Acute Exacerbation of the Chronic Heart Failure - Pathophysiology and Nursing Strategies

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

ACUTE EXACERBATION OF THE CHRONIC HEART FAILURE
1
Answer no 1.
Pathophysiology of the heart failure.
The acute exacerbation of the chronic heart failure has been diagnosed in Mrs Brown.
Concerning to pathophysiology of the heart failure, it can be said that it is related to malfunction
of the heart and circulation of blood. It is reported in the study of Ponikowski et al. (2016) heart
failure happen in the patient who is reported with several comorbidities like hypertension and
asthma. Activation of several compensatory mechanisms in an attempt for increasing cardiac
output can have detrimental effect on health of Mrs. Brown. The primary mechanism is
neurohormonal response that induces sympathetic nervous system and activation of RAAS.
In instance of carotid baroreceptors are seen to sense low blood pressure, a response is initiated
to activate SNS (Ponikowski et al. 2016). The activation of SNS s known to elevate the level of
norepinephrine and epinephrine that work on increasing the heart rate. In short term this can
work on increasing the cardiac output too. However, chronically, this leads to deleterious effect
causing decline in left ventricular systole.
It is also evident from the study of Kotecha and Piccini (2015) that heart failure can be
caused by narrowing of arteries, and interruption of signal transmission from SA node. As a
result arteries become narrow with due time and heart is not able pump blood efficiently (Sahle
et al. 2016). In case of Mrs. Brown the saturation level is 85% indicating dyspnea and signals the
heart to pump more blood causing pressure on the heart muscles. The lack of oxygen is primary
reason of hypoxia and shortness of breath in Mrs. Brown (Fenwick, 2015). The increase in
pressure of the heart muscles and even the arteries to pump the oxygen rich blood thereby
increasing the blood pressure 170/95 mm Hg.

ACUTE EXACERBATION OF THE CHRONIC HEART FAILURE
2
In the situation of heart failure, the whole mechanism of blood circulation is disturbed,
which is mainly influenced by the non-functioning of the cardiac cells. The outcome of such
affects the afterload and preload. According to Mentz and O'connor (2016) it can be reviewed
that afterload increase with increase in resistance of peripheral vascular which results in low
contraction of ventricles. The mechanism of contraction is altered when there is damage after
heart attack.
Heart failure is the consequence of two compensatory mechanisms, sympathetic nervous
system and renin angiotensin aldosterone system (RAAS) (Goldsmith, 2016). When heart
function is lowered, the RAAS system are activated and stimulates kidney to release renin, which
in turn causes release of angiotensin II. It is reported that angiotensin II and high level of
aldosterone causes vasoconstriction, high blood pressure and myocyte hypertrophy. They
increase the blood volume and cardiac output and damages the myocyte, thus resulting in fibrosis
and systolic heart failure.
Citing the instance of decrease in renal perfusion the kidney suspects hypovolemia.
Research conducted by Kotecha & Piccini (2015), provided the fact that low cardiac output can
limit renal perfusion. The mentioned compensatory mechanism can retain water and sodium for
RAAS. Angiotensin causes peripheral vasoconstriction, leading to rise in blood pressure of Mrs.
Brown.
Answer no 2.
Nursing strategy 1. To manage hypoxia and shortness of breath using Fowler position.
As reviewed from the case study, Mrs Brown was showing major sign for heart failure,
which includes severe dyspnoea, high rate of respiratory, low oxygen saturation level and atrial