Etiology and Pathogenesis
The primary factor in respiratory alkalosis is excessive ventilation. The rate of carbon dioxide (CO2) elimination exceeds its production, leading to reduced CO2 levels and a decrease in arterial partial pressure of CO2 (PaCO2).
Central Hyperventilation
Non-hypoxic Causes:
- Hyperventilation syndrome related to conditions such as hysteria.
- Brain trauma or disease, including trauma, infection, tumors, and cerebrovascular accidents.
- Drug toxicity due to substances such as salicylates or paraldehyde.
- Elevated body temperature or exposure to high ambient temperatures.
- Endogenous toxic metabolic products, such as in hepatic encephalopathy or metabolic acidosis.
Hypoxic Causes:
- Hypoxic conditions, such as those seen in high altitudes, diving, or intense physical exercise.
- Obstructive pulmonary diseases, including pneumonia, interstitial lung disease, bronchial obstruction, pleural or chest wall diseases, and emphysema.
- Insufficient blood supply, as in heart failure, shock, or severe anemia. Hypoxia triggers stimulation of the respiratory centers, resulting in hyperventilation.
Peripheral Hyperventilation
These include:
- Improper ventilator management.
- Shallow breathing due to post-thoracic or abdominal surgery pain.
- Chest trauma, including rib fractures.
- Sudden relief of airway obstruction.
- Pregnancy or progesterone use, which can also lead to hyperventilation.
Compensatory Mechanisms
With reduced CO2 levels, respiration becomes shallow and slow, leading to partial CO2 retention and an increase in carbonic acid (H2CO3) as compensation. Over prolonged periods, the kidneys reduce excretion of hydrogen ions (H⁺) and increase excretion of bicarbonate (HCO3-), consequently achieving equilibrium of the HCO3-/H2CO3 ratio at a lower level, a process known as compensated respiratory alkalosis.
Clinical Manifestations
The primary clinical feature is hyperventilation accompanied by rapid breathing. Alkalosis increases neuromuscular excitability. In mild acute cases, symptoms may include numbness and tingling of the lips and extremities, and muscle tremors. Severe cases can present with dizziness, syncope, blurred vision, and convulsions. Additional symptoms may include chest tightness, chest pain, dry mouth, and abdominal bloating. Under alkaline conditions, the dissociation of oxygen from oxyhemoglobin decreases, reducing oxygen delivery to tissues. This manifests as abnormal electroencephalogram (EEG) findings and impaired liver function.
Diagnosis and Differential Diagnosis
Respiratory alkalosis caused by various factors shares the common feature of hyperventilation. Hyperventilation syndrome due to hysteria is often easily recognized, whereas cases caused by high temperatures, fever, high altitudes, or postoperative conditions are more easily overlooked. Laboratory tests provide confirmation of the diagnosis:
PaCO2 is decreased, and CO2 combining power is reduced without metabolic influences, with actual bicarbonate (AB) being lower than standard bicarbonate (SB).
During the uncompensated phase, pH is elevated.
Prevention and Treatment
Management primarily focuses on treating the underlying cause. Psychological counseling can alleviate anxiety in patients with hysteria. Administration of oxygen and improved ventilator management are important. Treating the primary disease remains essential. Adjusting the respiratory rate and tidal volume during mechanical ventilation can significantly reduce pH. Covering the mouth and nose with a paper bag to allow rebreathing of exhaled CO2 can also help. Short-term forced breath-holding, inhalation of oxygen with 5% CO2, or oral administration of acetazolamide at 500 mg per day can promote bicarbonate excretion.
For patients with prolonged respiratory alkalosis, beta-adrenergic receptor antagonists may help slow the respiratory rate. In critically ill patients, under strict monitoring and with resuscitation measures in place, the use of muscle relaxants to block spontaneous breathing may be attempted. This is followed by endotracheal intubation for assisted ventilation to slow the respiratory rate and reduce tidal volume. Close monitoring of blood pH and PaCO2 is essential during this intervention.