Systolic Heart Failure Report 2022

Running head: SYSTOLIC HEART FAILURE
SYSTOLIC HEART FAILURE
Name of Student
Name of University

SYSTOLIC HEART FAILURE1
Author’s Note

SYSTOLIC HEART FAILURE2
Aetiology
Congenital heart
defect
High Blood Pressure
Cardiomyopathy
Heart attack Heart Valve
Disease
Emphysema
Irregular heart
rhythms
Diabetes
Pathogenesis
Hypertension leading to
increased heart rate thereby,
leading to heart failure
Mass Mitochondrial
Dysfunction, thereby reduced
oxygen, reduced work
efficiency and reduced exercise
capability, thus failure of
circulatory system
Clinical
Manifestations
SShortness of Breath,
tiredness, weakness,
dizziness, nausea, polyuria,
long lasting coughing, legs,
ankle and feet swelling,
reduced ability to exercise,
rapid weight gain, chest pain,
difficulty in concentrating and
lack of appetite
Insufficient delivery of oxygen
for metabolic needs due to
myocardial injury, which results
in impaired metabolic
vasodilation and Reduced
Skeletal Muscle
Treatment
Ivabradine
Furosemid
e
Glyceryl
Trinitrite
Pharmacothera
py Nursing & non-
pharmacotherapy
Monitoring the vital
signs of a patient with
heart failure
Effective Medication
and Oxygen Therapy
Diagnosis
Exercise test, BNP
and NT-proBNP
(NT-proB-type
Natriuretic
Peptide) blood
test
Chest x-ray Heart
catheterization
Patterns
of
Irregular
heartbea
t
Blood
test
Electrocar
diogram
Course of the
Disease
Prevent
ion
Stage A: High BP, Rheumatic
Fever, Diabetes
Stage B: Cardiomyopathy, Heart
attack, Valve disease
Stage C: Fatigue, shortness of
breath, Inability to perform
exercise
Stage D: Surgery options, heart
transplant, constant infusion of
intravenous inotropic drugs,
ventricular assist devices
Stop smoking,
Healthy
lifestyle,
weight loss,
effective
treatment
Systolic Heart Failure
When the left articular pump of
heart becomes bigger in size they
pump out less amount of blood, as
they become weak and cannot
perform contractions the way it
should
Acute Exacerbation of Heart
Failure

SYSTOLIC HEART FAILURE3
Question 1
Mrs. Brown (78 year old) was admitted to the hospital because of severe shortness of breath and the doctors were told about
her medical history of heart failure. In the case of a systolic heart failure, cardiac output is reduced as the size of the left ventricles
muscles increases and thereby loses the capability to pump adequate amount of blood efficiently (Alpert et al., 2014), leading to low
amount of oxygen, inability of the kidney to remove excess fluids, atrial fibrillation and increased heart rate. This oxygen loss further
results in various dysfunctions of the body, as oxygen is the primary source for the efficient metabolism and functioning of the body
and the reduced levels of oxygen results in the increased blood pressure, decreased oxygen saturation, increased heart rate and
increased respiration rate (Harjola et al., 2017). Due to the inactivity of the kidneys to remove excess fluids, the renin (also termed as
angiotensinogenase) release converts the Angiotensin 1 to Angiotensin 2 (Sayer & Bhat, 2014) by effectively participating in the
body's renin–angiotensin–aldosterone system, which is responsible for resolving the amount of excess fluid and vasoconstriction of
arteries (Clark, Krum & Hopper, 2014). Thereby increasing the blood pressure and increased aldosterone biosynthesis, thereby
increasing the reabsorption of salt and water and increased volume of extracellular fluid. Angiotensin 2 further leads the pituitary
gland to secrete huge amount of antidiuretic hormones. Antidiuretic hormones are responsible for maintaining the water balance in the
blood, thus increased amount of the hormone results in increased concentration of water in blood (Ter Maaten et al., 2015), which
thereby causes increase in volume and blood pressure. With the reduced amount of blood flow from heart, the carotid baroreceptor
starts responding to the changes of the pressure and blood flow amount of the heart (Ponikowski et al., 2014). The response of carotid