Acute and chronic breathlessness

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Breathlessness is the person's experience of uncomfortable breathing, not a diagnosis and not a direct proxy for oxygen saturation. The useful first division is acute versus chronic, followed by physiological severity. Acute threats include upper-airway obstruction, asthma or COPD with ventilatory failure, pneumonia and sepsis, pulmonary oedema, pulmonary embolism, pneumothorax, acute coronary disease, arrhythmia, anaphylaxis and metabolic acidosis. Chronic or progressive breathlessness is commonly multifactorial: airway disease, interstitial lung disease, pulmonary vascular disease, cardiac dysfunction, anaemia, obesity, neuromuscular weakness, medication effects and physical deconditioning can contribute simultaneously.

History should quantify function rather than rely on 'short of breath'. Establish onset, triggers, distance or stairs tolerated, recovery, positional symptoms, nocturnal attacks, cough, sputum, wheeze, chest pain, haemoptysis, fever, weight change and leg swelling. Record smoking and vaping, occupational and environmental exposure, thromboembolic risk, cardiac history, medicines and adherence. Examination then tests hypotheses: observe speech and breathing pattern, assess air entry and added sounds, look for congestion, murmurs, pulse irregularity, anaemia, clubbing, calf asymmetry, muscle weakness and signs of systemic disease.

Investigation should be sequential. Bedside physiology determines urgency; a compact first-line set detects common treatable causes; second-line tests answer residual questions. A mildly abnormal result is not necessarily causal, while two modest abnormalities may together explain severe limitation. Explicitly state which finding explains symptoms, which is incidental, and whether exertional testing is needed because resting physiology can be normal in exercise-induced disease.

Key points

Start with tempo: seconds to hours suggests obstruction, pulmonary oedema, embolism, pneumothorax, anaphylaxis or metabolic crisis; weeks to months broadens the differential to chronic lung, cardiac, anaemic, neuromuscular and deconditioning causes.
Measure respiratory rate, work of breathing, SpO2, pulse, blood pressure, temperature and mental state before assuming that a normal-sounding history means physiological stability.
Treat hypoxaemia to a prescribed target: usually 94-98%, or 88-92% pending blood gases when hypercapnic respiratory failure is a recognised risk; critical hypoxaemia still requires immediate oxygen.
A normal SpO2 does not exclude pulmonary embolism, metabolic acidosis, anaemia, early asthma, cardiac ischaemia or dysfunctional breathing, and supplemental oxygen can conceal worsening ventilation.
Use discriminating features: orthopnoea and congestion support heart failure; pleuritic pain and risk factors support embolism; wheeze supports but does not prove airway disease; inspiratory noise localises towards the upper airway.
First-line chronic assessment usually combines blood count, renal and thyroid profiles, ECG, chest radiograph and spirometry, adding natriuretic peptide, echocardiography, gas transfer, CT or exercise testing to answer specific questions.
Do not label unexplained breathlessness anxiety until dangerous and common organic causes have been assessed; panic and dysfunctional breathing may coexist with cardiopulmonary disease.
Trajectory is a test: document baseline exercise tolerance, compare previous observations and investigations, treat the leading cause, and define what lack of improvement will trigger reassessment.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Respiratory causes

Airway obstruction, infection, pleural disease, pulmonary vascular disease and interstitial or malignant lung disease impair ventilation, gas exchange or respiratory mechanics.

Cardiovascular causes

Heart failure, ischaemia, arrhythmia and valvular or pericardial disease reduce forward flow or raise pulmonary venous pressure, often overlapping with respiratory disease.

Systemic causes

Anaemia, metabolic acidosis, sepsis, endocrine disease and deconditioning increase ventilatory demand or reduce oxygen delivery despite structurally normal lungs.

Functional and perceptual factors

Anxiety, dysfunctional breathing and altered symptom perception can amplify breathlessness, but these diagnoses follow proportionate exclusion of dangerous physiological causes.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Increased ventilatory drive
Hypoxaemia, hypercapnia, acidosis, fever or exercise stimulates respiratory centres to increase rate and depth of breathing.
2
Mechanical loading
Airflow obstruction, stiff lungs, pleural restriction, obesity or muscle weakness increases the effort required to generate adequate ventilation.
3
Demand-capacity mismatch
Breathlessness intensifies when the neural command to breathe exceeds achievable ventilation, producing a conscious sense of unsatisfied inspiration or excessive effort.
4
Affective amplification
Fear and previous respiratory distress heighten attention to bodily signals, creating a feedback loop that may worsen symptoms without implying an imaginary illness.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Acute respiratory or airway threatRed flag

Stridor, inability to complete sentences, marked recession, silent chest, exhaustion, cyanosis, falling respiratory effort or reduced consciousness indicates threatened ventilation or airway patency. Treat immediately rather than sending an unstable patient for routine imaging.

