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

than left-sided. The patient may dismiss his or her pain as non-cardiac because it is not felt over the heart on the left side. It may radiate to the jaw or to the arms, but very rarely travels below the umbilicus. The severity of the pain varies.

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.

Ankle swelling

Some patients present with bilateral ankle swelling due to oedema from cardiac failure. Patients with the recent onset of oedema and who take a serious interest in their weight may have noticed a gain in weight of 3 kg or more. Ankle oedema of cardiac origin is usually symmetrical and worst in the evenings, with improvement during the night. It may be a symptom of biventricular failure or right ventricular failure secondary to a number of possible underlying aetiologies. As failure progresses, oedema ascends to involve the legs, thighs, genitalia and abdomen. There are usually other symptoms or signs of heart disease.

It is important to find out whether the patient is taking a vasodilating drug (e.g. a calcium channel blocker), which can cause peripheral oedema. There are other (more) common causes of ankle oedema than heart failure that also need to be considered (page 71). Oedema that affects the face is more likely to be related to nephrotic syndrome (page 213).

Risk factors for coronary artery disease

An essential part of the cardiac history involves obtaining detailed information about a patient’s risk factors—the patient’s cardiovascular risk factor profile (Questions box 4.4).

Previous ischaemic heart disease is the most important risk factor for further ischaemia. The patient may know of previous infarcts or have had a diagnosis of angina in the past.

Hypercholesterolaemia is the next most important risk factor for ischaemic heart disease. Many patients now know their serum cholesterol levels because widespread testing has become fashionable. The total serum cholesterol is a useful screening test, and levels above 5.2 mmol/L are considered undesirable. Cholesterol measurements (unlike triglyceride measurements) are accurate even when a patient has not been fasting. Patients with established coronary artery disease benefit from lowering of total cholesterol to below 4 mmol/L. An elevated total cholesterol level is even more significant if the high-density lipoprotein (HDL) level is low (less than 1.0 mmol/L). Significant elevation of the triglyceride level is a coronary risk factor in its own right and also adds further to the risk if the total cholesterol is high. If a patient already has coronary disease, hyperlipidaemia is even more important. Control of risk factors for these patients is called ‘secondary prevention’. Patients who have multiple risk factors for ischaemic heart disease (e.g. diabetes and hypertension) should have their cholesterol controlled aggressively. If the patient’s cholesterol is known to be high, it is worth obtaining a dietary history. This can be very trying. It is important to remember that not only foods containing cholesterol but those containing saturated fats contribute to the serum cholesterol level. High alcohol consumption and obesity are associated with hypertriglyceridaemia.

Smoking is probably the next most important risk factor for cardiovascular disease and peripheral vascular disease. Some patients describe themselves as non-smokers even though they stopped smoking only a few hours before. The number of years the patient has smoked and the number of cigarettes smoked per day are both very important (and are recorded as packet-years, page 6). The significance of a history of smoking for a patient who has not smoked for many years is controversial. The risk of symptomatic ischaemic heart disease falls gradually over the years after smoking has been stopped. After about 2 years the risk of myocardial infarction falls to the same level as for those who have never smoked. After 10 years the risk of developing angina falls close to that of non-smokers.

Hypertension is another important risk factor for coronary artery disease. Find out when hypertension was first diagnosed and what treatment, if any, has been instituted. The treatment of hypertension probably does reduce the risk of ischaemic heart disease, and certainly reduces the risk of hypertensive heart disease, cardiac failure and cerebrovascular disease. Treatment of hypertension has also been shown to reverse left ventricular hypertrophy.

A family history of coronary artery disease increases a patient’s risk, particularly if it has been present in first-degree relatives (parents or siblings) and if it has affected these people below the age of 60. Not all heart disease, however, is ischaemic; a patient whose relatives suffered from rheumatic heart disease is at no greater risk of ischaemic heart disease than anybody else.

A history of diabetes mellitus increases the risk of ischaemic heart disease very substantially. A diabetic without a history of ischaemic heart disease has the same risk of myocardial infarction as a non-diabetic who has had an infarct. It is important to find out how long a patient has been diabetic and whether insulin treatment has been required. Good control of the blood sugar level of diabetics reduces this risk. An attempt should therefore be made to find out how well a patient’s diabetes has been controlled.

Chronic kidney disease is associated with a very high risk of vascular disease. This is possibly related to high calcium-times-phosphate product and may be reduced by dietary intervention, ‘phosphate binders’, efficient dialysis, in renal transplant. Ischaemic heart disease is the most common cause of death in renal failure patients on dialysis.

The presence of multiple risk factors makes control of each one more important. Aggressive control of risk factors is often indicated in these patients.

