Class	Description	Risk of AMI/death in next year
I	New onset exertional angina; angina with less effort; no rest pain	7%
II	Angina at rest within the last month but no pain in last 48 hours	10%
III	Angina at rest in the last 48 hours	11%

Atypical presentations are common. Older patients, younger patients, women and diabetics are more likely to have presentations which are not immediately suggestive of myocardial ischaemia. Pain may be felt in the abdomen, jaw or arm (without chest pain) or an acute coronary syndrome may present only with dyspnoea, vomiting or syncope. Thus a high index of suspicion is necessary and the diagnosis of myocardial ischaemia should be considered (and an ECG done) in all patients in whom this diagnosis is possible.

There may be overlap with other chest pain syndromes. Some patients describe burning pain suggestive of gastro-oesophageal reflux, and while sharp, stabbing or even pleuritic-type pain makes myocardial ischaemia unlikely, it does not exclude this diagnosis. Pope et al found up to 22% of patients with the principal complaint of sharp stabbing pain had an acute coronary syndrome.^1,²

A number of diagnostic decision tools using history and ECG findings to assist with diagnosis have been proposed (e.g. the acute cardiac ischaemia (ACI) predictive instrument), which probably increase the accuracy of diagnosis.³ However a high index of suspicion is the most useful safeguard.

Risk factors

A previous diagnosis of myocardial infarction, stable angina and revascularisation procedures significantly increases the risk that a new presentation with chest pain is due to myocardial ischaemia. The presence of diabetes and increasing age are also important risks. It is not clear whether a history of other risk factors for atherosclerosis (smoking, hyperlipidaemia, family history) increases the risk that a new presentation with chest pain is due to myocardial ischaemia. This is because these findings are very common in the general population.

Other potentially life-threatening causes of chest pain

Aortic dissection

(See also Chapter 16, ‘Aortic and vascular emergencies’.)

This is an important but rare disorder leading to severe chest pain associated with a significant mortality. Typically the pain is of abrupt onset and is of maximum intensity immediately, as opposed to the pain of myocardial ischaemia which builds up over minutes. The pain of aortic dissection often radiates through to the back, which is unusual in myocardial ischaemia. The pain may be described as ‘tearing’ and can be very severe, needing large doses of narcotics for control of pain. The appearance of a patient with severe pain and a non-specific ECG who appears shocked, yet has a high blood pressure, is a strong clue to this disorder. Risk factors for aortic dissection include Marfan’s syndrome and other inherited disorders of connective tissue, hypertension, pregnancy and previous surgery involving the aorta.

Pneumothorax

(See also Chapter 8, ‘Respiratory emergencies: the acutely breathless patient’.)

Pleuritic chest pain varies with the respiratory cycle and is usually worse on inspiration. Pneumothorax (air in the pleural space) is an important cause of pleuritic chest pain and is frequently associated with dyspnoea. Primary spontaneous pneumothorax occurs most frequently in younger males who are tall and thin. Secondary spontaneous pneumothorax complicates chronic lung disease, especially COPD, asthma and cystic fibrosis.

Pulmonary embolism

(See also Chapter 10, ‘Pulmonary emboli and venous thromboses’.)

Pleuritic pain can also be caused by pulmonary embolism, where there is a complicating pulmonary infarction and pleural irritation; however, massive pulmonary embolism can also cause central chest discomfort suggestive of angina. This is often associated with dyspnoea and haemodynamic collapse, and may reflect acute right ventricular dysfunction.

Pneumonia

(See also Chapter 8.)

Pleuritic chest pain is a common feature of respiratory tract infections which involve the pleura.

Ruptured oesophagus

Severe anterior chest pain following vomiting is characteristic of oesophageal perforation (Boerhaave’s syndrome). While vomiting may occur in myocardial infarction, it usually follows the onset of chest pain rather than preceding it. Oesophageal perforation may also follow procedures, especially oesophageal dilatation.

Other causes of chest pain

Abdominal disease

(See also Chapter 25, ‘Gastrointestinal emergencies’.)

Upper abdominal disorders such as cholecystitis, peptic ulcer disease and pancreatitis can be associated with chest pain which dominates the presentation and may appear out of proportion to the abdominal findings. Some of these disorders may be associated with ECG abnormalities, further confusing the diagnosis. Upper abdominal pain may be an acute myocardial infarction (AMI).

