A 65-year-old man is admitted to the hospital for increasing shortness of breath and edema. Over the last 10 days, he has experienced progressively worsening shortness of breath occurring with modest exertion and a cough productive of a small amount of purulent sputum. He denies paroxysmal nocturnal dyspnea, orthopnea, fever, chills, and chest pain. He also reports a 4.5-kg (10-lb) weight gain. His medical problems include chronic obstructive pulmonary disease (COPD) , congestive heart failure due to coronary artery disease, type 2 diabetes mellitus, hypertension, degenerative joint disease, and obesity.
His blood pressure is 138/84 mm Hg, pulse is 96/min and regular, and respirations are 20/min. Pulse oximetry reveals an oxygen saturation of 94% while using nasal prongs at 2 liters of oxygen/min. His jugular venous pressure is 10-12 cm H₂O. Lung examination reveals diffusely decreased breath sounds with prolongation of the expiratory phase. There are no rales. Cardiac examination reveals an increased P2 and a grade 2/6 systolic murmur along the left sternal border. Abdominal examination is normal. There is 2-3+ bilateral pedal edema.
He is treated with intravenous furosemide and azithromycin, and his symptoms are gradually improving.
Laboratory results obtained 48 hours after admission are as follows:

Which of the following is most likely the cause of his acid-base disorder?

Question

A 65-year-old man is admitted to the hospital for increasing shortness of breath and edema. Over the last 10 days, he has experienced progressively worsening shortness of breath occurring with modest exertion and a cough productive of a small amount of purulent sputum. He denies paroxysmal nocturnal dyspnea, orthopnea, fever, chills, and chest pain. He also reports a 4.5-kg (10-lb) weight gain. His medical problems include chronic obstructive pulmonary disease (COPD) , congestive heart failure due to coronary artery disease, type 2 diabetes mellitus, hypertension, degenerative joint disease, and obesity.
His blood pressure is 138/84 mm Hg, pulse is 96/min and regular, and respirations are 20/min. Pulse oximetry reveals an oxygen saturation of 94% while using nasal prongs at 2 liters of oxygen/min. His jugular venous pressure is 10-12 cm H₂O. Lung examination reveals diffusely decreased breath sounds with prolongation of the expiratory phase. There are no rales. Cardiac examination reveals an increased P2 and a grade 2/6 systolic murmur along the left sternal border. Abdominal examination is normal. There is 2-3+ bilateral pedal edema.
He is treated with intravenous furosemide and azithromycin, and his symptoms are gradually improving.
Laboratory results obtained 48 hours after admission are as follows:

Which of the following is most likely the cause of his acid-base disorder?

Quizplus · Accepted Answer

This patient has a mixed acid-base disorder. He has alkalosis which can either be metabolic (high bicarbonate concentration) or respiratory (low PaCO2). Given his high bicarbonate concentration and high PaCO2, he has metabolic alkalosis, which sometimes complicates the course of diuretic therapy. One clue to the presence of a mixed acid-base disturbance is a lesser or greater degree of compensation than would be expected for the patient's primary acid-base disorder. In response to metabolic alkalosis, there is usually a 0.7 mm Hg increase in PaCO2 for each mEq/L increase in bicarbonate concentration. Therefore, in a patient with a bicarbonate level of 37 mEq/L, PaCO2 can increase up to a maximum of 50-55 mm Hg. This patient's PaCO2 of 63 mm Hg is significantly higher than would occur from metabolic alkalosis alone, suggesting the presence of underlying chronic respiratory acidosis, most likely due to chronic obstructive pulmonary disease (COPD). (Choice A) The acid-base disorder most commonly seen in association with diabetes is ketoacidosis. This patient is not acidemic and does not have an increase in his anion gap, making diabetic ketoacidosis implausible. The appropriate respiratory compensation to metabolic acidosis (not metabolic alkalosis) can be given by Winter's formula: PaCO2 = 1.5 × serum bicarbonate + 8 ± 2. (Choice B) With chronic respiratory acidosis from COPD, for every 10 mm Hg increase in PaCO2, the bicarbonate concentration increases by about 3 mEq/L. The degree of CO₂ retention in this patient would be expected to increase his bicarbonate concentration by approximately 8 mEq/L. His measured bicarbonate concentration is significantly higher, which suggests metabolic alkalosis. He is also alkalemic. The body does not "over-compensate" for any primary acid-base disorder, and the presence of alkalemia effectively excludes the simple acid-base disorder of respiratory acidosis. (Choice C) Congestive heart failure can be associated with several acid-base disorders depending upon the severity and associated comorbidities. Respiratory alkalosis is often seen due to the effect of hypoxemia to stimulate ventilation. Respiratory acidosis sometimes occurs when marked pulmonary edema is present. Since patients with heart failure are often treated with diuretics, metabolic alkalosis can also be seen. Rarely, lactic acidosis will be seen in association with cardiogenic shock. This patient's combined metabolic alkalosis and chronic respiratory acidosis are unlikely to be due to heart failure alone. (Choice E) Some diuretic agents can induce metabolic alkalosis. However, diuretic agents would not cause a combined metabolic alkalosis and respiratory acidosis. Educational objective: The presence of a mixed acid-base disorder is suggested by clinical history and when there is a lesser or greater degree of compensation than what typically occurs in response to the primary acid-base disorder. __________ References: Secondary responses to altered acid-base status: the rules of engagement. (http://www.ncbi.nlm.nih.gov/pubmed/20431042) Effect of metabolic alkalosis on respiratory function in patients with chronic obstructive lung disease. (http://www.ncbi.nlm.nih.gov/pubmed/21028)

A 65-Year-Old Man Is Admitted to the Hospital for Increasing