Case Study Analysis: Nursing Management of Heart Failure and Cardiogenic Pulmonary Edema

CASE STUDY ANALYSIS
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Introduction
Nursing management is essential in patient diagnosis and care process. This assessment
analysis focuses on patient Reggie aged 42 years old an indigenous Australia man. During
early childhood the patient was diagnosed with rheumatic heart disease, since then, there has
been a recurrent episode of recurrent acute decompensation of the heart failure condition.
This assessment reflects on two nursing issues for the patient with respect to the needed
urgent care needed for proper diagnosis. Identified nursing issues to force entail occurrence
and development of acute decompensation of the patient rheumatic disease linking to heart
failure and risk of heart failure in itself. Path physiology process of the two nursing problems
for the patient will be assessed and analyzed. In order to improve the patient status key,
nursing interventions have been identified for the patient so as to improve the overall disease
state of patient Reggie.
Assessment review
The first key nursing problem for the patient is heart failure, which refers to the
inability of the heart to pump enough blood to sufficiently maintain the blood flow to
maintain the overall needs of the body. The underlying rheumatic disease of the patient is
exuberating the heart failure state. Patient rheumatic heart disease state reflects on the overall
compilation of the rheumatic fever which the valves are damaged. The underlying disease of
the patient on the heart function is worsening the state and development of heart failure
which is a risk factor based on the patient status. Development of heart failure for the patient
has been increased by the underlying health issue on the patient status (Ponikowski et al.,
2016).
Underlying data assessment observed from the patient indicates a state of general
fatigue breathing difficulties and elevated weight in the previous months. The patient further
has pitting bilateral edema on his legs depicting accumulation of fluid and retention rate is
high. Further, the respiratory status depicts a state of elevated breathing rate due to the
weakened status of the heart at 28bs while there is low oxygen saturation at 92%.
Auscultation assessment of the patient reveals coarse crackles and increased high blood
pressure.
The Path physiology of acute heart failure depicts the state of clinical syndrome

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outcome brought about by the induced functional abnormalities occurring in the cardiac
leading to lowered output levels of cardiac output intracardiac diastolic pressures. The typical
occurrence of heart failure depicts a state of the hemodynamic model depicting downstream
hypoperfusion and the upstream congestion. Acute heart failure leads to acute
decompensation of the chronic heart failure caused due to the progressive congestion being
precipitated by various factors (Arrigo et al., 2017).
The induction of cardiac dysfunction leads to activation of the neuro-humoral pathway
in order to allow the counter the negative hemodynamic effects resultant due to heart failure.
The activation of neurohumoral leads to impairment of the sodium excretion in the kidneys
leading to accumulation of sodium and secondary accumulation of fluids (Essandoh et al.,
2015). Further, in persistence form, the neurohumoral activation leads to induction of
maladaptive processes which leads to remodeling of detrimental ventricles and dysfunction of
the organs (Arrigo & Rudiger, 2017).
The cascadation action of the congestive subclinical stage of the hemodynamic
congestion occurring as a result of cardiac filling and the venous pressures is followed by
fluids distribution into the lungs area and other visceral areas leading to overload signifying
clinical congestion. The correlation of the hydrostatic pressures and formation of edema is
poor. The accumulation of the chronic sodium in the heart leads to impairment on the
function of interstitial glycosaminoglycan network leading to a reduced capacity of the buffer
additional sodium and maintains of low interstitial edema (Nijst et al., 2015).
Many patients of AHF often display an elevated increase in body weight and
precipitation of the congestion due to sudden redistribution of the fluid. The activation of
sympathetic is shown to induce transient vasoconstriction leading to increased volume
displacement in the peripheral and the venous systems of the splanchnic of the pulmonary
circulation.
The resultant mismatch between the ventricular and vascular coupling relationship
leads to increased after load and lowered levels of venous capacitances leading to increased
alteration to of hypertensive AHF. The resultant fluid accumulation tends and redistribution
leads to the promotion of systematic congestion, but the occurring distribution carries based
on different situations of clinical activity (Jhund & McMurray, 2016).
The key patient problem, signs and symptoms are depicted by the patient status