A 58-year-old female smoker with end-stage chronic obstructive pulmonary disease and osteoarthritis is on ipratropium bromide and albuterol inhalers, and hydrocodone-acetaminophen. She presents with respiratory distress for 2 days accompanied by increased thick, yellow sputum production, low grade fever, and increasing confusion. On examination she is mildly obtunded but arousable, BP 160/100, pulse 115/min, RR 30/min, O2 saturation 84% on her usual 3 L/min nasal cannula oxygen. She is using accessory muscles to breath, has diffuse wheezing and rhonchi bilaterally, a prolonged expiratory phase, distant but regular heart sounds, and no peripheral edema.Arterial blood gases (ABGs) on arrival are as follows:pH: 7.20,PO2: 70 mm HgPCO2: 65 mm Hgcalculated HCO3 29 mEq/L.Electrolytes return shortly thereafter as follows:Na: 140 mEq/LK: 5.1 mEq/LHCO3: 29 mEq/LCl: 100 mEq/LBUN 20 mg/dL creatinine 1.5 mg/dLglucose 89 mg/dL.After prompt initiation of noninvasive positive pressure ventilation (Bi-pap), blood cultures, toxicology screen, intravenous fluids, and IV antibiotics, you have time to consider the patient's metabolic situation. Choose the answer which best describes the acid-base condition and its etiology.
Patients with severe COPD often have a baseline chronic respiratory acidosis with a PCO2 in the 50 to 60 mm Hg range. They are unable to ventilate sufficiently to correct the acidotic situation this creates. The kidney then compensates by retaining HCO3 . This results in a new steady state in which the patient has a near-normal pH on their blood gas despite the chronically elevated CO2 . In this question the further deterioration in the patient's respiratory status due to COPD exacerbation has caused further CO2 retention and a superimposed acute respiratory acidosis on top of the chronic respiratory acidosis. Salicylate overdose normally causes an anion gap acidosis and the AG is normal here. Volume depletion, especially due to recurrent vomiting, can lead to a contraction alkalosis, but this patient's acidosis indicates that the elevated bicarbonate level is caused by renal compensation for her chronic CO2 retention.
The patient has acute, severe respiratory acidosis caused by the sudden deterioration in her respiratory status.
The patient has an underlying metabolic acidosis caused by her renal insufficiency now compounded by a respiratory alkalosis.
The patient ingested abundant amounts of aspirin which caused a severe metabolic acidosis and respiratory failure.
The patient has a baseline chronic respiratory acidosis with metabolic compensation, now with a superimposed further respiratory acidosis caused by decreased ventilation.
Kidney