Difficulty breathing

Japanese: 呼吸困難

Concept Dyspnea is "a state in which effort is required to breathe and breathing is accompanied by a sense of discomfort." It is a symptom often observed in respiratory and circulatory diseases, and is a major cause of reduced quality of life (QOL) for patients. Patients may complain of a variety of symptoms, including "shortness of breath," "shortness of breath," "suffocation," "not enough air (oxygen)," "effort to breathe," and "difficulty inhaling (exhaling)," and can also be seen as a warning response indicating an abnormality in the body.
Pathophysiology Dyspnea is a sensation that occurs as a result of the overlap of various factors, and in order to interpret its pathology, it is necessary to understand the respiratory control mechanism.
1) Respiratory control mechanism:
Breathing is regulated by the _chemical regulatory system, the neuroregulatory system, and the behavioral regulatory system (Figure 2-31-1). The chemical regulatory system detects changes in arterial blood gases ( _PaO2 , _PaCO2 , pH) via peripheral chemoreceptors and central chemoreceptor fields, and these stimuli are transmitted to the respiratory centers in the brainstem, maintaining arterial blood gases within a certain range, _a so-called negative feedback mechanism. The neuroregulatory system acts via slowly adapting stretch receptors, irritant receptors, C-fiber endings, and muscle spindles in the respiratory muscles that are distributed in the lungs and airways. The behavioral regulatory system influences the respiratory centers from higher centers, and includes the effects on breathing of emotional changes such as excitement, anxiety, and stress, as well as mental tension.
2) Mechanism of respiratory distress:
Dyspnea can be understood as something that is detected when there is a discrepancy between the command to move the respiratory muscles (respiratory motor output or respiratory drive) and the actual length of the respiratory muscles that can move (respiratory muscle mechanics) (length-tension imbalance theory). In other words, dyspnea is likely to occur when the respiratory drive is strong but the respiratory movement is unable to keep up. It can also be explained that dyspnea is the same as the "sense of effort of breathing," and that information of the same strength as the respiratory drive (motor command) from the respiratory center is projected (copied) to the sensory center, causing this increase in respiratory drive to be perceived as dyspnea (motor command theory).
Assessment method Dyspnea is a subjective sensation and is difficult to assess objectively. In actual clinical practice, several assessment methods are used to assess the degree of dyspnea, mainly during exertion.
1)
Fletcher-Hugh-Jones classification (Table 2-31-1): This classification is widely used in clinical settings in Japan because it is simple. It is not an evaluation of dyspnea itself, but rather an indicator of the patient's exercise ability in daily life, so it should be kept in mind that it is easily influenced by factors other than dyspnea.
2) Medical Research Council (MRC) Shortness of Breath Scale:
It is used worldwide as an index for evaluating dyspnea and should be recommended in Japan as well. The original British Medical Research Council shortness of breath scale was used as a questionnaire for patients and was classified into five levels from 1 to 5, but recently the MRC shortness of breath scale, which has been shifted to five levels from 0 to 4, is often used (Table 2-31-2).
3) 6-minute walking test:
This test evaluates the maximum walking distance that a patient can walk in 6 minutes at a speed of their choice. Normally, along with the walking distance, the pre-exercise and minimum exercise values of transcutaneous oxygen saturation (S _p O ₂ ) are also evaluated at the same time. Although it is possible to rest along the way, patients are instructed to walk the maximum distance within the time limit. As with the Fletcher-Hugh-Jones classification, factors other than dyspnea also have an effect. Repeated measurements are useful for assessing the effectiveness of treatment and understanding the clinical course in patients with chronic respiratory disease. Recently, a shuttle walking test has also been performed, in which patients walk back and forth between 9 m markers in time with the tone of a CD.
