HEART FAILURE
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Ruth Kenney
Pathopharmacological Foundations for Advanced Nursing Practice
Western Governors University
HEART FAILURE
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Heart Failure
Investigated Disease Process
According to the CDC (2019), about 6.5 million adults in the United States have heart failure,
with an estimated annual cost of $30.7 billion.
Lesyuk et al. (2018), in their cost of illness study,
found that stage and comorbidities are the most common reasons for increasing cost, patients
with New York Heart Association (NYHA) stage IV are responsible for 70% of the annual cost
of heart failure. Comorbidities are the cause of 75% of all admissions related to heart failure.
"The lifetime risk of developing HF is 20% for Americans >
40 years of age” (Yancy et al., 2013,
p1501). Estimations show that in the next 15 years, heart failure will increase by 46%. Savarese
& Lund (2017), in their study of the global burden of heart failure, discuss the impact that an
aging population and improved heart failure survival rates will have on the hospitalization rates
and health care costs.
Heart failure carries not only a monetary value; maintaining the quality of
life is a challenge for many patients. Prevention, early identification, and intervention are
paramount to
successfully mitigating risk, and the rising cost associated with heart failure.
Pathophysiology
Heart failure is the result of a chronic progressive disease state.
Heart failure results from
physiologic changes that occur with various conditions such as hypertension, coronary artery
disease, myocardial infarction, valvular heart disease, and other cardiovascular conditions.
Smoking, obesity, diabetes, alcoholism, drug abuse, thyroid disease, and chemotherapeutic
agents also contribute to the development of heart failure. The Framingham study found that the
HEART FAILURE
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lifetime risk of developing HF was twice as high in subjects with a blood pressure
of≥160/100mmHg compared with ≤140/90mmHg (UpTo Date, 2020).
Myocardial dysfunction
results in reduced cardiac output, which activates the sympathetic nervous system causing
increased activity of the renin-angiotensin system which maintains perfusion to vital organs, over
time, this compensatory mechanism results in ventricular remodeling, disease progression, and
worsening functional abnormalities of the heart (Kirkwood &Paul, 2018).
Oxygen-rich blood travels from the lungs to the left atrium then to the left ventricle, which
pumps the blood out to the rest of the body.
In left-sided heart failure, the left ventricle has a
reduced ability to effectively pump the blood out of the heart to the rest of the body. The failure
of the left ventricle is broken down further into systolic failure or diastolic failure; systolic
failure is a result of the left ventricle's inability to contract normally, resulting in a decreased
ejection fraction (EF), so not enough blood is ejected out to the body.
In diastolic failure, the left
ventricle is too stiff and is unable to relax, which results in an inability of the ventricle to fill
during rest, causing a "backup" of blood into the right side of the heart. The Framingham study
