Controlling Fluid Retention Using Daily Weight Monitoring in Patients with Congestive Heart Failure - Research Proposal Example

Controlling Fluid Retention Using Daily Weight Monitoring in Patients with Congestive Heart Failure Background and Significance of Problem World Health Organization (2009) revealed that Cardiovascular Diseases (CVDs) are considered the number one cause of death worldwide than any other disease cause. An estimated of about 17.5 million people in 2005 had already died which represented the 30% of the total global deaths. Similarly, about 5.7 million deaths were due to stroke; while an estimated 7.6 million others were known to have been caused by coronary heart disease. The report further shows that, low- and middle-income countries had over 80% of CVD deaths which takes place equally both in men and women. Almost 20 million people will die due to CVDs in 2015 plus other related illnesses like hypertensive heart disease, experts projected. Similarly, hypertensive heart disease is ranked the leading cause of death (WebMD, 2008) related with high blood pressure which comprises the group of disorders such as ischemic heart disease, heart failure, and left ventricular hypertrophy. The illness set up the weak pumping power of the heart than normal or the heart changed to become less elastic. A patient with heart failure usually has blood that moves through the heart as well as body, however, less effectively and at the same time, pressure in the heart increases. This phenomenon can lead to inability of the heart muscles to pump enough nutrients and oxygen in order to meet the bodys needs. When this occurs, the chambers of the heart are expected to respond by stretching in order to hold more blood through the body, thus, augment the blood to keep moving. But eventually, the heart muscle walls deteriorate and are unable to strongly pump. Heart failure or HF (Healthology, 2008) is a stern condition whereby in the early stages, may not manifest symptoms and may have severe symptoms in the later stages. The term “heart failure” reinstates the older term “congestive heart failure” (Hunt, 2005) for the reason that patients with HF may not always be in a situation of fluid overload or pulmonary obstruction. It is basically a chronic and complex condition but is not considered as a disease. Instead, (Healthology, 2008) it is brought about by other conditions which damaged the heart. Symptoms include shortness of breath or dyspnea, if the person exercises, or even while at rest. Furthermore, in the case of heart failure, the kidneys will respond by enabling the body to retain quantities of fluid (water) and sodium that will build up in the arms, legs, lungs, ankles, feet, or other organs, until the body becomes congested, and results finally to congestive heart failure. Therefore, since kidney’s response to fluid retention can be affected by congestive heart failure, there is a great need to explore on the appropriate intervention as to how fluid retention in the patients’ body parts can be effectively controlled or prevented. Obviously, nurse clinicians need to be equipped about the current effective and evidence – based practice on the care management of congestive heart failure. The results of the study will serve as a very useful reference or source of information for nurses. Clinicians could design a better management decisions to patients with probable avert hospitalization among their patients with congestive heart failure. Family Perspective Analysis The impact of congestive heart failure on society as well as the health care system is enormous. This condition is an added burden to the patient’s health and his family physically, psychologically and economically. This common medical circumstance affects nearly 5 million Americans annually in the United States (Cowie, et. al, 1997) According to Cleland, et. al. (1999) the costs of inpatient and outpatient have reached approximately $40 million yearly, while almost 500 million dollars of which goes to the medications for heart failure alone. Furthermore, the estimated direct as well as indirect costs for Heart Failure in 2005 were about $27.9 billion. The incidence of hospital discharges with a primary diagnosis of HF leveled up by 155% over the last two (2) decades. Since the people are getting older, with more and more effective treatments for HF as well as myocardial infarction (MI), its more easy to view that in the next decade, the number of people distressed from HF will grow up exponentially (Riedinger, 2002). Epidemiology The American Heart Association or AHA (2005) was able to note that, more or less 5 million individuals live with heart failure. Hunt, et. al. (2006) added that, there are practically 550,000 new cases diagnosed every year; while there are about 1 million HF-associated hospitalizations yearly. A person can survive even with HF for several years, however, about two-thirds of all CHF patients die in 5 years of diagnosis (National Institutes of Health, 1997) and among those who have heart failure under 65 years of age, such those comprised by 80% of men and 70% of women, may not survive within 8 years (AHA, 2005). Pathophysiology According to the Guidelines for the Diagnosis and Management of Chronic Heart Failure for