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Shortness of breath
Other namesDyspnea, dyspnoea, breathlessness, difficulty (in/of) breathing; respiratory distress
Pronunciation
SpecialtyPulmonology

Shortness of breath (SOB), known as dyspnea (in AmE) or dyspnoea (in BrE), is an uncomfortable feeling of not being able to breathe well enough. The American Thoracic Society defines it as "a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity", and recommends evaluating dyspnea by assessing the intensity of its distinct sensations, the degree of distress and discomfort involved, and its burden or impact on the patient's activities of daily living. Distinct sensations include effort/work to breathe, chest tightness or pain, and "air hunger" (the feeling of not enough oxygen).[1] The tripod position is often assumed to be a sign.

Dyspnea is a normal symptom of heavy physical exertion but becomes pathological if it occurs in unexpected situations,[2] when resting or during light exertion. In 85% of cases it is due to asthma, pneumonia, reflux/LPR, cardiac ischemia, COVID-19, interstitial lung disease, congestive heart failure, chronic obstructive pulmonary disease, or psychogenic causes,[2][3] such as panic disorder and anxiety (see Psychogenic disease and Psychogenic pain).[4] The best treatment to relieve or even remove shortness of breath[5] typically depends on the underlying cause.[6]

Definition

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Dyspnea, in medical terms, is "shortness of breath".

The American Thoracic Society defines dyspnea as:

"A subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity."[7]

Other definitions describe it as "difficulty in breathing",[8] "disordered or inadequate breathing",[9] "uncomfortable awareness of breathing",[3] and as the experience of "breathlessness" (which may be either acute or chronic).[2][6][10]

Causes

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Further information: List of causes of shortness of breath

While shortness of breath is generally caused by disorders of the cardiac or respiratory system, others such as the neurological,[11] musculoskeletal, endocrine, gastrointestinal system (reflux/LPR),[12]hematologic, and psychiatric systems may be the cause.[13]

DiagnosisPro, an online medical expert system, listed 497 distinct causes in October 2010.[14] The most common cardiovascular causes are myocardial infarction and heart failure, while common pulmonary causes include chronic obstructive pulmonary disease, asthma, pneumothorax, pulmonary edema, and pneumonia.[2]

On a pathophysiological basis, the causes can be divided into (1) increased awareness of normal breathing such as during an anxiety attack, (2) an increase in the work of breathing, and (3) an abnormality in the ventilatory or respiratory system.[11] Ischemic strokes, hemorrhages, tumors, infections, seizures, and traumas at the brain stem can also cause shortness of breath, making them the only neurological causes of shortness of breath.[citation needed]

The tempo of onset and the duration of dyspnea are useful in knowing the etiology of dyspnea. Acute shortness of breath is usually connected with sudden physiological changes, such as laryngeal edema, bronchospasm, myocardial infarction, pulmonary embolism, or pneumothorax. Patients with COPD and idiopathic pulmonary fibrosis (IPF) have a mild onset and gradual progression of dyspnea on exertion, punctuated by acute exacerbations of shortness of breath. In contrast, most asthmatics do not have daily symptoms, but have intermittent episodes of dyspnea, cough, and chest tightness that are usually associated with specific triggers, such as an upper respiratory tract infection or exposure to allergens.[15]

Acute coronary syndrome

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Acute coronary syndrome frequently presents with retrosternal chest discomfort and difficulty catching the breath.[2] It however may atypically present with shortness of breath alone.[16] Risk factors include old age, smoking, hypertension, hyperlipidemia, and diabetes.[16] An electrocardiogram and cardiac enzymes are important both for diagnosis and directing treatment.[16] Treatment involves measures to decrease the oxygen requirement of the heart and efforts to increase blood flow.[2]

COVID-19

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Main article: COVID-19

People that have been infected by COVID-19 may have symptoms such as a fever, dry cough, loss of smell and taste, and in moderate to severe cases, shortness of breath.[citation needed]

Congestive heart failure

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Congestive heart failure frequently presents with shortness of breath with exertion, orthopnea, and paroxysmal nocturnal dyspnea.[2] It affects between 1 and 2% of the general United States population and occurs in 10% of those over 65 years old.[2][16] Risk factors for acute decompensation include high dietary salt intake, medication noncompliance, cardiac ischemia, abnormal heart rhythms, kidney failure, pulmonary emboli, hypertension, and infections.[16] Treatment efforts are directed toward decreasing lung congestion.[2]

Chronic obstructive pulmonary disease

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People with chronic obstructive pulmonary disease (COPD), most commonly emphysema or chronic bronchitis, frequently have chronic shortness of breath and a chronic productive cough.[2] An acute exacerbation presents with increased shortness of breath and sputum production.[2] COPD is a risk factor for pneumonia; thus this condition should be ruled out.[2] In an acute exacerbation treatment is with a combination of anticholinergics, beta2-adrenoceptor agonists, steroids and possibly positive pressure ventilation.[2]

Asthma

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Asthma is the most common reason for presenting to the emergency room with shortness of breath.[2] It is the most common lung disease in both developing and developed countries affecting about 5% of the population.[2] Other symptoms include wheezing, tightness in the chest, and a nonproductive cough.[2] Inhaled corticosteroids are the preferred treatment for children; however, these drugs can reduce the growth rate.[17] Acute symptoms are treated with short-acting bronchodilators.[citation needed]

Pneumothorax

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Main article: Pneumothorax

Pneumothorax presents typically with pleuritic chest pain of acute onset and shortness of breath not improved with oxygen.[2] Physical findings may include absent breath sounds on one side of the chest, jugular venous distension, and tracheal deviation.[2]

Pneumonia

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The symptoms of pneumonia are fever, productive cough, shortness of breath, and pleuritic chest pain.[2] Inspiratory crackles may be heard on exam.[2] A chest x-ray can be useful to differentiate pneumonia from congestive heart failure.[2] As the cause is usually a bacterial infection, antibiotics are typically used for treatment.[2]

Pulmonary embolism

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Pulmonary embolism classically presents with an acute onset of shortness of breath.[2] Other presenting symptoms include pleuritic chest pain, cough, hemoptysis, and fever.[2] Risk factors include deep vein thrombosis, recent surgery, cancer, and previous thromboembolism.[2] It must always be considered in those with acute onset of shortness of breath owing to its high risk of mortality.[2] Diagnosis, however, may be difficult[2] and Wells Score is often used to assess the clinical probability. Treatment, depending on the severity of symptoms, typically starts with anticoagulants; the presence of ominous signs (low blood pressure) may warrant the use of thrombolytic drugs.[2]

Anemia

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Anemia that develops gradually usually presents with exertional dyspnea, fatigue, weakness, and tachycardia.[18] It may lead to heart failure.[18] Anaemia is often a cause of dyspnea. Menstruation, particularly if excessive, can contribute to anaemia and consequential dyspnea in women. Headaches are a symptom of dyspnea in patients with anaemia. Some patients report a numb sensation in their head, and others have reported blurred vision caused by hypotension behind the eye due to a lack of oxygen and pressure; these patients have reported severe head pains, which can lead to permanent brain damage. Symptoms can include loss of concentration, focus, fatigue, language faculty impairment, and memory loss.[19][citation needed]

Cancer

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Shortness of breath is common in people with cancer and may be caused by numerous different factors. In people with advanced cancer, periods with severe shortness of breath may occur, along with a more continuous feeling of breathlessness.[20]

Treatments for breathlessness include both non-pharmacological and pharmacological approaches. Non-pharmacological interventions that have been shown to improve breathlessness include the use of fans, exercise, and pulmonary rehabilitation.[21]

Pharmacological treatments involve bronchodilators and corticosteroids to address the underlying causes of shortness of breath, as well as opioids or anti-anxiety medications to alleviate symptoms.[21] Integrative medicine options, including acupuncture, acupressure, reflexology, and meditation, have been found to have a beneficial effect.[21]

Additional interventions can help alleviate breathessnes when aligned with a patient's preferance and overall diagnosis. These may include medical procedures like stenting, thoracentesis, or pacement of pleura catheters to address bronchial obstructions or pleural effusions; cancer-directed treatments such as radiation therapy; and management of related symptoms often present in advanced cancer, including pain, can also influence the severity of breathlessness.[22]

While these treatments are effective in reducing breathlessness in cancer patients, a systematic view reported various treatment-related side effects including equipment-related distress, fatigue, and constipation.[23]

Psychological

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One common symptom of panic disorder is shortness of breath.[6][13] Panic attacks typically present with hyperventilation, sweating, and numbness.[6] Panic disorder is usually regarded as a diagnosis of exclusion in cases of shortness of breath.[13]

