Chronic Heart Failure: Causes, Diagnosis, and Treatment

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Table of Contents
Introduction................................................................................................................ 3
Aetiology.................................................................................................................... 3
Pathophysiology......................................................................................................... 4
Clinical Manifestation................................................................................................. 5
Diagnosis.................................................................................................................... 6
Clinical Course............................................................................................................ 7
Treatment................................................................................................................... 8
Conclusion.................................................................................................................. 9
References............................................................................................................... 10
Table 1: Types of Chronic Heart Failure......................................................................5
Figure 1: Pathogenesis of CHF.................................................................................... 7

Chronic Heart Failure
Introduction
Chronic heart failure is worldwide pandemic that affects more than 26 million people and
at least 300000 Australians (Taylor, Harrison, Britt, Miller, & Hobbs, 2017). Chronic heart
failure (CHF) is a lifelong limiting condition that is life threatening in the advance stage. CHF,
also known as congestive heart failure is a condition of ongoing inability of a person’s heart to
enough pump blood in all parts of the body and ensure that there is sufficient supply of oxygen
and nutrients (Atherton et al., 2018). The heart is unable to function efficiently and effectively to
enable the pumping of the blood through the body. CHF condition is different from heart attack
and cardiac arrest. Chronic heart failure involve heart muscles unable to pump blood properly
while cardiac arrest refer to heart stopping and having no pulse and heart attack refer to death of
heart muscle as a result of coronary artery blockage (Atherton et al., 2018). CHF is a serious
condition and cannot be cured but can be managed by right treatment for increased life
expectancy and improved quality of patient’s life. The following write-up discusses the chronic
heart failure aetiology, Pathophysiology and incidence of the condition in world and national
level. The write-up also discusses the CHF diagnostic tests, clinical course and prognosis,
treatment options and the public health implications.
Aetiology
Chronic Heart Failure is a condition caused by any condition in the human body that
damages the heart muscle. The first main cause of CHF is coronary artery disease. Coronary
arteries have an important role of supplying blood to the heart muscle. The blockage of coronary
arteries blocks or reduces blood supply in the heart muscle that reduce amount of oxygen and
nutrients supplied in the heart muscle. The heart muscle gets insufficient oxygen and nutrients
that are vital to enhancing the ability of the heart muscle to function properly. The second
aetiology of CHF is heart attack. Sudden blocks of coronary arteries as a result of heart attack
lead to scars in heart’s tissues. The scars in the tissues of the heart decrease how the heart
effectively pumps. The third cause of CHF is cardiomyopathy. Any damage on the heart muscle

other than blood flow or artery problems causes chronic heart failure. These other factors include
drug side effect or infections. Another cause of CHF is any condition that overworks the heart.
For instance, hypertension, valve disease, kidney disease, or diabetes conditions overwork the
heart muscles that cause CHF. The risk of CHF is increased by the following factors; obesity,
smoking, diabetes type 2, anaemia and amyloidosis.
There are around 30000 cases of CHF that are diagnosed every year in Australia with a
total of 4% of the Australian population living with the condition (Sahle, Owen, Mutowo, Krum,
& Reid, 2016). The rate of death and hospitalization as a result of CHF among Indigenous
Australian is 2-3 times more as compared to Non-Indigenous Australians. The incidence and
prevalence of CHF is more to ageing population as compared to younger people (Vongmany,
Hickman, Lewis, Newton, & Phillips, 2016).
Pathophysiology
The CHF syndromes occur as a result of abnormality in cardiac structure, rhythm,
function, or conduction. The CFC indicates the inability of a person’s heart to maintain enough
delivery of oxygen and a systematic response that attempt to compensate the inadequate oxygen
delivery. The cardiac output is impacted and the body expectation of oxygen delivery is not met.
CHF is caused by myocardial infarction, hypertension and amyloidosis that directly adversely
affect the heart muscles (Sager et al., 2016). The cardiac output is determined by the heart rate
and stroke volume. The stoke volume is determined by the volume of blood that enter the left
ventricle (preload), contractility, and blood flow from left ventricle (afterload). The heart work as
dynamic pump and depend on it inherent properties and what is pumped in and what must be
pumped against. Reduced contractility and impaired ventricular filling results to increased
systolic volume and decreased end diastolic stroke volume respectively. The reduced cardiac
output cause several changes in the heart and the whole body. One of the changes is in the
arterial blood pressure falling. This change dissimulates baroreceptors that are located in the
carotid sinus which is linked to nucleus tactus solitarii. This increases sympathetic activity that
release catecholamines in a person’s blood stream. The binding to apha-1 receptors lead to
arterial vasoconstriction that enables to restore blood pressure and has consequent effects of
increasing total peripheral resistance that increase the heart workload (Ul Haq, Wong, & Hare,
2015). The binding to beta-1 receptors inside the myocardium increased heart rate making