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Congestive Heart Failure

Develop a 5- to 10-slide PowerPoint presentation that addresses the following:
�Describe your selected disorder, as well as associated alterations. Explain the pathophysiology of the
alterations, including changes that occur in at least two body systems.
�Explain how genetics, gender, ethnicity, age, and behavior might impact the pathophysiology of the
alterations you identified, as well as diagnosis and treatment of your selected disorder.
�Construct a mind map for the disorder you selected. Include the epidemiology, pathophysiology of
alterations, risk factors, and clinical presentation, as well as the diagnosis and treatment of the disorder.

Congestive Heart Failure

Chronic heart failure refers to the inability of the heart to pump oxygenated blood to other vital organs in the

In the USA, about 5.5 million people suffer from chronic heart failure. According to Center for disease
control and prevention, CHF takes one life in every nine people diagnosed with CHF.

CHF is estimated to cost a total of $32 billion of the total health care costs to treat CHF condition.

CHF is a fatal medical disorder and the major reason of hospitalization as well as mortality rates in the USA
(Makaritsis et al., 2011).

Heart failure disorder is a multisystem disorder, which is described by numerous pathophysiological
alterations including skeletal muscles, cardiac muscle abnormalities, sympathetic nervous system.

Pathophysiology alterations in Mental
health systems

The main pathophysiological alterations include the alteration of neuro-hormones. Chronic heart failure
disease is progressive and entails a complex pathophysiological state.

The main clinical manifestation of CHF is the reduced left ventricular functions, which is caused by genetic
factors, hypertension, and myocardial infarction.

This impairs the cardiac muscle ability to pump blood effectively. The pathophysiology of CHF involves
neurohormonal model.

The hormones involved include aldosterone, angiotensin II, alpha tumor necrosis factor and
norepinephrine. These hormones are synthesized in and excreted into the blood circulation.

The increased concentration of the aforementioned hormones is also associated with anxiety and depression.

Pathophysiology alterations in Renal

The compensating mechanism used to maintain adequate arterial pressure involves the increase in filling

This involves the sympathetic nervous system activation, hypetrophy, as well as the remodeling of cardiac

Kidney is affected by the activation of rennin-angiotensin –aldosterone system (RAAS). This system results
to increase in retention of water and sodium salts.

These renal hemodynamic alterations make the glomerular filtrate (GFR) to be preserved. This is because the
angiotensin II constricts the efferent arteriole than the afferent one.

This causes the pressure in the intraglomerular capillary pressure to increase which increases the oncotic
pressure while reducing the hydrostatic intracapillary pressure, which results to renal failure.

Pathophysiology alterations in
Musco-skeletal systems

CHF patients often have difficulties to tolerance if exercise due to muscle fatigue and skeletal muscle.

These alterations are associated with the de-conditioning of the systemic neuro-hormonal changes and CHF
inflammation responses (Rehn et al., 2011)

Several studies highlight the histological abnormalities such as fiber type transformation and atrophy.

Other studies associate the transformation fiber type due to oxidative activity of the enzymes. These enzymes
are vital in regulation between utilization of energy and the energy produced.

However, researches are underway to understand the exact mechanism of the alterations and the impairment
i.e. whether the musco-skeletal impairment is due to oxidative stress, hypoxia, inflammation, and nutritional


Lifestyle behavior influences the extent of pathophysiological alterations.

For instance, increased intake of sodium in the diet causes excessive fluid retention, which causes the
activation of hormonal pathways. This causes renal dysfunction and weakening of the skeletal muscles.

Physical inactiveness also results in accumulation of harmful oxidants that affects the muscoskeletal system.
Regular exercise that is mild has been associated with increased blood flow in the muscles.

Fluid intake in CHF patient must be regulated. This is because there is risk of fluid retention that facilitates
renal dysfunction (Makaritsis et al., 2006).

Fluid retention also affects muscoskeletal system especially when fluid collects in the lower extremities.


Advance in age affects the cardiovascular function. For instance, older people show slight abnormalities
when performing submaximal loads, but their performance is low during exercises.

Elderly people are more likely to suffer renal dysfunction than young people are, which is attributed to the
hormonal imbalances associated with age (Goyal and Ehta, 2012).

Additionally, elderly people are more likely to present cognitive impairments and are more susceptible to
diseases due to reduced immune capacity.

This makes the elderly suffer psychological diseases, especially when they have to depend on others for their
daily activities of life such as cooking, bathing, and feeding.

This reduces their self-esteem and dignity


The study indicates that there is a higher relationship between CHF and ethnic group. The pathophysiology
alterations associated with ethnicity is influenced by external factors such as socio-economic status, which
influences access and utility of care (Aelebi et al., 2013).

Research indicates that African American people are more susceptible to renal dysfunction and stress.

The hormonal imbalances in the body reduce the kidney activities such as perfusion, which results to water
retention through the activation of rennin angiotensin aldosterone system (RAAS).

Most of the African American men are uninsured and thus access care when under critical condition. The
financial crisis and renal dysfunction makes the patient become depressed and increases their anxiety


CHF is defined as a complex syndrome, which includes myocardial function, congenital heart disease, and

CHF results in depression and dependency due to reduced quality of life. Research indicates that CHF
pathophysiological alterations affect sex differently.

However, the underlying mechanism on gender related differences is still unresolved, but there are
researches to unveil the root causes (Basile et al., 2013).

However, several studies highlights that women diagnosed with CHF present high chances of psychological
risks than male.

Renal dysfunction and muscoskeletal weakness are more common in males than in female. This is
attributable to different degree of self-care between the sexes.


Genetic polymorphisms have been used to study heart failure. Genes that directly affect CHF
have been identified (Susceptibility genes).

Polymorphisms are often located in promoter regions of a gene. This alters protein structure
and function.

This alters the fundamental role of neuro-hormonal
factors, which progresses the pathology of
alterations such as renal dysfunction, muscoskeletal muscles (Hypertrophy) and
neuro-hormonal genes (Alberti et al., 2013).

Mind concept


Alberti, L., Torlasco, C., Lauretta, L., Loffi, M., Maranta, F., & Salonia, A. et al. (2013). Erectile dysfunction in heart failure patients: a
critical reappraisal. Andrology, 1(2), 177-191.

Basile, G., Crucitti, A., Cucinotta, M., Figliomeni, P., Lacquaniti, A., & Catalano, A. et al. (2013). Impact of diabetes on cognitive
impairment and disability in elderly hospitalized patients with heart failure. Geriatrics & Gerontology International, 13(4), 1035-1042.

Extraordinarily Favorable Left Ventricular Reverse Remodeling through Long-Term Cardiac Resynchronization: Super-Response to
Cardiac Resynchronization. Pacing And Clinical Electrophysiology, 35(7), 870-876.

Goyal, B., & Mehta, A. (2012). Diabetic cardiomyopathy: Pathophysiological mechanisms and cardiac dysfuntion. Human &
Experimental Toxicology, 32(6), 571-590.

Makaritsis, K., Liakopoulos, V., Leivaditis, K., Eleftheriadis, T., & Stefanidis, I. (2006). Adaptation of Renal Function in Heart Failure.
Ren Fail, 28(7), 527-535.

Rehn, T., Munkvik, M., Lunde, P., Sjaastad, I., & Sejersted, O. (2011). Intrinsic skeletal muscle alterations in chronic heart failure
patients: a disease-specific myopathy or a result of deconditioning?. Heart Failure Reviews, 17(3), 421-436.

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