Research Paper on "Pathophysiology of Congestive Heart Failure"

Research Paper 7 pages (2102 words) Sources: 5

[EXCERPT] . . . .

Pathophysiology of congestive heart failure is incredibly complex, making it difficult for modern health care practitioners to define its conditions and leading the need to further explore the process of congestive heart failure. Still, with so many people around the world suffering from the life altering affects of congestive heart failure, it is important that contemporary medical practice remains active in defining the pathophysiology of the condition. This will ultimately help boost the general understanding of what symptoms look like and can help get patients the help they need faster.

Concepts within pathophysiology are bred from combining pathology with elements of physiology. Together, they blend in synergy in order to help give a more vivid picture of the affects of congestive heart failure among other serious conditions and diseases. Essentially, pathophysiology is concerned with observing and working towards solutions of the changes resulting from a condition or disease. Subsequently, the pathophysiology of congestive heart failure is at the same time active in defining symptoms as they occur and how other systems in the body are impacted by the presence of a serious cardiac condition, like congestive heart failure.

Congestive Heart Failure

In today's health environment, cardiac issues are one of the most serious faced by medical practitioners. There are a number of conditions that are covered in this larger concept term. Essentially, "heart failure is a clinical syndrome characterized by systemic perfusion inadequate to meet the body's metabolic demands as a result of impaired cardiac pump function" (Hobbs & Boyle, 2010). The more specif
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ied condition to be analyzed in this pathophysiological evaluation is the condition known as congestive heart failure. This is a type of heart failure that involves the swelling and congestion of blood in the heart because of an inability to properly pump blood to where it is needed throughout the body. Interestingly enough, "most patients with HF do not complain of symptoms at rest, but rather with physical exertion" (Borlaug & Paulus, 2011, p 674). This often makes it difficult to diagnose an early onset of the condition without a patient noticing potential pain or other symptoms during the daily events of their lives. The stress of exercise often activates abnormalities in the reserve functions of the heart (Borlaug & Paulus, 2011). Thus the normal and systolic reserves are impacted with exercise and are significantly impaired with conditions of heart failure. Still, it is a serious issue that cases massive degeneration of the other organs because of a lack of proper blood flow. Here, the research suggests that it starts "beginning as a single organ disease, it becomes a systemic disease during its evolution and progression" (Galli et al., 2010, p 155). Without the heart in full functioning capabilities, the other systems of the body are soon at risk when there has been a diagnosis of congestive heart failure.

There are a number of pathophysiological signs that can be noted in cases of congestive heart failure. Most patients have signs and symptoms of "fluid overload and pulmonary congestion, including dyspnea, orthopnea, and paroxysmal nocturnal dyspnea" (Hobbs & Boyle, 2010). These are some of the more obvious signs that there are cardiac issues potentially endangering the health and well being of the patient looking for a diagnosis. Moreover, more immediate symptoms of congestive heart issues can include "renal dysfunction, chachexia, valvular regurgitation, ventricular arrhythmias, higher NYHA heart failure class, lower LV injection fraction (LVEF), high catecholamine and B-type natriuretic pepdtide (BNP) levels, low serum sodium level, hypocholesterolemia, and marked LV dilation" (Hobbs & Boyle, 2010). One of the major signs is too much volume in the heart that is not being pushed out to the rest of the body which is in need of the oxygen in the blood. This is the primary cause for pulmonary and/or venous congestion. Congestive heart failure is a direct result of "depressed left-sided cardiac function" (Aucoin, 2011, p 12). The left side of the heart is overworked pumping out blood that is being blocked in and causing congestion to build up and cause abnormal functioning of the entire cardiac system. There is a dilation of the LV chamber, which "can cause mitral annular dilation and mitral regulation, leading to pulmonary congestion" (Hobbs & Boyle, 2010). As the left ventricular chamber continues to dilate, the rate of congestion within the heart increases, and thus the dangers of congestive heart failure also begin to increase.