Adult, formulated by the American College of Cardiology as well as the American Heart Association (ACC and AHA), Heart Failure is an intricate clinical syndrome that is caused by a few structural and/or functional cardiac disorder which can impair the ability of the heart ventricle to load with or eject blood (Hunt, 2005). Fluid retention is one sign; while dyspnea and fatigue are the common symptoms that may manifest. The fluid retention may upshot in increased occurrence of fluid in the lungs which is heard as crackles, and also as peripheral edema. In this case, fluid accumulation in the lungs can impair the gas exchange mechanism, thereby, leading to fatigue, and soon develop into dyspnea. These conditions will reduce exercise of the patient as well as activity tolerance. Note that in heart failure, the heart is incapable to supply sufficient oxygen to the tissues to meet up their metabolic needs. The etiology of heart failure is diverse and this condition can be the outcome of nonfunctioning myocardium injured by an MI, hypertension, or invasion of viruses which result in viral cardiomyopathy. When heart muscles are insufficiently flooded with oxygen supply, probably because of the narrow coronary arteries, this may cause damaged contractility of myocardial muscle that can also lead to HF. Heart failure can branch out or rooted from leaky valves or problematic intra-atrial or intraventricular septa. The right-sided HF may probably be caused by anything which increases pressure in the lungs, like emphysema, primary pulmonary hypertension, cancer, sarcoidosis, obstructive sleep apnea, and also mechanical ventilation. Added to that, the most common reason of right-sided failure is the left-sided failure. Patients may have heart failure that is aggravated by either systolic or diastolic dysfunction (Hunt, 2005). In 2001, the ACC/AHA introduced guidelines for system of classification in order to help practitioners sort out the different phases of heart failure (Hunt, 2001). This system is practically could guide practitioners in determining and treating patients who are at risk for HF or those with active disease. By detecting the illnesses at early stage, appropriate therapies or lifestyle choices can help reduce mortality and morbidity. Although, it is clearly emphasized that the classification system isnt purposely for replacement of the New York Heart Association classification of functional status, that describes the specific functional status of patients with HF. As far as classification of HF is concerned, HF has been classified into different types. Example is the low-output HF and the high-output HF. The low-output HF is one type in which the left ventricle is powerless to eject a regular volume of blood with every beat. The quantity of blood expelled is expressed as a portion of the amount of blood by which a ventricle accommodates. Normal ejection fraction is usually acceptable to be 60% to 75%. The Low-output HF is also known as a systolic dysfunction, which is normally characterized by a low expulsion fraction, typically less than 35%; this reduced capacity to eject blood is probably be due to weak point of the left ventricle (beginning an MI or a cardiomyopathy). This could also be brought about by the narrowing or thinning of the aortic valve aperture (aortic valve stenosis). Similarly, low-output heart failure can also stem from lowered volume of blood coming from a dysfunctional right ventricle, due to an MI or pulmonary hypertension (ACC/ & AHA Guidelines, 2001). On the contrary, in high-output heart failure not too much blood at the left ventricle is ejected. The disproportionate volume of blood leads to ventricle dilatation and the fluid backup towards the pulmonary vasculature, in due course leaking out going to the pulmonary interstitial spaces. There are certain conditions which cause high-output heart failure and these include: hyperthyroidism, anemia, aortic and mitral valve regurgitation, and hypervolemia, starting from an extrinsic cause (AHA, 2001). The biventricular failure can possibly occur whenever the backup of fluid from the weak left ventricle results in dilatation as well as failure of the right ventricle. The diastolic heart failure can be caused by the left ventricle being incapable to rest and fill. Typically it is caused by hypertension that leads in left ventricular hypertrophy. As to the compensatory mechanisms, if and when the patient has compensated heart failure, the body usually goes through numerous compensatory mechanisms to make the most of the functioning of the heart that has begun to pump not really that efficiently. Such mechanism includes stimulating the sympathetic nervous system to liberate nor epinephrine and epinephrine, by this means, increasing the heart rate to advance the cardiac output (AHA, 2001). Another process to increase cardiac output is to further boost up the stroke volume by escalating the total of circulating volume by activating neurohormone. Once the circulating blood volume or pressure lowers, the kidneys produce renin that is converted initially to angiotensin I, then later into angiotensin II in the existence of angiotensin converting enzyme (ACE). The angiotensin II will stimulate angiotensin II receptors on the vascular smooth muscle, following