臨床外科英語翻譯:休克(1)

Shock (1)

休克(1)

Shock is a state of organ hypoperfusion with resultant cellular dysfunction and death. Mechanisms may involve decreased circulating volume, decreased cardiac output, and vasodilation, sometimes with shunting of blood to bypass capillary exchange beds. Symptoms include altered mental status, tachycardia, hypotension, and oliguria. Diagnosis is clinical, including BP measurement. Treatment is with IV fluids, correction of underlying disorder, and sometimes vasopressors.

休克是因器官灌注不足，導致細胞機能障礙和死亡的一種狀態(tài)。休克生理機制涉及循環(huán)容量減少、心排量降低和血管擴張，有時伴血液分流，繞過毛細管交換床。癥狀包括精神狀態(tài)改變、心動過速、低血壓和少尿。臨床診斷包括量血壓。治療采靜脈輸液、糾正潛在疾病，有時使用血管升壓類藥物。

Pathophysiology

病理生理學

The fundamental defect in shock is reduced perfusion of vital tissues. Once perfusion declines so that O2 is inadequate for aerobic metabolism, cells shift to anaerobic metabolism with increased production of CO2 and accumulation of lactic acid. Cellular function declines, and if shock persists, irreversible cell damage and death occur.

休克的主要問題是生命組織灌注的減少。一旦組織灌注減少，細胞有氧代謝所需的氧氣就會不足，轉入無氧代謝，致使二氧化碳和乳酸積累壓增加，細胞功能下降。持續(xù)休克時就會發(fā)生不可逆的細胞損害和死亡。

During shock, both the inflammatory and clotting cascades may be triggered in areas of hypoperfusion. Hypoxic vascular endothelial cells activate WBCs, which bind to the endothelium and release directly damaging substances (eg, proteolytic enzymes) and inflammatory mediators (eg, cytokines, leukotrienes, tumor necrosis factor [TNF]). Some of these mediators bind to cell surface receptors and activate nuclear factor kappa B (NFκB), which leads to production of additional cytokines and also nitric oxide (NO), a potent vasodilator. Septic shock may be more proinflammatory than other forms because of the actions of bacterial toxins, especially endotoxin.

休克期間，可在組織灌注不足部位引發(fā)炎癥性和凝血性連鎖反應。低氧血管上皮細胞激活WEC，粘附在內皮上，直接釋放出破壞性物質（如蛋白水解酶)和炎癥介質（如細胞活素、白三烯、腫瘤壞死因子[TNF])。有些介質與細胞表面受體結合，活化核因子卡巴B(NFkB)，造成細胞活素和氧化亞氮（NO)生產增多。NO有強烈的血管擴張效果。由于細菌毒素的作用，尤其是內毒素，敗血癥性休克的促炎癥性反應強于其他休克。

Vasodilation of capacitance vessels leads to pooling of blood and hypotension because of “relative” hypovolemia (ie, too much volume to be filled by the existing amount of blood). Localized vasodilation may shunt blood past the capillary exchange beds, causing focal hypoperfusion despite normal cardiac output and BP. Additionally, excess NO is converted to peroxynitrite, a free radical that damages mitochondria and decreases ATP production.醫(yī)學全在線www.med126.com

容量血管擴張導致血液瘀積和因血容量“相對”減少（即現(xiàn)有血量充盈過度)而形成的低血壓，局部血管擴張使血液從毛細管交換床分流，造成局部血流灌注不足，但心排量和血壓均正常。此外，過多的NO被轉化成可破壞線粒體、降低APT生產的游離基――過亞硝酸鹽。

Blood flow to microvessels including capillaries is reduced even though large-vessel blood flow is preserved in settings of septic shock. Mechanical microvascular obstruction may, at least in part, account for such limiting of substrate delivery. Leukocytes and platelets adhere to the endothelium, and the clotting system is activated with fibrin deposition.

敗血癥性休克發(fā)作時，即使大血管血流未受影響，但微血管包括毛細管的血流卻減少了。微血管的機械性阻塞，至少可以部分說明酶解物輸送的受限原因。粒細胞和血小板粘附于內皮，凝血系統(tǒng)得以激活，纖維素沉積。

Multiple mediators, along with endothelial cell dysfunction, markedly increase microvascular permeability, allowing fluid and sometimes plasma proteins to escape into the interstitial space. In the GI tract, increased permeability possibly allows translocation of the enteric bacteria from the lumen to the blood stream, potentially leading to sepsis or metastatic infection.

多種介質，再加上內皮細胞功能障礙，明顯增加了微血管的滲透性，使液體及血漿蛋白溢入細胞間隙。胃腸道滲透性的增加致使腸道細菌易位，由腔體進入血流，并可能導致敗血癥或代謝性感染。

Neutrophil apoptosis may be inhibited, enhancing the release of inflammatory mediators. In other cells, apoptosis may be augmented, increasing cell death and thus worsening organ function.

嗜中性粒細胞的吞噬作用被抑制，炎癥介質釋放得到加強。也增強了其他細胞的吞噬作用，細胞死亡增多，從使器官功能惡化。

BP is not always low in the early stages of shock (although hypotension eventually occurs if shock is not reversed). Similarly, not all patients with “l(fā)ow” BP have shock. The degree and consequences of hypotension vary with the adequacy of physiologic compensation and the patient's underlying diseases. Thus, a modest degree of hypotension that is well tolerated by a young, relatively healthy person might result in severe cerebral, cardiac, or renal dysfunction in a patient with significant arteriosclerosis.

