Assessment of dyspnoea

Overview 
Theory 
Emergencies 
Diagnosis 
Resources 

In the acute or subacute presentation, an initial assessment for the severity of the clinical condition is the first step, using the Airway, Breathing, Circulation, Disability, Exposure (ABCDE) protocol.[12][13] See the Urgent considerations section for immediate management for life-threatening conditions.

Time course

Acute dyspnoea appears suddenly or in a matter of minutes. It typically indicates acute and severe conditions that may be life-threatening. Examples of conditions causing sudden-onset dyspnoea include acute pulmonary embolism, myocardial infarction, acute heart valve insufficiency, pneumothorax, anaphylaxis, foreign body aspiration, pulmonary oedema, or cardiac tamponade.[73]

Subacute dyspnoea develops over hours to days. Common causes include acute asthma, exacerbation of chronic obstructive pulmonary disease (COPD), or pulmonary oedema. Less common causes include myocarditis, superior vena cava syndrome, acute eosinophilic pneumonia, or cardiac tamponade.[73][74][75]

Chronic dyspnoea develops over weeks to months. It is associated with chronic pathology, such as congestive heart failure, COPD, cardiomyopathy, idiopathic pulmonary fibrosis, pulmonary vascular disease, pulmonary hypertension, valvular heart disease, or anaemia.[76] Less common causes of chronic dyspnoea include muscular dystrophies, kyphoscoliosis, amyotrophic lateral sclerosis, pulmonary alveolar proteinosis, chronic eosinophilic pneumonia, uraemia, or constrictive pericarditis.[75][77][78][79][80]

An acute/subacute worsening of dyspnoea in a patient with a known cardiovascular, pulmonary, or neuromuscular condition may represent a deterioration of the underlying condition or the appearance of a new problem.

Recurrent dyspnoea may indicate paroxysmal tachycardias or intermittent complete heart block.

Clinical history

The approach to the patient with dyspnoea depends on the severity of symptoms. Although careful history taking is crucial in the assessment of patients with all degrees of severity of dyspnoea, this tends to be much more focused and concise for people presenting acutely. Similarly, in the acute presentation, the physical examination and investigations focus on vital findings that may point to (or rule out) life-threatening pathology. The approach to the patient with chronic dyspnoea allows time for a more comprehensive, stepwise assessment.

The following factors need to be considered when taking a clinical history, although the time spent on asking questions and the degree of detail elicited will depend on the severity of the patient’s condition and the need for immediate investigations and treatment:

Severity

Dyspnoea is highly subjective, and, for a given level of functional impairment, severity varies widely. There is no universally agreed measure of dyspnoea; several scales are available in both research and clinical practice.[81] Although scales exist, their use in everyday practice is limited.
Severe dyspnoea in the acute presentation is typically associated with other symptoms and is more likely to be life-threatening (e.g., acute asthma, tension pneumothorax, acute upper airway obstruction, massive pulmonary embolism, or myocardial infarction).
Mild dyspnoea may be a sole symptom and may indicate a benign aetiology. It may be caused by stable COPD, deconditioning, non-critical airway obstruction, or normal ageing.
In the more chronic presentation, measurement of severity using three domains is suggested: sensory-perceptual (measuring what breathing feels like); affecting distress (measuring how distressing breathing feels); and symptom impact (measuring how dyspnoea affects functioning or quality of life).[1]
The Veterans Specific Activity Questionnaire (VSAQ) assesses the functional capability of the patient and estimates the aerobic capacity in metres.[82] The degree of impairment can then be inferred. The approach and testing for a 25-year-old with trouble running an 8-minute mile is different from that of an 80-year-old with trouble climbing a 12-step staircase. The VSAQ establishes the baseline function and provides an objective measure for longitudinal assessment of progress or the lack thereof.
Other classification schemes include the New York Heart Association functional classification and the Medical Research Council dyspnoea scale.[83][84]