The left ventricle is the side that is most impacted because it is the side which pumps out blood to the rest of the body. Essentially, blood is still being taken into the heart, but is having a hard time being pushed out. This can cause "diastolic LV dysfunction, which consisted of prolonged isovolumic LV relaxation, slow LV filling, and increased diastolic LV stiffness" (Borlaug & Paulus, 2011, p 671). Overall, such a process causes increased pressure in both ventricles, but more so on the left chamber that is a life line for the other organs in the body. During such cases of congestive heart failure, "the heart's ability to pump out a normal stroke volume" is severely impaired, causing major damage to the cardiac and other organ systems within the body (Aucoin, 2011, p 15). There is then an overall decrease in the blood that is being pumped out by the heart. This leads too many patients to suffer and die from "end-organ failure resulting from inadequate systemic organ perfusion, particularly to the kidneys" (Hobbs & Boyle, 2010).

Research by Li et al. (2012) looked at an even more specific instance of congestive heart failure to define its pathophysiology. In their work, the researchers explored the condition known as Dilated Cardiomyoptahy (DCM). It "is a cardiac muscle disorder characterized by systolic dysfunction and ventricular chamber dilation" and is "a major cause of congestive heart failure" (Li et al., 2012, p 1). This abnormality in the cardiac muscle is a result of risk factors, but also new research is showing that it can occur out of heredity. There have been findings which suggest a genetic link to DCM. Li et al. (2012) conclude with evidence showing clear signs of congestive HF, such as severe pulmonary edema and dyspnea associated with marked changes in myocardial expression of biomarkers of HF" (Li et al., 2012, p 5). Thus, certain elements of the pathophysiology of congestive heart failure go beyond life style factors and are determined by genetic biomarkers.

Impact on the Brain and Nervous System

It is clear that the cardiac system is intimately related with all the other organ systems in the body. As such, congestive heart failure not only impacts the heart and cardiovascular system, but other bodily systems as well. One of those major elements impacted by abnormal cardio functioning is cognitive functioning. Here, the research illustrates that "it has been demonstrated that depression is associated with poor prognosis in patients with HF, with higher prevalence rates of depression being associated with higher NYHA functional class" (Li et al., 2012, p 1). Li et al. (2012) associate this with a malfunction in serotonin release that is associated with the pathophysiology of congestive heart failure. Thus, the worse a patient's depression is, the worse the condition may end up to be based on the neurological connection between the brain's suppressor symptoms and abnormal cognitive functioning as a result of congestive heart failure factors.

The entire nervous system is also majorly impacted by the presence of such a damaging cardiac condition. Again looking at Li et al. (2012), it can be seen that the "autonomic areas of the lower brainstem and spinal cord that involve regulation of the cardiovascular system" can also show clear symptoms when a patient is in a state of congestive heart failure (Li et al., 2012, p 6). Thus, Li et al. (2012) "suggest that brain 5-HT dysfunction, due to at leas in part to the loss-of-function SNP C1473G in TPH2 gene, might play a promotive role in the development of congestive HF" (Li et al., 2012, p 6). Moreover, the pathophysiology of congestive heart failure also impacts the sympathetic nervous system as well. The sympathetic nervous system is activated and can cause tachycardia. This activation can also increase the myocardial oxygen consumption. The research shows how the sympathetic nervous system "increases heart rate and contractility, causes arteriolar vasoconstriction in nonessential vascular beds, and stimulates secretion of rennin from the juxtaglomerular apparatus of the kidney" (Hobbs & Boyle, 2010). When there are abnormal conditions in the cardiovascular system because of congestive heart failure, the sympathetic nervous system is also severely impacted. The sympathetic nervous system is activated "leading to peripheral vasoconstriction to preserve blood pressure homeostasis in vital areas and regulate sodium and water retention to preserve blood volume" (Galli et al., 2010, p 155). Peripheral vasoconstriction is often directly related to the condition's impact on the sympathetic nervous system. The body will begin to retain salt and water when the rennin-angiotensin system is activated. Fluid retention is one of the more obvious signs. Essentially, fluid… READ MORE

Quoted Instructions for "Pathophysiology of Congestive Heart Failure" Assignment:

Paper should be in APA 6th edition and include:

Introduction that identifies the topic , explains the significance, and describes the focus of the paper.

Body of paper: Review the literature regarding the topic , using subheadings to organize the work.

Discussion: Summarizes the body of paper and integrates scientific findings.

Significance to advanced nursing practice: Relate the topic to advanced practice nursing.

References:Minimum of 5 journal articles less than 4 years old!!(I will need a copy of each journal article emailed to me!)

PLEASE NOTE: THIS IS NOT A CLINICAL PAPER...IT IS A PATHOPHYSIOLOGY PAPER..THANKS! *****

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