Respiratory Alkalosis

Primary respiratory alkalosis is characterized by an arterial PCO 2 <35 mm Hg (4.7 kPa). Primary respiratory alkalosis must be differentiated from secondary respiratory alkalosis, which is a compensatory mechanism in the setting of primary metabolic acidosis (see Table 2). To maintain a normal ECF volume in the setting of increased urinary loss of sodium bicarbonate, the kidney retains sodium chloride. Therefore, patients with chronic respiratory alkalosis typically have hyperchloremia.

Common causes of respiratory alkalosis can be sorted by underlying pathology. Those involving the pulmonary vasculature include pulmonary hypertension and pulmonary embolism. Pulmonary parenchymal diseases are represented by pulmonary fibrosis, heart failure, and pneumonia. In patients with asthma, acute exacerbations of bronchospasm trigger an increased respiratory rate. Respiratory alkalosis also can result from conditions affecting ventilatory control (eg, anxiety, aspirin toxicity, sepsis, hypoxia, hepatic encephalopathy, pregnancy). Acute hypocapnia decreases cerebral blood flow and causes binding of free calcium to albumin in the blood. Mild respiratory alkalosis may cause lightheadedness and palpitations. More profound respiratory alkalosis may cause symptoms that resemble those of hypocalcemia, including paresthesias of the extremities and circumoral area and carpopedal spasm. Patients with ischemic heart disease may occasionally develop cardiac arrhythmias, ischemic electrocardiographic changes, and angina pectoris. In psychogenic hyperventilation, rebreathing air using a bag increases the systemic arterial PCO 2. This method also may help to rapidly reduce the pH in patients with mixed, severe alkalosis.