When the cause of breathlessness is psychological, a common symptom is excessive sighing.[13][24] This is sometimes referred to as "sigh syndrome"[24][25][26] or "sighing dyspnea".[25] Sigh syndrome is characterized by recurrent attempts to take a deep breath, prompted by a feeling of inability to do so, followed by a prolonged and often audible exhalation (i.e. a sigh).[24] Sigh syndrome is not dangerous and is usually self-limited, though it can be recurrent.[24]

Other

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Other important or common causes of shortness of breath include cardiac tamponade, anaphylaxis, interstitial lung disease, and pulmonary hypertension.[6][13][18] It is more common among people with relatively small lungs.[27] Around 2/3 of women experience shortness of breath as a part of a normal pregnancy.[9]

Cardiac tamponade presents with dyspnea, tachycardia, elevated jugular venous pressure, and pulsus paradoxus.[18] The gold standard for diagnosis is ultrasound.[18]

Anaphylaxis typically begins over a few minutes in a person with a previous history of the same.[6] Other symptoms include urticaria, throat swelling, and gastrointestinal upset.[6] The primary treatment is epinephrine.[6]

Interstitial lung disease presents with a gradual onset of shortness of breath typically with a history of predisposing environmental exposure.[13] Shortness of breath is often the only symptom in those with tachydysrhythmias.[16]

Neurological conditions such as spinal cord injury, phrenic nerve injuries, Guillain–Barré syndrome, amyotrophic lateral sclerosis, multiple sclerosis and muscular dystrophy can all cause an individual to experience shortness of breath.[11] Shortness of breath can also occur as a result of vocal cord dysfunction (VCD).[28]

Dyspnea can be a symptom of mast cell activation syndrome (MCAS).[29][30]

Sarcoidosis is an inflammatory disease of unknown etiology that generally presents with dry cough, fatigue, and shortness of breath, although multiple organ systems may be affected, with the involvement of sites such as the eyes, the skin, and the joints.[31]

In January 2025, Metro reported that vaping increases the risk of inflammation of the lungs by exposing users to the vaporized elements of the oil. Popcorn lung is considered to be one such inflammatory response, and it causes respiratory symptoms such as coughing and dyspnea.[32]

Pathophysiology

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Different physiological pathways may lead to shortness of breath including via ASIC chemoreceptors, mechanoreceptors, and lung receptors.[16]

It is thought that three main components contribute to dyspnea: afferent signals, efferent signals, and central information processing. It is believed the central processing in the brain compares the afferent and efferent signals; and dyspnea results when a "mismatch" occurs between the two: such as when the need for ventilation (afferent signaling) is not being met by physical breathing (efferent signaling).[33]

Afferent signals are sensory neuronal signals that ascend to the brain. Afferent neurons significant in dyspnea arise from a large number of sources including the carotid bodies, medulla, lungs, and chest wall. Chemoreceptors in the carotid bodies and medulla supply information regarding the blood gas levels of O2, CO2 and H+.[34] In the lungs, juxtacapillary (J) receptors are sensitive to pulmonary interstitial edema, while stretch receptors signal bronchoconstriction. Muscle spindles in the chest wall signal the stretch and tension of the respiratory muscles. Thus, poor ventilation leads to hypercapnia, left heart failure leading to interstitial edema (impairing gas exchange), asthma causing bronchoconstriction (limiting airflow) and muscle fatigue leading to ineffective respiratory muscle action could all contribute to a feeling of dyspnea.[33]

Efferent signals are the motor neuronal signals descending to the respiratory muscles. The most important respiratory muscle is the diaphragm. Other respiratory muscles include the external and internal intercostal muscles, the abdominal muscles, and the accessory breathing muscles.[35] As the brain receives its plentiful supply of afferent information relating to ventilation, it can compare it to the current level of respiration as determined by the efferent signals. If the level of respiration is inappropriate for the body's status then dyspnea might occur. There is also a psychological component to dyspnea, as some people may become aware of their breathing in such circumstances but not experience the typical distress of dyspnea.[33]

Diagnosis

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MRC breathlessness scale
Grade Degree of dyspnea
1 no dyspnea except with strenuous exercise
2 dyspnea when walking up an incline or hurrying on the level
3 walks slower than most on the level, or stops after 15 minutes of walking on the level
4 stops after a few minutes of walking on the level
5 with minimal activity such as getting dressed, too dyspneic to leave the house
Signs of respiratory distress illustration

The initial approach to evaluation begins with an assessment of the airway, breathing, and circulation followed by a medical history and physical examination.[2] Signs and symptoms that represent significant severity include hypotension, hypoxemia, tracheal deviation, altered mental status, unstable dysrhythmia, stridor, intercostal indrawing, cyanosis, tripod positioning, pronounced use of accessory muscles (sternocleidomastoid, scalenes) and absent breath sounds.[13]

A number of scales may be used to quantify the degree of shortness of breath.[36] It may be subjectively rated on a scale from 1 to 10 with descriptors associated with the number (The Modified Borg Scale).[36] The MRC breathlessness scale suggests five grades of dyspnea based on the circumstances and severity in which it arises.[37]

Blood tests

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Several labs may help determine the cause of shortness of breath. D-dimer, while useful to rule out a pulmonary embolism in those who are at low risk, is not of much value if it is positive, as it may be positive in several conditions that lead to shortness of breath.[16] A low level of brain natriuretic peptide is useful in ruling out congestive heart failure; however, a high level, while supportive of the diagnosis, could also be due to advanced age, kidney failure, acute coronary syndrome, or a large pulmonary embolism.[16]

Imaging

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A chest x-ray is useful to confirm or rule out a pneumothorax, pulmonary edema, or pneumonia.[16] Spiral computed tomography with intravenous radiocontrast is the imaging study of choice to evaluate for pulmonary embolism.[16]

Treatment

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The primary treatment of shortness of breath is directed at its underlying cause.[6] Extra supplemental oxygen is effective in those with hypoxia; however, this has no effect in those with normal blood oxygen saturations.[3][38]

Physiotherapy

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Individuals can benefit from a variety of physical therapy interventions.[39] Persons with neurological/neuromuscular abnormalities may have breathing difficulties due to weak or paralyzed intercostal, abdominal and/or other muscles needed for ventilation.[40] Some physical therapy interventions for this population include active assisted cough techniques,[41] volume augmentation such as breath stacking,[42] education about body position and ventilation patterns[43] and movement strategies to facilitate breathing.[42] Pulmonary rehabilitation may alleviate symptoms in some people, such as those with COPD, but will not cure the underlying disease.[44][45] Fan therapy to the face has been shown to relieve shortness of breath in patients with a variety of advanced illnesses including cancer.[46] The mechanism of action is thought to be stimulation of the trigeminal nerve.[citation needed]

Palliative medicine

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Systemic immediate release opioids are beneficial in emergently reducing the symptom severity of shortness of breath due to both cancer and non-cancer causes;[3][47] long-acting/sustained-release opioids are also used to prevent/continue treatment of dyspnea in palliative setting. There is a lack of evidence to recommend midazolam, nebulised opioids, the use of gas mixtures, or cognitive-behavioral therapy yet.[48]

Non-pharmacological techniques

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Non-pharmacological interventions provide key tools for the management of breathlessness.[20] Potentially beneficial approaches include active management of psychosocial issues (anxiety, depression, etc.), and implementation of self-management strategies, such as physical and mental relaxation techniques, pacing techniques, energy conservation techniques, learning exercises to control breathing, and education.[20] The use of a fan may be beneficial.[20] Cognitive behavioural therapy may also be helpful.[20]

Pharmacological treatment

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For people with severe, chronic, or uncontrollable breathlessness, non-pharmacological approaches to treating breathlessness may be combined with medication. For people who have cancer that is causing the breathlessness, medications that have been suggested include opioids, benzodiazepines, oxygen, and steroids.[20] Results of recent systematic reviews and meta-analyses found opioids were not necessarily associated with more effectiveness in treatment for patients with advanced cancer.[21][49]

Ensuring that the balance between side effects and adverse effects from medications and potential improvements from medications needs to be carefully considered before prescribing medication.[20] The use of systematic corticosteroids in palliative care for people with cancer is common, however, the effectiveness and potential adverse effects of this approach in adults with cancer have not been well studied.[20]

Epidemiology

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Shortness of breath is the primary reason 3.5% of people present to the emergency department in the United States. Of these individuals, approximately 51% are admitted to the hospital and 13% die within a year.[50] Some studies have suggested that up to 27% of hospitalized people develop dyspnea,[51] while in dying patients 75% will experience it.[33] Acute shortness of breath is the most common reason people requiring palliative care visit an emergency department.[3] Up to 70% of adults with advanced cancer also experience dyspnoea.[20]

Etymology and pronunciation

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English dyspnea comes from Latin dyspnoea, from Greek dyspnoia, from dyspnoos, which literally means "disordered breathing".[13][52] Its combining forms (dys- + -pnea) are familiar from other medical words, such as dysfunction (dys- + function) and apnea (a- + -pnea). The most common pronunciation in medical English is /dɪspˈniːə/ disp-NEE-ə, with the p expressed and the stress on the /niː/ syllable. But pronunciations with a silent p in pn (as also in pneumo-) are common (/dɪsˈniːə/ or /ˈdɪsniə/),[53] as are those with the stress on the first syllable[53] (/ˈdɪspniə/ or /ˈdɪsniə/).

