Santhirapala Vatshalan, Williams Louisa C, Tighe Hannah C, Jackson James E, Shovlin Claire L
Imperial College School of Medicine, Imperial College, London, United Kingdom; National Heart and Lung Institute (NHLI) Cardiovascular Science, Imperial College, London, United Kingdom; Respiratory Medicine, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London, United Kingdom.
Respiratory Medicine, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London, United Kingdom.
PLoS One. 2014 Mar 17;9(3):e90777. doi: 10.1371/journal.pone.0090777. eCollection 2014.
Oxygen, haemoglobin and cardiac output are integrated components of oxygen transport: each gram of haemoglobin transports 1.34 mls of oxygen in the blood. Low arterial partial pressure of oxygen (PaO2), and haemoglobin saturation (SaO2), are the indices used in clinical assessments, and usually result from low inspired oxygen concentrations, or alveolar/airways disease. Our objective was to examine low blood oxygen/haemoglobin relationships in chronically compensated states without concurrent hypoxic pulmonary vasoreactivity.
165 consecutive unselected patients with pulmonary arteriovenous malformations were studied, in 98 cases, pre/post embolisation treatment. 159 (96%) had hereditary haemorrhagic telangiectasia. Arterial oxygen content was calculated by SaO2 x haemoglobin x 1.34/100.
There was wide variation in SaO2 on air (78.5-99, median 95)% but due to secondary erythrocytosis and resultant polycythaemia, SaO2 explained only 0.1% of the variance in arterial oxygen content per unit blood volume. Secondary erythrocytosis was achievable with low iron stores, but only if serum iron was high-normal: Low serum iron levels were associated with reduced haemoglobin per erythrocyte, and overall arterial oxygen content was lower in iron deficient patients (median 16.0 [IQR 14.9, 17.4]mls/dL compared to 18.8 [IQR 17.4, 20.1]mls/dL, p<0.0001). Exercise tolerance appeared unrelated to SaO2 but was significantly worse in patients with lower oxygen content (p<0.0001). A pre-defined athletic group had higher Hb:SaO2 and serum iron:ferritin ratios than non-athletes with normal exercise capacity. PAVM embolisation increased SaO2, but arterial oxygen content was precisely restored by a subsequent fall in haemoglobin: 86 (87.8%) patients reported no change in exercise tolerance at post-embolisation follow-up.
Haemoglobin and oxygen measurements in isolation do not indicate the more physiologically relevant oxygen content per unit blood volume. This can be maintained for SaO2 ≥78.5%, and resets to the same arterial oxygen content after correction of hypoxaemia. Serum iron concentrations, not ferritin, seem to predict more successful polycythaemic responses.
氧气、血红蛋白和心输出量是氧运输的综合组成部分：每克血红蛋白在血液中运输1.34毫升氧气。动脉血氧分压（PaO2）和血红蛋白饱和度（SaO2）低是临床评估中使用的指标，通常是由于吸入氧浓度低或肺泡/气道疾病所致。我们的目的是研究在无并发低氧性肺血管反应性的慢性代偿状态下低血氧/血红蛋白的关系。
对165例连续入选的肺动静脉畸形患者进行研究，其中98例在栓塞治疗前后进行研究。159例（96%）患有遗传性出血性毛细血管扩张症。动脉血氧含量通过SaO2×血红蛋白×1.34/100计算。
在空气中SaO2有很大差异（78.5 - 99，中位数95）%，但由于继发性红细胞增多症及由此导致的红细胞增多，每单位血容量中SaO2仅解释动脉血氧含量变化的0.1%。低铁储备时可出现继发性红细胞增多，但前提是血清铁处于高正常水平：低血清铁水平与每个红细胞血红蛋白减少有关，缺铁患者的总体动脉血氧含量较低（中位数16.0[四分位间距14.9，17.4]毫升/分升，而18.8[四分位间距17.4，20.1]毫升/分升，p<0.0001）。运动耐量似乎与SaO2无关，但在血氧含量较低的患者中明显更差（p<0.0001）。一个预先定义的运动组的血红蛋白：SaO2和血清铁：铁蛋白比值高于运动能力正常的非运动员。肺动静脉畸形栓塞术可提高SaO2，但随后血红蛋白下降可精确恢复动脉血氧含量：86例（87.8%）患者在栓塞后随访时报告运动耐量无变化。
单独的血红蛋白和血氧测量并不能表明每单位血容量中更具生理相关性的氧含量。对于SaO2≥78.5%可维持该氧含量，低氧血症纠正后会重置为相同的动脉血氧含量。似乎是血清铁浓度而非铁蛋白可预测更成功的红细胞增多反应。
