Respiratory alkalosis is a type of hypocapnia characterized by a primary decrease in PCO₂ (<4.67 kPa) and an increase in pH (>7.45).

bubble_chart Etiology

1. Psychogenic hyperventilation This is a common cause of respiratory alkalosis, but it is generally not severe. Severe cases may present with dizziness, paresthesia, and occasionally convulsions. It is commonly seen in patients with hysteria episodes.

2. Abnormal metabolic processes In conditions such as hyperthyroidism and fever, ventilation can significantly increase beyond the amount of CO₂ that needs to be eliminated. This can lead to respiratory alkalosis, though it is usually not severe. However, it demonstrates that ventilation is not solely determined by the [H⁺] and Pco₂ in body fluids but is also related to metabolic intensity and oxygen demand. The hyperventilation in these cases may be caused by increased pulmonary blood flow triggering a reflex response.

3. Hypoxic hypoxia Hyperventilation during hypoxic hypoxia serves as compensation for the hypoxia but can also lead to excessive CO₂ elimination, resulting in respiratory alkalosis. This is commonly observed in individuals ascending to high altitudes, mountains, or high elevations, as well as in patients with thoracic or pulmonary conditions such as pneumonia, pulmonary embolism, pneumothorax, or pulmonary congestion, where stimulation of the thoracic, pulmonary vascular, or lung tissue afferent nerves causes reflex hyperventilation. Additionally, some congenital heart disease patients may develop hyperventilation due to increased right-to-left shunting, leading to hypotonic hypoxemia. These conditions all result in decreased plasma H₂CO₃ and the onset of respiratory alkalosis.

5. Salicylate poisoning Salicylates can directly stimulate the respiratory center, increasing its excitability and sensitivity to normal stimuli, thereby causing hyperventilation.

6. Gram-negative bacilli sepsis In patients with Gram-negative bacilli entering and proliferating in the bloodstream, significant hyperventilation may occur even before changes in body temperature or blood pressure. Pco₂ can drop as low as 17 mmHg. This change is highly diagnostic, though the mechanism remains unclear, as animal experiments have failed to replicate this phenomenon.

7. Excessive artificial ventilation.

8. Cirrhosis Patients with cirrhosis, ascites, and elevated blood NH₃ may exhibit hyperventilation, likely due to the stimulatory effect of NH₃ on the respiratory center. While ascites elevating the diaphragm can also stimulate respiration, non-cirrhotic ascites patients do not show hyperventilation.

9. Sudden correction of metabolic acidosis For example, when NaHCO₃ is used to correct metabolic acidosis, the extracellular [HCO₃^-] concentration rapidly returns to normal, but passage through the blood-brain barrier is slow (about 12–24 hours). During this time, the brain remains in a state of metabolic acidosis, so hyperventilation persists, leading to respiratory alkalosis due to excessively low H₂CO₃.

10. Pregnancy Moderate hyperventilation occurs during pregnancy, exceeding CO₂ production. This is currently attributed to the stimulatory effect of progesterone on the respiratory center, which is also observed with some synthetic progesterone preparations. During the early stages of pregnancy, vomiting and inadequate diet may lead to ketoacidosis, while respiratory alkalosis may develop later, sometimes causing hand and foot convulsions.

Due to decreased PCO₂, the respiratory center is inhibited, and the clinical manifestations include a shift from deep and rapid breathing to fast and shallow, short breaths, or even intermittent sigh-like respiration, indicating a poor prognosis. Due to tissue hypoxia, patients may experience headache, dizziness, and psychiatric symptoms. Due to decreased serum free calcium, paresthesia may occur, such as numbness and tingling around the mouth and limbs, or even convulsions, spasms, and a positive Trousseau sign. Laboratory findings: increased pH, decreased PCO₂ and CO₂CP, with SB, BE, and BB possibly decreased or normal.

bubble_chart Diagnosis

Based on the medical history and clinical manifestations, a preliminary diagnosis can be made. Blood gas analysis can confirm the diagnosis, showing increased blood pH, decreased P_CO2, and decreased [HCO₃^-].

bubble_chart Treatment Measures

1. Actively prevent and treat the primary disease.

2. Reduce the patient's hyperventilation. For example, sedatives can be used for psychogenic hyperventilation.

3. To increase blood PCO₂, cover the mouth and nose with a paper bag or a long tube bag to increase respiratory dead space and reduce the exhalation and loss of CO₂. Alternatively, inhale oxygen containing 5% CO₂ to achieve symptomatic treatment.

4. For patients with limb convulsions, intravenous calcium supplements can be administered in appropriate amounts to increase plasma [Ca⁺⁺] (slowly inject 10 ml of 10% calcium gluconate).