Respiratory alkalosis refers to a condition caused by excessive alveolar ventilation, leading to a decrease in arterial partial pressure of CO2 (PaCO2) and an increase in pH. It is primarily characterized by a decrease in plasma carbonic acid (H2CO3) concentration.
Etiology
Central Nervous System Stimulation
Disorders such as cerebrovascular accidents, encephalitis, brain trauma, or brain tumors may stimulate the respiratory center, resulting in hyperventilation. Hysterical episodes may lead to psychogenic hyperventilation. Certain medications, such as salicylates or ammonium salts, can directly excite the respiratory center and enhance ventilation. Improper use of mechanical ventilation with excessively high tidal volume may lead to severe respiratory alkalosis.
Increased Metabolic Demand
Conditions such as hyperthermia, hyperthyroidism, pain, trauma, or Gram-negative bacterial septicemia may cause metabolic hyperactivity, stimulating the respiratory center and leading to hyperventilation.
Hypoxia-Induced Stimulation
Low oxygen partial pressure in the environment or hypoxemia caused by various conditions can lead to enhanced respiratory activity and increased CO2 elimination due to hypoxic stimulation.
In acute respiratory alkalosis, compensation is primarily mediated through intracellular and extracellular ion exchange and intracellular buffering systems. Since the plasma H2CO3 concentration is reduced, bicarbonate (HCO3-) becomes relatively elevated. Hydrogen ions (H+) shift from the intracellular to the extracellular space and combine with HCO3- to lower plasma HCO3- concentration. Other intracellular buffering systems also contribute to compensation. In chronic respiratory alkalosis, renal compensatory mechanisms become operative. During sustained hypocapnia, tubular epithelial cells reduce the excretion of H+ and ammonia (NH3), resulting in increased urinary bicarbonate excretion and a compensatory decrease in plasma HCO3- concentration.
Clinical Manifestations
Most patients exhibit symptoms such as rapid breathing and increased heart rate. Alkalosis can increase neuromuscular excitability, causing symptoms such as numbness and tingling around the hands, feet, and mouth, as well as muscle tremors and carpopedal spasms. In addition, some patients may experience dizziness, apathy, or neurological impairments such as altered consciousness. Acute respiratory alkalosis in critically ill patients is often associated with poor prognosis and may indicate the potential development of acute respiratory distress syndrome (ARDS).
Diagnosis
Diagnosis can be made based on medical history and clinical presentation. Blood gas analysis in respiratory alkalosis reveals a decrease in PaCO2 and an increase in pH, with actual bicarbonate (AB) lower than standard bicarbonate (SB). After compensation, metabolic parameters show secondary decreases, including reductions in AB, SB, and buffer base (BB) values, while base excess (BE) becomes more negative.
Treatment
Management involves addressing the underlying condition and eliminating the causes of hyperventilation. In acute respiratory alkalosis, inhalation of a gas mixture containing 5% CO2 may be employed. Patients may also hold their breath repeatedly or rebreathe exhaled CO2 using a paper bag to maintain plasma H2CO3 levels, which can quickly alleviate symptoms. Sedatives may be considered for patients experiencing psychogenic hyperventilation. For hyperventilation caused by improper ventilator use, adjustments to respiratory rate and tidal volume may be necessary. Critically ill patients or those with central nervous system disorders causing rapid breathing may require pharmacological suppression of spontaneous respiration, with appropriately adjusted mechanical ventilation provided. For individuals with carpopedal spasms, intravenous administration of calcium gluconate may be used as a treatment.