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Assessment and treatment of chest pain pages 45-53 Multiple choice questions and submission instructions page 54 Practice profile assessment guide page 55

Assessment and treatment of chest pain

NS243 Tough J (2004) Assessment and treatment of chest pain. Nursing Standard. 18, 37, 45-53. Date of acceptance: April 27 2004. Aim and intended learning outcomes The aim of this article is to assist nurses in the management of chest pain in patients presenting in acute settings (A&E departments, acute admissions units and coronary care units). Through a structured approach of assessment, initiating investigations, treatment and delivering nursing care, life-threatening causes of chest pain can be identified, alerting medical staff immediately to these situations, and ensuring the most appropriate evidence-based treatment strategies are adopted. After reading this article you should be able to: I Identify the anatomy and physiology of organs associated with chest pain. I Identify the main causes of chest pain and differential diagnosis. I Describe the process for taking an accurate history from a patient with chest pain. I Identify the actions required to assess a patient with chest pain. I State the common treatment required for cardiac and life-threatening causes of chest pain. I Differentiate between acute myocardial infarction (AMI) and other acute coronary syndromes (ACS). I Identify life-threatening causes of chest pain and initiate appropriate nursing care and management of patients with ACS. I Identify the different types of reperfusion strategies available to patients with MI. Introduction Chest pain is one of the main causes of emergency admission to hospital in the UK. Between 30-35 per cent of all emergency medical admissions are for acute chest pain (Blatchford and Capewell 1997, Capewell and McMurray 2000). Patients with chest pain can be admitted to a variety of clinical areas for initial assessment. There are many different causes of chest pain requiring medical intervention, some of which can be life threatening. Patients who have MI and ACS and smaller numbers who have dissecting aortic aneurysm require urgent treatment. Differential diagnosis for chest pain can include pulmonary, gastric, musculoskeletal and non-organic causes. Through structured assessment and nursing intervention, it is possible to identify those at high risk and ensure rapid treatment is provided to patients most likely to benefit from reperfusion treatment. Anatomy and physiology of the chest and upper abdominal cavity Heart The heart lies in the thoracic cavity. It consists of four chambers divided by vertical septum. The upper chambers of the heart are the left and right atria, the lower chambers the left and right ventricles. The right atrium receives blood from the superior and inferior vena cave and coronary sinus. Blood passes through the tricuspid valve to the right ventricle; contraction enables blood to be pumped through the pulmonary valve to the lungs. The left atrium receives oxygenated blood from the four pulmonary veins. Blood is pumped into the left ventricle through the mitral valve. The left ventricle contracts and blood is forced through the aortic valve opening into the aorta and subsequently circulated around the body. The heart walls are composed of cardiac muscle; the myocardium (middle layer) is covered externally by the serous pericardium and lined internally with endocardium (Snell 2000). Aorta The aorta is the main arterial trunk and

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In brief Author Jackie Tough RGN, DipN, BSc(Hons), is nurse consultant, chest pain, James Cook University Hospital, Middlesbrough. Email: Summary Chest pain is one of the main reasons for emergency admission to hospital in the UK. Jackie Tough examines the causes and treatment of chest pain and offers a structured system for taking the patients history. Key words I Cardiovascular system and disorders I Chest pain I Heart disorders These key words are based on subject headings from the British Nursing Index. This article has been subject to double-blind review.

Online archive For related articles visit our online archive at: and search using the key words above.

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delivers oxygenated blood from the left ventricle to the body tissues. It is divided into the ascending aorta, arch of the aorta, descending thoracic aorta and the abdominal aorta. The coronary arteries arise from the ascending aorta. Lungs The lungs are positioned in the thoracic cavity, with each lung lying either side of the mediastinum, separated by the heart and great vessels. The right lung is larger than the left and has three lobes; the left has two. Oesophagus The oesophagus is a tubular structure approximately 10in long, which passes through the thoracic cavity and joins the stomach. Intercostal muscles The intercostal muscles consist of three layers external, internal and innermost, lying between each rib space. Their main function is to aid respiration. Stomach Although the stomach lies in the abdominal cavity, disease of the stomach can often be associated with chest discomfort (Snell 2000). The stomach lies in the left upper quadrant, epigastric and umbilical regions, much of it lying under the ribs. Pancreas The pancreas stretches across the posterior abdominal wall in the epigastric region. It consists of exocrine and endocrine cells producing a number of digestive enzymes including amylase. The endocrine pancreas produces insulin and glucagon (Snell 2000). Figure 1. The coronary circulation Ascending aorta Left coronary artery Left circumflex artery

