Disease Process: Heart Failure. Research Paper on Medicine.

It is a pathophysiologic state whereby the cardiac functioning of the heart develops abnormality such that it fails to perform its functions such as pumping blood at a rate proportional to the metabolic body process. It is one of the leading chronic diseases responsible for up to 5 million deaths, and a maximum of 38 billion medical cost in the US alone hence can translate to huge figure in global perspective.

A1: Pathophysiology

This section of the disease process explains the functional changes that accrue in the human body due to heart failure. According to Kemp and Conte (2012), pathophysiology of heart failures explores the functional variations in the human body parts that the disease affects such as neurohumoral status, blood volume, cardiac and systemic vascular functioning and integration. In summary, Kemp and Conte (2012) explain that heart failure causes cardiac dysfunction, which consequently causes alterations in the neurohumoral status, blood volume, and vascular function. The alterations have the role of acting as compensatory mechanisms through the application of systemic vasoconstriction that controls blood pressure and Frank-Starling mechanism for controlling cardiac output. McDonagh, Gardner, Clark, and Dargie, (2015), on the other hand, say that compensatory mechanism to include the changes in the myocyte through regeneration, augmentation of contractile mass tissue through myocardial hypertrophy, and neurohumoral systems activation. After a time, the compensatory mechanism deteriorates cardiac function demanding for the alternative intervention of heart failure; They include the application of treatment strategies that modulate non-cardiac factors like venous and arterial pressures using diuretic drugs and vasodilator administration. It is essential to comprehend the pathophysiology elements of heart failure for the main reason that, insights obtained become the foundation of therapeutic intervention

Cardiac Function

The reduction in the cardiac output after heart failure occurs due to the alterations in the cardiac function.The changes in the cardiac function include reduced stroke volume as a result of impairment of the either diastolic function, systolic function or both. When the heart loses contractility, systolic dysfunction occurs, and the causal factors are mainly the changes in the mechanisms responsible for signal transduction which plays a key role in the regulation of contractibility. When the heart failure trigger loss of significant contracting muscle as result of severe myocardial infarction, it similarly triggers systolic dysfunction. On the other hand, Kemp and Conte (2012) describes diastolic dysfunction to means a situation in which ventricle properties become stiffer or less compliant leading to the impairment and reduction of the ventricular filling.

There is a considerable reduction in blood ejection after ventricular filling. The resultant effect of both diastolic and systolic dysfunction is increased ventricular pressure hence serving as adaptation or compensatory mechanism through the utilisation of the Frank-Starling strategy to increase stroke volume. A different type of compensatory plan occurs in the dilated cardiomyopathy heart failure where there is automatic dilation of the heart ventricles which assists in normalising preload pressures. Some of the strategies that serve as therapeutic interventions for enhancing cardiac function includes the application of cardio-stimulatory drugs like digitalis and beta-agonists whose functions include stimulating contractility and heart rate. Vasodilator drugs similarly serve an essential purpose in improving cardiac functioning as they improve stroke volume by reducing ventricular afterload.

Changes in the Neurohumoral Status

Another pathophysiological change that occurs after a person contract heart failure is the alterations in the neurohumoral responses. Such changes the increment in the production of natriuretic peptides and antidiuretic hormones, and the activation of renin-angiotensin and sympathetic nerves. The overall effect of the neurohumoral status change is the production of arterial vasoconstriction that has the purpose of maintaining blood pressure. Other effects include the increment of blood pressure for subsequent enhancement of ventricular filling and venous constriction for increasing pressure in the venous system. It is for these reasons that the general observations of many scholars about neurohumoral responses leads to the common conclusion that they are compensatory mechanisms (McDonagh, Gardner, Clark, & Dargie, 2015).

The additional function of the neurohumoral responses is the intensification of heart failure due to the significant increase in the ventricular preload, which lowers the stroke volume while aggregating the preload to levels that trigger the occurrence of oedema, systemic and pulmonary congestion. Therapeutic intervention of heart failure in the perspective of the neurohumoral function is such that there should be the utilisation of drugs that have the ability to offset the neurohumoral alterations. Examples of useful treatment drugs include those that can prevent extreme activation of sympathetic nerves such as beta-blockers that have the predominant attributes of being good in the provision of significant long-term benefits. Others include the drugs that inhibit renin-angiotensin-aldosterone system activities such as aldosterone receptors, angiotensin receptor inhibitors and Angiotensin-converting enzyme blockers. Blood Volume

According to the frank-Starling, compensatory mechanism, the increment of stroke volume occurs due to the compensatory rise in blood volume for significant upsurge in ventricular preload. Amplification of blood volume occurs due to certain reasons including the decrement of urine output and fluid retention because of decreased renal perfusion results. Additionally, there is a stimulation of renin release in the situation where sympathetic kidney activation combines with reduced renal perfusion hence the activation of the renin-angiotensin system that has the considerable impact of enhancing aldosterone secretion.

