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Laura_Siford_s313017_NUR250 SS 2019 Assessment 1
Task 1
Non-ST elevation acute coronary syndrome (NSTEACS) is a condition in which there is an
acute reduction of blood flow to the myocardium without ongoing ST-segment-elevation
evident on electrocardiogram (ECG). NSTEACS is subdivided into unstable angina (UA) and
non-ST-elevation myocardial infarction (NSTEMI). NSTEMI is acute ischaemia caused by
partial occlusion of one or more coronary arteries (LeMone et al., 2017). ECG changes such
as ST depression, T wave inversion or transient ST elevation may or may not be evident in
both UA and NSTEMI. For a medical diagnosis of NSTEMI, elevated cardiac biomarkers must
also be present (LeMone et al., 2017; National Heart Foundation of Australia [NHFA],
2016a).
It is rare for a myocardial infarction to manifest in patients who do not have pre-existing
coronary heart disease (CHD) (LeMone et al., 2017). Atherosclerosis is the main cause of
reduced coronary blood flow, with the accumulation of lipoproteins and fibrous tissue
gradually narrowing the lumen of coronary arteries. The rupture or erosion of an
atherosclerotic lesion initiates the clotting process, that is platelet aggregation and
coagulation cascade, resulting in thrombus formation. This atherothrombosis significantly
impairs blood flow, causing the cardiac tissue that is supplied by the affected artery to
become ischaemic (LeMone et al., 2017). Myonecrosis then occurs if blood flow is not
restored. Myocardial injury results in the release of cardiac biomarkers, with troponin
having the highest sensitivity and specificity for myocardial damage (NHFA, 2016a).
CHD is the leading cause of death for Indigenous Australians, and Peter has an extensive
history of well-known risk factors for CHD, which has likely manifested in his current
condition of NSTEMI. The risk factors that predispose Peter to CHD are type 2 diabetes
mellitus (T2DM), hypertension, hyperlipidaemia and smoking (Alston, Peterson, Jacobs,
Allender, & Nichols, 2017; LeMone et al., 2017), each of which can damage arterial
endothelium, promoting atherosclerosis and subsequent atherothrombosis as previously
described. CHD is the most common cause of mortality in diabetics. Hypertension, common
in diabetics, doubles the risk for cardiovascular disease by placing extra pressure on arterial
walls and increasing the risk of atherosclerosis (NHFA, 2016b). Likewise, hyperlipidaemia has
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Laura_Siford_s313017_NUR250 SS 2019 Assessment 1
shown a significant correlation to an increased risk of premature CHD in diabetics. Diabetes
lowers HDL cholesterol and raises LDL cholesterol and triglycerides, increasing the risk of
atherosclerosis (LeMone et al., 2017). Smoking significantly increases the risk of developing
CHD in multiple ways. Vascular endothelium is damaged by carbon monoxide, leading to
atherosclerosis. Nicotine reduces HDL levels and increases platelet aggregation, contributing
to an increased risk of atherothrombosis. Nicotine also acts on the sympathetic nervous
system (SNS), increasing blood pressure, heart rate, myocardial contractility and oxygen
demand (Benowitz & Burbank, 2016; LeMone et al., 2017). It is clear that all four risk factors
are inextricably linked.
Peter also suffers from mitral valve regurgitation (MVR), a likely manifestation of rheumatic
heart disease, in which the mitral valve does not fully close. The cumulative effects on the
left atrium and left ventricle result in a reduced cardiac output (LeMone et al., 2017). MVR
therefore further contributes to Peter’s other high-risk features and may affect prognosis.
MVR also increases the risk of infective endocarditis, so if heamodynamic monitoring or
cardiac catheterisation is required to restore coronary blood flow, extra precautions must
be taken such as prophylactic antibiotics in addition to aseptic techniques (LeMone et al.,
2017; RHDAustralia, 2012).