on in vasoconstriction. The moment the adrenals recognize the raise in angiotensin II levels, they usually release aldosterone that causes the kidneys to keep hold of sodium and water, accordingly increasing circulating volume. After which, there will be two other neurohormones form into this mechanism; the posterior pituitary gland that releases vasopressin as a reaction to falling cardiac output and also the increase in circulating angiotensin II. In addition, vasopressin causes vasoconstriction as well as fluid retention. Following the previously stated processes is the release of endothelin from the endothelial inside layer of the bodys vasculature in reaction to angiotensin II, thrombin, cytokines, vasopressin, and shear forces (like with hypertension). In heart failure, endothelin hormone causes vasoconstriction because of the impaired release of nitric oxide in the vascular endothelium (Mann, 2004). Another compensatory mechanism would be the release of the amino acid peptides, particularly on the human atrial natriuretic hormone or hANP and the human brain’s natriuretic hormone or hBNP (ACC & AHA, 2001; Collin, 2001). Subsequently, human ANP is released by receptors in the atria as well as hBNP, which is released by stretch receptors found in the ventricles, as reaction to overload of blood volume. It should be emphasized that, the purpose of hANP and hBNP is to basically cause a loss of sodium and also of the water throughout the kidneys (ACC & AHA, 2001; Collin, 2001 and Yoshimura, 2001). Human BNP also supplies balanced vasodilatation of arteries, veins, and coronary arteries that reduces the blood pressure as well as improves blood flow. The human BNP lowers aldosterone levels, at the same time reduces hANP vasopressin levels. The moment a patient has successfully compensated heart failure, these mechanisms function together in a stable manner to take full advantage of cardiac output that prevents symptoms of decomposition. As soon as decompensation occurs in a certain time, the increased levels of angiotensin II, vasopressin, norepinephrine, other neurohormones, and low levels of nitric oxide may cause the endothelial lining of the blood vessels as well as the heart to become stiff and also noncompliant. This eventually undergoes hypertrophy, leading to endothelial lining dysfunction and also ventricular remodeling. Besides, decompensated heart failure is a hammering of balance between the mechanisms of HF as well as the bodys attempts to conquer the failure process (Collins, 2001) and as a result, the client begins to exhibit the symptoms and signs of the condition. HF can be on the right or left side of the heart. If it is a left-sided HF, it can be determined by crackles in the dorsal lung fields due to extreme preload (venous return to the heart). Thus, patients will be dyspneic, tachycardic, and tachypneic. They may also have a low down oxygen saturation level and will insist of having to use two to three (2-3) pillows at night for them to sleep (orthopnea). Patients might complain of waking up especially in the middle of the night, abruptly short of breath or paroxysmal nocturnal dyspnea. They may also experience an S3/S4 gallop during auscultation of the heart sounds (AHA, 2001) Additionally, through the mesenteric arteries, there may be low blood flow resulting in symptoms of very low blood flow going to the gastrointestinal tract. The said signs and symptoms are bloating, anorexia, nausea, and constipation. The low blood flow all the way through the renal arteries leads in reduced urinary output. There is vasoconstriction from angiotensin II, vasopressin, epinephrine, norepinephrine, and endothelin would be a source of being cool or cold, pale appearance, and possibly having ncyanotic extremities (increased afterload). Now, if patients have right-sided heart failure, the symptoms can be caused by an excessive preload particularly on the right side of the heart. Probably, there may be jugular venous tightness, liver ascites, engorgement, and sacral/pretibial/or pedal edema. Both identified types of HF are related to an increase in the patients weight, because of the excess water. Socio-economic Factors Extensive clinical studies have already documented major risk factors of heart and blood vessel (cardiovascular) disease. Contributing risk factors have also been identified. According to The American Heart Association (2009) some of the factors are the following: a) Increasing age, more than 83% of patients died due to coronary heart disease, with age 65 or older. More women had heart attacks, than men at older age; b) Gender, men have a bigger risk of heart attack at an early stage of life than women do; c) Heredity and Race, children whose parents suffered from heart diseases are also risk of having them; African Americans are more likely to have severe high blood pressure than the Caucasians. Heart disease risk is quite higher also among Mexican Americans, native Hawaiians, American Indians, and some Asian Americans. Other contributory factors include: 1) Tobacco smoke; 2) High blood cholesterol; 3) High blood pressure; 4) Physical inactivity; 5) Obesity and overweight; 6) Diabetes mellitus; and 7) Alcohol intake. General Management The approach in managing heart failure is