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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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 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 breath. 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 restriction. Past History Hypertension, Inferior Myocardial Infarction in 2020, Heart Failure, non-ischemic Cardiomyopathy, Permanent Pacemaker inserted 2021, DM Type II, GORD, Osteoarthritis. Current 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="" 135-147="" mmol/l="" potassium="" 3.9="" mmol/l="" 3.5-5.2="" mmol/l="" chloride="" 105="" mmol/l="" 95-107="" mmol/l="" urea="" nitrogen="" (bun)="" 14.0="" mmol/l="" 3.0-8.0="" mmol/l="" creatinine="" 147="" µmol/l="" 64="" -104="" µmol/l="" coagulation="" profile:="" result="" reference="" range="" 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="" 7.30="" 7.35-7.45="" pao2="" 75="" mmhg="" 80-100="" mmhg="" 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: Exacerbation 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 briefly 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 Library that may assist you. Please refer to the unit’s vUWS site for specific unit resources. 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 resources utilised during unit delivery
Answered Same DayApr 05, 2022

Answer To: Case Analysis- Case Study of an Acute Life-Threatening Condition Word Count There is a word limit of...

Dr. Saloni answered on Apr 05 2022
111 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 aberrations. Mr. Aloha Das's AHF might have been exacerbated by non-cardiac comorbidities, hypertension, and other variables. AHF has been most often triggered by severe decompensation underlying chronic heart failure, which is correlated 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 overrules 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 breathlessness, 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, breathlessness (associated with metabolic acidosis as well as cerebral 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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