Right coronary artery Left anterior descending artery I Pallor and sweating. I Hypotension with narrow pulse pressures. I Irregular pulse with extrasystole. Acute coronary syndromes (ACS) ACS refer to: I MI that can be divided into ST-elevation MI (STEMI) or non-ST-elevation MI (NSTEMI). I Unstable angina. The history should be consistent with MI or unstable angina. Electrocardiogram (ECG) changes and elevated cardiac markers, for example troponin T, will determine diagnosis. Check your local hospital guidelines for types of cardiac markers used and reference ranges. Angina Angina pectoris is the most common type of chest pain associated with heart disease and is caused by an imbalance between the blood supply to a portion of heart muscle and the requirements of the muscle for metabolism (Epstein et al 1999). Most patients will have a narrowing or stenosis of the coronary arteries and the pain is precipitated by an increase in metabolic requirements associated with physical exertion (Epstein et al 1999). Occasionally angina can be caused by aortic stenosis or hypertrophic cardiomyopathy. Pain that is similar in nature but occurs at rest or with increasing frequency may be caused by unstable angina (Epstein et al 1999). Symptoms that describe pain include: I Usually crushing, tight or constricting in nature. I Usually retrosternal. I Brought on by physical or emotional exertion. I Relieved by rest. I Often worse in cold weather or after eating. I Often relieved quickly by nitrates. Pericarditis Pericarditis is caused by inflammation of the pericardium, the serous sac that surrounds the heart, and can be a complication of MI. It may also result from viral or bacterial infection; coxsackie viral infections are the most common cause of

Draw a diagram of the internal chest organs and label the structures discussed above. Check your diagram using an anatomy and physiology textbook of your choice. Using your knowledge of the anatomy and physiology of the chest organs, write down the possible causes of chest pain.

Box 1. Causes of chest pain Cardiovascular I Myocardial infarction I Acute coronary syndromes I Angina I Pericarditis I Dissecting aortic aneurysm Pulmonary I Pleurisy I Pulmonary embolism I Pneumothorax I Pneumonia Musculoskeletal I Costochondritis I Trauma Gastrointestinal I Reflux I Ulcers I Gallstones I Pancreatitis Non-organic I Anxiety

Causes of chest pain There are numerous causes of chest pain, some of which are outlined in Box 1. Cardiovascular Myocardial infarction (MI) MI is usually caused by coronary thrombosis (Epstein et al 1999). The coronary thrombosis occurs at the site of a ruptured atheromatous plaque situated in the coronary arteries (Figure 1). The patient may previously have had angina but this is not always the case. The pain is severe, can occur at any time and persists even if the patient rests or uses nitrates. In patients who have diabetes mellitus or are older, MI can be relatively painless (Epstein et al 1999). Symptoms are (Epstein et al 1999): I Severe chest pain central, crushing, band like, similar to bad indigestion. I Persistent pain despite rest or use of nitrates. I Pain lasting more than 15-20 minutes is indicative of MI.

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pericarditis affecting young adults (Epstein et al 1999). Symptoms are (Epstein et al 1999): I Substernal constant soreness or sharp pain. I Worse when lying down and relieved by sitting forward. I Aggravated by deep inspiration. I Usually a fever if due to infection or MI. I Not usually made worse by exertion. I Unresponsive to nitrates. Dissecting aortic aneurysm Aortic dissection usually begins with a tear in the intima of the vessel; blood enters the median layer of the artery and splits the intima in two, leading to dissection. Dissection can originate in the ascending aorta and extend to the aortic arch, be confined to the ascending aorta or develop in the distal aorta and extend down the aorta. It is classified according to DeBakey type I, II and III (Kumar and Clark 2002). Symptoms are as follows (Epstein et al 1999): I Characteristic form of chest pain that is described as a tearing sensation. I Pain that radiates to the shoulder blades or back and into the neck and arms. I Can be mistaken for MI. I Shock. I Peripheral pulses may be absent. I The patient may be hypertensive. I Blood pressure measurements may vary between left and right arms. Pulmonary Pleurisy Pain from the pleura is often caused by the two pleural surfaces rubbing together. Inflammation of the pleura can result from pneumonia, pulmonary infarction or embolism and in some cases pneumothorax. Patients often say: I have to catch my breath (Snell 2000). Pain is localised, sharp or stabbing in nature and is worse on deep breathing or coughing (Kumar and Clark 2002). Pleural friction rub is heard on auscultation of the lungs. Pulmonary embolism Pulmonary embolism is caused as a result of a dislodged thrombus from systemic veins or occasionally the right side of the heart, which embolises in the pulmonary arterial system. Clots form as a result of sluggish blood flow, local injury or compression of the vein or a hypercoagulable state (Kumar and Clark 2002). There is sudden onset of unexplained dyspnoea. Pleuritic chest pain and haemoptysis are present only when infarction has occurred. Many pulmonary emboli can occur silently, but there are three typical clinical presentations (Kumar and Clark 2002): I Small or medium pulmonary embolism embolus in the terminal pulmonary vessel. I Massive pulmonary embolism sudden collapse due to acute obstruction of the right ventricular outflow tract. There is severe chest pain and cardiac ischaemia due to lack of coronary blood flow. I Multiple recurrent pulmonary emboli increasing breathlessness over weeks or months, syncope on exertion and occasionally angina. Pneumothorax Pneumothorax is air in the pleural space and can be spontaneous or occur as a result of trauma to the chest. Spontaneous pneumothorax is more likely to occur in young males as a result of a rupture of a pleural bleb, probably resulting from a congenital defect of the connective tissue of the alveolar walls (Kumar and Clark 2002). In individuals more than 40 years of age, the causes are related to chronic obstructive pulmonary disease (COPD), and more rarely bronchial asthma or carcinoma. The pneumothorax can be localised or generalised if the hemithorax contains air (Kumar and Clark 2002). The presenting symptoms are sudden onset of unilateral pleural pain and progressively increasing shortness of breath. In a large pneumothorax the patient may develop pallor and tachycardia. There may be few physical signs if the pneumothorax is small (Kumar and Clark 2002). Pneumonia Pneumonia is inflammation of the lungs. It presents as an acute illness and is often preceded by viral illness. It can be localised to one lobe or diffuse to both and can also occur as a result of aspiration of vomit (Kumar and Clark 2002). Patients experience cough, pleuritic chest pain, purulent sputum and fever. Musculoskeletal Costochondritis Costochondritis presents with anterior chest wall pain, which is caused by an irritated joint between the rib and sternum. It is often a result of repetitive minor trauma. It is harmless and usually disappears without treatment. Symptoms include localised tenderness, which is reproducible when applying pressure (ONeill et al 2002). Trauma Trauma to the chest occurs via blunt, penetrating or crush injuries. Myocardial contusion is direct, traumatic, myocardial damage without involvement of the coronary arteries. It is common in blunt trauma and is difficult to diagnose. It tends to occur in acceleration/deceleration and crush/compression injuries (Gomersall and Calcroft 1999). Symptoms include dyspnoea and chest pain. In severe cases cardiac tamponade can result in cardiogenic shock. Aortic and mitral valvular dysfunction may occur. ECG changes can be apparent such as ventricular ectopic beats, ST-segment and T wave changes (Gomersall and Calcroft 1999). Gastrointestinal Reflux Chest pain that results from gastro-oesophageal reflux disease (GORD) presents as a burning sensation. This is mainly due to direct stimulation of the hypersensitive oesophageal mucosa and can be due to spasm of the distal oesophageal muscle (Kumar and Clark 2002). Heartburn in the epigastric or central chest area is aggravated by bending, stooping or lying down and may be relieved by antacid medication. Ulcers Gastric ulcers are associated with gastritis and can be a result of local epithelial damage caused by Helicobacter pylori infection or abnormal mucus production (Kumar and Clark 2002). Pain associated with duodenal ulcers classically occurs at night but can occur during the day and is worse when may 26/vol18/no37/2004 nursing standard 47

