Case Study: Analyzing Mrs. Brown's Health, Treatments, and Outcomes

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Case Study
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This case study analyzes the case of Mrs. Brown, who presented with symptoms indicative of systolic heart failure. The analysis begins with the diagnosis, exploring the pathophysiology of the condition, including reduced cardiac muscle efficacy, potential causes like myocardial infarction, and the impact on the cardiac cycle. The study then delves into the patient's symptoms, such as severe dyspnea and pulmonary edema, linking them to physiological mechanisms like allergen responses and reduced ventilation capacity. It also discusses the effects of decreased oxygen delivery and hypoxemia. The case study further examines the activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system as contributing factors. The second part focuses on vital signs, identifying abnormalities in blood pressure, respiratory rate, pulse rate, and oxygen saturation. It prioritizes interventions such as oxygen administration and positioning to address hypoxemia and respiratory distress. The final part explores the use of medications like Furosemide and GTN, explaining their mechanisms of action and potential adverse effects. The case study references multiple research articles to support the analysis and recommendations.
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Running head: CASE STUDY
Health variation
Name of the Student
Name of the University
Author Note
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1CASE STUDY
Answer 1
On analysing the signs and symptoms manifested by Mrs. Brown it can be suggested
that she suffered from systolic heart failure. Also referred to as congestive heart failure, the
condition occurs when the body is not able to pump adequate amount of blood for meeting
the demands. The principle pathogenesis of systolic heart failure in the patient involved a
reduction in the efficacy of the cardiac muscles, thereby leading to overloading or damage.
Mrs. Brown is diagnosed to have suffered from systolic heart failure since the event occurred
during the systole that refers to the stage of the cardiac cycle that encompassed contraction of
the heart, followed by transfer of deoxygenated blood to their the lungs for purification, or
oxygenated blood to different body parts (Ter Maaten et al., 2015). This condition might have
occurred in the patient owing to numerous conditions such as, myocardial infarction that
result in deficiency of oxygen in the cardiac muscles, following which they cease to function.
Under normal circumstances the heart of an individual suffering systolic heart failure might
demonstrate a decreased force of cardiac contraction, which in turn can be accredited to
ventricle overloading. According to Mentz and O'connor (2016) among persons who have a
healthy heart, an increase in filling of ventricle subsequently leads to upsurge in force of
contraction, thereby raising the cardiac output. However, when Mrs. Brown suffered from
heart failure, the aforementioned mechanism failed, such that the ventricle got filled with
blood to an extent that reduced the efficiency of contraction of the cardiac muscles, thus
reducing the capability to form cross-link between myosin and actin filaments in the stretched
cardiac muscles (Morrow, 2017).
She manifested severe dyspnoea that can be associated with the presence of allergens
that might have triggered the release of numerous anti-inflammatory chemicals, thus causing
changes in the bronchiolar walls. Furthermore, onset of oedema in the lungs might have also
decreased ventilation spare capacity, thus making the lungs stiff and lowering gaseous
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2CASE STUDY
exchange efficiency (Kee et al., 2016). This in turn was mediated by an increase in distance
between blood and air, eventually causing shortness of breath or dyspnoea. Taking into
consideration the fact that the patient suffered from heart failure that disturbed the circulation
of bloodstream, the delivery of oxygen in the patient had decreased, thus causing tissue
hypoxia. The patient also reported signs of pulmonary oedema since congestive heart failure
prevented pulmonary circulation at a permissible rate, thus increasing the wedge pressure and
resulting in accumulation of fluid in the air spaces and tissues of the lungs, due to an
impairment in exchange of respiratory gases (Chioncel et al., 2016). Signs of low oxygen
saturation, also referred to as hypoxemia can be associated with the decrease in ejection
fraction or the percentage of blood that left the heart of the patient, each time it underwent
contraction. This in turn triggered the overload of fluid that caused hypoxemia, more
specifically, a deficiency of oxygen in arterial blood, which further worsened the health
condition of Mrs. Brown.
