THE PATIENT PRESENTS WITH

Transcription

1 B , THE PATIENT PRESENTS WITH 1. Chest pain 3 2. Dyspnoea Syncope Palpitations Peripheral oedema Heart murmur High blood pressure Fever associated with a cardiac symptom or sign 57 Evans

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3 Chest pain 1 Objectives By the end of this chapter you should: be able to take a clear history from a patient presenting with chest pain be aware of the differential diagnosis of chest pain be able to examine the patient with chest pain understand the appropriate investigations for a patient presenting with chest pain. DIFFERENTIAL DIAGNOSIS OF CHEST PAIN Chest pain is one of the most common presenting complaints seen by cardiologists. It is important to remember that: there are many causes of chest pain some causes of chest pain are life-threatening and require prompt diagnosis and treatment; other causes are more benign. The first differentiation to be made is between cardiac and non-cardiac chest pain ( Fig. 1.1 ). Position of the pain central or lateral/posterior Exacerbating factors exertion, emotion, food, posture, movement, breathing Radiation of the pain to neck, arms, head Quality of pain crushing, burning, stabbing. To get an idea of the severity of a patient s symptoms ask them about their effort tolerance how far can they walk on the flat? Do they have stairs at home, and does walking up them cause chest pain? HISTORY TO FOCUS ON THE DIFFERENTIAL DIAGNOSIS OF CHEST PAIN The differential diagnosis of chest pain is very diverse; a thorough history is, therefore, very important. PRESENTING COMPLAINT Differentiation depends on a detailed history of the pain, with particular emphasis on the following characteristics of the pain ( Fig. 1.2 ): Whether the pain is continuous or intermittent Duration of the pain Past medical history This can provide important clues: A history of ischaemic heart disease A history of peptic ulcer disease, or of frequent ingestion of non-steroidal anti-inflammatory drugs Recent operations cardiothoracic surgery can be complicated by Dressler s syndrome, mediastinitis, ischaemic heart disease or pulmonary embolus (PE) Pericarditis might be preceded by a prodromal viral illness PE can be preceded by a period of inactivity (e.g. a recent operation, illness or long journey) 3

4 Chest pain Fig. 1.1 Differential diagnosis of chest pain System involved Cardiac Vascular Respiratory (all tend to give rise to pleuritic pain) Gastrointestinal Musculoskeletal Neurological Pathology Myocardial infarction Angina pectoris Pericarditis Prolapse of the mitral valve Aortic dissection Pulmonary embolus Pneumonia Pneumothorax Pulmonary neoplasm Oesophagitis due to gastric reflux Oesophageal tear Peptic ulcer Biliary disease Cervical nerve root compression by cervical disc Costochondritis Fractured rib Herpes zoster Hypertension is a risk factor for both ischaemic heart disease and dissection of the thoracic aorta. Drug history, family history and social history Other risk factors for ischaemic heart disease, such as a positive family history and smoking, should be excluded. A history of heavy alcohol intake is a risk factor for gastritis and peptic ulcer disease. When a patient presents as a hospital emergency with cardiac chest pain, try to differentiate diagnoses for which thrombolysis is contraindicated from those for which it is indicated. Thrombolysis is contraindicated in pericarditis and dissection of the thoracic aorta. EXAMINATION OF PATIENTS WHO HAVE CHEST PAIN Points to note on examination of the patient who has chest pain are shown in Fig Inspection On inspection, look for: signs of shock (e.g. pallor, sweating) may indicate myocardial infarction (MI), dissecting aorta, PE laboured breathing may indicate MI leading to left ventricular failure (LVF) or a pulmonary cause signs of vomiting suggests MI or an oesophageal cause coughing suggests LVF, pneumonia. Cardiovascular system Note the following: Pulse and blood pressure is there any abnormal rhythm, tachycardia, bradycardia, hypotension, hypertension? Inequalities in the pulses or blood pressure between different extremities are seen in aortic dissection. Mucous membranes pallor could suggest angina due to anaemia; cyanosis suggests hypoxia. Any increase in jugular venous pressure a sign of right ventricular infarction or pulmonary embolus. Carotid pulse waveform a collapsing pulse is seen with aortic regurgitation, which can complicate aortic dissection. It is slow rising if angina is due to aortic stenosis. Displaced apex beat, abnormal cardiac impulses (e.g. paradoxical movement in anterior MI). Auscultation listen for a pericardial rub, third heart sound (a feature of LVF), mitral or aortic regurgitation (features of MI or dissection respectively), aortic stenosis (causes angina). Respiratory system Note the following signs: Breathlessness or cyanosis Unequal hemithorax expansion a sign of pneumonia and pneumothorax Abnormal dullness over lung fields a sign of pneumonia 4