Associated symptoms

Dyspnoea often occurs with other symptoms, and their co-existence may help to localise the origin of dyspnoea to the involved organ system and help to narrow the differential diagnosis.
Central chest pain is a common associated symptom in acute presentations and may suggest acute coronary syndrome, pulmonary embolism, pneumothorax, pneumomediastinum, or foreign body aspiration.[85] A more chronic history of central chest pain on exertion, lasting less than 20 minutes, not rapidly increasing, and relieved by rest or glyceryl trinitrate is more typical of stable angina.
Pleuritic chest pain may present acutely, subacutely, or chronically and may indicate pneumonia, pneumothorax, pulmonary embolism, a solitary fibrous tumour of the pleura, or pleuritis.[86]
Pericardial constriction and effusions are characterised by typical pericardial pain that is referred to the scapular region, worsened by position and changes in intrathoracic pressure, and relieved by leaning forwards.
Palpitations may be present in paroxysmal tachyarrhythmias, pulmonary embolism, valvular heart disease, or anxiety attacks.
Syncope may accompany dyspnoea associated with tachyarrhythmias or pulmonary embolism.
Fever manifests with dyspnoea in many infectious and inflammatory conditions, including pneumonia, bronchitis, laryngitis, viral syndromes (e.g., Hantavirus pulmonary syndrome and severe acute respiratory syndrome [SARS]), vasculitides, and sepsis.[87][88] Dyspnoea plus fever and cough may indicate community-acquired pneumonia or opportunistic infection in immunocompromised hosts. Post-obstructive pneumonia is possible in patients with foreign body aspiration or a chest malignancy.
Fatigue, anorexia, nausea, myalgia, sore throat, expectoration of sputum, confusion, dizziness, gastrointestinal disturbance, anosmia, dysgeusia, rhinorrhoea, and conjunctival congestion may occur with COVID-19. Patients who have recovered from COVID-19 may continue to experience dyspnoea.[89][90]
Night sweats, malaise and weight loss may occur with tuberculosis infection.
Wheezing in the acute or subacute presentation may indicate acute asthma, acute exacerbation of COPD, pulmonary oedema, bronchiolitis, or aspiration of a foreign body. Wheezing in the chronic presentation may indicate asthma, COPD, bronchiectasis, tracheobronchomalacia, or pulmonary or tracheobronchial tumours.
Cough may be present in acute bronchitis, acute infectious pneumonia, acute eosinophilic pneumonia, interstitial lung disease, COPD, asthma, bronchiectasis, tracheobronchomalacia, or chronic pneumonitis.[75] Chronic sputum production may indicate COPD or bronchiectasis, while large amounts of clear secretions may be present in bronchoalveolar carcinoma.[91]
Change in the pitch of the voice may accompany dyspnoea associated with pneumomediastinum, aortic aneurysm, retropharyngeal haematoma, lung cancer, or gastro-oesophageal reflux.[92][93]
Haemoptysis may accompany dyspnoea in patients with COVID-19, acute bronchitis, exacerbation of bronchiectasis, chest malignancies, vasculitides, acute infectious pneumonia, cryptogenic organising pneumonia, pulmonary embolism, cocaine toxicity, tuberculosis, or diffuse alveolar haemorrhage.[94][95][96][97][98][99]
Dysphagia or odynophagia may be present in a dyspnoeic patient with granulomatous laryngitis, pneumomediastinum, foreign body aspiration, tetanus, and epiglottitis.[100][101][102] In epiglottitis, dyspnoea may be additionally accompanied by drooling. Vomiting and diarrhoea may accompany dyspnoea in thyrotoxicosis or botulism.[103][104] Heartburn may be present in gastro-oesophageal reflux with aspiration.
Muscle weakness or myalgias associated with dyspnoea may indicate deconditioning, adverse effects of medications, muscular dystrophies, amyotrophic lateral sclerosis, acute polio or post-polio syndrome, Guillain-Barre syndrome, West Nile and other viral infections, leptospirosis, Cushing's myopathy, or botulism.[77][88][103][105][106][107][108][109][110]
Visual disturbances may occur with dyspnoea in myasthenia and tetanus, and headache may be present in carbon monoxide poisoning.[101][111][112]
Bone pain may be associated with acute chest syndrome due to sickle cell anaemia or fat embolism associated with long-bone fractures.[113]
Anxiety may be a reaction to dyspnoea of any aetiology but may also cause dyspnoea in acute panic or anxiety attacks.[114] Dyspnoea associated with stress may indicate anxiety, hyperventilation, or takotsubo cardiomyopathy.[115]
Abdominal pain, nausea, vomiting and diarrhoea may occur in patients with e-cigarettes, or vaping product use associated lung injury (EVALI). Gastrointestinal symptoms may precede respiratory symptoms of dyspnoea, cough and chest pain.[116][117][118]

Positionality

Orthopnoea is the presence of dyspnoea while supine, with an improvement in the upright position. It is characteristically linked with congestive heart failure but may also be present in asthma, COPD, inflammatory and degenerative neurological diseases, gastro-oesophageal reflux, pericardial effusion, or bilateral diaphragmatic paralysis.[77][119][120][121]
Platypnoea is the worsening of dyspnoea on assuming an upright position, with alleviation while supine. It is typical of patent foramen ovale, abdominal muscle deficiency, or hepatopulmonary syndrome.[122][123]
Trepopnoea is an infrequent finding in which dyspnoea is present only in the lateral decubitus position. It is associated with congestive heart failure, sinus of Valsalva aneurysms, or after a pneumonectomy.[124][125]
Variable positional changes in dyspnoea may also be seen in primary and metastatic cardiac tumours.[126][127]

Pattern of dyspnoea

Dyspnoea that appears during the working week and resolves over periods off work may be related to occupational exposure and suggests occupational asthma.[128][129] Occupational exposure may also be implicated in cases of asbestos-related lung disease and hypersensitivity pneumonitis.[130] A history of occupational or leisure exposure to aerosolised solvents, fumes, organic dust, moulds, and animals should be elicited and may be implicated in interstitial lung disease. Dyspnoea developing in indoor ice hockey players may reflect nitrogen dioxide or carbon monoxide toxicity from faulty ice resurfacing equipment.[131]
Seasonal dyspnoea or shortness of breath related to cold, pets, exercise, or non-specific irritants may suggest asthma or reactive airway disease.[132]
Dyspnoea occurring from the day prior to menses, and up to three days after menses, may indicate a catamenial pneumothorax.[133]

Past medical history

It is important to consider the possibility of comorbidities.

