shock

Japanese: ショック

Definition/Concept Shock is a condition in which tissue and organ cell function is impaired due to systemic circulatory disorder caused by some cause, and is a clinical syndrome that exhibits abnormalities in biological functions. While it is reversible in the early stages, if it persists it can become an irreversible systemic disease, leading to multiple organ failure and death. For this reason, it is essential to carry out early diagnosis and treatment appropriately and promptly.
In particular, shock remains a serious issue in the clinical setting of acute myocardial infarction. Even if early reperfusion of the infarcted myocardium is successful using catheter treatment, 50% of patients lose their shock in the CCU if they are unable to escape. This is a situation that we are still unable to escape from (Stegman et al., 2012).
The main sign of shock is a drop in blood pressure. Blood pressure is determined by cardiac output and peripheral vascular resistance, and homeostasis is maintained through the regulation of these two. In other words, blood pressure drops when cardiac output decreases, when peripheral vascular resistance decreases, or when both decrease. First, the cause of the drop in blood pressure must be identified, and early definitive intervention must be carried out.
Classification Shock can be broadly classified into 1) hypovolemic, 2) cardiogenic, 3) vaso-occlusive, and 4) blood distribution imbalance based on hemodynamic characteristics (Table 5-3-6). It can also be classified into stages I to III based on clinical severity (Teba et al., 1992) (Table 5-3-7).
1) Hypovolemic shock:
Causes include trauma, ruptured aortic aneurysm, gastrointestinal bleeding, bleeding due to surgery, severe pancreatitis, intestinal obstruction, diarrhea, vomiting, and burns. Loss of circulating blood volume or plasma volume reduces cardiac preload and leads to inadequate ventricular filling, resulting in reduced cardiac output and peripheral circulatory failure. Reactive sympathetic tone causes peripheral blood vessels to constrict. With a loss of 15% or less of circulating blood volume, blood pressure is maintained, but tachycardia occurs and pulse pressure decreases. With a loss of 20% or more, blood pressure falls, the skin turns pale, and cyanosis appears. The peripheral tissues suffer from circulatory failure. A loss of 40% or more is fatal.
2) Cardiogenic shock:
Impairment of the cardiac pumping function reduces cardiac output, resulting in peripheral circulatory failure. Reactive sympathetic nervous tone constricts peripheral blood vessels. Causes include myocardial contractile dysfunction and rhythm disorders. Mechanisms include: 1) a decrease in stroke volume due to a decrease in left ventricular contractility, 2) a decrease in heart rate, 3) a decrease in stroke volume due to a decrease in end-diastolic volume caused by tachycardia, and 4) a decrease in stroke volume due to a decrease in preload caused by right ventricular failure. Diseases include acute myocardial infarction, acute myocarditis, mitral regurgitation due to papillary muscle rupture, ventricular septal perforation, cardiac rupture, arrhythmia, dilated cardiomyopathy, and postoperative low cardiac output syndrome. Cardiogenic shock requires rapid diagnosis and treatment as the clinical course is rapid.
3) Vascular obstructive shock:
Peripheral circulatory failure occurs due to physical obstruction of the main blood flow. Examples of diseases that can cause this include pulmonary thromboembolism, cardiac tamponade, tension pneumothorax, left atrial myxoma, and supine hypotension syndrome caused by compression of the inferior vena cava by a pregnant uterus. It is necessary to release the obstruction that is causing the problem.
4) Distributive shock:
The above abnormalities are not observed, and shock occurs due to abnormal blood distribution. The main causes of the drop in blood pressure are 1) a decrease in systemic vascular resistance, 2) increased vascular permeability, and 3) a decrease in stroke volume due to a decrease in preload caused by dilation of the venous system. Other causes include sepsis, anaphylaxis, and neurogenic shock.