the patient is hungry. Patients may be symptomless until they present with haematemesis, melena or perforation (Kumar and Clark 2002). The patient may present with epigastric pain, nausea, anorexia and weight loss. Antacids can help relieve the pain of gastric and duodenal ulcers. Gallstones Gallstones are more common in women than men and are associated with increasing age (ONeill et al 2002). The three major factors leading to gallstone formation are: I Supersaturation of bile with cholesterol. I Impaired gall bladder motility. I Bile stasis. Symptoms include intermittent pain in the right upper quadrant, which occurs after food and lasts for several hours (ONeill et al 2002). Pancreatitis Pancreatitis can be acute or chronic and relapsing. It is usually associated with gallstones or high alcohol intake (ONeill et al 2002). The patient may present with central or epigastric pain radiating to the back, which can be severe. He or she may be distressed with pallor, sweating, hypotension and tachypnoea. There may be abdominal tenderness, rigidity and guarding (ONeill et al 2002). Non-organic Anxiety Left sub-mammary stabbing pain, known as Da Costas syndrome, is usually associated with anxiety (Kumar and Clark 2002). It often occurs in young adults at times of stress and hyperventilation, palpitations, sweating, tremor and effort fatigue are commonly associated with this type of pain. It can be differentiated from angina on the basis of history and ECG changes (Kumar and Clark 2002). A structured system of history taking Courses that teach nurses physical assessment and history-taking skills help to develop a structured approach to history taking. This is important when you need to decide rapidly the cause of chest pain. The following approach is useful as it guides the nurse through a question format. This should be used in conjunction with a visual and physical assessment as described by Ahern and Philpot (2002). Presenting complaint This should be identified as soon as the patient arrives in the receiving area. Chest pain is important because it requires urgent investigation to treat or exclude MI. Once chest pain has been established, the nurse needs to identify the history of the common symptoms associated with chest pain. The following prompts will help you to establish the cause of pain: I Site. I Radiation. I Character. I Exacerbating or relieving factors. I Duration. I Frequency. I Associated symptoms. Previous medical history Determining the patients previous medical history can help you to calculate the likelihood of this episode of chest pain having a cardiac origin. For example, individuals with previous MI or coronary heart disease (CHD) are at greater risk of having a further event. The Thrombolysis in Myocardial Infarction (TIMI) risk score is helpful in assessing the level of risk (Antman et al 2000) (Table 1). Previous medical history may also suggest alternative causes of chest pain. Risk factors This can play an important part in helping the nurse to confirm a cause of chest pain. There are significant risk factors for CHD (Epstein et al 1999): I Smoking. I Family history. I Hypertension. I Diabetes mellitus. I Hypercholesterolaemia. I Obesity. I Lack of physical exercise. Medication history Establishing the patients medication history is important to highlight existing cardiac-related drugs and previous administration of thrombolysis. A patient who has received thrombolysis in the past, with new ST elevation, will require different management strategies, especially if streptokinase was the thrombolytic agent used, as it cannot be re-administered. Social history This can provide details that may help in the decision-making process, as it can help to identify factors such as stress and lifestyle. Nursing interventions
(Antman et al 2000)