Asthma may be an extra-oesophageal manifestation of gastro-oesophageal reflux disease, while COPD often coexists with other conditions, such as cardiovascular diseases, gastro-oesophageal reflux, and lung cancer, which can make the differential diagnosis difficult.[26][93]
Dyspnoea may be associated with obesity or occur during a normal pregnancy. In pregnant patients dyspnoea may indicate the presence of a previously undiagnosed medical condition, such as valvular heart disease, pulmonary hypertension, alpha-1 protease inhibitor (alpha-1 antitrypsin) deficiency, pulmonary embolism, spontaneous pneumothorax or pneumomediastinum, progression of a pulmonary arteriovenous malformation, or deterioration of myasthenia.[134][135][136][137][138][139][140][141]
In a patient who is or recently was in labour, dyspnoea may indicate pulmonary embolism, septic or toxic shock, amniotic fluid or trophoblastic embolism, pneumothorax, or pneumomediastinum.[51][142]
Dyspnoea in the post-operative period may indicate pulmonary embolism, an acute coronary event, or pulmonary oedema related to fluid resuscitation. Less frequently a pneumothorax or previously unrecognised muscular dystrophy may be implicated.[143] Specific surgical interventions may be followed by dyspnoea due to fat embolism (liposuction, long-bone surgery), diaphragmatic paralysis (aortic valve surgery, lung surgery, and coronary artery bypass surgery), talc-induced acute lung injury (pleurodesis), or pulmonary vein stenosis (mitral valve surgery).[52][144][145] A history of previous venothromboembolic disease, inadequate anticoagulation, immobilisation, admission to hospital, long-distance travel, vascular access, or leg injury may indicate pulmonary embolism as the cause of dyspnoea.
The presence of a known autoimmune or rheumatological disease predisposes the patient to dyspnoea resulting from pulmonary embolism, pulmonary hypertension, interstitial lung disease, pleural effusion, or pulmonary haemorrhage.[146]
Known malignancy may cause dyspnoea through airway obstruction by the primary or metastatic tumour, malignant effusion, post-obstructive pneumonia, pulmonary tumour embolism, lymphangitic spread into the lung, or pericardial or endocardial involvement.[147][148]
History of rheumatological diseases, prior thromboembolic disease, uncorrected obstructive sleep apnoea, and obesity may indicate pulmonary hypertension.
Recurrent pneumonia may indicate gastro-oesophageal reflux with aspiration, a retained foreign body, benign or malignant tumours, or a vascular ring.[149][150][151]
Pleural effusions can accompany pneumonia, heart failure, pleural tuberculosis, malignancy, rheumatological diseases, or mesothelioma.
A history of thoracic radiation for malignancy should be elicited. Dyspnoea due to radiation pneumonitis typically appears 1 to 6 months after the radiation treatments.[152]
History of prior endotracheal intubation and prolonged mechanical ventilation may suggest subglottic scarring and stenosis.
Dyspnoea in a person with history of COVID may be a symptom of long COVID.[153]

Drug history

Medications may cause dyspnoea or contribute to it through a variety of mechanisms, including several forms of pulmonary toxicity (interstitial disease, pulmonary oedema, pulmonary haemorrhage, airways disease, pleural effusion, pulmonary vascular changes), induction of metabolic acidosis (nucleoside reverse-transcriptase inhibitors, topiramate), or induction of bradycardia and chronotropic insufficiency (digoxin, calcium-channel blockers, beta-blockers). Pneumotox on line: patterns - interstitial/parenchymal lung disease Opens in new window[154][155]
Beta-blockers may worsen airway obstruction in COPD and asthma.

Social history

A smoking history with documentation of the number of pack-years smoked is essential. Several smoking-related conditions, including COPD, lung cancer, and certain forms of interstitial lung disease, may produce dyspnoea.
No physical activity, being overweight or obese, and socioeconomic disadvantage are associated with chronic breathlessness.[156]
A history of e-cigarette or vaping product use, and the substances used (nicotine, cannabis, tetrahydrocannabinol) should be elicited. E-cigarette or vaping product use associated lung injury (EVALI) may present with dyspnoea.[116][118][157]
Excessive alcohol intake, injecting drug use, birth in a high-incidence country, and close contact with a person with active pulmonary tuberculosis are all risk factors for tuberculosis.[158]
A history of travel to, or residence in, a location reporting community transmission of COVID-19 disease during the 14 days prior to symptom onset should prompt the clinician to consider this diagnosis.

Physical exam

Careful physical examination helps to narrow the differential and rule in or out life-threatening conditions. Generally, dyspnoea with the presence of signs of acute distress ('dyspnoea that a doctor can see') fares worse than dyspnoea reported by a patient with a normal or near-normal physical exam.

Vital signs

Distress caused by acute dyspnoea typically leads to the appearance of several non-specific signs such as tachypnoea (rapid respiratory rate) and tachycardia (rapid heart beat). More specific changes in vital signs may point to specific pathologies.

A constellation of hypotension, tachycardia, and tachypnoea may indicate acute myocardial infarction, pulmonary embolism, aortic dissection, acute valvular insufficiency, cardiac tamponade, or an acute infectious process with sepsis.[159]
Hypertension in a dyspnoeic patient may point to hypertension-related diastolic heart failure with pulmonary oedema, hyperthyroidism, or phaeochromocytoma.[160]
Mental status change may be present with dyspnoea in some conditions, including hypoxaemic or hypercapnic respiratory failure related to congestive heart failure, pulmonary oedema, asthma, COPD, pneumonia, sepsis, or central nervous system infections.[161]
Pulsus paradoxus may be a sign of asthma, COPD, or cardiac tamponade.[73]

Vital signs may, however, be normal even when dyspnoea is caused by a potentially life threatening condition. A study of over 10,000 adults who attended the accident and emergency department with a chief complaint of dyspnoea reported that more than 50% of patients with acute coronary syndrome (ACS), asthma, and arrhythmia had oxygen saturations of 96% and above, and over half of patients with asthma, PE, arrhythmia, ACS, pneumonia, and COPD had a respiratory rate of <20 breaths per minute.[6] Therefore, normal vital signs are not sufficient to exclude these diagnoses.