In septic shock, various mediators (endotoxins, cytokines) are produced by bacteria (mainly Gram-negative bacteria) or bacterial components that have entered the bloodstream from the infection focus, which activates ATP-sensitive K channels in vascular smooth muscle and enhances nitric oxide (NO) production, causing peripheral vasodilation, resulting in a decrease in effective circulating blood volume and a drop in blood pressure. In the early stages, the patient experiences a high cardiac output, which is known as warm shock. However, if the shock state continues, plasma components leak out of the blood vessels due to vascular endothelial damage. Furthermore, peripheral circulatory failure causes acidosis due to enhanced lactate production. This reduces cardiac output, resulting in a state known as cold shock. As the condition worsens, disseminated intravascular coagulation (DIC) and acute respiratory distress syndrome (ARDS) occur, leading to multiple organ failure.
Anaphylactic shock occurs due to a decrease in effective circulating blood volume caused by vasodilation and plasma leakage, primarily due to a type I allergic reaction. Other systemic symptoms include laryngeal edema, airway smooth muscle contraction, and hives. Causative antigens include drugs and foods such as buckwheat, while direct acting substances include contrast agents, antibiotics, and narcotics. Neurogenic shock occurs when the sympathetic nervous system is suppressed or blocked, impairing nerve control of blood vessels, causing sudden blood vessel expansion and a decrease in effective circulating blood volume. Causes include transverse spinal cord injury, overdosing on sympathetic nerve suppressants, and cerebral herniation.
Stage I:
Compensated shock In the early stages of shock, the body employs compensatory mechanisms to maintain blood flow to vital organs such as the brain, heart, and kidneys. The patient remains conscious, with a slight drop in blood pressure, tachycardia, and tachypnea.
Phase II:
Decompensated shock: Due to insufficient compensatory response, organ perfusion is reduced. This can also lead to impaired consciousness, hypotension, and oliguria.
Stage III:
Irreversible shock
Sustained organ hypoperfusion leads to cellular necrosis and progressive multiple organ failure. Severe complications include disseminated intravascular coagulation and acute tubular necrosis.
Clinical symptoms: Signs and symptoms of decreased organ function due to a drop in blood pressure are observed. Common clinical symptoms include the 5p signs: pallor, perspiration, prostration, pulselessness, and pulmonary deficiency.
Diagnosis and Treatment If the systolic blood pressure is 90 mmHg or less, first determine whether or not the patient is in shock. In a state of shock, symptoms and signs due to organ hypoperfusion are observed. Vital signs (state of consciousness, blood pressure, pulse rate, respiratory rate, temperature), urine volume, skin findings, and peripheral circulation are monitored. Specifically, a clinical severity classification (Teba et al., 1992) (Table 5-3-7) and a shock score calculation method (Kanai et al., 2001) (Table 5-3-8) have been proposed. A total shock score of 4 or less is not considered shock, 5 to 10 is considered moderate, and 11 or more is considered severe. Since improvement of the state of shock and a detailed investigation of the cause are required immediately, treatment and diagnosis are carried out simultaneously. As emergency measures, airway and vascular access are immediately secured. For respiratory management, oxygen is administered, switching to NIPPV and, if necessary, artificial respirator management is performed. Pain is relieved with morphine or other medications. Medical history should include any history of heart disease or allergies, previous blood pressure values, medications taken, history of chest pain, shortness of breath, palpitations, etc., whether the patient has had hematemesis, bloody stool, diarrhea, abdominal pain, etc., possible infection, trauma, burns, or pregnancy. Tests should include blood and urine biochemistry tests, arterial blood gas analysis, 12-lead electrocardiogram, echocardiogram, and chest X-ray. If necessary, X-ray CT and CMR (cardiovascular magnetic resonance) tests should also be performed.
Treatment by cause
1) Hypovolemic shock:
It is important to evaluate the circulating blood volume, and parameters include the left ventricular end-diastolic diameter and the inferior vena cava diameter. This is evaluated using an echocardiogram. The left ventricular end-diastolic diameter is a reliable volume index, but caution is required as there are individual differences. The standard value is 40 to 55 mm. The standard value for the inferior vena cava diameter is around 10 mm, but if it completely collapses during inspiration, it can be determined that the circulating blood volume is insufficient. In tricuspid regurgitation, the inferior vena cava diameter expands, so caution is required. If a central venous catheter is placed, the central venous pressure can be measured. The standard value is 5 to 10 cmH ₂ O, but it is better to judge based on changes in pressure over time. If a Swan-Ganz catheter is placed, the pulmonary artery wedge pressure can also be measured. In addition, mixed venous oxygen saturation can be measured, which is an indicator of peripheral circulatory failure. Using the above as indicators, fluid infusion and blood transfusions are administered, and the cause of the loss of circulating blood volume is given priority.