Pulmonary vascular patternRed flag

Sudden unexplained breathlessness, pleuritic pain, haemoptysis, syncope, tachycardia or hypoxaemia with recent surgery, immobility, cancer, pregnancy, oestrogen exposure or previous venous thromboembolism raises pulmonary embolism probability; examination and chest radiograph may be non-specific.

Congestion and cardiac limitation

Orthopnoea, paroxysmal nocturnal dyspnoea, oedema, raised jugular venous pressure, basal crackles, a third heart sound or a new murmur supports heart failure or valve disease. Wheeze can accompany pulmonary oedema and should not automatically be called asthma.

Chronic pulmonary phenotype

Variable symptoms and triggers suggest asthma; smoking exposure with persistent obstruction suggests COPD; dry cough, fine inspiratory crackles and clubbing suggest interstitial disease; daily purulent sputum and recurrent infections suggest bronchiectasis. Objective testing must confirm the working phenotype.

Non-pulmonary and mixed causes

Pallor, bleeding history, weight gain, sleep-disordered breathing, proximal weakness, thyroid symptoms, acidosis, frailty or severe inactivity can explain or amplify breathlessness. Disproportionate symptoms with normal initial tests warrant broader assessment, not dismissal.

Dysfunctional breathing or panic

Episodic air hunger, tingling, sighing and an erratic breathing pattern may support dysfunctional breathing after physiological threats are excluded. Symptoms can be genuine and disabling and may coexist with asthma, pulmonary embolism history or cardiac disease.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
ABCDE observations, pulse oximetry and exertional toleranceFirst step
Why
Establish immediate severity and whether support or monitored care is required.
Interpretation and limitations
Trend respiratory rate, work, speech, pulse, pressure, temperature, consciousness and oxygen requirement. A normal resting saturation does not exclude serious disease; a reproducible exertional desaturation or marked tachycardia changes the differential and urgency.
02
Arterial or arterialised blood gas
Why
Measure ventilation, oxygenation and acid-base state when respiratory failure is possible.
Interpretation and limitations
Hypercapnia with acidaemia identifies acute ventilatory failure and may prompt non-invasive or invasive ventilation assessment. Hypocapnia can accompany embolism, sepsis or metabolic acidosis; interpret PaO2 against the documented oxygen device and concentration.
03
ECG and cardiac biomarkers
Why
Detect arrhythmia, ischaemia, right-heart strain or another cardiac driver.
Interpretation and limitations
An ECG may establish rapid atrial fibrillation or acute coronary disease but cannot exclude pulmonary embolism or heart failure. Use troponin for suspected myocardial injury and natriuretic peptide through the NICE heart-failure pathway when congestion or chronic cardiac limitation is plausible.
04
Chest radiograph
Why
Identify consolidation, oedema, effusion, pneumothorax, focal mass or important structural change.
Interpretation and limitations
Check projection and quality, compare prior images and integrate with examination. A normal film does not exclude embolism, asthma, early infection or important cardiac disease; persistent unexplained symptoms may require CT or functional testing.
05
Blood count, renal profile, liver profile, glucose and thyroid testing
Why
Find anaemia, infection, metabolic disturbance and systemic contributors.
Interpretation and limitations
Relate abnormalities to severity: mild anaemia rarely explains profound acute distress, whereas falling haemoglobin, severe acidosis or acute kidney injury may require immediate action. Eosinophilia can support an airway phenotype but is not diagnostic alone.
06
Spirometry, lung volumes and gas transfer
Why
Characterise airflow obstruction, restriction, gas-exchange impairment and air trapping in stable patients.
Interpretation and limitations
Confirm test quality before interpreting. Obstruction requires a reduced ratio; low FVC alone does not prove restriction, which needs total lung capacity. A low gas-transfer result may support emphysema, interstitial or pulmonary vascular disease and should be corrected for haemoglobin where appropriate.
07
Probability-led CTPA, echocardiography or high-resolution CT
Why
Answer a focused residual question after initial assessment.
Interpretation and limitations
Use NICE probability and D-dimer pathways before CTPA for suspected embolism. Echocardiography evaluates ventricular and valve disease but does not replace clinical assessment. High-resolution CT characterises diffuse lung disease when symptoms, crackles, gas transfer or radiography justify radiation exposure.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Acute pulmonary embolism

Abrupt unexplained dyspnoea, pleuritic pain, syncope or venous thromboembolism risk warrants probability-led assessment even when chest examination is unremarkable.