General exam

Cyanosis may indicate acute respiratory failure caused by exacerbation of COPD, pulmonary embolism, acute airway obstruction, acute drug toxicity, congenital cyanotic valvular disease, mechanical valve malfunction, cardiac tamponade, pulmonary arteriovenous malformations, aspiration, or methaemoglobinaemia.[159][162][163][164][165]
Jaundice may accompany dyspnoea in liver failure or leptospirosis.[109]
Facial oedema may be present in dyspnoeic patients with superior vena cava syndrome or anaphylaxis.
Urticarial rash may accompany dyspnoea in systemic anaphylaxis.[166] Purpura may indicate thrombotic thrombocytopenic purpura, meningococcaemia, or vasculitis.[167]
Laryngeal height of 4 cm or less is associated with a diagnosis of COPD.[168]
Increased abdominal girth may indicate congestive heart failure, hepatic cirrhosis with ascites and pleural effusions, or constrictive pericarditis.[169]
Clubbing may be present in lung cancer, interstitial lung disease, portopulmonary hypertension, or pulmonary arteriovenous fistulas.[170][171][172][173]
A goitre may accompany retrosternal goitre causing airway obstruction or may be the sign of Graves' disease with thyrotoxicosis.[174][175]
Kyphoscoliosis, either idiopathic or resulting from a neuromuscular process, may cause restriction of chest movement and subsequent dyspnoea.[78]

Cardiovascular exam

Neck vein engorgement may present in dyspnoeic patients with congestive heart failure, COPD, pneumothorax, or cardiac tamponade. Elevated jugular venous pressure and extra heart sound (S3 gallop rhythm) have specificities of 88% and 97% respectively for congestive heart failure.[176]
Chronic dyspnoea resulting from pericardial constriction and effusions may be accompanied by elevated neck veins, pulsus paradoxus, a pericardial knock, pericardial rub, and Kussmaul's sign.[177]
An irregular or fast heart beat may lead to a diagnosis of tachyarrhythmia or atrial fibrillation.
A loud S2 may be associated with pulmonary hypertension and cor pulmonale.
A systolic heart murmur may indicate acute valvular insufficiency, mechanical valve malfunction, or congenital or rheumatic valvular disease.[64][163]
Pulmonary hypertension is suggested by a loud P2 on auscultation.
Lower extremity oedema may indicate congestive heart failure with pulmonary oedema, volume overload, pulmonary thromboembolism, myocardial infarction, arrhythmias, constrictive pericarditis, pulmonary hypertension, inferior vena cava thrombosis, hypothyroidism, or cardiac tumours.[169][178]

Respiratory exam

The trachea may deviate away from the lesion in tension pneumothorax or a large pleural effusion.
Stridor in a dyspnoeic patient is usually caused by upper airway obstruction with a foreign body, infectious or inflammatory oedema (e.g., diphtheria, tetanus, epiglottitis, angio-oedema), dysfunction of the upper airway structures (vocal cord dysfunction, tetany), tumours of the airway wall (base of the tongue, larynx, oesophagus, trachea, and airway papillomatosis), or airway limitation by its extrinsic compression (subglottic stenosis, retrosternal goitre, thyroid cancer, lymphoma).[101][102][174][179][180][181][182][183][184]
Wheezing accompanies dyspnoea in asthma, COPD, anaphylaxis, vocal cord dysfunction, pulmonary congestion and oedema, cystic fibrosis, or pulmonary embolism.
Associated fever and difficulty in swallowing may indicate epiglottitis, while a characteristic cough in a child with an upper respiratory tract infection may indicate croup.
Pursed lip breathing may be present in a patient with COPD.
Hoarseness may accompany dyspnoea in laryngitis, laryngeal tumours, relapsing polychondritis, or unilateral idiopathic and benign (aortic aneurysm, Ortner's syndrome) or malignant vocal cord paralysis.[100][185][186]
Frequent sighing may accompany hyperventilation and anxiety states.[187][188]
A barrel chest (increased anteroposterior diameter) is seen in emphysema and cystic fibrosis.
Unilateral dullness to percussion may be due to pleural effusion, atelectasis, foreign body aspiration, unilateral diaphragmatic paralysis, pleural tumours, or pneumonia.[189] Hyper-resonance may indicate pneumothorax or severe emphysema. Subcutaneous emphysema may indicate the presence of pneumomediastinum.[85]
Unilateral decreased or absent breath sounds may be due to pleural effusion, atelectasis, foreign body aspiration, or pneumothorax.
Bronchial breath sounds may indicate pneumonia.
Distant breath sounds suggest a pleural effusion.[190]
Diminished tactile fremitus and diminished vocal resonance supports a diagnosis of pleural effusion.[191]
Asymmetric chest expansion is a specific, but not sensitive, sign of pneumonia and pleural effusion.[191]
A prolonged expiratory phase may be observed in asthma, COPD, cystic fibrosis, bronchiectasis, or bronchiolitis.
Pulmonary rales may indicate pulmonary congestion (fine, bibasal) or oedema, acute or chronic pneumonia, or some interstitial lung diseases, including sarcoidosis, hypersensitivity pneumonitis, or idiopathic pneumonitides. Velcro crackles should alert the clinician to the possibility of interstitial lung disease.

Neurological exam

Cranial nerve palsies may accompany dyspnoea in botulism.[103]
Ptosis may be present in myasthenia gravis, myotonic dystrophy, or botulism.[103][111][143]
Weakness, muscle wasting, and muscle fasciculations may be present in amyotrophic lateral sclerosis. Proximal greater than distal weakness with reduced muscle tone and subacute (days) dyspnoea may also indicate poliomyelitis secondary to enteroviral infections, West Nile virus, or vaccinations.[192]
Ascending, symmetrical weakness with absent tendon reflexes and progressive dyspnoea may be present in Guillain-Barre syndrome.[107][193]

Clinical decision tools for suspected pulmonary embolism

Clinical probability, assessed by a validated prediction rule and/or clinical judgment, is the basis for all diagnostic strategies for pulmonary embolism (PE).

In low-risk patients, guidance from the UK National Institute for Health and Care Excellence recommends considering use of the Pulmonary Embolism Rule-out Criteria (PERC) as part of the initial assessment to help exclude PE and determine whether further investigations are required.[56] Application of this rule to low-risk and very-low-risk populations has a sensitivity of 96% and 100% respectively, but low specificity.[194]

Investigations

Results of preliminary laboratory testing and radiographic investigations help to narrow the diagnosis. The choice of investigations is dictated by the clinical history and physical examination findings.