In the patient who demonstrated a decreased cardiac output, activation of the renin–
angiotensin-aldosterone (RAAS) system and neurohormonal imbalance acted as major factors
that lead to the development of maladaptive changes in the heart. This resulted in an increase
in filling pressure, and an overload that consequently increased left atrial stretch, thus
triggering conduction abnormalities in the heart (Kotecha & Piccini, 2015). This system
controls circulation owing to the action of angiotensin II that is a potent vasoconstrictor and
leads to narrowing of the blood vessels, thus increasing blood pressure. Furthermore, the
condition of Mrs. Brown can again be associated with abnormal activation of the sympathetic
nervous system (SNS) that resulted in worsening of the heart functions. This can be
associated to the fact that release of several catecholamine hormones like norepinephrine and
epinephrine resulted in an acceleration of the heart rate. Owing to the fact that Mrs. Brown
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3CASE STUDY
was affected with pulmonary oedema, there occurred a backup of blood, which eventually
increased blood pressure, resulted in fluid accumulation, thus causing bilateral basal crackles.
Answer 2
Vital signs have been identified as the most essential signs that provide an indication
about the vital life-sustaining functions of the human body (Lambe, Currey & Considine,
2017). In other words, taking vital signs measurement helped in assessing the general health
of Mrs. Brown, thus providing essential cues of her illness. On assessing the vital signs,
abnormalities were found in her blood pressure, respiratory rate, pulse rate, and oxygen
saturation. While she had a blood pressure of 170/95 mmHg, thus indicating hypertension,
85% SpO2 and 120 beats pulse suggested presence of hypoxemia and tachycardia (greater
than 100 beats/minute). Hence, the two priorities that require immediate implementation of
strategies are namely, (i) increasing oxygen saturation and (ii) preventing respiratory distress.
The first strategy that will be adopted is oxygen administration. Oxygen can be administered
to the patient through face mask or nasal cannula. The primary objective of this strategy can
be accredited to the fact that Mrs. Brown was suffering from hypoxemia. There is mounting
evidence for the fact that administration of supplemental oxygen helps in relieving dyspnoea
that occurs due to low levels of arterial oxygen (Sepehrvand & Ezekowitz, 2016).
Furthermore, the signs and symptoms manifested by Mrs. Brown increase her likelihood of
suffering rapid organ failure. Therefore, oxygen therapy will form a critical component of
resuscitation and will also prevent further deterioration of health condition. Pulse oximetry
will be performed in the patient to ensure that presence of 94–96% oxygen in the patient.
However, on observing oxygen levels more than 96%, the therapy will be immediately
stopped, in order to prevent clinical deterioration (Hofmann et al., 2017).
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4CASE STUDY
The second strategy would be to maintain the patient at semi- or high-fowler’s
position. In medical terms, fowler’s position refers to a standard position where the patient
Mrs. Brown will be seated at an angle of 45-60 degrees (semi-sitting position) with her knees
either straight or bent. In addition, semi-fowler would require the patient to be seated at 30-45
degrees (Kuhajda et al., 2015). This intervention will be used for promoting oxygenation by
facilitating maximum expansion of her chest, and will help in addressing the signs and
symptoms of respiratory distress. Research evidences elaborate on the fact that making a
patient sit at fowler’s position relaxes tension of the abdominal muscles, thus improving
breathing (Kubota, Endo, Kubota & Shigemasa, 2017). In other words, fowler's position will
lessen the chest compression in the patient that predominantly occurred due to gravity.
Besides facilitating easy breathing, it will also provide comfort to the patient during eating
and other activities, thus reducing respiratory distress.
Answer 3
Furosemide is used for treatment of hypertension, and fluid accumulation due to heart
failure owing to its action in the form of loop diuretics. This drug inhibits the luminal Na-K-
Cl cotransporter, located in the ascending limb of the loop of Henle. This inhibition is
mediated by binding of the drug to the chloride transport channel, thus leading to loss of
chloride, sodium, and potassium in urine. Furthermore, it also reduces transport of sodium in
macula densa, thus releasing renin that increases fluid retention in the body (Fenwick, 2015).
The nurse needs to keep a check on several adverse conditions such as, gout and
hyperglycaemia. In addition, the patient is also at a risk of suffering from thiamine deficiency
and hypokalaemia.
GTN or nitroglycerine is also administered for preventing chest pain, hypertension
and heart failure and functions through the production of nitric oxide 9NO), the active
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5CASE STUDY
metabolite from the nitrite ion. This NO activates guanylyl cyclase (GC) that leads to the
formation of cyclic guanosine monophosphate (cGMP), which causes myosin
dephosphorylation and causes smooth muscle relaxation (Atherton et al., 2018). Some
adverse events associated with this drug that need to be monitored are hypotension, headache,
and reflex tachycardia. It is anticipated that following the administration of the two drugs, the
patient will demonstrate stable blood pressure and reduced pulse rate.
