NR 507 Week 2: Discussion
Chamberlain University NR 507 Week 2: Discussion– Step-By-Step Guide
This guide will demonstrate how to complete the Chamberlain University NR 507 Week 2: Discussion 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
Whether one passes or fails an academic assignment such as the Chamberlain University NR 507 Week 2: Discussion 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
The introduction for the Chamberlain University NR 507 Week 2: Discussion 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
After the introduction, move into the main part of the NR 507 Week 2: Discussion 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
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
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
To differentiate between systolic and diastolic heart failure we need to understand the left ejection fraction (LVEF) as well as other terms such as stroke volume, cardiac output and end diastolic volume. Stroke volume is the the volume pushed out of the ventricles per beat (Bruss & Raja, 2022). For a 70kg male the normal stroke volume is 70ml/beat. Next we have the total volume of blood in heart during the relaxation phase or diastole which is referred to as the end diastolic volume (EDV). For the same 70kg male this is roughly 120ml. Next we have the end systolic volume which is the leftover blood volume in ventricles after contraction (ESV). On average this is around 50 ml. From this we can calculate our stroke volume which is the EDV minus the ESV which again equals 70ml/beat. Another term is cardiac output (CO) which represents the blood volume pumped out by the heart over one minute (Bruss & Raja, 2022). The CO is calculated by multiplying the stroke volume and the heart rate. Therefore the stroke volume equals the cardiac output divided by the heart rate. In our case we have an elevated heart rate of 110. This puts downward pressure the stroke volume. The left ejection fraction is calculated by dividing the stroke volume by the end diastolic volume. The LVEF is given as 25%.
In practice the LVEF can be calculated by utilizing an Echocardiogram (Oppedisano et al., 2021). The LVEF can be greatly affected by the stroke volume as listed above. As Oppedisano et al. noted, stroke volume is affected by the force of heart contraction (contractility), the pressure from blood volume during diastole (preload), and pressure in myocardium during heart contraction (after load) (2021). Stroke volume and therefore LVEF can be increased by elevated preload, contractility, and decreased after load. With heart failure, the amount of blood pumped out of the heart may be diminished (Oppedisano et al., 2021) like with dilated cardiomyopathy and valvular diseases. These lower the contractility of the heart and lower the stroke volume. This leads to diminished left ventricular ejection fraction below 40% consistent with systolic heart failure. Our case with LVEF of 25% is consistent with systolic heart failure. For comparison diastolic heart failure is seen with LVEF greater than 50%. The third heart sound is another verification of left ventricular dysfunction and left ventricular ejection fraction less than 50% (Calo et al., 2020).
Some of the symptoms of heart failure are related to the pathophysiology of heart failure as listed above. Jugular vein distention accompanies increased preload or specifically pressure in the superior vena cava (Nagueh,2021). As indicated in this article, dyspnea and orthopnea can reflect pulmonary hypertension from left atrial pressure increases. Crackles in bilateral bases reflect pulmonary congestion again from left atrial pressure. The article also noted that with a weak heart contraction, fluid may accumulate in the lower extremities leading to pitting edema. An elevated preload can also contribute to the fluid moving out of the peripheral dependent vasculature.
References:
Brass, Z., & Raja, A. (2022). Physiology, stroke volume. StatPearls Publishing, https:// http://www.ncbi.nim.nih.gov/books/NBK547686
Calo, L., Capucci, A., Santini, L., Pecora, D., Favale, S., Petracci, B., Molon, G. Bianchi, V., Cipolletta, L., deRuvo, E., Ammirati, F., Grecia, C., Campari, M., Valsecchi, S & D’Ononfrio, A. (2020). ICD+ measured heart sounds and their correlation with echocardiographic indexes of systolic and diastolic function. Journal of International Cardiac Electrophysiology, 58(1), 95 – 101. DOI: 10.1007/s10840-019-00668-y
Nagueh, S. (2021). Heart failure with preserved ejection fraction: insights into diagnosis and pathophysiology. European Society of Cardiology, 117(4), 999 – 1014. DOI: 10.1093/cvr/ cvaa228
Oppedisano, F., Mollie, R., Tavernese, A., Gliozzi, M., Musolino, V., Macri, R., Carres, C., Maiuolo, J., Serra, M., Cardomone, A., Voterai, M. & Mollace, V. (2021). PUFA supplementation and heart failure: effects on fibrosis and cardiac remodeling. Nutrients, 13(9), 2965. Https://doi.org/10.3390/nu13092965
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Sample Answer 2 for NR 507 Week 2: Discussion
Great job on this post. Differentiating systolic and diastolic heart failure involves different strategies in practice and while learning. The first step is understanding the left ejection fraction and other details. The details may include the stroke volume, which entails the volume pushed out of the ventricles per beat. Depending on the gender, the stroke volume is different. A normal stroke volume for the male is 70ml per beat. The following detail is the end-diastolic volume that involves the total blood volume while the heart is in its relaxation phase. A normal EDV for a male is roughly 120ml per beat. The end-systolic volume is the last detail used in the calculation. It involves the leftover blood volume in the ventricles after contraction. On average, a male has 50 ml per beat. Getting the details, the stroke volume is easily calculated by subtracting the ESV from the EDV. The cardiac output is another essential detail that will be calculated by multiplying the stroke volume by the heart rate.
