Acute coronary syndrome: role of the nurse in patient assessment and management
Intended for healthcare professionals
CPD    

Acute coronary syndrome: role of the nurse in patient assessment and management

Alison Malecki-Ketchell Lecturer and senior fellow of the Higher Education Academy, School of Healthcare, University of Leeds, Leeds, England

Why you should read this article:
  • To support you to recognise and differentiate between the various types of acute coronary syndrome (ACS)

  • To enhance your understanding of the assessment and management of ACS

  • To count towards revalidation as part of your 35 hours of CPD, or you may wish to write a reflective account (UK readers)

  • To contribute towards your professional development and local registration renewal requirements (non-UK readers)

Coronary heart disease is a leading cause of mortality, morbidity and hospitalisation in the UK and worldwide. Acute coronary syndrome (ACS) is a serious manifestation of coronary heart disease. ACS encompasses several conditions that represent acute injury or damage to the myocardium, including ST-elevation myocardial infarction (STEMI), unstable angina and non-ST elevation myocardial infarction (NSTEMI). Management may differ depending on the diagnosis, so prompt and accurate assessment is crucial to establish the patient’s condition and ensure timely initiation of the appropriate treatment. This article explains how ACS develops and what characterises its different types. It also outlines the assessment and management of patients with ACS, and explains the nurse’s role in these processes.

Nursing Standard. doi: 10.7748/ns.2022.e11877

Peer review

This article has been subject to external double-blind peer review and checked for plagiarism using automated software

Correspondence

a.c.ketchell@leeds.ac.uk

Conflict of interest

None declared

Malecki-Ketchell A (2022) Acute coronary syndrome: role of the nurse in patient assessment and management. Nursing Standard. doi: 10.7748/ns.2022.e11877

Published online: 24 January 2022

Aims and intended learning outcomes

The aim of this article is to provide nurses with an overview of acute coronary syndrome (ACS) and the nurse’s role in the assessment and management of patients with ACS. The article is based on the latest evidence and guidelines (National Institute for Health and Care Excellence (NICE) 2016, 2019, 2020, Ibanez et al 2018, Collet et al 2021), which will have informed the local policies and protocols that nurses need to follow. After reading this article and completing the time out activities you should be able to:

  • Explain the various types of ACS and the differences between them.

  • Recognise the importance of accurate and timely assessment and investigations to determine the correct ACS diagnosis.

  • Interpret electrocardiogram (ECG) findings in relation to ACS.

  • Understand what interventions are required in the immediate management of the different types of ACS and the rationale for such interventions.

  • Describe what the long-term management of ACS entails.

Key points

  • Acute coronary syndrome (ACS) encompasses several conditions that represent acute injury or damage to the myocardium

  • Prompt and accurate assessment is crucial to establish the correct diagnosis and initiate appropriate treatment in a timely manner

  • The immediate management of ACS may involve symptom relief, dual antiplatelet therapy, primary percutaneous coronary intervention and/or thrombolysis therapy

  • The long-term management of ACS aims to reduce the risk of further disease progression and acute cardiac events through secondary prevention medicines and cardiac rehabilitation

Introduction

ACS is an acute and serious manifestation of coronary heart disease (Eisen et al 2016). Coronary heart disease, also known as ischaemic heart disease, is a progressive condition where the coronary arteries become stiffened and narrowed by atherosclerosis, ultimately impeding blood flow to the cardiac muscle (myocardium) and impairing its function due to the imbalance between coronary blood supply and myocardial oxygen demand.

Atherosclerosis is a chronic condition in which arteries harden through the build-up of atherosclerotic plaques (Bergheanu et al 2017). It has been linked to modifiable risk factors such as cigarette smoking, hypertension, diabetes mellitus and a lack of exercise, as well as non-modifiable risk factors such as advancing age and a family history of atherosclerosis (Hajar 2017). High cholesterol, or hypercholesterolaemia, is considered one of the main risk factors for atherosclerosis (Bergheanu et al 2017).