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Laura_Siford_s313017_NUR250 SS 2019 Assessment 1
Task 2
Nursing Care Plan: Peter JONES
| Nursing problem: Acute Pain | |||
| Related to: myocardial ischaemia as evidenced by Peter’s report of 4/10 chest pain. | |||
| Goal of care | Nursing interventions | Rationale | Evaluation |
| Peter has an absence of pain by end of shift. |
1. Assess pain regularly using PQRST method; assess non-verbal signs of pain 2. Safely administer prescribed medications, repeating vital signs, pain assessment after administration; discuss analgesia escalation with doctor 3. Educate importance immediately reporting increase in or change in characteristics of pain 4. Administer supplemental oxygen as prescribed 5. Provide non-pharmacological pain control: comfortable; physical, psychological rest |
1. Pain subjective, comprehensive pain assessment provides objective baseline gauge effectiveness of/guide further interventions (ANMF, 2018; LeMone et al. 2017; Levett-Jones, 2018). 2. Paracetamol effective mild- moderate pain. GTN vasodilator reduces cardiac workload, improves blood flow to ischaemic area reducing pain. Morphine effective for pain not relieved by GTN, provides sedation, decreases cardiac workload. Change in vital signs/pain may indicate improvement/deterioration of condition (LeMone et al., 2017; NHFA, 2016a; Tiziani, 2017) 3. Delay reduces effective pain management; may result in deterioration of condition (LeMone et al., 2017; Levett-Jones, 2018) 4. Supplemental oxygen if sats <93%; increases myocardial oxygenation relieving ischaemic pain (LeMone et al., NHFA, 2016a) 5. Reduces perception/response to pain. Decreases SNS stimulation, cardiac workload, promoting comfort (LeMone et al., 2017) |
• Peter states pain score of zero • Peter appears comfortable with non verbal signs of pain absent • Peter’s vital signs are WNL |
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Laura_Siford_s313017_NUR250 SS 2019 Assessment 1
| Nursing problem: Risk of ineffective tissue perfusion | |||
| Related to: myocardial ischaemia as evidenced by Peter reporting central crushing chest pain. | |||
| Goal of care | Nursing interventions | Rationale | Evaluation |
| Peter demonstrates adequate perfusion throughout shift. |
1. Assess and document vital signs, escalating changes as per ADDS. 2. Safely administer medication and supplemental oxygen as prescribed 3. Attach cardiac monitoring and perform repeat 12 lead ECG’s as ordered, immediately reporting changes to doctor 4. Assess heart/breath sounds, LOC, skin, peripheral pulses, capillary refill, urine output 5. Minimise activity |
1. Reduction in CO may cause tachycardia, tachypnoea, vasoconstriction increasing cardiac workload (LeMone et al., 2017). ADDS ensures appropriate/timely clinical response (ACSQHC, 2012). 2. Aspirin and clopidogrel inhibit platelet aggregation maintaining/improving perfusion; GTN vasodilator improves blood flow to ischaemic tissue (NHFA, 2016a; Tiziani, 2017). Supplemental oxygen if sats <93% increases myocardial oxygenation reducing myocardial hypoxia (LeMone et al., 2017; NHFA, 2016a) 3. Increased risk arrhythmias due to infarction contribute to reduced myocardial blood flow/oxygenation; ECG valuable assessing myocardial perfusion/deterioration in condition (LeMone et al., 2017; NHFA, 2016a) 4. Abnormal changes may indicate impaired tissue perfusion (LeMone et al., 2017) 5. Reduces cardiac workload and myocardial oxygen demand (LeMone et al., 2017) |
• Peter’s vital signs WNL • Absence of ischaemia on Peter’s ECG • Peter’s skin warm and dry • Peter reports absence of chest pain |
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Laura_Siford_s313017_NUR250 SS 2019 Assessment 1
| Nursing problem: Anxiety | |||
| Related to: threat to health/lack of understanding as evidenced by Peter’s report of feeling tired and worried. | |||
| Goal of care | Nursing interventions | Rationale | Evaluation |
| Peter’s anxiety reduced by end of shift. |
1. Provide appropriate support e.g. ALO/professional interpreter 2. Identify, acknowledge source of anxiety, encouraging expression of worries 3. Educate on condition, expected process, outcomes, encouraging participation 4. Ensure confident demeanour, factual communication 5. Provide privacy, comfort, rest, education on non pharmacological methods to reduce anxiety such as deep breathing, distraction, visualisation, music |
1. Cultural needs met reducing anxiety; communication accuracy alleviates anxiety caused by lack of understanding (NMBA, 2016; Tiziani. 2017; AIHW, 2014) 2. Assist with coping, guide further interventions to relieve anxiety, reduce SNS stimulation that may increase anxiety (LeMone et al., 2017) 3. Consistent information and sense of control decreases anxiety providing predictability, relieving tension of unexpressed concerns, allowing patient to come to terms with situation (LeMone et al, 2017) 4. HCP’s can project additional anxiety onto patient; anxiety alleviated by honest explanations; strengthen therapeutic relationship (LeMone et al., 2017; NMBA, 2016) 5. Promotes relaxation, improves coping, reduces tension and anxiety (LeMone et al., 2017) |
• Peter verbalises feelings, identifies factors contributing to anxiety • Peter verbalises reduction in anxiety • Peter shows reduction in non-verbal signs of anxiety |
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Laura_Siford_s313017_NUR250 SS 2019 Assessment 1
Task 3
Suboptimal adherence to medications means the maximum benefit is not being achieved, which can be particularly harmful for those with
chronic conditions (Stanford, Charlton, McMahon & Winch, 2019). Given Peter has CHD, RHD, T2DM, hypertension and hyperlipidaemia,
ensuring compliance with his medication regime is of paramount importance. Ensuring Peter is free from pain and anxiety, and providing a
suitable environment with no interruptions is required for education to be effective (Tiziani, 2017). In addition to providing Peter with culturally
appropriate education and resources on the use, action and importance of taking his prescribed medications, dose administration aids (DAAs)
can be a useful strategy to improve medication adherence (de Dassel, Ralph & Cass, 2017). The Quality Use of Medicines Maximised for
Aboriginal and Torres Strait Islander People (QUMAX) programme provides subsidised DAAs to eligible Indigenous Australians, which may
further contribute to adherence (Couzos, Sheedy & Delaney Thiele, 2011).