Recording the above details, the left ejection fraction will be calculated by dividing the stroke volume and the end-diastolic volume. Since the details are different in practice, the LVEF will be calculated differently through an Echocardiogram (McCance & Huether, 2019). Through the above details, I agree that the LVEF will be greatly affected by the stroke volume. To increase the stroke volume and the LVEF, the preload and contractility will be elevated then the afterload is decreased. Considering a case of heart failure, the amount of blood pumped out of the heart may be diminished just as it happens when a patient suffers from valvular diseases and dilated cardiomyopathy. Therefore, leading to decreased contractility of the heart and stroke volume. The left ventricular ejection fraction will decrease below 40 percent, consistent with systolic heart failure.
References
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier.
Sample Answer 3 for NR 507 Week 2: Discussion
Thank you for sharing about this patient with systolic heart failure. Per a retrospective cohort study, both systolic and diastolic heart failure were inadequately cared for as evidence by nearly one in five patients with systolic heart failure and one in four patients with diastolic heart failure received zero prescriptions one year post diagnosis (Nguyen et al., 2020). Both these types of heart failure center around the extent of left ventricular ejection fraction. The subjective symptoms are similar in both types. As you indicated the ejection fraction is diminished in systolic heart failure (<40%). In addition to difference in medication compliance listed above the article noted that the comorbidity profile was different between systolic and diastolic heart failure. A higher number of systolic heart failure patients suffered with coronary heart disease and myocardial infarction while dislipidemia, hypertension, diabetes, and chronic kidney failure were more commonly seen with diastolic heart failure (Nguyen et al., 2020). The article concluded that hospital rates were higher with diastolic heart failure. Other factors that increased hospital admission for heart failure were being female and being over age 75. The article noted that administration of medications prior to heart failure diagnosis, for conditions such as hypertension reduced hospitalization rates due to heart failure.
Reference:
Nguyen, C., Zhang, X., Evers, T., Willey, V., Tan, H & Power, T. (2020). Real-world treatment patterns, healthcare resource utilization, and costs for patients with newly diagnosed systolic versus diastolic heart failure. American Health & Drug Benefits, 13(4), 166- 174. PMID: 33343816 PMC 7737726
Sample Answer 4 for NR 507 Week 2: Discussion
Thank you for your detailed post on systolic and diastolic heart failure. You provided an accurate explanation of the symptoms associated with each type of heart failure and their pathophysiology, as well as the significance of a 3rd heart sound and an ejection fraction of 25%. Your explanation of the 3rd heart sound was particularly informative. It is important to note that the presence of a 3rd heart sound has the potential to signify a more serious cardiovascular condition. It is also important to remember that the 3rd heart sound is a symptom of various conditions, and it is important to look at the patient’s history and perform tests and examinations to accurately diagnose the cause. In addition, you provided a clear explanation of the symptoms associated with systolic and diastolic heart failure. It is important to remember that the symptoms of each type of heart failure can be different, and it is important to recognize the signs and understand the underlying pathophysiology in order to provide the patient with the proper treatment.
It is also important to understand the potential treatments for systolic and diastolic heart failure. Treatment for systolic heart failure may involve medications such as ACE inhibitors, beta-blockers, and diuretics, as well as lifestyle changes such as exercise and dietary modifications (Tan & Thakur, 2022). Treatment for diastolic heart failure may involve medications such as calcium-channel blockers and nitrates, as well as lifestyle changes such as exercise and dietary modifications (Tan & Thakur, 2022). Additionally, some patients may require more advanced treatments such as surgery or implantable devices. It is important to discuss all available treatment options with the patient and their doctor in order to provide the best care and outcome. Thank you for your informative post!
References
Tan, J. L., & Thakur, K. (2022, August 8). Systolic hypertension – statpearls – NCBI bookshelf. Retrieved January 21, 2023, from https://www.ncbi.nlm.nih.gov/books/NBK482472/Links to an external site.