Pulse oximetry

Allows detection and ongoing monitoring of hypoxaemia with initiation of oxygen supplementation as necessary, while undertaking diagnostic work-up for its cause.

Peak expiratory flow (PEF)

Simple bedside test that may help differentiate between pulmonary and cardiac causes of dyspnoea.
Low peak flow is associated with obstructive lung disease such as asthma, COPD, and cystic fibrosis.[195]

Arterial blood gas (ABG)

Not all patients with dyspnoea display abnormal findings on ABG, and not all people with abnormal ABG results are dyspnoeic. However, the ABG results may help in constructing a differential diagnosis and, along with exertional oximetry, may be indicated to evaluate gas exchange abnormalities in conditions associated with hypoxaemia.
Hypercapnia (PaCO₂ >45 mmHg) may accompany dyspnoea in exacerbation of COPD, neuromuscular disease, upper airway obstruction, or obesity-hypoventilation syndrome.
Hypocapnia may be present in anxiety states and accompany any process that presents with hyperventilation, such as pulmonary embolism.
Hypoxaemia (PaO₂ <70 mmHg at sea level) has a broad differential, including conditions causing shunting (acute respiratory distress syndrome, pneumonia, pulmonary oedema, cyanotic valvular disease), ventilation-perfusion (V/Q) mismatching (COPD, asthma, pulmonary embolism), diffusion impairment (interstitial lung disease), or hypoventilation (COPD exacerbation, neuromuscular disease, upper airway obstruction, or obesity-hypoventilation syndrome).
The dyspnoea differentiation index, which combines the PaO₂ with PEF ([PEF x PaO₂]/1000), has a reported diagnostic accuracy of 79% in differentiating cardiac from pulmonary causes of dyspnoea.[195]
Acidosis (pH <7.36) is a potent stimulus of breathing and may accompany dyspnoea in the late phases of almost any process presenting with dyspnoea, including sepsis, pulmonary oedema, exacerbation of COPD, renal failure, and cyanide toxicity.[196] It may also be present in idiopathic or medication-induced renal tubular acidosis and thiamine deficiency.[197] Acidosis may result from using medications such as nucleoside reverse-transcriptase inhibitors and topiramate.[154][155]
Alkalosis may be a consequence of anxiety, panic attacks, dehydration, pulmonary embolism, ovarian hyperstimulation syndrome, or pulmonary leukostasis.[198][199]

Electrocardiogram (ECG)

ECG: this helps to diagnose acute coronary syndromes as the cause of dyspnoea with ST-T-segment changes. It also identifies complete heart block, bradycardias, and tachyarrhythmias, and detects changes suggestive of pericarditis, cardiac tamponade (low voltage), and pulmonary embolism.
Changes in the p-wave morphology may help diagnose right atrial enlargement (typical of a chronic pulmonary process) or left atrial enlargement (typical of valvular heart disease).
Change in the QRS axis may indicate right (COPD, pulmonary hypertension) or left (hypertension, valvular heart disease) ventricular enlargement or hypertrophy.

Spirometry

Simple clinic-based test allows the detection of an obstructive deficit, which is revealed by a disproportionate reduction in the forced expiratory volume in the first second of expiration (FEV1) in relation to the forced vital capacity (FVC).
Obstructive deficits are characteristic of asthma, emphysema, or chronic bronchitis.[25][26][200]
More symmetrical reduction in FEV1 and FVC may suggest restriction and warrants full pulmonary function testing, with measurement of lung volumes and DLCO (diffusing capacity of lung for carbon monoxide).[201]

FBC

Leukocytosis may accompany dyspnoea in any infectious process involving the respiratory system, as well as in sepsis, autoimmune disease, parasitic infections, and leukaemia.[198][202]
Eosinophilia may be present in a dyspnoeic patient with parasitic disease, certain vasculitides (e.g., Churg-Strauss syndrome), asthma, eosinophilic pneumonia, drug reaction with eosinophilia and systemic symptoms (DRESS), or cocaine use.[202][203][204][205][206]
Anaemia may be the primary reason for dyspnoea or may accompany it in drug-related lung injury, hereditary haemorrhagic telangiectasia, acute chest syndrome of sickle cell disease, pulmonary alveolar haemorrhage, or widespread infectious processes.[207][208]
Thrombocytopenia may be present with dyspnoea in viral infections, including influenza, SARS, and Hantavirus pulmonary syndrome.[87][88] It may also be due to adverse drug reactions, especially with chemotherapy.

C-reactive protein

Elevated in infection and other acute inflammatory states.

Electrolytes

Hyponatraemia may accompany dyspnoea in congestive heart failure, chronic kidney disease, liver failure, or hypothyroidism.

Thyroid function tests

Thyroid disease may present with dyspnoea.[10]

Liver function tests

Bilirubin may be elevated in dyspnoeic patients with liver failure, congestive heart failure, leptospirosis, and thoracic amoebiasis.[109][209][210]
Transaminases may be elevated in liver failure, acute myocardial infarction, atypical pneumonia (especially Legionella pneumonia), DRESS, and viral infections such as SARS and Hantavirus pulmonary syndrome.[87][88][206]

Kidney function tests

Dyspnoea accompanied by laboratory evidence of renal insufficiency may be due to metabolic acidosis, uraemic pleurisy, long-term volume overload with pleural effusions, pneumonia, DRESS, and several types of acute vasculitis.[206][211][212][213]

Cardiac enzymes

Elevated troponin I/T, myoglobin, and creatine kinase-MB may accompany acute myocardial infarction, myocarditis, takotsubo cardiomyopathy, DRESS, or rarely hypothyroidism.[214][215][216]
Troponin is the preferred biomarker in the evaluation of patients with suspected ACS. Myoglobin is a non-specific marker, with an early peak in activity following myocardial injury. Other markers have satisfactory sensitivity if measured 4-6 hours following the onset of symptoms. Troponin I and T, and CK-MB, are specific to the heart muscle.
May also reflect chronic coronary artery disease with superimposed physiological stress (e.g., sepsis, pulmonary embolism, chronic kidney disease).

