NR 507 Week 2: Discussion Part One
Chamberlain University NR 507 Week 2: Discussion Part One– Step-By-Step Guide
This guide will demonstrate how to complete the Chamberlain University NR 507 Week 2: Discussion Part One assignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.
How to Research and Prepare for NR 507 Week 2: Discussion Part One
Whether one passes or fails an academic assignment such as the Chamberlain University NR 507 Week 2: Discussion Part One depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.
After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.
How to Write the Introduction for NR 507 Week 2: Discussion Part One
The introduction for the Chamberlain University NR 507 Week 2: Discussion Part One is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.
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How to Write the Body for NR 507 Week 2: Discussion Part One
After the introduction, move into the main part of the NR 507 Week 2: Discussion Part One assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.
Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.
How to Write the Conclusion for NR 507 Week 2: Discussion Part One
After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.
How to Format the References List for NR 507 Week 2: Discussion Part One
The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.
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Sample Answer for NR 507 Week 2: Discussion Part One
What is the etiology of cystic fibrosis?
This topic is of great interest to me because of this subject that I will be doing my presentation on, so I did a detailed search. The peer review article revealed that according to Munder& Tummler (2015), cystic fibrosis lung disease result from impaired chloride and bicarbonate epithelial transport, defective mucociliary transport, and acidification of the airway-surface liquid. In many ways, the pathophysiological process differs according to the different evidenced-based practice. “The pathophysiology of cystic fibrosis is deduced from the loss or dysfunction of CFTR in the apical epithelial membrane” Stoltz, (2015). The contributing factor is an attenuated bacteria-killing capability has reported in monocytes and macrophages isolated from people with cystic fibrosis.
The response to the peer review is” We agree with Munder and Tümmler that abnormal function in myeloid cells (i.e., neutrophils, monocytes, or macrophages) may contribute to impaired host defense in cystic fibrosis.” Stoltz, 2015. The article contains other pertinent information to describe the depth of this disease. “Specific cell types involved (monocytes, neutrophils, or macrophages) and proposed mechanisms for defects (e.g., organelle acidification, complement-mediated phagocytosis, and intraphagosomal production of hypochlorous acid) vary substantially among studies.” Stoltz (2015).
Describe in detail the pathophysiological process of cystic fibrosis.
Cystic fibrosis is the abnormal secretions that obstruct the respiratory, digestive, and reproductive tract. According to (McCance et al., 2013) research shows that there may be additional CF-associated primary defects, such as a natural proinflammatory state and abnormal local immune defenses in the lungs. “Cystic fibrosis is also associated with cystic fibrosis transmembrane conductance regulator (CFTCR) gene mutation results in the abnormal expression of cystic fibrosis transmembrane conductance regulator (CFTCR) protein, which is a cyclic adenosine monophosphate (cAMP)–activated chloride channel present on the surface of many types of epithelial cells.” (McCance et al., 2013). These cells include the lining of the airways, bile ducts, the pancreas, sweat glands, and the vas deferens. Even though cystic fibrosis affects multisystem it ultimately most often affects the lung, which is the most critical site of involvement that leads to respiratory failure and death.
Identify hallmark signs identified from the physical exam and symptoms.
Cystic fibrosis often occurs primarily in the white population; it affects 1 in 29 whites in the united states. The symptoms typically start with the respiratory and digestive systems. Respiratory symptoms include a persistent cough or wheeze, sputum production, and recurrent or severe pneumonia, and chronic sinusitis and nasal polyps. “Persistence of infection incites chronic local inflammation, airway damage, bronchiectasis, microabscess formation, and foci of hemorrhagic pneumonia.
Describe the pathophysiology of complications of cystic fibrosis.
There is progressive damage to the typical architecture of the lung with a decline in pulmonary function.” (McCance et al., 2013. CF causes reduced hydration of airway mucus which results in increased adherence of mucus to the epithelium, making it easier for bacteria to stick to and increasing the chances of infection (McCance et al., 2013)
What teaching related to her diagnosis would you provide the parents?