The annual number of deaths from coronary heart disease has consistently declined in the UK, from 80,339 deaths in 2010 to 63,237 deaths in 2019 (British Heart Foundation 2021). This decline can be attributed to major advances in pharmacological and interventional management strategies. However, coronary heart disease remains a leading cause of mortality, morbidity and hospitalisation in the UK. In October 2021, ischaemic heart disease was the second leading cause of death in England and the leading cause of death in Wales (Office for National Statistics 2021).

TIME OUT 1

Stable angina is not classified as a type of ACS, but unstable angina is. How would you describe to patients the two conditions and how they differ from each other? Think about formulating your explanations in terms of the heart’s supply of, and demand for, oxygen

Defining acute coronary syndrome

ACS encompasses several conditions that represent acute injury or damage to the myocardium (Kotecha and Rakhit 2016):

  • ST-segment elevation myocardial infarction (STEMI).

  • Non-ST-segment elevation ACS, which encompasses unstable angina and non-ST-segment elevation myocardial infarction (NSTEMI).

Myocardial infarction

Myocardial infarction (MI) – commonly known as a heart attack – is defined pathologically as myocardial cell death (necrosis) due to prolonged restriction of blood supply (ischaemia) (Thygesen et al 2018). Thygesen et al (2018) described different types of MI according to the cause of infarction. One of these types is MI caused by atherothrombotic coronary artery disease, which is usually precipitated by atherosclerotic plaque disruption (rupture or erosion). Atherosclerotic plaque disruption leads to platelet activation, aggregation and adhesion, eventually resulting in thrombus (clot) formation and vessel occlusion.

Myocardial injury is defined as reversible damage caused by blood and oxygen deprivation, which may be resolved if blood flow is restored within 30-45 minutes. If the cessation of blood flow lasts longer than 45 minutes, the affected area of the myocardium becomes irreversibly damaged and necrosis occurs (Malecki-Ketchell 2016). Permanent necrotic damage to myocardial cells leads to cell fibrosis, electrical inactivity and loss of contractility (Konstantinidis et al 2012). Necrosis and the resultant infarction may be restricted to patchy areas of the myocardium or affect its full thickness (Akbar et al 2021).

MI typically, but not always, manifests as a sudden onset of ischaemic chest pain that is unrelieved by nitrates such as glyceryl trinitrate (GTN). Not all MIs present with classic ST-segment elevation, so MI is further categorised as STEMI or NSTEMI based on a 12-lead ECG. MI may also be indicated by new left bundle branch block or pathological Q waves on ECG. Therefore, giving a universal definition of acute MI is challenging and a combination of criteria need to be present to reach a definitive diagnosis. These criteria include (Thygesen et al 2018, Collet et al 2021):

  • Evidence of elevated cardiac troponin levels in the blood. Troponin is a biochemical marker of myocardial damage.

  • Additional evidence such as ischaemic alterations noted on ECG, thrombus noted at coronary angiography and/or loss of viable myocardium noted on imaging.

Unstable angina

Stable angina occurs when narrowed coronary arteries fail to meet an increase in demand for myocardial oxygen during exertion. Myocardial ischaemia ensues, giving rise to chest pain on exertion, which resolves with rest and/or coronary vasodilation with medicines such as GTN.

In contrast, unstable angina is defined as myocardial ischaemia at rest or on minimal exertion in the absence of acute myocardial injury and/or necrosis (Collet et al 2021). It gives rise to acute ischaemic chest pain that does not easily resolve with nitrates. In unstable angina, 12-lead ECG findings may be normal or abnormal. Abnormal findings may include ST-segment depression, transient ST-segment elevation or T-wave inversion, and there is no elevation of cardiac troponin levels (BMJ Best Practice 2021).

The emergence of high-sensitivity cardiac troponin (hs-cTn) blood assays has resulted in many patients who would have previously been diagnosed with unstable angina being diagnosed with NSTEMI, since elevated hs-cTn levels are seen in NSTEMI but not in unstable angina. This has resulted in a reduction in the incidence of unstable angina and an increase in the incidence of NSTEMI (Kotecha and Rakhit 2016).