休克初期，血壓并不總是很低的（盡管休克若不被逆轉，最終會發(fā)生低血壓)。同樣，并不是所有的“低”血壓病人都會休克。低血壓程度及其后果與生理代償是否充足及病人潛在疾病有關。因此，相對健康的年輕人可以忍受的輕度低血壓若發(fā)生在嚴重動脈硬化者向上，就可能導致嚴重的腦、心、或腎功能障礙。

Compensation: Initially, when O2 delivery (DO2) is decreased, tissues compensate by extracting a greater percentage of delivered O2. Current guidelines provide for interventions that will maintain mixed-venous O2 saturation above 30%. Additionally, low arterial pressure triggers an adrenergic response with sympathetic-mediated vasoconstriction and often increased heart rate. Initially, vasoconstriction is selective, shunting blood to the heart and brain. Circulating β-adrenergic amines (epinephrine, norepinephrine) also increase cardiac contractility and trigger release of corticosteroids from the adrenal gland, renin from the kidney, and glucose from the liver. Increased glucose may overwhelm ailing mitochondria, causing further lactate production.

代償：一開始，當輸氧（DO2)減少，組織通過增加氧氣提取量得到代償�，F(xiàn)有指南提供了一些措施，它可以使混合靜脈氧氣飽和度保持在30%以上。而且，低動脈壓觸發(fā)腎上腺素能反應，導致交感神經介導性血管收縮，常會使心率加快。開始時，血管收縮是選擇性的，血液被分流到心臟和大腦。循環(huán)系統(tǒng)中的β腎上腺素能胺（腎上腺素、去甲腎上腺素)也會增加心肌收縮性，觸發(fā)腎上腺釋放皮質激素，腎臟釋放腎素，肝臟釋放葡萄糖。葡糖增加可壓制虛弱的線粒體，導致乳酸鹽的進一步分泌。

Reperfusion: Reperfusion of ischemic cells can cause further injury. As substrate is reintroduced, neutrophil activity may heighten, increasing production of damaging superoxide and hydroxyl radicals. After blood flow is restored, inflammatory mediators may be circulated to other organs.

再灌注：缺血細胞再灌注可造成進一步傷害。再次導入酶解物，嗜中性細胞活動增強，增加破壞性超氧游離基和羥基的生產。血流恢復后，炎癥介質可能被循環(huán)到其他器官部位。

Multiple organ dysfunction syndrome (MODS): The combination of direct and reperfusion injury may cause MODS—the progressive dysfunction of 2 or more organs consequent to life-threatening illness or injury. MODS can follow any type of shock but is most common when infection is involved; organ failure is one of the defining features of septic shock. MODS also occurs in > 10% of patients with severe traumatic injury and is the primary cause of death in those surviving > 24 h.

多器官功能障礙綜合征（MODS)：直接損傷與再灌注損傷結合在一起就可能造成MODS――某個致命性疾病或損傷引起兩個或多個器官的進行性功能障礙。任何一種休克后都可發(fā)生MODS，但以感染型最常見，器官衰竭是敗血癥性休克的典型特征之一。10%以上的嚴重外傷病人也會得MODS，它也是存活＞24小時病人死亡的主要原因。

Any organ system can be affected, but the most frequent target organ is the lung, in which increased membrane permeability leads to flooding of alveoli due to capillary leaks. Progressive hypoxia may be increasingly resistant to supplemental O2 therapy. This condition is termed acute lung injury or, if severe, acute respiratory distress syndrome (ARDS).

可累及任何器官系統(tǒng)，最常見的靶器官有肺，肺膜滲透性增加導致毛細管滲漏，造成肺泡溢水。漸進性缺氧可逐步增強對補氧療法的阻力，這種情況被稱為急性肺損傷，嚴重時則為急性呼吸窘迫綜合征（ARDS)

The kidneys are injured when renal perfusion is critically reduced, leading to acute tubular necrosis and renal insufficiency manifested by oliguria and progressive rise in serum creatinine.

腎灌注嚴重減少則傷腎，導致急性腎小管壞死和腎機能不全，表現(xiàn)為少尿和血清肌酸酐的不斷上升。

In the heart, reduced coronary perfusion and mediators (including TNF and IL-1) may depress contractility, worsen myocardial compliance, and down-regulate β-receptors. These factors decrease cardiac output, further worsening both myocardial and systemic perfusion and causing a vicious circle often culminating in death.

若涉及心臟，冠狀動脈灌注減少和介質減少（包括TNF和IL－1)可抑制血管收縮性，心肌順應性變差，β受體功能下降。這些因素又會減少心排量，進一步惡化心肌和系統(tǒng)灌注，造成惡性循環(huán)，最終導致死亡。

The GI tract can develop ileus and submucosal hemorrhage. Liver hypoperfusion can produce focal or extensive hepatocellular necrosis, transaminase elevation, and decreased production of clotting factors.

胃腸道會發(fā)展成腸梗阻和粘膜下出血，肝臟灌注不足可產生局部性或廣泛性肝細胞壞死、轉氨酶升高及凝血因子產量減少。