Western Sydney University: Nursing Assignment on Heart Failure Care

This nursing assignment report focuses on the acute exacerbation of chronic systolic heart failure, using a case study of a patient named Mrs. Brown admitted to the Emergency Department (ED). The report delves into the pathophysiology of systolic heart failure, highlighting factors like preload, contractility, and afterload, and the role of the renin-angiotensin-aldosterone system (RAAS) and neurohormonal imbalances. It discusses the nursing strategies for managing patients in the ED, including assessment of heart rhythm, blood pressure, and oxygen saturation. The report also explains the mechanism of action of key medications, specifically IV furosemide and sublingual glyceryl trinitrate (GTN), used in the treatment of heart failure. The report is supported by various research articles and provides a comprehensive overview of the nursing care required for patients experiencing acute heart failure, emphasizing the importance of continuous monitoring and tailored interventions to improve patient outcomes.

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

1NURISNG ASSIGNMENT
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

2NURISNG ASSIGNMENT
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.

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Nursing strategies to manage the patient in Emergency department:
Heart failure is considered as the chronic and progressive condition that must be
managed and monitored by the skilled nurses who will aim to improve the health condition of
the patient by either managing their life style or by medication therapy. In this case scenario,
the patient exhibited low cardiac output that was the major cause of heart failure, hence it was
very crucial for the nurse to determine an appropriate nursing stagey that will manage and
control the cardiac output of the patient (Fenwick, 2015).
Since the patient was admitted to the Emergency Department (ED), it was very crucial
that the nurse will evaluate and assess the heart rhythm and heat rate of the patient and also
auscultate the apical pulse to note if any condition of tachycardia or atrial fibrillation is
present. This assessment will allow the nurse to identify if the patient is exhibiting any
symptoms of tachycardia, which is present in the resting period to recompense for reduced
ventricular contractility (Clark et al., 2016). The nurses can also identify the condition such
as premature atrial contractions (PACs), PVCs, paroxysmal atrial tachycardia (PAT), atrial
fibrillation (AF) and multifocal atrial tachycardia (MAT).
The other nursing strategy that can be used to manage the condition of the patient is to
continuously monitor the blood pressure and oxygen saturation of the patient. From the case
scenario, it was evident that the patient exhibited high blood pressure (hypertension) and high
oxygen saturation rate that is directly responsible for the onset of heart failure. Thus,
monitoring the blood pressure will help the nurses to asses the severity of heart failure as the
blood pressure usually elevates during chronic heart failure, where the patient body fail to
compensate and result in hypotension. By evaluating the patient’s pulse rate, the nurses can
also identify the condition of hypertension that happens due to renal failure and activation of

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renin-angiotensin mechanism associated with accumulation of excess fluid (Inamdar &
Inamdar, 2016). Therefore, it is evident that the above mentioned nursing strategies will help
the nurses to evaluate the health condition of the patient on basis of the vital sign and
accordingly develop the intervention that will be useful for treating the condition of severe
heart failure.
Mechanism of action of the drugs:
 Mechanism of action of IV furosemide: IV furosemide drug is a diuretic drug that
block the method of water reabsorption and is consumed for releasing the
accumulated fluid that accumulate due to heart failure and therefore helps the patient
in control their blood pressure. This medicine act by obstructing the transport of Na-
K-Cl into the ascending loop of henle, which result in inhibiting the transport of
sodium and lowering the total amount of sodium level in the cells. Hence, the
administration of this medication will be helpful for Mrs Brown to reduce the blood
pressure and contractibility of the cardiac cells (Ter et al., 2015).
 Mechanism of action of Sublingual glyceryl trinitrate (GTN): Sublingual glyceryl
trinitrate (GTN) is a vasodilator drug that is commonly consumed for relaxation of
vascular muscle. GTN underline the production of nitric oxide (NO) that activate the
guanylate cyclase and therefore result in the synthesis of CGM. This mechanism
activates the protein-kinase dependent pathway within cardiac muscle of the heart.
The action of de-phosphorylation also takes place that result in cardiac muscle
dilation leading to high amount of blood influx within the tissues, artery and veins
therefore reducing the blood pressure and increasing the blood flow in the
myocardium (Zhou & Parker, 2019).

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References
Clark, A. M., Wiens, K. S., Banner, D., Kryworuchko, J., Thirsk, L., McLean, L., & Currie,
K. (2016). A systematic review of the main mechanisms of heart failure disease
management interventions. Heart, 102(9), 707-711.
Fenwick, R. (2015). Management of acute heart failure in the emergency
department. Emergency Nurse, 23(8).
Floras, J. S., & Ponikowski, P. (2015). The sympathetic/parasympathetic imbalance in heart
failure with reduced ejection fraction. European heart journal, 36(30), 1974-1982.
Inamdar, A., & Inamdar, A. (2016). Heart failure: diagnosis, management and
utilization. Journal of clinical medicine, 5(7), 62.
Kotecha, D., & Piccini, J. P. (2015). Atrial fibrillation in heart failure: what should we
do?. European Heart Journal, 36(46), 3250-3257.
Mebazaa, A., Yilmaz, M. B., Levy, P., Ponikowski, P., Peacock, W. F., Laribi, S., ... &
McDonagh, T. (2015). Recommendations on pre‐hospital & early hospital
management of acute heart failure: a consensus paper from the Heart Failure
Association of the European Society of Cardiology, the European Society of
Emergency Medicine and the Society of Academic Emergency Medicine. European
journal of heart failure, 17(6), 544-558.
Mentz, R. J., & O'connor, C. M. (2016). Pathophysiology and clinical evaluation of acute
heart failure. Nature Reviews Cardiology, 13(1), 28.
Ter Maaten, J. M., Valente, M. A., Damman, K., Hillege, H. L., Navis, G., & Voors, A. A.
(2015). Diuretic response in acute heart failure—pathophysiology, evaluation, and
therapy. Nature Reviews Cardiology, 12(3), 184.

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Tham, Y. K., Bernardo, B. C., Ooi, J. Y., Weeks, K. L., & McMullen, J. R. (2015).
Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and
novel therapeutic targets. Archives of toxicology, 89(9), 1401-1438.
Zhou, K., & Parker, J. D. (2019). The role of vascular endothelium in nitroglycerin‐mediated
vasodilation. British journal of clinical pharmacology, 85(2), 377-384.