2) Cardiogenic shock:
If the condition is accompanied by acute myocardial infarction, emergency reperfusion therapy using a cardiac catheter is performed. Mechanical disorders such as acute mitral regurgitation due to papillary muscle rupture, left ventricular free wall rupture, and ventricular septal perforation require emergency surgical treatment. If the cause is arrhythmia, electrical defibrillation or a pacemaker is indicated. If shock is due to low cardiac output caused by myocarditis or dilated cardiomyopathy, catecholamines or phosphodiesterase (PDE) III inhibitors are used. If drug therapy does not improve hemodynamics, an auxiliary circulatory device called intra-aortic balloon pumping (IABP) is used. However, IABP is contraindicated in patients with aortic regurgitation and dissecting aortic aneurysm. Furthermore, if the effect is insufficient, the use of a percutaneous cardiopulmonary support (PCPS) or a left ventricular assist device should be considered. Systemic therapeutic hypothermia has also been attempted. Cardiac index and pulmonary artery occlusion pressure are assessed using a Swan-Ganz catheter, and the severity is assessed according to the Forrester classification (Figure 5-3-12) (Hayakawa et al., 2006). If the patient is in Subset II, diuretics and vasodilators are administered, and if the patient is in Subset III, fluid infusion is performed. If the patient is in Subset IV, in addition to diuretics and vasodilators, they are treated with inotropes and circulatory support devices, with the aim of progressing to Subset I as quickly as possible (Stegman et al., 2012; Topalian et al., 2008; Reynolds et al., 2008).
3) Vascular obstructive shock:
Many diseases present with sudden onset, so rapid diagnosis and treatment are necessary. The basis of treatment is to relieve the underlying obstruction. That is, in the case of cardiac tamponade, pericardial drainage should be performed as soon as possible, and in the case of tension pneumothorax, thoracic drainage should be performed as soon as possible.
4) Distributive shock:
In the early stages of septic shock, vascular resistance decreases due to vasodilation and arteriovenous shunts, and the skin appears warm and dry (warm shock). As the condition progresses, vascular resistance increases, peripheral circulatory failure becomes prominent, and the condition progresses to cold shock. If surgical removal of the source of infection is possible, the infected focus should be actively removed, bacterial tests such as blood cultures should be performed frequently, and antibiotics sensitive to the causative bacteria should be administered. Endotoxin adsorption therapy using polymyxin B immobilized columns has been attempted to treat endotoxin. Circulatory failure is treated with fluid infusion and administration of catecholamines.
In anaphylactic shock, it is essential to secure the airway, administer oxygen, and improve circulatory failure. If there is airway narrowing due to laryngeal edema or airway smooth muscle contraction, adrenaline is injected intramuscularly. In asthma attacks, aminophylline or steroids are administered. Circulatory failure is treated with fluid infusion and catecholamines. If a substance causing shock is being used, it should be discontinued immediately. Neurogenic shock requires treatment of the circulatory failure and the cause. Circulatory failure is treated with fluid infusion and dopamine. Atropine sulfate and adrenaline are effective for bradycardia. If shock persists, treatment of the cause is necessary. [Izumi Tohru]
■ References
Reynolds HR, Hochman JS: Cardiogenic Shock Current Concepts and Improving Outcomes. Circulation, 117: 686-697, 2008.
Stegman BM, Newby LK, et al: MD Post-Myocardial Infarction Cardiogenic Shock, Is a Systemic Illness in Need of Systemic Treatment. J Am Coll Cardiol, 59: 644–647, 2012.
Teba L, Banks DE, et al: Understanding circulatory shock. Postgrad Med, 91: 121-129, 1992.
Topalian S, Ginsberg F, et al: Cardiogenic shock. Crit Care Med, 36 (Suppl): S66–74, 2008.