Consider a patient in your clinical area who was admitted with chest pain. Review the signs and symptoms he or she experienced and how these helped to formulate the initial diagnosis. Table 1. TIMI risk score for ST-elevation MI (STEMI)
Historical Points Risk score 30-day mortality (per cent) 0.8 1.6 2.2 4.4 7.3 12.0 16.0 23.0 27.0 36.0

Age >75 years 65-74 years Diabetes mellitus, hypertension or angina Examination Systolic blood pressure <100mmHg Heart rate >100bpm Killip II-IV (heart failure classification in AMI) Weight <67kg Presentation Anterior ST elevation or left bundle branch block Time to treatment >4 hours Risk score total points (0-14)

3 2 1 3 2 2 1 1 1

0 1 2 3 4 5 6 7 8 >8

Observations Time is crucial when dealing with

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cardiac chest pain. The following observations are all equally important and should be performed within ten minutes of the patients admission: I Cardiac monitoring. I ECG recording (review by physician within ten minutes). I Blood pressure, pulse and respiration rate. It is helpful to record blood pressure in both left and right arms when a patient presents with chest pain. A difference of greater than 20mmHg may indicate aortic dissection and can assist in formulating diagnosis. I Oxygen saturation level. I Intravenous (IV) access and venepuncture for blood chemistry, blood count and cardiac markers. Cardiac monitoring has been discussed in detail previously by Hand (2002). Lead placement is discussed in detail. The principles of recording an ECG are straightforward and a good quality ECG can be obtained by complying with the procedures outlined in Box 2. The use of biochemical markers is standard practice to risk-stratify patients with suspected ACS. Cardiac markers should be used in conjunction with medical history, physical examination and 12-lead ECG recordings. Creatine kinase and myocardial bound isoenzyme a biochemical test are classical markers of myocardial necrosis. Levels rise within three to six hours and peak at 12-24 hours following myocardial necrosis or AMI, returning to normal over the next 48 hours. Troponin T and troponin I levels are highly specific for detecting myocardial necrosis, rising within four to eight hours and peaking at 12 hours. Myoglobin is a rapid change marker, released within two hours of onset of symptoms and peaking at six hours. It has an excellent negative predictive value and can be used to rule out MI in conjunction with more specific markers such as troponin (Braunwald et al 2000). Treatment of cardiac causes of chest pain An initial assessment should be as rapid as possible and treatment should be started immediately to provide prompt relief of symptoms, limit myocardial damage and risk of cardiac arrest. Initial treatment for patients presenting with ACS can be memorised using the mnemonic MONA: I Morphine IV titrated to avoid sedation and respiratory depression. I Oxygen in high concentration. I Nitroglycerin nitrate sublingual glyceryl trinitrate (GTN). I Aspirin 300mg orally as soon as possible. While initiating treatment according to MONA guidance, interpretation of the ECG is required to guide further management. If the ECG shows evidence of ST elevation, initial diagnosis of MI is highly likely and thrombolytic therapy should be considered immediately (Baigent et al 1998, Boersma et al 1996, FTT 1994). Treatment of ST-elevation MI STEMI is the term applied to the clinical presentation of AMI. While local guidelines may vary, common ECG criteria for thrombolysis are ST elevation of: I 1mm or more in two or more adjacent limb leads. I 2mm or more in two or more adjacent chest leads. The ECG leads consist of: I Limb leads I, II, III, AVR, AVL, AVF. I Inferior leads II, III, AVF. I Lateral leads I, AVL. I Precordial or chest leads V1V6, generally called the anterior leads but can be separated into right ventricle: V1, V2; ventricular septum: V3, V4; anterolateral left ventricle: V5, V6. The ST-elevation changes in the various ECG leads can be attributed to occlusion of specific arteries or infarct related artery (IRA) as follows: I Inferior MI represents occlusion of the right coronary artery. I Anterior MI represents occlusion of the left coronary artery (main stem) or left anterior descending artery. I Lateral MI represents occlusion of the circumflex coronary artery (Figure 1). ECG changes that may occur during infarction are displayed in Figures 3-5 (Turner and Turner 1995). Pathophysiology of CHD leading to AMI MI usually occurs in patients with coronary atheroma as a result of plaque rupture, resulting in thrombus formation. Atherosclerotic plaque forms over time in the arteries. The plaque consists of soft atheroma, Box 2. Recording an electrocardiogram (ECG) Preparing the skin I Remove any chest hair with a disposable razor I Dry the skin if sweating or wet Obtaining good contact with skin and electrodes I Slight abrasion of the skin before electrode placement to remove dry skin will improve the conduction signal I Apply slight pressure to ensure good contact between electrode gel and skin Placing the electrodes I Place an electrode on each arm and leg, avoiding large muscle mass Chest lead positions (Figure 2): V1 Fourth intercostal space right of the sternum V2 Fourth intercostal space left of the sternum V3 Midway between V2 and V4 V4 Fifth intercostal space mid-clavicular line V5 Fifth intercostal space in line with the anterior axillary line V6 Fifth intercostal space mid-axilla Eliminating muscle tremor and artifact I Placing the limb electrodes on bone rather than muscle can help to eliminate muscle tremor I Encourage the patient to stay still and relax to obtain a good quality trace I Maintain the patients dignity by covering the chest with a light blanket or sheet Colour coding of leads is universal to help the operator ensure lead connection errors are minimised. Always make sure you have placed the leads in the correct position (Figure 2). Common mistakes are made with the limb leads which can be mixed up

