Nirmalan M, Willard T, Edwards D J, Dark P, Little R A
MRC Trauma Group University of Manchester, University of Manchester, Oxford Road, Manchester M13 9PT, UK.
Br J Anaesth. 2003 Aug;91(2):224-32. doi: 10.1093/bja/aeg167.
The temporal evolution of lung injury following post-traumatic shock is poorly understood. In the present study we have tested the hypothesis that manifestations of pulmonary vascular dysfunction may be demonstrable within the first hour after the onset of shock.
Twenty-nine anaesthetized pigs (mean weight 27.4 kg; (SD) 3.2) were randomly allocated to three groups: control (C, n=9), shock resuscitated with either NaCl 0.9% (S, n=10), or 4% gelatine (G, n=10). Shock was maintained for 1 h followed by fluid resuscitation with either normal saline or 4% gelatine solution. Cardiac output (CO), mean arterial pressure (MAP), mixed venous saturation (Sv(O(2))), blood lactate concentration, mean pulmonary artery pressure (MPAP), MPAP/MAP, pulmonary vascular resistance (PVR), extravascular lung water index (EVLWi), Pa(O(2))/FI(O(2)), venous admixture (Q(.)(S)/Q(.)(T)), and dynamic lung compliance (C(dyn)) were measured at baseline, beginning of shock phase, end of shock phase, and post-resuscitation.
At the end of volume resuscitation CO was restored to control values in both shock groups. MAP remained significantly below control values (95% CI: C=70-95, S=28-52, G=45-69 mm Hg) in both shock groups. MPAP/MAP was significantly greater in both shock groups at the end of the shock phase (95% CI; C=0.15-0.24, S=0.28-0.38, G=0.32-0.42) and at the post-resuscitation phase (95% CI: C=0.12-0.30, S=0.43-0.61, G=0.32-0.49) indicating the presence of relative pulmonary hypertension. This was associated with a significant increase in PVR in Group S (F=3.9; P<0.05). There were no significant changes in Pa(O(2))/FI(O(2)), Q(.)(S)/Q(.)(T), EVLWi, or C(dyn). In a small cohort of animals a measurable increase in EVLWi (>30%) and reduction in C(dyn) (>10%) were observed.
Pulmonary vascular injury manifesting as relative pulmonary hypertension and increased PVR may occur within the first hour after the onset of shock. These changes may not be accompanied by overt changes in oxygenation, compliance, or EVLWi. Br J Anaesth 2003; 91: 224-32
创伤后休克后肺损伤的时间演变尚不清楚。在本研究中,我们检验了这样一个假设,即休克发作后第一小时内可能可证明肺血管功能障碍的表现。
29只麻醉猪(平均体重27.4 kg;标准差3.2)随机分为三组:对照组(C,n = 9)、用0.9%氯化钠复苏的休克组(S,n = 10)或用4%明胶复苏的休克组(G,n = 10)。维持休克1小时,然后用生理盐水或4%明胶溶液进行液体复苏。在基线、休克期开始、休克期末和复苏后测量心输出量(CO)、平均动脉压(MAP)、混合静脉血氧饱和度(Sv(O₂))、血乳酸浓度、平均肺动脉压(MPAP)、MPAP/MAP、肺血管阻力(PVR)、血管外肺水指数(EVLWi)、Pa(O₂)/FI(O₂)、静脉血掺杂(Q̇(S)/Q̇(T))和动态肺顺应性(C(dyn))。
在容量复苏结束时,两个休克组的CO均恢复到对照值。两个休克组的MAP仍显著低于对照值(95%置信区间:C = 70 - 95,S = 28 - 52,G = 45 - 69 mmHg)。在休克期末(95%置信区间;C = 0.15 - 0.24,S = 0.28 - 0.38,G = 0.32 - 0.42)和复苏后阶段(95%置信区间:C = 0.12 - 0.30,S = 0.43 - 0.61,G = 0.32 - 0.49),两个休克组的MPAP/MAP均显著升高,表明存在相对性肺动脉高压。这与S组PVR的显著增加相关(F = 3.9;P < 0.05)。Pa(O₂)/FI(O₂)、Q̇(S)/Q̇(T)、EVLWi或C(dyn)无显著变化。在一小群动物中,观察到EVLWi有可测量的增加(>30%)和C(dyn)有降低(>10%)。
休克发作后第一小时内可能发生表现为相对性肺动脉高压和PVR增加的肺血管损伤。这些变化可能不伴有氧合、顺应性或EVLWi的明显变化。《英国麻醉学杂志》2003年;91:224 - 32