Assignment On The Respiratory

Running head: NURSING
Nursing
Name of the Student
Name of University
Author’s note

1NURSING
Answer 1
The respiratory manifestation of Mrs Brown include hypoxia (SpO2: 85%), bi-basal
crackles, tachypnoea, dyspnoea The cardiac manifestations include hypertension (170/95), atrial
fibrillation and tachycardia.
Mrs Brown has a previous history of heart failure and she was admitted to the hospital
with increased respiratory rate (24 breaths per minute; normal: 16 to 20 beats per minute) and
pulse rate (120 beats per minute; normal up to 100 beats per minute). Her high blood pressure
might be attributed due to her poor oxygen saturation (Mentz&O'connor, 2016).These
parameters indicate that Mrs Brown is having low cardiac output (stroke volume X heart rate).
Under low cardiac output, neurohormonal compensatory mechanisms activate to increase cardiac
output. For example, sympathetic system increase the cardiac output by increasing the heart rate,
myocardial contractility, and peripheral vasoconstriction (Mentz&O'connor, 2016). Renin-
angiotensin-aldosterone system (RAAS) causes vasoconstriction (angiotensin) followed by an
increase in blood volume, and retention of salt and water (aldosterone). Activation of RAAS
increases the secretion of renin, plasma angiotensin II (ATII), and aldosterone. ATII is a potent
vaso-constrictor for efferent arterioles and thus increasing the peripheral vascular resistance and
and increasing the cardiac output. Peripheral vascular resistance used to create blood pressure in
the circulatory system, by the process of vasoconstriction (Reddy, Melenovsky, Redfield,
Nishimura & Borlaug, 2016). Rossi, Mascolo and Mollace (2017) stated that activation of RAAS
under sustained sympathetic stimulation leads to increased preload and after load of heart. RAAS
also increases plasma noradrenaline concentrations along with progressive retention of salt and
water leading to the formation of oedema. RAAS causes systemic hypertension and heart failure

2NURSING
along with the development of atrial fibrillation (AF) (Nair, Nery, Redpath & Birnie, 2014). AF
is evident in case of Mrs Brown as reported in her ECG report. It leads to decreased left
ventricular compliance along with thromboembolism (Marrouche et al., 2018). The blood clot of
thromboembolism results in the generation of heart failure. AF also increases the upper or the
systolic blood pressure as the heart now takes more efforts in pumping blood (vaso-constriction)
and thus providing justification regarding the high systolic blood pressure of Mrs Brown
(Atherton et al., 2018). Moreover, the BP of Mrs brown showed high systolic pressure. This
indicated disequilibrium in the end diastolic volume of Mrs Brown (volume of load in the right
and left ventricle at the end of diastole) and thus increased pressure over the cardiac muscles and
development of heart failure (Kerkhof, 2015). Heart failure occurs when heart is unable to pump
enough blood to different parts of body. It can occur due to narrowing of the arteries and
veins like artherosclerosis. Narrowing of arteries and veins give promotes ventricular re-
modelling. Ventricular re-modelling diminishes shape and size of heart along in decreased
contractility of the heart (systolic). This increases pressure over the blood vessels leading to
high systolic blood pressure as in case of Mrs Brown (Galli & Lombardi, 2016).
The backward failure of the decreased stroke volume as in case of systolic heart failure
results in the formation of congestion in the lungs. Congestion in the lungs along with renal
hypofunction causes pulmonary oedema. Pulmonary oedema results in the formation of hypoxia,
decrease oxygen saturation within the body (SpO2 of Mrs Brown is 85%)(Dunham-Snary et al.,
2017). Pulmonary oedema results in accumulation of fluid in the pulmonary cavity and this
causes failure of the pulmonary muscles to inflate properly and resulting in formation bi-basal
crackles mainly during the time of inhalation (Sellarés et al., 2016). The auscultation of lungs of
Mrs Brown identifies the presence of bi basal crackles. Sellarés et al. (2016) stated that older