01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Breathlessness is a perception rather than a diagnosis. It may reflect airway resistance, abnormal lung mechanics, impaired gas exchange, circulatory failure or a metabolic drive to breathe. Anxiety can accompany any of these mechanisms and should not be accepted as the explanation before significant physiological and clinical alternatives are considered.
The first distinction is between a patient who needs immediate support and one who can safely undergo staged diagnostic assessment. Loud wheeze is not a reliable measure of severity: an exhausted patient with little airflow may make very little noise. Equally, rapid deep breathing may be compensating for metabolic acidosis rather than representing primary lung disease.
Key points
- Assess speech, work of breathing, respiratory rate and conscious level before pursuing a diagnostic label.
- Prescribe oxygen to a target saturation, generally 94–98% or 88–92% with hypercapnic respiratory failure risk.
- A normal saturation on oxygen cannot exclude carbon-dioxide retention or respiratory fatigue.
- Consider airway obstruction, asthma, pulmonary oedema, pneumothorax, pulmonary embolism and severe infection early.
- Use blood gases when oxygenation, ventilation or acidaemia will change the support plan.
- Apply pulmonary-embolism probability tools only in the clinical populations and stability settings for which they are appropriate.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Respiratory causes
Airway narrowing, pneumonia, pneumothorax and other lung disorders increase respiratory load or impair gas exchange, often through more than one physiological mechanism.
Cardiovascular and systemic causes
Heart failure, pulmonary vascular obstruction, severe anaemia and metabolic acidosis can produce acute dyspnoea even when the principal problem is outside the airways.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Ventilation–perfusion mismatch
Poor matching of blood flow and alveolar ventilation impairs oxygen transfer; supplemental oxygen can improve the number without correcting the underlying lesion.
- 2Increased respiratory load
Narrowed airways or stiff lungs require greater effort for each breath, which can eventually exceed respiratory muscle capacity and lead to fatigue.
- 3Ventilatory drive
Acidaemia, hypoxaemia and altered central signalling increase the urge to breathe, explaining why respiratory rate must be interpreted with gas exchange and metabolic findings.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Stridor points toward upper-airway narrowing; wheeze and prolonged expiration suggest lower-airway obstruction. Poor air movement, exhaustion or altered consciousness are more dangerous than wheeze intensity alone.
Orthopnoea, widespread crackles and elevated jugular venous pressure suggest cardiac congestion. Severe hypertension or an acute coronary event may precipitate abrupt pulmonary oedema.
Sudden unilateral pain with asymmetric air entry suggests pneumothorax, while pleuritic pain, tachycardia or thrombotic risk may support pulmonary embolism. Neither diagnosis is excluded by an ordinary chest radiograph alone.
Fever, sputum and focal crackles support infection, but older or immunosuppressed people may lack fever. Anaemia, acidosis and neuromuscular weakness can cause dyspnoea without prominent chest findings.
05InvestigationsWhat to request, why it matters and how to interpret it.
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
Pulse oximetry and blood gasesFirst step - Why
- Assess oxygenation, carbon-dioxide handling and acid–base disturbance.
- Interpretation and limitations
- Record the oxygen device and concentration. Pulse oximetry does not measure ventilation; use a gas when hypercapnia, severe illness or treatment failure is possible.
- 02
ECG and chest imaging - Why
- Identify cardiac or thoracic causes and relevant alternatives.
- Interpretation and limitations
- ECG can reveal ischaemia or arrhythmia; radiography can show oedema, consolidation or pneumothorax. A normal radiograph does not exclude pulmonary embolism or early infection.
- 03
Probability-guided pulmonary-embolism testing - Why
- Choose D-dimer or imaging according to pre-test assessment.
- Interpretation and limitations
- For likely PE with Wells score above four, arrange immediate CTPA when possible. D-dimer is not a substitute for indicated imaging in this group.
- 04
Blood count, renal function and selected biomarkers - Why
- Identify systemic contributors and prepare safe disease-specific treatment.
- Interpretation and limitations
- Haemoglobin identifies anaemia, renal tests affect drug and contrast decisions, and natriuretic peptides can assist assessment of new suspected heart failure when interpreted in context.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Upper-airway obstruction
Stridor and altered voice suggest a proximal airway problem requiring urgent assessment; treating only presumed lower-airway bronchospasm would miss the key threat.
Metabolic acidosis
Deep rapid breathing may be appropriate compensation for accumulated acid, especially with ketoacidosis or shock; suppressing that ventilation can worsen acidaemia.
Neuromuscular weakness
A weak cough, shallow breathing and poor secretion clearance can signal failing ventilation despite relatively little audible chest abnormality during examination.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Immediate respiratory supportTreating the threatened airway or failing ventilationFirst stepSevere distress, hypoxaemia, fatigue or reduced consciousness makes waiting for complete investigation unsafe.+
- 1Obtain experienced help, position to support breathing when circulation allows, clear or support the airway and deliver oxygen appropriate to the immediate threat.
