Case Study Assessment: Congestive Heart Failure and Chronic Renal Failure

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Case study assessment
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Patient situation
This assessment is based on patient M.G aged 68 years old female having admission to
the emergency department with a diagnosis of congestive heart failure. She was discharged in
the hospital one and a half weeks ago and has just visited back due to complications arising
from her breathing ability and difficulty in walking. The patient assessment indicates inability
in following her fluid management and salt intake, further she has not been following her
medication correctly. Her past medical history indicates the presence of hypertension, chronic
renal failure, and anterior myocardial infection 4 years ago. Family history assessment shows
that she has lost both her parents, while she has a sister who is alive and well as well as a
brother age 62 years and 70 years respectively. The brother has been diagnosed with coronary
heart disease and hypertension. She has two children and six grandchildren.
Collecting information
Her medical assessments reveal that the blood pressure during discharge was bp140/90
while two weeks before discharge was BP156/94, which led to the commencement of
hydrochlorothiazide 25 mg PO. During patient admission, her pulse rate was irregular at 122,
BP 160/100, respiratory rate 26, temperature 37.3 Celsius degrees, and oxygen saturation
93% on room air. The patient presented with widespread palpitation on chest auscultation
examination in both lungs. Chest x-ray reveals widespread consolidation and cardiomegaly.
The apical pulse is elevated, skin assessment shows pink color while peripheral edema
present at a score of 2.
Electrolyte assessment indicates elevated potassium levels of 5.5mEq/l against normal
levels of 3.5-5.0 mEq/l which indicates mild hyperkalemia. Creatine assessment on the
functionality of the kidney shows impaired function. The patient creatine levels are 4.5mg/dl
against normal ranges of 0.6 to 1.2 ml/dL. The blood urea nitrogen indicates elevated levels
of signifying stress levels with a high of 43 mg/dl against normal ranges of around 7 to 20
mg/dL. Further CXR Assesment shows cardiomegaly presence signifying enlarged heart,
while a pulmonary score of a grade of 2 indicating fluid accumulation.

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Process information
Pathophysiology Congestive Cardiac Failure
Congestive heart failure occurs due to the inability of the heart to pump the blood
normally. Heart failure state reflects a pathophysiologic state where abnormal cardiac
function occurs. Heart failure can be linked to myocardial failure which leads to circulatory
failure. The pathophysiological occurrence of CHF occurs due to the state of the inability of
the heart to be able to acquire the normal maintenance of oxygen delivered. It indicates the
systematic response in an attempt to compensate for the inadequacy occurring. The stroke
volume is further assessed based on the preload and afterload in the left ventricular valves
(Harjola, et al., 2017).
The occurring significance of the heart in the reaction of the heart muscle through the
overload or damage reducing the efficiency of the heart leading to lower output levels while
myocardial dysfunction defined by the systolic and diastolic, acute or chronic depicts changes
of the heart. In assessing heart failure, various mechanisms take place which is activated
depending on the heart failure duration. Neurohormonal reflexes like the adrenergic system,
renal, peripheral alterations, and renin-angiotensin systems aim at restoring the cardiac output
and terminating the perfusion of tissue perfusions. The occurrence of stroke volume cannot
be removed from the left ventricle thus shifting the pressure-volume on to the systolic failure.
Filing of adequate cannot be achieved due to the occurrence of stiffness in the diastolic
region, thus shifting the diastolic pressure-volume curving upward without effects on the
diastolic pressure increasing without effects on the systolic volume-pressure curve, leading to
diastolic failure. The left ventricle heart failure often reflects the dominance of heart failure
syndrome while the right heart develops as an isolated failure, the occurrence of bi-
ventricular syndrome indicates an end-stage clinical assessment of the heart failure state
(Münzel, 2015).
In fluid mechanism congestion, the presence of cardiac dysfunction often leads to a
serious state of the neruo humoral pathway which entails changes on the nervous system,
vasopressin system; arginine activation and aldosterone system is activated by the negative
consequences of the heart failure on the delivery of oxygen to the peripheral tissues. The
activation of neurohumoral leads to impairment of sodium excretion regulation through eh
kidney organs which leads to increased levels of sodium and fluid accumulation, thus

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increasing cardiac filling pressures and congestion of the venous is observed recurrent
(McKie et al., 2011). The occurrence of venous congestion has often been indicated in
cardiac failure, it plays a crucial role in the overall pathophysiological process of cardiac
failure.
The association of cardiac function and renal dysfunction referred to as cardio-renal
syndrome occurs in CCF. The congestion of the venous is the key hemodynamic determinant
for the development of renal dysfunction and low index of cardiac functionality. The
increased occurrence of central pressure of the venous and low index of the cardiac is
particularly not favorable for renal function (Nijs et al., 2015).
The resultant effect of congestive heart failure leads to reduce contraction force due to
overloading of the ventricular. This leads to failure of ventricle lading with blood in the heart
muscle contraction reducing leading to reduced ability of the cross-link actin and myosin in
stretching the muscles of the heart (Arrigo, Parissis, Akiyama & Mebazaa, 2016).
Chronic renal failure
Chronic renal failure indicates the gradual loss of the kidney function. The kidney
performs filtration of waste and fluids from blood which is then excreted inform of urine. In
chronic disease advance stages, elevated levels of fluid, electrolytes and waste often build up
in the body. This occurs as a result of a progressive decline in kidney function ability. The
occurrence of modulation and adaptation occur at glomerular functionality which keeps the
kidney function normal, the remaining glomerular experience rise in pressure due to
hyperfiltration (Malek & Nematbakhsh, 2015).
The consequential release of the cytokines and growth factors yield hypertrophy and
hyperplasia, while the function of glomerular is hampered, leading to excess demand on
them. This leads to increase levels of permeability and proteinuria, while there is increased
permeability and proteinuria. The increased concentrations in the proximal tube lead to direct
nephrotoxins which deteriorate the state of the kidney function (DiLullo et al., 2015).
Chronic renal failure leads to the reduced ability of excretory functionality, leading to
accumulation of endogenous and other extraneous substances. This leads to
pharmacodynamic changes due to increased metabolic concentration leading to maximal
concentration capacity of the kidney is reduced.