ACUTE AND CHRONIC RESPIRATORY ALKALOSIS (CARBONIC ACID DEFICIT)
Respiratory alkalosis is a clinical condition in which the arterial pH is greater than 7.45 and the PaCO2 is less than 38 mm Hg. As with respiratory acidosis, acute and chronic conditions can occur.
Respiratory alkalosis is always due to hyperventilation, which causes excessive “blowing off” of CO2 and, hence, a decrease in the plasma carbonic acid concentration. Causes can include extreme anxiety, hypoxemia, the early phase of salicylate intoxication, gram-negative bacteremia, and inappropriate ventilator settings that do not match the patient’s requirements.
Chronic respiratory alkalosis results from chronic hypocapnia, and decreased serum bicarbonate levels are the consequence. Chronic hepatic insufficiency and cerebral tumors are predispos-ing factors.
Clinical signs consist of lightheadedness due to vasoconstriction and decreased cerebral blood flow, inability to concentrate, numb-ness and tingling from decreased calcium ionization, tinnitus, and at times loss of consciousness. Cardiac effects of respiratory alka-losis include tachycardia and ventricular and atrial dysrhythmias (Foster et al., 2001).
Analysis of arterial blood gases assists in the diagnosis of respiratory alkalosis. In the acute state, the pH is elevated above normal as a re-sult of a low PaCO2 and a normal bicarbonate level. (The kidneys cannot alter the bicarbonate level quickly.) In the compensated state, the kidneys have had sufficient time to lower the bicarbonate level to a near-normal level. Evaluation of serum electrolytes is in-dicated to identify any decrease in potassium as hydrogen is pulled out of the cells in exchange for potassium; decreased calcium, as se-vere alkalosis inhibits calcium ionization, resulting in carpopedal spasms and tetany; or decreased phosphate due to alkalosis, caus-ing an increased uptake of phosphate by the cells. A toxicology screen should be performed to rule out salicylate intoxication.
Patients with chronic respiratory alkalosis are usually asymp-tomatic, and the diagnostic evaluation and plan of care are the same as for acute respiratory alkalosis.
Treatment depends on the underlying cause of respiratory alka-losis (Foster et al., 2001). If the cause is anxiety, the patient is in-structed to breathe more slowly to allow CO2 to accumulate or to breathe into a closed system (such as a paper bag). A sedative may be required to relieve hyperventilation in very anxious patients. Treatment for other causes of respiratory alkalosis is directed at correcting the underlying problem.
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