Table 5-3-6
Shock Classification ">

Table 5-3-6

Table 5-3-7
Clinical Severity Classification ">

Table 5-3-7

Table 5-3-8
Shock score ">

Table 5-3-8

Fig. 5-3-12
Forrester Classification ">

Figure 5-3-12

Source : Internal Medicine, 10th Edition About Internal Medicine, 10th Edition Information

Japanese:

定義・概念
　ショックとは，何らかの原因により全身性の循環障害が起こったため，組織や臓器細胞機能低下を生じた状態であり，生体機能の異常を呈する臨床症候群である．早期では可逆性であるが遷延すれば不可逆性な全身疾患となり，多臓器不全から死に至る．このため，初期診断と治療を適切かつ迅速に行うことが肝要である．
　特に，急性心筋梗塞の臨床ではいまなおショックが重い課題となっている．たとえ，カテーテル治療により梗塞心筋への早期再灌流療法に成功したとしてもショックから脱することができないとその患者の50％をCCUで失っている．この現状からいまなお抜け出せずにいる（Stegmanら，2012）．
　ショックの主徴候は血圧低下にある．血圧は心拍出量と末梢血管抵抗により規定されており，その調節によりホメオスターシスが維持される．つまり，心拍出量が減少するか，末梢血管抵抗が低下するか，あるいは両者が低下した場合に血圧は低下する．まず，血圧低下の原因を明らかにし，早期の根治的介入を目指す．
分類
　ショックは血行動態的特徴から，①循環血液量減少性，②心原性，③血管閉塞性，④血液分布不均衡性に大別できる（表5-3-6）．また，臨床的重症度分類（Tebaら，1992）して，第Ⅰ期～第Ⅲ期に分類できる（表5-3-7）．
1）循環血液量減少性ショック（hypovolemic shock）：
原因としては，外傷や大動脈瘤破裂，消化管出血，手術による出血や重症膵炎，腸閉塞，下痢，嘔吐，熱傷などによる．循環血液量あるいは血漿量の喪失により心臓の前負荷が軽減し，心室充満が不十分となり，その結果，心拍出量が低下し，末梢循環不全を生じる．反応性の交感神経緊張により末梢血管は収縮する．　循環血液量の15％以下の喪失では，血圧は保たれているが，頻脈となり脈圧は減少する．20％以上の喪失で，血圧は低下し，皮膚は蒼白となり，チアノーゼが出現する．末梢組織は循環不全に陥っている．40％以上の喪失は致死的である．
2）心原性ショック（cardiogenic shock）：
心臓のポンプ機能障害により，心拍出量が低下し，末梢循環不全を生じる．反応性の交感神経緊張により末梢血管は収縮する．原因としては，心筋の収縮不全や調律不全がある．機序としては，①左心収縮力の低下による1回拍出量の低下，②心拍数の低下，③頻脈による拡張末期容量の減少に伴う1回拍出量の低下，④右心不全による前負荷減少に伴う1回拍出量の低下，があげられる．疾患では，急性心筋梗塞や急性心筋炎，乳頭筋断裂による僧帽弁閉鎖不全，心室中隔穿孔，心破裂，不整脈，拡張型心筋症や術後低心拍出量症候群などがあげられる．心原性ショックは，急激な臨床経過をとるため迅速な診断と治療を要する．
3）血管閉塞性ショック（obstructive shock）：
主血流の物理的な閉塞により，末梢循環不全を生じる．疾患として，肺血栓塞栓症や心タンポナーデ，緊張性気胸，左房粘液腫，妊娠子宮による下大静脈の圧迫によって生じる臥位低血圧症候群などがあげられる．原因となる閉塞を解除することが必要である．
4）血液分布不均衡性ショック（distributive shock）：
上記の異常は認めず，血液分布の異常によって生じるショックである．①体血管抵抗の減少，②血管透過性の亢進，③静脈系の拡張による前負荷減少に伴う1回拍出量の低下，が血圧低下の主因である．原因としては，敗血症やアナフィラキシー，神経性ショックなどがあげられる．
　敗血症性ショックは感染巣より血中に流入した細菌（おもにGram陰性菌）あるいは菌体成分により種々のメディエーター（エンドトキシン，サイトカイン）が産生され，血管平滑筋のATP感受性Kチャネルの活性化，一酸化窒素（NO）の産生亢進などにより末梢血管の拡張が起こり，有効循環血液量の低下をきたし血圧は低下する．初期は高心拍出量状態でいわゆるwarm shockであるが，ショック状態が持続すると，血管内皮障害により血管外へ血漿成分が漏出する．さらに末梢循環不全により乳酸の産生亢進によるアシドーシスが加わる．そのため心拍出量は低下しいわゆるcold shockとなる．重症化してくると，播種性血管内凝固症（disseminated intravascular coagulation：DIC）や急性呼吸促迫症候群（acute respiratory distress syndrome：ARDS）を引き起こし，さらに多臓器不全に陥る．
