Chronic Systolic Heart Failure: Pathogenesis, Nursing Strategies, and Drug Mechanisms

Running head: CHRONIC SYSTOLIC HEART FAILURE
ACUTE EXACERBATION OF CHRONIC SYSTOLIC HEART FAILURE
Name of Student:
Name of University:
Author’s Note:

CHRONIC SYSTOLIC HEART FAILURE
1
Answer 1- Pathogenesis of acute exacerbation of chronic systolic heart failure
Acute exacerbation of chronic systolic heart failure is the consequence of dysfunction of
heart which is related to rhythm, structure or conduction of signals. It is occurs when there is not
adequate pumping of blood and cardiac output required for normal functioning of body. The
major causes of chronic systolic heart failure are related to degenerative valve disease, alcoholic
cardiomyopathy and idiopathic cardiomyopathy. Heart failure mainly occur in elderly patient
who have been reported to have several comorbidities like angina, chronic lung disease, diabetes
and hypertension (Volpe, Carnovali & Mastromarino, 2016).
As evident from the case study Mrs Brown showed history of breathing difficulty,
dyspnoea with high blood pressure and low oxygen saturation level which depicts heart failure.
The chronic systolic heart failure is not only the incompetency of heart to maintain oxygen level,
it is also related to systematic response (Asgar, Mack & Stone, 2015).
The pathophysiology of the heart failure is related with volume of blood that enter the left
ventricle (preload) and outflow of blood from left ventricle (afterload). The heart failure outcome
with the activation of compensatory mechanism in order to increase the cardiac output. The two
main mechanism which is known as activation of sympathetic nervous system and activation of
renin-angiotensin aldosterone system are example of those compensatory mechanism. According
to Tham et al. (2015) it is known that when there is drop in blood pressure, the carotid
baroreceptor activate the sympathetic nervous system which in turn increase the level of
epinephrine and norepinephrine. The outcome of it result in high contraction of heart muscle,
high heart rate and afterload through peripheral vasoconstriction. This is deleterious effects
which causes decline of left ventricle systole and emergence of heart failure. In normal working

CHRONIC SYSTOLIC HEART FAILURE
2
heart, there is increase in filling of heart by the result of high contraction stated by law of Frank
starling. In heart failure, it is reported that the ventricles is loaded with less amount of blood due
to which the heart muscle contraction is less by less efficient action of myosin and action
filament (Harjola et al., 2017). Due to failure of systole, the stroke volume is decreased and
there is less contraction of heart. The impact of this is fundamentally determined by failure of
circulation of heart that result in less delivery of oxygen to the cell of body.
The pathophysiology of heart failure is also related to renin-angiotensin-aldosterone
system. Due to low cardiac output, there is decreased in renal perfusion and kidney assume
hypovolemia. The main compensatory mechanism to retain level of sodium and water result in
activation of renin-angiotensin-aldosterone system. When there is vasoconstriction, the level of
angiotensin increases that also increase the blood pressure. From the finding of (0) it can be said
that with the activation of renin-angiotensin-aldosterone system, there is adverse remodelling of
heart and cardiac function is impaired (Ter Maaten et al., 2015).
In systolic dysfunction, there is decrease in stroke volume resulting in incomplete
emptying of the blood. The major reason for such depends on two factors, impaired ventricular
contractility and high afterload. The impaired ventricular contractibility is because of abnormal
functioning of myocytes and fibrosis resulting due to necrosis, apoptosis, and inactivation of
contractile protein, enzymes and ion channels. When there is increase in resistance to flow of
blood, there is increase in outflow of blood from the ventricle. It is observed from the study of
Stembridge et al. (2015) that in heart failure is lack of transmission of signal from SA node
which does not depolarize and hyperpolarize the cell of the hearts. Due to such mechanism, the
ventricles are not able to contract well and blood does not get emptied with full efficiency. The
main All the above discussed rationale result in systolic heart failure.