NR 507 Week 3: Discussion Part Two
Chamberlain University NR 507 Week 3: Discussion Part Two– Step-By-Step Guide
This guide will demonstrate how to complete the Chamberlain University NR 507 Week 3: Discussion Part Two 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: Discussion Part Two
Whether one passes or fails an academic assignment such as the Chamberlain University NR 507 Week 3: Discussion Part Two 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: Discussion Part Two
The introduction for the Chamberlain University NR 507 Week 3: Discussion Part Two 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 3: Discussion Part Two
After the introduction, move into the main part of the NR 507 Week 3: Discussion Part Two 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: Discussion Part Two
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: Discussion Part Two
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 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.
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Sample Answer 2 for NR 507 Week 3: Discussion Part Two
What is the etiology of congestive heart failure?
Brashers (2014) explains how heart failure is a result of inadequate perfusion and cardiac output. Dysfunction of the left ventricle is also known as systolic and diastolic heart failure. Failing cardiac output results in inadequate perfusion of tissues or an increase of diastolic filling pressure of the left ventricle causing an increase in pulmonary capillary pressures. Ischemic heart disease and hypertension are two significant risk factors. Other risk factors include age, obesity, excessive alcohol intake, diabetes, kidney failure, valvular heart disease, congenital heart disease, and cardiomyopathies. Genes for cardiomyopathies, myocyte contractility, and neurohumoral receptors have also been linked to an increased risk for heart failure. Most commonly, causes of heart failure result in left ventricular dysfunction or systolic and diastolic heart failure. Right ventricle dysfunction usually occurs from lung disease. Cardiac output abnormalities can also cause heart failure although cardiac output may be normal or elevated.
Describe in detail the pathophysiological process of congestive heart failure.
Left heart failure or congestive heart failure (CHF), is also called heart failure with reduced ejection fraction (EF) or systolic heart failure. An EF less than 40% is diagnosed as systolic heart failure or CHF. In diastolic failure, EF is usually normal. In diastolic heart failure, there is an inability to perfuse to vital tissues due to reduced cardiac output. Heart rate and stroke volume are essential components in the heart’s ability to pump blood adequately. Stroke volume involves contractility, preload, and afterload. A myocardial infarction can reduce contractility as well as cardiomyopathies and myocarditis (Brashers, 2014).
Identify hallmark signs identified from the physical exam, diagnostic lab work, and symptoms.
Signs and symptoms based on the physical exam are dyspnea on exertion and fatigue. Dyspepsia with nausea and occasional epigastric pain and difficulty breathing while lyingflat at night are also signs of congestive heart failure (CHF). Hypertension, a predisposing factor of CHF, as evidenced by the patient’s current bp reading of 180/110.
The National Heart, Lung, and Blood Institute (NHLBI) (2018) describe the signs and symptoms of heart failure. Edema in feet, legs, liver, abdomen, and neck veins, shortness of breath, and fatigue or tiredness, and coughing are signs of heart failure.
Brashers (2014) describes how either an S3or S4gallop may be heard on auscultation, cyanosis, pulmonary edema, inspiratory crackles, and pleural effusion are signs of inadequate perfusion of the systemic circulation in heart failure.An ECG and troponin level should be done to rule-out acute ischemia. A chest x-ray, echo, and possibly heart catheterization can provide relevant information about heart size, congestion, cardiac output, and other coronary diseases. A serum BNP level can help determine the severity of heart failure and response to treatment. In emergent situations, administering oxygen, nitrates, and morphine will help lower preload through vasodilation. Diuretics and IV inotropic medications help to increase contractility and increase BP in those who are hypotensive. Digoxin may be used in those with atrial fibrillation along with anticoagulants and antithrombotics. In chronic left heart failure, the goal is to reduce preload and afterload. ACE inhibitors and beta blockers are popular drugs used in the treatment of left heart failure and reduce the mortality rate in patients.
In the American Family Physician (2014) journal, guidelines from the American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) recommend a series of lab work should be standard in making the diagnosis of CHF. A complete blood count, white blood cell count, urinalysis, fasting lipid, liver function, renal function, creatinine, glucose, thyroid function, and serum electrolytes should be part of the diagnostic evaluation for heart failure. B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) or both useful in supporting the clinical diagnosis of heart failure.
Describe the pathophysiology of complications of congestive heart failure.
