References:
- Saunders Comprehensive Review for the NCLEX-RN Examination, 9th Edition, ISBN 978-032-37-9530-2, by Linda Anne Silvestri, Angela E. Silvestri, and Jessica Grimm (Ch. 8, pp. 106-115)
A deficit of carbonic acid and a decrease in hydrogen ion concentration that results from the accumulation of base or from a loss of acid without a comparable loss of base in the body fluids. Its causes include:
| Cause | Description |
|---|---|
| Diuretics | The loss of hydrogen ions and chloride from diuresis causes a compensatory increase in the amount of bicarbonate in the blood. |
| Excessive vomiting or GI suctioning | Leads to an excessive loss of hydrochloric acid. |
| Hyperaldosteronism | Increased renal tubular reabsorption of sodium occurs, with the resultant loss of hydrogen ions. |
| Ingestion of and/or infusion of excess sodium bicarbonate | Causes an increase in the amount of base in the blood. |
| Massive transfusion of whole blood | The citrate anticoagulant used for the storage of blood is metabolized to bicarbonate. |
Assessment
- Neurological: lethargy, irritability, confusion, headache
- Cardiovascular: low blood pressure, tachycardia, dysrhythmias (same as in respiratory alkalosis)
- Gastrointestinal: anorexia, nausea, vomiting
- Neuromuscular: tetany, tremors, tingling of extremities, muscle cramps; hypertonic muscles, seizures
- Respiratory: decreased respiratory rate and depth as compensation (hypoventilation)
Intervention
- Monitor for signs of respiratory distress.
- Prepare to administer medications and intravenous fluids as prescribed to promote the kidney excretion of bicarbonate.
- Prepare to replace potassium as prescribed.