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Figure 2. Chest lead placement and colour coding

Refer to a physiology textbook and a recent article on haemostasis, anticoagulants and fibrinolysis (Casey 2003) and review the clotting mechanism. Relate this information to the pharmacological effects of thrombolytic agents on clot lysis.


V2 V3 V4 V5 V6

Perform a literature search on the benefits of thrombolysis in AMI, using the key words myocardial infarction, thrombolysis and mortality. Alternatively, review the section on thrombolysis in AMI in Yusuf et al (2003). Thrombolysis The fibrinolytic system acts to break down thrombus and it is this system that is activated by thrombolytic drugs. Releasing plasminogen activators causes plasminogen to be deposited on fibrin strands in the thrombus. Plasminogen activators cleave plasminogen to release plasmin, which digests fibrin and fibrinogen resulting in lysis of the clot. The aim is to recanalise the thrombolytic occlusion and restore blood flow (Rang et al 1999). Figure 3. Inferior ST-segment elevation
I II III II aVR aVL aVF V1 V2 V3 V4 V5 V6

an infiltration of white blood cells engulfs the lipids and forms foam cells and a fibrous cap. The plaque can rupture as a result of many factors, including stress from blood flow, inflammation, flexion or tension of the fibrous cap causing the plaque to become injured or thinned (McCance and Huether 1998). Rupture exposes sub-endothelial adhesion molecules and thrombus formation begins as adhesion molecules are exposed to flowing blood. This allows primary haemostasis to occur, resulting in platelet adhesion, platelet activation and aggregation (McCance and Huether 1998). The activation of the clotting cascade results in a mesh of fibrin strands around the platelet and thrombus formation (Figures 6 and 7) (McCance and Huether 1998). Reperfusion strategies Patients whose onset of major symptoms has occurred in the last 12 hours and who have ECG evidence of ST elevation should be considered for reperfusion therapy immediately. The type of reperfusion strategy offered is based on local resources and includes thrombolysis, which is the most common treatment in the UK. Percutaneous coronary intervention (PCI) is offered in some centres for individuals who have had a previous thrombolysed MI, or depending on the time of onset of symptoms to presentation. However, PCI is now being offered in some centres as the first-line treatment. Regardless of the reperfusion strategy adopted, the most important factor is to start treatment as quickly as possible this cannot be over-emphasised. Key phrases such as time is muscle and minutes mean myocardium have been used to encourage clinicians to act quickly. In addition, National Service Framework (NSF) for CHD targets relating to rapid delivery of treatment are monitored nationally, and include a door-to-needle time of 20 minutes (DoH 2000).

Figure 4. Anterior ST-segment elevation

I II III II aVR aVL aVF V1 V2 V3 V4 V5


Figure 5. Lateral ST-segment elevation

I II III II aVR aVL aVF V1 V2 V3 V4 V5 V6

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There is overwhelming evidence from large randomised controlled clinical trials conducted in the 1980s and 1990s of the benefits in terms of reduction in mortality for patients with AMI treated with thrombolytics. Early trials such as GISSI (1986) and ISIS-2 (1988) showed initial benefits from early thrombolysis. The GUSTO (1993) study and ISIS-3 (1992) confirmed that the speed at which thrombolysis is administered reduced mortality rate. The golden hour refers to the optimal timescale from onset of major symptoms to delivery of thrombolysis to achieve the greatest reduction in mortality (Boersma et al 1996). Subsequent studies, such as the Grampian Region Early Anistreplase Trial (GREAT) (Rawles 1996), have compared pre-hospital thrombolysis administered by GPs, with hospital-administered thrombolysis. This study demonstrated a median time from onset of symptoms for thrombolysis of 105 minutes in the pre-hospital group compared to 240 minutes for the hospital-thrombolysed group. Fiveyear mortality was 25 per cent in the pre-hospital group and 36 per cent in the hospital-treated group. The following figures represent the benefits in terms of lives saved by initiation of early thrombolysis (Boersma et al 1996): I 65 lives saved per 1,000: zero to one hour. I 37 lives saved per 1,000: one to two hours. I 26 lives saved per 1,000: two to three hours. I 29 lives saved per 1,000: three to six hours. Common thrombolytic agents include: I Streptokinase (infusion). I Alteplase (bolus and infusion). I Tenecteplase (single bolus - weight adjusted, now replacing alteplase). I Reteplase (double bolus). Heparin is given (usually intravenously) with all thrombolytic drugs except streptokinase. Figure 6. Pathophysiology in acute coronary syndromes Coronary atherosclerosis Plaque rupture Chronic stable angina Acute MI Thrombosis Unstable angina