NR 507 Week 3 Case Study
Pathophysiology and Clinical Findings
Question One
The patient’s spirometry results are consistent with obstructive pulmonary disease, as evidenced by the low forced expiratory volume in 1 second that ranges typically above 80%. The COPD diagnosis was considered since patient A.C. has presented with complaints of dry cough in the morning, dyspnea, sputum production, and history of exposure to tobacco smoke. However, the forced spirometry will demonstrate the presence of non-fully reversible airflow limitation using post-bronchodilator FEV1/FVC < 0.70 is compulsory to confirm the COPD diagnosis. A.C most likely pulmonary diagnosis is COPD based on the spirometry findings. The predicted results revealed that the Absolute FEV1/FVC ratio was 81%. Following the test, the pre-bronchodilator and post-bronchodilator predictions were 69% and 64%, which are less than 70% of the predicted value.
Question Two
Chronic obstructive pulmonary disease is a heterogeneous condition characterized by a wide range of chronic respiratory symptoms, which can be linked to airway abnormalities and alveoli that can cause persistent and airflow obstruction (Venkatesan, 2023). Emphysema can be characterized by the destruction of alveoli walls owing to the imbalance of proteinase–antiproteinase enzymatic activities (Leap et al., 2021). In healthy lung tissues, the protective antiproteinase counteracts the protein-degrading enzymes secreted by white blood cells. Under rare circumstances, a genetic condition, alpha-1 antitrypsin deficiency, could play a function in causing COPD. Persons living with the condition tend to have low alpha-1 antitrypsin, a protein produced in the liver. Chronic inflammation can be caused by chronic exposure to lung irritants, or long-term cigarette smoking recurrently recruits white blood cells into the alveoli (Dunphy et al., 2023). The burning of cigarettes produces a mixture of gases and chemicals that reach the alveoli and peripheral airways, where particles can easily collide with the surfaces and cause damage (Higham, et al., 2019). Counter to the atopic asthma processes, the COPD lymphocytic infiltration constitutes mainly of CD8+ T cells instead of CD4+ T-helper cells. Neutrophils and monocyte-/macrophage-derived proteins progressively destroy the alveolar walls and overcomes anti-proteinase defenses resulting in overdistended, hyperinflated, and weak elastic alveoli. As a result, there is air trapping, an increase in residual lung volume, low expiratory flow, and carbon dioxide retention.
Persons may experience hypercapnia but maintain adequate oxygenation in the early stages of the disease process. The desensitization of the central respiratory receptors to PCO2 occurs with long-term hypercapnia leading to the loss of normal respiratory stimulus to breathe independently and reliance on low oxygen levels to activate breathing. Chronic bronchitis is the more common pathological mechanism involved in COPD. Airflow obstruction is caused by bronchiole edema, mucus-producing goblet cell hyperplasia, and bronchiole smooth muscle hypertrophy (Dunphy et al., 2023). Chronic bronchitis is presented as long-term coughing or recurrent sputum production. Persons with cyanosis and hypoxia develop problems with ventilatory obstruction and suboptimal blood oxygen. Whereas, in chronic bronchitis, long-term hypoxia can lead to pulmonary vasoconstriction and pulmonary hypertension. The increased pulmonary resistance against the right ventricle leads to pulmonale or right ventricular failure. Chronic hypoxia stimulates renal erythropoietin that triggers and prolongs red blood cell synthesis in the bone marrow, increasing hemoglobin concentration and hematocrit. Acute exacerbations of chronic bronchitis are characteristic of COPD evidenced by Increased purulent sputum and worsened shortness of breath.
Question Three
The patient has presented with chief complaints of fatigue and increasing dyspnea on exertion for the last three months, but he did not seek medical help. In addition, he has been experiencing Dry, nonproductive cough in the morning. The patient has smoking history of 35 years. However, he has considerably reduced to one cigarette daily after the initiation of cardiac intervention.
Question Four
The chest ray exam has indicated signs of hyperinflation as both lungs are hyper-inflated and flattening of the diaphragm. The second objective finding is the presence of bilateral wheezing where there is forced exhalation and prolonging of expiratory phase. The vital signs reveal that respiratory rate and oxygen saturation is 22 and 93%. The patient has a history of cardiology consultation, rehabilitation, and successful angioplasty. Finally, the spirometry results reveal pre-bronchodilator and post-bronchodilator predictions for the FEV1/FVC ratio were 69% and 64%, which are less than 70% of the predicted value.
Management of COPD
Question One
The spirometric cut points have been proposed for simplicity in Table 2.5 of the GOLD standards. The spirometry results reveal that pre-bronchodilator and post-bronchodilator predictions for the FEV1 were 64% and 64%. The current classification is stage 2 moderate as stated in the GOLD criteria, where the FEV1 values are greater than 50 percent and lower than 80 percent (Global Initiative for Chronic Obstructive Lung Disease, 2023). After analyzing the patient CA’s well-managed symptoms, spirometry results, and assessment that reveals pulmonary decline is minimized, he can be considered stable.
