NR 507 Week 3: Case Study
Chamberlain University NR 507 Week 3: Case Study– Step-By-Step Guide
This guide will demonstrate how to complete the Chamberlain University NR 507 Week 3: Case Study 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 3: Case Study
Whether one passes or fails an academic assignment such as the Chamberlain University NR 507 Week 3: Case Study 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 3: Case Study
The introduction for the Chamberlain University NR 507 Week 3: Case Study 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.
Need a high-quality paper urgently?
We can deliver within hours.
How to Write the Body for NR 507 Week 3: Case Study
After the introduction, move into the main part of the NR 507 Week 3: Case Study 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 3: Case Study
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 3: Case Study
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.
Stuck? Let Us Help You
Completing assignments can sometimes be overwhelming, especially with the multitude of academic and personal responsibilities you may have. If you find yourself stuck or unsure at any point in the process, don’t hesitate to reach out for professional assistance. Our assignment writing services are designed to help you achieve your academic goals with ease.
Our team of experienced writers is well-versed in academic writing and familiar with the specific requirements of the NR 507 Week 3: Case Study assignment. We can provide you with personalized support, ensuring your assignment is well-researched, properly formatted, and thoroughly edited. Get a feel of the quality we guarantee – ORDER NOW.
Sample Answer for NR 507 Week 3: Case Study
Pathophysiology and Clinical Findings
Question One
The spirometry results for the patient in NR 507 Week 3: Case Study 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.
ALSO READ:
NR 507 Week 4: Alterations in Renal and Urinary
NR 507 Week 4: Open Forum Discussion
NR 507 Week 5: Discussion Part One
NR 507 Week 6: Recorded Disease Process Presentation Peer Review
NR 507 Week 7: Reflection Assignment
NR 507 Week 8: Genomes, Genetic Alterations, and Reproductive Disorders
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.
NR 507 Week 3: Case Study: 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.
NR 507 Week 3: Case Study 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
Sample Answer 2 for 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
Week 3: Discussion Part Two
In addition to the textbook, utilize at least one peer-reviewed, evidence-based resource to develop your post.
- 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.