Acute heart failure

Orthopnoea, oedema, raised venous pressure and pulmonary congestion support cardiac fluid overload, though wheeze and hypoxaemia may resemble airway disease.

Airway exacerbation

Wheeze, cough, variable or known obstruction and response to bronchodilation support asthma or COPD, while a quiet chest may signal critical obstruction.

Pneumonia or pleural disease

Fever, focal crackles, pleuritic pain, reduced breath sounds or new imaging abnormality suggests infection, effusion or pneumothorax.

Anaemia or metabolic disease

Pallor, bleeding history, renal or diabetic symptoms and laboratory abnormalities may explain disproportionate tachypnoea when cardiopulmonary imaging is unrevealing.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01ImmediateUnstable acute breathlessnessFirst stepAirway threat, severe work of breathing, shock, altered consciousness, cyanosis or rapidly worsening oxygen requirement.

1Call senior and critical-care help, use ABCDE, attach monitoring, gain access and obtain a bedside glucose; position and support the airway and ventilation before pursuing a detailed differential.
2Give oxygen to the appropriate target and obtain an early blood gas when hypercapnia or severe gas-exchange failure is possible; do not withhold oxygen from critical hypoxaemia because COPD is suspected.
3Treat the leading reversible emergency in parallel—bronchodilation for severe obstruction, adrenaline for anaphylaxis, decompression for tension pneumothorax, sepsis treatment, pulmonary-oedema support or the probability-led embolism pathway.
4EscalationReassess physiology after every intervention and set an explicit escalation plan for non-invasive ventilation, intubation, procedure or transfer; avoid transporting an unstable patient to unmonitored imaging.

02Initial diagnosisStable but unexplained acute breathlessnessNew breathlessness without immediate ABCDE compromise and without a secure diagnosis.

1Define onset and discriminators, examine lungs, heart and legs, record oxygenation and obtain ECG, chest radiograph and focused blood tests.
2Apply the relevant validated pathway rather than ordering every test: Wells and D-dimer for possible embolism, serial ECG and troponin for possible acute coronary disease, or natriuretic peptide for suspected new heart failure.
3Treat a supported cause and observe response; if symptoms and results conflict, reconsider pneumothorax, embolism, metabolic acidosis, anaemia, upper-airway disease and medication or toxin effects before discharge.
4Discharge only with stable observations, adequate function, a credible explanation or arranged urgent follow-up, and precise advice for recurrence, syncope, chest pain, haemoptysis or worsening work of breathing.

03ChronicStructured chronic breathlessness work-upBreathlessness lasting weeks or months without an established adequate explanation.

1Quantify functional limitation and tempo, review smoking, occupation, medicines and comorbidity, then obtain examination, blood count, renal/thyroid profile, ECG, chest radiograph and quality-assured spirometry.
2Second lineUse results to choose second-line tests: natriuretic peptide and echocardiography for cardiac suspicion; full lung function and CT for restriction or low transfer; sleep testing, muscle testing or ambulatory rhythm monitoring for specific phenotypes.
3When resting tests do not explain exertional symptoms, use a standardised walk test or cardiopulmonary exercise testing to reproduce limitation and separate ventilatory, gas-exchange, circulatory and deconditioning patterns.
4Treat all material contributors, including rehabilitation, smoking cessation, weight, anaemia and anxiety, then review function rather than assuming one diagnostic label will explain the whole symptom burden.

04Discordant resultsSymptoms greater than initial abnormalitiesFirst linePersistent disabling breathlessness with normal or mildly abnormal first-line tests.

