Previously, many groups established erroneous definitions of asphyxia based solely on low Apgar scores. hese prompted the American College of Obstetricians and Gynecologists and American Academy of Pediatrics (2017f) to issue a series of joint opinions with important caveats regarding Apgar score limitations. Certain elements of the Apgar score are partially dependent on the physiological maturity of the newborn, and a healthy, preterm neonate may receive a low score only because of immaturity. Other influencing factors include fetal malformations, maternal medications, and infection. Therefore, it is inappropriate to use an Apgar score alone to diagnose asphyxia. Moreover, the Apgar score alone cannot establish hypoxia as the cause of cerebral palsy, as discussed in Chapter 33 (p. 624).
Blood taken from umbilical vessels may be used for acid-base studies to assess the metabolic status of the neonate. Blood collection is performed following delivery by immediately isolating a 10-to 20-cm segment of cord with two clamps placed near the neonate and another two clamps positioned nearer the placenta. The cord is then cut between the two proximal clamps and then the two distal clamps (Blickstein, 2007).
Arterial blood is drawn from the isolated cord segment into a 1-to 2-mL commercially prepared plastic syringe containing lyophilized heparin or a similar syringe that has been flushed with a heparin solution containing 1000 U/mL. Once sampling is completed, the needle is capped and the syringe transported, on ice, to the laboratory. Although eforts should be made for prompt transport, neither the pH nor partial pressure of CO2 (pC02) values change significantly in blood kept at room temperature for up to 60 minutes (Lynn, 2007). Mathematical models have been developed that allow reasonable prediction of birth acid-base status in properly collected cord blood samples analyzed as late as 60 hours after delivery (Chauhan, 1994). Acid-base measurements can show signiicant variances between diferent analyzing devices (vlokarami,r2012).
he fetus produces both carbonic and organic acids. Carbonic acid (H2C03) is formed by oxidative metabolism of CO2. he fetus usually rapidly clears CO2 through the placental circulation. If CO2 clearance is lowered, then carbonic acid levels rise. This often follows impaired placental exchange. When H2C03
The Newborn 61 1 rently rise, the result is respiratoy acidemia.
In contrast, organic acids primarily include lactic and 3-hydroxybutyric acids. Levels of these increase with persistent placental exchange impairment, and they result from anaero bic glycolysis. These organic acids are cleared slowly from fetal blood. When they accumulate, without a concurrent increase in H2C03, the result is metabolic acidemia. With the develop ment of metabolic acidemia, bicarbonate (HC03 -) levels drop because it is used to bufer the organic acid. A rise in H2C03 concentrations accompanied by greater organic acid levels, relected by decreased HC03 -levels, causes mixed respiratoy metabolic acidemia.
In the fetus, respiratory and metabolic acidemia and ultimately tissue acidosis are most likely part of a progressively worsening continuum. his is diferent from adult pathophysiology, in which distinct conditions result either in respiratory acidosis-for example, pulmonary disease, or in metabolic acidosis-for example, diabetes. In the fetus, the placenta serves as both the lungs and, to a certain degree, the kidneys. One principal cause of fetal acidemia is a drop in uteroplacental perfusion. This creates retention of CO2, that is, respiratory acidemia, and if protracted and severe enough, yields a mixed or metabolic acidemia.