Due to the severity of the disease, it will be overwhelming and devastating to the parents, as an advanced clinical nurse I will provide them with all the information and videos available. I would also refer them to join a group of parents with children of a similar diagnosis. Advising the patient to prevent infection, adequate nutrition, and an increase in caloric intake is the primary goal to maintain a healthy lifestyle. Lastly, I would provide them with my information for them to call with any further questions.
References:
Antje Munder, M.D. Burkhard Tümmler, M.D., Ph.D.
Hanover Medical School, Hannover, Germany (2015)
tuemmler.burkhard@mh-hannover.de
David A. Stoltz, M.D., Ph.D. David K. Meyerholz, D.V.M., Ph.D.
Michael J. Welsh, M.D.
University of Iowa Carver College of Medicine, Iowa City, IA (2015)
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby.
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Sample Peer Response Answer 2 for NR 507 Week 2: Discussion Part One
Your post on cystic fibrosis (CF) is very informative. Your post explains the etiology, pathophysiology, and symptoms of cystic fibrosis in detail. I think we should also look to studying EBP nursing care plans to better assist our patients diagnosed with cystic fibrosis. Living with cystic fibrosis comes with many medical, social, and financial challenges for patients, their caretakers, and family members. Having a productive and fulfilling life with cystic fibrosis is possible, as long as patients are educated about how to cope with the condition. The Cystic Fibrosis Foundation (2018) outlines four areas they would like CF patients to focus on so they can live a their best lives: daily life, treatments and therapies, transitions, and CF resources. The Adult Guide to Cystic Fibrosis is a resource that helps adults with CF manage their lives, as adults with CF outnumber children with the disease. This guide discusses and makes recommendations for basic lung care, menopause, having a social life, birth control, pregnancy, exercise, traveling, having a career, and more. FNPs should also study this guide in order to create individual care plans for their CF patients.
Griesenbach and Alton (2015) mention that several therapies have progressed including amongst novel antibiotics (inhaled tobramycin and macrolides) and novel mucolytics (dornase alpha–a recombinant DNase) and hypertonic saline that have been approved through clinical trials and offered as mainstream treatment. New CF drug developments have progressed to CFTR correctors to treat classes I-III mutations (Griesenbach and Alton, 2015). Our understanding of cystic fibrosis pathophysiology and genetics has expanded tremendously and has led to vast improvements for patients. Griesenbach and Alton (2015) note the recent licensing of ivacaftor, a drug targeting the molecular defect in the CFTR protein in approximately 5 percent of cystic fibrosis patients, is one of the current treatments making a difference in treatment efforts.
References:
Griesenbach, U., & Alton, E. W. F. W. (2015). Recent advances in understanding and managing cystic fibrosis transmembrane conductance regulator dysfunction. F1000Prime Reports, 7, 64. http://doi.org/10.12703/P7-64
National Cystic Fibrosis Foundation. (2018). Adult Guide to Cystic Fibrosis. Retrieved from
Sample Peer Response Answer 3 for NR 507 Week 2: Discussion Part One
I could not agree more we need to educate everyone involved in the patients life so the patient can have a better quality of life. Kids with CF need more calories than other kids in their age group. The number of additional calories they need will vary according to each child’s lung function, activity level, and illness. A child’s calorie needs might be even higher during an illness (even a low-grade infection can significantly increase the calories required). A CF dietitian can help you determine how many calories your child needs each day, and track growth and weight gain over time to provide a good nutrition plan. The daycare or schools should be aware that the patient may need more attention or special considerations. The may need to go to the restroom often (digestive problems from CF can cause diarrhea and flatulence). Take oral or inhaled medication at school. Need to eat in class. Cough frequently to clear mucus from the lungs (CF is not contagious). The patient could become tired in class due to early-morning breathing therapy or staying awake from coughing at night. Helping others understand the problems that can occur is vital.
