Pathophysiology of Chronic Systolic Heart Failure and Nursing Strategies

This article explains the pathophysiology of chronic systolic heart failure and nursing strategies. It also discusses the mechanism of action of drugs used in the treatment of heart failure.

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1. Pathophysiology
The pathophysiology of chronic systolic heart failure is mainly determined by the failure
of the circulatory system for delivering sufficient oxygen for delivering the metabolic needs.
This is best explained by a complex interplay between the disruptive functioning of the
ventricular pump that restricts the supply of oxygen to the tissue that are metabolically active
(Chatterjee, 2015). The impairment of the ventricular muscles can be caused due to a number
of factors like high blood pressure. In such cases, the heart have to work harder for pumping
more blood through the body. It can also be caused due to chronic coronary heart diseases.
Cardiomyopathies are also responsible for damaging heart muscles. In a systolic heart failure,
dilation of the left ventricle occurs causing an increase in both the left ventricular end –
diastolic and the end systolic volumes (Katz, 2018). But as there is a greater increase in the
end –systolic than in the end diastolic volume, the left ventricular ejection fraction is
generally reduced. Hence, when the increase in the end –diastolic volume is not
proportionate, the ejection fraction can decrease despite of the normal left ventricular end
diastolic volume. Reduced ejection fraction in systolic heart failure may lead to the
backlogging of the fluid in to the lungs that can lead to pulmonary oedema (Macić-Dzanković
& Pojskić, 2017). In a systolic heart failure, a significant change in the shape of the ventricle
is caused. The shape of the left ventricle is normally ellipsoidal which changes to spherical in
a systolic heart failure (Macić-Dzanković & Pojskić, 2017).
It is evident from the case study, that Mrs. Brown had previous history of heart failure
that might have weakened the heart muscles. Contractility of the myocardium decrease with
previous history of myocardial infarction. Dys-functioning of the myocardial sarcomeres
might decrease the contractility, causing the stroke volume to be smaller and ultimately
decreasing the cardiac output. Failure of the left ventricular output leads to dyspnoea
(shortness of breath). Increasing chest tightness and shortness of breath is mainly due to the

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increased workload of the heart. Pulmonary oedema might be another cause of shortness of
breath in the patient as the accumulation of fluid reduces the movement of oxygen through
the lungs. The case study reveals that on diagnosis, the patient had been found to be having
arterial fibrillation. Atrial fibrillation might weaken the heart and cause heart failure
(Kataoka, 2017). This is a condition when circulation of the heart is impaired to meet the
oxygen demands of the body. Arterial fibrillation can be referred to as irregular and rapid
heart rate than can increase the risk of the strokes and other heart related conditions. During
the occurrence of arterial fibrillation, the two upper chambers of the heart beats chaotically
(Kotecha & Piccini, 2015). Clinical manifestations of arterial fibrillation includes palpitation
of the heart, shortness of breath. All these can be related to the symptoms displayed by Mrs.
Brown. The oxygen saturation level of Mrs. Brown is SpO2 85%, on room air which is quite
less than the standard value. As the heart muscles are weak, it is incapable of pumping more
blood causing oxygen deficiency in the cells. This causes the oxygen saturation to be low in
Mrs. Brown. The case study also reveals that the blood pressure of Mrs. Brown is also quite
high. Weka muscles of the heart causes the heart to work harder for pumping more blood
through the body. With this extra work, the muscles of the heart gets thicker and does not
work well.
Bilateral basal crackles can be heard in case of pulmonary oedema. Pulmonary
oedema is often caused by the occurrence of congestive heart failure. When the heart is not
being able to pump blood efficiently, the pressure on the blood vessels increase, which can
lead to the pushing of fluid in to the air spaces. These two factors can cause shortness of
breath and audible bilateral crackles (Kataoka, 2017). These can be related to the clinical
symptoms manifested by the patient.
2. High priority nursing strategies and their rationale