- 2Assess whether spontaneous ventilation is effective; assist ventilation and prepare advanced airway support when effort or conscious level is inadequate rather than simply increasing oxygen flow.
- 3Treat the suspected reversible lesion promptly, including severe bronchospasm or tension pneumothorax, and reassess respiratory effort, gas exchange and circulation after intervention.
02Obstructive airway branchInitial treatment of an acute severe asthma patternKnown or suspected asthma is accompanied by marked airflow obstruction and acute respiratory distress.+
- 1Give oxygen to maintain saturation 94–98%, an oxygen-driven salbutamol nebuliser and early systemic corticosteroid, assessing severity and treatment response repeatedly.
- 2Add the appropriate severe-asthma pathway measures, including inhaled ipratropium and senior consideration of intravenous magnesium when indicated by poor response.
- 3EscalationEscalate a silent chest, exhaustion, persistent hypoxaemia or an inappropriately normal PaCO2 of 4.6–6.0 kPa immediately; normal carbon dioxide in a severe attack already indicates a life-threatening pattern, while rising CO2 is more ominous.
03Cardiac and vascular branchSeparating pulmonary oedema from pulmonary embolismThe history, examination and early tests favour an acute cardiac or pulmonary vascular explanation.+
- 1For acute heart failure with congestion, give indicated IV diuretic and address precipitating ischaemia or arrhythmia; monitor pressure, renal function and urine response.
- 2For cardiogenic pulmonary oedema with severe dyspnoea and acidaemia, consider non-invasive ventilation without delay at presentation or after failure to respond to medical treatment. Do not use it routinely for every acute heart-failure admission.
- 3For suspected pulmonary embolism, use the appropriate diagnostic and interim-anticoagulation pathway, checking bleeding risk; haemodynamic instability requires urgent specialist assessment for reperfusion.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Salbutamol for acute severe asthma
Give 5 mg by oxygen-driven nebuliser initially; repeat according to the acute-asthma response pathway, often every 15–30 minutes for a poor early response while senior reassessment proceeds.Monitor pulse, potassium and lactate with intensive treatment. Persistent tachypnoea may reflect worsening obstruction or beta-agonist-associated lactic acidosis and requires reassessment.
Prednisolone for an adult asthma attack
Give 40–50 mg orally once daily until recovery, for a minimum of 5 days, provided the patient can swallow and absorb the medicine.Use an appropriate IV corticosteroid alternative if the oral route is unsuitable. Assess glucose and relevant infection risks; corticosteroids do not replace urgent ventilatory support.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Respiratory arrest
Progressive fatigue, airway obstruction or depressed respiratory drive can culminate in inadequate ventilation and arrest, particularly when deterioration is masked by supplemental oxygen.
Cardiac strain
Hypoxaemia, acidaemia and increased pulmonary vascular resistance can worsen cardiac function or trigger arrhythmia during a severe respiratory presentation.
Treatment-related harm
Excess oxygen in susceptible hypercapnic patients, excessive sedation and poorly monitored positive-pressure support can each worsen an otherwise treatable acute respiratory problem.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Record respiratory rate, speech and effort alongside oxygen requirement; improvement must include the patient’s work of breathing.
- Repeat blood gases when the initial gas is abnormal, oxygen treatment changes substantially or ventilation appears to deteriorate.
- Monitor fluid balance and renal function during diuresis, and potassium during repeated beta-agonist treatment.
- Before discharge, establish a working diagnosis, adequate stability and a follow-up plan with explicit return advice for recurrent or worsening breathlessness.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Pulmonary-embolism rule-out criteria
PERC may help when overall clinical suspicion is low and other diagnoses are feasible; it should not be used to dismiss a clinically likely embolism.
Acute-on-chronic disease
A person with COPD may have pneumonia, heart failure or pulmonary embolism as well as airflow obstruction; the existing label should not end the differential.
Pulse oximeter limitations
Poor perfusion, motion and skin-pigmentation-related measurement error can affect interpretation; use clinical findings and blood gases when readings do not fit.
Positive-pressure trade-offs
Non-invasive support can improve gas exchange but also affect venous return and conceal deterioration; poor airway protection or worsening instability requires prompt expert review.
11Common pitfallsFrequent interpretation and management errors.
- 01
Do not diagnose a panic attack solely because a breathless person appears frightened or has tingling.
- 02
Do not exclude severe asthma because wheeze becomes faint when the patient is tiring.
- 03
Do not request a D-dimer indiscriminately when a probability assessment already indicates pulmonary-embolism imaging.
- 04
Do not assume that all crackles need antibiotics or that all wheeze represents asthma.