Reference:
Katkin, J. (2017). Cystic fibrosis: Clinical manifestations and diagnosis. UpToDate. Retrieved from https://www.uptodate.com/contents/cystic-fibrosis-clinical-manifestations-and-diagnosis?source=search_result&search=cystic fibrosis&selectedTitle=1~150 (Links to an external site.)
Sample Peer Response Answer 4 for NR 507 Week 2: Discussion Part One
Reduced left ventricular pericardial effusion of 40% is a hallmark of systolic heart failure. This happens whenever the left ventricle cannot efficiently produce cardiac function to systemic pestle tissues sufficiently. Systolic heart failure is defined as having a heart that does not produce enough cardiac output to project vital organs adequately and has a lower ejection fraction. The left ventricular dilatation prevents the heart from pumping as much plasma as the body requires. This disorder is mainly brought on by previous myocardial injury and coronary artery diseases. The overall amount of blood expelled first from the ventricles is known as cardiac output, and it is influenced by the client’s stroke volume and pulse rate. Load capacity, volume overload, and ventricular dispensability all affect stroke volume. Contraction may be impacted whenever myocyte function is disturbed, like inflammatory conditions, cardiomyopathies, and myocardial ischemia. These inflammatory and immunological reactions culminate in ventricle simulation, which exacerbates contractility dysfunction. As contractility declines, left ventricular (LV) and left atrial (LA) preloads rise, increasing the intravascular volume that is ultimately driven into the pulmonary regions (Yancy et al., 2017). The cause of more significant breathlessness or dyspnea whenever a client exerts is an elevation in liquid in the pulmonary cells and a rise in heart rate. Whenever the client is lying down, the more significant pulmonary vascular obstruction may also cause orthopnea because the abdomen’s fluids push against the diaphragm, lowering the efficiency of the upper respiratory system. On the contrary, systolic heart damage can occur alone or in conjunction with diastolic dysfunction with maintained EF.
- Differentiate between systolic and diastolic heart failure.
Systolic heart failure is defined as having a lower evacuation component and not having the requisite heart rate to perfuse critical organs. The left ventricular dilatation prevents the heart from pumping as much blood as the body requires. This disorder is primarily brought on by previous myocardial injury and coronary heart disease (Yancy et al., 2017). After such a MI, the body’s non-infarcted region must adapt to the client’s price increases, which results in the reorganization of the cardiovascular system and adjustments to the organization and functionality of cardiomyocytes. The restructuring in the heart decreases the efficiency of the spasms, resulting in a reduction in cardiac function and an elevation in left ventricular pressure. On the contrary, systolic heart insufficiency may occur alone or with diastolic dysfunction with maintained EF (Shono et al., 2019). The chamber’s capacity is reduced because of the body’s inadequate ventricle emptying. Without considerable opposition and a rise in wall preservation, the inadequately lusitropic ventricle cannot absorb fullness with blood. Blood clots bring on atrial enlargement and atrial arrhythmias in the right atrium.
- State whether the patient is in systolic or diastolic heart failure.
Difficulty breathing, leg edema, sleep on several pillows, inability to work out owing to breathing difficulties, creaks on both sides, and JVD are indications of systolic heart failure. A predisposition heightened the client’s likelihood of heart problems to diabetes and hypertension. Ischemic cardiovascular disease, valve malfunction, and unexplained dilated cardiomyopathy are all linked to congestive cardiac failure.
- Explain the pathophysiology associated with the following symptoms: dyspnea on exertion, pitting edema, jugular vein distention, and orthopnea.
Jugular vein distention may be caused by excessive blood volume that could happen with cardiac arrest or other factors that prevent the right atrium from emptying or the blood from flowing into the right ventricle. Additionally, pitting edema in the lower limbs and orthopnea due to reduced cardiac function from the absence of pounding out of blood delivered from the lungs arise from the right ventricle of the heart becoming dysfunctional and fluid beginning to pool in the toes (Shono et al., 2019).
Dyspnea: DYSPNEA: In individuals with systolic heart disease, dyspnea results from pulmonary obstruction due to decreased cardiac features and increased pulmonary venous flow brought on by left ventricular malfunction (McCance & Huether, 2019). Breathing difficulties and the necessity to support oneself on pillows result from the circulatory blood shifting from the lower portion of the body to the airways when the client is sleeping.
