Metabolic acidosis, defined as a reduced pH (<7.25) and bicarbonate concentration (<18 mEq/L) accompanied by a normal or low Pco2 level, may be caused by hypoxia or by insufficient tissue perfusion. The origin of the disorder may be pulmonary, cardiac, infectious, renal, hematologic, nutritional, metabolic, or iatrogenic. The initial approach to metabolic acidosis is to determine the cause and treat the pathophysiologic problem. This approach may include, as in the sequence of therapy for hypoxia, increasing the inspired oxygen concentration; applying continuous positive airway pressure nasally; or initiating mechanical ventilation using positive end-expiratory pressure. Patients with hypotension produced by hypovolemia require fluids and may need inotropic or vasoactive drug support. If metabolic acidosis persists despite specific therapy, sodium bicarbonate (1 mEq/kg/dose) may be given by slow intravenous infusion. Near-normal or low Pco2 levels should be documented before sodium bicarbonate infusion. The buffering effect of sodium bicarbonate results in increased Pco2 levels, unless adequate ventilation is maintained.
Respiratory acidosis, defined as an elevated Pco2 level and reduced pH without a reduction in the bicarbonate concentration, may be caused by pulmonary insufficiency or central hypoventilation. Most disorders producing respiratory distress can lead to hypercapnia. Treatment involves assisted ventilation but not sodium bicarbonate. If central nervous system depression of respirations is caused by placental passage of narcotic analgesics, assisted ventilation is instituted first, then the central nervous system depression is reversed by naloxone.
RDS occurs after the onset of breathing and is associated with an insufficiency of pulmonary surfactant.
The lining of the alveolus consists of 90% type I cells and 10% type II cells. After 20 weeks of gestation, the type II cells contain vacuolated, osmophilic, lamellar inclusion bodies, which are packages of surface-active material (Fig. 61-1). This lipoprotein surfactant is 90% lipid and is composed predominantly of saturated phosphatidylcholine (lecithin), but also contains phosphatidylglycerol, other phospholipids, and neutral lipids. The surfactant proteins, SP-A, SP-B, SP-C, and SP-D, are packaged into the lamellar body and contribute to surface-active properties and recycling of surfactant. Surfactant prevents atelectasis by reducing surface tension at low lung volumes when it is concentrated at end expiration as the alveolar radius decreases; surfactant contributes to lung recoil by increasing surface tension at larger lung volumes when it is diluted during inspiration as the alveolar radius increases. Without surfactant, surface tension forces are not reduced, and atelectasis develops during end expiration as the alveolus collapses.
The timing of surfactant production in quantities sufficient to prevent atelectasis depends on an increase in fetal cortisol levels that begins between 32 and 34 weeks of gestation. By 34 to 36 weeks, sufficient surface-active material is produced by the type II cells in the lung, is secreted into the alveolar lumen, and is excreted into the amniotic fluid. The concentration of