Niinikoski J
Ann Clin Res. 1977 Jun;9(3):151-6.
Tissue hypoxia is an essential feature in the pathophysiology of hypovolaemic shock. In traumatized patients gross injury and haemorrhage may induce both general and local oxygen deficiency. Prolonged hypoxia can induce irreversible changes in tissues, inhibit wound healing, and increase susceptibility to infection. Correction of cardiac index and arterial PO2 does not necessarily ensure a normal tissue PO2, and therefore, arterial oxygen tension provides an inadequate index of peripheral tissue oxygenation. There are two methods currently available for clinical measurements of tissue gases: 1) mass spectrometry, and 2) tonometry with an implanted silicone rubber tube. These methods have shown that the tissue PO2 levels provide an excellent index of peripheral perfusion. During periods of experimentally induced low cardiac output, tissue PO2 decreases almost proportionally to decreases in cardiac output, whereas tissue PCO2 increases slightly. In experimental animals correction of short-term hypovolaemia restores tissue oxygen tensions to normal. However, in patients with multiple injury and hypovolaemic shock the tissue PO2 remains depressed for several days, despite the elevation of cardiac index above normal levels after extensive resuscitation. The poor tissue PO2 response, despite increased arterial PO2, clearly places the majority of the obstacle to oxygen delivery at the microcirculatory-cellular level.
组织缺氧是低血容量性休克病理生理学的一个基本特征。在创伤患者中，严重损伤和出血可导致全身和局部缺氧。长时间的缺氧可导致组织发生不可逆变化，抑制伤口愈合，并增加感染易感性。心脏指数和动脉血氧分压的纠正并不一定能确保组织氧分压正常，因此，动脉氧分压作为外周组织氧合指标并不充分。目前有两种临床测量组织气体的方法：1）质谱分析法，2）使用植入硅胶管的张力测定法。这些方法表明，组织氧分压水平是外周灌注的一个极佳指标。在实验诱导的心输出量降低期间，组织氧分压几乎与心输出量的降低成比例下降，而组织二氧化碳分压略有升高。在实验动物中，短期低血容量的纠正可使组织氧张力恢复正常。然而，在多发伤和低血容量性休克患者中，尽管经过大量复苏后心脏指数升高至正常水平以上，但组织氧分压仍会持续降低数天。尽管动脉氧分压升高，但组织氧分压反应不佳，这清楚地表明，氧输送的主要障碍存在于微循环 - 细胞水平。