Pitting edema: It is brought on by the stimulation of many body’s immune and neurohumoral pathways that encourage the kidneys’ reuptake of salt and water and the increase of interstitial environment (Shono et al., 2019). These support fluid impact conditions and the development of edema when combined with aberrant Starling pressures like high venous capillarity and reduced plasma oncotic tension.
Jugular vein distention: This indicates that the vena cava and central veins carry more blood than usual.
Orthopnea: When someone is resting flat, the strain in their lung vessels rises, which is when it occurs. When a person has HF or heart failure, their heart cannot allow blood to flow out from their body, which increases tension in the capillaries and pulmonary veins and causes blood to seep into their lungs, leading to orthopnea.
- Explain the significance of the presence of a 3rd heart sound and ejection fraction of 25%.
The third heartbeat indicates excessive background noise. It is associated with ventricular insufficiency. As with such a systolic heart failure client, the left ventricle enlarges because it cannot pump blood with sufficient power. A pericardial effusion of 25% means that every moment the client’s heart beats, 25% of his plasma is pumped out of the left ventricle, indicating that perhaps the heart is not functioning correctly. So, the body receives less oxygen from the blood (McCance & Huether, 2019).
Conclusion
Generally, Left ventricular insufficiency with intact ejection percentage is known as systolic heart failure. This heart insufficiency is defined by myocytes’ diminished capacity to transport calcium out of the cytoplasm, which impairs the ventricle’s stress relief capabilities. Due to stiffness and wall strain, the ventricle finds it challenging to absorb blood flow. Consequently, the left atrial pressure rises, which might cause respiratory failure and dyspnea when you strain yourself. If left-sided heart insufficiency is not addressed, the right side will also be impacted. Because of the undesirable reversal of intracardiac tissue perfusion, jugular vein distention is defined by venous return obstruction.
References
McCance, K.L. & Huether, S.E. (2019). Pathophysiology: The biologic basis for disease in
adults and children (8th ed.). Elsevier Health Sciences.
Shono, A., Mori, S., Yatomi, A., Kamio, T., Sakai, J., Soga, F., Tanaka, H., & Hirata, K. (2019).
Ultimate Third Heart Sound. Internal Medicine (Tokyo, 1992), 58(17), 2535–2538 https://doi.org/10.2169/internalmedicine.2731-19
Yancy, M., Jessup, M., Bozkurt, B., et al. (2017). 2017 ACC/AHA/HFSA focused update of the
2013 ACCF/AHA guideline for the management of heart failure: A report of the American College of Cardiology/American Heart Assocation Task Force on Clinical Practice Guidelines and the Heart Failure Society of America, Circulation, 136, e137-e161. https://doi.org/10.1161/CIR.0000000000000509Links to an external site.
Sample Peer Response Answer 4 for NR 507 Week 2: Discussion Part One
The thyroid gland regulates a wide range of physiological activities such as growth, metabolism, homeostasis, and cell proliferation and differentiation through the secretion of thyroid hormones. Thyroid diseases are among the most common endocrine disorders (Rafieian-Kopaei, M., Alizadeh, M., Safarzadeh, A., Bahmani, M., Beyranvand, F., Mohammadi, M., Azarbaijani, K., & Abbaszadeh, S., 2018). It can contribute to heart failure in various ways. Hypothyroidism is when the thyroid gland fails to sufficient thyroid hormone. The reduced levels also lead to various cardiovascular effects such as bradycardia, decreased cardiac contractility and increased systemic vascular resistance. When the heart starts struggling to pump blood the person begins to have symptoms of shortness of breath, fatigue, and fluid retention all of which are characteristics of heart failure. In hyperthyroidism the thyroid gland is producing an excessive amount of thyroid hormone. Excessive thyroid hormone levels can lead to increased cardiac output, left ventricular hypertrophy and eventually heart failure. In hyperthyroidism the increased level of T3 and T4 lead to high metabolic activity causing an increased heart rate and enhanced contractility. Over time the continuous strain on the heart can lead to detrimental effects because persistant cardiac output can induce arrythmias, cause dilated cardiomyopathy and eventually heart failure (Gluvic, Z. M., Zafirovic, S. S., Obradovic, M. M., Sudar-Milovanovic, E. M., Rizzo, M., & Isenovic, E. R., 2022). Thyroid hormones influence the vascular system greatly by affecting blood pressure, heart rate and circulation. The cardiovascular system is one of the main targets of thyroid hormones. Physiological levels of TH are necessary to maintain the normal function of the heart (Gluvic, Z. M., Zafirovic, S. S., Obradovic, M. M., Sudar-Milovanovic, E. M., Rizzo, M., & Isenovic, E. R., 2022). Therefore the intricate interplay between thyroid function and the cardiovascular system highlights the importance of managing thyroid disorders to prevent future cardiac complications.
