Case study: Patient admitted to accident and emergency with severe chest pain.
Debra Vickers, BSc (Hons), RN.
Thrombolysis Co-ordinator, Pennine Acute Hospitals NHS Trust (Rochdale), Lancashir
Professional Nurse 2003 Jan;18(5):293-5.
Jack Stewart, a 70-year-old retired grocer, presented to the accident and emergency (A&E) department following a 30-minute episode of severe central chest pain, which occurred while he was out shopping. He described his pain as a ‘central heaviness’, which radiated down his arms and into his jaw. The pain was associated with palpitations, dyspnoea, and sweating. His symptoms resolved shortly after resting.
Mr Stewart had experienced three episodes of similar pain over the previous 24 hours, lasting approximately 10-15 minutes each. He did not experience nausea or vomiting, nor was there any change in the pain with inspiration or movement.
His wife accompanied him to A&E.His medical history showed that he had several risk factors for coronary heart disease (CHD) (Wood et al, 1989).
He had been diagnosed with Type II diabetes five years previously, which was well controlled by diet, his sister had died of a myocardial infarction (MI) at the age of 65, he had a history of hypertension, and also smoked 5-10 cigarettes a day.
Chest pain must be treated as a medical emergency, therefore Mr Stewart was triaged ‘orange’ (urgent) and placed in the resuscitation bay of the A&E department. Throughout his assessment and treatment, he was offered reassurance, and interventions and treatments were explained. Care was taken to maintain his privacy and dignity during this time.
Mrs Stewart was invited to join him as soon as initial assessments were completed and, with the patient’s permission, assisted in providing information to the A&E department staff.
On physical examination he was anxious, and complaining of increasing central chest heaviness despite the fact that glyceryl trinitrate (GTN) 500mcg had been administered sublingually by ambulance service personnel on the journey to hospital.
The ambulance service personnel had also already given soluble aspirin 300mg. His blood pressure (BP) was 155/85, pulse 80bpm, and respiration rate 24/minute. His room air oxygen saturation was 96%, and temperature 37.2°C.
Oxygen therapy was started at 15 litres/minute (approximately 90% FiO2) administered via a non-rebreathe mask.Intravenous access was established via insertion of a cannula in the right antecubital fossa.
It is preferable that drugs are administered intravenously rather than intramuscularly as this may increase the risk of bleeding if the patient subsequently receives thrombolysis or glycoprotein inhibitors (Thompson, 1997).
Intramuscular injections may also damage muscle cells. These muscle cells release specific enzymes and so make some enzyme rises due to cardiac damage more difficult to interpret (Thompson, 1997).
Providing adequate pain relief at the earliest opportunity is of major importance. Initial drug therapy should aim to relieve pain and anxiety, as these may lead to a lowered threshold for cardiac arrhythmias, an increase in myocardial work, and provocation of coronary artery spasm (Thompson, 1997).
Diamorphine 5mg was therefore administered intravenously, at a rate of 1mg/minute, followed by metoclopramide 10mg intravenously, to prevent nausea. Mr Stewart reported that he was pain free 15 minutes later.
Continuous cardiac monitoring was begun, and a 12-lead ECG was recorded. The ECG showed significant ST-segment depression in leads V2, V3, V4 and V5. This was significant as a study of patients admitted with unstable angina with ST-segment depression >1mm had a significantly higher 90-day mortality (Lopez et al, 1998). As no ST-segment elevation was evident on the 12-lead ECG, thrombolytic therapy was not indicated at this point.
This type of treatment has not been shown to be of benefit in patients with acute coronary syndromes without ST-segment elevation (Fibrinolytic Therapy Trialists’ Collaborative Group, 1994).
An initial diagnosis of ‘acute coronary syndrome’ (non ST-elevation MI [NSTEMI] or unstable angina) was made, based on Mr Stewart’s clinical presentation and ECG findings. Arrangements were then made for the patient to be transferred to the coronary care unit (CCU) for further monitoring and investigation. Here he would continue on bed rest until stable.
A confirmed diagnosis of either unstable angina or NSTEMI can only be made once troponin testing has been completed and the result is known.Blood tests - Blood samples were taken for urea and electrolytes, glucose, clotting, cholesterol, and a chest X-ray was ordered. Imbalance of electrolytes such as potassium or magnesium can predispose the patient to cardiac arrhythmia and an elevated blood glucose is associated with increased mortality following acute MI (Malmberg et al, 1997).An initial laboratory glucose result of greater than 11mmol would necessitate an intensive glucose/insulin infusion for 24-48 hours (Malmberg et al, 1997).
A full blood count was taken in an attempt to identify pre-existing anaemia which in itself could be the cause of the chest pain. Random serum lipid levels indicate pre-existing hyperlipidaemia. A chest X-ray is important to rule out other serious causes of chest pain, such as pneumonia, thoracic aneurysm, pneumothorax, pulmonary oedema and to indicate heart size.A blood sample was also taken for cardiac troponin T. The cardiac troponins ‘T’ and ’ I’ are cardiac-specific enzymes and are independent markers associated with an increased risk of early death in patients with an acute coronary syndrome without ECG ST-segment elevation. The higher the cardiac troponin, the greater the risk of death within 30-42 days of presentation (Hamm et al, 1997; Stubbs et al, 1996).
