In acute breathlessness, the history, along with a rapid but careful examination, will usually suggest a diagnosis that can be confirmed by routine investigations including chest X-ray, 12-lead ECG and arterial blood gas (ABG) sampling.

Presentation

 A key feature of the history is the speed of onset of breathlessness. Acute severe breathlessness (over minutes or hours) has a distinct differential diagnosis list to chronic exertional breathlessness. The presence of associated cardiovascular (chest pain, palpitations, sweating and nausea) or respiratory (cough, wheeze, haemoptysis, stridor) symptoms can narrow the differential diagnosis yet further. A previous history of left ventricular dysfunction, asthma or exacerbations of chronic obstructive pulmonary disease (COPD) is important. A high temperature, cough (productive or non-productive) and/or viral prodrome may indicate respiratory infection and, if so, relevant infection control precautions should be taken from initial assessment. In the severely il patient, it may be necessary to obtain the history from accompanying witnesses. In children, the possibility of inhalation of a foreign body (Fig. 1) or acute epiglottitis should always be considered. There is often more than one underlying diagnosis; a thorough assessment should continue, even after a possible diagnosis has been reached, particularly if the severity of symptoms does not seem to be adequately explained.

Fig1. Inhaled foreign body A- Chest X-ray showing a tooth lodged in a main bronchus. B- Bronchoscopic appearance of inhaled foreign body (tooth) with a covering mucous film.

Clinical assessment

 Airway obstruction, anaphylaxis and tension pneumothorax require immediate identification and treatment. If any of these is suspected, treatment should not be delayed while additional investigations are performed, and anaesthetic support is likely to be required. In the absence of an immediately life-threatening cause, the following should be assessed and documented:

- level of consciousness

- degree of central cyanosis

- work of breathing (rate, depth, pattern, use of accessory muscles)

- adequacy of oxygenation (SpO₂ )

- ability to speak (in single words or sentences)

- cardiovascular status (heart rate and rhythm, blood pressure (BP) and peripheral perfusion).

 Pulmonary oedema is suggested by a raised jugular venous pressure and bi-basal crackles or diffuse wheeze, while asthma or COPD is characterised by wheeze and prolonged expiration. A hyper-resonant hemithorax with absent breath sounds raises the possibility of pneumothorax, while severe breathlessness with normal breath sounds may indicate PE. Leg sweling may suggest cardiac failure or, if asymmetrical, venous thrombosis.

The presence of wheeze is not always indicative of bronchospasm. In acute left heart failure, an increase in the left ventricular diastolic pressure causes the pressure in the left atrium, pulmonary veins and pulmonary capillaries to rise. When the hydrostatic pressure of the pulmonary capillaries exceeds the oncotic pressure of plasma (about 25–30 mmHg), fluid moves from the capillaries into the interstitium. This stimulates respiration through a series of autonomic reflexes, producing rapid, shallow respiration, and congestion of the bronchial mucosa may cause wheeze (sometimes known as cardiac asthma). Sitting upright or standing may provide some relief by helping to reduce congestion at the apices of the lungs. The patient may be unable to speak and is typically distressed, agitated, sweaty and pale. Respiration is rapid, with recruitment of accessory muscles, coughing and wheezing. Sputum may be profuse, frothy and blood-streaked or pink. Extensive crepitations and rhonchi are usually audible in the chest and there may also be signs of right heart failure.

Any arrhythmia may cause breathlessness, but usually does so only if the heart is structurally abnormal, such as with the onset of atrial fibrillation in a patient with mitral stenosis. In such cases, the classic mid-diastolic rumbling murmur may be heard. Patients sometimes describe chest tightness as ‘breathlessness’. However, myocardial ischaemia may also induce true breathlessness by provoking transient left ventricular dysfunction. When breathlessness is the dominant or sole feature of myocardial ischaemia, it is known as ‘angina equivalent’. A history of chest tightness or close correlation with exercise should be sought.

Initial investigations

 As shown in Box 1, amalgamation of a clear history and thorough clinical examination with chest X-ray, ECG and ABG findings will usually indicate the primary cause of breathlessness. In cases of suspected infection, a viral throat swab should be obtained early in the course of the assessment; increasingly point-of-care testing of viral throat swabs is available, providing important and rapid diagnostic information. If available, sputum should be sent for culture. If bronchospasm is suspected, measurement of peak expiratory flow will assist in the assessment of severity and should be performed whenever possible.

An ABG will often provide additional information to SpO₂ measurement alone, particularly if there is clinical evidence (drowsiness, delirium, asterixis) or a strong likelihood of hypercapnia. An acute rise in PaCO₂  will increase the HCO₃^-  by only a small amount, resulting in inadequate buffering and acidaemia. Renal compensation and a large rise in HCO 3 will take at least 12 hours. In acute type II respiratory failure , the rate of rise of PaCO₂ is a better indicator of severity than the absolute value. An ABG can also give a carboxyhaemoglobin level after smoke inhalation (although this can also be measured on a venous sample), and is central to the identification of metabolic acidosis or the diagnosis of psychogenic hyperventilation (see Box 1).

Box1. Clinical features in acute breathlessness

If pulmonary embolism is suspected, calculating pre-test probability is key. In a patient with a pre-test probability of less than 15%, the pulmonary embolism rule-out criteria (PERC) can rule out pulmonary embolism clinically, negating the need for further imaging, if none of the criteria listed in Box 2 is met.

Procalcitonin (PCT) and N-terminal pro-hormone brain natriuretic protein (NT-proBNP) can be measured in venous blood. While these biomarkers can give an indication of aetiology in shortness of breath, they are probably of more value in tracking clinical progression and response to treatment. Elevated PCT is a biomarker for bacterial infection and may be useful, in addition to clinical assessment, in helping decide the need for and duration of antibiotic therapy in patients with confirmed viral respiratory disease (such as COVID-19) who may have additional bacterial super-infection. Elevated NT-proBNP is suggestive of underlying left ventricular failure , although it can be elevated in other conditions such as renal failure, COPD, pulmonary hypertension and pulmonary embolism. Measurement of NT-proBNP may be considered if there is no clear-cut evidence of pulmonary oedema on a chest X-ray and can be particularly useful as a ‘rule-out’ test, as a normal NT-proBNP has high negative predictive value for heart failure. Individuals with suspected heart failure should undergo early echocardiography.

CT imaging (with or without pulmonary angiography) is a useful investigation in many respiratory conditions as interstitial changes, tumours or consolidation may not be evident on chest X-ray. If breath lessness is suspected to be an ‘angina equivalent’, objective evidence of myocardial ischaemia from stress testing may help to establish the diagnosis, although coronary artery angiography (either by CT or car diaccatheterisation) is often performed early in the investigation path way.

Box2. PERC rule for pulmonary embolism