Chapter 40: Chest pain

The presenting problem of chest pain is common yet very threatening to both patient and doctor because the underlying cause in many instances is potentially lethal, especially with chest pain of sudden onset. The causes of acute chest pain are summarised and presented in FIGURE 40.1.

The diagnostic strategy model (see TABLE 40.1) can be used to analyse chest pain according to the five self-posed questions.

Probability diagnosis

The commonest causes encountered in general practice are musculoskeletal or chest wall pain and psychogenic disorders. The former is a very important yet often overlooked cause and sometimes inappropriately referred to as fibrositis or neuralgia. Causes include costochondritis, muscular strains, dysfunction of the sternocostal joints and dysfunction of the lower cervical spine or upper thoracic spine, which can cause referred pain to various areas of the chest wall. Angina is common and must always be considered. If angina-like pain lasts longer than 15 minutes myocardial infarction must be excluded. The best predictor of coronary pain is chest pain with pain in both arms.

Serious disorders not to be missed

The usual triad of malignancy, myocardial ischaemia and severe infections (see TABLE 40.1) must be considered. In addition, other cardiovascular catastrophes, such as a dissecting aortic aneurysm and pulmonary embolus, must be excluded, although uncommon, especially in those at risk. Spontaneous pneumothorax should also be considered, especially in a young male of slight build. Malignancies of the lung are relatively common and may present as pain when the previously asymptomatic tumour invades nerves or the spine.

The severe infections that cause chest pain include pneumonia/pleurisy, pericarditis and mediastinitis.

Pitfalls

Unfortunately, myocardial infarction and angina are often missed. Referred pain from spinal dysfunction, especially if referred anteriorly, is commonly overlooked. Other pitfalls include a cough fracture of a rib, herpes zoster (prior to the eruption) and gastrointestinal disorders, including oesophageal spasm, reflux and cholecystitis. Oesophageal problems may be clinically indistinguishable from angina. Mitral valve prolapse can cause chest pain although the mechanism is unclear: think of it in an unwell female prone to palpitations and chest pain. The pain tends to be sharp, fleeting, non-exertional and located near the cardiac apex.

General pitfalls

General pitfalls include:

• not being ‘coronary aware’ in patients presenting with chest pain

• referred pain from spinal disorders, especially of the lower cervical spine—one of the great pitfalls in medical practice

• labelling chest pain as psychological in an anxious patient presenting with acute chest pain

• assuming that pain radiating down the inside of the left arm is always cardiac in origin

• being unaware that up to 20% of myocardial infarctions are silent, especially in elderly patients, and that pulmonary embolism is often painless if the main pulmonary veins are involved

Seven masquerades checklist

Of this group spinal dysfunction is possible. Disc lesions from the lower cervical spine are unlikely to cause chest wall pain, but dysfunction of the facet joints of this area of the spine and the upper thoracic spine are common causes of referred pain to the chest wall. Nerve root pain from spinal problems is rarely found in the chest wall. Pathological fractures secondary to osteoporosis or malignancy in the vertebrae cause posterior wall pain. Cocaine users can present with chest pain.

Psychogenic considerations

With psychogenic causes the pain can occur anywhere in the chest, and tends to be continuous and sharp or stabbing rather than constricting. Associated symptoms include palpitations, deep breathing, fatigue, tremor, agitation and anxiety. Abnormal stress, tension, anxiety or depression may precipitate the pain, which often lasts hours or days.

History

A meticulous history of the behaviour of the pain is the key to diagnosis. The pain should be analysed into its usual characteristics with the SOCRATES system. Association with serious medical problems such as diabetes, Marfan syndrome, anaemia and connective tissue disorders (e.g. SLE, RA) should be kept in mind. Consider coronary risk factors. The ability to take a detailed history will obviously be limited with severe acute pain.

Associated symptoms

• Syncope. Consider myocardial infarction, pulmonary embolus and dissecting aneurysm.

• Pain on inspiration. Consider pleuritis, pericarditis, mediastinitis, pneumothorax and musculoskeletal (chest wall pain).

• Thoracic back pain. Consider spinal dysfunction, acute coronary syndromes, angina, aortic dissection, pericarditis and gastrointestinal disorders such as a peptic ulcer, biliary colic/cholecystitis and oesophageal spasm.

Key questions

• Where exactly do you get the pain? Can you pinpoint it?

• Does the pain travel anywhere?

• Can you give me a careful description of the pain?

• How long did the pain last and could you do anything to relieve it?

• Is the pain brought on by exertion and relieved by rest?

• Do cold conditions bring it on?

• Do you have any other symptoms, such as breathlessness, faintness, fever, nausea or vomiting, dizziness, weight loss, sweating or back pain?

• Is the pain made worse by breathing or coughing, or by movement or pressing on that area?

• Is there any blood in any sputum you bring up?

• Is your pain associated with what you eat and drink? Or with a bitter taste in your mouth?

• Do you get the pain on stooping over and after lying in bed at night?

• Do antacids relieve your pain?

• Have you noticed a rash where you get the pain?

• Have you had a blow to your chest or an injury to your back?

Examination

The examination should focus on the following areas:

• general appearance—evidence of atherosclerosis (senile arcus, thickened vessels), pale and sweating (myocardial infarction, dissecting aneurysm or pulmonary embolus), hemiparesis (? aortic dissection)

• pulses—both radial and femoral—check for nature of pulse and absence of femoral pulses

• blood pressure

• temperature

• palpation of chest wall, lower cervical spine and thoracic spine—look for evidence of localised tenderness, pathological fracture, spinal dysfunction, herpes zoster

• palpation of legs—check for evidence of deep venous thrombosis

• examination of chest—check for evidence of pneumothorax

• auscultation of chest:

  • – reduced breath sounds, hyper-resonant percussion note and vocal fremitus → pneumothorax

  • – friction rub → pericarditis or pleurisy

  • – basal crackles → cardiac failure

  • – apical systole murmur → mitral valve prolapse

  • – aortic diastolic murmur → proximal dissection (aortic regurgitation)

Note: In the presence of a myocardial infarction, the examination may be normal but the patient, apart from being cold, clammy or shocked, may have muffled heart sounds, a gallop rhythm, a systolic murmur. With an aortic dissection the patient may also appear cold, clammy and shocked, but may show absent femoral pulses, hemiparesis and a diastolic murmur of aortic regurgitation.

