Nursing Assignment: Case Study of Acute Pulmonary Oedema in Ms. Foley

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This nursing assignment presents a comprehensive analysis of a patient, Ms. Martha Foley, suffering from acute pulmonary oedema following a car accident. The report is divided into two parts: the first part details Ms. Foley's history, clinical assessment, and treatment, including analysis of observation and fluid balance charts, a description of acute pulmonary oedema's pathophysiology, and nursing assessment implications. The second part focuses on the inter-professional model of care required for Ms. Foley, emphasizing risk management and the importance of team-based care, including pharmacological interventions like Frusamide and oxygen delivery methods. The report highlights nursing interventions, care plans, and the importance of quality improvement within the inter-professional healthcare setting, concluding with the implementation of an IPMPC© model.
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Running head: NURSING
NURSING ASSIGNMENT
Name of the student:
Name of the university:
Author note:
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Introduction and outline
This assignment is about a patient named Ms. Martha Foley, a 35 year old lady who is
suffering from acute pulmonary oedema and was admitted in the hospital prior to 5 days
because of post multi-trauma caused by a car accident. She is also suffering from multiple
fractures in both legs and smoke inhalation as being trapped in car for 15 minutes.
This paper has been divided into two parts. Part 1 contains the description of Ms.
Foley and her history along with the treatment in the hospital and the analysis of the
Observation Chart and Fluid Balance Chart. It also contains a brief description of acute
pulmonary oedema, its pathophysiology and the implications of nursing assessment of this
situation.
Part 2 contains the inter-professional model of care required for Ms Foley while in hospital.
Part 1
Clinical assessment
Ms. Foley is a full time worker at a supermarket and is a victim of domestic violence
from her former partner. She had a good relationship and support from her friends and co-
workers. The day of the accident she and her friend Ms. Annie Jones were travelling in the
same car. Ms. Jones was also admitted in the same hospital. Ms. Foley was a smoker of 10
cigarettes per day and also intake drugs such as methamphetamines IV and cocaine. But don’t
drink alcohol and is a vegetarian. She had suffered from left sided heart failure in the past and
is treated by cardiomyopathy.
Fluid balance chart describes that Ms. Foley is given compound Sodium acetate was
given intravenously from 01:00 am to 08:00 am at 200mls per hour and only 100mls is
drained out through urine. It has been shown in appendix 1.
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Observation chart describes about the general physical conditions of Ms. Foley during the
time of her admission in the hospital. The following things were measured:
Respiratory rate – 16-20 breathe/min
O2 Saturation – 95-97%
Air delivery method – RA
Blood pressure – 120/40-150/80 mmHg
Pulse rate – 70-90 beats /min
Temperature – 36.6-37.0
Consciousness/Sedation – 0
Pain score – 0-5
Application of pathophysiology
Acute pulmonary oedema is a type of disease in which the alveoli gets filled up with fluid
and the person is unable to breathe. As the fluid gets accumulated creates misbalance in
exchange of gases and leads to dyspnoea and hypoxia. Acute pulmonary oedema (APO) is
caused by two main mechanisms. The first mechanism is elevations in pulmonary pressures
due to severe increase in intra-cardiac pressure of chambers and second is severe lung injury
causing increase in pulmonary vascular permeability (Liesching et al. 2014).
Pulmonary oedema caused due to lung injury is termed as acute respiratory distress
syndrome (ARDS) while pulmonary oedema which is due to acute elevations in pulmonary
micro vascular pressures is termed acute cardiogenic pulmonary oedema (Lavin et al.
2015).
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The pathophysiology of these two types of oedema is almost different due to which
their treatments are also different. This document relates specifically to acute cardiogenic
pulmonary oedema (Zeiss 2016).
Pathophysiology
Acute cardiogenic pulmonary oedema is caused by an intense ischemic occasion
bringing about cardiovascular brokenness. Intense diastolic disappointment may likewise be
caused from hypertension and atherosclerosis. Less generally the intense sight might be
optional to other essential occasions, for example, intense valvular issue or arrhythmia (Elias
et al. 2015).