TIME OUT 2

List as many potential causes of chest pain as you can, then note down whether each of these causes is cardiac or non-cardiac. You may wish to access the following resources to assist you:

www.nhs.uk/conditions/chest-pain

patient.info/signs-symptoms/chest-pain-leaflet

What questions would you ask a patient presenting with chest pain to establish its underlying cause?

Assessment of patients with suspected acute coronary syndrome

The management of STEMI, NSTEMI and unstable angina may differ, so prompt and accurate assessment is crucial to establish the correct diagnosis and to initiate appropriate treatment in a timely manner.

The assessment of patients with suspected ACS follows a structured approach. It starts with taking a history of the patient’s presenting symptoms and investigating their past medical history, followed by a physical examination (Stephens 2019). Patients with ACS typically present with retrosternal chest pain radiating to one arm or both arms, the shoulders, neck, back and/or jaw, and a feeling of a tight band or heavy weight across the chest. In addition, patients often experience nausea, vomiting and sweating (cool, clammy skin) due to autonomic nervous system stimulation (Stephens 2019).

The nurse’s role may involve assessing the patient’s heart rate, regularity and rhythm, manually and via continuous 3-lead or 5-lead cardiac monitoring. The nurse’s role also includes measuring: blood pressure; respiratory rate, depth and regularity; and oxygen saturation of haemoglobin (SpO2). The findings of these may be within normal parameters. Tachycardia and tachypnoea may indicate anxiety or pain, or be a physiological consequence of hypotension mediated by low cardiac output. Hypertension may be a consequence of pain and/or anxiety, or of a diagnosed or undiagnosed underlying cause of coronary heart disease. Therefore, frequent and regular monitoring to establish trends is more useful than single measurements (NICE 2019).

To provide baseline values and rule out other potential conditions, all patients presenting with chest pain should routinely have venous blood samples taken for full blood count, urea and electrolytes, cholesterol, glucose, liver function tests and thyroid function tests. Cardiac troponin levels can be measured to confirm or exclude a diagnosis of MI. A clotting screen should be undertaken if warranted (NICE 2020).

Recording and interpreting a 12-lead electrocardiogram

A crucial aspect of the assessment and management of patients with ACS is the recording of a 12-lead ECG as early as possible on the patient’s presentation – presentation being the first contact with a healthcare professional, for example a nurse or a paramedic – as well as recording subsequent serial ECGs.

A 12-lead ECG provides a visual representation of the electrical activity of the heart from 12 different viewpoints. The P wave and QRS complex represent the depolarisation of myocardial cells, which triggers the contraction of the atrial and ventricular myocardium (Wei et al 2021). A period of electrical inactivity ensues, represented by a flat isoelectric ST segment, to enable complete ventricular emptying. Ventricular repolarisation then gives rise to the T wave (Meijborg et al 2014). Depolarisation and repolarisation occur sequentially as a result of the unique physiological ability of myocardial cells to produce their own electrical impulses. Figure 1 shows normal heart rhythm on ECG with a flat ST segment.

Figure 1.

Normal heart rhythm on electrocardiogram (ECG) with a flat ST segment

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In a 12-lead ECG, ten electrodes are placed strategically on the skin: six on specific chest area sites labelled V1 to V6, and one on each of the four limbs. These ten electrodes produce 12 different views of electrical activity in the myocardium, detecting depolarisation and repolarisation. In myocardial cells affected by ischaemia and/or injury, repolarisation may be delayed, which may show on ECG as an altered ST segment (depressed or elevated) and/or an altered T wave (Sampson 2018). ST-segment and/or T-wave alterations suggestive of myocardial ischaemia and/or injury can be attributed to a particular region of the heart, thereby assisting in identifying the affected coronary artery.

ST-segment elevation, usually accompanied by chest pain suggestive of myocardial ischaemia (persistent chest pain often radiating to the neck, lower jaw and left arm) and a history of coronary heart disease, supports a diagnosis of STEMI (Ibanez et al 2018). Box 1 details the ST-segment elevation values suggestive of ongoing coronary artery acute occlusion according to European Society of Cardiology guidelines (Ibanez et al 2018).