1Verify that tests were technically adequate and performed during the relevant state; compare previous imaging, spirometry and haemoglobin rather than accepting an isolated report summary.
2Look for exertional desaturation, pulmonary hypertension, inducible airway obstruction, arrhythmia, neuromuscular weakness and occult cardiac disease using targeted specialist tests.
3Assess breathing pattern, physical conditioning and fear-driven avoidance respectfully, while retaining a route back to organic reassessment if the trajectory changes.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Correct clinically important hypoxaemia while the underlying cause and need for ventilatory support are addressed.

Controlled oxygen

Titrate the delivery device to a prescribed saturation target of 94-98% for most acutely ill adults or 88-92% pending gases when hypercapnic respiratory failure risk is present.

Oxygen does not treat breathlessness without hypoxaemia and does not correct hypoventilation. Record device and flow, repeat blood gases when carbon-dioxide retention is possible, and escalate a rising oxygen requirement.

Reverse the supported pathophysiology rather than treating undifferentiated breathlessness with a routine medicine bundle.

Cause-specific emergency treatment

Use the current national and locally adopted protocol for the established emergency, such as severe asthma, anaphylaxis, pulmonary oedema, sepsis or venous thromboembolism.

Bronchodilator response does not prove asthma, diuresis can harm a non-congested patient, and anticoagulation carries bleeding risk. Verify diagnosis, contraindications, renal function and response.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Respiratory failure

An untreated cause may progress from increased work of breathing to hypoxaemia, hypercapnia, exhaustion and impaired consciousness.

Cardiovascular collapse

Massive embolism, tension pneumothorax, severe heart failure or sepsis can turn breathlessness into shock or arrest within minutes.

Functional decline

Chronic symptoms promote inactivity, muscle deconditioning and frailty, which further increase ventilatory demand during ordinary activity.

Diagnostic delay

Attributing symptoms prematurely to anxiety, obesity or known lung disease can postpone recognition of cancer, vascular disease or cardiac deterioration.

Psychological distress

Persistent air hunger commonly causes panic, sleep disturbance and loss of confidence, worsening disability even when physiological disease is stable.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

In acute illness trend respiratory rate, work of breathing, speech, SpO2 and oxygen device, pulse, blood pressure, temperature, mental state and urine output rather than documenting saturation alone.
Repeat blood gas after material oxygen or ventilation changes in hypercapnic-risk patients and sooner if consciousness, effort or haemodynamics worsen.
Track the disease-specific endpoint: peak flow in asthma, congestion and weight in heart failure, clot-related haemodynamics in embolism, or infection physiology in pneumonia and sepsis.
For chronic symptoms record functional distance, Medical Research Council dyspnoea grade, work or daily-activity impact and exacerbations so treatment benefit is clinically meaningful.
Review pending imaging and specialist tests through a named clinician; abnormal radiology and falling lung function require closed-loop action rather than passive filing.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Dyspnoea is multidimensional

Air hunger, excessive effort and chest tightness arise through different mechanisms. Asking which sensation predominates can distinguish ventilatory drive, mechanical loading and airway narrowing better than a single severity number.

Resting normality may be misleading

Early interstitial disease, pulmonary vascular disease, inducible laryngeal obstruction and chronotropic problems may appear only with exercise. A supervised test can expose the mechanism that resting CT, spirometry or saturation missed.

Hyperventilation has causes

A low carbon dioxide may represent pulmonary embolism, sepsis, pregnancy, liver disease, salicylate exposure or compensation for metabolic acidosis. Calling it anxiety without checking the pH and context is unsafe.

Mild abnormalities can add up

Obesity, moderate anaemia, diastolic dysfunction, modest obstruction and deconditioning may together cause major limitation. Multimorbidity requires treatment of contributors rather than a contest to identify one winner.

Oxygen and ventilation are different

A high saturation on supplemental oxygen can coexist with rising carbon dioxide and exhaustion. Work of breathing, consciousness and blood gas determine whether ventilation is failing.

11Common pitfallsFrequent interpretation and management errors.

01
Equating a normal oxygen saturation with absence of serious cardiopulmonary disease.
02
Diagnosing asthma from wheeze alone when pulmonary oedema, central obstruction or vocal-cord dysfunction remains possible.
03
Ordering CTPA for every breathless patient without pre-test probability and D-dimer reasoning.
04
Calling chronic breathlessness deconditioning before checking anaemia, cardiac disease, lung function and imaging.
05
Reporting several minor abnormalities without deciding whether any explains the patient's functional limitation.
06
Discharging after transient symptomatic improvement without a diagnosis, trajectory check or explicit return advice.