The acute cardiac dysfunction that happens from a background marked by myocardial
ischemia brings about expanded cardiovascular end diastolic weights which thus result in
hoisted pneumonic micro vascular weights and the improvement of intense cardiogenic
aspiratory oedema (Vlaar and Juffermans 2013). There is a decrease in cardiovascular yield
with ensuing solid enactment of the thoughtful sensory system and the renin-angiotensin
framework. This outcomes in lifted blood weights and expanded delayed consequences on
the heart starting a gooey cycle of expanded myocardial oxygen request and further lessening
in cardiovascular yield (Luks et al. 2014).
In the problems of heart failure there are homeostatic systems that prompt liquid maintenance
and pneumonic blockage. In APO there might be starting of liquid fill up, however the
essential pathophysiology won't be reliant on the benchmark liquid status. It is significant that
s number of these patients is hemoconcentrated on introduction because of the gathering of
up to 2 litres of liquid in their lungs (Spoletini et al. 2015). They may then show up
hemodiluted 24 hours after the fact when they are in the recuperation stage. As it were they
give off an impression of being enduring a more prominent plasma volume as of now, which
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is suggestive that the issue is not fundamentally a liquid over-burden issue. By and large of
APO the issue is less liquid abundance; rather it is an instance of liquid in the wrong
"compartment", (intra-alveolar, as opposed to intra-vascular) (Duffy et al. 2015).
Nursing care plan
The nursing care plan depends upon the appearance of the patient’s respiratory status. To
perform the assessment of nursing care for acute pulmonary oedema the nurse must observe
the individual’s responses (Akoumianaki et al. 2014).
1. To assess the respiratory rate, intensity, and effort, including nasal flaring, and
abnormal patterns of breathe.
2. To assess the lungs to locate the areas of decreased ventilation.
3. To monitor the mental status of the patient for beginning of agitation, confusion, and
extreme tiredness.
4. To monitor the symptoms of atelectasis: bronchial or tubular sounds of breathing,
crackles, reduced chest congestion, and shift of trachea to the affected side.
5. To monitor the alteration in Blood Pressure.
6. To observe the nail beds, skin cyanosis and mucous membranes of mouth.
7. To monitor oxygen saturation continuously, using pulse oximeter.
8. Monitor the effects changes in position during oxygenation (ABGs), venous oxygen
saturation and pulse oximetry.
9. To assess the ability of patient to excrete out mucous by coughing. Take note of the
quantity, colour, and consistency of the sputum.
10. Evaluate the patient’s hydration status.
11. Check on Hgb levels.
12. Monitor chest x-ray reports
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Nursing Interventions
The following are the therapeutic nursing interventions for acute pulmonary oedema:
1. A nurse must check the patient’s position regularly so that she must not fall from bed.
2. The nurse must turn the patient after every 2 hours and monitor the venous oxygen
diffusion after turning. If it drops below 10% or fails to return to baseline promptly,
turn the patient back into a supine position and evaluate oxygen status.
3. If patient is suffering from obesity then change the patient to Trendelenburg position
at 45 degrees which can be tolerated by the patient.
4. If the patient is extremely dyspnoeic, try the patient to lean over a bedside table, if it
is tolerable by patient.
5. Maintain the oxygen delivering device as per the instruction, which can maintain
oxygen saturation.
6. Avoid increasing the concentration of oxygen to the patients with COPD.
7. Encourage or assist with ambulation as per physician’s order.
8. Help the patient to take deep breath and control coughing. To support the patient to
inhale deeply, then holding the breath for some seconds, and cough for two to three
times by keeping the mouth open.
9. Encourage slow deep breathing using an incentive spirometer as indicated.
10. For postoperative patients, assist with splinting the chest.
Oxygen delivering devices
The initial management of patients with cardiogenic pulmonary edema (CPE) should
address the ABCs of resuscitation, that is, airway, breathing, and circulation. Oxygen should
be administered to all patients to keep oxygen saturation at greater than 90%. Any associated
arrhythmia or MI should be treated appropriately (Lumb 2016).
