）之间的差异，但对于这种分流差异在患者间变异性的机制和原因尚未完全了解。
对8例肝肺综合征患者进行研究，这些患者具有典型的肺弥散异常（一氧化碳弥散量为预测值的41±5（均值±标准误）%），且站立位与仰卧位相比（-10%±3）、运动时与静息时相比（-15%±2）动脉血氧饱和度（%）显著下降。所有患者静息时均存在低氧血症（动脉血氧分压8.2±0.6 kPa），吸入100%氧气后可部分纠正（48.2±8.8 kPa）。进行了肺血管造影，并通过两种独立方法测量右向左分流：（a）吸入100%氧气；（b）静脉注射放射性标记微球。
用99mTc标记的白蛋白大聚合体测量右向左分流证实存在显著的肺内微血管扩张，即“解剖学”分流相当于心输出量的32±4%。采用经典的100%氧气技术同时测量的分流明显较小（19±3%，p = 0.01）。对于个体而言，99mTc - 白蛋白大聚合体分流与100%氧气分流之间的差异绝对值在2%至30%之间，两者趋同表明存在较大的分流通道（纯解剖学分流），两者背离则代表解剖学分流与肺泡 - 毛细血管弥散受限（较小的微血管通道）的组合。
肝肺综合征中的低氧血症在功能上可能是由于右向左分流或弥散受限，这取决于肺微血管的扩张程度。
