Pain can be a very upsetting and distressing symptom and has to be managed instantaneously and effectively (Fife and Farr 1998). Successful pharmacological intervention and analgesic treatment can only be given when pain assessment is performed correctly (Thompson and Webster 1992). Some nurses submit unreliable pain assessments (O’Connor 1995), but this can improve with successful nurse education (Thompson et al 1994). Other nurses have a lack of knowledge about the pharmacology of narcotics or can underestimate the amount of opiates required in the treatment of AMI (Thompson and Webster 1992).
In common with other patients, Sam was told of the importance of reporting any instance of pain, as this can be a sign of continuing myocardial ischaemia. Opiates are the analgesics most frequently used here; normally in the form of diamorphine sulphate, which is administered intravenously. This acts on the nervous system to reduce anxiety; stimulates opiate receptors to sedate the central nervous system and produce primary analgesia; and decreases myocardial oxygen consumption by dilating venules in the peripheral circulation. Opiates are often administered in tandem with an antiemetic, which relieves the nausea and vomiting caused by reduced gut motility; and intravenous nitrates can act as a dilator of the coronary arteries and increase perfusion of the myocardium. The effectiveness of analgesic pain control should be closely monitored.
On admission, Sam exhibited dyspnoea, which pointed to hypoxia. In conjunction with the analgesics, he was given oxygen therapy to optimise the uptake of oxygen in his lungs and increase oxygen supply to the myocardium.
When administered during the course of a developing infarction, thrombolytic therapy can reduce in-care mortality by up to a quarter (Wilcox 1992). Thrombolysis can re-open the artery by dissolution of the ruptured atheromatous plaque that occludes it, reviving the affected area and providing reperfusion of the myocardial muscle before more damage occurs (Chamberlain 1989). This can be effective up to 12 hours after initial infarction, but the mortality rate is reduced significantly when it is administered promptly (ISSIS-2, cited by Fife and Farr 1998). The most commonly used thrombolytic agent is the bacterial protein streptokinase, though antibodies to it are produced in reaction by the body and opinions differ on how often it can be administered. Not all patients are suitable for thrombolytic therapy.
Administering aspirin, an antiplatelet drug, has also been found to reduce the mortality rate and prevents re-occlusion (ISSIS-2, cited by Fife and Farr 1998); a larger dose is normally given to the patient on admission to A&E. It is often administered on a daily basis or with streptokinase during thrombolysis.
Beta blockers can also be administered intravenously during the process of infarction, in small and frequent doses. They enhance the balance between oxygen supply and demand, reducing the heart rate, cardiac output, blood pressure and myocardial contractility. Thompson and Webster (1992) report Misinski’s (1987) findings that these agents can limit the size of the infarct and reduce mortality by up to 20 percent. The National Service Framework for CHD (DoH 2001) specified the prescription of beta-blockers for one year after AMI, and also ACE inhibitors, which reduce blood pressure by preventing the activation of angiotensin.
The DoH framework focused on the delivery of care to coronary patients and introduced 12 standards with milestones and goals to ensure equal access to coronary care across the NHS, regardless of region or socio-economic status. The key targets for medical intervention are reducing smoking, promoting healthy eating and physical activity, and reducing obesity.
Most patients will recognise AMI as a life crisis, and this will change their normal coping responses (Thompson and Webster 1992). Coping methods can vary wildly as the individual’s self-image begins to suffer. For example, women have different concerns from men (Radley et al 1998); hospital admission will have been unexpected; the sudden “sick role” may be difficult to accept; and the obligation of help from others can be problematic. The coping mechanisms of many patients may be ineffective without help from healthcare staff (Johnson and Morse 1990) and spousal / family support. Kubler-Ross (1970) produced a stage model of the process of adjustment: denial / isolation, anger, bargaining, depression, acceptance. Successful coping methods can include confrontation, optimism, self-reliance, support seeking, ventilation and “thinking things through” (Stewart et al 2000). Coping assistance should also extend to the spouse and to family members, who exhibit fear and anxiety for their loved ones.