In English, the various -pnea-suffixed words commonly used in medicine do not follow one clear pattern as to whether the /niː/ syllable or the one preceding it is stressed; the p is usually expressed but is sometimes silent depending on the word. The following collation or list shows the preponderance of how major dictionaries pronounce and transcribe them (less-used variants are omitted):

Group Term Combining forms Preponderance of transcriptions (major dictionaries)
good eupnea eu- + -pnea /juːpˈniːə/ yoop-NEE-ə[54][55][53][56]
bad dyspnea dys- + -pnea /dɪspˈniːə/ disp-NEE-ə,[55][56][57] /ˈdɪspniə/ DISP-nee-ə[54][53]
fast tachypnea tachy- + -pnea /ˌtækɪpˈniːə/ TAK-ip-NEE-ə[54][55][53][56][57]
slow bradypnea brady- + -pnea /ˌbreɪdɪpˈniːə/ BRAY-dip-NEE-ə[55][53][56]
upright orthopnea ortho- + -pnea /ɔːrˈθɒpniə/ or-THOP-nee-ə,[55][53][57][54]: audio  /ɔːrθəpˈniːə/ or-thəp-NEE-ə[53][54]: print 
supine platypnea platy- + -pnea /pləˈtɪpniə/ plə-TIP-nee-ə[54][55]
bent over bendopnea bend + -o- + -pnea /bɛndˈɒpniə/ bend-OP-nee-ə
excessive hyperpnea hyper- + -pnea /ˌhaɪpərpˈniːə/ HY-pərp-NEE-ə[54][55][53][56]
insufficient hypopnea hypo- + -pnea /haɪˈpɒpniə/ hy-POP-nee-ə,[54][55][56][57] /ˌhaɪpoʊˈniːə/ high-poh-NEE-ə[58][56]
absent apnea a- + -pnea /ˈæpniə/ AP-nee-ə,[54][55][53][56][57]: US  /æpˈniːə/ ap-NEE-ə[53][56][57]: UK 

See also

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Shortness of breath

View on Grokipedia
from Grokipedia
Shortness of breath, medically known as dyspnea, is the subjective sensation of difficult or uncomfortable , often described as an intense tightening in the chest, air hunger, or a feeling of suffocation. It represents a common symptom that can range from mild discomfort during , such as climbing stairs, to severe respiratory distress, affecting millions of individuals worldwide and significantly impacting . Dyspnea arises from complex interactions between the , peripheral chemoreceptors, and mechanoreceptors in the , triggered by factors such as hypoxia, , or acid-base imbalances. This symptom can manifest acutely, developing over hours to days, or chronically, persisting for more than four to eight weeks, and may occur at rest, during , or in specific positions like lying flat (). The most frequent causes stem from cardiopulmonary disorders, including , , (COPD), , and , though it can also result from , , physical deconditioning (lack of exercise), (GERD), anxiety disorders, or neuromuscular conditions. Mild exertional dyspnea, such as shortness of breath after climbing stairs, is often benign and attributable to physical deconditioning in otherwise healthy individuals, as the body's muscles and cardiovascular system require increased oxygen delivery during such activities. However, persistent, severe, or worsening symptoms warrant medical evaluation to rule out underlying pathology. For instance, heart-related issues like arrhythmias or impair oxygen delivery, while lung conditions such as or obstruct airflow. GERD can cause respiratory symptoms via reflux irritating the airways or leading to aspiration, and anxiety commonly causes air hunger and perceptual/visual changes (e.g., from hyperventilation). Non-respiratory factors, including panic attacks or , further contribute by altering breathing patterns or systemic oxygen demand. Evaluation of shortness of breath typically involves a detailed history, , assessment, and diagnostic tests such as chest X-rays, electrocardiograms (ECGs), , or gases to identify the underlying . Seek immediate medical attention for air hunger (shortness of breath) or visual instability if symptoms are sudden, severe, or accompanied by chest pain, rapid/irregular heartbeat, fainting, blue lips, confusion, severe headache, weakness/numbness, or difficulty speaking—these may indicate serious conditions like heart attack, pulmonary embolism, stroke, or other emergencies. For symptoms linked to known GERD or anxiety, consult a doctor promptly if they are new, worsening, persistent, interfere with daily life, or not improved with usual management (e.g., antacids for GERD, relaxation for anxiety). Although GERD can cause respiratory symptoms via reflux irritating airways and anxiety commonly causes air hunger and perceptual/visual changes (e.g., from hyperventilation), other serious causes must always be ruled out. Treatment focuses on addressing the root cause—ranging from and bronchodilators for acute respiratory issues to lifestyle modifications and medications for chronic conditions.

Definition and Terminology

Definition

Shortness of breath, medically termed dyspnea, is defined as a subjective of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity. This definition, established by the American Thoracic Society (ATS), emphasizes the personal and perceptual nature of the symptom, encompassing feelings such as increased effort or , chest tightness, and air hunger. Unlike objective measures of respiration, dyspnea reflects the individual's awareness of respiratory distress rather than physiological parameters alone. Dyspnea must be distinguished from related terms like and , which describe alterations in breathing patterns without implying subjective discomfort. refers to an increase in the depth and rate of breathing, often in response to metabolic demands such as exercise, while denotes a rapid , typically exceeding 20 breaths per minute in adults, and may occur without any perceived unease. In contrast, dyspnea is the distressing sensation accompanying these or other respiratory changes, and it should not be conflated with them in clinical assessment. The term "dyspnea" originates from the Greek "duspnoia," combining "dus-" (meaning bad or difficult) and "pnoē" (breath), reflecting its ancient in describing labored respiration. It entered English in the late , evolving from classical descriptions of difficulties to its modern clinical usage, where standardized definitions like the ATS statement guide and in contexts such as pulmonary and cardiovascular evaluations. Patients commonly describe dyspnea using vivid, personal phrases that highlight its qualitative aspects, such as "I can't get enough air," "I feel like I'm suffocating," or "My requires too much effort." Other frequent descriptors include a of chest , hunger for more air, or the inability to breathe out fully, which underscore the symptom's emotional and sensory dimensions. These expressions aid clinicians in assessing the severity and underlying contributors to the experience.

Etymology and pronunciation

The term "dyspnea," the primary synonym for shortness of breath, derives from the "δύσπνοια" (dyspnoia), composed of "δυσ-" (dys-, meaning bad or difficult) and "πνοή" (pnoē, meaning breathing or breath), literally signifying "difficult breathing." This entered Latin as "dyspnoea" before being adopted into English around the 17th century, with the earliest documented use appearing in 1681 in a table of hard words in texts. In modern usage, the spelling varies by regional convention: "dyspnea" predominates in , while "dyspnoea" is preferred in . The standard pronunciation is /dɪspˈniːə/ (disp-NEE-ə), with minor phonetic variations such as a more rounded in British accents (/dɪspˈnɪə/). Alternative lay and clinical terms include "breathlessness," which originated in late 14th-century from "breath" + the "-less," initially denoting an inability to breathe, and evolved to describe the sensation of labored respiration. This term gained traction in English during the , particularly in descriptions of cardiac and pulmonary conditions, serving as a more accessible to dyspnea for patient communication and early diagnostic texts. Over time, medical for shortness of breath has standardized around "dyspnea" in formal classifications, reflecting advances in respiratory . In the , 11th Revision (), it is designated as code MD12.0 for Dyspnoea, unspecified. also defines durations: acute dyspnoea (hours to 3 weeks), subacute dyspnoea (3 to 8 weeks), and chronic dyspnoea (more than 8 weeks).

