Respiratory acidosis refers to a condition where a decrease in pH occurs due to impaired carbon dioxide (CO2) elimination or excessive CO2 inhalation. It is primarily characterized by an increase in plasma carbonic acid (H2CO3) concentration.
Etiology
Central Respiratory Impairment
Conditions such as traumatic brain injury, cerebrovascular accidents, or the excessive use of respiratory depressants or anesthetics can lead to impaired CO2 elimination. Improper use of mechanical ventilators may also contribute.
Obstructive and Mechanical Causes
Acute conditions like laryngospasm, laryngeal edema, airway obstruction caused by foreign bodies, or drowning can result in acute respiratory acidosis. Chronic issues, including chronic obstructive pulmonary disease (COPD), bronchial asthma, severe chest wall deformities, respiratory muscle paralysis, pneumothorax, or pleural effusion, may lead to chronic respiratory acidosis.
Ventilation Impairments
Acute cardiogenic pulmonary edema, severe emphysema, critical pneumonia, or extensive pulmonary fibrosis can lead to ventilation insufficiency.
Environmental Factors
Environments with excessively high CO2 concentrations may cause excessive CO2 inhalation.
In acute respiratory acidosis, compensation primarily occurs through intracellular and extracellular ion exchange, as well as buffering systems within cells. However, these mechanisms are very limited and often result in decompensation. In contrast, chronic respiratory acidosis is characterized by sustained elevations in PaCO2 and hydrogen ion (H+) concentrations. Increased activity of carbonic anhydrase and glutaminase in renal tubular epithelial cells enhances renal excretion of H+ and ammonium (NH4+), as well as reabsorption of bicarbonate (HCO3+).
Clinical Manifestations
Severe acute respiratory acidosis often presents with rapid breathing, labored respiration, and prominent neurological symptoms. Initially, patients may experience headaches, blurred vision, restlessness, and agitation. Progression can lead to tremors, confusion, delirium, and even coma. Cerebral hypoxia may cause cerebral edema, brain herniation, or even respiratory arrest. A decrease in pH and hypercapnia (elevated CO2 levels) can lead to peripheral vasodilation, resulting in arrhythmias, hypotension, and other circulatory symptoms.
Chronic respiratory acidosis is commonly associated with underlying conditions such as COPD. Clinical manifestations are therefore often dominated by symptoms of the underlying diseases, including coughing, shortness of breath, respiratory distress, and cyanosis due to hypoxemia.
Diagnosis
A history of impaired respiratory function and the presence of the aforementioned symptoms can suggest respiratory acidosis. Blood gas analysis is key in confirming the diagnosis. Typical findings include increased arterial partial pressure of CO2 (PaCO2), decreased pH, and evidence of renal compensation. Metabolic parameters may show secondary increases, with elevated actual bicarbonate (AB), standard bicarbonate (SB), and buffer base (BB) values. AB values exceed SB, and base excess (BE) values are notably positive.
Treatment
Treatment for acute respiratory acidosis focuses on addressing the underlying causes of ventilation impairment and optimizing ventilation to facilitate CO2 elimination. In cases caused by respiratory arrest or airway obstruction, interventions such as airway intubation and mechanical ventilation can effectively improve ventilation and gas exchange. If respiratory depression is caused by morphine, intravenous administration of naloxone may help.
For patients with chronic respiratory acidosis, management involves treating the underlying condition and implementing targeted interventions such as infection control, bronchodilation, and facilitating sputum clearance. These measures aim to enhance ventilation function and alleviate the severity of acidosis.