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1. This Assessment task is based on the case scenario of ‘Mae Roberts’ and is shared with NSG2204 Professional Studies 4. Indigenous Culture and Health.
2. There are THREE separate QUESTIONS for NSG2201 Written Assessment task 2, that need to be answered in reference to the case scenario of ‘Mae’. Ensure you complete all three questions for this assessment task. Total word count for this task is 1500 words +/- 10%.
3. An introduction or conclusion are NOT REQUIRED for this assessment task; however, subheadings are encouraged
Mae Roberts is a 47-year-old Muti Muti and Dja Dja Wurrung Aboriginal woman from Robinvale in north-west Victoria, along the Murry River. Mae grew up in a large family (7 children), living with both her mother and grandparents.
Her mother was the 4th generation of the family to be part of Stolen Generation (Mae’s great-great grandparents being removed from Country and taken to Coranderrk with their children, near modern-Day Healsville).
Mae’s father was charged with shop- lifting when Mae was a small child, and died in remand prior to the charges coming to court. Mae does not remember him.
Mae separated from her husband as a young woman and raised her 3 children alone. She has 2 grandchildren, aged 3 years (a boy, Christopher) and 6 months (a girl, Amy). Mae lives with 2 of her children, their partners and her grandchildren in a 3 bedroom government-unit.
Her third child (Dennis) is currently serving time in prison for theft. Mae and her family are engaged with the local ACCHO (Aboriginal Controlled Community Health Organisation) Murray Valley Aboriginal Cooperative (MVAC), both for early learning for Christopher, and assistance with navigating the legal system through MVAC’s Justice Program, for Dennis.
Growing up, Mae’s mother experienced challenges with longstanding depression and substance use. Mae’s grandparents were very involved in all the children’s lives, and Mae feels a great sense of loss at their early deaths (from cardiovascular diseases, in their 40s and 50s).
Mae frequently experienced ill health as a child, including Acute Rheumatic Fever (ARF), when she was 6. Mae recalls her mother and grandmother talking about whether to take Mae to the doctor but being hesitant to do so.
She recalls her grandmother saying, “This is how it starts, you ask for help, and they say you’re not looking after your kids enough, and then the social worker comes and takes them away”.
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Mae has recently felt unwell, finding it harder to chase after Chirstopher and go to work (Mae usually does manual farm work at one of Robinvale’s local fruits growers). She has had increasing feelings of a racing heart and getting out of breath (tachycardia and dyspnoea). At times Mae has felt dizzy and needed to sit down. After this happened at work one day, the manager told Mae not to come back.
After Mae left work, she saw a doctor at MVAC who has said she needs to see a cardiologist urgently and organised an ambulance transfer to Mildura Base Hospital. The doctor has explained that Mae is likely to be there for at least several days and may need treatment in a larger hospital (such as Melbourne). Mae doesn’t know anyone in Mildura, states Mildura is “not my people, not my place” and is worried about having to go away from home, as her children don’t have a car.
• Acute Rheumatic Fever (ARF) at 6 years old post Group A streptococcal throat infection
• Chronic tonsillitis as a child and adolescent
• Hypertension
• Hypercholesterolemia
• Rheumatic Heart Disease (diagnosed 2011)
• Multigravida (3 live births)
Coronary Heart Disease Alcoholism
Depression
Type 2 Diabetes Mellitus (T2DM)
(Mother died at 44 years from cardiac failure?) Father unknown
Ramipril 10mg/day Pravastatin 40mg/nocte Panadol 1g/PRN
Benzathine Benzylpenicillin G (BPG or Bicillin) injection every 3-4 weeks
Information obtained on admission to Mildura Base Hospital………
Mae is seen by the Cardiologist and given a provisional diagnosis of Mitral valve stenosis, secondary to Rheumatic Heart Disease.
On Examination Mae appears anxious. RR – 22bpm
HR – 117 (irregular) BP – 110/64
Temp – 36.9 SpO2 – 94% RA
Results of Investigations/Diagnostic tests Pathology
UEC’s (Urea and Creatinine are slightly elevated) Echocardiogram - severe mitral stenosis; enlargement of left atria ECG – atrial fibrillation (115-125bpm)
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QUESTIONS:
1. Pathophysiology and Interpretation of Results (approx. 500-600 words)
a) Create a CONCEPT MAP (using the below link) describing the pathophysiology of the progression of Mae’s Rheumatic fever, to Rheumatic heart disease and the current diagnosis of mitral valve stenosis. Make links with risk factors relevant to the case scenario and represent this on the concept map. All elements of the concept map must be supported with evidence-based literature, and intext citations are required. The concept map must be submitted as a pdf document.
b) Provide a detailed description of what the results of the above investigations (Pathology, ECG and Echocardiogram) tell you about Mae’s current presentation and prognosis (the likely course of Mae’s medical condition). Your description should be linked with the above pathophysiology outlined in your concept map and MUST be supported with relevant evidence-based literature.
