This process paper will evaluate the complex relationship between disease pathophysiology and how it has progressed to the patient’s current state of health. It will include a comprehensive discussion of chronic and acute problems leading to the patient’s hospital admission, a complete description of interrelationships and pathophysiology for all medical diagnoses, a comprehensive discussion of the client’s signs and symptoms and results of all diagnostic studies to the underlying pathophysiology, and a comprehensive listing of all medications ordered at the time of admission with explanations of why each was ordered and identification of the most common side effects which may occur.
This paper will also identify and describe significant events that occurred during the patient’s hospital stay with support of explanation with evidence from signs and symptoms and diagnostic tests. Also, there will be a description of the client’s condition at the time of my care including medicines and other physician ordered interventions and explanation of reason each was instituted. Three nursing diagnoses will be identified for this client, each with measurable client goals, interdisciplinary interventions, and patient outcomes.
This paper will also provide a comprehensive description of the client’s illness on the individual, family and society, economically, socially, spiritually, emotionally, and the effects on family roles. In conclusion, the paper will end with the identification of a clinical or nursing practice problem related to the care of the client posed in the form of a nursing research question.
Complete explanation of the rationale for this problem and a review of the literature and synthesis of the findings from two research articles which are related to the research question will be provided. Introduction and History Discussion of relevant acute and chronic problems leading to admission to the hospital On October 17, 2010, D. S. was admitted to the hospital due to difficulty breathing and HF exacerbation. The patient states she was at home, but had increasing shortness of breath and then difficulty getting around to the bathroom. She is currently living at an assisted living home in Byron and is on supplemental oxygen there. Her admitting vital signs were T 98. 2, P 100, R 20, and BP 141/60.
The patient had recently been admitted to the hospital in September with these same complaints and suspected CHF and had some simple spirometry performed at her doctor’s office in May of this year. In May, her spirometry showed an FVC of 1. 97 L (72%), an FEV1 of 1. 26 L (72%), and an FEV1/FVC ratio of 64%. To determine whether airway obstruction or a restrictive process is causing a reduced FEV1, the FEV1/FVC ratio is the answer. A low FEV1 and a decreased ratio signify a predominantly obstructive process (Hyatt, Scanlon, Nakamura, 2003).
The patient has a history of emphysema and smoked one to two packs a day for thirty years before quitting twenty years ago. So in this case, her pulmonary function is decreased due to these processes. Also in May, a CT of her abdomen did show some questionable mild increased interstitial densities in the posterior aspect of the lungs at the bases, which might be indicative of possible early interstitial lung disease. In September, when she admitted for shortness of breath and suspected CHF, she underwent an ischemic workup and an echocardiogram was found to have no ischemia with a normal ejection fraction.
She was found to have right atrial enlargement, left atrial dilatation, moderate aortic valve sclerosis without stenosis, trace mitral regurgitation, mild mitral stenosis and mild tricuspid regurgitation as well as moderate pulmonary hypertension. D. S. is an 84 year old Caucasian female with a past medical history of chronic obstructive pulmonary disease (COPD), emphysema, congestive heart failure (CHF), hypertension (HTN), gastroesophageal reflux disease (GERD), chronic myeloid leukemia (CML), pulmonary hypertension, hypothyroidism, and anemia.
Her past surgical history includes an excision of a groin abscess, a cholecystectomy, a rotator cuff repair, and a breast biopsy. The patient’s family history is positive for hypertension and there is no family history of lung disease. Her father is deceased with muscular dystrophy and her mother is deceased with acute MI. She is allergic to sulfa, carbonic anhydrase inhibitors, thiazides, sulfonamide antibiotics, and sulfonylureas. Pathophysiology and Interrelationships In the following paragraphs, I will provide a comprehensive understanding of the diagnoses and how they relate to one another.
I will be discussing the medical diagnoses of COPD/Emphysema, congestive heart failure, pulmonary hypertension, HTN, chronic myeloid leukemia, anemia, hypothyroidism, and GERD. Each heading will include the definition, causes/etiology, risk factors, common signs and symptoms, common treatment methods, common labs and diagnostic studies, the patient’s history of the disease, the patient’s risk factors, the patient’s signs and symptoms, the patient’s course of treatment and whether or not the treatment is working, and the patient’s labs and diagnostic studies that confirm the diagnosis and efficacy of treatment.
COPD/Emphysema COPD is a general term for a group of conditions in which there is persistent difficulty in expelling air from the lungs (Olendorf, 2000). Emphysema is one of the most common conditions listed under the COPD umbrella. So for purposes of this paper, the rest of this section will focus mainly on emphysema. Emphysema is a respiratory disease characterized by breathlessness brought on by the enlargement, or overinflation of, the alveoli in the lungs. Emphysema is the most common cause of death from respiratory disease in the United States and is generally caused by several years of heavy cigarette smoking (Olendorf, 2000).
