In acute breathlessness, a careful history and examination will usually sug- gest a diagnosis that can be confirmed by CXR, ECG and ABG (Box 4.2).
Presentation
An important clue is the speed of onset. Acute severe breathlessness (onset in minutes to hours) has a different differential diagnosis to chronic exertional breathlessness (covered on p. 312). Associated cardiovascular or respiratory symptoms or a previous history of left ventricular dysfunc- tion, asthma or COPD can narrow the differential diagnosis. In severely ill patients, history from a witness may be helpful. Remember that there is often more than one underlying diagnosis, and continued re- evaluation is needed.
Clinical assessment
Upper airway obstruction, anaphylaxis and tension pneumothorax require immediate identification and treatment, which should not await inves- tigation; urgent anaesthetic airway support is usually required. In the absence of these life- threatening causes, document the following: level of consciousness, degree of central cyanosis, work of breathing (rate, depth, pattern, use of accessory muscles), oxygenation (SpO2), ability to speak (single words/ sentences) and cardiovascular status (HR, BP, JVP, perfusion).
Pulmonary oedema is suggested by a raised JVP and bibasal crackles, whereas asthma or COPD are characterised by wheeze and prolonged expiration. A resonant hemithorax with absent breath sounds indicates pneumothorax, whereas severe breathlessness with normal breath sounds suggests PE. Leg swelling may suggest cardiac failure or, if asymmetrical, venous thrombosis.
Although wheeze usually accompanies bronchospasm, it can also be found in acute left heart failure because of bronchial mucosal congestion (‘cardiac asthma’). In heart failure, pulmonary oedema stimulates breath- ing through vagal lung afferents, producing rapid, shallow breathing. An upright posture may ease the breathlessness. The patient may be unable to speak, distressed, agitated, sweaty and pale. Cough may yield frothy, blood- streaked or pink sputum. Crackles and wheezes are usually audible in the chest, and there may also be signs of right heart failure.
Any arrhythmia may cause breathlessness if the heart is structurally abnormal, for example, new atrial fibrillation in a patient with mitral ste- nosis. Patients sometimes describe chest tightness as ‘breathlessness’.
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Clinical assessment
Cardiorespiratory examination may reveal diagnostic signs. In suspected myocardial ischaemia, a 12- lead ECG is essential. Ongoing chest pain with shock, pulmonary oedema or ventricular arrhythmia or heart block on ECG should prompt urgent cardiology review and transfer to higher level care.
Chest pain with signs of increased intracardiac pressure (especially raised JVP) increases the likelihood of myocardial ischaemia or massive PE. The legs should be examined for signs of DVT.
A large pneumothorax should be evident on clinical examination, with absent breath sounds despite resonant percussion on the affected side. Uni- lateral bronchial breathing or crackles usually indicate respiratory infection, and a CXR should be expedited. Pleural disease may restrict rib movement, with a pleural rub on the affected side. Local chest wall tenderness usually indicates musculoskeletal pain, but also occurs in pulmonary infarction.
Pericarditis may be accompanied by a pericardial friction rub. In aor- tic dissection, there may be syncope, neurological deficit, asymmetrical pulses, features of Marfan’s syndrome (p. 290) or an early diastolic murmur representing aortic regurgitation.
Subdiaphragmatic inflammation (e.g. liver abscess, cholecystitis or ascend- ing cholangitis) can mimic pneumonia by causing fever, pleuritic pain and a sympathetic right pleural effusion. Likewise, acute pancreatitis can present with thoracic symptoms, and an amylase or lipase level may be diagnostic.
The abdomen must be examined in all patients with pleuritic chest pain.
Initial investigations
These are guided by the history and examination findings, but a CXR and ECG should be performed in most patients presenting to hospital with chest pain.
The CXR may reveal pneumonia, pneumothorax, rib fractures or met- astatic deposits. Careful review is needed to avoid missing small abnor- malities. A widened mediastinum suggests aortic dissection, but a normal CXR does not exclude this. In oesophageal rupture, more than 1 hour after symptom onset, the X-ray may show subcutaneous emphysema, pneumo- mediastinum or pleural effusion.
Acute chest pain with ECG changes of STEMI should trigger immediate reperfusion therapy. A history of cocaine or amphetamine use should be sought. If the history suggests MI but the ECG shows ischaemic changes not meeting STEMI criteria, regular repeat ECGs and treatment for NSTEMI/
unstable angina should begin. Serum troponin on admission is often helpful in unclear cases; however, if negative, it should be repeated 6 to 12 hours after maximal pain. Acute coronary syndrome may be diagnosed in patients with a convincing history of ischaemic pain and either ECG evidence of ischaemia or elevated serum troponin. Elevated serum troponin in a patient with an atypical history or a low risk of cardiac ischaemia may indicate myocarditis, PE, sepsis, hypotension, stroke or renal failure.
In chest pain without myocardial ischaemia, causes such as aortic dissection, massive PE and oesophageal rupture should be considered.
Thoracic CT or transoesophageal echocardiography are useful in sus- pected dissection. In massive PE, the CXR and ECG are commonly nor- mal; the classic S1Q3T3 ECG pattern is rare. If massive PE is suspected
and the patient is haemodynamically unstable, a transthoracic ECG may confirm right heart strain and exclude alternative diagnoses such as tamponade.
In patients at low risk of PE, a negative D- dimer effectively excludes the diagnosis. The D- dimer should be measured only if there is clinical suspi- cion of PE because false- positive results encourage unnecessary investiga- tions. If the D- dimer is positive, there is high clinical suspicion or there is other convincing evidence of PE (e.g. right heart strain on ECG), prompt CT pulmonary angiography should be arranged (p. 356 and Fig. 9.13).