BNP or N-terminal pro-BNP (NT-proBNP)

Elevated BNP and NT-proBNP have been associated with congestive heart failure, but also sepsis, coronary artery disease, pulmonary embolism, COPD with cor pulmonale, renal failure, liver cirrhosis, and hyperthyroidism.[217][218][219][220]
In emergency settings, natriuretic peptide biomarker levels may be more useful for ruling out than ruling in heart failure.[221] A low normal BNP level (<100 nanograms/L [<100 picograms/mL]) or a low NT-proBNP level (<300 nanograms/L [<300 picograms/mL]) is helpful in excluding congestive heart failure.[67]
NT-proBNP levels <400 nanograms/L (<400 picograms/mL) in an untreated person with chronic symptoms makes a diagnosis of heart failure less likely.[222]

D-dimer

D-dimer testing is particularly useful in patients with a low clinical probability assessment for PE.[50][223]
If there is high clinical suspicion of PE, or the patient does not satisfy the PERC rule, the Wells (or Geneva) Score may be used to categorise the patient as:
- ‘PE likely’ (Wells Score >4); D-dimer testing is not recommended because a negative result will not remove the need for definitive imaging (usually computed tomographic pulmonary angiography [CTPA] if available)[56][224][Figure caption and citation for the preceding image starts]: Original and simplified Wells Criteria (modified)Created by BMJ Knowledge Centre [Citation ends].
- ‘PE unlikely’ (Wells Score ≤4); D-dimer test is ordered.[56][224] A normal plasma D-dimer level safely excludes PE in patients with an unlikely pre-test probability of PE and no further investigation is required.[50][224]

D-dimer blood testing by enzyme-linked immunosorbent assay (ELISA) has a sensitivity and negative predictive value >95%, regardless of the calculated clinical probability, making it useful to rule out the presence of venous thromboembolism.[224] However, specificity is much lower, with estimates from 23% to 63%.[223]

Serological tests

High titre antibody against the suspected antigen supports a diagnosis of hypersensitivity pneumonitis. Common causative antigens include bacteria (thermophilic Actinomycetes, responsible for farmer’s lung and mushroom picker’s lung) and animal proteins (responsible for pigeon breeder’s lung and bird fancier’s lung).

Blood cultures

Blood cultures should be obtained in patients with severe community acquired pneumonia (CAP). Severe CAP is defined by the presence of one major criterion.[38]
- Septic shock with need for vasopressors
- Respiratory failure requiring mechanical ventilation, or three or more minor criteria:[38]
  - Respiratory rate ≥30 breaths/min
  - PaO₂/FiO₂ ratio ≤250
  - Multilobar infiltrate
  - Confusion or disorientation
  - Uraemia (blood urea nitrogen level ≥20 mg/dL)
  - Leukopenia (white blood cell count <4000 cells/microL)
  - Thrombocytopenia (platelet count <100,000/microL)
  - Hypothermia (core temperature <36°C)
  - Hypotension requiring aggressive fluid resuscitation
- Blood cultures should also be obtained in patients who are being treated empirically for MRSA or P. aeruginosa; patients with previous P. aeruginosa or MRSA infection; and patients who have been hospitalised and received parenteral antibiotics within the last 90 days.[38]
- Blood cultures have a yield of 2% to 9% in non-severe community-acquired pneumonia (CAP) and are not recommended in these patients.[38]

Sputum cultures

Sputum Gram stain and culture is recommended for patients with severe community-acquired pneumonia; patients who are being treated empirically for MRSA orP. aeruginosa; patients with previous P. aeruginosa or MRSA infection; and patients who have been hospitalised and received parenteral antibiotics within the last 90 days.[38]

Urine pneumococcal antigen and Legionella antigen

Randomised trials have failed to identify a benefit for urinary antigen testing for S. pneumoniae and Legionella.[225] There is concern that narrowing antibiotic therapy in response to positive urinary antigen tests could lead to increased risk of clinical relapse. Therefore urinary pneumococcal and Legionella antigen testing is only recommended for patients with severe CAP or if epidemiological factors increase risk of infection (e.g. recent travel, Legionella outbreak).[38]

Influenza virus tests

Influenza is a clinical diagnosis. The role of laboratory testing is to inform decisions about antiviral therapy, whether to perform other diagnostic testing, and the need to implement infection control measures. Not all patients with influenza require diagnostic testing.
Several available tests give results within 4 hours. These include molecular assays (rapid molecular assays; reverse transcription polymerase chain reaction [RT-PCR]) and antigen detection tests (rapid influenza diagnostic tests; immunofluorescence assays). Molecular assays are recommended for hospitalised patients with suspected influenza. They have a sensitivity of 90% to 95%.[226]
A nasal or nasopharyngeal swab, wash, or aspirate should be collected as soon as possible after the onset of illness. Virus shedding in the upper respiratory tract declines significantly 3 to 4 days after illness onset.[227]
Viral culture takes 3 to 10 days so results do not inform clinical management, but are helpful for surveillance and antigenic characterisation of new influenza strains.

Other respiratory viral testing

Nasopharyngeal secretions may be tested for respiratory syncytial virus (RSV), human metapneumovirus (hMPV), adenovirus, rhinovirus, and parainfluenza virus, by polymerase chain reaction (PCR).
Real-time RT-PCR for the detection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral RNA.