ST-segment depression and T-wave alterations – T-wave inversion being the classic change – are characteristic of non-ST-segment elevation ACS, but ECGs may be normal in more than 30% of patients with non-ST-segment elevation ACS (Collet et al 2021). Figure 2 shows heart rhythm on ECG with ST-segment elevation and Figure 3 shows heart rhythm on ECG with ST-segment depression.

Figure 2.

Heart rhythm on electrocardiogram (ECG) with ST-segment elevation

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Figure 3.

Heart rhythm on electrocardiogram (ECG) with ST-segment depression

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TIME OUT 3

The immediate management of ACS involves aggressive antiplatelet therapy. To understand the rationale for the use of antiplatelet therapy, revise the mechanisms of platelet activation, aggregation and adhesion, and the principles of the coagulation cascade, by watching these two videos:

Platelet activation and factors for clot formation: www.youtube.com/watch?v=R8JMfbYW2p4

Coagulation cascade: www.youtube.com/watch?v=cy3a__OOa2M

Immediate management of ST-segment-elevation myocardial infarction

In STEMI, the aim of immediate management is to salvage as much ischaemic and/or injured myocardium as possible by restoring the supply of oxygenated blood to affected cells and therefore limiting the size of infarction, reducing morbidity and mortality, and improving prognosis in survivors. A three-element approach is used:

  • Symptom relief.

  • Dual antiplatelet therapy (DAPT).

  • Primary percutaneous coronary intervention (PCI), or thrombolysis therapy if PCI cannot be delivered within 120 minutes of presentation.

Symptom relief

Chest pain and anxiety are associated with sympathetic nervous system activation and consequent vasoconstriction and tachycardia, leading to an increase in demand for myocardial oxygen. Therefore, pain relief and initial bedrest are crucial not only to alleviate symptoms, but also to reduce the risk of further myocardial damage. In what is an emotionally heightened time for patients and their significant others, it is important that nurses maintain a calm, reassuring approach and provide clear answers to their questions and concerns, since this can assist in relieving anxiety.

Ongoing pain assessment and management is an important aspect of the nurse’s role. The aim of administering analgesics is to achieve complete pain relief. Titrated intravenous (IV) morphine (5mg-10mg) is commonly prescribed for relieving ischaemic chest pain, accompanied by 10mg IV metoclopramide hydrochloride or an alternative antiemetic (Ibanez et al 2018). A numerical rating scale can be used to assess patients’ perception of pain and determine the efficacy of the analgesics administered.

Box 1.

ST-segment elevation values suggestive of ongoing coronary artery acute occlusion

ST-segment elevation seen on a 12-lead electrocardiogram is considered suggestive of ongoing coronary artery acute occlusion, in the absence of left ventricular hypertrophy or left bundle branch block, in the following cases:

  • In men aged >40 years, at least two contiguous leads with ST-segment elevation ≥2.5mm

  • In men aged ≤40 years, at least two contiguous leads with ST-segment elevation ≥2mm

  • In women, ST-segment elevation ≥1.5mm in leads V2 and V3 and/or ST-segment elevation ≥1mm in the other leads

(Adapted from Ibanez et al 2018)

According to the European Society of Cardiology guidelines (Ibanez et al 2018), there is little evidence for the routine use of nitrates to relieve ischaemic chest pain in STEMI, but nitrates may be useful for managing hypertension or heart failure in the acute phase and for managing residual angina symptoms beyond the acute phase. However, nitrates are recommended in the British National Formulary (Joint Formulary Committee 2021), and widely used in the UK, for relieving chest pain in patients with ACS. Nurses need to be aware of this discrepancy and follow local policy.

Another important aspect of the nurse’s role is continuous ECG monitoring to detect arrhythmias and provide prompt defibrillation and emergency pacing if necessary.

Patients with ACS may develop hyperglycaemia as a result of an inflammatory and adrenergic response to ischaemic stress (Senthinathan et al 2011, Angeli et al 2015), so their blood glucose levels need to be closely monitored. NICE (2020) guidelines recommend keeping blood glucose levels <11.0mmol/L while avoiding hypoglycaemia.

