Case Study on Pathogenesis of Clinical Manifestations, Nursing Strategies and Mechanism of Two Drugs for Heart Failure Patient

This case study discusses the pathogenesis of clinical manifestations, nursing strategies and mechanism of two drugs for heart failure patient. It covers the probable cause of dyspnea and high respiratory rate due to pulmonary congestion, nursing strategies for Mrs Brown, and mechanism of two drugs - IV Furosemide Lasix and Glyceryl Trinitrate (GTN).

Running head: NURSING
Case Study
Name of the Student
Name of the University
Author’s Note

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Table of Contents
Answer to question 1: Pathogenesis of clinical manifestations.................................................2
Answer to question 2: Nursing strategies for Mrs Brown..........................................................4
Answer to question 3: Mechanism of the two drugs..................................................................5
Reference-..................................................................................................................................7

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Answer to question 1: Pathogenesis of clinical manifestations
Mrs Brown presented with the symptoms of dyspnea, and lower oxygen saturation
(SpO2: 85%), with difficulty in breathing. Bilateral basal crackles in lungs and atrial
fibrillation with chronic heart failure is detected. She was also presented with acute
hypertension (170/95).
The congestive heart failure of Mrs Brown was associated with pulmonary crackles. It
can be a probable side effect of pulmonary oedema due to congestion. It is associated with
fluid build-up in the lungs. These can be probable symptoms of systolic heart failure.
Therefore, the most probable cause of Mrs Brown’s dyspnea and high respiratory rate is due
to pulmonary congestion. According to Platz et al, (2016), systolic heart failure or other
congestive heart conditions can severely increase the blood pressure of the individual,
permeating the heart valves, which makes the heart incompetent to pump blood and the blood
travels through the veins congesting the lungs of the individual. Hence, fluid or mucus along
with blood is accumulated in the lungs causing pulmonary oedema. Additionally, narrowing
of the arteries can also be caused that reduces the blood flow, and increased pressure,
resulting in the above pathological conditions. The pressure inside the blood vessels build-up,
that pushes the alveoli constricting its area, and diminishes the oxygen flow of the lungs. This
resulted in the less oxygen delivery to the tissues and organs causing dyspnea in Mrs Brown,
and progression of backward heart failure.
Mrs Brown was presenting an increased pulse rate (120 beats pm) and enhanced
respiratory rate (24 beats pm). Hence, it can be argued that Mrs Brown had declined cardiac
output (stroke volume* heart rate). As the blood flow is reduced due to systolic heart failure,
the end-diastolic volume and end-systolic volume of blood decreases that decreases the stroke
volume, which eventually diminished the cardiac output. In this stature, due to decreased

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cardiac output neurohormonal mechanisms can affect the situation to improve the cardiac
output. The increased blood pressure of Mrs Brown can further validate this. The Renin-
Angiotensin-Aldosterone System (RAAS) is a very important factor in regulating blood
volume and systemic vascular resistance. RAAS activation is highly sensitive to low cardiac
output, and low renal perfusion (decreased renal blood flow). So, the RAAS pathway is
activated as a compensatory mechanism. The reduced renal blood flow and more sodium
transport lead to the release of renin from distal tubule that cleaves angiotensin to form
angiotensin I (AI). Angiotensin converting enzyme (ACE) converts the AI to AII. With the
increase in AII in the tissue, the heart failure is progressed (Steenman & Lande, 2017).
RAAS also results in systemic hypertension that progress to being atrial fibrillation
(AF). RAAS has a role to play in the structural and electrical progression of the disease.
Angiotensin II increases the fibrillar collagen deposition, cardiac fibroblast functioning, and
stimulation of proliferating property of cardiac fibroblast that helps in atrial fibrosis and
maintenance of AF. Electrical remodelling by angiotensin II is very significant. The
prolonged burst pacing-induced paroxysms by RAAS sustains AF. The electrical
deregulation modifies the tissue types, shortens the atrial effective refractory period (AERP)
which reduces the action potential duration, downregulating the transient outward current and
L-type Ca2+ current. A proarrhythmic effect during alteration of gap junction results in
modulation of propagating impulses within cardiomyocytes that can lead to AF. The
Angiotensin II can delay the post-depolarization process accelerating the automatic rhythm of
pulmonary vein cardiomyocytes, which modulates the ectopic beats that cause AF. The ECG
report of Mrs.Brown provides clear evidence of AF (Hall, 2015).
Similarly, to compensate the lower cardiac output, Sympathetic Nervous system
(SNS) is activated that ensures ionotropic support to the heart, which enhances the stroke
volume and maintains the mean arterial perfusion, but ultimately helps in disease progression.

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The interplay between the beta-adrenergic receptor of the cardiovascular system and the
sympathetic nerves can help in the process of progression of heart failure. This can be
justified by high systolic blood pressure (170), followed by systolic heart failure in Mrs
Brown. The RAAS and SNS helped in the forward heart failure process in Mrs Brown
(Grassi, Mark & Esler, 2015).
Answer to question 2: Nursing strategies for Mrs Brown
According to the Heart Failure Guidelines (2018), standard 6.2 deals with the
administration of oxygen to patients whose saturation level is below 94%. In the case of Mrs
Brown, her oxygen saturation rate has been observed to be 85%. Administration of oxygen to
a critical patient, who is suffering from acute heart failure, helps in improving the tissue
oxygenation with resolve symptoms of dyspnea. The nurse who has been assigned to provide
care to her needs to monitor the saturation level by pulse oximetry. The patients who are
suffering from respiratory failure needs to be administered oxygen via the arterial blood gas
analysis tool (Cabello et al., 2016). The administration of oxygen will see a rise in the
saturation levels and should be provided unless it reaches 94% and above levels. Patients
suffering from myocardial infarction are often suggested to administer oxygen to improve
their medical condition. It is the responsibility of the nurse to carefully administer the tool to
the patient to provide relief from their distress. The nurses should provide the patient with the
best quality of care to relief the patient from their suffering.
The Nursing and Midwifery Board of Australia (2019) standard 1.2, suggests that a
nurse must fulfil her duty of providing comprehensive care to patients by intervening
efficiently. Mrs Brown can be prescribed to sit in a semi-Fowler’s position, and the nurse can
assist her to sit with her head raised at an angle of 450. The position can help in expansion of
the capacity of lungs, and thus helping in ventilation. The gravitational force acts as a

