Sympathetic overstimulation during critical illness: adverse effects of adrenergic stress.
Sympathetic overstimulation during critical illness: adverse effects of adrenergic stress.
复制标题
DOI：
10.1177/0885066609340519
复制
发表时间：
2009-09-01
影响因子：
3.1
通讯作者：
Hasibeder, Walter R
中科院分区：
文献类型：
--
作者：
Dunser, Martin W;Hasibeder, Walter R
“肾上腺素能的”这一术语源自“肾上腺素”，用于描述其作用与肾上腺素相似的激素或药物。肾上腺素能应激是通过肾上腺素能受体的刺激以及受体后通路的激活来介导的。危重病是交感神经系统的一种强烈刺激因素。不可否认的是，由肾上腺素能驱动的“战斗或逃跑反应”是一种在生理上有意义的反应，使人类在进化过程中得以生存。然而，在危重病中，交感神经系统的过度刺激在时间和范围上可能远远超过其有益作用。与脓毒症期间过度的免疫反应类似，危重病中的肾上腺素能应激可能失控并导致不良影响。几个器官系统可能会受到影响。心脏似乎最容易受到交感神经过度刺激的影响。有害影响包括舒张功能受损、心动过速和快速性心律失常、心肌缺血、心肌顿抑、细胞凋亡和坏死。在其他器官也观察到了儿茶酚胺的不良影响，比如肺部（肺水肿、肺动脉压升高）、凝血系统（高凝状态、血栓形成）、胃肠道（灌注不足、蠕动抑制）、内分泌系统（催乳素、甲状腺素和生长激素分泌减少）以及免疫系统（免疫调节、细菌生长刺激）和代谢（细胞能量消耗增加、高血糖、分解代谢、脂肪分解、高乳酸血症、电解质变化）、骨髓（贫血）和骨骼肌（细胞凋亡）。减少过度肾上腺素能应激的潜在治疗选择包括体温和心率控制、合理使用镇静/镇痛药物、设定合理的心血管目标、适当的液体治疗、使用左西孟旦、氢化可的松或补充精氨酸加压素。
The term ''adrenergic'' originates from ''adrenaline'' and describes hormones or drugs whose effects are similar to those of epinephrine. Adrenergic stress is mediated by stimulation of adrenergic receptors and activation of post-receptor pathways. Critical illness is a potent stimulus of the sympathetic nervous system. It is undisputable that the adrenergic-driven ''fight-flight response'' is a physiologically meaningful reaction allowing humans to survive during evolution. However, in critical illness an overshooting stimulation of the sympathetic nervous system may well exceed in time and scope its beneficial effects. Comparable to the overwhelming immune response during sepsis, adrenergic stress in critical illness may get out of control and cause adverse effects. Several organ systems may be affected. The heart seems to be most susceptible to sympathetic overstimulation. Detrimental effects include impaired diastolic function, tachycardia and tachyarrhythmia, myocardial ischemia, stunning, apoptosis and necrosis. Adverse catecholamine effects have been observed in other organs such as the lungs (pulmonary edema, elevated pulmonary arterial pressures), the coagulation (hypercoagulability, thrombus formation), gastrointestinal (hypoperfusion, inhibition of peristalsis), endocrinologic (decreased prolactin, thyroid and growth hormone secretion) and immune systems (immunomodulation, stimulation of bacterial growth), and metabolism (increase in cell energy expenditure, hyperglycemia, catabolism, lipolysis, hyperlactatemia, electrolyte changes), bone marrow (anemia), and skeletal muscles (apoptosis). Potential therapeutic options to reduce excessive adrenergic stress comprise temperature and heart rate control, adequate use of sedative/analgesic drugs, and aiming for reasonable cardiovascular targets, adequate fluid therapy, use of levosimendan, hydrocortisone or supplementary arginine vasopressin.