5 Investigation of patients who have chest pain 1 Fig. 1.2 Characteristics of different types of chest pain Characteristic Myocardial ischaemia Pericarditis Pleuritic pain Gastrointestinal pain Musculoskeletal Aortic dissection Quality of pain Crushing, tight or bandlike Sharp (may be crushing) Sharp Burning Usually sharp, although can be a dull ache Sharp, stabbing, tearing Site of pain Central anterior chest Central anterior Anywhere (usually very localized pain) Central Can be anywhere Retrosternal, interscapular Radiation To throat, jaw or arms Usually no radiation Usually no radiation To throat To arms or around chest to back Usually no radiation Exacerbating and relieving factors Exacerbated by exertion, anxiety, cold; relieved by rest and by glyceryl trinitrate Exacerbated when lying back; relieved by sitting forward Exacerbated by breathing, coughing or moving; relieved when breathing stops Peptic ulcer pain often relieved by food and antacids; cholecystitis and oesophageal pain are exacerbated by food Can be exacerbated by pressing on chest wall or moving neck Constant with no exacerbating or relieving factors Associated features Patient often sweaty, breathless and shocked; might feel nauseated Fever, recent viral illness (e.g. rash, arthralgia) Cough, haemoptysis, breathlessness; shock with pulmonary embolus Excessive wind Other affected joints; patient otherwise looks very well Unequal radial and femoral pulse and blood pressure; aortic regurgitant murmur may be heard on auscultation Any bronchial breathing or pleural rub signs of pneumonia and pleurisy. Gastrointestinal system Specifically look for: abdominal tenderness or guarding scanty or absent bowel sounds suggests an ileus (e.g. due to perforated peptic ulcer and peritonitis). INVESTIGATION OF PATIENTS WHO HAVE CHEST PAIN A summary of tests used to investigate chest pain is shown in Fig. 1.4 ; an algorithm is given in Fig Blood tests These include: cardiac biomarkers including cardiac troponin and creatine kinase cardiac troponin T and I are now commonly used to risk stratify patients presenting with acute coronary syndrome ( Fig. 1.6 ) full blood count anaemia may exacerbate angina renal function and electrolytes may be abnormal if the patient has been vomiting, leading to dehydration and hypokalaemia, or due to diuretic therapy arterial blood gases hypoxia is a sign of PE and LVF, hypocapnoea is seen with hyperventilation liver function tests and serum amylase deranged in cholecystitis and peptic ulcer disease. 5

6 Chest pain Fig. 1.3 Points to note when examining a patient who has chest pain. AR, aortic regurgitation; AS, aortic stenosis; BP, blood pressure; JVP, jugular venous pressure; LVF, left ventricular failure; MI, myocardial infarction; MR, mitral regurgitation; P2, pulmonary component of the second heart sound. neck carotid waveform elevated JVP and waveform BP hypotension (shock) hypertension difference between extremities pulse arrhythmia (tachy- or brady-) difference between extremities eyes xanthelasma (hypercholesterolaemia) face pallor (anaemia) cyanosis heart murmurs of AR (dissection) or AS (angina) pericardial rub audible murmur of MR (MI) 3rd heart sound (MI and LVF) right ventricular heave and loud P 2 (pulmonary embolus) displaced apex beat lungs pleural rub bronchial breathing reduced breath sounds abdomen abdominal tenderness or guarding reduced bowel sounds Fig. 1.4 First-line tests to exclude a chest pain emergency Test ECG CXR Biochemical markers Arterial blood gases Diagnosis If normal excludes MI, although evidence for this may emerge upon observation Widened mediastinum suggests aortic dissection; may show pleural effusion or pulmonary consolidation May be normal in first 4 h after MI, but CK-MB, cardiac troponins will then increase In the dyspnoeic patient severe hypoxaemia suggests pulmonary embolus, LVF or pneumonia CT scan Carry out urgently for suspected aortic dissection CK-MB, creatine kinase composed of M (muscle) and B (brain) subunits, which is found primarily in cardiac muscle; CT, computed tomography; CXR, chest radiography; ECG, electrocardiography; LVF, left ventricular failure; MI, myocardial infraction. ST depression in absence of BBB indicates myocardial ischaemia. At rest this equates with unstable angina or non-q wave infarction; on exertion this equates with effort-induced angina pectoris or tachyarrhythmias BBB if new this may be due to MI; if it is old, MI cannot be diagnosed from the electrocardiogram (ECG) fully developed Q waves indicate old MI (i.e. over 24-h old) atrial fibrillation secondary to any pulmonary disease or myocardial ischaemia. In the event of a large PE the classic changes are: sinus tachycardia (or atrial fibrillation) tall P waves in lead II (right atrial dilatation) right axis deviation and right BBB S wave in lead I, Q wave in lead III, and inverted T wave in lead III (SI QIII TIII pattern seen only with very large PE). Electrocardiography Findings may include: ST elevation in absence of bundle branch block (BBB) indicates acute MI (occasionally it is due to Prinzmetal s angina) Chest radiography The following signs may be seen: Cardiomegaly Widening of the mediastinum in aortic dissection 6