Clinical Presentation

Signs and symptoms

Shortness of breath, also known as dyspnea, is characterized by subjective sensations of uncomfortable breathing, often described as air hunger or the feeling of not being able to breathe deeply or quickly enough. Patients commonly report chest tightness, increased effort required to breathe, and fatigue that occurs even with minimal exertion. These experiences can range from mild discomfort during daily activities to a profound sense of suffocation that causes distress. In cases associated with anxiety, shortness of breath may be accompanied by perceptual or visual instability, such as blurred vision or tunnel vision, due to hyperventilation-induced hypocapnia. Objectively, healthcare providers may observe signs such as the use of accessory muscles, including the sternocleidomastoid, to assist with respiration, indicating increased . Other visible indicators include nasal flaring, to maintain airway pressure, and , where breathing becomes more difficult when lying flat, prompting patients to sit upright for relief. Associated symptoms vary with severity and may include , a bluish discoloration of the skin due to low oxygen levels, as well as wheezing or audible , which can signal underlying respiratory involvement. In obstructive lung diseases such as asthma and chronic obstructive pulmonary disease (COPD), shortness of breath is characteristically worse on exhalation (expiration) due to narrowed airways increasing resistance to expiratory airflow, leading to prolonged expiration, expiratory wheezing, and difficulty getting air out. The severity of shortness of breath is often assessed using the Modified Council (mMRC) dyspnea scale, a validated tool that grades breathlessness based on its impact on daily activities:
GradeDescription
0Not troubled by breathlessness except on strenuous exercise.
1Short of breath when hurrying on the level or walking up a slight hill.
2Walks slower than contemporaries on the level because of breathlessness, or has to stop for breath when walking at own pace.
3Stops for breath after walking about 100 meters or after a few minutes on the level.
4Too breathless to leave the house, or breathless when dressing or undressing.
This scale helps quantify the subjective burden of dyspnea. Symptoms may present acutely or develop chronically, influencing their pattern and persistence.

Acute versus chronic

Shortness of breath, or dyspnea, is classified temporally into acute, subacute, and chronic forms based on the duration of symptoms, which guides clinical urgency and approach. According to the , 11th Revision (), acute dyspnea encompasses symptoms lasting from hours to 3 weeks, subacute from 3 to 8 weeks, and chronic beyond 8 weeks. This helps differentiate immediate threats from ongoing conditions, with acute cases often signaling rapid physiological . Acute dyspnea features sudden onset over hours to days and is frequently life-threatening, requiring prompt evaluation to rule out emergencies such as anaphylaxis, pulmonary embolism, pneumothorax, heart attack, severe asthma attack, choking (airway obstruction), carbon monoxide poisoning, or acute decompensated heart failure. For instance, anaphylaxis can trigger rapid airway obstruction leading to severe breathlessness within minutes. Pulmonary embolism similarly causes abrupt vascular obstruction in the lungs, resulting in acute respiratory distress. Other life-threatening causes include choking, which leads to mechanical airway blockage; severe asthma attacks, which cause bronchospasm and inflammation; pneumothorax, which results in lung collapse; heart attack, which impairs cardiac function; carbon monoxide poisoning, which reduces blood oxygen transport; and acute decompensated heart failure, which leads to pulmonary congestion. Such episodes demand immediate medical intervention, including stabilization and diagnostic imaging, to prevent complications like hypoxia or . In acute presentations, symptoms like sudden wheezing may accompany the distress, emphasizing the need for rapid . Subacute dyspnea represents an intermediate category, developing over days to weeks, often bridging acute exacerbations and chronic progression without the same level of immediacy. This duration allows for somewhat less urgent but still thorough assessment to identify evolving issues. Chronic dyspnea involves persistent or recurrent symptoms lasting weeks to months or longer, typically arising from progressive diseases like (COPD) or . In COPD, ongoing airway inflammation and obstruction lead to sustained breathlessness, while causes fluid accumulation impairing and oxygenation over time. Management prioritizes long-term strategies, such as optimizing therapy for underlying conditions and improving through rehabilitation. This contrasts with acute forms by focusing on disease modification rather than acute resuscitation.

Causes

Cardiovascular causes

Cardiovascular conditions can lead to shortness of breath, or dyspnea, primarily through impairments in , increased pulmonary pressures, or reduced oxygen delivery to tissues. These etiologies often involve the heart's inability to effectively pump blood, resulting in fluid accumulation or inadequate perfusion that stimulates respiratory distress. In addition to pathological cardiovascular conditions, physical deconditioning—characterized by lack of physical fitness or weak muscles from inactivity—is a common cause of exertional shortness of breath, such as heavy breathing or dyspnea after climbing stairs. In deconditioned individuals, even moderate activities increase oxygen and energy demands significantly; muscles rely on anaerobic metabolism, producing lactic acid that stimulates ergoreceptors and heightens neural output to respiratory centers, accelerating breathing and causing breathlessness. This is often physiological and benign, particularly in sedentary people, and typically improves with regular exercise training. However, if the dyspnea is persistent, severe, occurs at rest, or is accompanied by symptoms such as chest pain, dizziness, or swelling, it may indicate an underlying condition requiring medical evaluation. Congestive heart failure is a leading cardiovascular cause of dyspnea, where the heart's weakened pumping action leads to fluid overload and subsequent . In this condition, systolic or diastolic dysfunction increases pulmonary venous pressure, causing fluid to transude into the lung alveoli and impair , which manifests as exertional or orthopneic shortness of breath. Fluid retention in the lungs reduces oxygen availability, prompting compensatory to meet tissue demands. This is particularly evident in acute decompensations, where dyspnea worsens with activity due to elevated left ventricular end-diastolic pressure. Acute coronary syndrome, encompassing and , induces dyspnea via myocardial ischemia that diminishes . Ischemia reduces the heart's contractility, lowering and systemic perfusion, which triggers dyspnea as the body attempts to augment oxygen delivery through increased respiratory effort. In such events, often accompanies shortness of breath, especially during exertion when myocardial oxygen demand exceeds supply. The resulting imbalance in oxygen supply-demand further exacerbates pulmonary congestion if left ventricular function is compromised. Arrhythmias, such as , contribute to dyspnea by disrupting coordinated atrial-ventricular contraction and impairing ventricular filling. Rapid or irregular rhythms reduce diastolic filling time, decreasing and leading to inadequate tissue oxygenation, which provokes breathlessness particularly during episodes of . In , loss of atrial kick further compromises preload, intensifying symptoms in patients with underlying heart disease. This can result in sudden-onset dyspnea, often positional or activity-related. Valvular heart disease, exemplified by , causes dyspnea through obstruction of blood flow and elevated left atrial pressure. Narrowing of the impedes left ventricular filling, increasing pulmonary capillary wedge pressure and promoting pulmonary congestion, which limits alveolar ventilation and induces shortness of breath. Regurgitant lesions, like , similarly back up blood into the lungs, worsening symptoms with exertion. Over time, chronic valvular issues lead to progressive dyspnea due to compensatory . Pericardial effusion results in dyspnea by compressing the cardiac chambers and restricting diastolic filling. Accumulation of fluid in the pericardial sac elevates intrapericardial pressure, limiting venous return and , which reduces and stimulates respiratory compensation. In severe cases, such as , this compression acutely heightens dyspnea alongside hemodynamic instability. The mechanism involves impaired right ventricular expansion, leading to systemic underperfusion and pulmonary backup.

