Week 5 – Acute coronary syndromes

Introduction
So far you have learned the essential elements of cardiac assessment, and rhythm and ECG analysis. In this section the focus is on
caring for the patient who is suffering acute coronary syndrome. This encompasses myocardial ischemia as well as acute myocardial
infarction (AMI). The nursing responsibilities in caring for a patient experiencing acute coronary syndrome includes community education
for early symptom recognition, prompt attention and prioritised management in the acute phase, discharge planning and cardiac
rehabilitation.
Learning outcomes for this section
Upon successful completion of this section, you should be able to:
identify assessment strategies for patients presenting with signs and symptoms of AMI
describe the differential diagnoses that may present with chest pain
relate the pathophysiology of heart disease to the anticipated plan of care for a patient experiencing an acute myocardial infarction
(AMI)
demonstrate an advanced physiological understanding of medication used in your practice setting
plan collaborative care that extends across the health care continuum for patients experiencing an uncomplicated AMI.
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Review
Acute coronary syndromes are most commonly associated with the rupture or erosion of an unstable atherosclerotic plaque and
subsequent formation of a platelet-fibrin thrombus. It is important to understand the pathophysiology of acute coronary syndromes
including the following:
Risk factors for the development of coronary artery disease.
Pathophysiology of the development of atherosclerosis.
The classifications of the different forms of angina.
The ECG characteristics of myocardial infarction from section 4.
Acute Coronary Syndrome (ACS) Patho…
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Readings (a choice)
Core text reading
Aitken, A, Marshall, A, & Chaboyer, W., chapter 9 ‘Cardiovascular alterations and management’, in ACCCN’s critical care nursing, Else
eReadings
Thompson, P 2011, Coronary care manual, 2nd edn, Elsevier, Australia.
Chapter 8 ‘Pathophysiology of atherosclerosis’, pp. 54-61.
Chapter 9 ‘Pathophysiology of coronary thrombosis’, pp. 62-71. – Click Here
Chapter 10 ‘Pathophysiology of myocardial infarction’, pp. 72-78.
Chapter 16 ‘Biochemical markers of myocardial necrosis’, pp.125-129 – Click Here
Chapter 60 ‘Prehospital coronary care’, pp. 454-458.
Chapter 61 ‘ACS: emergency department care’, pp. 459-466.
Chapter 62 ‘ACS: coronary care unit admission and care’, pp. 467-473. – Click Here
Chapter 63 ‘Management of ST elevation myocardial infarction’, pp. 474-484.
Chapter 64 ‘Management of non ST elevation ACS’, pp. 485-493.
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ACS in Women and ANZCOR Updates
eReading
Mehta, L.S., Beckie, T.M., DeVon, H.A., Grines, C.L., Krumholz, H.M., Johnson, M.N., Lindley, K.J., Vaccarino, V., Wang, T.Y., Watson,
Infarction in Women A Scientific Statement From the American Heart Association. Circulation, pp.CIR-0000000000000351. – Click He
Website
There have been some updates from the Australian and New Zealand Committee on Resuscitation (ANZCOR) (Australian Resuscitati
Australian and New Zealand Committee on Resuscitation: Guidelines Section 14: Acute Coronary Syndromes – Click Here
ANZCOR Guidelines Update on Acute Coronary Syndromes – Click here
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Safety and Quality ACS Clincial Care Standard
Australian Commission on Safety and Quality in Health Care. Acute Coronary Syndromes Clinical Care Standard. Sydney: ACSQHC, 2
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Classification of acute coronary syndromes
In the previous module you learned the ECG characteristics of acute MI. It is important to distinguish between unstable angina, non ST
elevation myocardial infarct (NSTEMI) and ST elevation myocardial infarct (STEMI). Patients with symptoms of ischemic discomfort may
present with or without ST segment elevation on an ECG. Patients who present without ST segment elevation are experiencing either
unstable angina or NSTEMI. The distinction between these is made by assessment of the presence of elevated serum cardiac markers.
