Assignment on Nursing 2022

Running head: NURSING ASSIGNMENT
NURSING ASSIGNMENT
Name of the Student:
Name of the University:
Author note:

NURISNG ASSIGNMENT1
Pathogenesis of acute exacerbation of chronic systolic heart failure:
The patient named, Mrs Brown, was suffering from the condition of systolic heart
failure that arises due to dysfunction within the rhythm, conduction of signals or structure of
the heart and affects the pumping activity of the heart. Systolic heart failure arises when the
heart is unable or fail to pump adequate amount of blood in the heart that in turn reduces the
cardiac output that is required for standard functioning of the human body. The prevalence
rate of heart failure is high among the older patients who have associated comorbidities such
as diabetes, angina, hypertension and prolonged lung illness (Mebazaa et al., 2015).
From the case scenario, it was evident that Mrs Brown had a past medical history of
breathlessness, dyspnoea associated with hypertension and reduce oxygen saturation level
that is responsible for leading the condition of heart failure. The patient was admitted to the
Emergency department (ED) and presently was dealing with severe condition of
breathlessness. The pathophysiology involved for the onset of heart failure is associated with
the total amount of blood which enters the human heart and reaches left ventricle and leaves
the heart through left ventricle (Tham et al., 2015).
There are various factors that result in the condition of heart failure and contribute
towards the contraction of heart namely preload, contractility and afterload that majorly
affects the stroke volume of the heart. Preload states the total amount of blood pumped into
the ventricles prior to heart contraction whereas afterload exhibits the pressure of pumping
out the blood from the ventricles that is majorly generated due to systemic and pulmonary
circulatory system. Contractility exhibit the capability of heart muscle to pump out the
complete blood present in the ventricles. The action of contractility is altered or hampered
due to damage caused by the first heart failure that therefore increase the possibility of severe
systolic heart failure (Mentz & O’connor, 2016). In the case scenario, the patient had already

NURISNG ASSIGNMENT2
suffered from heart failure two years ago and hence was under high risk of severe heart
failure due to damage heart muscle.
The systolic heart failure is defined as the condition when the human heart of unable
to pump adequate amount of blood and thus the activation of renin-angiotensin-aldosterone
system (RAAS) takes place. In case of systolic heart failure, the renin-angiotensin-
aldosterone system (RAAS) and neurohormonal imbalance is activated that result in different
physiological alterations such as increased afterload an filling pressure that further result in
fibrosis and atrial stretch contributing in the expansion of conduction irregularities and atrial
fibrillation. The patient had already suffered from heart failure, she might exhibit altered
level of calcium overloads and handling that further results in arrhythmia and after-
depolarization’s. Hence, the patient suffers from severe dyspnea due to impaired functional
activity of the heart and reduced cardiac output (Floras & Ponikowski, 2015). Since the
respiratory rate of the patient was very high approximately 24 breaths/minute, it was evident
that the patient great was beating very fast and the body was unable to fill adequate amount
of blood that resulted in atrial fibrillation.
The condition of atrial fibrillation is directly related to the onset of heart failure as the
loss of atrial systole takes place that alters the filling of blood in left ventricle and therefore
reduces the cardiac output of the person by 25% that result in the condition of systolic heart
failure. During low cardiac output, the sympathetic nervous system of the patient is activated
that stimulates the discharge of norepinephrine that ultimately triggers the beta-receptor to
enhance the heart rate of the patient and increases the speed and strength of muscle
contraction (Kotecha & Piccini, 2015). The muscle contraction result in high heart rate where
the ventricles thicken leading to hypertrophy and high level of collagen deposition that leads
to dysfunction and result in severe heart failure.