　アナフィラキシーショックは，Ⅰ型アレルギー反応を主とする血管拡張と血漿漏出による有効循環血液量の減少によって生じる．そのほかに喉頭浮腫や気道平滑筋収縮，じんま疹など全身症状が認められる．原因抗原としては，薬物やそばなど食物があり，直接作用するものとして造影剤や抗菌薬，麻薬などがあげられる．　神経原性ショックは，交感神経系が抑制または遮断されたことにより，血管への神経支配が障害され，血管が急激に拡張し，有効循環血液量の減少を生じるために起こる．原因としては，脊髄横断損傷や交感神経抑制薬の過剰投与，脳ヘルニアなどがあげられる．
第Ⅰ期：
代償性ショック（compensated shock）　ショック初期において人体は，脳や心臓，腎臓などの重要臓器への血流を維持しようとする代償機構が働く．意識は清明であり，血圧は軽度低下，頻脈，頻呼吸を認める．
第Ⅱ期：
非代償性ショック（decompensated shock）　代償反応が不十分のため，臓器灌流低下が認められる．そのため，意識障害や低血圧，乏尿も認める．
第Ⅲ期：
非可逆的ショック（irreversible shock）
　臓器灌流低下が持続したことによって，細胞壊死が生じ，多臓器不全が進行する．播種性血管内凝固症や急性尿細管壊死などの重篤な合併症が認められる．
臨床症状
　血圧低下に基づく臓器機能の低下や症状・徴候が認められる．一般的な臨床症状として，蒼白（pallor），冷汗（perspiration），虚脱（prostration），脈拍触知不能（pulselessness），呼吸不全（pulmonary deficiency）の5p徴候が知られている．
診断・治療
　収縮期血圧が90 mmHg以下であった場合，ショックか否かをまず診断する．ショック状態では臓器低灌流による症状や徴候が認められる．バイタルサイン（意識状態，血圧，脈拍，呼吸数，体温）や尿量，皮膚所見，末梢循環を把握する．具体的には，臨床的重症度分類（Tebaら，1992）（表5-3-7）やショックスコア算定法（金井ら，2001）（表5-3-8）が提唱されている．ショックスコアでは合計点が4以下ではショックではなく，5～10では中等度，11以上では重症のショックと判定する．　ショック状態の改善と原因精査が直ちに必要なため，治療と診断を同時に進める．救急処置として気道確保や血管確保を直ちに行う．呼吸管理としては酸素投与を行い，NIPPVに切り替え，必要であれば人工呼吸器管理を行う．疼痛はモルヒネなどにより緩和させる．　病歴聴取として，心疾患の既往やアレルギーの有無，以前の血圧値，服用薬物，胸痛・息切れ・動悸などの既往の有無，吐血・下血・下痢・腹痛などの有無，感染症の可能性の有無，外傷・熱傷・妊娠の有無などを聴取する．　検査としては，血液や尿の生化学検査，動脈血液ガス分析，12誘導心電図，心エコー図，胸部Ｘ線撮影を行う．必要であれば，X線CTやCMR（cardiovascular magnetic resonance）検査も行う．
原因別治療
1）循環血液量減少性ショック（hypovolemic shock）：
循環血液量の評価が重要であり，パラメーターとして左室拡張末期径，下大静脈径がある．心エコー図を用いて評価する．左室拡張末期径は容積指標として信頼性があるが，個人差があるので注意が必要である．標準値は40～55 mmである．下大静脈径は標準値は10 mm前後であるが，吸気時に完全に虚脱するようであれば，循環血液量が不足していると判断してよい．三尖弁閉鎖不全では下大静脈径が拡張するので，注意を要する．中心静脈カテーテルを留置すれば，中心静脈圧が測定可能となる．標準値は5～10 cmH₂Oであるが，圧の経時的変化で判断したほうがよい．Swan-Ganzカテーテルを留置すれば，肺動脈楔入圧も測定できる．さらに，混合静脈血酸素飽和度も測定でき，末梢循環不全の指標となる．以上を指標にしながら，輸液や輸血を行い，循環血液量が喪失している原因治療を優先させる．
2）心原性ショック（cardiogenic shock）：