2. Focused Physical Assessments and Medications. (approx. 600-700 words)
Please note that this question consists of TWO sections (Assessment & Medications)
a) Assessment
• Identify TWO relevant focused systems assessments (eg. CNS, GIT, Renal, etc) that you would perform on Mae; and provide a detailed rationale for your choices. Then Choose ONE of the above systems assessments and identify TWO abnormal findings you may note on performing this focused system assessment and provide a
rationale for each abnormal finding identified. This must be supported with relevant evidence-based literature.
• If Mae was to experience chest pain during her admission, identify ONE pain assessment tool you would use to assess her pain; and provide a brief explanation of why you would CHOOSE this tool, over other pain assessment tools. This must be supported with relevant evidence-based literature.
b) Medications
Mae has been prescribed two new Medications (Digoxin and Carvedilol) by the Cardiologist. Provide a detailed rationale for why Mae would be prescribed EACH of these medications, in the management of her current diagnosis/disease.
(For example, how do each of these medications assist in the management of this condition). This must be supported with relevant evidence-based literature.
3. Complications and Clinical deterioration (approx. 400 words)
a) Identify and describe TWO potential complications associated with Mae’s diagnosis/disease, providing a brief rationale for why Mae may be at risk of developing of EACH of these complications. This must be supported with relevant, evidence-based literature.
b) Identify THREE clinical cues (signs and symptoms) that would indicate deterioration (clinical deterioration) in Mae’s condition and provide a brief rationale for each. This must be supported with relevant, evidence-based literature.
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Mae Roberts has a complicated medical background, which sheds light on her current condition and outlook. It is clear from analysing the histology, ECG, and echocardiography results of her studies that Mae is experiencing significant heart difficulties, most likely as a result of her prior medical history.
To begin with, the pathology results show that there is an impaired renal function due to the high levels of urea and creatinine. Reduced renal perfusion—which is frequently observed in congestive heart failure—is frequently linked to elevated urea and creatinine levels.
Considering Mae's medical history of Rheumatic Heart Disease (RHD), these increased levels may be explained by a decrease in cardiac output, which in turn results in a reduction in renal blood flow.
Further highlighting the relationship between Mae's cardiac and renal manifestations is a research by Lo et al. (2019) that discovered cardiac anomalies, such as mitral stenosis, might exacerbate renal impairment.
An expansion of the left atria and significant mitral stenosis are shown on the echocardiography. The abnormal narrowing of the mitral valve, known as mitral stenosis, prevents blood from flowing from the left atrium into the left ventricle.
Mae's left atria have enlarged as a compensatory mechanism to the higher pressure gradient brought on by the stenosis. As a result of the atrial muscle fibres becoming overstretched and electrically unstable over time, this pressure overload can cause atrial fibrillation.
A major contributing element in this case is Mae's history of Acute Rheumatic Fever (ARF). A persistent inflammatory response that affects the heart valves, especially the mitral valve, can be brought on by ARF. This is in line with research by Pradhan et al. (2018), who found a significant association between ARF and the later onset of RHD, which can result in adult diseases such mitral stenosis.
This brings us to the ECG findings, which indicate atrial fibrillation (AF) with a heart rate of 115–125 beats per minute. An irregular and often fast heart rhythm, or AF, increases the risk of stroke and other heart-related problems. The left atrial enlargement noted earlier is directly related to Mae's presentation of AF.
The chaotic rhythm observed in atrial fibrillation (AF) is caused by erratic electrical activity from the strained atrial fibres. This arrhythmia can cause blood stasis in the left atrium, which raises the risk of clot formation and possible embolic events like stroke when paired with a stenotic mitral valve. The elevated heart rate aggravates Mae's dyspnea and tachycardia symptoms.
Mae has a dire outlook for her illness. When atrial fibrillation and severe mitral stenosis coexist, it may indicate a steadily declining heart condition. Mae may be more susceptible to heart failure, stroke, or other cardiac-related issues if she does not receive treatment.
Moreover, the renal dysfunction highlighted by the elevated urea and creatinine could progress, leading to further systemic complications. According to the Oliveira (2018), individuals with RHD-associated mitral stenosis and AF have a heightened risk of morbidity and mortality, emphasizing the urgency of appropriate medical intervention.
In conclusion, Mae Roberts' investigations paint a clear picture of a heart compromised by past infections and a lifetime of associated challenges. The echocardiogram and ECG results, in conjunction with her pathology, point towards a declining cardiac function with potential systemic repercussions.
Timely and comprehensive care is essential to manage and potentially reverse some of these changes, improving Mae's quality of life and long-term prognosis.
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Given Mae's presentation, the two most relevant focused systems assessments would be the Cardiovascular System (CVS) and Renal System.
Cardiovascular System (CVS): Mae's history of Rheumatic Heart Disease (RHD), recent diagnosis of mitral valve stenosis, atrial fibrillation, and her symptoms of tachycardia and dyspnoea highlight the urgent need for a thorough cardiovascular assessment.
Given the high prevalence of cardiac abnormalities in patients with a history of RHD, as supported by Watkins et al. (2018), a cardiovascular assessment is imperative to understand the extent and severity of Mae's cardiac issues.
Renal System: The elevated levels of urea and creatinine in Mae's pathology results indicate a compromised renal function. The close interplay between cardiac output and renal perfusion necessitates an in-depth renal assessment.
