Physiologic Effects
During fetal asphyxia, the PaO2
decreases from its normal value of 25 to 40 mm Hg to less than 5 mm Hg in about
Figure 59-3
The response of newborn monkeys to asphyxia. (From
Dawes GS: Foetal and Neonatal Physiology. Chicago, Year Book Medical Publishers,
1968.)
2 minutes ( Fig. 59-3
).
As a result of the severe hypoxia, anaerobic metabolism occurs. The PaCO2
rises rapidly. The pH quickly decreases to less than 7.0 because of a combined metabolic
and respiratory acidosis. In as little as 5 minutes, the pH may be less than 6.90,
the PaCO2
greater than 100 mm Hg, and
the PaO2
unmeasurable.[16]
[31]
Some of the metabolic acidosis may be caused
by reduced uptake of lactate by the liver rather than by increased lactate production.
[2]
Cardiac output is normal early in the course of asphyxia, but
its distribution is altered.[32]
[33]
[34]
Blood flow to the liver, kidney, gut, skin,
and muscle is reduced, and blood flow to heart, brain, adrenal glands, and placenta
is maintained constant or increased. This redistribution of blood flow to the heart,
brain, and adrenal glands helps maintain oxygenation and nutrition of the brain and
heart, even though the oxygen content of arterial blood is very low. Oxygen extraction
by tissues is greatly increased.[35]
In part, the
function of hypoxemic hearts is maintained by the metabolism of myocardial glycogen
and by the metabolism of lactic acid.[36]
When
these sources of energy fail, as they eventually do, the myocardium fails, and the
arterial blood pressure and cardiac output decrease. Myocardial function tends to
decrease when the pH is 7.0 or less. When the heart rate is below 100 beats/min
during asphyxia, cardiac output is significantly decreased. Central venous pressure
rises during asphyxia because the systemic capacitance vessels constrict and increase
the central blood volume and because the failing myocardium cannot effectively eject
the increased volume of blood. Fetuses and newborns may survive severe hypoxia because
they have large quantities of endogenous opiates in their blood.[37]
These substances, which increase during hypoxia,[38]
may reduce oxygen consumption. A normal response to catecholamines is also important
for survival from asphyxia, as discussed previously. Initial systemic circulatory
adaptations to hypoxia are mediated on a reflex basis.[39]
Normal responses to asphyxia include increased plasma adrenocorticotropic hormone,
glucocorticoids, catecholamines, atrial natriuretic factor, renin, arginine vasopressin,
and decreased insulin concentrations.[40]
[41]
[42]
Arginine vasopressin causes hypertension,
bradycardia,
and redistribution of systemic blood flow.[42]
Glycogenolysis maintains adequate blood glucose concentrations.[2]
Intrapartum asphyxia can result in hypervolemia or hypovolemia.
[43]
Asphyxia during labor usually causes hypervolemia
unless umbilical cord compression obstructs the umbilical vein more than it obstructs
the umbilical arteries (e.g., cord around the neck, cord compression by the head
coming later during a breech delivery), hemorrhage occurs from the fetal-placental
unit (e.g., abruptio placentae, transection of the placenta during cesarean section),
maternal hypotension occurs (e.g., shock, trauma, anesthesia), or asphyxia occurs
during the latter part of labor and delivery.
