Review Question - QID 213869

In emphysema, chronic CO2 retention results in respiratory acidosis with a compensatory metabolic alkalosis. This state is characterized by low pH, high PaCO2, and high [HCO3-] in the arterial blood.

A normal arterial blood gas (ABG) reading is pH =7.40 (7.35-7.45), PaCO2 = 40 mmHg (35-45), and [HCO3-] = 24mEq/L (22-28). Emphysema is characterized by retention of CO2, leading to hypercapnia and respiratory acidosis. In the setting of chronic disease, the kidneys can partially – never completely – compensate for this acidosis by excreting acid as well as both producing and reabsorbing more bicarbonate, resulting in a compensatory metabolic alkalosis. Thus, for this patient with chronic emphysema who does not appear to be having an acute exacerbation, an ABG would demonstrate elevated PaCO2, low pH, and elevated [HCO3-]. In a chronic respiratory acidosis such as this, the expected compensatory increase in bicarbonate is characterized by the equation delta[HCO3-] = 3.5*delta(PaCO2)/10.

Incorrect Answers:
Answer 1: This ABG (pH = 7.21, PaCO2 = 70, [HCO3-] = 27) is consistent with an acute respiratory acidosis, as might occur in an acute chronic obstructive pulmonary disease exacerbation, asthma attack, or opioid overdose (due to respiratory depression). In the acute setting, compensation is due to physiologic buffers such as hemoglobin and other proteins binding protons, which slightly increases the pH and [HCO3-], though the effect is minimal compared to the renal compensation that occurs in chronic respiratory acidosis. In acute respiratory acidosis, the expected change in bicarbonate is delta[HCO3-] = delta(PaCO2)/10.

Answer 3: This ABG (pH = 7.34, PaCO2 = 23, [HCO3-] = 12) represents metabolic acidosis with a concomitant respiratory alkalosis. Here, the low pH is explained by the low [HCO3-], indicating that this is primarily a metabolic acidosis. Respiratory compensation for metabolic acidosis involves blowing off CO2 by hyperventilation, resulting in an expected PaCO2 = 1.5*[HCO3-] + 8 +/- 2 (Winter’s formula). Here, the expected PaCO2 would be 24-28mmHg, and since the actual PaCO2 is 23, there must be a mild concomitant respiratory alkalosis. The fact that the pH, in this case, is so close to the normal range also hints at a concomitant acid/base derangement, since compensation alone does not normalize pH. This ABG could be from somebody with a crush injury who primarily has lactic acidosis but is also hyperventilating beyond normal respiratory compensation due to pain.

Answer 4: This is a simple metabolic alkalosis (pH = 7.53, PaCO2 = 54, [HCO3-] = 44) with appropriate respiratory compensation, such as might be seen in a patient with excessive vomiting. Elevated [HCO3-] explains the alkalotic pH, indicating that this is the primary derangement. In metabolic alkalosis, the expected change in PaCO2 is 0.7*delta[HCO3-] or 14mmHg. Thus, the measured PaCO2 is as expected and there is no secondary acid/base disorder.

Answer 5: This ABG (pH = 7.80, PaCO2 = 20, [HCO3-] = 50) is consistent with mixed respiratory and metabolic alkaloses. The fact that [HCO3-] and PaCO2 have moved in opposite directions means that a complex acid/base disorder is present. There is no primary derangement since both the elevated bicarbonate and the low CO2 are contributing to the high pH. This could occur in somebody who is both vomiting and hyperventilating due to a panic attack.

Bullet Summary:
Patients with emphysema chronically retain CO2, resulting in respiratory acidosis and compensatory metabolic alkalosis.