Figure 7. Thrombus formation Site of plaque rupture

Blood flow

Tunica intima (endothelium)

Tunica media

Tunica adventitia

Check your local hospital guidance and make a list of the contraindications to thrombolytic therapy. There are certain criteria that must be assessed to deliver thrombolysis safely; these are divided into absolute and relative contraindications (Box 3). The evidence regarding thrombolysis in MI has led to the guidance in the National Service Framework for Coronary Heart Disease being introduced (DoH 2000). Chapter three addresses MI and other ACS. It lays down standards and timescales in which to achieve them. Standard Five states: People with symptoms of a possible heart attack should receive help from an individual equipped with and appropriately trained in the use of a defibrillator within eight minutes of calling for help, to maximise the benefits of resuscitation should it be necessary (DoH 2000). Standard Six states that: People thought to be suffering from a heart attack should be assessed professionally and, if indicated, receive aspirin. Thrombolysis should be given within 60 minutes of calling for professional

help (DoH 2000). The NSF for CHD specifies the following time frames for treatment: I Call-to-help time response within eight minutes from calling for professional help. I Call-to-door time transfer to hospital within 30 minutes. I Door-to-needle time assessment and where necessary initiation of thrombolysis within 20 minutes of arrival in hospital. I Call-to-needle time initiation of thrombolysis in STEMI within 60 minutes of calling for help. The NSF for CHD expected 75 per cent of eligible patients to receive thrombolysis within 20 minutes (door-to-needle time) by April 2003. This has been difficult to achieve nationally and is reflected in the Myocardial Infarction National Audit Project (MINAP) data, which will be available in the public domain later this year. The door-to-needle time is important in the hospital setting, as it requires prompt assessment of patients presenting with chest pain to identify those with STEMI and commencement of thrombolysis within 20 minutes of arrival. The greatest improvements in mortality can be gained from call-to-needle time within 60 minutes of calling for help (DoH 2000). This is aimed at meeting the recommendations of Boersma et als (1996) study. For this reason local development plans are now concentrating on meeting the call-to-needle time of 60 minutes and this is being addressed primarily through the administration of pre-hospital thrombolysis by paramedics. Primary percutaneous coronary intervention (PCI) Primary PCI refers to angioplasty as the firstline treatment for STEMI where the IRA is reopened using a balloon catheter. A coronary stent may or may not be inserted to maintain vessel patency, may 26/vol18/no37/2004 nursing standard 51

depending on clinical need. A systematic review of ten clinical trials comparing primary PCI to thrombolysis showed a statistically significant reduction in mortality of 34 per cent in favour of PCI with a 47 per cent reduction in non-fatal reinfarction and substantial reduction in haemorrhagic stroke (Natarajan and Yusuf 2003). Primary PCI saves an additional 21 lives per 1,000, compared with thrombolytic therapy and 40-50 lives, compared with no therapy (Natarajan and Yusuf 2003), although thrombolysis within one hour from onset of major symptoms still appears to have the greatest reduction in mortality. Benefits of primary PCI are greater in patients presenting three to 12 hours from onset of symptoms (Steffenino et al 2003). However, availability of primary PCI in the UK is limited to certain regional cardiothoracic centres, therefore, early thrombolysis remains the first-line treatment in the UK. Treatment of AMI is in three stages, pre-hospital, hospital and continuing care: I In the pre-hospital stage, early resuscitation if necessary, oxygen therapy, pain relief, aspirin and thrombolysis (if available) are indicated (ATC 1994, Boersma et al 1996, FTT 1994). I In addition to the above, hospital treatment includes the administration of angiotensinconverting enzyme (ACE) inhibitors, beta blockers, glucose and insulin infusion where indicated (ACE Inhibitor Myocardial Infarction Collaborative Group 1998, Baigent et al 1998, Malmberg 1997, Yusuf et al 1985). I Continuing treatment includes low-dose aspirin, beta blockers, statins, ACE inhibitors, lifestyle modification, control of blood pressure and assessment for revascularisation (Oldridge et al 1988, Rihal et al 1998, Sacks et al 1996, Scandinavian Simvastatin Survival Study Group 1994, Wood et al 1998). Treatment of other ACS Initial assessment and treatment of patients presenting with typical cardiac chest pain in the absence of STEMI is as previously discussed according to MONA and baseline observations and tests. Further management will depend on ECG changes. ECG changes can manifest as ST depression in more than two leads and T wave inversion in leads where this would not normally occur. The history is usually consistent with increasing frequency or severity or angina at rest. Ongoing interventions include: I Aspirin. I Heparin subcutaneous low molecular weight. I Beta blockers. I Nitrates. I Glycoprotein IIb/IIIa inhibitors are recommended as part of initial management of unstable angina or NSTEMI in those at high risk of MI or death (NICE 2002). I Calcium antagonist (if beta blockers are contraindicated). I Continuing care is consistent with AMI discussed earlier. If any of the following risk factors are present, early angiography is indicated (DoH 2000): I Elevated troponin T levels. I Prolonged rest angina with ECG changes in more than two leads. I Pulmonary oedema or hypotension. I Angina not settling with medical treatment. I Second presentation of ACS within three months. Treatment with a non-steroidal anti-inflammatory drug such as indometacin may be sufficient for pain relief in pericarditis, but if pain is severe an opiate may be required (Sprigings and Chambers 2001).

