Mr. Appel has severe chronic obstruction pulmonary disease (COPD). He reports increasing dyspnea, increased sputum production, anxiety, weakness, and malaise. He routinely takes a diuretic (furosemide) and pulmonary medicines.

Patient Values

Electrolytes Measurements

Sodium (Na+) 140 mEq/L

Potassium (K+) 2.0 mEq/L

Chloride (Cl-) 105 mEq/L

pH- 7.25

PCO2-78 mm Hg

P02- 60

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 mm Hg

PO2 – 80-100 mm Hg

HCO3- 22-28 mEq/L

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

2. Interpret his ABG’s.

3. What would be the treatment?

Mr. Appel presents with increase shortness of breath anxious, weak with an increase production of sputum. His medication reconciliation is furosemide and pulmonary medications. Mr. Appel is having acute COPD exacerbation. Mr. Appel is placed on the cardiac monitor , pulse ox, 2/L of O2 obtain blood serum and ABG’s for diagnosis and a chest x-ray to rule out pneumonia . The ABG results indicate Partial Compensated Respiratory Acidosis. Causes are obvious from Mr. Appel history and physically examination. The calculation of the alveolar-arterial O2 gradient (inspired PO2 –([arterial PO2+ 5/4 arterial PCO2]) can assist and distinguish pulmonary from extra pulmonary disease. But we already have the history from Mr. Appel that he has diagnosis with COPD. COPD Chronic Obstructive Pulmonary disease is a chronic inflammatory lung disease that causes obstructive airflow from the lungs. One of the largest cause of COPD is a history of smoking cigarettes . Habitual smoking causes inflammation of the lining of the lungs, this makes the airways lose their elastic quality. There are other reasons an individual develops COPD such as exposure to air pollutants, second hand smoke, occupational chemicals. Heredity can also play a part. There is research that there is a alpha-1-antigen deficiency. Unfortunately this disease is progressive disease and does get more debilitating over time. Making lifestyle adjustments is a good place to start and encouraged and join programs with Cardiopulmonary Rehabilitation. Education with the patients for early signs and symptoms of exacerbation SOB, cough change in color of sputum headache malaise is a pearl and awareness of his disease process for the patient and should call his LIP. This is the result of the ABG obtained from Mr. Appel pH 7.25, PCO2 78 mmHg, PO2 60 mmHg, HCO3 30 mEq/L.

The pH is decrease normal 7.35-7.45, PCO2 78 is increased normal 35-45mmHg, PO2 60 mmHg is low normal 80-100, HCO3- is 30 increased normal 22-28 mEq/L . The respiratory system attempts to balance by increasing or decreasing the respiratory rate or deep breaths to “blow off CO2 “. If the pH is out of balance because of respiratory, it will be the renal system that attempts to correct the imbalance. This is compensation, compensation will not always be complete. Complete compensation returns the pH balance to normal 7.35-7.45. There are times when the imbalances is too large for compensation to restore the pH to normal this is called partial compensation, tis is what Mr. Appel has presented with this Partially Compensated Respiratory Acidosis. I would treat Mr. Appel with noninvasive positive pressure ventilation (recue BIPAP) , the use of O2 should be used cautiously maintain the O2 saturation 88-92%. Mr. Appel would be admitted to the ICU. Consult with pulmonologists and neurologist for assistance for treatment and evaluation of the partial respiratory acidosis. Pharmacologic therapy should be considered. Bronchodilators such as beta agonists such as albuterol, anticholinergic agents ipratropium bromide, and theophylline are helpful in treating obstructive airway disease and severe bronchospasm. The use of theophylline may improve contractility of the muscle of the diaphragm and stimulate the respiratory center. Respiratory stimulants may be used but have limited efficiency in respiratory acidosis. Medroxyprogestrone increases central respiratory center and stimulates ventilation in patients with COPD and alveolar hypoventilation. The electrolyte deficits are corrected Na+ 140 normal value (135-145) and K+ potassium 2.0 (3.1-5.1) with gentle hydration and replenish the potassium. Education of the patient and the family to have awareness of changes in his respiratory status to prevent further exacerbations in the future.

References

Lun CT, Tsui Ms, Cheng Sl. et al. Difference in baseline factors and survival between norocapnia compensated respiratory acidosis and decompensated respiratory acidosis in copd excerabation: A pilot study . Rspirology . 2016 Jan 21 (1) : 128-36. [Medline].

Zorrilla- Riveiro JG, Arnau-Bartes A, Rafate-Sellares R, Garcia-Perez D, Mas-Serra A, Fernadez-Fernandez R. Nasal Flaring as a clinical sign of respiratory acidosis in patients with dyspnea. Am J Emerg Med. 2017 Apr. 35 (4): 548-53. [ Medline].