Respiratory acidosis
Respiratory acidosis | |
ICD-10 | E87.2 |
---|---|
ICD-9 | 276.2 |
DiseasesDB | 95 |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.D. [2]
Overview
Respiratory acidosis is acidosis (abnormal acidity of the blood) due to decreased ventilation of the pulmonary alveoli, leading to elevated arterial carbon dioxide concentration (PaCO2).
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.
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 reabsorption is increased.
- 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.
- Chronic respiratory acidosis: HCO3- rises 3.5 mEq/L for each 10-mm Hg rise in PaCO2.
- The expected change in pH with respiratory acidosis can be estimated with the following equations:
- Acute respiratory acidosis: Change in pH = 0.008 X (40 - PaCO2)
- Chronic respiratory acidosis: 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.
Classification
Acute respiratory acidosis
- The PaCO2 is elevated above the upper limit of the reference range (over 6.3 kPa or 47 mm Hg)
- Accompanied with acidemia (pH <7.35)
Chronic respiratory acidosis
- The PaCO2 is elevated above the upper limit of the reference range
- Accompanied with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO3- >30 mm Hg).
Causes
Acute
- Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs.
- This failure in ventilation may be caused by
- Depression of the central respiratory center by cerebral disease or drugs,
- Inability to ventilate adequately due to neuromuscular disease (eg, myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barré syndrome, muscular dystrophy),
- Airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation.
Chronic
- Chronic respiratory acidosis may be secondary to many disorders such as
- COPD - Hypoventilation in COPD involves multiple mechanisms, including decreased responsiveness to hypoxia and hypercapnia, increased ventilation-perfusion mismatch leading to increased dead space ventilation, and decreased diaphragm function secondary to fatigue and hyperinflation.
- Obesity hypoventilation syndrome (i.e., Pickwickian syndrome), neuromuscular disorders such as amyotrophic lateral sclerosis, and severe restrictive ventilatory defects as observed in interstitial fibrosis and thoracic deformities.
- Lung diseases that primarily cause abnormality in alveolar gas exchange usually do not cause hypoventilation but tend to cause stimulation of ventilation and hypocapnia secondary to hypoxia. Hypercapnia only occurs if severe disease or respiratory muscle fatigue occurs.
Common Causes
Causes by Organ System
Causes in Alphabetical Order
Differential diagnosis of respiratory acidosis
For differential diagnosis of respiratory acidosis is consideration of the three structures involved in ventilation should be made: the chest cavity, central respiratory drive, and the lungs and airways.
Lung and airway
Chest cavity
- Neuromuscular disorder
- Muscular disorder
- Kyphoscoliosis
- Pleural effusion
- Flail chest
- Pneumothorax
Central respiratory drive
- Obstructive sleep apnea
- Sedation
- Narcotics
- Respiratory drive hypofunction secondary to infection, inflammation or infarction
References