4) Quantitative evaluation by category (Figure 2-31-2):
There are various scales, such as the Borg scale and visual analog scale (VAS), which allow for objective assessment of the absolute strength of the sensation. The Borg scale determines where the patient's perceived level of dyspnea falls when the degree of dyspnea is divided into approximately 10 categories. It is often used during exercise stress tests. The VAS shows the patient a horizontal line 10 cm (or 15 cm) high, with the left end representing no dyspnea and the right end representing very severe dyspnea, and the patient is asked to mark any point on the line depending on the level of dyspnea they feel. The level of dyspnea is assessed based on the distance from the left end. Both indices are useful for assessing the severity of the condition and the effectiveness of treatment.
Differential diagnosisFirst , determine whether there is an emergency. If so, perform diagnosis and treatment in parallel. The differential diagnosis should be made based on the medical history, physical examination findings, imaging findings, respiratory function, and other test results (Figure 2-31-3).
1) Medical History:
a) Time course of dyspnea: Differentiation should be made based on whether the condition is sudden, acutely progressive, chronic, or recurrent. Causes of sudden dyspnea include dyspnea due to pneumothorax, pulmonary thromboembolism, and acute myocardial infarction. Acute causes include acute left heart failure, bacterial or viral pneumonia, and acute interstitial pneumonia. Chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, and chronic heart failure cause chronically progressive dyspnea, but dyspnea progresses rapidly during acute exacerbations. Dyspnea associated with bronchial asthma and angina pectoris, and hyperventilation syndrome cause repeated paroxysmal dyspnea.
b) Causes of dyspnea:
Worsening during exertion: In most cases, dyspnea symptoms first appear during exertion, and as the condition progresses, dyspnea also appears at rest. It is necessary to differentiate not only respiratory diseases, but also exertional angina, etc.
Exacerbation depending on the time of day: In bronchial asthma, wheezing and dyspnea attacks tend to occur at night or early in the morning.
Exacerbation by posture: Dyspnea worsens in the supine position in patients with congestive heart failure and bronchial asthma, in the lateral position in patients with unilateral pleural effusion, atelectasis, and intratracheal tumors, and in the sitting position in patients with hepatopulmonary syndrome.
c) Accompanying symptoms:
Precordial tightness: angina pectoris, myocardial infarction, etc. Chest pain: pericarditis, pneumonia, pleurisy, pneumothorax, pulmonary embolism, etc. Other factors to note include the presence or absence of fever or cough, and the nature of phlegm.
2) Physical examination findings:
Fast and shallow breathing (decreased compliance of the pulmonary-thoracic system or inability to take a deep breath due to pain): interstitial pneumonia, congestive heart failure, pulmonary thromboembolism, pneumothorax Fast and deep breathing: diabetic ketoacidosis, acute renal failure, hyperventilation syndrome Wheezing and prolonged expiration, pursed lip breathing: obstructive pulmonary diseases such as bronchial asthma and COPD Other important factors to note include auscultatory findings (breath sounds, heart sounds), cyanosis, clubbing, the presence or absence of edema, and deformation of the thorax.
3) Chest imaging findings:
Hyperinflation and increased lung permeability: Emphysematous COPD
Diffuse interstitial shadows, ground-glass opacities, honeycomb lung, and reduced lung fields: pulmonary fibrosis, interstitial pneumonia. Dilation of pulmonary arteries and reduced pulmonary vascular shadows: pulmonary thromboembolism. Butterfly-shaped infiltrates and cardiomegaly: congestive heart failure, pulmonary edema. Other signs to look out for include infiltrates, pleural thickening, pneumothorax, and pleural effusion.