Myocardial dysfunction caused by infarction, ischemia, hypertension or other abnormalities cause a decrease in cardiac output and eventually low systemic blood pressure. Baroreceptors are activated which stimulate vasomotor regulation centers in the medulla. Vasomotor stimulation leads to an activation of the sympathetic nervous system (SNS). Catecholamines, epinephrine, and norepinephrine are released causing vasoconstriction which increases afterload, blood pressure and heart rate. The renal system is alerted to these changes and activates the renin-angiotensin-aldosterone system or RAAS. When the RAAS is activated renal perfusion decreases and peripheral vascular resistance increases. This action increases afterload and preload further. When the RAAS is activated, the release of aldosterone into the kidneys stimulates renin which is converted into Angiotensin I and Angiotensin II. The release of the chemicals further complicates things by causing a toxic effect on the myocardium. Remodeling of the ventricular wall, mediated by Angiotensin II, contributes to the breakdown and death of the collagen matrix which leads to decreased contractility, changes in myocardial compliance and ventricular enlargement. Other complex changes take place during CHF. Aldosterone causes salt and water retention, dysrhythmias, myocardial fibrosis, autonomic dysfunction, and prothrombotic effects. Hyponatremia caused by the action of arginine vasopressin or antidiuretic hormone causes vasoconstriction and renal fluid retention. Natriuretic peptides such as atrial and BNP’s are increased and may have protective properties in that they decrease pre-load, but inadequate in compensating for heart failure. Inflammatory cytokines like endothelial hormones and TNF-a and IL-6 contribute to hypertrophy and remodeling of the myocardium and contribute to weakness and weight loss. Changes in calcium ion channels affect normal transport function of calcium in and out of the myocyte. These calcium changes contribute to decreased contractility. Finally, insulin resistance in diabetes is a likely contributor to heart failure. Abnormal fatty acid metabolism and ATP generation causes a decrease in contractility and contributes to the remodeling effect. When the SNS and RAAS systems are activated in heart failure, they contribute to insulin resistance. The numerous changes that take place during heart failure increase morbidity and mortality rates (Brashers, 2014).
What teaching would you provide this patient to avoid heart failure symptoms?
Compliance with treatment plan may significantly reduce the severity of symptoms and mortality rates. A heart-healthy diet, weight reduction, and limited alcohol intake are some ways patients can reduce the severity of CHF and its’ manifestations. Routine lab tests to determine if treatment is working, such as a BNP level, cholesterol level, and blood sugar level are all critical in helping patients live longer, more active lives. It is also important to report any side effects of medication to the provider so that adjustments can be made. Getting flu and pneumonia vaccines, if not contraindicated, are essential in staying healthy. Discussing these preventive measures with the primary care provider is important and should be routine. Support groups may help living with CHF a little easier. Talking to professionals or other people who have the same experiences to ease feelings of anxiety or depression (National Heart, Lung, and Blood Institute, 2018).
References
American Family Physician. (2014, August 1). ACCF and AHA release guidelines on the management of heart failure. American Family Physician, 90(3), 186-189. https://www.aafp.org/afp/2014/0801/p186.html
Brashers, V. (2014). Alterations of cardiovascular function. In K. McCance, S. Huether, V. Brashers, & N. Rote, Pathophysiology: The Biologic Basis for Disease in Adults and Children 7th Edition Vol 2 (pp. 1175-1180). St Louis: Elsevier Mosby.
National Heart, Lung, and Blood Institute. (n.d.). Heart Failure. Retrieved July 2018, from National Heart, Lung, and Blood Institute: https://www.nhlbi.nih.gov/print/4955
Sample Answer 3 for NR 507 Week 3: Discussion Part Two
What is the etiology of congestive heart failure?
Brashers (2014) explains how heart failure is a result of inadequate perfusion and cardiac output. Dysfunction of the left ventricle is also known as systolic and diastolic heart failure. Failing cardiac output results in inadequate perfusion of tissues or an increase of diastolic filling pressure of the left ventricle causing an increase in pulmonary capillary pressures. Ischemic heart disease and hypertension are two significant risk factors. Other risk factors include age, obesity, excessive alcohol intake, diabetes, kidney failure, valvular heart disease, congenital heart disease, and cardiomyopathies. Genes for cardiomyopathies, myocyte contractility, and neurohumoral receptors have also been linked to an increased risk for heart failure. Most commonly, causes of heart failure result in left ventricular dysfunction or systolic and diastolic heart failure. Right ventricle dysfunction usually occurs from lung disease. Cardiac output abnormalities can also cause heart failure although cardiac output may be normal or elevated.
That was very thorough – nice job!
Describe in detail the pathophysiological process of congestive heart failure.