References
Gluvic, Z. M., Zafirovic, S. S., Obradovic, M. M., Sudar-Milovanovic, E. M., Rizzo, M., & Isenovic, E. R. (2022). Hypothyroidism and risk of cardiovascular disease. Current Pharmaceutical Design, 28(25), 2065-2072. https://doi.org/10.2174/1381612828666220620160516Links to an external site.
Rafieian-Kopaei, M., Alizadeh, M., Safarzadeh, A., Bahmani, M., Beyranvand, F., Mohammadi, M., Azarbaijani, K., & Abbaszadeh, S. (2018). Brucellosis: Pathophysiology and new promising treatments with medicinal plants and natural antioxidants. Asian Pacific Journal of Tropical Medicine, 11(11), 597. https://doi.org/10.4103/1995-7645.246336Links to an external site.
Week 3: Discussion Part Two
- What is the etiology of congestive heart failure?
Heart failure is a chronic disease where the left ventricle, the right ventricle, or both, are unable to squeeze effectively, be it from enlarged ventricles or myocardial hypertrophy or compromised cardiac output. If the left ventricle is unable to pump blood through the aorta to the body efficiently, a decrease in oxygenated blood to the body is present and blood back up into the lungs. If the right ventricle is not pumping efficiently, a decrease in blood to the lungs is present and there is a backup of blood into the right atrium and body. Risk factors for heart failure include any disease process that can reduce heart contracture or alter ventricle filling, such as hypertension, coronary heart disease, diabetes mellitus, stenosis, regurgitation, cardiomyopathies, and arrhythmias (Rogers & Bush, 2015). Even though this is a disease that can be caught early and managed well, its prevalence is a serious public health concern and accounts for countless hospitalizations each year (Marques de Sousa, dos Santos Oliveira, Oliveira Soares, Amorim de Araújo, & dos Santos Oliveira, 2017).
- Describe in detail the pathophysiological process of congestive heart failure.
In general, the pathophysiologic mechanisms of CHF in infants and children are very similar to those in adults. The same compensatory mechanisms are activated in the face of inadequate cardiac output. An acute decrease in blood pressure stimulates stretch receptors and baroreceptors in the aorta and carotid arteries, which in turn stimulate the sympathetic nervous system. With the release of catecholamines and the stimulation of β receptors, heart rate and the force of myocardial contraction increase (McCance et al., 2013). Venous smooth muscle tone also increases, which increases the return of venous blood to the heart. Sympathetic stimulation also decreases blood flow to the kidneys, skin, spleen, and extremities so that maximum flow to the brain, heart, and lungs can be maintained. Decreased blood flow to the kidneys causes the release of renin, angiotensin, and aldosterone. If chronic, this cycle results in retention of sodium and fluid by the kidneys, which in turn increases volume in the circulatory system (McCance et al., 2013). These neurohumoral and hemodynamic changes create abnormal ventricular wall stress and cause the myocardium to hypertrophy. The myocardial fibers also stretch to accommodate the increased volume. Hypertrophy and fiber stretch temporarily increase contractility and hence the force of ventricular contraction. These mechanisms eventually fail to maintain cardiac output as CHF progresses.
