“I pledge my honor that I have neither given nor received inappropriate aid on this assignment”
Heart Failure is a serious problem affecting millions of American’s. This paper focuses on describing Heart Failure and the patient that I cared for at Newark Beth Israel Hospital. Several different non-pharmacological interventions are discussed that can be used by nurses in the clinical or home care setting. Educating patients on other ways of coping with high levels of anxiety which may be secondary to their disease process is a crucial way to prevent recurrent exacerbations of a patient’s condition.
Heart Failure (HF) affects approximately 5.7 million people in the United States (US), according to the Center for Disease and Control and Prevention (CDC) ("CDC," 2012). This results in an estimated cost of 34.4 billion dollars every year for the US ("CDC," 2012). Many risk factors contribute to the exacerbation of HF. They can range from hypertension to coronary artery disease. It is the role of the nurse to be knowledgeable of pharmacological and non pharmacological interventions that can be implemented in the treatment of these patients. This topic was chosen in order to learn more about alternative forms of interventions that do not include medications. The focus of this paper will be on non pharmacological interventions, like animal assisted therapy, relaxation techniques, and exercise and its effect on patients with HF.
HF occurs when contraction or filling of the hearts chambers are not effectively ejecting blood throughout the body, therefore not meeting metabolic needs (Lewis, Dirksen, Heitkemper, Bucher, & Camera, 2011). When this occurs the heart beings to use compensatory mechanisms to try and correct the underlying problem. These mechanisms occur as a result of a decrease in cardiac output (CO) and stroke volume (Lewis et al., 2011). This leads to the sympathetic nervous system (SNS) releasing catecholamines which will increase the heart rate and CO. Yet, this type of compensation results in an increased need for oxygen by the heart if not corrected. Next, when the kidneys sense a decrease in blood flow, they activate a neurohormonal response. This is referred to as the rennin-angiotensin-aldosterone system (RAAS) (Lewis et al., 2011). The RAAS releases angiotension II which makes aldosterone discharge via the adrenal cortex. Because of this reaction, the body now retains sodium and water, constricts blood vessels and therefore raises the blood pressure in hope to disperse more blood throughout the body (Lewis et al., 2011). A third form of compensation is dilation, which results in a stretched left ventricle due to uncontrolled high blood pressure. The dilation mechanism is yet another way of the heart attempting to increase CO. However, this will result in the final compensation method; hypertrophy (Lewis et al., 2011). Hypertrophy normally takes a long time to occur and will initially contribute to an increase CO. Yet, in time CO will drop due to a hypertrophied left ventricle which results in poor systemic circulation (Lewis et al., 2011).
The clinical manifestations of HF vary depending on whether the individual has right or left sided HF. In a patient with right sided HF, peripheral edema, weight gain, jugular venous distention, hepatomegaly, ascites are symptoms normally seen (Lewis et al., 2011). In contrast, a patient with left sided HF, will display with, shortness of breath, dysrthymias, pulmonary edema, and decreased ejection fraction (Lewis et al., 2011).
Treatment for HF will normally start with diuretics. These include, loop diuretics, thiazide diuretics, and potassium sparring diuretics (Lewis et al., 2011). The primary goals of these drugs are to increase the secretion of water and sodium from the body. However, the patients potassium