Respiratory alkalosis is a primary decrease in Pco2 (hypocapnia) due to an increase in respiratory rate and/or volume (hyperventilation). Ventilation increase occurs most often as a physiologic response to hypoxia (eg, at high altitude), metabolic acidosis, and increased metabolic demands (eg, fever) and, as such, is present in many serious conditions. In addition, pain and anxiety and some central nervous system (CNS) disorders (eg, stroke, seizure [post-ictal]) can increase respirations without a physiologic need.
Respiratory alkalosis can be
Distinction is based on the degree of metabolic compensation. Excess HCO3− is buffered by extracellular hydrogen ion (H+) within minutes, but more significant compensation occurs over 2 to 3 days as the kidneys decrease H+ excretion.
Pseudorespiratory alkalosis is low arterial Pco2 and high pH in mechanically ventilated patients with severe metabolic acidosis due to poor systemic perfusion (eg, cardiogenic shock, during CPR [cardiopulmonary resuscitation]). Pseudorespiratory alkalosis occurs when mechanical ventilation (often hyperventilation) eliminates larger-than-normal amounts of alveolar carbon dioxide (CO2). Exhalation of large amounts of CO2 causes respiratory alkalosis in arterial blood (hence on ABG measurements), but poor systemic perfusion and cellular ischemia cause cellular acidosis, leading to acidosis of venous blood. Diagnosis is by demonstration of marked differences in arterial and venous Pco2 and pH and by elevated lactate levels in patients whose ABG measurement shows respiratory alkalosis; treatment is improvement of systemic hemodynamics.
Symptoms and signs depend on the rate and degree of fall in Pco2. Acute respiratory alkalosis causes light-headedness, confusion, peripheral and circumoral paresthesias, cramps, and syncope. Mechanism is thought to be change in cerebral blood flow and pH. Tachypnea or hyperpnea is often the only sign; carpopedal spasm may occur in severe cases due to decreased levels of ionized calcium in the blood (driven inside cells in exchange for hydrogen ion [H+]).
Chronic respiratory alkalosis is usually asymptomatic and has no distinctive signs.
Recognition of respiratory alkalosis and appropriate renal compensation (see Diagnosis of Acid-Base Disorders) requires ABG and serum electrolyte measurements. Minor hypophosphatemia and hypokalemia due to intracellular shifts and decreased ionized calcium (Ca++) due to an increase in protein binding may be present.
Presence of hypoxia or an increased alveolar-arterial (A-a) O2 gradient (inspired Po2− [arterial Po2+ 5/4 arterial Pco2]) requires search for a cause. Causes are often apparent based on history and examination findings. However, because pulmonary embolism often manifests without hypoxia, embolism must be strongly considered in a hyperventilating patient before ascribing the cause to anxiety alone.
Treatment is directed at the underlying disorder. Respiratory alkalosis is not life threatening, so no interventions to lower pH are necessary. Increasing inspired carbon dioxide through rebreathing (such as from a paper bag) is common practice but may be dangerous in at least some patients with CNS disorders in whom the pH of cerebrospinal fluid may already be below normal.
Respiratory alkalosis involves an increase in respiratory rate and/or volume (hyperventilation).
Hyperventilation occurs most often as a response to hypoxia, metabolic acidosis, increased metabolic demands (eg, fever), pain, or anxiety.
Do not presume anxiety is the cause of hyperventilation until more serious disorders are excluded.
Treat the cause; respiratory alkalosis is not life threatening, so interventions to lower pH are unnecessary.