When a person smokes, the body’s immune system tries to fight off the invading smoke by using certain substances. These substances can also attack the cells of the lungs, but normally the body is able to release other substances to prevent this. In the case of people who are smokers, this doesn’t happen and the original substances that were released to fight off the smoke also end up injuring the cells of the lungs as well. Eventually, the lungs will not be able to supply enough oxygen to the blood and a host of problems can occur with this.
Risk factors that have been identified for emphysema include exposure to tobacco smoke either through active or passive smoking (2nd hand smoke), occupational exposure such as dust or chemicals, ambient air pollution, or genetic abnormalities, including a deficiency of alpha-antitrypsin, an enzyme inhibitor that normally counteracts the destruction of lung tissue by certain other enzymes (Smeltzer, 2010). The symptoms of emphysema develop gradually over many years. It is generally characterized by three primary symptoms: chronic cough, sputum production, and dyspnea on exertion.
Other signs and symptoms include weight loss and the development of a “barrel chest” which occurs due to chronic hyperinflation of the lungs (Smeltzer, 2010). Respiratory insufficiency and failure are major life-threatening complications of COPD/emphysema. Respiratory insufficiency and failure may be acute or chronic in nature. Other complications of COPD/emphysema include pneumonia, chronic atelectasis, pneumothorax, and pulmonary arterial hypertension (cor pulmonale) (Smeltzer, 2010). Common non-pharmacologic treatment methods include quitting smoking, controlled coughing techniques, and mild exercise.
Pharmacologic treatments include the use of bronchodilators, corticosteroids, supplemental oxygen therapy, and antibiotics. In those with severe emphysema, lung transplantation may be the best course of treatment. Diagnostic studies used in the assessment and diagnosis of COPD/emphysema include pulmonary function tests, ABGs, a chest x-ray, and screening for alpha1-antitrypsin deficiency. Spirometry is the main pulmonary function test that is used to evaluate airflow obstruction, which is determined by the FEV1/FVC ratio briefly described in the opening paragraph. D. S. as been diagnosed with emphysema for a number of years, beginning in her 30’s or 40’s, as reported by the patient.
She stopped smoking about twenty years ago after having smoked one to two packs a day for the previous 30 years. The patient’s risk factors for this disease include her history of smoking and the fact that she worked as a shipping clerk during the war in some areas that may have had dust exposure. The patient does not recall any particular problem or respiratory issues back then. The patient presented to the hospital with shortness of breath especially on exertion and reports an occasional nonproductive cough.
The patient did not show any signs of a “barrel chest” and didn’t report any significant weight loss within the recent months. D. S. underwent a spirometry test back in May of this year. The results yielded an FVC of 1. 97 L (72%), an FEV1 of 1. 26 L (72%), and an FEV1/FVC ratio of 64%. A low FEV1 and a decreased ratio signify a predominantly obstructive process (Hyatt, Scanlon, Nakamura, 2003). A chest x-ray that was performed on October 20th, three days after her admission, showed evidence of mild interstitial pulmonary edema and small bilateral pleural effusions.
Her emphysema is a probable contributory factor to her history of pulmonary hypertension. The doctor’s believe that her emphysema is not the primary cause of her overall hypoxemia but believe that it is one of several contributory factors. D. S. ’s home medications that relate to COPD/emphysema include supplemental oxygen and albuterol PRN. The goal of supplemental oxygen therapy is to increase the baseline resting partial arterial pressure of oxygen (PaO2) to at least 60 mmHg at sea level and arterial oxygen saturation (SaO2) at least 90% (Smeltzer, 2010).
D. S. ’s oxygen saturation at the time of care was in the low- to mid-80s but would increase to 90% and above and a few deep breaths. Albuterol is a bronchodilator that relieves bronchospasm by altering smooth muscle tone, which in turn reduces airway obstruction by allowing increased oxygen distribution throughout the lungs and improving alveolar ventilation. Side effects associated with this medication include nervousness, shakiness, dizziness, nausea, tachycardia, chest pain, fever, pruritus, edema, and difficulty swallowing.
The medication does appear to be helping in the fact that the patient is not short of breath while lying in the bed, which is a common symptoms as COPD/emphysema progresses. Her oxygen saturation is still not where it should be. As stated earlier, her oxygen saturation hovered around the low-to mid-80s. For this reason, the doctor’s believe that her emphysema is not the primary cause of her hypoxemia, but fill that it is definitely a contributory factor. Hypertension Hypertension is defined as blood pressure measurements that repeatedly exceed 140 mmHg systolic and 90 mmHg diastolic.
Blood pressure is the product of cardiac output multiplied by peripheral resistance. Hypertension can result from an increase in cardiac output, an increase in peripheral resistance, or both. Structural and functional changes in the heart and blood vessels also contribute to increases in blood pressure that occur with aging. These changes include accumulation of atherosclerotic plaque, fragmentation of arterial elastins, increased collagen deposits, and impaired vasodilation (Smeltzer, 2010).
As blood flows through arteries it pushes against the inside of the artery walls. The more pressure the blood exerts on the artery walls, the higher the blood pressure will be. The cause of hypertension is not known in 90-95 percent of the people who have it; this is also called primary or essential hypertension. Risk factors for hypertension include age over 60, male sex, African American race, heredity (family history), salt sensitivity, obesity, inactive lifestyle, heavy alcohol consumption, smoking, and use of oral contraceptives.
