Case Analysis- Case Study of an Acute Life-Threatening Condition Word Count There is a word limit of 1000 words. Use your computer to total the number of words used in your assignment. However, do not...

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Case Analysis- Case Study of an Acute Life-Threatening Condition
Word Count
There is a word limit of 1000 words. Use your computer to total the number of words used in
your assignment. However, do not include the reference list at the end of your assignment in
the word count. In-text citations will be included in the additional 10%-word count. If you
exceed the word count by 10% (1100 words) the marker will stop marking.
Aim of assessment
The aim of this assessment is to enable students to:
1. Demonstrate knowledge by analysing the information provided in the case study.
2. Apply the clinical information provided in the case study and describe this clinical
information within a pathophysiological and patient focused framework.
3. Discuss nursing strategies and evidence-based rationales to manage a patient with acute
heart failure
4. Discuss the pharmacological interventions related to the management of a patient with
acute heart failure
Details
You are to answer all questions related to the case study provided. Your answers must be
directly related to the clinical manifestations that your patient presents with. You must submit
your work with a minimum of six references from the past 5 years including peer-reviewed
journal articles, textbook material or other appropriate evidence-based resources.
Case study
Mr. Aloha Das is a 68-year-old gentleman presenting to the emergency department at
0400hrs with worsening shortness of
eath. Onset 2 days ago and progressively worsening.
He also developed wheeze and right sided pleuritic chest pain this morning. Vomited x1,
ongoing nausea. Has history of non-compliance with medication and adherence to fluid
estriction.
Past History
Hypertension, Inferior Myocardial Infarction in 2020, Heart Failure, non-ischemic
Cardiomyopathy, Permanent Pacemaker inserted 2021, DM Type II, GORD, Osteoarthritis.
Cu
ent medications:
Furosemide 40mg OD, Captopril 6.25 mg TiD, Digoxin 0.125 mg BD, Metformin 500mg
TiD, Nexium 40 mg BD.
On 1.2 L fluid restriction; Echocardiogram results in 2021- systolic dysfunction, mild mitral
valve regurgitation, dilated left atrium and ejection fraction (EF) 33%.
Nursing Assessment
A. Clear, speaking in short sentences
B. RR 28 bpm, SpO2 90% RA, bilateral crackles, diffuse wheeze anteriorly and posteriorly
C. HR 120 bpm, peripherally cold, centrally warm, BP 186/108 mmHg, capillary refill<3 sec
D. GCS 15 (E4V5M6) PEARL
E. Patient looks distressed, diaphoretic, right JVP distension++, bilateral pedal pitting edema
2+
F. No IV fluids in progress
G. BGL 14.0mmol/L
Plan
• Continuous cardiac monitoring
• 12 lead ECG
• Blood pathology order
• Troponin I High Sensitivity
• Chest X-Ray
• Insert IVC right hand
• Furosemide 40mg IV Stat
• Echocardiogram

Results of Investigations:
Chest x- ray: Left ventricular hypertrophy, interstitial edema noted by Kerley B lines in the
costophrenic angle.
ECG:


