Chest pain

The mention of chest pain by a patient tends to provoke more urgent attention than other symptoms. The surprised patient may find himself whisked into an emergency ward with the rapid appearance of worried-looking doctors. This is because ischaemic heart disease, which may be a life-threatening condition, often presents in this manner (Table 4.2). The pain of angina and myocardial infarction tends to be similar in character; it may be due to the accumulation of metabolites from ischaemic muscle following complete or partial obstruction of a coronary artery, leading to stimulation of the cardiac sympathetic nerves.^1,2 Patients with cardiac transplants who develop coronary disease in the transplanted heart may not feel angina, presumably because the heart is denervated. Similarly, patients with diabetes are more likely to be diagnosed with ‘silent infarcts’.

TABLE 4.1 Cardiovascular history

^* Canadian Cardiovascular Society (CCVS) classification.

^† New York Heart Association (NYHA) classification.

TABLE 4.2 Causes (differential diagnosis) of chest pain and typical features

To help determine the cause of chest pain, it is important to ascertain the duration, location, quality, and precipitating and aggravating factors (the four cardinal features), as well as means of relief and accompanying symptoms (the SOCRATES questions; see Chapter 1).³

The term angina^a was coined by Heberden from the Greek and Latin words meaning ‘choking’ or strangling; and the patient may complain of crushing pain, heaviness, discomfort or a choking sensation in the retrosternal area or in the throat. It is best to ask if the patient experiences chest ‘discomfort’ rather than ‘pain’, because angina is often dull and aching in character and may not be perceived as pain.

The pain or discomfort is usually central rather

Angina characteristically occurs with exertion, with rapid relief once the patient rests or slows down. The amount of exertion necessary to produce the pain may be predictable to the patient. A change in the pattern of onset of previously stable angina must be taken very seriously.

These features constitute typical angina (Table 4.3).⁴ Although angina typically occurs on exertion, it may also occur at rest or wake a patient from sleep. Ischaemic chest pain is usually unaffected by respiration. The use of sublingual nitrates characteristically brings relief within a couple of minutes, but this is not specific as nitrates may also relieve oesophageal spasm and also have a pronounced placebo effect.

TABLE 4.3 Clinical classification of angina from the European Society of Cardiology

The pain associated with an acute coronary syndrome (myocardial infarction or unstable angina) often comes on at rest, is usually more severe and lasts much longer. Acute coronary syndromes are usually caused by the rupture of a coronary artery plaque which leads to the formation of thrombus in the arterial lumen. Stable exertional angina is a result of a fixed coronary narrowing. Pain present for more than half an hour is more likely to be due to an acute coronary syndrome than to stable angina, but pain present continuously for many days is unlikely to be either. Associated symptoms of myocardial infarction include dyspnoea, sweating, anxiety, nausea and faintness.

Other causes of retrosternal pain are listed in Table 4.2. Chest pain made worse by inspiration is called pleuritic pain. This may be due to pleurisy (page 110) or pericarditis (page 78). Pleurisy may occur because of inflammation of the pleura as a primary problem (usually due to viral infection), or secondary to pneumonia or pulmonary embolism. Pleuritic pain is not usually brought on by exertion and is often relieved by sitting up and leaning forwards. It is caused by the movement of inflamed pleural or pericardial surfaces on one another.

Chest wall pain is usually localised to a small area of the chest wall, is sharp and is associated with respiration or movement of the shoulders rather than with exertion. It may last only a few seconds or be present for prolonged periods. Disease of the cervical or upper thoracic spine may also cause pain associated with movement. This pain tends to radiate around from the back towards the front of the chest.

Pain due to a dissecting aneurysm of the aorta is usually very severe and may be described as tearing. This pain is usually greatest at the moment of onset and radiates to the back. These three features—quality, rapid onset and radiation—are very specific for aortic dissection. A proximal dissection causes anterior chest pain and involvement of the descending aorta causes interscapular pain. A history of hypertension or of a connective tissue disorder such as Marfan’s syndrome or Ehlers-Danlos syndrome puts the patient at increased risk of this condition.

Massive pulmonary embolism causes pain of very sudden onset which may be retrosternal and associated with collapse, dyspnoea and cyanosis

Table 4.4a Differential diagnosis of chest pain

(page 136). It is often pleuritic, but can be identical to anginal pain, especially if associated with right ventricular ischaemia.

Spontaneous pneumothorax may result in pain and severe dyspnoea (page 132). The pain is sharp and localised to one part of the chest.

Gastro-oesophageal reflux can quite commonly cause angina-like pain without heartburn. It is important to remember that these two relatively common conditions may co-exist. Oesophageal spasm may cause retrosternal chest pain or discomfort and can be quite difficult to distinguish from angina, but is rare. The pain may come on after eating or drinking hot or cold fluids, may be associated with dysphagia (difficulty swallowing) and may be relieved by nitrates.