Physical examination

Triage chest pain patients rapidly to urgent care. Important haemodynamic abnormalities should be recognised quickly. Apply oxygen and consider giving nitrates. Administer aspirin early as this has been shown to considerably decrease the mortality rate in myocardial infarction. Institute continuous cardiac monitoring and obtain IV access. Take a focused history as this is being implemented. An ECG should be done immediately. In addition look for:

1. Impaired level of consciousness, presence of respiratory distress, diaphoresis, pallor and peripheral hypoperfusion.

2. Signs of cardiac failure. Oedema is relatively non-specific but a raised jugular venous pressure (JVP) or third heart sound is very suggestive of heart failure. Signs of heart failure associated with an acute coronary syndrome place the patient in a high risk group.

3. Peripheral pulses. Peripheral vascular disease is strongly associated with coronary artery disease. Compare pulses in both arms and measure the blood pressure in both arms if aortic dissection is possible. A difference of greater than 10 mmHg is significant but non-specific.

4. The praecordium. Clinical cardiomegaly is suggestive of left ventricular dysfunction. Similarly, a third heart sound is usually abnormal. However, fourth heart sounds are common in the older population, particularly those with hypertension. Murmurs are frequently non-contributory but features of severe aortic stenosis, mitral valve prolapse or hypertrophic cardiomyopathy may suggest a cause for chest pain. A mitral regurgitation murmur that coincides with the patient’s pain and disappears with relief of pain is highly significant for high-risk ischaemia. A pericardial rub is an important sign but may be transient or only heard in certain postures.

5. The chest. Symmetry of breath sounds and deviation of the trachea should be sought. Look also for localised chest signs, particularly crackles, rubs, features of consolidation and evidence of pleural effusion. Chest wall tenderness is non-specific and is seen in many patients with and without important cardiorespiratory disorders.

6. Abdominal examination should be done routinely, particularly to look for a non-cardiac cause for the patient’s symptoms.

7. Limbs. Look for oedema, pulses and signs of deep venous thrombosis (DVT).

Investigations

Electrocardiogram (ECG)

All patients complaining of chest pain should have an ECG, and previous ECGs should be obtained for comparison. If the initial ECG is unhelpful and symptoms continue, a repeat ECG in 15 minutes may be diagnostic. The ECG helps to triage patients into high, intermediate and low risk for myocardial ischaemia and is crucial in the selection of treatment. ECG patterns are discussed in detail in Chapter 12, ‘Clinical electrocardiography and arrhythmia management’.

Cardiac enzymes, markers

Rapid troponin assays (including point-of-care tests) have revolutionised the care of chest pain patients. Troponins are now considered standard of care in this clinical setting. An elevated troponin confirms the diagnosis of an acute coronary syndrome and places the patient into a higher risk group. Two normal troponin values (on admission to the emergency department and 6 hours later) are very reassuring and may allow patients to be discharged safely from the emergency department.⁴

Editor’s comment

If still clinically suspicious or uncertain, in spite of tests, be safe—consult, keep for observation and reassessment.

Other tests

A chest X-ray is a simple and important test in patients presenting with chest pain. As well as identifying pulmonary pathology, cardiomegaly and pulmonary venous congestion may also be found in patients with acute ischaemic syndromes.

Bedside echocardiography can be very helpful in the assessment of acute chest pain. Increasingly ultrasound machines are available in emergency departments and many emergency physicians are now skilled in echocardiography. Detection of left ventricular wall motion abnormalities strongly suggests important ischaemia or previous infarction. Echocardiography may also detect pericardial effusion, aortic dilatation or even dissection, although transoesophageal echocardiography is far superior for aortic abnormalities.

Some emergency departments have access to facilities for early stress testing. Patients presenting with chest pain who have negative troponins and non-diagnostic ECGs may undergo an exercise stress test with or without nuclear medicine myocardial perfusion scanning. Negative results improve the probability that the cause of the chest pain is not ischaemic.

CT scanning is under intense investigation as a modality to assess chest pain patients. Coronary artery calcification on CT does correlate with atherosclerosis, but a definite role for this modality in the emergency department is still evolving. CT coronary angiography is also an evolving technology.

Figure 6.1 summarises an integrated approach to the work-up and disposition of the chest pain patient. A combination of symptoms, examination findings, ECG results and cardiac markers often allows a precise diagnosis in many patients. Perhaps even more importantly, the risk of adverse outcomes can be assessed. High-risk features include ongoing chest pain, an abnormal ECG and elevated troponins. These patients should be managed in a coronary care unit whereas lower risk patients might be admitted to a monitored ward bed or discharged for outpatient follow-up.