- Identify hallmark signs identified from the physical exam, diagnostic lab work, and symptoms.
57-year-old with dyspnea on exertion, fatigue, frequent dyspepsia, nausea, occasional epigastric pain, trouble breathing at night especially while lying on back, vital signs of 180/110 blood pressure. After a thorough assessment, to diagnosis heart failure and rule out other disease processes, such as valvular dysfunctions, a chest x-ray, and echocardiogram (Echo) would be ordered. A chest x-ray will reveal if the heart is enlarged and if there is any fluid in the lungs. An echo will measure the heart’s ability to pump, therefore conveying the EF. A serum BNP should be obtained to assess the severity of the disease (McCance et al., 2013). BNP is secreted via the ventricles when pressures within the ventricles change, the higher the serum level, the more severe the disease progression (McCance et al., 2013).
- Describe the pathophysiology of complications of congestive heart failure.
When heart failure occurs, they heart may not be strong enough to pump out as much blood as the body needs. As it tries to move more blood, the heart gets larger. It also pumps faster, and the blood vessels narrow to get more blood out to the body. As the heart works harder, it becomes weaker, and the damage increases. The body gets less oxygen, and the symptoms such as shortness of breath, swelling in the legs, and fluid buildup are present. In a normal heart, the upper chambers (called the atria) and lower chambers (the ventricles) squeeze and relax in turn to move blood through the body. If the ticker is weak, these chambers might not squeeze at the right time. The heart might beat too slowly, too quickly, or in an irregular pattern. When the rhythm is off, the heart can’t pump enough blood out to one body. Atrial fibrillation (AFib) is one type of abnormal heart rhythm that heart failure can cause. It causes the heart to quiver and skips instead of beating. An irregular heartbeat can lead to clots and cause a stroke. Also as the heart damage gets worse, the heart has to work harder to pump out blood, and it gets bigger and can damage the valves. Just like your other organs, they need a steady supply of blood to work as they should. Without the amount of blood, they need, they won’t be able to remove enough wastes from your blood. This is called kidney failure. Damaged kidneys can’t remove as much water from the blood as healthy ones. Consequently, the body will start to hold onto fluid, cause high blood pressure and make the heart work even harder.
- What teaching would you provide this patient to avoid heart failure symptoms?
To help prevent recurrence of heart failure symptoms in patients I would stress the importance of home control and monitoring of daily weight. Patients must be instructed to check their weight in the morning after urinating and before breakfast, wearing light clothes and using the same scale. An increase of 1.3 kg or more in body weight in two days, or of 1.3 – 2.2 kg in one week may be an indication of fluid retention (Roger & Bush, 2015). I would also educate on the use of their medication and diet. It is import to teach patients that they must always take their medication, even when they feel well in order to obtain efficient treatment. Also, fluid restrictions and managing salt intake would be highlighted. Most importantly, self-care education, including the control of non-pharmacological measures, would be part of the daily management, reinforcement, improvement, and evaluation of self-care abilities.
References:
Marques de Sousa, M., dos Santos Oliveira, J., Oliveira Soares, M.G., Amorim de Araújo, A., & dos Santos Oliveira, S.H. (2017). Quality of life of patients with heart failure: Integrative review. Journal of Nursing UFPE/Revista De Enfermagem UFPE, 11(3), 1289-1287. doi: 10.5205/reuol.10544-93905-1-RV.1103201720
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby.
McMurray, J. J., Gerstein, H. C., Holman, R. R., & Pfeffer, M. A. (2013). Heart failure: a cardiovascular outcome in diabetes that can no longer be ignored. The Lancet Diabetes & Endocrinology, 2(10), 843-851.
Rogers, C. & Bush, N. (2015). Heart failure: Pathophysiology, diagnosis, medical treatment guidelines, and nursing management. Nursing Clinics of North America, 50(4), 787-799.