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Respiratory alkalosis, pathophysiology and treatment


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 

• Direct measures (eg, treatment of pain, hypovolemia, fever, infection, or salicylate overdose) can be effective. A rebreathing device (eg, 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.

Respiratory alkalosis, pathophysiology and treatment Respiratory alkalosis, pathophysiology and treatment Reviewed by gafacom on June 07, 2019 Rating: 5

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