Assignment: The Map should be about Left-Sided Heart Failure

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Assignment: The Map should be about Left-Sided Heart Failure

Assignment: The Map should be about Left-Sided Heart Failure

Below are the Sub-heading that needs to be in the Concept Map.

Disease

Definition

AETIOLOGY

PATHOGENESIS

PATHOGENESIS

DIAGNOSIS

TREATMENT

COURSE OF DISEASE

PROGNOSIS

PREVENTION

Assignment: The Map should be about Left-Sided Heart Failure

Assignment: The Map should be about Left-Sided Heart Failure

· The separate Reference page for Concept Map. You may have more than 2 reference

· Visually Stimulating, add pictures in the background and visually attractive. Below is an sample example but this concept map needs to look unique and visually very appealing, please.

· Add pictures of heart, lungs what ever connects to the Map and its information.

· I have attached a sample of the concept map of another topic to guide you what information requires in the map.

· 500 words and it is worth 25 Marks.

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argument.

Abstract
Despite the advancement in medicine, management of heart failure (HF), which usually presents as a disease syndrome, has been a challenge to healthcare providers. This is reflected by the relatively higher rate of readmissions along with increased mortality and morbidity associated with HF. In this review article, we first provide a general overview of types of HF pathogenesis and diagnostic features of HF including the crucial role of exercise in determining the severity of heart failure, the efficacy of therapeutic strategies and the morbidity/mortality of HF. We then discuss the quality control measures to prevent the growing readmission rates for HF. We also attempt to elucidate published and ongoing clinical trials for HF in an effort to evaluate the standard and novel therapeutic approaches, including stem cell and gene therapies, to reduce the morbidity and mortality. Finally, we discuss the appropriate utilization/documentation and medical coding based on the severity of the HF alone and with minor and major co-morbidities. We consider that this review provides an extensive overview of the HF in terms of disease pathophysiology, management and documentation for the general readers, as well as for the clinicians/physicians/hospitalists.

Keywords: biomarker, heart failure, ICD 10, readmission, utilization
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1. Introduction
1.1. Background
Heart failure (HF) is a clinical syndrome caused by structural and functional defects in myocardium resulting in impairment of ventricular filling or the ejection of blood. The most common cause for HF is reduced left ventricular myocardial function; however, dysfunction of the pericardium, myocardium, endocardium, heart valves or great vessels alone or in combination is also associated with HF. Some of the major pathogenic mechanisms leading to HF are increased hemodynamic overload, ischemia-related dysfunction, ventricular remodeling, excessive neuro-humoral stimulation, abnormal myocyte calcium cycling, excessive or inadequate proliferation of the extracellular matrix, accelerated apoptosis and genetic mutations [1].

1.2. Classification of HFs
Heart failure can be classified as predominantly left ventricular, right ventricular or biventricular based on the location of the deficit. Depending on the time of onset, HF is classified as acute or chronic. Clinically, it is typically classified into two major types based on the functional status of heart: heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). In patients with HFpEF who are mostly females and older adults, EF is usually more than 50%; the volume of the left-ventricular (LV) cavity is typically normal, but the LV wall is thickened and stiff; hence, the ratio of LV mass/end-diastolic volume is high [2]. HFpEF is further categorized as borderline HF if the EF stays between 41% and 49% and improved HF if EF is more than 40% [1]. In contrast, in patients with HFrEF, the LV cavity is typically dilated, and the ratio of LV mass/end-diastolic volume is either normal or reduced. At the cellular level, both cardiomyocyte diameter and the volume of myofibrils are higher in HFpEF than in HFrEF [1]. As far as treatment and outcome are concerned, patients with HFrEF respond favorably to the standard pharmacological treatment regimen and demonstrate better prognosis. In contrast, patients with HFpEF have not been shown to respond to standard pharmacological treatments, except for nitrates, and therefore, have a poor prognosis, especially during the decompensated phase of HF [2,3,4]. In addition, based on cardiac output, HF is also classified as high-output failure and low-output failure. High-output failure is an uncommon disorder characterized by an elevated resting cardiac index of greater than 2.5–4.0 L/min/m2 and low systemic vascular resistance. The common causes of high output failure are severe anemia, vascular shunting, hyperthyroidism and vitamin B1 deficiency. This occurs as a result of ineffective blood volume and pressure, which stimulate the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS), causing the release of antidiuretic hormone (ADH), which all together ultimately lead to ventricular enlargement, negative ventricular remodeling and HF. Low output failure is much more common than high-output failure and is characterized by insufficient forward cardiac output, particularly during times of increased metabolic demand. Left ventricular dysfunction due to large MI, right ventricular dysfunction due to an acute pulmonary embolus and biventricular dysfunction are important causes of low output failure. More recently, exercise intolerance in HFpEF is proposed to be due to a decrease in oxygen delivery to or impaired oxygen utilization by the exercising skeletal muscles. Oxygen utilization is being calculated as the arterial–venous oxygen content difference (A-VO2 Diff), rather than reduced cardiac output (CO) [5,6]. Considering the slowed down oxygen uptake kinetics in HF along with peripheral muscle function impairment, exercise rehabilitation seems to be a logical and essential factor in improving the inflammatory imbalance, relieving elevated cardiac filling pressures, restoring exercise capacity, quality of life and reducing morbidity and mortality associated with HF. Hence, exercise training, mostly high intensity as opposed to moderate, in HFpEF patients has been significantly shown to improve rate of oxygen consumption or VO2 without affecting endothelial function [7,8].

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