Chest x-ray

Appropriate for most adults with acute and chronic dyspnoea.[9][11][228]
Chest x-ray is important to exclude spontaneous or secondary pneumothorax.
Pulmonary venous congestion and an enlarged heart suggest congestive heart failure.[221]
An enlarged cardiac silhouette may indicate valvular heart disease, a pericardial cyst, or cardiac tamponade.[73][229]
Dyspnoea accompanied by parenchymal infiltrates may be present in infectious pneumonia, pulmonary oedema, eosinophilic pneumonitis, radiation pneumonitis, some interstitial lung diseases (sarcoidosis, usual interstitial pneumonitis, non-specific interstitial pneumonitis, cryptogenic interstitial pneumonitis, lymphoid interstitial pneumonitis, acute interstitial pneumonitis, and pleuroparenchymal fibroelastosis), pneumoconioses (silicosis, asbestosis, berylliosis), drug-related lung disease, autoimmune disease-related lung disease (lupus, rheumatoid arthritis, scleroderma, polymyositis, vasculitis), metastatic lung disease and e-cigarette (or vaping product) use associated lung injury.[118][230][231][232][233][234]
Pleural effusion may accompany congestive heart failure, liver failure, uraemia, nephrotic syndrome, malignancy, pneumonia, pulmonary embolism, or pleuritis.
Pleural thickening and nodularity may be seen in pleural tumours and pleuroparenchymal fibroelastosis.[86][234]
Lung hyperinflation may be present in COPD, exacerbation of asthma, or foreign body aspiration.
Elevation of the hemidiaphragm may indicate its paralysis.
Unilateral lucidity may indicate pneumothorax or a diaphragmatic hernia.[235]
Prominent hilar vessels may be apparent in pulmonary hypertension.[236]
Chest x-ray may not be needed in an acute exacerbation of asthma if there is no suspicion of pneumothorax or pneumonia.[228]

Bedside ultrasonography of the chest

Point-of-care ultrasound (POCUS) examination of the heart, lungs, and inferior vena cava is an important tool in establishing the diagnosis of, or ruling out the presence of pleural effusion, pneumothorax, pulmonary oedema, pneumonia, and pulmonary embolism.[237][238][239]
Presence of B-lines on bedside ultrasonography in a patient with high pre-test probability of pulmonary oedema is suggestive of pulmonary oedema. Absence of B-lines in patients with low pre-test probability of pulmonary oedema almost rules out this diagnosis.[240]
Combining bedside echocardiography with ultrasonography of the chest may help further affirm the diagnosis of pulmonary oedema.[241]

Echocardiogram

Can detect pericardial disease and pulmonary hypertension.[236][242]
May also be used to delineate valvular heart disease, measure diastolic dysfunction, and differentiate between systolic and diastolic failure.
The diagnosis of constrictive and restrictive heart diseases with heart failure requires echocardiographic study.[228]

Computed tomographic (CT) angiography of the chest

CT pulmonary angiography confirms the diagnosis in most patients with suspicion of pulmonary embolism.
CT of the chest can also detect and help define the extent of pulmonary parenchymal disease (infectious and non-infectious infiltrates), suggest the presence of pulmonary oedema, define airway abnormalities (benign stenoses, foreign body, malignancy), define vascular abnormalities (congenital and acquired stenoses of the intrathoracic blood vessels, aneurysms), confirm the presence of pleural effusion, or evaluate other intrathoracic structures (thymus, retrosternal goiter).

High resolution CT chest

Necessary in evaluating interstitial lung disease, which is not excluded by a normal chest x-ray.
Prone position imaging helps rule out processes that are gravity-dependent: for example, vascular congestion.
Expiratory imaging should be included in patients with obstructive and mixed pulmonary function tests to rule in or rule out air-trapping and tracheomalacia.[11][243]

Ventilation-perfusion (V/Q) scan

Unmatched perfusion defects on V/Q scan suggest pulmonary embolism in an appropriate clinical setting.

Three-dimensional single-photon emission CT technology

Improves sensitivity and specificity of the V/Q scan.[244]

Lateral x-ray of the neck

May show an enlarged epiglottis, the 'thumb sign', which in an appropriate clinical scenario is suggestive of epiglottitis.

Chest fluoroscopy

Dynamic inspiration ('sniff manoeuvre', 'sniff test') under fluoroscopy helps detect a paradoxical movement of the diaphragm, typical of phrenic nerve paralysis.

CT coronary angiography

Coronary angiography is the conventional reference standard for diagnosis of coronary artery disease. Angiography also provides details about the overall coronary anatomy.
50% to 70% luminal diameter narrowing is considered coronary obstruction, although presence of lesser lesions is prognostically relevant.[245]
Risks include thrombosis or haemorrhage related to vascular access, arrhythmia, and atheroembolism.

Pulmonary function testing

Involves spirometry, measuring lung volumes, and evaluating the DLCO.
The two most common patterns of ventilatory defect are an obstructive deficit (low FEV1/FVC ratio, increased residual volume, increased total lung capacity), seen in asthma, bronchitis, and emphysema, and a restrictive deficit (symmetrical reduction of FEV1 and FVC, high FEV1/FVC ratio, low total lung capacity), seen in interstitial lung disease.
Less common patterns include a fixed or variable extrathoracic flow limitation in vocal cord obstruction and tumours, an isolated reduction of the DLCO in pulmonary hypertension and interstitial lung disease, and a low maximal voluntary ventilation in neuromuscular diseases.