Continuous non-invasive SpO2 monitoring is required, and the patient’s SpO2 should be maintained at ≥94%. Supplemental oxygen therapy is only recommended if SpO2 is <94% and/or if the patient shows signs of cardiac failure (O’Driscoll et al 2017).

Dual antiplatelet therapy

DAPT should be administered as soon as possible to reduce further platelet activation, aggregation and adhesion (Parodi et al 2013). Paramedics and nurses are often patients’ first contact with a healthcare professional, so they need to understand the action of DAPT.

A loading dose of 300mg of oral aspirin, ideally in chewable or dissolvable form for faster absorption, has a potent dual antiplatelet action, promoting vasodilation and impeding platelet aggregation. If primary PCI is planned, a P2Y12 adenosine diphosphate (ADP) receptor antagonist is administered alongside aspirin to inhibit ADP-mediated platelet aggregation and adhesion. An oral loading dose of 60mg prasugrel – or, in some instances, 180mg ticagrelor – is usually administered (Valgimigli et al 2018).

Primary percutaneous coronary intervention

The benefits of primary PCI are time dependent, so it must be offered within 12 hours of symptom onset and delivered at a PCI-capable centre within 120 minutes of the patient’s presentation (NICE 2020). Therefore, paramedics and nurses need to be trained to record a 12-lead ECG and either interpret it or transmit it for review, so that the suspected diagnosis can be confirmed as soon as possible. Pre-hospital triage enables patients to be directly transported to a PCI-capable centre, avoiding prolonged assessment times in the emergency department. PCI may be considered beyond 12 hours of symptom onset if STEMI is complicated by ongoing myocardial ischaemia, chest pain, arrhythmias, heart failure and/or cardiogenic shock (Ibanez et al 2018).

PCI is performed by interventional cardiologists in the cardiac catheter laboratory under X-ray control. There are two main approaches to PCI – transradial and transfemoral – and the transradial approach is generally favoured (Bhat et al 2017). A local anaesthetic is administered before the insertion of a short sheath into the radial artery, which is accessed at the wrist (Valgimigli et al 2015). A weight-adjusted bolus of IV unfractionated heparin is administered beforehand and an infusion of IV unfractionated heparin is administered during the procedure (Cavender and Sabatine 2014). In patients with heparin-induced thrombocytopenia, the direct thrombin inhibitor bivalirudin is used instead of unfractionated heparin (Ibanez et al 2018).

Figure 4 provides a summary of the procedure for PCI with stent insertion.

Figure 4.

Summary of the procedure for percutaneous coronary intervention with stent insertion

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Once the guidewire and balloon catheter have been withdrawn, the radial artery sheath is removed and manual digital pressure is applied on the puncture site to stop the bleeding. A transparent compression device is often applied over the area so that the puncture site remains visible. Around 90 minutes after the procedure, the compression device is gradually released and removed.

A drug-eluting stent is typically used for PCI, since it enables the slow release of medicines after the procedure to prevent cell proliferation, which would otherwise reduce the efficacy of the stent (Sabaté et al 2016).

Since the procedure is undertaken under local anaesthesia, patients can resume food and fluid consumption as soon as they feel able to. Post-procedural nursing care involves close monitoring of patients’ heart rate and rhythm, regular recording of their blood pressure and temperature, and checking the puncture site for bleeding for four hours or until bleeding has stopped. It is crucial that patients are encouraged to verbalise any chest pain and that a 12-lead ECG is performed immediately after PCI to check for post-procedural ischaemia, infarction or heart rhythm disturbances. Recording an ECG after the procedure is also useful for comparison with previous and future ECGs.

Thrombolysis therapy

If PCI cannot be delivered at a PCI-capable centre within 120 minutes of presentation, thrombolysis (fibrinolytic) therapy can be used as an alternative reperfusion strategy (NICE 2020). However, the benefits of thrombolysis therapy are also time dependent, so thrombolysis therapy must be commenced within 12 hours of symptom onset (NICE 2020). As time elapses, the potential benefits decrease and the clinical risks increase. The options for thrombolysis therapy are: an IV infusion of 1.5 million units streptokinase; a fibrin-specific thrombolytic such as IV weight-adjusted alteplase; or a bolus of IV tenecteplase (Ibanez et al 2018).

