Respiratory acidosis

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Respiratory acidosis
ICD-10	E87.2
ICD-9	276.2
DiseasesDB	95
MeSH	D000142

Template:Search infobox Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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).

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.

Classification

Respiratory acidosis can be acute or chronic.

• In acute respiratory acidosis, the PaCO₂ is elevated above the upper limit of the reference range (over 6.3 kPa or 47 mm Hg) with an accompanying acidemia (pH <7.35).
• In chronic respiratory acidosis, the PaCO₂ is elevated above the upper limit of the reference range, 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), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation.

Chronic

Chronic respiratory acidosis may be secondary to many disorders, including 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.

Chronic respiratory acidosis also may be secondary to obesity hypoventilation syndrome (ie, 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.

Causes in Alphabetical Order

• Alfentanil
• Fentanyl
• Obstructive sleep apnoea
• Oxygen, particularly in the patient with COPD
• Remifentanil
• Respiratory distress syndrome (neonatal)
• Respiratory failure type 2
• Sufentanil

Physiological response

Mechanism

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. A significant alteration in ventilation that affects elimination of CO₂ can cause a respiratory acid-base disorder. The PaCO₂ is maintained within a range of 39-41 mm Hg in normal states.

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.

In acute respiratory acidosis, compensation occurs in 2 steps.

• 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.
• 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.

Estimated changes

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)

Respiratory acidosis does not have a great effect on electrolyte levels. Some small effects occur on calcium and potassium levels. 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.