Respiratory acidosis is a state in which there is usually a failure of ventilation and an accumulation of carbon dioxide. The primary disturbance of elevated arterial PCO2 is the decreased ratio of arterial bicarbonate to arterial PCO2, which leads to a lowering of the pH. In the presence of alveolar hypoventilation, 2 features commonly are seen are respiratory acidosis and hypercapnia. To compensate for the disturbance in the balance between carbon dioxide and bicarbonate (HCO3-), the kidneys begin to excrete more acid in the forms of hydrogen and ammonium and reabsorb more base in the form of bicarbonate. This compensation helps to normalize the pH.
The respiratory centers in the pons and medulla control alveolar ventilation. Chemoreceptors for PCO2, PO2, and pH regulate ventilation. Central chemoreceptors in the medulla are sensitive to changes in the pH level. A decreased pH level influences the mechanics of ventilation and maintains proper levels of carbon dioxide and oxygen. When ventilation is disrupted, arterial PCO2 increases and an acid-base disorder develop. Another pathophysiological mechanism may be due to ventilation/perfusion mismatch of dead space.
Respiratory acidosis can be subcategorized as acute, chronic, or acute and chronic. In acute respiratory acidosis, there is a sudden elevation of PCO2 because of failure of ventilation. This may be due to cerebrovascular accidents, use of central nervous system (CNS) depressants such as opioids, or inability to use muscles of respiration because of disorders like myasthenia gravis, muscular dystrophy or Guillain-Barre Syndrome. Because of its acute nature, there is a slight compensation occurring minutes after the incidence. On the contrary, chronic respiratory acidosis may be caused by COPD where there is a decreased responsiveness of the reflexes to states of hypoxia and hypercapnia. Other individuals who develop chronic respiratory acidosis may have fatigue of the diaphragm resulting from a muscular disorder. Chronic respiratory acidosis can also be seen in obesity hypoventilation syndrome, also known as Pickwickian syndrome, amyotrophic lateral sclerosis, and in patients with severe thoracic skeletal defects. In patients with chronic compensated respiratory disease and acidosis, an acute insult such as pneumonia or disease exacerbation can lead to ventilation/perfusion mismatch.
Respiratory acidosis may cause slight elevations in ionized calcium and an extracellular shift of potassium. However, the hyperkalemia is usually mild. In chronic respiratory acidosis, renal compensation occurs gradually over the course of days.
The frequency of respiratory acidosis in the United States and worldwide varies based on the etiology. End-stage COPD patients are more prone to develop this acid-base disorder. It has also been noted that surgical patients are at a greater risk of developing respiratory acidosis.
Carbon dioxide plays a remarkable role in the human body mainly through pH regulation of the blood. The pH is the primary stimulus to initiate ventilation. In its normal state, the body maintains CO2 in a well-controlled range from 38 to 42 mm Hg by balancing its production and elimination. In a state of hypoventilation, the body produces more CO2 than it can eliminate, causing a net retention of CO2. The increased CO2 is what leads to an increase in hydrogen ions and a slight increase in bicarbonate, as seen by a right shift in the following equilibrium reaction of carbon dioxide:
The buffer system created by carbon dioxide consists of the following three molecules in equilibrium: CO2, H2CO3-, and HCO3-. When H+ is high, HCO3- buffers the low pH. When OH- is high, H2CO3 buffers the high pH. In respiratory acidosis, the slight increase in bicarbonate serves as a buffer for the increase in H+ ions, which helps minimize the drop in pH. The increase in hydrogen ions inevitably causes a decrease in pH, which is the mechanism behind respiratory acidosis.
The clinical presentation of respiratory acidosis is usually a manifestation of its underlying cause. Signs and symptoms vary based on the length, severity, and progression of the disorder. Patients can present with dyspnea, anxiety, wheezing, and sleep disturbances. In some cases, patients may present with cyanosis due to hypoxemia. If the respiratory acidosis is severe and accompanied by prolonged hypoventilation, the patient may have additional symptoms such as altered mental status, myoclonus, and possibly even seizures. Respiratory acidosis leads to hypercapnia, which induces cerebral vasodilation. If severe enough, increased intracranial pressure and papilledema may ensue, increasing the risk of herniation and possibly even death. Cases of chronic respiratory acidosis may cause memory loss, impaired coordination, polycythemia, pulmonary hypertension, and heart failure. Persistence of apnea during sleep can lead to daytime somnolence and headaches. In patients with an obvious source of respiratory acidosis, the offending agent needs to be removed or reversed.
An arterial blood gas (ABG) and serum bicarbonate level is necessary to evaluate patients with suspected respiratory acidosis. Other tests can be conducted to evaluate the underlying causes. In respiratory acidosis, the ABG will show an elevated PCO2 (>45 mmHg), elevated HCO3- (>30 mmHg), and decreased pH (<7.35). The respiratory acidosis can be further classified as acute or chronic based on the relative increase in HCO3- with respect to PCO2. In cases of acute respiratory acidosis, HCO3- will have increased by one mEq/L for every ten mmHg increase in PCO2 over a few minutes. In cases of chronic respiratory acidosis, HCO3- will have increased by four mEq/L for every ten mmHg increase in PCO2 over a time course of days. If the compensation does not occur in this pattern, a mixed respiratory-metabolic disorder may be present. In a patient who presents with unexplained respiratory acidosis, a drug screen may also be warranted.
Once the diagnosis has been made, the underlying cause of respiratory acidosis has to be treated. The hypercapnia should be corrected gradually because rapid alkalization of the cerebrospinal fluid (CSF) may lead to seizures. Pharmacologic therapy can also be used to help improve ventilation. Bronchodilators like beta agonists, anticholinergic drugs, and methylxanthines can be used in treating patients with obstructive airway diseases. Naloxone can be used in patients who overdose on opioid use.
Patients who are moribund, lethargic or confused need to be monitored in the intensive care unit (ICU). Those who exhibit hypoventilation will need endotracheal intubation and mechanical ventilation. The use of respiratory stimulants has not been shown to be effective in treating respiratory acidosis. Medroxyprogesterone has been used to stimulate the respiratory drive, but its benefits are questionable. Hypoxic patients, of course, need supplemental oxygen.
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