• upper abdominal palpation—check for tenderness suggestive of gall bladder disease or peptic ulceration

Possible findings on examination of a patient with chest pain are presented in FIGURE 40.2.¹

Investigations¹

The following investigations to aid diagnosis are available, although the majority are sophisticated and confined to hospitals with high-technology imaging departments. The fundamental tests that are readily available to the GP—ECG, chest X-ray and cardiac enzymes—should help confirm the diagnosis in most instances. All patients with undifferentiated chest pain should have a 12-lead ECG.

Electrocardiogram (ECG)

This may be diagnostic for ischaemia and myocardial infarction, although it is important to bear in mind that it may be normal with both, including the early minutes to hours of an acute infarction.

It can be helpful to differentiate between myocardial infarction, pulmonary embolism and pericarditis. The ECG in pulmonary embolism may be normal but if massive may show right axis deviation, right BBB and right ventricular strain. Pericarditis is characterised by low voltages and saddle-shaped ST segment elevation.

Exercise stress test

This is the key test for defining chest pain as cardiac in origin. Physical stress, such as the motor-driven treadmill or a bicycle ergometer, is used to elicit changes in the ECG to diagnose myocardial ischaemia.

Exercise thallium scan

This radionuclide myocardial perfusion scan using thallium can complement the exercise ECG.

Ambulatory ECG Holter monitor

This monitor is especially useful for silent ischaemia, variant angina and arrhythmias.

Chest X-ray

The routine CXR is taken in full inspiration. Ask for an expiration film if pneumothorax is suspected.

Blood glucose

Tests association with diabetes.

Haemoglobin and blood film

Anaemia is a possible associated factor.

Serum enzymes

Damaged necrosed myocardial tissue releases cellular enzymes, which are markers of this damage:

• troponin I and troponin T (the key marker)–on arrival and 2 hours later (ADAPT trial protocol)

• creatinine kinase (CK) and creatinine kinase– myocardial bound fraction (CK–MB)²

• myoglobin

Transthoracic echocardiography

This can be used in the early stages of myocardial infarction to detect abnormalities in heart wall motion, when ECGs and enzymes are not diagnostic. Stress echocardiography is a new technique that is useful where standard exercise testing has been unhelpful.

Transoesophageal echocardiography (TOE)

More sensitive and is the investigation for dissecting aneurysm (immediate diagnosis), prosthetic valves and embolisation.

Isotope scanning

1. Technetium-99m pyrophosphate studies:

   • myocardium—to diagnose posterolateral myocardial infarction in the presence of bundle branch block

   • pulmonary—to diagnose pulmonary embolism

2. Gated blood pool nuclear scan (radionuclide ventriculography)—this scan tests left ventricular function at rest and exercise in patients with myocardial ischaemia.

Angiography (arteriography)

Angiography, including CT angiogram, should be selective:

1. coronary—to evaluate coronary arteries

2. pulmonary—to diagnose pulmonary thromboembolism

3. coronary computed tomograph

4. MRI

Oesophageal studies

• Endoscopy

• Barium swallow

• Oesophageal manometry

• Radionucleide transit studies

Spine—X-ray

• Cervical spine

• Thoracic spine

Myocardial ischaemia¹

Coronary artery disease includes the acute coronary syndromes (unstable angina and myocardial infarction), stable angina and other variants of angina.

The typical retrosternal distribution of myocardial ischaemia is shown in FIGURE 40.3. Retrosternal pain or pain situated across the chest anteriorly should be regarded as cardiac until proved otherwise.

The wide variation of sites of pain, umbilicus to jaw, including neck, inside of arms, epigastrium and interscapular, should always be kept in mind (see FIG. 40.4). Pain is referred into the left arm more commonly than into the right arm. The best predictor of AMI is pain in both arms.

The quality of the pain is usually described as pressure, heaviness or tightness. The patient often uses the clenched fist sign to illustrate a sense of constriction.

The radiation of pain will assist in differentiating ischaemic pain from that caused by pericarditis. Enquiry about precipitating and relieving factors will enable a differentiation to be made between ischaemic pain and the almost identical pain caused by reference from the spine. Associated symptoms include dyspnoea, dizziness, nausea and vomiting and sweating (diaphoresis).

If a retrosternal pain almost identical with that of myocardial ischaemia is precipitated not by exertion but by bending, lifting, straining or lying down, oesophageal reflux and spasm is a possible diagnosis. This is frequently confused with ischaemic heart disease and can cause radiation into the left arm.

Stable angina. The pain of angina tends to last a few minutes only (average 3–5 minutes) and is relieved by rest and glyceryl trinitrate (nitroglycerine). The pain may be precipitated by an arrhythmia.

The types of acute coronary syndromes are summarised in TABLE 40.2.³

• Myocardial infarction. Ischaemic pain lasting longer than 15–20 minutes is usually infarction. However, it can resolve in a few minutes or within 24 hours. The pain is typically heavy and crushing, and can vary from mild to intense. Occasionally the attack is painless, typically in diabetics. Pallor, sweating and vomiting may accompany the attack.

• Unstable angina. This term includes rest angina, new onset effort angina, post infarct angina and post coronary procedure angina. Severe ischaemic chest pain can last 15–20 minutes or more. It is classified as low risk or high risk ‘minor myocardial damage’.