Anxiety and depression are widespread among AMI patients (Conn et al 1991). This can take the form of social withdrawal, sleeplessness, a lack of energy to carry on daily living activities, and feeling tearful. Sam became anxious, distressed and confused, and admitted to a fear of dying, which is a common and very real fear for AMI patients (Thompson et al 1995, Squillace and Delaney 1998). Subsequently, Sam said he felt that his role in the family and society had changed and that he felt unable to “take care of things”. Patients can experience many other types of fear such as fear of losing control, and fear of dependency. Depression can significantly delay recovery: Webster and Christman (1998) found that sufferers of continued anxiety post-AMI had higher mortality rates, were less likely to return to work, and were more likely to be re-admitted to hospital. For many AMI patients, anxiety can degenerate to anger: towards living their “unhealthy” lifestyle and not preventing the incident which had occurred so suddenly.
Fear of death and lack of function can also lead to anxiety before or during sexual intercourse. Stewart et al (2000) alleges that conflicting information is given to survivors and partners, who can avoid sexual activity because of concern about the side-effects of medication, or even for fear of causing another AMI. This can lead to relationship problems and then affect family bonds. Thompson and Webster (2000) recommend waiting a couple of weeks; Davidson (1999) presents a staged strategy lasting months. Most authors agree that sexual advice from health professionals is not forthcoming, but in Appendix Three the author has republished some guidelines issued by the Chiltern and South Bucks PCT.
“Type A” behaviour – polyphasic activity, the wish to achieve and the suppression of hostility and anger– makes individuals particularly vulnerable to stress (Leefarr 2000) and is known to increase tendency for thrombus formulation (Thompson and Webster 1992). Individuals exhibiting type A behaviour are more likely to suffer recurrent and fatal AMI (Gentry et al 1983). It is unclear whether prognoses can be altered by changing behaviour, though a follow-up study by Ragland and Brand (1988, cited by Thompson and Webster 1992) found a lower mortality level among 250 men. Nurses can assist the patient in identifying characteristics and working on a way of changing them.
Social issues facing AMI patients can be significant. Financial difficulties can be suffered during the initial period of rehabilitation if the patient has a well-paid job or was the breadwinner of the family. In the longer term, the patient can be fearful of their role in the workplace changing, or even losing their job, especially when there is a mortgage to pay. The role of the patient can also change in the home as the spouse or family become over-protective.
Changing dietary habits and regimes can be stressful, especially if the patient had previously enjoyed fatty foods, now considered inappropriate and even harmful. This can be in tandem with an increase in physical activity, an effort to reduce body mass and an attempt to moderate consumption of alcohol. Smoking may have been used to combat stressful situations, and also to fight anxiety, frustration, anger and negative feeling (Styles and McIntyre 1997), but is one of three main modifiable risk factors for CHD. All of these regimented changes can have a negative psychological effect. Before any advice can be given, the patient needs to display a motivation to make these changes.
Withdrawal from social routines can lead to negative reactions from friends and acquaintances, which can have a significant impact on rehabilitation and isolation. Stewart et al (2000) reported diminished energy for social activities and difficulty meeting friends following AMI. Patients can also avoid situations where the consumption of alcohol may be commonplace.
In conclusion, there have been major advances recently in the diagnosis and treatment of AMI, and, at the forefront of patient care, the nurse has a significant role to play in patient education and must keep abreast of these changes. As the management of the condition becomes more assertive, nurses must keep up with progress in therapy practices and be able to explicate these to the patient. There is much to be done pre-emptively here, too: nausea and vomiting can seem trifling complaints and such epigastric discomfort can be often wrongly interpreted by patients, with the appropriate medical help not sought quickly enough. Shortness of breath, severe restlessness and tachycardia can be other important signs to detect. Potential users can be informed about the importance of seeking medical help as urgently as possible.