7 Investigation of patients who have chest pain 1 Chest pain At rest Worse on exertion Consider pulmonary embolus in all patients Worse on inspiration Not worse on inspiration Investigate for angina pectoris (i.e. serial ECG, exercise ECG, coronary angiogram) Pleurisy secondary to pneumonia Pneumothorax Pulmonary embolus Dressler s syndrome Raised ST segment Central pain Lateral Consider MI ST depression T wave inversion T wave flattening Widespread concave ST elevation Musculoskeletal oesophagitis Musculoskeletal shingles (herpes zoster) Consider unstable angina and investigate further (i.e. serial ECGs, serial biochemical markers, exercise ECG, coronary angiogram) Pericarditis Fig. 1.5 Algorithm for investigation of chest pain. Fig. 1.6 Cardiac troponin Low risk Medium risk High risk Lung lesions Pleural and pericardial effusions Oligaemic lung fields in PE. Echocardiography This may reveal: Troponin T level <0.06 µg/l > month mortality (FRISC I) 4.3% 10.5% 16.1% pericardial effusion suggests pericarditis or dissection regional myocardial dysfunction a feature of MI or ischaemia aortic dissection with false lumen aortic or mitral valve abnormalities. Computed tomography and magnetic resonance imaging These are the most sensitive methods for excluding aortic dissection and should be performed urgently if this diagnosis is suspected. It is sometimes possible to visualize PE with spiral computed tomography (CT). Ventilation/perfusion scan This excludes PE in most cases if performed promptly. If the V/Q scan is negative and PE is strongly suspected, a more sensitive test is a pulmonary angiogram. 7

8 Chest pain Exercise tolerance test or myocardial perfusion scan This may be performed at a later date if angina is suspected. CENTRAL CHEST PAIN AT REST OF RECENT ONSET IN AN ILL PATIENT The importance of this subject is that this situation represents a medical emergency requiring rapid diagnosis and treatment. Contraindications to fibrinolytic therapy Absolute contraindications Haemorrhagic stroke or stroke of unknown origin at any time Ischaemic stroke in preceding 6 months Central nervous system damage or neoplasms Recent major trauma/surgery/head injury (within preceding 3 weeks) Gastrointestinal bleeding within the last month Known bleeding disorder Aortic dissection. Relative contraindications Transient ischaemic attack in preceding 6 months Oral anticoagulant therapy Pregnancy or within 1 week postpartum Non-compressible punctures Traumatic resuscitation Refractory hypertension (systolic blood pressure >180 mmhg) Advanced liver disease Infective endocarditis Active peptic ulcer. It is necessary in this situation to distinguish between the following: MI (see Ch. 10 ) Unstable angina (see Ch. 9 ) Pericarditis (see Ch. 17 ) Dissection of thoracic aorta PE Mediastinitis secondary to oesophageal tear Non-cardiac chest pain. Thrombolysis Conditions for which thrombolysis is contraindicated The following guidelines help differentiate MI from disorders in which thrombolysis can be fatal. Pericarditis In pericarditis: In the context of cardiac chest pain, ST elevation on the ECG is usually indicative of proximal occlusion of a major epicardial coronary artery. If untreated myocardial necrosis begins within 30 min. Urgent restoration of coronary blood flow (reperfusion) prevents further left-ventricular damage and improves prognosis. Two strategies are available: primary angioplasty and thrombolysis. The management will be discussed in Chapter 10. the patient may have a prodromal viral illness pain can be exacerbated by breathing movements there might be concomitant indications of infection. examination might reveal a pericardial rub an added sound (or sounds) in the cardiac area on auscultation. This has a scratchy quality and seems close to the ears. If complicated by pericardial effusion, there could be an: impalpable cardiac impulse increased cardiothoracic ratio on the chest radiograph, with a globular heart shadow the ECG shows characteristic concave upwards raised ST segments in all leads except AVR. Thrombolysis is contraindicated because it causes haemopericardium. Dissection of the thoracic aorta The pain is sharp and tearing. There is often radiation of the pain to the back. There might be a previous history of hypertension. On examination, the patient might be shocked and there could be delays between the major pulses (e.g. right brachial versus left brachial, brachial versus femoral). Chest radiography might show a widened mediastinum. The ECG will not show ST elevation unless the coronary ostia are dissected. Confirmation might require 8