Left heart failure or congestive heart failure (CHF), is also called heart failure with reduced ejection fraction (EF) or systolic heart failure. An EF less than 40% is diagnosed as systolic heart failure or CHF. In diastolic failure, EF is usually normal. In diastolic heart failure, there is an inability to perfuse to vital tissues due to reduced cardiac output. Heart rate and stroke volume are essential components in the heart’s ability to pump blood adequately. Stroke volume involves contractility, preload, and afterload. A myocardial infarction can reduce contractility as well as cardiomyopathies and myocarditis (Brashers, 2014).
That’s correct.
Identify hallmark signs identified from the physical exam, diagnostic lab work, and symptoms.
Signs and symptoms based on the physical exam are dyspnea on exertion and fatigue. Dyspepsia with nausea and occasional epigastric pain and difficulty breathing while lyingflat at night are also signs of congestive heart failure (CHF). Hypertension, a predisposing factor of CHF, as evidenced by the patient’s current bp reading of 180/110.
The National Heart, Lung, and Blood Institute (NHLBI) (2018) describe the signs and symptoms of heart failure. Edema in feet, legs, liver, abdomen, and neck veins, shortness of breath, and fatigue or tiredness, and coughing are signs of heart failure.
Brashers (2014) describes how either an S3or S4gallop may be heard on auscultation, cyanosis, pulmonary edema, inspiratory crackles, and pleural effusion are signs of inadequate perfusion of the systemic circulation in heart failure.An ECG and troponin level should be done to rule-out acute ischemia. A chest x-ray, echo, and possibly heart catheterization can provide relevant information about heart size, congestion, cardiac output, and other coronary diseases. A serum BNP level can help determine the severity of heart failure and response to treatment. In emergent situations, administering oxygen, nitrates, and morphine will help lower preload through vasodilation. Diuretics and IV inotropic medications help to increase contractility and increase BP in those who are hypotensive. Digoxin may be used in those with atrial fibrillation along with anticoagulants and antithrombotics. In chronic left heart failure, the goal is to reduce preload and afterload. ACE inhibitors and beta blockers are popular drugs used in the treatment of left heart failure and reduce the mortality rate in patients.
In the American Family Physician (2014) journal, guidelines from the American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) recommend a series of lab work should be standard in making the diagnosis of CHF. A complete blood count, white blood cell count, urinalysis, fasting lipid, liver function, renal function, creatinine, glucose, thyroid function, and serum electrolytes should be part of the diagnostic evaluation for heart failure. B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) or both useful in supporting the clinical diagnosis of heart failure.
Wow! Excellent work here.
Describe the pathophysiology of complications of congestive heart failure.
Myocardial dysfunction caused by infarction, ischemia, hypertension or other abnormalities cause a decrease in cardiac output and eventually low systemic blood pressure. Baroreceptors are activated which stimulate vasomotor regulation centers in the medulla. Vasomotor stimulation leads to an activation of the sympathetic nervous system (SNS). Catecholamines, epinephrine, and norepinephrine are released causing vasoconstriction which increases afterload, blood pressure and heart rate. The renal system is alerted to these changes and activates the renin-angiotensin-aldosterone system or RAAS. When the RAAS is activated renal perfusion decreases and peripheral vascular resistance increases. This action increases afterload and preload further. When the RAAS is activated, the release of aldosterone into the kidneys stimulates renin which is converted into Angiotensin I and Angiotensin II. The release of the chemicals further complicates things by causing a toxic effect on the myocardium. Remodeling of the ventricular wall, mediated by Angiotensin II, contributes to the breakdown and death of the collagen matrix which leads to decreased contractility, changes in myocardial compliance and ventricular enlargement. Other complex changes take place during CHF. Aldosterone causes salt and water retention, dysrhythmias, myocardial fibrosis, autonomic dysfunction, and prothrombotic effects. Hyponatremia caused by the action of arginine vasopressin or antidiuretic hormone causes vasoconstriction and renal fluid retention. Natriuretic peptides such as atrial and BNP’s are increased and may have protective properties in that they decrease pre-load, but inadequate in compensating for heart failure. Inflammatory cytokines like endothelial hormones and TNF-a and IL-6 contribute to hypertrophy and remodeling of the myocardium and contribute to weakness and weight loss. Changes in calcium ion channels affect normal transport function of calcium in and out of the myocyte. These calcium changes contribute to decreased contractility. Finally, insulin resistance in diabetes is a likely contributor to heart failure. Abnormal fatty acid metabolism and ATP generation causes a decrease in contractility and contributes to the remodeling effect. When the SNS and RAAS systems are activated in heart failure, they contribute to insulin resistance. The numerous changes that take place during heart failure increase morbidity and mortality rates (Brashers, 2014).