Blood Results:
Electrolyte, urea and creatinine:
Result Reference Range
Sodium 137 mmol/L XXXXXXXXXXmmol/L
Potassium 3.9 mmol/L XXXXXXXXXXmmol/L
Chloride 105 mmol/L XXXXXXXXXXmmol/L
Urea nitrogen
(BUN)
14.0 mmol/L XXXXXXXXXXmmol/L
Creatinine 147 µmol/L XXXXXXXXXXµmol/L
Coagulation profile:
Result Reference
ange
Partial thromboplastin time
(PTT)
35 sec 30-45 sec
Prothrombin time (PT) 12 sec 10-12 sec
Cardiac enzymes:
Result Reference range
High sensitivity Troponin T 25 ng/L 0-14 ng/L
Arterial blood gas analysis
Result Reference Range
pH XXXXXXXXXX
PaO2 75 mmHg XXXXXXXXXXmmHg
PaCO2 37 mmHg 35-45 mmHg
HCO3- 19 mmol/L 22-26 mmol/L
SpO2 94% >95%
BE -9 mmol/L -2 - +2mmol/L
Lactate 4mmol/L 0.5-1.6mmol/L
Impression: Exace
ation of Congestive Cardiac Failure and fluid volume overload
Question 1
In order to prioritise your nursing actions, you are expected to have a sound understanding of
the pathogenesis and pathophysiology.
Explain the pathogenesis and pathophysiology causing the clinical manifestations with which
Mr Das presents.
Question 2
Choose One high priority nursing intervention that you will perform for Mr Das
– Briefly explain why you chose this nursing intervention
– Explain how the nursing intervention will alleviate the clinical features of Mr Das
using physiological linking
– Describe
iefly the impact of not performing the intervention
Question 3
Mr Das has been prescribed Furosemide 40mg IV Stat and Glyceryl Trinitrate IV Infusion 10
mcg/min starting rate.
For both medications explain
– The mechanism of action
– Why your patient is receiving this medication in relation to his symptoms and diagnosis?
– What are the nursing considerations for this medication?
– What clinical response you expect?
– What continuing clinical observations will you need to undertake?
Submission
Refer to Section 2.5 of the Learning Guide- General Submission Requirements
Submit your assessment through Turnitin
Format
All assignments are to be typed
Typing must be according to the following format:
3 cm left and right margins, double spaced.
Font: Arial or Times New Roman
Font size: 12pt
See further submission requirements below
Submission Requirements
1. Electronic copy only. Students are to submit an electronic copy of the assessment. Students
are not required to submit the original hard copy of their assessment on campus
2. Submit your assessment electronically through the Turnitin link on the unit vUWS site.
3. Students are to upload the assessment with the following title:
Surname_Firstname_assessment title
4. Your assessment must be submitted in .doc, docx format.
5. This assessment is marked online; no paper copy will be accepted. Marks, comments and
the marking criteria will be released online. If you do not receive your marked assessment
when all others have been returned, it is your responsibility to contact the Unit Coordinator
for assistance.
Resources:
i. There are a number of textbooks and resources available through the Western Sydney
University Li
ary that may assist you. Please refer to the unit’s vUWS site for specific unit
esources.
ii. Assessments listed as individual assessments must be completed independently. Students
are advised to refer back to their notes, textbooks or appropriate academic, peer-reviewed
esources utilised during unit delivery
Answered Same DayApr 05, 2022

Solution

Dr. Saloni answered on Apr 05 2022
17 Votes
Running Head: Case Study of Mr. Das 1
Case Study of Mr. Das
Contents
Answer 1    3
Answer 2    4
Answer 3    5
References    7
Answer 1
An underlying issue of acute heart failure has been cardiac dysfunction (remodelling and primarily acute myocardial destruction), which is anticipated by pulmonary as well as systemic venous disruptions (including endothelial dysfunction), culminating in substantial acute hemodynamic abe
ations. Mr. Aloha Das's AHF might have been exace
ated by non-cardiac como
idities, hypertension, and other variables. AHF has been most often triggered by severe decompensation underlying chronic heart failure, which is co
elated with increased congestion affected by a multitude of conditions. To counter the detrimental hemodynamic repercussions of heart failure, cardiac dysfunction triggers a range of neuro-humoral pathways (Greenwood et al., 2018).
Persistent neuro-humoral engagement also initiates regressive processes that culminate in ventricular remodelling and organ failure. A subclinical level ove
ules observable complaints and predictors of volume abundance throughout the congestive cascade. Persistent salt deposition throughout heart failure disrupts the interstitial glycosaminoglycan system. Interstitial oedema also arises as a consequence of substantially increased hydrostatic forces. Sympathetic activation culminates in transient vascular constriction, enabling volume shifting from the splanchnic and peripheral vascular channels to the pulmonary circulation. Systemic constriction is influenced by a complex system of fluid retention and fluid redistribution during AHF (Holmes et al., 2020).
As per the recent findings, vascular constriction is more than merely a manifestation of heart failure; it also plays a critical role in the pathophysiology of AHF, initiating pro-inflammatory, hemodynamic, and pro-oxidant responses. Left-sided constriction induces
eathlessness, cough, orthopnoea, hypoxic state, tachypnoea, and poor lung auscultation (Greenwood et al., 2018). Right-sided constriction induces pleural effusions, ascites, hepatomegaly, stomach pain, vomiting, icterus, nausea, and diminished urine function. Hypo perfusion clinical manifestations have been infrequent. However, they do imply severity. Hypotension, weak pulses, anxiety, tachycardia, intellectual disorientation, weariness,
eathlessness (associated with metabolic acidosis as well as cere
al hypoxia), clammy extremities, cold, reduced urine function, and myocardial ischemia-related angina are indeed a few of the manifestations (Lello et al., 2019).
Answer 2
In the case of Mr. Das, one high-priority nursing intervention was to satisfy his oxygen...
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