Topic: Heart Failure Concept

Topic: Heart Failure Concept
Topic: Heart Failure Concept
Permalink:
Below are the Sub-heading that needs to be in the Concept Map.
Disease
Definition
AETIOLOGY
PATHOGENESIS
PATHOGENESIS
DIAGNOSIS
TREATMENT
COURSE OF DISEASE
PROGNOSIS
PREVENTION
· The separate Reference page for Concept Map. You may have more than 2 reference
· Visually Stimulating, add pictures in the background and visually attractive. Below is an sample example but this concept map needs to look unique and visually very appealing, please.
· Add pictures of heart, lungs what ever connects to the Map and its information.
· I have attached a sample of the concept map of another topic to guide you what information requires in the map.
· 500 words and it is worth 25 Marks.
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.
Topic: Left Sided Heart Failure Concept Map
influences
Aetiology
Depletion of blood flow in a cerebral artery resulting from a thrombus or embolus. (1)
Pathogenesis
Occlusion of cerebral artery production of ATP failure of energy pumps influx of sodium and calcium ions and efflux of potassium passive inflow of water cytotoxic oedema destruction of cells in infarct core.
Membrane depolarisation release of glutamate excessive calcium influx into neurons destruction of cells by lipolysis, proteolysis and free radicals.
infarct core and ischaemic penumbra
necrotic tissue not able to conduct impulses interrupting normal function such as motor and sensory transmission and speech.
Risk factors
· Obesity
· Smoking
· Sedentary lifestyle
· Age 1.
· ageg
Clinical features
· Right-sided hemiplegia and weakness
· 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
Diagnosis
· Complete history
· Physical and neurological examination
· Brain MRI or CT scan –differentiate cerebral haemorrhage from ischaemic stroke
· Other tests for vascular imaging – CT angiography, magnetic resonance angiography
Primary prevention
· Don’t smoke
· Diet high in fruit and vegetables
· Diet low in fats and salt
· 30 minutes of exercise daily
· Limit alcohol
1,7
Treatment
Medical
· Reperfusion Thrombolytic (tPA )
Nursing acute phase
· Frequent evaluation of neurological status and vital signs
· Oxygen saturations – administer oxygen if required
· Screen for swallowing – manage hydration and nutrition
· Manage activities of daily living
· Address appropriate communication strategies
· Prevent complications
Rehabilitation
· Passive and active movement
· Encourage activities provided by physiotherapists, speech and occupational therapists e.g. mobility, speech, ADL
· Education-
Secondary prevention
· Neuroprotection – e.g, aspirin
Course of disease
With reperfusion – blood restored to area, many symptoms gradually resolve
Without treatment – ischaemia extends to penumbra –symptoms worsen. Recovery may continue 6 months to a year but left with disability. Requires rehabilitation to optimise function 8
Complications
· Contractures
· Incontinence
· Falls
· Mood disturbances
· Dysarthria and aphasia
·
·
Death of brain tissue resulting from an occluded cerebral artery in the left side of the brain.. 6.
Prognosis
One in five likely to die within one month.
Of those who recover about 90% will experience some impairment. 9
causes
Atherosclerosis
Prevents formation of
4,7
6,7
5
1,2,4
1,2,3
Leads to need for immediate
diagnoses
Diagnosed by
Results in
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).

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