Respiratory acidosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
- Metabolism rapidly generates a large quantity of volatile acid (CO2) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of CO2. The CO2 combines with H2O to form carbonic acid (H2CO3).
- The lungs excrete the volatile fraction through ventilation, and acid accumulation does not occur.
- The PaCO2 is maintained within a range of 39-41 mm Hg in normal states.
- A significant alteration in ventilation that affects elimination of CO2 can cause a respiratory acid-base disorder.
- Respiratory acidosis is a clinical disturbance that is due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly, and failure of ventilation promptly increases the level of PaCO2.
- Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2 in turn decreases the HCO3-/PaCO2 and decreases pH.
- Hypercapnia and respiratory acidosis occur when impairment in ventilation occurs and the removal of CO2 by the lungs is less than the production of CO2 in the tissues.
- Central respiratory drive
- Alveolar ventilation is under the control of the central respiratory centers, which are located in the pons and the medulla.
- Ventilation is influenced and regulated by chemoreceptors for PaCO2, PaO2, and pH located in the brainstem,and in the aortic and carotid bodies as well as by neural impulses from lung stretch receptors and impulses from the cerebral cortex. Failure of ventilation quickly increases the PaCO2.
Compensation in acute respiratory acidosis
Acute cellular compensatory stage
- The initial response is cellular buffering that occurs over minutes to hours. Cellular buffering elevates plasma bicarbonate (HCO3-) only slightly, approximately 1 mEq/L for each 10-mm Hg increase in PaCO2.
- In acute respiratory acidosis, the acidosis can be severe and life threatening.
- Additionally, as the pCO2 increases, the partial pressure of O2 in the alveolus decreases. An inadequate oxygenation is one of the most concerning and dangerous aspects in the patients with acute respiratory acidosis.
- Starts in minutes to hours
- Less profound increase of HCO3 thus strong fall in pH
Chronic renal compensatory stage
- The second step is renal compensation that occurs over 3-5 days.
- With renal compensation, renal excretion of carbonic acid is increased and bicarbonate resorption is increased.
- Renal compensation is profound thus there is less drop in the pH.
- The prognosis of patients with chronic respiratory acidosis with acute respiratory acidosis is poor.
- Chronic respiratory acidosis is less dangerous.
- In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm Hg in PaCO2. The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:
- Acute respiratory acidosis:
- HCO3- increases 1 mEq/L for each 10-mm Hg rise in PaCO2.
- Change in pH = 0.008 X (40 - PaCO2)
- Chronic respiratory acidosis:
- HCO3- rises 3.5 mEq/L for each 10-mm Hg rise in PaCO2.
- Change in pH = 0.003 X (40 - PaCO2)
Effect of respiratory acidosis on electrolyte
- Acidosis decreases binding of calcium to albumin and tends to increase serum ionized calcium levels.
- In addition, acidemia causes an extracellular shift of potassium, but respiratory acidosis rarely causes clinically significant hyperkalemia.