Question Two
Pharmacological therapy is used to lessen symptoms, severity, and frequency of exacerbations and improve health status. The medication classes used to treat COPD are shown in Table 3.3. The choice in each medication class depends on the availability, cost, and clinical responses balanced against side effects. The clinician should individualize the treatment regimen since the relationship between symptom severity, airflow obstruction, and exacerbations differ between patients. The recommended medication classes are bronchodilators and antimuscarinic drugs. Examples of short-acting beta-agonists are Albuterol and long-acting beta-agonists are Formoterol. Examples of short-acting antimuscarinics, ipratropium and long-acting muscarinic antagonists are tiotropium and aclidinium.
Question Three
The available empirical data suggests that numerous pharmacological treatment options can reduce the mortality. The inhaled bronchodilators will be used to increase the FEV1 values and alter the other variables in the spirometric tests. The mechanism of action is alteration of the airway’s smooth muscle tone as well as improvements in expiratory flows, which can be reflected in the airways widening as opposed to changes in lungs elastic recoil. In addition, the bronchodilators can also lessen dynamic hyperinflation presented during resting periods and exercise and improvement in performance (Global Initiative for Chronic Obstructive Lung Disease, 2023). Specifically, the principal mechanism action of the beta2-agonist drugs is the relaxation of airways’ smooth muscles by the stimulation of beta2-adrenergic receptors to boost cyclic AMP and generate functional antagonism and bronchoconstriction. The short-acting beta2-agonists improve FEV1, and symptoms and effects usually wear off within four to six hours, while long-acting beta2-agonists improve FEV1, lung volumes, dyspnea, exacerbation rates, no hospitalizations, and health status. Secondly, the antimuscarinic medication class aids in blocking the bronchoconstrictor acetylcholine effect on the M3 muscarinic receptors within the airway smooth muscles. The short-acting antimuscarinic drugs block the inhibitory neuronal receptors M2 that trigger vagal- induced bronchoconstriction. At the same time, the long-acting muscarinic antagonists bind to M3 muscarinic receptors, which has faster dissociation from M2 muscarinic receptors, which prolongs the duration of bronchodilator effects.
Question Four
The available empirical data suggests that numerous non-pharmacological treatment options can reduce the mortality. The recommended non-pharmacological therapies for patient AC is smoking cessation and pulmonary rehabilitation. First, smoking cessation is considered the single most effective non-pharmacological treatment option to reduce the progression of COPD. The Lung Health Study conducted a randomized clinical trial including asymptomatic or mildly symptomatic COPD patients who were treated with a ten-week smoking cessation program and followed up for 14.50 years, where there was a reduction in overall mortality rate in the smoking cessation intervention group than regular care group (Global Initiative for Chronic Obstructive Lung Disease, 2023). Hence, the patient should be asked about the progress in all visits. Secondly, pulmonary rehabilitation is comprehensive intervention, which is based on thorough assessment followed by the delivery of patient-tailored therapies including exercise training, patient education, self-management interventions aiming at behavior changes. The program is designed to improve the psychological and physical condition of people and promote the long-term adherence to health-enhancing behaviors. The core components of the pulmonary rehabilitation will improve exercise capacity, prevent symptoms, and increase quality of life. Finally, participation in an outpatient pulmonary rehabilitation program will assist in improving the shortness of breath and overall health status.
References
Dunphy L. M. H. Winland-Brown J. E. Porter B. O. & Thomas D. J. (2023). Primary care: The art and science of advanced practice nursing – an interprofessional approach. F.A. Davis Company.
Global Initiative for Chronic Obstructive Lung Disease, Inc. (2023). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. https://goldcopd.org/wp-content/uploads/2023/01/GOLD-2023-ver-1.2-7Jan2023_WMV.pdf
Higham, A., Quinn, A. M., Cançado, J. E. D., & Singh, D. (2019). The pathology of small airways disease in COPD: historical aspects and future directions. Respiratory research, 20(1), 1-11. https://doi.org/10.1186/s12931-019-1017-y
Leap, J., Arshad, O., Cheema, T., & Balaan, M. (2021). Pathophysiology of COPD. Critical Care Nursing Quarterly, 44(1), 2-8. https://doi.org/10.1097/CNQ.0000000000000334
Venkatesan, P. (2023). GOLD COPD report: 2023 update. The Lancet Respiratory Medicine, 11(1), 18 https://doi.org/10.1016/S2213-2600(22)00494-5