Cholecystitis can cause chest pain and be confused with myocardial infarction. Right upper quadrant abdominal tenderness is usually present (page 170).

The cause of severe, usually unilateral, chest pain may not be apparent until the typical vesicular rash of herpes zoster appears in a thoracic nerve root distribution.

Dyspnoea

Shortness of breath may be due to cardiac disease. Dyspnoea (Greek dys ‘bad’, pnoia ‘breathing’) is often defined as an unexpected awareness of breathing. It occurs whenever the work of breathing is excessive, but the mechanism is uncertain. It is probably due to a sensation of increased force required of the respiratory muscles to produce a

Table 4.4b Differential diagnosis of chest pain

volume change in the lungs, because of a reduction in compliance of the lungs or increased resistance to air flow. Cardiac dyspnoea is typically chronic and occurs with exertion because of failure of the left ventricular output to rise with exercise; this in turn leads to an acute rise in left ventricular end-diastolic pressure, raised pulmonary venous pressure, interstitial fluid leakage and thus reduced lung compliance. However, the dyspnoea of chronic cardiac failure does not correlate well with measurements of pulmonary artery pressures, and clearly the origin of the symptom of cardiac dyspnoea is complicated.⁵ Left ventricular function may be impaired because of ischaemia (temporary or permanent reduction in myocardial blood supply), previous infarction (damage) or hypertrophy (often related to hypertension). As it becomes more severe, cardiac dyspnoea occurs at rest.

Orthopnoea (from the Greek ortho ‘straight’; see Table 4.5), or dyspnoea that develops when a patient is supine, occurs because in an upright position the patient’s interstitial oedema is redistributed; the lower zones of the lungs become worse and the upper zones better. This allows improved overall blood oxygenation. Patients with severe orthopnoea spend the night sitting up in a chair or propped up on numerous pillows in bed. The absence of orthopnoea suggests that left ventricular failure is unlikely to be the cause of a patient’s dyspnoea (negative likelihood ratio [LR] = 0.04⁶).

TABLE 4.5 Causes of orthopnoea

Paroxysmal^bnocturnal dyspnoea (PND) is severe dyspnoea that wakes the patient from sleep so that he or she is forced to get up gasping for breath. This occurs because of a sudden failure of left ventricular output with an acute rise in pulmonary venous and capillary pressures; this leads to transudation of fluid into the interstitial tissues, which increases the work of breathing. The sequence may be precipitated by resorption of peripheral oedema at night while supine. Acute cardiac dyspnoea may also occur with acute pulmonary oedema or a pulmonary embolus.

Cardiac dyspnoea can be difficult to distinguish from that due to lung disease or other causes (page 109)⁷. One should inquire particularly about a history of any cardiac disease that could be responsible for the onset of cardiac failure. For example, a patient with a number of known previous myocardial infarctions who develops dyspnoea is more likely to have decreased left ventricular contractility. A patient with a history of hypertension or a very heavy alcohol intake may have hypertensive heart disease or an alcoholic cardiomyopathy. The presence of orthopnoea or paroxysmal nocturnal dyspnoea is more suggestive of cardiac failure than of lung disease.

Dyspnoea is also a common symptom of anxiety. These patients often describe an inability to take a big enough breath to fill the lungs in a satisfying way. Their breathing may be deep and punctuated with sighs.

Palpitations

This is not a very precise term. It is usually taken to mean an unexpected awareness of the heartbeat.⁸ Ask the patient to describe exactly what he or she notices and whether the palpitations are slow or fast, regular or irregular, and how long they last (Questions box 4.2).

There may be the sensation of a missed beat followed by a particularly heavy beat; this can be due to an atrial or ventricular ectopic beat (which produces little cardiac output) followed by a compensating pause and then a normally conducted beat (which is more forceful than usual because there has been a longer diastolic filling period for the ventricle).

If the patient complains of a rapid heartbeat, it is important to find out whether the palpitations are of sudden or gradual onset and offset. Cardiac arrhythmias are usually instantaneous in onset and offset, whereas the onset and offset of sinus tachycardia is more gradual. A completely irregular rhythm is suggestive of atrial fibrillation, particularly if it is rapid.

It may be helpful to ask the patient to tap the rate and rhythm of the palpitations with his or her finger. Associated features including pain, dyspnoea or faintness must be inquired about. The awareness of rapid palpitations followed by syncope suggests ventricular tachycardia. These patients usually have a past history of significant heart disease. Any rapid rhythm may precipitate angina in a patient with ischaemic heart disease.