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One of the prime nursing strategy would be to monitor any change in the signs and the
symptoms, with respect to the treatment applied. They are accountable to monitor and
identify relevant changes in the clinical status of the patient. It necessary to auscultate the
apical pulse, assess the rate and the rhythm of the heart (Riley, 2015). Nurses should
document any account of dysrhythmias. The heart sounds has to be noted and the
peripheral pulses has to be palpated. Nurses should monitor the blood pressure and insect
for any kinds of cyanosis. The mental status and the level of consciousness of the patient
has to be assessed.
Rationale: The heart rate, apical pulse and dysrhythmia has to be noted as presence of
tachycardia normally indicates that the heart is compensating for the decrease ventricular
contractility. It is used to determine premature arterial contractions, paroxysmal atrial
tachycardia. Peripheral nerves pulses has to be palpated due to fact as diminished
popliteal, radial pulse and he post tibeal pulses migh6 indicate towards a decreased
cardiac output. Irregular pulses in patients might also be detected by the nurses. The main
rationale behind the continuous monitoring of the blood pressure is that high blood
pressure might indicate to increase SVR. Inspection of the skin for cyanosis is required
due to the fact that diminished pallor and blue skin may indicate towards venous
congestion. A continuous monitoring of the urine output is necessary as kidneys tends to
retain sodium and water if the cardiac output is reduced. The mental status of the patient
has to be monitored due to the fact, that the accumulation of the waste products in the
blood stream impairs the transport of oxygen and intake by the cerebral tissues that can
manifest itself as confusion, altered consciousness and lethargy.
Another nursing priority and strategy is to check the risk for impaired gas
exchange. Nurses should auscultate the breath sounds, wheezes and the crackles. They
encourage the patient in effective coughing (Riley, 2015). In order to facilitate lung

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expansion, nurses should ensure bed or chair rest keeping the head of the bed at an
elevated position; in a semi fowler position. In case the patient is experiencing extreme
breathlessness, supplemental oxygen can be given.
Rationale: Frequent changes in the position and placing the patient at a semi fowler
position assisted in preventing atelectasis and pneumonia. Maintaining a semi-fowler
position helps the patient to promote expansion of the chest (Riley, 2015). Supplemental
oxygen given to the patient reduces the congestion in the alveoli and enhances the
gaseous exchange.
3. Mechanism of action of the drugs
IV Furosemide (Lasix)
It is used as a diuretic that is used to eliminate water from the body. In the kidney, the
molecules are normally filtered in to the tubules of the kidney. The diuretic works by
blocking the absorption of chloride, sodium from the filtered fluid present in the kidney
(Pellicori, Kaur & Clark, 2015). The case study reveals that Mr Brown was suffering from
systolic heart failure, and pulmonary congestion might have been the reason for her
breathlessness. Hence, diuretic can help in preventing the water build-up in the body of the
person.
Sublingual Glyceryl Trinitrate (GTN)
Sublingual Glyceryl Trinitrate (GTN), is administered in case of congestive heart
failure. It is a nitrate drug acts as a vasodilation agent, causing the relaxation of the smooth
muscles, which causes a dose related relaxation of the arteries as well as the venous bed. The
venous dilation mainly predominates over the dilation of the arteries. Again, it also reduces
the systolic, diastolic and the man arterial pressure and the myocardial consumption of

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oxygen (Corstiaan & Brugts, 2015). Mr. Brown has been found to be suffering from
ventricular dysfunction, the drug causes dilation of the arteries and the ventricles, thus
reducing the systolic pressure and reducing the risk of heart attack.

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References
Chatterjee, K. (2015). Pathophysiology of systolic and diastolic heart.
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do?. European Heart Journal, 36(46), 3250-3257.
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Kotecha, D., & Piccini, J. P. (2015). Atrial fibrillation in heart failure: what should we do?.
European Heart Journal, 36(46), 3250-3257.

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Macić-Dzanković, A., & Pojskić, B. (2017). Acute heart failure after myocardial infarction.
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