Case Study Emphysema COPD FINAL

Topics: Asthma, Chronic obstructive pulmonary disease, Pulmonology Pages: 9 (1719 words) Published: March 6, 2015
Group Case Study: Emphysema

D.Z., a 65-year-old man, is admitted to a medical floor for exacerbation of his chronic obstructive pulmonary disease (COPD; emphysema). He has a past medical history of hypertension, which has been well controlled by Enalapril (Vasotec) for the past 6 years. He has had pneumonia yearly for the past 3 years, and has been a 2-pack-a-day smoker for 38 years. He appears as a cachectic man who is experiencing difficulty breathing at rest. He reports cough productive of thick yellow-green sputum. D.Z. seems irritable and anxious; he complains of sleeping poorly and states that lately feels tired most of the time. His vital signs (VS) are 162/84, 124, 36, 102 F, SaO2 88%. His admitting diagnosis is an acute exacerbation of chronic emphysema.

Physician's Orders
Diet as tolerated
Out of bed with assistance
Oxygen (O2 ) to maintain Sa O2 of 90%
IV of D5W 1/n NS with 20KCl meq/L to run at 50 ml/hr
Continuous ECG monitoring
Pulmonary function tests (PFT’s) in AM
Arterial blood gases (ABGs) in AM
CBC with differential and Na+ /K+ now
Basic metabolic panel (BMP) now and fasting in AM
Chest x-ray (CXR) on admit and QAM
Sputum culture now (obtain culture prior to starting anbiotics) Albuterol 2.5 mg plus ipratropium 250 mcg nebulizer treatment STAT Incentive Spirometery Q10x’s per hour while awake

1. Explain the pathophysiology of emphysema.
Abnormal permanent enlargement of lung spaces distal to terminal bronchioles accompanied by destruction of walls without obvious fibrosis. This leads to decline in alveolar surface area available for gas exchange. Loss of alveoli leads to airflow limitation in 2 ways: first, loss of the alvoelar walls results in a decrease in elastic recoil (leads to airflow limitation). Second, loss of the alveolar supporting structure leads to airway narrowing, which further limits airflow.

2. Are D.Z.'s vital signs and SaO2 appropriate? If not, explain why. vital signs (VS) are 162/84, 124, 36, 102 F, SaO2 88%.
Tachypnea and tachycardia indicates body is having trouble oxygenating tissues. SaO2 88% is too low. Orders are to administer O2 as needed to keep it >90% HTN: part of the COPD pathway is pulmonary hypertension, which then leads to cor pulmonale (R ventricular hypertrophy) These vital signs are expected for an exacerbation, but not necessarily “appropriate” (we would like to see oxygen sat above 90%, normal HR, RR, BP)

3. Describe a plan for implementing these physician's orders. Administer oxygen via nasal cannula to get SaO2>90% and put on continous ECG monitoring Call for lab draw for the following:
Basic metabolic panel now and fasting in AM
CBC with diff and Na+/K+
Sputum culture now
Pulmonary function test (pre-albuterol)
Albuterol 2.5 mg plus ipratropium 250 mcg nebulizer treatment STAT IV of D5W 1/NS with 20KCl meq/L to run at 50ml/hr (set up IV while nebulizer going) Pulmonary funciton test (pre-albuterol)
Chest x-ray QAM
Can have breakfast as tolerated. Wait ~30 minutes before Incentive Spirometry.

4. Identify three independent nursing actions you would try to improve D.Z.'s oxygenation. Administer low flow oxygen (humidified) (nasal cannula)
Sit upright (tripod; high fowlers if tripod not tolerated)
Incentive spirometry
Nebulizer treatments as perscribed
Turn, cough, deep breathe

LABS are as follows:
K+ -5.2

5. Based on these results, prioritize your next actions.
Priority 1: Potassium high
Call provider to discuss discontinuing IV fluids with 20KCl and possibly adding diuretic (since BP also high) Monitor EKG
Priority 2: WBC high
Call provider to discuss culture+sensitivity and possible antibiotics Low sodium
Expectd with high potassium, so if we decrease potassium (exp change IV fluids) then we can expect sodium excretion to slow down. Hct high (this is expected with COPD—body’s response to low oxygen) Hb high (this is expected with...
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