Thrombolysis therapy must be preceded or accompanied by DAPT with 300mg oral chewable aspirin and 300mg of the P2Y12 ADP receptor antagonist clopidogrel. After thrombolysis therapy, patients must receive anticoagulants until their discharge from hospital, with the options being: subcutaneous low molecular weight heparin such as enoxaparin sodium; IV unfractionated heparin; or a bolus of IV fondaparinux sodium followed by daily subcutaneous injections (Ibanez et al 2018). Coronary angiography, followed by PCI if indicated, is recommended within 24 hours of receiving thrombolysis therapy (Ibanez et al 2018).

Immediate management of non-ST-segment elevation acute coronary syndrome

In non-ST-segment elevation ACS, the aim of immediate management is to prevent further cardiac events and death (NICE 2020). However, management differs depending on the degree of cardiovascular risk.

The Global Registry of Acute Coronary Events (GRACE) 2.0 (Fox et al 2014) is an established risk-scoring system used to predict six-month mortality and the risk of cardiovascular events in patients with ACS. It considers patients’ medical history, physical examination findings, 12-lead ECG findings and results of venous blood tests including biochemical markers of myocardial injury.

Elevated hs-cTn levels are characteristic of NSTEMI. Elevated serum hs-cTn levels can be detected within 1-2 hours of the onset of myocardial injury (Collet et al 2021). Advances in the sensitivity and reliability of hs-cTn blood assays has substantially reduced the time to a diagnosis of NSTEMI, enabling immediate reperfusion with PCI where clinically appropriate (Collet et al 2021). Rapid ‘rule out-rule in’ protocols used in acute care settings require troponin testing immediately on presentation with suspected ischaemic chest pain and 1-2 hours after presentation, on the basis that early elevated troponin levels are predictive of changes at 3-6 hours (Chapman et al 2019).

The decision to proceed to immediate or urgent coronary angiography, followed by PCI if indicated, will be based on patients’ clinical condition, their GRACE score and the presence of ongoing ischaemia.

In patients with unstable angina or NSTEMI, NICE (2020) recommends:

  • Offering immediate coronary angiography to patients if their clinical condition is unstable.

  • Considering coronary angiography, followed by PCI if indicated, within 72 hours of first admission for patients with an intermediate or high risk of adverse cardiovascular events (predicted six-month mortality >3%).

  • Considering coronary angiography, followed by PCI if indicated, for patients initially assessed as being at low risk of adverse cardiovascular events (predicted six-month mortality ≤3%) if ischaemia is subsequently experienced or is demonstrated by ischaemia testing.

It is important to note that thrombolysis therapy should be avoided, since there is no evidence that it is beneficial in unstable angina and NSTEMI (Basit et al 2021).

Patients with a predicted six-month mortality of ≤3% on the GRACE risk-scoring system are thought to benefit from a more conservative management approach. Symptom relief should include coronary vasodilation with nitrates, such as sublingual GTN or more commonly an IV infusion of GTN titrated to systolic blood pressure. Patients should be prescribed DAPT in the form of a 300mg loading dose of aspirin followed by 75mg-150mg of aspirin daily, and either ticagrelor (loading dose 180mg followed by 90mg daily) or clopidogrel (loading dose of 300mg followed by 75mg daily) (Ibanez et al 2018).

Once patients are haemodynamically stable, further assessment of coronary heart disease – via investigations including an exercise treadmill or dobutamine stress test, computed tomography (CT) or magnetic resonance imaging (MRI) scans of the myocardium, and coronary angiography – should be conducted in the inpatient or outpatient setting. PCI will then be performed electively if indicated (NICE 2020).

TIME OUT 4

What are the long-term priorities for the care of patients who have been diagnosed with ACS and have undergone immediate management?