multidisciplinary in nature. First, device therapies are needed, and example is the Cardiac resynchronization therapy (CRT). Several studies have shown consistent progress while using CRT in self-reported quality of life, and exercise capacity. Studies have shown a decline in HF and causes of morbidity and mortality. ACC/AHA recommends that CRT must be provided for clients with EF equal or a lesser amount than 35%, NYHA class III, and QRS duration of higher than 0.12 milliseconds together with cardiac dyssynchrony on echo (Hunt, 2005) An internal cardiac defibrillator (ICD) also lengthened survival, even in clients EF of less than 30%, who had in no way experience sudden death event. ACC/AHA recommends that clinicians ought to offer ICDs to HF patients in order to prolong survival. Clearly there are numerous very important interventions that nurses must implement in relation to the effects of preload adjustments intended for the patient in HF. Primarily, patients clinical symptoms must be properly assessed through vital signs taking, as they present in HF. Next is giving the patient with supplemental oxygen. The weight the patient should also be monitored. Weight is important in evaluating therapies for each HF patient. Nursing measures must include proper positioning of the patient for comfort, and in general, semi-Fowlers or sitting on the border of the bed with arms assisted on the over-bed table. Health teaching the patient should also be carried out to restrict fluid to 1.5 to 2 liters, alongside with strategies for relieving the uneasiness of the oral dryness, like tooth brushing, using of mouthwash or other over-the-counter oral hygiene rinses. Nurses must remind patients that its necessary to calculate intake and output (I/O) to assess the success of the diuretic therapies. Make sure that the patient receives about 2-gram sodium diet together with diet education during his hospital stay. Again, evaluate the success of these therapies. Instruct the patient that if and when he or she experience less short of breath, it must immediately be reported. Blood pressure may fall or get better due to the diuresis. Crackles in the lung fields must be decreased, then, after 2 to 3 days, health care team should see a reduction in the area of jugular venous distention and same with edema. The Urine output must exceed intake of fluids; while the daily weights should match with the I/O. Now, if the I/O is 1 liter negative, therefore, the patient must be 2.2 pounds lighter the following morning. Note that, its very essential to monitor the blood pressure strictly with prescribed drugs. Even if the blood pressure is just 90 mm Hg systolic, continue giving the vasodilators, maintenance of the vasodilator will permit the after load to rise, causing the cardiac output to descend. On the other hand, if the systolic blood pressure goes down 90 mm Hg systolic and then the patient becomes dizzy, work together with the physician on a diverse plan. Remember to teach the patient regarding medications, low sodium diet, daily weights, fluid management, and smoking cessation, as suitable. Every now and then, patients return to the hospital because of recurrence of symptoms. These recurrent re-hospitalizations can be lowered if the patient takes all medications as recommended, and follows an exact fluid management as well as sodium reduction plan at home. The patient must always call the attention of his cardiologist the moment he wakes up at night with sudden feeling of shortness of breath, gains two (2) pounds over night and/or 5 pounds in a week. In addition, health care providers must consider the following if and when addressing comorbidities: 1) For patients with hypertension, drugs that are functional for both HF and hypertension must be used (examples, ACE inhibitors or beta-blockers); 2) Treat hypercholesterolemia; 3) Calcium channel blockers that has negative inotropic effects could be harmful in asymptomatic patients that has low EF and has no HF symptoms after an MI; 4) Help patients to stop smoking; 5) Discourage illicit drug use; 6) Encourage patients who take alcohol to stop; 7) To prolong life, clinicians must administer ACE inhibitors as well as beta-blockers (purposely carvedilol, metoprolol, or bisoprolol) to every patient without any contraindication or intolerance. Cited by the American Heart Association, Powell (2009), a lead investigator from University of Medical Center in Chicago stated that, the policy of contributing through self-management skills training as well as education did not provide promote education single-handedly on heart failure hospitalization or mortality in patients with mild to moderate levels of heart failure. Self-management training may successfully decrease death or heart failure re-hospitalization significantly in those with specific needs such as underprivileged functional capacity, little adherence to drugs as wells low income.  