The majority of patients with NSTEMI do not develop Q waves (indicating irreparable necrosis) on their ECG and you may hear referred to
as having a Non Q wave MI (NQWMI) although this terminology is no longer commonly used. However some patients with NSTEMI do
develop Q waves on their ECG, (QWMI). Patients experiencing STEMI can also develop Q waves on their ECG with a smaller number
experiencing NQWMI. With a strong current focus on client early action and early clinical intervention in this cohort of patients the number
of people exhibiting Q waves is decreasing.
Figure 5.1: Classification of acute coronary syndromes (Adapted from Thompson, P 2008, Coronary care manual, 2nd edn, Churchill
Livingstone, Australia, and White, HD & Chew, DP 2008, ‘Acute myocardial infarction’, Lancet, vol. 372, pp. 570–584.)
The presence of Q waves is often associated with transmural infarction, or one which extends through the full thickness of the
myocardium. However, Q waves are not a consistent indicator of transmural infarction. Similarly the presence of ST segment depression
without elevation elsewhere on the ECG is usually but not always associated with subendocardial injury. The lack of consistency of ST and
Q wave changes as indicators of subendocardial or transmural zones of injury has lead to the classification of acute coronary syndrome by
their ECG characteristics alone.
4/9/2020 Study plan: Week 5 – Acute coronary syndromes
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Clinical assessment: the patient with chest pain
Activity
Some disorders mimic the chest pain of AMI. Construct a table that describes the pain location, pain
characteristics and common assessment findings such as any ECG changes for each disorder listed below.
Disorders that may mimic the chest pain of AMI
pulmonary embolism pneumonia
aortic dissection pneumothorax
angina gastric reflux
Pericarditis
Approach to Chest pain
An Approach to Chest Pain
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Diagnosis of acute myocardial infarction
Acute cardiac care is a dynamic discipline. Research in regard to management strategies including diagnostic tools, drug therapy, invasive
and non-invasive treatments are under constant review by clinicians and researchers. Evidence based practice at this stage supports early
clinical presentation, cardiac enzymes and ECG changes as the standard for diagnosis of AMI. However, there are circumstances when
further intervention such as catheter lab or CT is required to confirm suspected diagnosis.
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Clinical presentation
The diagnosis and determination of the severity of an AMI is on a clinical diagnosis which requires a thorough history and physical
examination.
Pain, shortness of breath, diaphoresis are usually the most significant symptoms for most patients experiencing a STEMI or NSTEMI and
normally follow a characteristic pattern. However, some patients with acute coronary syndromes may not experience pain, and the
intensity of pain varies with the pain threshold of different patients. The intensity of the pain experienced is neither indicative nor diagnostic
of the severity of the ACS the patient may be experiencing.
Chest pain may be caused by many different conditions; however, it is important to remember that the patient with chest pain should be
considered cardiac in origin until proven otherwise. The patient who presents with acute chest pain requires prompt efficient nursing care
to help alleviate their suffering and the potential damage to the myocardium.
Myocardial Infarction in the ICU setting –
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Diagnostic tools and procedures
Activity

  1. Research the clinical signs which are common on presentation with an acute MI. Are there any signs or
    symptoms which are common with particular types or zones of infarction?
  2. Using your text find the sections that discuss the variety of diagnostic procedures and tools available for the
    diagnosis and treatment of Acute Coronary Syndromes. The list of investigations below can be performed to
    assist with the diagnosis and ongoing management of myocardial infarction and heart failure.
    Chest x-ray
    ECG
    Arterial blood gases
    Echocardiograph (two types and why use different methods?)
    Stress exercise electrocardiography
    Cardiac catheterisation: angiography and angioplasty
    Complete blood count
    Serum electrolytes/liver function tests/complete cholesterol screen
    Radionuclide studies
    Magnetic Resonance Imaging
  3. Provide information on why each test/procedure may be performed. (That is, what do you think the team is
    looking for or treating?) There could be more than one reason.
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    Biomarkers
    Knowledge of the purpose and significance of laboratory values assisting in the diagnosis and prognosis of AMI can enhance the quality of
    nursing care available to patients. Laboratory studies include routine blood analysis and special studies such as cardiac enzymes.