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Methods of oxygen delivery incorporate the utilization of a face covering, non-
intrusive pressure support ventilation (which incorporates bi-level positive aviation route
weight [BiPAP] and consistent positive airway pressure [CPAP]), and intubation and
mechanical ventilation (Stocker et al. 2014). The method that will be utilized relies upon the
proximity of hypoxemia and acidosis and on the patient's level of cognizance. For instance,
intubation and mechanical ventilation may end up noticeably important in instances of
tireless hypoxemia, acidosis, or changed mental status. The utilization of non-intrusive
weight bolster ventilation in acidotic patients with serious intense cardiogenic aspiratory
oedema does not give off an impression of being related with unfavourable results (early
mortality and intubation rates) in these patients (Adam, Osborne and Welch 2017).
Pharmacological uses of frusamide
Usual Adult Dose for oedema
Intravenous:
Initial dose: Frusamide is given intravenously and the dosage is 20-40 mg (slowly for 1 to 2
minutes) or may increase the dosage by 20 mg later by 2 hours after the previous dose until
the desired diuretic effect has been obtained.
Use: Treatment of oedema associated with congestive heart failure, cirrhosis of the liver, and
renal disease, including the nephrotic syndrome, especially when an agent with greater
diuretic potential is desired (Soni et al. 2017).
Oral:
Initial dose: 20 to 80 mg orally once; may repeat with the same dose or increase by 20 or 40
mg no sooner than 6 to 8 hours after the previous dose until the desired diuretic effect has
been obtained.
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Maintenance dose: Administer the dose that provided the desired diuretic effect once or
twice a day.
Maximum dose: 600 mg/day in patients with clinically severe oedematous states.
Comments:
-Oedema may be most efficiently and safely mobilized by giving this drug on 2 to 4
consecutive days each week.
-When doses greater than 80 mg/day are given for prolonged periods of time, careful clinical
observation and laboratory monitoring are particularly advisable.
Use: Treatment of oedema associated with congestive heart failure, cirrhosis of the liver and
renal disease, including the nephrotic syndrome, especially when an agent with greater
diuretic potential is desired.
Part 2
Inter-professional model of care
The Inter-Professional Model of Patient Care (IPMPC©) was introduced in 2006
when inter-professional collaboration started as a priority of policy agenda in Canada. This
model causes the experts to enhance better care the patients and their families which likewise
can manage the extra issues of human medicinal services. The models speak to a pedantic
program, a group based affair and a between proficient recreation encounter. The
instructional program stresses between proficient group building abilities, information of
callings, tolerant focused care, benefit taking in, the effect of culture on medicinal services
conveyance and a between proficient clinical segment (Maggiore et al. 2014).
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Nurses were ready for Ms Foley to attend her while she was lying flat on her bed,
trying to sit up, and gasping for air. She is worried, stating she is ‘scared’, and that she has a
weird feeling that she can only describe as ‘a sense of impending doom’. Vital signs taken
and are the following: Pulse 120bpm and regular, BP 100/50, RR 34, SaO2 92% on RA. Her
lips have started to turn blue and the nail beds on her fingers are cyanotic. She remains
dyspnoeic and desperate for air. She is coughing.
Risk management
The integral part of inter-professional care of nursing is quality improvement. ACHS
is a handbook which gives information of management of risks and improvement of quality
to assist organisations and to manage the risks at the organisational levels and to ensure that
quality of care and services are integrated (Powell et al. 2016).
Implication of Inter professional model of care
PE teams have found their place in health care. Teams do not replace the physician-
patient relationship, but rather enhance it—creating a more comprehensive, efficient, and
tailored health care experience (Short et al. 2014).
The care convention was created by the IP group amid a CPE workshop and
encouraged group gatherings. It was utilized as the guide by medical caretakers or doctors
associates who gave mind at the visits. Components of the IP mind convention included
visual signs, for example, publications on the exam room dividers that represent the body
frameworks affected by diabetes, and an envelope with data, worksheets and apparatuses
created by the IP group on parts of connecting with relatives for help, eating regimen,
exercise and medical administration.
Conclusion
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Thus through the above discussion it can be concluded that Ms. Martha Foley had an accident
and detected by acute pulmonary oedema which is a type of disease in which the lungs is
filled up with fluid. At first in this task there had been included clinical assessment tools;
pathophysiology and its applications; nursing care plan; nursing interventions;
pharmacological uses of frusamide; inter-professional model of care, its risk management and
its implications.
