Topic: Left Sided Heart Failure Concept Map

Place your order today and enjoy professional academic writing services—From simple class assignments to dissertations. Give us a chance to impress you.


Order a Similar Paper Order a Different Paper

Left Sided Heart Failure Concept Map

Number of Pages: 2 (Double Spaced)

Number of sources: 4

Save your time - order a paper!

Get your paper written from scratch within the tight deadline. Our service is a reliable solution to all your troubles. Place an order on any task and we will take care of it. You won’t have to worry about the quality and deadlines

Order Paper Now

Writing Style: APA

Type of document: Case Study

Academic Level:Undergraduate

Category:   Nursing

Dear Writer

More details attached.

Topic: Left Sided Heart Failure Concept Map
influences 4,7 6,7 5 1,2,4 1,2,3 Leads to need for immediate diagnoses Diagnosed by Results in
Topic: Left Sided Heart Failure Concept Map
Pathophysiology template Disease: Ischaemic stroke affecting the dominant left cerebral hemisphere Definition: An ischaemic stroke is death of brain tissue resulting from an occluded artery caused either by an atherosclerotic obstruction or embolus that interrupts blood supply to the area of the brain supplied by the occluded artery. The sudden loss of blood circulation results in a corresponding loss of neurologic function (Jauch, 2014). AETIOLOGY: A depletion of blood flow in a cerebral artery resulting from a: Thrombus –atherosclerotic plaque that has ruptured in a cerebral artery Embolus from heart e.g. left atrial thrombus, left ventricular thrombus, atrial fibrillation from carotid artery (Craft &Gordon,2011) PATHOGENESIS: Interruption of blood flow to cerebral tissue initiates a biochemical ischaemic cascade. Mitochondrial production of ATP ceases depolarisation  influx of sodium and calcium and efflux of potassium. Passive inflow of water into cells causes cytotoxic oedema and destruction of cells in infarct core. Membrane depolarization also stimulates the release of neurotransmitters. Glutamate release excessive calcium influx into nearby neurons (exocitotoxicity) destruction of cells by lipolysis, proteolysis and free radicals. Mitochondria break down releasing toxins and apoptotic factors. Injured brain tissue triggers inflammatory response release of inflammatory mediators cell death and oedema destruction of cells in infarct core necrosis ischaemic penumbra around core has diminished blood flow but preserved cellular metabolism. Areas of necrotic tissue are not able to conduct nerve impulses so functions such as initiating and conveying motor impulses, receiving and interpreting sensory information and speech control will be interrupted. (Bautista, 2014; Craft & Gordon, 2011; Maas & Safdieh,2009). CLINICAL MANIFESTATIONS: Just superior to the medullary junction, 90% of axons in the left pyramid cross to the right  right motor dysfunction. The middle cerebral artery supplies the frontal, temporal and parietal lobes as well as the basal ganglia and internal capsule. (Tocco,2011). Therefore specific clinical manifestations include: Hemiplegia and weakness on right side of body Sensory loss on right side Inability to see the right visual field of each eye Aphasia Apraxia Dysarthria Impaired reasoning Behavioural changes Problems with memory (Bautista, 2014; Craft & Gordon, 2011). DIAGNOSIS Complete history Physical and neurological examination Brain MRI or CT scan – Essential in differentiating cerebral haemorrhage from ischaemic stroke. MRI is superior as cerebral ischaemia can be identified within minutes and can identify small areas of stroke. Other tests for vascular imaging can be used e.g. CT angiography, magnetic resonance angiography (Silverman & Rymer, 2009). TREATMENT The emphasis of ischaemic stroke treatment is placed on salvaging potentially reversible ischemic penumbra brain tissue, preventing secondary stroke and minimising longterm disability. (Jaunch, 2014). Reperfusion thrombolytic agent (e.g.tPA) intra-arterial technique Neuroprotection -antithrombotic therapy (e.g. aspirin) Nursing management Acute phase frequent evaluation of neurological status frequent evaluation of vital signs Monitor oxygen saturation – administer oxygen if required Screen for swallowing deficits and manage appropriate hydration and nutrition strategies Manage activities of daily living Screen for communication deficits and address appropriate communication strategies Prevent complications e,g pressure areas, contractures, DVT Assess urinary and faecal continence and address appropriately Rehabilitation begin as early as possible by preventing complications, passive and active movement and mobilizing as early as possible. Support and encourage activities provided by physiotherapists, occupational therapists and speech therapists Education – e.g. lifestyle modification, adherence to medications (National Stroke Foundation, 2010). COURSE OF DISEASE With reperfusion – blood is restored to the area and signs and symptoms gradually resolve Without treatment – Course is determined by severity of stroke. Ischaemia will extend to penumbra as stroke evolves, signs and symptoms worsen. As cerebral oedema resolves, and with structural and functional reorganisation recovery may continue for 6 months to a year. (peak recovery in about 3 months). Requires rehabilitation to optimise function. (Teasell & Hussein, 2014). Complications Contractures Fatigue Incontinence Mood disturbances Falls Dysarthria and aphasia PROGNOSIS Stroke prognosis is influenced by factors such as age and stroke severity. One in five likely to die within one month of suffering ischaemic stroke. Of those who recover about 90% will experience some impairment (Dashe,2014) PREVENTION Eliminating modifiable risk factors will prevent an ischaemic stroke. Don’t smoke Diet high in fruit and vegetables, low in fats and salt 30 minutes of moderate-intensity physical activity on most days of the week Maintain healthy BMI Limit alcohol to no more than two standard drinks per day (National Stroke Foundation, 2010) If a history of atrial fibrillation – ensure adherence to anticoagulation therapy. References Bautista, C. (2014). Disorders of Brain Function. In S. Grossman & C. Porth (Eds), Porth’s pathophysiology: Concepts of altered health states (9th ed.). (pp489- 524). Philadelphia: Lippincott Williams & Wilkins. Craft, J. & Gordon, C. (2011), Alterations of Neurological Function across the Lifespan. In J.Craft, C.Gordon & A. Tiziani (Eds). Understanding Pathophysiology (pp 188-226). Sydney, Australia:Elsevier Australia. Dashe, J. F. (2014). Stroke prognosis in adults. UpToDate. Retrieved from: http://www.uptodate.com/contents/stroke-prognosis-in-adults Jaunch, E.C. (2014). Ischemic stroke treatment and management, Retrieved from: http://emedicine.medscape.com/article/1916852-overview Maas, E.B. & Rymer, M.M. (2009). Ischaemic stroke: Pathophysiology and Principles of Localization. Neurology 13 .Retrieved from: http://www.turner-white.com/pdf/brm_Neur_V13P1.pdf National Stroke Foundation (2010). Clinical guidelines for stroke management 2010. Melbourne Australia. Silverman, I.E. & Rymer, M.M. (2009). An atlas of investigation and treatment. Ischaemic stroke. Clinical publishing:Oxford,U.K. Teasell, R.& Hussein, N. (2014)Brain reorganization, recovery and organizecare. In Stroke rehabilitation clinician handbook 2014. Retrieved from: http://www.ebrsr.com/sites/default/files/Chapter%202_Brain%20Reorganization,%20Recovery%20and%20Organized%20Care_June%2018%202014.pdf Tocco, S. (2011). Identify the vessel recognize the stroke. American Nurse Today 9 (6).
Topic: Left Sided Heart Failure Concept Map
Assessment 1 – Concept map and guided questions. Information 1 – Getting started. Your first assessment is generating a concept map for left heart failure and answering three questions related to a case study about a patient who has an acute exacerbation of heart failure. When preparing your assignment refer to the criteria and standards in the Learning Guide. You can begin this assessment now by finding readings about heart failure and summarising the information under the headings of the pathophysiology template. This information can then be used for your concept map. Some readings that you may find helpful to start your assignment are: Your textbook: Craft,J.A., Gordon,C.J., Huether,S.E., McCance, K.L., Brashers, V.L. & Rote,N.E. (2015). Understanding pathophysiology – ANZ adaptation (2nd ed.). Chatswood, NSW: Elsevier Australia. Chapter 23. Also: Aitken, L., Marshall,A. & Chaboyer, W. (2015). ACCCN’s critical care nursing (3rd ed.). Chatswood, NSW: Elsevier Australia. Chapter 10. Wagner, K.D. (2014). High acuity nursing (6th ed.). Upper Saddler River, New Jersey: Pearson. Chapter13. (These books are available online from the Western Sydney University library). This is just to begin. You will then find more readings to add to your information. Remember that the information in your concept map and answers to the questions must correlate with the references that you cite so keep an accurate record when preparing your assignment. The marker of your assessment will check your citations. An example of a pathophysiology template for a left-sided ischaemic stroke and a concept map using this information has been attached to start you thinking about how you will approach your assignment. The concept map has been generated using Word. However, if you wish, you may prefer to use a concept map template that you may find on the web.

Writerbay.net

When writing your assignment, we aim to help you get an A, not just beat the deadline.


Order a Similar Paper Order a Different Paper