As underlined Kapoor and Bathon (2018), renal dysfunction can be a direct consequence of decreased cardiac output, commonly observed in congestive cardiac conditions.
Focusing on the Cardiovascular System assessment, two potential abnormal findings are:
Cardiac Murmurs: Given Mae's diagnosis of mitral valve stenosis, a murmur consistent with this condition might be detected on auscultation. This would typically be a diastolic rumble heard best at the apex.
Mitral stenosis results in turbulent blood flow across the narrowed mitral valve, producing this characteristic sound. Fahad et al. (2018) emphasise the correlation between valve abnormalities and the presence of murmurs.
Irregular Pulse: Mae's ECG confirmed atrial fibrillation, which would manifest clinically as an irregularly irregular pulse upon palpation. Atrial fibrillation disrupts the normal rhythmic contraction of the atria, leading to this irregular pulse. According to Duarte (2020), palpation of an irregular pulse is a primary clinical indicator of atrial fibrillation.
If Mae were to experience chest pain during her admission, the Numeric Rating Scale (NRS) would be an ideal pain assessment tool. Using a scale of 0 (no pain) to 10 (worst possible pain), the patient must rate their level of discomfort using this instrument.
The rationale behind the selection of NRS is its ease of use, effectiveness, and compatibility with adult patients, regardless of their cultural background.
Given Mae's history and any language or cultural hurdles, the NRS offers a simple, globally understandable way to measure pain intensity, as noted by Karcioglu et al. (2018). This makes it especially appropriate for Mae.
Digoxin: Patients with heart failure and atrial fibrillation are frequently administered this drug. It functions by enhancing cardiac output by lowering heart rate and strengthening heart contractions.
Digoxin would assist control Mae's heart rate, which would result in a more effective heart filling and pumping since she has atrial fibrillation. Digoxin has a strong literature base for treating atrial fibrillation and heart failure; Sethi et al. (2018) have confirmed Digoxin's effectiveness in treating both illnesses.
Carvedilol: A beta-blocker with extra alpha-blocking capabilities is called carvingilol. It is frequently used to treat hypertension and heart failure. The medication lowers heart rate, relaxes blood vessels, and lessens the burden on the heart.
Carvedilol would help Mae's heart function overall by reducing her hypertension and tachycardia. Toyoda et al. (2020) pointed out that its positive benefits on cardiac function and mortality reduction in heart failure patients are well-documented.
a) Complications
Heart Failure: Heart failure is one of the possible side effects of atrial fibrillation and mitral valve stenosis, both of which Mae has been diagnosed with. The heart finds it difficult to pump blood effectively in people with mitral stenosis because the left atrium and ventricle are blocked from receiving blood flow.
This can eventually cause the heart to weaken or stiffen, which can lead to cardiac failure. Furthermore, atrial fibrillation increases this risk by hindering the heart's capacity to pump blood efficiently due to irregular cardiac beats.
According to Akodad et al. (2019), there is a correlation between valve disorders such mitral stenosis and a higher risk of heart failure.
Stroke: Mae's condition, atrial fibrillation, raises the risk of stroke. Blood can pool in the heart as a result of abnormal cardiac beats, which can result in the production of clots.
If these clots are pumped out of the heart, they can travel to the brain and obstruct blood flow, resulting in a stroke. Mae's existing mitral stenosis further aggravates this risk, as stenosis can also contribute to blood stasis and clot formation.
The link between atrial fibrillation and an elevated stroke risk is well-established in the literature, with Choi et al. (2023) noting that atrial fibrillation multiplies the risk of stroke several-fold.
b) Clinical Cues Indicating Deterioration
Acute Dyspnoea and Orthopnoea: If Mae were to experience a sudden increase in breathlessness or finds it difficult to breathe when lying down, it could indicate a worsening of her cardiac function.
As heart failure progresses, fluid can accumulate in the lungs, leading to these symptoms. The association between acute dyspnoea, orthopnoea, and heart failure is underscored by Espinosa et al. (2023), who pinpoint these symptoms as classic indicators of decompensated heart failure.
Oedema: Swelling in the lower extremities, particularly the ankles and feet, can be a sign of Mae's deteriorating heart condition. As the heart's pumping efficacy diminishes, fluid can build up in the body's tissues, manifesting as oedema.
The presence of peripheral oedema as an indicator of worsening heart function is highlighted by Shoaib et al. (2019).
Decreased Urine Output: A reduction in urine output could indicate a further decline in Mae's cardiac function. As cardiac output drops, renal perfusion is compromised, leading to decreased renal function and urine production.
Zanoli et al. (2019) emphasize the interplay between reduced cardiac output and diminished renal function, underlining the importance of monitoring urine output in patients with cardiac abnormalities.
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Choi, S. E., Sagris, D., Hill, A., Lip, G. Y., & Abdul-Rahim, A. H. (2023). Atrial fibrillation and stroke. Expert review of cardiovascular therapy, 21(1), 35-56. https://www.tandfonline.com/doi/pdf/10.1080/14779072.2023.2160319
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