Aortic dissection

Chest pain is present in 75% of dissections. The pain, which is usually sudden, severe and midline, has a tearing or ripping sensation and is usually situated retrosternally and between the scapulae (see FIG. 40.5). It radiates to the abdomen, flank and legs. An important diagnostic feature is the inequality in the pulses (e.g. carotid, radial and femoral). There may also be occlusion of the coronary or kidney arteries with appropriate symptoms and signs. Hemiplegia, aortic incompetence or cardiac tamponade can occur. Consider a CT angiogram.

Pulmonary embolism³

This may have a dramatic onset following occlusion of the pulmonary artery or a major branch, especially if more than 50% of the cross-sectional area of the pulmonary trunk is occluded. There are three general types: massive (obstructive shock or BP< 90 mmHg), submassive (acute without hypotension but right ventricular dysfunction) and non-massive (low risk).

The diagnosis can present clinical difficulties, especially when dyspnoea is present without pain. It can be asymptomatic. Embolism usually presents with retrosternal chest pain (see FIG. 40.6) and may be associated with syncope and breathlessness. In addition, hypotension, acute right heart failure or cardiac arrest occurs with a massive embolus. The physical examination can be deceptively normal. Pulmonary infarction is generally less dramatic than embolism and it is usually accompanied by pleuritic chest pain and haemoptysis. It complicates embolism in about 10% of patients. The diagnosis is usually confirmed by a CT pulmonary angiogram (best) and/or V/Q scan (see later in chapter) and ECG (look for T wave inversion V1–V4). The D-dimer test may be useful.

Pleuritis⁴

Inflammation of the pleura is due to underlying pneumonia (viral or bacterial), pulmonary infarction, tumour infiltration or connective tissue disease (e.g. SLE).

Clinical features

• Often sudden onset

• Pain usually localised without radiation

• Sharp knife-like pain

• Continuous pain with sharp exacerbations

• Aggravated by inspiration, sneezing and coughing

• May be associated dyspnoea, cough, haemoptysis

Epidemic pleurodynia (Bornholm disease)

Unilateral severe knife-like intermittent chest pain and adjacent upper abdominal pain (‘the devil’s grip’) following an URTI—affecting any age. Other symptoms include fever, malaise, headache, malaise and tender truncal muscles. It is caused by a Coxsackie B virus. CXR is normal; diagnosis is by exclusion. It usually settles within a week with simple analgesics. Recurrences may follow.

Acute pericarditis⁵

The clinical presentation depends on the cause, whether viral (commonest), a connective tissue disorder, bacterial, uraemia or post-AMI. There may be fever, malaise, fatigue and anxiety.⁴

• Signs: friction rub, tachycardia, paradoxical pulse

• Investigations: ECG, CXR, echocardiography

Pericarditis causes three distinct types of pain:

1. pleuritic (the commonest), aggravated by cough and deep inspiration, sometimes brought on by swallowing; worse with lying flat, relieved by sitting up and leaning forward

2. steady, crushing, retrosternal pain that mimics myocardial infarction

3. pain synchronous with the heartbeat and felt over the praecordium and left shoulder

Occasionally, two and rarely all three types of pain may be present simultaneously (see FIG. 40.7).

The cardinal sign is a pericardial friction rub (often transient). Treatment depends on the cause—may be NSAIDs ± colchicine or corticosteroids.

Spontaneous pneumothorax

The acute onset of pleuritic pain and dyspnoea in a patient with a history of asthma or emphysema is the hallmark of a pneumothorax. It is due to a rupture of a subpleural ‘bleb’ or a small air-containing cyst. It often occurs in young, slender males without a history of lung disorders. The pain varies from mild to severe and can be felt anywhere in the chest, sometimes being retrosternal. Typical pain distribution is shown in FIGURE 40.8. The diagnosis is made on expiration film.

If a tension pneumothorax becomes painful and dyspnoea becomes rapidly more intense, urgent decompression of air is essential (see later in chapter). A comparison of the serious causes of acute chest pain is summarised in TABLE 40.3.

Oesophageal pain

Gastro-oesophageal reflux can cause oesophagitis characterised by a burning epigastric or retrosternal pain that may radiate to the jaw. The pain is aggravated or precipitated by lying flat or bending over, especially after meals, and is more frequent at night. The pain is worse if oesophageal spasm is present. Oesophageal motor disorders, including spasm, may occur in isolation. The pain may radiate uncommonly to the back (see FIG. 40.9). It may be precipitated by eating, especially hot or cold food and drink, and may be relieved by eating or by glyceryl trinitrate (nitroglycerine) and other nitrates. Features differentiating angina-like oesophageal pain and cardiac pain are presented in TABLE 40.4. Gastrointestinal causes of chest pain are summarised in TABLE 40.5.¹

Spinal pain

The commonest cause of pain of spinal origin is vertebral dysfunction of the lower cervical or upper dorsal region (see CHAPTER 37). The spinal problem may be a disc prolapse (relatively common in the lower cervical spine, but rare in the upper thoracic spine) or dysfunction of the facet joints or costovertebral joints causing referred pain. This referred pain can be present anywhere in the chest wall, including anterior chest, which causes confusion with cardiac pain (see FIG. 40.10). The pain is dull and aching. It may be aggravated by exertion, certain body movements or deep inspiration. The old trap for unilateral nerve root pain is herpes zoster.

Costochondritis⁴

This causes mild to moderate anterior chest wall pain that may radiate to the chest, back or abdomen. It is usually unilateral, sharp in nature and exaggerated by breathing, physical activity or a specific position. It may be preceded by exercise or a URTI and can persist for several months. It is diagnosed by eliciting tenderness at the costochondral junction of the affected ribs and needs to be differentiated from Tietze syndrome, where there is a tender, fusiform swelling at the costochondral junction (refer to CHAPTER 100).