Respiratory causes

Respiratory causes of shortness of breath, or dyspnea, predominantly arise from conditions affecting the airways, lung parenchyma, or pleural space, leading to impaired ventilation, , or increased respiratory effort. These disorders disrupt the normal mechanics of breathing, resulting in sensations of breathlessness that can be acute or chronic depending on the underlying . Chronic obstructive pulmonary disease (COPD), which includes and chronic bronchitis, is a leading respiratory cause of dyspnea due to irreversible limitation. In , destruction of alveolar walls diminishes the lung's surface area for oxygen diffusion, while chronic bronchitis involves persistent airway inflammation and excessive mucus production that narrows the bronchi. This combination increases the and reduces oxygen uptake, often worsening with or during exacerbations. Dyspnea is often worse on exhalation due to increased expiratory resistance from narrowed airways and air trapping, leading to prolonged expiration, expiratory wheezing, and a sensation of difficulty expelling air. Asthma manifests as reversible airway obstruction driven by , , and hyperresponsiveness to triggers such as allergens or irritants. The narrowed airways restrict airflow, particularly during exhalation, causing episodic dyspnea that may include expiratory wheezing, prolonged expiration, chest tightness, and a sensation of difficulty getting air out. In severe cases, this can progress to status asthmaticus, a life-threatening condition requiring immediate intervention. Acute bronchitis, typically viral in origin, causes bronchial inflammation and mucus hypersecretion, resulting in temporary airway narrowing and obstructive features. This can produce dyspnea worse on exhalation, often accompanied by prolonged expiration and expiratory wheezing. Symptoms usually resolve within weeks but may mimic or complicate other obstructive conditions. Intrathoracic airway obstructions, such as from foreign body aspiration, endobronchial tumors, or tracheobronchial stenosis, increase resistance particularly during expiration due to dynamic compression of the airways. This leads to dyspnea worse on exhalation, prolonged expiratory phase, and sometimes monophonic wheezing or audible expiration. These conditions may present acutely or progressively and require prompt diagnosis to prevent complications. Pneumonia, an of the tissue, leads to alveolar consolidation with fluid, , or inflammatory cells, severely impairing . This results in and increased to compensate, producing acute dyspnea often accompanied by fever, , and . Bacterial, viral, or fungal etiologies can all contribute, with being a common culprit. Pneumothorax occurs when air enters the pleural space, causing partial or complete collapse and preventing full expansion during . The resulting decrease in functional volume reduces ventilation and oxygenation, leading to sudden-onset dyspnea that intensifies with activity. It is more common in tall, thin individuals or those with underlying , and tension pneumothorax represents a due to mediastinal shift. Interstitial lung disease (ILD) encompasses a group of disorders characterized by and of the lung , stiffening the lung tissue and restricting expansion. This scarring hinders oxygen across the alveolar-capillary , causing progressive dyspnea that typically worsens over time and with physical effort. is a prominent example, where relentless leads to if untreated. In the context of recent pandemics, post-COVID-19 dyspnea has emerged as a significant respiratory , often stemming from or scarring following severe infection. This reduces and gas transfer capacity, persisting in 30-50% of hospitalized patients. As of 2025, meta-analyses indicate that persistent dyspnea affects approximately 12-25% of previously hospitalized patients at longer follow-ups (e.g., 3 years), reflecting impacts from and milder variants. Gastroesophageal reflux disease (GERD) can cause shortness of breath when acid reflux irritates the airways or larynx, leading to reflex bronchoconstriction, inflammation, or microaspiration of gastric contents into the lungs. This results in respiratory symptoms including dyspnea, which may be chronic, episodic, or associated with meals and recumbency. Respiratory manifestations can occur even without prominent heartburn.

Hematologic and metabolic causes

Hematologic and metabolic disorders can contribute to shortness of breath (dyspnea) primarily through impairments in oxygen transport, delivery, or utilization, as well as by altering respiratory drive or mechanics. These conditions often lead to tissue hypoxia or compensatory , manifesting as exertional or resting dyspnea depending on severity. , characterized by a reduction in count or levels, decreases the blood's oxygen-carrying capacity, resulting in inadequate oxygen delivery to tissues and subsequent dyspnea. This is particularly evident in severe cases, where patients experience shortness of breath during exertion or even at rest due to the body's inability to meet oxygen demands. Common types include , caused by insufficient iron for synthesis, and hemolytic anemias, where s are prematurely destroyed, both exacerbating tissue hypoxia and prompting increased respiratory effort. Carbon monoxide poisoning induces dyspnea by binding to with an affinity over 200 times greater than oxygen, forming that impairs oxygen transport and offloading to tissues. This leads to systemic hypoxia despite normal of oxygen in , often presenting with shortness of breath alongside and , as the reduced oxygen delivery triggers compensatory . The toxicity also shifts the oxyhemoglobin dissociation curve leftward, further hindering oxygen release at the cellular level. Metabolic acidosis, such as that occurring in (DKA), stimulates the to increase ventilation as a compensatory mechanism to eliminate excess and correct the acid-base imbalance. In DKA, uncontrolled leads to ketone production and , causing rapid, deep breathing (Kussmaul respiration) that manifests as shortness of breath, often accompanied by fruity breath odor. This aims to lower blood pH but can progress to respiratory fatigue if untreated. Obesity hypoventilation syndrome (OHS), also known as Pickwickian syndrome, arises in individuals with severe obesity ( ≥30 kg/m²) where excess mechanically restricts chest wall and diaphragmatic movement, leading to alveolar hypoventilation, , and . This results in chronic shortness of breath, particularly during exertion, as the impaired ventilation fails to meet oxygen needs, compounded by sleep-disordered breathing that worsens daytime dyspnea. Hyperthyroidism elevates basal metabolic rate and oxygen consumption through excess thyroid hormone, increasing overall tissue demand and often causing exertional dyspnea due to heightened cardiovascular workload and respiratory muscle fatigue. In conditions like , this can lead to , where and increased strain oxygen delivery, manifesting as shortness of breath alongside and weakness. The disorder may also weaken respiratory muscles, further contributing to ventilatory inefficiency.

Psychological and other causes

Psychological causes of shortness of breath often stem from anxiety and panic disorders, where perceived threats trigger and a sensation of air hunger. Anxiety can also lead to perceptual or visual changes, such as visual instability, blurred vision, or tunnel vision, often resulting from hyperventilation-induced hypocapnia causing cerebral vasoconstriction and altered cerebral blood flow. In , sudden episodes of intense fear are accompanied by physical symptoms including shortness of breath, chest tightness, and rapid heartbeat, affecting approximately 2-3% of the population annually. Similarly, can manifest as chronic dyspnea due to heightened autonomic arousal, mimicking organic respiratory distress but resolving with psychological interventions. These symptoms arise from the brain's misinterpretation of bodily signals, leading to overbreathing and reduced levels, which exacerbate the feeling of breathlessness. Seek immediate medical attention for air hunger (shortness of breath) or visual instability if symptoms are sudden, severe, or accompanied by chest pain, rapid/irregular heartbeat, fainting, blue lips, confusion, severe headache, weakness/numbness, or difficulty speaking—these may indicate serious conditions like heart attack, pulmonary embolism, stroke, or other emergencies unrelated to GERD or anxiety alone. For symptoms linked to known GERD or anxiety, consult a doctor promptly if they are new, worsening, persistent, interfere with daily life, or not improved with usual management (e.g., antacids for GERD, relaxation for anxiety). GERD can cause respiratory symptoms via reflux irritating airways, and anxiety commonly causes air hunger and perceptual/visual changes (e.g., from hyperventilation), but rule out other causes. Psychogenic dyspnea represents a somatoform presentation without identifiable organic , often linked to underlying stress or trauma. This condition involves subjective breathlessness not explained by pulmonary or cardiac dysfunction, potentially tied to or , where psychological factors amplify respiratory discomfort. Patients may experience episodic or persistent dyspnea that improves with reassurance and , distinguishing it from physiological causes through clinical history. Among other causes, neuromuscular disorders like (ALS) lead to shortness of breath through progressive weakening of respiratory muscles, impairing ventilation even in early stages. In ALS, diaphragmatic and intercostal causes , resulting in dyspnea that may precede limb symptoms and contribute to fatigue and anxiety. Respiratory symptoms such as dyspnea are reported by approximately 22% of patients prior to or at and worsen survival prognosis without ventilatory support. Cancer-related shortness of breath frequently occurs due to tumors or metastases that obstruct airways or compress tissue. In non-small cell with metastases, dyspnea prevalence reaches 70%, driven by tumor bulk, pleural effusions, or lymphangitic spread that limits . Primary tumors or secondary deposits from other sites similarly provoke breathlessness through mechanical interference or , often intensifying in advanced stages. Environmental factors, such as high altitude exposure or , can induce acute shortness of breath via hypoxic or irritant mechanisms. At altitudes above 2,500 meters, low oxygen levels trigger , characterized by rapid-onset dyspnea from fluid accumulation in the lungs. Inhalation of toxins like wildfire smoke causes airway inflammation and , leading to persistent respiratory distress that may persist post-exposure and exacerbate underlying conditions. Emerging post-2020 studies highlight as a psychoneurological contributor to chronic shortness of breath, where persistent dyspnea coexists with fatigue, brain fog, and anxiety following infection. In cohorts, dyspnea affects 20-40% of patients beyond three months, potentially involving autonomic dysfunction or central sensitization rather than residual lung damage alone. As of 2025, recent meta-analyses report dyspnea in about 24% of cases, with overall prevalence estimated at 7-36% in general populations. These symptoms, often overlapping with neuropsychiatric manifestations like depression, underscore the need for multidisciplinary management.

