Can anyone give me some ideas on this case study? thx

Nursing Students Student Assist

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You are a new graduate nurse on your second rotation in a 30-bed medical ward. It is 0800hrs during a morning shift, and you have been allocated the care of a 70-year-old female, who has been on your ward for the last week, recovering from an acute infective exacerbation of chronic obstructive pulmonary disease (copd).

Past medical history: ischaemic heart disease (ihd) and severe copd (with type ii respiratory failure).

When assisting the patient with breakfast you notice she has become increasingly breathless, only speaking in single words, and not interested in eating. A set of observations are taken:

SAO2 88% on np at 2l/min

bp 160/90, hr 144

resp rate 45 b/min, and

Temperature 37.2. auscultation of the lung fields reveals wide spread expiratory wheeze bilaterally.

lab results:

abg

uec's

fbc

ph 7.33

na 144mmol/l

hb 155 g/l

pa02 55 mmhg

k 4.5 mmol/l

wcc 11 x 109/l

pac02 70 mmhg

cl 109 mmol/l

plt 400 x 109/l

hc03 36 mmol/l

urea 8 mmol/l

creat 90 µmol/l

Questions

1. Using the information given in the (above) case study start by prioritizing and justifying your immediate care of this patient?

2. You also need to interpret both clinical and lab results, and

3. what physiological processes may be responsible for the abnormal clinical or lab results?

Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.

I agree with GrnTea. This patient, while a chronic COPD patient/respiratory failure Type II, something has caused an acute exacerbation in her condition.

What do you think first? The patient is eating and becomes hypoxic/tachypneic/tachycardic.......What is the first thing that comes to mind? Obstruction. Think ACB's. It is clear that this patient is in distress.......HR 144, RR45 Sat 88%. Now what do you do? Well in reality many things simultaneously. You will check and clear the airway. The patient can speak and isn't choking so......you are lead to believe the airway is clear right now. She is in distress and hypoxic... you have already gotten the ABGs on the present O2.

I would increase/titrate the O2 temporarily to try to achieve a Sat of approximately 90% and observe the patient closely for signs of decrease drive and LOC. I would start with 5/6 lpm NC and hopefully see some improvement in the saturation. I might condsider other more aggressive )2 like a Non re-breather if the patient remined hypoxis or continued to deteriorate........but I would probably opt for a venturi mask first to better titrate the concentration of O2 administered to the patient. After listening to the lungs you determine this is bronchospasm......I would call for a prn nebulizers and MD for other medical interventions. I would ask the MD for a stat portable CXR to be sure no aspiration occurs as that would affect the care/outcome/treatment of this patient.

It she continued in distress or depending on the facility I would call a Rapid Response. I would call the rapid response if that was the facilities procedure. Every culture is different. OP.....do they have Rapid respone units in the land down under? The patient is in distress as evidenced by a HR of 144 and a RR rate of 45....the icing on the cake is the Sat of 88% proving that this is NOT her living O2 saturation. Prepare for possible intubation and transfer to a higher level of care like ICU.

Specializes in Progressive, Intermediate Care, and Stepdown.

Between Mattnurse, bobbyzr7, Dixielee, Grntea, Esme12, and the OP, I've learned a lot from this discussion. I'm still a student and have limited experience with type of situation.

I really enjoy these types of discussions. I appreciate the experienced folks out there that take time to discuss this. I didn't even think of aspiration or the bronchospasm possibility. When I initially started nursing school, I wouldn't even have a clue where to begin. However, I feel somewhat in the loop right now. I think this type of discussion is a great way to enhance the critical thinking skills the program harps on. Nothing really beats clinical time and experience. I have yet to attain much of either.

Thanks again OP and thanks again all those folks out there helping us students out. :D

Along with what everyone else has said, my thoughts on the O2 and the COPD, is I would want to know what they were trending at prior to this episode. If they were trending at 96% on the 2 liters and now they are down to 88% on 2 liters, to me that is huge difference. If they are always at 89 to 90%, then not so much.

However, and I will stress this: Always treat the patient and how they are presenting.