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Appendices
Appendix One
Patient information
Sam is a 58-year-old man who works as an engineer in a big company. He lives with his wife and two adult children. Both his parents had died of coronary heart disease. Two years ago he was diagnosed with angina pectoris, which he has controlled with nitrates and beta blockers. He came to Accident and Emergency after experiencing severe chest pains across his left shoulder, which were not relieved by taking his usual regimen of sublingual glyceryl trinitrate (GTN) spray and not even by resting. An ECG was taken, which showed changes and indicated acute myocardial infarction. Blood tests were also taken to estimate cardiac enzyme levels.
Sam was also experiencing other symptoms, like sweating, nausea and vomiting, breathlessness, tachycardia, and hypotension. These are some of the clinical features of acute myocardial infarction. Pain relief and antiemetics were given, and thrombolytic therapy was started. Oxygen was prescribed and administrated. Observations such as blood pressure, pulse, oxygen saturation, respirations, heart rate, temperature and pain score were taken and recorded on a regular basis. Any changes were reported to the doctor.
Sam’s wife was with him throughout this experience and the fear and anxiety they were both experiencing was noticeable, so they needed reassurance, comfort and support. A few hours later Sam was transferred to a coronary care unit.
Appendix Two
Investigations
A number of clinical investigations can be used to detect any changes in order to diagnose acute myocardial infarction.
ECG-12 Lead
This is the most frequently performed investigation, because it is simple and quick. Taking several ECGs is helpful as they can change as time goes on. ECGs of AMI patients reveal an elevation in the ST segment (depression is a sign of ischaemia), a T-wave inversion and deep-set Q waves.
Blood Tests
Necrotic myocardium tissue releases enzymes into the blood that can be measured.
Cardiac Enzymes: Creatine Phosphokinase (CPK), also called Creatine Kinase (CK), is released within 36 hours of infarction. The isoenzymes CK-MM, CK-MB and CK-BB are found if damage has occurred to skeletal muscle, the myocardium or the brain. If CK-MB is elevated by more than 3% , a definite diagnosis of MI can be made. If over 5% myocardial necrosis is present. CK-MB starts to rise two to five hours following AMI and reaches a peak after about 12 hours. It returns to normal within two to four days.
Aspartate aminotransferase (AST) rises within eight to 12 hours, peaks in 18 to 36 hours and returns to normal up to six days post-infarction. It is also released by damage to the liver, brain, kidney and lung tissue.
Troponin T / Troponin I can only be detected when myocardial infarction has occurred. Troponin T can be discovered after four to six hours and peaks up to 24 hours after infarction, and can remain elevated for a number of weeks. Troponin I starts rising within three to five hours, peaks at 14 to 18 hours and remains elevated for five to seven days.
Lactic dehydrogenase (LDH) rises six to 12 hours after AMI reaches a peak between 48 and 72 hours. It remains elevated for five to 14 days. It has five isoenzymes: LDH1 and LDH2 indicate myocardial infarction.
Haematology Tests: In AMI the erythrocyte (red blood cell) sedimentation rate rises after the first few days and can remain elevated for several weeks after tissue necrosis.
The presence of leukocytes – or white blood cells (WBCs) – is usually elevated after AMI.
Platelet – or thrombocyte – aggregation can be a good indicator of coronary occlusion in infarction and can help play a role in determining the size of the AMI.
Glucose: Following AMI, hyperglycaemia due to stress may be common and may indicate previously undetected diabetes in 1 in 20 AMI patients.
Electrolytes: The imbalance of serum electrolytes such as potassium, calcium and sodium can indicate increased cell excitability.
Lipids: An initial cholesterol test should be taken within the first 24 hours and then a full lipied profile at six to eight weeks to indicate plasma cholesterol and triglyceride levels.
Appendix Three
Guidelines Following Cardiac Surgery: When Can I?
Chiltern and South Bucks Primary Care Trust (2001)
Appendix Four
References
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Appendix Five
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