Clinical Reasoning Cycle for a Patient with Health Complications

This case study discusses the clinical reasoning cycle for a patient with health complications. It covers the patient's health issues, pathophysiology, interventions, and patient empowerment techniques.

Running head: CASE STUDY
Clinical reasoning cycle
Name of the Student
Name of the University
Author Note

1CASE STUDY
Description
1. The first slide presents an overview of the purpose of the presentation and what it will
cover.
2. In the second slide we will discuss about the patient Mr. Joni and his health
complications. The patient is a resident of Inner West City, Melbourne and had been
referred for the annual health examination by his GP. He reports being an active
smoker and also has alcohol every week. Furthermore, he does not consume freshly
cooked food items and is dependent on takeaway food products. The health
complications identified during the assessment can be attributed to the fact that
prolonged smoking has caused significant damage to the lining of the arteries, thus
triggering a build-up of fatty material or atheroma, consequently making the arteries
narrow Daw, Margolis & Wright, 2017). This eventually led to AMI and an increase
in blood pressure. In addition, consumption of takeaway food products that are rich in
fat and cholesterol resulted in an increase in body weight, thus making him obese.
Accumulation of cholesterol in the flowing bloodstream also increased his risk of
cardiovascular complications (Annema et al., 2016).
3. In the third slide I shall be identifying the health issue that the patient is suffering
from. The patient’s condition can be accredited to the presence of atherosclerosis that
occur when the blood vessels that are responsible for carrying essential nutrients and
oxygen to the arteries from the heart become thickened and stiff. This hardening of
the arteries limits the flow of bloodstream to the body organs and tissues, thereby
triggering the onset of atherosclerosis, commonly known as hardening of arteries.
This atherosclerosis might have resulted in disruption in the blood supply. The
disruption generally occurred by contraction of the lumen of the blood vessels,
eventually causing a decrease of blood flow, thereby triggering the development of

2CASE STUDY
blood clots within the blood vessel (Bush et al., 2018). Furthermore, atherosclerosis
might have also increased his risk of suffering a stroke by releasing several
small emboli, which in turn occurred due to atherosclerotic plaque disintegration.
Furthermore, when these emboli entered the cerebral circulation, they resulted in the
onset of embolic infarction, thereby lodging in the blood vessels and blocking them.
Owing to the fact that the blood vessels located in the brain get blocked due to the
deposition of plaques, the brain will gradually get deprived of sufficient energy, and
therefore resort to utilising anaerobic metabolism in those brain cells and tissue that
are affected by ischemia.
4. In this fourth slide we will further discuss the pathophysiology of the complication
identified. Rupture of plaque that were developed in the arteries resulted in acute
myocardial infarction. In addition, commencement of anaerobic metabolism by the
brain results in the decreased production of adenosine triphosphate (ATP), however
triggers the release of lactic acid, a by-product (Fryer, Bain & Darryl, 2016). This acts
in the form of an irritant that would possibly destroy the cells by disrupting the acid-
base balance found in the brain. In addition, with depletion of glucose or oxygen in
the ischemic brain tissue, there occurs a failure in the production of adenosine
triphosphate (ATP), a high energy phosphate compounds, thus causing dysfunction of
energy-dependent ion pumping processes that are imperative for tissue cell survival.
In addition, ischemia in the patient might also induce oxygen free radical production,
which would damage the lining of the blood vessels (Fujiwara et al., 2016).
5. In the fifth slide we have established two goals for the patient which are to prevent
stroke and reduce hypertension.
6. The sixth slide talks about pharmacological interventions. Dipyridamole will prevent
blood clot formation by inhibiting phosphodiesterase enzyme that breaks down

3CASE STUDY
cAMP, thus increasing cellular cAMP levels and cGMP. It would also inhibit
reuptake of adenosine into red blood cells, platelets, and endothelial cells, increasing
the extracellular adenosine concentration (Barlas et al., 2018). In contrast, ACE
inhibitor would block transformation of Angiotensin I (ATI) to Angiotensin II (ATII),
thus decreasing arteriolar resistance and cardiac output, while subsequently increasing
venous capacity. Low resistance in the arteries and reduced ATII would hinder
aldosterone release, thus lowering blood volume and blood pressure (Hurford et al.,
2015).
7. In the seventh slide we would talk about non-pharmacological interventions. Mr. Joni
will be asked to perform aerobic exercise that will strengthen and enlarge his cardiac
muscles, and eventually enhance the blood pumping efficacy of the heart. On
performing exercise, his resting heart rate would also decrease, followed by reduction
of hypertension and improvement of circulation efficiency (Billinger, Boyne,
Coughenour, Dunning & Mattlage, 2015). Consuming a Mediterranean diet that is
rich in monounsaturated fat and dietary fiber, besides containing low saturated fat will
prevent stroke and also keep a check on body weight (Rosato et al., 2019).
8. The ninth slide talks about patient empowerment and education techniques. Teaching
patients about health condition and facilitating them to participate in self-management
is a significant feature of nursing care. Educational resources like leaflet can be
tailored and printed out for Mr. Joni that will contain information on stroke, its risk
factors, and management (Hennekens, Verheugt & Downey, 2016). Establishing
rapport, asking and answering questions, and considering particular patient concerns
and apprehensions about health condition is also imperative. His physical and
emotional impairments (if any) need to be considered and is family members will also
be involved during clinical decision making.