Long-term management of acute coronary syndrome

The long-term management of ACS involves reducing the risk of further disease progression and acute cardiac events, which is achieved through secondary prevention medicines and cardiac rehabilitation (Ibanez et al 2018, NICE 2020).

Long-term medical management

While the long-term medical management of ACS is not complex, it requires strict adherence to a regimen informed by current best practice guidelines and containing several medicines. An important aspect of the nurse’s role is to ensure that none of the required medicines are omitted from prescriptions and that patients adhere to their treatment.

An angiotensin-converting enzyme (ACE) inhibitor will have been prescribed, as appropriate, for those having had treatment for MI (NICE 2020) and titration commenced to a satisfactory blood pressure during the patient’s hospital stay. It will need to be continued in the community, so appropriate discharge communication to the community team is essential.

The long-term administration of an ACE inhibitor (such as ramipril or lisinopril) or an angiotensin receptor blocker (such as losartan potassium or valsartan) combined with a beta-blocker (such as metoprolol tartrate, atenolol or carvedilol) is associated with a significant survival benefit after STEMI (Ibanez et al 2018). However, there is a lack of evidence and a debate among healthcare professionals regarding the continuation of beta-blockers beyond 12 months after an MI, so nurses need to be aware of emerging evidence in this area.

An aldosterone antagonist should be prescribed to patients who have had an MI and who have signs or symptoms of heart failure or reduced left ventricular ejection fraction. All patients who have had an MI should also undergo echocardiography to establish left ventricular function (NICE 2020).

Long-term medical management of ACS also includes long-term DAPT with a combination of oral aspirin and a P2Y12 ADP receptor antagonist. The dosing, choice of P2Y12 ADP receptor antagonist and duration of treatment depend on the diagnosis and on an ongoing assessment of the risk of bleeding and stroke (Giustino et al 2015, NICE 2020).

Oral statins are recommended in the long-term management of patients in whom there is clinical evidence of cardiovascular disease (NICE 2016, Ibanez et al 2018). Elevated low-density lipoprotein cholesterol is a well-known risk factor for coronary heart disease (Ueda et al 2018). Therefore, high-intensity statins such as atorvastatin and rosuvastatin are generally recommended for the primary and secondary prevention of cardiovascular disease (NICE 2016).

All patients who have undergone PCI need outpatient follow-up care to investigate potential issues such as residual symptoms of ischaemia, adjust medicines as necessary and proceed to further assessment and/or treatment if required.

Cardiac rehabilitation

The aim of cardiac rehabilitation is to promote a healthy lifestyle and support behavioural change. Cardiac rehabilitation should start during the patient’s hospital stay and resume no later than ten days after their discharge. All patients regardless of age should be invited to attend a cardiac rehabilitation programme (NICE 2020), which may be based at home, in hospital or in the community. Such programmes should include exercise appropriate for patients’ age and ability as well as education, advice and support on physical exercise, diet, weight loss, smoking cessation, stress management, driving, flying and resuming sexual activity (British Association for Cardiovascular Prevention and Rehabilitation (BACPR) 2017).

Nurses have a crucial role in cardiac rehabilitation (BACPR 2017). Alongside other members of the multidisciplinary team – notably physiotherapists, dietitians, pharmacists and doctors – nurses are responsible for ensuring patients are enrolled on a cardiac rehabilitation programme, discussing its role and benefits.

Conclusion

Prompt and accurate assessment and management of ACS, informed by guidelines and protocols and conducted using a clear evidence-based approach, can significantly improve patient outcomes and prognosis. Therefore, it is crucial that nurses involved in the care of patients with ACS develop the knowledge, understanding and clinical expertise required to undertake their role and responsibilities effectively.

TIME OUT 5

Consider how the assessment and management of ACS relate to The Code: Professional Standards of Practice and Behaviour for Nurses, Midwives and Nursing Associates (Nursing and Midwifery Council 2018) or, for non-UK readers, the requirements of your regulatory body

TIME OUT 6

Now that you have completed the article, reflect on your practice in this area and consider writing a reflective account: rcni.com/reflective-account

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