Before transfer to the CCU standard drug therapy for acute coronary syndrome was introduced. The aims of treatment are to:
- Relieve chest pain;
- Improve prognosis by preventing progression to ST-elevation MI.
Low molecular weight heparin (LMWH) therapy was initiated because, although standard intravenous heparin has been shown to reduce the risk of death or MI in patients with acute coronary syndromes (Eikelboom et al, 2000), recent studies have shown that treatment with a LMWH is more effective in preventing further coronary events (ESSENCE, 1997).
Beta-blockers can reduce pain and ischaemia in patients with acute coronary syndromes, and randomised controlled trials show that they reduce the risk of MI by around 10% (McMurray and Rankin, 1994). Therefore a short-acting agent (metoprolol) was prescribed, at a dose of 50mg three times daily.
Mr Stewart’s cholesterol level was noted to be 6.0mmol/l, therefore lipid-lowering therapy was initiated. The major statin trials have clearly demonstrated that cholesterol lowering with this class of drugs reduces the risk of both coronary events and total mortality in patients with coronary disease (LIPID, 1998; Scandinavian Simvastatin Survival Study Group, 1994).
The rationale for the above treatments was explained to Mr Stewart and his wife, and they were reassured that more in-depth explanations and the provision of information would continue while he was an inpatient in the CCU.
Once settled in the CCU, Mr Stewart was advised to stay on bed rest, and to report any recurrence of his symptoms immediately.
Mr and Mrs Stewart were both introduced to the nursing, medical and cardiac rehabilitation staff who would be involved in his care, and time was taken to ensure that the explanations provided regarding his diagnosis, care and treatment were understood. Mr and Mrs Stewart were given opportunities to reflect and ask questions.
Continuous 12-lead cardiac monitoring ensured that any ST-segment changes or arrhythmias would be noted immediately. His heart rate remained stable at 80bpm. BP remained stable at 145/80. Blood test results showed that initial biochemistry, glucose, cardiac enzymes, full blood count and clotting were within normal limits. However, Mr Stewart’s troponin T was raised. A diagnosis was therefore made of NSTEMI.
Three hours after his transfer to the CCU Mr Stewart reported to the nursing staff that his chest tightness was beginning to recur. He was dyspnoeic, with a respiration rate of 24/minute, and his BP was slightly elevated from baseline recordings.
A repeat recording of a 12-lead ECG showed deepening of the previously noted ST depression in leads V1-V5. The use of intravenous nitroglycerin has been shown to relieve chest pain and ischaemia (Curfman et al, 1983). Therefore a GTN infusion was started, and the dose increased every 10 minutes (titrated to keep systolic BP >100mmHg) until the pain was relieved.
British Cardiac Society guidelines (BCS, 2001) state that certain patients with unstable angina/non-Q-wave MI are at high risk of progression to MI or death. Many of the circumstances associated with an increased risk of adverse outcome, that is age above 65 years; co-morbidity, especially diabetes; prolonged (>15 minutes) cardiac pain at rest; ischaemic ECG ST-segment depression on admission or during symptoms; and an increased troponin T, were found to be present in Mr Stewart’s case.
A small-molecule glycoprotein IIb/IIIa inhibitor was therefore prescribed, for a period of up to 96 hours, in accordance with National Institute for Clinical Excellence guidelines (NICE, 2002).Before beginning this infusion, Mr Stewart’s history was reviewed for potential contraindications (Box 1).
None were found, so the infusion began. Mr Stewart was carefully observed. In addition to 12-lead ECG and haemodynamic monitoring, and monitoring of symptoms, care was taken to observe for signs of bleeding, bruising and haematoma formation. Bloods were taken daily for a full blood count, observing for possible anaemia or thrombocytopaenia, urea and electrolytes, in order to identify an altered renal function, cardiac enzymes (CK) to detect further cardiac muscle damage through further myocardial ischaemia. Blood was also tested for glucose, to ensure adequate metabolic control of diabetes.
Once treatment with the glycoprotein IIb/IIIa inhibitor was started, Mr Stewart’s symptoms settled, and he remained pain free and haemodynamically stable. In accordance with British Cardiac Society guidelines (BCS, 2001), he was referred for coronary angiography, with a view to myocardial revascularisation for relief of symptoms. His coronary angiography took place two days later, at which time a stenosis in the left anterior descending coronary artery was discovered.
Coronary angioplasty was carried out, and a coronary stent inserted at the site of the lesion. Over the following week a structured mobilisation plan was followed and his levels of activity slowly increased.Before discharge, Mr Stewart was given advice about his modifiable risk factors, which included smoking, lack of physical activity, poor diet, being overweight and control of blood glucose levels.He was also offered advice and treatment to maintain his BP below 140/85mmHg, which is particularly important in patients with diabetes (DoH, 2000).
Low-dose aspirin and a beta-blocker were prescribed to be taken daily, in line with British Cardiac Society and National Service Framework guidelines (British Cardiac Society 2001; DoH, 2000).
Further dietary information was provided and statin therapy maintained, in order to achieve a serum cholesterol level of less than 5mmol/l.
Both Mr and Mrs Stewart were invited to join the hospital’s cardiac rehabilitation programme following discharge.
The patient’s name has been changed.
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