Table 4.6 Causes (differential diagnosis) of dyspnoea, palpitations and oedema

^* McGee S, Evidence-based clinical diagnosis, 2nd edn. St Louis: Saunders, 2007.

^† Khan NA, Rahim SA, Avand SS et al. Does the clinical examination predict lower extremity peripheral arterial disease? JAMA 2006 Feb 1; 295(5):536–546.

Table 4.7 Differential diagnosis of syncope and dizziness

Patients may have learned manoeuvres that will return the rhythm to normal. Attacks of supraventricular tachycardia (SVT) may be suddenly terminated by increasing vagal tone with the Valsalva manoeuvre (page 70), carotid massage, by coughing, or by swallowing cold water or ice cubes.

Syncope, presyncope and dizziness

Syncope is a transient loss of consciousness resulting from cerebral anoxia, usually due to inadequate blood flow. Presyncope is a transient sensation of weakness without loss of consciousness. (See Questions box 11.4, page 326.)

Syncope may represent a simple faint or be a symptom of cardiac or neurological disease. One must establish whether the patient actually loses consciousness and under what circumstances the syncope occurs—e.g. on standing for prolonged

If the patient’s symptoms appear to be postural, inquire about the use of anti-hypertensive or anti-anginal drugs and other medications that may induce postural hypotension. If the episode is vasovagal, it may be precipitated by something unpleasant like the sight of blood, or occur in a crowded, hot room; patients often sigh and yawn and feel nauseated and sweaty before fainting and may have previously had similar episodes, especially during adolescence and young adulthood.

If syncope is due to an arrhythmia, there is a sudden loss of consciousness regardless of the patient’s posture; chest pain may also occur if the patient has ischaemic heart disease or aortic stenosis.¹⁰ Recovery is equally quick. Exertional syncope may occur with obstruction to left ventricular outflow by aortic stenosis or hypertrophic cardiomyopathy. Profound and sudden bradycardia, usually a result of complete heart block, causes sudden and recurrent syncope (Stokes-Adams^c attacks^d). These patients may have a history of atrial fibrillation. Typically they have periods of tachycardia (fast heart rate) as well as periods of bradycardia (slow heart rate). This condition is called the sick sinus syndrome. The patient must be asked about drug treatment that could cause bradycardia, e.g. beta-blockers, digoxin, calcium channel blockers.

It is important to ask about a family history of sudden death. An increasing number of ion channelopathies are being identified as a cause of syncope and sudden death. These inherited conditions include the long QT syndrome and the Brugada syndrome. They are often diagnosed from typical ECG changes. In addition, certain drugs can cause the acquired long QT syndrome (Table 4.8).

TABLE 4.8 Drugs and syncope

Neurological causes of syncope are associated with a slow recovery and often residual neurological symptoms or signs. Bystanders may also have noticed abnormal movements if the patient has epilepsy. Dizziness that occurs even when the patient is lying down or which is made worse by movements of the head is more likely to be of neurological origin, although recurrent tachyarrhythmias may occasionally cause dizziness in any position. One should attempt to decide whether the dizziness is really vertiginous (where the world seems to be turning around), or whether it is a presyncopal feeling.

Intermittent claudication and peripheral vascular disease

The word claudication^e comes from the Latin meaning to limp. Patients with claudication notice pain in one or both calves, thighs or buttocks when they walk more than a certain distance. This distance is called the ‘claudication distance’. The claudication distance may be shorter when patients walk up hills. A history of claudication suggests peripheral vascular disease with a poor blood supply to the affected muscles. The most important risk factors are smoking, diabetes, hypertension and a history of vascular disease elsewhere in the body, including cerebrovascular disease and ischaemic heart disease. More severe disease causes the feet or legs to feel cold, numb and finally painful at rest. Rest pain is a symptom of severely compromised arterial supply. Remember the six P’s of peripheral vascular disease:

Popliteal artery entrapment can occur, especially in young men with intermittent claudication on walking but not running. Also, lumbar spinal stenosis causes pseudo-claudication: unlike vascular claudication, the pain in the calves is not relieved by standing still, but is relieved by sitting (flexing the spine) and may be exacerbated by extending the spine (e.g. walking downhill).

Fatigue

Fatigue is a common symptom of cardiac failure. It may be associated with a reduced cardiac output and poor blood supply to the skeletal muscles. There are many other causes of fatigue, including lack of sleep, anaemia and depression.

Teeth

A history of dental decay or infection is important for patients with valvular heart disease, since it puts them at risk of infective endocarditis. Dental caries may also be associated with an increased risk of ischaemic heart disease. Ask about the regularity of visits to the dentist and the patient’s awareness of the need for antibiotic prophylaxis before dental (and some surgical) procedures.