Chronic Obstructive Pulmonary Disease (COPD)

Mr. Appel has severe chronic obstructive pulmonary disease (COPD). He is admitted to the hospital with the complaint of increasing dyspnea, increased sputum, anxiety, and diaphoresis. He states he feels weak and tired. He routinely takes a diuretic (furosemide) and his pulmonary medications.

Mr Appel’s values
Sodium (Na+)140 mEq/L
Potassium (K+)2.0 mEq/L
Chloride (Cl–)105 mEq/L
Arterial blood gases (ABGs) pH- 7.25; PCO2, 78 mmHg; PO2, 60 mmHg; HCO3-, 30 mEq/L

Normal values
Sodium (Na+)136-146 mEq/L
Potassium (K+) 3.5-5.1 mEq/L
Chloride (Cl–)98-106 mEq/L
Arterial blood gases (ABGs) pH 7.35-7.45
PCO2 35-45 mmHg
PO2 80-100 mmHg
HCO3–22-28 mEq/L

A. What type of imbalance does Mr. Appel have?

Mr. Appel labs demonstrate an imbalance related hypokalemia. The lab result shows Mr. Appel potassium is at 2.0 mEq/L, where the typical values of potassium are 3.5-5.1 mEq/L. Additional, Mr. Appel arterial blood gases (ABG) show has respiratory acidosis. Mr. Appel is not pulling enough O2 from the atmosphere into his lungs, he is retaining carbon dioxide, and his K+ is low as well as his NA+.

B. Interpret his ABGs.

The labs Mr Appel Values WNL
pH 7.25 7.35-7.45 Acid
Pco2 78 mmHg 35-45 mmHg Acid
HCO3– 30 mEq/L 22-28 mEq/L Alkaline

Acid Normal Base
pH- 7.25 HCO3–
30 mEq/L
Pco2 -78 mmHg

The ABG tic-tac-toe lines up under acid related to pH and Pco2. The Pco2 suggests respiratory acidosis, partially compensated with the HCO3–30 mEq/L. Fully compensated would mean the pH being WNL. "Respiratory acidosis occurs when there is alveolar hypoventilation. Carbon dioxide is retained, increasing [H+] (as H2CO3), thus decreasing the ratio of HCO3- to Pco2, and producing acidosis… Body's compensation –Kidney's conserve HCO3- ions and eliminate H+ ions in acidic urine" (McCance, 2019, p. 128-129).

To achieve hemostasis, the body is continuously assessing changes in pH and Paco2. "When acidemia exists, the respirator rate increases (eliminating Co2 and reducing carbonic acid consecrations" (McCance, 2019, p. 124). This increased respiratory rate can lead to feelings of anxiety and diaphoresis. The respiratory system is working hard to excretes the increase in Co2 levels and normalize the acid-base balance.

Differential Diagnosis

Differential diagnosis of bronchiectasis should be ruled out. COPD and bronchiectasis shared similar signs and symptoms. They both present with difficulty breathing, cough with sputum, shortness of breath, and fatigue.

COPD and bronchiectasis share treatments – antibiotics, bronchodilators, anti-inflammatory drugs, chest physiotherapy, and use of oxygen.

The concerns to look for to start to rule out bronchiectasis would be:

•foul sputum (if not on antibiotics)
•Clubbing of fingers r/t chronic hypoxia.
•hemoptysis, large amounts

These similar and dissimilar factors should be relayed to the collaborating Attending Physician. A high- resolution CT should be ordered to help rule out the diagnosis of bronchiectasis.

C. What is the treatment?

Treatment:

1. Stat EKG.
2. Chest x-ray A/P and lateral.
3. Place him on telemonitoring.
4. Obtain a sputum specimen, complete a Culture and Sensitivity (C&S) – start appropriate antibiotic therapy. Consider Zithromax to decreases sputum. Zithromax dosing, initially, 500 mg PO as a single dose on day 1, followed by 250 mg daily on days 2 thru 5. Total cumulative dose id 1.5 g. Or for worsening COPD, 500 mg PO QD for three days.

Chronic antibiotic therapy is generally not indicated for patients with emphysema or CB. Macrolide [Zithromax] therapy, however, has been shown to have anti-inflammatory properties and may play a role in the treatment of those with CB. These therapies have been shown to inhibit proinflammatory cytokines, decrease neutrophil burst, inhibit migration and increase apoptosis, decrease eosinophilic inflammation, increase mucociliary transport, reduce goblet cell secretion, and decrease bronchoconstriction. (Ramos, Krahnke, and Kim, 2014, p. 147)

1. Give O2 via bilevel positive airway pressure - (BiPAP) helping to blow off CO2 and increase O2. Then O2 by NC, if below 92% call the provider. (If ABGs do not stabilize and O2 saturation's continue to drop, a pulmonologist or medical physician may need to be consulted.)
2. Provide potassium replacement - hang six bags of 10meq potassium in 100cc bag of normal saline. After 60 meq of potassium is given recheck CMP 1 hour afterward (with the addition of a magnesium level).

If potassium is < 2.5 mmol/L most protocols recommend IV repletion. Standard rates of IV potassium are 10meq/hr in a peripheral line and 20meq/hr in a central line. A maximum of 40 meq q 2-4 hrs should be given, and potassium levels should be rechecked. If potassium levels are still low, then continue to follow the hospitals' protocol. (Kardalas et al, 2018, p. 144)

1. Duo-nebs (ipratropium bromide and albuterol sulfate) q 4 hrs prn for dyspnea.
2. Discontinue furosemide as potassium excreting medication.
3. Start potassium-sparing diuretic, Spironolacone (Aldactone) at 25 mg to 100mg PO QD.
4. Serial labs – ABGs, CBC, CMP to revaluate status of respiratory acidosis and potassium replacement.
5. Chest physical therapy, deep breathing, a flutter valve, and postural drainage.
6. Provide patient teaching related to healthy nutrition (foods high in potassium), as well as "respiratory hygiene, recognition of early signs of infection, and techniques that relieve dyspnea, such as pursed-lip breathing, all of which may be useful in the treatment of COPD in selected individuals" (McCance, 2019, p. 1185).
7. Follow-up with collaborating Primary Care Physician (PCP) or Advanced Nurse Practitioner after discharge to verify the effectiveness of spironolactone and recheck CMP labs to insure that potassium level is within normal limits.

Sample Solution