Fractional exhaled nitric oxide testing

Measurement of a fraction of nitric oxide in exhaled air (FeNO, expressed in parts per billion [ppb]) can act as a non-invasive marker to detect eosinophilic inflammation of the airways. High FeNO level ( >40-50 ppb) supports the diagnosis of asthma.[200][246][247]Expert Panel Working Group of the National Heart, Lung, and Blood Institute (NHLBI) administered and coordinated National Asthma Education and Prevention Program Coordinating Committee (NAEPPCC)., Cloutier MM, Baptist AP, et al. 2020 Focused updates to the asthma management guidelines: a report from the National Asthma Education and Prevention Program Coordinating Committee Expert Panel Working Group. J Allergy Clin Immunol. 2020 Dec;146(6):1217-70. Cut-off values may vary according to age and location; consult local guidance.
The National Heart, Lung, and Blood Institute (NHLBI) suggests FeNO measurement in individuals aged >5 years:[247]Expert Panel Working Group of the National Heart, Lung, and Blood Institute (NHLBI) administered and coordinated National Asthma Education and Prevention Program Coordinating Committee (NAEPPCC)., Cloutier MM, Baptist AP, et al. 2020 Focused updates to the asthma management guidelines: a report from the National Asthma Education and Prevention Program Coordinating Committee Expert Panel Working Group. J Allergy Clin Immunol. 2020 Dec;146(6):1217-70.
- for whom the diagnosis of asthma is uncertain using history, examination, clinical course, spirometry, and bronchodilator responsiveness testing, or
- in whom spirometry cannot be performed.
The UK National Institute for Health and Care Excellence guidelines on asthma recommend that adults, young people and children aged 5-16 years with a possible diagnosis of asthma should be offered a fractional exhaled nitric oxide (FeNO) test initially, before spirometry, if available.[246]
The European Respiratory Society recommends that a FeNO test be offered to patients aged >18 years suspected of asthma, in whom the diagnosis has not been established based on the initial spirometry combined with bronchodilator reversibility testing.[200]

Bronchial provocation test

Inhalation of increasing doses of methacholine or histamine can be used to establish the presence of bronchial hyper-responsiveness.
Bronchial hyper-responsiveness is a sensitive, but not specific, feature of asthma.[200]

Nocturnal oximetry

Continuous nocturnal non-invasive measurement of oxygen saturation by pulse oximetry allows the detection of hypoventilation, sleep apnoea, or neuromuscular disease.

Holter monitoring

Continuous monitoring of the heart rate over a period of days or weeks allows for the detection of intermittent arrhythmias.

Cardiopulmonary exercise testing

Involves a detailed analysis of the cardiorespiratory response to exercise and allows the evaluation of cardiac function, pulmonary gas exchange, and ventilation, and the detection of cardiac ischaemia, exercise-related obstructive lung disease, and deconditioning.[248]
Subjective intensity of dyspnoea correlates closely with the magnitude and duration of respiratory effort during exertion.[249]

Electromyography

Signs of acute or chronic denervation or reinnervation may accompany amyotrophic lateral sclerosis.[250]

Lung biopsy

Thoracoscopic lung biopsy may be used to diagnose interstitial lung diseases. Lung biopsy may not be necessary if there are typical clinical and radiologic findings.
May also be used in diagnosing autoimmune or vascular diseases of the lung.
Transthoracic needle aspiration may be useful in confirming the malignant aetiology of intrathoracic nodules.

Needle decompression of tension pneumothorax animated demonstration

How to decompress a tension pneumothorax. Demonstrates insertion of a large-bore intravenous cannula into the fourth intercostal space in an adult.

Venepuncture and phlebotomy animated demonstration

How to take a venous blood sample from the antecubital fossa using a vacuum needle.

How to perform an ECG animated demonstration

How to record an ECG. Demonstrates placement of chest and limb electrodes.

Peak flow measurement animated demonstration

How to use a peak flow meter to obtain a peak expiratory flow measurement.

Radial artery puncture animated demonstration

How to obtain an arterial blood sample from the radial artery.

Femoral artery puncture animated demonstration

How to perform a femoral artery puncture to collect a sample of arterial blood.

Coronavirus disease 2019 (COVID-19)

Cough, fever, and dyspnoea are the most common symptoms of COVID-19. The cough is usually dry. Other symptoms include anosmia, ageusia, fatigue, anorexia, myalgia, and sore throat. There may be a travel history to an affected area or close contact with a suspected or confirmed case in the 14 days prior to symptom onset. The median time from onset of symptoms to hospital admission is reported to be approximately 7 days.[255]

Physical examination may detect fever (with or without chills/rigors) and obvious cough and/or difficulty breathing. Auscultation of the chest may reveal inspiratory crackles, rales, and/or bronchial breathing in patients with pneumonia or respiratory distress. Patients with respiratory distress may have tachycardia, tachypnoea, or cyanosis accompanying hypoxia.

The most common laboratory abnormalities in patients hospitalised with pneumonia include leukopenia, lymphopenia, leukocytosis, elevated liver transaminases, elevated lactate dehydrogenase, and elevated C-reactive protein. Other abnormalities include neutrophilia, thrombocytopenia, decreased haemoglobin, decreased albumin, and renal impairment.[255][256][257][258][259]

Blood and sputum specimens should be collected for culture in all patients to rule out other causes of lower respiratory tract infection and sepsis, especially in patients with an atypical epidemiological history. Specimens should be collected prior to starting empirical antimicrobials if possible.

Molecular testing is required to confirm the diagnosis. Diagnostic tests should be performed according to guidance issued by local health authorities and should adhere to appropriate biosafety practices.

A chest x-ray should be ordered in all patients with suspected pneumonia. Unilateral lung infiltrates are found in 25% of patients, and bilateral lung infiltrates are found in 75% of patients.[255][256][260] All imaging procedures should be performed according to local infection prevention and control procedures to prevent transmission.

See our Coronavirus disease 2019 (COVID-19) topic for current diagnostic advice.

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