急性心筋梗塞に伴う場合は，緊急に心臓カテーテルによる再灌流療法を施行する．乳頭筋断裂による急性僧帽弁閉鎖不全症や左室自由壁破裂，心室中隔穿孔などの機械的障害は緊急の外科的治療が必要となる．また，不整脈が原因である場合は，電気的除細動やペースメーカの適応となる．心筋炎や拡張型心筋症などによる低心拍出量によるショックであれば，カテコールアミンやホスホジエステラーゼ（PDE）Ⅲ阻害薬を用いる．薬物療法で血行動態の改善が得られない場合，補助循環装置である大動脈内バルーンパンピング（intra-aortic balloon pumping：IABP）を用いる．ただし，IABPは，大動脈弁閉鎖不全症や，解離性大動脈瘤では禁忌である．さらに，効果が不十分のときは，経皮的心肺補助装置（percutaneous cardiopulmonary support：PCPS）の併用や左心補助装置（left ventricular assist device）の適応を検討する．全身低体温療法（systemic therapeutic hypothermia）も試みられている．　Swan-Ganzカテーテルを用いて心係数および肺動脈楔入圧を評価し，Forrester分類（図5-3-12）（早川ら，2006）により重症度を評価する．SubsetⅡであれば，利尿薬や血管拡張薬を投与し，SubsetⅢであれば，輸液を行う．SubsetⅣであれば，利尿薬や血管拡張薬に加え，強心薬や補助循環装置を用いて治療し，SubsetⅠの状態に何としても速く移行させることを目指す（Stegmanら，2012；Topalianら，2008；Reynoldsら，2008）．
3）血管閉塞性ショック（obstructive shock）：
急激な病態を呈する疾患が多いため，迅速な診断と治療を要する．治療の基本は原因となる閉塞の解除である．即ち，心タンポナーデであれば心囊ドレナージを，緊張性気胸であれば胸腔ドレナージを可及的速やかに施行する．
4）血液分布不均衡性ショック（distributive shock）：
敗血症性ショックでは，初期に血管拡張や動静脈シャントによって血管抵抗が減少し，皮膚が温かく乾燥した状態（warm shock）を呈する．さらに進行すると，血管抵抗が上昇し，末梢循環不全が顕著化し，cold shockに移行する．感染源は外科的切除が可能な場合は，積極的に感染巣除去を行い，血液培養などの細菌検査を頻回に実施して，起因菌に感受性のある抗生物質を投与する．エンドトキシンに対しては，ポリミキシンB固定化カラムを用いたエンドトキシン吸着療法が試みられている．循環不全は輸液やカテコールアミン投与で対応する．
　アナフィラキシーショックでは，気道の確保と酸素投与，循環不全の改善が必須となる．喉頭浮腫や気道平滑筋収縮により気道狭窄がある場合は，アドレナリンを筋注する．喘息発作ではアミノフィリンやステロイドを投与する．循環不全に対しては輸液やカテコールアミンで対応する．ショックの原因物質を使用していたら直ちに中止する．　神経原性ショックは循環不全への対応と原因に対する対応を要する．循環不全に対しては輸液やドパミンで治療する．徐脈には硫酸アトロピンやアドレナリンが有効である．ショックが持続すれば原因治療を必要とする．［和泉　徹］
■文献
Reynolds HR, Hochman JS: Cardiogenic Shock Current Concepts and Improving Outcomes. Circulation, 117: 686-697, 2008.
Stegman BM, Newby LK, et al: MD Post-Myocardial Infarction Cardiogenic Shock, Is a Systemic Illness in Need of Systemic Treatment. J Am Coll Cardiol, 59: 644–647, 2012.
Teba L, Banks DE, et al: Understanding circulatory shock. Postgrad Med, 91: 121-129, 1992.
Topalian S, Ginsberg F, et al: Cardiogenic shock. Crit Care Med, 36 (Suppl): S66–74, 2008.

表5-3-6
ショックの分類">

表5-3-6

表5-3-7
臨床的重症度分類">

表5-3-7

表5-3-8
ショックスコア">

表5-3-8

図5-3-12
Forrester 分類">

図5-3-12

出典　内科学第10版内科学第10版について　情報

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