Specializes in ICU & LTAC as RN. FNP.

floridatrail2006

i feel that i learned something too from this discussion. i'm always open to learning from someone, whether it's a student, or an experienced nurse.

Specializes in Cardiac Care.

I am glad people took the time to answer the question and debate the interventions, instead of just saying do your own homework. Sharing information and providing alternative ideas is exactly what these boards are for! I for one know I learned quite a few things and also realized that I know some things myself!

Thanks for sharing!

Specializes in med-tele/ER.

Floridatrail2006

This is a little exerpt from the uptodate article "Use of oxygen in patients with hypercapnia" I read the whole article and quoted the part that I copied and pasted. It was interesting, I tried to PM you the full text but it says it is too long.

"Traditional teaching emphasizes that hypercapnia results from suppression of hypoxic ventilatory drive and warns that "patients will stop breathing" if given oxygen. However, this interpretation does not account for the many factors that contribute to the control of breathing in these patients, and has resulted in oxygen being withheld inappropriately from some patients with acute respiratory failure.

Regardless of the mechanism of hypercapnia, it is essential to administer oxygen to patients with significant hypoxemia to avoid the potentially life-threatening complications of a low PaO2. In addition, a meta-analysis of 31 studies confirmed that administering supplemental oxygen to hypoxemic patients reduced dyspnea and minute ventilation during exercise.

SUMMARY AND RECOMMENDATIONS — It is important to understand the goals of oxygen therapy and the multiple factors that can contribute to hypercapnia when considering the use of supplemental oxygen in the treatment of patients with ARF. An elevation in FiO2 may cause PaCO2 to rise, but it is unlikely to result in severe CNS depression unless the PaCO2 exceeds 85 to 90 mmHg. Many patients with acute on chronic respiratory failure have a chronic compensated respiratory acidosis (in which the arterial pH is only modestly reduced) and are at greater risk from hypoxemia than hypercapnia. The primary goal of therapy should be the maintenance of an SpO2 of 90 to 93 percent or a PaO2 of 8 to 9.3 kPa (60 to 70 mmHg) [21,32,33]. Further increases in the FiO2 above the level needed to achieve the latter goals do not add significantly to the oxygen content of blood but do increase the potential for more severe secondary hypercapnia.

Optimal oxygen therapy can be achieved using the following approach:

•Increase the inspired concentration of oxygen initially by 4 to 7 percent (eg, 32 to 36 percent FIO2) with close monitoring of both PaO2 and PaCO2. Venturi masks should be used when possible to permit tight regulation of FiO2 (figure 4) [34]. When using nasal cannula, the oxygen flow rate should generally be increased by 1 L per minute at a time; remembering that it is very difficult to predict the FIO2 when administering supplemental oxygen by nasal cannula. The goal is an oxygen saturation by pulse oximetry (SpO2) of 90 to 93 percent, and higher concentrations of inspired oxygen should be given if the SpO2 remains below 90 percent or the PaO2 below 8 kPa (60 mmHg).

•Simultaneous administration of bronchodilators and diuretics (if clinically indicated) should be considered for patients with COPD and ARF. (See "Management of acute exacerbations of chronic obstructive pulmonary disease".)

•The development of acute hypercapnia leading to significant acidemia (eg, pH

this was one of the references

Hypercapnia during oxygen therapy in acute exacerbations of chronic respiratory failure. Hypothesis revisited. Rudolf M, Banks RA, Semple SJ SO Lancet. 1977;2(8036):483.

And AZMOMO2,

I agree, while I do not want to do people's homework, I think the forums can spark interesting discussions where so many people can learn information. I very much appreciate the feedback from others. We can't know everything and read every update.

Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.

I love the inspired clinical debate and I will participate enthusiastically........but the OP hasn't even returned for the suggestions or to learn from the debate. When I answer homewrok questions I am careful to give enough information to either lead the poster in the right direction or, if I get return participation they can be lead to a great deal of information. I like posts like this.

Specializes in geriatrics.

this is an awesome post! classic example including a review of textbook from nursing school but also in depth critical thinking from experienced nurses.

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