Pathophysiology

Physiological mechanisms

Shortness of breath, clinically termed dyspnea, originates from integrated physiological processes that detect and respond to disruptions in respiratory balance, primarily through sensory inputs to the . These mechanisms involve stimulation of the respiratory centers, peripheral receptor activation, and central neural processing, culminating in the subjective awareness of breathing discomfort. Central to dyspnea is the stimulation of respiratory centers by chemoreceptors sensitive to gas levels. Peripheral chemoreceptors in the carotid bodies and , along with central chemoreceptors in the , detect (elevated arterial partial pressure of carbon dioxide, PaCO₂) and hypoxia (reduced arterial partial pressure of oxygen, PaO₂). These sensors trigger an increase in respiratory drive via the , enhancing ventilation to normalize gas tensions; however, persistent or excessive stimulation during high demand amplifies the sensation of breathlessness even in the absence of mechanical limitations. Mechanoreceptors in the and chest wall further contribute by monitoring respiratory mechanics. In the , slowly adapting stretch receptors () in the airways and rapidly adapting receptors (RARs) detect changes in lung volume and airway , relaying signals via vagal afferents to modulate breathing patterns. In the chest wall, Golgi tendon organs and muscle spindles in intercostal and diaphragmatic muscles sense increased effort or stiffness, providing feedback on mechanical load that intensifies dyspnea when the required effort exceeds normal capacity. Neurogenic factors, particularly vagal afferents from the airways and lungs, play a key role in signaling irritative or inflammatory stimuli that heighten respiratory discomfort. Unmyelinated C-fibers within the , originating from the nodose , respond to chemical mediators like , transmitting dyspnogenic signals to the that correlate with acute breathlessness. The fundamental relationship governing respiratory drive is the influence of PaCO₂ on , expressed as V=f(PaCO2)V = f(\mathrm{PaCO_2}), where ventilation rate (VV) increases nonlinearly with rising PaCO₂ to maintain , primarily through activation. This drive equation highlights how deviations in CO₂ levels directly escalate breathing effort and the associated sensation of dyspnea. Ultimately, the brain's perception of dyspnea involves cortical integration of these afferent signals. Inputs from chemoreceptors and mechanoreceptors converge in the nucleus tractus solitarius of the medulla, projecting via the to the and limbic structures, where a mismatch between centrally generated motor commands (efferent copy) and actual sensory feedback generates the conscious experience of respiratory distress.

Underlying processes in common conditions

In , dyspnea arises primarily from elevated pulmonary venous pressure, which exceeds the in pulmonary capillaries, leading to fluid transudation into the lung and resulting in interstitial edema. This edema stiffens the lung tissue, reducing pulmonary compliance and increasing the required to achieve adequate ventilation. The resultant mechanical disadvantage exacerbates the sensation of breathlessness, particularly during exertion when demands rise further. In (COPD), occurs due to loss of and premature airway closure during expiration, causing dynamic that flattens the diaphragm and impairs inspiratory muscle efficiency. This is compounded by ventilation-perfusion (V/Q) mismatch, where poorly ventilated alveoli receive disproportionate blood flow, leading to and stimulation of peripheral chemoreceptors that heighten the drive to breathe. The combination of mechanical load and inefficiency intensifies dyspnea, especially in advanced stages with significant emphysematous destruction. Anemia induces dyspnea through reduced oxygen-carrying capacity of the blood, resulting in tissue hypoxia despite normal pulmonary function and arterial oxygenation. This hypoxic state activates peripheral chemoreceptors and increases ventilatory drive, elevating and as a compensatory mechanism to enhance oxygen delivery to tissues. The effortful pattern reflects the body's attempt to offset the oxygen debt, often manifesting as exertional shortness of breath proportional to the severity of . Inflammatory cascades contribute to dyspnea in conditions like and by involving cytokines that amplify and airway inflammation. In , type 2 cytokines such as IL-4, IL-5, and IL-13, released from Th2 cells and , promote recruitment, mucus hypersecretion, and contraction, narrowing airways and increasing resistance to airflow. Similarly, in , proinflammatory cytokines like IL-6 and TNF-α drive influx and endothelial activation, exacerbating alveolar inflammation and impairing , which heightens the perception of breathlessness through both mechanical and neurogenic pathways. Recent insights from 2020s research highlight microvascular dysfunction as a key mechanism in dyspnea associated with , where persistent endothelial and impaired reduce pulmonary and systemic . Studies indicate that SARS-CoV-2-induced microvascular injury leads to altered recruitment and oxygen diffusion limitations, contributing to exertional breathlessness even in the absence of overt parenchymal damage. This dysfunction, often linked to ongoing low-grade , underscores the need for targeted vascular assessments in affected patients.

Diagnosis

History and physical examination

The evaluation of shortness of breath, or dyspnea, begins with a detailed to characterize the symptom and identify potential underlying causes. Clinicians inquire about the onset, which may be acute (over hours to days) or gradual, and the duration, distinguishing acute episodes from chronic symptoms lasting more than four to eight weeks. Triggers such as exertion, allergens, or positional changes are explored, along with associated symptoms including , , fever, , or , which help differentiate between pulmonary, cardiac, or other etiologies. Risk factors are systematically assessed, encompassing smoking , occupational exposures to dust or chemicals, family of cardiac disease, and medication use that could contribute to dyspnea. Red flags in the history warrant urgent evaluation; for instance, sudden onset dyspnea raises suspicion for , while or paroxysmal nocturnal dyspnea suggests congestive . These historical elements guide the subsequent and may prompt targeted diagnostic testing. The starts with , including to detect (typically >20 breaths per minute), heart rate for , , temperature, and to gauge severity. General inspection may reveal , use of accessory muscles, or body habitus contributing to symptoms. Lung assesses for adventitious sounds such as (rales) indicating or infection, wheezes suggesting airway obstruction, or diminished breath sounds in cases of effusion or . Cardiac evaluation involves and for jugular venous distention, an S3 gallop signifying ventricular dysfunction, murmurs, or a loud pulmonic second heart sound in . Additional findings like or further inform the .

Laboratory investigations

Laboratory investigations play a crucial role in evaluating shortness of breath by identifying underlying biochemical abnormalities that may indicate specific etiologies, such as , , , , , or cardiac ischemia. These tests are typically selected based on the patient's history and to narrow differential diagnoses efficiently. Arterial blood gas (ABG) analysis is a fundamental test that measures , partial pressure of arterial oxygen (PaO2), and partial pressure of arterial carbon dioxide (PaCO2) to assess oxygenation status, ventilation adequacy, and acid-base balance in patients with acute dyspnea. Low PaO2 indicates , which may stem from respiratory or cardiac causes, while elevated PaCO2 suggests , as seen in conditions like exacerbations. ABG is particularly useful when clinical suspicion for severe respiratory compromise exists, providing direct evidence of impairments. A (CBC) is routinely performed to detect through low levels, which can cause dyspnea due to reduced oxygen-carrying capacity, or via elevated counts, often indicating or other inflammatory processes. For instance, hemoglobin below 12 g/dL in women or 13 g/dL in men supports as a contributor to breathlessness. The CBC also evaluates platelet counts, which may be relevant in thrombotic conditions. B-type natriuretic peptide (BNP) or its N-terminal prohormone (NT-proBNP) levels are measured to evaluate for , where elevations above 100 pg/mL for BNP or 300 pg/mL for NT-proBNP strongly suggest cardiac origin of dyspnea, aiding in rapid differentiation from pulmonary causes. These biomarkers reflect ventricular wall stress and are particularly valuable in emergency settings for patients with acute onset symptoms, with levels under 100 pg/mL effectively ruling out heart failure in most cases. D-dimer testing is employed in low-risk patients suspected of to rule out the , as a negative result (typically <500 ng/mL) has a high negative predictive value, avoiding unnecessary . This is elevated in thromboembolic events but lacks specificity, so it is not recommended for high-probability cases where confirmatory tests are needed regardless. Guidelines emphasize its use within validated scoring systems like Wells' criteria to optimize diagnostic yield. Troponin levels, particularly cardiac or T, are assessed to detect myocardial ischemia, which can manifest as dyspnea without classic , especially in older adults or those with presentations. Elevations above the 99th upper reference limit indicate myocyte injury, supporting diagnosis when combined with clinical context. High-sensitivity assays, standardized in clinical practice since the , enable earlier detection of acute coronary syndromes by quantifying low-level elevations within hours of symptom onset, improving sensitivity for non-ST-elevation .