A key factor for controlling CHD risk factors is lifestyle modification (Woodruffe, Neubeck, Clark, Gray, Ferry, Finan, Sanderson & Briffa, 2015).
Peter should be provided with culturally appropriate education throughout his hospital stay on lifestyle modification strategies that he can
begin to implement in hospital, as well as on discharge home, to reduce his risk of further cardiac problems. In Australia, tobacco smoking is
the leading preventable cause of mortality and morbidity, with smokers up to four times more likely to die from CHD (Alston et al., 2017;
LeMone et al., 2017). Smoking cessation may have multiple benefits for Peter given its strong link not only to CHD, but diabetes, hypertension
and hyperlipidaemia. (LeMone et al., 2017). Evidence suggests nicotine replacement therapy (NRT) can increase success of quitting by up to
70%. As an Indigenous Australian living in a remote community, Peter is entitled to subsidised NRT through a prescription from his doctor,
which has been shown to contribute to success on this therapy (DiGiacomo, Davidson, Abbott, Davison, Moore & Thompson, 2011). It does
however also provide significant barriers for Peter, given limited access to and collaboration of health services, normalisation and high levels of
smoking in the community, and significant community distress and socioeconomic disadvantage (Tall, Brew, Saurman & Jones, 2015). It is
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Laura_Siford_s313017_NUR250 SS 2019 Assessment 1
therefore vital that a multifaceted approach tailored to Peter’s individual needs is implemented, including contact with Peter’s community
health service for ongoing support post-discharge (AIHW, 2014; LeMone et al., 2017).
Task 4
A new medication that Peter has been prescribed, when required, is glycerol trinitrate (GTN) sublingual spray. GTN is a potent vasodilator that
causes the relaxation of vascular smooth muscle. Dose related venous and arterial dilation occurs, with arterial dilation occurring at higher
doses. Vasodilation causes a reduction in preload, afterload, and myocardial oxygen consumption by decreasing arterial pressure and cardiac
output. GTN can also increase perfusion and oxygen delivery to areas of ischaemic myocardium. Sublingual administration allows for rapid
absorption, with an onset of action within 2-4 minutes, and duration of action less than 1 hour (LeMone et al., 2017; NHFA, 2016a; Tiziani,
2017). Peter has been prescribed GTN sublingual spray, as it is effective at reducing ischaemic chest pain. If pain is not achieved within 5
minutes, a second or third dose may be administered to Peter at 5-minute intervals provided hypotension does not occur (LeMone et al., 2017;
NHFA, 2016a).
Prior to GTN being administered to Peter, the prescribing doctor should correct the medication order, as mcg is not an acceptable abbreviation
for micrograms as it can easily be mistaken for milligrams (mg) and an incorrect dose administered (ACSQHC, 2016). A few potential drug
interactions may affect Peter. Ramipril can increase the effect of GTN on lowering blood pressure and increase risk of syncope. Close
monitoring must be undertaken to ensure he does not become hypotensive, which can lead to a reduction in coronary perfusion and an
increase in myocardial oxygen demand, potentially leading to ischaemic extension. Peter’s therapeutic response to GTN may be reduced due to
the administration of aspirin, so regular pain assessments must be performed to ensure adequate pain therapy is achieved (LeMone et al.,
2017; Tiziani, 2017).
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Laura_Siford_s313017_NUR250 SS 2019 Assessment 1
Ramipril is an angiotensin-converting-enzyme (ACE) inhibitor, which prevents angiotensin I converting to angiotensin II. This results in reduced
peripheral vascular resistance via vasodilation and a decrease in blood volume by decreasing aldosterone production. The net effect is a
reduction in blood pressure. Ramipril has a long duration of action of 24 hours. ACE inhibitors are associated with a reduction in MI associated
mortality and ventricular remodelling post MI, as well as a reduction in risk of subsequent heart failure and reinfarction. Peter has multiple
factors that may have indicated an ACE inhibitor being prescribed. In addition to its role in reducing BP in hypertension, given Peter is over 55
years old, has diabetes, hyperlipidaemia and is a current smoker, it also reduces his risk of MI, stroke, cardiovascular death or revascularisation
procedures (LeMone et al, 2017; Tiziani, 2017).
Whilst correcting the medication order for GTN, the doctor should also correct the medication order for ramipril as ‘daily’ should replace ‘OD’,
which is not an acceptable term for once daily (ACSQHC, 2016). In addition to the previously mentioned interaction with GTN, Peter has a few
other potential drug interactions. There is an increased risk of hyperkalaemia and decrease in hypotensive effect if given with aspirin. Given
Peter also has diabetes, which can affect kidney function and increase the risk of hyperkalaemia, blood potassium levels should be monitored.
Hyperkalaemia can further increase Peter’s risk of arrhythmias, and it is also a predictor of higher mortality in acute MI, so cardiac monitoring is
indicated. Metformin is another potential drug interaction, as in combination with ramipril, may cause clinically significant hypoglycaemia.
Careful monitoring of blood glucose levels is required (LeMone et al., 2017; Tiziani, 2017).
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Laura_Siford_s313017_NUR250 SS 2019 Assessment 1
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