Acute breathlessness
In acute breathlessness, a careful history and examination will usually sug- gest a diagnosis that can be confirmed by CXR, ECG and ABG (Box 4.2).
Presentation
An important clue is the speed of onset. Acute severe breathlessness (onset in minutes to hours) has a different differential diagnosis to chronic exertional breathlessness (covered on p. 312). Associated cardiovascular or respiratory symptoms or a previous history of left ventricular dysfunc- tion, asthma or COPD can narrow the differential diagnosis. In severely ill patients, history from a witness may be helpful. Remember that there is often more than one underlying diagnosis, and continued re- evaluation is needed.
Clinical assessment
Upper airway obstruction, anaphylaxis and tension pneumothorax require immediate identification and treatment, which should not await inves- tigation; urgent anaesthetic airway support is usually required. In the absence of these life- threatening causes, document the following: level of consciousness, degree of central cyanosis, work of breathing (rate, depth, pattern, use of accessory muscles), oxygenation (SpO2), ability to speak (single words/ sentences) and cardiovascular status (HR, BP, JVP, perfusion).
Pulmonary oedema is suggested by a raised JVP and bibasal crackles, whereas asthma or COPD are characterised by wheeze and prolonged expiration. A resonant hemithorax with absent breath sounds indicates pneumothorax, whereas severe breathlessness with normal breath sounds suggests PE. Leg swelling may suggest cardiac failure or, if asymmetrical, venous thrombosis.
Although wheeze usually accompanies bronchospasm, it can also be found in acute left heart failure because of bronchial mucosal congestion (‘cardiac asthma’). In heart failure, pulmonary oedema stimulates breath- ing through vagal lung afferents, producing rapid, shallow breathing. An upright posture may ease the breathlessness. The patient may be unable to speak, distressed, agitated, sweaty and pale. Cough may yield frothy, blood- streaked or pink sputum. Crackles and wheezes are usually audible in the chest, and there may also be signs of right heart failure.
Any arrhythmia may cause breathlessness if the heart is structurally abnormal, for example, new atrial fibrillation in a patient with mitral ste- nosis. Patients sometimes describe chest tightness as ‘breathlessness’.
4.2 Clinical features in acute breathlessness
Condition History Signs Chest X-ray ABG ECG
Pulmonary
oedema Chest pain, palpitations, or-
thopnoea, cardiac historya Central cyanosis, ↑JVP, sweating,
cool extremities, basal cracklesa Cardiomegaly, oedema/
pleural effusionsa ↓PaO2
↓PaCO2 Sinus tachycardia, is-
chaemiaa, arrhythmia Massive pulmo-
nary embolus Risk factors, chest pain, pleurisy, syncopea, dizzinessa
Central cyanosis, ↑JVPa, absence of signs in the lunga, shock (tachycardia, hypotension)
Often normal Prominent hilar vessels, oligaemic lung fieldsa
↓PaO2
↓PaCO2
Sinus tachycardia, RBBB, S1Q3T3 pattern
↑T(V1–V4) Acute severe
asthma History of asthma, asthma
medications, wheezea Tachycardia, pulsus paradoxus, cyanosis (late), →JVPa, ↓peak flow, wheezea
Hyperinflation only (unless complicated by pneumo tho rax)a
↓PaO2
↓PaCO2 (↑PaCO2 in extremis)
Sinus tachycardia (bradycardia in extremis) Acute exacerba-
tion of COPD Previous episodesa, smoker. If in type II respira- tory failure, may be drowsy
Cyanosis, hyperinflationa, signs of CO2 retention (flapping tremor, bounding pulses)a
Hyperinflationa, bullae, complicating pneumo- thorax
↓ or ↓↓PaO2
↑PaCO2 in type II failure ± ↑H+, ↑HCO3− in chronic type II failure
Normal, or signs of right ventricular strain
Pneumonia Prodromal illnessa, fevera,
rigorsa, pleurisya Fever, delirium, pleural ruba, con-
solidationa, cyanosis (if severe) Pneumonic consoli-
dationa ↓PaO2
↓PaCO2 (↑ in extremis) Tachycardia Metabolic
acidosis Evidence of diabetes mellitus or renal disease, aspirin or ethylene glycol overdose
Fetor (ketones), hyperventilation without heart or lung signsa, dehydrationa, air hunger
Normal PaO2 normal
↓↓PaCO2, ↑H+↓HCO3− Psychogenic Previous episodes, digital
or perioral dysaesthesia No cyanosis, no heart or lung
signs, carpopedal spasm Normal PaO2 normala
↓↓PaCO2, ↓H+a
aValuable discriminatory feature.
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However, myocardial ischaemia may induce breathlessness by provoking transient left ventricular dysfunction. Breathlessness as the dominant fea- ture of myocardial ischaemia is known as ‘angina equivalent’.
Initial investigations
Box 4.2 outlines how clinical features, ECG, CXR and ABG are used to distinguish the common causes of acute breathlessness. Serial peak expi- ratory flow is used to assess the severity of asthma. In COPD, ABG is more useful than SpO2 alone, as the PaCO2, arterial H+ and HCO3− indicate whether there is new or chronic type II respiratory failure (p. 320). ABG measurement is also useful in the assessment of asthma severity, metabolic acidosis and psychogenic hyperventilation.
If ‘angina equivalent’ is suspected, stress testing may reveal myocardial ischaemia.