    Enzymes are found in all living cells and act as catalysts in biochemical reactions. They are present in low amounts in the serum of
    healthy people. The loss of membrane integrity in myocardial cells undergoing necrosis allows intracellular molecules to diffuse out into
    the cardiac interstitium and subsequently the blood stream. Detection of the abnormal presence of biomarkers is the ultimate diagnostic
    criteria for distinguishing between unstable angina and NSTEMI. Some cardiac enzymes are present in other organs, so elevation of these
    enzymes is not always an indicator of cardiac damage.
    A biomarker, known as Troponin or, in correct terminology, ‘cardiac Troponin’ was discovered in the 1990’s and is used successfully today
    for assisting in the diagnosis of cardiac muscle damage. There are three different types of Troponin; Troponin I (TnI), Troponin C (TnC)
    and Troponin T (TnT), with Trop I and T used for detection of damage specifically to the cardiac muscle. Troponin is a protein consisting of
    three sub-units and plays a key role in muscle contraction alongside actin and myosin. These are known collectively as contractile
    proteins.
    Activity
    Consult the section on biomarkers in your prescribed text to find the answers to the following questions.
  4. Describe how Troponin (T/I) differs from existing cardiac enzymes, namely creatine kinase (CK), and the
    isoform of creatine kinase (CK-MB).
  5. Compose a table that lists all of the current biomarkers associated with AMI, the time they take to peak, and
    the duration of elevation.
  6. Consider how these and other investigations might be of some benefit in the diagnosis of myocardial
    infarction. Your list should include procedures such as laboratory assessments.
    It is important to note that the initial diagnosis of STEMI can be made by clinical and ECG criteria alone.
    It is not necessary to wait for results of biochemical markers to arrive before initiating therapy in patients
    at risk.
    4/9/2020 Study plan: Week 5 – Acute coronary syndromes
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    Management of the patient with acute coronary syndromes
    National Heart Foundation of Australia Website
    For professionals: Australian acute coronary syndromes – Click Here
    Australian acute coronary syndromes capability framework – Click Here
    Managing the patient with an acute coronary syndrome is an exciting area of clinical practice where you can really make a positive
    difference to patient and family outcomes.
    In the 1960’s specialised Coronary Care Units were introduced to hospitals across the world to offer closer monitoring and access of
    patients to specialty trained nursing staff and subsequently enhanced treatment of patients admitted with a myocardial infarction. Death
    rates due to pump failure or arrhythmia actively decreased and the focus turned to pre-hospital coronary care where paramedics offered
    clients early access to defibrillation and drug administration. Since these times Coronary Care Units, or Cardiac Care Units as they have
    been subsequently been termed, have developed into centres of research, clinical trials, advanced reperfusion and infarct limitation.
    Despite an international approach to cardiology as a specialty area of care and public health promotion campaigns, both national and
    internationally, ACS still remains one of the most common causes of acute medical admissions to the ED and the leading single cause of
    death.
    Web reading
    The National Heart Foundation in association with The Cardiac Society of Australia and New Zealand has developed evidence based
    acute coronary syndromes. An addendum to these guidelines has been published by the National Heart Foundation of Australia and th
    2011 and updated in 2016.
    Yancy, C.W., Jessup, M., Bozkurt, B., Butler, J., Casey, D.E., Colvin, M.M., Drazner, M.H., Filippatos, G., Fonarow, G.C., Givertz, M.M.
    ACC/AHA/HFSA focused update on new pharmacological therapy for heart failure: an update of the 2013 ACCF/AHA guideline for the
    report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Fa
    America. Circulation, 134(13), pp.e282-e293.
    This may be accessed at: http://circ.ahajournals.org/content/134/13/e282 or through the Heart Foundation Guidelines
    Figure: Algorithm for incorporating a high sensitivity troponin into the work-up of patients with suspected acute coronary
    syndromes (ACS).
    From: (2011) 2011 addendum to the National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand guidelines for
    the management of acute coronary syndromes (ACS) 2006. Heart, Lung and Circulation, 20(8), p 491.
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    Care priorities: minimising damaged tissue
    The patient with an acute coronary syndrome has impairment to coronary blood flow, most commonly from a ruptured plaque and
    subsequent thrombus formation. The extent of damage to the myocardium depends upon the extent to which this thrombus affects blood
    flow, the time that the myocardium has been ischaemic, the level of myocardial oxygen demand and the presence or lack of adequate
    collateral circulation.
