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DOWNLOAD PDFBecause there are numerous etiologies for respiratory alkalosis, the primary goal of therapy should be to address or identify the underlying cause.
Mechanically ventilated patients may develop respiratory alkalosis if the tidal volume or respiratory rate is set too high. Decreasing the ventilator's tidal volume or respiratory rate may restore the patient's acid-base balance.
In response to anxiety or pain, mechanically ventilated patients may experience hyperventilation and try to fight against the ventilator or breathe out of synchrony. This response leads to respiratory alkalosis and may be alleviated with adequate pain control and sedation. Relieving the patient's pain and anxiety will help them relax and stop hyperventilating.
Hyperventilation leads to excess loss of carbon dioxide and causes respiratory alkalosis. The administration of sedatives may help relieve hyperventilation by decreasing the amount of carbon dioxide loss. The medications will help the patient relax and stop deep rapid breathing causing the respiratory alkalosis.
Antidepressants depress the central nervous system and help slow down rapid breathing. Decreasing the patient's respiratory rate will stop hyperventilation and help restore normal acid-base balance. The administration of antidepressants is reserved for patients who are unresponsive to other techniques or decreasing psychological stress.
In response to decreased levels of CO2, the kidneys decrease bicarbonate reabsorption to help compensate the acid-base imbalance. The purpose of the compensatory drop in serum bicarbonate is to help lower the alkalinity of the blood.
Historically, during acute episodes of hyperventilation caused by panic or anxiety, a patient was instructed to breathe into a paper bag. This strategy is no longer recommended due to the risk of hypoxia. Calming breathing exercises like abdominal breathing is now considered the treatment of choice.
Patients with respiratory alkalosis should slowly correct CO2 levels to prevent rebound metabolic acidosis caused by a compensatory drop in serum bicarbonate.
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