Respiratory alkalosis treatment

It is imperative to identify serious causes of respiratory alkalosis and institute effective treatment. In spontaneously breathing patients, respiratory alkalosis is typically only mild or moderate in severity and no specific therapy is indicated. Severe alkalosis generally represents respiratory acidosis imposed on metabolic alkalosis and may improve with sedation. Patients receiving mechanical ventilation are treated with reduced minute ventilation achieved by decreasing the respiratory rate and/or tidal volume. If the alkalosis persists in the ventilated patient, high-level sedation or paralysis is effective. 

Treatment of mixed metabolic acidosis and respiratory alkalosis should be directed at the underlying cause. 

Contraindications Metabolic/respiratory alkalosis, current treatment with sedative-hypnotics, succinic semialdehyde dehydrogenase deficiency, hypersensitivity to sodium oxybate or any component of fhe formulaf ion... 

Animals may manifest toxicity to salicylates with signs and symptoms similar to those seen in humans. These may include fever, hyperpnea, seizures, respiratory alkalosis, metabolic acidosis, gastric hemorrhage, and kidney damage. Methemoglobinemia has also been seen in animals following salicylate toxicity. Activated charcoal has been used in animals. Methylene blue or ascorbic acid may be utilized for the treatment of methemoglobinemia. 

Mention of salicylate overdose is made here, even though its popularity seems to be in decline. Its treatment, presuming hemodialysis is not indicated, includes a classic type of beneficial drug interaction that is different from that of a specific antidote (cf. A -acetylcysteine, above). Furthermore, the combination of respiratory alkalosis... 

Treatment is by correction of the cause of the acidosis (e.g., insulin administration in diabetic ketoacidosis) and neutralization of the acid with NaHCOs, sodium lactate, or TRIS [tris(hydroxymethyl)aminomethane] buffer. Problems that may occur following alkali replacement therapy include development of respiratory alkalosis, particularly if the low CO2 tension persists, and further decline in the pH of CSF, which may decrease consciousness. The alkaline overshoot results from resumption of oxidation of organic anions (e.g., lactate, acetoacetate) with resultant production of bicarbonate from CO2. Severe acidosis should be corrected slowly over several hours. Potassium replacement therapy frequently is needed because of the shift of intracellular K" " to extracellular fluid and loss of K+ in the urine. 

This mixed disorder is often seen in patients with advanced liver disease, salicylate intoxication, and pulmonary-renal syndromes. The respiratory alkalosis decreases the PaC02 beyond the appropriate range of the respiratory compensation for metabolic acidosis. The plasma bicarbonate concentration also falls below the level expected in compensation for a simple respiratory alkalosis. In a sense, the defense of pH for either disorder alone is enhanced thus the pH may be normal or close to normal, with a low PaC02 and a low [HCOj]. Treatment of this disorder should be directed at the underlying cause. Because of the enhanced compensation, the pH is usually closer to normal than in either of the two simple disorders. 

Respiratory alkalosis is much less common than acidosis but can occur when respiration is stimulated or is no longer subjcci to feedback control (Fig. 4). Usually these are acute conditions, and there is no renal compensation. The treatment is to inhibit or remove the cause of the hyperventilation, and the acid-base balance should return to normal. Examples are ... 

The treatment of respiratory alkalosis involves rebreathing one s own exhaled air by breathing into a paper bag (not a plastic bag), administering carbon dioxide, and treating the underlying causes of the hyperventilation. 

The respiratory therapist and physician would be interested in the patient s respiratory acidosis, which is the excess CO resulting from inadequate alveolar ventilation. Respiratory alkalosis is a deficit of COj resulting from alveolar hypersensitivity. The area we will examine is the use of the spirometer and the accompanying charts for comparison. The medical terminology of inhalation therapy is more directed to pulmonary disease treatment, which one is attempting to prevent with the use of respirators. It should be noted that once the worker or person impairs his lungs, modem medicine cannot reinstate previous capacity. At best, present technology can only ease the pain. 

In metabolic alkalosis and respiratory acidosis, pH does not usually deviate significantly from normal, but treatment can be required to maintain Pao2 and PaC02 at acceptable levels. Treatment should be aimed at decreasing plasma bicarbonate with sodium and potassium chloride therapy, allowing renal excretion of retained bicarbonate from diuretic-induced metabolic alkalosis. 

In cases of acidosis in which correction of the underlying respiratory or metabolic cause will be delayed or prolonged, treatment with infusions of bases such as sodium bicarbonate may be used temporarily. Care should be taken not to overtreat the pH, particularly in respiratory acidosis, because the body s actions to correct the problem in combination with infusion of base can result in a metabolic alkalosis and related complications. 

Chronic pulmonary failure may be further complicated by metabolic disturbances tending to metabolic alkalosis or metabolic acidosis. The mechanism leading to alkalosis is not always clear, but among the factors that may influence it are the loss of hydrogen and Cl ions, because of vomiting or because of selective Cl and potassium depletion as a result of undernourishment, and prolonged treatment with diuretics. It is usually assumed that severe respiratory acidosis is always accompanied by metabolic acidosis. This reasoning is based on the fact that when the same CO2 tensions are achieved in the blood in vivo and in vitro,the plasma concentration of bicarbonate for identical pH s is lower in vivo than in vitro. In reality, this bicarbonate deficit seems to result because (I) the buffer curve of the blood CO2 has a lower slope in vivo than in vitro and (2) hyperventilation in vivo leads to lactic acid accumulation in he blood. 

---