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mediator that pulls the diaphragm helping in expansion of the volume of lungs allowing more
oxygenation. Pal, Tiwari and Verma (2017) suggested that there is an improvement in the
hemodynamic measurements in emergent patients. Song et al., (2017) revealed that relaxation
postures are mostly effective for controlling breathing problems and dyspnea. The semi-
fowler position was suggested to be most effective in patients for reducing the respiratory
output and dealing with dyspnea. It helps with a large range of physiological benefits, such as
heart rate, blood pressure, stroke volume, cardiac output, tidal volume among others. A
patient confined in bed can be seated in a semi- Fowler’s position for help in the process of
ambulation, hemodynamics observing, and for routine events like eating. Therefore, the semi-
Fowler’s position can help Mrs Brown clinically to reduce her dyspnea, and pulmonary
crackles and ease her situation.
Answer to question 3: Mechanism of the two drugs
Mrs Brown was intervened with IV Furosemide Lasix that can be useful against
pulmonary oedema, hypertension, and chronic heart failure. It is a loop diuretic drug, which
targets the sodium-potassium co-transporter (NKCC2) in the ascending loop of Henle of the
nephron of kidney, and blocks it by ceasing the water reabsorption procedure (Atherton et al.,
2018). The patient requires a high dosage of the drug, which increases the likelihood of
decreased renal activity. This is brought about by competitive inhibition of the chloride-
binding site of the NKCC2 that inhibits sodium transport and affects the osmotic gradient for
water-reabsorption. The maintenance of the sodium-potassium balance can regulate heart
health (Ding et al., 2016).
Mrs Brown was also treated with the Glyceryl Trinitrate (GTN) is a drug used for
treating heart disorders and hypertension. It is a vasodilating agent that diminishes the
pulmonary vascular resistance, thus releasing the extreme pressure of blood. The drug relaxes

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the vascular smooth muscles, and help in dilating the arterial and venous bed. Dilation of the
capillary beds can help in pooling of blood, decreasing the venous content thus relaxing the
diastolic pressure of the heart. This drug will reduce the mean arterial pressure along with the
systolic and diastolic pressure (Noack, 2019). A high dosage of nitrate administered in acute
heart failure patients has been observed to generate positive results within 48 hours. It has
also been observed to improve the stress levels in the myocardium with significant reductions
in the B-type natriuretic peptide. Light headache is experienced by people who have been
suffering from heart failure in their acute stages.

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Reference-
Atherton, J. J., Sindone, A., De Pasquale, C. G., Driscoll, A., MacDonald, P. S., Hopper, I.,
… Connell, C. (2018). National Heart Foundation of Australia and Cardiac Society
of Australia and New Zealand: Guidelines for the Prevention, Detection, and
Management of Heart Failure in Australia 2018. Heart, Lung and Circulation,
27(10), 1123–1208.
Cabello, J. B., Burls, A., Emparanza, J. I., Bayliss, S. E., & Quinn, T. (2016). Oxygen therapy
for acute myocardial infarction. Cochrane Database of Systematic Reviews, (12).
Ding, D., Liu, H., Qi, W., Jiang, H., Li, Y., Wu, X., ... & Salvi, R. (2016). Ototoxic effects
and mechanisms of loop diuretics. Journal of Otology, 11(4), 145-156.
Grassi, G., Mark, A., & Esler, M. (2015). The sympathetic nervous system alterations in
human hypertension. Circulation Research, 116(6), 976-990.
Hall, J. E. (2015). Guyton and Hall textbook of medical physiology e-Book. Elsevier Health
Sciences.
Noack, E. (2019, July). New pharmacological concepts concerning the active mechanism of
organic nitro-compounds. In Nitroglycerin 7: Progress in Therapy. Seventh Hamburg
Symposium November 24, 1990 (p. 21). Walter de Gruyter GmbH & Co KG.
Nursing and Midwifery Board of Australia. (2019). National Competency Standards for the
registered nurse. Access Date: 11th August. [Online]. Retrieved from: file:///D:/PPT
%20Materials/australia%20nurse.pdf

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Pal, A. K., Tiwari, S., & Verma, D. K. (2017). Effect of Recumbent Body Positions on
Dynamic Lung Function Parameters in Healthy Young Subjects. Journal of Clinical
and Diagnostic Research: JCDR, 11(5), CC08.
Platz, E., Lewis, E. F., Uno, H., Peck, J., Pivetta, E., Merz, A. A., ... & Cheng, S. (2016).
Detection and prognostic value of pulmonary congestion by lung ultrasound in
ambulatory heart failure patients. European heart journal, 37(15), 1244-1251.
Song, I. K., Park, H. S., Lee, J. H., Kim, E. H., Kim, H. S., Bahk, J. H., & Kim, J. T. (2017).
Optimal level of the reference transducer for central venous pressure and pulmonary
artery occlusion pressure monitoring in supine, prone, and sitting position. Journal of
clinical monitoring and computing, 31(2), 381-386.
Steenman, M., & Lande, G. (2017). Cardiac ageing and heart disease in humans. Biophysical
Reviews, 9(2), 131-137.