Respiratory Alkalosis

Introduction

Respiratory alkalosis is characterized by a decrease in Paco2 that leads to an increase in ph.

• Paco2 decreases when ventilatory CO2 excretion exceeds metabolic CO2 production, usually because of hyperventilation.
• Causes include increases in neurochemical stimulation via central or peripheral mechanisms, or physical increases in ventilation via voluntary or artificial means (e.g., mechanical ventilation).
• The earliest compensatory response is to chemically buffer excess bicarbonate by releasing hydrogen ions from intracellular proteins, phosphates, and hemoglobin. If prolonged (>6 hours), the kidneys attempt to further compensate by increasing bicarbonate elimination.

Clinical Presentation

Although usually asymptomatic, respiratory alkalosis can cause adverse neuromuscular, cardiovascular, and GI effects.

• Light-headedness, confusion, decreased intellectual functioning, syncope, and seizures can be caused by decreased cerebral blood flow.
• Nausea and vomiting can occur, probably due to cerebral hypoxia.
• Serum electrolytes can be altered; serum chloride is usually increased; serum potassium, phosphorus, and ionized calcium are usually decreased.

Treatment

Treatment is often unnecessary because most patients have few symptoms and only mild pH alterations (i.e., pH<7.50)

• Direct measures (e.g., treatment of pain, hypovolemia, fever, infection, or salicylate overdose) can be effective. A rebreathing device (e.g., paper bag) can help control hyperventilation in patients with anxiety/hyperventilation syndrome.
• Correct respiratory alkalosis associated with mechanical ventilation by decreasing the number of mechanical breaths per minute, using a capnograph and spirometer to adjust ventilator settings more precisely, or increasing dead space in the ventilator circuit.