    Damage progresses from the centre of the ischaemic zone out in a ‘wave’ firstly involving the subendocardium and eventually to the
    subepicardium. A patient left untreated can progress from a NSTEMI to a STEMI if left untreated. The major aim of management is to
    minimise the size of the ischaemic area by restoring blood flow to the affected area of cardiac muscle as quickly as possible. This can be
    achieved with various management strategies, drug therapies or surgery.
    Activity
    Below is a list of activities required to manage the patient who has just presented with chest pain. Analyse each
    activity and describe in detail how and why you would implement the care required for each. Sort this list in order
    of clinical priority. Remember your DRABCDEF priority principles; naturally some of these tasks will be done
    concurrently.
    Give oxygen if needed
    Evaluate chest pain
    Obtain vital signs
    Obtain an ECG
    Relieve the patient’s pain
    Prevent further pain
    Provide emotional support
    Obtain venous access
    Administer nitrates and aspirin.
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    Reperfusion strategies
    Following an ST elevation MI reperfusion is a high priority in order to minimise damage to the myocardium. The process of the area of
    necrosis from the subendocardium to the subepicardium is called the evolution of the MI (Huszar 2014).
    This has been divided into four phases as illustrated by the following table.
    Table 5.1: Four phases of acute MI
    (Adapted from Huszar 2014, Basic dysrhythmias: interpretation & management, revised 4th edn.)
    The goal of treatment is to begin reperfusion therapy within the first 30-60 minutes of the onset of the infarction. This can take the form of
    drug therapy or coronary intervention. The major groups of medication agents are listed in the following table.
    Hemostasis: Lesson 6 – Anticoagulatio…
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    Table 5.2: (Adapted from Huszar 2014, Basic dysrhythmias: interpretation & management, revised 4th edn.)
    Reperfusion strategies by percutaneous transluminal coronary angioplasty (PTCA) involve the insertion of a balloon tipped catheter into
    the occluded or narrowed vessel and inflation of the balloon to dilate the arterial lumen. Read the section in your text book on PTCA.
    Australian Resuscitation Council – ACS Reperfusion protocol – click here [scroll to the the bottom of the web page]
    Video Cardiac Catheterisation
    Activity
  7. Occlusion of the left anterior descending artery (LAD) causes which type of infarction? What are the potential
    complications?
  8. Occlusion of the right coronary artery (RCA) causes which type of infarction? What are the potential
    complications?
  9. What complications can occur as a result of coronary angioplasty? What are the possible treatment
    strategies for each?
  10. What are the long term management priorities for the patient recovering from and acute MI? Research the
    education and cardiac rehabilitation program offered by your hospital.
    Cardiac Cath with Angioplasty
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    Lifespan and Cultural Considerations
    Indigenous Australians
    Cardiovascular disease, particularly coronary heart disease, is the major cause of premature death for Aboriginal and Torres Strait
    Islander peoples, accounting for 26% of all deaths. Cardiovascular disease is also a major contributor to the gaps in life expectancy
    between Indigenous and non-Indigenous Australians, with recent statistics suggesting that Australian Aboriginal and Torres Strait Islander
    men and women can expect to live 10.6 and 9.5 fewer years, respectively, than other Australians.
    Acute coronary syndromes (ACS) include a broad spectrum of clinical presentations including ST-elevation myocardial infarction (STEMI),
    non-STEMI and an accelerated pattern of angina without evidence of myonecrosis (unstable angina); the latter two are often grouped as
    non-ST-elevation acute coronary syndromes (NSTEACS). Current National Heart Foundation of Australia/Cardiac Society of Australia and
    New Zealand guidelines highlight the importance of effective systems of care in delivering optimal management of ACS.
    In 2006, the Australian Institute of Health and Welfare (AIHW) released a landmark report on access to ACS treatment by Aboriginal and
    Torres Strait Islander patients. The report found that, compared with other Australians, Indigenous Australians hospitalised with ACS had:
    more than twice the rate of death from CHD
    a 40% lower rate of being investigated by angiography
    a 40% lower rate of percutaneous coronary intervention (PCI)
    a 20% lower rate of coronary artery bypass graft (CABG) surgery.
