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).  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)
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.
Arterial blood gas (ABG) analysis is necessary in the evaluation of a patient with suspected respiratory acidosis or other acid-base disorders.
The most common abnormal serum electrolyte finding in chronic respiratory acidosis is the presence of a compensatory increase in serum bicarbonate concentration.
A thyrotropin and a free T4 level should be considered in selected patients, since hypothyroidism may cause obesity, leading to obstructive sleep apnea (OSA) and sleep apnea–related hypoventilation.
Many patients with chronic hypercapnia and respiratory acidosis are also hypoxemic. These patients may have secondary polycythemia, as demonstrated by elevated hemoglobin and hematocrit values.
In patients without an obvious source of hypoventilation and respiratory acidosis, a drug screen should be performed. The effects of sedating drugs such as narcotics and benzodiazepines in depressing the central ventilatory drive and causing respiratory acidosis should be considered. These sedative drugs should be avoided, if possible, in patients with respiratory acidosis.
Radiography, computed tomography (CT) scanning, and fluoroscopy of the chest may provide helpful information in determining causes of respiratory acidosis. Radiologic studies (CT scanning and magnetic resonance imaging [MRI]) of the brain should be considered if a central cause of hypoventilation and respiratory acidosis is suspected.
Pulmonary function test measurements are required for the diagnosis of obstructive lung disease and for assessment of the severity of disease. Forced expiratory volume in 1 second (FEV1.0) is the most commonly used index of airflow obstruction.
Electromyography (EMG) and measurement of nerve conduction velocity (NCV) are useful in diagnosing neuromuscular disorders (eg, myasthenia gravis, Guillain-Barré syndrome, and amyotrophic lateral sclerosis [ALS]), which can cause ventilatory muscle weakness.
Measurement of transdiaphragmatic pressure is a useful diagnostic test for documenting respiratory muscle weakness. However, it is difficult to perform and is usually carried out only in specialized pulmonary function laboratories.
Pharmacologic therapies are generally used as treatment for the underlying disease process. Oxygen therapy is employed to prevent the sequelae of long-standing hypoxemia.
Therapeutic measures that may be lifesaving in severe hypercapnia and respiratory acidosis include endotracheal intubation with mechanical ventilation and noninvasive positive pressure ventilation (NIPPV) techniques such as nasal continuous positive-pressure ventilation (NCPAP) and nasal bilevel ventilation. The latter techniques of NIPPV are preferred treatment for obesity hypoventilation syndrome (OHS) and neuromuscular disorders, because they help to improve partial pressure of arterial oxygen (PaO2) and decrease the partial pressure of arterial carbon dioxide (PaCO2).
Noninvasive external negative-pressure ventilation devices are also available for the treatment of selected patients with chronic respiratory failure.
Rapid correction of the hypercapnia by the application of external noninvasive positive-pressure ventilation or invasive mechanical ventilation can result in alkalemia. Accordingly, these techniques should be used with caution.
Etiology and Pathophysiology
As noted (see Background), respiratory acidosis may have a variety of different causes, including the following:
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,  or pectus carinatum
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 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. 
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 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.
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)
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.  Respiratory acidosis, however, rarely causes clinically significant hyperkalemia.
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