Imaging and functional tests

A 12-lead electrocardiogram (ECG) is a standard initial functional test in the evaluation of dyspnea to identify potential cardiac etiologies. It can detect arrhythmias (e.g., , the most common arrhythmia causing dyspnea), ischemic changes, conduction abnormalities, , or signs of right heart strain such as in . A normal ECG has 89% sensitivity for ruling out . ECG is inexpensive, readily available, and guides further testing like or . Imaging and functional tests play a crucial role in the diagnostic evaluation of shortness of breath (dyspnea) by providing visual and quantitative assessments of respiratory and cardiac structures and functions, helping to identify underlying causes such as infections, vascular obstructions, or ventilatory impairments. These modalities are selected based on clinical suspicion, with chest radiography often serving as an initial, accessible tool, while advanced imaging like computed tomography and offers detailed insights into specific pathologies. Functional tests, including pulmonary function assessments, quantify airflow dynamics to differentiate between obstructive and restrictive lung diseases. Chest X-ray (CXR) is a first-line study in patients presenting with acute dyspnea, particularly when pulmonary or cardiac origins are suspected, as it can rapidly detect abnormalities like airspace opacification indicative of , with sensitivity ranging from 46% to 77% compared to computed . In cases of , CXR reveals a visible visceral pleural line with absent lung markings peripheral to it, though sensitivity may be reduced in patients, potentially missing over 30% of cases. For , CXR identifies an enlarged cardiac silhouette, often accompanied by signs of pulmonary venous congestion or bilateral pleural effusions, achieving up to 95% accuracy when interpreted by trained clinicians. Computed tomography pulmonary angiography (CTPA) is the gold standard for diagnosing (PE) in patients with dyspnea, offering high sensitivity (83-100%) and specificity (89-98%) by visualizing thrombi in pulmonary arteries down to the subsegmental level. It is particularly valuable when clinical probability scores, such as Wells criteria, suggest intermediate or high risk for PE, a common cause of acute shortness of breath, and provides rapid results to guide anticoagulation therapy. However, CTPA requires and may be contraindicated in patients with severe renal impairment (eGFR <30 mL/min/1.73 m²) due to the risk of contrast-induced nephropathy. Echocardiography, particularly transthoracic echocardiography (TTE), is essential for assessing cardiac contributions to dyspnea, measuring left ventricular (LVEF) to distinguish heart failure with reduced (HFrEF, LVEF ≤40%), mildly reduced (HFmrEF, LVEF 41–49%), or preserved (HFpEF, LVEF ≥50%), and guiding initial management with agents like beta-blockers or diuretics. It also evaluates valvular function through Doppler imaging, identifying abnormalities such as that elevate pulmonary pressures and contribute to in conditions like PE or . In undifferentiated dyspnea, bedside offers moderate sensitivity (53%) and high specificity (83%) for detecting right ventricular dysfunction suggestive of PE, aiding in rapid . Pulmonary function tests (PFTs), including , are key for quantifying ventilatory mechanics in chronic or subacute dyspnea, measuring forced expiratory in 1 second (FEV1), forced (FVC), and the to classify patterns of impairment. An below 0.70 indicates , such as (COPD) or , where airflow limitation reduces FEV1 disproportionately to FVC, often correlating with symptom severity in dyspnea. In contrast, a preserved greater than 0.70 with reduced FVC and total lung capacity (TLC <80% predicted) suggests restrictive disease, like , confirmed through full PFTs including lung measurements. Ventilation-perfusion (V/Q) serves as a reliable alternative to CTPA for evaluating suspected PE in patients with dyspnea and renal impairment, as it avoids and thus prevents further damage, with sensitivity up to 85% and specificity up to 97%. The test involves inhaled radioactive tracers for ventilation and intravenous macroaggregated for , identifying mismatched defects (normal ventilation with reduced ) that indicate , particularly useful in cases like where creatinine levels exceed 1.5 mg/dL. While non-diagnostic rates can reach 50% in the presence of comorbidities like , a high-probability V/Q scan strongly supports PE and prompts treatment.

Management

Initial assessment and supportive care

Sudden severe shortness of breath, including sudden inability to breathe, constitutes a life-threatening medical emergency requiring immediate intervention. Common causes include anaphylaxis (severe allergic reaction), choking or blocked airway, severe asthma attack, heart attack, pulmonary embolism, pneumothorax (collapsed lung), carbon monoxide poisoning, and acute heart failure. In such emergencies, call emergency services immediately (e.g., 911 or the local equivalent). While awaiting professional help, if the person is conscious, assist them to assume an upright sitting position of comfort, loosen tight clothing around the neck and chest, and monitor breathing and responsiveness. If choking is suspected and the responder is trained, deliver five back blows between the shoulder blades followed by five abdominal thrusts (Heimlich maneuver). If anaphylaxis is suspected and an epinephrine autoinjector (e.g., EpiPen) is available, assist in administering it as directed. If the person has a prescribed rescue inhaler for asthma, assist with its use. Stay with the person, provide reassurance, and if they become unresponsive with no normal breathing or pulse, begin CPR immediately. These are general first aid measures and do not substitute for professional medical care. The initial assessment of a presenting with shortness of breath prioritizes the ABC approach to ensure rapid stabilization. Airway patency is evaluated first by assessing for signs of obstruction such as or inability to speak, with interventions like head-tilt chin-lift or suctioning applied if needed to maintain a clear airway. support follows, involving assessment of (typically 12-20 breaths per minute), effort, and via , with supplemental oxygen delivered through (2-6 L/min) or face mask (5-10 L/min) to address . Circulation is then stabilized by checking pulse rate (60-100 beats per minute), blood pressure (systolic 100-140 mmHg), and capillary refill (<2 seconds), with measures like intravenous fluid infusion if is suspected. Supportive care includes positioning the patient upright or in a semi-Fowler's position (head elevated 30-45 degrees) to optimize expansion and reduce venous return, particularly beneficial in cases of heart failure-related dyspnea. Continuous monitoring with is essential, targeting an SpO2 of 94-98% in most acutely ill patients not at risk of hypercapnic failure, or 88-92% in those with conditions like COPD to avoid oxygen-induced . For patients with acute contributing to severe shortness of breath, such as (CPAP) or bilevel positive airway pressure (BiPAP) is recommended to reduce and risk, with strong evidence in hypercapnic exacerbations like COPD (reducing mortality by 37%) and cardiogenic (reducing mortality by 20%). In for acute refractory dyspnea, systemic opioids are recommended when non-pharmacologic measures are insufficient, as per 2021 ASCO guidelines building on 2020 evidence, with low doses (e.g., 2-5 mg orally or 1-2 mg IV) providing relief without significant respiratory depression in most cases.

Pharmacological interventions

Pharmacological interventions for shortness of breath primarily target the underlying pathophysiological mechanisms, such as , , fluid overload, , or anxiety-related , to provide symptomatic relief and improve respiratory function. Selection of therapy depends on the , with guidelines emphasizing rapid initiation for acute cases and maintenance regimens for chronic conditions. These treatments are tailored to individual patient factors, including severity and comorbidities, and are monitored for efficacy and adverse effects like or imbalances. Bronchodilators, especially short-acting beta-2 agonists such as albuterol, serve as cornerstone therapies for shortness of breath in and (COPD) . By stimulating beta-2 adrenergic receptors, these agents induce bronchodilation, enhancing airflow and reducing the sensation of dyspnea within 5-15 minutes of inhalation. Guidelines recommend albuterol as a first-line rescue medication, administered via or at doses of 2.5-5 mg every 20 minutes for up to three doses in acute settings. Long-acting beta-agonists, like salmeterol, are used for maintenance in stable COPD to sustain bronchodilation and decrease exacerbation frequency. In heart failure-associated shortness of breath, like address by inhibiting sodium reabsorption in the loop of Henle, promoting and reducing intravascular volume. This leads to decreased preload, alleviation of dyspnea, and improved oxygenation, particularly in acute decompensated states. Initial intravenous doses of 20-40 mg are standard, with adjustments based on response and renal function; guidelines advocate sequential nephron blockade with thiazides if needed for cases. Anticoagulants, notably unfractionated , are critical for managing shortness of breath due to by inhibiting and factor Xa, preventing further clot formation and . Administered intravenously with a bolus of 80 units/kg followed by infusion at 18 units/kg/hour, rapidly stabilizes and reduces recurrent embolic risk in acute presentations. Transition to oral agents occurs after 5-7 days, with treatment duration typically 3-6 months for provoked events. Corticosteroids mitigate shortness of breath in inflammatory airway diseases, such as exacerbations, by suppressing immune-mediated and . Systemic options like oral (40-60 mg daily for 5-7 days) or intravenous are recommended for moderate-to-severe cases, reducing hospitalization rates and relapse. Inhaled corticosteroids provide adjunctive maintenance therapy to prevent recurrent episodes. For psychogenic shortness of breath stemming from anxiety or , low-dose benzodiazepines such as (0.5-1 mg as needed) offer short-term relief by enhancing inhibition, thereby dampening and associated distress. Use is limited to second- or third-line after non-pharmacological strategies, due to risks of and dependency. Targeted biologics, including , represent therapies for severe eosinophilic , where traditional treatments are insufficient. Approved in 2018 for patients aged 12 and older with moderate-to-severe and elevated , and expanded to include children aged 6 to 11 years in 2021, dupilumab inhibits IL-4 and IL-13 signaling, significantly reducing rates by up to 67% and improving forced expiratory volume. Subcutaneous dosing every two weeks (300 mg) is standard for adults, with expanded approvals for younger patients as of 2025.