4) Respiratory function test findings:
Restrictive disorders (decreased vital capacity): pulmonary fibrosis, neuromuscular disease Obstructive disorders (decreased forced expiratory volume in 1 second, reduced forced expiratory volume in 1 second): bronchial asthma, chronic obstructive pulmonary disease Pulmonary diffusion disorder (decreased DLco): pulmonary fibrosis, COPD, pulmonary thromboembolism, pulmonary hypertension, anemia In addition, attention should be paid to the presence or absence of hypoxemia, hypercapnia, hypocapnia, and acidosis based on blood gas analysis.
5) Other tests:
The presence or absence of an inflammatory response in blood tests, the presence or absence of myocardial ischemia or right heart overload on an electrocardiogram, evaluation of left heart function by echocardiography, right ventricular dilation, and paradoxical movement of the ventricular septum are also important in differentiating between respiratory distress and other conditions.
Representative diseases
1)
Chronic obstructive pulmonary disease (COPD): If a patient has a history of smoking, has a lot of cough and phlegm, and is aware of chronically progressing dyspnea on exertion, this disease should be suspected and a respiratory function test should be performed. Beer barrel-like chest, pursed lip breathing, and clubbing are often observed. Hypoxemia and hypercapnia are not necessarily present at rest. Even in such cases, dyspnea on exertion is characteristic. The cause is not only hypoxemia on exertion, but also dynamic pulmonary hyperinflation. Since COPD patients have expiratory obstruction, when respiratory output increases during exertion, inspiration begins before sufficient expiration is completed, which leads to exacerbation of pulmonary hyperinflation. Under such circumstances, the diaphragm becomes lower, impeding efficient contraction, which leads to further increase in respiratory output and exacerbation of dyspnea. If dynamic pulmonary hyperinflation is improved, even partially, with bronchodilators or oxygen therapy, dyspnea on exertion will be alleviated.
2)
Pulmonary fibrosis:
Fine crackles are heard at the end of inspiration, and bilateral interstitial shadows are observed on chest X-ray and CT. Due to restrictive obstruction and pulmonary diffusion disorder, hypoxemia at rest and on exertion are prominent. Oxygen administration can reduce dyspnea during exertion.
3)
Bronchial asthma:
Attacks often occur at night or early in the morning or during exercise. Even in the absence of significant hypoxemia, increased airway resistance causes severe dyspnea. Moderate to severe attacks can cause orthopnea.
4)
Acute pulmonary embolism:
It frequently occurs after surgery, when a patient moves after being bedridden for a long period of time, or after a long flight, and often causes sudden dyspnea and is accompanied by chest pain. Obesity and cancer-bearing status are also risk factors. Hypoxemia accompanied by a decrease in _{P a} CO ₂ is observed. When sudden dyspnea and hypoxemia are present and no obvious abnormalities are found in the lung fields on chest X-ray, it is important to suspect this disease as a differential diagnosis.
5) Congestive heart failure, pulmonary edema:
Dyspnea and orthopnea are observed during exertion. Pulmonary congestion and fluid retention in the pulmonary interstitium decrease lung compliance and reduce vital capacity. Pulmonary interstitium edema also causes diffusion disorders, worsening hypoxemia. Furthermore, stimulation of C-fiber terminals causes tachypnea and exacerbates dyspnea. [Kimura Hiroshi]
■ References
American Thoracic Society: Dyspnea. Mechanisms, assessment, and management: a consensus statement. Am J Respir Crit Care Med, 159: 321-340, 1999.
Celli BR W, MacNee W, et al: Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper. Eur Respir J, 23: 932-946, 2004.
Hiroshi Kimura, Takayuki Kuriyama: Shortness of breath, dyspnea. Differential Diagnosis in Internal Medicine, 2nd ed., pp429-438, Asakura Publishing, Tokyo, 2003.