It is interesting to note that in the diagnosis of angina the patient’s description of typical symptoms is more discriminating than is the presence of risk factors which only marginally increase the likelihood that chest pain is ischaemic. Previous ischaemic heart disease is an exception. Certainly a patient who has had angina before and says he or she has it again, is usually right.

Treatment

The medications a patient is taking often give a good clue to the diagnosis. Find out about any ill-effects from current or previous medications. The surgical history must also be elicited. The patient may have had a previous angioplasty or coronary artery bypass grafting, and may know how many arteries were dilated or bypassed. If the patient is unable to provide a history, a midline sternotomy scar and scars consistent with previous saphenous vein harvesting support this diagnosis.

Past history

Patients with a history of definite previous angina or myocardial infarction remain at high risk for further ischaemic events. It is very useful at this stage to find out how a diagnosis of ischaemic heart disease was made and in particular what investigations were undertaken. The patient may well remember exercise testing or a coronary angiogram, and some patients can even remember how many coronary arteries were narrowed, how many coronary bypasses were performed (having more than three grafts often leads to a certain amount of boasting). The angioplasty patient may know how many arteries were dilated and whether stents (often called coronary stunts by patients and cardiac surgeons) were inserted. Acute coronary syndromes are now usually treated with early coronary angioplasty.

Patients may recall a diagnosis of rheumatic fever in their childhood, but many were labelled as having ‘growing pains’.¹¹ A patient who was put to bed for a long period as a child may well have had rheumatic fever. A history of rheumatic fever places patients at risk of rheumatic valvular disease.

Hypertension may be caused or exacerbated by aspects of the patient’s activities and diet (Questions box 4.5). A high salt intake, moderate or greater alcohol use, lack of exercise, obesity and kidney disease may all be factors contributing to high blood pressure. Non-steroidal anti-inflammatory drugs cause salt and fluid retention and may also worsen blood pressure. Ask about these, about previous advice to modify these factors, and about any drug treatment of hypertension when interviewing any patient with high blood pressure.

Social history

Both ischaemic heart disease and rheumatic heart disease are chronic conditions that may affect a patient’s ability to function normally. It is therefore important to find out whether the patient’s condition has prevented him or her from working and over what period. Patients with severe cardiac failure, for example, may need to make adjustments to their living arrangements so that they are not required to walk up and down stairs at home.

Most hospitals run cardiac rehabilitation programmes for patients with ischaemic heart disease or chronic heart failure. They provide exercise classes that help patients regain their confidence and physical fitness, along with information classes about diet and drug treatment, and can help with psychological problems. Find out if the patient has been enrolled in one of these and whether it has been helpful. Is this service used as a point of contact for the patient if he or she has concerns about new symptoms or the management of medications?

The return of confidence and self-esteem are very important issues for patients and for their families after a life-threatening illness.

Examination anatomy

The contraction of the heart results in a wringing or twisting movement that is often palpable (the apex beat) and sometimes visible on the part of the chest that lies in front of it—the praecordium (from the Latin prae ‘in front of’, and cor ‘heart’). The passage of blood through the heart and its valves and on into the great vessels of the body produces many interesting sounds, and causes pulsation in arteries and movement in veins in remote parts of the body. Signs of cardiac disease may be found by examining the praecordium and the many accessible arteries and veins of the body.

The surface anatomy of the heart and of the cardiac valves (Figure 4.1) and the positions of the palpable arteries (Figure 4.2) must be kept in mind during the examination of the cardiovascular system. In addition the physiology of blood flow through the systemic and pulmonary circuits need to be understood if the cardiac cycle and causes of cardiac murmurs are to be understood (Figure 4.3).

Figure 4.1 The areas best for auscultation do not exactly correlate with the anatomical location of the valves

Figure 4.2 Palpable arteries

Figure 4.3 Normal pressures (mmHg) and saturations (%) in the heart

The cardiac valves separate the atria from the ventricles (the atrioventricular or mitral and tricuspid valves) and the ventricles from their corresponding great vessels. Figure 4.4 shows the fibrous skeleton that supports the four valves and their appearance during systole (cardiac contraction) and diastole (cardiac relaxation).

Figure 4.4 The cardiac valves in systole (a) and diastole (b)

The filling of the right side of the heart from the systemic veins can be assessed by inspection of the jugular veins in the neck (Figure 4.5) and by palpation of the liver. These veins empty into the right atrium.

Figure 4.5 The jugular venous pressure (JVP) (a) Assessment of the JVP. The patient should lie at 45 degrees. The relationships between the sternomastoid muscle, the JVP, the sternal angle and the mid-right atrium are shown. (b, c) The anatomy of the neck showing the relative positions of the main vascular structures, clavicle and sternocleidomastoid muscle. See also Figure 4.6.

Figures (b) and (c) adapted from Douglas G, Nicol F, Robertson C, Macleod’s Clinical Examination, 11th edn. Edinburgh: Churchill Livingstone, 2005.

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