Theory Most of the research involving older adults can be link into the philosophy of self-efficacy beliefs, which has either been quantitative or qualitatively assessed. The said efficacy belief has over and over again supported the influence of those beliefs about the behavior. Although, it has not been particularly established how efficacy beliefs in reality influence motivation among older adults, or what sources or bases of the efficacy-enhancing information best facilitate and strengthen those beliefs (Resnick, 2000). This study is based on the premise of Barbara Resnick “The Theory of Self-efficacy” which states that, self-efficacy expectations as well as the outcome expectations are not just influenced by behavior, physiological sensations, verbal encouragement, and exposure to role models or the so called self-modeling play a very important contribution. The theory of self-efficacy adheres to the principle that the more patient believe, initiate or engage in the efficacy of his or her specific activity, the further likely (motivated) he or she is to perform that specific activity. Research Application The study primarily aims to establish significant effects of daily weight monitoring as an intervention in controlling fluid retention among patients who have heart failure, within a period of 18 months. It will further graph the patter of weight among the participants. Introduction and Defining Intervention to be Examined These monitoring systems on patients’ weight collect and transmit daily clinical information, and are being used often in diverse settings (Chumbler, Vogel, Garel, Qin, Kobb, and Ryan, 2005; Cavallerano, Cavallerano, Katalinic, Blake, Rynne M, Conlin, Hock, Tolson, Aiello, Aiello, 2005 and Shapiro, Izumi, Tanner, Moscato, Valanis, David, and Gullion, 2004). Moreover, this has been implemented in a widespread procedural project by the Centers for Medicare and Medicaid Services, involving 300 000 patients which mandates use of the said surveillance strategy (Super, 2004). Content Areas for Literature Review The underlying clinical science which will clarify or define the use, methods and outcomes of the prognostic importance of the surveillance information will be presented in the literature of the study. Although weight gain has long been considered by clinicians as an indicator of heart failure decompensation, however, in real setting, studies have not properly demonstrated and established he pattern of daily weight change which occurred among admitted patients for heart failure. The pattern and other mechanisms of daily weight change will be attempted to be explored in this study. Hypothesis Daily weight monitoring has no significant effects to the daily weight patterns among patients who have heart failure, within a period of 18 months. Operational Definitions of Research Variables For the purpose of clarity the following terms are define operationally: Controlling Fluid Retention, in this investigation means an intervention of a health practitioner to avoid renal vasoconstriction as well as the development of water and sodium retention, which are both hallmarks of early stages of congestive heart failure. Daily Weight Monitoring is a system to monitor the weight of the patient on a daily basis in order to help them reduce rates of hospitalization. The weight being measured is transmitted in real-time straightforwardly to their doctor’s office. Patients with Congestive Heart Failure Heart failure are clients admitted in home care under a physiologically delicate condition and are selected for a clinical trial for a therapy that is designed to obstruct the sodium retention. Statement of Research Design and Rationale The design of the study is experimental design. It shall utilize a quasi experimental design since it will include patient (voluntarily agreed to take part in the study) who were defined by the first occurrence of heart failure and who were initially been diagnosed for heart failure and other pre existing risks. Quasi-experiments may be a consequence from either investigating pre-existing groups; no random assignment can exists herein; no causal statements should be made. Settings The study may be conducted in either hospital setting or home care, provided that informed consent from authority and respondent will be sought. Sampling Strategy: Purposive Sampling. Research Design: Quasi Experimental Design. Data Collection Plan and Data Analysis Plan There will be an initial comparison of medical conditions (coronary artery disease, diabetes mellitus, hypertension, stroke/transient ischemic attack, and chronic obstructive pulmonary disease) among patients and their use of medications. Case patients will be recognized by the initial occurrence of their heart failure hospitalization throughout the 18-months. There will be evaluation of the independent effect of predecessor weight change in a 1-week period previous to heart failure hospitalization and the majority of the data will be treated with conditional logistic regression techniques. All analyses will be processed using SAS software version 9.1 (SAS Institute, Cary, NC). REFERENCES American Accreditation HealthCare Commission, 2008 Hypertensive heart Retrieved April 15, 2008 from http://health.nytimes.com/health/guides/disease/hypertensive-heart-disease/overview.html American College of Cardiology and the American Heart Association. (2001) ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult. American Heart Association. Heart disease and stroke statistics. (2005)Dallas, Tex: American Heart Association. American Heart Association. 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