Psychogenic pain

Psychogenic chest pain can occur anywhere in the chest, but often it is located in the left submammary region, usually without radiation (see FIG. 40.11). It tends to be continuous and sharp or stabbing. It may mimic angina but tends to last for hours or days. It is usually aggravated by tiredness or emotional tension and may be associated with shortness of breath, fatigue and palpitations.

Da Costa syndrome (effort syndrome) is recurrent attacks of stabbing left-sided submammary pain, usually associated with anxiety ± depression.

Takotsubo cardiomyopathy or ‘broken heart syndrome’ presents with acute chest pain and shortness of breath. It mimics an acute anterior myocardial infarction. It is caused by a major catecholamine discharge following an emotionally stressful event, resulting in apical left ventricular ballooning. Treatment is usually with aspirin, beta blockers and ACE inhibitors. Most patients recover completely.

Chest pain in children is rarely the result of serious pathology but is an important complaint, especially in adolescents. A US study has shown that the mean age for childhood chest pain is 11.9 years.⁵ Most cases are of unknown aetiology (probably psychogenic), while common causes include musculoskeletal disorders, cough-induced pain, costochondritis, psychogenic disturbance (includes hyperventilation) and asthma.⁶ See TABLE 40.6.

Chest pain in children younger than 12 years old is more likely to have a cardiorespiratory cause, such as cough, asthma, pneumonia or heart disease, while chest pain in adolescents is more likely to be associated with a psychogenic disturbance.

Causes of musculoskeletal pain include strains to pectoral, shoulder or back muscles after excessive exercise, and minor trauma from sports such as football or wrestling.

Breast problems can present as chest pain.

Cardiac causes

Myocardial ischaemia is very rare in children but should be considered in any child with exercise-induced chest pain, adolescents with long-standing diabetes and children with sickle-cell anaemia.

Precordial catch (Texidor twinge or stitch in the side)⁵

This complaint, which is common in children and adolescents, presents as a unilateral low chest pain that lasts usually 30 seconds to 3 minutes, typically with exercise, such as long-distance running. The pain is relieved by straightening up and taking very slow deep breaths followed by shallow breaths.

Chest pain is a very important symptom in the elderly as the life-threatening cardiovascular conditions—myocardial infarction and angina, dissecting aneurysm and ruptured aorta—are an increasing manifestation with age. In a community survey in Glasgow, 20% of men and 12% of women over 65 years were found to have ischaemic heart disease.⁸ The elderly patient presenting with chest pain is most likely to have angina or myocardial infarction. Other important disorders to consider are herpes zoster, cough fracture of the rib, malignancy, pleurisy, pulmonary embolus and gastro-oesophageal reflux.

Angina pectoris

Main features

• There is a 2–3% incidence between 25 and 64 years.⁹

• The history is the basis of diagnosis.

• Angina is an oppressive discomfort rather than a pain, typically transient and lasting <10 mins.

• It is mainly retrosternal: radiates to arms, jaw, throat, back.

• It may be associated with shortness of breath, nausea, faintness and sweating.

• It occurs during exercise, emotion, after meals or in cold.

• It is relieved within a few minutes with rest.

• Physical examination is usually not helpful, except during an attack.

• Mitral valve prolapse, oesophageal spasm and dissecting aneurysm are important differential diagnoses.

• The causes of angina are summarised in TABLE 40.7.

Note: Ensure that the patient is not anaemic or thyrotoxic. Fever and tachycardia also have to be excluded.

Variants^1,9

• Stable angina. Pain occurs with exertion and is usually predictable with no symptom change during the past month.

• Unstable angina (also referred to as crescendo angina, pre-infarct angina and acute coronary insufficiency). It is increasing angina (severity and duration) over a short period of time, precipitated by less effort and may come on at rest, especially at night. It may eventually lead to complete infarction, often with relief of symptoms. It is due to unstable plaque.

  • – Nocturnal angina. Pain occurs during the night. It is related to unstable angina.

  • – Decubitus angina. The pain occurs when lying flat and is relieved by sitting up.

  • – Variant angina or Prinzmetal angina or spasm angina.⁷ The pain occurs at rest and without apparent cause. It is associated with typical transient ECG changes of ST elevation (as compared with the classic changes of ST depression during effort angina). It can lead to infarction and cause arrhythmias. It is caused by coronary artery spasm.

Aids to diagnosis

This may be normal or show ischaemia or evidence of earlier infarction. During an attack it may be normal or show well-marked depression of the ST segment, symmetrical T-wave inversion (see FIG. 40.12) or tall upright T waves.

This is positive in about 75% of patients with severe coronary artery disease and should be performed if the diagnosis is in doubt, for prognostic reasons or to aid in the timing of additional investigations (e.g. coronary angiography). A normal stress test does not rule out coronary artery disease.

This test is helpful in some difficult circumstances such as in the presence of left branch bundle block (LBBB), old infarction and Wolff–Parkinson–White (WPW) syndrome (when exercise test is of little use) and with mitral valve prolapse, which gives high false positive tests. It helps determine the presence and extent of reversible myocardial ischaemia since thallium is only taken up by perfused tissue.

This may be useful in some patients.

This test assesses the ejection fraction, which is a reliable index of ventricular function and thus aids assessment of patients for coronary artery bypass surgery.

This assesses global and regional wall motion abnormalities and assesses valvular dysfunction and pericardium status.

This test accurately outlines the extent and severity of coronary artery disease. It is usually used to determine the precise coronary artery anatomy prior to surgery.

The relationship between the degree of angina and coronary artery disease is not clear-cut. Some people with severe angina have normal coronary arteries.