Another outstanding job!
What teaching would you provide this patient to avoid heart failure symptoms?
Compliance with treatment plan may significantly reduce the severity of symptoms and mortality rates. A heart-healthy diet, weight reduction, and limited alcohol intake are some ways patients can reduce the severity of CHF and its’ manifestations. Routine lab tests to determine if treatment is working, such as a BNP level, cholesterol level, and blood sugar level are all critical in helping patients live longer, more active lives. It is also important to report any side effects of medication to the provider so that adjustments can be made. Getting flu and pneumonia vaccines, if not contraindicated, are essential in staying healthy. Discussing these preventive measures with the primary care provider is important and should be routine. Support groups may help living with CHF a little easier. Talking to professionals or other people who have the same experiences to ease feelings of anxiety or depression (National Heart, Lung, and Blood Institute, 2018).
This week we learned a lot of great information such as the disorder of cystic fibrosis, fluid and electrolyte imbalances, and celiac disease. Another topic that was explored through discussion 2 was bronchitis. Two types of bronchitis exist, acute and chronic, which exhibits similar symptoms in the beginning but can progress to much worse symptoms if chronic occurs. Acute bronchitis usually is diagnosed after the patients presents with cough, fatigue, and possible yellow or green colored sputum. I was unaware that bronchitis does not require treatment with antibiotics unless chronic in which case antibiotics and steroids might be needed. For patients with chronic bronchitis effects can be much more serious leading to hypoxemia and or other conditions such as COPD. For patients with acute bronchitis treatment is essential and if symptoms do not resolve, he or she should promptly seek further treatment from a healthcare provider.
Discussion 1 and 2 both focused on disorders of the pulmonary system and this topic also made up a large portion of this weeks reading. This week we learned about the pulmonary system and how it works with the process to regulate fluids and electrolytes. We also discussed ventilation and perfusion which is a continuing cycle that ensures proper exchange of gasses across the cellular membranes. We learned about the many pulmonary disorders that an arise such as COPD, asthma, and tuberculosis. The pulmonary system is at risk for many disorders, some that are acute and treatable, while some are chronic and can be managed for best quality of life possible. Another factor that is very interesting to me is that each disorder seems to have symptoms that can range from mild to severe. An example is asthma, asthma can be a mild episode treated with medication but can also be serious and require mechanical ventilation such as with status asthmaticus. Another topic we learned is the disorders that arise in the pediatric patient. I am always very interested to learn about the disorders and treatments and how they are approached differently due to the age differences. I really enjoyed reading all the posts from my peers and the variety of additional information found by each individual. This week built on last week’s lesson and I look forward to seeing how next weeks lesson will continue to show how each system of the body must work with the others in order for full function to be achieved.
Sample Answer 4 for NR 507 Week 3: Discussion Part Two
I use to work on a telemetry floor for about two and half years, there were numerous occasions where I have taken care of the same patients more than once in a month’s span. As we know the term “frequent flyers”, one of the culprits in frequent re-admissions was congestive heart failure especially of our elderly population, who were 65 years old or older. The majority of these patients in my surrounding hospital community were living alone or lived in a nursing home, they didn’t have the financial or social resources. There are several factors that contribute to a patient’s readmission such as social, economics, language barrier, miscommunication, and the list can go on. Assessing all these needs when a patient is inpatient is crucial to help set up the success of a patient going home. It is projected that the prevalence of heart failure will increase 46% from 2012 to 2030, with more than 8 million adults living with the chronic condition (Ziaeian & Fnarow, 2016).
Hospitals all over the US are trying to find ways to decrease hospital readmissions in heart failure, such as medication reconciliation, patient education, discharge planning, scheduling follow-up, communicating with outside providers, and follow up telephone calls. In which all of these interventions play a crucial role in a heart failure patient. Nonetheless, improving communication during transitions in care from inpatient to outpatient require continued attention (Ziaeian & Fonarow, 2016). It was noted in the article that hospitals with higher nurse staffing ratios did have 41% lower odds of receiving Medicare penalties for excessive readmissions and follow up care within 7 days of discharge. Hopefully, this ongoing healthcare burden gets the strategies it needs to improve outcomes for these patents.
Ziaeian, B., & Fonarow, G. C. (2016). The prevention of hospital readmissions in heart failure. Progress in Cardiovascular Diseases, 58(4), 379–385. http://doi.org/10.1016/j.pcad.2015.09.004
NR 507 Week 3 Case Study
¨ºPathophysiology & Clinical Findings of the Disease
- Are the spirometry results consistent with obstructive or restrictive pulmonary disease? What is the most likely pulmonary diagnosis for this patient?