If left untreated, possible complications of hypertension include arteriosclerosis, heart attack, stroke, cardiomegaly, and kidney insufficiency or failure (Olendorf, 2000). Congestive Heart Failure Heart failure is defined as a condition in which the heart has lost the ability to pump enough blood to the body’s tissues. With too little blood being delivered, the organs and other tissues do not receive enough oxygen and nutrients to function properly (Olendorf, 2000). Heart failure that involves the buildup of fluid (edema) in the tissues is called congestive heart failure.
Heart failure results from a variety of cardiovascular conditions, including chronic hypertension, coronary artery disease, and valvular disease. The two major types of heart failure are left-sided heart failure (left ventricular failure) and right-sided heart failure (right ventricular failure). Atherosclerosis of the coronary arteries is the primary cause of heart failure (Smeltzer, 2010). Increasing age is a risk factor associated with the development of atherosclerosis.
As we age, our arteries go through vascular changes associated with aging such as increased thickening of the arteries, stiffness of central arteries, and general arterial remodeling (Birren, 2007). All of these contribute to the development of atherosclerosis in an otherwise healthy person as well as people with other conditions related to the development of heart disease. So while D. S. does not necessarily have a medical history of atherosclerosis, she may be experiencing some vascular changes. Other risk factors for heart failure include systemic and pulmonary hypertension, cardiomyopathy, valvular disease, and dysrhythmias.
The signs and symptoms associated with heart failure depend on the different types of heart failure. Signs and symptoms associated with left-sided HF include dyspnea, cough, pulmonary crackles, low oxygen saturation levels, an S3 heart sound, SOB on exertion, orthopnea, PND, oliguria, nocturia, pallor, tachycardia, fatigue, and activity intolerance. Signs and symptoms associated with right-sided heart failure include JVD, dependent edema, hepatomegaly, ascites, anorexia and nausea, and weakness and weight gain.
Pharmacologic therapy in the treatment of HF includes the use of ACE inhibitors, angiotensin II receptor blockers, beta-blockers, diuretics, digitalis, and calcium channel blockers, and anticoagulants. The patient is usually placed on a low-sodium diet and is advised not to drink an excessive amount of fluid. Additional therapy includes supplemental oxygen administration, placement of an implantable cardioverter defibrillator (ICD), implantation of a pacemaker, and in extreme cases, heart transplantation (Smeltzer, 2010).
Common lab and diagnostic studies used in the diagnosis and treatment of HF include BUN, creatinine, CBC, BNP, an echocardiogram, chest x-ray, and an electrocardiogram. D. S. was admitted to the hospital in September with similar complaints of shortness of breath on exertion as with this hospital visit. In September, she was also admitted with suspected CHF. For this current hospital admission she was admitted with the diagnosis of acute HF exacerbation. Her risk factors associated with the development of this condition include chronic hypertension, valvular disease, and increasing age.
The patient’s history of valvular disease includes moderate aortic sclerosis without stenosis, trace mitral regurgitation, mild mitral stenosis, and mild tricuspid regurgitation. The patient’s echocardiogram also showed right atrial enlargement as well as left atrial dilatation. The patient’s signs and symptoms include dyspnea, SOB on exertion, low oxygen saturation levels, tachycardia, bilateral pitting edema in the ankles, and anorexia. D. S. ’s home medications that relate to CHF include those used to control her hypertension and the diuretic, spironolactone (Aldactone).
The medications used to control her hypertension include amlodipine (Norvasc), atenolol (Tenormin), and lisinopril. Norvasc is a calcium channel blocker that lowers blood pressure by relaxing the blood vessels, which reduces systemic vascular resistance, so the heart does not have to pump as hard. Side effects associated with calcium channel blockers are generalized edema, dizziness, lightheadedness, drowsiness, dysrhythmias, and syncope (“Amlodipine,” 2010).
Atenolol is a beta-blocker that works by relaxing blood vessels and slowing heart rate to improve blood flow and decrease blood pressure. Side effects associated with beta-blockers include dizziness, nausea, lightheadedness, hypotension, bradycardia, shortness of breath, and syncope (“Atenolol,” 2010). Lisinopril is an ACE inhibitor that works by decreasing certain chemicals that constrict the blood vessels, so blood flows more smoothly and the heart can pump blood more efficiently.
The side effects associated with ACE inhibitors include dizziness, headache, weakness, cough, edema, difficulty breathing, syncope, chest pain, and jaundice (“Lisinopril,” 2008). Aldactone is a potassium-sparing diuretic that blocks the effects of aldosterone thereby causing the kidneys to eliminate unneeded water and sodium from the body into the urine. The side effects associated with this medication include dry mouth, thirst, dizziness, headache, restlessness, weakness, confusion, anorexia, jaundice, flu-like symptoms, blurred vision, and syncope (“Spironolactone,” 2009).