Chapter 048. Acidosis and Alkalosis (Part 14)

Chronic respiratory alkalosis is the most common acid-base disturbance in critically ill patients and, when severe, portends a poor prognosis. Many cardiopulmonary disorders manifest respiratory alkalosis in their early to intermediate stages, and the finding of normocapnia and hypoxemia in a patient with hyperventilation may herald the onset of rapid respiratory failure and should prompt an assessment to determine if the patient is becoming fatigued. Respiratory alkalosis is common during mechanical ventilation.The hyperventilation syndrome may be disabling. Paresthesia, circumoral numbness, chest wall tightness or pain, dizziness, inability to take an adequate breath, and, rarely, tetany may themselves be sufficiently...
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Chapter 048. Acidosis and Alkalosis (Part 14) Chapter 048. Acidosis and Alkalosis (Part 14) Chronic respiratory alkalosis is the most common acid-base disturbance incritically ill patients and, when severe, portends a poor prognosis. Manycardiopulmonary disorders manifest respiratory alkalosis in their early tointermediate stages, and the finding of normocapnia and hypoxemia in a patientwith hyperventilation may herald the onset of rapid respiratory failure and shouldprompt an assessment to determine if the patient is becoming fatigued. Respiratoryalkalosis is common during mechanical ventilation. The hyperventilation syndrome may be disabling. Paresthesia, circumoralnumbness, chest wall tightness or pain, dizziness, inability to take an adequatebreath, and, rarely, tetany may themselves be sufficiently stressful to perpetuatethe disorder. Arterial blood-gas analysis demonstrates an acute or chronicrespiratory alkalosis, often with hypocapnia in the range of 15–30 mmHg and nohypoxemia. Central nervous system diseases or injury can produce several patternsof hyperventilation and sustained Pa CO2 levels of 20–30 mmHg. Hyperthyroidism,high caloric loads, and exercise raise the basal metabolic rate, but ventilationusually rises in proportion so that arterial blood gases are unchanged andrespiratory alkalosis does not develop. Salicylates are the most common cause ofdrug-induced respiratory alkalosis as a result of direct stimulation of the medullarychemoreceptor (Chap. e34). The methylxanthines, theophylline, andaminophylline stimulate ventilation and increase the ventilatory response to CO 2.Progesterone increases ventilation and lowers arterial PaCO2 by as much as 5–10mmHg. Therefore, chronic respiratory alkalosis is a common feature of pregnancy.Respiratory alkalosis is also prominent in liver failure, and the severity correlateswith the degree of hepatic insufficiency. Respiratory alkalosis is often an earlyfinding in gram-negative septicemia, before fever, hypoxemia, or hypotensiondevelops. The diagnosis of respiratory alkalosis depends on measurement of arterialpH and PaCO2. The plasma [K+] is often reduced and the [Cl–] increased. In theacute phase, respiratory alkalosis is not associated with increased renal HCO 3–excretion, but within hours net acid excretion is reduced. In general, the HCO3–concentration falls by 2.0 mmol/L for each 10-mmHg decrease in PaCO2. Chronichypocapnia reduces the serum [HCO3–] by 4.0 mmol/L for each 10-mmHgdecrease in PaCO2. It is unusual to observe a plasma HCO3– < 12 mmol/L as aresult of a pure respiratory alkalosis. When a diagnosis of respiratory alkalosis is made, its cause should beinvestigated. The diagnosis of hyperventilation syndrome is made by exclusion. Indifficult cases, it may be important to rule out other conditions such as pulmonaryembolism, coronary artery disease, and hyperthyroidism. Respiratory Alkalosis: Treatment The management of respiratory alkalosis is directed toward alleviation ofthe underlying disorder. If respiratory alkalosis complicates ventilatormanagement, changes in dead space, tidal volume, and frequency can minimizethe hypocapnia. Patients with the hyperventilation syndrome may benefit fromreassurance, rebreathing from a paper bag during symptomatic attacks, andattention to underlying psychological stress. Antidepressants and sedatives are notrecommended. β-Adrenergic blockers may ameliorate peripheral manifestations ofthe hyperadrenergic state. Further Readings DuBose TD Jr: Acid-base disorders, in Brenner and Rectors The Kidney,8th ed, BM Brenner (ed). Philadelphia, Saunders, 2007, in press ———, Alpern RJ: Renal tubular acidosis, in The Metabolic andMolecular Bases of Inherited Disease, 8th ed, CR Scriver et al (eds). New York,McGraw-Hill, 2001 Galla JH: Metabolic alkalosis, in Acid-Base and Electrolyte Disorders—ACompanion to Brenner and Rectors The Kidney, TD DuBose, LL Hamm (eds).Philadelphia, Saunders, 2002, pp 109–128 Laski ME, Wesson DE: Lactic acidosis, in Acid-Base and ElectrolyteDisorders—A Companion to Brenner and Rectors The Kidney, TD DuBose, LLHamm (eds). Philadelphia, Saunders, 2002, pp 83–107 Madias NE: Respiratory alkalosis, in Acid-Base and ElectrolyteDisorders—A Companion to Brenner and Rectors The Kidney, TD DuBose, LLHamm (eds). Philadelphia, Saunders, 2002, pp 147–164 Wesson DE et al: Clinical syndromes of metabolic alkalosis, in The Kidney:Physiology and Pathophysiology, 3d ed, DW Seldin, G Giebisch (eds).Philadelphia, Lippincott Williams and Wilkins, 2000, pp 2055–2072