Indications for coronary angiography are presented in TABLE 40.8.

‘Ultrafast CT’ may replace traditional angiography.

Management of stable angina

Preventions

This is especially important for those with a positive family history and an unsatisfactory lifestyle. Modification of risk factors:

• no smoking

• weight reduction

• healthy eating/optimal low-fat diet

• exercise

• control of hypertension

• control of diabetes

• control of blood lipids

General advice for the stable angina patient

• Reassure patient that angina has a reasonably good prognosis: 30% survive more than 10 years;¹⁰ spontaneous remission can occur.

• Attend to any risk factors.

• If inactive, take on an activity such as walking for 20 minutes a day.

• Take regular exercise to the threshold of angina.

• If tense and stressed, cultivate a more relaxed attitude to life—consider a stress management/relaxation course.

• Avoid precipitating factors.

• Don’t excessively restrict lifestyle.

Medical treatment⁵

• Nitrates:

  glyceryl trinitrate 300–600 mcg tab sublingually, max 1800 mcg

  or

  glyceryl trinitrate SL 400 mcg metered dose spray: 1 spray; repeat after 5 minutes if pain persists (maximum three doses)

  or

  isosorbide dinitrate 5 mg sublingually; repeat every 5 minutes if pain persists (maximum 3 tablets)

  or

  nifedipine 5 mg capsule (suck or chew) if intolerant of nitrates

• Aspirin 150 mg (o)

  Tips about glyceryl trinitrate tablets:

• if pain persists for longer than 10 minutes despite two doses of nitrates, take a third dose and call for an ambulance

• warn patient about headache and other side effects

• sit down to take the tablet

• take ½ (initially) or 1 tablet every 5 minutes

• take a maximum of 3 tablets in 15 minutes

• tablets must be fresh

• discard the bottle after being opened for 3 months or after 2 days if carried on the person

• keep tablets out of light and heat

• if pain relieved quickly, spit out residual tablet

• advise patient to get medical advice if no relief after 3 tablets

Note: avoid nitrates if patient has taken sildenafil or vardenafil in the previous 24 hours or tadalafil in the previous 5 days.

Prevention of angina

Regular predictable attacks precipitated by moderate exertion. For prevention:

• add to aspirin (if not contraindicated) beta blocker, e.g. atenolol 25–100 mg (o) once daily

• or

• metoprolol 25–100 mg (o) twice daily plus nitrates

• glyceryl trinitrate (transdermal: ointment or patches) daily (use for 14 hours only)

• or

• isosorbide mononitrate 30 mg (o) SR tablet mane, increasing to 120 mg if required

• Note: Aim for a daily nitrate-free interval.

Not prevented by beta blocker:

• add

• a dihydropyridine calcium-channel blocker (CCB) nifedipine CR 30–60 mg (o) once daily

• or

• amlodipine 2.5–10 mg (o) once daily plus nitrates

• If beta blocker contraindicated (use a non-dihydropyridine calcium-channel blocker):

• diltiazem 30–90 mg (o) tds or CR 180–360 mg (o) daily

• or

• verapamil (according to directions)

Consider adding nicorandil 5 mg (o) bd, increasing after a week to 10–20 mg bd or replacing the CCB with perhexiline

• or

• ivabradine and seeking specialist advice

Includes onset of angina at rest, abrupt worsening of angina and angina following acute myocardial infarction.

• Should be hospitalised for stabilisation and further evaluation. May need IV nitrate therapy.

• The objectives are to optimise therapy and consider coronary angiography with a view to a corrective procedure.

Rules of practice

• For variant angina (spasm) use nitrates and calcium antagonist (avoid beta blockers).

• As a rule, avoid the combination of verapamil and a beta blocker (risk of tachycardia and heart block).

• Do not combine a dihydropyridine CCB with a non-dihydropyridine CCB.

• Tolerance to nitrate use is a problem, so 24-hour coverage with long-acting preparations is not recommended.

• Consider using the potassium channel opening vasodilator nicorandil 5 mg (o) bd to 10–20 mg (o) bd (after 1 week). Can use as alternative to long-acting nitrates. The new agent ivabradine can be considered.

• Nitrates can be used prophylactically prior to any exertion that is likely to provoke angina (e.g. glyceryl trinitrate spray or tablet or isosorbide dinitrate 5 mg tablet)

• Avoid nitrates if the patient has used a 5 phosphodiesterase inhibitor in the past 1–5 days.

Non-medical treatment⁵

One current technique is dilating coronary atheromatous obstructions by inflating a balloon against the obstruction—percutaneous transluminal coronary angioplasty (PTCA) (see FIG. 40.13) and maintaining patency with intracoronary stent devices.

Two complications of the balloon inflation angioplasty are acute coronary occlusion (2–4%) and restenosis, which occurs in 30% in the first 6 months after angioplasty.¹⁰

PTCA followed by stenting is now the most favoured procedure to maintain patency of the obstructed coronary vessel (see FIG. 40.14). Modern drug eluting stents, which include drugs such as primolimus, sirolimus or paclitaxel, can be used as well as the bare metal stent. Stent patients require long-term antiplatelet agents (e.g. aspirin plus clopidogrel) (specialist advice is required).

The main surgical techniques in current use are coronary artery bypass grafting (CABG) using either a vein (usually the saphenous) (see FIG. 40.15) or internal mammary arterial implantation (see FIG. 40.16) or both and endarterectomy.

Symptomatic patients with significant left main coronary obstruction should undergo bypass surgery, and those with two or three vessel obstruction and good ventricular function are often considered for angioplasty or surgery. A significant improvement in the quantity and quality of life can be expected.