Table 2-31-1
Fletcher-Hugh-Jones classification ">

Table 2-31-1

Table 2-31-2
Medical Research Council (MRC) Shortness of Breath Scale

Table 2-31-2

Figure 2-31-1
Scheme of respiratory control mechanism

Figure 2-31-1

Figure 2-31-2
Differential diagnosis of diseases causing respiratory distress

Figure 2-31-2

Figure 2-31-3
Differential diagnosis of diseases causing respiratory distress

Figure 2-31-3

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

Japanese:

概念
　呼吸困難とは「呼吸をするために努力が必要な状態で，呼吸に伴い不快感を自覚する状態」である．呼吸器疾患や循環器疾患においてしばしば観察される症状であり，患者にとっては生活の質（QOL）を低下させる大きな原因となる．患者の愁訴は，「息苦しい」，「息切れする」，「息が詰まる」，「空気（酸素）が足りない」，「呼吸をするのに努力がいる」，「息が吸いにくい（吐きにくい）」などさまざまであり，生体の異常を示す警告反応ともとらえることができる．
病態生理
　呼吸困難はさまざまな要因が重なり合って出現する感覚であり，その病態の解釈のためには呼吸調節機構の理解が必要である．
1）呼吸調節機構：
呼吸は化学調節系，神経調節系，行動調節系により調節されている（図2-31-1）．化学調節系は，動脈血液ガス（P_aO₂，P_aCO₂，pH）の変化を末梢化学受容器および中枢化学受容野が感知し，それらの刺激が脳幹部の呼吸中枢群へ伝達され動脈血液ガスが一定の範囲に保たれるという，いわゆるネガティブフィードバック機構を有する．神経調節系は，肺・気道系に分布するslowly adapting stretch receptor，イリタント受容器，C線維末端，呼吸筋に分布する筋紡錘を介して作用する．行動調節系は，高位中枢から呼吸中枢群へ影響を与えるものであり，興奮，不安，ストレスなどの感情の変化や精神的緊張による呼吸への影響が含まれる．
2）呼吸困難の発生メカニズム：
呼吸困難は，呼吸筋を運動させようとする指令（呼吸運動出力もしくは呼吸ドライブ）と，実際に可動する呼吸筋の長さ（呼吸筋メカニクス）との間に不一致が生じる際に関知するととらえることができる（長さ-張力不均衡説）．つまり，呼吸ドライブが強いにもかかわらず呼吸運動が追従できないときに呼吸困難が生じやすくなる．また，呼吸困難は「呼吸の努力感」と同一のものであり，呼吸中枢からの呼吸ドライブ（motor command）と同一強度の情報が感覚中枢へ投射（コピー）されることで，この呼吸ドライブの増加を呼吸困難と認識するとも説明される（モーターコマンド説）．
評価法
　呼吸困難は主観的な感覚であり，客観的に評価することは困難である．実際の臨床の現場ではおもに労作時の呼吸困難の程度を評価するため，いくつかの評価法が用いられている．
1）
Fletcher-Hugh-Jones分類
（表2-31-1）：簡便であるため日本では広く臨床の場で用いられている．呼吸困難そのものの評価ではなく，患者の日常生活における運動能力の指標であるため，呼吸困難以外の要因にも影響されやすいことを念頭におくべきである．
2）Medical Research Council（MRC）息切れスケール：
呼吸困難を評価する指標として世界的に使用されており，日本でも推奨されるべきものである．オリジナルのBritish Medical Research Council息切れスケールは患者への質問表として用いられ，１から5の5段階に分類されていたが，最近では0から4の5段階にシフトさせたMRC息切れスケールが使用されることが多い（表2-31-2）．