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6CASE STUDY
References
Atherton, J. J., Sindone, A., De Pasquale, C. G., Driscoll, A., MacDonald, P. S., Hopper, I., ...
& Thomas, L. (2018). National Heart Foundation of Australia and Cardiac Society of
Australia and New Zealand: Australian clinical guidelines for the management of
heart failure 2018. Medical Journal of Australia, 209(8), 363-369.
https://doi.org/10.5694/mja18.00647
Chioncel, O., Ambrosy, A. P., Bubenek, S., Filipescu, D., Vinereanu, D., Petris, A., ... &
Romanian Acute Heart Failure Syndromes study investigators. (2016). Epidemiology,
pathophysiology, and in-hospital management of pulmonary edema: data from the
Romanian Acute Heart Failure Syndromes registry. Journal of Cardiovascular
Medicine, 17(2), 92-104. doi: 10.2459/JCM.0000000000000192
Fenwick, R. (2015). Management of acute heart failure in the emergency
department. Emergency Nurse, 23(8). doi: 10.7748/en.23.8.26.s26
Hofmann, R., James, S. K., Jernberg, T., Lindahl, B., Erlinge, D., Witt, N., ... & Ravn-
Fischer, A. (2017). Oxygen therapy in suspected acute myocardial infarction. New
England Journal of Medicine, 377(13), 1240-1249. DOI: 10.1056/NEJMoa1706222
Kee, K., Stuart-Andrews, C., Ellis, M. J., Wrobel, J. P., Nilsen, K., Thompson, B. R., &
Naughton, M. T. (2016). Reply: Dyspnea in Heart Failure: A Multiheaded
Beast. American journal of respiratory and critical care medicine, 194(6), 775-776.
https://doi.org/10.1164/rccm.201604-0837LE
Kotecha, D., & Piccini, J. P. (2015). Atrial fibrillation in heart failure: what should we
do?. European Heart Journal, 36(46), 3250-3257. doi:10.1093/eurheartj/ehv513
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7CASE STUDY
Kubota, S., Endo, Y., Kubota, M., & Shigemasa, T. (2017). Assessment of effects of
differences in trunk posture during Fowler’s position on hemodynamics and
cardiovascular regulation in older and younger subjects. Clinical interventions in
aging, 12, 603. doi: 10.2147/CIA.S132399
Kuhajda, I., Djuric, D., Milos, K., Bijelovic, M., Milosevic, M., Ilincic, D., ... & Mpakas, A.
(2015). Semi-Fowler vs. lateral decubitus position for thoracoscopic sympathectomy
in treatment of primary focal hyperhidrosis. Journal of thoracic disease, 7(Suppl 1),
S5. https://dx.doi.org/10.3978%2Fj.issn.2072-1439.2015.01.29
Lambe, K., Currey, J., & Considine, J. (2017). Emergency nurses’ decisions regarding
frequency and nature of vital sign assessment. Journal of clinical nursing, 26(13-14),
1949-1959. https://doi.org/10.1111/jocn.13597
Mentz, R. J., & O'connor, C. M. (2016). Pathophysiology and clinical evaluation of acute
heart failure. Nature Reviews Cardiology, 13(1), 28.
https://doi.org/10.1038/nrcardio.2015.134
Morrow, T. (2017). Pathophysiology of Heart Failure.
https://digitalcommons.otterbein.edu/cgi/viewcontent.cgi?
article=1216&context=stu_msn
Sepehrvand, N., & Ezekowitz, J. A. (2016). Oxygen therapy in patients with acute heart
failure: friend or foe?. JACC: Heart Failure, 4(10), 783-790.
DOI: 10.1016/j.jchf.2016.03.026
Ter Maaten, J. M., Valente, M. A., Damman, K., Hillege, H. L., Navis, G., & Voors, A. A.
(2015). Diuretic response in acute heart failure—pathophysiology, evaluation, and
therapy. Nature Reviews Cardiology, 12(3), 184.
https://doi.org/10.1038/nrcardio.2014.215
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