Box 3. Absolute and relative contraindications to thrombolysis Absolute I Major surgery or trauma within six weeks I Known allergy to planned agent I Pregnancy I Proven active peptic ulcer or bleed within six months I Stroke within six months I Intracranial tumours I Bleeding disorder I Aortic dissection Relative I Extensive cardiopulmonary resuscitation I Severe hypertension I Diabetic retinopathy

REFERENCES ACE Inhibitor Myocardial Infarction Collaborative Group (1998) Indications for ACE inhibitors in the early treatment of acute myocardial infarction: systematic overview of individual data from 100,000 patients in randomised trials. ACE Inhibitor Myocardial Infarction Collaborative Group. Circulation. 97, 22, 2202-2212. Ahern J, Philpot P (2002) Assessing acutely ill patients on general wards. Nursing Standard. 16, 47, 47-54. Antiplatelet Trialists Collaborative (ATC) (1994) Collaborative overview of randomised trials of antiplatelet therapy I: Prevention of death, myocardial infarction and stroke by prolonged antiplatelet therapy in various categories of patients. British Medical Journal. 308, 6921, 81-106. Antman E et al (2000) The TIMI risk score for unstable angina/non-ST elevation MI: a method for prognostication and therapeutic decision making. Journal of the American Medical Association. 284, 7, 835-842.

Baigent C et al (1998) ISIS-2: 10-year survival among patients with suspected acute myocardial infarction in randomised comparison of intravenous streptokinase, oral aspirin, both, or neither. The ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. British Medical Journal. 316, 7141, 1337-1343. Blatchford O, Capewell S (1997) Emergency medical admissions: taking stock and planning for winter. British Medical Journal. 315, 7119, 1322-1323. Boersma E et al (1996) Early thrombolytic treatment in acute myocardial infarction: reappraisal of the golden hour. The Lancet. 348, 9030, 771-775. Braunwald E et al (2000) ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction: executive summary and recommendations. Circulation. 102, 10, 1193-1209. Capewell S, McMurray J (2000) Chest pain please admit: is there an

alternative? A rapid cardiological assessment service may prevent unnecessary admissions. British Medical Journal. 320, 7240, 951-952. Casey G (2003) Haemostasis, anticoagulants and fibrinolysis. Nursing Standard. 18, 7, 45-51. Department of Health (2000) National Service Framework for Coronary Heart Disease. London, The Stationery Office. Epstein O et al (1999) Clinical Examination. Second edition. London, Mosby. Fibrinolytic Therapy Trialists (FTT) Collaborative Group (1994) Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. The Lancet. 343, 8893, 311-322. GISSI (1986) Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nellInfarto

Miocardico (GISSI). The Lancet. 1, 8478, 397-402. Gomersall C, Calcroft R (1999) Chest Injuries. chest_injuries.htm. (Last accessed: May 7 2004.) GUSTO (1993) An international randomized trial comparing four thrombolytic strategies for acute myocardial infarction. The GUSTO investigators. New England Journal of Medicine. 329, 10, 673-682. Hand H (2002) Common cardiac arrhythmias. Nursing Standard. 16, 28, 43-52. ISIS-4 (1995) A randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group. The Lancet. 345, 8951, 669-685. ISIS3 (1992) Third International Study of Infarct Survival Collaborative Group ISIS-3: a randomised comparison of streptokinase vs tissue