3）6分間歩行テスト：
患者自身の任意の速度で6分間に歩行できる最大の歩行距離を評価するものである．通常は歩行距離とともに，経皮的酸素飽和度（S_pO₂）の運動前値と運動時最低値を同時に評価する．途中で休むことは可能であるが，制限時間内に最大限の距離を歩くように説明する．Fletcher-Hugh-Jones分類と同様，呼吸困難以外の要因も影響する．繰り返し測定することで，慢性呼吸器疾患患者における治療効果の判定や臨床経過の把握に有用である．最近では9 mの標識間をCDの発信音にあわせて往復歩行するシャトルウォーキング試験が行われることもある．
4）カテゴリーによる定量的評価（図2-31-2）：
Borgスケールやvisual analog scale（VAS）などがあり，感覚の絶対的な強さを客観的に評価することができる．Borgスケールは呼吸困難の程度をおよそ10段階のカテゴリーに分けたとき，患者が自覚する呼吸困難の程度がどこの位置にあるかを判定する．しばしば運動負荷試験に際して用いられる．VASは10 cm（あるいは15 cm）の水平線を患者に示し，呼吸困難をまったく感じない状態を左端，非常に強く呼吸困難を感じる状態を右端としたとき，患者が感じる呼吸困難の程度に応じて任意のところに印をつけてもらい，左端からの距離で呼吸困難の程度を評価する．いずれの指標も重症度判定や治療の効果判定に有用である．
鑑別診断
　まず緊急性があるかどうかを判断し，緊急性がある場合は診断と治療を並行して行う．病歴，身体所見，画像所見，呼吸機能その他の検査結果を参考にして鑑別診断を進める（図2-31-3）．
1）病歴：
　a）呼吸困難の時間経過：突発性か，急性進行性か慢性か，反復性かを参考にして鑑別を進める．突発性の呼吸困難の原因は，気胸や肺血栓塞栓症，急性心筋梗塞による呼吸困難などがある．急性のものには急性左心不全，細菌性・ウイルス性肺炎，急性間質性肺炎などがある．慢性閉塞性肺疾患（COPD）や肺線維症，慢性心不全などは慢性に進行する呼吸困難が出現するが，急性増悪時には急速に呼吸困難が進行する．また気管支喘息や狭心症に伴う呼吸困難，過換気症候群などでは発作性の呼吸困難を繰り返す．
　b）呼吸困難の誘因：
　労作時に増悪：ほとんどの呼吸困難はまず労作時に症状が出現し，病状が進行すると安静時にも呼吸困難が出現するようになる．呼吸器疾患だけではなく，労作性狭心症なども鑑別する必要がある．
　時間帯による増悪：気管支喘息では夜間～早朝に喘鳴・呼吸困難発作が出現しやすい．
　体位による増悪：うっ血性心不全，気管支喘息などでは仰臥位，片側胸水，無気肺，気管内腫瘍などでは側臥位，肝肺症候群などでは座位で呼吸困難が増悪する.
　c）随伴症状：
　前胸部絞扼感：狭心症，心筋梗塞など
　胸痛：心膜炎，肺炎，胸膜炎，気胸，肺血栓塞栓症など
　その他，発熱や咳の有無，痰の性状などに注意する．
2）身体所見：
　速くて浅い呼吸（肺胸郭系のコンプライアンスが低下しているか，痛みで大きく息を吸えない状態）：間質性肺炎，うっ血性心不全，肺血栓塞栓症，気胸
　速くて深い呼吸：糖尿病性ケトアシドーシス，急性腎不全，過換気症候群
　喘鳴と呼気延長，口すぼめ呼吸：気管支喘息，COPDなどの閉塞性肺疾患
　その他，聴診所見（呼吸音，心音），チアノーゼ，ばち指，浮腫の有無，胸郭の変形などに注意する．
3）胸部画像所見：
　過膨張と肺野の透過性亢進：気腫型COPD
　びまん性間質性陰影，すりガラス陰影，蜂巣肺，肺野の縮小：肺線維症，間質性肺炎
　肺動脈の拡張と肺野血管影の減少：肺血栓塞栓症
　バタフライ型浸潤影と心拡大：うっ血性心不全，肺水腫
　その他，浸潤影，胸膜肥厚，気胸や胸水などに注意する．
4）呼吸機能検査所見：
　拘束性障害（肺活量の低下）：肺線維症，神経筋疾患
　閉塞性障害（1秒率，1秒量の低下）：気管支喘息，慢性閉塞性肺疾患