Myocardial infarction

Clinical guidelines¹¹

• Variable pain; may be mistaken for indigestion

• Similar to angina but more oppressive

• So severe, patient may fear imminent death— angor animi

• About 20% have no pain. These have a high mortality rate

• ‘Silent infarcts’ in diabetics, hypertensives, females and elderly; one report (European Heart Journal, 14 February 2006, online) reported that 40% of infarcts were silent and undetected in older patients

• 60% of those who die do so before reaching hospital, within 2 hours of the onset of symptoms

• Hospital mortality is 8–10%¹⁰

• Like CVA, seems to peak at 6–10 am

Diagnosis is based on 2 out of 3 criteria: history of prolonged ischaemic pain, typical ECG appearance, and rise and fall of cardiac enzymes.

Aetiology

• Thrombosis with occlusion

• Haemorrhage under a plaque

• Rupture of a plaque

• Coronary artery spasm

Signs

These may be:

• no abnormal signs

• pale/grey, clammy, dyspnoeic

• restless and apprehensive

• variable BP with pain ↓ heart pump failure

• variable pulse: watch for bradyarrhythmias

• mild cardiac failure: third or fourth heart sound, basal crackles

Investigations

1. ECG. The ECG is valuable with characteristic changes in a full thickness infarction. The typical features (see FIG. 40.17) are:

   • the Q wave: broad (>1 mm) and deep >25% length R wave

     • – occurs normally in leads AVR and V1; III (sometimes)

     • – abnormal if in other leads

     • – occurs also with WPW and ventricular tachycardia (VT)

     • – usually permanent feature after full thickness AMI

   • T wave and ST segment:

     • – transient changes (inversion and elevation respectively)

     The typical progression is shown in FIGURE 40.18. Note:

   • Q waves do not develop in subendocardial infarction.

   • The strategies for management of AMI are based on the distinction between Q wave (transmural) or non-Q wave (subendocardial) infarction.

   • Q wave infarction has been proved to benefit from thrombolytic therapy, but non-Q wave infarction has not.

   • If new LBBB think AMI (in LBBB no Q wave).

   • A normal ECG, especially early, does not exclude AMI. Q waves may take days to develop.

2. Cardiac enzymes. The typical enzyme patterns are presented in FIGURE 40.19. As a rule, large infarcts tend to produce high serum enzyme levels. The elevated enzymes can help time the infarct:

   • troponin I or T:

     • – starts rising at 3–12 hours, peaks at 24 hours and persists for about 5–14 days

     • – now the preferred test

     • – positive in unstable angina

     • – raised in aortic dissection and kidney impairment

     • – may have to wait until 10 hours before recording a negative result

     • – not useful for repeat MI

     • – both proteins, I and T, provide same information

     • – reference interval <0.1 μg/L

   • creatinine kinase (CK):

     • – after delay of 6–8 hours from the onset of pain it peaks at 20–24 hours and usually returns to normal by 48 hours

     • – CK–MB: myocardial necrosis is present if >15% of total CK; unlike CK, it is not affected by intramuscular injections

3. Technetium pyrophosphate scanning

   • It is performed from 24 hours to 14 days after onset.

   • It scans for ‘hot spots’, especially when a posterolateral AMI is suspected and ECG is unhelpful because of pre-existing LBBB.

4. Echocardiography. This is used to assist diagnosis when other tests are not diagnostic.

Note: The clinical diagnosis may be the most reliable, as the ECG and enzymes may be negative.

Management of acute coronary syndromes

General principles^11,12

• Aim for immediate attendance if suspected.

• Pre-hospital: make diagnosis, assess risk, ensure stability. A 12-lead ECG should be arranged ASAP.

• Call a mobile coronary care unit.

• Achieve coronary perfusion and minimise infarct size.

• Prevent and treat cardiac arrest; have a defibrillator available to treat ventricular fibrillation.

• Optimal treatment is in a modern coronary care unit (if possible) with continuous ECG monitoring (first 48 hours) and a peripheral IV line (consider intranasal oxygen only if hypoxaemic <94% saturation).

• Pay careful attention to relief of pain and apprehension.

• Establish a caring empathy with the patient.

• Give aspirin as early as possible (if no contraindications): 300 mg chewed or dissolved sublingually.

• Prescribe a beta blocker and an ACE inhibitor early (if no contraindications).

Note: For a STEMI it is important to re-establish flow as soon as possible, usually by either thrombolytic therapy or primary angioplasty (preferably with stenting). Rescue angioplasty is usually used when large infarcts have not perfused at 60–90 minutes.⁵

Hospital management^5,11

• As for first-line management.

• Confirm ECG diagnosis: STEMI or NSTEACS.

• Take blood for cardiac enzymes, particularly troponin levels, urea and electrolytes.

• Organise an urgent cardiology consultation for risk stratification and a decision whether to proceed to coronary angiography and coronary reperfusion with PCI (or CABG) or with thrombolysis.

The optimal first-line treatment for the patient with a STEMI is urgent referral to a coronary catheter laboratory ideally within 60 minutes (the golden hour) of the onset of pain for assessment after coronary angiography for percutaneous transluminal coronary angioplasty (PTCA). If available and performed by an interventional cardiologist it has the best outcomes (level I evidence).

The principle is to achieve rapid reperfusion via primary angioplasty with a stent (optimal stent status currently under evaluation).

Adjunct therapy will include dual antiplatelet therapy—aspirin and a P2Y₁₂ inhibitor (clopidogrel, ticagrelor or prasugrel) and anticoagulation with low molecular weight heparin or unfractionated heparin, a statin and an ACE inhibitor.

Urgent reperfusion guidelines

• Within 60 minutes of symptom onset STEMI: PCI (optimal)

• Within 90 minutes of onset STEMI: PCI (acceptable)

• If these targets are not reached: fibrinolysis within 30 minutes of arrival

NSTEACS can progress to a STEMI; therefore all patients with NSTEACS should have ongoing monitoring in hospital and their risk stratified to direct management decisions.