    As highlighted in the 2006 AIHW and subsequent reports, the inhospital disparities in ACS care experienced by Aboriginal and Torres
    Strait Islander peoples warrant special consideration by health service providers.
    References
    Australian Bureau of Statistics. Life tables for Aboriginal and Torres Strait Islander Australians, 2010-2012. Canberra: ABS, 2013. (ABS
    Cat. No. 3302.0.55.003.
    Australian Institute of Health and Welfare. The health and welfare of Australia’s Aboriginal and Torres Strait Islander people: an overview,
  11. Canberra: AIHW, 2011. (AIHW Cat. No. IHW 42.)
    Paediatric Focus
    Kawasaki disease (KD) is the commonest cause of acquired heart disease in children in developed countries. The typical age at
    presentation is 6 months to 5 years of age and the highest incidence of Kawasaki disease is in Asian countries. An infectious etiology is
    likely, but a specific agent has not yet been identified. The immune system is extensively involved in disease pathogenesis. KD is
    associated with systemic vasculitis particularly affecting the coronary arteries, causing coronary artery aneurysms. KD is also potentially
    an important cause of long-term cardiac disease in adult life.The main sites of clinically important vascular involvement are the coronary
    arteries, although other vessels such as the axillary arteries can be involved. CAA occur in 15–25% of untreated cases, with additional
    cardiac features in a significant proportion of these including pericardial effusion, electrocardiographic abnormalities, pericarditis,
    myocarditis, valvular incompetence, cardiac failure and myocardial infarction.
    Reference:
    Dietz, S.M., Tacke, C.E., Hutten, B.A. and Kuijpers, T.W., 2015. Peripheral endothelial (dys) function, arterial stiffness and carotid intimamedia
    thickness in patients after Kawasaki Disease: A systematic review and meta-analyses. PloS one, 10(7), p.e0130913.
    Older Adult
    Advancing age is a risk factor for the development of coronary artery disease and is an important indicator of outcome after acute
    coronary syndrome. Guidelines for the management of older adults are the same as for their younger counterparts, with the proviso that
    treatments should be personalised. This includes an appreciation of functional status, co-morbidities, ischaemic and bleeding risk as well
    as the physiological changes associated with ageing such as impaired renal function. In older adults, the diagnosis of ACS is often
    challenging. ACS risk scores often classify older adults as high risk, this favours an early interventional strategy with prescription of
    appropriate secondary prevention medications. Older adults commonly present with autonomic symptoms including dyspnoea (49.3%),
    diaphoresis (26.2%), nausea and vomiting (24.3%), but also with pre-syncope and syncope (19.1%). Chest pain is present in ∼40% of
    those over 85 compared with nearly 80% in those under 65. Consequently, there is a reduced probability of ACS being diagnosed and an
    increased incidence of acute decompensation and in-hospital mortality.
    Delays to the provision and reporting of the initial ECG may delay diagnosis. Notably, more than two in five of ACS patients over 85 years
    of age do not have diagnostic ECG changes compared with a quarter of those under the age of 65 years. These factors may cloud the
    clinical picture and prevent timely diagnosis of ACS.
    In the case of STEMI, the myocardial infarction may be more evolved, with greater loss of myocardium and an increase in acute
    complications.
    The clinical presentation of ACS is often atypical in older patients and the initial ECG is often less commonly diagnostic in the older ACS
    patient; thus greater reliance is placed on the cardiac troponin assay for making the diagnosis. However, elevated troponin levels may
    occur incidentally in the absence of ACS or conditions such as myocarditis, pulmonary embolism or sepsis.
    Reference:
    4/9/2020 Study plan: Week 5 – Acute coronary syndromes
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    Veerasamy, M., Edwards, R., Ford, G., Kirkwood, T., Newton, J., Jones, D. and Kunadian, V., 2015. Acute coronary syndrome among
    older patients: A review. Cardiology in review, 23(1), pp.26-32.

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