Respiratory Acidosis

Updated: Aug 02, 2016
  • Author: Ryland P Byrd, Jr, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
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Overview

Background

Respiratory acidosis is an acid-base balance disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly and failure of ventilation promptly increases the partial pressure of arterial carbon dioxide (PaCO2). [1] The normal reference range for PaCO2 is 35-45 mm Hg.

Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3)/PaCO2 ratio, thereby decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the respiratory system is less than the production of carbon dioxide in the tissues.

Lung diseases that cause abnormalities in alveolar gas exchange do not typically result in alveolar hypoventilation. Often these diseases stimulate ventilation and hypocapnia due to reflex receptors and hypoxia. Hypercapnia typically occurs late in the disease process with severe pulmonary disease or when respiratory muscles fatigue. (See also Pediatric Respiratory Acidosis, Metabolic Acidosis, and Pediatric Metabolic Acidosis.)

Acute vs chronic respiratory acidosis

Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH < 7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate levels (ie, >30 mEq/L).

Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may result from depression of the central respiratory center by one or another of the following:

  • Central nervous system disease or drug-induced respiratory depression
  • Inability to ventilate adequately, due to a neuromuscular disease or paralysis (eg, myasthenia gravis, amyotrophic lateral sclerosis [ALS], Guillain-Barré syndrome, muscular dystrophy)
  • Airway obstruction, usually related to asthma or chronic obstructive pulmonary disease (COPD)

Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation in COPD involves multiple mechanisms, including the following:

  • Decreased responsiveness to hypoxia and hypercapnia
  • Increased ventilation-perfusion mismatch leading to increased dead space ventilation
  • Decreased diaphragmatic function due to fatigue and hyperinflation

Chronic respiratory acidosis also may be secondary to obesity hypoventilation syndrome (OHS—ie, Pickwickian syndrome), neuromuscular disorders such as ALS, and severe restrictive ventilatory defects such as are observed in interstitial fibrosis and thoracic skeletal deformities.

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Etiology and Pathophysiology

As noted (see Background), respiratory acidosis may have a variety of different causes, including the following:

  • COPD – Emphysema, chronic bronchitis, severe asthma [2, 3]
  • Neuromuscular diseases – ALS, diaphragm dysfunction and paralysis, Guillain-Barré syndrome, myasthenia gravis, muscular dystrophy, botulism
  • Chest wall disorders – Severe kyphoscoliosis, status post thoracoplasty, flail chest, and, less commonly, ankylosing spondylitis, pectus excavatum, [4] or pectus carinatum
  • Obesity-hypoventilation syndrome
  • Obstructive sleep apnea (OSA)
  • Central nervous system (CNS) depression – Drugs (eg, narcotics, barbiturates, benzodiazepines, and other CNS depressants), neurologic disorders (eg, encephalitis, brainstem disease, and trauma), primary alveolar hypoventilation, or congenital central alveolar hypoventilation syndrome (Ondine curse)
  • Other lung and airway diseases – Laryngeal and tracheal stenosis, interstitial lung disease
  • Lung-protective mechanical ventilation with permissive hypercapnia in the treatment of acute respiratory distress syndrome (ARDS); these patients typically are heavily sedated and may require paralytic agents

Metabolism

Metabolism rapidly generates a large quantity of volatile acid (carbon dioxide) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of carbon dioxide. The carbon dioxide combines with water to form carbonic acid (H2 CO3). The lungs excrete the volatile fraction through ventilation, and normally acid accumulation does not occur. [5]

A significant alteration in ventilation that affects elimination of carbon dioxide can cause a respiratory acid-base disorder. The partial arterial pressure of carbon dioxide (PaCO2) is normally maintained within the range of 35-45 mm Hg. [6, 7]

Alveolar ventilation

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, partial pressure of arterial oxygen (PaO2), and pH located in the brainstem, as well as by neural impulses from lung-stretch receptors and impulses from the cerebral cortex. Failure of ventilation quickly results in an increase in the PaCO2.

Physiologic compensation

In acute respiratory acidosis, the body’s compensation occurs in 2 steps. The initial response is cellular buffering that takes place over minutes to hours. Cellular buffering elevates plasma bicarbonate values, but 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.

The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:

  • Acute respiratory acidosis – Bicarbonate increases by 1 mEq/L for each 10-mm Hg rise in PaCO 2.The acute change in bicarbonate is, therefore, relatively modest and is generated by the blood, extracellular fluid, and cellular buffering system.
  • Chronic respiratory acidosis – Bicarbonate increases by 3.5 mEq/L for each 10-mm Hg rise in PaCO 2. The greater change in bicarbonate in chronic respiratory acidosis is accomplished by the kidneys. The response begins soon after the onset of respiratory acidosis but requires 3-5 days to become complete.

The expected change in pH with respiratory acidosis can be estimated with the following equations:

  • Acute respiratory acidosis – Change in pH = 0.008 × (40 – PaCO 2)
  • Chronic respiratory acidosis – Change in pH = 0.003 × (40 – PaCO 2)

Electrolyte levels

Respiratory acidosis does not have a great effect on serum electrolyte levels. Some small effects occur in 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. [8] Respiratory acidosis, however, rarely causes clinically significant hyperkalemia.

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