Reperfusion therapy^13,14

All patients with acute myocardial infarction should be considered for admission to a coronary care unit for monitoring and expert care. The decision of reperfusion therapy by PCI or fibrinolytic therapy will be determined by unit policy based on availability of PCI.

Fibrinolytic therapy

If angioplasty is unachievable either through timing or the unavailability of the service (such as in rural locations), thrombolysis is an indication for STEMI and the sooner the better, but preferably within 12 hours of the commencement of chest pain.^5,12 The decision should be made by an experienced consultant, especially as PCI is not usually possible once fibrinolytic therapy has been given.

Second-generation fibrin-specific agents (reteplase, alteplase or tenecteplase) are the agents of choice. Streptokinase can be used but it is inappropriate for use in Indigenous people and those who have received it on a previous occasion. There are several other contraindications for the use of fibrinolytic agents.

Further management strategies include:

• Full heparinisation for 24–36 hours (after rt-PA—not after streptokinase), especially for large anterior transmural infarction with risk of embolisation, supplemented by warfarin.

• Use LMW heparin (e.g. enoxaparin 1 mg/kg SC bd or unfractionated heparin 5000–7500 units SC 12-hourly).

Further management of STEMI (? myocardial infarction)

• Antiplatelet therapy: aspirin + clopidogrel

• Beta blocker (if no thrombolytic therapy or contraindications) as soon as possible: atenolol 25–100 mg (o) daily

  or

  metoprolol 25–100 mg (o) twice daily

• Consider glyceryl trinitrate IV infusion if pain recurs

• Start early introduction of ACE inhibitors (within 24–48 hours) in those with significant left ventricular (LV) dysfunction (and other indications)

• Statin therapy to lower cholesterol

• Treat hypokalaemia

• Consider magnesium sulphate (after thrombolysis)

• Consider frusemide

Post-AMI drug management

Proven:^1,12,13

• beta blockers—within 12 hours

• ACE inhibitors—within 24 hours

• aspirin 75–150 mg and clopidogrel 75 mg (o) daily or both (alternatives to clopidogrel: ticagrelor or prasugrel)

• lipid-lowering drugs (e.g. statins)

• warfarin

  Targets:

• BP <140/90; TC <4 mmol/L; LDLC <2 mmol/L; TG <2 mmol/L

Ongoing management

• Education and counselling

• Bed rest 24–48 hours

• Continuing ECG monitoring

• Check serum potassium and magnesium

• Early mobilisation to full activity over 7–12 days

• Light diet

• Sedation

• Beta blocker (o): atenolol or metoprolol

• Anticoagulation where indicated (certainly if evidence of thrombus with echocardiography)

• ACE inhibitors for left ventricular failure and to prevent remodelling

• monitor psychological issues (e.g. anxiety)

On discharge

• Rehabilitation program

• Continued education and counselling

• No smoking

• Reduce weight

• Encourage consumption of omega-3 fatty acids

• Regular exercise, especially walking

• Exercise test (to be considered)

• Continue beta blockers for 2 years

• Continue ACE inhibitors

• Aspirin 100–300 mg daily and clopidogrel 75 mg daily

• Anticoagulation where indicated (at least 3 months)

• Statin therapy

Special management issues

Indications for coronary angiography

• Development of angina

• Strongly positive exercise test

• Consider after use of streptokinase

Management of the extensive infarction

• ACE inhibitors (even if no CCF)

• Radionuclide studies (to assess left ventricular function)

• Beta blockers (proven value in severe infarction) if no contraindications or LV dysfunction

• Anticoagulation

Treating and recognising complications of STEMI

• Signs: basal crackles, extra (third or fourth) heart sounds, X-ray changes

• Treatment (according to severity) (refer to CHAPTER 88):

  • – oxygen

  • – diuretic (e.g. frusemide)

  • – morphine IV

  • – glyceryl trinitrate: IV, SL, (o) or topical

  • – ACE inhibitors

Requires early specialist intervention which may include:

• adrenaline—titrated to BP

• treat hypotension with inotropes

• intra-aortic balloon pump

• urgent angiography ± angioplasty/surgery

This occurs in first few days after AMI (usually anterior AMI), with onset of sharp pain.

• Signs: pericardial friction rub

• Treatment:⁹ anti-inflammatory medication (e.g. aspirin, indomethacin or ibuprofen for pain) with caution

Note: Avoid anticoagulants.

This occurs weeks or months later, usually around 6 weeks.

• Features: pericarditis, fever, pericardial effusion (an autoimmune response)

• Treatment: as for pericarditis

This is a late complication.

• Clinical: cardiac failure

• Features: arrhythmias, embolisation

• Signs: double ventricular impulse, fourth heart sound, visible bulge on X-ray

• Diagnosis: 2D electrocardiography

• Treatment:

  • – antiarrhythmic drugs

  • – anticoagulants

  • – medication for cardiac failure

  • – possible aneurysmectomy

This may accompany inferior MI and is life-threatening.

This presents with severe cardiac failure and a loud pansystolic murmur. Both have a poor prognosis and early surgical intervention may be appropriate.

All types are common with STEMI and require treatment according to guidelines in CHAPTER 70. Methods may include defibrillation, cardioversion and pacemaking. Past infarct prophylaxis with IV lignocaine is not indicated.^5,15

Patients require anticipatory guidance and support including education, reassurance and counselling. If necessary, anxiolytic agents and antidepressants may help recovery.

Aortic dissection

• Early definitive diagnosis is necessary: best achieved by transoesophageal echocardiography.

• 50% of patients are hypertensive; so need pharmacological control of hypertension with IV nitroprusside and beta blockers.

• Emergency surgery needed for many, especially for type A (ascending aorta involved).

Note: There is an increased incidence during pregnancy.