Non-pharmacological approaches

Non-pharmacological approaches to managing shortness of breath, also known as dyspnea, encompass a range of interventions aimed at improving respiratory function, reducing symptom intensity, and enhancing quality of life without relying on medications. These strategies are particularly beneficial for patients with chronic conditions such as chronic obstructive pulmonary disease (COPD) and are often integrated into comprehensive care plans to address underlying physiological limitations like hyperinflation and muscle fatigue. Evidence from systematic reviews indicates that such interventions are generally safe and associated with symptom relief in advanced disease states. Pulmonary rehabilitation is a multidisciplinary program that includes tailored exercise training, patient education, and nutritional counseling to enhance endurance and alleviate dyspnea. Exercise components, such as lower limb endurance training, have been shown to improve exercise capacity, health-related quality of life, and dyspnea scores in patients with stable COPD. Programs typically last 6-12 weeks and involve supervised sessions focusing on aerobic and strength exercises, which help counteract deconditioning and reduce the sensation of breathlessness during daily activities. High-quality evidence supports its efficacy, with moderate improvements in dyspnea reported across multiple randomized trials. Breathing techniques, including and , are simple, self-administered methods that decrease the and improve ventilation efficiency. involves inhaling through the nose for about 2 seconds and exhaling slowly through pursed lips for 4-6 seconds, which helps prevent airway collapse and reduces in conditions like COPD. , by contrast, emphasizes abdominal expansion during inhalation to engage the diaphragm more effectively, thereby lowering the effort required for breathing and alleviating dyspnea during exacerbations. These techniques are recommended by clinical guidelines for immediate symptom relief and long-term self-management, with evidence from controlled studies showing reductions in breathlessness intensity and improved tidal volumes. Long-term oxygen therapy (LTOT) is indicated for patients with chronic , such as those with severe COPD, to correct low blood oxygen levels and mitigate dyspnea. Administered via for at least 15 hours per day, LTOT has been demonstrated to prolong survival and enhance by reducing and improving exercise tolerance. Clinical trials, including landmark studies like the Nocturnal Oxygen Therapy Trial, confirm its benefits in hypoxemic patients with PaO2 ≤ 55 mmHg, though it does not benefit those without severe resting hypoxemia. Guidelines from respiratory societies strongly recommend LTOT based on moderate-quality evidence from randomized controlled trials. Surgical options, such as lung volume reduction surgery (LVRS), target severe by removing 20-30% of the most damaged lung tissue to reduce and improve diaphragmatic function. This procedure alleviates dyspnea by allowing healthier lung regions to expand more effectively, with evidence from randomized trials showing significant improvements in exercise capacity and in carefully selected patients with upper-lobe predominant . LVRS is typically reserved for those who respond poorly to other therapies, as it carries risks like prolonged air leaks, but long-term follow-up data indicate sustained dyspnea relief for up to 5 years in eligible candidates. Authoritative reviews emphasize patient selection based on heterogeneous distribution for optimal outcomes. Palliative measures provide symptomatic relief for refractory dyspnea, particularly in advanced or . Fan , involving directed airflow toward the face (often the cheek, adaptable for patients with a stoma), activates cutaneous and receptors to modulate the brain's perception of breathlessness, with randomized trials demonstrating reduced dyspnea intensity without adverse effects. Chest wall vibration, applied in-phase with inspiration using a handheld device, decreases the effort of in chronic respiratory diseases by enhancing sensory feedback and reducing neural drive, as supported by early controlled studies. Upright positioning, such as leaning forward with supported arms, optimizes diaphragm function and reduces the work of breathing in severe dyspnea, while relaxation techniques including mindfulness meditation help alleviate anxiety that exacerbates breathlessness. These low-cost interventions are safe for home use and are endorsed in guidelines for immediate comfort. Emerging digital applications for dyspnea self-management have gained traction in the , offering tools for tracking symptoms, guiding exercises, and providing personalized via smartphones. These apps, often integrated with wearables for real-time monitoring of and activity levels, have shown promise in improving adherence to self-management strategies and reducing exacerbation frequency in chronic lung diseases like COPD. Scoping reviews of recent studies highlight their feasibility and positive impact on empowerment, though larger trials are needed to confirm long-term efficacy.

Epidemiology and Prognosis

Prevalence and risk factors

Shortness of breath, or dyspnea, affects approximately 10-25% of adults in the general annually, with pooled estimates from systematic reviews indicating a of around 10% based on multiple studies. increases significantly with age, reaching up to 50% in individuals over 65 years, particularly in community-dwelling older adults where rates can range from 17% to 62% depending on severity assessments. Demographically, dyspnea is more common in women than men, with studies showing higher reporting rates and greater symptom burden in females across age groups. It is also more prevalent among smokers and individuals with comorbidities such as cardiovascular or respiratory diseases, where underlying conditions amplify the likelihood of experiencing breathlessness. Key risk factors include , which increases the risk of (COPD)—a major cause of dyspnea—by up to 10-fold in heavy smokers compared to never-smokers. elevates the odds of dyspnea with reported odds ratios of 1.5 to 5.7, depending on levels and activity context, due to reduced lung volumes and increased respiratory demand. Exposure to further heightens risk, as short-term inhalation of pollutants like particulate matter and can trigger acute episodes and contribute to chronic respiratory irritation. Recent trends show a notable rise in persistent dyspnea following , with 10-30% of survivors reporting ongoing breathlessness from 2020 to 2025, often linked to post-viral pulmonary sequelae. Regionally, prevalence is higher in low-income areas, where infections like contribute substantially; post-TB lung damage leads to elevated rates of dyspnea and associated conditions such as COPD in up to 30% of affected individuals.

Outcomes and complications

The of shortness of breath, or dyspnea, varies widely depending on its underlying cause, such as cardiac, pulmonary, or neuromuscular disorders, but the symptom itself serves as an independent predictor of all-cause across diverse populations. In longitudinal studies involving over 500 participants each, dyspnea has been associated with a 1.3- to 2.9-fold increased risk of , with hazard ratios consistently exceeding 1 even after adjusting for factors like age, , and function; follow-up periods ranged from 6 to 43 years, during which mortality rates varied from 5% to 39%. For chronic dyspnea lasting more than one month, the risk of 10-year mortality is 1.37 times higher than in the general population, particularly among those presenting to emergency departments without wheezing. In acute settings, such as prehospital assessments, outcomes can be severe, with approximately 11% of patients experiencing 30-day mortality, often linked to comorbidities like , , or (COPD) exacerbations. Men tend to have higher one-year mortality rates in these cohorts (p < 0.005), and over 60% of such patients require hospitalization, with time-critical diagnoses accounting for 11% of cases. Long-term cardiovascular outcomes are also adversely affected; in a 30-year of over 13,000 adults, even mild shortness of breath increased the risk of heart attack by 30%, while severe dyspnea more than doubled the likelihood of , , and heart attack. Complications of dyspnea often stem from its intensity and duration, leading to in acute presentations if untreated, particularly when show below 90% (observed in 35% of cases) or elevated respiratory rates (in nearly 49%). Chronic dyspnea contributes to psychological distress, including anxiety, depression, and (PTSD), with up to 39% of survivors reporting PTSD symptoms at one year, often triggered by sensations of air hunger. It also impairs , reducing physical functioning and work productivity; for instance, in adults with undiagnosed respiratory symptoms, higher dyspnea scores correlate with increased healthcare utilization (odds ratios of 1.011 for visits and 1.015 for visits) and greater . Additionally, persistent dyspnea can exacerbate , , and smoking-related comorbidities, further elevating morbidity in conditions like or COPD.

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