　肺拡散障害（DLcoの低下）：肺線維症，COPD，肺血栓塞栓症，肺高血圧症，貧血
　その他，血液ガス分析による低酸素血症，高炭酸ガス血症，低炭酸ガス血症，アシドーシスの有無に注意する．
5）その他の検査：
血液検査における炎症反応の有無，心電図による心筋虚血や右心負荷の有無，心エコーによる左心機能の評価，右室の拡張，心室中隔の奇異性運動なども呼吸困難の鑑別に重要である．
代表的疾患
1）
慢性閉塞性肺疾患
（chronic obstructive pulmonary disease：COPD）：喫煙歴があり，咳や痰が多く，慢性的に進行する労作時の呼吸困難を自覚する場合は本症を疑い，呼吸機能検査を施行する．ビア樽様の胸郭，口すぼめ呼吸，ばち指などをしばしば認める．必ずしも，安静時に低酸素血症や高炭酸ガス血症を伴わない．そのような場合でも労作時の呼吸困難が著しいのが特徴である．その原因は，労作時の低酸素血症だけではなく，動的肺過膨張に起因するものが大きい．COPD患者では呼気閉塞を伴うため，労作時の呼吸運動出力の増大の際に，十分な呼気が終了する前に吸気が開始され肺過膨張の増悪を招く．このような状況下では，横隔膜がより低位となり効率よい収縮が障害されるため，さらなる呼吸運動出力の増大がもたらされ呼吸困難が増悪する．気管支拡張薬や酸素療法により，部分的であれ動的肺過膨張が改善すると労作時呼吸困難が軽減する．
2）
肺線維症：
吸気末期にfine cracklesを聴取し，胸部X線，CTにて両側性の間質性陰影を認める．拘束性障害と肺拡散障害により，安静時の低酸素血症とともに，労作時の低酸素血症が顕著となる．酸素投与により労作時の呼吸困難を軽減させることができる．
3）
気管支喘息：
夜間～早朝や運動時に発作を生じることが多い．著明な低酸血症が存在しなくても，気道抵抗の増大により強い呼吸困難を生じる．中等度以上の発作では起坐呼吸をきたす．
4）
急性肺血栓塞栓症：
術後や長期臥床中の患者の体動後，長時間の飛行機搭乗後などに多く発症し，突発性の呼吸困難をきたし胸痛を伴うことが多い．肥満や担癌状態も危険因子となる．P_aCO₂の低下を伴う低酸素血症を認める．突発性の呼吸困難と低酸素血症があり，胸部X線にて肺野に明らかな異常を認めないときは，鑑別診断として本症の疑いをもつことが大切である．
5）うっ血性心不全，肺水腫：
労作時呼吸困難や起坐呼吸が認められる．肺うっ血や肺間質内での水分貯留により，肺コンプライアンスが減少し肺活量が低下する．また肺間質の浮腫により拡散障害が生じるために低酸素血症が悪化する．さらにC線維末端の刺激により頻呼吸を伴い呼吸困難が増悪する．［木村　弘］
■文献
American Thoracic Society: Dyspnea. Mechanisms, assessment, and management: a consensus statement. Am J Respir Crit Care Med, 159: 321-340, 1999.
Celli BR W, MacNee W, et al: Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper. Eur Respir J, 23: 932-946, 2004.
木村　弘，栗山喬之：息切れ，呼吸困難．内科鑑別診断学，第2版，pp429-438，朝倉書店，東京，2003.

表2-31-1
Fletcher-Hugh-Jones 分類">

表2-31-1

表2-31-2
Medical Research Council（MRC）息切れスケール">

表2-31-2

図2-31-1
呼吸調節機構のスキーム">

図2-31-1

図2-31-2
呼吸困難をきたす疾患の鑑別診断">

図2-31-2

図2-31-3
呼吸困難をきたす疾患の鑑別診断">

図2-31-3

出典　内科学第10版内科学第10版について　情報

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