Respiratory alkalosis is a loss of carbon dioxide (Pco2 <>2CO3) due to a marked increase in the rate of respirations. The two primary mechanisms that trigger hyperventilation are: hypoxemia and direct stimulation of the central respiratory center of the brain.
Compensatory mechanisms include decreased respiratory rate (if the body is able to respond to the drop in Paco2), increased renal excretion of bicarbonate, and retention of hydrogen. It is the most frequently occurring acid-base imbalance in hospitalized patients, with the elderly at increased risk because of high incidence of pulmonary disorders and alterations in neurological status.
Impaired Gas Exchange
May be related to
- Ventilation perfusion imbalance (e.g., altered oxygen supply, altered blood flow, altered oxygen-carrying capacity of blood, alveolar-capillary membrane changes)
Possibly evidenced by
- Dyspnea, tachypnea
- Changes in mentation
- Hypocapnia, tachycardia
- Demonstrate improved ventilation and adequate oxygenation of tissue as evidenced by ABGs within patient’s acceptable limits and absence of symptoms of respiratory distress.
- Verbalize understanding of causative factors and appropriate interventions.
- Participate in treatment regimen within level of ability/situation.
|Monitor respiratory rate, depth, and effort. Ascertain cause of hyperventilation if possible. Differentiate hyperventilation caused by anxiety, pain, or improper ventilator settings.||Identifies alterations from usual breathing pattern and influences choice of intervention.|
|Encourage patient to breathe slowly and deeply. Speak in a low, calm tone of voice. Provide safe environment.||May help reassure and calm the agitated patient, thereby aiding the reduction of respiratory rate. Assists patient to regain control.|
|Assess level of awareness or cognition and note neuromuscular status. Assess strength, tone, reflexes, and sensation.||Decreased mentation (mild to severe) and tetany or seizures may occur when alkalosis is severe.|
|Demonstrate appropriate breathing patterns, if appropriate, and assist with respiratory aids or rebreathing mask/bag.||Decreasing the rate of respirations can halt the “blowing off” of CO2, elevating Pco2 level and normalizing pH.|
|Provide comfort measures; encourage use of meditation and visualization. Use tepid sponge bath/cool cloths.||Promotes relaxation and reduces stress. Control and reduction of fever reduces potential for seizures and helps reduce respiration rate.|
|Provide safety and seizure precautions. Place bed in low position, pad side rails and do frequent observation of the patient.||Changes in mentation, CNS and neuromuscular hyperirritability may result in patient harm, especially if tetany or convulsions occur.|
|Discuss cause of condition (if known) and appropriate interventions and/or self-care activities.||Promotes participation in therapeutic regimen and may reduce recurrence of disorder.|
|Assist with identification and treatment of underlying cause.||Respiratory alkalosis is a complication, not an isolated occurrence; addressing the primary condition (hyperventilation of panic attack, organ failure, severe anemia; drug effect, such as with paraldehyde or epinephrine) promotes correction of the disorder and reduces likelihood of recurrence.|
|Monitor and graph serial ABGs, and pulse oximetry.||Identifies therapy needs and effectiveness.|
|Monitor serum potassium. Replace as indicated.||Hypokalemia may occur as potassium is lost (urine) or shifted into the cell in exchange for hydrogen in an attempt to correct alkalosis.|
|Provide sedation and pain medication, as indicated.||May be required to reduce psychogenic cause of hyperventilation.|
|Administer CO2, or use rebreathing mask as indicated. Reduce respiratory rate and tidal volume, or add additional dead space (tubing) to mechanical ventilator.||Increasing CO2 retention may correct carbonic acid deficit.|