As the volume of blood increases, there is also an increment in the circulation of antidiuretic hormone which plays a fundamental role in the retention of renal water which enhances humoral activation for increased reabsorption of renal water and sodium. Therefore, blood volume acts as a compensatory mechanism in that its upsurge assist in maintaining cardiac output but there are chances of the increased blood volume becoming deleterious due to the growing probability of raising the venous pressures which are the causal factor or systemic and pulmonary oedema (Mittman, Eschenhagen, & Scholz, 1998). The occurrence of oedema some body organs such as the lungs trigger exertional dyspnea hence the need for the heart failure patients receiving diuretic drugs as an intervention for reducing venous pressures and blood volume to avert the occurrence of oedema.

Systemic Vascular Function

One of the ways of compensating for the decreased cardiac in the case of heart failure is the application of feedback mechanism by activating the adrenergic system that constricts arterial resistance hence maintain the blood pressure at normal levels. The resistance of systemic vascular increases upon the activation of adrenergic nervous glands. On the other hand, the venal pressure becomes elevated as the veins constrict. Some of the essential elements of the compensatory feedback system include the arterial baroreceptors when there is a case of severe heart failure. The systemic vasoconstriction occurs due to humoral activation of the vasopressin hormone and renin-angiotensin system. Therapeutic intervention strategies in systemic vasoconstriction perspective entail the use of drugs that have the ability to block these mechanisms including enzyme inhibitors like angiotensin and blockers such as angiotensin receptors. These drugs should also enhance the volume of ventricular stroke through the reduction of ventricular afterload, and they include vasodilators like sodium nitroprusside and as hence the enhancement of cardiac output.

Cellular Changes

Heart attack at cellular levels entails the exploration of the spatial variability and beat-to-beat of the kinetics of calcium ions (Ca2+) which are at unprecedented levels during heart failure (McDonagh, Gardner, Clark, & Dargie, 2015). In the perspective of cellular changes, the definition of the term heart failure is that it is a health condition characterised by series of phenotypic alterations that accrue from the irregularities in the Ca2+ signals. The resultant abnormalities can either be electrophysiological or mechanical dysfunction. For the case of mechanical dysfunction, decreased systolic contractile mechanism characterise heart failure while electrophysiological dysfunction describes heart failure from the perspective of prolongation of QT interval prolongation, and augmented incidence of sudden cardiac death (SCD) and amplified ventricular beats. Ca2+ governs the interaction of electrophysiological and mechanical dysfunction by guiding how the depolarising pulse translates into mechanical contraction in the myocardial cells of the ventricles. Therefore, the dysfunction of the handling of intracellular Ca2+ trigger both electrophysiological and mechanical abnormalities.

A2. Standards of Practice for Heart Problem

Standard 1: Diagnosis

It is essential that correct diagnosis of patients suspected of suffering from heart failure be undertaken for the reversible causes to be addressed and treatment initiated in time. A detailed history and clinical examination are essential for the adequate diagnosis of HF. The common symptoms of heart failure are evident when the heart is unable to pump blood towards meeting the body needs adequately or able to discharge its roles under high cardiac pressure. The diagnosis of HF by the presence of characteristic symptoms, which include orthopnea, neck-vein distention, cardiomegaly, displaced apical impulse, acute pulmonary oedema, weight loss, rales, nocturnal cough, hepatomegaly, third heart sound, and pulmonary vascular congestion confirms the presence of HF (Steimle, 2007). It is important that physicians weigh some evidence, and consider the various conditions that cause heart failure towards achieving an adequate diagnosis. It has been noted over time that patients medical history and the results from physical, electrocardiography and chest x-ray examinations provide an accurate diagnosis in over 90% of cases (McDonagh, et al., 2011).

The various techniques of diagnosis include the review of the Neck Veins for Jugular Venous Pressure. Measuring the vertical distance of the internal vein above the sternal angle the pulsation on the right internal jugular vein is located with the normal pressure located 4cm above the sternal angle when the patient is at 45 degrees to the horizontal floor determines JVP (Steimle, 2007). According to McDonagh, et al. (2011), when HF is suspected based on medical history and examination results, it is important that any pieces of evidence of heart abnormality be determined. A routine test, in this case, is by echocardiography, which assesses the functions and structure of the valves and ventricles. Considering that heart failure rarely occurs in structurally normal hearts, any notable abnormalities through echocardiography provides the much-needed evidence for the diagnosis. Other factors that act as a baseline include the normal LVEF which is 50-70%, and mildly elevated pulmonary pressure of between 40-60mm Hg characterise HF