References
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Adam, S., Osborne, S. and Welch, J. eds., 2017. Critical care nursing: science and
practice. Oxford University Press.
Akoumianaki, E., Maggiore, S.M., Valenza, F., Bellani, G., Jubran, A., Loring, S.H.,
Pelosi, P., Talmor, D., Grasso, S., Chiumello, D. and Guérin, C., 2014. The application of
esophageal pressure measurement in patients with respiratory failure. American journal of
respiratory and critical care medicine, 189(5), pp.520-531.
Duffy, M., Jain, S., Harrell, N., Kothari, N. and Reddi, A.S., 2015. Albumin and
furosemide combination for management of edema in nephrotic syndrome: a review of
clinical studies. Cells, 4(4), pp.622-630.
Elias, B., Barginere, M., Berry, P.A. and Selleck, C.S., 2015. Implementation of an
electronic health records system within an interprofessional model of care. Journal of
interprofessional care, 29(6), pp.551-554.
Lavin, M., Harper, E. and Barr, N., 2015. Health information technology, patient safety,
and professional nursing care documentation in acute care settings. OJIN: The Online
Journal of Issues in Nursing, 20(2).
Liesching, T., Nelson, D.L., Cormier, K.L., Sucov, A., Short, K., Warburton, R. and Hill,
N.S., 2014. Randomized trial of bilevel versus continuous positive airway pressure for
acute pulmonary edema. The Journal of emergency medicine, 46(1), pp.130-140.
Luks, A.M., McIntosh, S.E., Grissom, C.K., Auerbach, P.S., Rodway, G.W., Schoene,
R.B., Zafren, K. and Hackett, P.H., 2014. Wilderness Medical Society practice guidelines
for the prevention and treatment of acute altitude illness: 2014 update. Wilderness &
environmental medicine, 25(4), pp.S4-S14.
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Lumb, A.B., 2016. Nunn's Applied Respiratory Physiology eBook. Elsevier Health
Sciences.
Maggiore, S.M., Idone, F.A., Vaschetto, R., Festa, R., Cataldo, A., Antonicelli, F.,
Montini, L., De Gaetano, A., Navalesi, P. and Antonelli, M., 2014. Nasal high-flow
versus Venturi mask oxygen therapy after extubation. Effects on oxygenation, comfort,
and clinical outcome. American journal of respiratory and critical care medicine, 190(3),
pp.282-288.
Powell, J., Graham, D., O’Reilly, S. and Punton, G., 2016. Acute pulmonary oedema.
Nursing Standard, 30(23), pp.51-60.
Short, K.R., Kroeze, E.J.V., Fouchier, R.A. and Kuiken, T., 2014. Pathogenesis of
influenza-induced acute respiratory distress syndrome. The Lancet infectious diseases,
14(1), pp.57-69.
Soni, L., Ansari, M., Thakre, N., Singh, A., Bhowmick, M. and Rathi, J., 2017.
Development and in-vitro evaluation of Furosemide Solid Dispersion using different
Water Soluble Carriers. International Journal, 6(2), pp.2571-2575.
Spoletini, G., Alotaibi, M., Blasi, F. and Hill, N.S., 2015. Heated humidified high-flow
nasal oxygen in adults: mechanisms of action and clinical implications. CHEST Journal,
148(1), pp.253-261.
Stocker, R., Lenzlinger, P.M. and Stover, J.F., 2014. Contemporary intensive care
treatment for patients with severe multiple trauma. In General Trauma Care and Related
Aspects (pp. 95-109). Springer Berlin Heidelberg.
Vlaar, A.P. and Juffermans, N.P., 2013. Transfusion-related acute lung injury: a clinical
review. The Lancet, 382(9896), pp.984-994.
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Zeiss, A.M., 2016. Cognitive Behavioral Therapy as an Integral Component of
Interprofessional Care. Cognitive and Behavioral Practice, 23(4), pp.441-445.
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APPENDIX 1
FLIUD BALANCE CHART
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APPENDIX 2
OBSERVATION CHART
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