DYSPNOEA

Dyspnoea is the unpleasant awareness of the work of breathing. Dyspnoea may or may not be associated with hypoxaemia and tachypnoea. Accurate assessment of the dyspnoeic patient depends on history, physical examination and appropriate tests, especially the chest X-ray. Physical signs in the severely distressed, breathless patient may be difficult to interpret. Many patients with acute cardiogenic pulmonary oedema have prominent wheezing, but wheezing is also a cardinal physical finding in patients with airflow obstruction.

Physical examination

An immediate assessment is necessary to differentiate the critically ill patient from those who are less sick. Look for:

1. General appearance—sweating, depressed level of consciousness, extreme respiratory distress and efficacy of ventilatory effort. Immediate ventilatory support may be necessary.

2. The presence of stridor, an important clue in the diagnosis of upper airway obstruction.

3. Vital signs including respiratory rate, heart rate and oximetry. Pulsus paradoxus may be present in severe airflow obstruction.

4. Cardiac examination. The presence of a third heart sound (gallop rhythm) and a raised jugular venous pulse are very suggestive of heart failure.

5. Respiratory examination. Important points include symmetry of chest movement, the presence of subcutaneous emphysema and focal signs in the chest

The chest X-ray

Examination of a chest X-ray is crucial in the assessment of the seriously ill patient with dyspnoea. Figure 6.2 summarises the interpretation of the chest X-ray in the breathless patient. Recall that portable chest X-ray machines have inherent technical limitations, in particular making assessment of heart size difficult.

Figure 6.2 Chest X-ray patterns in the breathless patient

Other tests

1. Arterial blood gases (ABGs). Indicated in all dyspnoeic patients to quantify the degree of hypoxaemia and demonstrate the presence of hypercarbia and acid–base abnormalities. A widened alveolar–arterial gradient may be a clue to subtle disorders such as pulmonary embolism; however, blood gas patterns are not specific for any disorder but do reflect the severity of the disease process.

2. ECG.

3. Spirometry. In patients who can cooperate, spirometry can diagnose and quantify airflow obstruction. Most modern electronic spirometers can display a flow–volume loop which can be helpful in the diagnosis of upper airway obstruction.

4. D-dimer. When combined with a clinical assessment of pre-test probability (e.g. using the Wells criteria), d-dimer can be helpful in the assessment of possible pulmonary embolism. A negative test in a patient with low pre-test probability makes pulmonary embolism unlikely. A positive test is non-specific.

5. Imaging tests for pulmonary embolism. Both CT pulmonary angiography and nuclear medicine ventilation–perfusion lung scanning are valuable in the diagnosis of suspected pulmonary embolism. Local availability may dictate which of these tests is used. Many emergency departments use protocols to select patients, based on pre-test probability and d-dimer, to limit inappropriate use of these expensive scans. Recall the significant radiation dose associated with CT scanning.

Disposition and management

Disposition and management depend on the underlying cause. Hypoxaemia should be treated with appropriate oxygen therapy, aiming to achieve adequate oxygen saturation as measured with pulse oximetry. Carbon dioxide narcosis should be suspected in the seriously ill dyspnoeic patient with a depressed level of consciousness, and careful titration of oxygen therapy based on serial blood gases may be necessary. In general, correction of hypoxaemia is an important goal in these seriously ill patients. Non-invasive ventilation should be used early in the distressed patient with impaired gas exchange.

HAEMOPTYSIS

Haemoptysis is defined as the coughing of blood from the respiratory tract. Usually it is clear that the blood is coming from the respiratory tract as the patient describes an associated cough. Sometimes differentiation from haematemesis is difficult, and blood loss from the upper airway, particularly the nose, may be difficult to exclude.

Most haemoptysis is minor, and should prompt a search for the cause, usually starting with a chest X-ray. In a stable patient with minor haemoptysis, investigations may be commenced in the emergency department and continued as an outpatient.

Large volume haemoptysis, defined as more than 600 mL in 24 hours,⁵ is life-threatening and frightening. It is often difficult for the patient to estimate the volume of blood loss. The immediate threat is not hypovolaemia, but hypoxaemia related to blood in the airways and lung parenchyma.