4CASE STUDY
9. The final slide talks about the summary of the entire presentation. An analysis of the
case scenario helped in identifying stroke as the major health complication for Mr.
Joni. Hence, the pathophysiology of the complication was discussed in details,
followed by providing explicit information about interventions that would help in
addressing the condition.
10. This is a list of reference of evidences used for the assignment
11. Thank you!

5CASE STUDY
References
Annema, W., Willemsen, H. M., de Boer, J. F., Dikkers, A., van der Giet, M., Nieuwland,
W., ... & Dullaart, R. P. (2016). HDL function is impaired in acute myocardial
infarction independent of plasma HDL cholesterol levels. Journal of clinical
lipidology, 10(6), 1318-1328. https://doi.org/10.1016/j.jacl.2016.08.003
Asgar, A. W., Mack, M. J., & Stone, G. W. (2015). Secondary mitral regurgitation in heart
failure: pathophysiology, prognosis, and therapeutic considerations. Journal of the
American College of Cardiology, 65(12), 1231-1248.
DOI: 10.1016/j.jacc.2015.02.009
Australian Institute of Health and Welfare. (2018). 3.7 Stroke.
https://www.aihw.gov.au/getmedia/56bb591f-6c56-4397-b928-8de6872e2cdd/aihw-
aus-221-chapter-3-7.pdf.aspx
Barlas, R. S., Loke, Y. K., Mamas, M. A., Bettencourt-Silva, J. H., Ford, I., Clark, A. B., ... &
Myint, P. K. (2018). Effect of antiplatelet therapy (aspirin+ dipyridamole versus
clopidogrel) on mortality outcome in ischemic stroke. The American journal of
cardiology, 122(6), 1085-1090. https://doi.org/10.1016/j.amjcard.2018.05.043
Billinger, S. A., Boyne, P., Coughenour, E., Dunning, K., & Mattlage, A. (2015). Does
aerobic exercise and the FITT principle fit into stroke recovery?. Current neurology
and neuroscience reports, 15(2), 519. https://doi.org/10.1007/s11910-014-0519-8
Bush, M., Stürmer, T., Stearns, S. C., Simpson Jr, R. J., Brookhart, M. A., Rosamond, W., &
Kucharska‐Newton, A. M. (2018). Position matters: Validation of medicare hospital
claims for myocardial infarction against medical record review in the atherosclerosis
risk in communities study. Pharmacoepidemiology and drug safety, 27(10), 1085-
1091. https://doi.org/10.1002/pds.4396

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Fryer, R. H., Bain, J. M., & Darryl, C. (2016). Mitochondrial encephalomyopathy lactic
acidosis and stroke-like episodes (MELAS): a case report and critical reappraisal of
treatment options. Pediatric neurology, 56, 59-61.
https://doi.org/10.1016/j.pediatrneurol.2015.12.010
Fujiwara, N., Som, A. T., Pham, L. D. D., Lee, B. J., Mandeville, E. T., Lo, E. H., & Arai, K.
(2016). A free radical scavenger edaravone suppresses systemic inflammatory
responses in a rat transient focal ischemia model. Neuroscience letters, 633, 7-13.
https://doi.org/10.1016/j.neulet.2016.08.048
Hennekens, C. H., Verheugt, F., & Downey, B. C. (2016). Overview of primary prevention of
coronary heart disease and stroke. UptoDated. Jun, 15.
https://www.uptodate.com/contents/overview-of-primary-prevention-of-coronary-
heart-disease-and-stroke
Hurford, R., Rezvani, S., Kreimei, M., Herbert, A., Vail, A., Parry-Jones, A. R., ... & Smith,
C. J. (2015). Incidence, predictors and clinical characteristics of orolingual angio-
oedema complicating thrombolysis with tissue plasminogen activator for ischaemic
stroke. J Neurol Neurosurg Psychiatry, 86(5), 520-523.
http://dx.doi.org/10.1136/jnnp-2014-308097
Mendelow, A. D., Lo, E. H., Sacco, R. L., FAAN, M. M. F., & Wong, L. K. (2015). Stroke:
pathophysiology, diagnosis, and management. Elsevier Health Sciences.
https://books.google.co.in/books?
hl=en&lr=&id=EmFyCgAAQBAJ&oi=fnd&pg=PP1&dq=stroke+management&ots=
fTb7AfDmLd&sig=QWkZ_dO4PJNdoWf2c0g_EgfChxg#v=onepage&q=stroke
%20management&f=false

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Rosato, V., Temple, N. J., La Vecchia, C., Castellan, G., Tavani, A., & Guercio, V. (2019).
Mediterranean diet and cardiovascular disease: a systematic review and meta-analysis
of observational studies. European journal of nutrition, 58(1), 173-191.
https://doi.org/10.1007/s00394-017-1582-0
Skelly, A. C., Hashimoto, R., Buckley, D. I., Brodt, E. D., Noelck, N., Totten, A. M., ... &
McDonagh, M. (2016). Noninvasive testing for coronary artery disease.
https://www.ncbi.nlm.nih.gov/books/NBK361148/