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If the cause of pericarditis is bacterial infection following thoracic surgery or trauma, antibiotics will be necessary after blood culture. An echocardiogram should be performed for signs of effusion and tamponade should be considered. Pericardiocentesis may be necessary (Sprigings and Chambers 2001). Treatment of life-threatening causes of chest pain Dissecting aortic aneurysm Dissection is a medical emergency requiring rapid intervention. Intravenous access and pain relief are required immediately. Blood pressure should be recorded in both arms and peripheral pulses assessed. A chest X-ray is required and, if available, transthoracic echocardiography. The aim is to maintain blood pressure at 100-120mmHg and a urine output of more than 30ml per hour; a urinary catheter is required to measure output. Management depends on the site of dissection if proximal and it will require urgent repair unless there are existing severe co-morbidities (Sprigings and Chambers 2001). Pulmonary embolism Pulmonary embolism should be treated according to severity. Heparin, either IV or subcutaneous, can be used depending on haemodynamic stability. In acute pulmonary embolism with signs of circulatory collapse, the patient should be connected to a cardiac monitor and fluid resuscitation should be started to maintain systolic blood pressure greater than 90mmHg. Inotropic support may be necessary with a dobutamine infusion. Thrombolysis is indicated in confirmed acute pulmonary embolism with persisting hypotension without response from the above interventions (Sprigings and Chambers 2001). Pneumothorax Treatment depends on the severity of symptoms and past medical history may help to identify the cause. Needle aspiration may be sufficient or a chest drain may be required. Tension pneumothorax can result in cardiorespiratory arrest (Sprigings and Chambers 2001). Trauma Treatment of traumatic chest injury depends on the severity of symptoms and damage to underlying organs, and can be minor or extensive and life threatening (Gomersall and Calcroft 1999). A chest X-ray is required and assessment of vital signs, oxygen saturation and arterial blood gases may be indicated. Assessment of fractured ribs or sternum and evidence of pneumothorax or haemopneumothorax should be considered. Cardiac tamponade or myocardial contusion may be indicated by ECG abnormalities and cardiac arrhythmias (Gomersall and Calcroft 1999). For general treatment of non-cardiac or non-lifethreatening causes of chest pain, refer to a medical text such as Kumar and Clark (2002). Conclusion Chest pain has multiple causes that can be urgent and life threatening or minor requiring simple relief of pain and reassurance. The nurse has a considerable role to play in ensuring patients are assessed and cared for using effective evidencebased strategies, not only assisting the doctor in diagnosis but also alerting medical colleagues to high-risk patients

Now that you have finished the article, you might like to write a practice profile. Guidelines to help you are on page 55.

plasminogen activator vs anistreplase and of aspirin plus heparin vs aspirin alone among 41,299 cases of suspected acute myocardial infarction. The Lancet. 339, 8796, 753-770. ISIS-2 (1988) Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. The Lancet. 13, 2, 349-360. Kumar P, Clark M (2002) Clinical Medicine. Fifth edition. Edinburgh, WB Saunders. Malmberg K (1997) Prospective randomised study of intensive insulin treatment on long-term survival after acute myocardial infarction in patients with diabetes mellitus. DIGAMI (Diabetes Mellitus, Insulin Glucose Infusion in Acute Myocardial Infarction) Study Group. British Medical Journal. 314, 7093, 1512-1515. McCance K, Huether S (1998)

Pathophysiology: the Biological Basis for Diseases in Adults and Children. Third edition. St Louis, Mosby. Natarajan M, Yusuf S (2003) Primary angioplasty for ST-segment elevation myocardial infarction: ready for prime time? Canadian Medical Association Journal. 169, 1, 32-35. National Institute for Clinical Excellence (2002) Glycoprotein IIb/IIIa Inhibitor Guidance for Acute Coronary Syndromes: Review (no 47). London, NICE. ONeill P et al (2002) Medicine. Edinburgh, Churchill Livingstone. Oldridge N et al (1988) Cardiac rehabilitation after myocardial infarction: combined experience of randomized clinical trials. Journal of the American Medical Association. 260, 7, 945-950. Rang H et al (1999) Pharmacology. Edinburgh, Churchill Livingstone. Rawles J (1996) Magnitude of benefit from earlier thrombolytic treatment in acute myocardial infarction: new evidence from Grampian Region Early Anistreplase Trial (GREAT).

British Medical Journal. 312, 7025, 212-215. Rihal C et al (1998) Chronic coronary heart disease: coronary artery bypass surgery vs percutaneous transluminal coronary angioplasty vs medical therapy. In Yusuf S et al (Eds) Evidence Based Cardiology. London, BMJ Books. Sacks F et al (1996) The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators. New England Journal of Medicine. 335, 14, 1001-1009. Scandinavian Simvastatin Survival Study Group (1994) Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). The Lancet. 344, 8934, 1383-1389. Snell R (2000) Clinical Anatomy for Medical Students. Fifth edition. Philadelphia PA, Lippincott Williams and Wilkins.

Sprigings D, Chambers J (2001) Acute Medicine: A Practical Guide to the Management of Medical Emergencies. Third edition. Oxford, Blackwell Science. Steffenino G et al (2003) Primary angioplasty, instead of thrombolysis, for all patients with acute STelevation myocardial infarction? Italian Heart Journal. 4, 4, 219-224. Turner D, Turner L (1995) Right ventricular myocardial infarction: detection, treatment and nursing implications. Critical Care Nurse. 15, 1, 22-27. Wood D et al (1998) On behalf of the Joint British Societies recommendations on prevention of coronary heart disease in clinical practice. Heart. 80, Suppl 2, S1-S29. Yusuf S et al (2003) Evidence Based Cardiology. Second edition. Cornwall, BMJ Books. Yusuf S et al (1985) Beta blockade during and after myocardial infarction: an overview of the randomised trials. Progress in Cardiovascular Diseases. 27, 5, 335-371.

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