From the Department of Anesthesiology, University of Maryland School of Medicine, Divisions of Trauma Anesthesiology and Critical Care Medicine, R Adams Cowley Shock Trauma Center, Baltimore, Maryland.
The Bizard Institute, Queen Mary University, London, United Kingdom.
Anesth Analg. 2021 Jul 1;133(1):68-79. doi: 10.1213/ANE.0000000000005552.
Vasopressor use in severely injured trauma patients is discouraged due to concerns that vasoconstriction will worsen organ perfusion and result in increased mortality and organ failure in hypotensive trauma patients. Hypotensive resuscitation is advocated based on limited data that lower systolic blood pressure and mean arterial pressure will result in improved mortality. It is classically taught that hypotension and hypovolemia in trauma are associated with peripheral vasoconstriction. However, the pathophysiology of traumatic shock is complex and involves multiple neurohormonal interactions that are ultimately manifested by an initial sympathoexcitatory phase that attempts to compensate for acute blood loss and is characterized by vasoconstriction, tachycardia, and preserved mean arterial blood pressure. The subsequent hypotension observed in hemorrhagic shock reflects a sympathoinhibitory vasodilation phase. The objectives of hemodynamic resuscitation in hypotensive trauma patients are restoring adequate intravascular volume with a balanced ratio of blood products, correcting pathologic coagulopathy, and maintaining organ perfusion. Persistent hypotension and hypoperfusion are associated with worse coagulopathy and organ function. The practice of hypotensive resuscitation would appear counterintuitive to the goals of traumatic shock resuscitation and is not supported by consistent clinical data. In addition, excessive volume resuscitation is associated with adverse clinical outcomes. Therefore, in the resuscitation of traumatic shock, it is necessary to target an appropriate balance with intravascular volume and vascular tone. It would appear logical that vasopressors may be useful in traumatic shock resuscitation to counteract vasodilation in hemorrhage as well as other clinical conditions such as traumatic brain injury, spinal cord injury, multiple organ dysfunction syndrome, and vasodilation of general anesthetics. The purpose of this article is to discuss the controversy of vasopressors in hypotensive trauma patients and advocate for a nuanced approach to vasopressor administration in the resuscitation of traumatic shock.
血管加压素在严重创伤患者中的使用受到抑制,因为担心血管收缩会恶化器官灌注,并导致低血压创伤患者的死亡率和器官衰竭增加。低血压复苏是基于有限的数据而提倡的,这些数据表明较低的收缩压和平均动脉压将导致死亡率降低。经典的理论认为,创伤后低血压和低血容量与外周血管收缩有关。然而,创伤性休克的病理生理学是复杂的,涉及多种神经激素相互作用,最终表现为最初的交感神经兴奋期,试图补偿急性失血,其特征是血管收缩、心动过速和平均动脉血压正常。在失血性休克中观察到的随后的低血压反映了交感抑制性血管扩张期。低血压创伤患者血流动力学复苏的目标是通过平衡的血液制品比例恢复足够的血管内容量,纠正病理性凝血功能障碍,并维持器官灌注。持续的低血压和低灌注与更严重的凝血功能障碍和器官功能障碍有关。低血压复苏的做法似乎与创伤性休克复苏的目标相悖,并且没有一致的临床数据支持。此外,过度的容量复苏与不良的临床结果有关。因此,在创伤性休克的复苏中,有必要在血管内容量和血管张力之间达到适当的平衡。似乎合乎逻辑的是,血管加压素在创伤性休克复苏中可能有用,可以对抗出血引起的血管扩张以及其他临床情况,如创伤性脑损伤、脊髓损伤、多器官功能障碍综合征和全身麻醉的血管扩张。本文的目的是讨论血管加压素在低血压创伤患者中的争议,并提倡在创伤性休克复苏中对血管加压素给药采取细致入微的方法。