9 Central chest pain at rest of recent onset in an ill patient 1 high-resolution spiral CT, echocardiography, or magnetic resonance imaging (which is the best investigation when available; Fig. 1.7 ). Thrombolysis is contraindicated because it causes massive bleeding from the aorta ( Fig. 1.8 ). Mediastinitis This is unusual and need not usually be considered unless there is a possibility of an oesophageal leak (e.g. after endoscopy or oesophageal surgery). Pulmonary embolus Pulmonary emboli can present as acute chest pain in an ill patient or as intermittent chest pain in a relatively well patient. For this reason it is crucial to suspect PE in all patients who have chest pain that is not typically anginal. The pain of a PE can be pleuritic or tight in nature and might be located anywhere in the chest. It can be accompanied by the following symptoms and signs: Fig. 1.7 Overview of dissection of the thoracic aorta Predisposing factors Hypertension Pathophysiology Classification Symptoms Signs Investigation Management Bicuspid aortic valve Pregnancy Marfan s, Turner s, Noonan s syndromes Connective tissue diseases SLE, Ehlers Danlos syndrome Men > women Middle age Damage to the media and high intraluminal pressure causing an intimal tear Blood enters and dissects the luminal plane of the media creating a false lumen Stanford classification: type A all dissections involving the ascending aorta; type B all dissections not involving the ascending aorta Central tearing chest pain radiating to the back Further complications as the dissection involves branches of the aorta: coronary ostia myocardial infarction; carotid or spinal arteries hemiplegia, dysphasia, or paraplegia; mesenteric arteries abdominal pain Shocked, cyanosed, sweating Blood pressure and pulses differ between extremities Aortic regurgitation Cardiac tamponade Cardiac failure CXR widened mediastinum ± fluid in costophrenic angle ECG may be ST elevation CT/MRI best investigations, show aortic false lumen Transoesophageal echo if available is also very sensitive Echocardiography may show pericardial effusion if dissection extends proximally; tamponade may occur Pain relief diamorphine Intravenous access central and arterial line Fluid replacement initially colloid then blood when available crossmatch at least 10 units Blood pressure control intravenous nitroprusside infusion or labetalol infusion if no cardiac failure keep blood pressure 120/80 mmhg Surgery for all type A dissections Medical management and possibly surgery or percutaneous treatment for type B CT, computed tomography; CXR, chest radiography; ECG, electrocardiography; MRI, magnetic resonance imaging; SLE, systemic lupus erythematosus. 9

10 Chest pain Fig. 1.8 Classification of aortic dissections. A B intimal tears true lumen false lumen I II III Dyspnoea Dry cough or haemoptysis Hypotension and sweating Sudden collapse with syncope. Massive PE will cause collapse with cardiac arrest. The ECG will show ventricular tachyarrhythmias or sinus rhythm with electromechanical dissociation. Patients will often experience a sense of impending doom or profound anxiety. Conditions predisposing to clot formation in the deep veins of the leg are associated with a high incidence of PE ( Fig. 1.9 ). As the mortality rate resulting from PE is approximately 10%, appropriate investigations to exclude PE should be carried out promptly and anticoagulation commenced using either intravenous heparin as an infusion or an appropriate low-molecularweight heparin preparation subcutaneously. Warfarin therapy should be commenced if PE is confirmed. Fig. 1.9 Conditions predisposing to deep venous thrombosis Condition Immobility Postoperative Haemoconcentration Hypercoagulable states Venous stasis (poor flow of venous blood) Examples Prolonged bed rest for any reason, long air journeys Abdominal and pelvic surgery, leg and hip surgery Diuretic therapy, polycythaemia Malignancy, oral contraceptive pill, protein C/protein S deficiency, etc. Congestive cardiac failure, atrial fibrillation (formation of thrombus in the right ventricle can result in PE) 10