Pulmonary embolus

Investigations to diagnose suspected pulmonary embolus (choose from):^4,17,18

• chest X-ray and ECG

• CT pulmonary angiography (first-line study)

• radionucleide imaging—the ventilation/perfusion (V/Q) study

• digital subtraction angiography

• D-dimer assay—useful but not specific

• Doppler sonography of lower limbs

• arterial blood gases

• Wells score: if >3, highly probable; if >6, diagnostic

Management (specialist care)

Needs supportive medical care and anticoagulation:

• heparin IV: 5000 U as immediate bolus, continuous infusion 30 000 U over 24 hours or 12 500 U (sc) bd

• or

• low molecular weight heparin

Note: The dose of heparin should then be adjusted daily to maintain the APTT at between 1.5 and 2 times control, or INR >2.

• Continue heparin 5–10 days.

• Warfarin (o) after 3–4 days or immediate; then continue heparin for 3 days after international normalised ratio (INR) at desired level.

Note: Thrombolytic therapy either IV or into the pulmonary artery can be used for major embolism. Surgical embolectomy is rarely necessary but needed if very extensive.

Pneumothorax

• Most episodes resolve spontaneously without drainage (at least 20% lung collapse).

• Drainage of the pleural space indicated for a large pneumothorax >25% pleural area, with persistent dyspnoea.

• Guidelines:

  • – <25% collapse, no symptoms: observe

  • – <25% collapse + persisting symptoms: drain

  • – >25% collapse: usually drain

• For recurrent attacks, excision of cysts or pleurodesis may be necessary.

• Statistics indicate a 30–50% recurrence rate of spontaneous pneumothorax (most within 12 months), 35% on the same side, 10–15% on the opposite side. Recurrence should not recur after a pleurodesis where the lung surface has been rendered adherent to the chest wall.

Acute tension pneumothorax

For urgent cases insert a 12–16 gauge needle into the pleural space through the second intercostal space on the affected side. Replace with a formal intercostal catheter connected to underwater seal drainage.

Gastro-oesophageal reflux

• Achieve normal weight if overweight.

• Avoid coffee, alcohol and spicy foods.

• Avoid large meals and overeating (keep to small meals).

• Use antacids or alginate compounds (e.g. Gaviscon, Mylanta Plus).

• If persistent:

  acid suppression—H₂-receptor blockers (e.g. cimetidine, ranitidine)

  or

  proton-pump inhibitors (e.g. omeprazole)

Oesophageal spasm¹⁹

• Long-acting nitrates (e.g. isosorbide dinitrate 10 mg tds)

• or

• Calcium-channel blockers (e.g. nifedipine CR 20–30 mg once daily)

Note: Attend to lifestyle and dietary factors, as for reflux.

There are many musculoskeletal causes, most of which can be eliminated by the history and physical examination. Some of the causes listed in TABLE 40.9 are very uncommon and often part of a general disorder, such as ankylosing spondylitis. Muscular tears or strains of the chest wall are quite common. A differential diagnosis is a fractured rib including a cough fracture.

Musculoskeletal chest pain is typically aggravated or provoked by movements such as stretching, deep inspiration, sneezing and coughing. The pain tends to be sharp and stabbing in quality but can have a constant aching quality.

Costochondritis is a common cause of anterior pain, which is generally well localised to the costochondral junction and may also be a component of an inflammatory disorder, such as one of the spondyloarthropathies.

Management is generally conservative with analgesics, gentle massage with analgesic creams and NSAIDs if there is an inflammatory component. Other measures that can help for very painful chest wall problems are localised injections of local anaesthetic with or without corticosteroids (with care not to penetrate the parietal pleura) and a modified support (especially for rib injuries) in the form of a special elasticised rib belt (called a universal rib belt) that gives excellent support and symptom relief while permitting adequate lung expansion.

Posterior chest (thoracic back) pain

Disorders of the musculoskeletal system represent the most common cause of thoracic (dorsal) back pain, especially dysfunction of the joints of the thoracic spine. Refer to CHAPTER 37 for more detail. Probably the commonest cause is costovertebral dysfunction caused by overstress of rib articulations with vertebrae (the costovertebral joints). This fact is clearly demonstrated with the midline thoracic back pain following cardiac surgery when these joints are compressed during sternotomy and splaying of the chest walls.

The back pain may be associated with simultaneous referred anterior chest pain or abdominal pain (see FIG. 37.3 in CHAPTER 37).

Acute thoracic back pain

Although posterior pain is invariably caused by vertebral dysfunction, there are several other important causes, including serious bone disease (leading to compression fractures) and life-threatening visceral and vascular causes. Refer to red flag pointers and TABLE 37.3 and management guidelines in CHAPTER 37.

Note:

• Intervertebral disc protrusions are rare in the thoracic spine.

• Rarely, a penetrating peptic ulcer can present with mid to lower thoracic back pain.

• Obvious or suspected myocardial infarction, especially with extensive infarction

• Transfer to major centre with complications of AMI:

  • – rupture of septum or papillary muscle

  • – aneurysm

  • – refractory arrhythmias

  • – cardiogenic shock

• Patients with persistent post-infarction angina

• Angina:

  • – patient with angina not responding to drug treatment

  • – patient with unstable angina

  • – angina lasting for longer than 15 minutes (unresponsive to sublingual nitrate) needs urgent hospital admission

• Suspected or proven pulmonary embolus or dissecting aneurysm or other serious life-threatening problem (after initial first-line measures, e.g. decompression of tension pneumothorax)

• Suspected oesophageal or other gastrointestinal disorder (e.g. duodenal ulcer), for endoscopy or appropriate gastroenterological evaluation

Hand-out sheets from Murtagh’s Patient Education 7th edition:

• Angina

• Cardiovascular (including coronary) risk factors