Considering the pre-bronchodilator FEV1/FVC ratio of 56%, which falls below the normal threshold of 70%, it suggests an obstructive problem in the patient. The TLC exceeding 120% indicates hyperinflation, and the criteria for obstructive pulmonary disease consider a TLC range within normal limits as being above 120% (Radovanovic, D., et. al., 2018). Based on these findings, my assessment is that the patient is likely experiencing chronic obstructive pulmonary disease (COPD).
- Explain the pathophysiology associated with the chosen pulmonary disease.
Per McCane & Huether (2019), COPD is airway obstruction disease that worsens with expiration. Use of the accessory muscles along with the added force or the time to expire the volume of air in the lungs, and the emptying of the lungs is slower with patients who have COPD (McCance & Huether, 2019). This condition is characterized by the infiltration of inflammatory cells into the lungs, leading to the release of various cytokines that contribute to airway damage and the production of mucus (McCance & Huether, 2019). They also experience heightened respiratory effort, a “mismatching of the ventilation-perfusion ratio,” and a reduction in the force of expiratory volume within one second (FEV1) (McCance & Huether, 2019). In COPD, the obstruction of airflow results from a combination of small airways disease, which raises airway resistance, and parenchymal destruction, specifically emphysema, diminishing the typical elastic recoil of the lung parenchyma (2024 GOLD Report). Everything together ends up leading to gas trapping and lung hyperinflation (2024 GOLD Report).
- Identify at least three subjective findings from the case which support the chosen diagnosis.
Three subjective observations include shortness of breath, fatigue, and dyspnea. Roughly 1% to 4% of visits to primary care offices involve complaints of dyspnea (Langan & Goodbred, 2020).
- Identify at least three objective findings from the case which support the chosen diagnosis.
The objective observations are quantifiable findings observed by the provider. Three objective findings consist of bilateral wheezes detected during forced exhalation, a hyperinflated state of the lungs with a flattened diaphragm, and Spirometry results indicating an FEV1/FVC (%) of 56 pre-bronchodilator & 52% post-bronchodilator which didn’t change much with bronchodilator use.
Management of the Disease
*Utilize the required Clinical Practice Guideline (CPG) to support your treatment recommendations.
- Classify the patient’s disease severity. Is this considered stable or unstable?
The 2024 GOLD Report states predicted post-bronchodilator FEV1 is 50%< FEV1 <80% predicted is Gold 2 Moderate. The patient’s post-bronchodilator FEV1 predicted is 64%. This patient’s disease severity is considered stable due to symptoms, assessment, spirometry results, and not needing to be hospitalized even though he spent three months with dyspnea.
- Identify two (2) “Evidence A” recommended medication classes for the treatment of this condition and provide an example (drug name) for each.
Evidence A recommended medication classes are Inhaled Bronchodilators an example is Albuterol which is a SABA (short acting beta agonist). Another medication class is Inhaled corticosteroids, example is beclomethasone dipropionate inhaled.
- Describe the mechanism of action for each of the medication classes identified above.
Inhaled Bronchodilators work by relaxing the respiratory smooth muscle and reducing airway resistance (COPD, (n.d.)). Inhaled corticosteroids reduce the inflammation in the airways activating anti-inflammatory genes (UpToDate. (n.d.)).
- Identify two (2) “Evidence A” recommended non-pharmacological treatment options for this patient.
Smoking cessation, pulmonary rehabilitation, physical activity (2021 GOLD Report).
References
COPD – Symptoms, Causes, Images, and Treatment Options. (n.d.). Epocrates.com. https://www.epocrates.com/online/diseases/7/copd
2024 GOLD Report. (2023, November 12). Global Initiative for Chronic Obstructive Lung Disease – GOLD. https://goldcopd.org/2024-gold-report/
Langan, R. C., & Goodbred, A. J. (2020). Office Spirometry: Indications and Interpretation. American Family Physician, 101(6). https://pubmed.ncbi.nlm.nih.gov/32163256/
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier.
Radovanovic, D., Santus, P., Blasi, F., Sotgiu, G., D’Arcangelo, F., Simonetta, E., Contarini, M., Franceschi, E., Goeminne, P. C., Chalmers, J. D., & Aliberti, S. (2018). A comprehensive approach to lung function in bronchiectasis. Respiratory Medicine, 145, 120–129. https://doi.org/10.1016/j.rmed.2018.10.031
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